One per cent Successful Long Term Weight Loss

-Robert Jeffrey and colleagues

"Dieting may be the major cause of obesity"

-Jean-Paul Deslypere, University of Ghent Professor of human nutrition

Obesity Gene Located


Adiposity is the result of an excessive number and/or size of white adipose cells.

Adiposity is caused by genetics and the environment. New chromosome variations causing obesity are constantly being added to the list. The latest, announced in 2011, is KLF14, a master gene that controls obesity, diabetes, and other maladies.

The importance of infection and early carbohydrate consumption in obesity is suppressed by dominant groups with religious and commercial agendas.

Maternal diabetes, maternal smoking, and malnutrition predispose the unborn to grow up fat. Early withdrawl of breast feeding and introduction of a high carbohydrate diet predispose the child to grow up fat. Sugar and monosodium glutamate (MSG) in infant formula are linked to later obesity. Exposure to certain bacteria and virii causes permament weight gain. Identical twins reared by different parents have the same weight, unless one has been exposed to a "fattening virus".
Vitamin B defecit in the mother may cause obesity. At two years young sheep were 25% fatter than normal, had greatly raised blood pressure, and showed signs of insulin resistance. They also appeared to have altered and hypersensitive immune systems.

A 2010 study in the Archives of Internal Medicine demonstrated that women who ate the highest amount of carbohydrates had a significantly greater risk of coronary heart disease than those who ate the lowest amount, and that carbohydrates from high-glycemic carbs were particularly assiciated with significantly greater risk for heart disease"

By the end of the yearlong trial, people in the low-carbohydrate group had lost about eight pounds more on average than those in the low-fat group. They had significantly greater reductions in body fat than the low-fat group, and improvements in lean muscle mass, even though neither group changed their levels of physical activity.

While the low-fat group did lose weight, they lost more muscle than fat. "They actually lost lean muscle mass, which is a bad thing," Dr. Mozaffarian said. "Your balance of lean mass versus fat mass is much more important than weight. And that's a very important finding that shows why the low-carb, high-fat group did so metabolically well."
-New York Times 9/1/2014

Some recent research indicates fructose is more damaging to the body than sucrose. Massive increases in dietary fructose correspond with the rise in obesity and diabetes. The only organ that can use fructose is the liver, which converts it to uric acid (high blood pressure, gout), de novo lipogenisis (fat), and an enzyme that interferes with the brain's metabolism of leptin, and increased inflammation.

A study by researchers at Duke University Medical Center found frequent consumption of fructose raises the risk for nonalcoholic fatty liver disease, inflammation and scarring.

" The obesity epidemic we are currently facing is the direct consequence of adding HFCS to food products." -Dr. David Brownstein, M.D
Definitive experiments (2010)
Click for more (2007)

Normal adults do not retain weight brought on by a period of simple overeating.

Conversely, individuals whose weight gain was not caused by overeating are rarely successful at long term weight loss. Furthermore, the weight they lose usually comes back with considerable "interest" (rebound). This rebound may be caused by an increase in fat cell numbers caused by the weight loss diet.

The new experimental drug Adipotide destroys the blood supply to unhealthy white adipose tissue. White adipose tissues are believed to promote cancer. The drug has brought on profound weight loss in primates with minimal side effects.

The world has almost as many diet plans as it has e-mail spammers, -Newsmax

High carbohydrate low fat diets for weight loss have been recommended for three millennia. Low fat high carbohydrate diets have been extensively studied for the last 5 decades. In the last decade Americans have reduced their fat intake only to get fatter than ever. For the first time in history, a majority of males are overweight.

Previously reported assocations between higher fat consumption and obesity have not held up to careful study. Previously reported associations between higher fat consumption and breast cancer have been refuted. A 14-year study of nearly 89,000 women found no evidence that a high-fat diet promotes breast cancer or that a low-fat diet protects against it. Women who ate the least fat appeared to have a 15 percent higher rate of breast cancer. (Journal of the American Medical Association 3/10/99)

Researchers from the Harvard School of Public Health found no evidence of an association between low-carbohydrate diets and cardiovascular risk, even when high in saturated animal fats.

Low-carb eating even seemed to protect against heart disease when vegetables were the main sources of fat and protein in the diet.

HDL (good cholesterol) had a 23 percent increase from low-carb dieting, twice that from low-fat. Gary Foster, director of Temple University's Center for Obesity Research and Education, led the federally funded 2 year study. Annals of Internal Medicine, May 2010

The low fat/low cholesterol diet is ineffective. Some researchers now think low-fat high carbohydrate diets are making us fat.

The Karolinska Institute in Sweden showed people who drink soft drinks or add sugar to their coffee increase their risk of developing pancreatic cancer.

If you're wondering why we don't have cyclamate these days, you can thank the Sugar Association, an industry group formed in 1943 to protect sugar's image from government rationing programs. Cyclamate cost 90% less than sugar and sweetened just as well. What to do if you're the sugar industry? Form the International Sugar Research Foundation and fund shady research looking to cast cyclamate as the bad guy. John Hickson, the research director of the ISRF, told the NYT. "If anyone can undersell you nine cents out of 10, you'd better find some brickbat you can throw at him." They found that brickbat, too - after burning through about $500,000 in the 70's ($4 million in today's money) they discovered cyclamate could cause bladder cancer in rats. This was followed promptly by a ban by the FDA. His job accomplished, Hickson then left to work for Big Tobacco. More recently it was discovered this was due to the pH in the bladder of rats, as well as an interaction with a certain protein. Turns out humans have a totally different pH and lack the protein that caused the cancer, so as long as you're a human, cyclamate is safe.

Meanwhile, traditional nutritionists have ignored last century's lowering of the age of female puberty from 17 to 13 years, revealing a tremendous increase in dietary carbohydrate.

In the future, drugs, antibodies to fat cells, and/or cellular removal will control adiposity. In the meantime, people at risk of adiposity would be wise to check with a competent endocrinologist to prevent the early rise in insulin levels that triggers adiposity, gout, and related diseases.

Adiposity 101 surveys the rapidly evolving field of adiposity research.


The Army is investigating transplants of brown adipose cells as a weight loss measure.

Readers of Adiposity 101 already know that the body's response to exercise is genetically defective in endomorphs. Recent reports on Aicar, PPAR-delta, and Resveratrol suggest that drugs will be able to transform endomorph metabolism into mesomorph or ectmorph metabolism.

It is also reported that PPAR-delta-mediated antiinflammatory mechanisms reduce the development of atherosclorsis. Perhaps the cardiovascular problems suffered by endomorphs are directly caused by genetic defects, not just as a result of obesity.

One can Google Aicar, PPAR-delta, and Resveratrol for more information.


Studies published in the journal Nature show that the type of bacteria in intestines may be the reason why some people have weight problems. A high carbohydrate diet is associated with a prevalence of fattening bacteria.


Though a low-fat diet is traditionally recommended by the U.S. Government and Heart Association, it caused the greatest decrease in energy expenditure, an unhealthy lipid pattern and insulin resistance.

Atins trumps Ornish and other diets in both weight loss and lipid improvements. --Journral of the American Medical Association, March 2007

NEW YORK, Feb 18 2000 (Reuters Health) -- The extremely carbohydrate-restricted Atkins diet is a safe, effective way to lose weight, according to studies presented at the Southern Society of General Internal Medicine in New Orleans.

In a press release, the researchers also say that their study did not find any of the safety concerns voiced by the American Dietetic Association, such as potentially dangerous effects on liver and kidney function.

"In four short months on the Atkins Diet, we were able to confirm scientifically what Dr. Atkins states he has seen in his practice over the past decades. The diet lowers cholesterol and triglycerides and raises HDL... which may represent an entirely new approach to the control and prevention of heart disease," said lead researcher Dr. Eric C. Westman, assistant professor of medicine at North Carolina's Duke University.

Low-Carb Diet Offers Second Tier Therapy for Type II Diabetics

Journal of the American College of Nutrition (1998;17:595-600)


Compound C75, developed for cancer treatment, inhibits feeding, but does not allow the metabolism to shut down. It tricks the animal into thinking it's well fed. It drops weight like a stone. C75 treated mice lost weight 45 per cent faster than untreated fasting mice. C75 also reversed a fat-related form of diabetes.

C75 blocks Fatty Acid Synthase, a powerful fat making enzyme. "This is the enzyme that turns your pasta into fat," Dr. Frank Kuhajda told United Press International. FAS is the last enzyme on an assembly line of about 25 enzymes that builds fat molecules to store energy. Kuhajda says that in a test tube, purified FAS will "make fat before your eyes" if given the right building blocks. This may have been very useful when primitive humans had to sprint across the savanna and kill an animal for supper. It has become a curse in the age of carbohydrate. "It makes us fat," Kuhajda says.

The latest Adiposity 101 is always available at


Chuck Forsberg

Obese and Normal Rodents


Obesity ruins the quality of life for more than 100 million Americans. Medical advances have circumvented the natural eugenic selection that previously limited the diabetic/obese to less than 10% of the population. Increases in obesity prone minorities and high carbohydrate gestation and suckling environments add to the weight.

Traditional weight control technology has changed little since Greek antiquity. 30 years of applied research into traditional weight control technology and the resulting recommendations have only made Americans fatter.

No study has ever shown dieting to extend the life of fat people, but more than twenty have reported ill effects from dietary weight cycling. For years dieters have complained that weight loss regimes made them fatter, but these observations fell on deaf ears. Recent research has shown that dieting is a major cause of obesity. While the long term success rate from dieting is less than one per cent, about 30 per cent of dieters regain more than they lose as a direct result of their dieting.

"In the last 25 years there has been no progress in treatment for obesity and the long-term results are miserable." (Marian Apfelbaum, University of Paris Professor of Nutrition) "dieting may be the major cause of obesity" (Jean-Paul Deslypere, University of Ghent Professor of human nutrition)

Recent obesity research has disproven public stereotypes and the conventional wisdom of most health professionals. Identical twins grow up with virtually the same body fatness, even when raised by different families, (those that don't may have been exposed to a virus that causes obesity) while adopted children raised by fat parents are no fatter than those raised by thin parents. The opposite would be true if adiposity were environmental instead of inborn. This evidence has yet to register on diet promoters and exercise gurus who continue to claim obesity is mostly caused by gluttony and sloth. When all you have to sell is a hammer every problem looks like a nail.

For the first time in history, research has placed true cures for human obesity within sight. But before this can happen, the public must first be weaned from its belief that the obese eat much more than other people, that this is the cause of their obesity, and that they could become lean and remain slender simply by eating normal amounts of food. This belief is particularly resistant to change since it was the accepted scientific position until recently. Misleading weight loss advertising perpetuates this belief, and the sheer volume of this commerce discourages the media from educating the public.

Less than one research dollar is spent for each overweight American compared to a thousand dollars for each HIV positive American. It is high time overweight Americans got their fair share of the billions and billions of tax dollars they pay for medical research. In addition, we should add a checkoff to income tax forms allowing taxpayers to earmark money for the research and deployment of new weight control technology.

In the meantime, the protections of the Americans with Disabilities Act should be extended to those Americans whose diligence in dieting has only made them fatter.

The purpose of this paper is to set out the case for new weight loss technology and thereby give hope to the millions of fat Americans for whom conventional weight loss technology has been ineffective or worse.

This paper is a summary of recent progress in obesity research. It identifies topics and issues concerning obesity. The reader should study the references given below if questions or doubts remain.

Many of the topics related to adiposity are interrelated. Since this document was only recently converted to hypertext, few links are available. The reader must carefully study the entirety of this document to understand adiposity.


    Set Point
    Obesity Virus
    Rats, Pigs and Blimps
    Brown Adipose Tissue (BAT)
    White Adipose Tissue (WAT)
    Size and Number of Fat Cells
    Fat Cell Receptors
    Fat and Carbohydrate Oxidation
    Muscle Fibre Type
    Types of Adiposity
    Syndrome X
    Maternal Environment
    Precocious Puberty
    Baby's Diet
    Personality Problems
    Health Problems
    Slow vs Rapid Weight Loss
    Behavior Modification
    Diet Side Effects
    Eat More to Lose Fat
    Artificial Sweeteners
    High Fiber Diet
    Low Fat Diets
    The Cornell Low Fat Study
    Dieting Gourmets
    The Lopez Diet / Eat like a Warrior
    Low Carbohydrate Diets
    Ornish and Atkins Compared
    Diets - the BOTTOM LINE
    Correlation .vs. Cause and Effect
    Flawed Sample Selection/Distribution
    Improper use of Ratios to Adjust Data
    Food Allergy Avoidance
    Stimulation of Thermogenesis (ECA STACK)
    Thyroid Receptor Correction
    Growth Hormone Treatment
    Growth Hormone Stimulation
    DHEA Treatment
    RU-486 Treatment
    CoPP Treatment
    Bromocriptine Treatment
    Circadian Lipostat Manipulation
    Testosterone Treatment
    Beta3-Adrenoceptor Agonists
    Serotonin Reuptake Inhibitors
    Fat Cell Removal by Surgery
    Fat Cell Removal by Immunological Manipulation


  • Anorectic: appetite suppression

  • Anorexiant: substance that suppresses appetite

  • Adipocyte Hyperplasia: Excessive number of fat cells, as much as ten times normal; an increase in the number of fat cells caused by diet induced weight cycling.

  • Adipose Cell: There are two types of adipose (fat) cells, White Adipose Tissue (WAT) and Brown Adipose Tissue (BAT). The body uses WAT to store energy for use in famines; BAT burns energy to maintain body temperature. Severe obesity is caused by too many White Adipose Cells. Human adipose tissue in vivo does not have the simple metabolic pattern that might be expected from studies of adipocytes in vitro. It is engaged in a variety of metabolic exchanges. TAG, glucose, oxygen, acetoacetate, and 3-hydroxybutyrate and acetate are all extracted from from the blood. NEFA, glycerol, lactate, and carbon dioxide are released. (Proceedings of the Nutrition Society 1992: 51, 409-418)

  • Bioavailability refers to the extent to which a medication or nutrient can actually be used by the body. Laboratory measurements of the protein, fat, and carbohydrate content of foodstuffs do not necessarily predict their effect on humans. Measurements of human response to foodstuffs indicate the bioavailability of dietary carbohydrate is greater in modern foods than in their traditional counterparts.

  • Body Mass Index (BMI) is a measure of the percentage of fat to total body mass. BMI is weight in kilograms divided by height in meters, squared. (Multiply by 704 if using inches and pounds.) BMI is a relatively height and bone-density independent measure of adiposity (fatness). BMI is more highly correlated with body fat than other indices of height and weight. BMI tends to overstate the fatness of mesomorphs and to understate the fatness of subjects whose lean tissue has been diminished by diet induced weight cycling.

  • CAREFUL RESEARCHERS a code phrase suggesting researchers reporting contrary results made errors in experimental design or deduction.

  • DHEA is a hormone that reduces fat tissue size and serum cholesterol in men. DHEA increases resting metabolism, directing dietary intake into heat instead of fat stores. Increased DHEA allows migration into colder environments. Results vary in women depending on their age.

  • ENDOMORPH a person with a heavy body build, in contrast to mesomorph (muscular) and ectomorph (skinny).

  • Fat Free Mass (FFM) is everything that is not fat. Water constitutes about 73 per cent of FFM. GLYCOGEN, another constituent of FFM, is stored in the liver and muscle as a reservoir of glucose for metabolic energy. Many papers do not distinguish between FFM and muscle tissue. To complicate the issue, obesity tissue contains significant protein and other substances in addition to fat. FFM measurements must be used with caution as controversy remains about its definition and measurement techniques.

  • GLUCOSE (dextrose), found in fruits and other foods, is the end product of carbohydrate digestion. Blood glucose is the primary source of energy in animals. Glucose is converted to glycogen and stored in the liver, muscles, and fat tissues. Blood glucose levels are of great interest in adiposity and diabetes. Low blood glucose from fasting or other dietary restriction can induce headaches, low spirits, and an innate compulsion to restore normal glucose levels by eating. Metabolic needs of the body are provided by the degradation of glucose and free fatty acids [FFA]. Most tissues can use both glucose and FFA for their energy needs, but the brain and nervous system can only use glucose (or ketones), but not fats. When dietary intake or fat stores do not permit sufficient production of glucose, body protein (lean tissue) is sacrificed to make it.

    To convert from the mmol/L SI units found in research papers to the familiar mg/dl used by American doctors, multiply by 18.

  • Hyperphagia: overeating

  • In vitro: in a test tube

  • In vivo: in the body

  • INSULIN has been called "the fattening hormone". Insulin promotes differentiation of white fat cells, fat deposition, lipoprotein lipase (LPL), inhibits growth hormone release, and inhibits the fat releasing action of catecholamines. Insulin inhibits the hormone-sensitive lipase that releases stored fat from adipose tissue. In normal individuals, insulin primarily increases glucose uptake by muscle tissue and lowers glucose production by the liver. In Syndrome X, the liver and muscles are resistant to insulin, forcing the production of more insulin to control blood glucose. This causes hyperinsulinaemia (too much insulin), shunting dietary energy to fat stores. A high level of insulin precedes obesity and hypertension in Syndrome X. Tight control in Type I diabetics increases average insulin concentration and causes weight gain. Since obesity is associated with resistance to insulin action, a vicious cycle of insulin->weight gain->more insulin is possible. High insulin levels appear to be a factor in development of high blood pressure, abnormal lipid levels and artherosclerosis. It is known that insulin induces the growth of human vascular smooth muscle and stimulates the proto-oncogene c-myc through the IGF-I receptor. And to top it all, high levels of insulin prevent the excretion of uric acid, leading to the painful condition of gout.

    Low levels of insulin caused by untreated type I diabetes can lead to lipoatrophy (loss of fat tissue). Dietary carbohydrate, but not fat or protein, increases plasma insulin levels.

  • KILOJOULE some papers use kilo Joules (kJ) to measure food energy instead of kilocalories (kcal), or "calories" as used by the lay press and food labels. To convert from kJ to kcal ("calories"), multiply by 0.24.

  • LEPTIN is a hormone (name derived from the Greek word for "thin") normally produced by the "ob" gene. Ob mice injected with shots of leptin quickly began losing fat cells, ate less food, spent more time exercising and generally became healthier. Obesity may be caused by insufficient leptin or an insensitivity to leptin.

    Leptin also plays a role in starvation. Rats fasted for 48 hours decreased leptin levels, delayed ovulation, decreased testosterone, decreased thyroid and increased stress hormones. These responses are thought to aid in surviving famine. This may explain some of the metabolic slowdowns seen in dieting humans. Fasted rats injected with leptin did not have these slowdowns.

    In humans, obesity may be caused by an insensitivity to leptin. Nonetheless, it may be possible to induce weight loss by adding enough leptin to overcome the insensitivity.

  • LIPOGENESIS Storing of energy in fat tissue

  • LIPOLYSIS Draining energy from fat tissue

  • LPL LIPOPROTEIN LIPASE Two major enzymes involved in the regulation of uptake and egress of fatty acids from fat cells are LipoProtein Lipase (LPL) (repartitions energy into fat) and Hormone Sensitive Lipase (HSL) (mobilizes fat).

  • Morbid obesity Obesity severe enough to directly affect the victim's health or quality of life.

  • NIDDM Non Insulin Dependent Diabetes Mellitus, or Insulin Resistance, a disease caused by a defect in insulin mediated glucose consumption.

  • PANNICULUS ADIPOSUS overhanging belly

  • PROINSULIN is one of many metabolically defective insulin- like substances produced by the pancreas in addition to insulin. The ability to distinguish insulin from the other substances is new and not widespread. Some now think most Type II diabetics are in fact insulin deficient because much of their "insulin" is actually proinsulin. (The Lancet, Feb 11 1989, 293--5) Several lines of evidence suggest proinsulin is not merely a weak insulin, but a unique hormone of its own specific target receptors, functions, and diseases. Proinsulin preferentially binds at proliferative target cells (lymphocytes, arterial smooth muscle cells, small gut crypt cells). It is thought to be an important cardiovascular risk factor. Predominately released already in small for date babies, aging, obesity, and type II diabetes, it may be an early marker if not pathogenic principle of Syndrome X (q.v.). Proinsulin is a potent risk factor in obesity. (5th European Congress on Obesity 10-12 June 1992)

  • PITUITARY GLAND releases Human Growth Hormone (HGH) in bursts, mostly during the early hours of sleep. Human Growth Hormone promotes muscle growth and fat loss. HGH is also called somatropin.

  • PROGRAMMING A permanent change in the structure or function of an organism resulting from a stimulus or insult acting at a critical period of early life.

  • REFACTORY Adjective indicating the condition reasserts itself, precluding long term relief.

  • VLCD: Very Low Calorie Diet
  • VLED: Very Low Energy Diet Both terms apply to diets severely restricted in energy content. The term "Low Calorie" is more popular than "Low Energy" because the latter has negative associations with tiredness and other diet related complaints.

  • WEIGHT REBOUND a net adiposity increase in a diet-regain cycle, sometimes confounded by loss of lean tissue.

  • YMMV: Your Mileage (results) May Vary.

    Interesting Parameters for Dietary Macronutrients

    Parameter Protein Fat Carbohydrate Ethanol
    Gross energy kcal/g 5.5 9.2 3.9 7.1
    Digestibility % 92 95 99 100
    Metabolic energy kcal/g 4 9 4
    Cost of storage kcal/g 6 1.4 3.4
    Weight change g/kcal ?? .21 to .12 .30 nil

    Nutritionists often compare the gross energy of fat, protein, and carbohydrate when selecting foods. Gross energy is the heat of combustion, useful information for investigating spontaneous combustion of humans.

    For the body to use these nutrients, they must be digested (an imperfect process). Some energy is required to convert carbohydrate to triglycerides in fat storage. Energy is also required to store dietary fat in adipose cells, and to store protein in lean tissue. (Obesity and Leanness - Basic Aspects)

    In the human body, dietary macronutrients affect fat stores (body weight) in individual ways. On a high-fat diet, 4703 to 8471 excess calories were required for each kilogram of added weight. (Department of HEW Pub NIH 75-708 Government Printing Office, 165-86) On a low carbohydrate VLCD, replacing fat calories with 8 g/day of equivalent carbohydrate calories reduced weight loss by 1.68 kg, corresponding to 3300 calories of carbohydrate/kilogram, possibly 2500 calories per kilogram for carbohydrate alone. (Am J of Clin Nutr 1992;56:217S-23S) The action of insulin and other hormones may account for the contradiction between the gross energy content of fat and carbohydrate compared with their dietary effects on human weight.

    Ethanol is another energy-providing substrate, at least in so far as energy is released when it is burnt in a bomb calorimeter. Some dietary studies show that increased ethanol consumption is not accompanied by the expected change in body weight. Pathways have been suggested by which ethanol may be oxidized without generation of useful energy. From a biochemical point of view, ethanol demonstrates the inapplicability of linking the "energy value" of a nutrient (kilocalories) with storage of lipids in fat tissue. After an overnight fast, there was no tendency for fat storage after a 1400 kJ ethanol load, in marked contrast to fat storage from a 1160 kJ monohydrate load. (Proc of the Nut Soc 1992 51, 409-18)



    One cannot understand current obesity research without some essential knowledge of human energy metabolism and how it is regulated. The body gets its energy from dietary protein, carbohydrate and fat. The body stores energy as glycerol, lean tissue and fat. The partitioning of available energy sources between energy output (work), muscle and fat storage vary greatly between individuals. These differences are primarily genetic in origin, but are also caused by metabolic and nutritional abnormalities during gestation and infancy, and certain infections.

    Muscle tissues burn carbohydrate and fat for energy. When energy expenditure exceeds dietary input, stored glycogen, fat stored in adipose cells, and lean tissue are cannibalized to make good the energy shortfall.

    Animals regulate their body fat stores within fairly narrow limits. This regulation is automatic, not requiring conscious intervention. Changes in energy balance are compensated for by changes in appetite and metabolism. A bout of flu reduces energy intake at the same time the body's fever increases energy expenditure; the lost weight is regained afterwards. Likewise a large Thanksgiving meal raises metabolism (that's why one feels warmer) and depresses appetite for a while. The usual body weight that a person maintains automatically is called the SET POINT weight.

    The SET POINT THEORY of body weight regulation postulates that a biological servo system affects energy expenditure, hormones, fat cell receptors, appetite, and other metabolic parameters to maintain a constant body weight (set point) resistant to changes in energy input or exertion.

    For many obese individuals, their set point is the stable weight to which they repeatedly return to after dieting. Set point theory explains why the calorie loss of moderate exercise provokes an increase in appetite and/or slowing of metabolism, preventing major weight loss. "Maintenance of a reduced or elevated body weight is associated with compensatory changes in energy expenditure, which oppose the maintenance of body weight that is different from the usual weight. These compensatory changes may account for the poor long-term efficacy of treatments for obesity." (NEJM 1995;332;621-8) The reduction in energy expenditure to a level 15 per cent below that predicted for the body composition, as a result of a 10 per cent (or larger) decrease in body weight, is large compared to the level of overeating resported in some studies.

    Healthy male subjects who have no history of dieting or weight concerns have a strong caloric compensation. (American Journal of Clinical Research subjects reduced intake of other foods after required eating of food containing 22%-52% of their baseline energy intake. Subjects compensated for the covert caloric dilution of one third of the available items by increasing intake of non diluted items. Nutrition 1992;55;331-42)

    The LPL study mentioned below supports the much-debated "set point" theory, which holds that inner mechanisms set a person's weight at a predetermined level and if anything is done to change the weight, the body will adjust to restore fat content to the set point.

    "I regard body temperature, which stays around 98.6 degrees F, to be a set point. Weight doesn't have a set point in that sense," says Xavier Pi-Sunyer, M.D., director of the Obesity Research Center at St. Luke's-Roosevelt Hospital Center in New York. If there is a set point for weight, it generally seems to move in one direction--that is, the body will not make adjustments to counteract a large weight gain but will fight efforts to lose the weight. "When a person gains weight and stays at that weight a while, the body will defend that weight. It becomes the new 'set point'," explains Pi-Sunyer.

    Aside from the action of LPL, the body uses other adaptive mechanisms when food intake is reduced. To cite just two of them: Dieting depresses the metabolic rate so that calories are burned more slowly, and as fat cells shrink, they become more responsive to the action of insulin and do not release their contents as readily. (FDA CONSUMER)

    The set point theory of body weight regulation is based on a large body of evidence. (Weigle DS; Human obesity - Exploding the myths. Western Journal of Medicine 1990 Oct; 153;421-428)

    Return to Nornal Weight A remarkable demonstration of the set point can be seen in the "Guru Walla" fattening session in the Massas ethnic group in Northern Cameroon. The subjects were fattened on a 6736 calorie (per day!) high carbohydrate diet. After the fattening session, the subjects' eating was entirely spontaneous. Average mean intake was 3081 calories. No dietary advice was provided. After 36 months the men returned to their starting body weights. (Am J of Clin Nut 1994;60:861-3)

    This suggests one's set point is misset if one cannot reach and maintain normal weight on 3000 calories per day.

    Is there an Obesity Virus?

    A preliminary study indicates 15 percent of obese people show signs of having caught obesity from a virus. The 2004 ficure is 30 per cent, compared to 10 per cent of lean people. Adenovirus-5 and adenovirus-37 were added to the list of fattening virii in 2005, so the percentage of fat people fattened by an obesity virus may be much higher than 30. Nikhil Dhurandhar at the University of Wisconsin at Madison claimed discovery of antibodies to this virus among the obese is the first significant finding in the field for years. UW endocrinologist Richard Atkinson admitted the idea of obesity as a viral disease is unconventional but noted that the idea of ulcers being caused by bacteria was just as outrageous 15 years ago. The study involved adenovirus 36, one of 50 adenoviruses, several of which are known to cause the common cold.

    Researchers at the University of Wisconsin in Madison have found that mice and chickens infected with a common human virus put on much more fat than uninfected animals. They have also discovered that the same virus is more prevalent among overweight people, a strong indication that it may also cause obesity in humans. In four experiments, the Wisconsin researchers inoculated chickens and mice with adenovirus-36, a member of a viral family that includes about 50 strains. Most adenoviruses cause colds, diarrhea or pinkeye. After several months, animals infected with adenovirus-36 weighed only 7 percent more on average than those without the virus, but their bodies contained more than twice as much fat.

    Aside from a day or two of cold-like symptoms, Atkinson said, the virus produced no observable effects besides obesity. Click here for longer article!

    CONCLUSION: As seen in experiment 1, Ad-36 infection can be transmitted horizontally from an infected chicken to another chicken sharing the cage. Additionally, experiment 2 demonstrated blood-borne transmission of Ad-36-induced adiposity in chickens. Transmissibility of Ad-36-induced adiposity in chicken model raises serious concerns about such a possibility in humans that needs further investigation.       International Journal of Obesity (2001) 25, 990996

    Rats, Pigs and Blimps

    Mice, rats and pigs are commonly used in adiposity research because their metabolisms resemble those of humans.

    Wild rats never exceed 10% body fat, even when fed high fat diets. Some strains have been bred to mimic the metabolism of obese humans. The best known strains are the obese ob/ob mouse and the fatty fa/fa Zucker rat. These strains become obese even when restricted by pair-feeding to the caloric intake of lean littermates. The genetically-obese rodents demonstrate the problems of the obese; they die easily in the cold, are often infertile, lack mobility, and will mobilize muscle in preference to fat when food is scarce.

    The ob/ob mouse fails to survive in the cold because it cannot generate sufficient heat by burning fat.

    The Tubby Mouse interests researchers because it models the course of human obesity more closely than other strains, in which the rodents overeat from birth. Tubby mice don't overeat; they gain weight slowly, as they age. Tubby mice also have imparied insulin metabolism.

    Nitrogen balance studies have shown that the obese Zucker rat tends to deposit amino acid carbon skeletons in the form of fat, rather than muscle protein. Their muscles are smaller and contain less protein than those of lean counterparts. The obese rat also has less lean body mass, a reduced rate of protein deposition, and a reduced rate of protein synthesis in skeletal muscle; the decreased rate of protein synthesis is already present in the obese rat before weaning. (Int J of Obes 1992,16: 213-8) Obesity in Zucker fa/fa rats is thought to result from the combination of two recessive genes (fa/fa). Zucker rats can survive in the cold, yet they attain the obese state with normal diet and exercise. "The obesity of the Zucker rat ... is inherited as an autosomal recessive mutation. It is thought to be the initiated by a single gene defect (fa) the nature of which remains totally unknown. These rats develop a syndrome that closely resembles human obesity. Hyperphagia, hyperinsulinemia and normoglycemia, hypertriglycemia, hypertrophy and hyperplasia of fat cells as well as the development of type II diabetes and renal complications are common features to both [rat and human] species." p. 679, Journal of Lipid Research, 1992. A 25- fold increase in the amounts of the enzyme adipose tissue Fatty Acid Synthetase (FAS) apparently causes this obesity. Mature adipocytes from genetically obese Zucker rats maintain their hyperactive lipid storage capacity when withdrawn from their in vivo environment, indicating an intrinsic alteration in these cells.

    High protein requirements could provide a partial explanation for the hyperphagia of genetically-obese Zucker rats. These mutants oxidize amino acids in preference to fats and therefore growth of lean body mass is limited. In order to obtain sufficient protein for normal growth the Zucker overeats, and the excess energy ends up as fat. It is claimed that the hyperphagia is almost completely abolished when these animals are fed very high protein diets, and weight gain is then diminished. (p. 33, Obesity and Leanness - Basic Aspects) "FAS overactivity will act as a metabolic drive, channeling dietary substrates [food energy] into adipose tissue fat stores; this would happen whatever the food intake level of the rats, in good keeping with the well-established observation that hyperphagia [overeating] is not a necessary precondition for the development of Zucker rat obesity. The shunting of nutrients into adipose tissue would entail two physiological consequences, a compensatory hyperphagia and a secondary hyperinsulinemia." Human FAS activity was higher in obese subjects than in lean controls. (Metabolism 1991;40;3:280- 5)

    The sand rat (Psammoys obesus) becomes obese, hyperinsulinaemic, and insulin resistant when shifted to a high energy diet, a syndrome which also affects Aboriginal Australians and Pima Indians.

    The choice of animal strain is important to obesity experiments. Results obtained with obese rats are more relevant to obese humans than results obtained with Wistar or Sprague-Dawley (genetically thin) rats.

    Brown Adipose Tissue (BAT)

    Brown Adipose Tissue (BAT) generates heat with Non Shivering Thermogenesis (NST) by burning calories without physical motion. In humans, brown adipose tissue size decreases with age, while in small mammals, the size remains constant or increases in preparation for hibernation.

    White Adipose Tissue (WAT)

    Obesity results from an excess of white adipose tissue (WAT).

    WAT cells are not simple storage tanks. They are active, living cells. They destroy DHEA and Growth Hormone. They convert steroids that promote muscle development to estrogen. White Fat cells compete with lean tissue for nutrients, impeding muscle development.

    Reduction of fat cell numbers (see below) causes permanent fat loss while weight loss techniques that do not reduce the number of fat cells are temporary. This suggests that fat cells themselves enforce the elevated set point in many individuals. "The evidence is strong that the defense of body weight against a reduction in diet palatability is much stronger in animals and humans with normal size or small fat cells than in individuals with enlarged fat cells. This seems to be the case regardless of fat cell number. One wonders, therefore, whether reduction in fat cell size might be the event that normally gives rise to the food hoarding response in food-deprived rats." (Clinical Neuropharmacology Vol 11 Suppl 1 p. S1-S7)

    not accounted for by the loss of muscle tissue.H 2 "Preadipocytes > Fat Cells" White fat cells begin life as PREADIPOCTYES. The human body contains a vast reserve of preadipocytes, but these cells are so tiny they only cause a problem when they differentiate (mutate) into the much larger adipocytes.

    Human adipose tissue contains a pool of tiny precursor cells (preadipocytes) which can be converted to adipocytes (fat cells) in the presence of glucocorticoids and insulin. (Journal of Clinical Endocrinology and Metabolism, 1987).

    The role of insulin in fat cell proliferation, reported in many papers, explains the effect of dietary sugar and carbohydrate on the development of obesity. This would also explain why excessive insulin levels in the gestating human baby induce obesity that appears after several years.

    The future adiposity of suckling pigs can be predicted by measuring the ability of the suckling's blood to differentiate preadipocytes into full size fat cells in a test tube. The preobese sucklings had low levels of growth hormone.

    Epidermal Growth Factor (EGF) dramatically inhibits differentiation of preadipocytes into fat cells. Obese mice have EGF levels as much as 80% less than their lean littermates. Fat pads of EGF treated rats weighed only half as much as untreated rats, contained only 25 percent as many mature adipocytes, and accumulated only 20 per cent as much lipid.

    Preadipocytes isolated from fat deposits in different parts of the anatomy appear to be different. This could explain the strong heritability of body fat distribution. Preadipocytes isolated from obese rat strains change into fat cells more easily than normal.

    Size and Number of Fat Cells

    Is obesity caused by an excess number of fat cells or by gross enlargement of a normal number of fat cells? The answer to this question has heavy implications for the possible success of various weight loss strategies.

    Lean individuals have 20 to 40 billion fat cells. Fat cells can expand to no more than twice normal size. Some obese subjects have ten times as many fat cells as normal. Bjorntorp and Sjostrom (METABOLISM V20;7;703) have observed an association between high fat cell numbers (hyperplasia), more severe obesity, and childhood onset obesity. A number of studies have found that subjects with childhood onset obesity have more difficulty losing weight and are more likely to regain more weight than they lose dieting, putting them at risk of hyperobesity from diet induced weight cycling.

    A study published in the Proceedings of the 5th International Congress on Obesity showed that obese subjects who had lost weight had fat cells 25 per cent smaller than those of marathon runners who had half the total body fat. The dieters had twice as many fat cells as the athletes.

    The defense of body weight against a reduction in diet palatability is much stronger in animals and humans with normal size or small fat cells than in individuals with enlarged fat cells. (Clinical Neuropharmacology Vol 11 Suppl 1 S1-7) This would explain why it is much more difficult for obese individuals to reach and maintain ideal weight.

    See "Weight Cycling" below for more information on how diets actually increase fat cell numbers.

    Fat Cell Receptors

    Fat cells gain and lose weight by passing lipids through receptors. One type of receptor removes lipids from the blood stream and another type allows the body to access the energy stored in the fat cells with a resulting loss of weight. Geographic distribution of fat, including "love handles" that do not respond to extreme dieting, is believed to result from local variations in these receptors.

    The numbers and efficiencies of fat cell receptor types change with repeated dieting, slowing weight loss on successive diets and promoting weight gain.

    Fat and Carbohydrate Oxidation

    A low metabolic rate is a risk factor for subsequent weight gain. A low ratio of fat to carbohydrate oxidation independent of energy expenditure is also a risk factor for weight gain. In response to weight gain, both the metabolic rate and fuel mix oxidation become "normal" for the new body weight. (Progress in Obesity Research 1990, p. 180)

    The lower thermic effect of food in the obese is uncorrected by weight loss, and thus it is a contributor to obesity rather than a consequence of obesity. (Am J of Clin Nutr 1992;55:924-33)

    Muscle Fibre Type

    The April 19 1990 Lancet reports that skeletal muscle fibre type is directly correlated with body fatness. Lean subjects have more "slow fibres" well endowed with mitochondria that use fatty acids as energy source. Corpulent subjects have fewer "slow fibres" but more "fast fibres" that only burn glucose; they cannot burn fat for energy. (See EXERCISE, below.) The proportion of fibre types is a nearly linear function of BMI. All of the subjects were sedentary, ruling out any effect from endurance training. (1D-5) (1D-7)

    A low ratio of fat to carbohydrate oxidation independent of energy expenditure is a risk factor for weight gain. (p. 180, Progress in Obesity Research 1990)

    It is now recognized that obese trauma patients require special dietary intervention because their bodies cannot use the energy stored in their fat for healing the way thin people do. (Journal of Clinical Investigations, Jan 1991) Growth Hormone treatment allows the obese patient's body to mobilize and utilize its fat stores. (METABOLISM 1993 42:2 185-190)


    Types of Adiposity

    Research over the last decade has shown that most fat people did not get fat because they ate too much, ate the wrong things, or exercised too little. Rather, they became fat because their bodies put too great a fraction of their food energy into fat. This research is discussed in later chapters.

    Experiments with controlled overfeeding of lean subjects demonstrate an increase in body metabolism that restores normal weight when overfeeding ceases. In a 1986 Dutch study, men who experienced many life events in a short period showed a gain in body mass. A year later this weight gain had disappeared in almost all subgroups of these men. The exception was the subgroup that tried to lose weight by dieting; those who dieted gained yet more weight. (International Journal of Obesity (1988), 12, 29-39.)

    Lean individuals' self-recovery from overeating is exploited in ads from Jennie Craig and other diet providers that claim long term weight loss. None of the well known "before/after" diet celebrities such as Art McMahon had childhood onset obesity.

    Much remains to be learned about human genetics, but it has already been learned that individuals with the HLA Aw30 allele have a 2.61 relative risk for obesity. (Human Heredity 1989;39(3):156-64)

    Experiments by Meier, Cincotta and Lovell suggest obesity and associated type II diabetes are the result of defective circadian [daily cycle] neuroendocrine rhythms.


    The conclusion of current research is that individual differences in Body Mass Index (BMI) are mostly the result of genetic factors. Discoveries of "obesity genes" continues at a fast pace, with the discovery of a fifth (the "tubby gene") reported in April 1996.

    Obesity is now thought to be the result of a pairing of normally recessive genes (fa/fa).

    "Previously, researchers at the University of Iowa found evidence of a recessive obesity gene (the child needs one copy of the gene from each parent to have the tendency towards overweight). A study of 277 school children and their families showed a pattern of obesity that followed the classic model for recessive inheritance.

    In December 1994 scientists from New York's Rockefeller University reported molecular identification of an obese gene in mice. A similar gene was also found in humans. The first identification of an obesity gene in both animal and humans excited obesity researchers and the lay public, if not nutritionists and exercise promoters.

    It is likely that a number of genetic mechanisms exert influence on weight, among them genes that dictate metabolism and appetite. One that is being investigated actively is the gene that codes for lipoprotein lipase (LPL), an enzyme produced by fat cells to help store calories as fat. If too much LPL is produced, the body will be especially efficient at storing calories [as fat].

    LPL is partly controlled by reproductive hormones (estrogen in women, testosterone in men), so gender-based differences in the activity of the enzyme also factor into obesity. In women, fat cells in the hips, thighs and breasts secrete LPL, while in men the enzyme is produced by fat cells in the midriff region. Fat cells in the abdominal area release their contents for quick energy, while fat in the thighs and buttocks are used for long-term energy storage. Thus, a man can often pare his paunch more readily than a woman can shed her saddlebags.

    LPL also makes it easier to regain lost weight, according to a study conducted at Cedars-Sinai Medical Center in Los Angeles and reported in the April 12, 1990, issue of the New England Journal of Medicine. Nine people who lost an average of 90 pounds had their LPL levels measured before dieting and after maintaining their new weights for three months. The researchers found that levels of the enzyme rose after weight loss, and that the fatter the person was to start with, the higher the LPL levels were--as though the body was fighting to regain the weight. They believe that weight loss activated the gene producing the enzyme. This may be one reason why it is easier for a dieter to regain lost weight than for someone who has never been obese to put weight on." (FDA CONSUMER) LPL plays a major role in the production of low density lipoproteins; this may partly explain the increased mortality associated with repetitive diet induced weight cycling. (Progress in Obesity Research 1990, 225)

    Two studies published in the New England Journal of Medicine illustrate the point.

    In "The body-mass index of twins who have been reared apart", the rearing environment was shown to have no effect on BMI. Adoptees of fat parents were no fatter then adoptees of skinny parents. In other words, if you're fat, it wasn't because your mother fed you too many cookies and it wasn't because your father didn't make you exercise.

    In a followup paper given at the 6th International Congress of Obesity, p. 670, the heritability estimate for obesity at age 45 comes to 0.84. Compare this to some other commonly accepted heritability estimates: Coronary, .49, Schizophrenia, .68, Hypertension, .57, Alcoholism, .57, Cirrhosis, .53, Epilepsy, 0.50.

    The plots of parent/offspring weights in the above study bear close inspection. The plot of biological parents and adoptees shows the (by now) well known nearly straight line relationship between parents' adiposity and that of their children. The plot of adoptive parent weight and adoptee weight shows a slight negative trend for females, and no trend for males. So much for fat mothers passing bad habits on to their children.

    "the genetic relationship fully accounts for the familial resemblance in body mass index among adults." [i.e., nothing to do with passing on bad eating habits or sedentary lifestyle] (Int J of Obesity 1992:16,227-36)

    A study of lean and overweight male Army personnel was designed to prove that the overweight valued good health less than normalweights, and practiced less healthy lifestyles. To the researchers' surprise, there were no significant differences between overweight and normalweights on these attitudes.

    "environmental effects shared among family members are irrelevant in the determination of weight and obesity." (International Journal of Obesity 1992 16 657-666)

    In "The response to long-term overfeeding in identical twins", 12 pairs of identical male twins were overfed and kept sedentary under close supervision. Those who gained the most fat gained less muscle than those who gained the least fat. Notwithstanding the wide differences in weight gain between pairs, among 10 of the 12 pairs weight gain was almost identical. There was a 3 to 1 ratio in weight gain between the easiest gainer and the slowest gainer.

    The overfeeding study is interesting because of its sample selection. None of the subjects had any history of obesity whatsoever, not even in their families. One can but imagine what that 3 to 1 difference in weight gain and 16 to 1 difference of lean/fat gain would have been if overweight subjects had been included.

    The appearance of these papers in the May 24 1990 New England Journal of Medicine prompted several submissions questioning the papers' findings. These letters and the authors' rebuttals were printed in the Oct 11 1990 edition.

    The Sep 1990 Science News reported a very wide difference in the amounts and types of tissues added in response to overfeeding. In this study, thin people actually added more weight than fat people did, but the thin people added weight mainly as lean tissue instead of fat. Data from "lean hungry" types that gained little weight were excluded!

    The obese (and pre-obese) differ from lean persons in other ways. Their muscle cells do not burn fat well. DHEA and growth hormone levels are low. Their fat cells spontaneously multiply under conditions when those of of lean persons do not. Metabolic differences are evident even before birth. These factors are described elsewhere in Adiposity 101.

    Insulin resistance is a survival advantage in famine, evidenced by the high prevalence of Syndrome X in populations that have experienced recent famines. The inhabitants of the Pacific Islet of Nauru have provided a practical object lesson in the genetics of obesity. The Nauruans were selected for the "thrifty genotype" when their ancestors reached the islands by long canoe voyages when fatter individuals escaped death by starvation. Droughts and crop failures were common in the past, and many died of starvation during the harsh Japanese occupation of 1942-5. Since then mining has made Nauru wealthy. Obesity and NIDDM became endemic after 1950, affecting two thirds of adults by age 55-64. NIDDM peaked in 1975-76 but has since decreased markedly as obesity and NIDDM prone people failed to reproduce. Diabetic women in Nauru had more stillbirths and less than half as many live births as healthy controls. Similar natural selection has reduced the prevalence of NIDDM in the West to about 8%. (NATURE VOL 357 4 June 92 363-3)

    Obese and lean persons do not share the same genetic heritage. Medical advances in managing gestational diabetes in the last few decades counteracting this natural selection have fattened the gene pool.


    "Syndrome X" or "insulin resistance syndrome" is defined as:

    1. resistance to insulin-mediated glucose uptake Fat cells release a hormone resistin that causes insulin resistance.
    2. glucose intolerance
    3. hyperinsulinemia
    4. increased very low density triglycerides (VLDL)
    5. decreased high-density lipoprotein cholesterol (HDL)
    6. hypertension
    7. elevated systolic BP during submaximal exercise
    8. adiposity
    Scientists used DNA samples from 2200 overweight volunteers to locate a section on chromosome 3 that may be the source of Syndrome X. Genes on those chromosomes probably control whether the body burns fat or stores it. ( Dec 19 2000)

    The inherited defect is insulin resistance in skeletal muscles, the other abnormalities are consequences. (American J of Obstet Gynecol July 1990 292-5) Since the differences in insulin resistance between Pima Indians and Caucasians remains even after matching for obesity, the increased insulin resistance could not be blamed on their obesity. (Progress in Obesity Research 1990: 361) In genetically prone individuals, insulin resistance is the earliest detectable defect. This defect may occur 15-25 years before the clinical onset of the disease. Insulin resistance constitutes an "intervening phenotype" as well as a marker for the disease. Initially the body attempts to compensate for this insulin resistance, but eventually the increased insulin secretion fails to compensate and type II diabetes results. (Diabetes 9/94 43:1066-83) This defect in insulin resistance in skeletal muscles may explain why fat people are less tolerant of extended exposure to cold; their bodies cannot burn energy quickly enough to maintain warmth.

    A study by teams in Australia and the United States confirms a genetic defect in certain populations with a high risk of developing obesity-linked disease such as diabetes. The research defined the defect in a critical metabolic step in the body's capacity to metabolise sugar. "this discovery is classed as a major breakthrough in that it has identified a genetic tendency which causes the disorder." Professor Paul Zimmet, director of the International Diabetes Institute (Reuter, July 2 1992)

    Some types of Type II diabetes in human were linked to gene locations in 1992.

    A connection between a gene and one type of diabetes with implications for hundreds of thousands of Americans was reported in February, 1993. "This is the first clear definition of a genetic cause of Type II diabetes," said Dr. Simon Pilkis, chairman of the Department of Physiology and Biophysics at the Stony Brook Health Sciences Center in New York. "Moreover, it may be one of the largest single-gene disorders described to date." "Tools are now available to screen for gene mutations, and it is only a matter of time before other genes implicated in Type II diabetes are identified," Pilkis said. "We will be able to screen different diabetic populations or the general population for these mutations, which will tell us whether someone has a predisposition to diabetes and what category they fall into." (UPI 02/28/1993)

    Miller and Colagiuri have pointed out that humans were primarily flesh-eating hunters consuming a low carbohydrate high protein diet until recently. insulin resistance offered a survival and reproductive advantage during the Ice Ages which dominated the last two million years of human evolution. The introduction of agriculture and subsequent food processing have raised the quantity and quality of dietary carbohydrates, reversing the dietary evolution of the last two million years, causing the recent epidemic of NIDDM. This is the only theory that explains why the prevalence of NIDDM is lower in European and Middle Eastern populations, which developed agriculture thousands of years ahead of the rest of the world. (Diabetologia (1994) 37;1280-6)

    Research has been accumulating on the fattening effect of high levels of insulin during gestation and infancy. High insulin levels are sometimes caused by excessive serum glucose in the mother's blood and leakage of a insulin- antibody pairs across the placenta. Obese individuals almost always exhibit high insulin levels.

    Hyperinsulinaemia itself could be one of the driving forces responsible for producing increased glucose utilization by white adipose tissue, increased total lipid synthesis with fat accumulation in adipose tissue and the liver, together with an insulin-resistant state in the muscles. (Biochemical Journal 1990 267:99-103)

    A decrease in glucose induced thermogenesis already exists at the onset of obesity. (Am J Clin Nutr 1993;57:851-6)

    One or two decades before type II diabetes is diagnosed, reduced glucose clearance (insulin resistance) is already present. This reduced clearance is accompanied by compensatory hyperinsulinemia, suggesting that the primary defect is in peripheral tissue response to insulin and glucose, not defective pancreatic beta cells. (Annals of Internal Medicine 1990 113:909-915)

    Slow glucose removal rate and hyperinsulinemia precede the development of Type II diabetes in the offspring of diabetic parents. (Annals of Internal Medicine 1990:113;909-15)

    insulin-mediated glucose disposal is reduced in otherwise healthy, lean normotensive subjects. insulin resistance is present in these hypertension-prone individuals before the development of hypertension. (Hypertension 1993:21; 273-9)

    "impairment of insulin sensitivity precedes both the development of overt hypertension and gain or redistribution of body fat. Therefore the concept that insulin sensitivity is low as a result of altered fat distribution has to be reconsidered" (Lancet 1993; 341: 327-31)

    "our data strongly support suggestion that hyperinsulinemia could be a common link between cardiological Syndrome X and recently postulated metabolic Syndrome X with the same characteristic finding - insulin resistance." (Kendereski et al, U of Beograd, Beograd, Yugoslavia, Abstracts, IJO 1993)

    Increased lipid oxidation is one of the earlier dysfunctions observed in recent-onset obesity; lipid oxidation may induce a decrease of glucose oxidation, insulin resistance, and increased fasting insulin secretion. (DIABETES 1993:42 1010-16) This increased lipid oxidation may explain the higher percentage of energy from dietary fat sometimes reported in fatter children.

    Muscle fiber composition changed with hyperinsulinemia, with more fast-twitch fibers and fewer slow-twitch fibers. (DIABETES 1993:42 1073-81)

    Hyperinsulinemia imposed on normal rats increased in vivo glucose utilization, lipogenesis and the fat accumulation in white adipose tissue, while producing an insulin resistant glucose transport im muscles. (Endocrinology 1990:127;6 3246-8)

    A large portion of middle aged and elderly people in Western countries suffer from a combination of metabolic disorders and cardiovascular risk factors. This combination includes hyperinsulinemia (elevated insulin levels), insulin resistance (reduced sensitivity to insulin), hyperlipidemia (elevated lipid levels), obesity, and hypertension. This combination is sometimes termed "Syndrome X" or "insulin resistance syndrome." Amlyin Pharmaceuticals scientists and others have observed that most subjects with hyperinsulinemia also have elevated amylin levels, or hyperamylinemia. The finding that amylin can stimulate renin [enzyme associated with hypertension] secretion is consistent with the idea that amylin may be a missing link between hypertension and the other metabolic disorders. (Amlyin Pharmaceuticals press release)

    insulin resistance and NIDDM are accompanied by a progressive deterioration of the microcirculation in many tissues, including the skeletal muscles that provide most of the body's insulin mediated glucose disposal. Vascular and circulatory changes causing a decline in muscle blood flow may be the cause of the metabolic disorder. (Diabetologia 1993;36:876-9)

    Maternal Environment

    What one's mother does or eats during or immediately before pregnancy affects one's BMI.

    Too much carbohydrate during gestation is Not Good. Gestating infants whose blood was highest in insulin (Measured indirectly by sampling the amniotic fluid.) (caused by elevated glucose in the mother's blood) were markedly obese by 6 years of age, independent of the mother's weight. This syndrome is thought to be a cause of Pima Indians' high incidence of obesity. (Archives of Disease in Childhood 1990; 65; 1050-2) Offspring of Diabetic Mothers exhibited an unusual pattern of fat growth; the baby is unusually fat at birth (macrosoma), but assumes normal weight at 1 year. Fat growth creeps in over the next several years, and accelerates at year 5 (girls) or 6 (boys). By age 8 both male and female offspring of diabetic mothers are markedly obese and getting fatter, correlating with insulin levels during gestation. (Diabetes, Vol 40, Suppl2, Dec 1991, 121-5)

    Mother's insulin is not thought to cross the placenta. However insulin injected into IDDM mothers raises antibodies, and these insulin-antibody pairs do cross the placenta. Once in the fetus, the insulin increases fat deposition, resulting in macrosoma. (NEJM Aug 2 1990 323:5 309-15)

    The May 1990 METABOLISM reported that changes in the rat sow's diet during early pregnancy had a permanent effect on pups' lipid metabolism.

    "Thus we propose that poor nutrition of the fetus and infant leads to permanent changes of the structure and function of certain organs and tissues. The timing and precise nature of the deficiencies determine the pattern of metabolic and functional abnormalities seen in later life, including diabetes and hypertension and possibly including some hyperlipidaemias and even insulin resistance. We suggest that poor early development of islets of Langerhans and Beta cells is a major factor in the aetiology of Type 2 diabetes." (Diabetologia 1992 35; 595-601) In some diabetic subjects defective insulin-like molecules constitute up to two thirds of the total concentration of insulin-like molecules in plasma that are measured as "insulin" by normal tests. Measuring the defective molecules as "insulin" can lead to misdiagnosis that a patient is insulin resistant when in fact he is insulin deficient.

    Pigs undernourished from 10 days to 1 year eventually became extremely fat. They had plenty of fat cells at 10 days of age, but these cells were completely empty and did not register by conventional cell counting at 1 year. However, as soon as plentiful food was supplied, the pigs became extremely fat; the longer the period of deprivation the fatter they tended to become. This finding refutes the commonly held belief view that an excessive number of adipocytes are formed only when overfeeding takes place in infancy. (Proceedings of the Nutrition Society 1992: 51, 353-65)

    Mothers who experienced caloric deprivation in a critical portion of pregnancy during the 1944 Netherlands Hungriwinter bore sons 2-3 per cent of which were obese at age 19, more than twice the normal incidence of obesity.

    Infant undernutrition caused by the mother's smoking may produce similar results.

    Precocious Puberty

    The average age of puberty in women has dropped in the past 100 years from 17 to 13. This has caused an increase in teen sexuality and pregnancy, but our interest here lies in its relationship to adiposity. Douglas L. Foster reported in the 1995 Experimental Biology meeting that blood glucose triggers the onset of puberty. He was able to delay puberty in sheep by reducing blood glucose, and induce puberty by increasing it. Since blood glucose is boosted by dietary carbohydrate, this reduction in the age of puberty indicates a major increase in bioavailable dietary carbohydrate in the last century.

    Baby's Diet

    A Case Western Reserve University study (4P-17) compared rat pups fed a milk-substitute formula (56% of calories from carbohydrates) with mother-fed controls (only 8% of calories from carbohydrates). The formula fed rats became fat. "The results show that alterations in the source of calories rather than the total caloric intake during the suckling period can have specific long-lasting effects on lipid metabolism in adulthood, leading to the development of obesity."

    Diet Change Result in adult
    Prematurely weaned to High Carbohydrate More prone to hypercholesterolemia
    Prematurely weaned to High Fat Prevents hypercholesterolemia
    Overnutrition* Elevated plasma cholesterol and insulin
    Undernutrition* Obesity

    [Prematurely weaned *3-10 days after birth] (FASEB Journal, June 1990, p. 2606)

    The fattening effect of a high carbohydrate diet at weaning is explained in a review of the influence of diet on the development of adiposity appearing in the 1992 Proceedings of the Nutrition Society.

    Laboratory reared rat pups fed a high carbohydrate formula have higher serum insulin and increased liver fat synthesis capacity compared with pups fed a high fat formula or reared naturally. Early exposure to a high carbohydrate diet predisposes an increased fat creation capacity in liver and adipose tissues and to the development of obesity later in life. (J Nutr. 123: 373-7, 1993)

    "an increase in carbohydrate-derived energy during the immediate post-natal period in the rat leads to the onset of obesity later in life. Chronic hyperinsulinemia and accumulation of fat is adipose tissues, resulting from increased lipogenic capacity in these rats, make this rat model unique in enabling study of the role of neonatal nutritional experience on the development of obesity in adult life." (Int J of Obesity 1993;17,495-502)

    Kramer found that breast feeding and delayed introduction of solid food protected against subsequent obesity. 95% of the obese had not been breast fed. (J Pediatr 1981 98: 883-7).

    In human, breast-fed infants are leaner than formula-fed infants at 1 year. The formula-fed infants were fatter because energy intake on high carbohydrate formula is higher. (Am J of Clin Nutr 1993;57:140-5) See Here

    The Amaerican Academy of Pediatrics recommends that most babies be exclusively breast fed for the first 6 months, and that mothers try to continue until 1 year.

    David Pettit of the National Institute of Diabetes and Digestive and Kidney Disease in Phoenix and colleagues studied 720 Pima Indians. The 325 who had been exclusively bottle-fed weighed "significantly" more than those who had been breastfed.

    These results support the assertion of a Reader's Digest article that breast feeding can "Fat Proof" one's baby (compared to formula feeding). Left unanswered is the question: at what age should the suckling's low carbohydrate diet evolve to the high carbohydrate diet currently favored by vegetarians and other low-fat diet evangelists? Insulin is the primary drive for the major increase in hepatic and adipose tissue lipogenesis that occurs during the early dynamic phase of obesity; dietary carbohydrates increase insulin levels.

    (Please refer to the discussions of adipose cell differentiation, reversion, and replication elsewhere in this document.)

    Breast milk contains human Epidermal Growth Factor (EGF) (discussed above), a potent inhibitor of obesity not present in infant formula and cow's milk.

    Children need dietary fat to insulate their nerve cells, prevent nerve crosstalk and brain damage. There is concern that infant formula does not provide certain long-chain lipids necessary for good cerebral and retinal development. (Acta Paediatr Scand Suppl 365: 58-67, 1990)

    "Children need fat and cholesterol for proper growth and brain development. Children under age two need fat and cholesterol every day - even if they look chubby. Breast-fed babies get what they need from breast milk, which draws 50% of its calories from fat." (Bottom Line Personal March 15 1995)

    Early exposure to cow's milk and solid foods in infancy increases the risk of diabetes in genetically predisposed babies. (DIABETES Feb 1993: 42: 288-95)


    Personality Problems

    As the causes of obesity become known, obesity is increasingly recognized as a cause of mental health problems rather than the result of mental problems.

    Obesity has been historically linked to emotional factors by clinicians and the lay public alike. Early psychiatric studies reinforced the popular perception that psychopathology is common among the overweight and plays an important role in the development of obesity. This notion has been challenged by recent investigations which suggest that psychological disturbances are more likely to be the consequences than the causes of obesity. Emotional difficulties faced by the obese may be largely attributable to an entrenched cultural contempt for the obese and a pervasive preoccupation with thinness. (Annals, New York Academy of Sciences, 1987)

    "There appear to be no global personality traits or profiles that are associated with obesity." (Am J of Clinical Nutrition July 1992)

    Health Problems

    Correlations between obesity and certain health problems have been widely reported in the media. Joint problems and sleep apnea are generally recognized direct effects of obesity.

    Obesity causes problems in pregnancy. Obese women have more cesarean deliveries, gestational diabetes, high blood pressure, and cesarean wound infections. Twice as many obese women's babies required convalescent or intensive care, compared to the newborns of lower-weight mothers. Over the centuries, these effects have selectively bred for thinness before today's medical technology was available.

    The effect of obesity on cardiovascular disease and diabetes is not well understood; both may be markers of basic underlying metabolic derangements. Controversy remains about the true cause and effect. There is no agreement in the scientific community that dieting provides a long term health improvement.

    "... even though we like to believe that weight loss in the obese is accompanied by a reduction in the mortality rate, it is important to keep in mind that no intervention study has yet dealt with this issue." (Letter to JAMA from Bouchard, Despres, and Tremblay)

    Metformin, a drug that improves insulin sensitivity, improves glucose, lipid metabolism, and reduces blood pressure, left ventricular mass, cholesterol, triglycerides, and fibrinogen in hypertensive, obese women. Levels of insulin, known to promote cardiovascular disease, dropped. Weight was not affected, and subjects did not experience the usual diet side effects. (DIABETES CARE 1993:16:10 1387-90)

    An Aug 5 1990 BBC broadcast reported that the size of a baby relative to the size of the placenta had a greater correlation on adult blood pressure than the combined effects of weight or alcohol consumption.

    A Norwegian study indicates moderate obesity (BMI < 35) does not greatly increase mortality except for diabetes. (Acta Med Scand, Suppl. 723; 17-21)

    Some of the correlation between obesity and health problems may be caused by common factors. For instance, DHEA and HGH help the healing process, help the immune system, block autoimmune disease, hyperglycemia, and neoplasia, promote muscle buildup and fat loss. The obese have much lower levels (order of magnitude) of Human Growth Hormone (HGH) and DHEA than normal subjects. Men with abdominal obesity have low testosterone values. Mice obesity genotypes are thought to promote various diseases. If both the obesity and poorer health result from common factors, only correction of the common factors will improve the patient's health outlook.

    Even is there is no great health risk from moderate corpulence, endomorphs would still wish for normal body composition simply because being fat in this society is an unmitigated bitch.

    Some of the health problems associated with obesity result not from the obesity itself but from the effects of dieting. As reported in the 1990 House hearings on the diet industry, studies consistently show an increase in mortality with dietary weight cycling. None have shown an improvement in long term health outcomes from dieting.

    Some obesity related health problems are the result of discrimination against obese patients by the medical establishment. Insurance companies discriminate against obese individuals, even those with no history of health problems. Insurance companies are forbidden to test applicants for HIV, a right of privacy not afforded to overweight applicants who are compelled to test and report their weight.

    The obese often get substandard medical treatment. In one case, symptoms of allergy induced asthma (post nasal drip) were attributed to obesity for several years, denying the patient effective treatment. Marginally overweight women are humiliated by male doctors. In one case, a surgeon "called the patient a fat bitch" and said "people like this do not deserve to live and that the only exercise she probably got was walking from the kitchen table to the refrigerator." Similar abuse was reported in a 1983 Nova program. It is incumbent of the AMA and regulatory bodies to monitor this abuse and institute corrective measures.

    "Some doctors can be as cruel as kids in a playground when faced with a fat patient." (Medical World News, May 1992)

    The University of Kentucky have a developed a course designed to correct the attitudes of doctors towards fat people. (IJO 1992 16, 859-868)

    "Now that prejudice against most formerly stigmatized groups has become unfashionable, if not illegal, one of the last acceptable forms of prejudice is that against obese persons. What is to be be done about this problem? The authors suggest the extension of the Americans with Disabilities Act to include the overweight, which would certainly be a beginning. Overt discrimination against overweight people is only part of the problem, however, and we in the medical profession are among the cheif offenders. Who among us has not heard the horror stories told by obese persons about their treatment at the hands of insensitive and prejudiced doctors? Studies documenting our role in the stigmatization of obesity have been available for years. Our education has done nothing ot relieve this problem. Not only house officers but also medical students are clearly prejudiced against obese persons." (EDITORIALS, New England Journal of Medicine, 1991;329:14;1037)


    Obesity prevalence estimates are virtually unchanged from the early 1960s, according to the Centers for Disease Control.

    As reported in the 1990 House hearings, there is no effective long term treatment for obesity.


    The correlation between exercise and thinness is well known and firmly established in cultural and media stereotypes. Victims of obesity are criticized for not engaging in physical activities enjoyed by thin people. Before prescribing an exercise regimen for weight loss, one must consider obesity's effect on ability to exercise and obtain pleasure from such activities. Overweight people, and the more overweight the more of a problem, are limited in the amount of exercise that they can endure. The lower athletic potential of obese individuals generally denies them the satisfaction of athletic success even if they manage to lose weight. Obese individuals may be unable to attain altered states such as "runner's high". These factors pose an alternative explanation for the reported correlations between exercise and thinness.

    Very few studies have attempted to identify the causality of this correlation. No relationship was found between baseline physical activity level and subsequent weight gain among either men or women. Recreational physical activity reported at the baseline interview had little relationship to later weight gain. There was little or no association between baseline physical activity and the risk of becoming obese, but a strong association with follow-up physical activity. (International Journal of Obesity 1993: 17; 279- 86)

    Individuals vary widely in their metabolic response to exercise. Reduction in body fat percentage varied from 49% to 1% for subjects placed on the same supervised exercise regime. VO2-max (liters/minute, a measure of fitness) change varied from 0% to 14%. The differences in these responses were mostly genetic. (Arteriosclerosis Vol 8, No 4) Mesomorphs' favorable responses to exercise programs tend not to accrue to endomorphs.

    Even after prolonged training program (6 mo), no pronounced effect on body fat was seen, whereas nonobese controls reduced their adipose deposit. (Metabolism 26:319, 1977) Obese subjects with fewer fat cells decreased in weight whereas patients suffering from severe obesity and an elevated number of fat cells even gained weight. (Metabolism 28:650, 1979)

    The fattening effects of exercise in hyperphagic obese may be explained by a post exercise peripheral tissue insulin resistance. (Journal of Clinical Endocrinology and Metabolism 1989 68:2 438-45)

    "The postexercise recovery phase may be an important period during which energy-saving may occur in chronically undernourished subjects." (May METABOLISM 1993 42:5 544-7)

    "The current low physical activity is possibly a result rather than a cause of higher body weight in old age." (Int J of Obesity, 1992, p. 199)

    An Italian study found correlations between the children's BMI and their fathers' BMI. A significant correlation between BMI and exercise was documented only in the group of girls. Heavier boys didn't get that way from lack of exercise.

    A study conducted by the Physical Education Association Research Centre and Schools of Education and Postgraduate Medicine, University of Exeter published in the July 28 1990 British Medical Journal found "No significant relation was detected between the level of habitual activity and skinfold thickness in either sex. Similarly, the children classified as overweight were not significantly less active than children who were not overweight."

    A Charlottsville VA study in the 1991 International Journal of Obesity reported: "Obese and nonobese children had similar levels of physical activity and attitudes toward activity"

    "Although many researchers and the lay press have argued that physical inactivity in children is strongly related to obesity and weight gain, the research is contradictory. ... One should have expected that, in the better done epidemiological studies such as in Tecumseh or in Finland, a strong consistent relationship should be found between activity and obesity. This was not found to be the case." (p. 563, Progress in Obesity Research 1990)

    A Minnesota Heart Health Program study noted a significant increase in obesity from 1980 to 1987. The data did not link changes in energy intake, fat intake, exercise, or cessation of smoking to this increase. (Int J of Obesity 1991 15,499-503)

    In a UC Davis study, a high level of exercise (marathon training) caused a modest weight loss, averaging 7 pounds when a permanent plateau was reached at 8 weeks.

    In a three month Swedish study of 60 minute exercise to 80 per cent of maximum capacity, obese men lost 2.9 kg of body fat, an amount of "borderline significance". Obese women did not lose fat except for some of the most obese subjects. (International Journal of Obesity 1991, 15, 75-81)

    Other studies did not show an increase in weight loss when aerobic and anerobic exercise was added to VLCD (Very Low Calorie Diet) and other diet programs. ("Lean Body Mass, Exercise and VLCD", International Journal of Obesity (1989), 13 (suppl. 2), 17-25.)

    "However, the addition of exercise does not affect total body mass loss. A net loss of FFM was observed in all groups, regardless of exercise modality [including resistance strength training]." (American Journal of Clinical Nutrition 1992: 11;2:152-8)

    Several years ago it was widely reported that working out left one with an "exercise afterglow" for up to 12 hours, during which body metabolism remained at least slightly elevated. More recent studies have shown that this effect requires a level of exercise attainable only by highly trained athletes. Moderate exercise does not increase the metabolism (BMR) of obese subjects.

    Exercise induces increased growth hormone levels in lean subjects. The obese do not release growth hormone in response to moderate exercise. In obese subjects, fenfluramine partially restores GH responsiveness to arginine but not growth hormone releasing hormone; fenfluramne may or may not restore GH responsiveness to exercise. Experimentation to determine the optimum timing between fenfluramine doses and exercise is needed.

    "Weight loss does not readily occur in women unless accompanied by caloric restriction. Further, the role of exercise in maintaining resting metabolic rate while dieting has only marginal support." (Journal of the American College of Nutrition 1993;12:4 363-7) has reported reading that individuals over 20% overweight should not exceed a pulse rate of 0.6 * (220 minus age). This guideline precludes robust exercise for the obese.

    Exercise is generally credited with reducing cholesterol and triglyceride levels. However, as reported in the October 10 1990 Journal of the American Medical Association, it may not work for the overweight. A 28 year old mildly overweight man went to a fitness center to begin an exercise program with the goal of losing 10 pounds. This man had recently had a physical in which the "usual values were normal". His fitness counselor put him on a exercise bike, a rowing machine, and then fast walking on treadmill for a total of thirty minutes of vigorous exercise. The next morning he couldn't get out of bed without help. On his next visit to the fitness center, the fitness counselor advised him to repeat the exercise program, which he did. The following day he was admitted to hospital with kidney failure. Emergency procedures restored his kidney function after 11 days. A long time later his blood pressure remains elevated, and he complains of headache, edema, and sleep problems. His triglyceride and cholesterol levels are also elevated.

    A UC Davis study reports that rats subjected to an exercise regime reach plasma triglyceride and adipose LPL levels greater than sedentary controls within 84 hours of exercise termination.

    The lean subjects had marked changes in lactate, pyruvate, FFA, and catecholamines, consistent with the need for rapid mobilization, uptake, and utilization of carbohydrate and fet-derived fuels. The responses of the obese subjects differed in insulin, FFA, glycerol, and, surprisingly, epinephrine. The postexercise hyperglycemic hyperinsulinemic state was more intense in the obese subjects and associated with higher plasma FFA and blood glycerol levels. After exercise, as in many other situations, obese subjects have insulin resistance. (J of Clin Endocrinology and Metabolism 1989 68:2 438-45)

    An alarming study published in the International Journal of Obesity (1992;16;519-527) reported Short-term exercise can reduce weight and fat gain in obese humans and animals. However, the beneficial effects are not long-lasting. After cessation of exercise, there was no difference in body weight, fat mass, and percentage body fat between exercised and sedentary OB rats. Unfortunately, the exercised rats had a significantly higher amount of internal fat and internal:subcutaneous fat ratio. Increased insulin sensitivity produced by exercise training has been reported previously, and this may be the cause of rapid fat gain; the same effect has been documented after dieting. Fat cell NUMBERS in some areas were actually increased compared to the sedentary rats. This increase in adiposity may pose health risks.

    Severely overweight subjects showed a 50 per cent impairment in FFA [Free Fatty Acid] mobilization in response to prolonged moderate exercise (level walking). This energy shortfall was made good at the expense of a drop in blood sugar (causing tiredness) and increase in lactate plasma (aching muscles). This represents a metabolic limitation on exercise by the obese. (See "fast fibres" above.) (1983 International Journal of Obesity pp 221-229.)

    "We tend to be thinner when we are young not because we consume fewer calories, but because we metabolize glucose more efficiently." (Valdimie Anisimov M.D., p. 26, October 1990 Omni)

    Contrary to the claims of Cable TV ads, there is no clinical evidence of spot reducing from any exercise.

    Nearly 80 percent of the exercise equipment sold in the US will be used seriously for six weeks or less. (Public Health Service/ Good Housekeeping 9/94)

    Unlike diets, exercise-only weight loss programs have not been reported to result in weight rebound. The small amount of weight loss may account for this.

    Exercise induced weight loss is temporary, but will be maintained as long as the intensity of exercise is maintained.

    The fragile bones of an old woman may develop early in a female athlete who pushes too hard to stay skinny and excel in her sport. These women have developed eating disorders, pushed their endurance workouts too hard, or both -- and have ceased to menstruate.

    "Exercise can produce a modest gain of Lean Body Mass (LBM) and loss of fat in weight-stable individuals, but it is important to realize that if much weight is lost during exercise there is a risk of erosion of the LBM. Data from both human and animal experiments show that exercise cannot conserve lean weight in the face of significant energy deficit" (Lead Review Article, Nutrition Reviews 50;6 June 92)

    "in older obese men, hypocaloric dieting combined with aerobic exercise does not attenuate the loss in fat-free mass that occurs during weight by hypocaloric dieting alone." (METABOLISM Vol 43 No 7 July 1994 867-71)

    High dropout rates and the low rates of weight loss (0.14 kg/week) in exercise studies by Brownell and Stunkard indicate the difficulties encountered in the use of exercise for weight control. Long-term data are not available about the value of exercise in obesity.

    "1) energy cost of exercise is minimal, 2) effects on thermic of food are negligible ... exercise may not prevent, and may even increase the fall of metabolic rate" (Am J of Clinical Nut, Feb 1992)

    It is hoped that eventual progress in the treatment and prevention of obesity will allow more people to enjoy the pursuit of more active pleasures.

    Will Power


    "The high prevalence of obesity in affluent societies, coupled with an increasingly lean aesthetic ideal, has resulted in unprecedented rates of dieting." (International Journal of Obesity 1990, 14, 373-383)

    Dieting is a natural idea given the obvious, if temporary, effects of famines and religious fasts. Energy deprivation as a method of obesity treatment had changed little since Greek antiquity.

    A supposition behind reducing diets is the conventional wisdom that overeating by the obese upsets the natural weight regulation enjoyed by the majority of humans.

    It is incorrect to assume that people eat more now than in historical times. The average calorie intake in the 13th century was up to 5000 calories a day. (Reuter)

    In distinction to the commonly accepted stereotype, research shows that the obese do not eat more than their lean counterparts. In addition, research has failed to demonstrate significant defect in obese subjects' hunger/satiety response to eating compared to that of lean subjects. (Int J of Obesity 1990,14: 219-33)

    There was no significant difference in energy intake at three months of age between babies of fat and thin mothers. The findings can be compared with those in the strains of genetically obese rodents used as models of human obesity, in which the development of fatness precedes any increase of energy intake. "Our findings suggest that the most appropriate approach to preventing obesity in susceptible infants may be to increase their energy expenditure, rather than decrease their energy intake." (NEJM Feb 25 1988)

    "Most people believe that the obese eat much more than other people, that this is the cause of their obesity, and that they could become lean and remain slender by eating "normal" amounts of food. This belief is particularly resistant to change since it was the accepted scientific position for many years and since there is little opportunity for spontaneous revision of generalizations about behaviors that show such great variability. Even if it were possible for the average person to make accurate observations of the habitual intakes of fat and lean acquaintances, and to recall them without distortion, it would be hard to perform the required arithmetic averaging operation in one's mind. Instead, it seems, people recall the behaviors that fit their preconceptions, remembering the large intakes of some obese people, while forgetting the modest intakes of others.

    In fact, the best data available suggest that the obese, as a group, eat no more than the lean." (American J of Clinical Nutrition 33: Feb 1980 p. 465)

    A number of studies compare the ratio of energy intake to some arbitrary measure of body parameters. Not surprisingly, the choice of body parameter to use in this "normalization" controls the outcome of the "study". Some studies use fat free mass (whose definition and measurement is itself controversial) for this normalization, ignoring actual body weight. Such an intellectual maneuver should be reassuring to fat people who have been warned that their fat strains their body. "There should be no doubt that simply walking, climbing stairs, or pumping blood through all of the excess tissue is a form of exercise." (IJO 1989;13;s2 17) A study of energy requirements of dieting men found that replacing lost body weight with equivalent lead weights reduced the fall in energy expenditure by more than 50%. Adipose tissue is more active than either lead weights or many components of FFM, so normalizations based on other than total weight must be regarded with cynicism.

    "Canadian researchers who studied the eating patterns of 80 women between the ages of 30 and 38 found that smaller eaters weighed an average of 10 pounds more than their larger-eating counterparts. ... Small eaters in the study had an average of 22 per cent more body fat than the large eaters." (F1, The Oregonian, 2/14/91)

    "Mean energy intakes were not significantly different between the lean and fat individuals. ... It does not appear that the obesity is caused by overeating." (Journal of the American Dietetic Association, 11/86)

    "Less expected was the raised SDS [obesity] among those consuming recommended caloric intakes. This indicates that obese children have a higher, probably genetically determined, weight level than the non-obese population." (The Lancet, Aug 26 1989)

    "[Professionl] Members of dietetic associations do not appear to differ from the general public with regard to weight control. Knowledge is obviously not enough for the health professional or their clientele." (American Journal of Clinical Nutrition, 6/92)

    "We found no significant relationship between obesity and the items documenting food consumption" (Int J of Obesity 1992, 16, 565-572) "The modest caloric intake of these men and the lack of correlation per cent body fat and total calories suggest that calorie differences are not the major causes of obesity in these men." (American Journal of Clinical Nutrition, 6/86)

    "There was no relationship between energy intake and adiposity" (American Journal of Clinical Nutrition, 9/90)

    "caloric intake per unit of lean body mass was constant regardless of the degree of obesity" (Journal of the American Dietetic Association, 2/92)

    "Comparisons of obese adolescents to normal peers have demonstrated comparable energy intake and nutrient distribution." (Journal of School Health 2/92)

    "No significant G effect was found for daily energy intake, daily intake per kg body weight, and for any of the nutrient intake (g/day)." (Recent Advances in Obesity Research: V 16-25)

    "Rural subjects were leaner, suffered less from diabetes and hypertension, and generally had higher cholesterol levels." (J of the American College of Nutrition, 1992, p 283-)

    "Studies on habitual food intake have failed to observe any consistent differences between obese and lean subjects." (p. 80, Obesity and Leanness - Basic Aspects)

    "Energy intake was inversely related to the 12-yr incidence of myocardial infarction. The correlation was independent of age, obesity, smoking, serum cholesterol, triglycerides, diabetes, systolic blood pressure, and physical activity. No correlation was found between dietary intake and incidence of stroke or overall mortality, nor was any correlation found between end-points and intake of fish, energy percentage from fat, protein, and carbohydrates." (Am J of Clinical Nutrition, Oct 1986)

    "the mean intake by the overweight subjects was less than that of the controls. ... Food intake has declined over the past decade when body weight and presumably fat stores have, on average, increased. From the epidemiologic data, it appears that increased caloric intake in the population can not explain the positive energy balance [obesity] observed in adult life in the United States, the Netherlands, or Sweden. ("Diet and Health: Implications for reducing chronic disease risk"; Committee on Diet and Health Food and Nutrition Board Commission on Life Sciences, National Research Council; National Academy Council, Washington D.C. )

    "the following aspects of weight are myths rather than reality: (a) There are objective definitions of obesity; (b) obesity is prevalent among women; (c) obese people take in more calories than the nonobese; (d) dieting is an effective way to reduce weight; (e) obesity is related to poor physical health." (J of Psychology, Jan 1990)

    "Discrepant findings in the literature concerning relationships between obesity and energy intake may be explained by reporting error and by the relative lean mass of obese vs nonobese women but not by systematic underreporting unique to obese subjects." (Am J of Clinical Nutrition Feb 1989)

    "Body mass index did not correlate with either current energy intake or energy expenditure. Smokers and drinkers had lower age-adjusted levels than non-smokers and abstainers. Since the excess body mass index levels associated with low socioeconomic status in women could not be explained after controlling for adverse health behaviors, further epidemiologic study of risk factors for obesity in Black women is recommended." (American J of Public Health, Jun 1992)

    We believe that eating behavior is more likely a secondary phenomenon, rather than a primary event in its etiology. The growing understanding of cellular physiology and biochemical genetics coupled with the repeated failures of dietary and behavioral forms of treatment speak for obesity being a disease of unknown etiology in which food intake is but link in a complex, causal chain. (Western Journal of Medicine Oct 1990; 153;421-428)

    Various techniques have been used to enforce diets, including appetite reducing drugs and surgical modification of the digestive system (balloons, staples, bypass, etc.). None of these has proven to improve the basic dynamics of the diet. Many have serious side effects beyond that of the diet itself, including immune system problems caused by low cholesterol levels.

    Lean and obese female Zucker rats were intermittently semistarved during their first 32 weeks of life, then fed ad libitum. "long-term caloric restriction during development appears to be effective in suppressing dietary obesity in animals that do not have a genetic predisposition to obesity, it appears not to be effective in animals that have a genetic predisposition to obesity."

    SLOW vs RAPID Weight Loss

    Since the body adapts to low calorie diets (LCD) by minimizing weight loss, very low calorie diets (VLCD) were developed. But even with the most advanced versions of these diets, proteins are not totally spared, particularly during the early weeks of dieting. It appears that a factor enables ground squirrels to lost large amounts of fat without losing lean tissue. (IJP 1994 18, 351-3)

    Controversy abounds about the efficacy of rapid vs slow weight loss. Many studies addressing this issue are flawed by sample selection problems. Slightly overweight subjects on mild diets do not reagain as much weight as massively overweight subjects placed on more stringent diets.

    Results are different when subject selection is randomized. Subjects on 1200 calorie and 800 calorie VLCD type diets had the same ratio of fat loss to lean tissue loss. The major effect of slowing the rate of weight loss was prolongation of the need to diet. Diet induced metabolic slowdown was a direct function of the amount of weight lost and nothing else. (International Journal of Obesity 1989, pp 179-181) Prolonged energy restriction reduces metabolism both by reducing lean tissue and by a reduction in oxygen consumption of the residual active tissue mass. (May METABOLISM 1993 42:5 544-7) Small doses of T3 (thyroid) during weight reduction prevented RMR reduction in obese women (5th European Congress on Obesity 10-12 June 1992)

    It does not appear that fasts are more difficult than moderate diets for many patients; indeed, many report considerably less hunger and a sense of well being. (American J of Clinical Nutrition 33: Feb 1980 p. 468)


    "The third aspect of treatment is maintenance of a stable caloric intake. It would seem that if anything has been clearly established in the research on behavioral treatment of obesity, it is that weight maintenance can be achieved with this therapy. The shortcoming of behavioral programs has been the small losses achieved; the record of maintenance is, by contrast, impressive. ... It should be noted that behavioral programs do not really have to contend with the problem of refeeding since the losses are usually quite small and achieved with minimal restriction." (American J of Clinical Nutrition 33: Feb 1980 p. 469)

    Diet Side Effects

    If you're genetically lean and otherwise healthy and active, there's nothing wrong [with being lean]. If you're lean because you're smoking, drinking or seriously dieting, there are some major problems. (Dr. Calloway, WSJ 10/21/95)

    A common result of reducing diets is weight regain. 95 per cent regain all the lost weight within 5 years.

    Thomas Wadden Ph.D., paid Optifast researcher and Director of the Weight and Eating Disorders Program at the University of Pennsylvania in Philadelphia estimates the long-term success rate for dieters not involved in clinical weight loss programs may be as high as 60 per cent. (Family Circle 6/4/96, 48)

    Robert Jeffrey and colleagues recently tried to study women who had maintained long term weight loss. They studied women from the general population, not limiting their study to participants in weight loss programs. Out of 30000 women studied, only 100 had lost significant weight and kept the weight off. 99.7 per cent did not. At least a third of women have tried to lose weight, so it is appropriate to adjust this 0.3 per cent figure to reflect only those who have tried to lose weight. Unfortunately, adjusting this 0.3 per cent figure still yields a success rate of one per cent (1%) or less. (U.S. News & World Report, 1/8/96)

    To see what dieters must do to keep weight off, Dr. Mary Klem of the University of Pittsburgh and researchers from the University of Colorado started the National Weight Control Registry of long-term weight losers. She reported the results in October 1996 at a meeting of the North American Association for the Study of Obesity. Among this small group of long term dieters, weight loss was maintained only by continued semistarvation. Average daily calories were 1,297 for women and 1,725 for men. This is hardly a normal life; many weight loss diets allow more food.

    A Swiss study compared various diets' effects on weight regain. Low caloric intake induces an adaptive increase in metabolic efficiency. Its persistence after slimming is an important factor in the ease with which the obese condition is regained. After body fat is reduced by feeding a low calorie diet, refeeding a similar caloric intake as weight- matched controls over a 2 week period results in a 15-20% lower energy expenditure, 3-fold increase in the rate of fat deposition, and a doubling of energetic efficiency. Isocaloric diets varying in protein content (8-40%), fat content (5-55%), differing fat types, and carbohydrate types were tested in search of an effective weight maintenance regimen. The elevated energetic efficiency during refeeding was partially reduced by low protein diets. Weight rebound was unaffected by the type of fat or the type of carbohydrate. Provided the diet provided adequate protein and did not exceed 35 per cent fat, no diet, including low fat, had an impact on the post weight loss reduction in energy expenditure that facilitates weight rebound.

    Refeeding was associated with a metabolic adaptation during which all of the fat lost during restricted feeding was subsequently deposited as body fat. Studies in both obese rats and obese humans show that fat superaccumulation with refeeding after energy restriction is a major factor contributing to relapsing obesity so often observed in humans. The liver seems to be particularly prone to reaccumulate fat stores after refeeding. Qualitative indication of super lipid accumulation in the liver after refeeding may be important in rebound obesity in humans after weight loss on VLEDs. (Am J Clin Nutr 1993;57:857-62)

    An Italian study (1P-115) indicates obese subjects with high insulin and triglyceride levels are more resistant to diets.

    Dieting does not reduce the number of fat cells, even in subjects carrying ten times the normal number. In fact dieting can increase the number of fat cells. In a Swiss study of lean and obese rats, reduced energy expenditure (EE) of obese rats with limited caloric intake resulted mostly from metabolic slowdown not related to reduction in lean body mass or activity levels. This metabolic slowdown continued after the obese rats returned to normal caloric intake (eating the same as lean rats) and regained the weight they had lost. (International Journal of Obesity 1991, 15, 7-16) Corticosterone induced inhibition of thermogenesis is suspected.

    Diet induced metabolic slowdown has two aspects: Resting Metabolism Rate (RMR) and Diet Induced Thermogenesis (DIT)/Thermic Effect of Food (TEF).

    The definitions and methodology for measuring and interpreting data on metabolism rates are not standardized, and it is no surprise that studies on diet induced decline in RMR are highly controversial. Furthermore, RMR studies may not distinguish between subjects in the depressed energy balance of weight suppression maintenance and subjects regaining lost weight. Until this these flaws are satisfactorily resolved, studies of RMR must be approached with the greatest of caution.

    A recent paper in the American Journal of Clinical Nutrition concluded that conflicting results that did not detect diet induced drop in RMR might be due to defects in their body composition assessment methods. Some studies that did not report diet induced metabolic slowdown were made on subjects who had already started weight regain, and were thus at a higher RMR than those losing or maintaining weight. "Further studies are required to investigate mechanisms of metabolic adaptation to hypocaloric diets because the phenomenon itself appears to be an established fact." Studies of DIT/TEF consistently report a metabolic slowdown with dieting not accounted for by the loss of muscle tissue.

    Studies that do not report diet induced metabolic slowdown may be measuring the post-diet metabolism while subjects are actively regaining weight. One study that did not make this mistake recorded a 27 per cent drop in weight stable caloric intake from 28.9 to 21.5 kcal/kg per day as the 175-270 pound subjects lost a modest 20 pounds. (Journal of Clinical Endocrinology & Metabolism 1987)

    Past studies that support or deny the existence of an adaptive metabolic component contributing to the low EE (metabolic slowdown) during chronic underfeeding have been inconclusive in experimental designs and data interpretations. The magnitude of the fall in EE during low calorie intake is similar to that recently shown to occur after slimming of grossly obese mice, as well as that reported in post-obese human subjects maintaining body weight on a restricted intake of food. This increase in metabolic efficiency may be important in the rapid relapse of obesity after slimming. (IJO 1993 17, 115-23)

    "Low and very low calorie diets have a common aim: to provoke a negative energy balance in order to diminish energy stored in adipose tissue. The purpose of people using them is less esoteric: to lose weight and to provoke morphological changes with the hope that this in turn will improve their health, their looks, and their sexual status. As a rule, the aim succeeds and the purpose fails. ... Adaptative changes in energy expenditure are the most intriguing feature. ... When the level of T3 is artificially maintained by an adequate addition of T3, the nitrogen balance is not modified and the BMR remains at its baseline level." (IJO 1993 17 (Suppl 1) S13-6)

    "Adaptive changes in metabolic rate in response to low caloric intake relies on complex and highly redundant readjustments of the thermoregulatory system including both behavioral and physiological regulations, and acting on both heat loss and heat production. It contributes to the rapid replenishment of fat stores as soon as an adequate amount becomes available again. It thus has a survival value in subsistence societies societies. In affluent societies it is a source of despair for the obese and of fortune for the authors of slimming programs." (IJO 1993 17 (Suppl 1) S3-S8)

    Dieting enhances or creates a fattening effect of some drugs. Propanolol reduced the metabolic energy expenditure of reduced-obese women but not that of nonobese women. (Am J clin Nutr 1992;56;662)

    The value of the postabsorptive RQ (Respiratory Quotient) may be a predictor of relapse of weight gain. After discontinuation of the low energy diet, an elevated RQ shows that the endogenous lipid oxidation is low, a condition favoring weight gain. This study confirms the great variability in the amount of weight regained after the cessation of a low-energy diet. (Am J Clin Nute 1993;57:35-42)

    Many dieters experience unpleasant side effects. The severity of side effects tends to be less for younger subjects and those whose weight gain was caused by overeating.

  • Risk of cancer from toxic chemicals released from fat cells during weight loss. (Science News Mar 15 1997) (Cancer Reseatch Mar 1 1997)
  • Substantial impairment of cognitive performance, 30 per cent and worse accuracy reduction on a standardized cognitive task. The cognitive impairment was related to the degree of weight loss. Heart rate immediately before and after testing was lowest in the current dieters with high weight loss. Lowered heart rate is typical of a chronic state of undernutrition. (Proceedings of the Nutrition Society 1992: 51, 343-51) One would hope mental performance would recover after weight loss, but this is not guaranteed. A study reported in the May 24 1997 Science news found a worsening of reaction time by dieters that accelerated during weight maintenance.
  • Some have reported experiencing various problems related to their nervous system that resolved with an increase in fat consumption.
  • Aggression and suicide. Lipids account for about half the dry matter of the brain. Monkeys on a low fat diet were significantly more aggressive than were controls on a normal diet. In six RANDOMISED, CONTROLLED primary prevention trials, there was a significant increase in mortality due to suicides or violence. Compared with control groups, the treated groups had 28 fewer deaths from CHD and 29 more deaths from suicide, homicide, and accident. Adolescents are thought to be more susceptible to these effects. Interventions to reduce cholesterol concentrations on a large scale could lead to a population shift to a more violent pattern of behaviour, which would result in more aggression, more abuse of children and partners, and generally more unhappiness. (Lancet 339: March 21 1992, p 727) A number of studies confirming the link between low choesterol and mood changes have been reported in Science News (3/11/95:p.157, 9/21/96:184). Low levels of DHA, a long-chain omega-3 fat, may explain the depressing effects of low-fat diets. (Science News 9-2-1995)
  • Schizophrenia. Depressed levels of certain fatty acids have been observed in patients with schizophrenia. The preliminary evidence for clinically effective dietary manipulation to correct such an abnormality opens up novel and exciting therapeutic possibilities. (Lipids, 1996 Mar, 31 Suppl:, S163-5)
  • Radical low fat diets deplete the body of essential fatty acids, and should not be used during pregnancy or lactation. The same concerns apply to childhood.
  • Cold Intolerance. "Cold intolerance is a significant problem aggravated by dieting in morbid obesity."

    Successive restriction and refeeding resulted in a defect in the utilization of energy intake, facilitating the development of obesity. (American Journal of Clinical Nutrition 1994;59;500-5)

  • Lack of energy. It has been reported that in the case of low carbohydrate diets, this condition resolves in a few weeks after the body adjusts to the diet. Others report increased energy on low carbohydrate diets.
  • Leaky Gut Syndrome may be caused or aggravated by high carbohydrate diets.
  • Low pulse rate and blood pressure. One symptom of low blood pressure from metabolic slowdown is dizziness when abruptly arising from a chair (postural hypotension).

    Normally, low resting pulse rate and blood pressure indicate a healthy body. Dieters and their doctors rejoice when energy deprivation lowers their high blood pressure and heart rate readings. Unfortunately, these lower numbers do not imply better health when lower pulse rate and blood pressure result from diet induced metabolic slowdown and not cardiovascular improvement.

    Lowered heart rate is typical of a chronic state of undernutrition. (Keys et al, The Biology of Human Starvation)

  • Menstrual Difficulties
  • Brusing is sometimes enhanced. It has been corrected with increased vitamin C and bioflavonoid supplements.
  • Leg cramps have been reported. Using potassium salt instead of table salt helps. So do potassium supplements.
  • Yeast Infections (Associated with high CHO diets) Dr. Atkins claims that high carbohydrate diets promote Candida Albicans overgrowth ("yeast infections"), which can interfere with weight management. Lab tests identified this condition in a third of his patients. A low carbohydrate diet often controls yeast infections.
  • Fluid Retention
  • Constipation. Constipation may be helped if you drink a lot more water, take more vitamin C, and add psyllium, flaxseed, or other fiber supplement to your diet.
  • Dry mouth
  • Sleep Disruptions (difficulty falling asleep, excessive sleepiness, disturbed sleep, vivid dreams)
  • Gout A few people report flareups of gout associated with ketosis. Others report alleviation of gout symptoms. 5 mg per day of folic acid twice a day has been reported to control gout.
  • Stomach Distress
  • Hair loss (iron+B-vitamin supplements may help) (Thyroid treatment may help) One correspondent reported hair loss provoked by a fen/phen diet regime was corrected by switching to an Atkins diet.
  • Ridged Nails (low fat diet vitamin or mineral deficiency) Adding fats and oils to the diet has been reported to correct this.
  • Dizzy spells
  • Weakness
  • Headaches (mostly women)
  • Hot flashes The reduction in adipose tissue from dieting may accelerate the drop in estrogen levels. One individual reports DHEA supplements greatly reduced her symptoms.
  • Depression (as measured in standardized tests).
  • Collagen generation as low as 5% of normal. (Collagen is the major protein of all connective tissues, a shortage of which is believed to cause wrinkles, etc. Collagen production is necessary for wound healing and normal growth.) This might explain the degraded appearance seen in some dieters.
  • Memory problems A London conference held by the British Psychological Society heard that people who fight the flab can become forgetful and have difficulty performing simple tasks. Until now scientists had thought only people with anorexia nervosa, the slimmer's disease, suffered mental impairment as a result of chronic undernourishment.
  • Diet induced metabolic changes include an increase in lipoprotein lipase (LPL), an enzyme that stores fat in fat cells by breaking down triglycerides in the blood. (Defects in LPL cause a wasting of fat tissue and high triglycerides.) LPL levels drop during the first few weeks of dieting, a time when when blood lipids often increase. Depending on the study, LPL levels remained normal or depressed for some time. Subjects with BMI < 35 or who lost less than 12% of their initial body weight did not show marked increases in LPL. But in the more obese subjects, LPL rose to 25 times normal, and remained elevated for at least 6 months. The fatter the person was to begin with, the more of the fattening enzyme they produced after weight loss. Kern's paper sheds insight on many issues related to the varied outcomes different people have to dietary weight cycling. (New England Journal of Medicine, Vol. 322 No. 15, Apr 12 1990)

    (See also: Metabolism: Clinical and Experimental, Jul 1987)

    Adipose cells have different receptors for storing and releasing fat. Weight loss diets worsen the ratio of fat cell receptors, promoting weight gain.

    Author's weight history in BMI showing massive weight rebound after a hospital resident doctor supervised weight loss program.

    A common side effect of dieting is the loss of lean tissue. Some lean tissue loss is considered acceptable because the lighter body's muscle needs are less. The low levels of growth hormone characteristic of obese persons impedes the body's regeneration of lean tissue. This may be a factor in the adverse health effects of repeated weight loss. Human Growth Hormone injections increase fat loss and drastically reduce lean tissue loss during dietary restriction. (J of Clinical Endocrinology and Metabolism, 1987, p. 878)

    Lipoprotein lipase (LPL), which increases dramatically during dieting, appears to increase the formation of low density lipoproteins in arterial walls (foam cell formation). LPL may enhance the interaction of plasma low density lipoprotein with arterial chondrotin sulfate protoglycan and dermatan sulfate protoglycan and thus facilitate low density lipoprotein retention in the artery wall. (J of Lipid Res 1993;34:1155-63)

    Dieters need drugs to suppress the excessive amounts of LPL, glucocorticoids, and runaway fat cell proliferation triggered by energy deprivation and dietary weight cycling. The experimental drug LY79771 has reduced post diet weight rebound in rats by about 20 per cent.

    Another side effect of dieting is bloating. A dieter with stomach distress may think she is overeating when in fact she is nearly experiencing slight symptoms of bloating caused by dieting. Bloating is rarely discussed in diet books, but is familiar to doctors working with famine victims. Extreme cases of bloating with distended stomachs are sometimes seen in TV documentaries of famine, the ultimate hypocaloric diet.

    A good guide to diet side effects (with recommendations for some) may be found in Appendix C of "The new, revolutionary Underburner's Diet, How to Rid Your Body of Excess Fat Forever" by Barbara Edelstein M.D. (c. 1987)

    A study in the November 1994 issue of the Journal of Abnormal Psychology shows a direct link between media exposure and eating disorders such as bulimia and anorexia nervosa.

    An important side effect of caloric restriction is the binging rebound. Diet evangelists talk of food as a substitute for love and other putative psychological upsets being a cause of binging. More commonly binging is a natural biological response to starving. It rarely appears in non dieting individuals.

    Binging is part of the body's set point servo system response to energy shortfall. Animal and human deprivation studies consistently demonstrate a period of markedly increased caloric input that tapers off as the body recovers from starvation. In one study of binging, the frequency of binges and the number of calories eaten approximated the diet's caloric deprivation, resulting in a near normal overall energy balance. Diet induced binging may be important in the onset of adipocyte hyperplasia associated with dietary weight cycling.

    Traditional wisdom on weight regulation holds that overeating and binging lead to obesity. In fact the reverse relationship exists, with dieting causing eating disorders. "dieting, rather than binging, is the disorder professionals should be attempting to cure." (Journal of School Health, Aug 1989)

    A definitive study on the subject appeared in the International Journal of Obesity. Binge eating almost disappeared after weight normalization by biliopancreatic diversion surgery. If binge eating were a mental problem, the surgically induced weight loss would not effect the binge eating. In most cases binge eating is not related to to neurotic personality, psychological distress, low self esteem or emotional instability. Rather, the dissatisfaction with one's shape and the continuous attempts to lose weight by chronic and strict dieting are the main factors compelling patients to binge. (IJO (1996) 20, 793-4)

    Eat More to Lose Fat

    Individuals unable to build muscle or lose fat on an aggressive diet/exercise regimen have reported success when they increase their energy intake. The number of such anecdotal reports reports suggests that a metabolic starvation protection mechanism was interfering with the weight loss one would normally expect from energy restriction. It may be relevant that studies of pre-obese children indicate lower energy intake (they eat less) than lean counterparts. It has also been reported that some women cannot reduce their "love handles" except when lactating.

    Weight Cycling

    For almost all dieters, starvation is not a normal state, and, unfortunately, neither is the associated weight loss. Many repeatedly attempt to shed their unwanted poundage.

    Many overweight people complain that dieting cycles cause net weight gain. They report excessive but relatively stable weight, except during dieting and subsequent weight regain "with interest".

    On the surface, animal studies of dietary weight cycling are contradictory, but there does seem to be a unifying concept: dietary perturbations increase the body's resistance to future perturbations in the same direction.

    When obesity is forced by overeating, cycles of weight fluctuation do not increase fatness. When rats are dieted below their set point, weight cycled rats regained weight more rapidly, regained more weight, but ate no more food than non cycled rats. (Int J of Obes; V12; N6)

    In humans, weight rebound induced by dietary weight cycling is clinically used to add fat to underweight patients who cannot to gain weight by overeating.

    Successive restriction and refeeding resulted in a defect in the utilization of energy intake, facilitating the development of obesity. (American Journal of Clinical Nutrition 1994;59;500-5)

    In "Variability of Body Weight and Health Outcomes in the Framingham Population", subjects with larger weight fluctuations had markedly higher BMIs and, what's worse, a higher slope of BMI increase over time (BMI/year). (N Engl J Med 1991; 324; 1839-44) A study of workers at Western Electric's Hawthorne Works in Chicago also reported higher BMI in weight cycling men. (Hamm et al. Large fluctuations in body weight during young adulthood and 25-yr risk of coronary death in men. American Journal of Epidemiology 1989, 129:312-318)

    In a 1986 Dutch study, men who experienced many life events in a short period showed a gain in body mass. A year later this weight gain had disappeared in almost all subgroups of these men. The exception was the subgroup that tried to lose weight by dieting; those who dieted had gained more weight. (International Journal of Obesity (1988), 12, 29- )

    "We have compared the body composition of obese women who only once lost no more than 10 kg, with a similar group of women who have had two or more cycles of weight loss and regain of more than 10kg. All weight losses were obtained on energy restriction by conventional diets. This retrospective study clearly demonstrates that the `dieters' had significantly lower lean body mass and more fat per kg body weight than non-dieters." (International Journal of Obesity (1989) 13 (suppl.2), 27-31)

    In a landmark study of the dieting loss-regain cycle, Drenick et al (1964; JAMA 187:100-105) and Johnson and Drenick (1977; Arch Intern Med 137:1381-1382) placed subjects on fasts. As with other types of diets, subjects with childhood onset obesity had the most trouble (poor weight loss, side effects) with the fast. At the conclusion of the fast, most of these patients maintained their weight loss for about a year. Half the subjects regained all their weight within two or three years, and almost all had regained their weight by 9 years. Patients with adult-onset and childhood-onset obesity gained weight at the same rate. Regain beyond original admission weight (weight rebound) was more common among the childhood-onset obese (42%) than adult-onset obese (26%). Eighty per cent developed diabetes; half of these cases were severe.

    Patients at a weight loss clinic lost 2.1 pounds a week on the second bout of dieting compared to 3.1 pounds per week the first time. This pattern also held true for a group of hospital inpatients whose food intake was carefully controlled.

    Obese rats took 21 days to lose their excess weight during their first cycle of food restriction, but took 46 days on the second cycle. The cycled animals showed significant increases in food efficiency (weight gain/calorie) in the second cycle. (Physiol Behav 1986;38;459-64)

    Bulemic patients with an average weight cycling of 17 kg had significantly lower metabolism than age, height, and weight matched controls. (Arch Gen Psychiatry 1990 47:144-8)

    An increase in the sensation of hunger and overeating after a period of chronic energy deprivation can be part of an autoregulatory phenomenon attempting to restore body weight. To gain insights into the role of fat and lean tissue depletion as determinants of such a hyperphagic response in humans, we reanalyzed the individual data on food intake and body composition available for the 12 starved and refed men in the classical Minnesota Experiment after a shift from a 12-wk period of restricted refeeding to an ad libitum refeeding period of 8 wk. For each individual, the following were determined: 1) the total hyperphagic response during the ad libitum refeeding period, calculated as the energy intake in excess of that during the prestarvation (control) period; 2) the degree of fat recovery and that of fat-free-mass (FFM) recovery before ad libitum refeeding, calculated as the deviation in fat and FFM from their respective prestarvation values (ie, the amount of fat or FFM before ad libitum refeeding as a percentage of fat or FFM during the control period); and 3) the deficit in energy intake before ad libitum refeeding, calculated as the difference between the energy intake during the period of restricted refeeding and that during the control period. The results indicate that 1) the total hyperphagic response is inversely correlated with the degree of fat recovery (r = -0.6) as well as with that of FFM recovery (r = -0.5), 2) the correlation between hyperphagia and FFM recovery persists after adjustment for fat recovery, and 3) the correlations between hyperphagia and fat recovery or FFM recovery persist after adjustment for the variance in the energy deficit during the preceding period of restricted refeeding. Taken together, these results in humans suggest that poststarvation hyperphagia is determined to a large extent by autoregulatory feedback mechanisms from both fat and lean tissues. These findings, which have implications for both the treatment of obesity and for nutritional rehabilitation after malnutrition and cachexia, have been integrated into a compartmental model of autoregulation of body composition, and can be used to explain the phenomenon of poststarvation overshoot in body fat. Am J Clin Nutr 1997;65:717-23.
    Abdul G Dulloo, Jean Jacquet, and Lucien Girardier
    Department of Physiology and Computer Unit
    Faculty of Medicine University of Geneva, Geneva, Switzerland

    Address reprint requests and correspondence to

    Diet evangelists cite a number of studies which found no serious bad effects from weight cycling. In one, a short term study of U.S. high school wrestlers who diet to "make weight" for matches reported that weight and metabolism returned to normal after the wrestling season. No long term followup was performed on these athletic mesomorphs who only lost a small amount of weight for very short periods. These elite athletes never met several of the conditions that trigger lipoprotein lipase (LPL, the "fattening hormone") overproduction in real world dieters. Subsequent studies have not noted impaired metabolism in the wrestlers who "dieted" to make weight. An incidental, but critical, finding of one investigation, was that in the minds of these athletes dehydration and dieting were synonymous. Their use of the word "diet" is in association with weight loss, not food restriction. Their "diets" lasted but two days, and only a few restricted food intake during this period. (Medicine and Science in Sports and Exercise, 1992; 1270-5)

    Diet evangelists are quick to assert that since the diets they recommend differ in one detail or another from the fasts used by Drenick et al, their diets will not provoke the same horrific long term results. There are few controlled studies comparing the safety and effectiveness of different types of diets, but those that have been made found no advantage to slowing the rate of weight loss.

    Experiments show that fat cells taken from massively obese subjects have much greater mitogenic (spontaneous cell replication) activity than cells taken from lean subjects. "When mature fat cells from massively obese persons give up their fat and revert in culture to forms similar to preadipocytes, they replicate significantly more rapidly than analogous cells from the lean. The reverted cells, therefore, retain the 'memory of their roots', indicating an inherent property of these cells." Prolonged nutrient energy restriction would lead to reversion of mature fat cells. This process would be increased by regular exercise. When the subject stops starving, the inherited program for excessive replication and differentiation creates even more fat cells. Thus, each diet cycle would lead to an even greater number of mature (large) fat cells, resulting in stepwise progression of massive obesity. (International Journal of Obesity, 1990, 14, 187-192)

    Mature (full) fat cells cannot replicate, but Sugihara has suggested that mature fat cells that have released their triglycerol as a result of dieting regain cell division ability. (Journal of Lipid Research 28, 1038-1045)

    The data of Bjorntorp and Sjostrom (METABOLISM V20;7;703) show a greater than 10 per cent increase in fat cell numbers from a single diet/partial regain cycle in some subjects with many fat cells. Fat cell numbers increased both during dieting (5%) and again during regain (5%). Subjects with fewer fat cells (normal range) did not experience this increase in fat cell numbers. The normal range is marked by the crosses at the lower left of the chart above.

    A paper appearing in The American Journal of Clinical Nutrition found "all three measures [of weight cycling] were significantly related to BMI (P < 0.01)." (Am J Clin Nutr 1992;55;641-4)

    In "Weight cycling: the experience of human dieters", Blackburn et al found a metabolic effect of dietary weight cycling, with slower rates of weight loss on a second diet. The Wadden/Optifast study on dietary weight cycling found a statistically significant correlation between dieting history and weight, BMI, fat mass, waist size, and hip size. The Wadden/Optifast study attempted to refute the Blackburn study by reporting that high diet cyclers lost weight as rapidly as low cyclers. Unfortunately, the high cyclers had three times the excess fat of low cyclers. Normally weight loss on a diet is strongly correlated with initial fatness, but Wadden's high cyclers, with three times the excess weight, only lost the same as the much thinner low cyclers. With half of their excess fat still remaining, Wadden's high cyclers reached a plateau and stopped losing weight on a 1000 calorie diet. (Am J Clin Nutr 1992;56;203S-8S)

    The Framingham study also found weight cyclers to be much fatter.

    To add injury to insult, dietary weight cycling may be bad for one's health. Weight cycling by dietary means may have a role in the development of chronic disease.

    A study by Jeffrey, Wing, and French published in the American Journal of Clinical Nutrition "adjusted" (fudged) the health risk data to "account" for the increased fatness of the diet cyclers. This inappropriate data adjustment (IDA) is barely mentioned and never justified in the paper. This adjustment is unwarranted in light of the observation that "without effort to diet, weight changes tend to be small over long periods of time" (Western Journal of Medicine Oct 1990; 153;421) Adjusting for current weight begs the question that dietary weight cycling increases obesity. Applicants experiencing negative health outcomes associated with weight cycling were excluded from the study. As an alternative to such exercises in manipulation, adjusting for weight history before the subjects' first diet would be credible.

    This and other studies that "adjusted" for weight gain did not report adverse results of weight cycling besides those commonly attributed to the excess weight from weight cycling. These negative studies are discussed in "Variability of Body Weight and Health Outcomes in the Framingham Population" by Lissner et al. With a cohort of 5127 and more detailed medical records, the Lissner study of the Framingham population supersedes the earlier, smaller, and more idiosyncratic studies.

    A newer study reported weight loss in 1963-1968 coincided with an increased incidence of coronary heart disease and diabetes mellitus and a declining level of serum total cholesterol. (American Journal of Epidemiology. 148(6):546-55, 1998 Sep 15.)

    With billions of dollars in diet sales and product liability litigation at stake, diet evangelists have bitterly attacked these studies. Diet evangelists insist that unknown factors other than dieting may have been responsible for these weight fluctuations. They have yet to suggest any credible alternative explanations for these weight cycles. Studies have shown that spontaneous weight loss is rare, occurring mainly from gastrointestinal disease or from very advanced cancer. (Ann Int. Med. , 198?)

    A careful reading of these papers will, however, reveal that these concerns were carefully considered and resolved during the study. This author raised this question with one of the Framingham study investigators in July 1992. He was confident that any cause of weight cycling other than yo-yo dieting widespread enough to affect the Framingham data would have been common knowledge to the doctors of Framingham, who would have diagnosed and treated any such conditions.

    ``A big surprise at the NIH meeting was a collection of of epidemiologic studies contradicting the conventional wisdom that extra fat shortens lives. David F. Williamson, Ph.D., an epidemiologist in the division of nutrition of the Centers for Disease Control, Atlanta, said that what "made people sit up and take notice" were 15 studies observing trends among several hundreds of thousands of people, all pointing to the possibility that dieting -- not being fat -- may increase a person's relative mortality risk about 1.5 to 2.5 times. "I was surprised by the consistency of the data," Dr. Williamson said. Another issue that "struck a number of us" was the strong relationship between weight loss and cardiovascular mortality, he said.'' (Medical World News, May 1992)

    Platelet volume is thought to be an independent risk factor for cardiovascular disease. Platelet volume significantly increased during an 8 week weight loss programme using nutrition protocols and weekly control visits. (5th European Congress on Obesity 10-12 June 1992) "This might result in an increased risk of thrombo-embolic ischaemic events in atherosclerotic patients. (IJO (1994) 18, 355-6) The heart is not spared from the catabolic effects of undernutrition, but is subject to the same degree of weight loss as skeletal muscle. Current data suggest the duration and level of caloric restriction are the main risk factors for fatal arrhythmic events. A very low calorie diet probably should not be combined with strenuous exercise, or other situations of high sympathetic drive. (Internation Journal of Obesity (1992) 16, 481)

    Obese weight cycling women develop left ventricular hypertrophy (LVH) more than obese non cyclers. LVH is a major predictor of cardiovascular morbidity. (5th European Congress on Obesity 10-12 June 1992) The same has been found in obese rats that weight cycled. (Hypertension 24:699-705, 1994).

    The mechanisms by which dietary weight cycling leads to negative health outcomes have not been intensively researched, but some have been implicated:

  • Diet induced hypercholesterolemia (American J Clin Nut 1991;53;1404-10)
  • Diet induced depletion of Omega-3 reserves, believed to protect against colon cancer, heart attack, etc.. (Phinney, Am J Clin Nut 1992;56;781-2)
  • Diet induced replacement of linoleic and alpha- linolenic acids with saturates and monounsaturates. (Zhen-yu Chen, Stephen C Cunnane, Dept. of Nut Sci, U of Toronto)
  • Decrease in HDL ("good") cholesterol
  • Loss of heart tissue
  • Loss of bone mass (USDA Grand Forks Human Nutrition Research Center)
  • Increase in fat cell numbers (Bjorntorp and Sjostrom METABOLISM V20;7;703)
  • Changes in fat cell receptors
  • Another ominous outcome is that the weight that is regained is more likely to be in the upper body than the lower, and for men at least, that type of weight distribution has been linked to an increased risk of heart disease. (University of California Berkeley Wellness Letter, 5;4)
  • Some studies on human weight cycling are tabulated below.

    Human Studies on Weight Cycling

    StudySubjects Sample Results WC>BMI Health Outcome
    (Dale)20 fSKEWEDIDAmatched(Short term study)
    Optifast50 fselectedIDAyesunknown
    TRIM88SKEWEDIDAyes(Short term study)
    Jequierf--yesSlowed Metabolism
    Baltimore846 mvolun.IDA?Glucose Intolerance
    WECO2107 malltrueyes?CHD
    Gothenburg2317randomtruen/aCHD, diabetes
    Lee (Harvard)11703 malumnitruen/aCHD, all
    Blair/MRFIT12866 mFEDERALn/an/aCHD
    Helsinki15830Finnishtruen/aCHD, all

    WC>BMI: Weight Cycling linked to increased fatness (BMI)

    IDA: Inappropriate Data Adjustment (see Improper use of Ratios to Adjust Data)

    A sample was judged SKEWED if subjects were selectively excluded from the cohort because they developed diabetes, CHD, morbid BMI, or other negative health outcomes linked to weight cycling after the commencement of weight cycling. Results were judged IDA if BMI was factored out, begging the question that dietary weight cycling may damage health because of the increase in obesity from weight cycling.

    A survey paper on weight cycling by the National Task Force on the Prevention and Treatment of Obesity has attracted considerable media attention. (JAMA 272:15 1196-1202) This report cited a number of studies on various types of weight cycling, including wrestlers who "make weight" by dehydrating without dieting. This group of nutritionists revaluated published studies on human weight cycling according to their own beliefs and decided dietary weight cycling had no adverse effect on metabolism. Centeral to their analysis is their belief that weight cycling does not cause weight gain. Statements such as "BMI, which is known to to be correlated with waist-to-hip ratio, was not adequately controlled for" (p. 1199) are based on the assumption diets never exacerbate obesity, a claim that is controversial at best. Such a belief is understandable in a group of nutritionists with long standing financial and professional commitments to energy restriction weight loss schemes. When all you have is a hammer, every problem starts to look like a nail; if you are a sincere craftsman you will not appreciate criticism of your stock in trade. Obesity researchers who have published papers detailing negative effects of dieting or calling for alternative therapies were excluded from this group.

    In writing its paper, the task force ignored studies showing bad effects from weight cycling, even one they cited in their bibliography (Lee et al). A study by Jeffrey, Wing (one of the task force members), and French reported all three weight-cycling measures were significantly related to BMI (P < 0.01), but this finding was not listed in the "Increased total body fat" entry in the Task Force report.

    The nutritionists' quasi-religious belief that dieting does not exacerbate obesity affected the writing of this paper. A paper by Rebuffe-Scrive et al (IJO 1004:18,655) was reported to have found no increased fasting plasma insulin, fasting glucose, or impaired glucose tolerance; in actuality, the paper showed marked increases in plasma glucose and insulin levels in response to an oral glucose load, an ominous portent to the induced diabetes reported in other dieting followup studies.

    Had the task force included other obesity researchers their conclusion might well have been different.

    A recent survey of European obesity experts showed they consider repeated dieting a greater causative factor for obesity than lack of will-power, physical inactivity, or depression leading to overeating.

    Weight cycling enhances weight gain in later life. The effects of repeated cycles of weight loss and regain on long-term weight development were studied in a national cohort of 1722 former elite male athletes, including 273 men engaged in power sports (weight cyclers) and 651 control men. The controls were age-matched fit conscripts from the time period of the athletes' active sporting carrers. The mean BMI at age 20 was identical for both groups of athletes and the control men.

    By 1985, the mean weight gain of the weight cyclers exceeded that of of the other athletes and that of controls. The prevalence of obesity (BMI > 30) among the weight cyclers was three times that among the other athletes and twice that among controls. The enhanced weight gain of the weight cyclers could not be explained by present habits. The results indicate weight loss and regain predispose to subsequent weight gain and obesity. (Rissanan, Kaprio, Sarna, Koshenvuo, Dept of Public Health, Univ of Helsinki, 5th European Congress on Obesity 10-12 June 1992)

    Dieting in childhood may not be any safer. The often reported impressive gains in body fat during recovery from malnutrition may result from enhancement in the efficiency of food utilization and a shift in energy partitioning in favor of fat storage. Children recovering from protein- energy malnutrition were fatter than well nourished children of the same age. (American Journal of Clinical Nutrition 1993:58:614-21)

    By considering the studies by Drenick et al, Lissner et al, and Bjorntorp and Sjostrom, it appears that obese (BMI > 35) individuals with childhood onset obesity (BMI > 20 at age 5) who lose 12% or more of their weight are at the greatest risk of gaining back more than they lose, with the attendant bad health effects. The risk is a serious one, a slope of .5 to .9 BMI/year weight gain (higher in some) compared to 0.25 for normal adults.

    A recent survey of European obesity experts showed they consider repeated dieting a greater causative factor for obesity than lack of will-power, physical inactivity, or depression leading to overeating. Most studies that did not report adverse effects from weight cycling have been flawed because they removed the effect of weight gain caused by weight cycling. To correct this flaw, studies must match dieters and non dieters according to their physical characteristics and history *BEFORE* their first diet.

    Weight loss studies should report the number and size of adipose cells before slimming, after slimming, and after weight regain stabilizes.

    Artificial Sweeteners

    There has been considerable media coverage of claims that artificial sweeteners hamper weight loss efforts. These appear to result from an American Cancer Society study that found a correlation between overweight and the use of artificial sweeteners. This correlation might better be explained by noting that people without weight problems generally avoid artificially sweetened products on account of cancer concerns, and unfamiliar taste. Some complain that artificially sweetened beverages don't give them their "sugar high". There is no "Diet Jolt Cola". It is likely that thin people read labels on artificially sweetened products warning that such products be used only by those desiring to reduce their caloric intake.

    A University of Toronto study on the effects of Aspartame sweetened diet soda on randomly assigned subjects found no effect on food selection at a meal 60 minutes afterwards. Subjects who consumed a half liter of a diet drink experienced reduced hunger for about 45 minutes.

    A New England Deaconess Hospital (1F-16) study found that aspartame facilitated greater weight loss among obese women on a multidisciplinary balanced deficit diet.

    A Harvard Medical School study indicated Aspartame facilitated long term weight maintenance in a multidisciplinary weight loss program. Among individuals consuming aspartame during a 19-week weight loss program, consuming more aspartame was associated with a greater weight loss. At weeks 71 and 156 of follow-up, aspartame was associated with better long term weight control.

    Concerns have been raised that ingestion of non-caloric beverages might trigger a hormonal response driven by a Pavlov response to the sweet taste. However, 12 subjects drinking 300 ml of diet Kool-Aid exhibited only a very small insulin response consistent with the residual carbohydrate content of the drink. (An J of Clin Nutr 1990;52:335-41)

    There was no evidence that aspartame promotes hunger or results in increased energy intakes in obese or in lean women. (IJO 1994 18, 570-578)

    A paper in a 2011 edition of The American Journal of Clinical Nutrition found that the observed correlation between obesity, diabetes and diet soda use was entirely the result of the dieters' health. In other words, adiposity and diabetes prompts people to switch to non caloric sweeteners, not the other way around.

    A number of anecdotal reports have appeared claiming that Nutrasweet consumption interferes with weight loss. Diet beverages are a major vehicle for Nutrasweet consumption. Almost all diet sodas contain citric acid which has been shown to interfere with ketosis.

    The sweet taste of nonnutritive sweeteners has been reported to increase hunger and food intake through the mechanism of cephalic-phase insulin release (CPIR). We investigated the effect of oral sensation of sweetness on CPIR and other indexes associated with glucose metabolism using nutritive and nonnutritive sweetened tablets as stimuli. Spontaneous oscillations in glucose, insulin, and glucagon concentrations were assessed as were increments (slopes) of fatty acid concentrations during the baseline period. The nature of the baseline (oscillations: glucose, insulin, and glucagon; and slopes: fatty acids) was taken into account in the analyses of postexposure events. No CPIR and no significant effect on plasma glucagon or fatty acid concentrations were observed after the three stimuli. However, there was a significant decrease in plasma glucose and insulin after all three stimuli. Only the consumption of the sucrose tablet was followed by a postabsorptive increase in plasma glucose and insulin concentrations starting 17 and 19 min, respectively, after the beginning of sucking. This study suggested that oral stimulation provided by sweet nonflavored tablets is not sufficient for inducing CPIR. Am J Clin Nutr 1997;65:737-43. The spontaneous oscillations noted above may explain the positive results reported by certain previous studies.

    A recent double-blind crossover study has suggested a portion of the population are slightly more likely to get headaches if consuming aspartame, but one subgroup of the experimental cohort reported fewer headaches when consuming aspartame. Another study raises the possibility that subjects with a history of clinical depression may react negatively to aspartame. Some assert that a litany of symptoms are associated with aspartame use. Since most of these symptoms have been associated with dieting, it is difficult to assign causality.

    Concerns have been raised about possible carcinogenic effects of Aspartame. One study reported a rise of 48 to 53 malignant brain tumors per million from 1984 to 1992. The Mayo Clinic notes that the incidence of brain tumors has been rising since the 1970's, long before aspartame was approved. A causal relationship has not been established. (Mayo Clinic Health Letter 3/97)

    While this author is not convinced that aspartame poses a risk to many, he does think the FDA should, with due diligence, approve alternatives to aspartame, performing any necessary research itself in the case of commodity materials for which a corporate sponsor is unavailable.

    Large numbers of dieters have reported difficulties in sustaining urinary ketones after consumption of dietetic beverages, such as diet cola, or slices of lemon in water. These difficulties disappear when when beverage intake becomes restricted to black coffee, black tea, or water. Although present only in small amounts, citric acid might be the offending substance because of the known ability of citrate to control carbohydrate metabolism at the subcellular level. Single-blind trials of citric acid added to drinking water indicated many were particularly sensitive to the citrate. (Am J of Clin Nutr 1992;56:217S-23S) 40-50% of people on ketogenic diets are sensitive to citric acid; they cannot tolerate the diet under these conditions. If difficulties arise, the only solution is to avoid fruits and beverages which contain citric acid, including most popular diet beverages. No test exists for this sensitivity. (Private conversation, 1992)

    High Fiber Diet

    High fiber diets have been proposed for weight loss from time to time. According to Consumers Reports, increasing fiber in one's diet does not induce long term weight loss.

    In 1990 the FDA proposed to ban guar gum in nonprescription diet drug products, citing safety problems.

    Not all fibers are equal. Most fiber types, including the fiber in oatmeal, do not have the metabolic effects of guar gum fiber.

    An increase in dietary fiber has been widely recommended for improving glucose homeostatsis, yet the amount of fiber is usually so high as to preclude the incorporation of such amounts into a palatable and acceptable diet. Many studies of dietary fiber are not well controlled; weight loss results from the gastric distress many people experience when switching to high fiber diets. One well controlled study assessed changes in dietary fiber while controlling for the intake of other macronutrients, and found no effect on plasma glucose or insulin. (Am J Clin Nutr 1995;62:426- 33)

    Low Fat Diets

    High carbohydrate low fat diets have been recommended since 1550 B.C. (Before Christ!). Low fat diets have been extensively studied for the last 5 decades.

    Concerns about cholesterol levels have prompted nutritional authorities to favor high carbohydrate low fat diets. The experiments that prompted these recommendations were often unrepresentative of normal human conditions; this fear of dietary fat may be oversimplistic.

    "studies suggest that it is the nature of the fatty acids rather than the amount of fat in the diet which is important" (Proceedings of the Nutrition Society 1992: 51, 397-408)

    NEW YORK Feb 11 2004 (Reuters Health) a moderate-fat diet tn low-fat hat contains plenty of healthy, plant-based fats may be a better choice for boosting cardiovascular health while shedding pounds, new research suggests. In a new study, people on low-fat and moderate-fat diets both lost weight, but those on the moderate-fat diet experienced a greater reduction in cardiovascular risk. "A heart-healthy weight-loss diet should include monounsaturated fats like those found in nuts, seeds, peanut and olive oils," lead author Dr. Christine L. Pelkman of the State University of New York at Buffalo told Reuters Health." Both the low- and moderate-fat diets led to weight loss, but the moderate-fat diet had a more positive influence on markers of cardiovascular health, the researchers report in the American Journal of Clinical Nutrition. Even though both groups of dieters experienced a drop in LDL, or "bad," cholesterol, the low-fat group also experienced a drop in levels of HDL, or "good," cholesterol after losing weight. HDL levels did not return to normal even after the 4-week weight-maintenance program. In contrast, HDL levels remained steady in people who consumed a moderate-fat diet. They also experienced other improvements in cardiovascular health, including a decrease in triacylglycerol, a fatty substance linked to heart disease.

    Beef fat, not beef itself, is associated with elevations in cholesterol concentrations. Lean beef can be included in cholesterol-lowering diets provided it is free of all visible fat. (Journal of the American College of Nutrition 1993 12: 1: 86-9) Stearic (beef) acid and saturated fats with fewer than 12 carbon atoms did not raise cholesterol. (METABOLISM 1965;14;776-86)

    A reduction in saturated fat, not total fat, is required to reduce serum total cholesterol and LDL-C levels. Provided that the total diet is low in saturated fat, these serum lipid responses can be achieved even when the diet is rich in fat-trimmed lean beef. (Journal of the American Dietetic Assn 1993;93:6 644-8)

    The negligible long term success rate of semistarvation diets has sparked interest in the weight loss possibilities of low fat diets.

    This interest springs from a number of observations.

  • Some ultra high fat (>>40% fat) diets cause weight gain in research rats. Low fat evangelists fail to note that high carbohydrate diets have proven even more fattening to these research rats. In addition, not all rats gain weight on the high fat diet, and most rats revert to normal weight when their diet is normalized. All of the high fat rat diets seen in the literature involve a profound increase in total energy intake, contrary to most obese humans who have normal or depressed energy intake.

    Replacing mother's milk (8% of calories from carbohydrates) with a milk-substitute formula (56% of calories from carbohydrates) grew fatter rats. (See "The Role of Baby's Diet", below.)

  • Decreased carbohydrate oxidation and increased lipid oxidation appears to have a primary role among the metabolic changes associated with the onset of obesity. (DIABETES, Vol 42, Jul 1993, 1010-6)

  • Obese subjects often exhibit a greater carving for fat than lean individuals. Fat craving is a common after effect of energy deprivation. Following food restriction, corpulent female rats had galanin (a substance that increases fat appetite) levels 40-50% higher than lean females or freely-fed corpulent females. Since most fat people have been on numerous diets, fat craving may be the result of the dietary restriction, not the initial fat inducing condition. (Diabetes Research 1990 15,1-7)

    Increased lipid oxidation is one of the earlier dysfunctions in recent onset obesity. Lipid oxidation may induce a progressive decrease of glucose oxidation, insulin resistance, and increased fasting insulin secretion. (DIABETES 42:1010-16, 1993)

    Studies show fat children obtain a slightly greater proportion of their energy input from fat than thin children do. This slight increase is overshadowed by their lower total energy intake. Pre-obese children consume less energy (50 calories/day average) than their lean counterparts.

  • Some studies suggest energy from fat additions to an otherwise neutral energy balance cause a weight increase short term, which may be more pronounced in the obese. This effect has not been demonstrated outside the context of induced overfeeding. In "Oxidative and nonoxidative macronutrient disposal in lean and obese men after mixed meals" (Am J of Clin Nut, 1992;55;630-6), Owen et al report "Significantly, there was no tendency for the obese men to have the defect in suppression of fat oxidation after mixed meals that had been reported by others".

    Use of a fat substitute at 10% of energy from dietary fat did not significantly reduce 24-h energy intake. (Am J or Clin Nutr 1993;58:326-3)

  • Low fat diets come in two types, semistarvation and ad libitum. Liquid Protein and VLCD diets are low fat; the Cambridge Food For Life Ultimate Weight Loss Formula provides 6% energy from fat (3% by weight). It has been argued that the infamous Dr. Atkins Diet is sometimes a low fat diet because some people do not like fatty foods that are not also high in carbohydrates. In fact, Dr. Atkins' 1992 book includes a low fat version of his low carbohydrate diet for those patients whose blood lipids do not respond favorably to his standard low carbohydrate diet.

    There is no epidemologic evidence indicating that total fat intake per se, independent of total caloric intake, is associated with increased adiposity in the population. Obesity itself has not been found to be associated with dietary fat in either inter- or intra- population studies. ("Diet and Health: Implications for reducing chronic disease risk"; Committee on Diet and Health Food and Nutrition Board Commission on Life Sciences, National Research Council; National Academy Council, Washington D.C. )

    "using a whole body calorimiter, we found no evidence of a decrease in 24-h energy expenditure on a high-fat diet compared with a high-carbohydrate diet." (American J of Physiology Feb 1990)

    A Rockefeller University study found no significant variation in energy need as a function of percentage of fat intake (0 to 70%), Confirming the results of a landmark 1930 study, a Rockefeller University study found no significant variation in energy need as a function of percentage of fat intake (0 to 70%). (American Journal of Clinical Nutrition 1992;55;350-5) The 1930 study found that the long-term effect on body weight of any diet is related only to the total energy content of the diet. Other features of the diet such as carbohydrate or fat content did not, in the long run, have consequential effects on body weight.

    "There is some problem in reconciling the short-term studies showing an association between high-fat diets and obesity with longer-term trials where there is no really strong evidence that high-fat diets do cause massive weight gain. There is the National Diet Heart Study in the United States, which lasted one year, and had men on diets varying in fat content from 40% to 20% of energy. The differences in body weight gain between these men were really very small" "Whatever happens to fat in terms of its being deposited preferentially on short-term overfeeding, there seems to be no difference between carbohydrate and fat supplements in terms of energy balance when you look over a period of 50 to 80 days." "If [dietary] fat is a promoter of weight gain and obesity, it is more likely to be through its effects on the hedonic characteristics of the food source [which would raise total caloric input] than because of any mysterious effect on intermediary metabolism" (Discussion, Nutrition Reviews, Vol. 50, No. 4)

    "Whether changing from a high-fat diet to an isoenergetic, low-fat, high-complex-carbohydrate diet results in thermogenic benefits is controversial. Brief dietary interventions and failure to account for the potential influence of body-fat distribution on energy metabolism could have confounded the interpretation of previous studies. ... No change in body composition, resting energy expenditure, overnight energy expenditure, or meal fat oxidation occurred. We conclude that isoenergetic shifts from dietary fat to dietary carbohydrate within the generally recommended range have little effect on energy metabolism" (Americal Journal of Clinical Nutrition 1994;60:470-5)

    "A diet of 20 to 25 per cent calories from fat has little effect on weight. The body has an amazing capacity to pick up carbohydrate calories if fat calories are lost." (Walter Willett, Chairman, Harvard University Nutrition Dept., Health, 5/94)

    "Comparisons of obese adolescents to normal peers have demonstrated comparable energy intake and nutrient distribution." (Journal of School Health 2/92)

    The anorectic effects of serotonin reuptake inhibitors and 5-hydroxtrytophan, potent weight control drugs, are evidenced by decreased carbohydrate intake, not decreased fat or protein intake.

    The Cornell Low Fat Study

    A Cornell University study "Weight loss on a low fat diet" has been widely quoted by low fat diet evangelists. This study is interesting primarily for what the mass media never reported about its methods and results.

    The Cornell study located 25 non-smoking women of greater than ideal weight who were not cognitively restricting their food intake to achieve weight control. "Unrestrained eaters were desired as subjects." Since virtually all overweight women desperately try to reduce their weight, this study's sample is hardly representative of real world overweight women. Of the 25 subjects that passed the initial screening, 9 were excluded from the study for unstated reasons, and another 3 dropped out during the low fat phase of the study, leaving only 13 subjects. Why all the fuss about sample selection? The researchers undoubtedly wanted to use subjects who were not truly obese (they don't respond to food the same as normalweights do). Neither did the researches wish to risk using women whose metabolisms had been depressed by previous diets.

    Subjects were randomly assigned to ad libitum diets with low fat (20% calories from fat) or high fat (40% calories from fat) foods. Subjects were placed on one diet or the other for 11 weeks. After an 7 week "washout period" the subjects switched diets. Subjects who first lost weight on the ad libitum 35-40% fat control diet subsequently failed to lose weight on the low fat diet.

    Caloric intake on the low fat diet was markedly depressed at the beginning, with an initial weight loss of almost a pound a week. Within 11 weeks, caloric intake on the low fat diet was increasing. The difference in calorie intake was cut in half, and weight loss nearly halted.

    "We are unable to explain the minimal effect that the low fat diet had in the second half of the study". The study paper also indicated that weight loss on the low fat diet was much less than expected from the caloric difference between the two diets, indicating a "metabolic disadvantage" compared to other diets.

    In addition, the media failed to report that the subjects regained twice as much weight in the 7 week period after the low fat diet as did the subjects on the control diet. The Cornell researchers have not seen fit to report any followups.

    Other Low Fat Diet Studies

    In a study of 171 women on a two year low fat diet, maximum weight loss of 3.2 kg was reported at 6 months. By year 2 some of the weight was regained. The standard deviation was more than twice the average weight loss. This shows that quite a few actually gained weight on the low fat diet, not counting the 13 that dropped out of the program. (Am J Clin Nutr 1991;54:821-8.)

    The Pritikin Institute promotes an ultra low fat diet to improve cardiovascular health. In a 1991 radio interview, a Pritikin Institute official characterized the weight loss effects of the Pritikin ultra low fat diet as "slight". Ann Louise Gittleman, Pritikin Longevity Center nutrition director, reported in 1992 that weight loss on the Pritikin diet was temporary for most.

    1993 saw Covert Bailey, inventor of the PBS infomercial, proclaim "diets don't work" as he shifted his endorsement to a line of exercise machines. Bailey's newer advertisments stress the fattening effects of diets. Careful observers of Bailey's recent infomercials have noted Bailey now uses baggy pants and wide ties to disguise his substantial paunch.

    Absent Bailey, the low fat weight loss mantra appears to have passed to Dr. Dean Ornish. Dr. Ornish is an ethical vegetarian and paid consultant to low fat meal producer ConAgra and author of the best seller "Eat More Weigh Less". In his paper (The Lancet July 21 1990) Ornish describes a mid-term resident program with a low-fat vegetarian diet and supervised exercise up to 80% of maximum. Ornish's data, while incomplete, suggest that changes in caloric intake and energy expenditure completely account for the reported weight loss. Apparently Ornish's "eat more, weight less" promise applies to roughage. Ornish claims to have partitioned the experimental cohort into two groups randomly, yet the initial weight difference between the two groups was comparable to the experimental group's weight loss. These results indicate the uncertainties caused by the small sample size.

    After 12 months of the ultra low fat vegetarian diet and rigorous supervised exercise, the the active group finished at about the same weight as the control group, but their triglycerides increased and their blood pressure reduction was less. A new study helps explain why the death rate amone Ornish's experimental subjects was greater than that of the controls. Dr. Ornish has not responded to repeated requests for clarifying information.

    A Rockefeller University study reported energy intake required to maintain body weight is not affected by wide variation in diet composition. Even with extreme changes in the percentage of energy from fat (0% - 70%) there was no detectable evidence of significant variation in energy need as a function of percentage fat intake. (American Journal of Clinical Nutrition 1992;55;350-5) "Sixty years ago, LH Newburgh and his colleagues examined the possibility that so-called endogenous obesity might be the result of special metabolic factors unrelated to energy intake or physical activity. They found no evidence for such purely endogenous obesity and also demonstrated that the long-term effect of any diet on body weight is related only to the total energy content of the diet. Other features of the diet such as carbohydrate or fat content did not, in the long run, have consequential effects on body weight."

    The incidence of obesity does not necessarily follow the amount of dietary fat. The average U.S. daily fat consumption is 2.52 ounces, with 10% of males obese; the average Australian daily fat consumption is much less at , but 14% are obese. (LONGEVITY, May 1992)

    "There is evidence that altering the proportion of the calories in the diet from fat, carbohydrate, and protein can have a limited effect on weight loss; however the effects appear to be quite small" (Methods for Voluntary Weight loss and Control, NIH Technology Assessment Conference Panel, Annals of Internal Medicine June 1992, 116;11)

    In the presence of dietary carbohydrate, the preferred fuel is glucose and the capacity to mobilize fat is limited. Factors that increase blood glucose during dieting may stimulate insulin release and all the metabolic sequelae of circulating insulin. Fatty acid synthesis is activated and lipolysis is profoundly inhibited by insulin even at very low concentrations of the hormone. (Am J of Clin Nutr 1992;56:217S-23S)

    Conventional wisdom holds that low fat diets improve insulin sensitivity. Unfortunately, this is true only after an ultra-low carbohydrate diet. No changes in glucose tolerance and substrate oxidation were measured after a high-carbohydrate low fat diet. In addition, these studies confirm a growing body of evidence that increasing dietary carbohydrate increases plasma triglycerides and decreases plasma high-density-lipoprotein (HDL), increasing the risk of cardiovascular disease. (METABOLISM 1993:42:365-70)

    "diets that are relatively low in fat and high in carbohydrate accenuate the abmormalities in glucose, insulin, VLDL, and HDL metabolism that are present in NIDDM. Because these results were observed in a population typical of those with NIDDM seen in most clinics, it seems reasonable to suggest that it is time to reappraise the clinical benefit of low-fat high-carbohydrate diets in these patients. This is not meant to question the aim of reducing saturated fat and cholesterol intake in patients with NIDDM but rather to indicate that this goal can be achieved without drastic reductions in total fat intake and reciprocal increases in carbohydrate consumption by simply substituting polyunsaturated and monounsaturated fat for saturated fat. ... We believe that the results no longer permit us to dismiss the deleterious metabolic effects of low-fat high-carbohydrate diets as purely transitory events in patients with NIDDM and [The results] require that dietary regimens that address the defects in carbohydrate and lipid metabolism that exist in these patients be evaluated." (DIABETES CARE 1989;12:2 94-101)

    "Our results do not support the recommendation of an isoenergetic high carbohydrate, low fat diet for improving peripheral insulin action in adults with glucose intolerance ... the increase in insulin action that we observed previously with vigorous exercise training was negated when combined with a diet high in carbohydrates and fiber. ... The subjects in this study are at increased risk for developing NIDDM" (Am J Clin Nute 1995;62:426-33)

    "the higher the fasting plasma insulin levels, the higher the mean annual CHD mortality rate" (Diabetes and Metabolism (Paris) 1987, 13: 350-353)

    The increased consumption of fructose in the Western diet has been linked to rising incidences of hypertriglycemia and hyperinsulinamia. (J Biol Chem 1992;267:14523-6) (Am J of Clin Nut 1993 116-117) We compared a cholesterol-free tofu- based frozen dessert containing high-fructose corn syrups with ice cream. The tofu dessert elicited a higher glycemic response, related to the substantial amount of total glucose in this "fructose" dessert. This highlights the error of using individual components of a commercially prepared food to recommend a product. (DIABETES CARE 13:382-85, 1990)

    Am J Clin Nutr. 2002 Nov;76(5):911-22.
    Fructose, weight gain, and the insulin resistance syndrome.
    Elliott SS, Keim NL, Stern JS, Teff K, Havel PJ.
    Department of Nutrition, University of California, Davis 95616, USA.
    This review explores whether fructose consumption might be a contributing
    factor to the development of obesity and the accompanying metabolic
    abnormalities observed in the insulin resistance syndrome. The per capita
    disappearance data for fructose from the combined consumption of sucrose and
    high-fructose corn syrup have increased by 26%, from 64 g/d in 1970 to 81
    g/d in 1997. Both plasma insulin and leptin act in the central nervous
    system in the long-term regulation of energy homeostasis. Because fructose
    does not stimulate insulin secretion from pancreatic beta cells, the
    consumption of foods and beverages containing fructose produces smaller
    postprandial insulin excursions than does consumption of glucose-containing
    carbohydrate. Because leptin production is regulated by insulin responses to
    meals, fructose consumption also reduces circulating leptin concentrations.
    The combined effects of lowered circulating leptin and insulin in
    individuals who consume diets that are high in dietary fructose could
    therefore increase the likelihood of weight gain and its associated
    metabolic sequelae. In addition, fructose, compared with glucose, is
    preferentially metabolized to lipid in the liver. Fructose consumption
    induces insulin resistance, impaired glucose tolerance, hyperinsulinemia,
    hypertriacylglycerolemia, and hypertension in animal models. The data in
    humans are less clear. Although there are existing data on the metabolic and
    endocrine effects of dietary fructose that suggest that increased
    consumption of fructose may be detrimental in terms of body weight and
    adiposity and the metabolic indexes associated with the insulin resistance
    syndrome, much more research is needed to fully understand the metabolic
    effect of dietary fructose in humans."

    "If ever proof were needed that the proposition that there is a cause-and-effect relationship between diet and breast cancer far exceeds scientific data, the US National Institutes of Health's plan to conduct a $10 million clinical trial is proof indeed. Despite abundant evidence that dietary fat bears no relation to development of cancer of the breast, the NIH intends (under the fashionable umbrella of "women's health") to initiate a study of 40,000 women (half of whom will be randomly assigned to consume no more than 20 per cent of their calories in fat) to try once again to prove a link that is probably not there. ... Why then does NIH insist on spending $10 million on a study whose hypothesis seems to be little more than wishful thinking? Is it only because of the faddish infatuation with fat as the root of all dietary evil? In the United States, as elsewhere, money for scientific research is in short supply. There are many ways the NIH could better spend its $10 million." (Editorial in NATURE - VOL 359 - 29 OCTOBER 1992)

    Two large studies published in the April 2000 New England Journal of Medicine failed to find any evidence that eating low-fat high fiber food lowered the rick of colon cancer.

    There is some concern that low-fat diets induce depletion of the body's Omega-3 reserves, believed to protect against colon cancer, heart attack, etc., and to promote lipolysis ("fat burning").

    N-3 fatty acids (FAs) are essential in early human development. Fish and shellfish are the main food sources of HDA. Women who consume fish have more DHA in their breast milk than do those who do not eat seafood. Infant formulas contain only LNA, which may not be suitable. "Pregnant and nursing women should be encouraged to consume seafood on a regular basis during pregnancy and lactation to furnish DHA for their infants." (Journal of the American Dietetic Assoc 1993;93:58-64)

    A number of fatty acids appear to lower blood lipids. (J Am Col Nut 1991:10(6);593-601) The loss of these nutrients on a low fat diet may explain the increase in triglycerides seen on high carbohydrate low fat diets.

    Dieting Gourmets

    A diet designed by Michel Montignac restricts the eating of certain kinds of foods together. Fat and proteins marry well, but not with carbohydrates. Even a single French fry is forbidden, as is sugar.

    Montignac satisfies his sweet tooth with artificially sweetened desserts or low-sugar chocolate mousse.

    The diet's basis is the relationship between insulin and the creation of stored fat. For example, the carbohydrate in several slices of whole-wheat bread at breakfast will not cause weight gain, but adding butter will.

    The method recommends plenty of fresh and cooked vegetables, meat, poultry and fish, and up to three glasses of red wine per meal.

    Montignac encourages dieters to eat carbohydrates as main courses. Fruit, which must be delayed until three hours after a meal, becomes a morning or midnight snack, not a dessert.

    "The man who put France on a diet" has drawn fire from the nutrition establishment. Gerard Pascal, head of nutrition and food hygiene at the National Institute of Food Research, says Montignac's method is dangerous and scientifically unfounded. Pascal urged the overweight to eat a bit of everything. "That's difficult and unspectacular, but in the long run, it's the only valid rule to follow."

    Montignac is not sure his method will thrive in the United States, where fast food and sugar-laced packaged foods are dietary staples. (APn 01/23/1993) Scientific papers on this diet technique, is any, have yet to come into prominence.

    The Lopez Diet / Eat like a Warrior

    J. Ignacio Lopez de Arriortua's pamphlet on "Feeding the Warrior Spirit" achieved must-read status at General Motors before he left for VW.

    How to Eat Like A Warrior

    + No sugar, potatoes, or white flour

    + Fruit must be eaten alone, not with other foods

    + In the morning, eat only fruit, but as much as you like

    + Don't mix carbohydrates and protein at the same meal

    + Drink only good wine

    Low Carbohydrate Diets

    Low carbohydrate weight loss diets have been used for centuries. Sugar consumption is lower, low carbohydrate diets are more popular, and the incidence of hyperobese individuals is lower in Europe than in the U.S. (International Journal of Obesity 1992, 16,565-572)

    A number of short term studies, mostly in the 50's and 60's, showed a marked advantage in weight loss from high protein, low carbohydrate diets compared to diets higher in carbohydrate.

    In addition, low carbohydrate diet is more effective than low fat diet in reducing the prevalence of efficient, fat-producing Firmicute bacteria.

    Weight Loss on 1800 kcal Diets varying in Carbohydrate Content
    Carbohydrate (g/day) Fat Loss (kg) Lean Body Mass Loss Tiredness
    104 8.38 24.7 % 1
    60 10.20 15.9 % 2
    30 14.85 4.9 % 3

    Each group had 3 subjects. All three diets had 115 grams of protein per day. Tiredness indicates the number of subjects reporting this symptom. (Am J of Clin Nut 1971 290-6)

    Another study compared two 590 kcal diets. The "ketogenic" diet had 52g protein, 10g CHO, and 38g fat. The other diet had 50g protein, 10g fat, and 76g CHO. The ketogenic diet did not exhibit any advantages. At 590 kcal/day neither of these diets was representative of popular "low carbohydrate" regimens. (METABOLISM, 1992 41:4: 406-14)

    Compared to high carbohydrate diets, a high protein low carbohydrate diet preserved lean body mass and improved glucose oxidation. (METABOLISM Dec 1994 43:12 1481-7)

    In the presence of carbohydrate, the preferred fuel is glucose and the capacity to mobilize fat is limited. Factors that increase blood glucose during dieting may stimulate insulin release and all the metabolic sequelae of circulating insulin. Fatty acid synthesis is activated and lipolysis is profoundly inhibited by insulin even at very low concentrations of the hormone. (Am J or Clin Nut 1992;56;217S-23S)

    These studies indicate a low carbohydrate diet with generous protein allowance provides superior fat loss, reduced lean tissue loss compared to other types of weight loss diets. The main disadvantage is a greater incidence of tiredness, not unexpected considering the dramatically greater fat loss.

    Of particular interest is the famous "Atkins Diet Revolution" developed by Dr. Robert Atkins, a New York cardiologist.

    Dr. Atkins claims that 95% of excess adiposity is metabolic and not an eating disorder. His solution is to limit sugar and other carbohydrates to the dietary levels man experienced before the agricultural revolution.

    Dr. Atkins claims that high carbohydrate diets promote Candida Albicans overgrowth ("yeast infections"), which can interfere with weight management. His lab tests confirmed this condition in a third of his patients.

    Low carbohydrate dieters sometimes report remission of allergies and hearburn.

    At the start, the Atkins diet severely restricts carbohydrates. As weight loss proceeds, carbohydrates are increased to modulate the rate of weight loss. Except for carbohydrates, Atkins dieters eat ad libitum.

    The media attention afforded Dr. Atkins' Diet Revolution and Dr. Atkins' claim that high carbohydrate consumption promoted obesity and insulin resistance triggered a heated response from the American Medical Association Council on Foods and Nutrition. The Council, whose members and their links to high carbohydrate food producers were not disclosed, blasted the Dr. Atkins diet in the June 4 1973 Journal of the American Medical Association. While Dr. Atkins rebuts many of the Council's points in his 1992 sequel "Dr. Atkins' NEW Diet Revolution," (ISBN 0-87131- 679-X) the Council's observation that "It is unfortunate that no reliable mechanism exists to help the public evaluate and put into proper perspective the great volume of nutritional information and misinformation" is, sadly, as true in 1993 as it was in 1973.

    Since the AMA Council on Foods and Nutrition put the Atkins diet off limits, few if any investigations of the Atkins diet have appeared in the literature. Consumer Reports' Rating the Diets has rated Atkins as "absolutely not recommended"; ironically their top rated diet (Nutri/Systems) was the first to make payments on product liability lawsuits, and has made hundreds of settlements.

    Critics blast the Atkins diet as a high-fat regimen that increases serum lipids. Dr. Atkins, a cardiologist, responds: ``Am I advocating a high-fat diet? Not in the long run. As my critics twenty years ago were forced to acknowledge when they looked into the matter, and as Professor John Yudkin proved, this isn't a high-fat diet. The average person on a low-carbohydrate diet eats less fat than he was eating on his previous "balanced" diet - the average diet in America today.''

    ``the AMA [Council on Foods and Nutrition] said they were "deeply concerned about any diet that advocates the unlimited intake of saturated fats and cholesterol-rich foods." Then they scrutinized all the medical literature they could bring to bear and came up with a single case described in 1929. "This was the study of the Arctic explorer, Vilhjalmur Stefansson, who, impressed with the health of the native Eskimos he observed, volunteered with an associate to be observed for a year on an all animal food diet. In this study, one of the two subjects cholesterol levels did go up but the other's dropped. The AMA inaccurately reported that both men had cholesterol increases."

    Let's look at their language: "Individuals responding to such a diet with a rise in blood fat will have an increased risk of coronary heart disease." Absolutely, All I can say is: "I agree, and individuals who jump off a curb with a parachute and are thereupon attacked by an enraged bull will have an increased risk of torn garments." The AMA's ad hoc nutrition panel had to phrase it that way, because they knew, of course, that they could not find any evidence that would have allowed him to make a stronger statement.

    I think it is clear from their circumspect language that the AMA was aware of the difference between the results when fat and cholesterol are added to a high-carbohydrate diet and the results that occur when they are added to a low-carbohydrate lipolytic diet. In the usual scenario, when carbohydrates are a large part of the diet, the undesirable lipid reading may get worse if there is an increased intake of fat as well; on the Atkins diet, such a result is rare indeed.'' (Chapter 15, Dr. Atkins NEW DIET REVOLUTION, 1992)

    It should be noted that serum cholesterol increases are encountered with other types of diet. (American Journal of Clinical Nutrition 1991;53;1404-10)

    Low-fat high carbohydrate diets similar to those recommended by the American Dietetic Association, have serious metabolic effects when consumed by patients with NIDDM for 15 days. The dietary recommendations of the ADA may actually increase the risk of coronary artery disease in patients with NIDDM. Hyperglycemia, hyperinsulinemia, hypertriglycemia, and reduced plasma HDL have been identified as factors predisposing to the risk of coronary heart disease.

    Furthermore, these same four metabolic abnormalities have been shown to be exaggerated following ingestion of a high- carbohydrate, low-fat diet. (American Journal of Medicine 1987:82 213-220)

    High-carbohydrate diets lead to several changes in carbohydrate and lipid metabolism in patients with NIDDM that could lead to an increased risk of coronary artery disease. These effects persist for more than six weeks. It seems reasonable that the routine recommendation of low-fat high carbohydrate diets be reconsidered. (Diabetes Care 12:94-101, 1989)

    In the obese NIDDM, ketones generated by VLCD or low carbohydrate diets suppress hepatic glucose output and fasting blood sugar. (O619, IJO 1994 165)

    Tiredness is a common, but hardly universal, complaint on low carbohydrate diets. Some of these problems may be related to citric acid interacting with the Atkins diet (see "Artificial Sweeteners", above). Several Usenet readers have reported abandoning the Atkins diet as a result of side effects and bad publicity in the press.

    Other problems include palatability, inconvenience and expense of obtaining low-carbohydrate foods.

    Dr. Atkins' 1992 book claims "the 10,000 active patients at the Atkins Center for Complimentary Medicine in New York are living testimonials to the major health improvements derived from a low-carbohydrate diet." Dr. Atkins advertises books and vitamins on a syndicated radio talk show (WOR radio, (1-800-2-ATKINS, 1-800-6-ATKINS).

    This author has not been able to find a single study of the Atkins multistage ad libitum low carbohydrate type of diet in the scientific literature. The available low carbohydrate studies have used energy restricted diets profoundly different from Atkins' regime. A nearly definitive study by Kekwick and Pawan appeared in METABOLISM vol. 6, pp. 447-60. This study carefully checked for the weight loss that almost always occurs upon hospital admission as well as the possible effect of fluid loss or retention on weight figures. Kekwick and Pawan found that a low carbohydrate diet was much more effective for fat loss in the obese than a low fat high carbohydrate diet with the same energy. Atkins' diet differs from that used by Kekwick and Pawan in that Atkins limits carbohydrates, not total calories.

    A relatively recent paper appeared in the Feb 1973 American Journal of Clinical Nutrition, "Response of body weight to a low carbohydrate, high fat diet in normal and obese subjects". This paper is unusual for diet studies in that it discloses the individual results of each of its obese subjects instead of hiding them in the arithmetic mean. "we treated obese subjects with high fat, low carbohydrate diets. If the carbohydrate content of the diet was not more than 50 to 60 g/day and the fat content approximately 150 g/day, an average daily weight reduction of 0.3 kg was achieved. The cholesterol and triglyceride concentrations in the serum, which had been raised at the beginning of the experiment, invariably showed a tendency towards normalization under this dietary program."

    A Scottish study found lowering carbohydrate intake doubled weight loss, increased fat oxidation, and reduced metabolic slowdown compared to lowering fat intake.

    Some studies did not find any advantages to low carbohydrate diets. Many of the regimens failed to follow the recommendation of a 1984 study that indicated increased protein requirements during dieting. (Journal of Clinical Investigations 1984;73: 750-8)

    These papers appear to confirm Atkins' claim that his diet has a "metabolic advantage" over other types of diets. The idea behind "metabolic advantage" is that a suitable low carbohydrate diet provides weight loss at a much higher caloric intake than other types of diets, with much less lean tissue loss. By comparison, the Cornell low fat diet study discussed above found weight loss was much less than expected from the measured reduction in caloric intake.

    In the presence of dietary carbohydrate, the preferred fuel is glucose and the capacity to mobilize fat is limited. Factors that increase blood glucose during dieting may stimulate insulin release and all the metabolic sequelae of circulating insulin. Fatty acid synthesis is activated and lipolysis is profoundly inhibited by insulin even at very low concentrations of the hormone. (Am J of Clin Nutr 1992;56:217S-23S) Several recent papers have reported low carbohydrate diets to be better than the generally accepted low fat diet for control of type II diabetes (insulin resistance). Click here to visit the Low Carbohydrate - Diabetes page at St. John's University

    One of the Council's criticisms of the Atkins diet was loss of appetite. Such a criticism calls into question the judgement, if not the honesty, of the Council's members. Atkins considers appetite reduction a virtue of his diet, as would most dieters. However, if this loss of appetite is sufficient to decrease energy input below maintenance levels, then studies of energy restricted low carbohydrate diets may be relevant. These studies did not find a long term "metabolic advantage" to carbohydrate restriction. It remains to be seen if the anorectic effect of the Atkins diet is powerful enough to reduce energy input to the low levels used in these studies.

    Another criticism is the diet's ketogenic tendency, which Atkins calls "Benign Dietary Ketosis" to distinguish the mild ketosis caused by his diet with the dangerous form associated with diabetes emergencies. People on very-low-calorie diets go into ketosis without carbohydrate restriction. Pregnant women are in ketosis most of the time. Endurance athletes who've been running for an hour or more go into ketosis. A ketogenic diet has been successful in controlling childhood seizure disorders (EPILEPSY DIET TREATMENT, John Hopkins University Press).

    Atkins estimates that less than a third of individuals in his diet are "fat-sensitive" and will develop a less favorable cholesterol level on a high-fat [low-carbohydrate] diet than on a low-fat diet. His 1992 book includes procedures for testing for sensitivity to various types of fat and appropriate diet modifications.

    Dr. Atkins reports long term results that are much better than those obtained with other diets. He has offered to make his patient records available to researchers, something Weight Watchers, Nutri/Systems, et al refuse to do. His favorable results, however, may be the result the same selective dropout mechanisms that generate spurious positive results in other diet studies.

    In early August 1993, A complaint was filed by Dr. Paul Gennis, who treated an Atkins patient in Jacobi Hospital's emergency room for an embolism that he said had formed in her brain. This led to a suspension of Atkins' license, an event that was reported with obvious glee by some of Atkins' detractors. These people apparently do not think the reversal of this diagnosis and suspension nearly so newsworthy.

    Ornish and Atkins Compared

    We need large scale randomized studies comparing low fat and low carbohydrate diets. Until such studies is published, we must compare results reported by Ornish and Atkins themselves. The Ornish figures are the average of the Ornish Experimental group (n=22) carefully selected from hundreds of applicants. The Atkins data (n=1) is from page 150 of his 1992 book. Neither of these samples is necessarily representative of the overweight population. However, the starting age, weight, and body mass index of Atkins' sample resembles those of Ornish's experimental group much more closely than Ornish's own control group, lending credence to the comparison.

    The changes in metabolic risk factors agree with those reported in the METABOLISM and DIABETES CARE studies discussed above, suggesting the differences between low-fat and low-carbohydrate diets reported in those papers are applicable to a wider population.

    Ornish and Atkins Diets Compared
    (low fat)
    (low carbohydrate)
    Age 56 55
    Starting weight 201 195
    Body Mass Index 28.4 28.1
    (low fat)
    (low carbohydrate)
    Cholesterol change -24% -13%
    HDL (GOOD) Cholesterol - 3% +60%
    Triglycerides (BAD) +75% -82%
    Weight -12% -19%

    Further confirmation of Atkins' data comes from Dr. Ronald Krauss, chairman of the American Heart Association's Nutrition Committee. In some men with normal-sized LDL cholesterol particles, a very low-fat diet can cause changes in the cholesterol profile that indicate an increased heart disease risk. In one study, 36 out of 87 men with normal-sized LDL particles switched to the small-particle abnormalities when their dietary fat was lowered from 46 percent of calories from fat to 24 percent. One sign of the switch was a rise in their ratio of total cholesterol to "good" HDL cholesterol, which implies a higher heart disease risk. (API 7/16/96)

    Diets - the BOTTOM LINE

    "weight will return toward its baseline level whenever a previously instituted perturbation (such as diet, exercise, modified protein fast, behavior modification, or jaw wiring) has been completed. In this case, continued diet, exercise, and behavior modification also did not help the subjects to avoid regaining lost weight."

    "Both the medical profession and society look with disfavor on obese people and obesity in general. For example, students at a well-known university preferred a number of less savory people to obese individuals as potential marriage partners. Obese people are treated negatively in cartoons and in literature. Many believe that obese people need only to "close their mouths" and to be more motivated to lose weight. Thus use of medications to correct a the public, deemed inappropriate."

    "Unfortunately, a lack of understanding of both the natural history of obesity and its diversity adds to the pejorative view of obese people and of anorexiants. Some health professionals are not aware of data concerning mechanisms present in the human organism that act to countervene perturbations in body weight and that may account for the apparent failure of interventions, including medications." (Clin Pharmacol Ther, May 1992)

    A paper by William Bennett in the Annals, New York Academy of Sciences, (book length issue on Human Obesity) gives the bottom line on diets. "Data on the dietary treatment of obesity have been accumulating since 1931. Nothing in the chronicle suggests that worthwhile progress has been made by pursuing efforts to teach people more effective ways to restrict their food intake. There now is enough information to permit the prediction that results will be mediocre in the short run and after several years the results will be less than acceptable. The burden should now be on the investigator to establish a strong reason for undertaking yet another study of intake restriction, including studies employing behavior modification aimed primarily at altering eating behaviors.

    Committees reviewing the use of human subjects in these experiments should not assume that they are ethically uncomplicated. The low probability that information of therapeutic value will result from such a study should weigh heavily in any deliberation on whether to authorize it."

    "I can see little reason for intake restriction to receive continued support, either as a subject of research or as an accepted therapy for obesity. Bloodletting as a therapy for pneumonia was abandoned about a century before penicillin was discovered. It required a modicum of courage and good sense on the part of practitioners who turned away from the practice, but there is no reason to believe their patients suffered from this lack of therapy."

    "A survey of studies published 1977-1986 and reporting on dietary or behavioral treatment of obesity reveals that the maximum percentage of body weight lost is, on average, 8.5 percent - no different from the value, 8.9% in similar studies from 1966-1976, as reviewed by Wing and Jeffery."

    "The goals and research methods of studies on dietary treatments for obesity are overdue for ethical as well as scientific reevaluation. The same may be said for the numerous programs providing such treatment outside the context of research."

    A final footnote on combining diets and exercise. A Harvard Health letter compared results of 1982 and 1991 surveys of doctors' lifestyles. Since 1982 the doctors reduced their consumption of red meat, fat, and cholesterol. They increased their dietary fiber and exercised more. Unfortunately, the increased attention to diet and exercise did not produce leaner bodies; the proportion reporting weight problems increased from 29 to 39 per cent.

    While diet evangelists continually assert that new wrinkles in 60+ year old treatments are improving weight loss outcomes, the long term success rate of even the best available weight loss programs using diet, exercise, and behavior modification remains less than five per cent. (NIH conference on voluntary weight loss, Mar 30-Apr 1 1992)


    The quality of diet research and media coverage of adiposity leaves much to be desired. The vast majority of this research is so poor it would never be accepted by the FDA as proof of an ethical drug's efficacy and safety.

    A pervasive problem in published research is the refusal of authors to disclose financial and other conflicts of interest. An article in the Feb 2 1999 Wall Street Journal reported that almost every researcher publicly supporting a new drug had financial ties to the drug manufacturers. Most troubling, none of these conflicts of interest were disclosed.

    The reader should beware of three common flaws in popular obesity studies:

    Correlation .vs. Cause and Effect

    A typical correlation study might show that joggers are thinner than couch potatoes. This is a *correlation*. Such data are generally cited as proof that obesity is caused by lack of exercise, with the implication that fat couch potatoes will become thin if only they get off their lazy butts and exercise.

    What is the error in drawing such a conclusion? The error is the unstated assumption that the correlation proves a particular cause and effect. In fact, other cause and effect relationships may be involved. Conventional wisdom concludes: Lack of exercise causes obesity. Another explanation for the observed correlation is: Obesity and associated impaired athletic performance makes sports activities unpleasant and frustrating, forcing a more sedentary lifestyle.

    "While the link between exercise and health in some large epidemologic studies seems powerful, intervention and outcome studies suggest a more qualified correlation. ... Yet we still have no clinical trial to demonstrate that increasing activity in a group of sedentary people reduces the rate of disease vs sedentary controls," says William Haskell, PhD, also a member of the Stanford faculty. (JAMA June 12, 1991)

    Correlation studies that draw conclusions or make recommendations without properly evaluating alternative models of causality are fundamentally flawed and must be treated with suspicion.

    Flawed Sample Selection/Distribution

    Non-random selection or partitioning of the sample population flaws many studies that otherwise appear to be well designed.

    One cannot allow subjects to select which experimental group they will join because the selection process may be stronger than the experimental intervention. News media might not understand the implications, but the study will be flawed.

    For example, a study on the mortality effects of obesity was based on patients who had repeatedly lost and regained weight, compared to lean individuals. Was the higher mortality caused by obesity, by the dieting, did weight cycling cause both, or did genetic factors cause all three?

    Studies comparing the relative success of alternative treatments rarely assign subjects to the alternatives at random. The factors that determined sample selection and partitioning may be more important than the alleged independent variable.

    Diet studies typically exclude dropouts from their data. This is not acceptable in weight loss research because dropouts have lower weight loss and greater weight regain. Excluding even a few such data points distorts the experiment because the variability between subjects is much greater than the average weight loss.

    EXAMPLE: Let us put 15 subjects through a thought experiment. 5 lose 20 pounds on the New Fat or Fit program, 5 gain 20, and 5 end up the same. The average weight loss is (5x20-5x20 +0 = 0) 0, about as well as real diet programs. But before the 5-year weigh-in, two of the subjects who regained their weight and three of the unfortunates that gained twenty gave up on Fat or Fit and went on an Atkins' diet. The five that dropped 20 are of course eager to report the success of their superior will power to the researchers. So now we have (5x20 -2x20 +3x0 = 60/10 subjects = 6) 6 pounds average loss. That 6 pound loss is completely bogus, but that's how diet papers are put together.

    Diet studies sometimes mistake genetic differences for dietary intervention. Compared with women in Western cultures, traditional Asian women start menstruating later, give birth at a younger age and gain far less weight in adulthood - all factors that decrease breast-cancer risk. (Dr. Michelle D. Holmes, an instructor of medicine at Harvard Medical School and Brigham and Women's Hospital in Boston. )

    Improper use of Ratios to Adjust Data

    The use of ratios of variables (frequently called "index" variables) is common in obesity and related research. The use of such "adjustments" is invalid if the intercept is nonzero or if the relationship is nonlinear. The article explains a number of other factors which can cause the use of ratios to cause interpretive difficulties. (International Journal of Obesity 1995 19,644-52) In common language, such adjustments may constitute serious FUDGING of the data.


    The honesty and integrity in life sciences research has increasingly come under question.

    We understand the pressure on a corporation or trade institute to manage information about the safety and efficacy of its products and services. Such pressures are not limited to the corporate sector. Weight loss researchers live by the "publish or perish" syndrome. Exaggeration of weak results is sometimes a necessary expedient to secure continuing research funding. "When all you have is a hammer, everything starts to look like a nail" applies to research projects.

    "It is seldom necessary to list individual results in a paper. Data can usually be summarized by a measure of location and a measure of dispersion. A common practice is to list the arithmetic mean, standard deviation (S.D.) and the number of observations (n) used to estimate these statistics. If only a few observations are available the dispersion is better indicated by the range. If the distribution is significantly skewed [not a "normal distribution"] both the median [50th percentile] and range [minimum and maximum] should be cited." (Journal of Endocrinology, 1992)

    How can one spot "fudged" research? One way is to look at the way data is presented. If mean (average) values for the experimental groups are presented, check the standard deviation values. The standard deviation must be small compared to the reported differences between groups. If the standard deviation is comparable to the differences between groups, the data can not be used to analyize individuals.

    Diet evangelists dismiss or downplay the importance of genetics and other inborn differences affecting the development of obesity. Large standard deviations highlight the biological differences between fat and thin people. If the standard deviation is not disclosed, the researcher is hiding something from the reader. "the mean net weight gain in 1423 women as a consequence of pregnancy was found ... to be small (0.5 kg). Nevertheless, this seemingly modest increase concealed the fact that 15% of these women had actually gained more than 5 kg" (IJO 16, 935) Diet studies typically exclude dropouts from their data. This is not valid in weight loss research because subjects tend to drop out after frustration with poor weight loss. Dropouts have lower weight loss and greater weight regain. Excluding even a few such data points generates a false positive finding because the variability between subjects is much greater than the average weight loss (SD >> M). Goal directed programs and programs that dogmatically insist subjects will succeed if only they follow the regimen provoke highly skewed dropouts.

    Weight loss studies often present the average weight loss of a subset of the experimental cohort. Most such samples are not representative of the overweight population, yet vital questions of relevance to the overweight population are rarely addressed. What portion of the overweight population was not eligible for or excluded from the program, thus introducing selection bias? (Williamson & Levy, Int J of Obesity, 1988, 12, 579-83)

    Long term studies pose further problems for studies without a non-dieting control group. Williamson and Levy analyzed weights recorded for medical purposes at two clinic visits separated by intervals of 1 to 5 years. These were 332 adult patients who were initially at least 20 per cent overweight. The 59 patients measured over a 5 year interval showed an "apparent weight loss" for 31 per cent of this group with a mean decrease of 7.3 kg. This long term random weight loss is comparable to the positive results reported by some diet and behavior programs. "Some variation in an individual's body weight is expected to occur over time for a variety of reasons including mood swings, health status, seasonal variations in food intake, amount of exercise, tobacco smoking, pregnancy, and dieting attempts. These intervening variables have not been well controlled in long-term weight loss follow-up studies.

    The sub-group of subjects who maintain a weight loss is usually reported in isolation without comparison to the majority of overweight subjects who originally entered the survey or program. These results suggest the degree of variation that a [non-dieting] control group would contribute both to the proportion of overweight subjects who would have naturally decreased in weight at a specific re- measurement interval and the mean amount of weight by which they would have decreased. The sample size in this study exceeds that of most long-term follow-up studies reported in the literature."

    Few studies are available of body composition changes after weight losses from standard dieting programs. Weight losses beyond the initial glycogen and water shifts have proven difficult to achieve. (Weight loss of 5kg (11 pounds) or less may not involve any loss of fat!) When they do occur it is difficult to verify the actual protocol the subjects followed. Subjects often report they often became `stuck' on traditional protocols and resorted to some more drastic form of food restriction to achieve weight loss. They are often reluctant to report such behavior at the time of the actual diet. (Am J of Clin Nutr 1992;56:217S-23S)

    Unless a significant loss beyond baseline is demonstrated by weight loss studies and programs, no effect should be attributed to the program. Control groups that account for random weight changes (mostly from unsupervised dieting) are essential in studying the long-term maintenance of weight loss.

    Any study that takes weight loss as a goal should include the following information:

  • Weight, height, and Body Mass Index (BMI) for subjects at entry, then weight and BMI at each follow-up time.

  • Number and size of fat cells before slimming, after slimming, and after weight regain.

  • When expressed as means, these values should be accompanied by the standard deviation, not the standard error.

  • Data for males and females should always be separated.

  • If the study contains more than one experimental group and/or a control group, subjects must be randomly assigned to each group.

  • If the study contains more than one experimental group and/or a control group, the data should be presented for each group.

  • Studies with 50 or fewer subjects should present individual data.

  • Data should include followup for a minimum of three years after treatment ends.

  • If there are drop-outs, the remaining number of subjects should be recalculated and reported along with the mean weight at follow-up. Almost all drop-outs regain their weight loss or more, and must be calculated this way.
  • Weight loss studies should report the number and size of adipose cells before slimming, after slimming, and after weight regain.
  • (Based on recommendations by by William Bennett, Harvard Medical School Health Letter)


    Heavy advertising, a "thin is in" ethic, media preoccupation with unusually obese individuals, and built-in repeat business have bloated the diet industry into a 33 billion dollar a year enterprise.

    The media often sensationalize studies confirming public stereotypes while ignoring research that disproves those stereotypes. The following news release is typical: "Why Johnnie gets fat CHICAGO, Reuter - Television may be contributing to a near epidemic of obesity among American children because it drives metabolism dramatically lower, even below levels found in youngsters who are simply resting, researchers said on Monday. The metabolic lowering -- caused by a still unknown mechanism -- may combine with the high-fat snacks that often accompany the hours so-called couch potatoes spend in front of the tube, according to a study published in the February issue of the medical journal Pediatrics. It said obesity affects as many as one out of every four U.S. youngsters, as well as about 30 per cent of adults." While entranced by the sedating effect of a "The Wonder Years" episode on 31 children measured for a Master's thesis, the media completely ignored the lead article in the same issue. A 1250 child study by Stanford and NICH that concluded that "television viewing time appears to have only weak, if any, meaningful associations with adiposity". (Pediatrics 1993; 91:273-80)

    As Professor Garner's 1990 testimony before the House of Representatives indicated, deceptive advertising is standard operating procedure in the weight loss industry. While an isolated deceptive diet/exercise ad may not be too misleading to the public at large, the collective effect of such deception (Nazi Big Lie effect) creates great damage.

    Weight Watchers, Nutri/Systems and other diet promoters refuse to divulge their long term weight loss data.

    Misleading advertising is, unfortunately, normal for the diet industry. The majority of diet food products tested for the New York state Consumer Protection Board contained more calories than listed on their package labels. 80 percent of the diet food products tested exceeded claimed calories, some by as much as 73 calories per serving. Added sugar has been found in 25% of orange juice brands described as pure and unsweetened.

    Advertising ethics are no better in the related exercise industry. A NordicTrack ad claimed a fat person could lose up to 1100 calories per hour, several times what an endomorph with middle age spread could reasonably expect.


    Food Allergy Avoidance

    Food allergies may be responsible for some adiposity according to an article in the American Journal of Bariatric Medicine (1996/?). Subjects with weight problems lost fat and gained muscle after eliminating foods to which they are allergic as identified by tests. Information on food intolerance testing using The ALCAT Test is available from AMTL Corp. at 1-800-881-2685. Other articles and books on food allergies have appeared over the years.


    Thermogenesis refers to the generation of body heat in muscle and brown adipose tissue (BAT).5 Lean subjects increase thermogenesis in response to meals, exercise, and cold weather. Obese subjects show less of each of these responses than lean subjects. Obese subjects are less tolerant to long term cold exposure because of their inferior thermogenesis capability.

    These facts have prompted many investigations into the possibility of reducing obesity by increasing thermogenesis in the obese.

    In their book "Life Extension Weight Loss", Pearson and Shaw suggest thermogenesis enhancing drugs and cold exposure as ways to burn up fat.

    Caffeine, ephedrine, nicotine and other materials have been shown to increase metabolism in humans. Aspirin increases the thermogenic effectiveness of ephedrine in obese but not lean women. Some are associated with weight loss during the treatment period. Common side effects of such treatment include high blood pressure and heart palpitations.

    Ephedrine quadrupled the weight loss of obese women whose metabolisms had been depressed by previous dieting. (International Journal of Obesity, 1987: 163-8)

    A double-blind Danish study reported that ephedrine 20mg + caffeine 200mg administered three times daily dramatically increased fat loss and fat oxidation (see "fast fibres") and reduced loss of fat-free mass. Three of the 8 patients on E+C complained of insomnia, palpitations, and tremor, respectively. (Metabolism, 41;7 July 1992)

    A combination of ephedrine(75-150mg), caffeine(150mg), and asprin(330mg), in divided premeal doses, supports modest, sustained weight loss even without prescribed caloric restriction, and may be more effective combined with diet. (IJO 1993 17 (Suppl 1) S73-8)

    Caffeine consumption is controversial. Some diet books recommend it, some forbid it. Early Atkins books allowed it, the 1992 sequel does not. Caffeine and ephedrine are known to increase blood pressure, so caution is advised. The FDA has warned against dietary supplements containing ephedrine (Wall Street Journal, B5, 4/11/96). The FDA is considering regulating ephedrine (1997).

    "Love maketh lean the fatte mens tumor, so doth Tobacco" (Tobias Hume, The First Part of Ayres, London, 1605)

    "Light a Lucky and you will never miss sweets that make you fat." -Constance Talmadge, silent movie star in 1929 Lucky Strike ad

    Smokers gain weight when they quit smoking, up to 60 pounds. Average is 16.7 pounds for men, 19.2 for women after 5 years (Am jr of Epidiemology Nov 1998). Their final weight averages the same as that of non smokers. This suggests nicotine reversibly depresses weight, 6 to 7 per cent according to University of Wisconsin researcher Richard Keesey. Nicotine reduces weight by increasing metabolism, not by reducing appetite or food intake. A growing number of young women have discovered this, and cigarette smoking is gaining popularity as a weight control measure.

    Pearson and Shaw recommend nicotinic acid to increase thermogenesis and as a recreational drug.

    A study of obese women on a swimming program suggests their heat loss to water had the opposite effect, increasing their fat stores. It's been reported that women gain 10 pounds in less than a week's time when they move to Alaska; they lose this weight when they move back to a warmer climate. This weight gain may be the result of BAT lipogenesis.

    It has been suggested that early exposure to cold might promote adult leaness. (p. 75, Obesity and Leanness - Basic Aspects) Improvements in household heating in this century may contribute to an increase in obesity.


    While most research into obesity has focused on appetite suppression, some have decided to look for ways to help burn more energy, but do it in the safest way possible.

    Whole body oxygen consumption, a measure of metabolism, was increased in animals given KB-141 and the monkeys had a 7 percent loss of body weight in a week without affects on the heart, the researchers reported.


    (Also called somatropin, or ST.)

    Maximally effective doses of ST can reduce lipid accretion rates and adipose tissue mass by as much as 80%, and increase protein (lean tissue) deposition by 50%. ST affects numerous target tissues to effect marked changes in nutrient partitioning. Many of the metabolic effects are a direct action of ST, involving a variety of tissues and the metabolism of all nutrient classes, i.e., CHO, lipid, protein and minerals.

    These metabolic changes are important because they: (1) establish the rate of lipid accretion and, therefore, the extent to which ST affects body composition in a growing animal, (2) play a key role in redirecting nutrients (e.g., glucose), normally destined to be deposited as lipid, to other tissues thereby supporting the nutrient needs for lean tissue accretion during growth. When animals are in positive energy balance, ST causes a reduction in lipogenic rate. The ability of ST to reduce lipid accretion in growing pigs is the result of a decrease in insulin sensitivity of fat cells, which reduces lipid synthesis. The effects of ST are chronic rather than acute. (Proceedings of the Nutrition Society (1992) 51, 419-31)

    Human Growth Hormone promotes muscle growth and fat loss. Growth Hormone restricts glucose incorporation into fat cells. The pituitary gland releases Human Growth Hormone (HGH) in bursts, mostly during the early hours of sleep. The obese produce fewer HGH bursts, and each burst is much smaller than normal. Reduction of plasm insulin levels does not restore GH to normal in obese children.

    Obesity is associated with reduced 24 hour integrated concentrations of growth hormone (IC-GH) and elevated concentrations of insulin (IC-I) compared to lean individuals. The difference in growth hormone levels is greatest in childhood. The difference in growth hormone between lean and obese children are typical of poorly growing children with classical growth hormone (GH) deficiency. In contrast to children with classical GH deficiency, obese children are generally normal or above average for height, growth rate, osseous maturation and IGF-1 levels.

    A study reported in the Dec 3 1990 Wall Street Journal reported that short children treated with growth hormone lost a "drastic 76 per cent of body fat" while gaining as much as 25% lean body mass (compared to untreated controls).

    Obese individuals normally release very little or no detectable HGH bursts. Even under the most strenuous exercise, obese individuals release only a small fraction of the HGH lean sedentary individuals release in normal sleep.

    A study of lipid metabolism in lean and pre-obese swine (pigs of normal weight which will become fat) indicated low levels of growth hormone at least until sexual maturity, and an enhanced deposition of blood lipids as fat compared to lean subjects. (International Journal of Obesity 1990, 14, 21-29) This enhanced deposition is significant in two ways. First there is the direct accumulation of fat. Secondly this deposition of fat "short circuits" metabolism of blood lipids into cholesterol and steroid hormones. This theory helps explain why destruction of fat tissue allows animals to grow up with more muscle mass than identical but untreated controls.

    Growth Hormone deficiency in adults is associated with psychosocial maladjustment, reduced muscle strength and reduced exercise capacity. Body composition is significantly altered with increased fat and decreased muscle volume as compared to healthy subjects. Epidemiological data suggest premature mortality from cardiovascular disease. Short-term GH treatment trials have shown improved psychosocial performance, normalization of body composition, increased muscle strength, improved exercise capacity, and increased cardiac performance. (Christiansen & Jorgensen, Univ Dept of Endocrinology and Int Med, Aarhus Kommunehospital, Denmark)

    In a recent study, administration of synthetic growth hormone to elderly male patients with low HGH levels to normalize their HGH levels resulted in significant muscle gain and fat loss.

    A Dutch study 8 GH deficient patients reported that 6 months GH therapy increased lean body mass and decreased fat mass. The sense of well-being improved in most patients. Cholesterol levels decreased. (Clinical Endocrinology 1992 37, 79-87)

    A study at St. Thomas' Hospital in London found that patients with hypopituitarism have altered body composition and quality of life. In comparison with a matched control group such patients had considerably reduced lean body mass and increased fat mass and waist to hip ratio. A number were significantly depressed, sufficient to justify therapy. "We conclude that there is a morbid syndrome associated with growth hormone deficiency in adult life which responds dramatically to hormone replacement. To be effective this therapy has to be continued indefinitely."

    Exogenous GH increases lean tissue and reduces body fat in obese women in the absence of significant energy restriction. (Hormone Research 1991, 19-24) Obese men manifest fewer GH secretory bursts per 24 h and accelerated HGH disposal rates. (Journal of Clinical Endocrinology and Metabolism 72:1 p. 51)

    5 weeks HGH treatment reduced the fat mass of obese women 2 kg as it increased lean body mass 3 kg. LPL activity was reduced 50 per cent. (5th European Congress on Obesity 10- 12 June 1992)

    In the future, pre-obese individuals might be treated with HGH and DHEA to keep them from becoming fat.

    Growth Hormone Stimulation

    Human growth hormone is expensive, and side effects are an issue. An alternative to HGH injection is to stimulate the body to excrete HGH.

    Pearson and Shaw recommend stimulation of human growth hormone (HGH) excretion with arginine amino acid supplements as a weight loss method. Long term propranolol therapy increases body weight in heart attack patients (2P-14); this may modify some of Pearson and Shaw's recommendations.

    Normal people require as much as 18 grams of arginine to increase HGH secretion. Unfortunately, the references given in their book indicate their recommended amino acid megadosage is still orders of magnitude too small to cause the obese to release detectable amounts of HGH. The obese have a high threshold which must be surpassed by strenuous exercise (to the point of exhaustion) or "incredible" doses of amino acids (orders of magnitude more than even Pearson&Shaw recommend) before any stimulation of HGH release is noted. HGH levels achieved under these exceptional conditions are still only a fraction of what lean subjects spontaneously produce in their sleep. reports that double-blind studies with weight lifters have shown NO benefit.

    The antiobesity drug fenfluramine normalizes obese subjects' human growth hormone (HGH) response to arginine. (Hormone Research 1987: 27; 190-194)

    "Chronic ingestion of L-dopa (an HGH releaser) leads to sustained but reversible weight loss in both lean and obese Zucker rats."

    GH Secretion in response to all provocative stimuli is decreased in the obese; the precise mechanism of this impairment in unknown. Administration of GHRH (Growth Hormone Releasing Hormone) and the synthetic compound GHRP-6 causes a massive GH release, indicating that impaired GH secretion in the obese is a functional state that might be corrected by suitable medication. (J of Clin Endo & Metab 1993:Apr 819-23)

    "We conclude that obese patients are highly sensitive to the lipolytic and calorigenic actions of exogenous GH; however, administration of exogenous GH is associated with a distinct resistance to the actions of insulin on glucose matabolism." (METABOLISM Vol 43 No 7 July 1994 872-7)

    Netnews postings report that oral arginine is mostly destroyed in the stomach. Instances of acromegaly associated with arginine use have been reported.


    Dehydroepiandrostone (DHEA) reduces weight gain in the hypercorticosteronemic Zucker fatty rat, an animal of genetic obesity. Its chronic anti-obesity effect is thought to reflect a chronic antiglucocorticoid activity. (Int J of Obesity, 1992, 579-)

    University of Wisconsin researchers treated normal and 19 spontaneously obese dogs with DHEA. The normal weight dogs did not reduce weight or energy intake. Two-thirds of the obese dogs lost 20 percent of their excess body weight and dropped cholesterol levels by nearly 25 percent without reduction in food intake. (Int J of Obesity 1990, 14,95- 104)

    The 1990 Journal of Nutrition reported that DHEA treatment reversed dietary induced obesity (from a mixture of corn oil and condensed milk) as well as genetically induced obesity (fa/fa rat).

    In premenopausal obese women, DHEA levels are inversely proportional to BMI. Adipose cells remove DHEA from the bloodstream; enhanced removal of DHEA in severely obese may account for their impaired sensitivity to caloric restriction [inability to lose weight as expected]. (Metabolism, Feb 91, p 187)

    The author of "The Vitamin Bible" reports successful personal weight loss with DHEA but gives no sources or details.

    Pearson & Shaw claim the "DHEA" sold by health food stores is bogus. It has been noted on the net that pharmacologically-inert plant sterols found in Mexican yam can be used by pharmaceutical manufacturers as raw material to synthesize a wide variety of medicinally-useful steroids, but the human body can't do the same feat. Vendors of such "yam precursors" are either very confused or they're being duplicitous.

    DHEA administration may have adverse effects in some women. (Lancet, 343(8911);1479-81, 1994 Jun 11.) An article in the Jan 20 1997 Wall Street Journal was quite pessimistic about DHEA's prospects, and reported that DHEA accelerated prostate cancer. Until more is known about the benefits and dangers of DHEA one should not use this steroid without competent medical supervision.

    Check DHEA and Melatonin Web Page


    RU-486 completely reversed the obesity of genetically obese (fa/fa) rats by blocking the effects of glucocorticoids and insulin causing excessive fat cell proliferation. RU-486 reduced fat storage from 1907 kj to 102 kj, while increasing protein (lean tissue) storage from 44 kj to 217 kj. (American Journal of Physiology 1990, R539-43)

    RU-486 (mifepristone) reduces the deposition of fat tissue and increases the deposition of lean tissue, but only in obese subjects. RU-486 also causes obese mice to lose weight by increasing BAT thermogenesis. Reportedly RU-486 can help cure Cushing's syndrome, a gland disorder characterized by obesity and hypertension. "Potentially the most potent anti-aging drug available." (Longevity, Jan 1991)

    A paper in the 1992 International Journal of Obesity reports that Norepinephrine (the neural transmitter, not the asthma drug) inhibits rat pre-adipocyte proliferation.


    Obese and Normal Rodents The 1990 Pharmacology reported that injections of cobalt- protoporphyrin completely reversed the obesity of Zucker fa/fa fatty rats. Unlike diets, lean tissue is not affected. Untreated rats that were fed the same amount of food as the CoPP treated rats for the first 42 days reverted to the same weight as untreated fatty rats by day 60. This indicates CoPP caused a long term reduction in the rats' set point. Typical CoPP treated (left) and untreated (right) Zucker fatty rats are shown.


    27 hyperprolactinaemic obese women (BMI 38.7) lost 1.2-1.5 kg per week when treated with bromocriptine. (5th European Congress on Obesity 10-12 June 1992)


    Some obesity and type II diabetes may be caused by defective circadian [daily cycle] neuroendocrine rhythms.

    Albert Meier, professor of zoology at Louisiana State University, initiated a study of bromocriptine after 25 years of research on animals' body rhythm biology during migration and hibernation. What he attempted to translate to humans was the finding that many animals reduce or increase their body fat without altering food intake or activity levels. (Insight, Mar 26 1990)

    Meier, Cincotta and Lovell have dramatically reduced body fat with oral bromocriptine taken orally at times calculated to reset circadian hormone rhythms to phase relationships that cause loss of body fat. Bromocriptine is a dopamine agonist used to suppress lactation and in treatment of Parkinson's disease.

    "The phase of the prolactin rhythm differs in lean and fat sparrows, fish, rats, and humans. Daily injections of prolactin in animals at times when the daily peaks occur in the plasma of lean and fat animals produce the appropriate decrease or increase in fat stores within two weeks."

    In early clinical trials, without food restriction, body fat was reduced equivalent to a 420 calorie VLCD, but without the loss of lean body mass caused by weight loss diets. Studies with Syrian hamsters investigating whole body protein turnover indicate this treatment enhances protein synthesis, redirecting anabolic activities from lipid to protein. Apparently the timed bromocriptine treatment alters the genetically controlled partitioning of nutrients described in "The response to long-term overfeeding in identical twins" discussed above.

    In the second study reported in Experientia 48 (March 1992 p. 248-), 15 diabetic subjects were given timed bromocriptine treatment. As with the non-diabetic subjects, all 15 diabetic subjects lost fat (That *all* subjects lost fat is significant. In energy deprivation diet studies, some subjects invariably fail to lose weight. In long term diet followup, the standard deviation is two or three times as great as the average weight loss because a large minority gain weight, sometimes a great amount. Without individual data or the standard deviation, one simply cannot judge the true effectiveness of the experimental intervention. Many diet studies suppress this information as it would cause the reader to discount the validity of the claimed results.) Blood glucose dropped significantly. Oral hypoglycemic medication was was discontinued in 3 participants, and glucose levels remained near normal for at least two months after treatment. Doses of hypoglycemic drugs and insulin were reduced in three other subjects during treatment.

    Blood pressure was also reduced, allowing blood pressure medication to be discontinued in several.

    In a telephone conversation (June 1992) Dr. Meier reported that a third series of clinical trials was underway as part of the FDA process to approve the treatment as safe and effective. He strongly emphasized how critical TIMING is to fat loss; correct dosage given in the wrong rhythm actually increases body fat. The timing calculation is a process patented by Louisiana State University and licensed to Ergo INC, Newport RI. Drs. Meier and Cincotta have financial interest in the process.

    "Our studies also indicate that a cause-effect relationship between overfeeding and obesity is oversimplistic and that food intake and lipid synthesis may be regulated in a concerted fashion by circadian neuroendocrine activities."


    Besides bromocriptine, other dopamine agonists may be useful in the fight against Syndrome X. Ergo researchers found that a combination of dopamine Dl/D2 agonists improved blood levels of insulin, glucose, lipids and free fatty acids. They also had positive effects on proteins, enzymes and other measures related to diabetes, obesity and cardiovascular health. The findings are to be presented to the American Diabetes Association June 21-24 1997.


    Testosterone has been shown to decrease adipose tissue mass by several mechanisms. Young men with high testosterone secretion have low visceral fat mass. Testosterone and HGH synergistically promote beta-adrenergic receptor mediated lipolysis of fat cells. Men with abdominal obesity have low testosterone values and insulin resistance.

    An 8 month study at the Sahigren's Hospital in Goteborg, Sweden tested 23 men aged 40-65 years in a fully controlled, double blind experiment in restoring testosterone levels to normal. The testosterone treated group improved in waist size, blood pressure, plasma lipids, fasting glucose, and insulin sensitivity. The treated group reported improvements of well-being and energy. Normalization of testosterone levels reduced many of the health warning signs associated with obesity. No adverse functional side-effects were found. (International Journal of Obesity 1992 16:991- 7)

    Some reports of negative side effects from oral testosterone have been reported; it is thought that the liver is the cause of these problems, and that application by skin patch to the scrotum avoids this problem.


    Animal studies on several Beta3-agonists show they fulfill many of the properties of the ideal anti-obesity drug. These compounds produce selective loss of body fat mass with a preservation of lean tissue. In addition, the changes in body composition are accompanied by favourable metabolic changes including improvement in glucose tolerance, reduction of hyperinsulinemia and hyperlipidaemia. (S18-3)


    "The genesis of this project was an invitation to discuss anorexiant medications with the house officers in the Medical Clinic as Strong Memorial Hospital. The colleague who invited me was dismayed that the treatment options used in the medical clinic were not helping people lose weight." Michael Weintraub, MD "both the medical profession and society look with disfavor on obese people and obesity in general. ... Obese people are treated negatively in cartoons and in literature. Many believe that obese people need only to "close their mouths" and be more motivated to lose weight. The use of medications to correct a characterologic defect is, in the opinion of physicians and the public, deemed inappropriate.

    Unfortunately, a lack of understanding of both the natural history of obesity and its diversity adds to the perjorative view of obese people and of anorexiants. Some health professionals are not aware of data concerning mechanisms present in the human organism that act to contravene perturbations in body weight and that may account for the apparent failure of interventions, including medications."

    To provide longer-term data, Weintraub et al developed a 4 year multimodal program using state-of-the-art behavior modification, caloric restriction, and exercise as the "placebo" for the entire duration of the four year study. Subjects attended nearly 100 visitations with health professionals during the study. When reading reports on The National Heart, Lung, and Blood Institute funded Multimodal Intervention Study, please keep in mind that this "state- of-the-art" treatment was the "placebo". (State of the diet/exercise/shrink art, that is!) "From the end of the second double-blind phase at week 190 through week 210, we monitored study participants to see what happened without medication but with continuing behavior modification, caloric restriction, and exercise therapy. ... One measure of the excellence of the ancillary [placebo] therapy in this study was that it enabled participants treated with placebo to lose just 0.01 kg/week less than participants receiving active therapy in the 18 studies that lasted at least 8 weeks reviewed by Scoville for the FDA."

    121 subjects, 18 to 60 years old, mean BMI of 33.4 +- 2.2, three fourths female, entered the medication phase of the study after 6 weeks of behavior mod, diet and exercise. 69 per cent had been on six or more diets previously.

    Subjects on medication lost about three times the weight as those only receiving behavior modification, diet and exercise. There was no indication of tolerance or abuse potential of the medication. There was no indication that use of anorexiant inhibits the learning of behavior modification.

    As reported by the New York Times New Service, Dr. Albert Stunkard, an obesity researcher at the University of Pennsylvania, said he knew of no other study that had elicited such a dramatic and sustained weight loss. It ``points to the way things are going to go,'' he said.

    The investigators found their patients could not maintain their weight loss without the drugs.

    The final 30 weeks of the program assessed what happened when all the patients were weaned from the drugs, relying on continued diet, exercise and behavior control. They gradually regained almost all the weight they had lost, despite the continuing program of diet, exercise and behavior modification.

    Some who believe that the essential defect in obesity is will power have asserted that the weight regain was from subjects' going "off the diet" when medication was withdrawn, instead of the diets' poor long term performance. A number of facts argue against this assertion:


  • Fenfluramine's appetite reducing effect wears off within a week. Any increased eating from cessation of the anroectic effect would have occurred much earlier.

  • Patients were on moderate diets, up to 1800 calories/day for men, 1200 for women. Most of the patients were veterans of a half dozen or more diet attempts. With this amount of metabolic slowdown, the traditional (diet/exercise/behavior mod) part of the program may not have been able to induce much long-term weight loss without benefit of the drugs' lowering of set point.

  • Lipid profiles, primarily affected by the diet and exercise, confirmed the weight regain was not caused by cheating on the diet.

    When the study was over, and subjects taken off the drugs were nearly as fat as they were initially, many tried to get the drug combination from their private doctors and ran into skepticism over the treatment.

    Some experts on weight loss hailed the studies, saying they could mark a pronounced shift in the way obesity is studied and treated.

    These experts said the results showed obesity could be treated the way chronic diseases like high blood pressure or arthritis are. In those diseases, drugs must be taken indefinitely to keep symptoms in check.

    ``This is a landmark study,'' said Dr. George Blackburn, an obesity researcher at New England Deaconess Hospital in Boston, author of the 1989 paper "Weight cycling: the experience of human dieters".

    Study VI of the report discusses individual outcomes. One subject did not reach goal weight (120% of ideal) but he was able to maintain his weight loss even after medication ceased. Some others did reach goal weight but gained it all back, or more. Most lost at least some weight but regained after medication ceased, despite continuing behavior modification, diet and exercise. Some lost little or no weight, or gained weight. Many of the failures were due to the experimental protocol which did not allow for individual adjustments that would have been made in a health care setting. Diet evangelists who do not appreciate the deep biological diversity of fat people should study this paper (and the papers on identical twins) carefully.

    Serotonin-reuptake inhibiting agents include flouxetine (Prozac), fenfluramine, and d-fenfluramine (dexfenfluramine, dF).

    In France and England, fenfluramine has been used in the treatment of human obesity for 25 years. No unequivocal report of major health hazards has appeared with fenfluramine in spite of extensive worldwide prescription for decades. Dexfenfluramine is the dextro stereoisomer of fenfluramine, and is a more potent antiobesity agent with fewer side effects. Tiredness and drowsiness were the most commonly reported unwanted side effects of treatment, but occurred as frequently with placebo treatment as with dexfenfluramine." (Clinical Neuropharmacology Vol 11 Suppl 1 S179)

    Over five million people have benefited from dexfenfluramine over the past seven years. "It's proven itself over and over again." (Dr. Rudolf Noble, Dir. Cathedral Hill Obesity Clinic, San Francisco)

    The conventional characterization of d-fenfluramine as an appetite suppressant is hopelessly oversimplified at best, if not downright inaccurate. "Our calorimeteric data indicate that dexfenfluramine induced anorexia and body weight reduction is a consequence of activated lipid oxidation" (Boschmann, Frenz, Noack, German Inst. of Human Nutrition, 5th European Congress on Obesity 10-12 June 1992))

    "According to most authors, tolerance to the anorectic effects of d-fenfluramine in rats rapidly sets in; food intake is depressed or only 2 to 6 days ... However, as long as the drug is administrated, the weight deficit persists." (Clinical Neuropharmacology Vol 11 Suppl 1 S105)

    "Following approximately a week of daily ingestion of fenfluramine, the body weight of female rats is reduced and remains chronically suppressed for as long as treatment is continued. This chronic suppression of body weight by fenfluramine cannot be explained by the anorectic effects of fenfluramine, since food intake returns to normal after about a week. Part of this chronic suppression of body weight lies in the ability of fenfluramine to enhance the thermic effect of food. Fenfluramine ingested by a fasted rat causes no change in metabolic rate. However, following the ingestion of the meal consisting of mixed nutrients or only carbohydrates, the thermic effect of the food is significantly greater than that of the meal without fenfluramine. A similar observation was observed in humans. These observations when combined with the negligible effects of dieting as a means of controlling body weight, argue for the chronic use of fenfluramine as a therapeutic technique to produce sustained weight loss in humans." (Clinical Neuropharmacology Vol 11 Suppl 1 S90-2)

    Is fenfluramine's anorectic effect essential to its antiobesity properties? When body weight was reduced in rats prior to treatment with fenfluramine, administration of the drug was followed by a rapid increase in food intake with maintenance of the reduced weight. The reduced body weight in fenfluramine-treated rats is defended; when animals are force fed to a higher weight and then allowed to eat ad libitum their food intake drops and body weight drops. (Recent Advances in Obesity Research: V 290)

    Fenfluramine normalizes obese subjects' human growth hormone (HGH) response to arginine. Normally obese subjects generate negligible amounts of HGH in response to arginine stimulation. (Hormone Research 1987: 27; 190-194)

    Fluoxetine, another serotonin-reuptake inhibiting agent, has been shown to improve insulin sensitivity and other metabolic actions.

    Dexfenfluramine is a related drug that increases metabolic rate (MR), diet induced thermogenesis (DIT), decreases blood pressure, and enhances glucose clearance. Dexfenfluramine reduces or prevents weight regain after slimming. The drug appears well suited for use in hypertensive or diabetic obese patients. (Clinical Neuropharmacology Vol 11 Suppl 1) (Progress in Obesity Research 1990) In rat, d-fenfluramine improves the insulin action of reducing the liver's glucose output. (DIABETES Apr 1989)

    The Weintraub study maintains a level of experimental design, reportage, disclosure and honesty that distinguishes it from most studies of traditional weight loss techniques. It is the longest weight control study of any type. It underscores the abject failure of traditional weight loss technology to improve the quality of life for most fat people.

    Free reprints of this 65 page supplement are available.

    Consumers Reports discounted the significance of the Weintraub study in their June 1993 issue on diets. CR would have served its overweight readers better if they had applied the same criteria to the marginal nostrums they recommended.

    Another study is underway at the Veterans Administration Medical Center in Hampton, Va. "This is comparable or superior to any medical treatment of obesity," said the study's author, Dr. Richard L. Atkinson. Atkinson and his colleagues gave the two drugs to 506 women and 57 men, most of whom have been followed for at least six months, and some for more than a year. Blood pressure in 49 subjects with high blood pressure dropped to normal. Twenty-four patients with high cholesterol saw those levels fall to normal, Atkinson said. And blood sugar -- an indication of diabetes -- also dropped to normal. "That's dramatic stuff." "We're fixing high blood pressure, high sugar and high fats by treating the underlying disease -- obesity," Atkinson said. The study underscores the growing belief among obesity researchers that diet, exercise and behavior change are not enough in most cases to produce long-term weight loss in overweight people. "We need to look for additional treatments," Atkinson said.

    Numerous papers on the antiobesity properties of serotonin- reuptake inhibiting agents appeared in Vol 11 Supplement 1 of Clinical Neuropharmacology (1988).

    A three year German study reported on a four year group therapy weight loss study. During the first year dexfenfluramine was administered to half of the group double-blind. Three years after cessation of drug treatment, the cholesterol, triglycerides, blood glucose and systolic blood pressure of both groups were above baseline values. The fenfluramine group lost more weight than the placebo group on group therapy, but suffered weight rebound after the drug was withdrawn. (IJO 1994 18, 391-5)

    The ultimate application of serotonin-reuptake inhibiting agents may be to prevent or minimize weight regain that usually follows dieting. (Am J Clin Nutr 1992:56: 195S-8S)

    Animal experiments have raised concerns about potential brain damage from some of these drugs. These experiments may not be relevant to human usage for weight loss.

    Study results presented Dec. 10, 1998 at the annual EUROECHO meeting showed no statistically significant increase in heart valve regurgitation or cardiovascular physical findings and outcomes when patients previously treated with fenfluramine or placebo for approximately three months were compared.

    Dr. Ravin Davidoff of Boston University Medical Center presented echocardiographic data and cardiovascular evaluations of women who had previously taken fenfluramine or placebo as part of a smoking cessation trial. Patients took the drug as part of that study approximately four years ago at The Fred Hutchinson Cancer Research Center in Seattle.

    Fenfluramine was frequently prescribed as part of the diet drug combination known as phen-fen. Fenfluramine, which was sold in the United States as Pondimin(R), was voluntarily withdrawn from the marketplace by Wyeth-Ayerst Laboratories on Sept. 15, 1997.

    "The study represented a unique opportunity to evaluate patients years after their participation in a placebo-controlled study with fenfluramine," Dr. Davidoff said. "After an average of 4.4 years following cessation of drug, there were no statistically significant increases in the prevalence of echocardiographic valvular abnormalities, cardiovascular physical findings and outcomes between fenfluramine-treated patients and placebo."

    Data were presented on 530 female patients (276 fenfluramine, 254 placebo) who participated in the smoking cessation trial. The echocardiographic portion of the study focused primarily on the FDA-defined criteria of mild or greater aortic regurgitation and moderate or greater mitral regurgitation.

    "These results are consistent with other data from controlled studies involving use of anorexigens for less than three months," Dr. Davidoff said.

    The withdrawl of these drugs and the massive lawsuit that resulted may be another result of today's widespread use of junk science and general abandoning of critical thinking in legal actions.


    Fat Cell Removal by Surgery

    Surgery is the only currently available fat reduction treatment that has demonstrated long term success in a majority of patients.

    Unfortunately, the amount of fat removed by currently accepted surgical procedures is too small to be useful for mainstream weight reduction purposes.

    A newspaper recently reported an increase in breast size for women who had "love handles" removed. It is possible the breast size was recovering from the effects of stringent dieting undertaken in unsuccessful attempts to spot reduce the "love handles".

    A South African study of freely-eating, non-obese liposuction patients showed no increase in fat cell size, metabolic efficiency, or regional adipose distribution 1 to 2 months after surgery.

    Surgical removal of fat in Cushing's Syndrome patients (4F- 21) resulted in an increase in lean tissue mass, and no fat regain.

    In adult male rats, having combined subcutaneous and epididymal lipectomy ("adipectomy") removing 24% of all fat, there was no difference in cell size between any fat depots compared to sham-operated animals at sacrifice after 12 weeks. There was no evidence of redistribution or compensatory growth of adipose tissues after lipectomy. (Acta Med Scand, Suppl. 723: 225-31)

    Diabetic patients receiving abdominal liposuction have reduced insulin requirements (dose reduced from 20 to 10 units). (Unpublished data) 11 obese patients with truncal obesity treated with abdominal lipectomy which removes subcutaneous fat. 4.5 month later, triglycerides, LDL, plasma insulin, and C Peptides were lowered. (Cazes et al, U of Toronto, IJO 1994 O617) By 1995 obese Type II diabetics will be treated with liposuction. This procedure is intended to lower the need for insulin by reducing the total number of fat cells in the diabetic's body. (Longevity Jan 1993; Fred Glazer M.D.)

    Ultrasonic suction lipectomy was applied to 205 patients with varying degrees of obesity. Triglyceride and blood glucose were improved 30 days after surgery. Late postoperative improvement in the blood glucose tolerance test was seen in 3 of the cases.

    Some efforts are underway to develop surgical procedures to significantly normalize fat cell numbers.

    Fat Cell Removal by Immunological Manipulation

    The Hannah Research Institute in Scotland have developed a treatment to reduce adiposity by targeting cytotoxic antibodies to fat cells. In early experiments, rat fat cell plasma was injected into sheep. The resultant antibodies were filtered and introduced into the rats. The treated rats lost fat.

    The treated rats also had more lean tissue than untreated controls. This suggests fat cells deprive lean tissue of nutrients necessary for growth.

    After treatment ended, the rats gained fat in other areas, restoring a normal amount of fat. This suggests some higher level mechanism prevents adipose mass from falling below norms. Normal weight rats were used in these experiments; results may be better for obese humans with diet induced adipocyte hyperplasia.

    In a 1991 telephone conversation this author was told Hannah's research is proceeding very well toward its goal of producing leaner animal meat. Human application in the near future was thought unlikely due to risk of malpractice lawsuits. A followup conversation in December 1996 found the previous pissimism regarding human application replaced by optimism coupled with an understandable reticence to disclose proprietary information. The specificity of antigens no longer appears to be an insurmountable problem. Cambridge Antibody Technology are cooperating with Obesus, and some of the large pharmaceuticals are interested in human applications of this technology.

    Other researchers, using monoclonal antibodies, report success in longer term suppression of fat cell numbers. (Private conversation, 1992)


    Some of the current obesity epidemic will be traced to nutritional and hormonal problems during pregnancy and/or infancy. Pregnancies with gestational diabetes and other problems that previously failed now produce preobese children. The introduction of high carbohydrate baby formula and sugary baby foods in this century will also be a factor.

    Low Energy weight loss diets applied early in life will also be implicated. Within the decade, prescription of energy restriction weight loss diets for patients with childhood onset obesity will be recognized as a violation of the Hippocratic Oath.


    Popular attitudes on obesity are based on the notion that obesity is caused by sloth and gluttony. Recent research has discredited this stereotype and suggested possibilities for effective prevention or treatment in the future.

  • Add a $5 checkoff to income tax forms allowing taxpayers to earmark money for the research and deployment of new weight control technology.

  • Truth in Advertising must be enforced on all weight loss claims. Advertising must accurately and graphically depict the long term results obtained by typical users, accurately reporting the prevalence of long term weight regain and rebound.

  • In the meantime, the protections of the Americans with Disabilities Act should be extended to fat Americans whose diligence in dieting has made them so heavy.

  • Diagnostic procedures are needed to identify the 1 per cent of overweight subjects for whom weight loss diets provide long term benefits.

  • Policies and public education are urgently needed to reduce diet induced adipocyte hyperplasia. This is an area where malpractice and product liability lawyers can do some good. The recent lawsuit settlements by Nutri-System Weight Loss Inc. are a promising start. A meeting on the subject at a recent Trial Lawyers' convention bodes well for the future. President Clinton's links to trial lawyers and his refusal to criticize malpractice suits may encourage this development.

  • Effective interventions to correct human obesity must be developed and deployed. One hundred million American endomoprphs deserve more than a few dimes' worth of legitimate obesity research.

  • Accurate information on medications' weight gain side effects must be provided. Non fattening alternatives should be developed.

  • Medical interventions must be developed to replace the natural selection against obese/diabetic offspring that has been short circuited by modern medicine. Neither eugenics nor today's discrimination are acceptable.

  • Since impaired insulin sensitivity often precedes obesity and other complications of Syndrome X, infants and children should be routinely screened for insulin sensitivity or high insulin levels. Prompt corrective action to normalize insulin sensitivity is needed to ward off obesity, NIDDM, and other complications of Syndrome X. At risk children should also be screened for testosterone, thyroid, growth hormone, cortisol, and fat cell numbers.

  • Doctors should properly diagnose and properly treat the medical conditions of their obese patients instead of insisting on unrealistic weight loss as an alternative or precondition to treatment.

  • Doctors should ascertain patients' fat cell numbers and sizes before prescribing weight loss regimens. They should disclose the long term effects of their proposed regimens on fat cell number. They should disclose the long term reduction (if any) of patients' fat cell sizes.

  • Doctors must monitor collagen, essential fatty acid, and serotonin levels during dietary restriction and correct as necessary to avoid the unhealthy dieting consequences documented in the medical literature.

  • Regulatory interference in the development and deployment of effective new treatments must abate. Public health would be better served if regulators shifted their attention to the abuses of the traditional weight loss industry.

  • Mothers should limit carbohydrate and sugar consumption during pregnancy and lactation to prevent excessive insulin levels.

  • When possible, mothers should exclusively breast feed 6 to 12 months or longer. Exclusive breast feeding decreases the development of eventual obesity. In cases where breast milk is unavailable, the infant's diet should have the same macronutrient composition as human breast milk.

  • Infants should not be fed a high carbohydrate diet unless repeated measurements of their insulin levels demonstrate they can tolerate high levels of carbohydrate consumption.
  • "We recognize that the message we have for endocrinologists and metabolic specialists is a somber one, difficult to the sufferer from obesity. On the other hand, it seems to us most consonant with the true state of affairs. Our understanding of genetic mechanisms is progressing rapidly and the interaction between genetic endowment and early environment will be under intensive study in the next decade. This is the hopeful side of the problem." (CLINICAL REVIEW 28: A Biological Basis for Human Obesity, Journal of Clinical Endocrinology and Metabolism, 1991.)


    Dr. Bernstein's Diabetes Solution (Not only for diabetics)

    Human Obesity: Exploding the Myths The Western Journal of Medicine Oct 1990; 153;421-428

    The carnivore connection: dietary carbohydrate in the evolution of NIDDM (Diabetologia (1994) 37;1280-6)

    Annals, New York Academy of Sciences, book length issue on

    Human Obesity

    LONG TERM WEIGHT CONTROL: The National Heart, Lung, and Blood Institute funded multimodal intervention study, Clin Pharmacol Ther, May 1992 Reprints of the entire supplement are available at no charge. Direct requests to: Michael Weintraub MD Department of Community and Preventive Medicine University of Rochester School of Medicine PO Box 644 Rochester NY 14642

    Information on the medications used may be obtained with a self addressed stamped envelope mailed to: DIET STUDY University of Rochester Medical Center POB 643 Rochester NY 14642

    OBESITY AND LEANNESS, Basic Aspects, ISBN 0 86196 0173

    Never Say Diet? article by Ruth Papazian, FDA CONSUMER, article downloaded from the Food and Drug Administration Bulletin Board. For copies contact the FDA Publications Staff at 301-443-3220.

    "Making Peace with Food", Susan Kano, 1989, Harper & Row, ISBN 0-06-096328-X

    Proceedings of the Nutrition Society (1992) Vol 51, pp 400 ff. (special issue on the Manipulation of Adiposity)

    SYMPOSIUM ON OBESITY: Metabolic Study in Human Obesity with Isocaloric Diets High in Fat, Protein, or Carbohydrate METABOLISM 6 (1957) 447-60


    References such as (4F-21) refer to paper designations in the Tokyo International Congress on Obesity abstracted in the International Journal of Obesity. Some of these papers appear in Progress in Obesity Research 1990 (Proceedings of the 6th International Congress on Obesity), John Libbey & Sons ISBN 0 86196 274 5

    References to the 5th European Congress on Obesity are abstracted in the International Journal of Obesity v.17 Supplement 2. "Recent Advances in Obesity Research: V" ISBN 0-86196-072-6

    "CLINICAL REVIEW 28: A Biological Basis for Human Obesity", Journal of Clinical Endocrinology and Metabolism, 1991.

    "Progress in Obesity Research 1990" ISBN 0 86196 274 5

    "Obesity in Europe 88" ISBN 0-86196-167-6

    International Journal of Obesity (Periodical)

    "Fat Chance" Nova episode broadcast on PBS (1983)

    Annals, New York Academy of Sciences, book length issue on Human Obesity

    The Callaway Diet, Bantam non fiction paperback, ISBN-0- 553-28708-7

    "Diet and Health: Implications for reducing chronic disease risk"; Committee on Diet and Health Food and Nutrition Board Commission on Life Sciences, National Research Council; National Academy Council, Washington D.C. 1989.

    Progress in Obesity Research 1990 (Proceedings of the 6th International Congress on Obesity), John Libbey & Sons ISBN 0 86196 274 5

    "Number and Size of Adipose Tissue Fat Cells in Relation to Metabolism in Human Obesity" Page 703, Metabolism, Vol 20 No 7 July 1971.

    "Lean Body Mass, Exercise and VLCD", International Journal of Obesity (1989), 13 (suppl. 2), 17-25.

    "Super Nutrition for Women", Ann Louise Gittleman, Santa Monica Pritikin Longevity Center nutrition director, Bantam Books, 1991


    Low Carb FAQ

    Index of research articles

    Banting's 1869 Letter on Corpulence

    Long article on insulin

    The Low Carb Retreat

    Online Guide to Low-Carb Diet Resources

    Insulin and its Metabolic Effects (backup copy)

    Canadian Low Carb Site

    The World's Biggest Fad Diet

    The latest Adiposity 101 is available at

    Low Carbohydrate & Ketogenic Diet Resources
    Insulin Resistance (Syndrome X) Information
    Low Carbohydrate Diets Web Page
    Paul on Fat (Low Carb Advice)
    Hypoglycemics' Diet
    Dr. Barry Sears' The Zone Web Page
    Diabetic Neuropathy - A New Approach
    Glycemic Index Web Page
    Lipid Metabolism
    Altered Immunity and the Leaky Gut Syndrome
    DHEA Web Page
    DHEA and Melatonin Web Page
    American Journal of Clinical Nutrition
    Paul McAleer's Fat Acceptance Page

    Other resources
    Other resources
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    Dangers of Trans-Fatty Acids
    Diet and Human Evolution

    ©1997 Chuck Forsberg. This page may be freely linked to, mirrored, or redistributed provided it is not modified.

    End of Adiposity 101

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Tue Aug 12 06:35:55 1997 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from Message-Id: <> Received: from Date: Mon, 11 Aug 1997 22:30:06 -0700 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Ray Audette Organization: Paleolithic Press Subject: Re: restricting calories[via LSMTP - see] To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R > >I have tried deluding myself for years that I am genetically > >predisposed for being fat, and I can't help it, but I've lost weight > >enough times to know that I can't do it unless I'm restricting > >calories, exercising more than just moderately, and restricting > >carbs to ward off binges. Many species including Man are predisposistioned to store fat. This is a biological necesitity given the seasonal availability of almost any food source anywhere in the world. The body must have some mechanism to determine when to store fat and when to burn the stored fat. This fat must be stored no matter how much the food supply may vary from year to year, so calories are not useful to this process in the long run. By varing the overall metabolic rate, energy is conserved to store fat when the signal is given regardless of caloric intake levels. The signal to store fat in many ominovores (including bears and humans) is the presence of high-carbohydrate vegetable foods available in the spring and summer. Herbavores also store fat this way and store fat until the late fall and early winter when the carbohydrate levels in their food start to fall dramaticly. Pre-technology, Man had limited access to vegetable foods for much of the year. In temperate climates winter cold killed most vegetation and in more temperate zones the dry season had the same effect. Even in tropical rain forests, edible fruits becomes scarce for much of the year. Without technology-dependent foods (grains,beans,potatoes,dairy and refined sugars and vegetable oils) all that is available for Man to eat is fatty winter meat. This signals the body that it is time to raise the metabolic rate and burn stored fat. This higher metabolic rate makes game easier to catch and is useful for withstanding harsh conditions. But even in winter, a reduction in calories will result in a slowing of the metabolic rate and slow the burning of stored fat to forstall starvation. In our constant supermarket summer, it's no wonder most humans are overweight by hunter-gather (the thinnest people in the world) standards. Convince your body that the proverbial "rainy day" of winter has arrived by lowering carbs and watch it do what it was designed to do! Ray Audette Author "NeanderThin:A Caveman's Guide to Nutrition"
    One of the principle sources for dietary fat in Americans is milk and milk products. A coralation between fat and cancer may indict milk because of its' contribution to total fat. But is it the fat or the proteins in milk that causes the problem? Milk proteins have been implicated in the immune reaction that causes Type 1 diabetes in children. They also are the source of one of the most common food alergies. The May '97 issue of the Harvard Women's Health Watch (newsletter)had an article that abstracted a couple of studies that showed an increased risk (2.5-3.5X) for breast cancer in women with high bone denisity. High bone denisity is usually seen as a reliable indicator of high milk consumption. We know that milk contains several proteins that promote growth and have seen the effects of lactation on breast tissue growth. Proteins are more likely candidates as mutatagens than are lipids as they are more unique to each species and thus more likely to produce an immune system response (see Ames,B.N. "Paleolithic Diet, Evolution and Carcinogens", Science 238(Dec. 18,1987)1633-34. Bruce Ames (U.C. Berkley)is considered by many to be the leading authority on cancer causation. Ray Audette Author "NeanderThin:A Caveman's Guide to Nutrition" Alan Silverstein wrote: > > In particular I got to ask him about fat in the diet versus cancer risk: > What's the deal?
    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Wed Oct 8 09:22:56 1997 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id JAA18706 for ; Wed, 8 Oct 1997 09:22:52 -0700 (PDT) Message-Id: <> Received: from by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Wed, 8 Oct 1997 12:22:21 -1300 Date: Wed, 8 Oct 1997 12:16:36 -0400 Reply-To: LowCarb Low-Carbohydrate Technical Discussion Sender: LowCarb Low-Carbohydrate Technical Discussion From: Dean Esmay Subject: Re: Some Low Carb concerns/questions To: LOWCARB@MAELSTROM.STJOHNS.EDU In-Reply-To: <> Status: RO Covert Bailey spreads a whole lot of misinformation. His overriding philosophy that exercise is the only sure way to lose fat ignores one important fact: every single study on exercise to date, regardless of the type of exercise, (aerobic, anaerobic, resistance training, split routines & combo approaches, etc.) has shown that exercise almost always fails to alleviate obesity--whether combined with hypocaloric and/or low fat diet or not. People have gotten angry with me many times for saying this. But none of them ever point to any research refuting this point--because there isn't any. Or if it's there, I have yet to find it, and no one who argues with me has found it either. So far anyway. There are, of course, numerous benefits to health and well-being for exercise, including moderate fat loss and lean tissue gains. People with only 10 pounds or so to lose may get all the weight loss benefits they need from exercise. But anyone who claims that exercise is the key to solving weight problems in the chronically obese is simply not telling the complete truth about what the actual research on the subject has shown.
    Sweden-Obesity Copyright, 1997. The Associated Press. All rights reserved. The information contained in this news report may not be published, broadcast or otherwise distributed without the prior written authority of The Associated Press. STOCKHOLM, Sweden (AP) -- A new study provides more evidence that obesity is an inherited condition for many, researchers at the Karolinska Institute said Tuesday. The results may not help overweight people slim down, but could comfort them by showing they are not to blame for their weight problem. The study of 200 women showed that a particular gene mutation was seven times more common in overweight women than in women of normal weight. Overall, 15 percent of the women had the gene, and all but three of them were obese. On average, those who carried the mutated gene had 44 pounds more fatty tissue than those with the normal form of the gene, according to the study, performed at the institute that awards the Nobel Prize in medicine. Research leader Peter Arner said identifying the gene mutation could be useful in predicting whether a child is likely to be susceptible to obesity. "It's fascinating," the Swedish news agency TT quoted him as saying. "You can ask why this is so, but so far we can't answer that." The study follows work done earlier by Arner and colleagues that linked the difficulty in shedding excess weight to a particular hormone receptor. The new study, to be published in the Journal of Clinical Investigation, shows that the gene for that receptor is mutated in many people.
    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Sat Nov 15 05:30:36 1997 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id FAA28122 for ; Sat, 15 Nov 1997 05:30:31 -0800 (PST) Message-Id: <> Received: from by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Sat, 15 Nov 1997 8:30:29 -1300 Date: Fri, 14 Nov 1997 18:40:01 -0500 Reply-To: LowCarb Low-Carbohydrate Technical Discussion Sender: LowCarb Low-Carbohydrate Technical Discussion From: Ilya Subject: Re: Slow loss To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R This is a response to all three messages about slow weight loss, not just this one. I have converted quite a few people to low carbing within the last year. Counting people converted by my converts I am probably responsible for 3 dozen by now (if not more). Several people report slow/no loss. WITHOUT FAILING THE CAUSE HAS BEEN THE SAME - not enough food and not enough fat. It's hardest to convince women to eat more, especially more fat. Even those who buy into low carbing will still try to pursue a fairly low calorie/low fat diet. Eat more fat! See my rough estimate for your calories per day and comments below: Florence Cameron wrote: > > In a message dated 97-11-14 07:08:51 EST, Anita writes: > > << Seems I'm "converting" all my family and friends to lowcarbing. My > 27 yo > daughter started 3 weeks ago. She's been up and down the scale - > most > recently lost her weight on phen-phen then stopped when all the bad > press > was > released (pshew!!). Anyway, she promptly regained about 25 lbs. On > Atkins > she reports feeling better and purple sticks but only 2 lbs lost in 3 > weeks. > That's so different than my experience. Has anyone had her > experience... > would appreciate the sharing to encourage her. anita >> > > My weight loss is only slightly better. I lost only 3 lbs in the > first 10 > days (and I have a total of 100 lbs to lose)!! I am 5'6" and I'm > about 230 > lbs. > > My stick is not showing purple or is trace when I wake up. By mid > afternoon, > it's in the moderate zone, where it stays until sometime after dinner. > By > bedtime, it's back down to trace. > > A typical day's diet for me is: > > 7:30 3 eggs, 8-10 sticks bacon, a tablespoon of sour cream, diet > Coke 470 calories (according to one calorie guide) > 12:30 2 small sized bacon cheeseburgers served on lettuce, 1 slice > tomato > OR > a 3 egg cheese and onion omelet with 3-4 slices of bacon, > lettuce, > 1 slice > tomato, diet Coke about 450 calories (for the omlette) > 3:00 about 2-3 oz. hard cheese, maybe 1 or 2 sugar free Jellos, > each with > a > dab of heavy whipped cream 200-300 calories + ? for heavy cream (not sure how big a dab is) > 4:00 coffee, 1 Equal, 1teaspoon heavy cream > > 6:30 about 8 oz steak or beef, usually 2 tablespoons of sour cream, > about 2 > oz > of hard cheese, diet Dr. Pepper 600 cal for beef (about, depends on the cut), 50 cal for sc, 200 for cheese > 8:00 either 2 oz. hard cheese or 2 Sugar Free jellos each with a dab > of > heavy > whipped cream 200 for cheese The total for the day: 470 + 450 + 250 + 850 + 200 = 2220 calories per day Not sure how big you are right now, but this would be fine only if you are rather small. Remember, if you are in ketosis you aren't even getting all these calories (you only get about 5 calories/gram out of fat if it's not burned completely, and if you show purple on the stix then it's not burned completely). The other problem is not having enough fat even if you get enough calories. I am running out the door right now and don't have time to check the fat % in your food, but it should be at 70 % or higher. Even better, just figure out how much protein you need per day and the rest should be fat (with trace carbs). If you have too much protein then your body may start burning it as carbs (making glucose out of them). My quick guess is that your diet does not have high enough % of fat in it. Two remaining hints - drink more water. You often will not be thirsty, but if you try to drink it will taste good. In that case - drink more. (If you try to drink and don't feel like it or the water doesn't taste good to you at that point, then don't). If you are in more than trace ketosis you will probably loose more fat by drinking more weight. Your body will stop burning fat if it can't get rid of excess ketones to avoid too high levels of ketones in blood. The other hint is try eliminating nutrasweet (you seem to be consuming a fair bit of it). Some people have problems with it, especially on low carb diets. Ilya
    > >Nancy Humeniuk wrote: > >>Ann, how does this explain those of us who are not over-weight but >>>still > >>have insulin resistance? > >I don't really know, beyond the glib generality that these things are > >probably multi-factorial. How was your insulin resistance measured? Hi The following is my response to this thread. It is the text of a letter I wrote to a colleague on the topic of Ovarian Dysfunction Allen E Gale Dec3'97 TOMCAN/AEG/BSJ-B November 21, 1997 Part of the problem with insulin resistance/metabolic syndrome is the diversity of clinical features which are associated. As Reaven first stated in his benchmark lecture back in 1986 (?87) - it was the "Banting Memorial Lecture". He said, or words to the effect - "at first blush it appears outlandish to suggest an association between hyperinsulinaemia, hypertension and hypertriglyceridemia". Hyperinsulinaemia has now of course been clearly associated with infertility and ovarian dysfunction and I enclose** a photostat of an article from the Advertiser in which Professor Norman publicly acknowledges this phenomenon; it is now recognised by the Heart Foundation (enclosed**) as being an important piece in the jigsaw puzzle of coronary vascular disease and it is now quite clearly accepted by the AMA in two recent articles which appeared in the Messenger Press(enclosed**) - both of which refer clearly to insulin resistance. Unfortunately understanding of insulin resistance is bedevilled by the extreme complexity of the endocrine orchestra. I thought it would be helpful to set the following points down. In my reading, the (gynecological) clinical features associated with insulin resistance include eclampsia, impaired intrauterine growth and intravascular abnormalities of the clotting mechanism as well as gestational diabetes, generalised pruritus, vaginitis, menstrual irregularities, chronic candidal vulvovaginitis, large babies (>9 lb or 4.1kg), polyhydramnios, preeclampsia, or unexplained foetal losses. Another angle in the jigsaw puzzle of IR in women is illustrated by a case that recently has come under my care. A woman who has had repeated foetal losses where I was unable to display convincing evidence of insulin resistance in the mother but the father has clearcut insulin resistance on glucose/insulin tolerance testing. This immediately raised the question of the impact of a foetus bearing the thrifty gene inutero of a woman who under the physiological responses of pregnancy becomes normally insulin resistant - insulin resistance being part of the normal physiological response to pregnancy. Such a mother, in the absence of the thrifty gene may well get through the pregnancy without progressing to gestational diabetes even though her diet contains a high intake of refined carbohydrate. However what is the impact of that on the foetus? Insulin has been aptly described as a "dangerous peptide" and again what would be the impact on the mother of rising insulin levels in the foetus. You may know of the work of the Austrian physician in relation to measurement of amniotic insulin levels. I have not had a chance to follow up this lead but I could send further details later.** But I digress! My purpose in writing was to suggest that whilst we need to measure both glucose and insulin levels, the diagnosis of insulin resistance/metabolic syndrome may often rest entirely on clinical grounds. The failure to get consistent results does not mean that we should not do the test but rather suggests that there are several wild-cards which have not yet declared their presence. To recapitulate my understanding of insulin resistance, it runs this way:- and I welcome your comments/criticisms and suggestions and comments and criticisms from the others who receive and may still be reading this letter!:- Insulin resistance (IR) may be pre-receptor, receptor or post-receptor; pre-receptor IR may be due to insulin antibodies - this appears to be rare and is reported to be associated with acanthosis nigricans and the HAIR-AN Syndrome. I have found a number of patients with the pigmentation which is supposed to be classical of acanthosis nigricans but have not found one patient with insulin antibodies (the question is:- are we missing the antibodies because of faulty laboratory technique or is this condition rare?). Receptor IR may be any one of over 40 different mutations of the insulin receptor. It would appear purely on clinical grounds that the body uses IR as a physiological response to the needs for a high blood sugar level - in the teenage years, in pregnancy, during acute and chronic stress associated with infection, trauma, surgery and of course emotional stress. Also on purely clinical grounds it would appear that these mechanisms of IR due to mutations of the receptor are switched on and off to achieve certain physiological processes - presumably much as elevation of the body temperature is part of the body's defence against infection. Does the diversity of different mutations of the insulin receptor reflect the diversity of clinical features associated with insulin resistance - the list growing almost daily and ranging from the original deadly triad of Reaven to diabetes and polycystic ovary disease, to name the commonest. Then there is the post-receptor IR. At my last rain-check there were over 7 different glucose transporter proteins - glut 4 being the active transporter in all cells except the gut, red cells and brain; glut 4 production being stimulated to be produced by the mitochondria of the cell by the excitation of the insulin receptor by attachment of the insulin molecule. But the scenario only just begins with the above, insulin itself is opposed by glucagon secreted from the alpha cells of the pancreas; Somatostatin also secreted by the pancreas opposes both insulin and glucagon and another wild-card is pancreatic peptide whose function eludes me; then Somatastotin is also secreted by the gut. Then of course there is the whole list of insulin-like growth factors which presumably become fixed in tissues and have insulin-like activity and capable of pulling down glucose. Finally there is this protein referred to as "PC-1"** produced by the obese cells. This apparently is capable of inducing a post-receptor defect in blocking the action of glucose transporter protein. I am sure there are other post-receptor mechanisms of IR which I have not discovered as yet in the literature. My brief attempt to tie the features together has not attempted to link in leptin and the other mediators. Certainly a claim could be made for the recognition of insulin assays as a useful adjunct in the evaluation of insulin resistance. As you may know, I have been forced to consider measurement of insulin assays as a research tool in view of the opposition I have encountered from my endocrine colleagues and the questions I have been asked by the Health Insurance Commission to validate my use of this test. (Incidentally I am out of trouble with the Health Commission since all of my patients now pay for the insulin assays). An interesting comment came to me from one pathologist. He stated that there are so many undiagnosed individuals in the community with insulin resistance that if they were all diagnosed accurately it would bankrupt the health care system! The bottom line of course remains how do we treat these individuals. This would appear to be through diet, exercise and weight control, the latter only coming when there is correct diet and exercise. Correct diet remains a controversy and it is interesting that our American friends are talking about a class action against dietitians and nutritionists for mis-information in relation to the high carbohydrate low-fat diet! Heaven spare us from such litigious thinking but the message is there; the medical profession should adopt an open and inquiring mind and whilst these newer topics must be regarded as research, it is those who ridicule such thinking that should be the ones to put themselves at risk of litigation! I would draw your attention to an article from the low carb list giving quotes from a review of diets in prevention of heart disease; I will send it later.** ** the above references are currently only in hard copy, but I will get them typed up and sent to the list! --------------------------------- Now to throw in a whole new concept, have alook at the following abstract; this comes into line with the above concepts if Godfrey's subjects are mothers with normal gestational IR but the foetus carries the thrifty gene from the father. Fascinating! --------------------------------------Abstract-------------------------- FETAL PROGRAMMING AND ADULT DISEASE Keith Godfrey MRC Environmental Epidemiology Unit, University of Southampton UK The "fatal origins" hypothesis states that adult coronary heart disease, and the associated disorders stroke, non-insulin dependent diabetes and hypertension are programmed by undernutrition in utero. Animal Studies: Experimental studies have long since established the principle that stimuli applied at critical, sensitive periods of early life can have permanent effects on a range of physiological processes,1 a phenomenon termed "programming". Numerous experiments in animals have shown that undernutrition in utero leads to persisting changes in blood pressure, cholesterol metabolism, insulin responses to glucose, and in a range of metabolic, endocrine and immune parameters. Epidemiological studies: Evidence that coronary heart disease, hypertension and diabetes are programmed initially came from longitudinal studies of 25,000 UK men and women in which size at birth was related to the occurrence of disease in middle age.2 People who were small or disproportionate (thin or short) at birth had high rates of coronary heart disease, raised blood pressure and cholesterol levels, and abnormal insulin metabolism. These relations have been shown to reflect fetal growth retardation rather than premature birth. Repeated replication of the UK findings has led to wide acceptance that low rates of fetal growth are associated with cardiovascular disease in later life. Associations with coronary heart disease have, for example, been shown in studies from the USA, India and Finland;3 in different populations, associations with raised blood pressure and with non-insulin dependent diabetes have been replicated in 23 studies4 and in 8 studies respectively.5.6 Clinical studies: Detailed clinical studies of adults with known body proportions at birth are beginning to unravel the mechanisms that might link fetal exposures with later disease. Thinness at birth, for example, is thought to reflect fetal undernutrition in mid-late gestation;7 it is associated with insulin resistance and coronary heart disease in adult life. Magnetic resonance spectroscopy has shown that the adults who were thin at birth have reduced rates of glycolysis in their muscles. This could indicate persistence of a fetal glucose sparing adaptation. Persisting alterations in metabolism may be partly mediated by programmed changes in the production of hormones or in tissue sensitivity to them: programming of the hypothalamic-pituitary-adrenal axis is one current focus of research.8 Fetal undernutrition: Small size at birth and disproportion in head size, length and weight are thought to be surrogate markers for the influences that programme the human fetus. Several lines of evidence suggest that nutritional influences may underlie cardiovascular programming: (1) fetal undernutrition programmes physiology and metabolism in animals; (2) fetal growth is essentially regulated by nutrient supply; (3) alterations in fetal and placental growth that predict cardiovascular disease in humans are related to nutrition in pregnancy and can be experimentally induced in animals; (4) diet in pregnancy is associated with altered blood pressure levels in the offspring; and (5) maternal body composition in pregnancy has been linked with coronary heart disease in the offspring. The future: We need to progress beyond epidemiological associations to define the underlying cellular and molecular processes, and to determine how these programmed changes become translated into pathology. We need to identify the specific aspects of maternal body composition, metabolism and nutrient intake that lead to fetal undernutrition, and to understand the consequent fetal adaptations. Further research requires a strategy of interdependent clinical, animal and epidemiological studies. 1. McCance RA, Widdowson EM (1974) The determinants of growth and form. Proc R Soc London 185:1-17. 2. Osmond C, Barker DJP, Winter PD, Fall CHD, Simmonds SJ (1993) Early growth and death from cardiovascular disease in women. BMJ 307:1519-24. 3. Forsen T, Eriksson JG, Tuomilehto J, Teramo K, Osmond C, Barker DJP (1997) Mother's weight in pregnancy and coronary heart disease in a cohort of Finnish men: follow up study. BMJ 315:837-840. 4. Law CM, Shiell AW (1996) Is blood pressure inversely related to birth weight? The strength of evidence from a systematic review of the literature. J Hyperten 14:935-941. 5. Hales CN, Barker DJP, Clark PMS, Cox LJ, Fall CHD, Osmond C, Winter PD (1991) Fetal and infant growth and impaired glucose tolerance at age 64. BMJ 303:1019-22. 6. Lithell HO, McKeigue PM, Berglund L, Mohsen R, Lithell UB, Leon DA (1996) Relation of size at birth to non-insulin dependent diabetes and insulin concentrations in men aged 50-60 years. BMJ 312:406-10. 7. Barker DJP, Gluckman PD, Godfrey KM, Harding JE, Owens JA, Robinson JS (1993) Fetal nutrition and cardiovascular disease in adult life. Lancet 341:938-41. 8. Edwards CRW, Benediktsson R, Lindsay RS, Seckl JR (1993) Dysfunction of placental glucocorticoid barrier: link between fetal environment and adult hypertension? Lancet 341:355-7. 9. Campbell DM, Hall MH, Barker DJP, Cross J, Shiell AW, Godfrey KM. (1996) Diet in pregnancy and the offspring's blood pressure 40 years later. Br J Obstet Gynaecol 103:273-280. Godfrey K, Robinson S, Barker D, Osmond C, Cox V. (1996) Maternal nutrition in early and late pregnancy in relation to placental and fetal growth. BMJ 312:410-414. From:- The Australian Society for Medical Research 36th National Scientific Conference Adelaide Convention Centre, Adelaide, SA. 23-26 November, 1997. ---------------------------------------------------------------------------- -------------- Incidentally, in view of my interest in growing Shiraz in the Flinders Ranges, I wonder where the benefits of red wine in relation to coronary vascular disease fits in? Apparently studies have also suggested reduced mortality in those who drink white but the major benefit appears to come from the red wine. Is it just the anti-oxidants or is it some more subtle effects on the metabolic pathways. Of some anecdotal interest is one patient I had who had severe hyperinsulinaemia and he was concerned whether he should cease his enjoyment of wine. I sent him to the laboratory to consume a half bottle of white wine on an empty stomach! Neither his blood glucose or insulin levels made any great changes but he certainly was not fit to drive at the end of 2 hours! But then someone the other day was saying that alcohol elevates blood triglycerides? Some have suggested that alcohol elevates blood triglycerides. But is this wine or beer; this is why "Longbrew" beer has entered the market; the carbs have been fermented to a low level, and this reduces the tendency for beer to increase intra-abdominal fat. I suspect, from my understanding of IR, that the real danger of alcohol only starts when the drinker is on a high carbohydrate diet. We need more data. Cheers Allen Dec7'97 Date: Fri, 23 Jan 1998 16:39:44 -0500 From: Dana Carpender To: LOWCARB@MAELSTROM.STJOHNS.EDU > . All are men except my daughter. > (Youth?) Probably. Doesn't it make you crazy? :-) Yes, men and the young do both lose more easily than mature women. > My sister in law and I have not lost any weight other than the > initial water loss. Does anyone have any ideas or read about > comparisons that may help > answer our dilemma? Thanks. Are you taking the pill? Or, if you're older than that, are you on ERT? Both can have a big effect on insulin, and render the diet ineffective. I know more than one woman who has gained twenty pounds or more from going on the pill. If you're taking it, I'd switch over to barrier methods or the IUD. (Norplant and Depoprovera won't help.) If you're on ERT, talk to a doctor about trying DHEA instead. (If you're over 35 or so, you might look at taking DHEA anyway. I went on it two years ago, at 37, and felt dramatically better -- more energetic and better moods -- within a few days. My muscle tone improved, my athletic stamina increased, and I dropped 7 lbs in 10 days. You'd need a gun to get the stuff away from me!!) Steroid medications, like prednisone, can be a problem. They mimic the action of some of the adrenocortical hormones that encourage water retention and fat deposition. (The weight creep I complained about several weeks back turned out to be due to an adrenal-stimulating herbal tonic I had started taking for allergies. Helped the allergies, but made me grow like a Ballpark Frank that plumps when you cook it! I'd rather have allergies.) Food sensitivities can be a real problem, too. I'm having a much easier time keeping my weight down now that I've figured out that peanuts make me blimp up. Doesn't seem to be the carbs, I wasn't eating enough for that to be the problem. I just seem to have an idiosyncratic reaction -- eat peanuts, get a double chin in fifteen minutes. (BUMMER!!) Another spoiler is candida. If you've had a lot of antibiotics in your life, and have a lot of gas and bloating, fatigue, brain fog, and constipation and/or diarrhea, you might look at this. Unfortunately, if this is the problem, you'll have to restrict the diet even further -- no cheese, vinegar or other fermented foods, mushrooms, etc. Probably have to take nystatin or caprylic acid, too. The *last* thing I'd look at is portion control. There are a few people who have to control *both* carbs and portions, although they can eat more calories on a lowcarb diet than they could on lowfat/high carb. But if any of this other stuff has rung a bell, I'd start there first. Dana (who hates the very *thought* of portion control!) At 10:20 AM 4/6/98, Beverly Meyer wrote: >I have read many times that protein uses more energy (calories?) in >digestion than it actually produces. If true, can anyone explain this? Not thermodynamically possible. Protien does have a higher Specific Dynamic Action (SDA) than carbs or fat. Ingestion of protein will cause an expenditure of 25% as many caloreis as are consumed. So if you eat 100 caloreis of protein, you will burn 25 calories digetion them. Carbs have a SDA ~15-20%, fat about 3%. Lyle McDonald, CSCS "The ketogenic diet simulates the metabolism of a fasting body....As a fasting body burns it own fat for energy, so a person on a ketogenic diet derives energy principally by burning fat rather than from the more common energy source, carbohydrate." John Freeman M.D. in "The Epilepsy Diet Treatment- An Introduction to the Ketogenic Diet"
    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Sat Apr 18 06:28:20 1998 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id GAA00051 for ; Sat, 18 Apr 1998 06:28:18 -0700 (PDT) Message-Id: <> Received: from by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Sat, 18 Apr 1998 9:22:28 -1300 Date: Sat, 18 Apr 1998 06:58:08 EDT Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Elbrams Subject: Re: LOWCARB Digest - 14 Apr 1998 to 17 Apr 1998 (#1998-27) To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: RO In a message dated 98-04-17 16:40:20 EDT, you write: << a stimulant that works by making the neurotransmitter dopamine more available in the brain, >> I have ADHD and had lowcarbing recommended to me by my physician because he learned at a nutritional conference that the diet also boosts the production of dopamine. Have been on it for 15 mos. Not only lost 50lbs, but have my ADHD under control for the first time in my life!!! (I'm 52 y.o.) Am eternally grateful. Hope others have experienced similar results. Anita

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Sat Apr 18 14:08:55 1998 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id OAA03151 for ; Sat, 18 Apr 1998 14:08:51 -0700 (PDT) Message-Id: <> Received: from by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Sat, 18 Apr 1998 17:03:34 -1300 Date: Sat, 18 Apr 1998 17:03:05 -0400 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Don Wiss Subject: Re: pointer to article on cholesterol versus diet To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R Todd Moody wrote: >Well, I lost 40 pounds fairly quickly on a lowcarb diet, and my >cholesterol went from 226 to 302, almost all of the increase as >LDL. Since then, I have checked it a few times and it appeared >to be slowly dropping. Todd you have often posted your total cholesterol. Last Fall Edward Campbell posted the following to this list: The 10/21/97 issue of Circulation contained an article called: "Fasting Triglycerides (TG) and HDL and Risk for Myocardial Infarction". This Harvard study concluded that the ratio of TG:HDL was the most significant risk factor in developing CHD. The TG:HDL ratio was a better predictor than total cholesterol (TC), better than TC:HDL ratio, and better than LDL:HDL ratio. Note that the TG:HDL ratio they claim is most predictive ignores LDL. It is very possible that on your lowcarb diet you have a fine TG:HDL ratio. It makes sense as a high carb diet increases TG, and a low fat diet decreases HDL. After going on the Paleolithic diet my total also went up some, but with a TG of 78 and HDL of 76 I'm not concerned. Don.

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Sun Apr 19 11:49:17 1998 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id LAA11618 for ; Sun, 19 Apr 1998 11:49:14 -0700 (PDT) Message-Id: <> Received: from by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Sun, 19 Apr 1998 14:43:51 -1300 Date: Sun, 19 Apr 1998 13:43:38 -0500 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Lyle McDonald Subject: Re: Glucagon and Insulin To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R At 2:41 AM 4/19/98, RST CA wrote: >As I recall from the book, Glucagon (the fat-removing hormone) is produced >most in two scenarios: when you eat protein, and when you eat a combination of >fat and protein. If I recall correctly, the "Protein only" ingestion >produced the highest amount of glucagon. If I am wrong, this whole posting >makes no sense, so please correct me! Protein is odd in that it causes both an insulin AND glucagon increase. I would expect protein and fat to inrease glucagon more but only because the fat should decrease the insulin response to protein. >But here's what I am thinking-- the VERY lowfat, AND very low carb diets are >fabulously effective. This may be not from the calorie deficit as is usually >thought, but from the increased output of Glucogan. The fat loss is ultimateily related to both hormonal and caloric effects. Any diet that is low in calories will cause weight loss. The primary difference will be in the quality of weight loss. Below a certain calorie threshold, a lower carb diet will cause greater fat loss and less muscle loss than a higher carb diet. This is because the reduction in insulin allows ketosis to develop which serves to spare glucose (and protein) while maximizing fat utilization (since insulin is kept low allowing maximal rates of lipolysis). assuming adequate protein intake (which is 1.5 g protein/kg body weight OR 150 grams whichever is greater), a ketogenic very low calorie diet will show les protein losses than a non-ketogenic diet at that same calorie level. the problem is the inevitable drop in metaboli rate due to low calories. >If a large part of low-carb low-fat success is from the increased glucagon >production from eating straight protein, perhaps that could be incorporated >into a low-carb routine, but in such as way as NOT to create an abysmally low >calorie level that would eventually lower metabolism levels. Total starvation will raise glucagon the most (since insulin will be the lowest) but you'll lose body protein. When you add protein (which stimulates both insulin AND glucagon release), you develop as deep of ketosis and you have a PSMF. But you have problems with metabolic slowdown. So you add dietary fat as a (fairly) hormonally neutral nutrient to get calories up. Hence the ketogenic diet. Lyle McDonald, CSCS "Come get some!" Duke Nukem

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Wed May 13 07:03:36 1998 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id HAA03524 for ; Wed, 13 May 1998 07:03:26 -0700 (PDT) Message-Id: <> Received: from by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Wed, 13 May 1998 9:58:36 -1300 Date: Mon, 11 May 1998 22:14:02 -0400 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Todd Moody Subject: Effects of lowcarb To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R My sister just sent me the "Good Calorie Diet", by Philip Lipetz. She wanted my comments on it, since she knows that I am caught up in this nutrition stuff. For those who don't know of Lipetz or this diet, it is basically a diet that emphasizes low glycemic index foods, for reasons familiar to most low-carb people: control of blood sugar and consequent control of insulin. The difference is that this diet emphasizes low-GI *carbohydrates*, such as certain legumes. No surprise there either. He does, however, make a claim that I find interesting, namely that saturated fats not only increase insulin resistance but that insulin resistance itself inhibits the release of glucagon. If this is true, it would tend to undermine the effectiveness of lowcarb diets high in saturated fats, since these increase insulin resistance. He also states that high protein and high fat meals dramatically increase one's blood sugar response to future carb-containing meals, citing research from 1927 (J.S. Sweeney, Arch. Int. Med. 40:818-30) and 1935 (H.P. Himsworth, Clin. Sci. 2:67-94). These are old studies, but they seem to fit the experience of many people on low-carb diets, namely that they become even more "carbohydrate intolerant." The following study, cited by Lipetz, may also be of interest, particularly with respect to the effect of dietary protein on glucagon. Todd Moody ----------------------------------------------------------- Title Circulating amino acids and pancreatic endocrine function after ingestion of a protein-rich meal in obese subjects. Author Schmid R; Schusdziarra V; Schulte-Frohlinde E; Maier V; Classen M Address Department of Internal Medicine II, Technical University of Munich, West Germany. Source J Clin Endocrinol Metab, 68(6):1106-10 1989 Jun Abstract We measured plasma amino acid together with insulin, glucagon, pancreatic polypeptide (PP), and glucose concentrations after the ingestion of a protein meal in lean and obese subjects. The basal plasma amino acid levels were similar in both groups. The postprandial increase in the plasma amino acid levels in the obese subjects was only 15-50% of that in the lean subjects. The mean basal and peak postprandial plasma insulin levels were significantly higher (72 and 165 pmol/L) in the obese group than in the lean group (36 and 115 pmol/L; P less than 0.05-0.01). The postprandial rise in plasma glucagon was largely attenuated in the obese subjects, and there was no difference in plasma PP and glucose levels in the 2 groups. To further evaluate the role of circulating amino acids on pancreatic endocrine function in obese and lean subjects, an amino acid mixture consisting of 15 amino acids was infused iv. During the infusion the plasma amino acid levels were comparable in both groups. Plasma insulin rose by 36 +/- 7 (+/- SE) pmol/L (5 +/- 1 microU/mL) in the lean and 129 +/- 22 pmol/L (18 +/- 3 microU/mL) in the obese subjects, whereas plasma glucagon, PP, and glucose levels were similar in both groups. In view of the 3.6-fold greater insulin responses in the obese subjects, it is likely that circulating amino acids contribute to their hyperinsulinemia in spite of the reduced postprandial rise of amino acids in this group (50-85%). Thus, under physiological conditions amino acids have to be considered as an important regulatory component of postprandial insulin release in obese subjects.

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Thu May 21 14:11:54 1998 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id OAA15525 for ; Thu, 21 May 1998 14:11:37 -0700 (PDT) Message-Id: <> Received: from by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Thu, 21 May 1998 17:06:06 -1300 Date: Thu, 21 May 1998 16:02:02 -0500 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Lyle McDonald Subject: Re: Ketones, insuli and glucagon To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R At 2:59 PM 5/21/98, Todd Moody wrote: >I understand, although I also see this as reason not to strive >for "deep ketosis", as it is sometimes called. I theorized many months ago (and experience working with individuals bears this out) that deeper ketosis will actually be WORSE for fat loss. the reason being that high level of ketones in the blood not only stimulate insulin but also direclty inhibit further fat breakdown (these are the two feedback loops that prevent runaway ketoacidosis in non-diabetics). Most seem to lose fat MUCH more effectively if they maintain right at trace ketosis (I use this since it's the lowest ketone concentration that we can measure by Ketostix and still be sure that we are getting the adaptations from ketosis). >As I see it, the main advantage of a ketogenic diet for weight >loss is that it apparently allows for the maximum retention of >muscle during the weight-loss period. I think the main >disadvantage is that ketogenic diets involve consumption of a lot >of calorically dense foods, making it fairly easy to plateau at a >caloric break-even point that is still substantially above ideal >weight. But numerous studies show that people who are instructed to reduce carbs to below 50 grams per day, but eat 'all they want of protein and fat' will automatically reduce caloric intake, thus creating a caloric deficit and lose weight. I find that many individuals reduce calories TOO much, slowing metabolism and fat loss. >Of course, all weight-loss diets face the same problem. As one >loses weight one uses fewer calories just to get around, and so >the break-even point slowly falls, unless one increases activity >levels and muscle mass to compensate. Increasing activity levels >itself tends to stimulate appetite. The data on this is far from conclusive. My experience (working with a lot of people as a trainer) is this: when people start exercise programs, they tend to get hungrier. The reason is that their bodies are very good at using glucose for fuel, and very bad at using fat. Lowering blood glucose tends to send a hunger signal to the brain to eat more. After several weeks of training, as the body's ability to use fat increases, hunger is typically blunted by exercise. AS well, some studies (not all) show that the increase in eating does not compensate for the calories burned by exercise. That is, individuals who increase exercise to burn an additional 500 cal/day (or whatever) may only eat 300 cal/day more. >I don't think these problems are insurmountable, but they can >make fat loss more difficult than one would expect from reading >even low-carb diet books. I've read the major lowcarb diet books and most are truly piss poor. the only one I even had marginal respect for (in terms of actually presenting human physiology as it really is, rather than making crap up to sell more books) is "Protein Power" by the Eades. I had some minor quibbles about some of their details (tho' I understood why they had to simplify some concepts to make it more readable) but much less than the other lowcarb books (won't name names). Diet book authors seem to feel that they can make up human physiology as they go along, making such basic mistakes that it sickens me (as I wrote before, a basic biochemistry/physiology book would be a good investment for would be diet book authors). I can only assume that most figure the average reader won't care to examine the details for claims being made. Let's face it, the stupidest diet book can sell a million copies if they have a good marketing plan. Tell people what they want ot hear, wrap it in some logical sounding (but not necessarily correct) arguments, and you've got a bestseller. Incidentelly this is also why I think the mainstream has come down so hard on purveyors of lowcarb diet books. The claims being made, and the rationale being given for those claims, are so out of jibe with human physiology that most diet books are a joke. I *hope* to change that with my book though I know that lowcarb diets will never be accepted totally. I can defend, with human research available to anyone who wants to look for it, any claim I make about ketogenic diets. When I can't defend something with science, or there just isn't enough data to support something, I'm going to point it out. And unlike most diet books, I'm not going to paint lowcarb diets in any light other than a purely objective one. I'm presenting the physiological facts about what happens in ketosis, both good and bad. I won't sell as many copies if I wrote a piece of dung diet book promising easy weight loss without exercise but I hope that at least some RD's and MD's will get some of their damn facts straight about ketosis and ketogenic diets. I want people to be able to take this book to their MD or RD (who of course will be telling them how awful ketosis is) and say "Read this, it's the facts". That's why I'm only using research (have around 650 studies right now, got a few more to get), not testimonials or any other crap like that. Of course all of this is predicated on me actually finishing the damn thing.
    Lyle McDonald wrote: > > >What are "orthostatic symptoms"? > > Orthostatic hypotension refers to a quick drop in blood pressure when > invidiuals go from sitting to standing (or otherwise change posture). These symptoms will also happen if standing up for a prolonged period of time (though going from sitting to standing is usually easier to notice). > What I find kind of interesting about ketogenic diets is that individuals > with hypertension (high blood pressure) tend to normalize their BP on a > ketogenic diet, presumably from the same effects. Doubt it. Orthostatic hypotension occurs because of the low levels of aldosterone (and to some degree cortisol). Going low carb allows adrenals to recover. Most tests will not show exhausted adrenals. That's because they look at current levels of cortisol and such. What one needs to look at is the level during a period of increased demand. Patients with chronic fatigue , for example, respond very differently to exercise than normal people - their cortisol drops after a stationary bike ride. As an aside, it is quite possible to have both orthostatic hypotension and hypertension at the same time. For those interested in looking into orthostatic hypotension you might want to look up neurally mediated hypotension (basically the same thing, diagnosed on the tilt table instead). Ilya
    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Fri Jul 24 17:06:08 1998 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id RAA26287 for ; Fri, 24 Jul 1998 17:06:04 -0700 (PDT) Message-Id: <> Received: from by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Fri, 24 Jul 1998 20:05:58 -1300 Date: Fri, 24 Jul 1998 19:48:35 EDT Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Susie McDonald Subject: Re: low carb and psychiatric patients To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R research@SPEEDNET.COM.AU (Duff Watkins) writes: << Is anyone aware of any research done regarding the effects of a low carb diet upon psychiatric in-patients? My observation is that inpatients probably have the worst diet in the world, compounded by heavy duty psychotropic medication. So I'm curious about what a low carb diet would do for this population. >> I don't know if this will be helpful to you, but I found this: A strong correlation exists between schizophrenia and deficiencies in fats, especially in the n-3 series. Schizophrenics who naturally eat lots of Omega-3 fats tend to have less severe symptoms than those who don't. Supplementation with extra fats in the Omega-3 group significantly improves symptoms of schizophrenia in most patients. Close relatives of schizophrenics show similar deficiencies in Omega-3 fats. The possibility that diets generally low in fat might worsen schizophrenia or even bring on the condition among those already predisposed to it is hard to ignore. (Laugharne JD; Mellor JE; Peet M. Fatty acids and schizophrenia. Lipids, 1996 Mar, 31 Suppl:, S163-5. See also Peet M et. al. Essential fatty acid deficiency in erythrocyte membranes from chronic schizophrenic patients, and the clinical effects of dietary supplementation. Prostaglandins Leukot Essent Fatty Acids, 1996 Aug, 55:1-2, 71-5)

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Sat Jul 25 17:33:16 1998 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id RAA04397 for ; Sat, 25 Jul 1998 17:33:13 -0700 (PDT) Message-Id: <> Received: from by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Sat, 25 Jul 1998 20:33:03 -1300 Date: Sat, 25 Jul 1998 19:34:35 -0400 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Dana Carpender Subject: Re: low carb and psych To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R Automatic digest processor wrote: Is anyone aware of any research done regarding the effects of a low carb > diet upon psychiatric in-patients? My observation is that inpatients > probably have the worst diet in the world, compounded by heavy duty > psychotropic medication. So I'm curious about what a low carb diet > would do > for this population. When I was on the lowcarb diet support list a couple of years back, there was one lister whose psychiatrist had prescribed a ketogenic diet specifically for treatment of chronic depression. Unfortunately, some folks played amateur shrink, made him/her angry, and they didn't stay on the list, so I didn't hear how it turned out. > I am keenly interested in this same question.....particularly as it > applies to > alcoholism......well all of the psychiatric DX. There was an article in the local paper a few months back -- I now rue that I didn't clip it -- saying that a study had strongly correlated a "sweet tooth" with alcoholism; said it was the strongest predictor. This jibes with my personal experience. Also remember reading years ago of rat studies, where rats fed sugar and other refined carbs chose, when given a choice, to drink alcohol, while rats on a whole foods diet chose water. In the book Megavitamin Therapy, a Dr. Frank Butler is cited as having successfully treated alcoholism by tube-feeding a high protein diet with substantial vitamins and minerals. Says the study was published in The Journal of The American Geriatrics Society in Sept. '67. This book cites a number of studies of this sort. > A strong correlation exists between schizophrenia and deficiencies in > fats, > especially in the n-3 series. And there is apparently a cholesterol/serotonin connection as well, which is suspected to be involved in the increased levels of violence in folks with very low blood cholesterol. If anyone knows more about the cholesterol/serotonin connection, I'd sure like to hear about it. > Try "Diet and Disease" (Cheraskin, Ringsdorf, and Clark) for studies > on = > food and mental illness. Psychodietics, also by Cheraskin and Ringsdorf, is the first book I ever read on nutrition. Worth digging up. I had been in counseling for years; after reading it, I quit sugar and white flour (didn't go low carb yet) and found that what I thought were psychological problems pretty much evaporated. But then, when I went thru Cheraskin and Ringsdorfs list of 48 symptoms of hypoglycemia, I had 40. > > There have been several ancedotal observations (and I think there > are > > published studies) on the effectiveness of using diet modification > to help > > control ADD, according to a university psychiatrist whom I know. > I have a friend with ADD. He feels normal and does not have problems > when > he is low carbing. He does cheat periodically, and when that happens > the > symptoms return. I also have another friend who was prescribed prozac. > > He also feels well when low carbing. Unfortunately for him he often > can't low carb and the symptoms usually return. Have a dear friend with ADHD who finds that eating low carb/high protein is *essential* to controling his brain chemistry. Also finds DMAE very helpful. Have a family member who has been able to drop Prozac after going low carb, and adding several supplements, also including DMAE, high Bs, some ginkgo, etc. Says he feels better than when on Prozac. I don't believe that everyone's mental problems can be cleared up with nutrition. I do think that if Lilly had tried, they couldn't have come up with a better way to market Prozac than to push a low fat/high carb diet. Dana
    At 11:17 PM 8/30/98, Donna H wrote: >Lyle wrote: << Additionally, very high free fatty acid and ketone >levels raise insulin>> > >Thanks very much for that interesting discourse. Could you remind us >again what raises free fatty acid levels? I assume intake of fats is >not necessarily what contributes to them in the blood, exclusively? FFA levels do raise with dietary fat intake (of course the dietary triglyceride has to be hydrolyzed first to glycerol + free fatty acids) but I'd probably the say the main source of blood borne FFA is from fat cells. Fat is stored in adipose tissue as triglycerides which is glycerol + three free fatty acids (hence, tri = three, and glyceride = glycerol). The triglyceride must be broken down (hydrolyzed) to glycerol + three free fatty acids, which occurs under the action of something called Hormone Sensitive Lipase (HSL). HSL is activated primarily by the catecholamines (adrenaline/noradrenaline or epinephrine/norepinephrine depending on what side of the pond you live on) although growth hormone, cortisol and glucagon play small roles. HSL is almost totally inactivated by insulin (which also stimulates something called lipoprotein lipase or LPL which tells the fat cell to synthesize triglycerides). When HSL is activated (by low insulin and high catecholamine levels) it signals the fat cell to break down triglycerides to glycerol and FFA. The glycerol is released into the bloodstream and can be turned into glucose in the liver. FFA enters the bloodstream, probably boudn to albumin, where it travels to various tissues to be burned (i.e. the liver, muscle tissue). So you're goin to get maximal blood FFA levels under conditions of low insulin and high catecholamines whih is during fasting. The next highest would be a ketogenic diet. As you add carbs, insulin goes up and the catecholamines go down, and you get progressively less blood borne FFA, an hence less fat burning. Lyle McDonald, CSCS This space for lease At 9:48 AM 9/8/98, Chuck Forsberg WA7KGX wrote: >Your comment that aerobic exercise is ineffective for weight loss >is interesting. It would be more accurate to say that the amount of exercise which will/can be realistically done by the average person is ineffective for significant weight loss. Sure, runners are very thin but you're looking at running volumes of 1-2 hours/day. The current recommendations for 30' of aerobic exercise a few times a week as an effective modality for weight loss are a joke. It may make you healhier (again, see Paffenberg) but it won't cause any body composition changes. the impact calorically of aerobic exercise on various parameters of weight loss is severely overstated (see C. Zelasko "Exercise for weight loss: What are the facts?" J Am Diet Assoc (1995) 95: 1414-1417. for a brief review). The caloric burn of aerobic exercise, especially at the intensities that most can sustain, is low, perhaps 5 cal/minute. So you're looking at 300 cal/hour, fairly insignificant. Contrary to popular belief, aerobic exercise does NOT raise metabolic rate after training. And after an average training bout, the number of caloris burned after exercise may be 5-10 calories at most. Even after exhausting exercise, it's only 150 calories. Beyond that, aerobic exercise doesn't do a lot to spare protein losses or prevent the drop in metaboli rate during dieting (some studies say yes, some studies say no). Probably the biggest benefit of aerobics is that it improves the muscles ability to use fat for fuel, by inreasing mitochondrial density and the activity/number of aerobic enzymes. To the contrary, while the caloric burn of weight training isn't very high either (perhaps 9 cal/minute), there are long term increases in metabolic rate (approximating 35-40 cal/lb of msucle gained although starvation diet may prevent this, by decreasing calories burned/kg active tissue), and there is a moderately significant increase in metabolic rate after weight training reflecting increased ATP use, coming primarily from fat stores, for protein synthesis. This increase in protein synthesis lasts at least 36 hours. Put more practically, I have seen very few individuals (esp. women) do much to change their body composition by performing aerobic exercise only, unless they are doing extreme amounts (multiple hours per week). If they are consuming a lot of carbohydrate at the same time, they amy still not get any effect (it depends on the intensity of the exercise). To the contrary, I have seen (and trained) many individuals whom weight training and diet or the combo of weight training and aerobics did affect body composition. If anything, this effect is more pronounced in women, because they are starting with less muscle mass (generally) than men and have more to gain from it. As well, the glycogen depletion (that I discussed a few posts back) from weight training enhances fat utilization by the muscle. An excellent paper that I highly recommend is: JP Flatt "Integration of the overall response to exercise" Int J Obes (1995) 19 (suppl): S31-S40. also, JP Flatt "Glycogen levels and obesity" Int J Obes (1996) 20 (suppl): S1-S11. JP Flatt "Body composition, respiratory quotient, and weight maintenance" Am J Clin Nutr (1995) 62(suppl): 1107S-1117S. Gives some insight into why lowered carb diets tend to work well for fat loss for many individuals (although he does not draw this conclusion in his papers). Flatt's premise (and he has written numerous papers on this, as well as some textbook chapters on this topic) is that the fatpoint (the level at whch bodyfat will be habitually set) is in part determined by where muscle glycogen levels are maintained (obviously this isn't the whole story). If you habitually maintain high glycogen levels (high carb diet + inactivity), your body will have a higher fat point than if you lower glyogen levels (low carb diet and/or glycogen depleting exercise). If you can chronically maintain muscle/liver glycogen at lower levels, you will shift your fat point downwards. Another part of his premise is that, for fat loss to occur, fat oxidation (Fox, determined by factors such as diet especially carb intake, insulin level, genetics) must exceed fat intake (Fin, determined by fat intake) (once again, basic thermodynamics). Basically: Net fat loss = Fox - Fin This leads him to recommend (illogically IMO) that fat intake should be minimized to allow for a differential between Fox and Fin. this makes no sense because high carb diets also reduce Fox. By decreasing carb intake (and depleting muscle glycogen), you increase Fox, making it easier to create a differential between Fox and Fin. along with this, see: Schrauwen P, et. al. "Role of glycogen-lowering exercise in the change of fat oxidation in response to a high-fat diet." Am J Physiol 1997 Sep;273(3 Pt 1):E623-E629 and Schrauwen P, et al. "Fat balance in obese subjects: role of glycogen stores. " Am J Physiol. 1998 Jun; 274(6 Pt 1): E1027-E1033. both of which found that depleting muscle glycogen (with exhaustive cycling, although weight training would ahve been mor efficient) made it easier for the body to adapt to a 'high fat' diet (which was almost ketogenic in this study). Because depletion of glycogen increased fat oxidation. And they made sure to study both lean and obese subjects to see if there was any inherent defect in obese individuals that prevented the observation that had been made in lean individuals. There wasn't. Lyle McDonald, CSCS This space for lease I only know from personal experence. When I feel an energy drain, I eat a high fat food and feel more energy within a few minutes. Stefansson conducted studies for the U.S. military on pemmican consumption and its effects on physical endurance. After a adaptation period, stamina improved as it did in a recent study of fat consumption and athletic performance which I will endevor to find for you. Many people try to limit fat because of concerns about cardiovascular health. These concerns have been eliminated lately by many studies. This article on stroke prevention shows what I'm talking about. 12/24/97,Reuters- "Higher Fat Diet Reduces Stroke Risk?" In a surprising new study, the editorial's authors, Drs. Roger Sherwin and Thomas Price of the University of Maryland School of Medicine indicate that dietary fat does not increase the risk of the most common type of stroke. Also, certain types of fat - including saturated fat and monounsaturated fat - may even decrease the risk of stroke in middle-aged men. Further studies are necessary to confirm this. This finding is in conflict with other studies linking heart disease with a high fat diet. "In the new study, the risk of having a stroke dropped 15% for every 3% increase in energy gained from total fat and dropped 9% for every 1% increase in saturated fat, the type found in meat and dairy products. The stroke risk declined 11% for every 1% increase in monounsaturated fat intake, the type of fat found in canola, nut and olive oil, according to a report in the current issue of The New England Journal of Medicine. There was no protective effect of polyunsaturated fat, which is found in fish and vegetable oils." Ray Audette Author "NeanderThin:A Caveman's Guide to Nutrition"
    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Tue Sep 22 10:27:19 1998 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id KAA17570 for ; Tue, 22 Sep 1998 10:27:15 -0700 (PDT) Message-Id: <> Received: from by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Tue, 22 Sep 1998 13:26:06 -0500 Date: Tue, 22 Sep 1998 19:03:48 -0700 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Ray Audette Organization: Paleolithic Press Subject: Re: Lack of ovulation solved by Ketogenic Diet? To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R cleckler wrote: I am curious if anyone can shed some > light on my situation and explain why the diet has this effect. I was told that I don't menstruate because of high testosterone levels. > This was posted to the low-carb support list today: From: "Nancy P. Hemenway" Stein and Levanthal first described PCO is 1935 -- it is a condition which basically is characterized by persistent annovulation (lack of ovulating). There are a variety of characteristics women with PCOS share. Women with PCOS produce an overproduction male hormones -- testosterone and androstenedione. The typical senario is irregular menstrual cycles, onset of hirsutism in the teens or early 20s, and gradually worsening excess hair growth. Also, women with PCOS develop a quantity of small cysts on the ovaries. The ovaries will have a particular "look" on ultrasound examination. The characteristic PS ovary arises when annovulation occurs over and over for a length of time. The basic problem is that although these ovaries contain many follicles with eggs, - the eggs are immature unlike the "normal" ovary that develops one egg each month that releases mid cycle. ( One of the major biochemical features of polycystic ovary syndrome is insulin resistance accompanied by compensatory hyperinsulinemia (elevated fasting blood insulin levels). There is increasing data that hyperinsulinemia produces the hyperandrogenism of polycystic ovary syndrome by increasing ovarian androgen production, particularly testosterone and androstenedione and by decreasing the serum sex hormone binding globulin concentration. The high levels of androgenic hormones interfere with the pituitary ovarian axis, leading to increased LH levels, anovulation, amenorrhea, and infertility. According to Mark Perloe, MD (a reproductive endocrinologist in Atlanta) Drs. Velazquez, Nestler and Dunaif have shown that lowering serum insulin concentrations with METFORMIN (Glucophage 1500 mg a day) or troglitazone (Rezulin 400 mg a day) ameliorates hyperandrogenism, by reduction of ovarian enzyme activity that results in male hormone production. These medications have been shown to reverse the endocrine abnormalities seen with polycystic ovary syndrome within two or three months. They can result in decreased hair loss, diminished facial and body hair growth, normalization of elevated blood pressure, regulation or menses, weight loss and normal fertility. We have seen pregnancies result in less than two months in woman who conceived in their very first ovulatory menstrual cycle. Ray Audette Author "NeanderThin:A Caveman's Guide to Nutrition"

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Thu Sep 24 20:30:40 1998 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id UAA07880 for ; Thu, 24 Sep 1998 20:30:38 -0700 (PDT) Message-Id: <> Received: from by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Thu, 24 Sep 1998 23:29:57 -0500 Date: Thu, 24 Sep 1998 19:41:27 -0700 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Donna H Subject: Re: Lack of ovulation solved on ketogenic diet? X-To: cleckler@MCI2000.COM To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R This was a really interesting post. You may do well to read up on PCO (also called PCOS) on the web-- polycystic ovarian syndrome. This is where a woman does not ovulate-- and high insulin levels are found very often, also most or many PCOS patients are obese. From what I understand, researchers aren't sure if high insulin is the cart or the horse in this disorder. But perhaps your situation is related to this, since by low-carbing you're most certainly lowering insulin production. Another thought, just possibly, is that if you were very low-fat in terms of diet before, the higher fat content of a typical low-carb diet may be giving you more basic cholesterol for your body to make sex hormones out of. Not to mention the protein and iron that are important in regular cycles. I don't recall if it was mentioned on this list or elsewhere, but one study someone cited noted that women tend to 'do better' somehow on larger amounts of dietary fat than men. Given our intricate sex hormone production situation, that makes sense to me. Perhaps someone can point to the study, who remembers it? Congrats on the normalization. Donna _________________________________________________________ DO YOU YAHOO!? Get your free address at

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Thu Oct 1 17:25:12 1998 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id RAA03751 for ; Thu, 1 Oct 1998 17:25:09 -0700 (PDT) Message-Id: <> Received: from by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Thu, 1 Oct 1998 20:23:23 -0500 Date: Thu, 1 Oct 1998 11:31:14 -0700 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Doug Skrecky Subject: high protein diet spares muscle mass To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R Authors Piatti PM. Monti F. Fermo I. Baruffaldi L. Nasser R. Santambrogio G. Librenti MC. Galli-Kienle M. Pontiroli AE. Pozza G. Institution Istituto Scientifico San Raffaele, Dipartimento di Chimica e Biochimica Medica, Milano, Italy. Title Hypocaloric high-protein diet improves glucose oxidation and spares lean body mass: comparison to hypocaloric high-carbohydrate diet. Source Metabolism: Clinical & Experimental. 43(12):1481-7, 1994 Dec. Abstract The aim of the study was to investigate the effects of two hypocaloric (800-kcal) diets on body weight reduction and composition, insulin sensitivity, and proteolysis in 25 normal glucose-tolerant obese women. The two diets had the following composition: 45% protein, 35% carbohydrate (CHO), and 20% fat (HP diet, 10 subjects), and 60% CHO, 20% protein, and 20% fat (HC diet, 15 subjects); both lasted 21 days. A euglycemic hyperinsulinemic (25 mU/kg/h) clamp lasting 150 minutes combined with indirect calorimetry was performed before and after the diet. Both diets induced a similar decrease in body weight and fat mass (FM), whereas fat-free mass (FFM) decreased only after the HC diet. 3-Methylhistidine (3-CH3-HIS) excretion was reduced by 48% after the HP diet and remained unchanged after the HC diet (P < .05). A significant correlation was found between the changes in FFM and in 3-CH3-HIS excretion after the diet (rs = .50, P < .02). Blood glucose remained unchanged, while insulin decreased in both diets. Free fatty acids (FFA) significantly increased only after the HC diet (P < .05). During the clamp period, glucose disposal and glucose oxidation significantly increased after the HP diet and significantly decreased after the HC diet. Opposite results were found when measuring lipid oxidation. In conclusion, our experience suggests that (1) a hypocaloric diet providing a high percentage of natural protein can improve insulin sensitivity; and (2) conversely, a hypocaloric high-polysaccharide-CHO diet decreases insulin sensitivity and is unable to spare muscle tissue.

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Wed Dec 2 06:42:38 1998 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id GAA13944 for ; Wed, 2 Dec 1998 06:42:35 -0800 (PST) Message-Id: <> Received: from by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Wed, 2 Dec 1998 9:36:04 -0500 Date: Wed, 2 Dec 1998 07:29:01 -0500 Reply-To: Sender: Low-Carbohydrate Technical Discussion From: "Elizabeth A. Koch" Subject: Re: Why Low Carb Eating Works To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: RO I don't very often add my opinion, but here goes. I have been on low carb eating for four months now, and have never, ever had a more pleasant dieting or eating experience. I was on low, low fat for over six years and could not convince my M.D. that I was sticking to low fat. My cholesterol was in the 400 range, my triglycerides were high, and all in all, I was a mess. After only one month on low carbs, my cholesterol dropped 100 points, I lost 20 plus pounds, am hardly ever hungrey. I used to be "starved" all of the time. I think it definitely has to do with my insulin level and blood glucose. But in the long run, I don't care why it works, I just know that it does. Elizabeth

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Fri Dec 18 05:54:49 1998 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id FAA23172 for ; Fri, 18 Dec 1998 05:54:46 -0800 (PST) Message-Id: <> Received: from by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Fri, 18 Dec 1998 8:51:58 -0500 Date: Thu, 17 Dec 1998 23:52:36 -0800 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Stef Maruch Subject: Re: Zoloft To: LOWCARB@MAELSTROM.STJOHNS.EDU In-Reply-To: <> from Dana Carpender at "Dec 17, 98 05:24:40 pm" Status: R Dana Carpender writes: >Also wondering if any of the folks using it have noticed any mood >improvement from the diet itself. I am taking less zoloft than before I began lowcarbing, but I sure as heck haven't been able to drop it entirely. As for mood improvement, it's hard to say what-all contributed to that -- I began lowcarbing as a result of a diabetes diagnosis. I also doubled my exercise and lost weight. Maybe the diet itself helps my mood, but I think being in better shape and having my blood sugars more in control helps it more than the diet. >Do think that a low fat, high carb diet -- >especially one high in sugar and refined flour products, which suck B >vitamins out of the body -- is practically designed to cause mood >destabilization. I remember the first week on such a diet (prescribed by my doctor for high cholesterol). One day I felt utterly hopeless. One bowl of ice cream cured the feeling within fifteen minutes. -- Stef ** rational/scientific/philosophical/mystical/magical/kitty ** ** <*> ** - - - - - - - - - - - - - - - - - - - - - - - - - - - -

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Fri Dec 18 14:06:49 1998 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id OAA26064 for ; Fri, 18 Dec 1998 14:06:45 -0800 (PST) Message-Id: <> Received: from by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Fri, 18 Dec 1998 17:03:09 -0500 Date: Fri, 18 Dec 1998 16:01:12 -0600 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Lyle McDonald Subject: Re: Protein conversion To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R At 11:47 AM 12/16/98, Matt Kirkwood wrote: >This may be the source of my misunderstanding. I think I read (probably in >Atkins) that fat has an even lower glucose conversion rate than protein, >so a very small portion of the fat we eat can be converted by the liver >into glucose (or glycogen, or whatever). Yes, glycerol (which is the backbone of triglycerides, aka fat) can be converted to glucose. ON average, 10% of the total fat broken down will reapper in the bloodstream as glucose (i.e. 180 grams of fat = 18 grams of glucose). >Since glucose is the body's >energy source, if you can't get much glucose out of the fat, you can't get >much energy. (?) I'm probably totally lost. :-) The body can make glucose in the lier from: 1. certain amino acids 2. glycerol 3. lactate/pyruvate (breakdown products of glycogen in the muscle and liver) glycerol contributes minimally (~18-20 grams/day), and lactate and pyruvate contribute about 40 g/day. The rest of the body's glucose requirements (which are about 140 grams/day at the beginning of a ketogenic diet and drop to about 80 grams/day after 3 weeks) come from the conversion of protein. So you're looking at about 70 grams of glucose to be made from protein. Now, you can either let your body break down stored body protein (muscle, etc) or you can give it sufficient dietary protein to spare body protein losses. At a 58% conversion rate of protein to glucose, it takes about 150 grams protein/day to eliminate body protein losses during the first few days of ketosis (150 * 0.58 = 87). After a few weeks in ketosis, it should only take about 50 grams of protein to eliminate protein losses. This assumes that someone is not exercising, which increases protien requirements. >I think I read in a Covert Baily book that body fat is liberated to refill >glycogen stores after excercise. I'll look for it again tonight. I sure hope Bailey didn't say that, because he's dead wrong. >Atkins argues that this isn't true. He says the calorie balance math >doesn't work unless you pay attention to the diet makeup. This might not >be true, but it would fit with my reasoning that if you can't get glucose >out of it, you can't get energy out of it. I'm not sure I agree with my >own reasoning, however. Atkins makes no distinction between weight loss and fat loss. He is basing his comments on early studies showing much greater weight loss for low carb diets, but it's all water. Lyle McDonald, CSCS No .sig needed

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Sat Dec 19 17:20:23 1998 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id RAA05037 for ; Sat, 19 Dec 1998 17:20:18 -0800 (PST) Message-Id: <> Received: from by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Sat, 19 Dec 1998 20:16:44 -0500 Date: Sat, 19 Dec 1998 15:57:27 -0500 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Ilya Subject: Re: Protein conversion To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R Todd Moody wrote: > First, it is my understanding that an > all-protein diet will probably make you sick. I believe this is true, but not because of... > There must be an > upper limit to how much protein the body can process in a day. Bodybuilders have been eating huge amounts of protein with no apparent damage to the body. I have read about upwards of 500gm per day (no idea how anecdotal this is and if it is an exageration) which would give 2000 calories or so. > Second, even if there is a glucose deficit, it doesn't follow > that there is an energy deficit. Fat can be burned, and it > doesn't have to be *body* fat. I think it might be helpful to differentiate fat loss from fat gain. (No 'duh' jokes please :) Without insulin fat will not be stored in any appreciable amounts. This is confirmed by my own (and a few others) experience where I would eat 5000 calories per day and not gain weight, as long as I didn't have any carbs and didn't allow myself to slip into deep ketosis. (I am right now probably around 175lbs, so 5000 calories per day for me on a continous basis is a lot). Since fat LOSS is determined more by other hormones, e.g. various adrenal hormones, such as glucagon, insulin would need to be lowered (since it suppresses glucagon). But that is only a necessary, not a sufficient condition for fat loss. So, being in ketosis is likely to result in fat loss if you have a lot to lose, but if you are already fairly lean, then that may not be enough to lose the last bits of fat. > Third, I don't think fat can help to refill glycogen stores. About 5% or so of fat (by calories) on average can be turned into glucose (the glycerol molecule can be converted). This depends on the type of fat. In very short chain fats this is higher. I believe it doesn't go above 10% for fats encountered in foods (the most common food containing decent amounts of short chain fats is butter). (Sorry, I don't remember where I have read the percentage values, they might be a little off). > > So while a low carb diet may contain lots of calories and volume of food, > > the "bioavailable" energy in the diet is much lower than in a high carb > > diet with the same amount of calories. > > Well, fat is just as bioavailable as glucose. Suppose you eat > just fat for a while, but in calorically massive amounts. If > there is no caloric deficit, why should your body tap its stored > fat when there is an abundance of dietary fat to use for fuel? So you probably wouldn't lose any weight, but likely not gain much either. YMMV of course. Ilya
    Message 23: From owner-lowcarb@MAELSTROM.STJOHNS.EDU Thu Dec 24 22:09:52 1998 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Date: Wed, 23 Dec 1998 06:19:35 -0500 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: eloise campbell Subject: Re: your hi to the low carb list To: LOWCARB@MAELSTROM.STJOHNS.EDU Hi, after a year of low-carbing and lurking on this list, I have finally decided to contribute! The posts on Cushinoid tendancies, PCOS and infertility really interest me. After my initial weight loss of 50 lbs in about 4 months (I'm 42) I noticed further changes over the ensuing months. All my life, physicians have remarked on my poor muscle tone, hirsutism and Cushingoid features. Anyway, looking over photos over the last year, it is really dramatic to see how my face has changed...I have cheekbones and you can actually see a jaw line. These changes progressed AFTER my weight loss! Also the mild acne on my cheeks completely cleared and absolutely no more PMS. Frequent headaches and arthritic symptoms are completely gone. Excess hair is starting to lessen as well. Mood swings and mild depression are a thing of the past. Muscle tone is also better, and my dentist has commented on the health of my gums. So, I can't say enough good things about the low-carb regimen and, when I get the usual lectures about what I'm doing to my health, I just have to SMILE! I've never been healthier or felt better. Helen -----Original Message----- From: Donna H [SMTP:dhdonna@YAHOO.COM] Sent: Saturday, December 19, 1998 12:42 AM To: LOWCARB@MAELSTROM.STJOHNS.EDU Subject: Re: your hi to the low carb list Nicole, Welcome to the list-- it's a great list. What you mentioned about PCOS was of great interest to me. I was reading up on different things (besides not eating properly) that can cause obesity, read about PCOS and got very curious. I have so many of the symptoms except that my periods are very normal and my ovaries appear so too. But I still think there's some link somewhere. When I went from low-calorie to low-carb, I noticed my skin got better and a tiny bit of dark hair I had above my lip thinned out a LOT. With that in mind, I was really ready to suspect hyperinsulinism, which as it sounds like you know, is routinely part of PCOS. Based on that I persuaded my good doc to let me do a trial run of a diabetes med called Metformin... it's supposed to sensitize your body to its own insulin and many diabetics lose weight on it. Also among the PCOS population, many women I've read posts of are being prescribed it to restore their fertility (you could hit the infertility newsgroup and find out about that there). Anyhow... haven't lost weight on Metformin after about a month (darn!!), but hoping over a few months it will stabilize out my hormones and perhaps THEN. What I did notice was a quick effect for softer skin, my nearly lifelong body acne has dramatically cleared, and that little dark hair has too. <> Interesting. Only after a LOT of reading did I run across discussion of Cushingoid tendencies in SOME PCOS patients (some have high prolactin levels too). Anyhow, I'm not sure if you meant the uppermost part of your back, in the quote above, or some other area, but I had always thought I had a mildly annoyingly shaped upper back (too slopey and too much), and after say a week or two on Metformin what can I say, the shape of my neck and shoulders just looks a LOT more like other people's. It's weird that it could happen, but anyway, the Metformin seems to have addressed something needed in my body, and it IS used in PCOS, if you're curious. Maybe the lowcarbing will do the trick for you, though. If you want to read up on PCOS, there are a few great sites easily found with your fave search engine. Best wishes, Donna _________________________________________________________ DO YOU YAHOO!? Get your free address at
    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Thu Dec 24 22:09:52 1998 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id WAA25241 for ; Thu, 24 Dec 1998 22:09:49 -0800 (PST) Message-Id: <> Received: from by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Fri, 25 Dec 1998 1:06:24 -0500 Date: Wed, 23 Dec 1998 06:19:35 -0500 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: eloise campbell Subject: Re: your hi to the low carb list To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R Hi, after a year of low-carbing and lurking on this list, I have finally decided to contribute! The posts on Cushinoid tendancies, PCOS and infertility really interest me. After my initial weight loss of 50 lbs in about 4 months (I'm 42) I noticed further changes over the ensuing months. All my life, physicians have remarked on my poor muscle tone, hirsutism and Cushingoid features. Anyway, looking over photos over the last year, it is really dramatic to see how my face has changed...I have cheekbones and you can actually see a jaw line. These changes progressed AFTER my weight loss! Also the mild acne on my cheeks completely cleared and absolutely no more PMS. Frequent headaches and arthritic symptoms are completely gone. Excess hair is starting to lessen as well. Mood swings and mild depression are a thing of the past. Muscle tone is also better, and my dentist has commented on the health of my gums. So, I can't say enough good things about the low-carb regimen and, when I get the usual lectures about what I'm doing to my health, I just have to SMILE! I've never been healthier or felt better. Helen -----Original Message----- From: Donna H [SMTP:dhdonna@YAHOO.COM] Sent: Saturday, December 19, 1998 12:42 AM To: LOWCARB@MAELSTROM.STJOHNS.EDU Subject: Re: your hi to the low carb list Nicole, Welcome to the list-- it's a great list. What you mentioned about PCOS was of great interest to me. I was reading up on different things (besides not eating properly) that can cause obesity, read about PCOS and got very curious. I have so many of the symptoms except that my periods are very normal and my ovaries appear so too. But I still think there's some link somewhere. When I went from low-calorie to low-carb, I noticed my skin got better and a tiny bit of dark hair I had above my lip thinned out a LOT. With that in mind, I was really ready to suspect hyperinsulinism, which as it sounds like you know, is routinely part of PCOS. Based on that I persuaded my good doc to let me do a trial run of a diabetes med called Metformin... it's supposed to sensitize your body to its own insulin and many diabetics lose weight on it. Also among the PCOS population, many women I've read posts of are being prescribed it to restore their fertility (you could hit the infertility newsgroup and find out about that there). Anyhow... haven't lost weight on Metformin after about a month (darn!!), but hoping over a few months it will stabilize out my hormones and perhaps THEN. What I did notice was a quick effect for softer skin, my nearly lifelong body acne has dramatically cleared, and that little dark hair has too. <> Interesting. Only after a LOT of reading did I run across discussion of Cushingoid tendencies in SOME PCOS patients (some have high prolactin levels too). Anyhow, I'm not sure if you meant the uppermost part of your back, in the quote above, or some other area, but I had always thought I had a mildly annoyingly shaped upper back (too slopey and too much), and after say a week or two on Metformin what can I say, the shape of my neck and shoulders just looks a LOT more like other people's. It's weird that it could happen, but anyway, the Metformin seems to have addressed something needed in my body, and it IS used in PCOS, if you're curious. Maybe the lowcarbing will do the trick for you, though. If you want to read up on PCOS, there are a few great sites easily found with your fave search engine. Best wishes, Donna _________________________________________________________ DO YOU YAHOO!? Get your free address at
    Authors Yaari S. Goldbourt U. Institution Computing Center, Bar-Ilan University, Ramat-Gan, Israel. Title Voluntary and involuntary weight loss: associations with long term mortality in 9,228 middle-aged and elderly men. Source American Journal of Epidemiology. 148(6):546-55, 1998 Sep 15. Abstract Recent studies have suggested that weight loss in middle-aged persons antecedes increased mortality. Therefore, the authors sought to examine the association between changes in body weight and subsequent mortality, according to self-reported dieting status. The authors followed 9,228 men aged 40-65 years in 1963, for whom weight changes between 1963 and 1968 were recorded and extensive clinical, anthropometric, biochemical, and dietary assessments were made. Of these men, 2,471 reported being on a diet when first examined in 1963, and 636 were dieting primarily to lose weight. Mortality follow-up covered an 18-year period (1968-1986). Men who lost 5 kg or more between 1963 and 1968 ("extreme weight losers") exhibited the following age-pooled risks of mortality relative to the stable weight group: for total mortality, 1.36 (95% confidence interval (CI) 1.20-1.55); for all cardiovascular disease mortality, 1.40 (95% CI 1.16-1.69); for all non-cardiovascular disease mortality, 1.33 (95% CI 1.11-1.59); for coronary heart disease mortality, 1.55 (95% CI 1.25-1.93); and for cancer mortality, 0.90 (95% CI 0.65-1.24). After adjustment for differences in coronary heart disease risk factor levels and morbidity between these groups at the end of the weight change period (1968), the excess risks associated with extreme weight loss declined by approximately one third. They declined further if adjustment was made for 1963 (pre-weight-change period) morbidity and risk factor levels. Being on a slimming diet, as reported in 1963, was associated with an approximate doubling of excess mortality in men with extreme weight loss. Weight loss in 1963-1968 coincided with an increased incidence of coronary heart disease and diabetes mellitus and a declining level of serum total cholesterol. This and other studies indicate that both voluntary and involuntary weight loss might be associated with a small increase in the risk of all-cause mortality.
    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Thu Mar 11 15:06:22 1999 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id PAA29543 for ; Thu, 11 Mar 1999 15:06:20 -0800 (PST) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Thu, 11 Mar 1999 18:04:30 -0500 Date: Thu, 11 Mar 1999 13:03:10 -0600 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Eileen Subject: Insulin Receptors To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R Hi all- I just read a very interesting article in the issue of Science which just came across my desk (Science, vol. 283, pp. 1544-8, 1999). (News and Views, p. 1423). Researchers in Canada found that by inactivating the enzyme which dephosphorylates the insulin receptor (PTP-1B) in a transgenic mouse model, that the mice were able to maintain normal blood glucose levels following a meal, even though they had half as much insulin in their blood. When fed a diet 10X higher in fat (and also calories) than control mice, they were resistant to weight gain and the development of diabetes relative to the control mice. While the next step will be to see what inactivating this enzyme does in a diabetic animal model(and person,etc.), it is a very encouraging result that has identified a new target for drug therapy. Maybe one day we will all be able to eat carbs again if we can take a drug that will restore insulin sensitivity to our insulin receptors (idea is that phosphorylated form of the insulin receptor will actively take up glucose, while the dephosphorylated form is inactive, i.e. 'insulin resistant', so if we could design a drug to keep the IR phosphorylated, we could improve insulin sensitivity). Other good news is the animals have been healthy for 2 years, no signs of cancer or other abnormalities from disrupting this molecule that could function in multiple signal transduction pathways. *********************************************************************** Eileen: 36.4% body fat(165#)/ 28.3% body fat(155#)(5'5" size 10)/ 22% body fat; 41 y.o, PP

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Fri Mar 12 07:39:43 1999 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id HAA05287 for ; Fri, 12 Mar 1999 07:39:41 -0800 (PST) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Fri, 12 Mar 1999 10:31:17 -0500 Date: Fri, 12 Mar 1999 09:30:09 EST Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Jerry Stegenga Subject: Re: Dietary fat and breast cancer To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: RO In a message dated 3/12/1999 12:11:36 AM Eastern Standard Time, blpatcai@EROLS.COM writes: << Add to that a different race which presumably indicates more genetic differences than just appearance, different lifestyles--exercise patterns, for example--and many many dietary differences including different foods, different cooking methods, and different eating patterns. The studies I find most convincing aren't the massive ones comparing one country to another (shouldn't we all eat like the French? --great for the tastebuds and the heart but not so good for the liver--talk about a tradeoff!) but those comparing descendants who have adapted to a different lifestyle--as in Asians versus Americans of Asian extraction. OTOH, as a third-generation presumably-assimilated American, I keep many aspects of my ancestral culture including diet, as do my friends from other cultural backgrounds, so I know from personal observation that there may still be significant differences--if we could figure out just what is significant. Barbara >> Many books and papers have been written on what happens to various "Native" populations when they become "civilized" and processed foods are introduced into their diets. The most remarkable is a book written by Weston A. Price, D.D.S. entitled "Nutrition and Physical Degeneration" which records the general health and dental conditions of peoples all over the world who adopted the "Civilized " diet. It is well worth reading. Most of the other publications have appeared in the Lancet. The conclusion of these findings was that 10 to 20 years after adopting the "civilized(western)" diet chronic illnesses began to appear that were unknown before. Weston A. Price"s book is available from Amazon. Jerry TARFN

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Thu Apr 8 05:58:55 1999 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id FAA24594 for ; Thu, 8 Apr 1999 05:58:49 -0700 (PDT) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Thu, 8 Apr 1999 8:56:14 -0500 Date: Thu, 8 Apr 1999 22:10:48 +1000 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Dr Keith H Charlton Subject: Re: LOWCARB Digest - 6 Apr 1999 to 7 Apr 1999 - Special issue(#1999-81) To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: RO Sorry I've tried to delete the bulk of the prompting text and can't. I'm a Brisbane chiropractor with an interest (qualification, even), in clinical epidemiology/evidence-based medicine. I've also been fat since 8 years of age, and am now 49. I recently lost 30Kg on Atkins, and my Type II diabetes. Effortlessly. Yesterday I received Dr Bernstein's book on diabetes (thank God for And read it. Today I called and talked to him. He has been an MD since about 1980 (mature student). He's been diabetic for over 50 years. His approach is a refined version of Atkins. I care for people with mostly MS disorders, but I have a goodly number of patients whom I am privileged to serve who struggle daily with the low fat paradigm. Since I've just spent the last five years in Oxford and spent time with the godfather of evidence-based medicine (David Sackett), I was dismayed to return to Bris and find the Oz god of low fat is alive and well (as in the UK and the US, where I've recently spent time). Some of you may know of the Cochrane Collaboration, which provides, quarterly, a database of systematic reviews of treatment effectiveness. Using this, asking a Professor of Cardiology here, a clinical methods reviewer for the CC (Paul Glasziou, with whom I will soon be teaching medical students evidence based medicine), a research based endocrinologist who worked recently for the Garvan Institute in Sydney, ALL admit that there is no clinical evidence supporting low fat diets. In fact, if any of you search PubMed at NIH, you will find a long list of papers showing harm from low fat diets (elevated triglycerides, increased insulin resistance, etc). My clinical chemistry is a quarter century old, and I'm not an academic. There is no evidence supporting either low fat or low carb (other than the infamous Ornstein trial (I can talk to you directly if you want a critical appraisal of trial design and external validity issues). The biologically plausible way to proceed with obese, or type II diabetic persons, clearly seems to be low carb, until someone does suitably designed trials suggesting otherwise. The non-trial evidence against low fat seems compelling at this stage (perversely enough, I knew Nathan Pritikin personally and hostd him to dinner in Brisbane 15+ years ago). Surely it's time for those of you better qualified than me to mount at least a semblance of criticism at this parlous state of affairs supporting low fat diets. I enjoy the LC discussions here (I'm a lurker), but is there an endocrinologist or diabetologist who is willing to speak up? Those of us privileged to care for patients directly should calculate the plausibility gap (we should be evidence-based, surely) and come clean. Nobody I know in Oz is prepared to do so. MDs here with whom I share the techniques for accessing PubMed and Cochrane are routinely shocked at the paucity of the evidence base for low fat. Are there any more of you out there? Keith Charlton DC MPhil ---------- > From: Dean Esmay > To: LOWCARB@MAELSTROM.STJOHNS.EDU > Subject: Re: LOWCARB Digest - 6 Apr 1999 to 7 Apr 1999 - Special issue(#1999-81) > Date: Thursday, 8 April 1999 13:34 > > Most of these issues have been addressed--with extensive references and > referrals to clinical experience of seasoned physicians--on this list over > the last two years. However: > > >There are no magic diets, simply thermodynamics - > >eat less than you burn and you will lose weight. > > There is not one peer-reviewed study to support any claim that a > low-calorie diet, whether combined with exercise or not, is an effective > long-term treatment for affecting more than very moderate weight loss in a > majority of subjects. > > This is not an opinion. It is a fact. If you doubt it, I invite you to > discuss the matter with any professional obesity researcher. Or to simply > try to find any study which refutes what I say. I'd be very surprised if > you could find one. -Several- studies have looked at calorie-restricted > diets combined with exercise and "lifestyle modification" over a period of > 1 year, two years, and even five years, and -all- have shown abysmal > failure in the vast majority of subjects. > > >I also agree that there > >are many unanswered questions about ketosis and a high protein diet. What > >are the effects on bone density for females? > > The long-term answer to this is unknown. This is also true of almost all > dietary approaches. > > There are, however, a number of studies on people who live their entire > lives eating diets of up to and even beyond 50% protein on a daily basis, > with almost no evidence of osteoporosis among either male or female > populations, nor indeed any evidence of any substantial health problems or > decreased longevity. > > There are studies which indicate no substantial calcium loss from natural > animal proteins. There are, on the other hand, short-term lab studies > which indicate high calcium loss when ingesting large quantities of soy > protein isolates. > > In general the evidence that there is a meaningful danger to bone density > rom a high protein diet is quite limited, with much contrary data. Again > many of these studies have been discussed at great length here over the > last two years. > > >What are the long-term effects of ketosis? > > Define "long term." Several studies have looked at people in ketotic > states over periods of weeks, months, and in a few cases (mostly > epileptics) years. To date there is no substantial evidence of long-term > health damage. > > Dr. Richard Bernstein, a respected diabetic researcher (and a man who's > lived with IDDM for about 30 years) is a good clinical example. Not only > has he been on a ketogenic diet for decades, but he's been in medical > practice almost as long, treating his diabetic patients with this same > diet. So far he's managed to avoid losing his license, going to jail, or > getting sued for killing his patients--who in general seem to do > extraordinarily well on his program. > > As most people (aside from severe diabetics) will not remain in a ketotic > state for more than a few months, it therefore seems silly to insist that > there is a grave danger to their health. > > If you spend any time on the support lists for ketogenic diets, where > literally hundreds of dieters help each other on such diets, you will find > no recorded cases of hospitalization due to acidosis--this in support > groups that have been around over four years, with literally thousands of > members. Indeed, while ketogenic diets have been used for as much as 20 > years by some diabetics, there is still to date no recorded evidence of > long-term damage. > > Despite widespread claims that the moderate dietarily-induced ketosis > induced by carbohydrate starvation is dangerous, the explosion in > popularity of ketotic diets over the last five years has yet to produce ANY > significant increase in reports of patients being hospitalized or dying due > to ketoacidosis. > > Those who continue to suggest that moderate dietarily-induced ketosis is > dangerous look more and more foolish every year. Very much like physicians > who were claiming all throughout the 1970s that anabolic steroids cannot > possibly increase muscle mass. Which was the consensus opinion of the AMA, > medical textbook authors, and most physicians. > > >How about ketosis and pregnancy? > > Speak to an obstetrician about this, or to a diabetologist. Many if not > most pregnant women are naturally in a state of moderate ketosis throughout > their pregnancies. Most obstetricians consider anything less than heavy > ketosis to be fairly normal and simply ignore it, or make a note to do > nothing more than monitor it at each checkup. > > In populations where carbohydrate intake is zero to none (such as in the > Inuit) there is no evidence of any negative fetal effects. > > What, by the way, are the long-term effects of low-fat, low-protein, > high-carbohydrate diets? Can you document them with evidence? > > >(the standard answer to this > >is no-one should diet while pregnant, however I have heard of pregnant > >women on ketogenic diets - not for weight loss, but cause they think it is > >healthy) > > Indeed, I know one physician who specializes in diabetics who routinely > keeps all his pregnant diabetic patients in on a ketogenic diet, being sure > merely to keep them in no deeper than the moderate-to-light ketosis that is > normal for pregnancy anyway. Bernstein does this. There remains to date > very little evidence that such a state is dangerous; what hypothetical > danger there is may well be offset by the counter-danger that high insulin > and blood sugar levels may offer to both child and mother. > > My own wife was in moderate ketosis throughout most of her pregnancy. Our > 18 month old son has been in excellent health and been ahead of the growth > and development curve since his birth. > > The Inuit have traditionally eaten diets of under 7% carbohydrate--with > most of the year spent eating practically no carbohydrate at all--and yet > there has never been any evidence that they suffer any substantially > increased level of stillbirth, miscarriage, fetal deformity, or > childbirth-related death. > > Does this mean ketosis is absolutely safe? No. But it does indicate that > extreme fear is unjustified. But it would be unwise to advise a pregnant > woman to intentionally seek to put herself into ketosis for no particular > reason--just as much as it would be unwise to advise a pregnant woman to > take almost any medication unnecessarily. > > >I heard an MD state that some fetal deaths had been attributed to > >ketosis, but have not found any references to date. > > I have been searching for over two years for the evidence that there is an > association between fetal deaths and ketosis. Up to and including directly > questioning professional researchers on the subject. The entirety of the > evidence in this regard appears to be based on two things: > > 1) There is evidence of extreme maternal and fetal danger from > KETOACIDOSIS, a state of extremely heavy ketosis accompanied by extremely > high glucose levels seen in Type I diabetics. In this state, both ketone > levels and blood sugar levels are many times higher than anything that > could be achieved due to simple carbohydrate starvation. > > 2) There are a couple of studies which indicate that abnormally high ketone > leves have a teratogenic effect on lab rats. > > There remains no evidence that the light to moderate ketosis that is caused > by ketogenic diets is any significant danger to healthy adults. > > > >I subscribe to this > >list because I am interested. I know my opinions are different from the > >majority who subscribe, but I am trying to logically look at what my > >patients are subject to. > > This list exists to give physicains, dieticians, professional trainers, > medical researchers, and others a place to discuss these issues. There's > nothing wrong with raising these questions, although there is some > frustration at having to repeat discussions we've already had. On the > other hand, perhaps it's wise to periodically review these matters. Or put > together another FAQ like the one at > -- Alas I have no time. > -=- > > "It is impossible for a man to learn what he thinks he already knows." > Epictetus (50-138 A.D.)

    From owner-lowcarb*caf**OMEN*-COM@MAELSTROM.STJOHNS.EDU Mon Apr 26 09:45:33 1999 Return-Path: owner-lowcarb*caf**OMEN*-COM@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id JAA09956 for ; Mon, 26 Apr 1999 09:45:28 -0700 (PDT) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Mon, 26 Apr 1999 12:42:38 -0500 Date: Mon, 26 Apr 1999 11:42:28 -0400 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Dana Carpender Subject: Re: Early Low Carb To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R > > Many years ago, I read a book written in either the 50's or 60's by a > gentleman who supported general LC theory and included the drinking of > polyunsaturated oils on a daily basis. > > Later, when I read Dr. Atkin's first book, I noted that much of his theory > seemed to be derived from the book I had read earlier. > > Can anyone tell me the gentleman's name who wrote that early book? Some > info on later studies that either back up or tear down his theories would > also be appreciated. Dr. Herman Taller, _Calories Don't Count_, '62, if I remember correctly. Long out of print, but worth reading if you can find it. Earlier than that was Dr. Richard McKarness, _Eat Fat And Grow Slim_, which came out in the '50s, and again was very similar to Atkins or PP. Has a forward by the wife of polar explorer and low carb fan Vihljamer Steffanson. (For that matter, I have a copy of a book from 1914 called _Eat and Grow Thin_, also a low carb book. Recommends the most *amazing* dinners -- three courses minimum, all protein of some sort.) Dana

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Sat May 1 06:17:16 1999 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id GAA18936 for ; Sat, 1 May 1999 06:17:10 -0700 (PDT) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Sat, 1 May 1999 9:14:08 -0500 Date: Sat, 1 May 1999 08:52:55 -0400 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: April Willmore Subject: Re: Candida: dietary and nutritional supplement protocols To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R Excerpted from an article at the website of John Vlok DOMmisse, MD, FRCP(C), a nutritional & metabolic medical practitioner, link courtesy of Amy, LC-Diabetes list: Diet: Without strict adherence to the following diet, no anti-candida drug or treatment will succeed: (1) Avoid added sugars.... (2) Avoid white-starch foods, like white bread, cakes, cookies, white pasta, white rice, potatoes w/o their skins, and all refined flours, etc.... (3) Increase your intake of essential oils, esp. omega-3 oils, which are very lacking in the Western World's diet. These include: Fish oils, and oily fish, like salmon, mackerel, tuna-in-oil, sardines-in-oil, etc.; Flax-seed, borage and evening primrose oils.....Avocadoes, nuts, olives and olive-oil, canola and other vegetable oils are mostly omega-6, which are also good but not as lacking in our diets. (4) Avoid antibiotics and cortisone-type prescriptions if at all possible.

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Wed May 26 18:50:27 1999 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id SAA09640 for ; Wed, 26 May 1999 18:50:25 -0700 (PDT) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Wed, 26 May 1999 21:46:42 -0500 Date: Wed, 26 May 1999 15:48:16 EDT Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Betsy Walits Subject: Re: Healthy government diet programs To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R In a message dated 5/26/99 2:21:32 AM !!!First Boot!!!, esmay@SYNDICOMM.COM writes: << Aside from the irony of the piece, I'm probably not the only one here who notes how unhealthy that food regimen is. A packet of juice and cereals anly, eh? Not exactly setting the kids up for a lifetime of healthy eating. No wonder diabetes is at such epidemic levels in the inner cities. >> Good point... I was one of those mothers who didn't produce enough milk, so I supplemented with formula. After realizing the benefits of reduced carb (and having my first child be chunky like me), I supplemented my second child with protein enriched formula. By adding protein powder to his formula, I believe that I produced my first thin kid. And he's still thin and now he's three. Accordingly, for those who must use formula, I always recommend that protein powder be added. For me, I added enough protein to make it 30% of calories. BTW, I also regularly added fat, usually olive oil. None of that good stuff is in the government Wic forumlas. BTW, regarding cereals, I also used protein enriched oatmeal while my baby was little. Betsy

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Fri May 28 04:12:49 1999 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id EAA20445 for ; Fri, 28 May 1999 04:12:47 -0700 (PDT) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Fri, 28 May 1999 7:09:05 -0500 Date: Wed, 26 May 1999 22:10:59 -0400 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: April Willmore Subject: Re: "Healthy" government diet programs, kids, and seniors To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: RO > Dean writes: > Aside from the irony of the piece, I'm probably not the only one here who > notes how unhealthy ..A packet of juice and cereals ... No wonder > diabetes is at such epidemic levels in the inner cities. > Betsy writes: > Good point... I .. supplemented with formula. After realizing the benefits of > reduced carb (and having my first child be chunky like me), I supplemented my > second child with protein enriched formula. By adding protein powder to his > formula, I believe that I produced my first thin kid. And he's still thin and > now he's three. I supplemented both my boys with "whole milk no added carbs yogurt" from an infa-feeder. The first has always had a weight problem, but has been better since ours became a lowcarb household. The second has always been slender, and they are now graduating from high school in two weeks, and starting high school next fall, respectively. I supplemented two clients yesterday with my (mayo, egg, and soy) egg salad in whole wheat pitas. They are live-at-home seniors who routinely eat juice and cereal, plus white bread and jelly and Ensure throughout the day. One said he slept better than he had in weeks last night, and was noticeably stronger this morning, and the other was more alert and oriented, with fewer memory lapses. Think about seniors eating all those carbs because it's easy, and kids eating it because it's what the government and mom provide. It is a miracle anyone in this country is in any state whatsoever approaching decent health. April

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Wed Jun 2 22:31:28 1999 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id WAA05851 for ; Wed, 2 Jun 1999 22:31:14 -0700 (PDT) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Thu, 3 Jun 1999 1:26:29 -0500 Date: Thu, 3 Jun 1999 16:09:34 -0700 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Ray Audette Organization: Paleolithic Press Subject: Re: diabetes type 2 versus lowcarb To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R Alan Silverstein wrote: > > They just don't get it... > It says in part: "After three months on a low-fat, high-carbohydrate, > high-fibre diet, "Effects of Varying Carbohydrate Content in Patients with Non-Insulin-Dependent Diabetes Mellitus" JAMA, vol.271,#18(May 11 1994)pgs.1421-1428 After less than 6 weeks on a low-fat, high carbohydrate diet, diabetic subjects averaged a 24 percent increase in LDL cholesterol and a 23 percent increase in tryglycerides. The study was discontinued in fear of subjects safety. Ray Audette Author "NeanderThin" St. Martin's Press Nov.'99

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Thu Jun 17 04:58:14 1999 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id EAA12872 for ; Thu, 17 Jun 1999 04:58:12 -0700 (PDT) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Thu, 17 Jun 1999 7:55:00 -0500 Date: Thu, 17 Jun 1999 06:30:33 -0400 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: "Ann B. Mullikin" Subject: Hi-fat/Lowcarb for Diabetes To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R Hi List; The Endocrinologists have been holding a meeting recently and some of the stuff that came out of it is quite interesting. ie, "Diabetics Improve Health With Very High-Fat, Low Carb Diet" Not new to us, but remarkable to be coming from such a mainstream group. The dawn is breaking? ---------------------------------------------------------------------------- ----------------------- DG-DISPATCH - ENDO 99: Diabetics Improve Health With Very High-Fat, Low Carb Diet ---------------------------------------------------------------------------- ---- ---------------------------------------------------------------------------- ---- By Cameron Johnston Special to DG News SAN DIEGO, CA -- June 15, 1999 -- A very high-fat, low-carbohydrate diet has been shown to have astounding effects in helping type 2 diabetics lose weight and improve their blood lipid profiles. The results of three studies involving such a diet, which is similar to, but has a few key differences from the famous "Dr. Atkins Diet", were presented today at the annual meeting of the Endocrine Society. Dr. James Hays, an endocrinologist and director of the Limestone Medical Center in Wilmington, DE, admitted that the concept of a high-fat diet in people who are already at higher risk of cardiovascular disease might seem incongruous. Nonetheless, this study of 157 men and women with type 2 diabetes showed an impressive benefit in body mass index (BMI) triglycerides, HDL, LDL and HbA1c. ---------------------------------------------------------------------------- ------- The complete article can be found at: Best regards ann

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Tue Aug 10 18:24:51 1999 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id SAA00738 for ; Tue, 10 Aug 1999 18:24:48 -0700 (PDT) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Tue, 10 Aug 1999 21:24:55 -0500 Date: Mon, 9 Aug 1999 23:24:37 -0700 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Doug Skrecky Subject: floor test To: LOWCARB@MAELSTROM.STJOHNS.EDU In-Reply-To: <> Status: R Elzi Volk wrote: > >One place where I would start on the definition of obesity is strictly from > >a functional criteria. Put the person laying in the middle of a floor > >without any furniture nearby. He has five seconds to stand up, and he > >can't use anything to help him. Hockey players are able to do this easily > >on ice. And no, I can't pass this test, I take the better part of a minute > >if I make it at all. > > This is somewhat irrelevant (I'm being very polite). > I can't get up from a prone lying position in 5 seconds, Alex, and it has > absolutely nothing to do with obesity, but a function of muscle imbalances, > connective tissue limitations and joint instability. Although I am no > longer at 12% bodyfat (I'm now at 19%), I was even less able to do so then. > Does this mean I was (and am) obese?? > I rather like this simple physical test for physical fitness. Thanks for suggesting it. It would not surprise me if it correlated with treadmill performance. Since physical fitness as measured on a treadmill has been demostrated to be responsible for the variations in mortality associated with different body weights, it might be decent test to determine your expected life expectancy, even if it does not always work to measure obesity (need a scalefor that.) FYI - to keep that muscle mass up while dieting, consume extra protein. This has been demostrated in scientific intervention studies to block the loss of muscle mass, which usually occurred on high carb weight loss diets. It is loss of muscle mass, not bodyfat that has been associated with increased mortality in dieters. A "healthy" low protein diet is a contradiction in terms.

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Sun Sep 12 19:51:47 1999 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id TAA03608 for ; Sun, 12 Sep 1999 19:51:45 -0700 (PDT) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Sun, 12 Sep 1999 22:51:57 -0500 Date: Fri, 10 Sep 1999 14:14:22 -0700 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Doug Skrecky Subject: weight loss: beneficial or detrimental? To: LOWCARB@MAELSTROM.STJOHNS.EDU In-Reply-To: <> Status: RO Barbara Pollack wrote: > they tweaked the lowest-weight group by > excluding smokers and those with cancer and other illnesses but left the > groups alone--and then reported that the skinnies were the longest-lived. > More recently unhealthy people at all BMIs have been segregated out in several large studies. The findings were that healthy people live longer, but BMI has no effect on longevity after health status is accounted for. In short if you can jog around the block, and don't have high blood pressure, losing weight will not make you live longer - although it make make you more attractive to the opposite sex........

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Fri Oct 1 04:10:06 1999 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id EAA25682 for ; Fri, 1 Oct 1999 04:10:05 -0700 (PDT) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Fri, 1 Oct 1999 7:09:18 -0500 Date: Wed, 29 Sep 1999 16:39:12 +0200 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Alison Kamffer Subject: Re: protein diet w/ single kidney... To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R If Her single kidney is functioning nomally,then she should have no problem with a low carb diet. If in doubt, better check her creatinine clearance, ie renal function 1st.Remember 1 kidney can do the job of 2, but the problem is to have 2 kidneys which only have 1/2 function!We have now screened 1000's of urea and creatinines,prior to a low cho programme; those slightly raised[e.g.urea < 10] always return to normal at the 4 week check. We don't take people with obviously poor renal function tho.

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Fri Oct 8 03:14:14 1999 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id DAA01055 for ; Fri, 8 Oct 1999 03:13:59 -0700 (PDT) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Fri, 8 Oct 1999 6:14:19 -0500 Date: Thu, 7 Oct 1999 20:57:05 -0700 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Doug Skrecky Subject: a high protein diet helps dieters lose a few pounds To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R Authors Skov AR. Toubro S. Ronn B. Holm L. Astrup A. Institution Research Department of Human Nutrition, The Royal Veterinary and Agricultural University, Copenhagen, Denmark. Title Randomized trial on protein vs carbohydrate in ad libitum fat reduced diet for the treatment of obesity. Source International Journal of Obesity & Related Metabolic Disorders. 23(5):528-36, 1999 May. Abstract OBJECTIVE: To study the effect on weight loss in obese subjects by replacement of carbohydrate by protein in ad libitum consumed fat-reduced diets. DESIGN: Randomized dietary intervention study over six months comparing two ad libitum fat reduced diets (30% of total energy) strictly controlled in composition: High-carbohydrate (HC, protein 12% of total energy) or high-protein (HP, protein 25% of total energy). SETTING AND PARTICIPANTS: Subjects were 65 healthy, overweight and obese subjects (50 women, 15 men, aged 18-55 y) randomly assigned to HC (n = 25), HP (n = 25) or a control group (C, n = 15). All food was provided by self-selection in a shop at the department, and compliance to the diet composition was evaluated by urinary nitrogen excretion. MAIN OUTCOME MEASURE: Change in body weight, body composition and blood lipids. RESULTS: More than 90% completed the trial. Weight loss after six months was 5.1 kg in the HC group and 8.9 kg in the HP group (difference 3.7 kg, 95% confidence interval (CI)(1.3-6.2 kg) P < 0.001), and fat loss was 4.3 kg and 7.6 kg, respectively (difference 3.3 kg (1.1-5.5 kg) P < 0.0001), whereas no changes occurred in the control group. More subjects lost > 10 kg in the HP group (35%) than in the HC group (9%). The HP diet only decreased fasting plasma triglycerides and free fatty acids significantly. CONCLUSIONS: Replacement of some dietary carbohydrate by protein in an ad libitum fat-reduced diet, improves weight loss and increases the proportion of subjects achieving a clinically relevant weight loss. More freedom to choose between protein-rich and complex carbohydrate-rich foods may allow obese subjects to choose more lean meat and dairy products, and hence improve adherence to low-fat diets in weight reduction programs.

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Mon Oct 18 08:11:40 1999 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id IAA29380 for ; Mon, 18 Oct 1999 08:11:38 -0700 (PDT) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Mon, 18 Oct 1999 11:11:30 -0500 Date: Fri, 15 Oct 1999 16:41:11 EDT Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Ellen Carpenter Subject: Changes in BMR after low carb To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: RO Is there any evidence out there to document a correlation between the increase in BMR as a result of low carbs (x 18 months) and an increase in core temperature? What used to be a sub-normal baseline temp (97.6) has become elevated (100.0) consistently for several months without any known source. Insulin levels dropped from 65 to 30, combined with 100+ lb weight loss. Any thoughts?? Ellen, RN

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Wed Oct 20 10:28:45 1999 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id KAA17919 for ; Wed, 20 Oct 1999 10:28:36 -0700 (PDT) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Wed, 20 Oct 1999 13:27:53 -0500 Date: Wed, 20 Oct 1999 13:26:06 -0400 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: April Willmore Subject: correct URL for Goldberg diet, was ..Atkin's diet, fat sources To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R not

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Tue Oct 26 14:28:24 1999 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id OAA11754 for ; Tue, 26 Oct 1999 14:28:22 -0700 (PDT) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Tue, 26 Oct 1999 17:28:06 -0500 Date: Mon, 25 Oct 1999 13:45:45 -0700 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Pat Sonnenstuhl Subject: Re: Fat sources To: LOWCARB@MAELSTROM.STJOHNS.EDU In-Reply-To: <> Status: R An n excellent book for this information is Eat Fat, Lose Weight by Ann Louise Gittleman. Easy to read and I've seen it at Target. There is definitely a trick to eating the 'right type' of fat. Pat Sonnenstuhl, ARNP, CNM "Let your heart instruction you. Listen well: you will know your way." mary anne radmacher-hershey -----Original Message----- From: Low-Carbohydrate Technical Discussion [mailto:LOWCARB@MAELSTROM.STJOHNS.EDU]On Behalf Of Barrett Butler Sent: Wednesday, October 06, 1999 10:23 AM To: LOWCARB@MAELSTROM.STJOHNS.EDU Subject: Fat sources Has anyone collected data on the sources or choices most have made in going to a higher fat diet? Maybe they haven't changed their fats but eat more of them. -still what are those foods. This may be important in looking at impacts on blood lipid profiles. Possibly steering toward healthy fats may make a more positive change in health factors. I get the feeling that many people are choosing to eat way too much saturated and altered fats in the way of hydrogenated oils, fried food, bacon, pork rinds, hotdogs etc. B. Butler ISSA CFT

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Tue Nov 23 05:27:09 1999 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id FAA11385 for ; Tue, 23 Nov 1999 05:27:03 -0800 (PST) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Tue, 23 Nov 1999 8:27:00 -0500 Date: Mon, 22 Nov 1999 23:22:37 -0800 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Doug Skrecky Subject: moderate exercise ineffective in weight loss To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R Int J Sport Nutr 1998 Sep;8(3):213-22 Influence of diet and/or exercise on body composition and cardiorespiratory fitness in obese women. Utter AC, Nieman DC, Shannonhouse EM, Butterworth DE, Nieman CN Department of Health, Leisure, and Exercise Science, Appalachian State University, Boone, NC 28608, USA. The purpose of this study was to measure the influence of diet, exercise, or both on body composition and cardiorespiratory fitness in obese women. Ninety-one obese subjects were randomized into one of four groups: diet (D) (4.19-5.44 MJ or 1,200-1,300 kcal/day), exercise (E) (five 45-min sessions at 78.5+/-0.5% maximum heart rate), exercise and diet (ED), and controls (C). Maximal aerobic power and body composition were measured in all subjects before and after a 12-week diet intervention period. Subjects in D and ED lost 7.8+/-0.7 and 8.1+/-0.6 kg body mass, with no significant change for E relative to C. Losses of percent body fat and fat mass were significantly greater in D and ED but not in E relative to C. The change in VO2max was greater in ED and E but not D when compared to C. Results indicate that moderate aerobic exercise training during a 12-week period has no discernible effects on body composition but does improve cardiorespiratory fitness in dieting obese women.

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Sat Dec 18 12:32:53 1999 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id MAA08482 for ; Sat, 18 Dec 1999 12:32:51 -0800 (PST) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Sat, 18 Dec 1999 15:32:51 -0500 Date: Sat, 18 Dec 1999 15:02:19 -0500 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Thomas Incledon Subject: Omnivorous better than lactoovovegetarian diet? To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R This just came out. Thought some may enjoy reading it. Tom Incledon TITLE: Effects of an omnivorous diet compared with a lactoovovegetarian diet on resistance-training-induced changes in body composition and skeletal muscle in older men [In Process Citation] AUTHORS: Campbell WW; Barton ML Jr; Cyr-Campbell D; Davey SL; Beard JL; Parise G; Evans WJ AUTHOR AFFILIATION: Nutrition, Metabolism, and Exercise Laboratory, Donald W Reynolds Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock. SOURCE: Am J Clin Nutr 1999 Dec;70(6):1032-9 [MEDLINE record in process] CITATION IDS: PMID: 10584048 UI: 20051097 ABSTRACT: BACKGROUND: Very limited data suggest that meat consumption by older people may promote skeletal muscle hypertrophy in response to resistance training (RT). OBJECTIVE: The objective of this study was to assess whether the consumption of an omnivorous (meat-containing) diet would influence RT-induced changes in whole-body composition and skeletal muscle size in older men compared with a lactoovovegetarian (LOV) (meat-free) diet. DESIGN: Nineteen men aged 51-69 y participated in the study. During a 12-wk period of RT, 9 men consumed their habitual omnivorous diets, which provided approximately 50% of total dietary protein from meat sources (beef, poultry, pork, and fish) (mixed-diet group). Another 10 men were counseled to self-select an LOV diet (LOV-diet group). RESULTS: Maximal strength of the upper- and lower-body muscle groups that were exercised during RT increased by 10- 38% (P < 0.001), independent of diet. The RT-induced changes in whole- body composition and skeletal muscle size differed significantly between the mixed- and LOV-diet groups (time-by-group interactions, P < 0. 05). With RT, whole-body density, fat-free mass, and whole-body muscle mass increased in the mixed diet group but decreased in the LOV- diet group. Type II muscle fiber area of the vastus lateralis muscle increased with RT for all men combined (P < 0.01), and the increase tended to be greater in the mixed-diet group (16.2 +/- 4.4 %) than in the LOV diet group (7.3 +/- 5.1%). Type I fiber area was unchanged with RT in both diet groups. CONCLUSION: Consumption of a meat-containing diet contributed to greater gains in fat-free mass and skeletal muscle mass with RT in older men than did an LOV diet.

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Sun Jan 9 02:35:59 2000 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id CAA22896 for ; Sun, 9 Jan 2000 02:35:58 -0800 (PST) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Sun, 9 Jan 2000 5:36:04 -0500 Date: Sat, 8 Jan 2000 16:01:29 PST Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Jack Goldberg Subject: Re: LOWCARB Digest - 6 Jan 2000 to 7 Jan 2000 (#2000-4) To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R . To support this, there is much anecdotal >evidence ..... My suspicion is that it is cell-mediated, The evidence is in the fermented milk product medical literature. Do a search on Medline. Lactobacillus is known to boost immunity through cytokine mechanisms. My references are in the book. Anecdotally, and from just my own personal experience the following have occurred in the almost 4 years I've been on the GO-Diet. 1. I have not had one cold in that time.( I used to suffer from 4 to 5 colds every year.) 2. No sick days except for one broken leg which cost me three hours in the ER. 3. No more athletes foot. A chronic problem of people who use the locker rooms at health clubs. 4. All yellowing nailbeds have whitened. (yellowing of the nailbeds is a common phenomenon caused by fungal infection of the nail). To me this adds up to an immune boost. Jack Goldberg, Ph.D. Co-author The GO-Diet. Now available from Amazon and Barnes and Noble on line. ______________________________________________________ Get Your Private, Free Email at

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Sun Jan 9 10:32:47 2000 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id KAA25804 for ; Sun, 9 Jan 2000 10:32:43 -0800 (PST) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Sun, 9 Jan 2000 13:32:29 -0500 Date: Sun, 9 Jan 2000 10:36:59 -0700 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Elzi Volk Subject: Re: LOWCARB Ketodiets and immune system continued To: LOWCARB@MAELSTROM.STJOHNS.EDU In-Reply-To: <> Status: R At 04:01 PM 1/8/00 PST, you wrote: >Anecdotally, and from just my own personal experience the following have >occurred in the almost 4 years I've been on the GO-Diet. >1. I have not had one cold in that time.( I used to suffer from 4 to 5 colds >every year.) >2. No sick days except for one broken leg which cost me three hours in the >ER. >3. No more athletes foot. A chronic problem of people who use the locker >rooms at health clubs. >4. All yellowing nailbeds have whitened. (yellowing of the nailbeds is a >common phenomenon caused by fungal infection of the nail). This is what puzzles me. Many on the lowcarb-l list report they have fewer colds, etc while on a keto diet. Although not all report 100% resistance (I have one now), the relative incidence is less. Conversely, those who do become sick with a flu or cold while on a keto diet report increased time for recovery. So while some of the anecdotal evidence (lack of allergy symptoms, articles, etc) imply suppression of immune system, some of the reports (lack of colds, etc) also imply increased immune system. This is what has be stumped. There are also some studies that have mentioned reducing glucose/insulin levels increases auto- and xenograft survival in patients. As well as decrease chronic inflammation such as in rheumatoid arthritis. It has been postulated that it may decrease symptoms of lupus as well. This points to an auto-immune specific mechanism, as someone mentioned privately. And this may be, but this still does not fully explain reactions to allergies, which is not completely an auto-immune reaction. >To me this adds up to an immune boost. Many others also report control of systemic bacterial and fungal infections, such as candida etc. This may also be more specific to a requirement of glucose by fungal and bacterial organisms rather than specifically an immune boost. It is reported that lack of glucose reduces tumor growth, and is not solely a function of the immune system. Glucose and insulin are indirectly and directly required for expression of many genes. Lack of one or the other serves to regulate gene expression of certain proteins that consequently regulate the growth of tumors. As well as intrinsic, there is a humoral effect. Low plasma glucose and insulin shift many endocrine/paracrine/autocrine factors that contribute to decreased tumor growth. I cannot lend any reputable credence to my hypotheses as you cannot to yours unless someone actually investigates immune markers in the body while on a ketodiet. We can make assumptions from the anecdotal observations we all have, but immunology is quite complex and multifactoral. We must approach reductive conclusions with care. I have been meaning to contact a researcher in dietary nutrients and immunology (she's in the UK) on this subject, but it has been near the bottom of my priority list (work and grad school are on top). Elzi Volk, SSSR "To be in the state of 'hambre del alma', a starved soul, is to be made relentlessly hungry."

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Mon Jan 10 15:57:41 2000 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id PAA07901 for ; Mon, 10 Jan 2000 15:57:39 -0800 (PST) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Mon, 10 Jan 2000 18:57:29 -0500 Date: Mon, 10 Jan 2000 18:51:31 -0500 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Dana Carpender Subject: Re: immune system To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: RO Automatic digest processor wrote: Is there any non-anecdotal data on this? "Colds" are vague things, and > people often will have selective memories about them. Also, as people > get older, they may have fewer contacts with carriers (especially > chidren). And also have developed immunities to many of the common strains of cold. Still, my subjective experience is that I catch less stuff since I've gone low carb. Possibly useful data points, from _Get the Sugar Out_ by Ann Louise Gittleman, M.S., C.N.S.: "Sugar is a known immunosuppressant. This is frightening considering that our ability to withstand all diseases (from the common cold to AIDS) depends on having an active, healthy immune system. No matter what form it takes, sugar paralyzes the immune system in a variety of ways: 1. It has been proven to destroy the germ-killing ability of white blood cells for up to five hours after ingestion. 2. It reduces the production of antibodies, proteins that combine with and inactivate foreign invaders in the body. 3. It interferes with the transport of vitamin C, one of the most important nutrients for all facets of immune function. 4. It causes mineral imbalances and sometimes allergic reactions, both of which weaken the immune system. 5. It neutralizes the action of essential fatty acids, thus making cells more permeable to invasion by allergens and microorganisms. -- Dana W. Carpender

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Mon Jan 31 18:48:43 2000 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id SAA11574 for ; Mon, 31 Jan 2000 18:48:41 -0800 (PST) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Mon, 31 Jan 2000 21:48:38 -0500 Date: Mon, 31 Jan 2000 20:07:15 -0500 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Leanne Ridley Subject: Study re: insulin and GH response To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: RO I figured that, with the recent discussions concerning growth hormone, this recent study would be of interest: Leanne Ridley ****************************** Title Elevated insulin levels contribute to the reduced growth hormone (GH) response to GH-releasing hormone in obese subjects. Author Lanzi R ; Luzi L ; Caumo A ; Andreotti AC ; Manzoni MF ; Malighetti ME ; Sereni LP ; Pontiroli AE Address Istituto Scientifico San Raffaele, Divisione di Medicina Interna, Unit`a di Bioingegneria, Universit`a degli studi di Milano, Milan, Italy. Source Metabolism, 48(9):1152-6 1999 Sep Abstract We have recently presented experimental evidence indicating that insulin has a physiologic inhibitory effect on growth hormone (GH) release in healthy humans. The aim of the present study was to determine whether in obesity, which is characterized by hyperinsulinemia and blunted GH release, insulin contributes to the GH defect. To this aim, we used a simplified experimental protocol previously used in healthy humans to isolate the effect of insulin by removing the interference of free fatty acids (FFAs), which are known to block GH release. Six obese subjects (four men and two women; age, 30.8 +/- 5.2 years; body mass index, 36.8 +/- 2.8 kg/m2 [mean +/- SE]) and six normal subjects (four men and two women; age, 25.8 +/- 1.9 years; body mass index, 22.7 +/- 1.1 kg/m2) received intravenous (i.v.) GH-releasing hormone (GHRH) 0.6 microg/kg under three experimental conditions: (1) i.v. 0.9% NaCl infusion and oral placebo, (2) i.v. 0.9% NaCl infusion and oral acipimox, an antilipolytic agent able to reduce FFA levels (250 mg at 6 and 2 hours before GHRH), and (3) euglycemic-hyperinsulinemic clamp (insulin infusion rate, 0.4 mU x kg(-1) x min(-1)). As expected, after placebo, the GH response to GHRH was lower for obese subjects versus normals (488 +/- 139 v 1,755 +/- 412 microg/L x 120 min, P < .05). Acipimox markedly reduced FFA levels and produced a mild reduction of insulin levels; under these conditions, the GH response to GHRH was increased in both groups, remaining lower in obese versus normal subjects (1,842 +/- 360 v 4,871 +/- 1,286 microg/L x 120 min, P < .05). In both groups, insulin infusion yielded insulin levels usually observed under postprandial conditions and reduced circulating FFA to the levels observed after acipimox administration. Again, the GH response to GHRH was lower for obese subjects versus normals (380 +/- 40 v 1,075 +/- 206 microg/L x 120 min, P < .05), and in both groups, it was significantly lower than the corresponding response after acipimox. In obese subjects, as previously reported in normals, the GH response to GHRH was inversely correlated with the mean serum insulin (r = -.70, P < .01). In conclusion, our data indicate that in the obese, as in normal subjects, the GH response to GHRH is a function of insulin levels. The finding that after both the acipimox treatment and the insulin clamp the obese still show higher insulin levels and a lower GH response to GHRH than normal subjects suggests that hyperinsulinemia is a major determinant of the reduced GH release associated with obesity. Language Eng Unique Identifier 99411857

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Thu Feb 17 18:38:58 2000 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id SAA07744 for ; Thu, 17 Feb 2000 18:38:56 -0800 (PST) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Thu, 17 Feb 2000 21:39:03 -0500 Date: Thu, 17 Feb 2000 14:21:16 +0100 Reply-To: Sender: Low-Carbohydrate Technical Discussion From: Tanya Zilberter Organization: Subject: Re: High LDL Question To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R -----Original Message----- >as TGL goes down, so does the amount of small, dense LDL in the >overall LDL fraction. It is still disputed, however, whether the >small, dense LDL is an independent risk factor for heart disease. >Todd Moody "A very low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins." (A J Clin Nutr. 69(3):411-8, 1999) -- Tanya Zilberter, PhD Weight Loss Guide

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Sat Feb 19 12:38:32 2000 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id MAA23666 for ; Sat, 19 Feb 2000 12:38:30 -0800 (PST) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Sat, 19 Feb 2000 15:38:41 -0500 Date: Sat, 19 Feb 2000 14:49:32 +0000 Reply-To: Sender: Low-Carbohydrate Technical Discussion From: "M. Coole" Subject: Low birth weight and insulin resistance To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R Low Birthweight Linked to Insulin Resistance Syndrome Later in Life in China Read it Here WESTPORT, Feb 16 (Reuters Health) - Chinese infants with low birthweight are more likely than those with normal birthweight to develop the insulin resistance syndrome as adults, according to a report in the February 15th issue of Annals of Internal Medicine. Dr. Catherine Law from Southampton General Hospital, UK, and colleagues explain that in developed countries, low birthweight has been associated with increased prevalence of the insulin resistance syndrome of hyperglycemia, hyperinsulinemia, hypertriglyceridemia, and high blood pressure. They hypothesized that the increasing prevalence of insulin resistance syndrome in developing countries might be explained by maternal undernutrition and reduced fetal growth, as well as increasing body mass index among adults. The investigators studied 627 Chinese men and women, mean age 45, whose birthweights were known and whose mothers' heights and weights had been recorded during pregnancy. They note that the subjects were born in Beijing between 1948 and 1954, "when much of the population was chronically malnourished." The higher a subject's blood pressure, the lower his or her birthweight had been, the results indicated. Each decrease in birthweight of 1 kg was associated with a systolic blood pressure rise of 2.9 mm Hg and a diastolic rise of 1.7 mm Hg. Similarly, low weight at birth was associated with higher blood sugar, insulin, and triglyceride levels in adult life, the authors report. All these consequences of low infant birthweight were accentuated in those who had high body mass index as adults. As expected, the investigators note, lower infant birthweight was closely associated with lower body mass index of the mother, suggesting "that thinness of the mother during pregnancy is associated with insulin resistance and reduced glucose tolerance in adult offspring." "Prevention of adult obesity remains an important strategy for decreasing the incidence of the insulin resistance syndrome, particularly in the immediate future," the authors conclude. "Our study suggests that in the longer term, benefit may also be derived from increasing women's body mass index to optimal levels before pregnancy." Ann Intern Med 2000;132:253-260.

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Sun Feb 20 19:23:34 2000 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id TAA05324 for ; Sun, 20 Feb 2000 19:23:32 -0800 (PST) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Sun, 20 Feb 2000 22:23:42 -0500 Date: Sun, 20 Feb 2000 19:20:38 -0600 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Liz H Subject: Studies Suggest Atkins Diet is Safe To: LOWCARB@MAELSTROM.STJOHNS.EDU In-Reply-To: <> Status: R Studies Suggest Atkins Diet is Safe New York, Feb 18/00 (Reuters Health) The extremely carbohydrate-restricted Atkins diet is a safe, effective way to lose weight, according to studies presented at the Southern Society of General Internal Medicine in New Orleans. A study of the diet conducted at the Durham VA Medical Center in North Carolina showed that on average, mildly obese people lost about 21 pounds in four months on the diet, and had positive changes in heart risk factors such as reduced cholesterol and increased HDL or "good cholesterol." These results are supported by a second study from researchers at the Atkins Center for Complementary Medicine in New York. The Durham study included 41 mildly obese, healthy people who attended an outpatient clinic. The study participants followed a program that reduced carbohydrate intake to less than 20 grams per day, and included vitamin supplements, fish oil supplements and 20 minutes of exercise at least three times per week. Over four months on the diet, the participants lost an average of 21.3 pounds, and showed a 6.1% drop in cholesterol, and almost a 40% drop in the level of triglycerides in their blood. In addition, their HDL levels increased by about 7%. In a press release, the researchers also say that their study did not find any of the safety concerns voiced by the American Dietetic Association, such as potentially dangerous effects on liver and kidney function. "In four short months on the Atkins Diet, we were able to confirm scientifically what Dr. Atkins states he has seen in his practice over the past decades. The diet lowers cholesterol and triglycerides and raises HDL... which may represent an entirely new approach to the control and prevention of heart disease," said lead researcher Dr. Eric C. Westman, assistant professor of medicine at North Carolina's Duke University. The study is continuing in order to assess the long-term effects of the diet. Reporting the results of the second study, Colette Heimowitz, director of nutrition at the Atkins Center in New York, said that it was based on 319 overweight or obese patients treated at the Center for at least a year. Investigators collected information on weight, blood pressure, cholesterol, kidney and liver function and other parameters during the study. "What we found is what we already knew from anecdotal data," Heimowitz told Reuters Health in an interview after the meeting on Friday. " There were some pretty impressive benefits in body composition, HDL levels went up, LDL levels went down and blood pressure decreased," she reported. Where HDL is the good cholesterol for its association with reduced heart risk, LDL has earned the name of being the "bad" cholesterol because high levels are associated with heart disease. "We now have data for the scientific community" on the healthful benefits of the Atkins diet, Heimowitz asserted. The Atkins diet severely restricts carbohydrate intake to induce a state of ketosis, or metabolic starvation. Dieters are encouraged to measure urinary ketone excretion as an indication of how effective the diet is in inducing fat breakdown. "Ketosis is a benign byproduct of fat burning," Heimowitz asserted. "With an adequate protein and fat intake, there is no loss of muscle mass...There is no change in (blood) pH if the diet is properly done," she said. However the diet is not for everyone, Heimowitz warned. "It's for those who need a correction in their sugar and carbohydrate metabolism...We encourage (vitamin) supplementation and an intake of 'good' fats, such as fish oil," Heimowitz commented. Liz H. ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Mon Feb 28 17:33:33 2000 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id RAA01178 for ; Mon, 28 Feb 2000 17:33:31 -0800 (PST) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Mon, 28 Feb 2000 20:33:43 -0500 Date: Mon, 28 Feb 2000 20:28:31 -0500 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: April Willmore Subject: Re: cats and grain diets was Anxiety and Depression To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: RO listmember wrote: > (Grover) was > hyperthyroid, and the vet told me that when soy products are primary in cat > food, some cats will develop hyperthyroidism. And when cats are fed a commercial food high in rice/other grains, they get diabetes. Go figure! (Cats are, after all, carnivores.) I don't understand how educated individuals like vets are so brainwashed into recommending the major commercial products, all of which are primarily carbs. Even the ones that say, "our #1 ingredient is meat (or protein)" have three kinds of corn following the #1 ingredient, meat, so that when you look at the overall make-up of the food, it is a high percentage of carbohydrate. (If it seems I am posting a disproportionately high number of e-mails, I just came off a 6-week assignment, so have a little time to write. This commercial dog and cat food issue is a pet peeve of mine.) April

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Wed Mar 1 07:51:55 2000 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id HAA16055 for ; Wed, 1 Mar 2000 07:51:52 -0800 (PST) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Wed, 1 Mar 2000 10:51:56 -0500 Date: Wed, 1 Mar 2000 06:19:59 -0800 Reply-To: Low-Carbohydrate Technical Discussion Sender: Low-Carbohydrate Technical Discussion From: Pat Sonnenstuhl Subject: New Books ! To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R I was at the book store the other day and found several new books. Anyone heard of them? I didn't buy any of them, but would like to review them.: Two with the title Syndrome X, one by Reaven, the individual that has done so much research at Stanford, and quoted by Barry Sears, one Eat Fat, Be Healthy, and another Metabolize. I'm also aware of another book coming out this spring: Sugars and Fours. I also found an amazing website, which perhaps you have found also: Pat Sonnenstuhl, ARNP, CNM "Long-term planning is not about making long-term decisions. It is about understanding the future consequences of today's decisions." -- Gary Ryan Blair

    From owner-lowcarb@MAELSTROM.STJOHNS.EDU Wed Apr 5 11:00:16 2000 Return-Path: owner-lowcarb@MAELSTROM.STJOHNS.EDU Received: from ( []) by (8.8.5/SCO5) with ESMTP id LAA25361 for ; Wed, 5 Apr 2000 11:00:14 -0700 (PDT) Message-Id: <> Received: from ( by (LSMTP for OpenVMS v1.1a) with SMTP id <>; Wed, 5 Apr 2000 12:59:10 -0500 Date: Wed, 5 Apr 2000 12:00:09 -0600 Reply-To: Alan Silverstein Sender: Low-Carbohydrate Technical Discussion From: Alan Silverstein Subject: Overweight Teens Benefit from High-Fat Diet To: LOWCARB@MAELSTROM.STJOHNS.EDU Status: R In the local newspaper on 3/24 (just getting around to it), and article by Ridgely Ochs, Newsday. Too long to type it all in, but here are some quotations, and some comments from me. "...researchers have found that overweight teens on a high-fat, high-protein diet lost more weight than adolescents on a traditional low-fat diet." Hmm... I bet most of those teens were overweight due to hyperinsulinemia, hence self-selected to benefit from low-carb. "...the teens' cholesterol levels improved..." "...Center for Atherosclerosis Prevention at Schneider's Children's Hospital in New Hyde Park, NY... presented Thursday at the Society for Adolescent Medicine meeting in Washington, DC." "...22 people ages 12-18 who were 20-100 pounds overweight... lost an average of 19 pounds in 12 weeks, compared to those on a low-fat diet who lost about 8.5 pounds. Overall cholesterol levels dropped in both groups..." "...triglycerides... fell 33% in the (first group), compared to 17% in the low-fat diet group... and levels of HDL... also increased more..." "'The idea of controlling carbohydrates has been around for 20 years but no one has done a controlled trial.'" "...wasn't surprised by the greater weight loss... but 'was frankly surprised by the lipids. We didn't expect that.'" The dropout rate was about 30% in both groups. Caloric intake was higher in the low-carb group (1830 versus 1100). Both exercised 30 min 3x/week. The article does mention suppression of insulin. One negative counterpoint offered (as usual): "'...small, short-term study... we need to know what happens to the cardiovascular system over the long term... I worry about telling kids to go on nothing but a high-fat diet. That's bad news... We're not talking about teaching kids over the long-term to eat a healthy diet. This kind of scares me.'" Harumph. As usual, it's just not that simple! Alan Silverstein
    From: (Dr. Jai Maharaj) Subject: A DIET TO HELP DEFEAT DIABETES Date: Sat, 24 Feb 2001 00:15:27 GMT A diet to help defeat diabetes By Barry Hailstone, Medical Reporter The Advertiser, Australia Thursday, February 22, 2001 A team of CSIRO scientists in Adelaide is conducting the world's first study into ways of preventing diabetes. It is believed but not proven that healthy eating and controlling weight will prevent type-2 diabetes, a non- insulin dependent form of the disease that usually strikes in midlife. The head of the CSIRO's SA-based clinical research unit, Peter Clifton, has recruited more than 60 South Australians for the study. The CSIRO is giving the recruits portion-controlled food for about 16 weeks and the volunteers overweight men and women aged from 20 to 65 must stay off alcohol and stick to the diet to achieve a substantial weight loss. Dr Clifton said yesterday the study involved eating specially prepared high-protein, low-carbohydrate foods, losing weight and regular blood tests for about four months. "The object is to develop a technique for identifying people who are likely to suffer type-2 diabetes by measuring the insulin in their body and using diet and weight control to prevent the disease from occurring in later life," Dr Clifton said. People with high insulin levels in their blood had a high chance of acquiring diabetes. "It ticks away like a time bomb," Dr Clifton said. "At this stage we are selecting people with high insulin levels who are at high risk of type-2 diabetes and then giving them a high protein carbohydrate-reduced diet which includes a variety of dairy and meat foods to see if it influences their insulin level and improves their metabolism of food. "If it results in them having a lower insulin level then such a diet may protect them in future from diabetes." One in 12 Australians was diagnosed with diabetes and one in 20 did not know they had it. "It's a rapidly increasing 'fat society disease' now occurring in a younger age group, men and women in their early forties," he said. News Plus Om Shanti From: Howard Lee Harkness Newsgroups:, Subject: Re: Scared to death WRT diet after heart attack Organization: YGBSM! Message-ID: NNTP-Posting-Date: Mon, 03 Mar 2003 23:00:31 GMT Date: Mon, 03 Mar 2003 23:00:31 GMT Xref: MIME-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit "Dr. Andrew B. Chung, MD/PhD" wrote: >Howard Lee Harkness wrote: > >> And, as already mentioned, normal, all healthy humans who are not >> *gaining* weight are in ketosis for a substantial part of every day. > >Incorrect. Yet another diet-guru-wannabe with an MD who is unfamiliar with the work of Lyle McDonald. Ketosis is clinically defined as a blood concentration of 0.02 mmol/dl, a level typically substantially exceeded in 20 minutes of aerobic exercise. ... or 5-6 hours after a meal, especially if it contains some fat, and does not contain excess carbs. Ketones are generally present at all times at a minimum level of at least 0.01 mmol/dl in most healthy people, and ketone concentration in most people will peak sometime after midnight, when most normal, healthy (non-IR) people will be in clinical ketosis. Yes, ketone production (and lypolysis in general) is inhibited by insulin, which will be be present in high levels if the person is consuming excess carbs, especially if that person is insulin resistant, in which case the person WILL BE GAINING WEIGHT due to lack of lypolysis. Weight loss requires lypolysis, and the corresponding production of ketones. Normal, healthy people who are maintaining a steady weight alternate between fat storage and fat burning twice or more times per day. >Ketosis is not good for arteries. If ketosis is bad for you, it follows that you should avoid aerobic exercise. (That's about as silly as the "two-pound diet") I'm still waiting for long-term studies showing that ketosis (not DKA) is bad for you. However, I know that the only thing I can expect from Dr. Chung on that subject is a priori wishful thinking. From McDonald: "Somewhat difficult to understand is why ketogenic diets have been readily accepted as medical treatment for certain conditions but are so equally decried when mentioned for fat loss[...] Pediatric epilepsy patients are routinely kept in deep ketosis for periods of up to 3 years, and occasionally longer, with few ill effects." None of the observed ill effects have anything to do with damage to the arteries, BTW, which leads me to conclude that Dr. Chung's statement that ketosis is hard on the arteries was basically pulled out of his ass. Or maybe he's just confused from following his "two-pound diet".