ADIPOSITY 101
Chuck Forsberg caf@omen.com
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.
Some recent research indicates fructose is much 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.
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.
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.
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.
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. http://www.nytimes.com/2008/08/01/science/01muscle.html?ref=dining
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. http://jama.jamanetwork.com/article.aspx?articleid=1199154
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.
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.
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.
| 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)
This suggests one's set point is misset if one cannot reach and
maintain normal weight on 3000 calories per day.
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,
990–996
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) 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.
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.
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 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.
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)
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)
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:
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)
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.
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."
SET POINT
Is there an Obesity Virus?
Rats, Pigs and Blimps
Brown Adipose Tissue (BAT)
White Adipose Tissue (WAT)
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.
Fat Cell Receptors
Fat and Carbohydrate Oxidation
Muscle Fibre Type
FORTUNE OF BIRTH
Types of Adiposity
GENETICS or ENVIRONMENT?
SYNDROME X
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. (Foxnews.com Dec 19 2000)
Maternal Environment
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
| 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)
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)
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)
Keithf.Lynch@f8.n135.z1.fidonet.org 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.
"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.
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."
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)
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.
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.
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)
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.
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)
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:
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.
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)
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.
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 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.
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)
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.
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 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.
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)
"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.
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.
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 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.
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, www.audionet.com)
(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.
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.
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)
"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:
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.
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. )
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:
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 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.
"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.
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.
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.
Dblake@bme.jhu.edu 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 www.ceri.com/dhea.htm
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.
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:
>MENU>
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.
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.
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.
"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
Banting's 1869 Letter on Corpulence
Online Guide to Low-Carb Diet Resources
Insulin and its Metabolic Effects
(backup copy)
The latest Adiposity 101 is available at www.omen.com
Low Carbohydrate & Ketogenic Diet Resources
Other resources
©1997 Chuck Forsberg.
This page may be freely linked to, mirrored, or redistributed
provided it is not modified.
Personality Problems
Health Problems
TRADITIONAL TREATMENT
EXERCISE
DIETS
SLOW vs RAPID Weight Loss
BEHAVIOR MODIFICATION
Diet Side Effects
Author's weight history in BMI showing massive weight rebound
after a hospital resident doctor supervised weight loss program.
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
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 abdul.dulloo.unige.ch.
Human Studies on Weight Cycling
Study Subjects Sample Results WC>BMI Health Outcome
(Dale) 20 f SKEWED IDA matched (Short term study) Optifast 50 f selected IDA yes unknown Blackburn 57 cyclers true yes n/a TRIM 88 SKEWED IDA yes (Short term study) Jequier f - - yes Slowed Metabolism Baltimore 846 m volun. IDA ? Glucose Intolerance WECO 2107 m all true yes? CHD Gothenburg 2317 random true n/a CHD, diabetes Framingham 5127 random true yes CHD Lee (Harvard) 11703 m alumni true n/a CHD, all Blair/MRFIT 12866 m FEDERAL n/a n/a CHD Helsinki 15830 Finnish true n/a CHD, all
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.
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)
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.
High Fiber Diet
Low Fat Diets
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.
Other Low Fat Diet Studies
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."
Dieting Gourmets
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.
Low Carbohydrate Diets
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 Ornish and Atkins Compared
INITIAL CONDITIONS ORNISH
(low fat)ATKINS
(low carbohydrate)Age 56 55 Starting weight 201 195 Body Mass Index 28.4 28.1 DIET RESULTS ORNISH
(low fat)ATKINS
(low carbohydrate)Cholesterol change -24% -13% HDL (GOOD) Cholesterol - 3% +60% Triglycerides (BAD) +75% -82% Weight -12% -19% Diets - the BOTTOM LINE
FLAWED RESEARCH
Correlation .vs. Cause and Effect
Flawed Sample Selection/Distribution
Improper use of Ratios to Adjust Data
TRUTH IN RESEARCH PAPERS
MEDIA DISTORTION
NEW TECHNOLOGY
Food Allergy Avoidance
THYROID ISSUES
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.
GROWTH HORMONE TREATMENT
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.
DHEA TREATMENT
Check DHEA and Melatonin Web Page
RU-486 TREATMENT
CoPP TREATMENT
BROMOCRIPTINE TREATMENT
CIRCADIAN LIPOSTAT MANIPULATION
DOPAMINE AGONISTS
TESTOSTERONE TREATMENT
BETA3-ADRENOCEPTOR AGONISTS
SEROTONIN REUPTAKE INHIBITORS
FAT CELL REMOVAL
Fat Cell Removal by Surgery
Fat Cell Removal by Immunological Manipulation
PREDICTIONS
RECOMMENDATIONS FOR ACTION
REQUIRED READING
RECOMMENDED READING
INTERESTING WEB PAGES
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
WWW.Weight.com
DHEA Web Page
DHEA and Melatonin Web Page
American Journal of Clinical Nutrition
Paul McAleer's Fat Acceptance Page
Other resources
Other resources
Other resources
Other resources
Other resources
Other resources
Dangers of Trans-Fatty Acids
Diet and Human Evolution
End of Adiposity 101
