ADIPOSITY 101
Chuck Forsberg caf@omen.com
Adiposity is caused by genetics and the environment. New chromosome variations causing obesity are constantly added to the list. Identical twins reared by different parents have the same weight, (unless one has been exposed to a "fattening virus").
Maternal diabetes, 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.
Monosodium glutamate (MSG) in infant formula has been linked to obesity.
Exposure to certain virii causes permament weight gain.
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 glucose. 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. Click for more
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. The weight they lose usually comes back with considerable "interest" (rebound). This rebound may be caused by a diet induced increase in fat cell numbers.
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.
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 and related diseases.
Adiposity 101 surveys the rapidly evolving field of adiposity research.
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
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 environmental. 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.
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 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)
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 hyperph 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