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1. FOREWORD
This is a summary of adiposty information I've gleaned from
forays to the Med School library and other sources. I hope
it provides you with some useful information on obesity
research. Some of you may be able to fill in some of the
gaps mentioned here.
2. BACKGROUND
Set Point Theory: the body adjusts appetite, energy
expenditures, and other characteristics to restore a
constant weight, somewhat resistant to either dieting or
overfeeding.
In vitro: in a test tube (more or less). In vivo: in the
body.
Rats and pigs are commonly used in adiposty research because
their fat mechanisms resemble those of humans.
Body Mass Index (BMI) is a measure of the percentage of fat
to total body mass used as a height and bone-density
independent measure of adiposty.
3. SOURCES
"Recent Advances in Obesity Research: V" ISBN 0-86196-072-6
"Obesity in Europe 88" ISBN 0-86196-167-6
International Journal of Obesity
4. TYPES OF ADIPOSTY
4.1 Transient Adiposty
One source of obesity is overeating from emotional stress.
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, some 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
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subgroups, except those that tried to lose weight by
dieting.
4.2 Chronic Adiposty
My area of interest is chronic adiposty, in which the
subject is heavier than average for most of his life.
5. MEDIA DISTORTION
As Professor Garner's 1990 testimony before the House of
Representatives indicated, false advertising is rampant in
the diet industry. While an individual deceptive diet ad
may not be too damaging to the public at large, the
collective effect of such deception (Nazi Big Lie effect)
creates great damage.
6. FLAWED RESEARCH
I've become acutely aware of the wide variance in quality of
research and media coverage on the problem of adiposty. The
reader should beware of two common flaws in obesity studies.
6.1 Correlation .vs. Cause and Effect
A correlation study might show that joggers are thinner than
couch potatoes. This is a *correlation*. Almost
invariably, this data is used to "prove" that obesity is
caused by lack of exercise, that fat couch potatoes will
become thin if only they get off their duffs and exercise.
What is the error in drawing such a conclusion? The error
is the unstated assumption that the correlation proves a
particular cause and effect. In fact, there are two
possible cause and effect relationships at play. The common
assumption is: Lack of exercise causes obesity. The other
possibility is that obesity is a handicap that frustrates or
precludes sports activities.
Correlation studies that draw conclusions or make
recommendations without properly evaluating alternative
models of causality are fundamentally flawed and should be
treated with suspicion.
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6.2 Flawed Sample Selection/Distribution
Non-random selection or partitioning of the sample
population flaws many otherwise convincing studies.
A study on the mortality of obesity was based on patients
who had lost and regained weight. Was the increase in
mortality caused by the obesity, or by the dieting?
Diet program studies typically exclude dropouts from their
data.
Studies comparing the relative success of alternative
treatments do not always assign subjects to the alternatives
at random. Factors that determined sample selection and
partition may be more important to the outcome than the
nominal independent variable.
7. BIOLOGY OF ADIPOSTY
7.1 White Adipose Tissue (WAT)
Obesity results from an excess of white adipose tissue.
WAT cells are no mere storage tanks. These living cells
compete with lean tissue for nutrients, generate and destroy
hormones.
The fact that reduction of fat cell numbers by surgery or
immune attack causes a permanent fat loss while weight loss
techniques that do not reduce the number of fat cells are
temporary suggests that white fat cells themselves
constitute the "set point" regulator.
7.2 Brown Adipose Tissue (BAT)
The other type of fat is Brown Adipose Tissue (BAT) whose
main purpose appears to be the generation of heat
(thermogenisis).
7.2.1 Preadipocytes_>_Fat_Cells White fat cells begin life
as PREADIPOCTYES. Hormones control the differentiation of
preadipocytes into fat cells. The adiposty of individual
pigs can be predicted by measuring the ability of the
suckling's {*filter*} to differentiate preadipocytes in a test
tube. The preobese sucklings had low levels of fetal growth
hormone and high levels of triiodothyronine.
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7.2.2 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.
The literature indicates a number of factors complicate
measurement of the number and size of fat cells. This is an
evolving methodology.
A study published in the Proceedings of the 5th
International Congress on Obesity showed that obese subjects
who had lost weight in a combined diet/exercise program had
fat cells 25 per cent smaller than those of endurance
athletes who had half the fat. In other words, the dieters
had twice as many fat cells as the athletes.
7.3 Fat Cell Receptors
Fat cells gain and lose size by passing lipids through
receptors. One type of receptor removes lipids from the
{*filter*} stream and another type allows the body to access the
energy stored in the fat cells with a resulting loss of
weight.
The relative numbers and efficiencies of these two receptor
types change with dieting, promoting weight gain.
Geographic distribution of fat, including "love handles"
that do not respond to extreme dieting, is believed to
result from local variations in these receptors. No diet or
exercise has been shown to have any geographic specificity
in fat reduction.
7.4 The Role of Genetics
The conclusion of current research is that individual
differences in Body Mass Index (BMI) are mostly the result
of genetic factors.
Two studies published this year 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 had no effect on the BMI.
In other words, whether your mother fed you cookies or
celery made no difference on how fat you became as an {*filter*}.
In "The response to long-term overfeeding in identical
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twins", 12 pairs of identical male twins were overfed and
kept sedentary under close supervision. There was a 3 to 1
ratio in weight gain between the easiest gainer and the
slowest gainer. Those who gained the most fat gained less
muscle than those who gained the least fat. Ten of the 12
pairs of identical twins gained almost identical amounts of
weight.
This study is especially interesting because or its sample
selection. All subjects were sedentary and none of the
subjects had a history of obesity. One can but imagine the
results if a few marathon runners and a few Nutrisystem
graduates had been included.
There is a possibility one's maternal environment (what your
mother ate during pregnancy) may have an effect on lipid
metabolism and possibly obesity.
8. EFFECTS OF OBESITY
The correlation between psychological problems and obesity
is well known. Obesity is increasingly recognized as a
cause of psychological problems instead of the result of
mental problems.
The correlation between obesity and health problems is well
known.
But some of the mortality associated with obesity results
not from the obesity itself but from the effects of weight
loss. (This should not be confused with rare acute
reactions to specific types of diets.) As reported in the
recent House hearings on the diet industry, some studies
show in increase in mortality with weight loss.
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. The privacy of HIV antibody status is protected
as civil right, a right denied to obese applicants who might
prefer to omit their weight from insurance forms.
The obese sometimes get substandard medical treatment. In
one case, symptoms of allergy induced asthma (post nasal
drip) were attributed to obesity. I have also heard reports
of marginally overweight women humiliated by male doctors.
It would be appropriate for the AMA or regulatory bodies to
survey the incidence of such excesses.
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9. TREATING OBESITY
As reported in the recent House hearings in the diet
industry, there is no effective long term treatment for
obesity.
9.1 DIETS
Caloric restriction (semistarvation) appears to be the
oldest method of obesity treatment. Dieting is a natural
idea given the appearance of famine victims and the effects
of religious fasts. In distinction to widespread
stereotype, research shows that the obese do not eat more
than their lean counterparts.
Heavy advertising, the "thin is in" ethic, media
preoccupation with unusually obese individuals, and endemic
repeat business have swollen the diet industry into a 33
billion dollar a year enterprise.
A number of techniques have been used to enforce diets,
including appetite reducing {*filter*} and surgical modification
of the digestive system. None of these has proven to
improve the basic dynamics of the diet.
The major side effect of reducing diets is weight regain.
Despite a level of expenditure that would have produced
several space stations and a mission to Mars, the long term
success rate remains less than five per cent.
Controversy abounds about the efficacy of rapid vs slow
weight loss. Some studies addressing this issue are flawed
by sample selection problems. Subjects on 1200 calorie and
800 calorie VLCD type diets had the same ratio of fat loss
to lean tissue loss. Diet induced metabolic slowdown was a
direct function of the amount of weight lost.
(International Journal of Obesity 1989, pp 179-181)
It is sometimes reported that dieting cycles induce net
weight gain. Correction of chronic underweight by diet
cycling constitutes the singular instance of effective
dietary weight modification. However, I have not found any
relevant clinical research on this issue. My personal
observations suggest weight gain exceeding total weight loss
is most likely if the dieter approaches ideal weight and/or
is younger than 20-30 years.
Diet induced problems include an increase in lipoprotein
lipase and a worsening of the ratio of fat cell receptors,
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both of which promote weight gain.
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.
Dieting itself may be the more serious upset to the
patient's natural balance.
Rare instances of toxic side effects of certain diets have
received media attention. Compared to the assumed health
risks of obesity, none of these problems appears widespread
enough to warrant the attention they have received.
There has been considerable media coverage of claims that
artificial sweeteners hamper weight loss efforts. As far as
I can determine, these result from an American Cancer
Society study that found a correlation between overweight
and the use of artificial sweeteners. This correlation can
better be explained by noting that people without weight
problems generally prefer sugar sweetened beverages because
of taste and "sugar high". People may also read the labels
on some artificially sweetened products suggesting they be
used only by those desiring to reduce their caloric intake.
9.2 EXERCISE
Exercise is generally considered to be good for one's
health. 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. For
some individuals 7 pounds is sufficient, but not for others.
that those over 20% overweight should not exceed a pulse
rate of 0.6 * (220 minus age). This does not permit robust
exercise.
Exercise induces a period of raised metabolism and growth
hormone levels in lean subjects. These effects are reduced
or missing in the obese.
Severely overweight subjects showed a 50 per cent impairment
in FFA [free fatty acid] mobilization in response to
prolonged moderate exercise. This energy shortfall was made
good at the expense of a drop in {*filter*} sugar and increase in
lactate plasma (the enzyme that makes your muscles ache?).
This represents a metabolic limitation on exercise by the
obese. (1983 International Journal of Obesity pp 221-229.)
Contrary to the claims of Cable TV ads, there is no clinical
evidence of spot reducing effects from exercise.
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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.
9.3 Stimulation of Thermogenisis
Thermogenisis refers to the generation of body heat in
muscle and brown adipose tissue (BAT). Lean subjects
increase thermogenisis in response to meals, exercise, and
cold. Obese subjects show less of each of these responses
than lean subjects. Obese subjects are less tolerant to
long term cold exposure because of their inferior
thermogenisis capability.
In their book "Life Extension Weight Loss", Pearson and Shaw
suggest thermogenisis enhancing {*filter*} and cold exposure as
ways to burn up fat. A study of obese women on a swimming
program suggests their heat loss to water had the opposite
effect, increasing their fat stores.
9.4 Growth Hormone
Human Growth Hormone promotes muscle growth and fat loss.
In a recent study, administration of synthetic growth
hormone to elderly male patients resulted in significant fat
loss.
Pearson and Shaw recommend stimulation of human growth
hormone (HGH) excretion with arginine amino acid supplements
as a weight loss method. Unfortunately, references given in
their book indicate the recommended amino acid dosage is an
order of magnitude too small to cause the obese to release
any detectable HGH.
The obese have a high threshold of grueling exercise (to the
point of exhaustion) or megadoses of arginine which must be
surpassed before stimulation of HGH release is noted. HGH
levels achieved under these exceptional conditions are still
only a fraction of what lean subjects spontaneously produce
in their sleep.
GHR may be useful in reducing diet-induced loss of lean
tissue.
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9.5 DHEA
DHEA is a steroid hormone which has demonstrated marked
weight reducing ability in animal studies. It is claimed
that the "DHEA" sold by health cooking.net">food stores is bogus. The
author of "The Vitamin Bible" reports successful personal
weight loss from DHEA but gives no sources.
9.6 Surgery
Surgery is the only currently available fat reduction
treatment available today that offers a significant long
term success factor. Unfortunately, the amount of fat
removed by currently accepted surgical procedures is too
small to be useful for weight reduction purposes.
9.7 Passive Immunization
The Hannah Research Institute in Scotland is developing a
method to reduce long term adiposty with passive
immunization to fat cell plasma. In the earliest
experiments, rat fat cell plasma was injected into sheep.
The resultant antibodies were filtered and introduced into
the rats. The treated rats showed a permanent reduction in
the size of fat deposits compared to the controls.
Surprisingly, the treated rats had more lean tissue than
untreated controls. This indicates fat cells deprive lean
tissue of nutrients necessary for normal growth.
In a telephone conversation this year I was told Hannah's
research is proceeding very well toward its goal of
producing leaner meat animals, but human application in the
near future is unlikely due to the risk of malpractice
lawsuits.
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