From: caf@omen.UUCP (Chuck Forsberg WA7KGX)
Subject: New Adiposity 101 1/2
Organization: Omen Technology Inc
Date: Thu, 13 Aug 1992 07:32:49 GMT

Here's the latest edition of Adiposity 101.  Updated information has been
added to many chapters, esp. diet safety and effectiveness as well as a
disturbing study on exercise for weight loss.




                       Adiposity 101

                       Chuck Forsberg

                      Portland Oregon


1.  FOREWORD

Obesity ruins the quality of life for millions of Americans.

Traditional weight control technology has changed little
since Greek antiquity.  30 years of applied research and
more than $100 billion of public expenditure have not helped
most fat Americans.  Indeed, more may have been hurt than
helped.

Genetics, gestation and suckling environments produce
individuals with profoundly different tendencies to gain and
lose muscle and fat.  Obesity is now known to be one of the
most inheritable of diseases.

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.

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


2.  ROSETTA STONE

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

Adipose Cell: There are two types of adipose (fat) cells,
White Adipose Tissue (WAT) and Brown Adipose Tissue (BAT).
The body uses WAT to store energy for use in hard times; BAT
burns energy to maintain body temperature.

Permanent changes in WAT number can be induced during the
suckling period.  It is thought that permanent changes in
BAT can be induced after weaning.

Fat Free Mass (FFM) is everything that is not fat.  Water
constitutes about 73 per cent by weight of FFM.  Glycogen,
another constituent of FFM, is stored in the liver and
muscle as a reservoir of glucose for metabolic energy.  Many
papers do not distinguish between FFM and muscle tissue.

Glucose: (dextrose) found in fruits and other foods, is the
end product of carbohydrate metabolism.  Blood glucose is



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the primary source of energy in animals. Glucose is
converted to glycogen and stored in the liver, muscles, and
fat.  Blood glucose levels are of great interest in
adiposity and diabetes.  Low blood glucose from fasting or
other dietary restriction can induce headaches, low spirits,
and compulsion to restore normal glucose levels by eating
more.  To convert from the trendy mmol/L SI units found in
research papers to the familiar mg/dl used by American
physicians, multiply by 18.

Adipocyte Hyperplasia:  Excessive number of fat cells, as
much as ten times normal.

Hyperphagia: overeating

Body Mass Index (BMI) is a measure of the percentage of fat
to total body mass.  BMI is weight in kilograms divided by
height in meters, squared.  (Multiply by 704 if using inches
and pounds.) BMI is a height and bone-density independent
measure of adiposity (fatness).  BMI is more highly
correlated with body fat than other indices of height and
weight.  BMI should not be used in individual cases unless
confirmed by unretouched photographs or other indications.
BMI does not distinguish between mesomorphs and somewhat
overweight men.

Fat Free Mass (FFM): everything but fat.  FFM includes
bones, water, etc. and is not quite the same as lean tissue.

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

Refactory: Adjective indicating the condition reasserts
itself, precluding long term relief.

Two major enzymes involved in the regulation of uptake and
egress of fatty acids from fat cells are LipoProtein Lipase
(LPL) (stores fat) and Hormone Sensitive Lipase (HSL)
(mobilizes fat).

The pituitary gland releases Human Growth Hormone (HGH) in
bursts, mostly during the early hours of sleep.  Human
Growth Hormone promotes muscle growth and fat loss.

DHEA is a hormone that reduces fat and cholesterol.

Metabolic needs of he body are provided by the degradation
of glucose and free fatty acids [FFA].  Most tissues can use
both glucose and FFA for their energy needs, but the brain
and nervous system can only use glucose.  When dietary
intake does not permit sufficient production of glucose,



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body protein is sacrificed to make it.

Kilo Joule: some papers use kilo Joules (kJ) to measure food
energy instead of kilocalories (kcal), or "calories" as used
by the lay press and food labels.  The kJ is a smaller unit
of energy than the kcal, and diet portions expressed in kJ
don't seem as small as those expressed in "calories".  To
convert from kJ to kcal ("calories"), multiply by 0.24.

Programming: A permanent or long-term change in the
structure or function of an organism resulting from a
stimulus or insult acting at a critical period of early
life.



3.  THE BIOLOGY OF ADIPOSITY

3.1  SET POINT

One cannot appreciate 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.  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.  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 abnormalities
during gestation.

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.



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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, limiting weight loss.

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.  Healthy male subjects who have
no history of dieting or weight concerns have a strong
caloric compensation. (American Journal of Clinical
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 empiric evidence.  (Weigle DS; Human obesity -
Exploding the myths.  Western Journal of Medicine 1990 Oct;
153;421-428)

3.2  Rats, Pigs and Blimps

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

Wild rats never exceed 10% body fat, even when fed high fat



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diets.  Some strains have been bred to mimic the metabolism
of obese humans.  The most common 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 ob/ob mouse fails to survive in the cold because it
cannot generate sufficient heat by burning fat.

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,
hypertriglyceridemia, 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.

High protein requirements could provide a partial
explanation for the hyperphagia of genetically-obese Zucker
rats.  These mutants oxidise 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."

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





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3.3  Brown Adipose Tissue (BAT)

Brown Adipose Tissue (BAT) generates heat (thermogenisis) by
burning calories without physical motion.

3.4  White Adipose Tissue (WAT)

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

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

Reduction of fat cell numbers (see below) causes permanent
fat loss while weight loss techniques that do not reduce the
number of fat cells are temporary at best.  This suggests
that fat cells themselves enforce the elevated "set point"
in many individuals.

3.5  Preadipocytes > Fat Cells

White fat cells begin life as PREADIPOCTYES.

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 creation, as reported in
many papers, explains the effect of dietary sugar and
carbohydrate on the delayed development of obesity.  This
would also explain why excessive amniotic insulin levels
cause fatter offspring.

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 fetal
growth hormone and high levels of triiodothyronine.

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.

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.



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Preadipocytes isolated from obese rat strains change into
fat cells more easily than normal.

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

Lean individuals have 20 to 40 billion fat cells.  As
reported in a 1983 Nova program, fat cells can expand to no
more than twice normal size.  Obese subjects have up to 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 gain more
weight than they lose dieting, putting them at risk of
hyperobesity from diet cycling.

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 marathon runners
who had half the total body fat.  In other words, the
exercise/dieters had twice as many fat cells as the
athletes.

3.6  Fat Cell Receptors

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

The numbers and efficiencies of fat cell receptor types
change with repeated dieting, promoting weight gain.

3.7  Fat and Carbohydrate Oxidation

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




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3.8  Muscle Fibre Type

The April 19 1990 Lancet reports that skeletal muscle fibre
type is directly correlated with BMI.  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 fat for healing the way thin people do.
(Journal of Clinical Investigations, Jan 1991)


4.  FORTUNE OF BIRTH

4.1  Types of Adiposity

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

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.  "However, 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)

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

Experiments with controlled overfeeding of lean subjects
demonstrate an increase in body metabolism that restores
normal weight when overfeeding ceases.




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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.

4.2  GENETICS

The conclusion of current research is that individual
differences in Body Mass Index (BMI) are mostly the result
of genetic factors.  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.

However, 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.

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



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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)

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
to their children.

"the genetic relationship fully accounts for the familial
resemblance in body mass index among adults."

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.

In "The response to long-term overfeeding in identical
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



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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.

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 when those of lean persons do not.
Metabolic differences are evident even before birth.  These
factors are described elsewhere in this document.

Obese and lean persons do not share the same genetic
heritage, essentially they are a distinct race.

4.3  Maternal Environment

What one's mother does or eats during or immediately before
pregnancy affects one's BMI.  The May 1990 METABOLISM
reported that changes in the rat sow's diet during early
pregnancy had a permanent effect on pups' lipid metabolism.

As reported in the Health InfoCom Network News Volume  3,
Number 36 December  5, 1990, Dr. Bernard Silverman of
Children's Memorial  Hospital in  Chicago says a study of
124 children whose mothers were either diabetic before
pregnancy or became diabetic during it showed:  Children at
normal weight at age 1.  Many were obese by 6 to 8.  At 8,
the median weight was 71 pounds for boys;  normal median -
56 pounds. Median for girls was 68 pounds; normal medium 55
pounds.  A study in the December 1990 Archives of Disease in
Childhood reported that infants whose amniotic fluid was



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highest in insulin were markedly obese by 6 years of age,
independent of the mother's weight.  This syndrome may be
the cause of Pima Indian's high incidence of obesity.

"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 inactive 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 inactive molecules as "insulin" can
lead to misdiagnosis that a patient is insulin resistant
when he is insulin deficient.

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.  That is more than twice the normal incidence of
obesity.

Infant undernutrition caused by smoking may produce similar
results.

























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4.4  Baby's Diet

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

_____________________________________________________________
|Diet Change       | Result in adult                         |
|__________________|_________________________________________|
|High Carbohydrate | More prone to hypercholesterolemia      |
|High Fat          | Prevents hypercholesterolemia           |
|Overnutrition     | Elevated plasma cholesterol and insulin |
|Undernutrition    | Obesity                                 |
|__________________|_________________________________________|

(FASEB Journal, June 1990, p. 2606)

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 low fat diet currently
favored by 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 discussion of adipose cell 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 also need sufficient dietary fat to insulate their
nerve cells, prevent nerve crosstalk and brain damage.


5.  EFFECTS OF OBESITY









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5.1  Personality Problems

The correlation between psychological problems and obesity
is well known.  Many psychiatrists' couches have been filled
with patients wishing to lose weight.  As the nature and
causes of obesity become known, obesity is increasingly
recognized as a cause of mental health problems rather than
the result of mental problems.


5.2  Health Problems

The correlation between obesity and certain health problems
has been widely documented.  Joint problems and sleep apnea
are generally recognized direct effects of obesity.

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.

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 weight 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.

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.

Some of the health problems associated with obesity result
not from the obesity itself but from general effects of
dieting.1 As reported in the 1990 House hearings on the diet


__________

 1. This does not refer to gall bladder and other acute
    problems some subjects have with specific diets.  Gall
    bladder problems are common in obesity.



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industry, some studies show an 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.  Insurance companies are forbidden to test
applicants for HIV antibodies, 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.  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)


6.  TRADITIONAL TREATMENT

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.

"... 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)















                       Adiposity 101







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6.1  EXERCISE

The correlation between exercise and thinness is well known
and firmly established in cultural and media stereotypes.
As a result, 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.

"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)




                       Adiposity 101







                           - 17 -



A Minnesota Heart Health Program study noted a significant
increase in obesity from 1980 to 1987.  The data suggest
that change in energy intake, fat intake, exercise, or
cessation of smoking was not responsible for this increase.

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.)

Several years ago it was widely reported that working out
left one with an "exercise afterglow" of 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 of obese subjects.

Exercise induces increased growth hormone levels in lean
subjects.  The obese do not release growth hormone in
response to moderate exercise.

Keithf.Lynch@f8.n135.z1.fidonet.org has reported reading
that those over 20% overweight should not exceed a pulse
rate of 0.6 * (220 minus age).  This guideline would
preclude robust exercise.

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



                       Adiposity 101







                           - 18 -



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.

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 this rapid fat gain
as it is after dieting.  Fat cell NUMBERS in some areas were
actually increased compared to the sedentary rats.  This
increase in adiposity may increase 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.

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

Exercise induced weight loss is temporary, but will be
maintained as long as the level 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.



                       Adiposity 101







                           - 19 -



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.

"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)

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.

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































                       Adiposity 101







                           - 20 -



6.2  DIETS

"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
is the oldest known method of obesity treatment.

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.

In distinction to the commonly accepted stereotype, research
shows that the obese do not eat more per pound 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.

"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)

"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 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.
1989.)

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.

Lean and obese female Zucker rats were intermittently
semistarved during their first 32 weeks of life, then fed ad



                       Adiposity 101







                           - 21 -



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."


6.3  SLOW vs RAPID Weight Loss

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)


6.4  Diet Side Effects

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

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.

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



                       Adiposity 101







                           - 22 -



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 thermogenisis is suspected.

Diet induced metabolic slowdown has two aspects: Resting
Metabolism Rate (RMR) and Diet Induced Thermogenisis
(DIT)/Thermic Effect of Food (TEF).  Studies on diet induced
decline in RMR are contradictory, with no agreement on
definitions and methodology.  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
when losing or maintaining lower 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.

Diets have unpleasant side effects for some.

  + Dry mouth

  + Sleep Disruptions (difficulty falling asleep, excessive
    sleepiness, disturbed sleep, vivid dreams)

  + Cold Intolerance.  "Cold intolerance is a significant
    problem aggravated by dieting in morbid obesity."

  + Lack of energy.

  + Menstrual Difficulties

  + Yest Infections

  + Fluid Retention





                       Adiposity 101







                           - 23 -



  + Low pulse rate and blood pressure.  One symptom of low
    blood pressure from metabolic slowdown is dizziness when
    abruptly arising from a chair.

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

  + Constipation

  + Stomach Distress

  + Hair loss

  + Ridged Nails (low fat diet vitamin or mineral
    deficiency)

  + Dizzy spells

  + Weakness

  + Headaches (mostly women)

  + Hot flashes

  + Depression (as measured in standardized tests).

  + Collagen generation as low as 5% of normal.  (Collagen
    is the major protein of all connective tissues, a
    shortage of which is believed to cause wrinkles, etc.
    Collagen production is necessary for wound healing and
    normal growth.) This might explain the degraded
    appearance seen in some dieters.

Diet induced metabolic changes include an increase in
lipoprotein lipase (LPL), an enzyme that stores fat in fat
cells.  LPL levels drop during the first few weeks of
dieting.  Depending on the study, LPL levels remained normal
or depressed for some time after dieting.  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 remain elevated
for at least 6 months.  The fatter the person was to begin
with, the more of the fat-regaining enzyme they produced
after weight loss.  Kern's paper sheds insight on many
issues related to the varied outcomes different people have
to diet cycling.  (New England Journal of Medicine, Vol. 322



                       Adiposity 101







                           - 24 -



No. 15, Apr 12 1990)

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

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)

Dieters need drugs to suppress the excessive amounts of LPL,
glucocorticoids, and runaway fat cell proliferation
triggered by energy deprivation and diet 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)

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, and 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 lost weight is
regained.  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.  Binging may be important in the onset of



                       Adiposity 101







                           - 25 -



adipocyte hyperplasia associated with diet 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)


6.4.1  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
present in some individuals was interfering with the weight
loss one would normally expect from energy starvation.  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.


6.5  Diet Cycling

For 95 per cent of 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".

Animal studies of weight cycling are contradictory.  When
obesity is forced by induced overeating, cycles of weight
fluctuation do not increase fatness.  When rats are reduced
below 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 diet cycling is
clinically used to add fat to underweight patients who
cannot to gain weight by overeating.

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 (BMI/year).  (N Engl J Med 1991; 324;
1839-44) A study of workers at Western Electric's Hawthorne



                       Adiposity 101







                           - 26 -



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 Epidemiolology 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 gained yet more
weight.  (International Journal of Obesity (1988), 12, 29-
39.)

"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 total fasts.  As with other types of diets,
subjects with childhood onset obesity had the most trouble
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 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 with 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.

Diet evangelists cite a number of studies which found no
serious bad effects from weight cycling.  In one, a short
term study of high school wrestlers who diet to "make
weight" for matches reported that weight and metabolism
returned to normal after the wrestling season.  No long term
followup was performed on these athletic mesomorphs who only



                       Adiposity 101







                           - 27 -



lost a small amount of weight for very short periods.  These
wrestlers never met several of the conditions that trigger
lipoprotein lipase (LPL, the "fattening hormone")
overproduction in serious dieters.

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

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

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

The data of Bjorntorp and Sjostrom (METABOLISM V20;7;703)
show greater than 10 per cent increase in fat cell numbers
from a single diet/partial regain cycle in subjects with
many fat cells.  Subjects with fewer fat cells (normal
range) did not suffer the same increase in fat cell numbers.

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

The Wadden study on diet cycling found a statistically
significant correlation between dieting history and weight,
BMI, fat mass, waist size, and hip size.  (Am J Clin Nutr
1992;56;203S-8S)



                       Adiposity 101







                           - 28 -



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

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

A study by Jeffrey, Wing, and French published in the
American Journal of Clinical Nutrition "adjusted" (fudged)
the health risk data to "account" for the increased fatness
of the diet cyclers.  This and other studies that "adjusted"
for weight gain did not report adverse results of diet
cycling besides those commonly attributed to the excess
weight from diet cycling.  These negative studies are
discussed in "Variability of Body Weight and Health Outcomes
in the Framingham Population" by Lissner et al.  With a
cohort of 5127 and more detailed medical records, the
Lissner study of the Framingham population supersedes the
earlier, smaller, and more idiosyncratic studies.

Diet evangelists have attacked these studies as bitterly as
the Tobacco Institute attacks studies linking smoking and
disease.  Diet evangelists insist that unknown factors other
than dieting may have been responsible for these weight
fluctuations.  (They have yet to suggest any credible
alternatives to dieting.) A careful reading of these papers
will, however, reveal that these concerns were carefully
considered and resolved before publishing.  I raised the
question with one of the Framingham study investigators in
July 1992.  He was confident that any cause of weight
cycling other than yo-yo dieting widespread enough to affect
the data on weight cyclers would have been known to
Framingham doctors.

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

The heart is not spared from the catabolic effects of
undernutrition, but is subject to the same degree of weight



                       Adiposity 101





-- 
Chuck Forsberg WA7KGX          ...!tektronix!reed!omen!caf 
Author of YMODEM, ZMODEM, Professional-YAM, ZCOMM, and DSZ
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