Monster Media 1993 #3/MONSTER.ISO/textfile/adipobv.101

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                       Adiposity 101

                       Chuck Forsberg

                      Portland Oregon


1.  FOREWORD

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 hope to the millions
of fat Americans for whom conventional weight loss
technology has been ineffective at best.

Formatted 11-12-93.


2.  ROSETTA STONE

Anorectic: appetite suppression

Anorexiant: substance that suppresses appetite

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

Careful researchers: a roundabout way of stating that
researchers reporting contrary results made errors in
experimental design or deduction.

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

Hyperphagia: overeating

In vivo: in the body  In vitro: in a test tube

Lipogenesis: Storing of energy in fat tissue

Lipolysis: Draining energy from fat tissue

Panniculus adiposus: overhanging belly

Weight rebound: a net adiposity increase in a diet-regain
cycle, sometimes confounded by a net loss of lean tissue.

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











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burns energy to maintain body temperature.  Severe obesity
is caused by too many White Adipose Cells.

Human adipose tissue in vivo does not have the simple
metabolic pattern that might be expected from studies of
adipocytes in vitro.  It is engaged in a variety of
metabolic exchanges.  TAG, glucose, oxygen, acetoacetate,
and 3-hydroxybutyrate and acetate are all extracted from
from the blood.  NEFA, glycerol, lactate, and carbon dioxide
are released.  (Proceedings of the Nutrition Society 1992:
51, 409-418)

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

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

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

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











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Morbid obesity: Obesity severe enough to directly affect 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).

@ Insulin promotes differentiation of white fat cells, fat
deposition, lipoprotein lipase (LPL) activity, inhibits
growth hormone release, and inhibits the fat releasing
action of catecholamines.  In normal individuals, insulin
increases glucose uptake by muscle tissue and lowers glucose
production in the liver.  In Syndrome X, the the liver and
muscles are resistant to insulin, forcing the production of
more insulin to control blood glucose.  This causes
hyperinsulinaemia (too much insulin), shunting dietary
energy to fat stores.  A high level of insulin precedes
obesity and hypertension (Syndrome X).  Tight control in
Type I diabetics increases average insulin concentration and
causes weight gain.  Since obesity is associated with
resistance to insulin action, a vicious cycle of insulin-
>weight gain->more insulin is possible.  High insulin levels
may be a factor in development of high blood pressure,
abnormal lipid levels and artherosclerosis.  It is known
that insulin induces the growth of human vascular smooth
muscle and stimulates the proto-oncogene c-myc through the
IGF-I receptor.  Low levels of insulin caused by untreated
type I diabetes can lead to lipoatrophy (loss of fat
tissue).  Dietary carbohydrates, but not fat or protein,
increase insulin concentration.

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











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potent risk factor in obesity.  (5th European Congress on
Obesity 10-12 June 1992)

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.  HGH is
also called somatropin.

DHEA is a hormone that reduces fat tissue size and serum
cholesterol.

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.  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.

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

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


3.  ENERGY BASICS

@
     Interesting Parameters for Dietary Macronutrients

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

Gross energy is the heat of combustion, possibly useful
information when investigating spontaneous combustion of
humans.











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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 energy content of fat and carbohydrate compared with
their dietary effects on human weight control.

@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)


4.  THE BIOLOGY OF ADIPOSITY

4.1  SET POINT

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.












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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.

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











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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)

4.2  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
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.

@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











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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.
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.

















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4.3  Brown Adipose Tissue (BAT)

Brown Adipose Tissue (BAT) generates heat with Non Shivering
Thermogenesis (NST) by burning calories without physical
motion.

4.4  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.  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)

4.5  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 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.











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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.

4.5.1  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.  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 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 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.

4.6  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











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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.

4.7  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)

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)

4.8  Muscle Fibre Type

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

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

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
















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5.  FORTUNE OF BIRTH

5.1  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.

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.


5.2  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.











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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 [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)

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.












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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.  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.

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











Adiposity 101                15                     11-12-93



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 this
document.

Obese and lean persons do not share the same genetic
heritage.

5.3  SYNDROME X

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

1   resistance to insulin-mediated glucose uptake

2   glucose intolerance

3   hyperinsulinemia

4   increased very low density triglycerides (VLDL)

5   decreased high-density lipoprotein cholesterol (HDL)

6   hypertension

6a  Elevated systolic BP during submaximal exercise

7   increased fat mass
The inherited defect is insulin resistance in skeletal
muscles, the other abnormalities are consequences.
(American J of Obstet Gynecol July 1990 292-5)

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)

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











Adiposity 101                16                     11-12-93



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)

@ 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 clucose 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 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











Adiposity 101                17                     11-12-93



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
Sybdrome 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)

@ 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, the 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.
(From an 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)














Adiposity 101                18                     11-12-93



5.4  Maternal Environment

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

@ Too much carbohydrate during gestation is Not Good.
Gestating infants whose blood was highest in insulin 1
(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


__________

 1. Measured indirectly by sampling the amniotic fluid.












Adiposity 101                19                     11-12-93



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 was directly
opposed to the 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.








































Adiposity 101                20                     11-12-93



5.5  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                         |
|________________________|_________________________________________|
|PW to High Carbohydrate | More prone to hypercholesterolemia      |
|PW to High Fat          | Prevents hypercholesterolemia           |
|Overnutrition*          | Elevated plasma cholesterol and insulin |
|Undernutrition*         | Obesity                                 |
|________________________|_________________________________________|

PW = 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;16,495-502)

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).












Adiposity 101                21                     11-12-93



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 oc
Clin Nutr 1993;57:140-5)

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 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 need dietary fat to insulate their nerve cells,
prevent nerve crosstalk and brain damage.  Nw 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)

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)


6.  EFFECTS OF OBESITY

6.1  Personality Problems

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

Obesity has been historically linked to emotional factors by
clinicians and the lay public alike.  Early psychiatric
studies reinforced the popular perception that
psychpathology 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











Adiposity 101                22                     11-12-93



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)

6.2  Health Problems

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

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











Adiposity 101                23                     11-12-93



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.2 As reported in the 1990 House hearings on the diet
industry, studies consistently show an increase in mortality
with 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


__________

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












Adiposity 101                24                     11-12-93



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 certainy 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 physicans?  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)



7.  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.






























Adiposity 101                25                     11-12-93



7.1  EXERCISE

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 supervided 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)












Adiposity 101                26                     11-12-93



"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 suggest
that change in energy intake, fat intake, exercise, or
cessation of smoking were not responsible for 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.











Adiposity 101                27                     11-12-93



(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)

[e-mail] 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











Adiposity 101                28                     11-12-93



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











Adiposity 101                29                     11-12-93



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 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)

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.















Adiposity 101                30                     11-12-93



7.2  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
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.

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











Adiposity 101                31                     11-12-93



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)

"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











Adiposity 101                32                     11-12-93



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.
1989.)

"the following aspects of weight are myths rather than











Adiposity 101                33                     11-12-93



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.  CONCLUSIONS> Since the excess body mass index
levels associated with low socioeconomic status in women
could not be explained after controlling for adverse health
behaviors, further epidemiologic study of risk factors for
obesity in Black women is recommended." (American J of
Public Health, Jun 1992)

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

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

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













Adiposity 101                34                     11-12-93



7.3  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)
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)


7.4  BEHAVIOR MODIFICATION

"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 redeeding since the losses are usually
quite small and achieved with minimal restriction."
(American J of Clinical Nutrition 33: Feb 1980 p. 469)


7.5  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











Adiposity 101                35                     11-12-93



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.

@A Refeeding was associated with a metabolic adaptation
during which all of the fat saved 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 have important applications in rebound obesity
seen 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).












Adiposity 101                36                     11-12-93



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 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.

@ Studies that do not report diet induced metabolic slowdown
may be measuring the post-diet metabolism while subjects are
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











Adiposity 101                37                     11-12-93



intriguing feature. ... When the level of T3 is artifically
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.

  + Dry mouth

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

  + @ Substantial impairment of cognitive performance, 30
    per cent and worse accuracy reduction on a standardized
    cognitive task.  The cognitive impairment was related to
    the degree of weight loss.  Heart rate immediately
    before and after testing was lowest in the current
    dieters with high weight loss.  Lowered heart rate is
    typical of a chronic state of undernutrition.
    (Proceedings of the Nutrition Society 1992: 51, 343-51)

  + @ Aggression and suicide.  Lipids account for about half
    the dry matter of the brain.  Monkeys on a low fat diet











Adiposity 101                38                     11-12-93



    were significantly more aggressive than were controls on
    a normal diet.  In six randomised, controlled primary
    prevention trials, there was a significant increase in
    mortality due to suicides or violence.  Compares with
    control groups, the treated groups had 28 ferer deaths
    from CHD and 29 more deaths from suicide, homicide, and
    accident.  Adolescents are thought to be more
    susceptible to these effects.  Interventions to reduce
    cholesterol concentrations on a large scale could lead
    to a population shift to a more violent pattern of
    behaviour, which would result in more aggression, more
    abude of children and partners, and generally more
    unhappiness.  (Lancet 339: March 21 1992, p 727)

  + Radical low fat diets deplete the body of essential
    fatty acids, and should not be used during pregnancy or
    lactation.  The same concerns apply to childhood.

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

  + Lack of energy.

  + Menstrual Difficulties

  + Yest Infections

  + Fluid Retention

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

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

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

  + Constipation

  + Stomach Distress

  + Hair loss












Adiposity 101                39                     11-12-93



  + 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.

  + Memory problems A London conference held by the British
    Psychological Society heard that people who fight the
    flab can become forgetful and have difficulty performing
    simple tasks.  Until now scientists had thought only
    people with anorexia nervosa, the slimmer's disease,
    suffered mental impairment as a result of chronic
    undernourishment.

Diet induced metabolic changes include an increase in
lipoprotein lipase (LPL), an enzyme that stores fat in fat
cells by breaking down triglycerides in the blood.  (Defects
in LPL cause a wasting of fat tissue and high
triglycerides.) LPL levels drop during the first few weeks
of dieting, a time when when blood lipids often increase.
Depending on the study, LPL levels remained normal or
depressed for some time.  Subjects with BMI < 35 or who lost
less than 12% of their initial body weight did not show
marked increases in LPL.  But in the more obese subjects,
LPL rose to 25 times normal, and remained elevated for at
least 6 months.  The fatter the person was to begin with,
the more of the fattening enzyme they produced after weight
loss.  Kern's paper sheds insight on many issues related to
the varied outcomes different people have to diet 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 regain.











Adiposity 101                40                     11-12-93



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)

Nw Lipoprotein lipase (LPL), which increases dramatically
during dieting, appears to increase the formation of low
density lipoproteins in arterial walls (foam cell
formation).  (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 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 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











Adiposity 101                41                     11-12-93



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)


7.5.1  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.


7.6  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".

On the surface, animal studies of weight cycling are
contradictory, but there does seem to be a unifying concept;
diet 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 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











Adiposity 101                42                     11-12-93



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
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 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
(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
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.

Obese rats took 21 days to lose their excess weight during
their first cycle of food restriction, but took 46 days on











Adiposity 101                43                     11-12-93



the second cycle.  The cycles 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)

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
lost a small amount of weight for very short periods.  These
elite athletes never met several of the conditions that
trigger lipoprotein lipase (LPL, the "fattening hormone")
overproduction in real world dieters.  @Subsequent studies
have not noted impaired metabolism in the wrestlers who
"dieted" to make weight.  An incidental, but critical,
finding of one investigation, was that in the minds of these
athletes dehydration and dieting were synonymous.  Their use
of the word "diet" is in association with weight loss, not
food restriction.  Their "diets" lasted but two days, and
only a few restricted food intake during this period.
(Medicine and Science in Sports and Exercise, 1992; 1270-5)

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

Experiments show that fat cells taken from massively obese
subjects have much greater mitogenic (spontaneous cell
replication) activity than cells taken from lean subjects.
"When mature fat cells from massively obese persons give up
their fat and revert in culture to forms similar to
preadipocytes, they replicate significantly more rapidly
than analogous cells from the lean.  The reverted cells,
therefore, retain the 'memory of their roots', indicating an
inherent property of these cells." Prolonged nutrient energy
restriction would lead to reversion of mature fat cells.
This process would be increased by regular exercise.  When
the subject 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











Adiposity 101                44                     11-12-93



Obesity, 1990, 14, 187-192)

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

The data of Bjorntorp and Sjostrom (METABOLISM V20;7;703)
show a greater than 10 per cent increase in fat cell numbers
from a single diet/partial regain cycle in subjects with
many fat cells.  Alarmingly, fat cell numbers increased both
during dieting (5%) and again during regain (5%).  Subjects
with fewer fat cells (normal range) did not experience this
increase in fat cell numbers.

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

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

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

To add injury to insult, 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 adjustment is barely mentioned
and never justified in the paper.  This adjustment is
unwarranted in light of the observation that "without effort
to diet, weight changes tend to be small over long periods











Adiposity 101                45                     11-12-93



of time" (Western Journal of Medicine Oct 1990; 153;421)
Adjusting for current weight begs the question that diet
cycling increases obesity.  Applicants experiencing negative
health outcomes associated with diet cycling were excluded
from the study.  As an alternative to such exercises in
manipulation, adjusting for weight history before the
subjects' first diet would be credible.

This and other studies that "adjusted" for weight gain did
not report adverse results of 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.  (Diet evangelists have yet to suggest any
credible alternative explanations for these weight cycles.)
A careful reading of these papers will, however, reveal that
precisely these concerns were carefully considered and
resolved during the study.  Finally, this paper's author
raised this question with one of the Framingham study
investigators in July 1992.  He was confident that any cause
of weight cycling other than yo-yo dieting widespread enough
to affect the Framingham data would have been common
knowledge to the doctors of Framingham, who would have
diagnosed and treated any such conditions.

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

Nw Platelet volume is thought to be an independent risk
factor for cardiovascular disease.  Platelet volume











Adiposity 101                46                     11-12-93



significantly increased during an 8 week weight loss
programme using nutrition protocols and weekly control
visits.  (5th European Congress on Obesity 10-12 June 1992)

The heart is not spared from the catabolic effects of
undernutrition, but is subject to the same degree of weight
loss as skeletal muscle.  @Current data suggest the duration
and level of caloric restriction are the main risk factors
for fatal arrhythmic events.  A very low calorie diet
probably should not be combined with strenuous exercise, or
other situations of high sympathetic drive.  (Internation
Journal of Obesity (1992) 16, 481)

@ Obese weight cycling women develop left ventricular
hypertrophy (LVH) more than obese non cyclers.  LVH is a
major predictor of cardiovascular morbidity.  (5th European
Congress on Obesity 10-12 June 1992)


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

   + Diet induced hypercholesterolemia (American J Clin Nut
     1991;53;1404-10)

   + Diet induced depletion of Omega-3 reserves, believed to
     protect against colon cancer, heart attack, etc..
     (Phinney, Am J Clin Nut 1992;56;781-2)

   + Decrease in HDL ("good") cholesterol

   + Loss of heart tissue

   + Loss of bone mass (USDA Grand Forks Human Nutrition
     Research Center)

   + Increase in fat cell numbers (Bjorntorp and Sjostrom
     METABOLISM V20;7;703)

   + Changes in fat cell receptors

   + Another ominous outcome is that the weight that is
     regained is more likely to be in the upper body than
     the lower, and for men at least, that type of weight
     distribution has been linked to an increased risk of
     heart disease.  (University of California Berkeley
     Wellness Letter, 5;4)

Some studies on human diet cycling are tabulated below.












Adiposity 101                47                     11-12-93



              Human Studies on Weight Cycling

___________________________________________________________________________
|Study       | Subjects    Sample    Results   WC>BMI    Health Outcome    |
|____________|_____________________________________________________________|
|(Dale)      |     20 f    SKEWED    FUDGED    matched    (short term)     |
|Optifast    |     50 f   selected   FUDGED      yes        unknown        |
|Blackburn   |       57   cyclers     true       yes          n/a          |
|TRIM        |       88    SKEWED    FUDGED      yes      (short term)     |
|Jequier     |        f      -          -        yes      slow metab.      |
|Baltimore   |    846 m    volun.    FUDGED       ?      glucose intol     |
|WECO        |   2107 m     all       true      yes?          CHD          |
|Gothenburg  |     2317    random     true       n/a     CHD, diabetes     |
|Framingham  |     5127    random     true       yes          CHD          |
|Harvard     |  11703 m    alumni     true       n/a        CHD, all       |
|Blair/MRFIT |  12866 m   FEDERAL      n/a       n/a          CHD          |
|Helsinki    |    15830   Finnish     true       n/a        CHD, all       |
|____________|_____________________________________________________________|

  WC>BMI: Weight Cycling linked to increased fatness (BMI)
A sample was judged SKEWED if subjects were selectively
excluded from the cohort because they developed diabetes,
CHD, morbid BMI, or other negative health outcomes linked to
diet cycling after the commencement of diet cycling.
Results were judged FUDGED if BMI was factored out, begging
the question that diet cycling may damage health because of
the increase in obesity from diet cycling.

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

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

By 1985, the mean weight gain of the weight cyclers exceeded
that of of the other athletes and that of controls.  The
prevalence of obesity (BMI > 30) among the weight cyclers
was three times that among the other athletes and twice that
among controls.  The enhanced weight gain of the weight
cyclers could not be explained by present habits.  The
results suggest that weight loss and regain predispose to
subsequent weight gain and obesity.  (Rissanan, Kaprio,











Adiposity 101                48                     11-12-93



Sarna, Koshenvuo, Dept of Public Health, Univ of Helsinki,
5th European Congress on Obesity 10-12 June 1992)

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

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

As explained above, all the available studies that did not
report adverse effects from diet cycling have been flawed
because they removed the effect of weight gain caused by
diet cycling.  To correct this flaw, studies must match
dieters and non dieters according to their physical
characteristics and history *BEFORE* their first diet.

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

7.6.1  Artificial Sweeteners  There has been considerable
media coverage of claims that artificial sweeteners hamper
weight loss efforts.  These appear to result from an
American Cancer Society study that found a correlation
between overweight and the use of artificial sweeteners.
This correlation might better be explained by noting that
people without weight problems generally avoid artificially
sweetened products on account of cancer concerns, unfamiliar
taste.  Some complain that artifically sweetened beverages
don't give them their "sugar high".  Can you imagine a Diet
Jolt Cola?  Undoubtedly, some thin people may read labels on
artificially sweetened products suggesting such products be
used only by those desiring to reduce their caloric intake.

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











Adiposity 101                49                     11-12-93



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

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

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

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


7.7  High Fiber Diet

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

Guar Gum, an agent for adding fiber to the diet, has been
banned by the FDA.

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











Adiposity 101                50                     11-12-93



7.8  Low Fat Diets

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

@"studies suggest that it is the nature of the fatty acids
rather than the amount of fat in the diet which is
important" (Proceedings of the Nutrition Society 1992: 51,
397-408) @Beef fat, not beef itself, is associated with
elevations in cholesterol concentrations.  Lean beef can be
included in cholesterol-lowering diets provided it is free
of all visible fat.  (Journal of the American College of
Nutrition 1993 12: 1: 86-9) Stearic (beef) acid and
saturated fats with fewer than 12 carbon atoms did not raise
cholesterol.  (METABOLISM 1965;14;776-86) @ A reduction in
saturated fat, not total fat, is required to reduce serum
total cholesterol and LDL-C levels.  Provided that the total
diet is low in saturated fat, these serum lipid responses
can be acheived even when the diet is rich in fat-trimmed
lean beef.  (Journal of the American Dietic Assn 1993;93:6
644-8)

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

This interest springs from a number of observations.

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

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

   + Obese subjects often exhibit a greater carving for fat
     than lean individuals.  Fat craving is a common after
     effect of energy deprivation.  Following food
     restriction, corpulent female rats had galanin (a











Adiposity 101                51                     11-12-93



     substance that increases fat appetite) levels 40-50%
     higher than lean females or freely-fed corpulent
     females.  Since most fat people have been on numerous
     diets, fat craving may be the result of dietary
     restriction, not the initial fat inducing condition.
     (Diabetes Research 1990 15,1-7)

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

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

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

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

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

There is no epidemologic evidence indicating that total fat
intake per se, independent of total caloric intake, is
associated with increased adiposity in the population.
Obesity itself has not been found to be associated with











Adiposity 101                52                     11-12-93



dietary fat in either inter- or intra- population studies.
("Diet and Health:  Implications for reducing chronic
disease risk"; Committee on Diet and Health Food and
Nutrition Board Commission on Life Sciences, National
Research Council; National Academy Council, Washington D.C.
1989.)

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

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

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

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

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











Adiposity 101                53                     11-12-93



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

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

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

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

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

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

In a study of 171 women on a two year low fat diet, maximum
weight loss of 3.2 kg was reported at 6 months.  By year 2











Adiposity 101                54                     11-12-93



some of the weight was regained.  The standard deviation was
more than twice the average weight loss. In other words,
quite a few actually gained weight on the low fat diet, not
counting the 13 that dropped out of the program.  (Am J Clin
Nutr 1991;54:821-8.)

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

1993 saw the inventor pf the PBS infomercial, Covert Bailey
proclaim "diets don't work" as he shifted his endorsement to
a line of exercise machines.

Absent Bailey, the low fat weight loss mantra appears to
have passed to Dr. Dean Ornish, consultant to low fat meal
producer ConAgra and author of the best selling "Eat More
Weigh Less".  In his paper (The Lancet July 21 1990) Ornish
describes a mid-term resident program with a low-fat
vegetarian diet and supervised exercise up to 80% of
maximum.  Ornish's data, while incomplete, suggest that
changes in caloric intake and energy expenditure completely
account for the reported weight loss.  Apparently Ornish's
"eat more, weight less" promise applies to roughage.  Ornish
claims to have partitioned the experimental cohort into two
groups randomly, yet the initial weight difference between
the two groups was comparable to the experimental groups
weight loss.  These results indicate the uncertainties
caused by the small sample size.  After 12 months of the
ultra low fat vegetarian diet and rigorous supervised
exercise, the the active finished at about the same weight
as the control group, but their triglycerides increased and
their blood pressure reduction was less.

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











Adiposity 101                55                     11-12-93



content of the diet.  Other features of the diet such as
carbohydrate or fat content did not, in the long run, have
consequential effects on body weight."


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

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

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

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

"diets that are relatively low in fat and high in
carbohydrate accenuate the abmormalities in glucose,
insulin, VLDL, and HDL metabolism that are present in NIDDM.
Because these results were observed in a population typical
of those with NIDDM seen in most clinics, it seems
reasonable to suggest that it is time to reappraise the
clinical benefit of low-fat high-carbohydrate diets in these
patients.  This is not meant to question the aim of reducing
saturated fat and cholesterol intake in patients with NIDDM
but rather to indicate that this goal can be acheived
without drastic reductions in total fat intake and
reciprocal increases in carbohydrate consumption by simply
substituting polyunsaturated and monounsaturated fat for
saturated fat. ... We believe that the results no longer











Adiposity 101                56                     11-12-93



permit us to dismiss the deleterious metabolic effects of
low-fat high-carbohydrate diets as purely transitory events
in patients with NIDDM and [The results] require that
dietary regimens that address the defects in carbohydrate
and lipid metabolism that exist in these patients be
evaluated." (DIABETES CARE  1989;12:2 94-101)

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

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

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

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

N-3 fatty acids (FAs) are essential in early human
development.  Fish and shellfish are the main food sources
of HDA.  Women who consume fish have more DHA in their











Adiposity 101                57                     11-12-93



breast milk than do those who do not eat seafood.  Infant
forumulas contain only LNA, which may not be suitable.
"Pregnant and nursing women should be encouraged to consume
seafood on a regular basis during pregnancy and lactation to
furnish DHA for their infants." (Journal of the American
Dietic Assoc 1993;93:58-64)

7.9  Dieting Gourmets

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

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

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

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

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

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

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

7.9.1  The Lopez Diet / Eat like a Warrior  J. Ignacio Lopez
de Arriortua's pamphlet on "Feeding the Warrior Spirit"
acheived must-read status at General Motors before he left
for VW.

How to Eat Like A Warrior











Adiposity 101                58                     11-12-93



 + No sugar, potatoes, or white flour

 + Fruit must be eaten alone, not with other foods

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

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

 + Drink only good wine


7.10  Low Carbohydrate Diets

Low carbohydrate weight loss diets have been used for
centuries.  Sugar consumption is lower, low carbohydrate
diets are more popular, and the incidence of hyperobese
individuals is lower in Europe than in the U.S.3

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

Weight Loss on 1800 kcal Diets with varying CHO (grams/day)

_______________________________________________________
|Carbohydrate | Fat Loss (kg)   % LBM Loss   Tiredness |
|_____________|________________________________________|
|    104      |      8.38          24.7          1     |
|     60      |     10.2           15.9          2     |
|     30      |     14.85           4.9          3     |
|_____________|________________________________________|

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

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

@ In the presence of carbohydrate, the preferred fuel is


__________

 3. International Journal of Obesity 1992, 16,565-572












Adiposity 101                59                     11-12-93



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

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

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

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

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

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

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

Since the AMA Council on Foods and Nutrition put the Atkins











Adiposity 101                60                     11-12-93



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

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

   ``the AMA [Council on Foods and Nutrition] said they were
   "deeply concerned about any diet that advocates the
   unlimited intake of saturated fats and cholesterol-rich
   foods." Then they scrutinized all the medical literature
   they could bring to bear and came up with a single case
   described in 1929.4 "This was the study of the Arctic
   explorer, Vilhjalmur Stefansson, who, impressed with the
   health of the native Eskimos he observed, volunteered
   with an associate to be observed for a year on an all
   animal food diet.  In this study, one of the two subjects
   cholesterol levels did go up but the other's dropped.
   The AMA inaccurately reported that both men had
   cholesterol increases."

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

   I think it is clear from their circumspect language that
   the AMA was aware of the difference between the results
   when fat and cholesterol are added to a high-carbohydrate


__________

 4. See Dr. Atkins' footnote on this study.












Adiposity 101                61                     11-12-93



   diet and the results that occur when they are added to a
   low-carbohydrate lipolytic diet.  In the usual scenario,
   when carbohydrates are a large part of the diet, the
   undesirable lipid reading may get worse if there is an
   increased intake of fat as well; on the Atkins diet, such
   a result is rare indeed.'' (Chapter 15, Dr. Atkins NEW
   DIET REVOLUTION, 1992)

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

@ Low-fat high carbohydrate diets similar to those
recommended by the American Dietic Association, have serious
metabolic effects when consumed by patients with NIDDM for
15 days.  The dietary recommendations of the ADA may
actually increase the risk of coronary artery disease in
patients with NIDDM.  Hyperglycemia, hyperinsulinemia,
hypertriglycemia, and reduced plasma HDL have been
identified as factors predisposing to the risk of coronary
heart disease.  Furthermore, these same four metabolic
abnormalities have been shown to be exaggerated following
ingestion of a high-carbohydrate, low-fat diet.  (American
Journal of Medicine 1987:82 213-220)

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

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

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

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

This author has not been able to find a single study of the











Adiposity 101                62                     11-12-93



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

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

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

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

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

In the presence of dietary carbohydrate, the preferred fuel
is glucose and the capacity to mobilize fat is limited.
Factors that increase blood glucose during dieting may











Adiposity 101                63                     11-12-93



stimulate insulin release and all the metabolic sequelae of
circulating insulin.  Fatty acid synthesis is activated and
lipolysis is profoundly inhibited by insulin even at very
low concentrations of the hormone.  (Am J of Clin Nutr
1992;56:217S-23S) Several recent papers have reported low
carbohydrate diets to be better than the generally accepted
low fat diet for diabetic control.

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

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

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

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


















Adiposity 101                64                     11-12-93



7.11  Ornish and Atkins Compared

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

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

_______________________________________________________________________
|DIET RESULTS           | ORNISH (low fat) | ATKINS (low carbohydrate) |
|_______________________|__________________|___________________________|
|Age                    | 56               | 55                        |
|Starting weight        | 201              | 195                       |
|Body Mass Index        | 28.4             | 28.1                      |
|_______________________|__________________|___________________________|
|Cholesterol change     | -24%             | -13%                      |
|HDL Cholesterol (GOOD) | - 3%             | +60%                      |
|Triglycerides (BAD)    | +75%             | -82%                      |
|Weight                 | -12%             | -19%                      |
|_______________________|__________________|___________________________|

7.12  Diets - the BOTTOM LINE

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

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










Adiposity 101                65                     11-12-93



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


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

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

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

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

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











Adiposity 101                66                     11-12-93



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

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


8.  FLAWED RESEARCH

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

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

8.1  Correlation .vs. Cause and Effect

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

What is the error in drawing such a conclusion?  The error
is the unstated assumption that the correlation proves a
particular cause and effect.  In fact, other cause and
effect relationships may be involved.  Conventional wisdom
concludes: Lack of exercise causes obesity.  The other
explanation for the observed correlation is: Obesity and
associated impaired muscle development makes sports
activities unpleasant and frustrating if not impossible.

"While the link between exercise and health in some large
epidemologic studies seems powerful, intervention and
outcome studies suggest a more qualified correlation. ...
Yet "we still have no clinical trial to demonstrate that
increasing activity in a group of sedentary people reduces











Adiposity 101                67                     11-12-93



the rate of disease vs sedentary controls," says William
Haskell, PhD, also a member of the Stanford faculty." (JAMA
June 12, 1991)

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

8.2  Flawed Sample Selection/Distribution

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

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

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

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

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

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











Adiposity 101                68                     11-12-93



9.  TRUTH IN RESEARCH PAPERS

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

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

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

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

Diet evangelists dismiss or downplay the importance of
genetics and other inborn differences affecting the
development of obesity.  Large standard deviations highlight
the biological differences between fat and thin people.  If
the standard deviation is not disclosed, the researcher is
hiding something from the reader.  @"the mean net weight
gain in 1423 women as a consequence of pregnancy was found
... to be small (0.5 kg).  Nevertheless, this seemingly
modest increase concealed the fact that 15% of these women
had actually gained more than 5 kg" (IJO 16, 935)

Diet studies typically exclude dropouts from their data.
This is not valid in weight loss research because subjects
tend to drop out after frustration with poor weight loss.
Dropouts have lower weight loss and greater weight regain.
Excluding even a few such data points generates a false











Adiposity 101                69                     11-12-93



positive finding because the variability between subjects is
much greater than the average weight loss (SD >> M).  Goal
directed programs and programs that dogmatically insist
subjects will succeed if only they follow the regimen
provoke highly skewed dropouts.

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

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

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

@Few studies are available of body composition changes after
weight losses from standard dieting programs.  Weight losses
beyond the initial glycogen and water shifts have proven
difficult to achieve.  (Weight loss of 5kg (11 pounds) or
less may not involve any loss of fat!) When they do occur it
is difficult to verify the actual protocol the subjects
followed.  Subjects often report they often became `stuck'











Adiposity 101                70                     11-12-93



on traditional protocols and resorted to some more drastic
form of food restriction to achieve weight loss.  They are
often reluctant to report such behavior at the time of the
actual diet.  (Am J of Clin Nutr 1992;56:217S-23S)

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

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

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

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

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

   + Data for males and females should always be separated.

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

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

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

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

   + If there are drop-outs, the remaining number of
     subjects should be recalculated and reported along with
     the mean weight at follow-up.  Almost all drop-outs
     regain their weight loss or more, and must be
     calculated this way.

   + Weight loss studies should report the number and size
     of adipose cells before slimming, after slimming, and
     after weight regain.
(Based on recommendations by by William Bennett,  Harvard











Adiposity 101                71                     11-12-93



Medical School Health Letter)


10.  MEDIA DISTORTION

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

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

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

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

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












Adiposity 101                72                     11-12-93



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


11.  NEW TECHNOLOGY

11.1  STIMULATION OF THERMOGENESIS

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

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

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

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

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

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



__________

 5. There is some controversy about the location of
    thermogenesis in adults (BAT or muscle tissue).












Adiposity 101                73                     11-12-93



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

Caffeine consumption is controversial.  Some diet books
recommend it, some forbid it.  Early Atkins books allowed
it, the 1992 sequel does not.  Caffeine and ephedrine are
known to increase blood pressure, so caution is advised.

Smokers gain weight when they quit smoking; their final
weight averages the same as that of non smokers.  This
suggests nicotine reversibly depresses weight, 6 to 7 per
cent according to University of Wisconsin researcher Richard
Keesey.  Nicotine reduces weight by increasing metabolism,
not by reducing appetite or food intake.  A growing number
of young women have discovered this, and cigarette smoking
is gaining popularity as a weight control measure.

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

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

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

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

11.2  GROWTH HORMONE TREATMENT

(Also called somatropin, or ST.)

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












Adiposity 101                74                     11-12-93



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

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

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

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

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

A study of lipid metabolism in lean and pre-obese swine
(pigs of normal weight which will become fat) indicated low
levels of growth hormone at least until sexual maturity, and
an enhanced deposition of blood lipids as fat compared to
lean subjects. (International Journal of Obesity 1990, 14,
21-29) This enhanced deposition is significant in two ways.
First there is the direct accumulation of fat.  Secondly











Adiposity 101                75                     11-12-93



this deposition of fat "short circuits" metabolism of blood
lipids into cholesterol and steroid hormones.  This theory
helps explain why destruction of fat tissue allows animals
to grow up with more muscle mass than identical but
untreated controls.

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

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

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

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

Exogenous GH increases lean tissue and reduces body fat in
obese women in the absence of significant energy
restriction.  (Hormone Research 1991, 19-24)

Obese men manifest fewer GH secretory bursts per 24 h and
accelerated HGH disposal rates.  (Journal of Clinical
Endocrinology and Metabolism 72:1 p. 51)

@ 5 weeks HGH treatment reduced the fat mass of obese women
2 kg as it increased lean body mass 3 kg.  LPL activity was











Adiposity 101                76                     11-12-93



reduced 50 per cent.  (5th European Congress on Obesity 10-
12 June 1992)

In the future, high risk babies might be given lipid
tolerance tests, and pre-obese individuals treated with HGH
and DHEA to keep them from becoming fat.

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

Pearson and Shaw recommend stimulation of human growth
hormone (HGH) excretion with arginine amino acid supplements
as a weight loss method.  Unfortunately, the references
given in their book indicate their recommended amino acid
megadosage is still orders of magnitude too small to cause
the obese to release detectable amounts of HGH.

The obese have a high threshold which must be surpassed by
strenuous exercise (to the point of exhaustion) or
"incredible" doses of amino acids (orders of magnitude more
than even Pearson&Shaw recommend) before any stimulation of
HGH release is noted.  HGH levels achieved under these
exceptional conditions are still only a fraction of what
lean subjects spontaneously produce in their sleep.

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

Long term propranolol therapy increases body weight in heart
attack patients (2P-14); this may modify some of Pearson and
Shaw's recommendations.

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

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
















Adiposity 101                77                     11-12-93



11.3  DHEA TREATMENT

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

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

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

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

Pearson & Shaw claim the "DHEA" sold by health food stores
is bogus.  The author of "The Vitamin Bible" reports
successful personal weight loss with DHEA but gives no
sources or details.

11.4  RU-486 TREATMENT

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

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

A paper in the 1992 International Journal of Obesity reports











Adiposity 101                78                     11-12-93



that Norepinephrine (the neural transmitter, not the asthma
drug) inhibits rat pre-adipocyte proliferation.




























































Adiposity 101                79                     11-12-93



11.5  CoPP TREATMENT

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

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Typical CoPP treated (left) and untreated (right) Zucker
fatty rats.  Look at this from a distance to get the best
effect.  (B/W Xerographic photocopy of original color plate
was scanned, converted to GIF format by XView, converted to
ASCII with ASCGIF.)

11.6  BROMOCRIPTINE TREATMENT

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
















Adiposity 101                80                     11-12-93



11.7  CIRCADIAN LIPOSTAT MANIPULATION

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

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

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

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

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

In the second study reported in Experientia 48 (March 1992
p. 248-), 15 diabetic subjects were given timed
bromocriptine treatment.  As with the non-diabetic subjects,
all 15 diabetic subjects lost fat.6 Blood glucose dropped


__________

 6. That *all* subjects lost fat is significant.  In energy
    deprivation diet studies, some subjects invariably fail
    to lose weight.  In long term diet followup, the
    standard deviation is two or three times as great as the
    average weight loss because a large minority gain
    weight, sometimes a great amount.  Without individual











Adiposity 101                81                     11-12-93



significantly.  Oral hypoglycemic medication was was
discontinued in 3 participants, and glucose levels remained
near normal for at least two months after treatment.  Doses
of hypoglycemic drugs and insulin were reduced in three
other subjects during treatment.

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

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

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

11.8  TESTOSTERONE TREATMENT

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

An 8 month study at the Sahigren's Hospital in Goteborg,
Sweden tested 23 men aged 40-65 years in a fully controlled,
double blind experiment in restoring testosterone levels to
normal.  The testosterone treated group improved in waist
size, blood pressure, plasma lipids, fasting glucose, and
insulin sensitivity.  The treated group reported
improvements of well-being and energy.  Normalization of


____________________________________________________________

    data or the standard deviation, one simply cannot judge
    the true effectiveness of the experimental intervention.
    Many diet studies suppress this information as it would
    cause the reader to discount the validity of the claimed
    results.












Adiposity 101                82                     11-12-93



testosterone levels reduced many of the health warning signs
associated with obesity.  No adverse functional side-effects
were found.  (International Journal of Obesity 1992 16:991-
7)

11.9  BETA3-ADRENOCEPTOR AGONISTS

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

11.10  SEROTONIN REUPTAKE INHIBITORS

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

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

To provide longer-term data, Weintraub et al developed a 4
year multimodal program using state-of-the-art behavior
modification, caloric restriction, and exercise as the
"placebo" for the entire duration of the four year study.
Subjects attended nearly 100 visitations with health
professionals during the study.  When reading reports on The
National Heart, Lung, and Blood Institute funded Multimodal
Intervention Study, please keep in mind that this "state-
of-the-art" treatment was the "placebo".  (State of the
diet/exercise/shrink art, that is!) "From the end of the
second double-blind phase at week 190 through week 210, we
monitored study participants to see what happened without











Adiposity 101                83                     11-12-93



medication but with continuing behavior modification,
caloric restriction, and exercise therapy. ... One measure
of the excellence of the ancillary [placebo] therapy in this
study was that it enabled participants treated with placebo
to lose just 0.01 kg/week less than participants receiving
active therapy in the 18 studies that lasted at least 8
weeks reviewed by Scoville for the FDA."

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

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

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

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

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

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

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

   + Patients were on moderate diets, up to 1800
     calories/day for men, 1200 for women.  Most of the
     patients were veterans of a half dozen or more diet
     attempts.  With this amount of metabolic slowdown, the
     traditional (diet/exercise/behavior mod) part of the











Adiposity 101                84                     11-12-93



     program may not have been able to induce much long-term
     weight loss without benefit of the drugs' lowering of
     set point.

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

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

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

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

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

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


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

In France and England, fenfluramine has been used in the
treatment of human obesity for 25 years.  No unequivocal
report of major health hazards has appeared with
fenfluramine in spite of extensive worldwide prescription
for decades.  Dexfenfluramine is the dextro stereoisomer of











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fenfluramine, and is a more potent antiobesity agent with
fewer side effects.  Tiredness and drowsiness were the most
commonly reported unwanted side effects of treatment, but
occurred as frequently with placebo treatment as with
dexfenfluramine." (Clinical Neuropharmacology Vol 11 Suppl 1
S179)

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


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

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

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

Is fenfluramine's anorectic effect essential to its
antiobesity properties?  When body weight was reduced in
rats prior to treatment with fenfluramine, administration of











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the drug was followed by a rapid increase in food intake
with maintenance of the reduced weight.  The reduced body
weight in fenfluramine-treated rats is defended; when
animals are force fed to a higher weight and then allowed to
eat ad libitum their food intake drops and body weight
drops.  (Recent Advances in Obesity Research: V 290)

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

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

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

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

Free reprints of this 65 page supplement are available.

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

Another study is underway at the Veterans Administration
Medical Center in Hampton, Va.  "This is comparable or
superior to any medical treatment of obesity," said the
study's author, Dr. Richard L. Atkinson.  Atkinson and his
colleagues gave the two drugs to 506 women and 57 men, most
of whom have been followed for at least six months, and some
for more than a year.  Blood pressure in 49 subjects with
high blood pressure dropped to normal.  Twenty-four patients
with high cholesterol saw those levels fall to normal,











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Atkinson said. And blood sugar -- an indication of diabetes
-- also dropped to normal.  "That's dramatic stuff." "We're
fixing high blood pressure, high sugar and high fats by
treating the underlying disease -- obesity," Atkinson said.
The study underscores the growing belief among obesity
researchers that diet, exercise and behavior change are not
enough in most cases to produce long-term weight loss in
overweight people.  "We need to look for additional
treatments," Atkinson said.

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

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

11.11  FAT CELL REMOVAL

11.12  Surgery

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

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

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

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

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

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











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(Acta Med Scand, Suppl. 723: 225-31)

Diabetic patients receiving abdominal liposuction have
reduced insulin requirements (dose reduced from 20 to 10
units).  (Unpublished data) @ By 1995 obese Type II
diabetics will be treated with liposuction.  This procedure
is intended to lower the need for insulin by reducing the
total number of fat cells in the diabetic's body.
(Longevity Jan 1993; Fred Glazer M.D.)

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

11.13  Immunological Manipulation

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

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

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

In a 1991 telephone conversation this author was told
Hannah's research is proceeding very well toward its goal of
producing leaner animal meat.  Human application in the near
future was thought unlikely due to risk of malpractice
lawsuits.

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


12.  PREDICTIONS

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











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formula and sugary baby foods in this century will also be a
factor.

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


13.  RECOMMENDATIONS FOR ACTION

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

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

   + In the meantime, the protections of the Americans with
     Disabilities Act should be extended to fat Americans
     whose diligence in dieting has made them even heavier.

   + Diagnostic procedures are needed to identify the 5 per
     cent of overweight subjects for whom weight loss diets
     provide long term benefits.

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

   + Effective interventions to correct human obesity must
     be developed and deployed.  Significant candidates
     include immunization to fat cell plasma, CoPP, RU-486,
     correction of low EGF, testosterone, DHEA and Growth
     Hormone levels.  One hundred million American
     endomoprphs deserve more than a few dimes' worth of
     legitimate obesity research.













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

   + Doctors should ascertain patients' fat cell numbers and
     sizes before prescribing traditional weight loss
     regimens, which cannot permanently suppress the size of
     adipose cells much below normal.

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

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

   + Mothers should limit carbohydrate and sugar consumption
     during pregnancy and lactation.

   + Mothers should breast feed the full recommended time.

   + Infants should not be fed a high carbohydrate diet.

"We recognize that the message we have for endocrinologists
and metabolic specialists is a somber one, difficult to the
sufferer from obesity.  On the other hand, it seems to us
most consonant with the true state of affairs.  Our
understanding of genetic mechanisms is progressing rapidly
and the interaction between genetic endowment and early
environment will be under intensive study in the next
decade.  This is the hopeful side of the problem." (CLINICAL
REVIEW 28: A Biological Basis for Human Obesity, Journal of
Clinical Endocrinology and Metabolism, 1991.)


14.  REQUIRED READING

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

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

LONG TERM WEIGHT CONTROL:
The National Heart, Lung, and Blood Institute funded
multimodal intervention study, Clin Pharmacol Ther, May 1992











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Reprints of the entire supplement are available at no
charge.  Direct requests to:
Michael Weintraub MD
Department of Community and Preventive Medicine
University of Rochester School of Medicine
PO Box 644
Rochester NY 14642

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


OBESITY AND LEANNESS, Basic Aspects, ISBN 0 86196 0173

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

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

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

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


15.  RECOMMENDED READING

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

References to the 5th European Congress on Obesity are
abstracted in the International Journal of Obesity v.17
Supplement 2.

"Recent Advances in Obesity Research: V" ISBN 0-86196-072-6

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











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

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

International Journal of Obesity (Periodical)

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

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

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

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

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

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

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

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

































                          CONTENTS


 1.  FOREWORD...........................................   1

 2.  ROSETTA STONE......................................   1

 3.  ENERGY BASICS......................................   4

 4.  THE BIOLOGY OF ADIPOSITY...........................   5
     4.1    SET POINT...................................   5
     4.2    Rats, Pigs and Blimps.......................   7
     4.3    Brown Adipose Tissue (BAT)..................   9
     4.4    White Adipose Tissue (WAT)..................   9
     4.5    Preadipocytes > Fat Cells...................   9
     4.6    Fat Cell Receptors..........................  10
     4.7    Fat and Carbohydrate Oxidation..............  11
     4.8    Muscle Fibre Type...........................  11

 5.  FORTUNE OF BIRTH...................................  12
     5.1    Types of Adiposity..........................  12
     5.2    GENETICS....................................  12
     5.3    SYNDROME X..................................  15
     5.4    Maternal Environment........................  18
     5.5    Baby's Diet.................................  20

 6.  EFFECTS OF OBESITY.................................  21
     6.1    Personality Problems........................  21
     6.2    Health Problems.............................  22

 7.  TRADITIONAL TREATMENT..............................  24
     7.1    EXERCISE....................................  25
     7.2    DIETS.......................................  30
     7.3    SLOW vs RAPID Weight Loss...................  34
     7.4    BEHAVIOR MODIFICATION.......................  34
     7.5    Diet Side Effects...........................  34
     7.6    Diet Cycling................................  41
     7.7    High Fiber Diet.............................  49
     7.8    Low Fat Diets...............................  50
     7.9    Dieting Gourmets............................  57
     7.10   Low Carbohydrate Diets......................  58
     7.11   Ornish and Atkins Compared..................  64
     7.12   Diets - the BOTTOM LINE.....................  64

 8.  FLAWED RESEARCH....................................  66
     8.1    Correlation .vs. Cause and Effect...........  66
     8.2    Flawed Sample Selection/Distribution........  67

 9.  TRUTH IN RESEARCH PAPERS...........................  68

10.  MEDIA DISTORTION...................................  71



                           - i -











11.  NEW TECHNOLOGY.....................................  72
     11.1   STIMULATION OF THERMOGENESIS................  72
     11.2   GROWTH HORMONE TREATMENT....................  73
     11.3   DHEA TREATMENT..............................  77
     11.4   RU-486 TREATMENT............................  77
     11.5   CoPP TREATMENT..............................  79
     11.6   BROMOCRIPTINE TREATMENT.....................  79
     11.7   CIRCADIAN LIPOSTAT MANIPULATION.............  80
     11.8   TESTOSTERONE TREATMENT......................  81
     11.9   BETA3-ADRENOCEPTOR AGONISTS.................  82
     11.10  SEROTONIN REUPTAKE INHIBITORS...............  82
     11.11  FAT CELL REMOVAL............................  87
     11.12  Surgery.....................................  87
     11.13  Immunological Manipulation..................  88

12.  PREDICTIONS........................................  88

13.  RECOMMENDATIONS FOR ACTION.........................  89

14.  REQUIRED READING...................................  90

15.  RECOMMENDED READING................................  91
































                           - ii -









                       Adiposity 101


                       Chuck Forsberg

                      Portland Oregon


                          ABSTRACT



Obesity ruins the quality of life for millions of Americans.
Genetics, gestation and suckling environments produce
individuals with profoundly different amounts of muscle and
fat.

Traditional weight control technology has changed little
since Greek antiquity.  30 years of applied research into
traditional weight control technology and more than $100
billion of public expenditure have helped very few fat
Americans.

We now know that more have been hurt than helped.  Not a
single study has ever shown weight loss to extend life, and
more than twenty have reported ill effects from weight loss.
Recent research has shown that dieting is a major cause of
obesity.  Dieters have for years complained that weight loss
regimes made them fatter, but these observations fell on
deaf ears.  Now malpractice lawyers have begun to speak more
loudly.

Recent obesity research has disproven public stereotypes and
the conventional wisdom of most health professionals.  For
the first time in history, research has placed a cure for
human obesity within sight.  Before this can happen, the
public must 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 reducating the
public.

For each overweight American, less than one dollar is spent
for legitimate obesity research, compared to a thousand
dollars spent 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.
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