New Adiposity 101 1/2 
Author Message
 New Adiposity 101 1/2

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

                       Adiposity 101

                       Chuck Forsberg

                      Portland Oregon


Obesity ruins the quality of life for millions of Americans.

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

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

This paper is a summary of recent progress in obesity
research.  It identifies topics and issues concerning
obesity. The reader should study the references given below
if questions or doubts remain.

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


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

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

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

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

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

                       Adiposity 101

                           - 2 -

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

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

Hyperphagia: overeating

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

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

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

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

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

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

DHEA is a hormone that reduces fat and cholesterol.

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

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                           - 3 -

body protein is sacrificed to make it.

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

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



One cannot appreciate current obesity research without some
essential knowledge of human energy metabolism and how it is
regulated.  The body gets its energy from dietary protein,
carbohydrate and fat.  The body stores energy as glycerol,
lean tissue and fat.  Muscle tissues burn carbohydrate and
fat for energy.  When energy expenditure exceeds dietary
input, stored glycogen, fat stored in adipose cells, and
lean tissue are {*filter*}ized to make good the energy
shortfall.  The partitioning of available energy sources
between energy output (work), muscle and fat storage vary
greatly between individuals. These differences are primarily
genetic in origin, but are also caused by abnormalities
during gestation.

Animals regulate their body fat stores within fairly narrow
limits.  This regulation is automatic, not requiring
conscious intervention.  Changes in energy balance are
compensated for by changes in appetite and metabolism.  A
bout of flu reduces energy intake at the same time the
body's fever increases energy expenditure; the lost weight
is regained afterwards.  Likewise a large Thanksgiving meal
raises metabolism (that's why one feels warmer) and
depresses appetite for a while.  The usual body weight that
a person maintains automatically is called the SET POINT

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.

                       Adiposity 101

                           - 4 -

For many obese individuals, their set point is the stable
weight to which they repeatedly return to after dieting.
Set point theory explains why the calorie loss of moderate
exercise provokes an increase in appetite and/or slowing of
metabolism, limiting weight loss.

Research subjects reduced intake of other foods after
required eating of">food containing 22%-52% of their baseline
energy intake.  Subjects compensated for the covert caloric
dilution of one third of the available items by increasing
intake of non diluted items.  Healthy male subjects who have
no history of dieting or weight concerns have a strong
caloric compensation. (American Journal of Clinical
Nutrition 1992;55;331-42)

The LPL study mentioned below supports the much-debated "set
point" theory, which holds that inner mechanisms set a
person's weight at a predetermined level and if anything is
done to change the weight, the body will adjust to restore
fat content to the set point.

"I regard body temperature, which stays around 98.6 degrees
F, to be a set point. Weight doesn't have a set point in
that sense," says Xavier Pi-Sunyer, M.D., director of the
Obesity Research Center at St.  Luke's-Roosevelt Hospital
Center in New York.  If there is a set point for weight, it
generally seems to move in one direction--that is, the body
will not make adjustments to counteract a large weight gain
but will fight efforts to lose the weight. "When a person
gains weight and stays at that weight a while, the body will
defend that weight.  It becomes the new 'set point',"
explains Pi-Sunyer.

Aside from the action of LPL, the body uses other adaptive
mechanisms when">food intake is reduced. To cite just two of
them: Dieting depresses the metabolic rate so that calories
are burned more slowly, and as fat cells shrink, they become
more responsive to the action of insulin and do not release
their contents as readily.  (FDA CONSUMER)

The set point theory of body weight regulation is based on a
large body of empiric evidence.  (Weigle DS; Human obesity -
Exploding the myths.  Western Journal of Medicine 1990 Oct;

3.2  Rats, Pigs and Blimps

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

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

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                           - 5 -

diets.  Some strains have been bred to mimic the metabolism
of obese humans.  The most common are the obese ob/ob mouse
and the fatty fa/fa Zucker rat.  These strains become obese
even when restricted by pair-feeding to the caloric intake
of lean littermates.

The ob/ob mouse fails to survive in the cold because it
cannot generate sufficient heat by burning fat.

Obesity in Zucker fa/fa rats is thought to result from the
combination of two recessive genes (fa/fa).  Zucker rats can
survive in the cold, yet they attain the obese state with
normal diet and exercise.  "The obesity of the Zucker rat
... is inherited as an autosomal recessive mutation.  It is
thought to be the initiated by a single gene defect (fa) the
nature of which remains totally unknown.  These rats develop
a syndrome that closely resembles human obesity.
Hyperphagia, ...

read more »

Mon, 30 Jan 1995 15:32:49 GMT
 New Adiposity 101 1/2

Fri, 19 Jun 1992 00:00:00 GMT
 New Adiposity 101 1/2

                           - 29 -

loss as skeletal muscle.  (Internation Journal of Obesity
(1992) 16, 481)

Some studies on human diet cycling are tabulated below.
              Human Studies on Weight Cycling

|Study      | Subjects   Sample     Results   WC>BMI    Health Outcome    |
|(Dale)     | 20 f       SKEWED     FUDGED    matched   (short term)      |
|Wadden     | 50 f       selected   FUDGED    yes       unknown           |
|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     |

  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.

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 {*filter*}s.

As explained above, studies that do not report adverse
effects from diet cycling are flawed because they filter out
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 *BEFORE*
their first diet.

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

                       Adiposity 101

                           - 30 -

6.5.1  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, inferior
taste, and the lack of "sugar high". 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.

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

A Harvard Medical School study indicated Aspartame
facilitated long term weight maintenance in a
multidisciplinary weight loss program.

6.6  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.

6.7  Low Fat Diets

Concerns about cholesterol levels have focused attention on
low fat diets.  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.

   + 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

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                           - 31 -

     the high fat rat diets seen in the literature involve a
     profound increase in total energy intake, contrary to
     most obese humans who have depressed energy intake.

     Replacing mothers 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.  Since fat craving is a common
     after effect of energy deprivation, and most fat people
     have been on numerous diets, fat craving may be the
     result of dietary restriction, not the initial fat
     inducing condition.  Studies show fat children obtain a
     slightly greater proportion of their energy input from
     fat than thin children do.  This slight increase is
     decisively 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".

Low fat diets come in two types, semistarvation and ad
libitum.  Most 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 Atkins Diet is also a low fat diet because many
(not all) people do not like fatty foods that are not also
high in carbohyrdrates.

A Rockefeller University study appearing in the American
Journal of Clinical Nutrition (1992;55;350-5) found no
significant variation in energy need as a function of
percentage of fat intake (0 to 70%), confirming a 1930
study.  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.

                       Adiposity 101

                           - 32 -

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

"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 hig-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 differenced 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 than because of
any mysterious effect on intermediary metabolism"
(Discussion, Nutrition Reviews, Vol. 50, No. 4)

6.7.1  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 the">food the same as
normalweights do).  Neither did the researches wish to risk

read more »

Mon, 30 Jan 1995 15:34:53 GMT
 New Adiposity 101 1/2

Fri, 19 Jun 1992 00:00:00 GMT
 New Adiposity 101 1/2
Chuck, do you suppose you could post a file that has the new
stuff in it or in some other way highlight the new stuff?
I've read the thing several times now and I do want to see
what you've added, but hate to read the old stuff again.
I suppose I could try to use diff on it, but maybe you
have a better idea.

Gordon Banks  N3JXP      | "Skepticism is the chastity of the intellect, and


Wed, 01 Feb 1995 01:02:35 GMT
 New Adiposity 101 1/2

Fri, 19 Jun 1992 00:00:00 GMT
 New Adiposity 101 1/2

> Chuck, do you suppose you could post a file that has the new
> stuff in it or in some other way highlight the new stuff?

I would like that also.  Chuck digs up some interesting


Wed, 01 Feb 1995 03:35:13 GMT
 New Adiposity 101 1/2

Fri, 19 Jun 1992 00:00:00 GMT
 New Adiposity 101 1/2

>Chuck, do you suppose you could post a file that has the new
>stuff in it or in some other way highlight the new stuff?
>I've read the thing several times now and I do want to see
>what you've added, but hate to read the old stuff again.
>I suppose I could try to use diff on it, but maybe you
>have a better idea.

Aside from that, AD101 has changed so much I gave up on change
markings shortly after the previous posting.  Organizing it has
been a bear - should the Weintraub study be discussed under
traditional technology because it decisively shows the failure
thereof, or under new technology because of the data on the
drug treatment?

The subchapter on Nutrasweet hasn't changed.

The part on Atkins is about the same as the draft I posted - I
still haven't found any reports of independent clinical trials
of the Atkins diet.  The attitude of one researcher I talked to
was that testing Atkins isn't worth risking one's carrer butting
heads with the AMA.  I added Atkins to Adiposity 101 because it
seems to be the only major diet type that hasn't been thoroughly

As you read the (mostly new) information on obesity/diabetes
aftereffects of gestational undernutrition, think about the
connection between low birthweight babies and smoking.

Chuck Forsberg WA7KGX          ...!tektronix!reed!omen!caf
Author of YMODEM, ZMODEM, Professional-YAM, ZCOMM, and DSZ
  Omen Technology Inc    "The High Reliability Software"
17505-V NW Sauvie IS RD   Portland OR 97231   503-621-3406

Fri, 03 Feb 1995 11:06:23 GMT
 [ 9 post ] 

 Relevant Pages 

1. New Adiposity 101

2. Adiposity 101

3. Obesity research dollars (was Adiposity 101)

4. Need Adiposity 101 article

5. Correction to Adiposity 101

6. Adiposity 101 4/4

7. Updated Adiposity 101 (long)

8. Adiposity 101 (Part 1 of 2)

9. Adiposity 101

10. Adiposity 101 (Part 2 of 2)

11. Adiposity 101 (Part 2 of 2)

12. *Job Posting* Sr Biostatistician, New Jersey, ERG#101

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