Adiposity 101 (Part 1 of 2) 
Author Message
 Adiposity 101 (Part 1 of 2)

                              Adiposity 101

                              Chuck Forsberg

                             Portland Oregon

       1.  FOREWORD

       Some themes have begun to emerge from papers published over
       the years.  The quality of research varies widely, with
       weight loss industry reports often ignoring relevant
       information published years ago.

       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 barely a summary of recent progress in obesity
       research.  While it identifies topics and issues concerning
       obesity, the reader should throughly study the trail of
       references given below if questions or doubts remain.

       I hope this summary will provide useful information on
       obesity.

       2.  BACKGROUND

       2.1  Rats, Pigs and Blimps

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

       The Zucker fa/fa rat is the John Goodman of rats.  Zucker
       rats attain the obese state with normal diet and exercise.
       This research rat strain has been bred to mimic the
       metabolism of fat humans.  Obesity in humans and Zucker rats
       is thought to result from the combination of two recessive
       genes (fa/fa).

       BHE/cdb rats, while not genetically obese, have hepatic
       lipogenic (liver fat deposition) capacity greater than that
       of Sprague-Dawley or Wistar rats, and resemble humans more
       closely.

       The choice of rat strain is important to obesity
       experiments.  Results obtained with fa/fa rats are relevant
       to obese humans.  Results obtained with Wistar or Sprague-
       Dawley rats are more relevant to humans whose genetic makeup
       protects them from overweight.

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       2.2  Rosetta Stone

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

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

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

       Set Point Theory: A biological servo system controls energy
       expenditures, hormones, fat cell receptors, appetite, and/or
       other metabolic parameters to return the body to a constant
       weight (set point) after periods of underfeeding or
       overfeeding.

       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.  BMI is a somewhat height and
       bone-density independent measure of adiposity (fatness).

       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).

       3.  TYPES OF ADIPOSITY

       One source of obesity is overeating from emotional stress.

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

       Lean individuals' self-recovery from overeating is exploited
       in ads from Jennie Craig and other diet providers that claim
       long term weight loss.

       In a 1986 Dutch study, men who experienced many life events
       in a short period showed a gain in body mass.  A year later

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       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.

       Science has discovered that most fat people do not get fat
       because they eat wrong or exercise too little.  They get fat
       because their bodies' fat cells take too much of their cooking.net">food
       energy, starving their lean tissues and lowering their
       metabolisms.

       It is now recognized that obese trauma patients require
       special dietary intervention because their bodies cannot use
       the energy stored in fat for healing the way thin people do.
       (Journal of Clinical Investigations, Jan 1991)

       4.  THE BIOLOGY OF ADIPOSITY

       4.1  Brown Adipose Tissue (BAT)

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

       4.2  White Adipose Tissue (WAT)

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

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

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

       4.3  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).

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

       The future adiposity of suckling pigs can be predicted by
       measuring the ability of the suckling's {*filter*} to
       differentiate preadipocytes into full size fat cells in a
       test tube.  The preobese sucklings had low levels of fetal
       growth hormone and high levels of triiodothyronine.

       Epidermal Growth Factor (EGF) dramatically inhibits
       differentiation of preadipocytes into fat cells.  Obese mice
       have EGF levels as much as 80% less than their lean
       littermates.

       Preadipocytes isolated from different fat deposits 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.

       4.3.1  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.

       As reported in a 1983 Nova program, fat cells can expand no
       more than twice normal size.  Obese subjects have up to ten
       times as many fat cells as normal.

       A study published in the Proceedings of the 5th
       International Congress on Obesity showed that obese subjects
       who had lost weight in a combined diet/exercise program had
       fat cells 25 per cent smaller than those of marathon runners
       who had half the total body fat.  In other words, the
       exercise/dieters had twice as many fat cells as the
       athletes.

       4.4  Fat Cell Receptors

       Fat cells gain and lose weight by passing lipids through
       receptors.  One type of receptor removes lipids from the
       {*filter*} stream and another type allows the body to access the
       energy stored in the fat cells with a resulting loss of
       weight.

       Geographic distribution of fat, including "love handles"
       that do not respond to extreme dieting, is believed to
       result from local variations in these receptors.

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

       4.5  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

       4.6  Muscle Fibre Type

       The April 19 1990 Lancet reports that skeletal muscle fibre
       type is directly correlated with BMI.  Lean subjects have
       more "slow fibers" well endowed with mitochondria that use
       fatty acids as energy source.  Corpulent subjects have fewer
       "slow fibers" but more "fast fibers" that only burn glucose;
       they cannot burn fat for energy. (See EXERCISE, below.) The
       proportion of fiber 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)

       5.  THE ROLE OF GENETICS

       The conclusion of current research is that individual
       differences in Body Mass Index (BMI) are mostly the result
       of genetic factors.  Obesity is now thought to be the result
       of a pairing of normally recessive genes (fa/fa).

       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, {*filter*}ism, .57,
       Cirrhosis, .53, Epilepsy, 0.50.

       Most obese individuals repeatedly undertake diets trying to
       control their weight.  This cyclic weight variation

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       depresses measured heritability figures by injecting a
       spurious variability that does not indicate a real
       difference in obesity.

       The plots of parent/offspring weights in the above study
       bears close inspection.  The plot of biological parents and
       adoptees shows the (by now) well known nearly straight line
       relationship.  The plot of adoptive parent weight and
       adoptee weight shows a negative trend for females, and no
       trend for males.  So much for fat mothers passing bad habits
       to children.

       A study of lean and overweight male Army personnel was
       designed to prove that the overweight valued good health
       less than normalweights, and practiced less healthy
       lifestyles.  To the researchers' surprise, there were no
       significant differences between overweight and normalweights
       on these attitudes.

       In "The response    to long-term overfeeding in identical
       twins", 12 pairs    of identical male twins were overfed and
       kept sedentary under close supervision.  There was a 3 to 1
       ratio in weight gain between the easiest gainer and the
       slowest gainer.  Those who gained the most fat gained less
       muscle than those who gained the least fat.  Ten of the 12
       pairs of identical twins gained almost identical amounts of
       weight.

       The overfeeding study is interesting because of its sample
       selection.  None of the subjects had any history of obesity
       whatsoever, not even in their families. One can but imagine
       what that 3 to 1 difference in weight gain and 16 to 1
       difference of lean/fat gain would have been if overweight
       subjects had been included.

       The appearance of these papers in the May 24 1990 New
       England Journal of Medicine prompted several submissions
       questioning the papers' findings.  These letters and the
       authors' rebuttals were printed in the Oct 11 1990 edition.

       The Sep 1990 Science News reported a very wide difference in
       the amounts and types of tissues added in response to
       overfeeding.  In this study, thin people actually added more
       weight than fat people did, but the thin people added weight
       mainly as lean tissue instead of fat.  Data from "lean
       hungry" types that gained little    weight were excluded!

       The obese (and pre-obese) differ from lean persons in other
       ways.  Their muscle cells do not burn fat well.  DHEA and
       growth hormone levels are low.  Their fat cells
       spontaneously multiply when those of lean persons do not.

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       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, they are a distinct race.

       5.1  The Role of Maternal Environment

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

       As reported in the Health InfoCom Network News Volume  3,
       Number 36 December  5, 1990, Dr. Bernard Silverman of
       Children's Memorial  Hospital in  Chicago says a study of
       124 children whose mothers were either diabetic before
       pregnancy or became diabetic during it showed:  Children at
       normal weight at age 1.  Many were obese by 6 to 8.  At 8,
       the median weight was 71 pounds for boys;  normal median -
       56 pounds. Median for girls was 68 pounds; normal medium 55
       pounds.  Some researchers say the pre{*filter*}s' obesity may be
       due to excess insulin in the amniotic fluid surrounding them
       during gestation.  A study in the December 1990 Archives of
       Disease in Childhood reported that infants whose amniotic
       fluid was highest in insulin were markedly obese by 6 years
       of age.

       Mothers who experienced caloric deprivation in a critical
       portion of pregnancy during the 1944 Netherlands
       Hungriwinter bore sons 2-3 per cent of which were obese at
       age 19.  That is more than twice the normal 1-2 per cent
       incidence of obesity.

       5.2  The Role of Baby's Diet

       A Case Western Reserve University rat study (4P-17) compared
       rat pups fed a milk-substitute formula (56% of calories from
       carbohydrates) with mother-fed controls (who received 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 {*filter*}hood, leading to the
       development of obesity."

       This result supports the assertion of a Reader's Digest
       article that {*filter*} feeding can "Fat Proof" one's baby.
       Left unanswered is the question: at what age should the
       suckling's low carbohydrate diet evolve to the high
       carbohydrate low fat diet currently favored by diet

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       faddists?  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.)

       {*filter*} milk contains human Epidermal Growth Factor (EGF)
       (discussed above), a potent inhibitor of obesity not present
       in infant formula and cow's milk.

       Children also need sufficient dietary fat to insulate their
       nerve cells, prevent nerve crosstalk and brain damage.

       6.  EFFECTS OF OBESITY

       6.1  Personality Problems

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

       6.2  Health Problems

       The correlation between obesity and certain health problems
       has been widely documented.  Controversy remains about the
       true cause and effect suggested by this correlation.

       Some of the correlation between obesity and health problems
       may be caused by common factors.  For instance, DHEA and HGH
       help the healing process, help the immune system, block
       autoimmune disease, hyperglycemia, and neoplasia, promote
       muscle buildup and fat loss.  The obese have much lower
       levels (order of magnitude) of Human Growth Hormone (HGH)
       and DHEA than normal weight subjects.  Men with abdominal
       obesity have low testosterone values.  Mice obesity
       genotypes are thought to promote various diseases.  If both
       the obesity and poorer health result from common factors,
       only correction of the common factors will improve the
       patient's health outlook.

       An Aug 5 1990 BBC broadcast reported that the size of a baby
       relative to the size of the placenta had a greater
       correlation on {*filter*} {*filter*} pressure than the combined
       effects of weight or {*filter*} consumption.

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       Some of the health problems associated with obesity result
       not from the obesity itself but from general effects of
       dieting.1 As reported in the recent House hearings on the
       diet industry, some studies show an increase in mortality
       with weight loss.

       Some obesity related health problems are the result of
       discrimination against obese patients by the medical
       establishment.  Insurance companies discriminate against
       obese individuals, even those with no history of health
       problems.  Insurance companies are forbidden to test
       applicants for HIV antibodies, a right of privacy not
       afforded to overweight applicants who are compelled to
       measure 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.  I have also
       heard reports of marginally overweight women humiliated by
       male doctors.  Similar abuse was reported in a 1983 Nova
       program.  It is incumbent of the AMA and regulatory bodies
       to monitor this abuse and institute corrective measures.

       7.  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 sloppy it would never
       be accepted by the FDA as proof of an ethical drug's
       efficacy.

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

       7.1  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 accepted 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.

       __________

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

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       What is the error in drawing such a conclusion?  The error
       is the unstated assumption that the correlation proves a
       particular cause and effect.  In fact, there are other
       possible cause and effect relationships at play.
       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.

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

       7.2  Flawed Sample Selection/Distribution

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

       One cannot use people as their own controls.  One cannot
       allow subjects to select which experimental group they will
       join.  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, or by dieting?

       Weight loss program studies typically exclude dropouts from
       their data.

       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.

       8.  TRUTH IN RESEARCH PAPERS

       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.

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

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            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.
       (Based on recommendations by by William Bennett,  Harvard
       Medical School Health Letter)

       9.  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.

       As Professor Garner's 1990 testimony before the House of
       Representatives indicated, false advertising is rampant in
       the diet industry.  While an individual deceptive diet ad
       may not be too misleading to the public at large, the
       collective effect of such deception (Nazi Big Lie effect)
       creates great damage.

       10.  TREATING OBESITY

       Obesity prevalence estimates are virtually unchanged from
       the early 1960s, according to the Centers for Disease
       Control.

       As reported in the recent House hearings, there is no
       effective long term treatment for obesity.

                              Adiposity 101

                                  - 12 -

       "... even though    we like to believe that weight loss in the
       obese is accompanied by a reduction in the mortality rate,
       it is important to keep in mind that no intervention study
       has yet dealt with this issue." (Letter to JAMA from
       Bouchard, Despres, and Tremblay)

                              Adiposity 101

--
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



Tue, 02 Aug 1994 23:05:32 GMT
 
 [ 1 post ] 

 Relevant Pages 

1. Adiposity 101 (Part 2 of 2)

2. Adiposity 101 (Part 2 of 2)

3. New Adiposity 101

4. Adiposity 101

5. Obesity research dollars (was Adiposity 101)

6. Need Adiposity 101 article

7. Correction to Adiposity 101

8. Adiposity 101 4/4

9. Updated Adiposity 101 (long)

10. Adiposity 101

11. New Adiposity 101 1/2

12. Andiposity 101


 
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