Adiposty 101 
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 Adiposty 101

                                  - 1 -

       1.  FOREWORD

       This is a summary of adiposty information I've gleaned from
       forays to the Med School library and other sources.  I hope
       it provides you with some useful information on obesity
       research.  Some of you may be able to fill in some of the
       gaps mentioned here.

       2.  BACKGROUND

       Set Point Theory: the body adjusts appetite, energy
       expenditures, and other characteristics to restore a
       constant weight, somewhat resistant to either dieting or

       In vitro: in a test tube (more or less).  In vivo: in the

       Rats and pigs are commonly used in adiposty research because
       their fat mechanisms resemble those of humans.

       Body Mass Index (BMI) is a measure of the percentage of fat
       to total body mass used as a height and bone-density
       independent measure of adiposty.

       3.  SOURCES

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

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

       International Journal of Obesity


       4.1  Transient Adiposty

       One source of obesity is overeating from emotional stress.
       Experiments with controlled overfeeding of lean subjects
       demonstrate an increase in body metabolism that restores
       normal weight when overfeeding ceases.

       In a 1986 Dutch study, some men who experienced many life
       events in a short period showed a gain in body mass.  A year
       later this weight gain had disappeared in almost all

                               Adiposty 101

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       subgroups, except those that tried to lose weight by

       4.2  Chronic Adiposty

       My area of interest is chronic adiposty, in which the
       subject is heavier than average for most of his life.


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


       I've become acutely aware of the wide variance in quality of
       research and media coverage on the problem of adiposty.  The
       reader should beware of two common flaws in obesity studies.

       6.1  Correlation .vs. Cause and Effect

       A correlation study might show that joggers are thinner than
       couch potatoes.  This is a *correlation*.  Almost
       invariably, this data is used to "prove"       that obesity is
       caused by lack of exercise, that fat couch potatoes will
       become thin if only they get off their duffs and exercise.

       What is the error in drawing such a conclusion?  The error
       is the unstated assumption that the correlation proves a
       particular cause and effect.  In fact, there are two
       possible cause and effect relationships at play.  The common
       assumption is: Lack of exercise causes obesity.  The other
       possibility is that obesity is a handicap that frustrates or
       precludes sports activities.

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

                               Adiposty 101

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       6.2  Flawed Sample Selection/Distribution

       Non-random selection or partitioning of the sample
       population flaws many otherwise convincing studies.

       A study on the mortality of obesity was based on patients
       who had lost and regained weight.  Was the increase in
       mortality caused by the obesity, or by the dieting?

       Diet program studies typically exclude dropouts from their

       Studies comparing the relative success of alternative
       treatments do not always assign subjects to the alternatives
       at random.  Factors that determined sample selection and
       partition may be more important to the outcome than the
       nominal independent variable.


       7.1  White Adipose Tissue (WAT)

       Obesity results from an excess of white adipose tissue.

       WAT cells are no mere storage tanks.  These living cells
       compete with lean tissue for nutrients, generate and destroy

       The fact that reduction of fat cell numbers by surgery or
       immune attack causes a permanent fat loss while weight loss
       techniques that do not reduce the number of fat cells are
       temporary suggests that white fat cells themselves
       constitute the "set point" regulator.

       7.2  Brown Adipose Tissue (BAT)

       The other type of fat is Brown Adipose Tissue (BAT) whose
       main purpose appears to be the generation of heat

       7.2.1  Preadipocytes_>_Fat_Cells       White fat cells begin life
       as PREADIPOCTYES.  Hormones control the differentiation of
       preadipocytes into fat cells.  The adiposty of individual
       pigs can be predicted by measuring the ability of the
       suckling's {*filter*} to differentiate preadipocytes in a test
       tube.  The preobese sucklings had low levels of fetal growth
       hormone and high levels of triiodothyronine.

                               Adiposty 101

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

       The literature indicates a number of factors complicate
       measurement of the number and size of fat cells.  This is an
       evolving methodology.

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

       7.3  Fat Cell Receptors

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

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

       Geographic distribution of fat, including "love handles"
       that do not respond to extreme dieting, is believed to
       result from local variations in these receptors.  No diet or
       exercise has been shown to have any geographic specificity
       in fat reduction.

       7.4  The Role of Genetics

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

       Two studies published this year in the New England Journal
       of Medicine illustrate the point.

       In "The body-mass index of twins    who have been reared
       apart", the rearing environment had no effect on    the BMI.
       In other words, whether your mother fed you cookies or
       celery made no difference on how fat you became as an {*filter*}.

       In "The response    to long-term overfeeding in identical

                               Adiposty 101

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

       This study is especially interesting because or its sample
       selection.  All subjects were sedentary and none of the
       subjects had a history of obesity. One can but imagine the
       results if a few marathon runners and a few Nutrisystem
       graduates had been included.

       There is a possibility one's maternal environment (what your
       mother ate during pregnancy) may have an effect on lipid
       metabolism and possibly obesity.


       The correlation between psychological problems and obesity
       is well known.  Obesity is increasingly recognized as a
       cause of psychological problems instead of the result of
       mental problems.

       The correlation between obesity and health problems is well

       But some of the mortality associated with obesity results
       not from the obesity itself but from the effects of weight
       loss.  (This should not be confused with rare acute
       reactions to specific types of diets.)  As reported in the
       recent House hearings on the diet industry, some studies
       show in increase in mortality with weight loss.

       Some obesity related health problems are the result of
       discrimination against obese patients by the medical
       establishment.  Insurance companies discriminate against
       Obese individuals, even those with no history of health
       problems.  The privacy of HIV antibody status is protected
       as civil right, a right denied to obese applicants who might
       prefer to omit their weight from insurance forms.

       The obese sometimes get substandard medical treatment.  In
       one case, symptoms of allergy induced asthma (post nasal
       drip) were attributed to obesity.  I have also heard reports
       of marginally overweight women humiliated by male doctors.
       It would be appropriate for the AMA or regulatory bodies to
       survey the incidence of such excesses.

                               Adiposty 101

                                  - 6 -


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

       9.1  DIETS

       Caloric restriction (semistarvation) appears to be the
       oldest method of obesity treatment.  Dieting is a natural
       idea given the appearance of famine victims and the effects
       of religious fasts.  In distinction to widespread
       stereotype, research shows that the obese do not eat more
       than their lean counterparts.

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

       A number of techniques have been used to enforce diets,
       including appetite reducing {*filter*} and surgical modification
       of the digestive system.  None of these has proven to
       improve the basic dynamics of the diet.

       The major side effect of reducing diets is weight regain.
       Despite a level of expenditure that would have produced
       several space stations and a mission to Mars, the long term
       success rate remains less than five per cent.

       Controversy abounds about the efficacy of rapid vs slow
       weight loss.  Some studies addressing this issue are flawed
       by sample selection problems.  Subjects on 1200 calorie and
       800 calorie VLCD type diets had the same ratio of fat loss
       to lean tissue loss.  Diet induced metabolic slowdown was a
       direct function of the amount of weight lost.
       (International Journal of Obesity 1989, pp 179-181)

       It is sometimes reported that dieting cycles induce net
       weight gain.  Correction of chronic underweight by diet
       cycling constitutes the singular instance of effective
       dietary weight modification.  However, I have not found any
       relevant clinical research on this issue.  My personal
       observations suggest weight gain exceeding total weight loss
       is most likely if the dieter approaches ideal weight and/or
       is younger than 20-30 years.

       Diet induced problems include an increase in lipoprotein
       lipase and a worsening of the ratio of fat cell receptors,

                               Adiposty 101

                                  - 7 -

       both of which promote weight gain.

       A supposition behind reducing diets is the conventional
       wisdom that overeating by the obese upsets the natural
       weight regulation enjoyed by the majority of humans.
       Dieting itself may be the more serious upset to the
       patient's natural balance.

       Rare instances of toxic side effects of certain diets have
       received media attention.  Compared to the assumed health
       risks of obesity, none of these problems appears widespread
       enough to warrant the attention they have received.

       There has been considerable media coverage of claims that
       artificial sweeteners hamper weight loss efforts.  As far as
       I can determine, these result from an American Cancer
       Society study that found a correlation between overweight
       and the use of artificial sweeteners.  This correlation can
       better be explained by noting that people without weight
       problems generally prefer sugar sweetened beverages because
       of taste and "sugar high". People may also read the labels
       on some artificially sweetened products suggesting they be
       used only by those desiring to reduce their caloric intake.

       9.2  EXERCISE

       Exercise is generally considered to be good for one's
       health.  In a UC Davis study, a high level of exercise
       (marathon training) caused a modest weight loss, averaging 7
       pounds when a permanent plateau was reached at 8 weeks.  For
       some individuals 7 pounds is sufficient, but not for others.

       that those over 20% overweight should not exceed a pulse
       rate of 0.6 * (220 minus age).  This does not permit robust

       Exercise induces a period of raised metabolism and growth
       hormone levels in lean subjects.  These effects are reduced
       or missing in the obese.

       Severely overweight subjects showed a 50 per cent impairment
       in FFA [free fatty acid] mobilization in response to
       prolonged moderate exercise.  This energy shortfall was made
       good at the expense of a drop in {*filter*} sugar and increase in
       lactate plasma (the enzyme that makes your muscles ache?).
       This represents a metabolic limitation on exercise by the
       obese.  (1983 International Journal of Obesity pp 221-229.)

       Contrary to the claims of Cable TV ads, there is no clinical
       evidence of spot reducing effects from exercise.

                               Adiposty 101

                                  - 8 -

       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

       9.3  Stimulation of Thermogenisis

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

       In their book "Life Extension Weight Loss", Pearson and Shaw
       suggest thermogenisis enhancing {*filter*} and cold exposure as
       ways to burn up fat.  A study of obese women on a swimming
       program suggests their heat loss to water had the opposite
       effect, increasing their fat stores.

       9.4  Growth Hormone

       Human Growth Hormone promotes muscle growth and fat loss.
       In a recent study, administration of synthetic growth
       hormone to elderly male patients resulted in significant fat

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

       The obese have a high threshold of grueling exercise (to the
       point of exhaustion) or megadoses of arginine which must be
       surpassed before stimulation of HGH release is noted.  HGH
       levels achieved under these exceptional conditions are still
       only a fraction of what lean subjects spontaneously produce
       in their sleep.

       GHR may be useful in reducing diet-induced loss of lean

                               Adiposty 101

                                  - 9 -

       9.5  DHEA

       DHEA is a steroid hormone which has demonstrated marked
       weight reducing ability in animal studies.  It is claimed
       that the "DHEA" sold by health">food stores is bogus.  The
       author of "The Vitamin Bible" reports successful       personal
       weight loss from DHEA but gives no sources.

       9.6  Surgery

       Surgery is the only currently available fat reduction
       treatment available today that offers a significant long
       term success factor.  Unfortunately, the amount of fat
       removed by currently accepted surgical procedures is too
       small to be useful for weight reduction purposes.

       9.7  Passive Immunization

       The Hannah Research Institute in Scotland is developing a
       method to reduce long term adiposty with passive
       immunization to fat cell plasma.  In the earliest
       experiments, rat fat cell plasma was injected into sheep.
       The resultant antibodies were filtered and introduced into
       the rats.  The treated rats showed a permanent reduction in
       the size of fat deposits compared to the controls.

       Surprisingly, the treated rats had more lean tissue than
       untreated controls.  This indicates fat cells deprive lean
       tissue of nutrients necessary for normal growth.

       In a telephone conversation this year I was told Hannah's
       research is proceeding very well toward its goal of
       producing leaner meat animals, but human application in the
       near future is unlikely due to the risk of malpractice

                               Adiposty 101

Sat, 26 Dec 1992 19:22:34 GMT
 [ 1 post ] 

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