NetNews Usenet Archive 1992 #27/NN_1992_27.iso/spool/sci/med/21127

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Newsgroups: sci.med
Path: sparky!uunet!omen!caf
From: [e-mail] (Chuck Forsberg)
Subject: Adiposity 101 2/3
Archive-Name: adiposity.101/part02
Organization: Omen Technology Inc
Date: Tue, 17 Nov 1992 13:41:07 GMT
Message-ID: <[e-mail]>
Submitted-By: caf@omen
Lines: 1469

---- Cut Here and feed the following to sh ----
#!/bin/sh
# this is fat.02 (part 2 of adiposity.101)
# do not concatenate these parts, unpack them in order with /bin/sh
# file adiposity.101 continued
#
if test ! -r _shar_seq_.tmp; then
    echo 'Please unpack part 1 first!'
    exit 1
fi
(read Scheck
 if test "$Scheck" != 2; then
    echo Please unpack part "$Scheck" next!
    exit 1
 else
    exit 0
 fi
) < _shar_seq_.tmp || exit 1
if test ! -f _shar_wnt_.tmp; then
    echo 'x - still skipping adiposity.101'
else
echo 'x - continuing file adiposity.101'
sed 's/^X//' << 'SHAR_EOF' >> 'adiposity.101' &&
X
#"We found no significant relationship between obesity and
the items documenting food consumption" (Int J of Obesity
1992, 16, 565-572)
X
#"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
in these men." (American Journal of Clinical Nutrition,
6/86)
X
#"There was no relationship between energy intake and
adiposity" (American Journal of Clinical Nutrition, 9/90)
X
#"caloric intake per unit of lean body mass was constant
regardless of the degree of obesity"  (Journal of the
American Dietetic Associtation, 2/92)
X
#"Comparisons of obese adolescents to normal peers have
demonstrated comparable energy intake and nutrient
distribution." (Journal of School Health 2/92)
X
#"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-)
X
#"Studies on habitual food intake have failed to observe any
consistent differences between obese and lean subjects." (p.
80, Obesity and Leanness - Basic Aspects)
X
#"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
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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)
X
#"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.)
X
#"the following aspects of weight are myths rather than
reality:
(a) There are objective defintitions 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)
X
#"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)
X
#"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)
X
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..
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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."
X
X
6.3  SLOW vs RAPID Weight Loss
X
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.
X
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)
X
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.
(Americal J of Clinical Nutrition 33: Feb 1980 p. 468)
X
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6.4  BEHAVIOR MODIFICATION
X
#"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 behavoral treatment
of obesity, it is that weight maintenance can be achieved
with this therapy.  The shortcoming of behavorial 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."
(Americal J of Clinical Nutrition 33: Feb 1980 p. 469)
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6.5  Diet Side Effects
X
A common result of reducing diets is weight regain.  95 per
cent regain all the lost weight within 5 years.
X
A Swiss study compared various diets' effects on weight
regain.  Low caloric intake induces an adaptive increase in
metabolic efficiency.  Its persistence after slimming is an
important factor in the ease with which the obese condition
is regained.  After body fat is reduced by feeding a low
calorie diet, refeeding a similar caloric intake as weight-
matched controls over a 2 week period results in a 15-20%
lower energy expenditure, 3-fold increase in the rate of fat
deposition, and a doubling of energetic efficiency.
Isocaloric diets varying in protein content (8-40%), fat
content (5-55%), differing fat types, and carbohydrate types
were tested in search of an effective weight maintenance
regimen.  The elevated energetic efficiency during refeeding
was partially reduced by low protein diets.  Weight rebound
was unaffected by the type of fat or the type of
carbohydrate.  Provided the diet provided adequate protein
and did not exceed 35 per cent fat, no diet, including low
fat, had an impact on the post weight loss reduction in
energy expenditure that facilitates weight rebound.
X
An Italian study (1P-115) indicates obese subjects with high
insulin and triglyceride levels are more resistant to diets.
X
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.
X
In a Swiss study of lean and obese rats, reduced energy
expenditure (EE) of obese rats with limited caloric intake
resulted mostly from metabolic slowdown not related to
reduction in lean body mass or activity levels.  This
metabolic slowdown continued after the obese rats returned
to normal caloric intake (eating the same as lean rats) and
regained the weight they had lost.  (International Journal
of Obesity 1991, 15, 7-16) Corticosterone induced inhibition
of thermogenisis is suspected.
X
Diet induced metabolic slowdown has two aspects: Resting
Metabolism Rate (RMR) and Diet Induced Thermogenisis
(DIT)/Thermic Effect of Food (TEF).  Studies on diet induced
decline in RMR are contradictory, with no agreement on
definitions and methodology.  #A recent paper in the
American Journal of Clinical Nutrition concluded that
conflicting results that did not detect diet induced drop in
RMR might be due to defects in their body composition
assessment methods.  Some studies that did not report diet
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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.
X
Diets have unpleasant side effects for some.
X
X  + Dry mouth
X
X  + Sleep Disruptions (difficulty falling asleep, excessive
X    sleepiness, disturbed sleep, vivid dreams)
X
X  + Cold Intolerance.  "Cold intolerance is a significant
X    problem aggravated by dieting in morbid obesity."
X
X  + Lack of energy.
X
X  + Menstrual Difficulties
X
X  + Yest Infections
X
X  + Fluid Retention
X
X  + Low pulse rate and blood pressure.  One symptom of low
X    blood pressure from metabolic slowdown is dizziness when
X    abruptly arising from a chair.
X
X    Normally, resting pulse rate and blood pressure indicate
X    a healthy body.  Dieters and their doctors rejoice when
X    energy deprivation lowers their high blood pressure and
X    heart rate readings.  Unfortunately, these lower numbers
X    do not imply better health when lower pulse rate and
X    blood pressure result from diet induced metabolic
X    slowdown and not cardiovascular improvement.
X
X  + Constipation
X
X  + Stomach Distress
X
X  + Hair loss
X
X  + Ridged Nails (low fat diet vitamin or mineral
X    deficiency)
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X  + Dizzy spells
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X                       Adiposity 101
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X  + Weakness
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X  + Headaches (mostly women)
X
X  + Hot flashes
X
X  + Depression (as measured in standardized tests).
X
X  + Collagen generation as low as 5% of normal.  (Collagen
X    is the major protein of all connective tissues, a
X    shortage of which is believed to cause wrinkles, etc.
X    Collagen production is necessary for wound healing and
X    normal growth.) This might explain the degraded
X    appearance seen in some dieters.
X
Diet induced metabolic changes include an increase in
lipoprotein lipase (LPL), an enzyme that stores fat in fat
cells.  LPL levels drop during the first few weeks of
dieting.  Depending on the study, LPL levels remained normal
or depressed for some time after dieting.  Subjects with BMI
< 35 or who lost less than 12% of their initial body weight
did not show marked increases in LPL.  But in the more obese
subjects, LPL rose to 25 times normal, and remain elevated
for at least 6 months.  The fatter the person was to begin
with, the more of the fat-regaining enzyme they produced
after weight loss.  Kern's paper sheds insight on many
issues related to the varied outcomes different people have
to diet cycling.  (New England Journal of Medicine, Vol. 322
No. 15, Apr 12 1990)
X
(See also: Metabolism: Clinical and Experimental, Jul 1987)
X
Adipose cells have different receptors for storing and
releasing fat.  Weight loss diets worsen the ratio of fat
cell receptors, promoting weight regain.
X
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)
X
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.
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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.
X
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)
X
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.
X
Binging is part of the body's "set point" servo system
response to energy shortfall.  Animal and human deprivation
studies consistently demonstrate a period of markedly
increased caloric input that tapers off as lost weight is
regained.  In one study of binging, the frequency of binges
and the number of calories eaten approximated the diet's
caloric deprivation, resulting in a near normal overall
energy balance.  Binging may be important in the onset of
adipocyte hyperplasia associated with diet cycling.
X
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)
X
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6.5.1  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.
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6.6  Diet Cycling
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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.
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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".
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Animal studies of weight cycling are contradictory.  When
obesity is forced by induced overeating, cycles of weight
fluctuation do not increase fatness.  When rats are reduced
below set point, weight cycled rats regained weight more
rapidly, regained more weight, but ate no more food than non
cycled rats. (Int J of Obes; V12; N6)
X
In humans, weight rebound induced by diet cycling is
clinically used to add fat to underweight patients who
cannot to gain weight by overeating.
X
In "Variability of Body Weight and Health Outcomes in the
Framingham Population",  subjects with larger weight
fluctuations had markedly higher BMIs and, what's worse, a
higher slope of BMI (BMI/year).  (N Engl J Med 1991; 324;
1839-44) A study of workers at Western Electric's Hawthorne
Works in Chicago also reported higher BMI in weight cycling
men.  (Hamm et al. Large fluctuations in body weight during
young adulthood and 25-yr risk of coronary death in men.
American Journal of Epidemiolology 1989, 129:312-318)
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In a 1986 Dutch study, men who experienced many life events
in a short period showed a gain in body mass.  A year later
this weight gain had disappeared in almost all subgroups of
these men.  The exception was the subgroup that tried to
lose weight by dieting; those who dieted gained yet more
weight.  (International Journal of Obesity (1988), 12, 29-
39.)
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"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)
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In a landmark study of the dieting loss-regain cycle,
Drenick et al (1964; JAMA 187:100-105) and Johnson and
Drenick (1977; Arch Intern Med 137:1381-1382) placed
subjects on total fasts.  As with other types of diets,
subjects with childhood onset obesity had the most trouble
with the fast.  At the conclusion of the fast, most of these
patients maintained their weight loss for about a year.
Half the subjects regained all their weight within two or
three years, and almost all had regained their weight by 9
years.  Patients with adult-onset and childhood-onset
obesity gained weight at the same rate.  Regain beyond
original admission weight was more common among the
childhood-onset obese (42%) than adult-onset obese (26%).
Eighty per cent developed diabetes; half of these cases were
severe.
X
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.
X
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
wrestlers never met several of the conditions that trigger
lipoprotein lipase (LPL, the "fattening hormone")
overproduction in serious dieters.
X
Diet evangelists are quick to assert that since the diets
they recommend differ in one detail or another from the
fasts used by Drenick et al, their diets will not provoke
the same horrific long term results.  There are few
controlled studies comparing the effectiveness of different
types of diets, but those that have been made found no
advantage to slowing the rate of weight loss.
X
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.
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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
Obesity, 1990, 14, 187-192)
X
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)
X
#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
during dieting as well as maintenance.  Subjects with fewer
fat cells (normal range) did not suffer this increase in fat
cell numbers.
X
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)
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The Wadden study on diet cycling found a statistically
significant correlation between dieting history and weight,
BMI, fat mass, waist size, and hip size.  (Am J Clin Nutr
1992;56;203S-8S)
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The Framingham study also found weight cyclers to be much
fatter.
X
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.
X
#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.  Adjusting for current weight begs the
question that diet cycling increases obesity.  Subjects
experiencing negative health outcomes associated with diet
cycling were excluded.  As an alternative, adjusting for
weight history before the subjects' first diet would be
credible.
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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.
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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.
X
#Diet evangelists have attacked these studies as bitterly as
the Tobacco Institute attacks studies linking smoking and
disease.  Diet evangelists insist that unknown factors other
than dieting may have been responsible for these weight
fluctuations.  (They have yet to suggest any credible
alternatives to dieting.) A careful reading of these papers
will, however, reveal that 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 data on diet cyclers
would have been known to Framingham doctors.
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#``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)
X
#The heart is not spared from the catabolic effects of
undernutrition, but is subject to the same degree of weight
loss as skeletal muscle.  (Internation Journal of Obesity
(1992) 16, 481)
X
#The mechanisms by which diet cycling leads to negative
health outcomes have not been intensively researched, but
some have been noted:
X
X   + Diet induced hypercholesterolemia
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X   + Diet induced depletion of Omega-3 reserves (Phinney, Am
X     J Clin Nut 1992;56;781-2)
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X   + Decrease in HDL ("good") cholesterol
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X   + Loss of heart tissue
X
X   + Loss of bone mass (USDA Grand Forks Human Nutrition
X     Research Center)
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X   + Increase in fat cell numbers (Bjorntorp and Sjostrom
X     METABOLISM V20;7;703)
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X   + Changes in fat cell receptors
X
X   + Another ominous outcome is that the weight that is
X     regained is more likely to be in the upper body than
X     the lower, and for men at least, that type of weight
X     distribution has been linked to an increased risk of
X     heart disease.  (University of California Berkeley
X     Wellness Letter, 5;4)
X
Some studies on human diet cycling are tabulated below.
X
X              Human Studies on Weight Cycling
X
__________________________________________________________________________
|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     |
|Framingham | 5127       random     true      yes       CHD               |
|Harvard    | 11703 m    alumni     true      n/a       CHD, all          |
|___________|_____________________________________________________________|
X
X  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.
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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.
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#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.
X
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.
X
#Weight loss studies should report the number and size of
adipose cells before slimming, after slimming, and after
weight regain.
X
6.6.1  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, 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.
X
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.
X
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.
X
A Harvard Medical School study indicated Aspartame
facilitated long term weight maintenance in a
multidisciplinary weight loss program.
X
X
X
X
X
X
X
X                       Adiposity 101
X
X
X
X
X
X
X
X                           - 35 -
X
X
X
6.7  High Fiber Diet
X
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.
X
6.8  Low Fat Diets
X
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.
X
This interest springs from a number of observations.
X
X   + High fat (>>40% fat) diets cause weight gain in
X     research rats.  Low fat evangelists fail to note that
X     high carbohydrate diets have proven even more fattening
X     to research rats.  In addition, not all rats gain
X     weight on the high fat diet, and most rats revert to
X     normal weight when their diet is normalized.  All of
X     the high fat rat diets seen in the literature involve a
X     profound increase in total energy intake, contrary to
X     most obese humans who have depressed energy intake.
X
X     Replacing mothers milk (8% of calories from
X     carbohydrates) with a milk-substitute formula (56% of
X     calories from carbohydrates) grew fatter rats.  (See
X     "The Role of Baby's Diet", below.)
X
X   + Obese subjects often exhibit a greater carving for fat
X     than lean individuals.  #Fat craving is a common after
X     effect of energy deprivation.  Following food
X     restriction, corpulent female rats had galanin (a
X     substance that increases fat appetite) levels 40-50%
X     higher than lean females or freely-fed corpulent
X     females.  (Diabetes Research 1990 15,1-7)
X
X     Since most fat people have been on numerous diets, fat
X     craving may be the result of dietary restriction, not
X     the initial fat inducing condition.  Studies show fat
X     children obtain a slightly greater proportion of their
X     energy input from fat than thin children do.  This
X     slight increase is decisively overshadowed by their
X     lower total energy intake.  Pre-obese children consume
X     less energy (50 calories/day average) than their lean
X     counterparts.
X
X
X
X
X
X                       Adiposity 101
X
X
X
X
X
X
X
X                           - 36 -
X
X
X
X   + Some studies suggest energy from fat additions to an
X     otherwise neutral energy balance cause a weight
X     increase short term, which may be more pronounced in
X     the obese.  This effect has not been demonstrated
X     outside the context of induced overfeeding.  In
X     "Oxidative and nonoxidative macronutrient disposal in
X     lean and obese men after mixed meals" (Am J of Clin
X     Nut, 1992;55;630-6), Owen et al report "Significantly,
X     there was no tendency for the obese men to have the
X     defect in suppression of fat oxidation after mixed
X     meals that had been reported by others".
X
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 Dr. Atkins Diet is also a low fat diet because some
people do not like fatty foods that are not also high in
carbohydrates.
X
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 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.)
X
#"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)
X
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 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)
X
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.
X
X
X
X
X                       Adiposity 101
X
X
X
X
X
X
X
X                           - 37 -
X
X
X
"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 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)
X
"Comparisons of obese adolescents to normal peers have
demonstrated comparable energy intake and nutrient
distribution." (Journal of School Health 2/92)
X
6.8.1  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.
X
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.
X
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
more weight on the low fat diet.
X
X
X
X                       Adiposity 101
X
X
X
X
X
X
X
X                           - 38 -
X
X
X
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 almost halted.
X
#"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, suggesting a "metabolic disadvantage"
compared to low carbohydrate diets.
X
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.
X
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
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.)
X
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.
X
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
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."
X
X
X
X                       Adiposity 101
X
X
X
X
X
X
X
X                           - 39 -
X
X
X
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)
X
"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)
X
"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)
X
X
6.9  Low Carbohydrate Diets
X
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 much lower in Europe than in the U.S.2
X
A number of short term studies, mostly in the 50's and 60's,
showed a marked advantage in weight loss from low
carbohydrate diets compared to diets higher in carbohydrate.
X
X
X
__________
X
X 2. International Journal of Obesity 1992, 16,565-572
X
X
X
X
X                       Adiposity 101
X
X
X
X
X
X
X
X                           - 40 -
X
X
X
Of particular interest is the "Atkins Diet" developed by Dr.
Robert Atkins, a New York cardiologist.
X
Dr. Atkins claims that 95% of overweight 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.
X
Dr. Atkins claims that high carbohydrate diets promote
Candida Albicans overgrowth ("yeast infections"), which can
interfere with weight management.  His lab tests confirmed
yeast infections in a third of his patients.
X
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, dieters are encouraged to eat ad libitum.
X
The wide media attention afforded Dr. Atkins' Diet
Revolution and Dr. Atkins' claim that high carbohydrate
consumption 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,"
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 1992
as it was in 1973.
X
Since the AMA Council on Foods and Nutrition put the Atkins
diet off limits, few 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.
X
Critics blast the Atkins diet as a high-fat regimen that
increases serum lipids.  Dr. Atkins, trained as 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.''
X
``the AMA [Council on Foods and Nutrition] said they were
X
X
X
X                       Adiposity 101
X
X
X
X
X
X
X
X                           - 41 -
X
X
X
"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 1929.3 "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."
X
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.
X
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 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 have
observed with other types of diet.  (American Journal of
Clinical Nutrition 1991;53;1404-10)]
X
Problems reported with the Atkins diet include weakness,
palatability, inconvenience and expense of obtaining low-
carbohydrate and sugar-free foods.  Several Usener readers
have reported abandoning the Atkins diet as a result of side
effects and the bad publicity.
X
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
X
X
__________
X
X 3. See Dr. Atkins' footnote on this study.
X
X
X
X
X                       Adiposity 101
X
X
X
X
X
X
X
X                           - 42 -
X
X
X
from a low-carbohydrate diet." Dr. Atkins advertises books
and vitamins on his nationally syndicated radio talk show
(1-800-2-ATKINS, 1-800-6-ATKINS).
X
This author has not able to find a single study of the
Atkins ad libitum carbohydrate restricted type of diet in
the medical scientific literature.  The available low
carbohydrate studies have used energy restricted diets
profoundly different from Atkins' recommendations.
X
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."
X
A Scottish study found lowering carbohydrate intake doubled
weight loss, increased fat oxidation, and reduced metabolic
slowdown compared to lowering fat intake.  This appears 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 much less
than expected from the reduction in caloric intake.
X
Several recent papers have reported low carbohydrate to be
better than the generally accepted low fat diet for diabetic
control.
X
One of the Council's criticisms of the Atkins diet was loss
of appetite.  Atkins considers this 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.
X
X
X
X
X                       Adiposity 101
X
X
X
X
X
X
X
X                           - 43 -
X
X
X
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
results, however, may be the result the same selective
dropout problems that affect other diet studies.
X
6.10  Diets - the BOTTOM LINE
X
"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."
X
"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."
X
"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)
X
X
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.
X
X
X
X                       Adiposity 101
X
X
X
X
X
X
X
X                           - 44 -
SHAR_EOF
true || echo 'restore of adiposity.101 failed'
fi
echo 'End of adiposity.101 part 2'
echo 'File adiposity.101 is continued in part 3'
echo 3 > _shar_seq_.tmp
exit 0
--
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