- 13 -

       10.1  DIETS

       "The high prevalence of obesity in affluent societies,
       coupled with an increasingly lean aesthetic ideal, has
       resulted in unprecedented rates of dieting." (International
       Journal of Obesity 1990, 14, 373-383)

       Dieting is a natural idea given the temporary effects of
       religious fasts.  Caloric restriction (semistarvation) is
       the oldest known method of obesity treatment.

       A supposition behind reducing diets is the conventional
       wisdom that overeating by the obese upsets the natural
       weight regulation enjoyed by the majority of humans.

       In distinction to the commonly accepted stereotype, research
       shows that the obese do not eat more than lean counterparts.
       In addition, research has failed to demonstrate significant
       defect in obese subjects' hunger/satiety response to eating
       compared to that of lean subjects.

       "Canadian researchers who studied the eating patterns of    80
       women between the ages of 30 and 38 found that smaller
       eaters weighed an average of 10 pounds more than their
       larger-eating counterparts.  ...  Small eaters in the study
       had an average of 22 per cent more body fat than the large
       eaters."    (F1, The Oregonian, 2/14/91)

       Various techniques have been used to enforce diets,
       including appetite reducing {*filter*} 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.

       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."

       10.1.1  Diet Side Effects  A common side effect of reducing
       diets is weight regain.  95 per cent regain their weight
       within 5 years.

       A Swiss study compared various diets' effects on weight
       regain.  Low caloric intake induces an adaptive increase in
       metabolic efficiency.  Its persistence after slimming is an

                              Adiposity 101

                                  - 14 -

       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 effect 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.

       An Italian study (1P-115) indicates obese subjects with high
       insulin and triglyceride levels are more resistant to diets.

       Dieting does not reduce the number of fat cells, even in
       subjects burdened with ten times the normal number.  In fact
       dieting can increase the number of fat cells.

       Controversy abounds about the efficacy of rapid vs slow
       weight loss.  Many studies addressing this issue are flawed
       by sample selection problems.  Slightly overweight subjects
       on mild diets do not reagain as much weight as massively
       overweight subjects placed on more stringent diets.

       Results are different when subject selection is randomized.
       Subjects on 1200 calorie and 800 calorie VLCD type diets had
       the same ratio of fat loss to lean tissue loss.  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)

       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 and not from a
       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.

       Diet induced metabolic slowdown has side effects.

         + Intolerance to prolonged exposure to cold.

                              Adiposity 101

                                  - 15 -

         + Lack of energy.

         + Low resting pulse rate and {*filter*} pressure are generally
           considered signs of good health.  Unfortunately, diet
           induced metabolic slowdown also causes low pulse rate
           and {*filter*} pressure.  One symptom of low {*filter*} pressure
           from metabolic slowdown is dizziness when abruptly
           arising from a chair.

         + Hair loss

         + Dizzy spells

         + Weakness

         + Headaches

         + Hot flashes

         + Depression (as measured in standardized tests).

         + Collagen generation as low as 5% of normal.  Collagen is
           the major protein of all connective tissues, shortage of
           which is believed to cause wrinkles, etc.
       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, but then rise 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.  (New England Journal of
       Medicine, 322, 15, Apr 12 1990) (This LPL activity could
       explain the initial rapid weight loss, frustrating plateaus,
       and eventual weight regain experienced by most dieters.)

       Adipose cells have different receptors for storing and
       releasing fat.  Energy shortfall diets worsen the ratio of
       fat cell receptors, further promoting weight gain.

       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 and preobese persons
       largely prevent the body from regenerating lean tissue,
       causing some of the adverse health effects of repeated
       weight loss.  Human Growth Hormone injections have been
       shown to reduce dieting induced loss of lean tissue.

       Dieters need {*filter*} to suppress the excessive amounts of LPL,
       glucocorticoids, and runaway fat cell proliferation
       triggered by the energy shortfall weight loss cycle.  The

                              Adiposity 101

                                  - 16 -

       drug LY79771 reduced post diet weight rebound in BHE/cdb
       rats by about 20 per cent.

       Another side effect of dieting is bloating.  Bloating is
       familiar to third world doctors working with famine victims,
       whose distended stomachs are sometimes seen in TV famine
       documentaries.  This subject is rarely discussed in diet
       books.  Bloating confuses dieters who can not distinguish
       bloating from overfeeding symptoms.  A dieter may think she
       is overeating when in fact she is nearly bloating from
       dieting.

       10.1.2  Diet Cycling  For 95 per cent of dieters, starvation
       is an unnatural transitory state, and so is the associated
       weight loss.  Many repeatedly attempt to shed their unwanted
       poundage.

       It is widely reported that dieting cycles cause net weight
       gain, but relevant experiments and hard clinical data are
       hard to find.

       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)

       Experiments show that fat cells taken from massively obese
       subjects have much greater mitogenic (spontaneous cell
       replication) activity than cells taken from lean subjects.
       "When *mature* fat cells    from massively obese persons give
       up their fat and revert in culture to forms similar to
       preadipocytes, they replicate significantly more rapidly
       than analogous cells from the lean.  The reverted cells,
       therefore, retain the 'memory of their roots', indicating an
       inherent property of these cells." "Prolonged nutrient
       energy restriction would lead to reversion of mature fat
       cells.  This process would be accentuated by regular
       exercise. ...  When the subject resumes overeating and a
       sedentary pattern, the inherited program for excessive
       replication and differentiation would be recalled, resulting
       in an even higher degree of adipocyte hyperplasia.  Thus,
       each cycle of compliance and relapse would lead to an even
       greater number of mature (large) fat cells, resulting in
       stepwise progression of the massive obesity." (International
       Journal of Obesity, 1990, 14, 187-192)

       Weight rebound induced by reducing diets is clinically used
       to add fat to underweight patients who cannot gain
...

read more »

This mentality drives me nuts. Seems like everybody in America
is striving for victimhood. How will we compete with Japan with
such an attitude?

Brian

I merely repeated Dr. Callaway's assessment that bloating is a
common side effect of dieting that is not adequately addressed by
the diet establishment.  Dr. Callaway made the connection with third
world nutrition disorders.

I have often experienced bloating when dieting, and for a long
time erroneously confused that discomfort with that caused by
infrequent overeating.  I suspect other dieters have made this
same mistake.

If Brian had followed the reading recommendations in Adiposity
101, he would have discovered that the former director of the
Nutrition and Lipid Clinic at The Mayo Clinic, former director
of the George Washington University Medical Center Center for
Clinical Nutrition, who has held prominent positions with the
U.S. Department of Helth and Human Services, and the National
Institutes of Health warned that combining dieting and exercise
can exacerbate dieting's harmful side effects.
--
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

]This mentality drives me nuts. Seems like everybody in America
]is striving for victimhood. How will we compete with Japan with
]such an attitude?

The victimology of america is certainly annoying. However, Chuck's A-101
looks to me like a natural response to the discrimination and
mistreatment that the obese (especially women) suffer from:
  -they are "unattractive" and find it harder to get a job or a mate.
  -they are viewed as "weak willed" and pigs, and people let them
   know about it.
  -those who have not experienced obesity will often imply "get off your
   lazy {*filter*}and exercise, and you won't be so ugly" without ever
   considering WHY the person may have difficulty exercising.

As far as I can tell, the treatment of the obese (and in general of
the physically unattractive or inept) is every bit as damaging as
racist behavior - and yet it is condoned by our society.

I think that many MD's tend to be overachievers and ascetics, and have
great difficulty understanding those who are not.

One thing is certain: obesity in America is something that medical
science has great difficulties dealing with. Dr's can say "exercise
and don't overeat" which is good advice, but they have almost no success
in long term treatment of obesity The statistics on weight loss make
quitting cigaretes seem easy, and my personal experience backs that up!

While A-101 seems very selectively edited (similar to Durk and Sandy
Pearson's Life Extension), it does mention some studies that sound
interesting. Rather than just slashing at it, why not directly address
the issues that were raised - ie the studies cited, problems with them,
counter-studies, etc. Certainly there are mysteries in the difficulty
of treatment of obesity, and a good discussion (rather than a flame fest)
would be of interest to those of us dealing with this problem.

I have the following question: I have read that whole body calorimeter
studies find no difference in metabolic rate (as measured by heat
balance) between obese and non-obese. I have read this interpreted
as saying that difficulty in weight loss is thus not a matter of
different metabolisms, but rather behavior. While this may be true,
the deductive path seems fallacious: it assumes that conversion of
calories to heat (or not converting them) is the only significant
issue - ie, conservation of energy between input caloric content
of food, output caloric content of wastes, and heat. Is it really
this simple, or can the calories be stored or converted in other ways?
--
John Moore NJ7E, 7525 Clearwater Pkwy, Scottsdale, AZ 85253  (602-951-9326)

 - - Affirmative Action is Racism by another name - -
 - - Support ALL of the bill of rights, INCLUDING the 2nd amendment! - -

The essential problem in obesity is that the obese body
partitions too much of the available energy to the production
and maintenance of adipose tissue.  As with the thin body, the
obese body normally regulates its weight with remarkable
precision.  How precise?  Less than a pat of butter per day.

When an obese person goes on a diet, his/her metabolism drops
soon after.  The rat experiment mentioned in Adiposity 101
found that most of this metabolic retardation was not caused by
loss of lean tissue.   Metabolism remain depressed until after
the weight was regained.

Energy restriction for weight control has been the subject of
scientific study for over 60 years.  Energy restriction has
cured neither fat rats nor fat humans of their affliction.

New in the 1992 Adiposity 101 are the reports on apparently
successful experiments to prevent the development of the obese
state in genetically obese rats.  After 60 years of dead end
research, alternative obesity treatmnets are finally beginning
to show promise.
--
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

                                  - 13 -

       10.1  DIETS

       "The high prevalence of obesity in affluent societies,
       coupled with an increasingly lean aesthetic ideal, has
       resulted in unprecedented rates of dieting." (International
       Journal of Obesity 1990, 14, 373-383)

       Dieting is a natural idea given the temporary effects of
       religious fasts.  Caloric restriction (semistarvation) is
       the oldest known method of obesity treatment.

       A supposition behind reducing diets is the conventional
       wisdom that overeating by the obese upsets the natural
       weight regulation enjoyed by the majority of humans.

       In distinction to the commonly accepted stereotype, research
       shows that the obese do not eat more than lean counterparts.
       In addition, research has failed to demonstrate significant
       defect in obese subjects' hunger/satiety response to eating
       compared to that of lean subjects.

       "Canadian researchers who studied the eating patterns of    80
       women between the ages of 30 and 38 found that smaller
       eaters weighed an average of 10 pounds more than their
       larger-eating counterparts.  ...  Small eaters in the study
       had an average of 22 per cent more body fat than the large
       eaters."    (F1, The Oregonian, 2/14/91)

       Various techniques have been used to enforce diets,
       including appetite reducing {*filter*} 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.

       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."

       10.1.1  Diet Side Effects  A common side effect of reducing
       diets is weight regain.  95 per cent regain their weight
       within 5 years.

       A Swiss study compared various diets' effects on weight
       regain.  Low caloric intake induces an adaptive increase in
       metabolic efficiency.  Its persistence after slimming is an

                              Adiposity 101

                                  - 14 -

       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 effect 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.

       An Italian study (1P-115) indicates obese subjects with high
       insulin and triglyceride levels are more resistant to diets.

       Dieting does not reduce the number of fat cells, even in
       subjects burdened with ten times the normal number.  In fact
       dieting can increase the number of fat cells.

       Controversy abounds about the efficacy of rapid vs slow
       weight loss.  Many studies addressing this issue are flawed
       by sample selection problems.  Slightly overweight subjects
       on mild diets do not reagain as much weight as massively
       overweight subjects placed on more stringent diets.

       Results are different when subject selection is randomized.
       Subjects on 1200 calorie and 800 calorie VLCD type diets had
       the same ratio of fat loss to lean tissue loss.  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)

       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 and not from a
       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.

       Diet induced metabolic slowdown has side effects.

         + Intolerance to prolonged exposure to cold.

                              Adiposity 101

                                  - 15 -

         + Lack of energy.

         + Low resting pulse rate and {*filter*} pressure are generally
           considered signs of good health.  Unfortunately, diet
           induced metabolic slowdown also causes low pulse rate
           and {*filter*} pressure.  One symptom of low {*filter*} pressure
           from metabolic slowdown is dizziness when abruptly
           arising from a chair.

         + Hair loss

         + Dizzy spells

         + Weakness

         + Headaches

         + Hot flashes

         + Depression (as measured in standardized tests).

         + Collagen generation as low as 5% of normal.  Collagen is
           the major protein of all connective tissues, shortage of
           which is believed to cause wrinkles, etc.
       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, but then rise 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.  (New England Journal of
       Medicine, 322, 15, Apr 12 1990) (This LPL activity could
       explain the initial rapid weight loss, frustrating plateaus,
       and eventual weight regain experienced by most dieters.)

       Adipose cells have different receptors for storing and
       releasing fat.  Energy shortfall diets worsen the ratio of
       fat cell receptors, further promoting weight gain.

       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 and preobese persons
       largely prevent the body from regenerating lean tissue,
       causing some of the adverse health effects of repeated
       weight loss.  Human Growth Hormone injections have been
       shown to reduce dieting induced loss of lean tissue.

       Dieters need {*filter*} to suppress the excessive amounts of LPL,
       glucocorticoids, and runaway fat cell proliferation
       triggered by the energy shortfall weight loss cycle.  The

                              Adiposity 101

                                  - 16 -

       drug LY79771 reduced post diet weight rebound in BHE/cdb
       rats by about 20 per cent.

       Another side effect of dieting is bloating.  Bloating is
       familiar to third world doctors working with famine victims,
       whose distended stomachs are sometimes seen in TV famine
       documentaries.  This subject is rarely discussed in diet
       books.  Bloating confuses dieters who can not distinguish
       bloating from overfeeding symptoms.  A dieter may think she
       is overeating when in fact she is nearly bloating from
       dieting.

       10.1.2  Diet Cycling  For 95 per cent of dieters, starvation
       is an unnatural transitory state, and so is the associated
       weight loss.  Many repeatedly attempt to shed their unwanted
       poundage.

       It is widely reported that dieting cycles cause net weight
       gain, but relevant experiments and hard clinical data are
       hard to find.

       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)

       Experiments show that fat cells taken from massively obese
       subjects have much greater mitogenic (spontaneous cell
       replication) activity than cells taken from lean subjects.
       "When *mature* fat cells    from massively obese persons give
       up their fat and revert in culture to forms similar to
       preadipocytes, they replicate significantly more rapidly
       than analogous cells from the lean.  The reverted cells,
       therefore, retain the 'memory of their roots', indicating an
       inherent property of these cells." "Prolonged nutrient
       energy restriction would lead to reversion of mature fat
       cells.  This process would be accentuated by regular
       exercise. ...  When the subject resumes overeating and a
       sedentary pattern, the inherited program for excessive
       replication and differentiation would be recalled, resulting
       in an even higher degree of adipocyte hyperplasia.  Thus,
       each cycle of compliance and relapse would lead to an even
       greater number of mature (large) fat cells, resulting in
       stepwise progression of the massive obesity." (International
       Journal of Obesity, 1990, 14, 187-192)

       Weight rebound induced by
...

read more »

I've never experienced such "bloating", so I can't comment on how
distressful it is.  Was it enough to make you quit the diet?

--
----------------------------------------------------------------------------
Gordon Banks  N3JXP      | "I have given you an argument; I am not obliged

----------------------------------------------------------------------------

--
----------------------------------------------------------------------------
Gordon Banks  N3JXP      | "I have given you an argument; I am not obliged

----------------------------------------------------------------------------

--
----------------------------------------------------------------------------
Gordon Banks  N3JXP      | "I have given you an argument; I am not obliged

----------------------------------------------------------------------------

Your taking my comment out of context is also unappreciated.

By trying to talk people out of exercise because they are "exercise-
impaired" you can deprive people of a very valuable thing. If you
have two working legs and no other serious health problem other than
obesity, chances are, you can at least *walk*. People don't need
more excuses to avoid exercise.

Even if this person is saying this, there are hundreds of other
"authorities" who are advocating exercise. You do no-one a service
by putting down exercise.

Brian

The connection with third world nutrition disorders was not
intended to imply that bloating experienced by "yuppie first
world dieters" is as severe as some of the maladies of famine
victims on the verge of death.  It was intended to suggest that
caloric deprivation weight loss programs have more in common
with famine than simple weight loss.

To address your concerns, I have added the following to A-101:

        It is hoped that eventual progress in the treatment and
        prevention of obesity will allow more people to enjoy the
        pursuit of more and more active pleasures.

--
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

Many is the body builder (and admirer too, no doubt) that wishes
that nature saw fit to devote as many resources to building up
spare muscle tissue on a body, instead of fat tissue.

Was there a spot on CNN about a year ago where "whole body calorimetry"
was done on a group of Pima Indians?  The reported results were that
obese and lean subjects had the same metabolisms, so the news was
"If you're fat it's your fault", or some equally catchy phrase.
(This is TV news, not journals.)

But it seems the whole business of whole body calorimetry is in
doubt, based on several other postings.  Can anyone else post
more information on this measurement technique?

I don't think the whole story on adipose tissue will be uncovered
without serious consideration of what BENEFITS fat tissue bestows.

We all know that muscle tissue -- indeed many tissues -- will atrophy
from "disuse".  What might the body's definition of "disuse" of adipose
tissue be?

== Bob Yazz ==
--
"Well you can put lipstick on a hog and call it 'Monique',
but it's still a pig." -- Texas Gov. Ann Richards

A point that has never been adequately addressed is the percentage
of the population that is successful in dieting without help.
They don't get into studies, yet the net experience is that there
are a lot of them out there that have had long-term success.
These people never present themselves to obesity researchers
and so aren't included in studies.
--
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Gordon Banks  N3JXP      | "I have given you an argument; I am not obliged

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