- 1 -

       1.  FOREWORD

       This is a summary of information on the causes and treatment
       of overweight I've gleaned over the years from forays to the
       Med School library and from other sources.  I hope this
       summary provides useful information on obesity.

       2.  BACKGROUND

       Adipose Cell: There are two types of adipose (fat) cell,
       White Adipose Tissue (WAT) and Brown Adipose Tissue (BAT).

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

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

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

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

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

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

       3.  TYPES OF ADIPOSITY

       One source of obesity is overeating from emotional stress.

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

       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
       subgroups, EXCEPT the subgroup that tried to lose weight by
       dieting; those who dieted gained yet weight.

                              Adiposity 101

                                  - 2 -

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

       4.  THE BIOLOGY OF ADIPOSITY

       4.1  Brown Adipose Tissue (BAT)

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

       4.2  White Adipose Tissue (WAT)

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

       WAT cells are not simple storage tanks.  These are active,
       living cells.  They destroy DHEA and Growth Hormone.  They
       convert hormones to estrogen.  White Fat cells compete with
       lean tissue for nutrients, interfering with normal muscle
       development.

       The fact that reduction of fat cell numbers (see below)
       causes permanent fat loss while weight loss techniques that
       do not reduce the number of fat cells are temporary suggests
       that fat cells themselves enforce the "set point" in many
       situations.

       4.3  Preadipocytes > Fat Cells

       White fat cells begin life as PREADIPOCTYES.

       Adipose tissue from {*filter*} humans contains a pool of tiny
       precursor cells (preadipocytes) which can be converted to
       adipocytes (fat cells) in the presence of glucocorticoids
       and insulin.  (Journal of Clinical Endocrinology and
       Metabolism, 1987).

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

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

                              Adiposity 101

                                  - 3 -

       As reported in a 1983 Nova program, fat cells can expand to
       about twice normal size.  Obese subjects have up to ten
       times as many fat cells as normal.

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

       4.4  Fat Cell Receptors

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

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

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

       4.5  Muscle Fibre Type

       The April 19 1990 Lancet reports that skeletal muscle fibre
       type is directly correlated with BMI.  Lean subjects have
       more "slow fibers" well endowed with mitochondria that use
       fatty acids as energy source.  Corpulent subjects have more
       "fast fibers" that cannot burn fat for energy. (See
       EXERCISE, below.) (1D-5) (1D-7)

       5.  THE ROLE OF GENETICS

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

       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 was shown to have no effect
       on BMI.  In other words, if you're fat, it wasn't because
       your mother fed you too many cookies and it wasn't because

                              Adiposity 101

                                  - 4 -

       your father didn't make you exercise.

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

       This study is interesting because of its sample selection.
       None of the subjects had any history of obesity whatsoever,
       not even in their families. One can but imagine what that 3
       to 1 spread would have been if subjects with a history of
       weight problems had been included.

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

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

       The obese (and pre-obese) differ from lean persons in other
       ways.  Muscle cells do not burn fat.  DHEA and growth
       hormone levels are low.  Fat cells spontaneously multiply
       when those of lean persons do not.  These factors are
       described elsewhere in this document.

       Obese and lean persons do not share the same genetic
       heritage.

       5.1  The Role of Maternal Environment

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

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

       As reported in the Health InfoCom Network News Volume  3,

                              Adiposity 101

                                  - 5 -

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

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

       5.2  The Role of Baby's Diet

       A Case Western Reserve University rat study (4P-17) compared
       rat
...

read more »

I agree things look bleak for enabling most obese patients to lose
weight.  However, there are people, some of them right here on this
net who have gone from being morbidly obese (more than double
their ideal weight) to a normal weight and gotten fit through
diet and exercise.  Furthermore, some of these people have kept
their weight down over a long period of time.  So I don't want
people to assume that it can't be done.

                                  - 1 -

       1.  FOREWORD

       This is a summary of information on the causes and treatment
       of overweight I've gleaned over the years from forays to the
       Med School library and from other sources.  I hope this
       summary provides useful information on obesity.

       2.  BACKGROUND

       Adipose Cell: There are two types of adipose (fat) cell,
       White Adipose Tissue (WAT) and Brown Adipose Tissue (BAT).

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

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

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

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

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

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

       3.  TYPES OF ADIPOSITY

       One source of obesity is overeating from emotional stress.

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

       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
       subgroups, EXCEPT the subgroup that tried to lose weight by
       dieting; those who dieted gained yet weight.

                              Adiposity 101

                                  - 2 -

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

       4.  THE BIOLOGY OF ADIPOSITY

       4.1  Brown Adipose Tissue (BAT)

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

       4.2  White Adipose Tissue (WAT)

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

       WAT cells are not simple storage tanks.  These are active,
       living cells.  They destroy DHEA and Growth Hormone.  They
       convert hormones to estrogen.  White Fat cells compete with
       lean tissue for nutrients, interfering with normal muscle
       development.

       The fact that reduction of fat cell numbers (see below)
       causes permanent fat loss while weight loss techniques that
       do not reduce the number of fat cells are temporary suggests
       that fat cells themselves enforce the "set point" in many
       situations.

       4.3  Preadipocytes > Fat Cells

       White fat cells begin life as PREADIPOCTYES.

       Adipose tissue from {*filter*} humans contains a pool of tiny
       precursor cells (preadipocytes) which can be converted to
       adipocytes (fat cells) in the presence of glucocorticoids
       and insulin.  (Journal of Clinical Endocrinology and
       Metabolism, 1987).

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

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

                              Adiposity 101

                                  - 3 -

       As reported in a 1983 Nova program, fat cells can expand to
       about twice normal size.  Obese subjects have up to ten
       times as many fat cells as normal.

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

       4.4  Fat Cell Receptors

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

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

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

       4.5  Muscle Fibre Type

       The April 19 1990 Lancet reports that skeletal muscle fibre
       type is directly correlated with BMI.  Lean subjects have
       more "slow fibers" well endowed with mitochondria that use
       fatty acids as energy source.  Corpulent subjects have more
       "fast fibers" that cannot burn fat for energy. (See
       EXERCISE, below.) (1D-5) (1D-7)

       5.  THE ROLE OF GENETICS

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

       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 was shown to have no effect
       on BMI.  In other words, if you're fat, it wasn't because
       your mother fed you too many cookies and it wasn't because

                              Adiposity 101

                                  - 4 -

       your father didn't make you exercise.

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

       This study is interesting because of its sample selection.
       None of the subjects had any history of obesity whatsoever,
       not even in their families. One can but imagine what that 3
       to 1 spread would have been if subjects with a history of
       weight problems had been included.

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

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

       The obese (and pre-obese) differ from lean persons in other
       ways.  Muscle cells do not burn fat.  DHEA and growth
       hormone levels are low.  Fat cells spontaneously multiply
       when those of lean persons do not.  These factors are
       described elsewhere in this document.

       Obese and lean persons do not share the same genetic
       heritage.

       5.1  The Role of Maternal Environment

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

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

       As reported in the Health InfoCom Network News Volume  3,

                              Adiposity 101

                                  - 5 -

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

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

read more »

Your mileage may vary in other states, but in Oregon one can be refused
health insurance for overweight.

I have been told that health insurance companies in Oregon can
not insist on an HIV test.  None of the insurance companies I
applied to asked for an HIV test, all required a weight test.

-forbidding insurance being written according to actual risk, giving
-preferential treatment to those who carry the risks.  This should
-be recognized, however, as a transfer of wealth from the average
-customer to the exceptional one (obese or whatever).  

There is a deeper issue here.  If it is allowed to discriminate
according to weight, then fairness demands all risk factors be
included, including race.

-
-
->       The obese often get substandard medical treatment.  In one
->       case, symptoms of allergy induced asthma (post nasal drip)
->       were attributed to obesity for several years.  I have also
->       heard reports of marginally overweight women humiliated by
->       male doctors.  Similar abuse was reported in a 1983 Nova
->       program.  The AMA and regulatory bodies should survey the
->       incidence of such abuses.
-
-Obesity is a health risk.  It is modifiable through changing one's

Missed the point here.  The above paragraph did not concern treatment
for obesity.  It described instances of intellectually lazy doctors
failing to properly diagnose a common health problem in a patient that
happnes to be fat, because that patient is fat.

-
->       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 and nothing
->       else.  (International Journal of Obesity 1989, pp 179-181)
-
-
-This has been my experience.  One should state it more accurately
-that in most experiments, metabolic rate is proportional to the
-lean body mass at a given time in a given individual.  It is impossible
-to lose fat alone without losing some lean tissue, but some of the
-extreme starvation diets (much less than 800 cal) can produce
-too much lean tissue loss and lower the metabolism too much.  Exercise
-is an excellent way of increasing LBM and also burning up calories.

Missed the main point again.  Reduction of lean body mass accounts for
only a portion of the reduced metabolism.  Please read the paper in
International Journal of Obesity 1991, 15, 7-16 for details.

-
-
->       Weight rebound induced by reducing diets is clinically used
->       to add fat to underweight patients who cannot gain weight by
->       overeating.
->
-This is a very stupid thing to do.  I can think of only a few instances

That is precisely the point of my original posting.

-
-
->       My personal observations suggest weight rebound is most
->       likely when the fat cell size is severely reduced.  How long
->       the fat cells remain without the triglycerol that prevents
->       them from dividing controls the amount of adipocyte
->       hyperplasia, not how quickly a diet brings the fat cells to
->       that state of stress.  Thus, losing weight slowly does not
->       reduce weight rebound compared to rapid weight loss.
-
-
-I don't follow this.  How did you measure your cell size?  Did you
-control for lean body mass?

This was a summary of what I've learned from my research on the subject.
I've listed the most pertinent articles in my original posting to allow
the reader to investigate for oneself.

-
-
->       Dieters need {*filter*} to suppress the excessive amounts of LPL,
->       glucocorticoids, and runaway fat cell proliferation
->       triggered by severe weight loss.
->
-
-Could you document this?  I've never seen any increase in LPL when dieting.

The main paper appeared in the New England Journal of Medicine, 322, 15,
Apr 12 1990.  If you have data from your personal experience, might you
share it with us, along with a complete background?

-
->       "I can see little reason for intake restriction to receive
->       continued support, wither as a subject of research or as an
->       accepted therapy for obesity.  {*filter*}letting as a therapy for
->       pneumonia was abandoned about a century before penicillin
->       was discovered.  It required a modicum of courage and good
->       sense on the part of practitioners who turned away from the
->       practice, but there is no reason to believe their patients
->       suffered from this lack of therapy."
->
-
-There are only three possible approaches: intake restriction,
-output enhancement, and efficiency alteration.  I would agree
-with the statement that voluntary intake restriction looks like

Where did "voluntary" come from??  That is a fundamental misquote one
should NOT have made after reading Bennett's paper.  Bennett's paper
covered many forms of diet restriction, voluntary and otherwise.

If you have access to a good library, do try to read the article by
William Bennett in the Annals, New York Academy of Sciences, (book length
issue on Human Obesity).
--
"Many such [diet] programs proffer treatment as though it were established as
effective and safe.   Nothing in the results published by research programs
authorizes anyone to make such claims."
        -William Bennett,   Harvard Medical School Health Letter

Actually, the terms "output enhancement" and "efficiency alteration"
seem particularly ill-defined to me.  Where does "generation of heat"
come in?  There's deliberate heat generation (brown fat thermogenesis,
which has only been know about for a decade or so -- my own favorite area
of bariatric research).  And there's exercise, what I suspect you meant
(at least in part) by output enhancement.

Other than the quite real issues of binging or "food abuse", intake
restriction looks to me like a time-honored formula for failure.

For all the research that shows obesity is a health risk, has the underlying
assumption that it is a Cause, rather than  just a (very obvious) marker for
something else, ever been proven?

Best Wishes
--

Payphone ripoff?  Californians call Pac Bell at 800/352-2201, M-F, 8-5.
From elsewhere try the FCC's enforcement division at 202/632-7553.

(1) Bring eating habits roughly within the normal range, i.e., eat
only when hungry (or plan on eating a reasonable quantity of cooking.net">food and
eat only that). In my case I never actually worked out a diet, I
simply stopped allowing myself to eat because of stress, anxiety,
etc. or any cause other than hunger. (Or to eat only very small snacks
under such circumstances.)

(2) Then treat weight control as a side effect of a general increase
in exercise. My main goal is to be (reasonably) fit and well exercised,
rather than to lose weight. Weight does tend to go down when this is
done, however.

But then, I was never more than about 30% overweight.  I really don't
know what life is like for people who weigh, say, 300 pounds.
--
-------------------------------------------------------
Michael A. Covington | Artificial Intelligence Programs
The University of Georgia  |  Athens, GA 30602   U.S.A.
-------------------------------------------------------

Edison Wong
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Inquiring minds want to know:  just how did he do that???

One speculation of mine about the increased indidence of adiposity in
developed countries is the disruption of the light/dark cycle which is
provided by electricity.  I suspect that brown fat thermogenesis is
heavily influenced by the brain's notion of "time of year".  (Kindly
note that this speculation is clearly labelled as such.)
--

Payphone ripoff?  Californians call Pac Bell at 800/352-2201, M-F, 8-5.
From elsewhere try the FCC's enforcement division at 202/632-7553.

Again, I ask that people at least read Bennett's paper before continuing
this nonsense.
--
"Many such [diet] programs proffer treatment as though it were established as
effective and safe.   Nothing in the results published by research programs
authorizes anyone to make such claims."
        -William Bennett,   Harvard Medical School Health Letter

I suspect that brown fat thermogenesis is

BTW, amputation may sound silly, but people
still have stomach surgery and liposuction to reduce adiposity...
--
- -    0 0    o o
 |      >      >
===    <=>    \_/
Inquiring minds want to know:  just how did he do that???

I can see it now.  The SUGAR DIET.  (Sugar is carbohydrate, no?)

--
"Many such [diet] programs proffer treatment as though it were established as
effective and safe.   Nothing in the results published by research programs
authorizes anyone to make such claims."
        -William Bennett,   Harvard Medical School Health Letter

The problem is the 95% statistics are accrued from people who present
to obesity researchers.  These are people who almost always have
failed to be able to lose weight on their own after many tries.  Those
who can lose and keep it off by diet and exercise don't show up at
obesity clinics where this sort of data is gathered.  It would take a
huge population study to find out what percentage can lose on their own.
We probably should do the study to try to find out what is responsible
for the success cases if we can.

Unfounded assumption??

-failed to be able to lose weight on their own after many tries.  Those
-who can lose and keep it off by diet and exercise don't show up at
-obesity clinics where this sort of data is gathered.  It would take a

How Many who regain their weight don't show up either?

-huge population study to find out what percentage can lose on their own.
-We probably should do the study to try to find out what is responsible
-for the success cases if we can.

A good point.  Be sure to normalize for the biological factors that
distinguish the chronically obese from normal subjects.

-per week.  My fat relatives and I can eat like there was no tomorrow.

This puts you in a minority of fat people.  The research cited indicates
obese individuals do not eat more than average, and many eat less than
average.

-Surveys of reduced obese have documented in almost every case improvement
-in objective measures of health such as lower {*filter*} glucose, {*filter*}
-pressure, {*filter*} lipids, etc.  The fact that so few obese in these
-studies stay reduced long term makes it harder to make statements
-about their outcome.  Most people feel that it is positive, however.

The fact remains: no controlled intervention study has shown long term
health improvement resulting from dieting.  For each long term dieting
success there appear to be several unfortunates who end up fatter and
less healthy for their efforts.
--
"Many such [diet] programs proffer treatment as though it were established as
effective and safe.   Nothing in the results published by research programs
authorizes anyone to make such claims."
        -William Bennett,   Harvard Medical School Health Letter