X-Message-Number: 24284
Date: Mon, 21 Jun 2004 20:40:19 -0700 (PDT)
From: Doug Skrecky <>
Subject: better to be obese than thin

[Everyone "knows" that being fat is unhealthy. Learned Professors talk
about the anti-aging effect of adult-onset caloric restriction. "If you
want to live longer", "you'll have to lose weight", is the general
consensus. Well, it's reality-check time. Below is a good article by John
Luik, followed by some Pubmed abstracts, with a few additional comments.]

Better to be obese than thin (Junk Science)  by John Luik
  The shocking headlines appear almost daily in any newspaper:
"International Consensus Suggests BMI Over 25 is a Serious Risk": "Being
Overweight a Serious Risk to Your Health"; "Obesity Said to Reduce
Lifespan By Up to 20 years."
  All of these purport to tell a story, based on a scientific study, in
which fat always plays the role of villain and diet, exercise and weight
loss star as the heroes. But is it true? Does fat really cause premature
death, for example the 300,000 U.S. deaths per year, supposedly linked to
obesity? Or is the fat=premature death connection something closer to
propaganda - carefully crafted, neatly selected to tell a particular
story and nicely packaged - but ultimately a distortion bearing little
relationship to reality.
  Ever since Louis Dublin of the Metropolitan Life Insurance Company
proclaimed in 1951 that "obesity is America's number one health problem,"
there has been a steady stream of scietific studies, now numbering in the
hundreds, that have shown thinner is not always healthier and that
overweight is not a primary cause of increased mortality. One of the most
important and famous of these is the Framinham Study, which started in
1950 as a longitudinal investigation of the causes of cardiovascular
disease. Some 5,209 women and men, ages 30-59, were followed over the
course of 30 years. In 1979, three of the study's lead researchers
published their data on the impact of obesity. For men, the strongest
risk - that is the worst life expectancy - was for the thinnest men, with
the men who were 25% to 40% fatter than the Met's ideal weight tables
living the lonest. Forwomen, mortality was elevated only for the very thin
and the very fat.
  Nor was the Framingham study data a fluke. A 14-year study involving
1,233 employees from the People's Gas Company in Chicago found that,
contrary to the ideal weight tables, the best weight for a 5 foot 9 inch
man in his middle 50's was 198 pounds - more than 40 pounds heavier than
the life insurnace tables suggested was ideal. Indeed, in a series of
studies, Reubin Andres of the U.S. National Institute on Ageing found the
entire notion of ideal weights was nothing more than a statistical
fiction. According to Mr. Andres, none of the scientific studies
supported the claim that individuals with excessive weights of 10% to 30%
had elevated mortality rates. Weight-mortality graphs, Mr. Andres argued,
were not linear as the anti-fat activists argued but rather U-shaped,
with the highest longevity linked to a variety of weights making up the
base of the U.  Alongside Mr. Andre's work was that of Ancel Keys, the
proponent of the cholesterol-heart disease theory, who over 25 years
looked at fat and mortality rates in Japan, Greece, Itality, Yugoslavia,
the Netherlands, Finland and the United States. Published as the Seven
County study in 1980, Mr Keys found the risk of premature mortality due to
excessive weight increased only at the extremes of over and under weight.
Nor have Mr. Key's findings been over-turned with time. A recent study
looking at a group of Europeans from his original data found men with
BMI's of less than 18.5 - that is thin men - had almost twice the
mortality rate of either normal or overweight men, even controlling for
smoking. The study further found that being overweight - a BMI of 25-29.9
- had no effect on mortality and even those men who were obese still had
lower death rates than the thin men.
  Another longitudunal study involving almost two million Norwegians
followed for 10 yearsfound those with BMI's from 26-28 (overweight
according to current standards) had the highest life expectancy, while
those with BMI of 18-20 - normal weight - had a higher risk for premature
mortality than those who were obese with BMI's of 34-36. A similar pattern
was found in a 1996 U.S. study that re-analzed data from previous studies
involving more than 600,000 people. The study found white males with
BMI's in the normal range of 19-21 had the same mortality rate as those
with BMI's of 29-31, which is overweight to obese. Again, for non-smoking
white males, the lowest mortality rate was found with BMI's of 23-29, a
range that includes the overweight.
  But what about that famous claim in the Journal of the American Medical
Association, repeated thousands of times in the media, that obesity
causes 300,000 excess deaths in the United States per year? Here, too,
the risk curve is U shaped, and the data simply does not support the
claims being advanced. Individuals with a "normal" BMI of 20 have the same
mortality risk as those with a BMI of 30 - the obese. Moreover, both
those with normal BMI's and those with obese BMI's have risk higher than
that of someone who is overweight - BMI 25. But then one would never
discover this from reading the author's discussion of their data or indee
reading the headlines about the study.
  A similar junk science treatment is to be found in a 1995 study of
115,000 U.S. nurses, which is, along with the JAMA study, one of the most
frequently used pieces of research to justify the claim that
fat=premature death. Despite the author's claims that even being mildly
overweight increases the risk of premature death, a close analysis of the
data suggest this is not the case. What the study found was that for the
two groups of women who made up more than 80% of the study, those with
BMIs of 19-24.9 - normal - and those with BMIs of 25-31.9 - overweight
and obese - had almost the same mortality rates.
  Given the money to be made and power to be gained from publishing the
obesity epidemic, it is probably unreasonable to hope we might be spared
a costly, intrusive and ultimately unsuccessful war against fat. As the
anti-fat crusaders hit their stride, our only consolation may be in
knowing the fat problem has more to do with junk science than with junk
food.
  John Luik is a health policy analyst.


[Scientists are human as well. In the following abstract, the authors
just could not bring themselves to say that the actual intentional weight
loss itself was not associated with reduced mortality.]

Diabetes Care. 2004 Mar;27(3):657-62
Trying to lose weight, losing weight, and 9-year mortality in overweight
U.S. adults with diabetes.
  OBJECTIVE: The aim of this study was to examine the relationships
between intention to lose weight, actual weight loss, and all-cause
mortality among overweight individuals with diabetes. RESEARCH DESIGN AND
METHODS: We performed a prospective analysis among 1,401 overweight
diabetic adults aged > or =35 years sampled in the National Health
Interview Survey. The previous year intention to lose weight and weight
change were assessed by self-report. Nine-year mortality rates were
examined according to intent to lose weight and weight loss, which were
adjusted for age, sex, education, ethnicity, smoking, initial body weight,
and diabetes complications. RESULTS: Individuals trying to lose weight
had a 23% lower mortality rate (hazard rate ratio [HRR] 0.77, 95% CI
0.61-0.99) than those who reported not trying to lose weight. This
association was as strong for those who failed to lose weight
(0.72, 0.55-0.96) as for those who succeeded in losing weight (0.83,
0.63-1.08). Trying to lose weight was beneficial for overweight (BMI
25-30 kg/m2) individuals (0.62, 0.46-0.83) but not for obese (BMI>30)
individuals (1.17, 0.72-1.92). Overall weight loss, without regard to
intent, was associated with an increase of 22% (1.22, 0.99-1.50) in the
mortality rate. This increase was largely explained by unintentional
weight loss, which was associated with a 58% (1.58, 1.08-2.31) higher
mortality rate. CONCLUSIONS: Overweight diabetic adults trying to lose
weight have a reduced risk of all-cause mortality, independent of whether
they lose weight. Actual weight loss is associated with increased
mortality only if the weight loss is unintentional.

[The authors below say that intentional weight loss probably decreases
mortality rate. Guess what they failed to mention.]

Obes Rev. 2003 Feb;4(1):9-16.
Weight loss causes increased mortality: cons.
Short-term studies indicate that intentional weight loss (IWL) among
obese persons significantly improves health variables that are often
precursors or markers of chronic diseases (e.g. heart diseases, type-2
diabetes). Hence, it is logical to assume that IWL among obese persons
would lead to increased longevity. On the whole, epidemiological studies,
including recent ones that use conservative analytic approaches such as
distinguishing between apparently IWL and unintentional weight loss
(UWL), adjusting for potential confounders and excluding apparently
unhealthy subjects, indicate that apparently IWL appears to neither
increase nor decrease mortality rate. However, it is important to note
that none of the existing studies were designed specifically to test the
hypothesis that IWL reduces mortality rate, and given methodological
problems, these studies do not provide a satisfactory way to address the
body mass index (BMI)-mortality question. Several controlled clinical
trials suggest that IWL may reduce mortality rate. However, even in these
studies, it is important to acknowledge that subjects are randomized to
conditions that produce more or less weight loss and not to distinct
levels of weight loss per se. Nevertheless, while we await additional
data from better designed studies, given our incomplete knowledge, we
conclude that it seems more likely than not that IWL achieved by
medically recommended methods does not increase and probably decreases
mortality rate.

[In the study below the relative mortality risk of chubby BMIs of
23.0-24.9 was 1.0. Somehow the risk of BMIs in the range of 25.0-26.9
failed to be mentioned.]

Int J Obes Relat Metab Disord. 2002 Apr;26(4):529-37.
Under- and overweight impact on mortality among middle-aged Japanese men
and women: a 10-y follow-up of JPHC study cohort I.
  OBJECTIVE: Although obesity is a major health problem in Western
countries, its impact may differ in another culture. This paper examines
the association between body mass index (BMI; kg/m2) and mortality in
Japan, where the mortality profile and BMI distribution differ
substantially from Western countries. DESIGN: The JPHC Study cohort I, a
population-based prospective study in four public health center areas,
started in 1990 and was followed-up to the end of 1999. SUBJECTS: A total
of 19,500 men and 21,315 women aged 40-59 y who submitted their body
weight and height and did not report any serious disease at baseline.
MEASUREMENT: Risk of death by category of BMI. RESULTS: During 10 y of
follow-up, 943 and 483 deaths were documented in the men and women,
respectively. The association between BMI and all-cause mortality was
U-shaped: compared with a category of 23.0-24.9, the statistically
significant elevations in relative risk were observed in both under- and
overweight categories (2.26 in 14.0-18.9, 1.57 in 19.0-20.9, 1.33 in
21.0-22.9 and 1.38 in 27.0-29.9, 1.97 in 30.0-39.9 in men, 1.94 in
14.0-18.9 and 1.91 in 30.0-39.9 in women) after adjustment for possible
confounders and weight change. The U-shaped association did not change
after excluding deaths occurring in the first 5 y of follow-up or even
after excluding subjects who reported a weight loss of 5 kg or more since
20-y-old, or after stratifying subjects by smoking status. CONCLUSION:
Both under-and overweight are important determinants of premature death
among the Japanese population.

[The authors of the below study finally fess-up in the last sentence.]

Int J Epidemiol. 2001 Aug;30(4):777-86
Weight change, body weight and mortality: the impact of smoking and ill
health.
  OBJECTIVES: This paper examines the influence of cigarette smoking and
ill health on the relationship between weight change, body weight and
subsequent mortality to determine whether weight loss and leanness in
middle to older age is deleterious to health. METHODS: Men aged 40-59
years at screening drawn from one general practice in each of 24 British
towns, who completed a questionnaire 5 years after screening (Q5) and
provided full information on changes in weight and smoking status (n =
7065) were then followed up for an average of 13.8 years. RESULTS: In all
men a shallow U-shaped relationship was seen between body mass index (BMI)
at Q5 and all-cause mortality rates. Weight loss and substantial weight
gain (> or =10%) were associated with increased mortality rates compared
to the stable weight group. The increased risk associated with weight
loss was seen in long- term non-smokers (n = 4101) and recent ex-smokers
(n = 722) but not in current smokers (n = 2242) after adjustment for a
wide range of potential confounders. However, the increased risk was
markedly attenuated after exclusion of those with ill health (relative
risk [RR] = 1.16, 95% CI : 0.84-1.59 and RR = 0.79, 95% CI : 0.29-2.20 for
long-term non-smokers and recent ex-smokers, respectively). Moderate
weight gain (4-10%) was associated with lower risk of mortality than
observed in those with stable weight but only in recent ex-smokers and in
current smokers, not in long-term non-smokers. A positive association was
seen between BMI at Q5 and all-cause mortality in non-smokers and this
was strengthened by exclusion of men with weight loss. CONCLUSION: The
increased risk of mortality associated with weight loss or low body
weight in middle-aged and older men appears to be a direct consequence of
ill health leading to weight loss and leanness. In healthy non-smoking
men weight loss and leanness are not associated with increased mortality
and moderate weight gain (4-10%) was neither deleterious nor beneficial.

[Finally we have an abstract, that is not too far off-base!]

Med Sci Sports Exerc. 1999 Aug;31(8):1118-28.
Thinness and weight loss: beneficial or detrimental to longevity?
  This review examined the hypotheses that 1) low body mass index (BMI) is
optimal for longevity and 2) weight loss reduces mortality rates. The
preponderance of epidemiological evidence fails to support either of
these hypotheses. Indeed, a number of studies show that thinness and
weight loss (regardless of initial BMI) are associated with increased
mortality rates. These findings cannot be attributed to smoking status or
to weight loss resulting from subclinical disease. The effect of
intentional weight loss on mortality rates depends upon health status.
For overweight individuals in good health, there is no compelling evidence
to show that mortality rates are reduced with weight loss. Even among
overweight persons with one or more obesity-related health conditions,
specific weight loss recommendations may be unnecessary: 1) the reduction
in mortality rate associated with intentional weight loss is independent
of the amount of weight loss, 2) the reductions in all-cause mortality
rate associated with increased physical activity and fitness (23-44%),
independent of changes in body weight, are greater than that reported for
intentional weight loss (approximately 20%), and 3) many obesity-related
health conditions (e.g., hypertension, dyslipidemias, insulin resistance,
glucose intolerance) can be ameliorated independently of weight loss. In
view of the potential risks associated with weight loss and weight
cycling, it is suggested that public health may be better served by
placing greater emphasis on lifestyle changes and less attention to
weight loss per se.

[Finally we have a cook-the-book classic. In 1980 Walford found that
caloric restriction after weaning was ineffective at increasing the
maximum lifespan of male C57BL/6J mice (186.4 versus 187.4 weeks). The
experiment was repeated in 1982, and lo and behold, it failed to work
again. However another control group with a decreased lifespan was run.
All of a sudden, relative to this new control group,  maximum lifespan
was found to increase by 21%. (32 versus 40 months) Hello increased
funding!]

Science. 1982 Mar 12;215(4538):1415-8.
Dietary restriction in mice beginning at 1 year of age: effect on
life-span and spontaneous cancer incidence.
Weindruch R, Walford RL.
  Lifelong dietary restriction beginning at 3 to 6 weeks of age in rodents
is known to decelerate the rate of aging, increase mean and maximum
life-spans, and inhibit the occurrence of many spontaneous cancers.
Little is known about the effects of dietary restriction started in
middle age. In the experiments now reported the food intake of 12- to
13-month-old mice of two long-lived strains was restricted by using
nutrient-enriched diets in accordance with the concept of "undernutrition
without malnutrition." The mice on the restricted diet averaged 10 to 20
percent increases in mean and maximum survival times compared to the
control mice. Spontaneous lymphoma was inhibited by the food restriction.

Exp Gerontol. 1980;15(4):237-58.
Survival and disease patterns in C57BL/6J mice subjected to undernutrition.
Cheney KE, Liu RK, Smith GS, Leung RE, Mickey MR, Walford RL.

[In a few humans, caloric restriction has been implimented  as an
middle-aged-onset intervention. The rationale for this self-induced
anorexia is that adult-onset CR in mice and rats retards their aging, and
extends their lifespan. This sounds reasonable, except that the premise
unfortunately, is based more on myth than reality.]

Aging (Milano). 1995 Apr;7(2):136-9
Is late-life caloric restriction beneficial?
Caloric restriction initiated in young mice and rats results in increases
in mean and median life span. When caloric restriction is implemented in
older animals, an increase in life span is still observed; however, the
magnitude of the increase is not as great as that observed in animals
calorie restricted since they were young. Here we report the results of a
pilot study in which caloric restriction was initiated in mature, older
rats. Survival rates and terminal pathology were characterized and
compared between a cohort of 17 continually ad libitum fed Long Evans
rats and a cohort of 18 Long Evans rats, which were gradually introduced
to 33% restriction in diet consumption at 18 months of age. No difference
in the median life span was observed between the two groups. The data
suggest there may be a level of maturity, or a stage in the aging
process, after which caloric restriction no longer increases longevity.

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