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Ann. Rev. Med. 1981. 32:221-31

Copyright © 1981 by Annual Reviews Inc. All rights reserved

THE PROBLEM OF OBESITY .7394

Faith T. Fitzgerald, M.D.

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Department of Medicine, University Hospital, University of Michigan,

Ann Arbor, Michigan 48109

INTRODUCTION

Any physician who cares for patients recognizes the painful problem of
obesity. It is estimated that 25--45% of the American population over 30
years of age is "overweight" (1). Doctors see obesity in the clinic,the office,
the hospital, and on the street. And even if we avoid direct patient involve­
ment by engaging in nonclinical activities, we still worry about it in our­
selves and in our families.
Examination of the scientific and lay literature about obesity finds it
predominantly echoing Ayer's statement of over 20 years ago: "Practically
everyone will agree that obesity is the number one health problem to­
day. . . ." (2). But are there well-established data that support this pro­
nouncement? Is there a firm scientific foundation to the national, almost
obsessive, opposition to fatness? Is the medical community, in particular,
justified in its continuing efforts to promote weight reduction among the
obese?
This review presents three theses for your consideration. The iconoclastic
views that are suggested are hardly new, nor do they lack for substantial
evidence. They are:
1. Obesity, as we commonly use the term, may be more an aesthetic and
moral problem than one of physical health (3-5).
2. The therapy of obesity may be, in some circumstances, more morbid
than fatness (6-11).
3. There may be some advantages, in medical and other senses,to being fat
(3).

MORAL PROBLEMS

What do we mean when we say someone is obese? By some criteria, up to

60% of Americans aged 40-60 years are over their "best weight" by more
221
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 222 FITZGERALD

than 10% (12). One third of our nation's people are said to be more than
20% over their "ideal weight" (1). Yet a state cannot be called abnormal
in any statistical sense if it is characteristic of so large a number of the
population under study. It would seem to call for a redefinition of what is
normal.
Obesity has also been defined as a state of excess body fat. Studies by
cadaver analysis showed the "average" young man to possess 15% of his
total body weight as fat, and the "average" young woman 25%. (13). But
these percentages come from a total of but eight cadavers (14),which casts
doubt on their universal applicability. Moreover, this sort of analysis is
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obviously impractical in the doctor's office and of little aid to the individual
physician trying to diagnose obesity in the individual patient. Assessment
of body density, and thus of the proportion of fat to lean by the Ar­
chimedian method of immersion and water displacement (15, 16) suffers
from inaccuracies of method (3, 14) and is too cumbersome and sloppy a
technique to use in clinic. Isotope or chemical dilution studies of fat and
volumes of distribution are best suited to research laboratories (17, IS).
Anthropomorphic measurements used in studies of large populations of
fat people use skin-fold thicklless, height-weight ratios, ponderal indices,
and the like, all compared to arbitrary normals (14). For practical purposes,
the most frequently cited criteria for normal weight refer to height-weight
comparisons for each age and sex category (19). These charts are generally
based on the Society of Actuaries report of 1959, which analyzed persons
insured from 1935 to 1953 and showed a linear relationship between over­
weight and excess mortality. In this survey, the aggregate mortality for men
and women more than 20% overweight was found to be about 150% that
of the insured population of average weight (19).
It has been argued, however, that these insurance data are seriously
flawed (20-22). Lower socioeconomic classes,which tend to be heavier, are
less likely to be insured. The health awareness and performance of the newly
insured population may be unusual. Height and weight estimates of this
group were notoriously bad; moreover, the insurance data do not consider
body weight in terms of adiposity,but only of raw weight in relation to age,
height,and sex. There is no distinction between those who were heavy with
muscle and those burdened with fat. These same data could be used to label
body building as a major health hazard.
A recent review compares these actuarial data with six other epidemi­
ologic studies. The results are strikingly different. There may actually be a
negative relationship between body weight and mortality. The obese, in
some age categories, may live longer than the lean (23).
Most physicians do not habitually use reference charts and probably
could not quote the ideal weight for a 5 foot-5 inch woman in 2-inch heels
 OBESITY 223

with medium frame. Most doctors, like most lay people, diagnose obesity
by eyeball analysis. Well-established experts in the field of obesity are
untroubled by recommending superficial observation (12) or the "mirror
test" (14}-100king at one's naked body in the mirror (24}-as a reasonable
way to estimate obesity. Do the patients seem fat to us? Then fat they are.
And in this method of diagnosis we are biased by culture: What an Ameri­
can fashion model calls chubby a Russian grandmother considers patholog­
ically thin.
Self-perception of obesity is common in our weight-conscious society. In
one sample of 500 Californians, 32% of the men and 46% of the women
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described themselves as too heavy (14). This is generally perceived as a

perjorative, and can be potentially harmful.
Because of the cultural equation of beauty with goodness, the aesthetic
aspects of overweight blend into the moral. A fat man says, "Just looking
at myself in a store window makes me feel terrible. It has gotten so that I
am very careful not to look by accident. It's a feeling that people have a right
to hate me and hate anyone who looks as fat as me. As soon as 1 see myself,
1 feel an uncontrollable burst of hatred. 1 just look at myself and say, 'I hate
you: you're loathesome' " (25).
It is clear from reading magazines or watching television that public
derision and condemnation of fat people is one of the few remaining sanc­
tioned social prejudices in this nation freely allowed against any group
based solely on appearance. Personality profiles of obese adolescent girls
show that they respond very like oppressed minorities in their acceptance
of dominant values in the culture and their passive withdrawal (26). It has
been documented that all of us-the general public, social workers, employ­
ers, graduate schools admissions officers, nurses, and physicians-feel nega­
tively toward the obese (4, 27-29). Obesity is a moral crime and one of the
few remaining sinful diseases: one is fat because of "weakness of the will"
(30). The fat are denied jobs, promotions, educational opportunities (14),
and, recently, challenged in their right to adopt a child until they lose
weight (31).

MEDICAL PROBLEMS

Are we as a profession justified in shaming the fat into losing weight, in

promising them an improved state of health if they do? Why is being fat
bad for you?
There are three major categories of physical risk associated with obesity:
(a) the increased mechanical burden of obesity; (b) the dangers of increased
food intake, or of the "wrong sort" of food; and (c) the miscellaneous
complications and associations of obesity.
 224 FITZGERALD

Increased Mechanical Burden

In this category are those disorders attributed to the stresses placed by extra
pounds upon the skeletal frame and cardiovascular system of the fat person.
Degenerative joint disease is accelerated by obesity, especially marked in
the spine, knees, ankles, and hips. This is probably mediated by the trauma
of increased weight-bearing (24, 32). Many modem sports may be shown
to have this same effect.
Respiratory compromise is held to be common in the fat. Certainly,
dyspnea is a common symptom among the obese. This has been attributed
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to an increased oxygen demand (33, 34), increased intraabdominal pressure

with decreased diaphragmatic activity (35), and the increased work of
breathing occasioned by the mass of the fat thorax (36). Other investigators
have described upper airway obstruction (37) and a decreased sensitivity to
carbon dioxide (38) or oxygen (39, 40). But there is no good correlation
between the presence or severity of dyspnea or alveolar hypoventilation and
the body weight (39, 41). The physiologic responses of the respiratory
system to weight loss are variable and ill explained (36, 42-44). The Pick­
wick syndrome (43) may occur in massive obesity, of course, and is proba­
bly due to a combination of mechanical and central nervous system factors.
Much more work is necessary on sleep apnea in the lean (45) before any
definitive statements can be made about its relationship to fatness.
Cardiomegaly occurs in the obese (41, 46). There is evidence that the
cardiac enlargement of the obese is roughly proportional to the increase in
body mass. This is associated with an increased blood volume and an
increased cardiac output, which are also proportionate to the increased
tissue mass (46, 47). In the moderately obese, this "work. hypertrophy"
might be the fat person's equivalent of exercise-induced cardiac enlarge­
ment, an "athlete's heart" (46). Whether the "athlete's heart" is a good or
a bad thing remains controversial even in athletes (48). "Fatty heart," or
degenerative intramyocardial fat droplets, are not present in the obese as
a rule. There may be increased subepicardial fat and fat between myocardial
muscle bundles in the very obese, but the clinical significance of this finding
is uncertain (46, 49).
Surgery is more dangerous in the obese because of mechanical and anes­
thetic-respiratory difficulties (50, 51). There may also be a problem of
delayed diagnosis of intraabdominal disease because of the increased diffi­
culty of adequate physical examination.

Increased Food Intake

It should be noted that fat people do not continually gorge themselves. If
they did, they'd perpetually gain weight. An obese individual may gain by
 OBESITY 225

"overeating" but,having achieved a stable weight level,will take in as many

calories as are necessary to support that weight at any given level of exer­
cise. There are data showing no marked difference in the caloric intake of
a cohort of stable obese people from that of a group of normal weight (52).
If a fat person exercises very little, he or she may actually eat less than a
very active lean person (53).
It has been proposed that the fat are ruled by appetite-the titillation of
the taste, smell, or appearance of food-more than they are by hunger
(54-57). If this is true, they may be attracted to good-tasting foods such as
sweets and animal fats more than the lean individual: they may have a
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proportionately greater intake of delicious but "unhealthy" foods.

Coronary vascular disease and its relationship to obesity has stimulated
much interest, conflict, and controversy. There is evidence from the Fra­
mingham study that angina and sudden death are more common in the
obese (58) with an effect that varies with age. A number of other epidemi­
ologic studies have demonstrated little influence of obesity alone on the
development of coronary heart disease (59-61). It appears that obesity
alone,in the absence of hypertension or hypercholesterolemia,is not a risk
factor for atherosclerotic coronary heart disease. If either or both conditions
are present, however, risk is magnified by obesity (58,62). There is a better
correlation between positive caloric balance and high serum lipid levels (63)
than between stable obesity and serum cholesterol levels (59, 64). Since a
large number of fat people go through cyclic diets and refeeding, this
potential risk of hypercholesterolemia during refeeding raises the theoreti­
cal possibility that diet therapy, with an almost invariable recidivism to
obesity, may be risky.
Gallstones afDict the fat. Saturation of gallbladder bile with cholesterol
(rendering it more lithogenic) is greater in the obese, and is decreased at a
stable reduced weight (65). The active phase of weight reduction, however,
may actually transiently increase the risk of gallstones, since fasting in­
creases the saturation of gallbladder bile (66). Once gallstones are present,
there is no evidence they are ameliorated by weight loss.

Miscellaneous Complications
Hypertension is one of the most commonly cited concomitants of obesity
(67). Though some studies show only slight association of obesity with
blood pressure elevation (59), the obese are probably at higher risk for
hypertension than the lean. The degree of obesity is not well correlated with
the severity of hypertension (41,59),and increased pressures associate more
with body weight and shape than with adiposity per se (68). Since hyperten­
sion and obesity may be genetically rather than causually related, it remains
to be demonstrated that sustained weight loss leads to a sustained decrease
 226 FITZGERALD

in hypertension or its complications. Though a number of studies show

diminution of blood pressure in a significant number of patients (14) when
they lose weight (67,69),the mechanism of the hypotensive effect of weight
loss remains controversial, the degree variable, and the effect on prognosis
obscure (3, 14).
The relationships between elevations in blood pressure and obesity obvi­
ously need further study. What we do know at present suggests that weight
loss, often impossible for the patient, ought not to be a prerequisite by
physicians for the institution of antihypertensive medications (70).
Diabetes mellitus is held to be a major feature of obesity. A difficulty in
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the interpretation of epidemiologic data is in knowing what is meant by

"diabetes" in each study. There is a difference in the glucose tolerance
curves of the fat compared to the lean, and this difference is lessened by
weight loss (71-74). What this means is not immediately evident,since the
"normals" for the standard glucose tolerance curves were established in
lean young people and then applied to the obese and elderly (75). If diabetes
mellitus is defined only by a glucose tolerance curve that differs from those
in the lean, then many fat people are "diabetic." Yet there is no good
evidence that microvascular diabetes is increased in the fat, nor that angi­
opathy is improved by weight loss. It is also clear that the obese differ from
genetic diabetics in that circulating insulin increases as obesity increases
(74).
Though one may argue that "decreased" glucose tolerance in the obese
is normal for their weight, it would still seem prudent to advise attempts
at weight reduction in those patients who have glycosuria, increased infec­
tions, cataracts, or neuropathy.
Gynecologic and obstetric influences of obesity assume added significance
in that most obese people are women (76). Obese women may be at in­
creased risk for certain complications of pregnancy, including glucose intol­
erance, hypertension, and thromboembolic disease (77). The detrimental
effects of maternal starvation on fetal well-being are such, however, that
obese pregnant women are not advised to lose weight during pregnancy,but
rather to gain proportionate to their stage of pregnancy much as any
nonobese woman would (78).
Obesity in women is associated with menstrual irregularities (79).
Whether this is due to periodic dieting, the emotional stresses of obesity,
or a fundamental disturbance of endocrine function in the fat woman is not
yet apparent. A relationship between teenage obesity and endometrial car­
cinoma (80) requires further elucidation.
Hyperuricemia and gouty arthritis are increased in the obese and decline
with weight loss (81,82). In assessing hyperuricemia,especially in the obese
 OBESITY 227

woman, the clinician should take care to exclude thiazide diuretics (an
ingredient of some diet pills) as contributory to the increased serum urate
(82).
Nephrotic syndrome has been reported in four patients with massive
obesity (83). What significance this has to the less-than-massively obese is
uncertain.
Fatty liver may occur in fat people. A recent study (84) demonstrates
fatty hepatitis, fatty fibrosis, and fatty cirrhosis in 29 overweight patients
referred for study of hepatomegaly or abnormal liver functions. The ques­
tion of the prevalence of fatty liver disease in the obese population not
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selected for evident hepatic dysfunction was not addressed. Moreover,while

the 29 patients were questioned concerning potential hepatotoxic illness,
alcohol, or drug abuse, none were evidently questioned about their diets.
Since the obese frequently fast in attempts to lose weight, and since starva­
tion causes fatty hepatopathy and cirrhosis, it again becomes questionable
whether the obesity or its therapy was responsible for the perceived morbid­
ity.
Psychological stresses are commented upon in many discussions of
obesity (3-5,15,25-31). Might social attitudes concerning the obese actu­
ally create or contribute to some of its morbidity? Stress has been convinc­
ingly argued to have major influence on heart disease and cancer,
cerebrovascular and circulatory disease (85). It is with these same morbid
states that obesity is said to correlate. More study is called for, since, if we
do stress our patients by categorizing them as diseased, we may be con­
tributing to their disease. Perhaps our major thrust in therapy should be to
change attitudes about the obese rather than their shapes.

THE V ALUE OF THERAPY

In extreme, life-threatening,or immobilizing obesity,extreme measures are

surely acceptable. But unnecessary dieting in mild to moderately fat people
may kill them (7, 11). The multitude of complications reported from intesti­
nal bypass surgery (6) make it inappropriate for most, if not all patients,
and certainly unwarranted for cosmetic reasons alone. Addiction was (and
perhaps still is) a major danger of the use of amphetamine in the therapy
of obesity (86). What contribution the more potent amphetamines may have
made to the increased blood pressure and possible heart disease of the obese
has not been well explored.
A relatively infrequently addressed but highly significant complication of
the therapy of obesity is the financial morbidity incurred by fat individuals
and the nation. It is conservatively estimated that Americans spend over 10
 228 FITZGERALD

billion dollars a year in reduction schemes of one sort or another (14). Diet
foods, machines, exercises, spas, camps, clinics, pills, and corsets may drain
thousands of dollars from the individual fat man or woman. What do they
get for this money? Not much. it seems. Estimates are that 75-95% of all
schemes for weight reduction fail (87). Even if the patients do lose weight,
they rapidly regain it. And in the successful 5-25%, we really don't know
what's been gained so far as health is concerned. The irony is that the
therapy of obesity is generally so ineffectual that clinical studies relating
weight loss to the relief of conditions in which obesity is implicated as
pathogenic are nearly impossible to do (3).
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It seems reasonable that one should try to treat obesity when we treat the
degenerative joint disease, dyspnea, hyperglycemia, congestive heart failure.
angina, or hypertension of the obese. But should we frustratingly insist on
weight loss in the nonhypertensive asymptomatic obese patient?

THE ADVANTAGES OF OBESITY

The recent review of epidemiologic studies that suggested decreased mortal­

ity among the obese (13) logically raises the question of a possible selective
advantage to obesity. Data exist suggesting that fat people may have better
survival with cancers and tuberculosis than do the lean (14). Surprisingly,
the obese also commit suicide less frequently (14). There are psychiatric
testing studies which maintain that the obese may be better problem solvers
and more perceptive receivers of external stimuli than the lean (55).
A well-adapted animal has the ability to store fat during periods of
abundant food supply in preparation for the inevitable intervals of famine
(88). It may be, then, that the prevalence of obesity in the United States is
due to the conjunction of millions of years of evolutionary thrust with a
remarkable sufficiency of food available at minimal exertion. The fat may
be the most highly evolved among us. And should food become scarce
through natural disaster, war, or shortages of energy, the fat may be the
most likely survivors.

SUMMARY

In view of the conflicting data, the patent cultural biases under which we
labor, and the possible harmful effects of therapy, it seems best that physi­
cians examine the problems of obesity with the same keen scepticism and
science they apply to other unsettled issues. To treat disease in the obese
is obviously good. To treat simple obesity as a disease may be another
matter entirely

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