O Nutrition and Health

One hypothesis suggests the ability to store excess calories as fat in adipose
tissue was useful during prehistoric times as a protection against food
shortages. However, this ability later became a handicap in industrialized
societies. The industrial revolution allowed food to be available consis-
tently and reduced the physical effort needed to obtain, process, and
prepare it. Increased control of infectious diseases, modern transportation,
and increasingly sedentary patterns of work and recreation contributed to
the presence of the current high level of obesity in the United States.

Moderate obesity was considered a sign of health in this country until the
present century, and many societies still consider it healthy. The positive
attributes of body fat were extolled by early fertility symbols (e.g., the
Venus of Willendorf from prehistoric times), by the ancient Greeks, and by
Shakespeare. On the other hand, Dickens described the association of
extreme obesity with poor health in the character of Mr. Pickwick, who
suffered from the cardiorespiratory syndrome that now bears his name.
These concerns eventually led life insurance companies to develop and use
rate structures based on tables of body weight-for-height (Rittenbaugh
1982).

Widespread interest in studying body fat (adipose tissue) was stimulated by
the publication in 1940 of “Adipose Tissue: A Neglected Subject” (Wells
1940). A subsequent prophetic observation correlated the distribution and
size of body fat cells with the development of atherosclerosis: fat cells
concentrated in the trunk region were more likely to be linked to heart
disease than were those on the arms or legs (Bjurulf 1959). In 1965, the
American Physiological Society published a large compendium of informa-
tion on adipose tissue that is still a good source of information (Renold and
Cahill 1965).

The first data using weight tables to predict life expectancy were collected
by the life insurance industry in 1913 (Association of Life Insurance
Medical Directors and Actuarial Society of America 1913), but tables of
ideal or desirable weight did not appear until the Metropolitan Life Insur-
ance Company published its first tables of ideal or desirable weight in the
1940’s (Simopoulos and Van Itallie 1984). Concurrently, modern epi-
demiologic techniques began to identify obesity as a risk factor for some of
the major diseases of modern times: cardiovascular disease, diabetes,
hypertension, and cancer. The most recent epidemiologic data on obesity
as a health hazard were the subject of a national conference (NIH 1985) and
are reviewed in this chapter.

276
Obesity O

Significance for Public Health

Obesity is one of the most prevalent diet-related problems in the United
States. It affects about 34 million adults ages 20 to 74 (NCHS 1987), with
the highest rates observed among the poor and minority groups (Van Itallie
1985; Van Itallie and Abraham 1985). :

Population data for heights and weights (and, ‘therefore, obesity) among
Americanis derive from three national surveys: the National Health Exam-
ination Survey (NHES I) of 1960-62 (DHEW 1964), the first National .
Health and Nutrition Examination Survey (NHANES I) of 1971-74
(DHEW 1973), and NHANES II of 1976-80 (McDowell et al. 1981; NCHS
1987). In addition, data are available from the Framingham Heart Study
(Hubert et al. 1983) and from the American Cancer Society Study of
1959-62 (Lew and Garfinkel 1979). ,

The 1971-74 NHANES found that 23.7 percent of men and 26.0 percent of
women ages 20 to 74 were overweight. These figures were based on a
definition of overweight that included persons whose weights met or
exceeded the 85th percentile of the body mass index, or BMI (weight in
kilograms divided by height in meters squared for men, and for women,
divided by height to the power 1.5) for individuals ages 20 to 29. The BMI is
discussed in more detail below. Because body weights increase with age,
population rates of overweight that have been reported for adults ages 25 to
74 (and age-adjusted) are higher—26.0 percent of men and 29.4 percent of
women (NCHS 1986).

NHANES II reported 25.6 percent of Americans ages 20 to 74. as over-
weight. Age-adjusted rates for blacks (36.6 percent) exceeded those for
whites (24.6 percent), and those for females of all races (26.7 percent)
exceeded those for males (24.4 percent). Although the rate for black males
(26.3 percent) was only slightly higher than that for white males (24.4
percent), the rate for black females of 45.1 percent was highest of all—
almost twice that of the 24.6 percent for white females (NCHS 1987). Rates
of obesity in the United States appear to be higher than those observed in
England, Canada, or Australia, at least among certain age groups (Bray
1985; Millar and Stephens 1987). The reasons for these differences have not
been established.

The peak overweight rates for men occur from ages 35 to 64, whereas rates
for women continue to increase throughout the ages in which they are

277
ie Nutrition and Health

measured. The percent of adults classified as overweight increases from a
low of 5.5 percent among black males ages 20 to 24 to a high of 61.2 percent
among black women ages 45 to 54 (NCHS 1987).

NHANES II data also identified individuals at or above the 95th percentile
BMI for a reference population ages 20 to 29. By this criterion, 9.3 percent
of all Americans were classified as severely overweight, with the rate for
blacks (15.5 percent) almost twice that for whites (8.8 percent). Here too,
rates for females (10.6 percent) were higher than for males (8.0), with a
much higher prevalence among black females than among white females
(19.7 and 9.6 percent, respectively). The highest prevalence of severe
overweight was the 26.3 percent observed among black females ages 35 to
44: the lowest was the 3.4 percent rate seen in white females ages 20 to 24
(NCHS 1987). When adjustments were made for differences in age dis-
tribution among populations between surveys, the age-adjusted propor-
tions of men and women severely overweight (95th percentile by BMI) in
1976-80 significantly exceeded those in 1961-62 (Van Itallie and Abraham
1985).

The influence of poverty on the prevalence of overweight in women has
been established. For example, in the 45 to 54 age range, 54.1 percent of
poor women were overweight compared with 32.5 percent in the general
female population (Van Itallie 1985).

Severe overweight increases the risk for high blood cholesterol, high blood
pressure, and diabetes and, hence, for diseases for which these conditions
are risk factors (see chapters on diabetes, coronary heart disease, high
blood pressure, neurologic disorders, and kidney diseases). It also in-
creases the risk for gallbladder disease (see chapter on gastrointestinal
diseases) and for some types of cancer (see chapter on cancer). Its psycho-
social consequences are significant (see chapter on behavior). The great
prevalence of obesity and its physical and mental health consequences
suggest that its prevention should be a high public health priority.

Perhaps for these and other reasons, many Americans try to lose excess
weight. According to data from the 1985 National Health Interview Sur-
vey, 27 percent of males and 46 percent of females were trying to lose
weight by reducing caloric intake, increasing physical activity, or both
(Stephenson et al. 1987). The health consequences of these activities are
also of public health concern and are reviewed in this chapter.

278
Obesity |

Key Scientific Issues

@ Definition of Obesity

@ Health Consequences of Obesity
@ Causes of Obesity

@ Treatment of Obesity

Definition of Obesity

An ideal, health-oriented definition of obesity would be based on the
degree of excess body fat at which health risks to individuals begin to
increase. No such definition currently exists. Instead, the most commonly
used methods estimate body fat as a percentage of total body weight
(underwater weighing), establish an index of body fat level (skinfold thick-
ness or waist-to-hip circumference measurements), compare weight-for-
height measurements (height and weight tables), or compute an index of
body weight as a function of height (BMI) in reference to population
standards.

Much of the scientific disagreement about the level of body fat associated
with increased health risks to individuals or to populations can be at-
-ributed to the difficulties in measuring body fat content and in defining
dverweight and obesity. Even underwater weighing, which measures body
‘at as a percent of total body weight and which is too cumbersome and
2xpensive to use in population studies, can produce inaccurate results
Barnes 1987). The easily available measurements of heights, weights, and
skinfold thicknesses, which are more frequently used in epidemiologic
itudies for assessing obesity and its effects, can be even less accurate.

Reference Body Weight Standards

An ideal body weight-for-height based on minimal health risks has not yet
seen defined for either individuals or populations. Instead, weight-for-
1eight is usually compared with standards based on survey populations.
The accuracy of such determinations, therefore, depends on the size and
ype of the reference population, as well as on the precision and appropri-
iteness of the measures used.

deight and Weight Tables. The reference standards most commonly used
0 define obesity are those based on actuarial data from the Metropolitan

279
O Nutrition and Health

Life Insurance Company (MLIC), in which “desirable” or “ideal” weight is
the weight-for-height of insured persons with the longest lifespans. The
original 1949 tables were revised in 1959 (MLIC 1959) based on the Build
and Blood Pressure Study of 1959 (Society of Actuaries 1960), and again in
1983 (MLIC 1983) based on the Build Study of 1979 (Society of Actuaries
and Association of Life Insurance Medical Directors of America 1980).

Tables of heights and body weights derived from several studies are given in
Table 6-1. These tables present ranges of weight-for-height associated with
the lowest mortality rates. The midpoint of the range is usually used as the
standard for ideal or desirable weight. As seen in Table 6-1, Metropolitan
desirable weights of 1983 are higher than those for 1959 in nearly all height
categories but especially in those that are shorter. Both sets of data present
as “desirable” body weights that are significantly lower than average
weights measured in population surveys.

Relative Weight. Relative weight refers to actual weight as a percent of the
desirable weight defined in the tables. A relative weight of 100 would thus
be a desirable weight. As commonly used, a relative weight of 120 percent
of that desirable is considered overweight, and relative weights of 140
percent or more are considered severely overweight (NIH 1985; Foster and
Burton 1985). The desirable weights were slightly more liberal in the 1983
Metropolitan tables than in the 1959 tables, particularly for persons of short
stature; weights for the shortest men in the 1983 table were heavier by 12 Ib
and for the shortest women by 14 Ib.

These tables are handicapped by major flaws in the data from the studies on
which they are based. For example, the tables present heights and weights
with shoes and clothing but whether heights and weights were obtained
with or without clothes and shoes was not consistent. The data for the
Metropolitan tables were drawn from persons who could afford life insur-
ance and were predominantly white and from middle-class males of young
and middle age; thus, they were not necessarily representative of other
groups. For these and other reasons, some experts believe that these tables
are limited in value (Knapp 1983).

Body Mass Index. Ratios of weight to height estimate total body mass
rather than fat mass, but they correlate highly with amount of body fat
(Revicki and Israel 1986). The most commonly used ratio is known as
Quetelet’s index, or the BMI, and is usually defined as body weight in
kilograms divided by the square of the height in meters (wt/ht?). A simple
nomogram to facilitate calculation of the BMI is given in Figure 6-1. In

280
Obesity )

population studies such as NHANES, this index is modified to reflect body
composition differences between men and women.

A great advantage of such an index is the capability to evaluate and
compare not only individuals but populations or subgroups within popula-
tions. Thus, various experts have recommended that the degree of obesity
be defined by the BMI and have established reference standards for its use.
These standards were derived from the same studies used to construct the
Metropolitan tables. The BMI equivalent to a relative weight of 100 was 22
kg/m? for men and 21.5 kg/m? for women (Simopoulos and Van Itallie
1984). Table 6-2. shows the equivalent body mass indices derived from the
three reference populations in common use: the 1959 and 1983 Metropoli-
tan tables of desirable weights (MLIC 1959, 1983) and the 1976-80
NHANES (NCHS 1987). The indices in Table 6-2 are translated from the
85th and the 95th percentile weight distribution of NHANES II and from
the 120 percent and 140 percent overweight cutoff points of the Metropoli-
tan tables of 1959 and 1983. These indices are in rather close agreement.
While some experts suggest that the body mass indices based on the 1959
Metropolitan tables, 26.4 for men and 25.8 for women, be considered the
upper limits of normal weight (NIH 1985), others favor the higher levels
derived from the more rigorous national probability sample of NHANES II
(NCHS 1987).

The term overweight rather than obesity is used in this discussion because,
although the BMI correlates highly with body fat, it does not distinguish
between body fat and lean body tissue. While excess fat tissue is generally
assumed to account for the additional weight and, therefore, the additional
mortality among overweight individuals, excess weight can also include
lean body mass (which weighs more than fatty tissue) (Van Itallie 1985;
Forbes and Welle 1983) or a larger body frame size (Simopoulos and Van
Itallie 1984). Such problems limit the use of the BMI as a standard for
health risk (Garn, Leonard, and Hawthorne 1986). Its clinical significance,
discussed below, has also been questioned (Callaway 1984).

Body Composition. Careful measurements of skinfold thickness made with
calipers generally correlate well with body fat content. The sums of the
scapular and triceps skinfolds that correspond to the 85th percentile of the
NHANES II population were 45.5 mm in men and 70.1 mm in women (Van
Itallie 1985). The lean body mass (or fat-free weight) can be calculated as
the difference between total body weight and the weight of adipose tissue
estimated from skinfold thickness or other methods. Elbow breadth and
wrist circumference may be useful indicators of body frame size (Si-
mopoulos and Van Itallie 1984).

401
Table 6-1
Comparison of Metropolitan Desirable Weights With Average Weights
From U.S. Cohort Studies

 

Average Weight for Age 40-49 y, kg (Ib)

 

Insured Lives
Metropolitan Tables@ (Medium Build and Blood
Frame), Weight in Kilograms pressure Study Build Study

 

American Cancer Health and Nutrition

Height (Without Society Study Examination Survey

 

WOH PuE CONLIN Fy

78Z

 

Shoes), cm (ft (Pounds) (Without Clothing) 19596 1979> 1979¢ (HANES I, 1979)¢
in) 19598 1983 (1935-1953)e (1950-1971) (1959)¢ (1971-1974)e
Men
156 (5 1) 50-55 (111-122) 57-62 (126-136) 60 (133) 61 (135) _ _
159 (5 2) 52-57 (114-126) 58-63 (128-138) 62 (137) 63 (139) 67 (148) 66 (145)
162 (5 3) 53-59 (117-129) 59-64 (130-140) 64 (141) 65 (144) 68 (149) 68 (150)f
164 (5 4) 54-60 (120-132) 60-65 (132-143) 66 (145) 68 (149) 69 (153) 73 (162)
167 (5 5) 56-62 (123-136) 61-66 (134-146) 68 (149) 69 (153) 71 (156) 72 (159)
169 (5 6) 58-64 (127-140) 62-68 (137-149) 70 (154) 72 (158) 73 (160) 75 (166)
172 (57) 59-66 (131-145) 64-69 (140-152) 72 (158) 73 (162) 74 (163) 78 (173)
174 (5 8) 61-68 (135-149) 65-70 (143-155) 73 (162) 76 (167) 77 (169) 79 (174)
177 (59) 63-69 (139-153) 66-72 (146-158) 76 (167) 78 (171) 78 (173) 79 (175)
179 (5 10) 65-72 (143-158) 68-73 (149-161) 78 (171) 80 (176) 80 (177) 83 (184)
182 (5 11) 67-74 (147-163) 69-75 (152-165) 80 (176) 82 (181) 83 (182) 85 (188)
185 (60) 68-76 (151-168) 70-77 (155-169) 82 (180) 85 (187) 85 (187) 88 (194)
187 (6 1) 0-78 (155-173) 72-78 (159-173) 84 (185) 87 (192) 87 (192) 92 (203)
190 (6 2) 73-81 (160-178) 73-80 (162-177) 86 (190) 90 (198) 90 (198) 92 (203)
192 (6 3) 75-83 (165-183) 75-83 (166-182) 89 (196) 92 (203) 92 (203) —
£87

Women

146 (4 9) 43-48 (94-106) 48-54 (106-118) 54 (120) 52 (115) _ 58 (127)f
149 (4 10) 44-49 (97-109) 48-54 (106-120) 56 (123) 54 (118) 52 (115) 59 (131)f
151 (4 11) 45~51 (100-112) 50-56 (110-123) 57 (126) 54 (120) 55 (421) 62 (136)
154 (5 0) 47-52 (103-115) 51-57 (112-126) 59 (129) 56 (124) 57 (126) 64 (141)
156 (5 1) 48-54 (106-118) 52-59 (115-129) 60 (132) 57 (126) 58 (128) 63 (138)
159 (5 2) 49-55 (109-122) 54-60 (118-132) 62 (136) 59 (130) 60 (132) 64 (141)
162 (5 3) 51-57 (112-126) 55-61 (121-135) 63 (139) 60 (133) 62 (136) 67 (148)
164 (5 4) §3~59 (116-131) 56-63 (124-138) 65 (143) 62 (136) 63 (139) 68 (151)
167 (5 5) 54-61 (120-135) 58-64 (127-141) 67 (147) 64 (140) 64 (142) 71 (156)
169 (5 6) 56-63 (124-139) 59-65 (130-144) 68 (151) 65 (144) 66 (146) 71 (156)
172 (5 7) 58-65 (128-143) 60-67 (133-147) 70 (155) 67 (147) 68 (150) 72 (158)
174 (5 8) 60-67 (132-147) 62-68 (136-150) 73 (160) 70 (152) 71 (156) 78 (172)
177 (5 9) 62-68 (136-151) 63-69 (139-153) 75 (165) 70 (155) 73 (161) _

179 (5 10) 64-70 (140-155) 64-71 (142-156) 77 (170) 72 (159) 75 (165) _—

 

@Not age specific: 1959 tables recommended for ages 25 and older; 1983 tables for ages 25 to 59 years.
bWithout shoes or clothing.

cValues are means for age groups 40 to 44 and 45 to 49. Self-reported heights without shoes and weights with indoor clothing.

dValues are means for age groups 35 to 44 and 45 to 54. Measured without shoes; clothing ranged from 0.20 to 0.62 Ib (not deducted from
weights shown).

eYears when measurements taken.

fEstimated values obtained from linear regression equations.

Source: Manson, J.E.; Stampfer, M.J.; Hennekens, C.H.; and Willett, W.C. 1987. Body weight and longevity. A reassessment. Journal of the
American Medical Association 257:353-58. Copyright 1987, American Medical Association, reprinted with permission.

5 Aus3qQ
Ld Nutrition and Health

Weight Height
kg lb Body cm_ in
so Mass 1
ode Index er
300 =
120 ya [wt/(ht)2] 130
120-360 70 qT
110-F 949 60 wer
100-220 50 140-55
95 +
=e wd
85 40 Women “0 Men +
oe E170 1907
*s ‘a0 Obese - Obese 4-60
—_—
150 : q
: Vv q
+140 Overweight _Overweight_ 160
60+ 439 A +
cceptable J
55-120 Acceptable 20 P > +*
170
50-110 4
175
45 100 4-70
95 180.
40 90 +
85 185}
80 10 +
3 190-4.
5 75 L 75
70 195
30-65 200-4.
60 20st”
25-55 210
“85

Figure 6-1.

 

 

 

 

 

 

A nomogram for determining body mass index (BMI). To
use this nomogram, place a ruler or other straight edge
between the column for height and the column for weight
connecting an individual's numbers for those two variables.
Read the BMI in kg/m* where the straight line crosses the
middie tines when the height ang weight are connected.
Overweight: BMI of 25-30 kg/m“; obesity: BMI above 30
kg/m“. Heights and weights are without shoes or clothes.

Source: Bray, G.A. 1985. Obesity: definition, diagnoses and disadvantages.
The Medical Journal of Australia 142:S2-S8. Copyright 1985,
The Medical Journal of Australia, reprinted with permission.

284
Obesity @)

Table 6-2
Body Mass Index (kg/m?) Used to Define Desirable Weight and
Overweight According to Three Different
“Ideal” Reference Populations

 

BMI for “Ideal” Reference Population

 

 

“Ideal” . Severe
Reference Mean Overweight — Overweight
Study® Population Men Women Men Women Men Women

 

NHANES II 20- to 29-

year-olds 24.3 23.1 27.8 273 3i.l 32.3
Metropolitan Desirable weight
1959 insured 72.0 21.5 264 © 25.8 30.8 30.1
Metropolitan Desirable weight
1983 insured 22.7 22.4 27.2 269 318 31.4

 

aThe NHANES I! data define overweight as the 85th percentile or more of the distribution
of BMI for men and women ages 20 to 29 and severely overweight as the 95th percentile
for that reference population (NCHS 1987). The Metropciitan 1959 data are taken from
the 1959 Metropolitan Life Insurance tables. Weights and heights were adjusted to ap-
proximate those without shoes or clothing (Simopoulos and Van Itallie 1984; NIH 1985).
The Metropolitan 1983 data are taken from the 1983 Metropolitan tables. Height and
weight were with shoes and light clothes (Van Itallie 4985; NIH 1985). For both the 1959
and the 1983 Metropolitan data, the weights for midpoint of medium-frame persons were
used, and for both studies overweight and severe overweight were defined as 20 percent
and 40 percent, respectively, over desirable weight.

Types of Obesity

Hyperplastic vs. Hypertrophic. Obesity is associated with too many
adipose cells (hyperplastic obesity), adipose cells that are too large (hyper-
trophic obesity), or both (Hirsch and Batcheloer 1976). Studies on differ-
ences and changes in fat cell sizes and numbers have led to the hypothesis
that while changes in the size of adipose cells may occur at any age, the
number of adult cells may be fixed and determined by weight gain during
certain periods of childhood development; fat cell number is established by
late adolescence (Knittle et al. 1979) and, once established, does not
decline. These suggestions have been interpreted to imply that the poten-
tial for sustained weight reduction in adulthood may depend, in part, on the
number of adipose cells present. That is, because people with excessive
numbers of fat cells may expect only limited success in weight reduction,
prevention of adult obesity should begin with limits on excessive weight
gain during childhood (Hirsch and Batcheloer 1976).

This hypothesis has received limited support. Although adult-onset
obesity is more commonly due to an increase in the size of a normal number

285
C Nutrition and Health

of adipose cells than to an increase in their number (Krotkiewski et al.
1983), adipose cell number also increases in response to excessive weight
gain at any time throughout adult life (Sjostrom 1980). Some studies have
reported better treatment outcome among hypertrophic than hyperplastic
obese subjects (Bjorntorp et al. 1975), but others have not observed any
such difference (Strain et al. 1984), and the clinical significance of differ-
ences in fat cell size and number remains to be determined.

Upper Body vs. Lower Body. Women generally have been observed to have
more subcutaneous fat than men, but men appear to suffer a greater
cardiovascular risk from a given degree of fat than women (Bjorntorp 1983).
The distribution of body fat may be an indicator of this difference. More
men than women accumulate large fat cells in the abdominal region. This
distribution around the abdomen with increased waist-to-hip ratio, referred
to as upper body obesity, is associated with increased cardiovascular risk
factors such as hypertriglyceridemia and impaired glucose tolerance
(Krotkiewski et al. 1983). Lower body obesity is more typical of women,
who tend to accumulate fat in the hips, gluteal regions, and extremities, a
distribution that does not appear to be associated with increased cardiovas-
cular risk factors (Krotkiewski et al. 1983), perhaps because fat on the hips
is not well mobilized (Rebuffe-Scrive et al. 1985). Adipose cells are insulin-
resistant in the abdominal region but usually are insulin-sensitive in the
gluteal region (Maugh 1982). Studies of siblings ranging in relationship from
identical twins to adoptive suggest that these differences in adipose cells
may be genetically determined (Bouchard et al. 1985). Accordingly, women
with upper body obesity with a waist-to-hip ratio similar to that of men are,
like men, at increased risk for hypertriglyceridemia, hyperinsulinemia,
diabetes, and cardiovascular disease (Krotkiewski et al. 1983).

Regardless of gender, a high waist-to-hip ratio predicts an increased risk for
cardiovascular disease and diabetes. Measurements made in 1967 of waist-
to-hip circumference of 792 54-year-old men in Gothenberg were positively
correlated 13 years later with deaths from stroke and ischemic heart
disease (Larsson et al. 1984). Other indices of body fatness such as the
BMI, the sum of three skinfolds, or either waist or hip circumference alone
showed no such correlation. A 12-year study of 1,462 women found the
waist-to-hip ratio to be a better predictor of myocardial infarction, angina
pectoris, stroke, and death than any other anthropometric measurement
obtained (Lapidus et al. 1984). In both of these studies, persons whose
waist-to-hip ratio was in the top quintile of distribution (greater than 1.0 for
men or 0.8 for women) suffered the greatest incidence of cardiovascular
disease.

286
Obesity le

Childhood Obesity. Obesity and extreme obesity in children have been
defined in several studies by a triceps or scapular skinfold thickness greater
than or equal to the 85th or 95th percentile, respectively, of children in the
same age group and sex between the baseline and a later year of measure-
ment in national surveys (Dietz 1986). Increased weight-for-height above
the 85th percentile for a defined population has also been used and can be
deduced from standard growth charts (see chapter on maternal and child
nutrition). Obesity in children can cause psychosocial dysfunction, ortho-
pedic problems, abnormal glucose tolerance, hypertension, and elevated
cholesterol and triglycerides that may persist into adulthood (Dietz 1986;
Freedman et al. 1985). It also can increase the risk of obesity in adulthood
(Garn 1985a, 1985b; Shear et al. 1988; Sorensen and Sonne-Holm 1988).
According to a comparison of children studied in the NHES Cycle II and
Cycle III between 1963 and 1970 and children studied later in NHANES I
and II from 1971 to 1980, obesity and extreme obesity in children appear to
be increasing by as muchas 54 and 98 percent, respectively, in 6- to 1 l-year-
olds and by 39 and 64 percent, respectively, in 12- to 17-year-olds
(Gortmaker et al. 1987).

Health Consequences of Obesity

Excess Mortality

Numerous studies have examined the effects of excessive body weight on
mortality. The best known studies include the Build and Blood Pressure
Studies of 1959 and 1979 (Society of Actuaries 1960; Society of Actuaries
and Association of Life Insurance Medical Directors of America 1980) and
the American Cancer Society Study (Lew and Garfinkel 1979; Lew 1985).
Several smaller studies include the Manitoba Study (Rabkin, Mathewson,
and Hsu 1977), the Chicago People’s Gas Company (Dyer et al. 1975), the
Seven Countries Study (Keys 1980), the Longshoremen Study (Borhani,
Hechter, and Breslow 1963), and the Provident Mutual Life Study (Blair
and Haines 1966). This subject has been reviewed extensively (Simopoulos
and Van Itallie 1984; NIH 1985; Manson et al. 1987).

In most of these studies, mortality increased with increasing weight. This
effect can be expressed as the mortality ratio, defined as the actual number
of deaths as a percent of expected deaths for the population as a whole. The
mortality ratio has been shown to increase with degree of obesity, and with
its duration, from 110 among persons 5 to 15 percent overweight to 227
among those 55 to 65 percent overweight (NIH 1985). Extreme (morbid)
obesity, defined in this instance as either 100 percent or 100 Ib over

287
C Nutrition and Health

desirable weight (Kral 1985), has been reported in one small series to be
associated with a mortality ratio of 1,200 percent (NIH 1985).

Although experts generally agree that excessive body weight is associated
with increased mortality (NIH 1985), the body weight associated with the
lowest mortality still lacks precise definition. Several important meth-
odologic issues contribute to this uncertainty. These include the failure to
control for cigarette smoking and inappropriate control for biologic effects
of overweight such as hypertension, hyperlipidemia, and hyperglycemia,
for weight loss due to subclinical disease (Manson et al. 1987), for weight
history, for body fatness, or for duration of the condition (Simopoulos and
Van Itallie 1984).

Several studies, for example, have reported a higher mortality at the lower
as well as the higher range of fatness. This J- or U-shaped curve was found
in the Build Study of 1979 (Society of Actuaries and Association of Life
Insurance Medical Directors of America 1980; Van Itallie and Abraham
1985), the Framingham Heart Study (Hubert et al. 1983; Garrison and
Castelli 1985), the American Cancer Society Study (Lew and Garfinkel
1979), and the Hawaiian Japanese Study (Rhoads and Kagan 1983). The
increased mortality at lower weights was related to several types of cancer
(Lew and Garfinkel 1979). The J-shaped curve was markedly reduced but
still observable when adjusted for smoking history (Garrison and Castelli
1985), as well as for serum cholesterol level, blood glucose level, and
systolic blood pressure (Harris et al. 1988).

In the Build and Blood Pressure Study of 1959 (Society of Actuaries 1960),
optimal weight for all ages, judged by survival, was close to that of 20- to
29-year-olds. Older cohorts were heavier, and the increase in relative
weight with increasing age was associated with increased mortality. Data
from the Framingham Heart Study confirm that being overweight in-
creases health risks for older people (Harris et al. 1988). Implicit in this
trend is the undesirable effect of weight gain beyond desirable weight after
maturity and the suggestion that weight gain acquired during adult life
might be more detrimental than the degree of overweight. In fact, one study
has reported the highest rates for cardiovascular and renal disease among
overweight adults who were below average weight as children but who
developed late-onset obesity (Abraham, Collins, and Nordsieck 1971).
However, in the Build Study of 1979, the effect of overweight on mortality
was more marked in obese men issued insurance policies between ages 15
and 39 than for equally obese men issued insurance policies between ages
40 and 69. A problem with both the 1959 and 1979 studies was the rather

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short average duration of time that policyholders were observed—6.6
years for the latter study. In the Build Study of 1979, the adverse effects of
underweight became evident in a relatively shorter time than the adverse
effects of overweight (Society of Actuaries and Association of Life Insur-
ance Medical Directors of America 1980).

The studies that do not show increased risk from obesity, such as the Seven
Countries Study and the Longshoremen Study, have limitations because
they were too short in duration, too small in sample size, Or did not
consider the adverse effects of smoking or of preexisting illness (Si-
mopoulos and Van Itallie 1984; Van Itallie and Abraham 1985; Manson et
al. 1987). Under these circumstances, the adverse effects of overweight
would be obscured and of underweight exaggerated. Prospective data from
the Framingham Heart Study, in which a cohort was followed for 26 years,
clearly show the adverse effect on mortality of as little as 10 percent
overweight, using the 1959 Metropolitan tables (Hubert et al. 1983). Bear-
ing in mind data limitations, minimal mortality appears to occur ata weight
10 percent below the U.S. averages as shown in Table 6-1 (Manson et al.
1987).

Other Health Consequences

Relative body weights above 100 to 109 percent of desirable are associated
with increased mortality as well as morbidity from heart disease, cancer,
diabetes, digestive diseases, and cardiovascular disease. The higher the
relative weight, the greater the risk for these conditions (Lew and Garfinkel
1979). From the NHANES II data, rates of hypertension and diabetes were
nearly tripled for persons 20 percent or more overweight, and hyper-
cholesterolemia was 50 percent more common (Van Italie 1985). Obesity
is associated with reduced levels of high density lipoproteins but with
elevated levels of triglycerides and atherogenic lipoproteins (Albrink et al.
1980). The large American Cancer Society Study found mortality from
various causes to increase according to the degree of overweight. Data
from this study are shown in Table 6-3. Of all obesity-related diseases,
noninsulin-dependent diabetes is most clearly and strongly associated with
obesity. The details of these relationships are discussed in the chapter on
diabetes.

Many other serious conditions such as gallstones, sleep apnea, osteo-
arthritis, and other disabling disorders of locomotion bear a direct relation-
ship to obesity, although causality is not necessarily proved by these
associations.

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Table 6-3
Mortality Ratios for All Ages Combined in Relation to the Death
Rate of Those 90 to 109 Percent of Average Weight

 

Weight Index
Sex <080 080-089 090-109 110-119 120-129 130-139 140+

 

Total deaths M_ 1.25 1.05 1.00 1.15 1.27 1.46 1.87
F 4.19 0.96 1.00 1.17 1.29 1.46 1.89
Coronary M_ 0.88 0.90 1.00 1.23 1.32 1.55 1.95
heart F 1.01 0.89 1.00 1.23 1.39 1.54 2.07
disease
Cancer, M 1.33 1.13 1.00 1.02 1.09 1.14 1.33
all sites F 0.96 0.92 1.00 1.10 1.19 1.23 1.55
Diabetes M 0.88 0.84 1.00 1.65 2.56 3.51 5.19
F 0.65 0.61 1.00 1.92 3.34 3.78 7.9
Digestive Ms 1.39 1.28 1.00 1.45 1.88 2.89 3.99
diseases F 1.58 0.92 1.00 1.66 1.61 2.19 2.29
Cerebral Ms 1.21 1.09 1.00 1.15 1.17 1.54 2.27
vascular F 1.33 0.98 1.00 1.09 1.16 1.40 1.52
disease

 

Source: Lew, E.A., and Garfinkel, L. 1979. Variations in mortality by weight among
750,000 men and women. Joumal of Chronic Diseases 32:563—76. Copyright
1979, Pergamon Press, Ltd., reprinted with permission.

Causes of Obesity

The causes of obesity are incompletely understood, so that effective treat-
ment is difficult. Obesity is the net result of an excess of energy consump-
tion over expenditure. Factors that must be considered as contributing to
causation are: (1) heredity, (2) primary overeating, (3) altered metabolism
of adipose tissue, (4) defective or decreased thermogenesis (the process by
which calories are converted into heat), (5) decreased physical activity
without an appropriate reduction in food intake, and (6) certain prescribed
medications. These potential causes can interact with one another. Of the
six factors, individuals may have some control of overeating and underac-
tivity.

Genetic Causes

Some studies of incidence of obesity among population groups, and among
individuals within population groups, suggest that the tendency for obesity
is inherited. On the other hand, separating genetic from cultural and
environmental contributions is difficult—a fact brought out by studies of
American Indians and blacks (Van Itallie and Abraham 1985; Van Itallie

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Obesity O

1985), two populations that display higher levels of obesity than other
groups. To explore the question of environment versus heredity, investiga-
tors have examined the weight characteristics of twins and adopted sib-
lings. In addition, studies of reduced energy expenditure in overweight
infants and adults, as reviewed later in this chapter, have provided evidence
in support of a geneti¢ basis for obesity.

One study measured the body fatness of 871 biologic and adopted siblings
of French descent, including 87 pairs of monozygotic twins, and found that
the amount and distribution of fat were related to the closeness of the
genetic relationship. Similarities were not observed between adopted sib-
lings. The genetic effect was particularly noted in measurements of skin-
fold thicknesses and in lean body mass. At the same time, a substantial
environmental, or cultural, effect was also observed (Bouchard et al. 1985).
Aerobic capacity in response to submaximal exercise also appeared to be at
least partially genetically determined because similarities were greater
among twins than among siblings or adopted siblings (Bouchard et al.
1984). Although these findings do not entirely rule out effects of early
learned practices, they do make it tempting to speculate that for genetic
reasons, some persons are less able to benefit from exercise and are thus
more susceptible to obesity than others.

Another recent study provided even broader evidence for the genetic
determination of obesity. In a study of 4,071 pairs of twins, investigators
estimated that 80 percent of the contribution to obesity could be explained
by genetics (Stunkard, Foch, and Hrubec 1986). Evidence for a smaller but
still substantial genetic contribution was provided by investigations on 540
Danish adoptees (Stunkard et al. 1986). In this latter study, the BMI of the
adoptees correlated strongly with that of their biologic parents but not at all
with that of their adoptive parents, an observation that suggests that in this
Danish population, early family environment had apparently little influ-
ence in determining the degree of fatness.

Overeating

Overeating is clearly a prominent contributor to obesity. Yet, obese per-
sons do not necessarily consume more calories for their weight than lean
individuals. Nutrient intake, established by dietary interview of a probabil-
ity sample of 6,219 male and nonpregnant female adults selected from
NHANES |, did not correlate with the degree of obesity (Braitman, Adlin,
and Stanton 1985). Although underreporting of food intake by the obese
could not be ruled out, the authors sugges.ed that factors other than
overeating, such as decreased levels of physical activity. be given increased

consideration in the etiology of obesity.

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Additional factors include complex controls of feeding behaviors at the
biologic and behavioral levels. At the biologic level, feeding behavior is
regulated in part by the brain hypothalamus (Dallman and Bray 1986) and
its interactions with brain neurotransmitters, nervous impulses from the
intestinal tract or from higher brain centers, circulating nutrients absorbed
from the intestinal tract, and certain hormones. While anatomic or bio-
chemical lesions in the brain can cause obesity, more frequent and likely
causes of overweight are improper signals coming to the brain, particularly
those from the adipose tissue and the intestinal tract (Stricker 1984),

Feeding behavior occurs in response to hunger and to appetite induced by
the presence of food. Satiety and the resulting cessation of eating occur in
Tesponse to certain hormones, nervous impulses, and absorbed nutrients
signaling the brain (Dallman and Bray 1986). Whether specific foods affect
feeding and satiety and, consequently, over- or undereating is uncertain.
Laboratory animals overeat and become obese if offered highly palatable
foods, especially those high in fat and sugar and low in fiber. The same may
be true of some humans (Herman and Polivy 1984). Foods low in fat and
high in naturally occurring fiber appear to induce satiety in humans at lower
levels of caloric intake than do high-fat, low-fiber foods (Heaton et al. 1983;
Duncan, Bacon, and Weinsier 1983).

Psychologic and behavioral factors also influence eating behavior, although
their precise role has been difficult to define. Suggestions that obese
persons were more dependent on external cues than internal signals of
physiologic hunger (Schachter 1971) or were more restrained (and, there-
fore, overcompensated) in their eating behavior (Herman and Polivy 1984)
have not proved as useful in diagnosis and treatment as was once thought
(Stunkard and Messick 1985). The effects of peer pressure (Herman 1978)
are also not well established.

Altered Adipose Cell Metabolism

Obesity might result from a metabolic error in energy balance in which an
unusually high proportion of available dietary calories is directed to
adipose tissue for storage. In humans and in many animals, adipose tissue
is not as active in fat synthesis as other tissues but instead depends largely
on circulating triglycerides for its fat content. These, in turn, originate from
chylomicrons derived from absorbed dietary fat or from very low density
lipoproteins synthesized by the liver from excess nutrients not immediately
needed as fuel.

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Obesity Q

Lipoprotein Lipase. The removal of circulating triglyceride and its deposi-
tion in adipose tissue depends on lipoprotein lipase, an enzyme in adipose
tissue. In studies of genetically obese strains of experimental animals, the
observed increase in fat mass at the expense of lean body mass, even with
caloric restriction, has been attributed to an excess of adipose tissue
lipoprotein lipase (Greenwood and Vasselli 1981). Too much of this enzyme
appeared to “pull” triglyceride into the adipose tissue, cause deprivation of
other tissues (such as muscle), and lead to overeating. Thus, the over-
production of adipose tissue lipoprotein lipase might account for human
obesity. Increased synthesis of lipoprotein lipase has been observed in the
adipose tissue of obese persons who are losing weight, which could explain
the rapid regain of weight lost with dieting (Schwartz and Brunzell 1981).
However, other observers have reported no increase of adipose tissue
lipoprotein lipase activity in response to caloric restriction. Instead, they
report a decline in the enzyme with reduced calories and an increase with
return to higher caloric intake (Rebuffe-Scrive, Basdevant, and Guy-Grand
1983). Until these inconsistencies can be resolved, the role of lipoprotein
lipase in human obesity remains uncertain.

Hormones. In times of caloric need, as in fasting or during exercise,
lipoprotein lipase is inactivated and adipose tissue is mobilized. Many
hormones stimulate lipolysis (breakdown of lipid), but epinephrine released
from the adrenal medulla and norepinephrine released from sympathetic
nerve endings are probably the chief activators of lipolysis during exercise
and stress, respectively. A genetic component to epinephrine-stimulated
lipolysis has been identified (Despres et al. 1982), which suggests that an
inherited impairment of epinephrine response during exercise could ac-

count for the observed failure of obese individuals to lose weight with
exercise (Ribeiro et al. 1984).

Insulin is another hormone that modifies energy balance and may contrib-
ute to obesity (Dallman and Bray 1986). Hyperinsulinemia and insulin
resistance, for example, can occur in all types of obesity and may be a link
between hypertension, obesity, and glucose intolerance (Modan et al.
1985). Plasma insulin, which increases in response to feeding, promotes
uptake of circulating triglycerides by adipose tissue and inhibits fat mobi-
lization, thereby favoring storage of excess calories as fat. These reactions
are reversed during fasting, when insulin levels are low. As discussed in the
diabetes and high blood pressure chapters, weight loss often is followed by
acorrection of these abnormalities; when weight is regained, the problems
return.

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C Nutrition and Health

Whether human obesity is caused by a primary abnormality i in adipose
tissue or in the hormones that regulate its deposition is unknown at this
time. However, adipocyte precursors obtained from massively obese sub-
jects release a factor that, when added to rat adipose cells in tissue culture,
causes cells to multiply (Lau, Roncari, and Hollenberg 1987). This finding
suggests that metabolic effects may indeed play a role.

Altered Thermogenesis

Set Points. The weight of most people remains remarkably stable over the
adult years, despite large fluctuations in dietary intake. Experiments in
animals indicate that body weight is stabilized at a specific set point that is
maintained without conscious control by variations in metabolic rate in
response to food intake (Keesey 1986). A possible mechanism for such
stability is a change in body heat production, or thermogenesis, to compen-
sate for changes in energy intake (James 1983). Although human body
weight often appears to be regulated at a set point, its controlling mecha-
nism has not yet been demonstrated.

Heat production is an accurate measure of energy expenditure or metabolic
rate. Because measurement of actual heat production is cumbersome and
expensive, metabolic rate is usually determined by indirect calorimetry,
which converts measurements of oxygen consumption into calories,
ideally expressed per unit of lean body mass. Lean body mass is the body
compartment containing the most metabolically active tissues and ac-
counts for most energy expenditure. Thus, accurate methods for estimating.
lean body mass are essential (Horton 1983) as are those for measuring the
degree of physical activity.

Metabolic Rate. The measure of the energy used for running the body’s
essential metabolic machinery and for maintaining body temperature is the
resting metabolic rate (RMR), obtained when the subject is resting com-
fortably several hours after the last meal or physical activity. The basal
metabolic rate (BMR) is the energy the body needs when the subject is at
complete rest, before arising in the morning and 12 hours or more.after the
last meal (Horton and Danforth 1982). The RMR is much more convenient
to obtain, and although it is slightly higher than the BMR, it provides a
reasonable estimation of the BMR. At stable body weights, BMR and RMR
are higher in obese persons than in normal-weight persons because of the
increased body size. It is uncertain, however, whether the RMR of the
obese is the same (Himms-Hagen 1984; Blaza and Garrow 1983) or lower
(Danforth 1983) than that of normal-weight persons when it is expressed i in
terms of lean body weight.

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Obesity @

Diet-Induced Thermogenesis. The energy generated metabolically when
food is digested, called diet-induced thermogenesis, rises with increased
food ingestion. Adaptive thermogenesis is the increase in RMR that occurs
with increased food intake. Together, these forms of thermogenesis ac-
count for only about 10 percent of total energy expended. Failure to
increase thermogenesis with overeating could result in obesity, but
whether obese persons have defective thermogenesis has not been estab-
lished. In the Vermont Prison Study, thin prisoners required many more
calories to increase their body fat than could be calculated from the caloric
value of the food ingested (Sims et al. 1973). These results suggest that in
normal-weight individuals, extra calories are readily metabolized to heat
when they are not needed.

In persons of normal weight, thermogenesis increases following a meal and
is proportional to meal size (Rothwell and Stock 1986). The type of carbo-
hydrate consumed may affect heat production; sucrose appears to be more
thermogenic than glucose in normal-weight—but not obese—persons
(Sharief and Macdonald 1982). Other macronutrients may also be impor-
tant. The thermogenic effect of dietary protein, carbohydrate, and fat has
been estimated to be 25, 10, and 3 percent of calories ingested, respectively
(James and Trayhurn 1981). The small amount of heat lost when fat is
processed may account for the importance of dietary fat as an inducer of
obesity. Despite these findings, other investigators found a very small
increase in total heat output with overfeeding and have concluded that any
such adaptation to carbohydrate (but not fat) intake is very small (James
1983).

Effect of Weight Loss. In studies using continuous indirect calorimetry.
reduced glucose-induced thermogenesis was found after obese subjects
lost 9 to 33 kg (compared with controls), suggesting that defective ther-
mogenesis is one of the factors causing relapse of obesity after weight loss
(Schutz et al. 1984). In another study, energy expenditure was measured in
a respiration chamber before and during weight reduction in obese sub-
jects, and it declined as fat was lost; results were based on lean body mass
(Ravussin et al. 1985). Other investigators analyzed the caloric content of
measured liquid formula diets fed to obese and lean (never obese) patients
during long-term hospital stays of many months’ duration under metabolic
ward conditions. They found that obese and lean subjects required similar
amounts of energy per square meter of surface area per day. After weight
loss and stabilization to a lower body weight, the obese subjects showed a
28 percent decrease in calories required to maintain body weight at the new
level (Leibel and Hirsch 1984).

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O Nutrition and Health

Other researchers, however, have identified problems with methodology or
experimental design in such studies of defective thermogenesis in the obese
(James 1983). For example, measurement of thermogenesis over periods of
time longer than a few hours is only feasible where calorimetry chambers
are available. Although people can reside in such chambers and move about
freely for days at a time, activity is far from normal. Moreover, the need to
express oxygen consumption in terms of lean body mass presupposes
accuracy of methods of measuring body composition. Changes in heat
production when dieting subjects are re-fed also complicate these studies.
Although some evidence favors the hypothesis that adaptive ther-
mogenesis occurs with weight change and is mediated by thyroid activity
and the sympathetic nervous system (Danforth 1983; Landsberg and Young
1983: Horton 1983), the effect appears to be small and the role of ther-
mogenesis in weight loss must be considered unsettled.

Lack of Exercise

Various studies have shown that physical inactivity in adult life shortens life
expectancy (Paffenbarger et al. 1986), perhaps because underactivity with-
out concomitant decrease in food intake can result in obesity. The very
large difference in caloric expenditure between the most inactive and most
active occupations, 2,300 to 4,400 kcal daily (Joint FAO/WHO Ad Hoc
Expert Committee 1973), suggests that exercise could help manage and
prevent obesity. Obesity may be a disease of inactivity, but that hypothesis
has been difficult to prove (Stern 1984). Direct methods of measurement of
daily physical activity are lacking, and current methodology for evaluating
activity at home cannot detect whether inactivity contributes to obesity
(Garrow 1978). Most studies that have compared the activity patterns of
lean and obese subjects are based on questionnaires.

Epidemiologic data from the Lipid Research Clinics Prevalence Study
show relatively low energy intakes to be coupled with increasing body
weight, particularly in women (Dennis et al. 1985). Other epidemiologic
data support this finding (Braitman, Adlin, and Stanton 1985). These and
other investigators attribute the finding to decreased activity level. In
another study, persons who participated in vigorous weekend activity were
leaner than those who did not (Morris et al. 1980). A correlation also has
been reported in young adolescents between degree of obesity and number
of hours of television watched per week (Dietz and Gortmaker 1985).

Another interesting, but as yet unvalidated, aspect of the relationship

between physical activity and body weight is involuntary movement—
spontaneous fidgeting or moving, which varies widely from individual to

296
Obesity Q

individual. In one study, for example, that measured energy expenditure in
unselected subjects, very large individual differences in energy—100 to 800
kcal/day—were attributed to differences in spontaneous activity (Ravussin
et al. 1986). Among infants, energy expenditure at age 3 months was more
than 20 percent lower in those who became overweight than in infants
whose weight remains normal (Roberts et al. 1988). A reduced 24-hour
energy expenditure in adults correlated strongly with subsequent weight
gain in southwestern American Indians with a high prevalence of obesity
(Ravussin et al. 1988). Much is still to be learned about the relationship
among physical movement, caloric expenditure, and body weight, but the
cumulative effects of physical activity over time could be important in
preventing or correcting obesity (Black 1983).

Prescribed Medications

Many drugs prescribed for clinical conditions other than obesity may cause
weight gain. Such drugs include propranolol, clonidine, and related medi-
cations prescribed for hypertension and other cardiovascular diseases that
may change metabolic rates and decrease levels of energy expenditure.
Adrenal steroids such as prednisone, prescribed as anti-inflammatory
agents, cause hypertrophic obesity. Some people experience weight gain
with tranquilizers such as amitriptyline and diazepam, certain anti-
histamines such as cyproheptadine, and birth control pills. These and other
issues related to medications are reviewed in the chapter on drug-nutrient
interactions.

Treatment of Obesity

To lose weight. one must decrease caloric intake, increase caloric expendi-
ture. or do both. Thus, the chief approaches to weight reduction involve
behavior change related to diet and exercise, drugs to decrease hunger or
increase satiety. and surgical or mechanical intervention designed to re-
duce food intake. To date. none of these methods has proved to be entirely
effective. and none is without tisk.

Weight loss reduces health risks in the obese. In theory, it should be
accomplished easily, but in practice, traditional diet therapy has not been
very successful: people who lose weight tend to gain it back (Stunkard

1986). Thus. a combination of diet and exercise seems the most sensible

approach to treatment (Stricker 1984). Because obesity is a condition

requiring continuous attention, any behavior changes required to maintain
weight loss must be lifelong.

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CO Nutrition and Health

Behavior Modification

Behavior changes to induce weight loss were based initially on the theory
that faulty eating behavior caused obesity and could be corrected by a
program.of record keeping, stimulus control, and reinforcement of appro-
priate behaviors. The early programs focused on the importance of eating
behavior and introduced specified behavioral procedures to change eating
patterns. Weight losses, however, were modest, and behavior therapy is
now used as part of broader programs that include nutrition education,
exercise, and cognitive restructuring (Stunkard 1987). Such programs form
the basis of many commercial efforts that treat a substantial number of
mildly obese people in this country (Brownell 1986). Current approaches
are trying to increase the amount and duration of weight loss by combining
various behavior modification techniques with low-calorie diets (Wadden,
Stunkard, and Brownell 1983). The results have not been evaluated from a
long-term perspective.

Drugs and Surgical Methods

Thus far, no drug therapy has induced long-term weight loss. Drugs are
aimed at decreasing hunger or increasing satiety, usually by mimicking
certain neurotransmitters or hormones that play a physiologic role in
feeding behavior (Sullivan and Triscari 1985). One problem is that weight
lost with drug therapy is more often regained than with other methods,
suggesting that appetite-suppressant drugs lower the set point level at
which body weight is regulated and only secondarily suppress appetite
(Stunkard 1982). Regardless, weight loss would be expected to occur only
during the period of drug therapy, suggesting the need for chronic treat-
ment.
t

Surgical intervention appears appropriate only for selected persons with
massive obesity or with its severe complications who have not responded
to more conservative treatment. Jejunoileal bypass has been largely aban-
doned because of unfavorable side effects. Other procedures such as
gastric balloons and gastric surgery, which reportedly cause substantial
weight loss—although rarely to ideal weight—in morbidly obese persons
(Kral 1985), require further study before their long-term effects are known.

Dangers of Dieting

Extremely low-calorie diets, 300 or 400 kcal per day, have resulted in deaths
due, at least in part, to the effects of dietary deficiencies on the heart
muscle (Van Itallie and Abraham 1985). Short-term studies indicate that the
same problems are less likely to occur with diets higher in calories (range of

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Obesity O

800 kcal) and with better quality protein (Wadden, Stunkard, and Brownell
1983). Nevertheless, such higher calorie diets still require careful medical
supervision.

Another possible risk of dieting is the effect of repeated attempts on long-
term prospects for weight Icss. One study of rats has suggested that cyclic
weight reduction may increase the difficulty of losing weight. Obese rats
subjected to two repeated episodes of weight reduction and weight gain lost
less weight during the second cycle and regained it more easily and with a
lower food intake (Brownell et al. 1986). Whether similar effects occur in
humans is as yet uncertain.

Fad weight loss regimens of unscientific merit have been estimated to cost
consumers $5 billion annually (Herbert 1981). While such diets attract
many people’s attention they may be dangerous, especially when they
provide less than the full complement of essential nutrients (Dwyer 1985).
This danger is discussed in greater detail in the chapter on dietary fads and
frauds.

Depression brought on by dieting is a serious condition affecting many
obese persons (Stunkard and Rush 1974). Preoccupation with being thin
may lead to two related and often serious eating disorders, anorexia ner-
yvosa and bulimia, that occur most commonly in adolescent girls (Herzog
and Copeland 1985). Anorexia nervosa is characterized by an extreme fear
of becoming obese, with severe diet restriction and weight loss sometimes
to the point of cachexia and death. Bulimia is a syndrome of secretive binge
eating followed by self-induced vomiting or purging. These conditions are
discussed in detail in the chapter on behavior.

Implications for Public Health Policy

Dietary Guidance

General Public

Excess weight or overweight occurs when too few calories are expended
and too many consumed for individual metabolic requirements. The ex-
traordinarily high prevalence of obesity in the United States—one-fourth of
American adults are overweight and nearly one-tenth are severely over
weight—coupled with its role as a risk factor for diabetes. hypertension,
coronary artery disease and stroke, gallbladder disease. and some types of
cancer, suggests that a reduction in the average weight of the general
e Nutrition and Health

population would improve the Nation’s health. Americans, in general,
would benefit from a lifestyle that includes more physical activity and a diet
containing fewer calories.

Because fat contains more than twice the caloric value per gram of either
protein or carbohydrate, the general public would benefit from reduced fat
intake. In addition, it may be difficult to meet essential vitamin and mineral
requirements on low-calorie diets. Because sugar and alcohol provide
calories from carbohydrate but no other nutrients, individuals seeking to
attain and maintain desirable body weight should use these substances
sparingly.

Evidence indicates that exercise burns calories, increases the proportion of
lean to fat body mass, and, therefore, raises the metabolic rate. Therefore,
increased levels of physical activity are important for attaining desirable
body weights among the general population.

Special Populations

Qualified health professionals should evaluate overweight persons for the
presence of chronic disease risk factors—especially elevated blood choles-
terol, blood glucose, or blood pressure. Such evaluation is important for
individuals whose excess body fat is distributed mainly on the abdomen.
This pattern is more typical for men than for women, and it increases risks
for diabetes, high blood pressure, hyperlipidemia, and heart attacks.

Health professionals should work with obese persons to restrict caloric
intake and to increase caloric expenditure. Such advice should also be
provided to overweight persons, with or without other significant risk
factors, to help reduce their risk for heart disease, stroke, some kinds of
cancers, and many other diseases and to prevent or reduce psychosocial
complications of obesity. Professional guidance is recommended because
many popular means to reduce weight may themselves pose risks to health
and because unsupervised efforts to control obesity usually fail over the
long term. Although excess body fat is difficult to lose, current research
suggests that long-term individual or group programs that facilitate behav-
ioral changes in diet and exercise are most likely to be effective. The
intensity of these programs and the precise goal for weight loss should
depend on the patient’s degree and distribution of overweight, weight
history, chronic disease risk factors, health status, and personal choices.

Current evidence is insufficient to recommend similar programs for over-
weight children. Obesity in infancy and childhood increases the risk for

300