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OCR for page 57
Factors That Influence Body Weight
There are numerous factors that can influence body weight. The individual
has no control over some of these factors, including developmental determin-
ants, genetic makeup, gender, and age. Other factors that influence body weight
over which the individual has potential control include level of physical activity,
diet, and some environmental and social factors. This chapter explores the
relationship between each of these factors and body weight.
DEVELOPMENTAL DETERMINANTS
It has been postulated that there are times during people's lives when
exposure to certain factors may increase their risk for the onset of obesity. These
times have been termed "critical periods." If these critical periods, along with
the influential factors, can be clearly defined, it may be possible to identify
individuals at increased risk for the development and persistence of overweight
and obesity in adulthood. The prenatal period, the period of adiposity rebound,
and adolescence have been proposed as critical periods in childhood (Dietz,
1994~; pregnancy and the immediate postpartum period have been proposed as
critical periods for women in adulthood.
Prenatal Factors
Although the data are subject to a variety of interpretations, it has been
documented in both animals and humans that females who are severely food
restricted during the first one to two trimesters of pregnancy have progeny who
have a higher prevalence of obesity, diabetes, insulin resistance, and hyperten-
sion later in life. Progeny of survivors of the Dutch famine in World War II
demonstrated a higher prevalence of obesity and diabetes (Ravelli et al., 1976),
although this conclusion was questioned by later studies (Jackson et al., 1996;
Susser and Stein, 19941. Malnutrition in utero also has been reported to result in
57
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58
WEIGHT MANAGEMENT
increased obesity and its complications later in life (Stanner et al., 1997). Lower
birth weights also seem to be associated with increased upper body visceral
adiposity in later life with its attendant increased risk of cardiovascular disease
(Oken and Gillman, 2003; Rogers, 2003~. Since individuals from a lower socio-
economic background are more likely to be exposed to malnutrition during
gestation or early childhood, the prevalence of obesity in such subgroups might
be expected to be higher.
Adiposity Rebound
Adiposity increases from birth until approximately 1 year of age, then de-
clines to a minimum at approximately 6 years of age. The term "adiposity re-
bound" refers to the increase in body mass index (BMI) and body fat that occurs
after this nadir in children between the ages of 5 and 7 years. Children experi-
encing adiposity rebound at an earlier age appear to have a three- to sixfold
greater risk of increased adult BMI than do other children (Whitaker et al.,
1998~. He and Karlberg (2002) demonstrated, through the development of prob-
ability charts based on 3,650 children followed from birth to 18 years of age,
that children who experienced this rebound before 8 years of age have a higher
risk of adulthood obesity. However, Guo and coworkers (2000), using serial
BMI data from the Fels Longitudinal study demonstrated that while there was no
association between early age at adiposity rebound and adult BMI status in men,
after controlling for effects of birth weight, adult physical activity, alcohol and
cigarette use, there was approximately twice the risk for overweight with early
rebound in women.
Causes of early adiposity rebound have been variously attributed to ad-
vanced skeletal maturity (Roland-Cachera et al., 1984; Williams and Dickson,
2002), high protein intake (Roland-Cachera et al., 1995), and parental BMI
(Dorosty et al., 2000~. Cameron and Demerath (2002) concluded after extensive
review of the available scientific literature that the evidence is still not clear
about whether age at adiposity rebound is a critical period for the development
of obesity, but that early adiposity rebound might well be a statistical predictor
of later obesity because of its strong relationship with early adiposity and accel-
erated maturation, both of which are established markers of later risk of obesity.
Adolescence
Although only 30 percent of adult obesity begins during childhood, 70 per-
cent of the adult obesity that begins in childhood may start during adolescence
(Dietz, 1994~. Adolescent obesity is associated with a variety of adverse health
effects in adulthood, including early mortality in men and increased risks of
coronary heart disease, diabetes, and colorectal cancer (Miller, 1988; Must et al.,
1992; Wylie-Rosett, 1988~. Most of these risks were only slightly attenuated by
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FACTORS THAT INFLUENCE BODY WEIGHT
59
adjustment for adult obesity, which suggests that obesity during adolescence
may determine the risk of these later complications regardless of whether or not
the individuals are obese adults.
While total fatness is an important consideration when evaluating develop-
mental aspects of obesity, an additional consideration is adipose tissue distribu-
tion. Visceral adipose tissue has an independent effect on obesity-associated
comorbidities (Emery et al., 1993) that is separate Mom that of total body fat,
although the developmental aspects of visceral adipose tissue deposition have
not been well studied. Among children, visceral adiposity appears to be
associated with an increased risk of cardiovascular risk factors such as elevated
triglycerides and reduced high-density lipoproteins that are independent of total
body fat (Caprio et al., 1996; Gutin et al., 1994~. However, the ages at which
these relationships appear remain unclear. Cross-sectional studies suggest that
visceral adipose tissue deposition is not marked before adolescence, but
increases rapidly at that time.
Adulthood
The period after adolescence has not been intensively studied, although
approximately two-thirds of adult obesity begins after adolescence. Whether
additional critical periods exist in adulthood is less certain, but pregnancy and
postpartum may constitute one such period for a subset of women (Williamson
et al., 1994~. Postpartum weight retention appears to range from 0.5 to 4.8 kg for
most women (Johnston, 1991), but ADican-American mothers may be twice as
likely to retain 9.1 kg (20 lb) or more postpartum than Caucasian mothers
(Parker and Abrams, 1993~. Boardley and colleagues (1995) found that African-
American women ate more and were less physically active postpartum than
were the Caucasian women in their sample. When the possible confounding
factors of prepregnancy weight, gestational weight gain, prenatal physical
activity, parity, and socioeconomic status were controlled, African-American
women still retained more weight in the postpartum period than did Caucasian
women. Results of several recent studies suggest that possible genetic factors
may be involved in the tendency to retain weight postpartum. One study found
that in women with normal prepregnancy BMIs, high first-trimester serum leptin
concentrations (a protein hormone encoded by the obese gene) correlated with
increased gestational weight gain and postpartum weight retention (Stein et al.,
1998~. In another study, women within 12 months of the birth of their first child
who were homozygous for the 825T allele of the G-protein J33, considered a
"thrifty" genotype, had significantly higher BMIs and postpartum weight
retention than women who did not carry the genotype (Gutersohn et al., 2000~.
No effect of the genotype was observed among women who had never given
birth, suggesting a pregnancy-specific phenomenon. In addition, this relation-
ship was only observed among women who engaged in low levels of physical
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60
WEIGHT MANAGEMENT
activity, supporting the idea that physical activity may mitigate effects of genetic
endowment on the potential for postpartum weight retention. Whether this
particular genetic variation in this specific G protein is causally linked to the
observed differences in BMI and weight retention or is merely a marker for the
responsible mutation, as well as what the mechanism might be, are both
questions that require further investigation (Feldman and Hegele, 2000~.
GENETIC DETERMINANTS
The understanding of the genetic influences on overweight and obesity in
humans has increased dramatically. Individuals show significant heterogeneity
in their body weight and body fatness responses to altered energy balance,
dietary components, and changing activity levels. It is now well-established that
overweight and obesity have a significant genetic component, with estimates of
the contribution of genetic variation to observed variation in obesity-related
phenotypes (such as BMI, fat mass, and leptin levels) ranging from 30 to 70
percent (Comuzzie et al., 1993, 1994, 1996~. However, little is yet known about
the specific causes of heterogeneity (Perusse and Bouchard, 1999~. It seems
clear that energy metabolism and neural control of appetite are involved in
regulating body weight and may contribute to the etiology of obesity. Studies of
resting metabolic rate show that the variation within families is less than the
variation among families (Bogardus et al., 1986~.
Several studies have evaluated the potential mechanisms by which genetic
factors may contribute to obesity. One of the mechanisms by which differences
in energy metabolism may contribute to obesity may involve defects in
uncoupling proteins (UCP). Several types of uncoupling proteins have been
identified. Fleury and colleagues (1997) first described human uncoupling
protein 2 (UCP-2) and its links to obesity and hyperinsulinemia. Bouchard
(1997) noted that markers near the UCP-2 gene in humans are linked to
differences in resting metabolic rate. Thus, genetic differences in UCP-2, and
perhaps other UCPs, may contribute to human obesity.
There is a group of at least 20 Mendelian syndromes in which obesity is a
component, including Prader-Willi, Bardet-Biedl, Borjeson, Cohen, and Wilson-
Turner (Gunay-Aygun et al., 1997; Reed et al., 1995~. These genetic disorders
are rare, and family studies do not suggest that the genes responsible for these
syndromes are involved in the common forms of human obesity. For more than
99 percent of obese humans, the genetic basis of their obesity is unknown.
Animal Models of Genetic Obesity
The strongest evidence for genetic weight-regulating mechanisms is the re-
cent elucidation of single gene defects that are associated with excessive weight
gain in animals. Single gene mutations can indisputably cause obesity in both
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FA CTORS THA T. lNFL UENCE BOD Y. WEIGHT
61
rodent models and in humans. In rodents, such mutations have been identified in
at least five genes: the obese gene for the circulating adipose tissue-secreted
factor leptin; the db gene for the receptor of leptin; the agouti yellow mutation,
which controls hair color in mice through the production of melanin pigments
(with its human equivalent, agouti signaling protein gene); the fat mutation in
the carboxipeptidase E gene, which is a prohormone processing enzyme; and the
tub mutation, the function of which has yet to be determined. Of the five gene
products that currently have been associated with weight regulation, leptin is the
best characterized. Genetic defects in leptin are associated with extreme obesity
in both humans and laboratory animals. In addition, serum concentrations of
leptin are elevated in close proportion to body fat in obese people with no defect
in the leptin gene. Recent studies show that administration of recombinant leptin
to lean and obese individuals results in dose-dependent weight loss (Heymsfield
et al., 1999~. Further research is needed to assess the potential role of leptin in
obesity treatment.
Familial Aggregation of Risk for Obesity
Using the comprehensive Danish adoption registry, Stunkard and colleagues
(1986) found that adopted children who were raised separately from their
biological parents had body weights closer to those of their biological parents
than to those of their adoptive parents. The children in this study were separated
from their parents at a very early age, generally before 3 months, so the oppor-
tunity for the biological parents to instill eating and activity habits was very
limited. Another study of adoptees showed a significant genetic influence on
obesity, but none of the environmental indicators evaluated were found to
contribute, although a number of the conditions considered have previously been
associated with obesity (Sorensen et al., 1998~. Stunkard and colleagues (1986)
estimated that as much as 70 percent of the variance in the occurrence of obesity
could be attributed to genetic factors, but other authors have postulated that as
little as 20 percent of the variance is due to genetic factors. The general consen-
sus is that genetic factors account for about 30 to 50 percent of the variance in
the occurrence of obesity (Bouchard, 1997~.
Twin studies provide the most impressive clinical evidence that genetic
factors play an important role in the etiology of obesity in humans. Stunkard and
colleagues (1990) studied identical and nonidentical twins who were reared
together and others who were reared apart. They found a high correlation of
body weight among identical twins, even if they were reared apart. Bouchard
and colleagues (1990) studied twins who were isolated in the Canadian wilder-
ness with no access to foods other than those provided by the investigators.
Identical twins were overfed for a period of 100 days, and their gains in body
weight and adipose tissue were evaluated. There was a closer association of both
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62
WEIGHT A'IANAGEMENT
body weight and intra-abdominal adipose tissue (visceral fat) within twin pairs
than among twin pairs.
The maximal heritability of obesity has been estimated to range from 30 to
50 percent, based on a review of family studies (Chagnon et al., 2000~. Although
extensive efforts have been made to identify mutations in the genes identified as
obesity-associated in rodents and in other candidate genes for obesity in humans,
to date only a handful of individuals have been identified with mutations in any
of the genes that have produced obesity in rodents. Specifically, several humans
have been identified with mutations in the leptin gene or its receptor, but no
individuals have yet been found with mutations in the other genes identified in
rodents.
In total, single gene mutations have been identified as responsible for
obesity in 25 persons, with these mutations appearing in 7 genes (12 different
mutations) (Perusse et al., 1999) or in 5 genes (Chagnon et al., 2000~. Studies of
quantitative trait loci (QTL) in rodents have suggested at least 98 different QTLs
associated with obesity (Chagnon et al., 20009.
Currently, the major effort in the search for specific genes that contribute to
human overweight and obesity is based on the use of genome scanning. In
genome scanning, linkage analysis is conducted to identify QTLs that affect the
specific phenotype under study. The use of genome scanning has provided
evidence of QTLs that influence body weight and the number of fat cells
(Chagnon et al., 2000~.
Comparison of the risks of obesity in spouses and in first-degree relatives
has suggested that genetic factors may be of greater prominence in more severe
obesity (Katzmarzyk et al., 2000~. Among the members of families that contain
at least one morbidly obese person, a major gene effect was transmitted in a
codominant fashion, suggesting a gene-environment interaction (Rice et al.,
19994. Both multifactorial and major gene effects have been suggested. Efforts
are ongoing to identify the genetic and molecular basis of overweight and
obesity, and it is likely that many genes (and within these genes and their
promoters, many different mutations or variants) that are responsible for the
genetic variation of obesity in humans will be identified.
The development of obesity likely involves a combination of shared
environment and shared genetic propensities. The rapid increase in prevalence
of obesity in the United States, as well as in many other countries, across all age
groups may reflect a removal of environmental constraints (e.g., high levels of
daily activity and food availability) on the expression of obesity genotypes.
Knowledge of the genetic components of obesity is not likely to be useful to the
military in the near term, but identification of markers of potential risk of
obesity may well have implications for future screening.
OCR for page 63
FACTORS THE T INFLUENCE BODY WEIGHT
-
45 -1
0
~ 40
._
>
~ O
I an
I
i
. _
._
I ~
~ 1 0
30
a, 25
a,
0 20
15
63
20-29 30-39 40~9 50-59 60~9 70-79 > 80
Age Group
G pre-obesity
·cIass ~
·cIass I!
· cIass Ill
FIGURE 3-1 The prevalence (%) of overweight and obesity of men and women by age
in the U.S. population. Preobesity = body mass index (BMI) of 25-29.9, class I obesity =
BMI of 3~34.9, class II obesity = BMI of 35-39.9, and class III obesity = BMI > 40.
SOURCE: Third National Health arid Nutrition Examination Survey, 1988-1994, Must et
al. (1999).
AGE
Cross-sectional and longitudinal studies indicate a gradual increase in the
average BMI of Americans up to the ages of 50 to 60 years (IOM, 19951. This
trend is similar, with some variation, across males and females and across all
evaluated ethnic groups. Population studies also indicate a decline in body
weight and BMI among the elderly, usually in the seventh and eighth decades
(IOM, 1995; Kuczmarski et al., 1994; NHLBI, 1998~. The same trends have
been identified in changes in total body fat and percent body fat (Chumlea et al.,
20021. Overweight and obesity thus reach maximal rates among middle-aged
adults. This pattern is shown in Figure 3-1.
The age-related body mass increase up to the fifth and sixth decades is
accompanied by additional anatomical, structural, and body compositional
changes. Stature declines from about age 30 onward, with rates in women faster
than those in men and for postmenopausal women faster than their premeno-
pausal counterparts. Declining stature accounts for a small portion of the age-
related increase in BMI (Gallagher et al., 1996~.
-
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64
WEIGHT MANAGEMENT
Many weight-management experts agree that body weight becomes pro-
gressively more difficult to maintain with age, but there appears to be little
rationale for increasing the upper BMI range consistent with good health as
individuals become older. Williams (1997) indicated that body weight and
associated circumferences would increase with advancing age unless food intake
is reduced and physical activity is substantially increased.
A large number of cross-sectional studies, however, do demonstrate that
body fat increases with age, even after controlling for changes in body weight
and physical activity levels (Baumgartner et al., 1995; Flynn et al., 1989;
Forbes, 1987; Forbes and Reina, 1970; Gallagher et al., 1996, 1997; Noppa et
al., 1980; Novak, 1972; Steen et al., 19799. Gallagher and colleagues (1996)
demonstrated that the mean body-fat content in nonexercising civilian women
with a BMI of 25 increased from 30 percent for those between the ages of 17
and 20 years to 36 percent for those ages 40 years and older. The implication of
this is that lean body mass and, frequently, skeletal mass, decrease with age.
Additionally, partitioning of adipose tissue between the subcutaneous and
visceral compartments is also moderated by age (Borkan et al., 1983~. Men have
more visceral adipose tissue than do women at all ages, and the rate of visceral
adipose tissue increase with age is greater in men than in women (Bleak, 2001).
In contrast to body fat, skeletal muscle mass declines with age beginning
around the third decade of life (Dutta and Hadley, 1995~. This observation is
true not only for the general population, but it is also evident in military
personnel (USAF, 1975~. The rates of decline may accelerate after the onset of
menopause in women (Aloia et al., 1991) and for both genders in the seventh
and eighth decades (Flynn et al., 1989~. Losses of skeletal muscle parallel
changes in skeletal minerals with advancing age and are present even after
controlling for loss in body weight (Gallagher et al., 2000~. The mechanisms of
body composition change with aging are multifactorial and include physical
inactivity, diet, and hormonal and cytokine alterations. The loss of lean mass
and gain in fat mass occur even with no apparent change in body weight. Since
lean mass contributes the larger share of metabolic activity, total energy
expenditure during rest or low activity will also decrease proportionally with the
loss of lean mass.
Total energy expenditure and thus, energy requirements, decrease with
advancing age (Tzankoff and Norris, 1978~. Physical activity levels are lower in
older individuals, which account for a portion of the energy expenditure
reduction that comes with aging. Resting energy requirements are also lower in
the elderly, due largely to decreases in all metabolically active tissues, including
skeletal muscle, brain, and visceral organs. In laboratory animals, the heat
produced by tissues per unit of mass decreases with age (a decrease in the
specific resting energy expenditure of organs), but it remains uncertain whether
this observation also applies to humans. The practice of resistance training by
people over the age of 50 years may enhance fat-free mass, primarily skeletal
OCR for page 65
FACTORS THAT INFLUENCE BODY WEIGHT
65
muscle, and thereby help offset the age-related decline in resting metabolic rate
(Hill and Saris, 1998; Tzankoff and Norris, 19774. In women, loss of ovarian
function accounts for a lower rate of overall heat production compared with that
observed in premenopausal women (Poehlman and Tchernof, 1998~. Thus, both
older men and women have lower rates of energy expenditure and, unless
counterbalanced by increased physical activity and reduced food intake, older
individuals, in general, will gain weight over time.
RACE/ETHNICITY
Whether there are racial/ethnic differences in response to the various
components of weight management is a legitimate research question that has
been explored to only a moderate extent. Data from National Health and
Nutrition Examination Surveys (NHANES) clearly indicate that there are
racial/ethnic differences in the prevalence of overweight and obesity. Flegal and
coworkers (2002), reporting on 1999-2000 NHANES data, determined that in
men 20 years of age and older, the prevalence of overweight (BMI ~ 25) was
67.4 percent for non-Hispanic whites, 60.7 percent for non-Hispanic blacks, and
74.7 percent for Mexican Americans. The differences were not statistically
significant, but sample sizes were relatively small. However, for women ages 20
years and older, the prevalence of overweight was 57.3 percent in non-Hispanic
whites, 77.3 percent in non-Hispanic blacks, and 71.9 percent in Mexican
Americans. The difference in prevalence between non-Hispanic white and non-
Hispanic black women was statistically significant (Flegal et al., 20024. The
causes of these differences in the prevalence of overweight have not been clearly
identified, but are likely to be a combination of physiology, culture, and
behavior.
The relationship of BMI to percent body fat is also affected by race/
ethnicity. Fernandez and colleagues (2003) recently reported the results of an
analysis of l l cross-sectional studies involving body composition assessments
of African-American men and women, Hispanic-American men and women,
and European-American men and women. The average age ranged from 42.6 to
50.8 years, and the average BMI ranged from 25.1 (European-American
women) to 29.8 (African-American women). Total body fat was measured using
dual-energy X-ray absorptiometry. There were no differences in the estimation
of percent body fat from BMI for men across ethnic groups. However, for
women with BMIs less than 30, Hispanic-American women had a significantly
higher percent of body fat at a given BMI than did African-American or
European-American women. However, at BMIs greater than 35, European-
American women had a higher percent body fat than either of the other two
groups of women. Some earlier studies have reported greater fat free mass in
African-American women compared with Caucasian women with the same
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66
WEIGHT MANAGEMENT
BMI, primarily due to the greater skeletal mass in ADican-American women
(Gallagher et al., 1996; Ortiz et al., 1992~.
A number of studies have examined possible physiological reasons for these
race/ethnic differences. Foster and colleagues (1997) explored differences in
resting energy expenditure (REE) between obese African-American women and
Caucasian-American women. They found that REE was most closely correlated
to body weight and that Ahican-American women had lower REE than
Caucasian-American women. Melby and coworkers (2000) examined behavioral
and physiological characteristics related to obesity risk in young, sedentary,
nonobese African-American and Caucasian-American women. The two groups
were similar in age and anthropometric characteristics. Parameters examined
included REE, respiratory exchange rates (RER), insulin sensitivity, and
maximal oxygen consumption. REE was 3 to 4 percent lower in African-
American women, but the difference was not statistically significant. However,
the resting RER was significantly lower in African-American women. The
African-American women also had significantly lower insulin sensitivity values
that resulted in higher acute phase insulin response to glucose. Total daily
energy expenditure and physical activity energy expenditure were significantly
lower in the African-American women.
Tanner and coworkers (2002) recently identified a relationship between
muscle fiber type and obesity. In a study of lean and obese African-American
and Caucasian women, type I muscle fibers (slow twitch, oxidative muscle
fibers) were significantly reduced in obese women compared with the lean
women, and type IIb fibers (fast twitch, glycolytic muscle fibers) were
significantly increased. These differences between lean and obese women were
greater in African-Americans than in Caucasians. The type IIb phenotype is
insulin resistant and deficient with regard to lipid disposal. The authors
speculated that the prevalence of the type II fibers might result in partitioning
lipid toward storage in skeletal muscle or adipose tissue rather than oxidation
within the skeletal muscle, resulting in a positive fat balance.
A number of studies have also examined social and behavioral factors that
may contribute to the difference in the prevalence of overweight between
African-American and Caucasian women (Kumanyika et al., 1993; Stevens et
al.' 1994~. Attitudinal and behavioral factors that limit the ability of some
African-American women to lose weight or maintain weight loss have been
identified. Regardless of whether or not they were overweight, ADican-Ameri-
can women were half as likely as Caucasian women to consider themselves
overweight. There is a much greater cultural tolerance of overweight among
African-Americans, and they have different body image perceptions. Although
African-American women responded physiologically to a weight-reduction
program in the same manner as Caucasian women, their drop-out rate from the
program was double that of Caucasian women (Glass et al., 2002~.
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I~-ACTORS THAT lNFLUENCE BODY WEIGHT
PHYSICAL ACTIVITY
67
While recent studies point to the importance of genetic factors in the
etiology of obesity (Bouchard, 1997; Chagnon et al., 2000), the rapid rise in the
prevalence of overweight and obesity in the last 20 years likely reflects major
environmental shifts in exercise habits and food availability, which can be
controlled.
Physical activity represents an important component of volitional energy
expenditure. Modern transportation and other conveniences have reduced the
need for energy expenditure in the form of physical exertion. Reductions in
physical activity over the past several decades likely contribute to the evolution
of the positive energy balance and weight-gain characteristics of all industrial-
ized societies. Lack of physical activity begins in youth, with television
watching time correlated with BMI, as well as with both prevalence and severity
of overweight (Dietz and Gortmaker, 1985; Katzmarzyk et al., 1998; Tanasescu
et al., 2000~. A reduced emphasis on school physical education classes has been
accompanied by a gradual decline in childhood fitness (Luepker, 1999~. Indeed,
physical inactivity is a major risk factor for development of obesity in children
and adults (Astrup, 1999; Goran, 2001~. Among adults who have maintained
weight loss over time, a common factor is increased physical activity (Klem et
al., 1997~.
The effects of physical activity on weight and health may be influenced by
age. Owens and coworkers (1992) evaluated the effects of physical activity on
both weight change and the risk factors for cardiovascular disease during the
perimenopausal period. Women who increased their activity levels during the 3-
year study period (as measured using the Paffenbarger Physical Activity
Questionnaire) had the smallest increases in body weight and the smallest
decrement in high-density lipoprotein cholesterol.
Flatt (1987) has pointed out that to avoid increased fat deposition, both
energy balance and macronutrient balance (especially fat balance) are necessary.
When dietary fat is elevated, there is limited capacity to reduce total body fat by
fat oxidation. Exercise, especially in bouts of 30 minutes of activity or more
(Pate et al., 1995), can promote fat oxidation because the substrate that is
preferentially oxidized switches Mom carbohydrate to fat. Thus, chronic
extended bouts of exercise may, in effect, substitute for expansion of the adipose
tissue, allowing the physically active individual to achieve fat balance while
maintaining a lower body-fat mass than the sedentary individual (Flats, 1987~.
3akicic and coworkers (1995) initially demonstrated that over the short term,
four 1 0-minute bouts of exercise per day, four times per week is more effective
in reducing body weight than a single 30 to 40 minute period of exercise.
However, the long-term data indicated that the short-term bouts of exercise were
not as effective as the long bouts in reducing weight and maintaining weight loss
(Jakicic et al., 1999~.
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68
WEIGHT MANAGEMENT
Most fatty-acid oxidation in the human body occurs in muscle (Calles-
Escandon and Poehlman, 1997~. The intrinsic capacity of muscle to oxidize fat
can be impaired by physical inactivity and possibly by loss of estrogen in
women, but it is amenable to partial correction by exercise training (Calles-
Escandon and Poehlman, 1997~. A decrease in aerobic capacity and fat-free
mass, rather than aging per se, is responsible for the decrease in fat oxidation
seen in elderly women (Calles-Escandon and Poehlman, 1997~. Exercise
training increases oxidative disposal of fatty acids and improves muscle
metabolism in both young and old individuals. However, the elderly do not
increase fat utilization in response to exercise to the same extent as the young,
despite performing exercise to the same intensity and for the same duration
(Bleak, 2000; Calles-Escandon and Poehlman, 1997~.
In a study of 970 healthy, female twins with a wide range of percent body
fat, both total body fat and central adiposity were associated with physical
activity (Samaras et al., 1999~. Moderate-intensity sports of 1 and 2 hour
durations accounted for within-pair differences of 1.0 kg and 1.4 kg,
respectively, of total body fat. Among participants in whom one of a pair of
twins was overweight, higher levels of physical activity were still associated
with 3.96 kg lower total body fat and 0.53 kg lower central abdominal fat. In
other words, even persons with an apparent genetic predisposition to adiposity
showed an effect of physical activity on body-fat mass (Samaras et al., 1999~.
Studies of energy expenditure in individuals and families show that differences
are greater between families than within families (Bogardus et al., 1986~. Some
differences in energy expenditure between families are due to genetic factors
and some are due to differences in activity patterns.
Hormones affect the relationship of physical activity, body fat, and fat-free
mass. Guo and coworkers (1999) found that associations between physical
activity and fat-free mass were more pronounced in postmenopausal women
than in premenopausal women, and that hormone replacement therapy had
beneficial effects on body composition. Monozygotic twin pairs who were
concordant for smoking and hormone replacement therapy status, but discordant
for moderate-intensity activity, showed greater within-pair differences in total
body fat than those who were concordant for activity level (Samaras et al.,
1999), suggesting that the effect of physical activity is greater than that of
hormonal status.
Habitual physical activity also affects other physical characteristics. Gilliat-
Wimberly and coworkers (2001 ) found that an association exists between
habitual physical activity and maintenance of resting metabolic rate in middle-
aged women. Physical activity also may reduce the incidence of chronic diseases
by favorably altering blood lipid profiles, reducing body fat, and improving lean
body mass (Eliakim et al., 1997; Schwartz et al., 1991; Wei et al., 1997; Wilbur
et al., 1999~.
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FACTORS THA T INFLUENCE BODY WEIGHT
FOOD
Intake
69
In conjunction with the importance of physical activity levels, energy intake
must be matched to energy expenditure. Positive energy balance results if
energy intake is greater than energy expenditure. Increased energy consumption,
decreased energy expenditure, or both can result in positive energy balance.
While the etiology of obesity is multifactoral, the common characteristic of
all obese people is excessive energy storage in the form of body fat. Whether
obese people consume more energy than do lean people has been a major source
of controversy. Studies in modern respiratory chambers using doubly-labeled
water have shown that weight-stable obese people have a higher resting
metabolic rate and total 24-hour energy expenditure than do lean people (Jequier
and Schutz, 1983; Ravussin et al., 1982; Zed and James, 1986), which
demonstrates that average energy intake must indeed be higher in the obese.
Some differences in energy expenditure, and consequently in energy intake,
among families are due to genetic factors and differences in activity patterns.
Social and cultural factors also contribute to individual food intake differences
(de Castro, 1999~.
Since the energy in food is derived from the macronutrients protein, fat, and
carbohydrate (CHO), plus the optional energy source, alcohol, diets that are high
in fat tend to be low in complex CHOs such as fiber. There is still considerable
controversy over whether the role of diet composition or simply total energy
intake is important in maintaining a healthy body weight.
Composition
A high energy intake or an energy intake that is not adjusted downward
with declining physical activity or age-related decreases in lean body mass is
associated with the development of overweight or obesity in susceptible individ-
uals. In addition to total energy intake, the character of the diet may play a role
in the etiology of obesity. High-fat diets may promote increased energy intake or
may be associated with metabolic changes that promote the deposition of
adipose tissue.
Dietary Fat
Research in both animals and humans suggests that high-fat (low in
complex CHOs) diets promote obesity (Astrup et al., 2000; Bahceci et al., 1999;
Blundell and Cooling, 2000; Cheverud et al., 1999; Maffeis et al., 2001~.
Because fat is more energy dense than other foods (9 kcal/g versus 4 kcal/g for
protein and CHO), eating high-fat foods results in a greater energy intake than
would eating a similar quantity of lower-fat foods. Fat modifies the taste of food
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WEIGHT MANAGEMENT
and, in some people, promotes excess intake. Fatty foods tend to be easier to
chew or may not require chewing, thus making larger quantities easier to eat in a
shorter time than foods that require more mastication. Dietary fat also has a
weaker satiation effect than CHOs, which results in the over consumption of fat
(Rolls and Hammer, 1995; Rolls et al., 1999~.
Some of the difference in weight gain on a high-fat versus a low-fat diet
may be explained by differences in the metabolic processing of fat. Compared
with dietary fat, CHOs require additional energy expenditure for digestion,
assimilation, and conversion to fat. When energy intake exceeds expenditure, 23
percent of energy consumed is required to convert and store CHO as fat,
compared with only 3 percent to store fat. Two studies in laboratory animals
have demonstrated this effect of dietary fat on body weight and body
composition (Donato and Hegsted, 1985; Lin et al., 1979~.
The link between dietary fat and obesity in humans is not conclusive
because of difficulties in accurately measuring or controlling the food intake and
energy expenditure of individuals and the need to rely on estimates of body
composition. Nonetheless, increasing evidence from clinical studies suggests
that dietary fat promotes weight gain in humans as well as in animals. Studies in
which people were overfed diets varying in the proportion of energy Mom fat
(40 to 53 percent of kcal as fat) showed that high-fat diets promoted weight gain
more efficiently than did lower-fat diets (Sims et al., 1973~.
A positive correlation between the proportion of fat in the diet and the
incidence of obesity has been noted among various cultures, as well as within
ethnic groups that have migrated to the United States and adopted American
dietary patterns (Curb and Marcus, 1991; Kushi et al., 1985~. While these
correlations all point to a causal role for dietary fat in obesity, they are subject to
confounding variables such as differences in energy intake and expenditure,
health status, and genetic and environmental influences. However, based on
information such as that described above, Danforth ( 1985) recommended
shifting to a higher-CHO and lower-fat diet to reduce the high prevalence of
obesity in affluent societies such as the United States.
Obesity is more closely correlated with the level of dietary fat than with
total energy intake (Dreon et al., 1988; Romieu et al., 19883. A low incidence of
obesity has been observed among vegetarians who typically consume low-fat,
high-CHO diets (Knuiman and West, 1982; Sacks et al., 1975~. However, those
who adhere to vegetarian diets for religious rather than nutritional reasons
probably have a higher-fat diet (Dhurandhar and Kulkarni, 1993), and the
prevalence of obesity among these types of vegetarians is high compared with
that of omnivores (Dhurandhar and Kulkarni, 1992~.
Some studies have failed to demonstrate an association between fat intake
and body weight in free-living populations. On the basis of food frequency
questionnaires, Macdiarmid and colleagues (1994) stratified 1,800 people by
their fat consumption (high was considered to be 45 percent or more kcal as fat
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FACTORSTHATlNFLUENCEBODY WEIGHT
71
and low was considered to be 35 percent or less kcal as fat) and found no
statistically significant difference in age, BMI, or social class between the two
groups. However, the high-fat group rated their general diet and health as
poorer. The high-fat group also consumed significantly more protein and total
energy, but less CHO and fiber; consumed meat and high-fat dairy products
more frequently; and consumed fewer fruits, vegetables, and cereals.
Results of a small study suggest that the amount of energy required to
maintain body weight may be related to the proportion of fat in the diet,
regardless of an individual's weight status (Prewitt et al., 1991~. These findings
suggest that dietary fat may promote greater weight gain and body-fat accumula-
tion than expected on the basis of energy intake alone. In contrast, Leibel and
colleagues (1992) found no relationship between the ratio of dietary fat/CHO
and the total energy required to maintain body weight. CHO ranged from 15 to
85 percent of total intake, and kcal from fat ranged from 0 to 70 percent of total
intake. The disparity between findings of these two studies may be due to the
shorter duration of the second study (33 days average and ranging from 15 to 56
days compared with 140 days in the Prewitt study). Differences among the
normal-weight patients in the study of Prewitt and colleagues (1991) were not
seen consistently before 13 to 16 weeks. Also, body composition was not
assessed in the Leibel study, and results of animal studies suggest that isocaloric
diets of varying fat content may produce differences in percent of body fat
without changing body weight (Boozer et al., 1990, 1993~.
The arguments for whether dietary fat promotes obesity were summarized
in two recent, competing editorials. Willett (1998a, 1998b) argues that obesity
has increased in the United States despite reductions in intake of dietary fat and
that ecological studies have found no relationship between fat intake and
obesity. In contrast, Bray and Popkin (1998) argue that individuals who gained
weight may not have decreased (or may have increased) their intake of dietary
fat. They also argue that ecological studies may not be appropriate to study the
relationship between fat intake and obesity, that body weight is a poor measure
of body fatness, and that most of the previous studies focused on outcomes other
than obesity. Although the literature is not clear, results of studies on laboratory
animals and the small number of human studies suggest that dietary fat does
promote obesity. Recently, Astrup and colleagues (2002) reviewed evidence on
the effects of low-fat diets. Four meta-analyses of weight change occurring on
low-fat diets in intervention trials with overweight subjects were reviewed.
These analyses consistently demonstrated significant weight loss in both
normal-weight and overweight subjects.
C(zrl~ohydrates
Several rationales have been postulated for the use of high-protein, low-
CHO diets: (1 ) intake of a high proportion of kcal as CHO has adverse physio-
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WEIGHT MANAGEMENT
logical consequences, such as increasing insulin secretion, promoting fat deposi-
tion, and increasing serum triglycerides levels; (2) low-CHO diets can lead to a
"ketogenic"-state, which has been hypothesized to suppress appetite; (3) a high-
protein diet preserves lean body mass during weight loss; and (4) the ther-
mogenic effect of protein is the highest of the three macronutrients, resulting in
increased energy expenditure for a similar intake.
There is at least some scientific rationale for the above hypotheses (Skov et
al., 1999a, l999b). ~ high-protein diet has been found to: stabilize blood glu-
cose during nonabsorptive periods and reduce insulin response following test
meals (Layman et al., 2003b), improve glucose oxidation (Piatti et al., 1994),
decrease lipid oxidation (Piatti et al., 1994), produce positive changes in blood
lipids (Layman et al., 2003b), and provide greater satiety than diets higher in
CHO (Layman et al., 2003a). Although more research is needed on the subject
of amino acid flux measurements and how it relates to blood glucose levels, data
from Layman and colleagues (2003b) support the idea that the ratio of dietary
protein and CHO can have a significant effect on metabolic balance and specifi-
cally on glucose homeostasis during weight loss.
The role of CHO in soft drinks in producing obesity is controversial. Some
studies suggest that an increase in the consumption of soft drinks may have
contributed to the increased prevalence of obesity (French et al., 2000; Troiano
et al., 2000), whereas others do not support this hypothesis (Gibson, 2000;
Macdiarmid et al., 1998; O'Brien et al., 1982~.
Portion Size
There is little research available on the role of portion size in the increasing
prevalence of overweight in the United States. However, common sense dictates
that it is a contributing factor. For example, a single serving of meat is con-
sidered to be 3 to 4 oz based on the Dietary Guidelines and the U.S. Food Guide
Pyramid. However, in restaurants (where Americans are spending a greater
portion of their food dollars), an 8-oz portion of red meat would be considered a
"petite" serving; the standard serving would be 12 to 16 oz. Thus, an individual
consuming a 16-oz steak in a restaurant would be likely to report (if asked in a
dietary survey) consuming a single serving of red meat, when in reality 4 to 5
servings were consumed.
The intake of soft drinks has increased dramatically in the last 40 years, as
has the trend towards larger portion sizes (Hill and Peters, 1998~. While a
standard serving of a soft drink in 1960 consisted of one 6-oz serving, the
standard size serving today is 12 oz. and many vendors sell 20-oz bottles almost
exclusively. Fountain drinks have also increased to the "superjumbo" 32- to 64-
oz sizes. It is not unusual for individuals to consume some 500 to 1,000 kcal per
day from soft drinks in addition to their usual solid-food diet.
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FA CTORS THA T INFL UENCE BOD Y WEIGHT
73
The change to larger portion sizes has been particularly apparent in fast-
food restaurants where portion size has been used as a competitive tool. Full-
service restaurants also have adopted the practice of serving larger meals.
Similar to the increase in sonic drink portions sizes, fast-food restaurants now
offer "super-size" portions for a minimal increase in cost. For example, a
"jumbo super-size" order of a large hamburger, french fries, and soft drink at a
fast-food restaurant may now contain more than 1,500 kcal for a single meal
(Nielsen and Popkin, 2003; Young and Nestle, 2002, 2003~. One of the
distinguishing features of dining out in Europe compared with the United States
is the difference in restaurant portion sizes, a factor that may contribute to the
lower prevalence of obesity in Europe.
A recent trend analysis of portion size was conducted by Nielsen and
Popkin (2003~. Data were taken from four national food-consumption surveys
covering the period 1977 to 1996. Food consumption was estimated as energy
intake in kcal and as average portion sizes using food models to assist
respondents in identifying portion size. Results demonstrated that for foods
eaten both inside and outside the home, portions sizes have increased for salty
snacks, desserts, soft drinks, fruit drinks, French fries, hamburgers, cheese-
burgers, and Mexican food.
Meal Patterns and Eating Habits
Eating patterns that are appropriate for an active lifestyle may continue after
the individual changes to a more sedentary lifestyle. Individuals for whom this
observation has been made include athletes and a large percentage of people
with increasing age and changing occupational responsibilities. Athletes who are
in training expend large amounts of energy each day and, for many organized
sports, are encouraged to eat large quantities to maintain their weight at an
artificially high level. When activity declines, the eating pattern established
during training may not be adjusted to meet the new lower energy needs. The
same is true of military personnel. During initial entry training, advanced
individual training, and special forces training, large amounts of energy are
expended on a daily basis. By the time training is completed, individuals have
been habituated to consume large amounts of food over a very short period of
time.
In many occupations, tasks that require more physical activity are assigned
to younger workers. As these workers age and acquire more responsibility, their
work may become more sedentary, but eating patterns may not change. This
pattern of decreased occupational energy expenditure with job promotion may
be common in the military as well. Privates, airmen, and junior noncom-
missioned officers are more active than senior officers and noncommissioned
officers. Despite strong commitments to engage in daily physical fitness, which
may be unchanged or even increased in more senior individuals, the decrease in
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WEIGHT MANAGEMENT
activities of daily living and job performance can lead to a positive energy
balance unless particular care is taken to reduce energy intake.
The ubiquitousness of vending machines and fast-food outlets ensures
constant access to foods at work—usually foods with a high caloric content
largely in the form of fat or refined CHO. A major contributing factor to the
epidemic of obesity in recent years is likely the rise in the proportion of meals
eaten away from home (eating out), along with the increase in access to foods in
virtually all locations. These changes have contributed in several ways to
promoting obesity. Because more families include two-wage earners, adults
spend more time out of the home and do not have time to prepare meals as they
customarily did in the past. Meals consumed at restaurants tend to be larger and
have a higher caloric content than those consumed at home, mainly because of
hillier fat content and larger portion sizes (Young and Nestle, 20034. In
addition, a high percentage of meals eaten away from home are eaten in fast-
food restaurants or consist of fast-food take-out. The presence of food in
virtually every circumstance of daily life, from fast-food outlets to vending
machines, encourages and allows individuals to consume multiple calorically
dense meals and snacks per day (Bell et al., 1998; Rolls, 2000~.
PHYSIOLOGICAL FACTORS
A number of phenotypic characteristics have been associated with the risk
of weight gain, notably alterations in nonvolitional components of energy
expenditure. Energy expenditure can be divided into three main components:
.
Resting metabolic rate (RMR), the rate of energy expended at rest, un-
der thermo-neutral conditions, and in a post-absorptive state.
Thermic effect offending, the incremental increase in energy expendi-
ture after a meal is consumed due to the energy costs of absorption and the
transport of nutrients, as well as the synthesis and storage of protein, fat, and
CHO. Some of the thermic effect of feeding may be mediated by sympathetic
nervous system activity.
.
Energy expended for physical activity' including involuntary move-
ments associated with shivering, fidgeting, and postural control.
RMR accounts for 60 to 75 percent of total energy expended in most adults.
RMR is primarily related to the maintenance of fat-free mass, reflecting such
activities as protein synthesis and breakdown, temperature and cellular
homeostasis, and cardiovascular, pulmonary, and central nervous system
function. Metabolism associated with visceral organ mass makes the largest
contribution to RMR, followed by that of skeletal muscle mass and adipose
tissue (Gallagher et al., 1998~. RMR is consistently greater in men than in
women due to the greater lean tissue mass of males. A low RMR relative to
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FACTORS THATINFLUENCE BODY WEIGHT
75
body size was found to predict weight gain (Ravussin et al., 1988) in both men
and women, although some studies have not confirmed this observation
(Weinsier et al., 2000~. RMR begins to decrease with age in the middle of the
fourth decade. Gilliat-Wimberly and coworkers (2001) found that an association
exists between physical activity and maintaining RMR in middle-aged women.
The thermic effect of feeding usually accounts for 5 to 10 percent of daily
energy expenditure and varies between lean and obese individuals (Astrup,
19961. Extensive studies have been inconsistent in supporting the view that ex-
cessive weight gain is secondary to a reduced thermic effect of food (Tataranni
et al., 19959~
Recent studies support the view that small, nonvolitional physical activities
such as fidgeting may account for individual differences in energy expended
with changes in energy balance (Levine et al., 1999; Zurlo et al., 19924.
Although relatively small in caloric magnitude, these activities may account for
some of the between-individual differences observed in the regulation of body
weight.
These three phenotypic energy expenditure characteristics serve as markers
for potential weight gain over the long term. Many factors may contribute to
these individual energetic differences, and the origin of these differences is the
basis of intensive study.
ENVIRONMENTAL FACTORS
Smoking and Alcohol
Cigarette smoking increases metabolic rate and may limit food intake, and
weight gain is a common consequence of smoking cessation (Perkins, 1993;
Russ et al., 2001~. The use of alcoholic beverages may also have an impact on
body weight. Energy consumed as alcohol that is in excess of need is converted
to and stored as fat. Drinking alcohol has been shown to be associated with a
greater energy intake than drinking nonalcoholic beverages, perhaps due to
increased appetite (Tremblay and St-Pierre, 1996; Tremblay et al., 1995~.
A recent, large prospective study of a cohort of men ages 40 to 59 with a 5-
year follow-up found that mean BMI increased significantly from the light-to-
moderate to the very-heavy alcohol intake group. The study concluded that
heavy alcohol intake (defined as 2 30 g/day of alcohol) contributed directly to
weight gain and obesity, regardless of the type of alcohol consumed (Wanna-
methee and Shaper, 2003~.
Pharmacological Agents That Produce Weight Gain
Numerous drugs can produce weight gain and fat gain. These include
glucocorticoids (e.g., prednisone), hypoglycemic agents (e.g., insulin, sulfonyl-
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WEIGHT MANA CEMENT
ureas), certain antihypertensive agents (e.g., prazocin), anti-allergens (e.g.,
cyproheptadine), and numerous drugs that affect the central nervous system
(e.g., thorazine, tricyclic antidepressants, valproic acid, lithium). Most of these
drugs are used for diseases that mandate separation from the military, but there
are a number of drugs that may be taken by military personnel that are not
deemed a rationale for separation.
SOCIAL FACTORS
Americans live in a culture in which food is abundant. A well-developed
and efficient food transportation and storage system assures a readily available
and affordable food supply throughout the entire year.
The relative affluence of Americans has led to an increase in consumption
of snack foods (Morgan and Goungetas, 1986) and an increase in the proportion
of foods of animal origin compared with that of foods of plant origin (Senauer,
1986~. Foods of animal origin are likely to be higher in energy and fat than
comparable quantities of foods of plant origin.
The availability and abundance of food in the U.S. marketplace has
accelerated dramatically in the past 30 years. The per capita energy content of
food entering the American marketplace increased about 500 calories on a daily
basis during this time period. In addition, fat intake has also increased steadily,
although the relative intake of fat has been decreasing since the 1970s (Putnam
and Allshouse, 1999~. This decrease in fat intake has been associated with an
increase in average total energy intake (Bray and Popkin, 1998~. Food-supply
studies indicate that the increase in the number of calories consumed is
accompanied by a shift in macronutrient consumption that reflects an increase in
refined CHO consumption and a decrease in consumption of fruits and
vegetables (Putnam and Allshouse, 1999~.
Family and Ethnicity
Eating is an intensely social activity, and many eating habits are acquired in
a familial or ethnic setting. People tend to imitate the eating habits of their
parents, so quantity and quality of foods eaten and meal patterns tends to be
established early. Traditions that arise around eating patterns in a more agrarian
or active society may favor excess consumption. Ethnic groups differ in their
perceptions about appropriate body size and what constitutes overweight
(Bhadrinath, 1990; Root, 1990~.
Studies of changes in diet with immigration and acculturation show, for
example, that Japanese who migrated to California and Hawaii have tended to
abandon the traditional low-fat Japanese diet for American food patterns
(Burchfiel et al., 1995; Curb and Marcus, 1991; Goodman et al., 1992; Hara et
al., 1996; Ziegler et al., 1996~. The result has been a marked increase in weight
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t-A CTORS THA T INFL UENCE BODY WEIGHT
77
among these immigrants. Similarly, Japanese children who remain in Japan, but
whose diet is increasingly western, are also getting heavier (Murata, 2000;
Takada et al., 1998~. Thus, dietary change is strongly associated with increased
weight in both of these carefully studied population groups. The same phenome-
non is observed in studies of South Asians who have migrated to the United
Kingdom and who have modified their diet and physical activity patterns
(McKeigue et al., 1992~.
Socioeconomic Status
Social class and socioeconomic status (SES) influence the prevalence of
overweight. In many countries of the world, lower SES is linked to increased
body weight (Molarius et al., 20004. In contrast, in some developing countries
and primitive societies, obesity is considered a sign of affluence or fertility
(Molarius et al., 2000~. However, some researchers who contend that obesity
decreases economic status have disputed the belief that lower SES causes
obesity in the United States. For example, one study reported that women who
were overweight in late adolescence or early adult life were more likely to have
lower income, greater levels of poverty, and decreased rates of marriage than
were normal-weight women with comparable degrees of disability (Gortmaker
etal., 1993~.
The Potential Role of Viruses in the Etiology of Obesity
The possibility exists that at least some cases of human obesity are due to
viral infection. Five viruses and scrapie agents cause obesity in animals (Bernard
et al., 1988, 1993; Carp et al., 1998; Carter et al., 1983a, 1983b; Dhurandhar et
al., 1990, 1992, 1997, 2000; Gosztonyi and Ludwig, 1995; Lyons et al., 1982;
Nagashima et al., 1992~. One of these viruses is a human adenovirus, Ad-36,
which has been shown to produce a syndrome of increased body fat and
paradoxically decreased serum cholesterol and triglycerides in chickens and
mice (Dhurandhar et al., 2000~. Preliminary data have been reported that
demonstrated similar results in monkeys (Atkinson et al., 2000~. Other prelim-
inary studies suggest that humans with serum antibodies to Ad-36 have a higher
BMI and lower serum lipids than do Ad-36 antibody-negative individuals
(Atkinson et al., 1998~.
Humans in Bombay, India, who had serum antibodies to SMAM-l, an avian
adenovirus, were noted to be significantly heavier and to have lower serum
lipids compared with antibody-negative individuals. Viral antigen was found in
the serum oftwo ofthe individuals with SMAM-1 antibodies (Dhurandhar et al.,
1997~.
More research is needed to confirm the hypothesis generated from the
above data that some cases of human obesity might be due to a viral infection.
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WEIGHT MANA CEMENT
Since adenoviruses are common cold viruses, the possibility of the spread of
Ad-36 and perhaps other obesity-producing viruses in the military community
may be of significant concern.
SUMMARY
The brief review of factors influencing body weight presented in this chap-
ter demonstrate that maintaining a healthy body weight is an extremely complex
issue. Maintenance of fitness and appropriate body-fat standards by military
personnel is affected by each individual's genetics, developmental history,
physiology, age, physical activity level, environment, diet, ethnicity, and social
background.
Representative terms from entire chapter:
physical activity
