Which Factor Determines The Size Of The Body Frame

In that location are numerous factors that can influence body weight. The private has no control over some of these factors, including developmental determinants, genetic makeup, gender, and age. Other factors that influence body weight over which the private has potential command include level of physical activeness, diet, and some ecology and social factors. This chapter explores the human relationship between each of these factors and torso weight.

DEVELOPMENTAL DETERMINANTS

It has been postulated that there are times during people's lives when exposure to certain factors may increment their run a risk for the onset of obesity. These times have been termed "critical periods." If these critical periods, along with the influential factors, tin can be clearly divers, 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 boyhood accept been proposed equally critical periods in childhood (Dietz, 1994); pregnancy and the immediate postpartum menstruum accept been proposed equally critical periods for women in machismo.

Prenatal Factors

Although the data are subject area 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 2 trimesters of pregnancy have progeny who have a college prevalence of obesity, diabetes, insulin resistance, and hypertension after in life. Progeny of survivors of the Dutch famine in World War Two demonstrated a higher prevalence of obesity and diabetes (Ravelli et al., 1976), although this decision was questioned by after studies (Jackson et al., 1996; Susser and Stein, 1994). Malnutrition in utero too has been reported to event in increased obesity and its complications afterwards in life (Stanner et al., 1997). Lower birth weights too 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 socioeconomic background are more probable to be exposed to malnutrition during gestation or early childhood, the prevalence of obesity in such subgroups might be expected to be college.

Adiposity Rebound

Adiposity increases from nativity until approximately i year of historic period, then declines to a minimum at approximately six years of age. The term "adiposity rebound" refers to the increase in body mass index (BMI) and body fatty that occurs later on this nadir in children between the ages of 5 and 7 years. Children experiencing adiposity rebound at an earlier age appear to have a iii- 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 probability charts based on 3,650 children followed from birth to 18 years of age, that children who experienced this rebound before eight years of age have a higher risk of adulthood obesity. Nevertheless, Guo and coworkers (2000), using serial BMI information from the Fels Longitudinal study demonstrated that while there was no clan between early historic period at adiposity rebound and adult BMI status in men, afterwards controlling for effects of nascency weight, adult physical activity, booze and cigarette use, at that place was approximately twice the take a chance for overweight with early rebound in women.

Causes of early adiposity rebound have been variously attributed to avant-garde 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 testify is yet non clear well-nigh whether historic period at adiposity rebound is a critical menses for the evolution of obesity, but that early adiposity rebound might well be a statistical predictor of later on obesity because of its strong relationship with early on adiposity and accelerated maturation, both of which are established markers of afterward risk of obesity.

Adolescence

Although just xxx pct of adult obesity begins during babyhood, lxx percent of the developed obesity that begins in childhood may start during adolescence (Dietz, 1994). Boyish obesity is associated with a multifariousness of agin health effects in adulthood, including early on bloodshed in men and increased risks of coronary heart disease, diabetes, and colorectal cancer (Miller, 1988; Must et al., 1992; Wylie-Rosett, 1988). Almost of these risks were only slightly attenuated by adjustment for adult obesity, which suggests that obesity during boyhood may decide the hazard of these after complications regardless of whether or not the individuals are obese adults.

While total fatness is an important consideration when evaluating developmental aspects of obesity, an additional consideration is adipose tissue distribution. Visceral adipose tissue has an independent effect on obesity-associated comorbidities (Emery et al., 1993) that is split from that of total trunk fat, although the developmental aspects of visceral adipose tissue deposition accept not been well studied. Amongst children, visceral adiposity appears to be associated with an increased risk of cardiovascular take chances factors such every bit elevated triglycerides and reduced high-density lipoproteins that are independent of full trunk 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 boyhood, but increases quickly at that time.

Adulthood

The period later adolescence has not been intensively studied, although approximately two-thirds of developed obesity begins later adolescence. Whether boosted disquisitional periods exist in adulthood is less certain, just pregnancy and postpartum may institute one such catamenia for a subset of women (Williamson et al., 1994). Postpartum weight memory appears to range from 0.v to 4.8 kg for most women (Johnston, 1991), but African-American mothers may exist twice as likely to retain nine.1 kg (20 lb) or more postpartum than Caucasian mothers (Parker and Abrams, 1993). Boardley and colleagues (1995) institute that African-American women ate more and were less physically agile 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 than weight in the postpartum period than did Caucasian women. Results of several contempo studies propose 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 commencement-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 Thousand-protein ß3, considered a "thrifty" genotype, had significantly higher BMIs and postpartum weight retentiveness than women who did not bear the genotype (Gütersohn et al., 2000). No effect of the genotype was observed amidst women who had never given nascence, suggesting a pregnancy-specific phenomenon. In addition, this relationship was but observed amongst women who engaged in low levels of physical action, supporting the idea that physical activeness 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 machinery might exist, 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 prove meaning heterogeneity in their trunk weight and body fatness responses to altered energy remainder, dietary components, and changing activeness 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 equally BMI, fat mass, and leptin levels) ranging from 30 to 70 percent (Comuzzie et al., 1993, 1994, 1996). Even so, little is yet known virtually the specific causes of heterogeneity (Pérusse and Bouchard, 1999). It seems articulate that energy metabolism and neural command of appetite are involved in regulating body weight and may contribute to the etiology of obesity. Studies of resting metabolic rate evidence 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) start described homo uncoupling protein 2 (UCP-two) and its links to obesity and hyperinsulinemia. Bouchard (1997) noted that markers most the UCP-2 gene in humans are linked to differences in resting metabolic rate. Thus, genetic differences in UCP-ii, and maybe other UCPs, may contribute to man obesity.

At that place is a group of at to the lowest degree 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 unit studies do non suggest that the genes responsible for these syndromes are involved in the common forms of human obesity. For more than 99 per centum of obese humans, the genetic basis of their obesity is unknown.

Fauna Models of Genetic Obesity

The strongest bear witness for genetic weight-regulating mechanisms is the contempo elucidation of single cistron defects that are associated with excessive weight proceeds in animals. Single gene mutations tin can indisputably crusade obesity in both 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 poly peptide cistron); the fat mutation in the carboxipeptidase E gene, which is a prohormone processing enzyme; and the tub mutation, the function of which has withal to be adamant. 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 add-on, serum concentrations of leptin are elevated in close proportion to torso fatty 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). Farther inquiry is needed to assess the potential role of leptin in obesity treatment.

Familial Assemblage 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 trunk 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, and so the opportunity for the biological parents to instill eating and activity habits was very limited. Another report of adoptees showed a significant genetic influence on obesity, simply none of the environmental indicators evaluated were found to contribute, although a number of the atmospheric condition considered accept previously been associated with obesity (Sorensen et al., 1998). Stunkard and colleagues (1986) estimated that as much as seventy percent of the variance in the occurrence of obesity could be attributed to genetic factors, but other authors have postulated that every bit trivial every bit 20 percent of the variance is due to genetic factors. The general consensus is that genetic factors business relationship for well-nigh thirty to 50 pct of the variance in the occurrence of obesity (Bouchard, 1997).

Twin studies provide the most impressive clinical show that genetic factors play an important function 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, fifty-fifty if they were reared autonomously. Bouchard and colleagues (1990) studied twins who were isolated in the Canadian wilderness with no access to foods other than those provided by the investigators. Identical twins were overfed for a catamenia of 100 days, and their gains in body weight and adipose tissue were evaluated. There was a closer clan of both body weight and intra-intestinal adipose tissue (visceral fat) within twin pairs than amongst twin pairs.

The maximal heritability of obesity has been estimated to range from thirty to 50 percent, based on a review of family studies (Chagnon et al., 2000). Although all-encompassing efforts take been fabricated to identify mutations in the genes identified every bit obesity-associated in rodents and in other candidate genes for obesity in humans, to engagement merely a scattering of individuals take been identified with mutations in whatever of the genes that take 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 full, unmarried gene mutations have been identified as responsible for obesity in 25 persons, with these mutations actualization in seven genes (12 dissimilar mutations) (Pérusse et al., 1999) or in v 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., 2000).

Currently, the major try in the search for specific genes that contribute to homo overweight and obesity is based on the utilise of genome scanning. In genome scanning, linkage assay is conducted to identify QTLs that impact the specific phenotype under written report. 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 showtime-degree relatives has suggested that genetic factors may be of greater prominence in more severe obesity (Katzmarzyk et al., 2000). Amidst the members of families that contain at least one morbidly obese person, a major gene issue was transmitted in a codominant fashion, suggesting a gene-environment interaction (Rice et al., 1999). Both multifactorial and major cistron furnishings take been suggested. Efforts are ongoing to identify the genetic and molecular footing of overweight and obesity, and it is likely that many genes (and inside 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 probable involves a combination of shared environment and shared genetic propensities. The rapid increase in prevalence of obesity in the Us, as well as in many other countries, across all age groups may reverberate a removal of environmental constraints (e.k., high levels of daily activity and food availability) on the expression of obesity genotypes. Cognition of the genetic components of obesity is non probable to be useful to the military in the near term, just identification of markers of potential risk of obesity may well have implications for hereafter screening.

Historic period

Cross-sectional and longitudinal studies indicate a gradual increment in the average BMI of Americans upwards to the ages of fifty to threescore years (IOM, 1995). This trend is similar, with some variation, across males and females and beyond all evaluated indigenous groups. Population studies also point a reject in body weight and BMI amongst the elderly, ordinarily in the seventh and 8th decades (IOM, 1995; Kuczmarski et al., 1994; NHLBI, 1998). The same trends accept been identified in changes in total trunk fatty and percent body fat (Chumlea et al., 2002). Overweight and obesity thus reach maximal rates amidst middle-anile adults. This pattern is shown in Figure 3-1.

FIGURE 3-1

The prevalence (%) of overweight and obesity of men and women by age in the U.South. population. Preobesity = torso mass index (BMI) of 25–29.ix, class I obesity = BMI of 30–34.ix, class Two obesity = BMI of 35–39.9, and grade III obesity (more than...)

The historic period-related trunk mass increase upward 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 premenopausal counterparts. Declining stature accounts for a small portion of the age-related increase in BMI (Gallagher et al., 1996).

Many weight-direction experts concur that torso weight becomes progressively more difficult to maintain with age, but there appears to exist piddling rationale for increasing the upper BMI range consistent with good health every bit individuals become older. Williams (1997) indicated that body weight and associated circumferences would increment with advancing age unless food intake is reduced and physical activity is substantially increased.

A big number of cross-exclusive studies, withal, do demonstrate that body fat increases with age, even after controlling for changes in torso weight and concrete action 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., 1979). Gallagher and colleagues (1996) demonstrated that the mean body-fat content in nonexercising noncombatant women with a BMI of 25 increased from 30 pct for those between the ages of 17 and twenty years to 36 percent for those ages 40 years and older. The implication of this is that lean body mass and, frequently, skeletal mass, subtract with historic period. Additionally, partitioning of adipose tissue betwixt the subcutaneous and visceral compartments is likewise moderated by age (Borkan et al., 1983). Men take more visceral adipose tissue than do women at all ages, and the charge per unit of visceral adipose tissue increase with historic period is greater in men than in women (Blaak, 2001).

In dissimilarity to body fat, skeletal muscle mass declines with age beginning around the 3rd decade of life (Dutta and Hadley, 1995). This observation is truthful not only for the general population, but it is also evident in armed services 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 7th and eighth decades (Flynn et al., 1989). Losses of skeletal musculus parallel changes in skeletal minerals with advancing age and are present fifty-fifty after controlling for loss in trunk 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 alter in torso weight. Since lean mass contributes the larger share of metabolic activity, full energy expenditure during remainder or low activity volition likewise subtract proportionally with the loss of lean mass.

Full energy expenditure and thus, energy requirements, decrease with advancing age (Tzankoff and Norris, 1978). Concrete action levels are lower in older individuals, which business relationship for a portion of the free energy expenditure reduction that comes with crumbling. Resting energy requirements are likewise lower in the elderly, due largely to decreases in all metabolically active tissues, including skeletal musculus, 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), just it remains uncertain whether this observation also applies to humans. The do of resistance preparation past people over the age of l years may enhance fat-complimentary mass, primarily skeletal muscle, and thereby assistance first the age-related reject in resting metabolic rate (Hill and Saris, 1998; Tzankoff and Norris, 1977). In women, loss of ovarian function accounts for a lower charge per unit of overall rut production compared with that observed in premenopausal women (Poehlman and Tchernof, 1998). Thus, both older men and women accept lower rates of energy expenditure and, unless counterbalanced past 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 but a moderate extent. Information 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 twenty years of age and older, the prevalence of overweight (BMI ≥ 25) was 67.4 percent for non-Hispanic whites, 60.7 pct for non-Hispanic blacks, and 74.vii percentage for Mexican Americans. The differences were not statistically meaning, 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.ix percent in Mexican Americans. The divergence in prevalence between not-Hispanic white and non-Hispanic black women was statistically significant (Flegal et al., 2002). The causes of these differences in the prevalence of overweight have not been clearly identified, but are likely to be a combination of physiology, civilization, and behavior.

The relationship of BMI to percentage body fat is also affected by race/ ethnicity. Fernandez and colleagues (2003) recently reported the results of an analysis of 11 cross-exclusive studies involving body limerick 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 fifty.8 years, and the boilerplate BMI ranged from 25.1 (European-American women) to 29.8 (African-American women). Full trunk fatty was measured using dual-energy X-ray absorptiometry. There were no differences in the estimation of percent body fatty from BMI for men across indigenous groups. However, for women with BMIs less than 30, Hispanic-American women had a significantly higher per centum of trunk fat at a given BMI than did African-American or European-American women. Nonetheless, at BMIs greater than 35, European-American women had a higher percent body fat than either of the other two groups of women. Some before studies have reported greater fatty free mass in African-American women compared with Caucasian women with the same BMI, primarily due to the greater skeletal mass in African-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 African-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 2 groups were similar in age and anthropometric characteristics. Parameters examined included REE, respiratory commutation rates (RER), insulin sensitivity, and maximal oxygen consumption. REE was iii to 4 percent lower in African-American women, but the difference was not statistically significant. Still, the resting RER was significantly lower in African-American women. The African-American women besides had significantly lower insulin sensitivity values that resulted in higher astute 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 musculus fiber type and obesity. In a study of lean and obese African-American and Caucasian women, type I musculus fibers (slow twitch, oxidative musculus fibers) were significantly reduced in obese women compared with the lean women, and blazon 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 blazon 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 as well 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, African-American women were half as likely equally Caucasian women to consider themselves overweight. There is a much greater cultural tolerance of overweight among African-Americans, and they have different trunk image perceptions. Although African-American women responded physiologically to a weight-reduction program in the same manner as Caucasian women, their driblet-out rate from the programme was double that of Caucasian women (Glass et al., 2002).

PHYSICAL Activeness

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 xx years likely reflects major ecology shifts in exercise habits and food availability, which can be controlled.

Physical activity represents an important component of volitional free energy expenditure. Mod transportation and other conveniences have reduced the need for free energy expenditure in the form of physical exertion. Reductions in concrete activity over the past several decades likely contribute to the evolution of the positive energy balance and weight-gain characteristics of all industrialized societies. Lack of physical activity begins in youth, with tv set watching time correlated with BMI, as well every bit with both prevalence and severity of overweight (Dietz and Gortmaker, 1985; Katzmarzyk et al., 1998; Tanasescu et al., 2000). A reduced accent on school concrete education classes has been accompanied by a gradual refuse in childhood fitness (Luepker, 1999). Indeed, physical inactivity is a major hazard 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 action on weight and wellness may be influenced by age. Owens and coworkers (1992) evaluated the effects of concrete activity on both weight alter and the gamble factors for cardiovascular disease during the perimenopausal period. Women who increased their action levels during the 3-yr report period (every bit measured using the Paffenbarger Physical Action Questionnaire) had the smallest increases in body weight and the smallest decrement in loftier-density lipoprotein cholesterol.

Flatt (1987) has pointed out that to avoid increased fat deposition, both energy residuum and macronutrient balance (especially fat balance) are necessary. When dietary fat is elevated, there is limited chapters to reduce total body fatty by fat oxidation. Do, specially 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 from saccharide to fatty. Thus, chronic extended bouts of exercise may, in consequence, substitute for expansion of the adipose tissue, allowing the physically active individual to reach fat balance while maintaining a lower body-fatty mass than the sedentary private (Flatt, 1987). Jakicic and coworkers (1995) initially demonstrated that over the brusque term, four x-infinitesimal bouts of exercise per day, four times per calendar week is more constructive in reducing body weight than a single 30 to forty minute period of exercise. However, the long-term information indicated that the short-term bouts of exercise were non equally effective every bit the long bouts in reducing weight and maintaining weight loss (Jakicic et al., 1999).

Almost fatty-acid oxidation in the human torso occurs in muscle (Calles-Escandon and Poehlman, 1997). The intrinsic capacity of musculus to oxidize fatty can be impaired by concrete inactivity and possibly past loss of estrogen in women, only it is amenable to partial correction past practise training (Calles-Escandon and Poehlman, 1997). A decrease in aerobic chapters and fatty-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 fat acids and improves muscle metabolism in both young and one-time individuals. However, the elderly do not increase fat utilization in response to practice to the same extent as the young, despite performing do to the same intensity and for the same duration (Blaak, 2000; Calles-Escandon and Poehlman, 1997).

In a study of 970 healthy, female person twins with a wide range of per centum torso fatty, both total body fat and primal adiposity were associated with physical action (Samaras et al., 1999). Moderate-intensity sports of one and 2 60 minutes durations accounted for within-pair differences of 1.0 kg and 1.4 kg, respectively, of full trunk fatty. Among participants in whom i of a pair of twins was overweight, college levels of physical activeness were still associated with 3.96 kg lower total body fat and 0.53 kg lower primal abdominal fatty. 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 evidence 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 bear on the human relationship of physical activity, body fatty, and fat-free mass. Guo and coworkers (1999) found that associations betwixt concrete action and fatty-free mass were more pronounced in postmenopausal women than in premenopausal women, and that hormone replacement therapy had beneficial effects on trunk limerick. 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 fatty than those who were concordant for activity level (Samaras et al., 1999), suggesting that the upshot of concrete activity is greater than that of hormonal status.

Habitual concrete action also affects other physical characteristics. Gilliat-Wimberly and coworkers (2001) found that an association exists betwixt habitual physical activity and maintenance of resting metabolic rate in middle-aged women. Concrete activity as well 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).

FOOD

Intake

In conjunction with the importance of physical activity levels, free energy intake must be matched to energy expenditure. Positive energy residue results if energy intake is greater than energy expenditure. Increased energy consumption, decreased free energy expenditure, or both tin can outcome in positive free energy balance.

While the etiology of obesity is multifactoral, the mutual characteristic of all obese people is excessive energy storage in the course of body fat. Whether obese people swallow more energy than practise 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 exercise lean people (Jequier and Schutz, 1983; Ravussin et al., 1982; Zed and James, 1986), which demonstrates that boilerplate free energy intake must indeed be college in the obese. Some differences in free energy expenditure, and consequently in free 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 poly peptide, fat, and carbohydrate (CHO), plus the optional energy source, alcohol, diets that are high in fatty tend to exist depression in complex CHOs such as fiber. There is yet considerable controversy over whether the function of diet composition or simply full energy intake is of import 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 torso mass is associated with the evolution of overweight or obesity in susceptible individuals. In addition to total energy intake, the grapheme of the nutrition may play a role in the etiology of obesity. Loftier-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 (depression 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 fatty is more energy dumbo than other foods (9 kcal/chiliad versus iv kcal/chiliad for protein and CHO), eating loftier-fat foods results in a greater energy intake than would eating a similar quantity of lower-fat foods. Fatty modifies the taste of food and, in some people, promotes backlog intake. Fat foods tend to be easier to chew or may not require chewing, thus making larger quantities easier to consume in a shorter fourth dimension than foods that crave more mastication. Dietary fat also has a weaker satiation issue than CHOs, which results in the over consumption of fatty (Rolls and Hammer, 1995; Rolls et al., 1999).

Some of the departure in weight gain on a loftier-fat versus a low-fatty nutrition may exist explained by differences in the metabolic processing of fat. Compared with dietary fatty, CHOs require additional free energy expenditure for digestion, assimilation, and conversion to fat. When energy intake exceeds expenditure, 23 percent of energy consumed is required to catechumen and store CHO every bit fatty, compared with only 3 per centum to shop fatty. Ii studies in laboratory animals have demonstrated this effect of dietary fat on trunk weight and torso composition (Donato and Hegsted, 1985; Lin et al., 1979).

The link between dietary fatty 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 demand to rely on estimates of torso limerick. Nonetheless, increasing prove from clinical studies suggests that dietary fat promotes weight gain in humans also as in animals. Studies in which people were overfed diets varying in the proportion of energy from fat (forty 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, equally well as within ethnic groups that have migrated to the The 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 bailiwick to confounding variables such every bit differences in energy intake and expenditure, wellness status, and genetic and environmental influences. However, based on information such every bit that described in a higher place, 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 than closely correlated with the level of dietary fat than with total energy intake (Dreon et al., 1988; Romieu et al., 1988). A low incidence of obesity has been observed among vegetarians who typically consume depression-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 take a college-fat diet (Dhurandhar and Kulkarni, 1993), and the prevalence of obesity among these types of vegetarians is loftier compared with that of omnivores (Dhurandhar and Kulkarni, 1992).

Some studies have failed to demonstrate an clan betwixt fat intake and body weight in free-living populations. On the basis of nutrient frequency questionnaires, Macdiarmid and colleagues (1994) stratified 1,800 people by their fatty consumption (high was considered to be 45 percentage or more kcal every bit fat and low was considered to be 35 percent or less kcal as fat) and found no statistically significant difference in age, BMI, or social course between the two groups. Even so, the loftier-fatty group rated their general diet and health as poorer. The loftier-fat group likewise consumed significantly more than protein and total energy, but less CHO and cobweb; consumed meat and loftier-fat dairy products more ofttimes; 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 private's weight status (Prewitt et al., 1991). These findings advise that dietary fat may promote greater weight gain and body-fat accumulation than expected on the basis of energy intake alone. In contrast, Leibel and colleagues (1992) plant no relationship betwixt the ratio of dietary fatty/CHO and the total energy required to maintain trunk weight. CHO ranged from xv to 85 percent of total intake, and kcal from fat ranged from 0 to seventy pct of total intake. The disparity betwixt findings of these two studies may exist 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 non seen consistently before 13 to 16 weeks. Also, trunk limerick 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 of america despite reductions in intake of dietary fat and that ecological studies take found no human relationship between fatty intake and obesity. In dissimilarity, Bray and Popkin (1998) contend that individuals who gained weight may non have decreased (or may have increased) their intake of dietary fat. They also debate that ecological studies may not be appropriate to study the relationship between fat intake and obesity, that body weight is a poor measure out of body fatness, and that nearly of the previous studies focused on outcomes other than obesity. Although the literature is non articulate, results of studies on laboratory animals and the small number of man studies suggest that dietary fat does promote obesity. Recently, Astrup and colleagues (2002) reviewed evidence on the effects of low-fat diets. Iv meta-analyses of weight change occurring on low-fatty diets in intervention trials with overweight subjects were reviewed. These analyses consistently demonstrated meaning weight loss in both normal-weight and overweight subjects.

Carbohydrates

Several rationales have been postulated for the utilise of high-protein, depression-CHO diets: (1) intake of a loftier proportion of kcal as CHO has adverse physiological consequences, such as increasing insulin secretion, promoting fat degradation, and increasing serum triglycerides levels; (2) low-CHO diets can atomic number 82 to a "ketogenic" state, which has been hypothesized to suppress appetite; (iii) a loftier-protein diet preserves lean torso mass during weight loss; and (iv) the thermogenic 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 in a higher place hypotheses (Skov et al., 1999a, 1999b). A high-protein nutrition has been found to: stabilize blood glucose 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 enquiry is needed on the subject of amino acid flux measurements and how it relates to claret glucose levels, data from Layman and colleagues (2003b) support the idea that the ratio of dietary protein and CHO can have a significant result on metabolic balance and specifically 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 accept contributed to the increased prevalence of obesity (French et al., 2000; Troiano et al., 2000), whereas others exercise not support this hypothesis (Gibson, 2000; Macdiarmid et al., 1998; O'Brien et al., 1982).

Portion Size

There is picayune research available on the role of portion size in the increasing prevalence of overweight in the United States. All the same, mutual sense dictates that it is a contributing cistron. For instance, a single serving of meat is considered to be 3 to 4 oz based on the Dietary Guidelines and the U.S. Food Guide Pyramid. All the same, 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 eatery would exist probable 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 concluding 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 six-oz serving, the standard size serving today is 12 oz, and many vendors sell 20-oz bottles about exclusively. Fountain drinks accept also increased to the "super-jumbo" 32- to 64-oz sizes. It is not unusual for individuals to eat some 500 to 1,000 kcal per day from soft drinks in add-on to their usual solid-nutrient diet.

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 accept adopted the practice of serving larger meals. Similar to the increase in soft potable portions sizes, fast-nutrient restaurants now offer "super-size" portions for a minimal increase in cost. For case, a "jumbo super-size" guild of a large hamburger, french fries, and soft drink at a fast-food restaurant may at present contain more than 1,500 kcal for a single repast (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 divergence 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). Information were taken from four national nutrient-consumption surveys covering the catamenia 1977 to 1996. Food consumption was estimated every bit energy intake in kcal and every bit average portion sizes using food models to assistance respondents in identifying portion size. Results demonstrated that for foods eaten both inside and outside the dwelling house, 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 advisable for an agile lifestyle may go along 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 grooming expend large amounts of free energy each day and, for many organized sports, are encouraged to eat large quantities to maintain their weight at an artificially loftier level. When action declines, the eating blueprint established during training may not be adjusted to run across the new lower free energy needs. The same is true of military personnel. During initial entry training, avant-garde individual grooming, and special forces training, large amounts of energy are expended on a daily basis. By the time grooming is completed, individuals have been habituated to eat large amounts of food over a very brusque catamenia of time.

In many occupations, tasks that require more physical activeness are assigned to younger workers. As these workers age and larn more responsibility, their work may become more sedentary, just eating patterns may not alter. This blueprint of decreased occupational free energy expenditure with job promotion may be common in the military as well. Privates, airmen, and junior noncommissioned officers are more agile than senior officers and noncommissioned officers. Despite strong commitments to appoint in daily physical fitness, which may be unchanged or fifty-fifty increased in more senior individuals, the subtract in activities of daily living and task operation can lead to a positive energy residual unless particular care is taken to reduce energy intake.

The ubiquitousness of vending machines and fast-food outlets ensures constant admission to foods at work—ordinarily foods with a loftier caloric content largely in the form of fatty 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 abroad from home (eating out), along with the increase in access to foods in nigh all locations. These changes have contributed in several ways to promoting obesity. Because more families include two-wage earners, adults spend more fourth dimension out of the home and do non accept time to prepare meals every bit they customarily did in the past. Meals consumed at restaurants tend to be larger and accept a higher caloric content than those consumed at home, mainly considering of higher fat content and larger portion sizes (Young and Nestle, 2003). In addition, a loftier percentage of meals eaten away from home are eaten in fast-nutrient restaurants or consist of fast-food take-out. The presence of nutrient in virtually every circumstance of daily life, from fast-food outlets to vending machines, encourages and allows individuals to consume multiple calorically dumbo meals and snacks per solar day (Bell et al., 1998; Rolls, 2000).

PHYSIOLOGICAL FACTORS

A number of phenotypic characteristics have been associated with the gamble 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 free energy expended at balance, under thermo-neutral conditions, and in a post-absorptive state.
Thermic outcome of feeding, the incremental increase in energy expenditure after a meal is consumed due to the energy costs of absorption and the transport of nutrients, likewise as the synthesis and storage of protein, fat, and CHO. Some of the thermic effect of feeding may be mediated by sympathetic nervous arrangement activity.
Energy expended for physical action, including involuntary movements associated with shivering, fidgeting, and postural command.

RMR accounts for 60 to 75 percentage of total energy expended in most adults. RMR is primarily related to the maintenance of fatty-free mass, reflecting such activities as protein synthesis and breakdown, temperature and cellular homeostasis, and cardiovascular, pulmonary, and cardinal nervous system role. 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 body size was found to predict weight gain (Ravussin et al., 1988) in both men and women, although some studies accept 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 normally accounts for v to 10 percent of daily free energy expenditure and varies between lean and obese individuals (Astrup, 1996). Extensive studies take been inconsistent in supporting the view that excessive weight gain is secondary to a reduced thermic outcome of food (Tataranni et al., 1995).

Contempo studies support the view that small, nonvolitional concrete activities such as fidgeting may business relationship for private differences in free energy expended with changes in free energy remainder (Levine et al., 1999; Zurlo et al., 1992). Although relatively small in caloric magnitude, these activities may business relationship for some of the between-private 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 private energetic differences, and the origin of these differences is the ground of intensive study.

ENVIRONMENTAL FACTORS

Smoking and Alcohol

Cigarette smoking increases metabolic charge per unit and may limit food intake, and weight gain is a common event of smoking abeyance (Perkins, 1993; Russ et al., 2001). The use of alcoholic beverages may as well have an touch on trunk weight. Free 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 free energy intake than drinking nonalcoholic beverages, possibly due to increased appetite (Tremblay and St-Pierre, 1996; Tremblay et al., 1995).

A contempo, big prospective study of a cohort of men ages 40 to 59 with a 5-year follow-up institute that mean BMI increased significantly from the light-to-moderate to the very-heavy alcohol intake grouping. The study concluded that heavy booze intake (defined equally ≥ thirty one thousand/twenty-four hours of alcohol) contributed direct to weight gain and obesity, regardless of the type of alcohol consumed (Wannamethee and Shaper, 2003).

Pharmacological Agents That Produce Weight Gain

Numerous drugs can produce weight gain and fat gain. These include glucocorticoids (east.chiliad., prednisone), hypoglycemic agents (e.g., insulin, sulfonylureas), certain antihypertensive agents (due east.grand., prazocin), anti-allergens (e.g., cyproheptadine), and numerous drugs that touch on the central nervous system (e.m., thorazine, tricyclic antidepressants, valproic acid, lithium). Most of these drugs are used for diseases that mandate separation from the armed forces, but there are a number of drugs that may be taken by armed forces 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 organization assures a readily available and affordable food supply throughout the entire year.

The relative abundance 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 fauna origin are likely to be college in energy and fat than comparable quantities of foods of institute origin.

The availability and abundance of nutrient in the U.S. marketplace has accelerated dramatically in the past thirty years. The per capita energy content of food entering the American market place increased about 500 calories on a daily footing during this fourth dimension catamenia. In add-on, fatty 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 point 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 subtract in consumption of fruits and vegetables (Putnam and Allshouse, 1999).

Family unit and Ethnicity

Eating is an intensely social activeness, and many eating habits are acquired in a familial or ethnic setting. People tend to imitate the eating habits of their parents, and then quantity and quality of foods eaten and repast patterns tends to be established early. Traditions that arise around eating patterns in a more agrarian or active order may favor excess consumption. Indigenous groups differ in their perceptions about appropriate body size and what constitutes overweight (Bhadrinath, 1990; Root, 1990).

Studies of changes in diet with clearing and acculturation show, for example, that Japanese who migrated to California and Hawaii take tended to abandon the traditional low-fat Japanese nutrition 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 issue has been a marked increase in weight among these immigrants. Similarly, Japanese children who remain in Japan, but whose diet is increasingly western, are besides 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 phenomenon is observed in studies of Southward Asians who accept migrated to the United Kingdom and who have modified their diet and physical activity patterns (McKeigue et al., 1992).

Socioeconomic Status

Social grade and socioeconomic status (SES) influence the prevalence of overweight. In many countries of the world, lower SES is linked to increased trunk weight (Molarius et al., 2000). In contrast, in some developing countries and archaic societies, obesity is considered a sign of affluence or fertility (Molarius et al., 2000). However, some researchers who contend that obesity decreases economic condition 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 probable to take lower income, greater levels of poverty, and decreased rates of matrimony than were normal-weight women with comparable degrees of disability (Gortmaker et al., 1993).

The Potential Role of Viruses in the Etiology of Obesity

The possibility exists that at to the lowest degree 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 man adenovirus, Advertizing-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 information have been reported that demonstrated like results in monkeys (Atkinson et al., 2000). Other preliminary studies suggest that humans with serum antibodies to Ad-36 have a college BMI and lower serum lipids than practice Ad-36 antibiotic-negative individuals (Atkinson et al., 1998).

Humans in Bombay, India, who had serum antibodies to SMAM-1, an avian adenovirus, were noted to exist significantly heavier and to have lower serum lipids compared with antibody-negative individuals. Viral antigen was found in the serum of two of the individuals with SMAM-1 antibodies (Dhurandhar et al., 1997).

More research is needed to confirm the hypothesis generated from the higher up data that some cases of human being obesity might exist due to a viral infection. Since adenoviruses are cold viruses, the possibility of the spread of Ad-36 and peradventure other obesity-producing viruses in the military community may be of significant business.

SUMMARY

The brief review of factors influencing body weight presented in this chapter demonstrate that maintaining a healthy body weight is an extremely complex upshot. Maintenance of fitness and appropriate trunk-fatty standards by armed forces personnel is affected by each individual's genetics, developmental history, physiology, age, physical activeness level, environment, nutrition, ethnicity, and social groundwork.