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The Journal of Nutrition Vol. 128 No. 2 February 1998,
pp. 411S-414S
New England Medical Center, Boston, MA 02111
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ABSTRACT |
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Abstract
Introduction
References
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Few studies have examined the long-term effects of childhood obesity on adult disease. Nonetheless, obesity present in childhood or adolescence seems to increase the likelihood of adult morbidity and mortality. In men who were obese during adolescence, all-cause mortality and mortality from cardiovascular disease and colon cancer were increased. In both men and women obese during adolescence, rates of cardiovascular disease and diabetes were increased. Among women but not men obese during adolescence, obesity has a variety of adverse psychosocial consequences. These include completion of fewer years of education, higher rates of poverty, and lower rates of marriage and household income. These effects seem related both to the persistence of obesity and to the effects of childhood or adolescent obesity on the quantity and location of body fat deposition. Approximately 50% of obese adolescents with a body mass index at or above the 95th percentile become obese adults. Furthermore, the risk factors for adult disease that are associated with obesity in children and adolescents persist into adulthood or increase in prevalence if weight gain occurs. Although both total body fat and regional fat deposition could account for the association of childhood or adolescent obesity with adult disease, no studies to date have examined cardiovascular risk factors and related them to visceral fat, controlled for total body fat.
KEY WORDS: obesity · children · adolescents · adults · morbidity
Few longitudinal studies have examined the effects of childhood onset obesity on adult morbidity and mortality. In this review, I will examine the effects of childhood obesity on the prevalence of adult morbidity and mortality. Furthermore, based on the presumption that persistence of childhood obesity into adulthood increases the risk of adult morbidity and mortality, I will examine the risk of persistent obesity for obesity present at different ages in childhood. Finally, I will explore the potential mechanisms by which childhood onset obesity can lead to adult disease.
Few studies have examined the effects of childhood or adolescent onset obesity on adult morbidity and mortality. In part, the lack of such studies reflects the difficulties in the maintenance of a cohort for the time necessary for adult disease to occur. One exception is the Third Harvard Growth Study. In this study, children were enrolled in 1922 as they entered first or second grade of public school in three middle-class cities north of Boston. Subjects were then measured annually until they either left or completed high school in 1935. More than 1800 children received a minimum of eight or more years of measurements.
The likelihood that obesity present at earlier ages will persist and induce morbidity and mortality has important implications for the cut-off point used to assess obesity in children and adolescents and for how aggressive therapy directed at obesity should be. Few studies have carefully examined the likelihood of persistence of obesity in the same cohort at different intervals throughout childhood.
Few long-term studies have been performed that establish the mechanism by which obesity present in childhood or adolescence predisposes to the morbidity or mortality that occurs in adulthood. Nonetheless, several candidate mechanisms exist. The most likely of these mechanisms relates to the effects of childhood or adolescent obesity on total body fat in adults. Approximately twice as many individuals who reported that they were "considered a fat child" were greater than 155% of ideal body weight as young adult women (Rimm and Rimm 1976
INTRODUCTION
Abstract
Introduction
References
EFFECTS OF CHILDHOOD OBESITY ON ADULT MORBIDITY AND MORTALITY
). We designated overweight subjects as those who had two or more measurements of their body mass index (BMI) during high school in excess of the 75th percentile (Cronk and Roche 1982) for subjects of the same age and sex from the first National Health and Nutrition Examination Survey (NHANES 1). We designated as lean subjects those who maintained their BMI between the 25th and 50th percentile throughout their high school years. Results were corrected for smoking status and self-reported weight; these data were collected when the subjects were approximately 55 y old.
). As discussed below, the effects of adolescent obesity on adult morbidity and mortality can be explained either by the locus of fat deposition during adolescence or by the independent effect of total body fat on some of the morbidities examined.
View this table:
Table 1.
Risk of mortality among males and females overweight during their high school years1
). In a large sample studied during the National Longitudinal Survey of Youth (Gortmaker et al. 1993), we demonstrated that obesity present in late adolescent females had severe social consequences 7 y later. Consequences included lower rates of marriage, fewer years of education completed, lower family incomes and higher rates of poverty. The persistence of these results when controlled for the income and educational levels of the family of origin and for self-esteem suggested that obesity in women was a determinant rather than a consequence of these socioeconomic correlates.
). Over a period of 15 y, correlation coefficients ranged from r = 0.28 to r = 0.56, depending on the variable, age, sex and ethnicity of the subjects sampled. Blood pressure and dyslipidemia cluster in obese children and adolescents, and insulin probably represents a significant mediator of these interactions (Bao et al. 1996). Although obesity in childhood seems to influence all of these relationships in young adulthood, weight change seems to exert a more powerful effect (Gidding et al. 1995). Unfortunately, because the analyses in the studies cited above were not stratified by age, it is not clear whether these relationships vary with age of onset of obesity or grow stronger with advancing age.
LIKELIHOOD THAT CHILDHOOD OBESITY
WILL PERSIST
). The period of adiposity rebound defines a period when the BMI begins to increase after a nadir in early childhood, generally between 4 and 8 y of age. Although excess weight in adulthood appears consistently associated with early adiposity rebound (Rolland-Cachera et al. 1987), no data have been published to date that allow the calculation of the odds ratio for subsequent obesity for children with early adiposity rebound.
. As shown in Table 2, the odds ratio for the persistence of obesity rises with age among obese children. The substantial instability in the odds ratios during adolescence probably reflects the small samples of obese individuals present at each age. Furthermore, the low prevalence of obesity makes it impossible to determine the increased risk of persistence among individuals with more severe obesity. However, the likelihood of persistent obesity among individuals of different ages at the first incidence of obesity cannot be determined from the data presented.
View this table:
Table 2.
The odds ratios (95% CI) for the persistence of obesity among obese (BMI >95th percentile) males and females
of different ages compared with the non-obese
(BMI = 50th percentile)1
are concordant with other studies that suggest that obesity will persist in a substantial proportion of obese children. As shown in Table 3, obesity will persist in approximately 50% of overweight children or adolescents, regardless of the measure used (Freedman et al. 1987a, Mossberg 1989, Stark et al. 1981). Because predictive value is affected by the prevalence of a disease, and because many of these studies examined cohorts initiated before the recent increase in the prevalence of obesity among children and adolescents (Troiano et al. 1995), the predictive values shown in Table 3 likely underestimate the likelihood that obesity will persist among children who are overweight today. Nonetheless, the likelihood that obesity will persist in 50% of children or adolescents identified by a BMI 
95th percentile, or by a weight-for-height of 130%, which is slightly greater than a BMI 95th percentile, suggests that a BMI 95th percentile for children of the same age and sex represents a reasonable cutoff point to identify obesity.
View this table:
Table 3.
Predictive value (PV) of childhood obesity for obesity in early adulthood
MECHANISMS BY WHICH CHILDHOOD AND ADOLESCENT OBESITY CAUSE ADULT DISEASE
), compared with women who did not report that they were "considered a fat child." However, persistent obesity from childhood accounts for approximately one-third of adult obesity (Braddon et al. 1986). Because children who are overweight may grow up to be more obese as adults, their risk of morbidity and mortality in adulthood may be increased. However, as we indicated above, control for the effect of weight during adulthood only mildly attenuated the effects of adolescent overweight on adult morbidity and mortality (Must et al. 1992).
), activity (Tremblay et al. 1990), cigarette smoking (Shikomata et al. 1989) and alcohol (Troisi et al. 1991) also contribute significantly. As in adults, waist circumference or waist:hip ratio correlate poorly with visceral adipose tissue (Fox et al. 1993) in adolescents.
), systolic and diastolic blood pressure (Shear et al. 1987), and the 1-h insulin response to an oral glucose tolerance test (Freedman et al. 1987b). In the most sophisticated of these studies (Caprio et al. 1996), visceral fat measured by magnetic resonance imaging correlated with basal insulin concentrations, triglycerides, and HDL cholesterol concentrations. Furthermore, the insulin response to a euglycemic insulin clamp demonstrated that basal insulin secretion, stimulated insulin secretion and insulin resistance were all correlated with visceral adipose tissue (Caprio et al. 1995).
). However, until both total body fat and visceral fat distribution are measured in the same subjects, the independent contribution to adult morbidity and mortality of visceral adiposity that begins in childhood will remain unclear. Second, the distribution of body fat and therefore its associated consequences may be affected by the age or developmental stage of the child. No study of adult morbidity or mortality has yet examined this possibility. Finally, the effects of obesity have not clearly been distinguished from the factors that promote obesity or the regional deposition of fat. For example, only recently has cardiovascular fitness been measured in a fashion independent of weight (Gutin et al. 1997). Interestingly enough, this study demonstrated that obesity was the principal factor that accounted for the adverse effects of childhood obesity on cardiovascular risk factors.
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FOOTNOTES |
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LITERATURE CITED |
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Abstract
Introduction
References
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