Development Of Overweight

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The likelihood that childhood overweight will persist, and therefore the likelihood of adverse consequences of childhood obesity in adulthood, may be related to its age of onset (70). There is a growing body of evidence that two periods and possibly a third appear to constitute specific periods of increased risk for persistence and subsequent disease: the prenatal period, "adiposity rebound,'' and the period of adolescence. At present, the mechanisms entrained at these periods to promote the increased risk of persistence of obesity or its complications remain poorly understood. In addition, stunting during childhood appears to put children at risk for the development of overweight; this will briefly be discussed in this section.

The most compelling data to suggest that the prenatal period constitutes a period of increased risk for persistent adiposity derive from studies of infants of mothers who had diabetes during pregnancy. Regardless of whether their diabetes was gestational, insulin-dependent, or non-insulin-dependent, these infants tend to be fatter at birth than those whose mothers were nondiabetic or prediabetic during pregnancy (71). Long-term follow-up of infants whose mothers had diabetes suggests they have an increased prevalence of obesity at later ages that extends through adolescence (72). Shorter-term studies further suggest that body weight in such infants normalizes by about 1 year of age but subsequently begins to be higher than the norm between ages 5 and 7 years (73). Pregravid overweight status of the mother has been associated with macro-somia independent of maternal age, smoking status, race/ethnicity, height, parity, gestational age, and sex of infant (74). In turn, children who were large for gesta-tional age at birth have greater and progressively increasing adiposity through 3-6 years of age than do their normal-size counterparts (75).

The argument that fetal life represents a critical period for adiposity has not been totally resolved, the evidence from the infants of mothers with diabetes notwithstanding. Several large studies have shown an association between high birth weight and child adiposity (75-78) or adult adiposity after controlling for gestational age (77,78), but most did not adjust for confounding variables such as parental fatness, maternal smoking, gestational diabetes, or socioeconomic status (79). Conversely, low birth weight may be associated with an increase in intra-abdominal fat deposition that may in turn account for an increased likelihood of risk factors for cardiovascular disease, including hypertension, diabetes, and hyperlipidemia (80). However, the association between lower birth weight and the development of overweight has not been clearly demonstrated. Although babies with lower birth weight have been shown to have an increased risk of syndrome X and of heart and pulmonary disease in adulthood (81), it is not clear that these consequences are mediated by excess adiposity.

The second period of apparent increased risk for later obesity, "adiposity rebound,'' involves early acceleration of the BMI after its nadir at 4-7 years of age. This phenomenon appears to be associated with an increased risk of later obesity (82,83). That infants of mothers with gestational or insulin-dependent diabetes during pregnancy also appear to have onset of overweight during this period (74) raises questions as to whether early acceleration of the BMI after its nadir is a risk for later obesity. Other research shows that parental obesity is also associated with early adiposity rebound (84) and that early rebound may reflect overweight associated with maternal diabetes. Thus, whether there exists a true period of risk for the development of overweight at this time, independent ofmaternal diabetes and/or parental overweight, remains unclear.

Although adiposity rebound has been associated with adult adiposity, this may only be an epiphenom-enon (85). Increased BMI at rebound has not yet been associated with higher body fat, nor do we know whether the increased BMI observed in adults who have had early rebound is attributable to greater body fat. In addition, whether age at rebound or the size of the BMI at rebound has the greater influence on adult BMI remains unclear. New evidence shows that the BMI at age 7 years and age at rebound both predict adult BMI (86), and a positive association has been found between childhood height at age 5 years and adult BMI (87).

The final developmental stage of increased risk, adolescence, may be much more of a concern for females than for males. Females, who mature earlier, are at increased risk for greater BMIs as adults (88,89); the relationship for males is less clear. In addition, while ~30% of obesity present in 36-year-old-women may begin in adolescence, only about 10% may begin then in males (32).

Some evidence from developing countries indicates an increase in overweight among stunted children, but this may be a spurious finding due to limitations in the indices used to define overweight and metabolic differences. As indicated in the first section of this chapter, indices used for evaluating relative weight, such as BMI and weight-for-height, do not directly measure body fat. In the case of stunted children, those with increased BMIs may have an excess of body fat, heavier bones, or larger muscles. On the other hand, metabolic defects may contribute. In Brazil, mild stunting was associated with the percentage of energy from fat and weight gain, suggesting that stunted children may be more susceptible to the effects of a high-fat diet than other children (90). Still another possibility is that stunted children may be more likely to have impaired fat oxidation (91). Evidence from a longitudinal study in Guatemala has shown that severely stunted children have increased abdominal fatness as adults, after controlling for fatness and other confounders (92).

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