onset. Indeed, the results of one such twin study suggested that the intra-uterine environment is a critical period for the development of adult height, but not for adult BMI .
Likewise, new research, so far only in the animal model, is emerging that suggests that maternal obesity during pre- and postnatal periods can have profound, genotype-specific effects on the development of obesity in offspring that is genetically predisposed to obesity (B. Levin, 2005: Oral presentation at the Society for the Study of Ingestive Behavior).
The first year of life may be an especially interesting period to study with respect to longer term obesity. Rapid weight gain during the first 4 months of life is a risk factor for obesity in childhood and adulthood. In one study of 300 full-term African American infants, rapid weight gain was defined as an increase in weight-for-age ≥ 1 SD between birth and 4 months . After adjusting for confounding factors, infants who had experienced rapid weight gain by 4 months of age were 5.22 times more likely to be obese at 20 years of age compared to infants who did not experience rapid weight gain. In a separate analysis of 19,397 infants, results indicated that both birth weight and rate of weight gain were associated with an increased probability of childhood overweight at 7 years of age ; within each strata of birth weight, increased rate of weight gain was associated with increased childhood overweight prevalence. Potential genetic and home environmental influences on early life rate of weight gain are poorly understood and may be an important area for future research.
Additional studies that evaluate the heritability of, or specific genes associated with, refined behavioral phenotypes related to obesity. Very little is known about the heritability of behavioral traits that are associated with obesity, particularly those reviewed in Section 4. Studies that clarify the genetic-environmental architecture of these traits would elucidate the extent to which those behavioral traits are genetically influenced, as well as the nature of environmental influences that influence those behaviors (i.e., shared vs. nonshared environmental effects). Such designs could also address important multivariate questions, including the extent to which the correlations between behaviors and body fat is influenced by the same genes (i.e., “genetic correlations”) or the same environmental factors (i.e., “environmental correlations”). Especially interesting would be heritability studies of laboratory-based behavioral traits, such as the reinforcing value of food [90, 157], delayed satiation , disinhibition , or eating in the absence of hunger [48, 162], which have been linked to obesity status.
One of the difficulties in identifying obese phenotypes and associated eating behaviors lies in the existence of several subpopulations of over-