pects of the environment are rarely directly measured in behavioral genetics studies of obesity. Consequently, investigators generally could not test the influence of putative social-environmental factors when modeling genetic influences on fat mass.
Heritability of BMI has been estimated from a variety of designs, but most commonly from twin and adoption studies that compared phenotypic correlations for body fat between groups of individuals varying in genetic relatedness. To the extent that fat mass is genetically influenced, phenotypic correlations will be greater among individuals who are more genetically similar (e.g., monozygotic, MZ, twins) than less genetically similar (e.g., dizyogotic, DZ, twins). Using biometric statistical models, heritability is estimated along with the magnitude of shared and nonshared environmental factors.
Maes et al.  put forward a most comprehensive review of this literature, the results of which provide indisputable support for a heritable component to BMI and fat mass. Heritability estimates fall in the range of 20 to 80 percent when estimated from family studies that compared parent-child and sibling correlations, 20 to 60 percent when estimated from adoption studies, and 50 to 90 percent when estimated from twin studies. Although the heritability estimates vary sizably, the most accurate estimates arguably come from twin studies, which have methodological strengths over other designs . Also, studies of twins reared apart (i.e., twins separated during childhood and therefore not exposed to the same home environment) generally yield some of the higher heritability estimates. Stunkard et al.  conducted the first study of twins reared apart, the results of which estimated heritability at ~65 to 75 percent for BMI. Allison et al.  obtained comparable heritability estimates when pooling an international sample of twins reared apart from seven countries. Finally, the inconsistent results that have been reported across studies were likely due to small sample sizes.
Results of longitudinal behavior genetic studies suggest that there are age-specific genetic effects on BMI, such that different obesity-promoting genes may become active at different ages across the lifespan. This has been documented throughout the lifespan [121, 122]. Thus, although some genes exert a consistent influence over time and are partially responsible for the “tracking” of BMI, other genetic influences may appear at different stages of a child’s development. Apropos to the theme of this paper, considering developmental milestones may be especially important for future studies testing the interplay of genetic and social-environmental influences on obesity.
Beyond heritability, unmeasured genotype studies have provided clues into the nature of environmental influences on obesity. First, most studies find no evidence for shared home environmental influences on fat mass variability in adulthood. Rather, most environmental influences on fat