economic progress amplifies mismatch. Much of the literature on the developmental origins of health anddisease focuses on chronic diseases. However, given thestrong association between chronic diseases and obesity,particularly central obesity, this evidence is highly relevant and provides a strong rationale for obesity prevention efforts in populations that have experienceddramatic changes in the nutritional environment as aconsequence of nutrition transition.Mechanisms may include effects on the number ofnephrons in the kidney,36 glucocorticoid exposure subsequent to maternal stress, or poor nutritional status potentially programming the insulin and hypothalamicpituitary axes for high levels of metabolic efficiency28 andepigenetic changes.Maternal stress and specific aspects ofdiet (for example, intake of folate and other methyldonors) can affect DNA methylation and geneexpression.37–39 Ongoing studies in places such as Indiaare examining the role of maternal micronutrient intakeon epigenetic changes that affect child adiposity.39,40Research in India has provided other important insights.For example, Indian infants with poorly nourishedmothers are born with weight deficits, but in relativeterms the deficits in lean mass are greater than those inadiposity. In later life, when modern high-energy andhigh-fat diets are consumed, the previously “thin-fat”babies also have greater central adiposity.41,42It is apparent from studies of the developmentalorigins of disease that there is a strong intergenerationalcomponent to health.While much of the literature on theearly origins of obesity and associated risk has focused onundernutrition, there is also substantial evidence thatmaternal overweight and obesity in pregnancy influencedisease risk among offspring. For example, gestationaldiabetes is related to offspring body composition andincreased risk of insulin resistance and diabetes in offspring.43,44 Thus, there is concern about an intergenerational amplification of diabetes risk. Women who weremalnourished as children are at increased risk of beingcentrally obese and having impaired glucose tolerance asadults. If these conditions affect a woman’s pregnancy, heroffspring will be at increased risk of early development ofobesity and diabetes. As obesity develops at younger andyounger ages, the likelihood that adolescents and youngwomen who become pregnant will experience complications associated with gestational diabetes and hypertension will increase dramatically. There is growing evidencethat maternal obesity, even without gestational diabetes,isa risk factor for child obesity through a pathway related tofetal overnutrition (see the review by Fall45).