Within the Western world's aging and increasingly overweight population, we are seeing an increasing prevalence of adult-onset, lifestyle-related disease such as diabetes, hypertension and atherosclerosis. There is significant evidence that suboptimal nutrition in pregnancy can lead to an increased risk of these diseases developing in offspring, and that this increased risk can be heritable. Thus, poor in utero nutrition may be a major contributor to the current cycle of obesity. While the molecular basis of this phenomenon is unknown, available evidence suggests that it can be mediated by epigenetic changes to gene expression. Here, we discuss epigenetics as a mediator of disease risk in response to nutritional cues. The potential for maternal nutrition to heritably alter epigenetic states may have implications for population health and adaptive evolution.