In the early 1980s, David Barker and others noted a paradox: although overall rates of cardiovascular disease increase with rising national prosperity, the least prosperous residents of a wealthy nation suffer the highest rates. He and others proposed over a series of studies that an adverse fetal environment followed by plentiful food in adulthood may be a recipe for adult chronic disease, a claim referred to as the Barker Hypothesis. These studies generally correlated birth weight and other infant parameters to the incidence of adult disease. Detractors, including an editorial in BMJ in 1995, complained that “[e] arly nutrition is inferred indirectly from fetal and infant growth, and fetal growth especially is a doubtful surrogate measure”(1). Most of the epidemiological studies were also vulnerable to confounding factors, particularly social class, that influence both intrauterine and adult environment, which delayed acceptance of the hypothesis. In PNAS, Rooij et al.(2) present another chapter in the ongoing study of the children of the Dutch Hunger Winter, a key test of the hypothesis (2). They show that, in addition to the previously shown effects of food restriction in utero on metabolism and cardiovascular health, there are effects on age-associated decline of cognitive functions. In the winter and spring of 1944 after a railway strike, the German occupation limited rations such that people, including pregnant women, in the western region of The Netherlands, including Amsterdam, received as little as 400–800 calories/d. The famine affected people of all social classes and was followed by growing prosperity in the postwar period. Thus, the Dutch Hunger Winter study, from which results were first published in 1976, provides an almost perfectly designed, although tragic, human experiment in the effects of intrauterine deprivation on subsequent adult health. This study has provided crucial support and fundamental insights for the growing field of the developmental origins of health and disease (DOHaD).