Iron is involved in the functional conformation of hemoglobin; it facilitates hemoglobin binding to oxygen. Iron also has a critical role in erythropoiesis. When erythroblasts proliferate and differentiate, they require large amounts of iron for hemoglobin synthesis. The heme moiety of erythroblasts requires iron for synthesis, and it regulates globin production. Thus, iron deficiency (ID) causes anemia, which is associated with many diseases. Because ID in the adult has a detrimental influence on erythrocyte function, maternal ID affects fetal development; thereafter, many physiological functions may be altered in the offspring. In rats fed a low-iron diet, although maternal ID did not cause severe anemia in the dam, brain development in the offspring was profoundly impaired; their offspring showed an increased auditory brainstem response time later in life, which suggested an impairment in brain development (1). Thus, subclinical anemia in the mother during early pregnancy may be a risk factor for abnormal central nervous system development in the fetus. The authors also showed that there was a time window for the susceptibility of brain development to ID (1). The fetal stage was thought to be the most vulnerable stage during development (2). The bottom line was that, when a fetus had experienced maternal ID, health problems become manifest in adulthood, despite adequate adult nutrition. Although animals are resistant to diet-induced obesity under normal circumstances, feeding with a high-fat diet (HFD) induces obesity in many experimental animals. Therefore, HFD is widely used as a model for the Western diet, which is thought to be an important risk factor for obesity. In turn, obesity increases the risk for metabolic syndrome, which includes cardiovascular disease. Therefore, the relationship between obesity and the Western diet has a profound impact on public health. Because the time range of highest vulnerability in brain development occurs in the fetal stage, one might expect that some abnormal development of the brain at that time could affect the adult’s susceptibility to obesity (3). In fact, the thrifty phenotype hypothesis proposed that poor nutrition in early life causes subsequent development of the metabolic syndrome in adults (4). It is now recognized that intrauterine undernutrition or excessive maternal feeding, including a HFD, affects the developmental programming of the offspring, and changes can be manifest in adulthood (5). Thus, the risk for adult health problems, particularly metabolic syndrome, can be markedly influenced by fetal and prenatal environmental exposures. Interestingly, many abnormal feeding behaviors are manifest only with the HFD. For example, heterozygote carriers of the proopiomelanocortin gene mutation are predisposed to obesity. Under normal feeding conditions, these mice maintained a normal weight; however, when fed a HFD, these mice became significantly obese (6). This also occurred with pharmacological receptor manipulations (7). Similar responses were observed in neuropeptide Y knockout mice. When fed normal chow, they look healthy, but when fed a HFD, they become obese (8). These are only a few examples, but they showed that the HFD is useful for revealing diseases. In this issue of Endocrinology, Bourque et al. (9) reported that mouse offspring exposed to maternal ID during the gestational period developed a susceptibility to HFD-induced obesity; in addition, they developed glucose intolerance and increases in blood pressure. These symptoms are indicative of metabolic syndrome. Dams fed a