We found that exposure to Chinese famine during fetal life and early childhood was associated with a higher risk of metabolic syndrome in later life. These associations were stronger in subjects who had a Western dietary pattern and subjects who were overweight in adulthood.
Barker et al. (12
) and Gluckman and Hanson (13
) suggested that environmental factors during fetal life and infancy play a role in the origin of the metabolic syndrome and its components. A mismatch between fetal and postnatal environments might exacerbate this effect. To support this hypothesis, the Dutch famine study found that prenatal exposure to famine was associated with higher BMI, higher waist circumference, lower glucose tolerance, higher risk of coronary heart disease, more atherogenic lipid profile, and increased levels of plasma fibrinogen in later life (21
). Men who had experienced the siege of Leningrad (1941–1944) during early life had increased mortality from ischemic heart disease and stroke in their adulthood (22
). Early life exposure to Chinese famine (1959–1961) was also associated with the increased risk of overweight (9
), hyperglycemia (8
), and hypertension (3
) in adult life. The current study provides further evidence that both fetal and infant exposure to severe famine increased the clustering of the metabolic risk factors that predispose a person to type 2 diabetes and cardiovascular disease.
The association between fetal exposure to famine and higher risk of metabolic syndrome was exacerbated by a nutritionally rich environment in later life represented by Western dietary pattern and overweight. This dietary pattern was characterized by high intake of meat, eggs, dairy, sugary beverages, and edible oils and a low intake of vegetables (18
). Our results provide evidence to support the hypothesis that the mismatch between the early life starve environment and later life rich environment magnified the risk of metabolic diseases in later life.
A potential limitation of this study is resident migration across different regions in China, which might lead to misclassification of famine exposure. However, the mobility of the population in rural China is relatively low because relocation of permanent residents needed to be approved by authorities. According to the 2000 China National Population Census, only 2.68% of the rural population lived in provinces other than their birthplaces (23
). Therefore, we do not expect that intraprovince migration led to serious misclassification in famine exposure. Another limitation of our study is the lack of birth weight data, which precludes us from examining the interactions between birth weight and adult overweight or dietary patterns on risk of metabolic syndrome.
Despite these limitations, the current study provided a unique opportunity to test the hypothesis of the joint association between early life famine exposure and later life environment with the risk of metabolic syndrome in adulthood. When compared with other famine studies, the Chinese famine lasted much longer and affected more people.
In conclusion, we found that exposure to severe famine in fetal life and infant period was associated with higher risk of metabolic syndrome in adulthood. A nutritionally rich environment, represented by a Western dietary pattern and overweight, further strengthened the association. Our study indicates that both the early life environment and later life overnutrition are critical for the cardiometabolic health in adult life.