This chapter reviews the causes and health consequences of the Irish famine, the China famine, and the Dutch Hunger Winter, and the genetic and biocultural mechanisms that link the early exposure to famine and health risks in later life. Famine survivors suffer from adverse health consequences such as metabolic abnormalities, cancer, and premature death. We review four hypotheses that may explain the health consequences of experiencing famine: the thrifty gene hypothesis, the thrifty phenotype hypothesis, the epigenetic changes, and the cultural food-related changes. The thrifty gene hypothesis argues that those who can absorb and process food efficiently have survival advantages during a historical time when human were subject to frequent cycles of feast and famine. Such trait, however, becomes maladaptive in an environment with constant abundance of food, leading to metabolic diseases. The thrifty phenotype hypothesis argues that prenatal malnutrition is detrimental to pancreas development, elevating the risk of type 2 diabetes. Epigenetics mechanisms suggest that fetal environment influence the expression and non-expression of genes, resulting in different states of phenotypes in later life. Finally, studies show that those who experienced food restrictions tend to engage in overeating, thus the traumatic experience might influence people’s health through behavioral mechanisms. We argue that a better understanding of how early life adversity influence health in later life could inform the intervention programs that promote the maternal and infant health.
|Original language||English (US)|
|Title of host publication||The SAGE Handbook of Social Studies in Health and Medicine|
|Editors||Susan Scrimshaw, Sandra Lane, Robert Rubinstein, Julian Fisher|
|Publisher||SAGE Publications Ltd|
|State||Accepted/In press - Oct 15 2020|