Early life stress and metabolism

Exposure to stress is a normal and constant facet of life. However, excessive or chronic stress at particular phases of brain development can have lasting detrimental effects on many aspects of physiology, including appetite regulation and metabolism. A specific window of vulnerability to the lasting effects of stress is the early life period, in utero and immediately postnatally. At these times, excessive psychological stress, such as parental withdrawal or a bereavement in the family, can influence hypothalamic-pituitary-adrenal (HPA) axis development, resulting in excessive glucocorticoid production throughout life. Although additional mechanisms contribute to aberrant programming of feeding and metabolism with early life stress, HPA axis dysregulation can play a major role, with excess glucocorticoids contributing to a chronically stimulated appetite for palatable foods, as well as increased fat deposition. Here we will review recent work examining the impact of early life stress on metabolic function in animal models and in humans, we will examine some of the glucocorticoid-mediated mechanisms by which this might occur, and we will highlight those cases of metabolic resilience in the face of early life stress.