Prenatal psychosocial stress exposure is associated with insulin resistance in young adults

Entringer, Sonja, Wüst, Stefan, Kumsta, Robert, Layes, Irmgard, Nelson, Edward, Hellhammer, Dirk and Wadhwa, Pathik (2008) Prenatal psychosocial stress exposure is associated with insulin resistance in young adults. American Journal of Obstetrics and Gynecology, 199 (5), 498e1-498e7. (doi:10.1016/j.ajog.2008.03.006).

Abstract

Context: epidemiological studies across the world have reported strong associations between markers of an individual’s birth phenotype (e.g., birth weight) and subsequent risk for type 2 diabetes mellitus. Prenatal stress has been proposed as one of the underlying processes contributing to both birth phenotype and the physiology of the developing organism that underlies health and disease risk in later life.
Objective: to determine the association between maternal psychosocial stress exposure during pregnancy and measures of glucose-insulin metabolism in the adult offspring. Design and Participants: Healthy young adults whose mothers experienced major stressful life events during their pregnancy (n=36, Prenatal Stress, PS group) and a comparison group (n=22, CG) underwent an oral glucose tolerance test (OGTT). Main Outcome Measures: Plasma glucose, insulin and C-peptide levels in response to the OGTT.
Results: glucose levels were not significantly different across the groups, however, PS subjects showed significantly elevated 2h insulin (p=.01) and C-peptide levels (p=.03), and a trend for a higher homeostatic model insulin resistance index (p=.07). These differences were independent of birth phenotype, family history of type 2 diabetes mellitus, gestational diabetes, body mass index, pro-inflammatory state, and smoking.
Conclusions: higher insulin responses reflect relative insulin resistance in these prenatally-stressed young adults and may predispose them to subsequently develop type 2 diabetes mellitus. To the best of our knowledge, this study is the first to provide evidence for a direct link in humans between prenatal psychosocial stress and alterations in glucose-insulin metabolic function.

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