Abstract
During the last 2 decades evidence suggesting a role for prenatal diet in the development of adult disease has built up. One of the mechanisms that has been proposed to mediate this association is fetal programming of the stress response. It has been hypothesized that poor nutritional circumstances during gestation can alter the set points of the stress response resulting in lifelong over- or underactivation of the response, which subsequently causes disease. Support for the fetal programming of the stress response hypothesis has come from animal experiments as well as from human studies. Animal studies have mainly been performed in rats, guinea pigs, and sheep. In these studies, pregnant animals were fed a restricted diet after which functioning of the stress systems, the Hypothalamic–Pituitary–Adrenal (HPA)-axis and the Autonomic Nervous System (ANS), was measured in the offspring. Overall, results show that maternal food restriction induces growth retardation in the offspring as well as several alterations in the development of the HPA-axis and the ANS. Due to obvious ethical constrictions to manipulate the maternal diet research in humans has mainly focused on the effects of birth weight as an indirect measure of the fetal environment. Most birth-weight studies have shown an overactive HPA-axis and ANS in response to stress in people with low birthweight. Only two studies in humans have directly measured the effects of prenatal diet on stress responsiveness in later life. The Motherwell Study found that fasting cortisol concentrations and cortisol responses to a psychological stress protocol were elevated in men and women whose mothers consumed a diet consisting of high meat and fish intake and low green vegetables intake. The Dutch Famine Birth Cohort Study investigated the effects of prenatal exposure to the Dutch famine, which happened at the end of World War II in the Netherlands. Men and women who were exposed to the famine in utero did not show altered functioning of the HPA-axis. However, men and women exposed to the famine during early gestation did show greater blood pressure responsiveness to a psychological stress protocol. It can be concluded that prenatal diet definitely affects stress responsiveness in later life. The exact effect, how it happens, to what extent, and which factors are of importance, remains to be clarified. It seems justified though, to inform women of the importance of a balanced diet during pregnancy for the health of their babies.
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Abbreviations
- ACTH:
-
AdrenoCorticoTropic Hormone
- ANS:
-
Autonomic Nervous System
- AVP:
-
Arginine VasoPressin
- CRH:
-
Corticotropin-Releasing Hormone
- Dex:
-
Dexamethasone
- FR:
-
Food Restricted
- GR:
-
Glucocorticoid Receptor
- HPA-axis:
-
Hypothalamic–Pituitary–Adrenal axis
- PVN:
-
ParaVentricular Nucleus
- TSST:
-
Trier Social Stress Test
- 11β-HSD:
-
11 Beta-Hydroxy Steroid Dehydrogenase
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Rooij, S.R.d. (2011). Prenatal Diet and Stress Responsiveness. In: Preedy, V., Watson, R., Martin, C. (eds) Handbook of Behavior, Food and Nutrition. Springer, New York, NY. https://doi.org/10.1007/978-0-387-92271-3_130
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