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Fetal origins of stress-related adult disease.
Ann N Y Acad Sci. 2006 Nov; 1083:11-27.AN

Abstract

During the past decade, a considerable body of evidence has emerged showing that circumstances during the fetal period may have lifelong programming effects on different body functions with a considerable impact on disease susceptibility. The purpose of this article is to provide a synopsis of these findings and their role in explaining the development of stress-related adult disease. In the context of Per Björntorp memorial symposium, stress-related disease will be interpreted broadly, including cardiovascular disease and components of the metabolic syndrome, for which the evidence of fetal origins is most abundant. It has however become evident that early-life programming has a much broader potential effect on an individual's health. For example, perinatal variables, such as low birth weight, have been associated with increased prevalence of depressive symptoms. Mechanistic studies in animals and humans have shown that lifelong programming of the hypothalamic-pituitary-adrenal axis (HPAA) function by fetal life conditions is likely to be a key factor in mediating associations with these disorders, which frequently are characterized by HPAA overactivity. Preliminary observations suggest a similar important role for early-life programming of sympathoadrenal function. Reduced HPAA activity is characteristic of a number of stress-related disorders, including posttraumatic stress disorder; chronic pain; fatigue; and atypical, melancholic depression. It is therefore highly plausible that susceptibility to these disorders originates in a similar manner during early life, although direct evidence is to a great deal lacking. Important targets for future research include distinction between the effects of different pregnancy conditions, such as maternal malnutrition, preeclampsia, and maternal infection, which may have dissimilar late-life consequences. This will be a crucial step when the associations that are currently emerging will be translated into disease prevention.

Authors+Show Affiliations

National Public Health Institute, Mannerheimintie 166, 00300 Helsinki, Finland. eero.kajantie@helsinki.fi

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

17148730

Citation

Kajantie, Eero. "Fetal Origins of Stress-related Adult Disease." Annals of the New York Academy of Sciences, vol. 1083, 2006, pp. 11-27.
Kajantie E. Fetal origins of stress-related adult disease. Ann N Y Acad Sci. 2006;1083:11-27.
Kajantie, E. (2006). Fetal origins of stress-related adult disease. Annals of the New York Academy of Sciences, 1083, 11-27.
Kajantie E. Fetal Origins of Stress-related Adult Disease. Ann N Y Acad Sci. 2006;1083:11-27. PubMed PMID: 17148730.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fetal origins of stress-related adult disease. A1 - Kajantie,Eero, PY - 2006/12/7/pubmed PY - 2007/3/8/medline PY - 2006/12/7/entrez SP - 11 EP - 27 JF - Annals of the New York Academy of Sciences JO - Ann N Y Acad Sci VL - 1083 N2 - During the past decade, a considerable body of evidence has emerged showing that circumstances during the fetal period may have lifelong programming effects on different body functions with a considerable impact on disease susceptibility. The purpose of this article is to provide a synopsis of these findings and their role in explaining the development of stress-related adult disease. In the context of Per Björntorp memorial symposium, stress-related disease will be interpreted broadly, including cardiovascular disease and components of the metabolic syndrome, for which the evidence of fetal origins is most abundant. It has however become evident that early-life programming has a much broader potential effect on an individual's health. For example, perinatal variables, such as low birth weight, have been associated with increased prevalence of depressive symptoms. Mechanistic studies in animals and humans have shown that lifelong programming of the hypothalamic-pituitary-adrenal axis (HPAA) function by fetal life conditions is likely to be a key factor in mediating associations with these disorders, which frequently are characterized by HPAA overactivity. Preliminary observations suggest a similar important role for early-life programming of sympathoadrenal function. Reduced HPAA activity is characteristic of a number of stress-related disorders, including posttraumatic stress disorder; chronic pain; fatigue; and atypical, melancholic depression. It is therefore highly plausible that susceptibility to these disorders originates in a similar manner during early life, although direct evidence is to a great deal lacking. Important targets for future research include distinction between the effects of different pregnancy conditions, such as maternal malnutrition, preeclampsia, and maternal infection, which may have dissimilar late-life consequences. This will be a crucial step when the associations that are currently emerging will be translated into disease prevention. SN - 0077-8923 UR - https://www.unboundmedicine.com/medline/citation/17148730/Fetal_origins_of_stress_related_adult_disease_ L2 - https://doi.org/10.1196/annals.1367.026 DB - PRIME DP - Unbound Medicine ER -