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Developmental origins of adult health and disease: the role of periconceptional and foetal nutrition.

Abstract

The 'developmental origins of adult health and disease' hypothesis stated that environmental factors, particularly maternal undernutrition, act in early life to programme the risks for adverse health outcomes, such as cardiovascular disease, obesity and the metabolic syndrome in adult life. Early physiological tradeoffs, including activation of the foetal hypothalamo-pituitary-adrenal (HPA) axis, confer an early fitness advantage such as foetal survival, while incurring delayed health costs. We review the evidence that such tradeoffs are anticipated from conception and that the periconceptional nutritional environment can programme the developmental trajectory of the stress axis and the systems that maintain and regulate arterial blood pressure. There is also evidence that restriction of placental growth and function, results in an increased dependence of the maintenance of arterial blood pressure on the sequential recruitment of the sympathetic nervous system and HPA axis. While the 'early origins of adult disease' hypothesis has focussed on the impact of maternal undernutrition, an increase in maternal nutritional intake and in maternal body mass intake has become more prevalent in developed countries. Exposure to overnutrition in foetal life results in a series of central and peripheral neuroendocrine responses that in turn programme development of the fat cell and of the central appetite regulatory system. While the physiological responses to foetal undernutrition result in the physiological trade off between foetal survival and poor health outcomes that emerge after reproductive senescence, exposure to early overnutrition results in poor health outcomes that emerge in childhood and adolescence. Thus, the effects of early overnutrition can directly impact on reproductive fitness and on the health of the next generation. In this context, the physiological responses to relative overnutrition in early life may directly contribute to an intergenerational cycle of obesity.

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  • Authors+Show Affiliations

    ,

    Early Origins of Adult Health Research Group, Sansom Research Institute, School of Pharmacy and Medical Science, University of South Australia, Adelaide, SA, Australia. caroline.mcmillen@unisa.edu.au

    , , , ,

    Source

    MeSH

    Adipose Tissue
    Adult
    Cardiovascular System
    Embryonic Development
    Female
    Fetal Development
    Humans
    Neurosecretory Systems
    Obesity
    Pregnancy
    Prenatal Exposure Delayed Effects
    Prenatal Nutritional Physiological Phenomena

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't
    Review

    Language

    eng

    PubMed ID

    18226059

    Citation

    McMillen, I Caroline, et al. "Developmental Origins of Adult Health and Disease: the Role of Periconceptional and Foetal Nutrition." Basic & Clinical Pharmacology & Toxicology, vol. 102, no. 2, 2008, pp. 82-9.
    McMillen IC, MacLaughlin SM, Muhlhausler BS, et al. Developmental origins of adult health and disease: the role of periconceptional and foetal nutrition. Basic Clin Pharmacol Toxicol. 2008;102(2):82-9.
    McMillen, I. C., MacLaughlin, S. M., Muhlhausler, B. S., Gentili, S., Duffield, J. L., & Morrison, J. L. (2008). Developmental origins of adult health and disease: the role of periconceptional and foetal nutrition. Basic & Clinical Pharmacology & Toxicology, 102(2), pp. 82-9. doi:10.1111/j.1742-7843.2007.00188.x.
    McMillen IC, et al. Developmental Origins of Adult Health and Disease: the Role of Periconceptional and Foetal Nutrition. Basic Clin Pharmacol Toxicol. 2008;102(2):82-9. PubMed PMID: 18226059.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Developmental origins of adult health and disease: the role of periconceptional and foetal nutrition. AU - McMillen,I Caroline, AU - MacLaughlin,Severence M, AU - Muhlhausler,Beverly S, AU - Gentili,Sheridan, AU - Duffield,Jaime L, AU - Morrison,Janna L, PY - 2008/1/30/pubmed PY - 2008/2/23/medline PY - 2008/1/30/entrez SP - 82 EP - 9 JF - Basic & clinical pharmacology & toxicology JO - Basic Clin. Pharmacol. Toxicol. VL - 102 IS - 2 N2 - The 'developmental origins of adult health and disease' hypothesis stated that environmental factors, particularly maternal undernutrition, act in early life to programme the risks for adverse health outcomes, such as cardiovascular disease, obesity and the metabolic syndrome in adult life. Early physiological tradeoffs, including activation of the foetal hypothalamo-pituitary-adrenal (HPA) axis, confer an early fitness advantage such as foetal survival, while incurring delayed health costs. We review the evidence that such tradeoffs are anticipated from conception and that the periconceptional nutritional environment can programme the developmental trajectory of the stress axis and the systems that maintain and regulate arterial blood pressure. There is also evidence that restriction of placental growth and function, results in an increased dependence of the maintenance of arterial blood pressure on the sequential recruitment of the sympathetic nervous system and HPA axis. While the 'early origins of adult disease' hypothesis has focussed on the impact of maternal undernutrition, an increase in maternal nutritional intake and in maternal body mass intake has become more prevalent in developed countries. Exposure to overnutrition in foetal life results in a series of central and peripheral neuroendocrine responses that in turn programme development of the fat cell and of the central appetite regulatory system. While the physiological responses to foetal undernutrition result in the physiological trade off between foetal survival and poor health outcomes that emerge after reproductive senescence, exposure to early overnutrition results in poor health outcomes that emerge in childhood and adolescence. Thus, the effects of early overnutrition can directly impact on reproductive fitness and on the health of the next generation. In this context, the physiological responses to relative overnutrition in early life may directly contribute to an intergenerational cycle of obesity. SN - 1742-7843 UR - https://www.unboundmedicine.com/medline/citation/18226059/Developmental_origins_of_adult_health_and_disease:_the_role_of_periconceptional_and_foetal_nutrition_ L2 - https://doi.org/10.1111/j.1742-7843.2007.00188.x DB - PRIME DP - Unbound Medicine ER -