Early Development Origins of Adult Disease Caused by Malnutrition and Environmental Chemical Substances

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Author(s)

Abstract

We observed that maternal exposure to diesel exhaust (DE) and diesel exhaust particles (DEPs) damaged the reproductive and central nervous systems in mice and rats. These observations suggest that impairment of early development induced by maternal exposure to DE and DEP causes several disorders after growing up. To elucidate the effects of maternal exposure to environmental substances, we review here a hypothesis of fetal and early developmental origins of adult disease. Recent studies influenced by Dr. Barker's Thrifty Phenotype Hypothesis have led to advances in understanding how fetal and infant malnutrition can permanently and adversely alter the development of tissues and organs. Several epidemiological surveys in humans have uncovered links between maternal malnutrition and effects on the organs such as the kidney, pancreas, liver, muscles, adipocytes, and the hypothalamic-pituitary-adrenal (HPA) axis. These observations were examples of critical period programming. The idea has been applied to examining possible fetal and early origins of other diseases. Interestingly, many reports showed that similar phenomena were induced by perinatal exposure to airborne environmental pollutants. Studies have shown that maternal DE exposure disrupts reproductive development and damages the central nervous system. In addition, perinatal exposure to tobacco smoke has been linked to several respiratory disorders. These results show that early development is a critical determinant of adult physiology and much care should be taken to ensure the proper environment for fetal development. This idea is especially topical currently, where rapid industrialization in Asia has accelerated changes in environment and increased pollution.

Journal

  • Journal of Health Science

    Journal of Health Science 55(1), 11-19, 2009-02-01

    The Pharmaceutical Society of Japan

References:  60

Cited by:  3

Codes

  • NII Article ID (NAID)
    110007055942
  • NII NACSIS-CAT ID (NCID)
    AA11316464
  • Text Lang
    ENG
  • Article Type
    Journal Article
  • ISSN
    13449702
  • NDL Article ID
    9782049
  • NDL Source Classification
    ZS17(科学技術--医学--衛生学・公衆衛生)
  • NDL Call No.
    Z54-J464
  • Data Source
    CJP  CJPref  NDL  NII-ELS  J-STAGE 
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