Environment and origin of disease
- Vasantha Padmanabhan
- … show all 1 hide
Rent the article at a discountRent now
* Final gross prices may vary according to local VAT.Get Access
Growth and reproduction exert pervasive effects on individuals and society as a whole. On an individual basis, they are regulated by a delicate balance between well-integrated gene-dependent mechanisms and the external environment, with daily changes in nutritional availability, stressors and life choices profoundly affecting integration of complex biologic pathways. A developing fetus is especially vulnerable to changes in the maternal environment from external conditions and to circumvent any detrimental consequences, it develops compensatory mechanisms that may be adaptive or disruptive, based upon whether they provide survival advantages or disadvantages, respectively. The developmental origin of disease concept, or Barker hypothesis, highlights this conflict . The alarming increase in the prevalence of some common diseases may partially represent the introduction of medical interventions, environmental pollutants, and lifestyle choices that adversely alter preprogrammed develop
- Barker DJ. Programming the baby. In: Mothers, babies, and disease in later life. London: BMJ Publishing Group; 1994. p. 14–36.
- Ong KK, Dunger DB. Perinatal growth failure: the road to obesity, insulin resistance and cardiovascular disease in adults. Best Pract Res Clin Endocrinol Metab 2002;16:191–207. CrossRef
- Cianfarani S, Germani D, Branca F. Low birth weight and adult insulin resistance; the “catch-up growth” hypothesis. Arch Dis Child Fetal Neonatal Ed 1999;81:F71–3. CrossRef
- Nathanielsz PW. Life in the womb. Origin of adult diseases. Ithaca, NY: Promethean Press; 1999.
- Gluckman PD, Hanson MA. Maternal constraint of fetal growth and its consequences. Semin Fetal Neonatal Med 2004;9:419–25. CrossRef
- Dupont J, Holzenberger M. Biology of insulin-like growth factors in development. Birth Defects Res 2003;69:257–71. CrossRef
- Gatford KL, Quinn KJ, Walton PE, Grant PA, Hosking BJ, Egan AR, et al. Ontogenic and nutritional changes in circulating insulin-like growth factor (IGF)-I, IGF-II and IGF-binding proteins in growing ewe and ram lambs. J Endocrinol 1997;155:47–54. CrossRef
- McLellan KC, Hooper SB, Bocking AD, Delhanty PJD, Phillips ID, Hill DJ, et al. Prolonged hypoxia induced by the reduction of maternal uterine blood flow alters insulin-like growth factor-binding protien-1 (IGFBP-1) and IGFBP-2 gene expression in the ovine fetus. Endocrinology 1992;131:1619–28. CrossRef
- Tarantal AF, Castillo A, Ekert JE, Bischofberger N, Martin RB. Fetal and maternal outcome after administration of tenofovir to gravid rhesus monkeys (Macaca mulatta). J Acquir Immune Defic Syndr 2002;29:207–20.
- Friedman JM, Halaas J. Leptin and the regulation of body weight in mammals. Nature 1998;395:763–70. CrossRef
- Centers for Disease Control and Prevention. CDC growth charts: United States. http://www.cdc.gov/nchs/about/major/nhanes/growthcharts/datafiles.htm.
- Meisel RL, Ward I. Fetal female rats are masculinized by male littermates located caudally in the uterus. Science 1981;213:239–42. CrossRef
- IPCS. Global assessment of the state-of-the-science of endocrine disruptors International Programme on chemical safety. Geneva, Switzerland: World Health organization; 2002.
- Colborn T, vom Saal FS, Soto AM. Developmental effects of endocrine-disrupting chemicals in wildlife and humans. Environ Health Perspect 1993;101:378–84. CrossRef
- Bennetts HW, Underwood EJ, Shier FL. Specific breeding problem of sheep on subterranean clover pastures in Western Australia. Aust Vet J 1946;22:2–12.
- EPA630R-96012. Special report on environmental endocrine disruption: an effects assessment and analysis; 1997. p. 88–9.
- Crews D, McLachlan JA. Epigenetics, endocrine disruption, heath, and disease. Endocrinology 2006;147:S4–10. CrossRef
- Allegrucci C, Denning CN, Burridge P, Steele W, Sinclair KD, Young LE. Human embryonic stem cells as a model for nutritional programming: an evaluation. Reprod Toxicol 2005;20:353–67. CrossRef
- Pennisi E. Environmental epigenomics meeting. Supplements restore gene function via methylation. Science 2005;310:1761. CrossRef
- McKay JA, Williams EA, Mathers JC. Folate, DNA methylation during in utero development and aging. Biochem Soc Trans 2004;32:1006–7. CrossRef
- Environment and origin of disease
Reviews in Endocrine and Metabolic Disorders
Volume 8, Issue 2 , pp 67-69
- Cover Date
- Print ISSN
- Online ISSN
- Springer US
- Additional Links
- Industry Sectors
- Author Affiliations
- 1. Department of Pediatrics, University of Michigan, Ann Arbor, MI, 48105, USA