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The fetal origins hypothesis questioned
- Piet H. Jongbloet (4 July 2005)
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Piet H. Jongbloet, Dr. Radboud University Nijmegen Medical Centre (252), P.O. Box 9101, 6500 HB Nijmegen, the Netherlands
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Eriksson (1) endeavours to reconcile the rapid increase in body weight during early childhood with preceding thinness at birth as a major play in the game of coronary heart disease, as reported by Rich-Edwards et al. in the longitudinal nurses’ health study. (2) He argues that a relation between low birth weight and long term health outcomes, i.e. the fetal origins hypothesis, has been confirmed in many populations. This, however, does not imply a causal relationship. Apart from many other incompatibilities,(3),(4) birth size being just one snapshot of the trajectory of fetal growth and the need to consider modifiers working later in life might be the impetus to shift our attention away from birth and to target the conception as possible genuine cause of low birth weight, excessive weight gain and threatened life expectancy. (5) It has become evident that optimal birth weight and size, equal male:female ratio and survival are clustered during the seasonally-bound major birth peak in February-April and the minor peak in September. In contrast, reduced birth weight, preterm death and high sex ratios (very often associated with constitutional pathology) are accumulated during the increasing and decreasing slopes of these birth peaks. These phenomena correspond with optimal versus critical stages of oocyte maturation during the alternating ‘ovulatory’ and ‘anovulatory’ seasons which are a relic from our ancestors, as formulated in the seasonally-bound optimally ripening of the oocyte (SOptRO-) hypothesis versus the seasonally-bound pre-ovulatory overripeness ovopathy (SPrOO-) hypothesis. These occurrences are also met during the other transitional stages in which the ovulatory pattern and oocyte maturation are at stake, such as postmenarcheal and premenopausal age, postpartum restoration, undernourishment, etc. (6),(7) This “conception origin” hypothesis looks to be in the better position to explain intrauterine growth retardation and the self perpetuating cycle of progressive functional loss leading to disease. Competing interests: None declared Piet Hein Jongbloet, PhD Department of Epidemiology and Biostatistics, University Medical Centre Nijmegen, the Netherlands, PO Box 9101, 6500 HB Nijmegen, the Netherlands Tel: (00)31-024-3619132 Fax: (00)31-024-3613505 1 Eriksson JG. The fetal origins hypothsis–10 years on. BMJ 2005;330:1096-7. 2 Rich-Edwards JW, Kleinman K, Michels KB, Stampfer MJ, Manson JE, Rexrode KM et al. Longitudinal study of birth weight and adult body mass index in predicting risk of coronary heart disease and stroke in women. BMJ 2004;318:1115-8. 3 William S, Poulton R. Birth size,growth, and blood pressure between the ages of 7 and 26 years: failure to support the fetal origins hypothesis. Am J Epidemiol 2002;155:849-52. 4 Huxley R, Neil A, Collins R. Unravelling the fetal origins hypothsis: is there really an inverse association between birth weight and subsequent blaad pressure? Lancet 2002;360:659-65. 5 Jongbloet PH. “Conception Origin” versus “Fetal Origins” hypothesis and sstroke. Stroke 2004;35:e1-2 6 Jongbloet PH (1975) The effects of preovulatory overripeness of human eggs on development. In Blandau RJ (ed); Aging gametes. Their Biology and pathology. International Symposium, Seatle, 1973. Karger, Basel,pp.300- 329. 7 Jongbloet PH (2004) Over-ripeness ovopathy - A challenging hypothesis for sex ratio modulation. Hum Reprod 19,769-764. Competing interests: None declared |
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