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The fetal origins hypothesis—10 years on

BMJ 2005; 330 doi: https://doi.org/10.1136/bmj.330.7500.1096 (Published 12 May 2005) Cite this as: BMJ 2005;330:1096

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The fetal origins hypothesis questioned

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

Competing interests: No competing interests

04 July 2005
Piet H. Jongbloet
Dr.
Radboud University Nijmegen Medical Centre (252), P.O. Box 9101, 6500 HB Nijmegen, the Netherlands