RE: "WHY EVIDENCE FOR THE FETAL ORIGINS OF ADULT DISEASE MIGHT BE A STATISTICAL ARTIFACT: THE ‘REVERSAL PARADOX’ FOR THE RELATION BETWEEN BIRTH WEIGHT AND BLOOD PRESSURE IN LATER LIFE"

Matthew W. Gillman

Department of Ambulatory Care and Prevention, Harvard Medical School, and Harvard Pilgrim Health Care, Boston, MA 02215

Regarding the interchange between Tu et al. and Weinberg (1Go–3Go) about the "fetal origins" hypothesis, I fear that both sets of authors come to the wrong conclusions. As Weinberg (2Go) observes, Tu et al. (1Go) are simplistic in their arguments. In perinatology, birth weight itself—or more accurately, fetal size at birth or length of gestation—has intrinsic meaning. Avoiding restricted fetal growth or increasing length of gestation can prevent neonatal morbidity and mortality. In the "fetal origins" paradigm, however, birth weight itself is not a causal factor. One only has to recognize that higher birth weight is related to higher body mass index, and higher body mass index predicts higher blood pressure, to understand that the factors underlying that pathway must be different from those that explain any possible inverse association of birth weight with later blood pressure. Thus, trying to estimate the overall "effect" of birth weight on blood pressure is nonsensical.

Weinberg's clarification touches on these issues (2Go), but she concludes, inexplicably, that we should investigate whether dizygotic twins have adult blood pressures that are different from those of singletons, because twins and singletons have different birth weights. This suggestion just returns us to the imprudent emphasis on birth weight, this time in the much more complicated physiologic system of twin pregnancy (4Go). The better way forward in fetal/developmental origins research is to examine putative prenatal determinants directly, through both observational and experimental designs (5Go–7Go). Birth weight got us into fetal origins research, but it cannot lead us forward.


    ACKNOWLEDGMENTS
 
Conflict of interest: none declared.


    References
 TOP
 References
 

  1. Tu YK, West R, Ellison GTH, et al. Why evidence for the fetal origins of adult disease might be a statistical artifact: the "reversal paradox" for the relation between birth weight and blood pressure in later life. Am J Epidemiol 2005;161:27–32.[Abstract/Free Full Text]
  2. Weinberg CR. Invited commentary: Barker meets Simpson. Am J Epidemiol 2005;161:33–5.[Free Full Text]
  3. Tu YK, Ellison GTH, West R, et al. Tu et al. respond to "Barker meets Simpson." Am J Epidemiol 2005;161:36–7.[Free Full Text]
  4. Morley R, Willinger M, Hankins H, eds. Investigation of fetal origins of adult health in twin cohorts. Paediatr Perinat Epidemiol 2005;19(suppl 1):1–59.[ISI][Medline]
  5. Gillman MW. Epidemiological challenges in studying the fetal origins of adult chronic disease. Int J Epidemiol 2002;31:294–9.[Free Full Text]
  6. Belizan JM, Villar J, Bergel E, et al. Long term effect of calcium supplementation during pregnancy on the blood pressure of offspring: follow up of a randomised controlled trial. BMJ 1997;315:281–5.[Abstract/Free Full Text]
  7. Gillman MW, Rifas-Shiman SL, Kleinman KP, et al. Maternal calcium intake and offspring blood pressure. Circulation 2004;110:1990–5.[Abstract/Free Full Text]




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