Sex-Specific Effects of Fetal Exposure to the 1959–1961 Chinese Famine on Risk of Adult Hypertension
- 491 Downloads
Previous research is inconsistent about the effects of prenatal famine exposure on risk of adult hypertension. Follow-up of persons exposed to the 1959–1961 Chinese famine, the largest in human history, provides an opportunity to examine the long-term impact of prenatal famine exposure on adult cardiovascular disease (CVD). We investigated the effects of fetal-infant exposure to the famine on risk of hypertension in adulthood. We included 1,415 participants from the 2009 China Health and Nutrition Survey born September 1, 1956–December 31, 1964. Blood pressure (BP) measurements, self-reported previous diagnosis of hypertension and current anti-hypertension drug use were obtained from the survey. Differences in mean BP and risk of adult hypertension by famine exposure status were determined using linear and logistic regression analyses, after adjusting for confounders. Women with fetal-infant exposure to famine had higher mean systolic blood pressure (4.24 mmHg; 95 % confidence interval (CI) 1.50–6.98) than those unexposed. They also had increased odds of a prior diagnosis of hypertension (odds ratio (OR) 2.16; 95 % CI 1.16–4.02), and were more likely to be currently taking anti-hypertensive medications (OR 2.81; 95 % CI 1.32–5.97) than unexposed women after adjusting for covariates. No statistically significant increases in mean BP or hypertension were seen among men. Exposure to famine during the fetal-infant period or early childhood has deleterious effects on adult health, but the effects may be greater for women. Gender-specific intervention strategies for CVD may be warranted for populations exposed to under-nutrition during critical time periods of fetal development.
KeywordsFetal exposure Gender difference Hypertension Blood pressure Chinese famine
This research uses data from the China Health and Nutrition Survey (CHNS). We thank the National Institute of Nutrition and Food Safety, China Center for Disease Control and Prevention; the Carolina Population Center, University of North Carolina at Chapel Hill; the National Institutes of Health (NIH; R01-HD30880, DK056350, and R01-HD38700); and the Fogarty International Center, NIH, for financial support for the CHNS data collection and analysis files since 1989. We thank those parties, the China-Japan Friendship Hospital, and the Ministry of Health for support for CHNS 2009.
Conflict of interest
- 6.Beard, J. L. (2008). Why iron deficiency is important in infant development. The Journal of Nutrition, 138, 2536–2543.Google Scholar
- 7.Lucas, A. (1991). Programming by early nutrition in man. In G. Bock & J. Whelan (Eds.), The childhood environment and adult disease. Ciba Foundation Symposium 156 (pp. 38–50). Chichester: Wiley.Google Scholar
- 21.Cohen, J., Cohen, P., West, S. G., et al. (2003). Applied multiple regression/correlation analysis for the behavioral sciences. Mahwah: Lawerence Erlbaum Associates.Google Scholar
- 25.Zambrano, E., Martinez-Samayoa, P. M., Bautista, C. J., et al. (2005). Sex differences in transgenerational alterations of growth and metabolism in progeny (F2) of female offspring (F1) of rats fed a low protein diet during pregnancy and lactation. Journal of Physiology, 566, 225–236.CrossRefPubMedCentralPubMedGoogle Scholar
- 26.Zambrano, E., Bautista, C. J., Deas, M., et al. (2006). A low maternal protein diet during pregnancy and lactation has sex- and window of exposure-specific effects on offspring growth and food intake, glucose metabolism and serum leptin in the rat. Journal of Physiology, 571, 221–230.CrossRefPubMedCentralPubMedGoogle Scholar