Barker’s Hypothesis Among the Global Poor: Positive Long-term Cardiovascular Effects of In-utero Famine Exposure

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Population Center Working Papers (PSC/PARC)
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Barker hypothesis
in utero
cardiovascular health
Demography, Population, and Ecology
Family, Life Course, and Society
Inequality and Stratification
Medicine and Health
Social and Behavioral Sciences
We gratefully acknowledge the generous support for the Mature Adults Cohort of the Malawi Longitudinal Study of Families and Health (MLSFH-MAC) by the the Swiss Programme for Research on Global Issues for Development (SNF r4d Grant 400640_160374). We also gratefully acknowledge support by National Institute of Child Health and Human Development (NICHD, Grant Nos. R03 HD05 8976, R21 HD050653, R01 HD044228, R01 HD053781) and National Institute on Aging (NIA, Grant No. R21 AG053763), as well as support through the Population Studies Center (supported by NICHD R24 HD-044964) and Population Aging Research Center (supported by NIA P30 AG12836) at the University of Pennsylvania.
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An influential literature on the Barker's hypothesis (or the Developmental Origins of Health and Disease, DOHaD) has documented that poor conditions in utero lead to higher risk of hypertension, diabetes, stroke and heart disease in middle age in middle- and high-income contexts. One of the main explanations is that periods of high calorie intake after birth are inconsistent with the adaptations that the fetus makes to prepare for a poor resources environment (thrifty phenotype hypothesis). Using data from a persistently low-income country, Malawi, we find that individuals exposed in utero to a substantial famine in 1949, have lower levels of blood pressure and blood sugar and less symptoms associated with stroke over half a century later. These findings may be explained by a prolonged period of malnutrition following the famine in contrast to most of the contexts studied in the previous literature.

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