Fetal origins of cardiovascular disease

David J.P. Barker

Annals of Medicine · 1999 · 421 citations · 28 references

DOIFull text

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Concepts

TL;DR

Low birthweight, thinness, and short stature at birth are linked to higher adult cardiovascular disease and diabetes risk, a relationship explained by the fetal origins hypothesis that suggests undernutrition induces lasting cardiovascular, metabolic, or endocrine adaptations. Prevention of these diseases may rely on avoiding fetal growth imbalances, mismatches between prenatal and postnatal growth, or nutrient supply disruptions.

Abstract

Low birthweight, thinness and short body length at birth are now known to be associated with increased rates of cardiovascular disease and non-insulin dependent diabetes in adult life. The fetal origins hypothesis proposes that these diseases originate through adaptations which the fetus makes when it is undernourished. These adaptations may be cardiovascular, metabolic or endocrine. They permanently change the structure and function of the body. Prevention of the diseases may depend on prevention of imbalances in fetal growth or imbalances between prenatal and postnatal growth, or imbalances in nutrient supply to the fetus.

References

28