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There is much evidence of a link between low birthweight and elevated risk of adult cardiovascular disease, from humans and experimental animals. However, if one relies on data linking birthweight to coronary heart disease to estimate the public health implications of this association, the effects are likely to be modest. The focus on birthweight may be misplaced, because reduced size at birth may not be in the causal pathway linking gestational factors to disease in adult offspring. We need to know more about this before we can estimate the public health implications of gestational factors and assess the potential for intervention. The most studied gestational factor is maternal nutrition. We review here evidence for and against birthweight being in the causal pathways between suboptimal maternal nutrition and increased risk of adult disease in the offspring and provide evidence suggesting that birthweight is not in all of them. From a public health point of view, we suggest that future research in this field should focus on modifiable gestational exposures that may be linked to adult disease, whether or not they influence size at birth.

Type

Journal article

Journal

Paediatr perinat epidemiol

Publication Date

07/2002

Volume

16

Pages

194 - 199

Keywords

Adult, Animals, Australia, Biomarkers, Birth Weight, Coronary Disease, Female, Fetal Growth Retardation, Humans, Male, Maternal Exposure, Pregnancy, Public Health, Risk Factors, Starvation