Journal
JOURNAL OF DEVELOPMENTAL ORIGINS OF HEALTH AND DISEASE
Volume 14, Issue 2, Pages 242-248Publisher
CAMBRIDGE UNIV PRESS
DOI: 10.1017/S2040174422000538
Keywords
Birth weight; discordant twin study; cardiometabolic health; UK Biobank
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This study used a discordant twin study design to investigate the association between birth weight and later-life cardiometabolic risk factors. The results showed that there was no strong evidence of association between within-pair differences in birth weight and most cardiometabolic risk factors in MZ twins, except for nominal associations with C-reactive protein and insulin-like growth factor 1.
One of the longstanding debates in life-course epidemiology is whether an adverse intrauterine environment, often proxied by birth weight, causally increases the future risk of cardiometabolic disease. The use of a discordant twin study design, which controls for the influence of shared genetic and environmental confounding factors, may be useful to investigate whether this relationship is causal. We conducted a discordant twin study of 120 monozygotic (MZ) and 148 dizygotic (DZ) twin pairs from the UK Biobank to explore the potential causal relationships between birth weight and a broad spectrum of later-life cardiometabolic risk factors. We used a linear mixed model to investigate the association between birth weight and later-life cardiometabolic risk factors for twins, allowing for both within-pair differences and between-pair differences in birth weight. Of primary interest is the within-pair association between differences in birth weight and cardiometabolic risk factors, which could reflect an intrauterine effect on later-life risk factors. We found no strong evidence of association in MZ twins between the within-pair differences in birth weight and most cardiometabolic risk factors in later life, except for nominal associations with C-reactive protein and insulin-like growth factor 1. However, these associations were not replicated in DZ twin pairs. Our study provided no strong evidence for intrauterine effects on later-life cardiometabolic risk factors, which is consistent with previous large-scale studies of singletons testing the potential causal relationship. It does not support the hypothesis that adverse intrauterine environments increase the risk of cardiometabolic disease in later life.
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