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Birth weight and risk of angina pectoris: analysis in Swedish twins
A Hubinette1, S Cnattingius, A L V Johansson
1Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden. anna.hubinette@mep.ki.se
Insights
Low birth weight is linked to a higher risk of angina pectoris, especially in dizygotic twins. Genetic factors may influence this association between fetal growth and heart disease risk.
Area of Science:
- Cardiology
- Twin Studies
- Epidemiology
Background:
- Intrauterine nutrition, indicated by birth weight, is inversely associated with coronary heart disease (CHD) risk.
- Investigating discordant twin pairs minimizes genetic and early environmental influences.
Purpose of the Study:
- To examine the association between birth weight and angina pectoris in same-sexed twins.
- To reduce confounding by genetic and early environmental factors using twin pair analysis.
Main Methods:
- Utilized the Swedish Twin Registry for population-based study.
- Collected self-reported birth weight and angina pectoris data via telephone interviews (1998-2000).
- Analyzed 4594 twins in cohort analysis and discordant twin pairs (55 dizygotic, 37 monozygotic) for within-pair analysis.
Main Results:
- Low birth weight (<2.0 kg) showed a trend towards increased angina risk in the cohort (OR: 1.46), which diminished after adjustments.
- Within dizygotic twin pairs discordant for angina, low birth weight significantly increased risk (adjusted OR: 5.73).
- No significant association was found between low birth weight and angina within monozygotic twin pairs (adjusted OR: 1.20).
Conclusions:
- Findings suggest genetic differences related to fetal growth may influence the observed birth weight-CHD associations.
- The study highlights the role of genetic factors in the relationship between early life conditions and adult cardiovascular disease risk.
Objective:
Intrauterine nutrition approximated by birth weight has been shown to be inversely associated with risk of coronary heart disease (CHD). By investigating the association within twin pairs discordant for disease, the influence of genetic and early environmental factors is substantially reduced.
Methods:
We have investigated the association between birth weight and angina pectoris in same-sexed twins with known zygosity included in the population-based Swedish Twin Registry. Self-reports of birth weight and angina pectoris were collected in a telephone interview between 1998 and 2000. The cohort analyses were based on 4594 same-sexed twins, and the within-pair analyses included 55 dizygotic and 37 monozygotic twin pairs discordant for angina pectoris. Odds ratios (OR) and 95% confidence intervals (CI) were calculated by logistic regression.
Results:
Compared with birth weight between 2.0 and 2.9 kg, low birth weight (<2.0 kg) was associated with increased risk of angina pectoris in the twin cohort, (OR: 1.46; 95% CI: 1.14-1.87), but after adjustment for potential confounders the risk decreased, and did not reach significance. Within twin pairs discordant for angina pectoris, low birth weight was significantly associated with increased risk of angina pectoris within dizygotic twins (adjusted OR: 5.73; 95% CI: 1.59-20.67), but not within monozygotic twins (adjusted OR: 1.20; 95% CI: 0.40-3.58).
Conclusions:
The results suggest that genetic differences associated with foetal growth and adult risk of CHD may have affected previously reported associations between birth weight and CHD.
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