Can cardiovascular risk be predicted by newborn, childhood, and adolescent body size? An examination of longitudinal data in urban African Americans

Objective: Recent retrospective studies of older adults have demonstrated a correlation between lower birth weight and hypertension and insulin resistance. We tested this finding in our sample of urban African Americans with prospective data on growth and blood pressure and also tested other variables (in addition to birth weight) for their relationship to adult cardiovascular risk. Study design: ii prospective study or birth weight, growth, and blood pressure (Philadelphia Perinatal Collaborative Project) followed a sample of 137 African Americans, with nine examinations from birth through 28.0 +/- 2.7 years. Metabolic measurements (oral glucose tolerance testing, euglycemic hyperinsulinemic clamp, and plasma lipid concentration) were performed on the subjects as adults. Bivariate correlations among parameters were computed using the Pearson r. The chi-squared statistic was used to determine associations of outcomes with birth weight, Stepwise multiple linear regressions were computed using newborn, early childhood, adolescent, and young adult parameters to predict adult outcomes. Results: Birth weight and blood pressure at age 28 rears are not correlated (Pearson r = 0.06). Birth weight is also unrelated to adult obesity. However, weight at 0.3 years and after and body mass index al 7 years and after are correlated with adult weight. Furthermore, weight at age 14 years is significantly negatively correlated with measures of insulin-stimulated glucose use, indicating that obese adolescents may be at greater risk than nonobese adolescents for development of non-insulin dependent diabetes in adulthood. Conclusions: We found no relationship between birth weight and adult outcomes pertaining to cardiovascular risk in this sample of adult African Americans, However, we did iind evidence thar somatic growth (body weight and body mass index) is significantly related to obesity and attenuated insulin-stimulated glucose utilization in adulthood. These findings indicate that the origins of adult cardiovascular disease are related to somatic growth, but not intrauterine growth, and are evident during childhood.