Chronic Exposure of Grandparents to Poverty and Body Mass Index Trajectories of Grandchildren: A Prospective Intergenerational Study

The purpose of this study is to evaluate the validity of BMI based on self-reported data by comparison with technician-measured BMI and biomarkers of adiposity. We analyzed data from 10,639 National Health and Nutrition Education Study III participants > or =20 years of age to compare BMI calculated from self-reported weight and height with BMI from technician-measured values and body fatness estimated from bioelectrical impedance analysis in relation to systolic blood pressure, fasting blood levels of glucose, high-density lipoprotein-cholesterol, triglycerides, C-reactive protein, and leptin. BMI based on self-reported data (25.07 kg/m2) was lower than BMI based on technician measurements (25.52 kg/m2) because of underreporting weight (-0.56 kg; 95% confidence interval, -0.71, -0.41) and overreporting height (0.76 cm; 95% confidence interval, 0.64, 0.88). However, the correlations between self-reported and measured BMI values were very high (0.95 for whites, 0.93 for blacks, and 0.90 for Mexican Americans). In terms of biomarkers, self-reported and measured BMI values were equally correlated with fasting blood glucose (r = 0.43), high-density lipoprotein-cholesterol (r = -0.53), and systolic blood pressure (r = 0.54). Similar correlations were observed for both measures of BMI with plasma concentrations of triglycerides and leptin. These correlations did not differ appreciably by age, sex, ethnicity, or obesity status. Correlations for percentage body fat estimated through bioelectrical impedance analysis with these biomarkers were similar to those for BMI. The accuracy of self-reported BMI is sufficient for epidemiological studies using disease biomarkers, although inappropriate for precise measures of obesity prevalence.

Retrospective studies show that childhood adversity is associated with systemic inflammation in adulthood. Few prospective studies have examined whether childhood adversity influences inflammation in an observable manner during childhood or adolescence and if these effects are sustained over time. Using longitudinal data from the Avon Longitudinal Study of Parents and Children, we examined associations between acute adverse events at seven time points prior to age 8 and inflammation at ages 10 and 15. Inflammatory markers at age 10 included interleukin-6 (IL-6; N=4655) and C-reactive protein (CRP; N=4647), and CRP was measured again at age 15 (N=3286). We further evaluated whether body mass index (BMI), depression, or cigarette smoking mediated associations between adverse events and inflammation. Adverse events in middle childhood (occurring between ages 6 to 8), as well as cumulative adversity from birth to 8 years, were associated with higher levels of IL-6 and CRP at age 10. Adverse events reported in early childhood (1.5years) or middle childhood, and cumulative adversity from birth through 8years predicted increased levels of CRP at age 15, and these associations persisted after adjustment for CRP at age 10. Some, but not all, of these associations were mediated by BMI. This study documents that exposure to adverse events prior to age 8 is associated with elevated inflammation at age 10 and in mid-adolescence. These findings provide prospective evidence for a biological mechanism by which early experiences may shape long-term health. Future studies with earlier assessments of inflammation are necessary in order to elucidate potential sensitive periods and mechanisms that link childhood adversity to later disease vulnerability. Copyright © 2012 Elsevier Ltd. All rights reserved.

Using data from three waves of the Children of the National Longitudinal Surveys of Youth data set (1986, 1988, 1990), we examine the dynamic relationship between children's family histories of poverty and their developmental trajectories of mental health. Children who were poor in 1986 or who had prior histories of poverty had higher levels of depression and antisocial behavior in that year. Furthermore, subsequent poverty histories were also related to children's mental health trajectories. The number of years that children were poor between 1986 and 1990 correlates significantly with changes in children's antisocial behavior during those years. Finally, rates of increase in antisocial behavior were substantially higher for children with histories of persistent poverty during those years than for transiently poor or nonpoor children. These results demonstrate the accelerating behavioral disadvantages faced by persistently poor children.