Association of Parental Obesity with Concentrations of Select Systemic Biomarkers in Non-obese Offspring: The Framingham Heart Study

Abstract

Objective: Parental obesity is a risk factor for offspring obesity. It is unclear whether parental obesity also confers risk for obesity-associated conditions (e.g., a pro-inflammatory or pro-thrombotic state) in the absence of offspring obesity.

Research Design and Methods: We compared concentrations of multiple biomarkers representing distinct biological pathways, (C-reactive protein [CRP], aldosterone, renin, B-type natriuretic peptide, N-terminal proatrial natriuretic peptide, fibrinogen, and plasminogen activator inhibitor-1) in non-obese Framingham Offspring study participants with none (n=665), one (n=488) or two (n=119) parents with obesity (body mass index ≥30 kg/m²).

Results: Non-obese offspring with both parents with obesity had higher CRP levels (median: 2.16 mg/L) compared with offspring with one (median: 1.58 mg/L) or no (median: 1.35 mg/L) parents with obesity. After multivariable adjustment, a non-linear relation with parental obesity became evident: compared to people without parental obesity, CRP levels were higher in offspring with two obese parents (p=0.04) but not in offspring with only one obese parent (p=0.76). Renin levels were more linearly related to parental obesity status, being significantly higher in offspring with one (p=0.04) or two parents (p=0.09) with obesity (p=0.02 for trend). The other systemic biomarkers did not vary according to parental obesity status (all p>0.05).

Conclusions: Our findings suggest that offspring with a high risk of developing obesity have an altered biomarker profile, characterized by systemic inflammation and increased neurohormonal activity, even in the absence of obesity. This is consistent with the notion, that parental obesity may confer an increased susceptibility to other adiposity-associated traits.