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 proinflammatory or prothrombotic 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, NH 2-terminal proatrial natriuretic peptide, fibrinogen, and plasminogen activator inhibitor-1)in nonobese Framingham Offspring Study participants with no parents(n = 665), one parent(n = 488), or two parents(n = 119)with obesity(BMI >30 kg/m 2). RESULTS-Nonobese offspring with both parents with obesity had higher CRP levels(median 2.16 mg/l)than offspring with one parent(1.58 mg/l)or no parents(1.35 mg/l)with obesity. After multivariable adjustment, a nonlinear relationship with parental obesity became evident: compared with those 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 parent(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 neurohor-monal 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.
ASJC Scopus subject areas
- Internal Medicine
- Endocrinology, Diabetes and Metabolism