Why the study?
Central obesity is associated with cardiometabolic dysfunction and cardiovascular disease, but CVD burden may vary by metabolic phenotype among affected adults.
Does metabolically unhealthy central obesity increase prevalent cardiovascular disease in U.S. adults with central obesity?
Does metabolically unhealthy central obesity increase prevalent cardiovascular disease in U.S. adults with central obesity?
Among U.S. adults with central obesity, a greater burden of metabolic abnormalities is associated with a step-wise increase in prevalent cardiovascular disease, underscoring the need for phenotype-based risk stratification beyond waist circumference.
May inform phenotype-specific CVD risk assessment in central obesity; leaves open prospective validation and causal inference.
Background: Central obesity is strongly associated with cardiometabolic dysfunction and cardiovascular disease (CVD), yet CVD burden may vary by metabolic phenotype among affected adults. This study examined whether metabolically unhealthy central obesity (MUCO) is associated with higher CVD prevalence than metabolically healthy central obesity (MHCO), whether CVD increases in a dose-response manner with metabolic abnormality burden, and whether associations vary by age, sex, and race/ethnicity. Methods: We conducted a cross-sectional analysis of NHANES 2011-March 2020, including adults ≥20 years with central obesity (≥102 cm (40″) in men; ≥88 cm (35″) in women). Metabolic phenotype was defined by four abnormalities: elevated blood pressure (≥130/85 mmHg or antihypertensive use), dysglycemia (HbA1c ≥ 5.7%, self-reported diabetes, or diabetes medication use), low HDL cholesterol (<40 mg/dL in men or <50 mg/dL in women), and hypercholesterolemia (physician diagnosis or lipid-lowering therapy). Participants were classified as MHCO (0-1 abnormality) or MUCO (≥2 abnormalities); abnormalities were summed (0-4) to assess dose-response. The outcome was self-reported physician-diagnosed CVD (coronary heart disease, myocardial infarction, stroke, heart failure, or angina). Survey-weighted Poisson regression estimated adjusted prevalence ratios (PRs) and 95% confidence intervals (CIs). Results: Among 11,657 adults with central obesity, 6,997 were MHCO and 4,660 MUCO, representing 128.4 million U.S. adults. Weighted CVD prevalence was higher in MUCO than MHCO (15.7% vs 7.3%). After adjustment, MUCO was associated with higher CVD prevalence (PR 1.48; 95% CI 1.30-1.68; p < 0.001). Each additional metabolic abnormality increased CVD prevalence by 29% (PR 1.29; 95% CI 1.21-1.38; p < 0.001). The association was strongest among adults aged 20-39 years (PR 3.89; 95% CI 2.22-6.81), despite low absolute prevalence. Conclusions: Among U.S. adults with central obesity, metabolic dysfunction is associated with higher CVD prevalence, with a clear dose-response relationship. These findings support phenotype-based cardiovascular risk stratification beyond waist circumference and emphasize early identification and management of metabolic abnormalities, particularly in younger adults.
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Donkor et al. (2026) studied this question.
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