Abstract WE521: Clinical Obesity: Prevalence, Cardiometabolic Risk, and Response to Lifestyle Intervention

An expert commission proposed novel diagnostic criteria distinguishing between preclinical and clinical obesity, recommending treatment indications for the latter. However, their relative proportions in adults with obesity and associated disease risks are unknown. We aimed to quantify the prevalence of preclinical and clinical obesity, investigate their associations with incident cardiovascular diseases (CVD) and type 2 diabetes (T2D), and assess remission from clinical obesity after lifestyle intervention. We used the nationally representative NHANES 2017-2018 survey cycle (n=5,265) and a random subcohort of the population-based EPIC-Potsdam study (n=2,500) to estimate prevalence of preclinical and clinical obesity. We assessed risk of CVD and T2D across the defined obesity groups in established CVD and T2D case-cohorts (including 403 CVD and 778 T2D cases) in EPIC-Potsdam using weighted Cox proportional hazard regression. Remission from clinical obesity was investigated in the Tuebingen Lifestyle Intervention Program study (n=150) after a 9-months lifestyle intervention focused on weight loss. In NHANES 2017-2018 and EPIC-Potsdam, among those with BMI-defined obesity (≥30kg/m 2 ), 100% were confirmed to have obesity by at least one other anthropometric measure (waist circumference, waist-to-height, waist-to-hip ratio, or DXA-measured body fat). More than 80% of adults with confirmed obesity met the proposed diagnostic criteria for clinical obesity, depending on age, BMI and metabolic criteria used. Compared to adults without obesity and not fulfilling proposed diagnostic criteria, adults with clinical obesity had increased risk of CVD (HR: 2.78, 95%CI: 1.78-4.34) and T2D (7.88, 5.56-11.2). Adults with preclinical obesity had no elevated risk of CVD, but T2D risk was markedly increased (4.32, 1.77-10.5). In adults with a weight loss >3% (median 7.4%) by the lifestyle intervention, prevalence of clinical obesity decreased from 71% to 57%, and that of prediabetes (as component of the metabolism criterion) from 52% to 29%. Age and liver fat content, but not BMI or visceral fat mass, independently predicted remission of clinical obesity. In conclusion, our findings indicate that a very large proportion of adults with BMI-based obesity had clinical obesity. This proportion varied depending on BMI and criteria used. Weight loss moderately decreased prevalence of clinical obesity, but improved metabolic health in many who may not be classified to clinical obesity.