Eating disorders, nutrient intake, and cardiometabolic risks: a cross-sectional study in Turkish adults

BACKGROUND: Eating disorders can cause endocrine-metabolic complications, and comorbidities, potentially leading to obesity, type 2 diabetes, and cardiovascular disease (CVD). This study aimed to examine the associations between eating disorders, nutrient intake, and the risk of CVD and diabetes in adults aged 40–75 years. METHODS: This study included 3181 healthy Turkish adults aged 40–75 years. CVD risk was assessed using the Systematic Coronary Risk Evaluation (SCORE) and Atherosclerotic Cardiovascular Disease (ASCVD) Risk Estimator Plus. Type 2 diabetes risk was evaluated using the Finnish Diabetes Risk Score (FINDRISC), eating disorders were assessed with the Eating Disorder Examination Questionnaire (EDE-Q), and dietary intake was measured via 24-hour food recall. RESULTS: In the sample (50.4% male, mean age 50.33 ± 7.79 years), individuals at borderline 10-year ASCVD risk (estimated 5–7.4% 10-year risk) presented significantly greater body weight, body mass index, neck circumference, and waist-hip ratio than did those at low risk (p < 0.001). Additionally, the total EDE-Q scores of individuals with borderline 10-year ASCVD risk were significantly lower than those of individuals with low risk (p < 0.001). Total EDE-Q scores of individuals at very high risk of diabetes were higher than those of individuals at moderate risk (p < 0.05). SCORE and ASCVD risk were significantly weakly positively correlated with dietary cholesterol (r = 0.050, r = 0.064, respectively) and protein intake (r = 0.093, r = 0.142, respectively) (p < 0.05). Interestingly, and contrary to expectations based on previous literature, the total EDE-Q score was weakly negatively correlated with both SCORE (r = -0.101) and ASCVD (r = -0.092) risk scores (p < 0.001). This unexpected correlation could reflect selection bias, as healthier individuals exhibiting subclinical symptoms may have been more inclined to participate. In contrast, it was weakly positively correlated with the FINDRISC score (r = 0.163) (p < 0.001). CONCLUSIONS: Increased anthropometric measurements were associated with elevated risks of CVD and diabetes. Higher dietary cholesterol and protein intake showed weak positive associations with CVD risk factors. Notably, eating disorders were positively associated with diabetes risk but unexpectedly showed a negative association with CVD risk. These findings suggest that disordered eating behaviors may influence cardiometabolic outcomes. Further research is warranted to explore the mechanisms underlying these associations. Given the cross-sectional nature of this study, causality cannot be inferred.