DOI: 10.26650/iuitfd.2000721 ISSN: 1305-6441

THE OBESITY PARADOX IN DIABETIC CORONARY ARTERY DISEASE: IS BODY MASS INDEX ALONE SUFFICIENT?

Gazi Çapar
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Dear Editor,I have read with great interest the recently published article entitled "The Obesity Paradox in the Coexistence of Diabetes and Coronary Artery Disease" by Aydoğan et al. (1). The authors demonstrated that obese individuals with diabetes mellitus had significantly lower SYNTAX scores than their non-obese counterparts, suggesting an inverse association between obesity, as defined by body mass index, and angiographic coronary disease complexity (1). Although obesity is widely recognized as a major risk factor for diabetes mellitus and atherosclerotic cardiovascular disease, numerous observational studies over the past two decades have paradoxically reported more favorable clinical outcomes among overweight or obese patients after the development of cardiovascular disease (2). Nevertheless, the underlying mechanisms responsible for this paradox remain incompletely understood. In this context, we believe that several issues deserve further consideration.Body mass index (BMI) is a limited anthropometric measure that does not adequately reflect body fat distribution or body composition. In particular, visceral adiposity has been shown to be more strongly associated with chronic inflammation, insulin resistance, endothelial dysfunction, and adverse cardiovascular outcomes than BMI itself. Therefore, incorporating additional parameters such as waist circumference, waist-to-height ratio, body fat percentage, or imaging-based assessment of visceral adipose tissue may provide a more accurate evaluation of cardiometabolic risk (3).Furthermore, reverse causation and residual confounding may substantially contribute to the observed obesity paradox. A lower BMI may reflect sarcopenia, occult malignancy, chronic inflammatory disorders, or advanced chronic diseases rather than indicating a genuinely protective effect of obesity. Consequently, the greater angiographic disease complexity observed in non-obese individuals may partly reflect differences in frailty, muscle mass, comorbidity burden, or underlying disease severity (4). Although the authors acknowledged the study’s methodological limitations, including its retrospective design and small sample size, future prospective multicenter studies incorporating nutritional status, skeletal muscle mass, and markers of metabolic health may provide a more comprehensive understanding of this phenomenon.

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