Central obesity refers to the accumulation of visceral fat around the abdomen and internal organs. Unlike subcutaneous fat, which sits closer to the skin, visceral fat is metabolically active and has been linked to a range of cardiometabolic complications.
A recent study explored whether central obesity may be more relevant to heart failure risk than overall body weight. The findings suggest that fat distribution—not simply body size—could be a more meaningful marker when evaluating future cardiovascular risk.
The study included nearly 2,000 adults without heart failure at baseline and followed them for about 7 years. Researchers assessed several anthropometric measures, including body weight, BMI, waist circumference, and waist-to-height ratio. High-sensitivity C-reactive protein (hs-CRP) was used as a marker of systemic inflammation.
Over the follow-up period, higher hs-CRP levels were associated with worse heart failure-free survival, indicating that greater inflammation was linked to a higher likelihood of developing heart failure.
Importantly, both waist circumference and waist-to-height ratio were significant predictors of heart failure risk, whereas BMI was not significantly associated with heart failure in this analysis. These findings suggest that abdominal fat may be more clinically relevant than overall body weight alone when assessing risk.
The investigators also performed a mediation analysis to better understand the role of inflammation in the relationship between central obesity and heart failure.
The results showed that hs-CRP accounted for 25.4% of the effect of waist circumference on heart failure risk and 28.5% of the effect of waist-to-height ratio. This suggests that systemic inflammation may partially explain why excess abdominal fat is associated with a greater risk of heart failure.
However, the authors cautioned that this does not prove hs-CRP itself directly causes heart failure. Statistical mediation can identify a potential pathway, but it cannot confirm whether hs-CRP is a true biological mediator or simply a marker reflecting other inflammatory processes, such as IL-6 or TNF-α.
One of the key practical messages from the study is that BMI alone may miss important cardiovascular risk in some individuals. A person may have a “normal” BMI while still carrying excess abdominal fat that contributes to metabolic dysfunction and inflammation.
As a result, the findings support a broader cardiometabolic assessment that includes waist circumference or waist-to-height ratio, especially in patients who appear healthy based on BMI alone.
Although the study does not prove that reducing central obesity will directly prevent heart failure, the findings reinforce the importance of targeting visceral fat and inflammation as part of long-term cardiovascular prevention.
Experts noted that the most effective strategies are those that improve overall metabolic health, including regular physical activity, a combination of aerobic and resistance exercise, a diet rich in whole foods, fiber, fruits, vegetables, and healthy fats, better sleep, and limiting excess sugar and ultra-processed foods.
The study has several limitations. It focused only on African American participants, which may limit how broadly the findings can be applied to other populations. The analysis was also limited by the lack of a standardized heart failure definition, incomplete biomarker assessment, and missing imaging and biometric data. As with many observational studies, residual confounding cannot be excluded.
Overall, the findings suggest that central obesity measures, particularly waist circumference and waist-to-height ratio, may be more informative than BMI for predicting heart failure risk. The study also highlights systemic inflammation as a possible pathway linking abdominal fat to heart failure. When assessing cardiovascular risk, a normal BMI may not tell the whole story.
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