You Can Have a Normal Weight and Still Be at Risk for Heart Failure

Research Highlights

• Fat stored around the waist, often called belly fat or visceral fat, showed a much stronger link to heart failure risk than body mass index (BMI), making waist size a more revealing measure of risk.
• Inflammation throughout the body emerged as a major factor connecting abdominal fat to heart failure, accounting for roughly one-quarter to one-third of that increased risk.
• Because inflammation plays such a central role, targeting and reducing inflammation could become an important strategy for lowering heart failure risk in people with excess belly fat.

Belly Fat and Heart Failure Risk

New findings presented at the American Heart Association’s EPI|Lifestyle Scientific Sessions 2026 suggest that excess fat around the waist (central obesity or visceral fat) may raise the risk of heart failure, largely due to inflammation. The conference, held in Boston from March 17 to 20, highlights the latest research on prevention, lifestyle, and cardiometabolic health.

Waist Size vs BMI in Predicting Risk

Researchers reported that higher levels of visceral fat were more closely associated with heart failure risk than overall body weight. Larger waist measurements were linked to increased risk even among individuals whose body mass index (BMI) fell within a normal range. The results indicate that fat distribution may play a more important role than total weight. Inflammation appears to be a key factor that helps explain why fat stored around the abdomen is particularly harmful to the heart. These findings suggest that measuring waist size could improve how clinicians identify people at higher risk, rather than relying on BMI alone.

“This research helps us understand why some people develop heart failure despite having a body weight that seems healthy,” said Szu-Han Chen, lead author of the study and a medical student at National Yang Ming Chiao Tung University in Taiwan. “By monitoring waist size and inflammation, clinicians may be able to identify people with higher risk earlier and focus on prevention strategies that could reduce the chance of heart failure before symptoms begin.”

Inflammation as a Key Driver

A 2025 scientific statement from the American Heart Association on risk-based primary prevention of heart failure emphasizes that systemic inflammation, or inflammation throughout the body, is a major contributor to heart disease. It can interfere with the immune system, damage blood vessels, and promote the formation of scar tissue in the heart. The Association has also pointed to evidence that higher inflammation levels are linked to greater heart disease risk, even in people with normal cholesterol.

Key Study Findings

The study reported several important results:

• 112 adults developed heart failure over a median follow-up of 6.9 years
• Higher levels of excess fat around the waist were associated with increased heart failure risk, while higher BMI was not
• Both waist circumference and waist-to-height ratio were linked to greater risk
• Participants with higher inflammation levels, based on blood tests, were more likely to develop heart failure during the nearly seven-year follow-up
• Inflammation explained about one-quarter to one-third of the relationship between abdominal fat and heart failure risk

Implications for Prevention and Care

“This study highlights the importance of integrating measures of central adiposity such as waist circumference into routine preventive care. Understanding upstream drivers of heart failure risk including central adiposity is key to recognizing and modifying risk,“ said Sadiya S. Khan, M.D., M.Sc., FAHA, volunteer chair of the American Heart Association’s 2025 Scientific Statement: Risk-Based Primary Prevention of Heart Failure.

“This study builds on prior research that highlights the importance of excess or dysfunctional adiposity in the development of heart failure, which informed the inclusion of body mass index into the PREVENT-HF risk equations to estimate risk of heart failure. However, future research should identify if central adiposity has greater predictive utility beyond strength of association.”

Khan, who was not involved in the study, is also Magerstadt Professor of Cardiovascular Epidemiology and an associate professor of cardiology and preventive medicine at Northwestern University’s Feinberg School of Medicine in Chicago.

Study Limitations and Future Research

The researchers noted that they were unable to analyze specific types of heart failure, so the findings apply to heart failure overall. Future studies are needed to explore how visceral fat and inflammation may affect different forms of heart failure and whether reducing inflammation could lower risk.

Study Details and Design

The analysis included data from 1,998 African American adults living in urban and rural areas of Jackson, Mississippi, who participated in the Jackson Heart Study. None had heart failure at enrollment between 2000 and 2004.

Participants ranged in age from 35 to 84, with an average age of 58, and 36 percent were women. They were followed for a median of 6.9 years, through December 31, 2016.

Researchers evaluated body fat using several measures, including weight, body mass index (BMI), waist circumference, and waist-to-height ratio. Blood samples were also analyzed to measure high-sensitivity C-reactive protein, a widely used marker of inflammation.

The study was conducted under the guidance of Professor Hao-Min Cheng at Taipei Veterans General Hospital and National Yang Ming Chiao Tung University.

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Study links large body size during childhood to diabetes and CAD later

Researchers have found in a new study that child body size is linked to risk of heart disease and diabetes in later life. The increased risk is most likely when large body size persists into adulthood.
Having a large body size in childhood is associated with an increased risk of coronary artery disease and type 2 diabetes, particularly when it persists into adult life. The new study has been published by The BMJ today.

The results also suggest that a larger early life body size may help protect women against breast cancer in later life. 

Obesity in children is widely recognised as a global public health crisis, yet levels continue to rise. 

Having a high body mass index (BMI) in early life is thought to increase the risk of various health conditions in later life. But it is unclear whether an individual can reverse the impact of childhood obesity through lifestyle changes, particularly as those who are obese in early life tend to remain obese as adults.

So researchers at the University of Bristol used a technique called Mendelian randomisation to examine the genetic influence of body size in early life on risk of four diseases in later life - coronary artery disease, type 2 diabetes, breast and prostate cancer.

 Their findings are based on more than 450,000 people from the UK Biobank database using measures of BMI in adulthood (average age 57) and self-reported perceived body size at age 10 and over 700,000 individuals from four large scale genome-wide association studies.

Analysing genetic information in this way avoids some of the problems that may hinder traditional observational studies, making the results less prone to unmeasured (confounding) factors, and therefore more likely to be reliable. An association that is observed using Mendelian randomisation therefore strengthens the inference of a causal relationship. 

The researchers found that early life body size is associated with an increased risk of coronary artery disease and type 2 diabetes. However, when early life body size was analysed together with adult body size, the effects were considerably reduced, suggesting that the increased risk is most likely in those with a large body size in childhood that persists into later life.

They also found strong evidence that larger early life body size has a protective effect on risk of breast cancer, although they say timing of puberty might play an important role here and this requires further investigation before firm conclusions can be made. 

However, no strong evidence was found of a causal effect of either early or later life measures on prostate cancer.

The authors point to some study limitations, such as relying on self reported early life body size which may have affected the accuracy of their estimates. However, strengths include the large number of participants and the sophisticated analytical methods used.

 As such, they say their findings suggest that the positive association between body size in childhood and risk of coronary artery disease and type 2 diabetes in adulthood can be attributed to individuals remaining large into later life.

"Our approach therefore yields insight into the pathway between early life risk factors such as BMI and disease outcomes," they conclude.

 This study suggests that the effect of self-reported adiposity at age 10 on coronary artery disease and type 2 diabetes "can be obviated by achieving and maintaining a normal body mass index (BMI) in adulthood," writes Professor Mary Schooling in a linked editorial.

The study used sophisticated and up-to-date mendelian randomization methods. Nevertheless, she says its findings "need careful interpretation and contextualization before they can be applied to population health."

 She points to adolescence - the transition from childhood to adulthood - as a key point of intervention, and suggests that "puberty might be a key time to reduce adiposity."

This is only for your information, kindly take the advice of your doctor for medicines, exercises and so on.     

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