October 31, 2025

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The Silent Killer in MASLD? It's Not Diabetes, Says New Study

A new study published in Clinical Gastroenterology and Hepatology has identified high blood pressure,Type 2 diabetesor pre-diabetes, and low HDL as the deadliest cardiometabolic risk factors for patients with metabolic dysfunction-associated steatotic liver disease (MASLD). MASLD occurs when excess fat accumulates in the liver in conjunction with at least one of five cardiometabolic risk factors:obesity, Type 2 diabetes, high blood pressure, high blood sugar, and low HDL cholesterol. These conditions impact either cardiovascular or metabolic health and significantly elevate the risk of complications such as advancedliver, kidney, and heart disease. To better understand which of these risk factors most strongly predict mortality in MASLD patients, researchers analyzed data from the U.S. National Health and Nutrition Examination Survey (NHANES), spanning from 1988 to 2018. Out of more than 134,000 participants aged 20 and older, about 21,000 met the criteria for MASLD. Researchers tracked all-cause mortality rates in relation to individual risk factors. The study found that high blood pressure increased the risk of death by 40%, diabetes or pre-diabetes by 25%, and low HDL by 15%. Dr. Matthew Dukewich, lead author of the study, noted, “Until now, it was commonly thought that diabetes was the most pressing health problem for MASLD patients, which is a key insight.” Obesity, while the most common risk factor, also showed increased mortality risk depending on body mass index (BMI). Moreover, the study found that each additional cardiometabolic risk factor raised the risk of death by 15%. Looking forward, the authors plan to explore the influence of genetics, diet, and alcohol use on MASLD outcomes. Reference:Differential Effects of Cardiometabolic Risk Factors on All-Cause Mortality in US Adults with Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD), Dukewich, Matthew et al. Clinical Gastroenterology and Hepatology, Volume 0, Issue 0

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