A groundbreaking study from The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, in collaboration with multiple research institutions, challenges the long-standing belief that high cholesterol directly correlates with coronary artery disease (CAD) in metabolically healthy individuals. The research, published today in the Journal of the American College of Cardiology: Advances, specifically targets a population known as Lean Mass Hyper-Responders (LMHRs), individuals who develop elevated levels of LDL cholesterol after following a low-carbohydrate ketogenic diet.
The study included 100 LMHRs who adopted a ketogenic diet over an extended period. Despite significant increases in LDL cholesterol levels—often considered a key risk factor for heart disease—the researchers found no direct association between elevated cholesterol markers, such as ApoB and LDL-C, and either the baseline presence of heart disease or its progression. This new finding suggests a need for further investigation into personalized treatment strategies and a reassessment of existing cardiovascular risk models.
Cardiovascular disease remains the leading cause of death globally, making accurate diagnosis and risk assessment crucial. The prevailing “lipid hypothesis,” which attributes elevated ApoB and LDL-C levels to a higher risk of cardiovascular disease, has long guided medical treatment and prevention efforts. However, the findings of this study cast doubt on the validity of this hypothesis in metabolically healthy individuals whose cholesterol rises as a result of a low-carb diet. Many of these individuals adopt such diets to address mental or physical health challenges, such as diabetes or inflammatory disorders.
As therapeutic carbohydrate reduction gains recognition for its benefits in treating a variety of chronic conditions—ranging from diabetes to bipolar disorder—concerns about its impact on heart health have lingered. Despite the significant health improvements observed in individuals following ketogenic diets, doctors often discourage the approach due to fears of increased cardiovascular risk.
The study focused on LDL-C and ApoB levels in individuals with the LMHR metabolic profile, which includes elevated cholesterol but otherwise normal metabolic markers, such as low triglycerides, high HDL, low blood pressure, low insulin resistance, and a healthy body mass index. The research team found no connection between cholesterol levels and the progression of coronary artery plaque. Instead, the primary factor predicting plaque growth was the initial plaque burden, rather than cholesterol levels or changes in those levels.
These findings support previous research by the team, which showed that individuals with the LMHR phenotype have similar coronary plaque levels as those with normal cholesterol levels, further suggesting that increased LDL in response to a ketogenic diet may not necessarily indicate a higher risk of coronary plaque buildup.
The study was co-led by Dr. Matthew Budoff, MD, an investigator and program director at The Lundquist Institute, and senior author of the paper. Dr. Budoff, who also serves as a professor of medicine at the David Geffen School of Medicine at UCLA, emphasized the importance of personalized, data-driven approaches to assessing cardiovascular risk. “It is crucial for clinicians and the public to recognize that risk assessments should be tailored to individual conditions,” he said. “The existence of this phenotype highlights the need for alternative markers or tests to assess metabolic health in some cases.”
The research calls for a shift toward personalized cardiovascular risk assessments, with an emphasis on cardiac imaging. The researchers advocate for a multidisciplinary approach to understanding the cardiovascular risks of LMHR individuals, many of whom rely on low-carbohydrate and ketogenic diets to manage chronic conditions and maintain their health.
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