New research from the University Of Pittsburgh School Of Medicine suggests that while high-protein diets are often considered beneficial for athletes and those aiming to build muscle, consuming excessive amounts of protein may have negative effects on heart health.
According to the study, diets high in protein, especially those with over 22% of daily calories from protein, may increase the likelihood of developing atherosclerosis, a condition marked by arterial narrowing and hardening due to plaque accumulation.
The recent study involved human trials, along with animal and cellular studies, unveiling a complex molecular mechanism. This mechanism indicates that high protein intake can activate immune cells linked to atherosclerotic plaque formation, raising the risk of heart disease.
Increasing protein intake for improved metabolic health may not be a cure-all, as it could potentially harm arteries, according to Dr. Babak Razani, a professor of cardiology at the University of Pittsburgh. The study emphasizes the need for precise dietary modifications to influence body function at a molecular level and mitigate disease risks.
The study highlights leucine, an amino acid abundant in animal-based foods like beef, eggs, and milk, as a significant factor in promoting atherosclerosis pathways. This finding reveals insights into the role of protein-rich diets in cardiovascular risk, suggesting possibilities for tailored nutritional approaches to reduce disease risk.
This study examines the increasing trend of high-protein diets, commonly believed to offer health advantages such as muscle maintenance and weight loss. However, it challenges the assumption that higher protein intake is always beneficial, warning against potential negative health effects, particularly from excessive reliance on animal-based protein sources.
Researchers conducted experiments to investigate the impact of amino acids from protein on disease processes, focusing on macrophages, immune cells crucial in atherosclerosis. High protein intake was found to disrupt macrophage function, leading to cellular debris accumulation in arterial walls and worsening plaque formation. Dr. Bettina Mittendorfer from the University of Missouri highlighted amino acids’ role in disease signaling and cell metabolism alteration.