Recent research from the University of Pittsburgh School of Medicine sheds light on a potential downside of high-protein diets, revealing how excessive protein consumption, particularly involving the amino acid leucine, may elevate the risk of atherosclerosis, a condition characterized by hardened arteries.
Published in Nature Metabolism on February 19, the study presents findings suggesting that consuming over 22% of daily calories from protein could trigger increased activation of immune cells involved in the formation of arterial plaque, thereby heightening the risk of atherosclerosis.
Lead author Babak Razani, M.D., Ph.D., professor of cardiology at Pitt, underscores the importance of understanding the molecular mechanisms underlying dietary choices and their impact on cardiovascular health. He warns against the common misconception that boosting protein intake is universally beneficial, emphasizing the need for precision in dietary modifications to mitigate disease risks effectively.
The study, which incorporated small human trials alongside experiments in mice and cell cultures, revealed that high dietary protein intake, particularly from animal sources, is prevalent in the average American diet. Approximately a quarter of the population derives over 22% of their daily calories from protein, a trend driven by the belief in the health benefits of protein consumption.
Building upon previous research indicating a link between excess dietary protein and atherosclerosis risk, the current study sought to elucidate the underlying mechanisms. Collaborating with metabolism expert Bettina Mittendorfer, Ph.D., from the University of Missouri, Columbia, Razani’s team conducted a series of experiments across different models to investigate the cellular and molecular pathways involved.
Their research unveiled that amino acids, the building blocks of proteins, can activate specific signaling mechanisms within immune cells known as macrophages, contributing to the development of atherosclerosis. Notably, the amino acid leucine, abundant in animal-derived foods like beef, eggs, and milk, emerged as a key player in driving abnormal macrophage activation and exacerbating atherosclerosis risk.
The study highlights the importance of precision nutrition in navigating protein consumption for cardiovascular health. Razani cautions against blindly increasing protein intake, particularly in vulnerable populations, and advocates for a balanced approach to dietary recommendations. He suggests that personalized diet modifications, informed by the understanding of individual leucine levels and dietary sources, could offer potential avenues for mitigating cardiovascular risks.
Looking ahead, the research prompts further exploration into optimal protein intake levels and their implications for cardiovascular health. Razani emphasizes the need for a comprehensive understanding of dietary patterns to guide future dietary guidelines effectively, particularly in clinical settings where protein-rich diets are often recommended to preserve muscle mass in patients.
As the scientific community continues to unravel the complexities of diet and cardiovascular health, the study underscores the importance of informed dietary choices and tailored interventions in promoting overall well-being.