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In a breakthrough study published in Nature Metabolism, researchers from the University of Pittsburgh School of Medicine have uncovered a molecular mechanism connecting excessive dietary protein to an increased risk of atherosclerosis. Based on a combination of small human trials, experiments in mice, and cell studies, the findings highlight the potential dangers of consuming over 22% of dietary calories from protein. Furthermore, the researchers showed that one amino acid — leucine — seems to have a disproportionate role in driving the pathological pathways linked to stiff, hardened arteries or atherosclerosis.
Senior and co-corresponding author Babak Razani, M.D., Ph.D., a professor of cardiology at Pitt, emphasized the importance of the study in challenging the notion that increasing protein intake is universally beneficial for metabolic health. The research indicates that such dietary habits could lead to actual damage to arteries, raising concerns about the long-term impact on cardiovascular health.
The study, building on previous research from 2020 that linked excess dietary protein to atherosclerosis risk in mice, delved deeper into the potential mechanism and its relevance to the human body. Working in collaboration with Dr. Bettina Mittendorfer from the University of Missouri, Columbia, the researchers conducted a series of experiments across various models, from cells to mice to humans.
According to a survey of the average American diet over the last decade, Americans consume a lot of protein, mainly from animal sources. Further, nearly a quarter of the population receives over 22% of all daily calories from protein alone. That trend is likely driven by the popular idea that dietary protein is essential to healthy living, says Razani. However, he and other groups have shown that over-reliance on protein may harm long-term health.
The research revealed that consuming more than 22% of daily dietary calories from protein can activate immune cells involved in atherosclerotic plaque formation, thereby increasing the risk of cardiovascular disease. Notably, the study identified leucine, an amino acid found in animal-derived foods like beef, eggs, and milk, as a significant contributor to abnormal immune cell activation and elevated atherosclerosis risk.
Razani stressed the need for a nuanced approach to dietary choices, cautioning against unquestioningly increasing protein intake. Instead, he advocated for considering the overall diet and promoting balanced meals, especially for individuals at risk of heart disease and vessel disorders.
The study’s findings raise crucial questions about the optimal level of protein consumption. While the USDA recommends around 15% of daily calories from protein, the study prompts further investigation into the potential ‘sweet spot’ that maximizes protein benefits, such as muscle gain, without triggering detrimental molecular events leading to cardiovascular disease.
The research implications extend to hospital settings, where nutritionists often advise protein-rich foods to preserve muscle mass and strength in critically ill patients. The study challenges this approach, suggesting that a more balanced and personalized dietary recommendation may be essential, especially for individuals with cardiovascular risk factors.
Additionally, Razani pointed out that the research suggests differences in leucine levels between diets enriched in plant and animal proteins, indicating variations in their effects on cardiovascular and metabolic health. This aspect of the study opens up exciting possibilities for future dietary guidelines that consider the molecular mechanisms involved.
In conclusion, this groundbreaking research adds a crucial layer to our understanding of the relationship between dietary protein, molecular processes, and cardiovascular health. As conversations about nutrition evolve, the study emphasizes the importance of precision nutrition and personalized nutritional recommendations to mitigate potential risks associated with excessive protein intake.
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