Excessive Dietary Protein is Bad For the Arteries, Increases Risk of Atherosclerosis

In Western societies, high protein intake is usually promoted as part of a healthy lifestyle. However, a series of clinical studies suggests that too much protein can actually be bad for the arteries.

Protein Consumption in the US

Protein is one of the three essential macronutrients needed by the human body, together with fats and carbohydrates. It is an important building block of the body which is also used to build and repair damaged tissues.

A survey of the American diet over the last decade revealed that Americans generally consume lots of protein, mostly from animal sources. Almost a quarter of the population received more than 22% of all daily calories from protein alone.

This trend is even driven by the popular idea that dietary protein is important to healthy living. However, previous studies have shown that overreliance on protein may not be really good for long-term health.

The amount of protein a person needs depends on various factors, such as age, muscle mass, activity level, and overall health. The U.S. Food and Drug Administration suggests that most American adults need about 50 grams of protein daily.

Why Too Much Protein Is Bad

At the University of Pittsburgh School of Medicine, researchers unveiled the molecular mechanism by which excessive protein can lead to atherosclerosis. Their findings are discussed in the study "Identification of a leucine-mediated threshold effect governing macrophage mTOR signalling and cardiovascular risk".

The research involves a series of clinical studies on male and female participants with combined experiments in mice. It was found that consuming more than 22% of dietary calories from proteins can cause an increase in the activation of immune cells that contribute to formation of atherosclerotic plaque. Moreover, an amino acid known as leucine seems to play a role in driving the pathological pathways related to hardened arteries.

The mechanistic studies have shown that amino acids can actually trigger disease through specific signaling mechanisms and alter the metabolisms of these cells. For example, small immune cells in the vasculature known as macrophages can trigger the development of atherosclerosis.

The initial experiments on human participants for determining the timeline of immune cell activation after the ingestion of protein-enriched meals was used in simulating similar conditions in mice and in human macrophages. It was shown that excessive intake of dietary protein can affect macrophages which clear out cellular debris and worsen atherosclerotic plaques.

Analysis of circulating amino acids also show that leucine is primarily responsible for abnormal macrophage activation and risk of atherosclerosis. This indicates a potential avenue for further research on personalized diet modification.

The research findings are particularly beneficial in hospital settings, where nutritionists usually recommend protein-rich foods to preserve muscle mass and strength. According to Razani, the negative part of protein consumption is blindly increasing the load. Instead, he suggests looking at the diet as a whole and suggests balanced meals that do not exacerbate cardiovascular conditions.

The findings suggest that differences in leucine levels between diets enriched in plant and animal protein could explain the differences in their effect on metabolic and cardiovascular health. The researchers are hopeful that this type of mechanistic research may help inform dietary guidelines in the future.