The Role of Protein in the Progression of Atherosclerosis

Recent research featured in Nature Metabolism indicates that dietary protein, especially a specific amino acid, significantly contributes to atherosclerosis. This disease leads to the buildup of plaques along the walls of arteries, triggering heart attacks and strokes, and accounts for a quarter of all fatalities worldwide.

Protein intake from our diet is essential for our body’s ability to synthesize its own proteins, yet the optimal quantity of dietary protein is still debated. Evidence from animal studies shows that limiting protein intake can significantly increase lifespan, with some human epidemiological research suggesting similar outcomes. Conversely, protein plays a crucial role in muscle development, crucial for preventing sarcopenia, a condition characterized by muscle loss.

A 2020 investigation by the same researchers found that in a mouse model of atherosclerosis, consuming high amounts of protein worsened the condition by triggering the activity of mTORC1 protein in macrophages. These immune cells are attracted to emerging lesions on artery walls, where they play a healing role by clearing away dangerous debris and LDL cholesterol. Unfortunately, these macrophages can sometimes consume excessively, transforming into engorged foam cells that become lodged within the atherosclerotic plaque, thereby exacerbating its expansion.

The mTORC1 protein facilitates the synthesis of additional proteins in the presence of abundant nutrients and hinders autophagy, the cellular process for eliminating internal waste. When nutrient levels drop, mTORC1 activity diminishes, leading cells to enter a state focused on maintenance and conservation. This shift from growth to repair mode is believed to be a key factor behind the lifespan extension observed with caloric restriction and the use of rapamycin, an effective mTORC1 blocker, in animal studies. The 2020 research indicated that excessive protein intake impairs the efficiency of macrophages by stimulating mTORC1 and reducing autophagy.

Leucine, which is plentiful in animal-based proteins, may explain why some studies find plant-based proteins to be healthier. These findings highlight that protein consumption implications extend beyond muscle mass, crucial as it is. Focusing on the intake of specific amino acids seems to be a prudent approach, as demonstrated by studies where limiting methionine and isoleucine has been linked to enhanced healthspan and lifespan in animals.

The research has identified a process where elevated protein consumption leads to an increase in blood leucine levels, which in turn activates mTORC1. This activation suppresses the autophagic capabilities of monocytes and macrophages, leading to the development of atherosclerosis. Given the widespread acceptance of protein intake levels exceeding the minimum daily recommendation of 0.8 gr per kg of body weight as safe and beneficial, these findings hold significant implications for clinical practices and public health policies. Thus, increasing protein consumption with the aim of improving metabolic health might not be a cure-all strategy and could potentially harm your arterial health.

To view the original scientific study click below:
Identification of a leucine-mediated threshold effect governing macrophage mTOR signalling and cardiovascular risk