Researchers have found that in mice, high protein diets may help with weight loss and muscle building, but it could also lead to more plaque in the arteries. Plaque contains a mix of fat, cholesterol, calcium deposits, and dead cells.
This new research has also shown that high-protein diets spur unstable plaque. This is the plaque that is most prone to rupturing and causing blocked arteries, particularly if it is unstable, increasing the risk of a heart attack.
“There are clear weight-loss benefits to high-protein diets, which has boosted their popularity in recent years,” said senior author Babak Razani, MD, PhD, an associate professor of medicine. “But animal studies and some large epidemiological studies in people have linked high dietary protein to cardiovascular problems. We decided to take a look at whether there is truly a causal link between high dietary protein and poorer cardiovascular health.”
For the study, researchers fed mice a high-fat diet to deliberately induce atherosclerosis, or plaque build-up in the arteries. Mice must eat a high-fat diet to develop arterial plaque, so some of the mice received a high-fat diet that was also high in protein. And others were fed a high-fat, low-protein diet for comparison.
“A couple of scoops of protein powder in a milkshake or a smoothie adds something like 40 grams of protein — almost equivalent to the daily recommended intake,” Razani said. “To see if protein has an effect on cardiovascular health, we tripled the amount of protein that the mice receive in the high-fat, high-protein diet — keeping the fat constant. Protein went from 15% to 46% of calories for these mice.”
More Plaque in the Arteries
Researchers found that the mice on the high-fat, high protein diet developed 30% more plaque in the arteries than the mice on the mice on the high-fat, normal-protein diet, despite the fact that the mice who consumed more protein did not gain weight, unlike the mice on the high-fat, normal-protein diet.
“This study is not the first to show a telltale increase in plaque with high-protein diets, but it offers a deeper understanding of the impact of high protein with the detailed analysis of the plaques,” Razani said. “In other words, our study shows how and why dietary protein leads to the development of unstable plaques.”
“This work not only defines the critical processes underlying the cardiovascular risks of dietary protein but also lays the groundwork for targeting these pathways in treating heart disease,” he said.
Ph.D., Razani and his colleagues studied the path protein takes after it has been digested and broken down into amino acids. They found that excess amino acids from a high-protein diet activate a protein in macrophages called mTOR, which tells the cells to grow. These cells then have their ability to shut down, unable to clean up the toxic waste of plaque.
“In mice on the high-protein diet, their plaques were a macrophage graveyard,” Razani said. “Many dead cells in the core of the plaque make it extremely unstable and prone to rupture. As blood flows past the plaque, that force — especially in the context of high blood pressure — puts a lot of stress on it. This situation is a recipe for a heart attack.”
More research is needed to understand how high dietary protein might increase plaque complexity. But it does offer a new understanding of how a high protein diet may impact cardiovascular risk in some people.