They discover why only humans are prone to heart attacks

Every year almost 20 million people die from cardiovascular diseases. Is the first cause of death among children under 70 and, in most cases, it is due to atherosclerosis, an obstruction of the arteries because of fat deposits.

Now, a study of scientists from the University of California San Diego School of Medicine, published in PNAS, reveals that the loss of a single gene more than two or three million years ago in our ancestors may be the cause of an increased risk of cardiovascular diseases in all human beings as a species, while creating a additional risk for people who eat red meat.

Professors Nissi Varki and Ajit Varki have been studying these diseases for more than a decade. Together with other colleagues, they noted at the beginning of their investigation that the coronary attacks of natural origin due to atherosclerosis were virtually non-existent in other mammals, including chimpanzees that share risk factors similar to humans, such as sedentary lifestyle or hypertension. But the 'heart attacks' of chimpanzees were due to a still unexplained scar of the heart muscle.

A missing gene

Now, Varkis and Professor Philip Gordts and the rest of researchers have found that mice modified to be deficient (like humans) in a sialic acid sugar molecule called Neu5Gc showed a significant increase in atherogenesis compared to control mice, which retain the CMAH gene that produces Neu5Gc.

Researchers, members of the Center for Research and Training in Glycobiology and / or the Center for Research and Academic Training in Anthropogenesis at the University of California, San Diego, believe that a mutation that deactivated the CMAH gene It happened a few million years ago in hominid ancestors, an event possibly linked to a malaria parasite that Neu5Gc recognized.

In their findings, the research team has verified that the elimination of human-type CMAH and Neu5Gc in mice caused a almost twice increase The severity of atherosclerosis compared to unmodified mice.

The mutation that deactivated the CMAH gene would have occurred millions of years ago in hominid ancestors

Ajit Varki explains that "the increased risk seems to be driven by multiple factors, including hyperactive white blood cells and a tendency to diabetes in human-type mice. This may help explain why even vegetarian humans without any other obvious cardiovascular risk factors they are still very prone to heart attacks and strokes, while other evolutionary relatives are not. "

A greater predisposition

But consume red meat, humans are also repeatedly exposed to Neu5Gc, which researchers say causes an immune response and a chronic inflammation called xenosialitis. In their tests, human-type mice modified to lack the CMAH gene received a diet rich in Neu5Gc fats and subsequently suffered an additional 2.4-fold increase in atherosclerosis, which could not be explained by changes in fats or sugars in the blood.

In previous work, Varkis and his colleagues had shown that The Neu5Gc diet also promotes inflammation and cancer progression in mice deficient in Neu5Gc, which suggests that the non-human sugar molecule, which is abundant in red meat, may at least partially explain the relationship between consumption of red meat and certain types of cancer.

Interestingly, the evolutionary loss of the CMAH gene seems to have produced other significant changes in human physiology, including reduction of human fertility and greater ability to run long distances. The authors conclude that "the human evolutionary loss of CMAH probably contributes to a predisposition to atherosclerosis due to intrinsic and extrinsic (dietary) factors and future studies could consider the use of this more human model."