Millions of years ago a genetic mutation in humans would have made them much more vulnerable to atherosclerosis, responsible for a third of deaths from cardiovascular disease.
L’atherosclerosis is characterized by the deposit of a plaque essentially composed of lipids on the wall of the arteries. Eventually, these plaques can damage the arterial wall, lead to obstruction of the vessel or even rupture. Thus, atherosclerosis is responsible for one third of deaths from cardiovascular diseases.
If many known risk factors such as physical inactivity, age, hypertension, obesity or even smoking, about 15% of cardiovascular problems linked to atherosclerosis cannot be explained by these. According to a study published on July 22 in the journal PNAS, this could be due to the loss of a gene in humans two or three million years ago. And heavy consumers of red meat are at even greater risk, the researchers note.
About ten years ago, scientists at the University of San Diego School of Medicine noticed that heart attacks due to atherosclerosis did not exist in other mammals, even in our cousins the chimpanzees. . And yet, those studied shared common human risk factors such as hypertension and physical inactivity. In conclusion, the researchers had noted that the heart attacks of the animals were due to a scar of the heart muscle with unexplained origins.
Elimination of the CMAH gene
Based on these results, they have decided to work today on mice that they have modified by removing, like humans, the CMAH gene which produces a sugar molecule called Neu5Gc. They were then able to observe that the modified rodents showed a significant increase in atherogenesis, which produces atheroma, plaques made up of lipids attaching themselves to the inner wall of the arteries, compared to mice in the control group. Therefore, knockout of the CMAH gene resulted in nearly twice the severity of atherosclerosis compared to unmodified animals.
Thus, the mutation that deactivated the CMAH gene would have taken place several million years ago in our hominid ancestors, possibly due to a parasite recognizing Neu5Gc, the researchers suggest.
“The increased risk appears to be caused by many factors, including overactive white blood cells and a tendency to diabetes in the modified mice,” says Ajit Varki, co-author of the study. “This could help explain why even vegetarian humans without obvious cardiovascular risks are still very susceptible to heart attacks and strokes, unlike other animal species.”
Heavy red meat lovers more at risk
However, heavy red meat lovers remain more exposed to Neu5Gc which has an immune response and leads to chronic inflammation. Indeed, during the study, modified mice fed a Neu5Gc-rich diet suffered from 2.4 times more atherosclerosis. “Loss of CMAH in human evolution likely contributes to a susceptibility to atherosclerosis through intrinsic and extrinsic (dietary) factors,” the researchers conclude.
In the past, the latter had already shown that a diet rich in Neu5Gc also promoted inflammation and cancer in mice that did not have this molecule. Thus, the non-human sugar molecule, abundant in red meat, could explain, in part, a link between its consumption and certain cancers. In addition to cardiovascular diseases and cancers, the evolutionary loss of CMAH in humans also seems to have led to a reduction in fertility or even an increased ability to run over long distances.
But while cardiovascular problems are far more common in humans, animals are not completely spared. Thus, thousands of dogs around the world die each year of a heart attack. Besides atherosclerosis, the problem can occur if the animal suffers from bacterial infection, nephrotic syndrome, hypothyroidism, tumor or vasculitis.
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