Our ancestors began to have atherosclerosis and heart attack about two or three million years ago due to mutations in the gene that malaria is used to invade the human body. Scientists said in PNAS magazine.
"The loss of CMAH does not only lead to the risk of atherosclerosis caused by an unhealthy diet, but also to the development of cardiovascular disease. This should be taken into account in experiments. Experiments on animals, " said scientist Ajit Varki from the University of California, San Diego (USA).
According to WHO statistics, atherosclerosis and heart and vascular diseases are still one of the major causes of death in most countries around the world, despite all efforts to treat these diseases. As usual, the disease begins to develop from the accumulation of cholesterol in blood vessel walls, which then leads to thickening of the blood vessel walls, accumulation of calcium and loss of flexibility.
Inflammation develops in the walls of blood vessels leading to fat accumulation inside the cells that cause atherosclerosis.
Until now, scientists have not elucidated the mechanism of forming cholesterol plaques and liming deposits in blood vessel walls. Some researchers suggest that changes in the activity of genes involved in fat metabolism lead to "bad" cholesterol buildup in the blood, which is responsible for the development of atherosclerosis. circuit. Other biologists say that "pathogens" are other things.
For example, Russian biologists have recently discovered that the cause of atherosclerosis development is not disorders of fat metabolism, but inflammation that develops in the wall. Blood vessels lead to fat accumulation inside cells.
Ten years ago, scientist Ajit Varki and his colleagues studied the behavior of chimpanzees and other animals, and found that they never really got atherosclerosis and did not have related issues, regardless of which diet they have. This discovery led scientists to look for differences in the activity of vascular cells, the immune system and the endocrine glands.
It turns out, chimpanzees and humans have a difference in this area: a small mutation in the CMAH gene . This gene is responsible for producing N-glycolylneuraminic acid (Neu5Gc) . This substance and similar molecules act as sieves, with holes to allow molecules to pass through to enter the cells.
A few years ago, American biologists discovered that CMAH-modified mice are more likely to have diabetes, and their immune cells start to behave abnormally. This led Mr. Ajit Varki and his colleagues to think that other mutations in this gene could also affect the body's activity and are related to the development of heart disease.
To clarify this issue, scientists conducted two series of experiments, causing a mutation related to the lack of CMAH gene and how this gene loss affects the life and activity of The cardiovascular system of mice fed normal and fat foods did not contain Neu5Gc.
Research results show that, in both cases, the mice began to have atherosclerosis - the rate of accumulation of cholesterol plaque in their arterial walls was doubled, as well as the rate of inflammation. The removal of all Neu5Gc molecules in mice with the help of special antibodies caused the immune system to struggle with this substance has led to similar results.
Interestingly, if a large amount of this acid is added to the food, it is not helpful but only aggravates the health status of the mouse with the damaged CMAH gene. In their bodies, this acid does not normalize immune system activity, but in turn makes it more aggressive to attack blood vessel walls and causes inflammation.
'It seems that the risk of atherosclerosis increases is related to many' internal 'and' external 'factors in the damaged CMAH gene. This explains why many non-meat and fat vegetarians can become victims of heart attacks and strokes, while this is not a typical phenomenon with chimpanzees and other animals. ' , Mr. Ajit Varki concluded
Why did humans lose this useful gene? The problem is that some viruses, such as influenza or malaria, use neuraminic acid (such as Neu5Gc) to enter cells in the human body.
The fight against these viruses, as the researchers suggest, led to the fact that the CMAH gene was irreversibly damaged during the evolution of Homo. That helped humans survive, but it was intended for people to die from heart disease.