Ancestors of ancestors who would be Homo sapiens from 2 million years ago to 3 million years ago "lost" their genes. In fact, the function of the CMAH gene has been completely neutralized by the body. This trait was conveyed along the chain of evolution, and this governor caused Homo sapiens 200,000 years ago.
We have evolved. We are developing. However, this inactivated HMA has a characteristic that is not good for our species: heart attack or technically acute myocardial infarction.
This is a major discovery of research this week by researchers at the University of California School of Medicine in San Diego, USA. This material has been published by the Journal of the National Academy of Sciences (PNAS).
According to researchers, this explains why coronary heart disease is common in humans and explains that "it does not really exist" in other mammals, including chimpanzee relatives. There are signs of heart attack for sperm whales and dolphins, but they are rarely.
Cardiovascular disease is the leading cause of premature death, the leading cause of death in the world under the age of 70. According to the World Health Organization (WHO), they kill 17.9 million people, or 31 percent of all deaths in the world. It is expected to increase to 23 million by 2030 every year.
Most of these occur as a complication of atherosclerosis – roughly the plaque formation of the arteries that carry our blood. Ajit Varki, a professor and researcher at the University of California, said: "This results in a narrowing of the arteries and a significant decline in blood vessels to critical organs.
Here are the reasons why heart attacks actually happen to humans, according to researchers – Photo: C. Bickel / Courtesy / BBC
And a major discovery. The loss of the CMAH gene promotes the onset of one of the major complications that constitute the leading cause of death worldwide, he noted.
According to the researchers, the tendency induced by inactive genes is for everyone, but for people who eat red meat there is an increased potential or an additional risk.
There are many behaviors that increase the risk of heart attacks such as cholesterol, no physical activity, older age, hypertension, obesity and smoking in 15% of cardiovascular diseases, but the study points out. , The patient does not have these factors. There may be only genetic markers.
In a previous study in which Ajit Varki, one of the authors, published 10 years ago, scientists observed that atherosclerosis does not actually exist in other animals. At that time, captive mammals such as chimpanzees were observed. The idea was to analyze whether human common risk factors such as hypertension, hypertension, and low physical activity could cause heart attacks in human relatives.
Nothing of type was recorded. Rare chimpanzee heart attacks are caused by scarring of the heart muscle that can not be explained until now. Therefore, it is not related to atherosclerosis.
Researchers emphasize that other animals do not develop atherosclerosis in their natural environment. They suffer from cardiovascular problems only if they are genetically modified to cause the presence of human risk factors, or feed for study with stratospheric and unnatural amounts of cholesterol.
Brazilian biologist Frederico Alisson da Silva of UFRJ participated in a previous study on this subject at the University of California. – Photo: Personal Collection / BBC
Brazilian biologist Frederico Alisson da Silva, a professor and researcher at the Department of Immunology at the Institute of Microbiology at the University of Rio de Janeiro (UFRJ), worked for the Varki Institute at the University of California.
On Monday (22) in a conversation with BBC News Brazil he recalled previous research as a starting point for the announced findings.
"observe [de dez anos atrás] Studies have shown that loss of the human – specific MAHC helps explain this apparent discrepancy in heart attacks that occur in Homo sapiens, he said.
Dr. Varki and his team used genetically modified mice in a study published on Monday.
Like humans, rodents have been engineered to inactivate the CMAH gene. Controls with the same living conditions were maintained as normal functioning genes. Genetically modified rats showed at least twice as much blood fat accumulation even though they fed the same routine and routine.
CMAH produces molecules called Neu5Gc, a kind of sialic acid. As scientists have discovered, the lack of this material is beneficial to the development of atherosclerosis. Because humans can not synthesize Neu5Gc, they do not have that gene and can cause heart attacks.
Researchers are still unsure about the evolutionary pressures that homo sapiens ancestors inactivate genes. – Photo: Ohio State University's ex-medical center
There is still no certainty when a hominid ancestor lost this ability. One hypothesis developed by scientists is that some parasites attack our ancestors, drawn by Neu5Gc. By natural selection, people who have not synthesized matter have become more and more survivors. And it gradually destroyed all the characteristics of hominid derived from this ancestor.
"There are several scenarios that explain why inactivation of the CMAH gene in homozygotes is fixed," the doctor said. "One possible scenario is that by injecting Neu5Gc generated by the CMAH gene into the cell surface and selecting a lethal and efficient pathogen that invades our cells, it can cause a disastrous epidemic and make the ancestor expressing the gene a negative choice Functional CMAH. "
Another explanation would be "selective fertility through female immunity to paternal Neu5Gc," he said. "In this case, females deficient in CMAH were able to produce their offspring as CMAH-deficient males, so we chose CMAH aggressively I can not. "
Varki, however, does not rule out the randomness of the phenomenon. "We can not rule out scenarios in which the inactivation of the MAHC occurs randomly and eventually setstled in a small group that causes modern people," he said.
It was not even known whether any poor ancestor left us the gene for this disorder. "Accurate scoring is currently impossible because we do not know the exact moment the gene is deactivated," says Varki.
Scientists also point out that the lack of Neu5Gc increases the risk of other health problems such as the possibility of diabetes and stroke. "Increased risk appears to be influenced by many factors," Varki said. "But it helps explain why even vegetarians without other obvious cardiovascular risk factors are susceptible to heart attacks and strokes and other evolutionary relatives are not. Will be.
Studies have shown that other animals at risk for red meat consumption are not vulnerable to heart attack. – Photo: Heather Luis / US Department of Agriculture
The researchers also found how the body of Homo sapiens responds to Neu5Gc. According to scientists, humans are mainly exposed to molecules when they eat red meat.
But the results are not good.
This study pointed out that it would stimulate the "immune response" because it is a foreign substance to a person. It is thought to cause inflammation in the bloodstream called xenosialitis. In a study of modified rodents, people fed a diet rich in Neu5Gc showed a 2.4-fold increase in atherosclerosis.
The human evolutionary loss of the CMAH gene has contributed to a reduction in atherosclerosis caused by endogenous and exogenous (dietary) factors, the researchers wrote in the journal.
The immune response to this substance is believed to be able to explain why high red meat intake is often associated with a larger tendency to suffer from certain cancers. But more research is needed.
In the laboratory of the Federal University of Rio de Janeiro, biologist Frederico Alisson da Silva is studying another front about research in North America. And he found evidence that the fact that there is no MAHC already has a higher chance of getting cancer. "In studies leading to me from Rio, we are studying whether gene inactivation is associated with the risk of colon cancer at the end of the human digestive system, and whether it is associated with red meat consumption," he said.
"The fact that we have deactivated MAHC causes our bodies to see Neu5Gc as an antigen and cause chronic inflammation mediated by antibodies produced by Neu5Gc."
"A study of atherosclerosis shows that this inflammation is related to the development of atherosclerosis," the Brazilians continue. "According to our unpublished research, this mechanism is contributing to humans with high carcinoid incidence but no other carnivorous mammal species."
On the other hand, the loss of MACH in human evolution has brought other characteristics. Researchers have identified two factors: long distance travel and reduced fertility.
Assuming that research will help to better understand the case of heart attack, scientists believe that the findings can help improve future cardiovascular treatment.
"We provide evidence that our constitution can cause atherosclerosis and cardiovascular disease more easily because of the loss of AMH function in humans," Varki says. "Our analysis can help explain why people may have more cardiovascular complications than others, even though they have similar risk factors."
He also pointed out that Neu5Gc produced by other species is considered "foreign" in human organisms and that "we develop antibodies to it." Especially in red meat with abundant substance.
"We have shown that the immune response worsens and accelerates the progression of atherosclerosis," he added, adding that the risk of cardiovascular disease is associated with high consumption of red meat.
Varki also argued that further research on the CMAH gene would hope to be able to offer new treatments for the treatment of cardiovascular disease.