The researchers believe a mutation that inactivated the CMAH gene occurred a few million years ago in hominin ancestors, an event possibly linked to a malarial parasite that recognised Neu5Gc. They said human-like elimination of CMAH and Neu5Gc in mice caused an almost two-fold increase in the severity of atherosclerosis compared to unmodified mice.
"The increased risk appears to be driven by multiple factors, including hyperactive white cells and a tendency to diabetes in the human-like mice," said Ajit Varki, a professor at UC San Diego "This may help explain why even vegetarian humans without any other obvious cardiovascular risk factors are still very prone to heart attacks and strokes, while other evolutionary relatives are not," Ajit said.
However, in consuming red meat, humans are also repeatedly exposed to Neu5Gc, which researchers said prompts an immune response and chronic inflammation they call "xenosialitis. In their tests, human-like mice modified to lack the CMAH gene were fed a Neu5Gc-rich, high-fat diet and subsequently suffered a further 2.4-fold increase in atherosclerosis, which could not be explained by changes in blood fats or sugars.
"The human evolutionary loss of CMAH likely contributes to a predisposition to atherosclerosis by both intrinsic and extrinsic (dietary) factors, and future studies could consider using this more human-like model,"
Ajit said loss may also have set up a further risk for red meat-eating humans, said researchers at University of California (UC) San Diego School of Medicine in the US Atherosclerosis -- the clogging of arteries with fatty deposits -- is the cause of one-third of deaths worldwide due to cardiovascular disease, they said There are many known risk factors, including blood cholesterol, physical inactivity, age, hypertension, obesity and smoking.
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