It’s always been a puzzle to scientists why cardiovascular diseases such as heart attacks are more common among humans compared to the other animals that inhabit our planet. Carnivores feast on meat, raw meat, so why aren’t they dying in droves from coronary heart disease?
An evolutionary gene loss among humans two to three million years ago could be the answer and explains why coronary events are so common in humans and so rare in other animals, according to researchers at the University of California San Diego School of Medicine.
How the loss of a single gene led to heart attacks becoming the top killer of people in the developed world is outlined in a study published Monday in the peer-reviewed multidisciplinary scientific journal PNAS, or the Proceedings of the National Academy of Sciences of the United States of America.
Naturally occurring coronary heart attacks due to atherosclerosis are virtually non-existent in other mammals, a bewildering phenomenon that challenged Nissi Varki, MD, professor of pathology at UC San Diego School of Medicine, with co-author Ajit Varki, MD, Distinguished Professor Of Medicine and Cellular And Molecular Medicine, and their colleagues.
The researchers were members of the Glycobiology Research and Training Center and/or the Center for Academic Research and Training in Anthropogeny at UC San Diego.
These other mammals include closely related chimpanzees in captivity that share human-like risk factors, such as high blood lipids, hypertension and physical inactivity. Instead, chimp “heart attacks” were due to an as-yet unexplained scarring of the heart muscle.
The study shows 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 that retained the CMAH gene that produces Neu5Gc.
Researchers believed a mutation that inactivated the CMAH gene occurred a few million years ago in hominin ancestors. This unfortunate event was possibly linked to a malarial parasite that recognized Neu5Gc.
The study pointed out that human-like elimination of CMAH and Neu5Gc in mice caused an almost two-fold increase in 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 Varki. “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.”
Humans consuming red meat are also repeatedly exposed to Neu5Gc. This molecule prompts an immune response and chronic inflammation researchers called “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 that 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,” wrote the authors, “and future studies could consider using this more human-like model.”
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