Evolutionary Gene Loss May Help Explain Why Only Humans Are Prone To Heart Attack

An anonymous reader quotes a report from ScienceDaily: A decade ago, 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 colleagues noted that naturally occurring coronary heart attacks due to atherosclerosis are virtually non-existent in other mammals, including closely related chimpanzees in captivity which 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. In the new study, the Varkis, and Philip Gordts, PhD, assistant professor of medicine, and others report 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, who retain the CMAH gene that produces Neu5Gc. The researchers — members of the Glycobiology Research and Training Center and/or the Center for Academic Research and Training in Anthropogeny at UC San Diego — 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 recognized Neu5Gc. In their findings, the research team said human-like elimination of CMAH and Neu5Gc in mice caused an almost 2-fold increase in severity of atherosclerosis compared to unmodified mice. The researchers note that humans are repeatedly exposed to Neu5Gc when they consume red meat, as it 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,” reports ScienceDaily. The study has been published in the journal PNAS.