Ajit Varki: On the origin of maladies

In India, Varki was a physician–scientist at the Christian Medical College in Vellore. After a few years he moved to the United States where he specialized in hematology, later became a leading glycobiologist, and most recently caught the evolution bug. He now codirects the Glycobiology Center at the University of California in San Diego and the Center for Academic Research and Training in Anthropogeny (the study of human origins). Varki's interest in evolution began a decade ago while he was studying sialic acids—sugars that coat cell surfaces and modulate a variety of physiological and pathological process. He discovered that humans can't synthesize one kind of sialic acid (Neu5Gc) that other mammals can. However , in experiments conducted partly on himself, Varki found that humans incorporate Neu5Gc into their bodies when they eat red meat (1) and that this incorporation has implications for disease. For example, it may explain why diets rich in steaks and burgers might predispose some people to toxins (2) or lead to chronic inflammation (3). Meanwhile , sialic acid changes that are unique to humans help explain why we are susceptible to certain diseases, like P. falciparum malaria (4). With each new finding, Varki drills deeper into the question of what makes us human. How did you transition from glycobiology into chimp biology? After I found a sialic acid diff erence between chimps and humans, I wanted to know more about what makes humans diff erent. I went to the Yerkes National Primate Research Center to educate myself about chimpanzees. I had assumed that because they're genetically so similar to us, their diseases were going to be similar to ours. But that wasn't the case! I learned that most of the common cancers of humans had never been reported in the great apes. Their heart attacks were completely diff erent than ours. And things like bronchial asthma and rheuma-toid arthritis, which are common in humans, were uncommon in apes. Instead they tended to get strange types of renal failure, a diff erent kind of cardiac disease, and so on. Then I thought, well, if we're genetically so similar, but our diseases are so diff erent, at least this should be a tractable problem. And you approach this problem by comparing chimp and human genomes? Yes, but not just the genomes. There's a complex interaction between our ge-nomes, our phenomes [the set of possible phenotypes], and our environment. …