Cochran, who has a doctorate in physics, developed satellite imaging systems and other optics hardware for Hughes Aircraft in El Segundo, California, in the 1980s. When the Cold War ended and defense budgets shrank, he moved his family to Albuquerque and became an optics consultant while indulging his amateur interest in biology. He worked for a while with evolutionary biologist Paul Ewald on theories that common disorders such as heart disease and Alzheimer’s are caused by germs. The pair courted controversy by postulating that some unidentified pathogen prompts a hormonal imbalance that makes babies more likely to become gay.

Cochran became intrigued by the deadly Ashkenazi diseases: Tay-Sachs, a neurological disorder that debilitates children before killing them, usually by age 4; Canavan disease, which turns the brain into spongy tissue and typically claims its victims before they can start kindergarten; Niemann-Pick Type A, in which babies accumulate dangerous amounts of fats in various organs and suffer profound brain damage and death before age 2.

He was struck by the fact that so many Jewish diseases involved problems with processing the same fat molecules, called sphingolipids, that transmit nerve signals. This seemed an unlikely coincidence. Genetically isolated groups often have higher rates of certain diseases. But of the more than 20,000 human genes, only 108 are known to be involved in sphingolipid metabolism. The odds of Ashkenazi Jews having four sphingolipid storage disorders by random chance are less than 1 in 100,000, he calculated.
He talked it over with Harpending, an expert in human population genetics. They came to believe this was an example of heterozygote advantage—where having two copies of a mutated gene can mean disaster but one copy is helpful.

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