Raw Internet power may solve this illness if Google has its way

Buried deep within each cell in Sergey Brin's body—in a gene called LRRK2, which sits on the 12th chromosome—is a genetic mutation that has been associated with higher rates of Parkinson's. Illustration: Rafa Jenn

Wired – Several evenings a week, after a day’s work at Google headquarters in Mountain View, California, Sergey Brin drives up the road to a local pool. There, he changes into swim trunks, steps out on a 3-meter springboard, looks at the water below, and dives.

Brin is competent at all four types of springboard diving—forward, back, reverse, and inward. Recently, he’s been working on his twists, which have been something of a struggle. But overall, he’s not bad; in 2006 he competed in the master’s division world championships. (He’s quick to point out he placed sixth out of six in his event.)

The diving is the sort of challenge that Brin, who has also dabbled in yoga, gymnastics, and acrobatics, is drawn to: equal parts physical and mental exertion. “The dive itself is brief but intense,” he says. “You push off really hard and then have to twist right away. It does get your heart rate going.”

There’s another benefit as well: With every dive, Brin gains a little bit of leverage—leverage against a risk, looming somewhere out there, that someday he may develop the neurodegenerative disorder Parkinson’s disease. Buried deep within each cell in Brin’s body—in a gene called LRRK2, which sits on the 12th chromosome—is a genetic mutation that has been associated with higher rates of Parkinson’s.   

Not everyone with Parkinson’s has an LRRK2 mutation; nor will everyone with the mutation get the disease. But it does increase the chance that Parkinson’s will emerge sometime in the carrier’s life to between 30 and 75 percent. (By comparison, the risk for an average American is about 1 percent.) Brin himself splits the difference and figures his DNA gives him about 50-50 odds.

That’s where exercise comes in. Parkinson’s is a poorly understood disease, but research has associated a handful of behaviors with lower rates of disease, starting with exercise. One study found that young men who work out have a 60 percent lower risk. Coffee, likewise, has been linked to a reduced risk. For a time, Brin drank a cup or two a day, but he can’t stand the taste of the stuff, so he switched to green tea. (“Most researchers think it’s the caffeine, though they don’t know for sure,” he says.) Cigarette smokers also seem to have a lower chance of developing Parkinson’s, but Brin has not opted to take up the habit. With every pool workout and every cup of tea, he hopes to diminish his odds, to adjust his algorithm by counteracting his DNA with environmental factors.

“This is all off the cuff,” he says, “but let’s say that based on diet, exercise, and so forth, I can get my risk down by half, to about 25 percent.” The steady progress of neuroscience, Brin figures, will cut his risk by around another half—bringing his overall chance of getting Parkinson’s to about 13 percent. It’s all guesswork, mind you, but the way he delivers the numbers and explains his rationale, he is utterly convincing.

Brin, of course, is no ordinary 36-year-old. As half of the duo that founded Google, he’s worth about $15 billion. That bounty provides additional leverage: Since learning that he carries a LRRK2 mutation, Brin has contributed some $50 million to Parkinson’s research, enough, he figures, to “really move the needle.” In light of the uptick in research into drug treatments and possible cures, Brin adjusts his overall risk again, down to “somewhere under 10 percent.” That’s still 10 times the average, but it goes a long way to counterbalancing his genetic predisposition.

It sounds so pragmatic, so obvious, that you can almost miss a striking fact: Many philanthropists have funded research into diseases they themselves have been diagnosed with. But Brin is likely the first who, based on a genetic test, began funding scientific research in the hope of escaping a disease in the first place.

His approach is notable for another reason. This isn’t just another variation on venture philanthropy—the voguish application of business school practices to scientific research. Brin is after a different kind of science altogether. Most Parkinson’s research, like much of medical research, relies on the classic scientific method: hypothesis, analysis, peer review, publication. Brin proposes a different approach, one driven by computational muscle and staggeringly large data sets. It’s a method that draws on his algorithmic sensibility—and Google’s storied faith in computing power—with the aim of accelerating the pace and increasing the potential of scientific research. “Generally the pace of medical research is glacial compared to what I’m used to in the Internet,” Brin says. “We could be looking lots of places and collecting lots of information. And if we see a pattern, that could lead somewhere.”

In other words, Brin is proposing to bypass centuries of scientific epistemology in favor of a more Googley kind of science. He wants to collect data first, then hypothesize, and then find the patterns that lead to answers. And he has the money and the algorithms to do it.

Brin’s faith in the power of numbers—and the power of knowledge, more generally—is likely something he inherited from his parents, both scientists. His father, Michael, is a second-generation mathematician; his mother Eugenia is trained in applied mathematics and spent years doing meteorology research at NASA. The family emigrated from Russia when Brin was 6. At 17, he took up mathematics himself at the University of Maryland, later adding a second major in computer science. When he reached Stanford for his PhD—a degree he still hasn’t earned, much to his parents’ chagrin—he focused on data mining. That’s when he began thinking about the power of large data sets and what might come of analyzing them for unexpected patterns and insights.

Around the same time, in 1996, Brin’s mother started to feel some numbness in her hands. The initial diagnosis was repetitive stress injury, brought on by years of working at a computer. When tests couldn’t confirm that diagnosis, her doctors were stumped. Soon, though, Eugenia’s left leg started to drag. “It was just the same as my aunt, who had Parkinson’s years ago,” she recalls. “The symptoms started in the same way, at the same age. To me, at least, it was obvious there was a connection.”

At the time, scientific opinion held that Parkinson’s was not hereditary, so Brin didn’t understand his mother’s concern. “I thought it was crazy and completely irrational,” he says. After further tests at Johns Hopkins and the Mayo Clinic, though, she was diagnosed with Parkinson’s in 1999.

Even after the LRRK2 connection was made in 2004, Brin still didn’t connect his mother’s Parkinson’s to his own health. Then, in 2006, his wife-to-be, Anne Wojcicki, started the personal genetics company 23andMe (Google is an investor). As an alpha tester, Brin had the chance to get an early look at his genome. He didn’t find much of concern. But then Wojcicki suggested he look up a spot known as G2019S—the notch on the LRRK2 gene where an adenine nucleotide, the A in the ACTG code of DNA, sometimes substitutes for a guanine nucleotide, the G. And there it was: He had the mutation. His mother’s 23andMe readout showed that she had it, too.

Brin didn’t panic; for one thing, his mother’s experience with the disease has been reassuring. “She still goes skiing,” he says. “She’s not in a wheelchair.” Instead, he spent several months mulling over the results. He began to consult experts, starting with scientists at the Michael J. Fox Foundation and at the Parkinson’s Institute, which is not far from Google’s headquarters. He quickly realized it was going to be impractical to keep his risk from the public. “I can’t talk to 1,000 people in secret,” he says. “So I might as well put it out there to the world. It seemed like information that was worthy of sharing and might even be interesting.”

So one day in September 2008, Brin started a blog. His first post was called simply “LRRK2.”

“I know early in my life something I am substantially predisposed to,” Brin wrote. “I now have the opportunity to adjust my life to reduce those odds (e.g., there is evidence that exercise may be protective against Parkinson’s). I also have the opportunity to perform and support research into this disease long before it may affect me. And, regardless of my own health, it can help my family members as well as others.”

Brin continued: “I feel fortunate to be in this position. Until the fountain of youth is discovered, all of us will have some conditions in our old age, only we don’t know what they will be. I have a better guess than almost anyone else for what ills may be mine—and I have decades to prepare for it.”

In a sense, we’ve been using genetics to foretell disease risk forever. When we talk about “family history,” we’re largely talking about DNA, about how our parents’ health might hint at our own. A genetic scan is just a more modern way to link our familial past with our potential future. But there’s something about the precision of a DNA test that can make people believe that chemistry is destiny—that it holds dark, implacable secrets. This is why genetic information is sometimes described as “toxic knowledge”: Giving people direct access to their genetic information, in the words of Stanford bioethicist Hank Greely, is out and out “reckless.”

It’s true that in the early days of the science, genetic testing meant learning about a dreaded degenerative disease like Huntington’s or cystic fibrosis. But these diseases, although easy to identify, are extremely rare. Newer research has shown that when it comes to getting sick, a genetic predisposition is usually just one factor. The vast majority of conditions are also influenced by environment and day-to-day habits, areas where we can actually take some action.

But, surprisingly, the concept of genetic information as toxic has persisted, possibly because it presumes that people aren’t equipped to learn about themselves. But research shows this presumption to be unfounded. In 2009, The New England Journal of Medicine published results of the Risk Evaluation and Education for Alzheimer’s Disease study, an 11-year project that sought to examine how people react to finding out that they have a genetic risk for Alzheimer’s. Like Parkinson’s, Alzheimer’s is a neurodegenerative condition centering on the brain. But unlike Parkinson’s, Alzheimer’s has no known treatment. So learning you have a genetic predisposition should be especially toxic.

In the study, a team of researchers led by Robert Green, a neurologist and geneticist at Boston University, contacted adults who had a parent with Alzheimer’s and asked them to be tested for a variation in a gene known as ApoE. Depending on the variation, an ApoE mutation can increase a person’s risk for Alzheimer’s from three to 15 times the average. One hundred sixty-two adults agreed; 53 were told they had the mutation.

The results were delivered to the participants with great care: A genetic counselor walked each individual through the data, and all the subjects had follow-up appointments with the counselor. Therapists were also on call. “People were predicting catastrophic reactions,” Green recalls. “Depression, suicide, quitting their jobs, abandoning their families. They were anticipating the worst.”

But that isn’t what happened. People told that they were at dramatically higher risk for developing Alzheimer’s later in life seemed to process the information and integrate it into their lives, often choosing to lead more healthy lifestyles. “People are handling it,” Green says. “It doesn’t seem to be producing any clinically apparent distress.”

In other experiments, Green has further challenged the conventional wisdom about the toxicity of genetic information: He has begun questioning the need for counselors and therapists. “We’re looking at what happens if you don’t do this elaborate thing. What if you do it like a lab test in your doctor’s office? We’re treating it more like cholesterol and less like Huntington’s disease.”

In other words, given what seems like very bad news, most of us would do what Sergey Brin did: Go over our options, get some advice, and move on with life. “Everyone’s got their challenges; everyone’s got something to deal with,” Brin says. “This is mine. To me, it’s just one of any number of things that I could get in old age. And the most important factor is that I can do something about it.”

For the rest of the story, see Wired