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  But the deeper I looked, the more I realized that, in fact, most of us have the opposite of longevity genes—and that much of our DNA dearly wants to kill us.

  Chapter 6

  THE HEART OF THE PROBLEM

  Men are born soft and supple; dead, they are stiff and hard. Plants are born tender and pliant; dead, they are brittle and dry. Thus whoever is stiff and inflexible is a disciple of death. Whoever is soft and yielding is a disciple of life. The hard and stiff will be broken. The soft and supple will prevail.

  —Lao Tzu

  You’re gonna get stabbed a number of times,” Bill Vaughan said by way of greeting when I appeared at the door of his house in the Berkeley Hills. “But it’s all in the interest of research.”

  Despite only having known Vaughan for twenty-four hours, I was already accustomed to taking abuse from him. When we’d sat down to lunch the previous day, he’d announced, “You want to understand aging? I’ll show you aging!”

  And with that, he’d pinched the back of my hand, hard. It felt like a hornet sting. As I looked at him in shock, he did the same to himself.

  “Look!” he said, thrusting his hand almost in my face. “See the difference?”

  On my hand, the pinch mark had disappeared almost instantly, like a ripple on a pond. But on his hand a persistent little fold of skin lingered.

  He leaned back in his seat. “That’s aging!” he said. “It’s elasticity—the loss of elasticity. That’s what it’s all about.”

  The difference came down to two molecules: collagen, a tough, rubbery substance that gives structure to lips and tendons and skin; and elastin, which lets our skin snap back from a smile or a frown, rather than remaining there as a wrinkle. But Vaughan wasn’t talking about wrinkles. Elasticity, to him, is a much broader concept, maybe even the key to aging. “It affects lung function,” he said, “it affects heart function. And we still don’t really understand it.”

  Vaughan was seventy-seven but didn’t look it, with his shock of dark hair and broad, unlined face. My first impression was that he sort of resembled the actor Christopher Walken, which turned out to be some of his friends’ first impressions of him, too. In the early 1980s, as an underemployed biochemistry PhD, Vaughan had used his wife’s kitchen mixer to whip up a kind of gluey energy food for athletes that eventually became known as the PowerBar. He sold out to his business partner and co-inventor before PowerBar became a household name, but he never regretted it. “He just worked all the time,” he says of the partner, whose name was Brian Maxwell. “And he dropped dead of a heart attack when he was fifty-one.”

  Pause.

  “In a post office.”

  A few years later, Vaughan revved up the KitchenAid again, this time looking for a better way to feed his daughter Laura while she was running (and winning) ultramarathon races of one hundred miles or more. She needed to get calories into her body, but her stomach could not handle any kind of solid food while she was running, often for twenty-four hours at a time. Not even a PowerBar (“It just sits in your stomach,” Vaughan said). So he came up with a kind of sugary gel, enhanced with a secret mix of vitamins, electrolytes, amino acids, and herbs, that he would dispense to her from plastic flasks at key points along the course. Vaughan eventually dubbed the mixture GU, and it hit the market in 1994 as the world’s first athletic energy gel. Sold in little foil packets to runners, cyclists, and any other athlete in need of a quick shot of fuel, GU changed the world of sports nutrition as radically as the PowerBar had.

  Today there are dozens of energy bars and gels on the market, but both billion-dollar product categories originated in Vaughan’s own kitchen. “I’m a problem solver,” he told me. “The problem that I had to address was that my kids were going off to running practice at six in the morning, with nothing in their stomach, and then not eating until noon. They were not created with marketing in mind.”

  He eventually sold GU to his son Brian, which let him retire to his house in the Berkeley Hills and turn his attention to “the ultimate problem,” the one that had consumed his mind since he was a graduate student: aging. His homegrown basement laboratory was famous among Berkeley’s elite athletes, who often come there to be tested for their performance potential—but it is even better known among the Bay Area’s large and growing community of amateur aging scientists and do-it-yourself “health hackers,” who monitor their own vital signs and take action accordingly. To the “quantified self” movement, the folks who track themselves with Fitbits and complicated scales and such—and even send out their own feces to be analyzed—Vaughan is like patient zero, because there in his basement lab he has been doing his own self-studies for decades. I was dying to see it.

  He was serious about the research. The shelves of his downstairs office were lined with notebooks, some marked ATHLETES, others AGING STUDIES; a printout of his wife’s latest test results lay atop another binder labeled FAMILY. On a lab bench in the next room sat the white KitchenAid mixer that had given birth to both the PowerBar and GU. Vaughan had gotten into self-testing while he was still a graduate student, way before anyone had ever uttered the phrase quantified self. He was studying biochemistry in the building where HDL cholesterol was first identified, and like his fellow graduate students he was often drafted as a guinea pig for studies. He caught the research bug, and the notebooks on his shelves now held five decades’ worth of data on his own blood chemistry—his own, personal version of The Blast.

  He isn’t selfish, either. Once in a while, he hosts parties where his aging-conscious friends get their blood drawn and compete at the “lung function test,” a surprisingly painful exercise where you take in as much air as possible and then blow it out—all of it—into a white plastic tube connected to a computer. I’d done the same thing at The Blast, and it was about as much fun as trying to make yourself vomit. The test is supposed to measure lung capacity—which depends, of course, on elasticity. (The older we get, the stiffer our lungs.) Those results go into the notebooks, too, and I silently prayed that Vaughan served a lot of good booze at these “parties.”

  We got down to business quickly. First up was the cholesterol test. Within minutes, Vaughan was swabbing my middle finger with alcohol and then—ka-chinch!—punching a hole in my fingertip with a disposable plastic lancet. “Let’s see if you’re a bleeder,” he said, holding my finger firmly as a drop of blood began to form. “Okay, good.”

  In a smooth, practiced motion, he suctioned off the blood into a thin glass pipette and transferred it to a small rectangular cartridge, which he then placed in the open tray of a small beige machine that looked like a parking-ticket validator but was, in fact, a state-of-the-art blood analyzer, normally found only in high-end medical offices. The machine began whirring.

  Vaughan performed this ritual on himself at least once a week, he said, and the benefits more than justified the machine’s $1,300 price tag. Rather than having to go to the doctor’s office to get blood work done once a year, he simply does it himself, whenever he wants. “I use it to see whether my various dietary interventions have any effect,” he explained. “A DIYer like me can find out what works and what doesn’t in a few weeks—what works for me, not as a statistic.”

  Like Suzanne Somers, he’s become his own personal science project, the main difference being that Vaughan has an actual science degree (also, he skips the hormones). He pays special attention to his LDL cholesterol—the “bad” kind—which tends to be extremely low in centenarians. If he keeps his LDL low, he reasons, then he might stand a chance of living to be a hundred, too. The machine lets him monitor it closely: If it gets too high, he’ll cut back on the carbohydrates and perhaps up his dose of red yeast rice, a natural statin that lowers LDL. He used to run a lot, until his aging knees forced him to quit, and now he spends a good chunk of each day sitting on a Lifecycle, scrolling through the latest research studies on the PubMed database. When his cholesterol drops down to a comfortably centenarian-like level, he half joked, “I eat a piece
of cheesecake.”

  “Maintenance is tough,” he admitted. “You gotta be on it, as you get up there, and you’ve got to spend much more time on it.” He spends nearly all his time either combating aging, via exercise and yoga, or studying it: I’d run into him at conference after conference, and he was always up on the latest research.

  The machine beeped, and the digital readout flashed to life. “There you are!” he said, leaning in to check the number.

  “Two hundred thirty-five,” he read slowly. “Wow!”

  This was not a good “Wow!”

  According to the latest guidelines from the American Heart Association, a total cholesterol level of more than 240 is defined as dangerously high; ideally, it should be less than 200. My numbers got worse from there. My HDL cholesterol—the “good” kind, the higher the better—came in at fifty-six, which was okay but not great. Next was LDL, the one I’d been waiting for. Under one hundred is good. Vaughan has beaten his down to around thirty-five, which is centenarian territory. Mine rang the bell at a gelatinous 154.

  Maybe I shouldn’t have eaten that Double-Double at In-N-Out Burger last night, I thought to myself.

  “That’s high,” he said, frowning.

  “That sucks!” I yelped.

  “Yeah.”

  Three months after my visit to Bill Vaughan, I found myself sitting in a waiting room in Fort Lee, New Jersey, crowded shoulder-to-shoulder with more than a dozen senior citizens who were kvetching in at least four different languages. It was close to ten on a Friday morning, and we were all here to get our blood tested. Things had not been going smoothly, and the crowd was getting restive. “She got here aftah we did!” one well-made-up matron snarled as another lady was ushered into the back room. Meanwhile, the middle-aged woman next to me reassured her septuagenarian mother, “You want your doctor to be younger than you are.”

  I had come to see a youngish cardiologist named Nathan Lebowitz, to try to get a handle on the whole cholesterol issue. High cholesterol seems to run in my family—my grandfather’s had hovered up around three hundred, and my little visit to Bill Vaughan’s home lab had finally motivated me to get checked out. I was eager not to join the roughly six hundred thousand Americans who die of heart disease every year, more than from any other cause. Cancer runs a close second, but here’s the thing: Every one of those cancer patients, as well as stroke victims, and respiratory-disease sufferers, and the rest, also died because, eventually, their hearts stopped beating. Your heart quits, and you’re done. Obviously.

  I picked Lebowitz not because he regularly made “Top Docs” lists but because he focused strongly on prevention, which studies had long identified as key to fighting heart disease. He was also known for taking his time to explain things to patients, far more than the six minutes of face time that insurance companies typically allow. I didn’t need to hear my doctor tell me that my cholesterol “should be lower” one more time. I wanted to know more. “You can catch things incredibly early,” Lebowitz had said on the phone, still sounding like the native Brooklynite he is. “Why wait?”

  Why indeed. Everything we know tells us that heart disease has a long, long prologue. In one famous study from the 1950s, serious coronary arteriosclerosis—thickening and stiffening of the main artery leading from the heart—was found in 77 percent of a group of three hundred patients. These were not old or even middle-aged men, either: They were young soldiers who had been killed in Korea, and their average age was just twenty-two. Yet serious heart problems often go undiagnosed; in two-thirds of male patients, the first sign of heart disease is actually a heart attack. For women, that number is more like half, which is still alarmingly high.

  Much of what we know about heart disease comes from the famous Framingham study, which is like a heart-focused version of The Blast that has been going on for more than fifty years in Framingham, Massachusetts, covering multiple generations of people. It was Framingham that first revealed the link between high cholesterol and the likelihood of heart attacks, along with four other key risk factors: obesity, diabetes, high blood pressure, and smoking. Scientists have been poring over Framingham data for decades, but in 2006 a team of epidemiologists laid out the bottom line in a major study published in Circulation, the journal of the American Heart Association: “Even the presence of a single major risk factor at 50 years of age is associated with substantially increased lifetime risk of CVD [cardiovascular disease] and markedly shorter survival.”

  Gulp.

  So as I drew near the magic tipping point of fifty, I found myself the proud owner of not just one, but two out of the five Framingham risk factors: high-ish cholesterol and not-so-low-ish blood pressure (140 over 90, and climbing with each successive draft of this book). Even though I fancied myself some sort of athlete, I was still not immune. Legions of middle-aged athletes have keeled over dead from heart attacks, including the running guru Jim Fixx and thousands of others whom you’ve never read about.

  My sky-high LDL number was particularly worrisome. The problem is that goopy LDL particles tend to get stuck in tiny fissures in the artery walls, creating “plaques” that then capture more cholesterol and other cellular junk as it passes by in the bloodstream, the way a tree falling into a river will snag all sorts of debris in its branches. Those plaques can then harden and constrict blood flow, a condition called atherosclerosis (which is different from arteriosclerosis, which is hardening of the artery tissue itself). The plaques are full of bad stuff, and if one of them should suddenly rupture and break off, the bad stuff travels directly to the heart, and then it’s good-bye, Uncle Billy.

  For the last few decades, the main goal of cardiology (and pharmacology) was to try to get those cholesterol numbers down, usually via statin drugs, which cut down LDL; our frenzy to lower cholesterol quickly made statin drugs like Lipitor and Crestor the best-selling class of drugs ever. And we succeeded, to a remarkable degree: Since 1960, death rates from cardiovascular disease have been cut in half.

  But there had to be more to it. For one thing, while statins did appear to help patients with existing heart disease, who were already sick, widespread use of the drugs for prevention has not really lowered overall mortality rates among healthy people. That is, statins only seem to help those with existing problems, but don’t work as primary prevention. “You should see a decline in overall mortality, and you don’t,” says Nir Barzilai. “So that, to me, means that statins kill them in another way.”

  More recently, there’s been some doubt as to whether cholesterol is really the whole story. A major study of 136,000 patients who had experienced a coronary “event” found that half of them actually had low LDL cholesterol, according to then-current guidelines. TV newsman Tim Russert was one of them: When he died of sudden heart attack in 2008, his LDL was a saintly sixty-eight. Although his weight was an obvious risk factor, and he was on blood pressure medication, he betrayed no serious symptoms before an arterial plaque ruptured and killed him at age fifty-eight.

  This is not to say that heart disease has no warning signs. High blood pressure, which Russert had, is an easy one. Less obvious is simply whether or not someone looks old. Data from the decades-long Copenhagen City Heart Study shows that people who display certain outward signs of aging, such as fatty deposits around the eyes, creased earlobes, and baldness or receding hairline (uh-oh), had more than a 50 percent greater risk of a heart attack. Another one: Slower reaction time, which Bill Vaughan also measures in his basement lab, has also been shown to predict risk of death from cardiovascular disease. And finally, there is one bellwether of heart trouble that on reflection should be obvious: erectile dysfunction. Viagra was originally developed as a blood-pressure medication, before its other life-enhancing effects were detected. A 2012 study showed that, in fact, men with more severe erectile dysfunction were also more likely to have preventable heart disease. Like the ads say, “It could be a question of blood flow.”

  But cholesterol remains the most obvious, most quantifiab
le risk factor. The bad news is that, in all likelihood, your doctor (like mine) has been measuring it the wrong way. “The regular cholesterol blood test that we’ve been doing forever, that’s not the real story,” Dr. Lebowitz said when I finally managed to get in to see him. “It’s an attempt to represent the real story.”

  He began by setting me straight on one big point: Not all cholesterol is bad. Cholesterol is actually a molecule essential to life, crucial for making cell membranes as well as producing hormones like testosterone and estrogen; that’s why it’s in our blood to begin with. Cholesterols are also required for brain function, so it’s neither possible nor desirable to Lipitor them completely out of existence. Moreover, cholesterol comes in all sorts of shapes and sizes, not just the big three (good, bad, and triglycerides). And just to make things even more complicated, he said, not all bad cholesterol is so bad—and not all good cholesterol is good.

  Lebowitz opened a folder and peered at my lab results. To get a better idea of his patients’ true risk profile, he relies on a sophisticated array of blood tests called the Boston Heart panel, which measures a bewildering array of parameters. My results took up three full pages, but they told a slightly more hopeful story than Bill Vaughan’s home blood-test machine. Since my visit to Berkeley, my LDL had dropped; that was the good news. The not-so-good news is that it had only fallen by 6 points, from 154 to, erm, 148.

  Lebowitz frowned. Cholesterol numbers can bounce around from day to day, but this was pretty bad. Still, all hope was not lost. The important thing with LDL is not just the total number, he explained. All that LDL has to be carted around in special carrier molecules, which vary considerably in size. As he put it, a small number of large carrier molecules is better than a large number of small carriers, in the same way that it would be safer to transport fifty tourists around Rome in a single large bus rather than on fifty separate mopeds. Just as the mopeds would be much more likely to get into accidents, a bunch of small carrier molecules would have more opportunities to stick into my artery walls and cause plaques that might eventually kill me. “Just playing the percentage odds, more of them are gonna hit your artery wall, and some of them are gonna stick, and wiggle their way into the cracks, and cause problems,” he said.