Spring Chicken Page 11

  Each carrier molecule is marked by a protein called apolipoprotein B, or ApoB, which shows up on tests. Major studies going back nearly fifteen years have shown that ApoB is a much better predictor of risk than plain old LDL, and some researchers have suggested that doctors should focus more on ApoB instead. Such testing is now routine in Europe, but unfortunately, the latest U.S. cholesterol guidelines do not even mention it.

  How important is particle size? One function of the CETP “longevity gene” identified by Nir Barzilai in his centenarians is to increase their LDL particle size. One-hundred-eight-year-old Irving Kahn’s LDL cholesterol probably gets shipped around in particles the size of jumbo jets. Unfortunately, I don’t have the right CETP gene, so my ApoB score was 101, a good bit above the risk threshold of 90. So, apparently, my LDL rolls around in rusty pickup trucks flying the Confederate flag.

  Luckily my HDL cholesterol number was also high, which is good because one function of HDL is to “sweep” cholesterol away from the heart and back to the liver. Better yet, most of my HDL particles seemed to be large, a type called A-1, which are the more effective sweepers. (Best of all: red wine is thought to burst HDL.) Lebowitz scribbled on my sheet, “Great!”

  Still, it wasn’t that great: my HDL and LDL numbers would technically make me a candidate for “cholesterol lowering,” he said, which usually means a statin drug. It’s almost a rite of middle-aged passage, that moment when your doctor writes your first Lipitor prescription. But I was not eager to take a statin, especially with Nir Barzilai’s words ringing in my ear. Mainstream cardiologists almost uniformly believe that their advantages greatly outweigh any downsides, but my latent Christian Science genes nevertheless objected to a long-term medication—not yet. Luckily, a little more digging proved that I didn’t need one.

  There are actually two kinds of cholesterol in your body, the stuff you produce and what you absorb from your diet. The latter actually makes up a relatively small portion of the total, yet our bodies are remarkably good at preserving and recycling it. “Remember, our genes still think it’s three thousand years ago and we’re starving, so these mechanisms for preserving cholesterol are still going strong,” Lebowitz said.

  The thing is, a statin drug would only reduce the cholesterol I produced, but the fancy test showed that my particular type of cholesterol was mostly absorbed from my diet (apparently, they can tell the difference). So a statin wouldn’t do much. This was good news: I could use something less potent, a drug like Welchol or Zetia, which simply helps transport cholesterol out of the intestines. (Oat bran fiber does much the same thing, absorbing cholesterol in the gut and escorting it out of the body.) But I still demurred, so he began quizzing me about my eating habits.

  “Do you eat a Mediterranean diet?” he asked.

  “Sort of,” I hemmed.

  “Do you like French fries?” he prodded.

  “Once a week,” I lied.

  “Noooooo—that’s not acceptable.”

  “Steak once a week?” I ventured.

  He kind of grimaced at that news, too.

  Red meat has long been known to be a risk factor for heart disease, originally because of its fat content. More recent research has more or less exonerated fat (which turns out to be relatively good for you), while identifying another possible culprit in carnitine, an amino acid found in red meat. In the body, carnitine is metabolized to a chemical called TMAO that causes atherosclerosis (think: Tenderloining My Ass Off). In a recent small study, researchers pinpointed particular gut microbes in most people that are responsible for producing TMAO—but longtime vegetarians, who don’t have those particular microbes, also don’t make TMAO when they eat red meat.

  Translation: According to this study, it is apparently only safe to eat meat if you’re a vegetarian.

  Which I wasn’t. Nor was I about to become one. But I wasn’t up for taking medication, either, so I instead vowed to eliminate burgers and French fries from my diet. Mostly. I could have gone further, and cut out all processed meats—which have been shown, in at least one large recent study, to increase heart failure risk more than unprocessed red meats. But I like prosciutto too much. That was enough to convince Lebowitz to let me escape from his office (I’d been there a full hour), although I’m sure he knew that, like most cardiac patients with middling numbers, I wasn’t quite ready to do anything to change—and possibly even save—my life.

  Then I did still more research, and that’s when I really got freaked out.

  Heart disease is typically thought to be a purely modern ailment, a function of our newly rich diets; back in the good old days, before we ate French fries and trans fats and tenderloined our asses off all the time, it supposedly didn’t exist. But that actually isn’t quite true.

  In 1909, a French British scientist in Cairo named Marc Ruffer dissected and analyzed a group of ancient Egyptian mummies to which he had finagled access. He styled himself a “paleopathologist,” one who studied ancient diseases, and in these dried-up old corpses, he found several. Some of the mummies carried eggs of the waterborne parasite that causes bilharzia, while at least one appeared to have pustules consistent with smallpox. Most interesting of all, he also found that several of the mummies appeared to suffer from what was thought to be a brand-new condition: atherosclerosis.

  At the time, heart disease was just emerging as a leading cause of death in the industrial world—which it has remained, for more than a century. For years, the presence of arterial disease in these ancient mummies was thought to be a function of their decadent royal lifestyle, since only kings and queens and high-status individuals got to be mummified. But a little over a century after Ruffer, a multinational team shattered that view by reporting in the Lancet that they had found similar degrees of arterial hardening not only in dozens more Egyptian mummies—even some who were only in their late twenties at death—but also in numerous other mummified corpses from Peru, the American Southwest, and the Aleutian Islands in Alaska. (Atherosclerosis also afflicted Otzi the “Iceman,” who was entombed in a glacier 5,000 years ago.)

  Unlike the Egyptian dead, these individuals were far from royalty; in Peru, especially, mummification of the dead was a common practice. “In the same way I have my portrait of my Newport banker grandfather in my house, they would keep the mummy around,” says Caleb “Tuck” Finch, a USC gerontologist who was part of the Lancet team. “Some of them were two thousand years old.” The hope was that someday, perhaps, mummified Great-Great-Great-Great-Grandma would magically come back to life, like Ted Williams’s cryonically frozen head.

  The crucial difference was that the Peruvian mummies, and also the North American ones, were largely hunter-gatherers, eating a “healthy” and authentically Paleo diet—yet they, too, suffered from the beginnings of cardiovascular disease. Atherosclerosis affected women and men, at all age brackets, and all levels of ancient societies, and so the Lancet study raised a troubling question: Are humans somehow hardwired for heart disease?

  Short answer: Yes, we probably are. That explains why those poor dead young American soldiers had arteriosclerosis before they turned twenty-five. In a sense, we are almost programmed to develop a certain degree of hardening of the arteries—if we live long enough. And that’s not all: Our hearts themselves stiffen and atrophy with age. That was what had happened to my dog Theo, his poor heart prematurely aged by the strain of feeding his blood-hungry tumor. But the thing is, it happens to all of us eventually.

  The most fascinating moment of The Blast, and also the most unnerving, came on my second day, when I lay down on a gurney in a darkened office, while a technician lathered my chest with a greenish gel. Then he pressed the cold metal end of an ultrasound wand into the puddle of goop and turned his computer screen toward me. Up popped a ghostly green image of my beating heart, something I had never seen. It looked bizarre, the valves flopping and waving around in a complex, fluid dance, like some kind of deep-sea animal.

  It was doubly weird because the ultra
sound revealed only a slice of an image, as though he had shone a flashlight into a dark, watery cave where my heart happened to be beating. We sat there and watched my heart work through every beat, the valves fluttering and wobbling before they finally snapped into place and allowed the chamber to fill. It was beyond strange to watch the single muscle, heretofore invisible, that had sustained my entire life.

  We were watching elasticity in action: The heart muscle must stay strong enough to swoosh blood throughout the 60,000 miles (!) of blood vessels in a typical human body, contracting and expanding up to 180 times per minute at peak exercise intensity. Yet the arteries themselves must also remain flexible enough to handle all that flow—like a water balloon, they can only take so many fillings before the rubber starts to get sketchy. Over time, we lose that flex. And not just because of atherosclerosis, but because our hearts—like the rest of us—are subject to damage from intrinsic aging, the same way the fuel pump in your old car will eventually wear out and need to be replaced. It just gets old. It was never meant to last that long.

  Like that old pump, your heart performs less and less well with age. Although your resting heart rate doesn’t change much, except in response to endurance training, maximum heart rate declines pretty much in a straight line with age. So does VO2 max, as I learned in The Blast. The heart muscle weakens and can’t throw out as much blood per stroke. It still lasts much longer than any part of any automobile ever manufactured—it’s a miraculous little machine, in fact—but the truth is that the human heart only lasts so long. Which is why the biggest, most serious, and least modifiable “risk factor” for heart disease is age itself.

  As he moved the chilly ultrasound wand around on my chest, the Blast technician would periodically stop and press a button on his computer, capturing images of certain parts of my heart. He was essentially taking its measurements, paying special attention to the left ventricle, one of the parts of the “pump” that first shows signs of age. Over time, thousands and millions of contractions, the muscle tends to become thickened and enlarged, which you might think was good news. Bigger, stronger heart = more blood pumped, right?

  Wrong. Actually, a larger left ventricle is a classic symptom of cardiac disease and high blood pressure, as the pump has to work harder to keep things moving through your stiffening circulatory system. As it pumps harder, it makes more muscle, and thus it gets bigger—and a lot less efficient. That was Theo’s problem. He was only able to seem healthy, despite his huge tumor, because he had been so athletic all his doggy life. Aging is hiding in our bodies.

  Long-term aerobic exercise and/or strength training can actually reduce one’s risk of cardiac hypertrophy—although exercise started later in life is much less effective. If you let it go, an enlarged heart can segue into heart failure, which is one of the main reasons why older people run out of gas, as Luigi Ferrucci noted. Says Richard Lee, a Harvard cardiologist and stem-cell researcher, “Nature probably cares more about hair loss in the forties than it does about heart failure in the eighties—but now our hospitals are filled with people who are in heart failure in their eighties.”

  What can be done? Controlling blood pressure in general seems to help, either with medication—or with meditation, which has actually been shown to work in studies, believe it or not. Data from the BLSA has also pointed to abdominal fat—my kind—as another possible cause or contributor to left ventricle problems. So getting rid of that would be a good next step (one we’ll explore further in a few chapters). But those only take you so far. The fact remains that like the components of your car, your heart simply was not designed to last forever.

  Neither were our arteries. Next, the technician applied the wand to the inside of my neck, and waggled it around a bit. Now he was measuring something called “intimal medial thickness,” or the thickness of the wall of my carotid artery. Over time, our artery walls tend to grow thicker—and less flexible. Hence we get high blood pressure, and cardiac hypertrophy, in a vicious feedback loop. Dr. Lebowitz had done the same measurements and while he found no actual plaques, which was good, he nonetheless concluded that my “arterial age” was fifty-nine, which shocked me.

  Over time, data from The Blast has shown that by far the biggest contributor to heart disease and heart failure is our own aging biology—the way our heart muscle and arterial walls themselves change over time, making us more susceptible to athero- and arterio-sclerosis. Processes inside our own cells create various kinds of junk, including so-called cross-linked proteins and excess deposits of things like calcium and collagen.

  We actually want calcium and collagen in our bones and our skin—but in our hearts, they cause hardening and stiffening and other bad things. And there seems to be no way to avoid them: The longer we live, the more of this junk gets deposited in our most important muscle. Worse, that muscle does not really regenerate, because heart-muscle cells do not divide. (Nor do neurons, the other most important kind of cell in our bodies.) And as more of us live beyond the traditional heart-attack risk range of our fifties and sixties, more people are living with aged hearts.

  “You’re just not gonna get a Pinto to do four hundred thousand miles,” says Lee of Harvard. “You may get a Volvo or a Subaru, but you’re just not gonna get a Pinto to do that. And some parts of the heart are probably like that.”

  So the trick becomes, can you change a Pinto into a Volvo?

  Chapter 7

  BALDNESS AS METAPHOR

  A moist eye, a dry hand, a yellow cheek, a white beard, a decreasing leg, an increasing belly… your voice broken, your wind short, your chin double, your wit single, and every part about you blasted with antiquity.

  —Shakespeare

  Somehow, I managed to escape Baltimore without having to fill the Downton Abbey hat. My microbiome will go unanalyzed, at least for the next three years. But the good people at The Blast also ignored one other biomarker of aging that, for me at least, seems all too obvious: my hair. More specifically, the lack thereof. It’s the moment I most dread, when my hipster barber hands me the mirror to “take a look at the back” and the creeping bald spot that an LA standup comic once called a “flesh-colored yarmulke.”

  I’d been obsessing about my flesh-colored yarmulke since earlier in the summer, when I drove up to my college reunion (let’s just call it a “significant” reunion). I was there partly out of curiosity about what kinds of adults my pimply classmates had turned into, but also for the usual, time-honored reason: to see how old everyone else looks. Over a June weekend, a few hundred of us congregated on Ye Olde College Greene to get reacquainted. We bunked in the old dorms, traipsed around to the old landmarks, and remarked on how our favorite professors now seemed so aged which is precisely what the students were thinking about us. In the evening we sipped rather than chugged our beers under white tents and tried to sustain conversations with people we hadn’t seen in decades. One major question was always left unspoken: What in the hell happened to your hair?

  Before I left, I had dug out the old “Freshman Facebook.” I am so old that back then it was an actual, physical book, with a photo and basic information on every single member of the class of [REDACTED]. But what jumped off the page—almost literally—was the hair. We had so much of it, incredible, thick, dense masses of hair sprouting so far down our foreheads that it almost merged with our eyebrows. In many photos, it seemed as if some kind of furry animal had nested on the person’s head.

  Granted, those photos were taken in the 1980s, sort of a lost golden age for hair. But still: There was a lot of hair. And now, for most of us, it was at best a vestige of its former self. Many of the guys had surrendered to the inevitable and just buzzed their skulls; others, including yours truly, were still in denial. Not just the men, either, but many of the women had also lost the sheen and luster of their youthful tresses. But not all of us were so afflicted, at least not yet: A select few classmates still sprouted—nay, flaunted—their luxuriant manes, perhaps with a few gray flecks, but otherwise
little changed from their freshman shots, except that the rest of us now hated them.

  So what had happened? Why was our hair going bad, just two decades after its glorious, shaggy peak? And was this some sort of marker, a sign that the rest of our bodies were also dying, withering, falling apart?

  Seeking answers, I went to visit Dr. George Cotsarelis, a professor at the University of Pennsylvania and a leader in the science of hair regeneration. It’s not that our hair disappears, he explained, in a soothing voice practiced on thousands of panicked patients, who may or may not include Donald Trump. A grip-and-grin shot of Cotsarelis and Trump adorned the office bookshelf, right next to one with President Obama, but he would neither confirm nor deny that he was the genius behind The Donald’s famous mane. I didn’t press the issue. I had deeper concerns.

  Hair loss is not really loss, Cotsarelis explained. It’s more an issue of shrinkage. The good news is that our hair follicles have not disappeared, even in my flesh-colored-yarmulke zone. The bad news is that those follicles have “miniaturized” to the point where the hairs they produce are microscopic. In other words, bald guys aren’t really bald; their hair is merely invisible. But beyond that, he didn’t really have many answers. “We don’t really know much about why it happens,” he admitted. “We really don’t.”