Spring Chicken Read online

  Instead, I tried to refocus on the delicious lobster rolls we would be eating later, at Sam’s Chowder House. With some fries and a nice, warm beer…

  “You only live once,” Todd said, intruding on my reverie.

  Or something like that. I don’t really remember everything that happened next, except that I zipped off the hoodie, said “Screw it!” and took off running for the water’s edge.

  A human being exposed to cold water can die in one of two ways: quickly, or slowly. The former generally involves the cold-shock response, where blood pressure and heart rate suddenly skyrocket, resulting in a heart attack (or, as the press release will put it, a “massive cardiac event”). This is especially popular among middle-aged triathletes, and it is infinitely preferable to the slow way, where the cold water simply sucks heat out of your body—twenty-six times faster than when skin is exposed to air, by the way—until you eventually lose consciousness and drown. According to the Coast Guard, that generally happens when one’s core temperature drops to below eighty-seven degrees, or about forty degrees warmer than the water in Half Moon Bay.

  So I needed to be convinced that this cold-water plunge was going to be worth it, and not merely an “invigorating” exercise that I would hate, if it didn’t kill me. Were there other benefits to short-term cold exposure—or was Todd just some kind of masochist? You know, the kind who deliberately takes a cold shower every day, and enjoys it?

  I didn’t have to dive very deep into the database to find some hints that a shot of cold might actually be good for you. Some of the longest-lived creatures on earth thrive in very cold water, for one thing. Lobsters can live for decades, if they are clever enough to stay out of lobster pots. Blue whales have been known to live for 200 years or so, and then of course there was Ming, the 507-year-old Icelandic ocean clam, may she rest in peace. Cold water may also explain why certain species of rockfish (a family that includes snapper and striped bass) essentially appear to be ageless, showing no signs of age-related deterioration at all. But whether cold water is responsible for their longevity, who knows?

  Nematode worms, however, are pretty easy to keep in the lab, and studies on them suggest that cold water might help increase their longevity. For a long time, it was thought that this had to do with the simple fact that colder temperatures slowed down the chemical reactions that eventually lead to aging. New research, however, suggests that something much more profound might be going on. In a recent paper published in the journal Cell, scientists from the University of Michigan found that cold temperatures activated a longevity-promoting pathway in the worms.

  The good news is that humans actually have the same genetic pathway. That may help explain why Katharine Hepburn, who swam every day in Long Island Sound, winter or summer, lived to the age of ninety-six. In a Finnish study of cold-water swimmers, subjects were analyzed at the beginning of the “winter swimming season” (yes, there is such a thing), and then again at the end, five months later. After months of regular cold swimming, the study subjects had much higher levels of natural antioxidant enzymes in their blood. They also had higher red-blood-cell counts, and more hemoglobin—in short, there was more blood in their blood. Their bodies truly had adapted to the stress of cold-water immersion, in good ways.

  Even more interesting was research showing that exposure to cold water could activate brown fat, which burns energy and helps generate heat (for example, when we do stupid stuff like jump into frigid water). Unfortunately, brown fat is also relatively rare in adults, making up only a tiny fraction of our total fat stores; in most of us, it’s limited to a few small pockets on our upper back, between our shoulder blades. It kicks into action in cold conditions in order to help keep us warm, but it also exerts beneficial effects on metabolism, mainly by burning white fat more quickly and efficiently than exercise or dieting. The more you are exposed to cold, studies have shown, the more brown fat you create. This is a good thing.

  Finally, on a much more basic level, heat is bad for us; the fact that we are warm-blooded creatures actually accelerates our aging. It’s part of the price we pay for not being reptiles. The reason has to do with our proteins—not the kind we eat in the form of meat or tofu, but the proteins that form the most basic currency of our cells. (Basically, everything that goes on in our cells depends on proteins.) The thing is, excessive heat causes our proteins to lose their three-dimensional structure, known as their “folding,” which is crucial to their proper functioning. When they “unfold,” then they can no longer do their jobs. We can observe this while cooking breakfast: “Crack the egg, it goes into frying pan, and the proteins unfold,” explains Gordon Lithgow.

  These “misfolded” proteins then become useless to our bodies, like empty wine bottles sitting around in our house. They have to be thrown out, or recycled, by a complex array of cellular garbage-disposal and protein-recycling machinery called the proteasome. But even at lower temperatures—say, around 98.6 degrees Fahrenheit—the same thing is happening: Our proteins are literally cooking.

  This is thanks to a phenomenon called the Maillard reaction (named for the French guy who discovered it a hundred years ago), which we have all observed: It’s why bread crusts are brown, why steaks get charred on the grill, and why cooked rice smells good. The Maillard reaction happens when amino acids combine with sugars under heat, and it makes food yummy. Unfortunately, the same reaction is taking place inside our bodies, a kind of slow-motion Maillard that produces nasty things called advanced glycation end-products, or AGEs—which really do help promote some diseases of aging, notably macular degeneration but also atherosclerosis, diabetes, and Alzheimer’s. AGEs in our blood vessels, we know, are a leading cause of stiffer arteries and higher blood pressure, for example.

  Bottom line, then: My proteins were loving the cold water. So was my brown fat. And while other parts of me weren’t enjoying it quite as much, my brain knew enough to trust that Todd had done his homework and was maybe on to something. So I vowed to do my best to stay in that F*7@ki*g freezing Half Moon Bay as long as I possibly could.

  It burned, at first. At least, that’s what it felt like: wading into hot lava. That sensation didn’t last more than a couple of seconds before the chilly reality hit. It was breathtaking, literally; I could not breathe. I shrieked, then panicked and stopped at about waist-deep. “Can’t breathe!” I croaked, turning to bolt for shore.

  Todd dove into a wave, ignoring me. I had no choice but to follow or get knocked down. When I surfaced, a strange thing happened: It got better. Sort of. The impulse to flee had faded, anyway. Another wave rose up, and we dove into that. I whooped for joy now; this was fun. Frisbee Guy had stopped his masturbatory throwing and was staring at us.

  “It’s important to move around a lot,” Todd said—not to stay warm, mind you, but to make it even colder. “Otherwise you generate a little warm layer next to your skin,” he added, like that was a bad thing. We jogged in place and body-checked the incoming waves, laughing and shouting like kids. My skin tingled all over; my legs were numb from the knees down. My heart pumped furiously, trying to keep my core warm, while robbing blood from my extremities. Like my testicles, which ached fiercely, as if in the grasp of a vengeful ex-girlfriend. “My balls hurt!” I blurted.

  “Yeah,” said the World’s Toughest Nerd, with a knowing nod. “That happens.”

  The rest of me felt pretty good. A strange calm settled in, and I relaxed into the water, as if it were the same balmy Pacific that caresses Hawaii (which it is, technically). As I plunged into yet another hypothermic wave, I wondered, Is this what happens when you die? I almost felt too good. I looked at my watch, which said we’d been in the water for four minutes and change. It was cold, but I didn’t mind so much. A short while later, a decent-size wave came along, and I bodysurfed it in to shore. I’d stayed in for almost six minutes, and, weirdly, I had enjoyed it immensely. It was the most exciting sort-of-dangerous thing I’d done all month.

  “Nice job!” Todd said when
he got out of the water after six more refreshing minutes. We toweled off, feeling like the biggest badasses on the beach, and got in the truck to go for lunch. A lobster roll had never tasted so good, but it was the thrill of the cold water that made it that way.

  “It’s like this gold mine, that people are not taking advantage of,” he sighed over lunch. “It’s so obvious to me, I don’t understand it.”

  Back home, I tried the cold-showering thing a few times, telling myself that our city tap water wasn’t nearly as frigid as Half Moon Bay. It would be easy! Also, the case for the benefits of cold water seemed pretty strong. And even if I did not end up living forever, it definitely started the day with a zing. And, often, a yelp.

  It felt great after a hard bike ride on a hot day, or when I needed a bigger jolt of energy than yet another cup of coffee could provide. Once in a while. But my enthusiasm for it as a daily practice pretty quickly shrank, you might say. Standing under an ice-cold shower just wasn’t as much fun as splashing around in the ocean. So while I will gladly jump into almost any cold body of water now, without fear or hesitation, in my daily life I went back to hot showering.

  It was thus a relief to learn that just as cold can be good for you, small doses of heat are also beneficial in certain ways. Heat activates something in our cells called heat-shock proteins, which sound bad but aren’t. Their job is basically to help repair cellular proteins, which tend to come unglued or unfolded in hot or stressful conditions. Studies in smaller animals like worms have shown that this response can be “trained”—worms that have experienced stress in their lives develop a more powerful heat-shock response.

  Heat-shock proteins are especially important in exercise. To compress a very long and complicated story: Certain heat-shock proteins, such as the ones produced in high-intensity exercise, actually help our cells clean house, which lets them function better for longer. Every time he cranked up the intensity in his Spinning classes, for example, Phil Bruno was creating heat-shock proteins that helped repair his own cells—and also reduce his insulin resistance, another way in which exercise counteracts diabetes.

  But my encounter with Todd Becker did get me thinking more about the topic of stress in general. And as I delved into the literature about stress and hormesis, I began to realize that much of what we think we know about stress is, in a nutshell, completely wrong.

  Stress is a bit of a catchall term: We use it to describe how we feel when we’re under pressure at work, driving on Los Angeles freeways, or churning toward a book deadline; we also “stress out” over getting to the airport on time, vacationing with in-laws, or anything to do with raising teenagers. This psychological stress can give rise to biological stress: One way is by triggering the release of stress hormones like cortisol, which helped our Paleolithic ancestors engage their fight-or-flight survival response and store more calories as energy for long, hungry journeys into exile. In the modern world, alas, cortisol merely makes people in office jobs get fat. Stress also appears to shrink our telomeres, those thingymabobs that protect our chromosomes. Another very interesting study found that people who were lonely, which is one of the most intense forms of psychological stress, had their genes for inflammation activated at a much higher rate than those who felt more socially connected.

  The most common kind of biological stress is one that you have probably also heard about: oxidative stress, which is caused by free radicals. And if you know anything about oxidative stress, you know that it is bad, but that these free radicals can be—must be—combated by taking antioxidants, either as supplements or in our food. Which is why, when you go to the grocery store, nearly everything from fruit juice to breakfast cereal to dog food brags about its antioxidant content on the package. Antioxidants, most of us believe, somehow “soak up” or counteract the effects of free radicals. They’re a good thing, as everyone knows. Except they’re not.

  The discovery of oxidative stress was one of the unsung dividends of the race to build the atomic bomb. During research for the Manhattan Project, things sometimes got a little sloppy, safety-wise, and many people were accidentally exposed to large doses of radiation. When that happened, these poor radiation victims seemed to grow old extremely rapidly: Their hair fell out, their skin wrinkled, and they developed various kinds of cancers in short order.

  Scientists pretty quickly found that ionizing radiation created large amounts of free radicals, which are oxygen molecules with one free electron. The unpaired electron makes them chemically angry, and they rampage around, looking for nice innocent molecules to react with and corrupt. This chemical bullying results in oxidation, which is also why exposed metal rust and cut apples turn brown; this “browning” is also happening inside our bodies. (And it’s different from the “browning” that takes place in the Maillard reaction.) Free radicals also damage cellular DNA, leading to cancer (among other things). The atomic scientists figured out they could help victims of radiation poisoning by feeding them “radioprotective” compounds, which basically scooped up all the excess free radicals. These were the first antioxidants. And they worked, sort of.

  But free radicals were not thought to have any link to aging until one morning in November 1954, when a young scientist named Denham Harman was sitting around his Berkeley lab, not doing much work. Back then, scientists did not have to spend every waking moment writing grant applications, like they do now, so they could spend time in the very productive enterprise of just sitting and thinking about stuff. Harman had been coming into the office like this for four months, just mulling over the single problem that consumed him: aging. Since every animal grew old and died, Harman believed, “there had to be some common, basic cause that was killing everything,” he told an interviewer decades later. That morning, the answer dawned on him in one blinding moment: “Free radicals flashed through my mind,” he later recalled.

  Harman was ultimately able to prove that all oxygen-consuming life-forms produce free radicals, negatively charged oxygen molecules that chemists now call reactive oxygen species, or ROS, in their mitochondria. These molecules, he believed, caused the DNA damage and other cellular harm that drove the aging process—and also caused cancer. In particular, he believed, oxidized LDL cholesterol (“bad” cholesterol) appeared to be responsible for forming arterial plaques. They also damage proteins in our cells. But because ROS are an unstoppable, inevitable consequence of aerobic respiration, this oxidative damage is the price we pay for living in an oxygen-rich atmosphere. Or, to put it another way: Breathing kills.

  Which is a depressing thought. But Harman had a solution: antioxidants. In one famous experiment, he fed mice food that was laced with the preservative BHT, which also happens to be a strong antioxidant, and they lived 45 percent longer. He did this again and again with other compounds, including vitamins C and E. His theory got a big boost from Nobel laureate Linus Pauling, who embraced vitamin C—one of the most powerful natural antioxidants—as a cure to all ailments, from the common cold to cancer.

  The free radical theory of aging was the perfect 1960s theory, pitting “free radicals” against the forces of order, in the form of antioxidants. It was seductive in its simplicity: Aging was thus reduced to a chemical reaction that could be slowed, perhaps even stopped, simply by consuming a few pills. Harman himself took large amounts of vitamins C and E, the two most common antioxidants; he also ran two miles every single day, well into his eighties. He passed away in November 2014 in a nursing home in Nebraska, but his theory has taken over the world. More recently, health-foodies have embraced more exotic antioxidants, from beta-carotene to various phytochemicals found in blueberries, pomegranates, and red wine grapes, to name a few. More than 50 percent of the American public consciously takes some sort of antioxidant supplement, according to some estimates. Dr. Oz celebrates them daily on his show. The free radical theory, it’s safe to say, has been almost universally accepted by the public.

  But there was one nagging problem, gerontologists began to realize in the 1
990s: Antioxidants didn’t really seem to extend lifespan in lab animals. Even Harman was slightly troubled by the fact that, while he could increase average lifespan, he was unable to extend the animals’ maximum lifespan as he had in his experiments. It was not clear that his antioxidant compounds were affecting the actual aging process. If they really were slowing down aging, by absorbing free radicals, then the longest-lived mice should have lived longer. (Linus Pauling, on the other hand, consumed massive doses of vitamin C, and lived to be ninety-three.)

  Others had a difficult time replicating Harman’s results. And in human studies—particularly the double-blind, randomized clinical trials that are the gold standard for medical science—antioxidant supplements have had a mixed track record at best. A massive JAMA review of sixty-eight clinical trials of antioxidants, covering a total of more than 230,000 subjects, found a huge disparity in results: A handful of studies showed that antioxidants reduced mortality risk, but overall the majority of well-run studies found that people who took vitamin A, vitamin E, and beta-carotene actually seemed to increase their risk of death. Beta-carotene in particular, once the darling of nutrients, was strongly associated with increased cancer risk. The data on vitamin C was less conclusive, and there was some indication that selenium might be slightly beneficial.

  But, still: WTF? The antioxidant theory had seemed so simple and elegant. And now it appeared to be wrong. If free radicals really did cause cellular damage, and thence aging, then why didn’t antioxidants seem to help?

  In 2009, a maverick German scientist named Michael Ristow shed some light on the issue with a simple but subversive experiment: His team recruited forty young people to a regular exercise program where they worked out for more than ninety minutes, five days a week. Half the subjects were given an antioxidant supplement with high doses of vitamin C and vitamin E, while the other half unknowingly took a placebo pill.