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Thinking about it makes you a better person, not a worse one

The Economist Magazine Oct 5th 2013

The love of money”, St Paul memorably wrote to his protégé Timothy, “is the root of all evil.” “All” may be putting it a bit strongly, but dozens of psychological studies have indeed shown that people primed to think about money before an experiment are more likely to lie, cheat and steal during the course of that experiment.

Another well-known aphorism, ascribed to Benjamin Franklin, is “time is money”. If true, that suggests a syllogism: that the love of time is a root of evil, too. But a paper just published in Psychological Science by Francesca Gino of Harvard and Cassie Mogilner of the University of Pennsylvania suggests precisely the opposite.

In the first test they were asked to make, within three minutes, as many coherent sentences as they could out of a set of words they had been presented with. What they were not told was that each of them had been assigned to one of three groups. Some volunteers’ word sets were seeded with ones associated with money, such as “dollars”, “financing” and “spend”. Some were seeded with words associated with time (e.g., “clock”, “hours”, “moment”). And some were seeded with neither. Thus unknowingly primed, the volunteers were ready for the second test.

This was mathematical. They were given a sheet of paper with 20 matrices which each contained 12 numbers, two of which added up to ten (for example, 3.81 and 6.19). They had to write down, on a separate answer sheet, how many of these pairs they could manage to find in five minutes. They were also given a packet of money and told they could reward themselves with a dollar for each pair they discovered.

Crucially, they were not asked to show their workings on the answer sheets—and the matrix sheets, on which those workings might have appeared, carried no identifier and were ostentatiously discarded once the test was done. Nevertheless, by hiding an identification code in a sample matrix on the answer sheet, Dr. Gino and Dr. Mogilner knew which matrix sheet each candidate had been given and thus who had cheated and who had not. They found that 88% of those who had been primed with money-related words in the first test cheated, as did 67% of those given neutral words. Of those primed with time-related words, though, only 42% cheated.

Nor, despite St Paul’s aphorism, was the lure of lucre during the experiment (as opposed to the effect of thinking about it as a result of being primed) necessary as a corrupting influence. A similar trial on different participants showed that presenting the matrix as a test of intelligence also caused those primed with the idea of money to cheat more than those primed with the idea of time—though, intriguingly, that did not apply if the matrix was presented as a test of personality.

This led Dr. Gino and Dr. Mogilner to suspect that self-reflection played a part in controlling unethical behavior during the test. They therefore conducted a third test in which, for half the volunteers, there was a mirror in the cubicle they were sitting in when doing the experiment.

Volunteers primed to think about money cheated 39% of the time when a mirror was present but 67% when it was not. Those primed to think about time cheated 32% of the time in the presence of the mirror and 36% in its absence—results that are statistically indistinguishable.

Finally, a fourth experiment asked primed volunteers to fill in a questionnaire before tackling the matrix. In among “filler” questions intended to disguise what was happening this asked them to rate how they felt about self-reflective statements like, “Right now, I am thinking about who I am as a person.”

As in the previous tests, those primed with money words cheated more often than those primed with neutral words and far more often than those primed with time words. But whether someone cheated was also related to how strongly he felt about the self-reflective statements presented to him in the questionnaire.

It seems, then, that thinking about time has the opposite effect on people from thinking about money. It makes them more honest than normal, rather than less so. Moreover, the more reflective they are, the more honest they become. There must be an aphorism in that.

Bill Briggs CNBC.com Oct. 24, 2013

For men of a certain age who feel lethargic, lumpy and maybe a tad limp, it is — they are convinced — T time.

In record numbers, American guys are turning to testosterone boosters to repair their pep, revive their sex drive, even erase their erectile issues. Annual sales of the prescription hormone have more than doubled since 2008, according to IMS Health, Inc., reaching $1.6 billion last year, en route to $5 billion by 2017, some analysts predict. And that doesn’t include testosterone supplements purchased over the counter or via the mail.

“We are seeing a very dramatic increase,” in men taking testosterone supplements and drugs, said Dr. Edmund Sabanegh, chair of the urology department at the Cleveland Clinic.

But the quick medical fix many seek for nagging male ills that come as naturally as receding hairlines also can bring on side effects including blood clots and infertility.

After age 30, testosterone levels dip about 1 percent each year. As internal stores of that hormone decline, men can experience a loss of muscle mass and strength, depression, lethargy and a waning interest in sex.

“The symptoms of low testosterone are kind of what many of us feel when we get older: maybe a little decrease in energy, a little erectile problem, a little drop in libido,” Sabanegh said. “Often, those are normal” for men in their 40s, 50s or older.

“And when that’s the situation, we just talk about making lifestyle changes, taking a few pounds off, getting on a regular exercise program, improving their diets,” Sabanegh added. “Those sorts of things can, in many patients, give them the kind of effect they were hoping for in the testosterone.”

For Sabanegh to place a patient on testosterone therapy, he said the man must exhibit the saggy-draggy clinical symptoms of low testosterone. Then, a lab test must confirm that the patient’s hormone level has slumped to an abnormal number. Although that line varies by individual, typically Low T means the count is less than 300 nanograms per deciliter.

While supplements can boost a man’s energy and get his sexual enthusiasm back to normal, the problem is many men’s testosterone use isn’t monitored by a physician. Sabanegh has treated patients who show up suffering the side effects from hormone dosing. “On occasion,” he said, “…I have seen acne and elevated red blood cell counts” – which can cause blood clots. Simply stopping the medication will end those side effects.

One testosterone user who has not suffered any such symptoms is Dan Nobel, 61, a nutrition store owner in St. Louis. In fact, the only changes he has noticed, he said, are a happier lifestyle and strength improvements.

A competitive bodybuilder, Nobel routinely scrutinizes his meals and his weight, 165 pounds. Last year, he decided to try his first over-the-counter testosterone supplement, 2TX, simply because he had reached age 60. (He’s never had his testosterone count checked by a physician, he said.)

“At the gym, when I did a squat (press) or a bench press, I went up 10 pounds. My libido seemed better too. And that was just after like two days of being on it,” Nobel said. “I thought, wow, this does seem to make a difference.”

Recently, at a local bodybuilding competition, Nobel won his division – men aged 60 to 69.

Meanwhile, anti-aging clinics catering to men (and women) in that same age bracket have sprung up across the nation, with many promoting testosterone drugs to their male clients.

At Vitality Logix, a wellness center specializing in aging in New York City, founder Joshua Gizersky said the key to “successful therapy” is diagnosing the reason testosterone is low “and judiciously replacing (it) to levels consistent with a 25-year-old male.”

“Guys in their early 20s are thought to have some of the highest testosterone levels in their lifetime and commonly surpass (a count of) 800,” said Gizersky, a doctor of osteopathic medicine. Consequently, “this age is chosen as the ideal target, especially when using testosterone for age-management reasons in older men.”

That can mean prescribing enough extra testosterone to propel a man’s count from about 250 to twice or as much as four times that amount, Gizersky said.

The range for “normal” testosterone in a healthy male is 300 to 1,200 nanograms per deciliter, according to the National Institutes of Health.

In addition, users of oral (typically, over-the-counter) testosterone supplements — like the one Nobel has taken — should be wary, both doctors warned. Some over-the-counter forms of testosterone taken orally are known to cause liver damage when the supplements are metabolized, Sabanegh said.

“Most of the people working at GNCs and Vitamin Shoppes have very little education on this subject matter,” Gizersky said. “Many are high school kids or college students without any concept of what they are selling and certainly no knowledge of the human physiology involved, nor the production methods used in these products — which makes for a very dangerous situation.”

The World’s First Hamburger Made From Lab-Grown Meat Has Just Been Served

The Economist Magazine Aug 10th 2013

AS FREEBIES go, it was a disappointment. Of the hundred-odd representatives of the world’s media who crammed into a television studio in London on August 5th, none got so much as a bite of the food on offer. What they did get, though, was a taste of what may prove to be the future of eating. The meal they gathered to witness other people digest consisted of the world’s first hamburger made of meat grown from scratch in a laboratory.

What the 140-gram patty lacked in heft it made up for in price. At more than $330,000, a tab partly picked up by Google’s co-founder, Sergey Brin, it must rank among the most expensive dishes in history. After sizzling in a pan for a few minutes under the watchful eye of a chef, the burger was served to two preselected tasters—a nutrition scientist and a food writer. Their verdict, “like meat” but “not that juicy”, did not perturb Mark Post of Maastricht University, who grew the beef. In fact, Dr Post, who also savored some of his creation (and is pictured holding it), had every reason to call it “a good start”.

Besides powdered egg and breadcrumbs (for binding) and beetroot juice and saffron (to enhance color), the patty was composed entirely of cultured muscle cells. To make it, Dr Post began with stem cells taken from two live cows (a Blanc Bleu Belge and a Blonde d’Aquitaine). He multiplied these cells a trillion fold and then merged them into myotubes (in essence, artificial muscle fibers), each less than 3mm long. This done, he wrapped the myotubes around hubs of agarose, a gel-like polymer extracted from seaweed, and fed them a diet of amino acids, sugars and fats (all derived from plants) to make them big and strong.

Muscle cells’ natural tendency to contract and relax meant that the myotubes bulked themselves up into rings of muscle tissue through continual movement. When each ring had grown sufficiently (this took three months, which is, as Dr. Post points out, “faster than a cow”), he cut it free to create a strand. He used 20,000 of these strands to make the historic burger.

The result was a far cry from a Porterhouse or a fillet steak. Cultivating something like that would mean growing the cells into big three-dimensional structures—which would in turn entail delivering nutrients deep inside the tissue. To do so would require blood vessels or some artificial equivalent. A real steak would also contain fat cells, the absence of which explained the lack of juiciness. Such cells are harder to culture than muscle. Dr. Post and his team are working on both these points.

Carnivores should cheer. The world’s appetite for meat is forecast to rise by 70% by 2050. Nearly a third of the world’s ice-free land is already used to raise livestock or grow fodder for these animals. Without a radical technological shift the new demand will be hard to satisfy. Vegetarians, too, have reason to egg Dr. Post on. A single sample of stem cells could, he reckons, yield 20,000 tons of “cultured beef”. This is enough to make 175m quarter-pounders, a number that would require 440,000 cattle to be slaughtered.

In addition, animal husbandry is responsible for 18% of the world’s greenhouse-gas emissions, since cattle produce prodigious quantities of methane—a gas whose warming potential is 20 times that of carbon dioxide’s over the course of a century. Growing meat in factories would help reduce these emissions. And if home-based meat kits eventually became available, it would give a whole new meaning to the phrase “hand-reared”.

Standing Orders: Real Science Lies Behind the Fad for Standing Up at Work

The Economist Magazine – Science and Technology – Aug 10th 2013

WINSTON CHURCHILL knew it. Ernest Hemingway knew it. Leonardo da Vinci knew it. Every trendy office from Silicon Valley to Scandinavia now knows it too: there is virtue in working standing up. And not merely standing. The trendiest offices of all have treadmill desks, which encourage people to walk while working. It sounds like a fad. But it does have a basis in science.

Sloth is rampant in the rich world. A typical car-driving, television-watching cubicle slave would have to walk an extra 19km a day to match the physical-activity levels of the few remaining people who still live as hunter-gatherers. Though all organisms tend to conserve energy when possible, evidence is building up that doing it to the extent most Westerners do is bad for you—so bad that it can kill you.

That, by itself, may not surprise. Health ministries have been nagging people for decades to do more exercise. What is surprising is that prolonged periods of inactivity are bad regardless of how much time you also spend on officially approved high-impact stuff like jogging or pounding treadmills in the gym. What you need as well, the latest research suggests, is constant low-level activity. This can be so low-level that you might not think of it as activity at all. Even just standing up counts, for it invokes muscles that sitting does not.

Researchers in this field trace the history of the idea that standing up is good for you back to 1953, when a study published in the Lancet found that bus conductors, who spend their days standing, had a risk of heart attack half that of bus drivers, who spend their shifts on their backsides. But as the health benefits of exercise and vigorous physical activity began to become clear in the 1970s, says David Dunstan, a researcher at the Baker IDI Heart & Diabetes Institute in Melbourne, Australia, interest in the effects of low-intensity activity—like walking and standing—waned.

Over the past few years, however, interest has waxed again. A series of epidemiological studies, none big enough to be probative, but all pointing in the same direction, persuaded Emma Wilmot of the University of Leicester, in Britain, to carry out a meta-analysis. This is a technique that combines diverse studies in a statistically meaningful way. Dr Wilmot combined 18 of them, covering almost 800,000 people, in 2012 and concluded that those individuals who are least active in their normal daily lives are twice as likely to develop diabetes as those who are most active. She also found that the immobile are twice as likely to die from a heart attack and two-and-a-half times as likely to suffer cardiovascular disease as the most ambulatory. Crucially, all this seemed independent of the amount of vigorous, gym-style exercise that volunteers did.

Correlation is not, of course, causation. But there is other evidence suggesting inactivity really is to blame for these problems. One exhibit is the finding that sitting down and attending to a task—anything from watching television to playing video games to reading—serves to increase the amount of calories people eat without increasing the quantity that they burn. Why that should be is unclear—as is whether low-level exercise like standing would deal with the snacking.

A different set of studies suggests that simple inactivity by itself—without any distractions like TV or reading—causes harm by altering the metabolism. One experiment, in which rats were immobilized for a day (not easy; the researchers had to suspend the animals’ hind legs to keep them still) found big falls in the amount of fats called triglycerides taken up by their skeletal muscles. This meant the triglycerides were available to cause trouble elsewhere. The rats’ levels of high-density lipoprotein (HDL) fell dramatically as well. HDL is a way of packaging cholesterol, and low levels of it promote heart disease. Other studies have shown the activity of lipoprotein lipase—an enzyme that regulates levels of triglycerides and HDL—drops sharply after just a few hours of inactivity, and that sloth is accompanied by changes in the activity levels of over 100 genes.

Papers which focus on people rather than laboratory animals have found similar effects. Happily, this research also suggests the changes can be reversed by small amounts of fairly relaxed activity. A study published last year by Dr Dunstan found that breaking up prolonged periods of sitting with two minutes of walking every 20 minutes made a big difference. After feeding his volunteers a sugary meal, he discovered that people who had been walking in this way had blood-glucose levels almost 30% lower than those of people who had remained seated.

For some scientists, this combination of epidemiology, animal experiments and human trials suggests that light-to-moderate exercise—standing up, walking around and the like—is something qualitatively different from an energetic, high-intensity workout. But not everyone is convinced. Many of the human studies are small-scale. (Dr. Dunstan’s paper, for example, involved just 19 participants.) And not every study that has gone looking for the ill effects of inactivity has found them.

Still, the potential size of the problem means not everyone is prepared to wait for definitive proof. Sellers of standing desks are, naturally, jumping on the latest research findings to advertise their wares. And it is surely only a matter of time before the first law suit from a sickly cubicle slave reaches court.

The Economist, Oct 19th 2013 

 

A SIMPLE idea underpins science: “trust, but verify”. Results should always be subject to challenge from experiment. That simple but powerful idea has generated a vast body of knowledge. Since its birth in the 17th century, modern science has changed the world beyond recognition, and overwhelmingly for the better.

But success can breed complacency. Modern scientists are doing too much trusting and not enough verifying—to the detriment of the whole of science, and of humanity.

What a load of rubbish

Even when flawed research does not put people’s lives at risk—and much of it is too far from the market to do so—it squanders money and the efforts of some of the world’s best minds. The opportunity costs of stymied progress are hard to quantify, but they are likely to be vast. And they could be rising.

One reason is the competitiveness of science. In the 1950s, when modern academic research took shape after its successes in the second world war, it was still a rarefied pastime. The entire club of scientists numbered a few hundred thousand. As their ranks have swelled, to 6m-7m active researchers on the latest reckoning, scientists have lost their taste for self-policing and quality control. The obligation to “publish or perish” has come to rule over academic life. Competition for jobs is cut-throat. Full professors in America earned on average $135,000 in 2012—more than judges did. Every year six freshly minted PhDs vie for every academic post. Nowadays verification (the replication of other people’s results) does little to advance a researcher’s career. And without verification, dubious findings live on to mislead.

Careerism also encourages exaggeration and the cherry-picking of results. In order to safeguard their exclusivity, the leading journals impose high rejection rates: in excess of 90% of submitted manuscripts. The most striking findings have the greatest chance of making it onto the page. Little wonder that one in three researchers knows of a colleague who has pepped up a paper by, say, excluding inconvenient data from results “based on a gut feeling”. And as more research teams around the world work on a problem, the odds shorten that at least one will fall prey to an honest confusion between the sweet signal of a genuine discovery and a freak of the statistical noise. Such spurious correlations are often recorded in journals eager for startling papers. If they touch on drinking wine, going senile or letting children play video games, they may well command the front pages of newspapers, too.

Conversely, failures to prove a hypothesis are rarely even offered for publication, let alone accepted. “Negative results” now account for only 14% of published papers, down from 30% in 1990. Yet knowing what is false is as important to science as knowing what is true. The failure to report failures means that researchers waste money and effort exploring blind alleys already investigated by other scientists.

The hallowed process of peer review is not all it is cracked up to be, either. When a prominent medical journal ran research past other experts in the field, it found that most of the reviewers failed to spot mistakes it had deliberately inserted into papers, even after being told they were being tested.

If it’s broke, fix it

All this makes a shaky foundation for an enterprise dedicated to discovering the truth about the world. What might be done to shore it up? One priority should be for all disciplines to follow the example of those that have done most to tighten standards. A start would be getting to grips with statistics, especially in the growing number of fields that sift through untold oodles of data looking for patterns. Geneticists have done this, and turned an early torrent of specious results from genome sequencing into a trickle of truly significant ones.

Ideally, research protocols should be registered in advance and monitored in virtual notebooks. This would curb the temptation to fiddle with the experiment’s design midstream so as to make the results look more substantial than they are. (It is already meant to happen in clinical trials of drugs, but compliance is patchy.) Where possible, trial data also should be open for other researchers to inspect and test.

The most enlightened journals are already becoming less averse to humdrum papers. Some government funding agencies, including America’s National Institutes of Health, which dish out $30 billion on research each year, are working out how best to encourage replication. And growing numbers of scientists, especially young ones, understand statistics. But these trends need to go much further. Journals should allocate space for “uninteresting” work, and grant-givers should set aside money to pay for it. Peer review should be tightened—or perhaps dispensed with altogether, in favour of post-publication evaluation in the form of appended comments. That system has worked well in recent years in physics and mathematics. Lastly, policymakers should ensure that institutions using public money also respect the rules.

Science still commands enormous—if sometimes bemused—respect. But its privileged status is founded on the capacity to be right most of the time and to correct its mistakes when it gets things wrong. And it is not as if the universe is short of genuine mysteries to keep generations of scientists hard at work. The false trails laid down by shoddy research are an unforgivable barrier to understanding.

Toward the end of “The Sports Gene” (Penguin/Current), David Epstein makes his way to a remote corner of Finland to visit a man named Eero Mäntyranta. Mäntyranta lives in a small house next to a lake, among the pine and spruce trees north of the Arctic Circle. He is in his seventies. There is a statue of him in the nearby village. “Everything about him has a certain width to it,” Epstein writes. “The bulbous nose in the middle of a softly rounded face. His thick fingers, broad jaw, and a barrel chest covered by a red knit sweater with a stern-faced reindeer across the middle. He is a remarkable-looking man.” What’s most remarkable is the color of his face. It is a “shade of cardinal, mottled in places with purple,” and evocative of “the hue of the red paint that comes from this region’s iron-rich soil.”

Mäntyranta carries a rare genetic mutation. His DNA has an anomaly that causes his bone marrow to overproduce red blood cells. That accounts for the color of his skin, and also for his extraordinary career as a competitive cross-country skier. In cross-country skiing, athletes propel themselves over distances of ten and twenty miles—a physical challenge that places intense demands on the ability of their red blood cells to deliver oxygen to their muscles. Mäntyranta, by virtue of his unique physiology, had something like sixty-five per cent more red blood cells than the normal adult male. In the 1960, 1964, and 1968 Winter Olympic Games, he won a total of seven medals—three golds, two silvers, and two bronzes—and in the same period he also won two world-championship victories in the thirty-kilometre race. In the 1964 Olympics, he beat his closest competitor in the fifteen-kilometre race by forty seconds, a margin of victory, Epstein says, “never equaled in that event at the Olympics before or since.”

In “The Sports Gene,” there are countless tales like this, examples of all the ways that the greatest athletes are different from the rest of us. They respond more effectively to training. The shape of their bodies is optimized for certain kinds of athletic activities. They carry genes that put them far ahead of ordinary athletes.

Epstein tells the story of Donald Thomas, who on the seventh high jump of his life cleared 7′ 3.25″—practically a world-class height. The next year, after a grand total of eight months of training, Thomas won the world championships. How did he do it? He was blessed, among other things, with unusually long legs and a strikingly long Achilles tendon—ten and a quarter inches in length—which acted as a kind of spring, catapulting him high into the air when he planted his foot for a jump. (Kangaroos have long tendons as well, Epstein tells us, which is what gives them their special hop.)

Why do so many of the world’s best distance runners come from Kenya and Ethiopia? The answer, Epstein explains, begins with weight. A runner needs not just to be skinny but—more specifically—to have skinny calves and ankles, because every extra pound carried on your extremities costs more than a pound carried on your torso. That’s why shaving even a few ounces off a pair of running shoes can have a significant effect. Runners from the Kalenjin tribe, in Kenya—where the majority of the country’s best runners come from—turn out to be skinny in exactly this way. Epstein cites a study comparing Kalenjins with Danes; the Kalenjins were shorter and had longer legs, and their lower legs were nearly a pound lighter. That translates to eight per cent less energy consumed per kilometre. (For evidence of the peculiar Kalenjin lower leg, look up pictures of the great Kenyan miler Asbel Kiprop, a tall and elegant man who runs on what appear to be two ebony-colored pencils.) According to Epstein, there’s an evolutionary explanation for all this: hot and dry environments favor very thin, long-limbed frames, which are easy to cool, just as cold climates favor thick, squat bodies, which are better at conserving heat.

What we are watching when we watch élite sports, then, is a contest among wildly disparate groups of people, who approach the starting line with an uneven set of genetic endowments and natural advantages. There will be Donald Thomases who barely have to train, and there will be Eero Mäntyrantas, who carry around in their blood, by dumb genetic luck, the ability to finish forty seconds ahead of their competitors. Élite sports supply, as Epstein puts it, a “splendid stage for the fantastic menagerie that is human biological diversity.” The menagerie is what makes sports fascinating. But it has also burdened high-level competition with a contradiction. We want sports to be fair and we take elaborate measures to make sure that no one competitor has an advantage over any other. But how can a fantastic menagerie ever be a contest among equals?

During the First World War, the U.S. Army noticed a puzzling pattern among the young men drafted into military service. Soldiers from some parts of the country had a high incidence of goitre—a lump on their neck caused by the swelling of the thyroid gland. Thousands of recruits could not button the collar of their uniform. The average I.Q. of draftees, we now suspect, also varied according to the same pattern. Soldiers from coastal regions seemed more “normal” than soldiers from other parts of the country.

The culprit turned out to be a lack of iodine. Iodine is an essential micronutrient. Without it, the human brain does not develop normally and the thyroid begins to enlarge. And in certain parts of the United States in those years there wasn’t enough iodine in the local diet. As the economists James Feyrer, Dimitra Politi, and David Weil write, in a recent paper for the National Bureau of Economic Research:

Ocean water is rich in iodine, which is why endemic goiter is not observed in coastal areas. From the ocean, iodine is transferred to the soil by rain. This process, however, only reaches the upper layers of soil, and it can take thousands of years to complete. Heavy rainfall can cause soil erosion, in which case the iodine-rich upper layers of soil are washed away. The last glacial period had the same effect: iodine-rich soil was substituted by iodine-poor soil from crystalline rocks. This explains the prevalence of endemic goiter in regions that were marked by intense glaciation, such as Switzerland and the Great Lakes region.

After the First World War, the U.S. War Department published a report called “Defects Found in Drafted Men,” which detailed how the incidence of goitre varied from state to state, with rates forty to fifty times as high in places like Idaho, Michigan, and Montana as in coastal areas.

The story is not dissimilar from Epstein’s account of Kenyan distance runners, in whom accidents of climate and geography combine to create dramatic differences in abilities. In the early years of the twentieth century, the physiological development of American children was an example of the “fantastic menagerie that is human biological diversity.”

In this case, of course, we didn’t like the fantastic menagerie. In 1924, the Morton Salt Company, at the urging of public-health officials, began adding iodine to its salt, and initiated an advertising campaign touting its benefits. That practice has been applied successfully in many developing countries in the world: iodine supplementation has raised I.Q. scores by as much as thirteen points—an extraordinary increase. The iodized salt in your cupboard is an intervention in the natural order of things. When a student from the iodine-poor mountains of Idaho was called upon to compete against a student from iodine-rich coastal Maine, we thought of it as our moral obligation to redress their natural inequality. The reason debates over élite performance have become so contentious in recent years, however, is that in the world of sport there is little of that clarity. What if those two students were competing in a race? Should we still be able to give the naturally disadvantaged one the equivalent of iodine? We can’t decide.

Eyesight can be improved—in some cases dramatically—through laser surgery or implantable lenses. Should a promising young baseball player cursed with normal vision be allowed to get that kind of corrective surgery? In this instance, Major League Baseball says yes. Major League Baseball also permits pitchers to replace the ulnar collateral ligament in the elbow of their throwing arm with a tendon taken from a cadaver or elsewhere in the athlete’s body. Tendon-replacement surgery is similar to laser surgery: it turns the athlete into an improved version of his natural self.

But when it comes to drugs Major League Baseball—like most sports—draws the line. An athlete cannot use a drug to become an improved version of his natural self, even if the drug is used in doses that are not harmful, and is something that—like testosterone—is no more than a copy of a naturally occurring hormone, available by prescription to anyone, virtually anywhere in the world.

Baseball is in the middle of one of its periodic doping scandals, centering on one of the game’s best players, Alex Rodriguez. Rodriguez is among the most disliked players of his generation. He tried to recover from injury and extend his career through illicit means. (He has appealed his recent suspension, which was based on these allegations.) It is hard to think about Rodriguez, however, and not think about Tommy John, who, in 1974, was the first player to trade in his ulnar collateral ligament for an improved version. John used modern medicine to recover from injury and extend his career. He won a hundred and sixty-four games after his transformation, far more than he did before science intervened. He had one of the longest careers in baseball history, retiring at the age of forty-six. His bionic arm enabled him to win at least twenty games a season, the benchmark of pitching excellence. People loved Tommy John. Maybe Alex Rodriguez looks at Tommy John—and at the fact that at least a third of current major-league pitchers have had the same surgery—and is genuinely baffled about why baseball has drawn a bright moral line between the performance-enhancing products of modern endocrinology and those offered by orthopedics.

The other great doping pariah is Lance Armstrong. He apparently removed large quantities of his own blood and then re-infused himself before competition, in order to boost the number of oxygen-carrying red blood cells in his system. Armstrong wanted to be like Eero Mäntyranta. He wanted to match, through his own efforts, what some very lucky people already do naturally and legally. Before we condemn him, though, shouldn’t we have to come up with a good reason that one man is allowed to have lots of red blood cells and another man is not?

“I’ve always said you could have hooked us up to the best lie detectors on the planet and asked us if we were cheating, and we’d have passed,” Lance Armstrong’s former teammate Tyler Hamilton writes in his autobiography, “The Secret Race” (co-written with Daniel Coyle; Bantam). “Not because we were delusional—we knew we were breaking the rules—but because we didn’t think of it as cheating. It felt fair to break the rules.”

“The Secret Race” deserves to be read alongside “The Sports Gene,” because it describes the flip side of the question that Epstein explores. What if you aren’t Eero Mäntyranta?

Hamilton was a skier who came late to cycling, and he paints himself as an underdog. When he first met Armstrong—at the Tour DuPont, in Delaware—he looked around at the other professional riders and became acutely conscious that he didn’t look the part. “You can tell a rider’s fitness by the shape of his ass and the veins in his legs, and these asses were bionic, smaller and more powerful than any I’d ever seen,” he writes. The riders’ “leg veins looked like highway maps. Their arms were toothpicks. . . . They were like racehorses.” Hamilton’s trunk was oversized. His leg veins did not pop. He had a skier’s thighs. His arms were too muscled, and he pedalled with an ungainly “potato-masher stroke.”

When Hamilton joined Armstrong on the U.S. Postal Service racing team, he was forced to relearn the sport, to leave behind, as he puts it, the romantic world “where I used to climb on my bike and simply hope I had a good day.” The makeover began with his weight. When Michele Ferrari, the key Postal Service adviser, first saw Hamilton, he told him he was too fat, and in cycling terms he was. Riding a bicycle quickly is a function of the power you apply to the pedals divided by the weight you are carrying, and it’s easier to reduce the weight than to increase the power. Hamilton says he would come home from a workout, after burning thousands of calories, drink a large bottle of seltzer water, take two or three sleeping pills—and hope to sleep through dinner and, ideally, breakfast the following morning. At dinner with friends, Hamilton would take a large bite, fake a sneeze, spit the food into a napkin, and then run off to the bathroom to dispose of it. He knew that he was getting into shape, he says, when his skin got thin and papery, when it hurt to sit down on a wooden chair because his buttocks had disappeared, and when his jersey sleeve was so loose around his biceps that it flapped in the wind. At the most basic level, cycling was about physical transformation: it was about taking the body that nature had given you and forcibly changing it.

Hematocrit, the last of those variables, was the number they cared about most. It refers to the percentage of the body’s blood that is made up of oxygen-carrying red blood cells. The higher the hematocrit, the more endurance you have. (Mäntyranta had a very high hematocrit.) The paradox of endurance sports is that an athlete can never work as hard as he wants, because if he pushes himself too far his hematocrit will fall. Hamilton had a natural hematocrit of forty-two per cent—which is on the low end of normal. By the third week of the Tour de France, he would be at thirty-six per cent, which meant a six-per-cent decrease in his power—in the force he could apply to his pedals. In a sport where power differentials of a tenth of a per cent can be decisive, this “qualifies as a deal breaker.”

For the members of the Postal Service squad, the solution was to use the hormone EPO and blood transfusions to boost their hematocrits as high as they could without raising suspicion. (Before 2000, there was no test for EPO itself, so riders were not allowed to exceed a hematocrit of fifty per cent.) Then they would add maintenance doses over time, to counteract the deterioration in their hematocrit caused by races and workouts. The procedures were precise and sophisticated. Testosterone capsules were added to the mix to aid recovery. They were referred to as “red eggs.” EPO (a.k.a. erythropoietin), a naturally occurring hormone that increases the production of red blood cells, was Edgar—short for Edgar Allan Poe. During the Tour de France, and other races, bags of each rider’s blood were collected in secret locations at predetermined intervals, then surreptitiously ferried from stage to stage in refrigerated containers for strategic transfusions. The window of vulnerability after taking a drug—the interval during which doping could be detected—was called “glowtime.” Most riders who doped (and in the Armstrong era, it now appears, nearly all the top riders did) would take two thousand units of Edgar subcutaneously every couple of days, which meant they “glowed” for a dangerously long time. Armstrong and his crew practiced microdosing, taking five hundred units of Edgar nightly and injecting the drug directly into the vein, where it was dispersed much more quickly.

Link to Original Story:

http://www.newyorker.com/arts/critics/atlarge/2013/09/09/130909crat_atlarge_gladwell