On April 20, 1994, three cyclists from the Italian Gewiss-Ballan team made a mockery of the pro peloton with 30 miles remaining in the 127-mile Belgian classic La Flèche Wallonne. Entering the center of Huy, a city of 14th-century churches and cobbled squares straddling a languid loop in the Meuse River, the field jolted onto the precipitous Chemin des Chapelles, also known as the Mur de Huy. As the road headed up, Moreno Argentin, Giorgio Furlan, and Evgeni Berzin flicked their shifters into gears that only they possessed. By the top of the 1.3-kilometer climb, the trio had a 14-second gap on the field. The peloton never saw them again. After a 30-mile final loop through the rolling Ardennes countryside, the Gewiss-Ballan trio started their final climb to the finish atop the Mur de Huy. There was no need for them to send a fleeting prayer for victory toward one of the ascent’s six roadside chapels; Argentin won with Furlan and Berzin taking second and third. The trio’s nearest competitor, 1991 and 1992 road world champion Gianni Bugno, rolled in 1:14 later. Two and a half minutes drained from the clock before 1993 world champion Lance Armstrong finished.
Even before the Gewiss-Ballan threesome crossed the finish line, fans and riders were suspicious. Pull up the race on YouTube and you’ll see why. It is a show of effortless, inhuman domination. When the teammates attack, they float away with a fluid animation a universe apart from the bobbing and heaving field gasping behind. That spring day in Belgium broadcast the awesome, performance-enhancing potential of EPO.
Following the race, a French sportswriter named Jean-Michel Rouet spoke to the Gewiss-Ballan team’s Italian doctor, Michele Ferrari. The physician was rumored to be a keen proponent of the relatively new blood-boosting anemia treatment drug, recombinant human erythropoietin, or EPO, and his riders’ unbelievable victory made Rouet eager to pin down the Italian. Reporting on their encounter in the April 22, 1994, issue of the French sports daily L’Équipe, Rouet raised the widely accepted rumor that EPO had caused a rash of Dutch cyclists to die in their sleep. Referring to events that many accepted but none stopped to challenge, Rouet all but accused Ferrari of trying to kill athletes. “A dozen Dutch riders died a few years ago,” the journalist asserted. When Ferrari demurred, Rouet pressed on. “In any case, it is dangerous!” he said.
Ferrari would have none of it. “EPO is not dangerous,” he retorted. “Its abuse is.” Ferrari then added, “It is also dangerous to drink ten liters of orange juice.”
Ferrari was a protégé of Italian blood-doping pioneer Francesco Conconi—a man whose groundbreaking research into autologous blood boosting helped Francesco Moser shatter the hour record in 1984. For most reading this exchange, Ferrari’s response to Rouet’s interrogation immediately became evidence of the doctor’s cavalier attitude toward anti-doping laws. When growing moralism about drug use in sport was superimposed upon Ferrari’s statement of fact—EPO isn’t dangerous, its abuse is—the Italian’s willingness to challenge hardened anti-doping orthodoxies also became a sign of moral treachery. Sure, orange juice was benign, but just pick up a newspaper or cycling magazine and you’d see—EPO was a killer set loose among the peloton.
Ferrari became a poster boy for the mortal dangers of EPO and its distributors. While the Dutch riders Rouet referred to were never conclusively linked to death by EPO, the fabrication served a larger anti-doping moral agenda and the missionary effort to impose purity on sport. After the IOC expanded its definition of performance-enhancing substances and took a more aggressive approach to doping in response to the 1984 Olympic blood-boosting scandal, the characterization of sports doping as a plague gained speed. As historian Paul Dimeo explains, through the 1980s, “the construction of doping as an evil, a plague, a cancer or a temptation” was kept alive by the myth that sports were inherently good and drugs were a corrupting temptation that had to be beat out of the athletic garden of Eden. By daring to speak the truth about a drug—that under a doctor’s supervision, it is safe—Ferrari fell short of the newly emboldened anti-doping evangelists. Pointing out that Ferrari was correct would have been to spit in the soup of anti-doping outrage that was becoming a nurturing broth for journalists and anti-doping administrators alike.
Three years before Lance Armstrong finished La Flèche Wallonne over two minutes down on the Ferrari-charged trio, on May 19, 1991, the New York Times startled readers with news of a killer stalking the roadways and velodromes of Europe. “A genetically engineered drug that was created for people suffering from kidney failure has become the latest substance to be abused by athletes seeking enhanced stamina and performance,” Times journalist Lawrence Fisher reported. “The consequences, in some cases, may be deadly.” Ominously titled “Stamina-Building Drug Linked to Athletes’ Deaths,” the piece connected the death of 18 European pro cyclists over a four-year period to EPO. Although the Times headline gripped readers by their lapels and yanked them into the dirty world of European pro cycling, the story’s claim that the drug was responsible for 18 cyclist deaths was based on speculation. EPO can theoretically cause stroke, hypertension, and myocardial infarction when used by dehydrated athletes, especially when taken without a doctor’s supervision. Evidence also suggests that the hormone may have an anti-inflammatory and tissue-repairing effect that can aid with recovery. What was not provable in 1991, or today, is that the drug killed a rash of cyclists.
The number of red blood cells, or erythrocytes, in our body is controlled by a feedback loop between an oxygen sensor in our kidneys and our bone marrow—the factory that produces blood cells. Erythrocytes don’t have a nucleus and can’t repair themselves. After about 120 days of service, they are shot, and the spleen shuffles these red blood cells out of circulation at a rate of 2 to 3 million erythrocytes per second. Like a manager calling down to the production line when a new order for widgets comes across his desk, when the kidneys sense that our red-blood-cell count is getting low (our hematocrit level), EPO signals the bone marrow to crank up blood cell production. Stem cells start a chain of sequential divisions that eventually results in fresh new erythrocytes eager to cart oxygen to our muscles for four months. A hormone, erythropoietin, works as the middleman in this process; it binds with blood-cell receptors and triggers the creation of erythrocytes.
Like a second temporary factory manager who suddenly appears on the floor with a megaphone and starts barking out orders for more product, when a doctor injects synthetic EPO into your body, the artificial hormone tricks the stem cells in the bone marrow into creating more red blood cells. It can be a life-saving event when natural erythropoietin levels wane due to pathologies like bone marrow cancer or kidney failure.
This process also works in healthy people, only instead of fooling an ailing body into boosting its flagging red-blood-cell count back up to normal, injecting EPO into a healthy human causes the bone marrow to produce more red blood cells than are normally needed. The resulting surplus of these oxygen-carrying cells can increase endurance by as much as 10 percent. The ideal adult hematocrit percentage varies between individuals and genders, but it is generally in the 40 to 54 percent range at sea level, and about 5 percent higher than that for people who live at altitude. When athletes figured out that exogenous EPO could juice their red-blood-cell count, they got the same performance-enhancing benefit as living at altitude or sleeping in a hypoxic chamber. Describing the effect of EPO on his performance, cyclist Tyler Hamilton said in his 2012 book, The Secret Race, “That holy place at the edge of your limits gets edged out—and not just a little.”
Although endurance athletes probably began experimenting with this new synthetic hormone during the drug’s clinical trials in 1986, its use as a potential performance enhancer was first recognized in the early 1950s. Beginning in 1953, a University of Chicago biochemist named Eugene Goldwasser set about understanding how the human body created and regulated red blood cells. Solving this problem had tremendous life-saving potential. Inventing a way to artificially replace the body’s EPO would be a boon for millions of patients affected by kidney failure. After three decades of research, Goldwasser isolated the erythropoietin gene, thereby opening the door to its synthesis.
In his autobiography, A Bloody Long Journey, Goldwasser recalls that not long after he began his 1953 investigations, a man with racehorses to sell came looking for equine EPO. Horses that ran faster and longer commanded premium prices, and the horseman wanted to inject his stock with EPO to increase their performance in claiming races—events where horses are sold based on their placings. As Goldwasser recalls, “He had done his homework and knew that for short races, increasing red cells was no help . . . but in longer races, having a bigger erythron [red-blood-cell count] was an advantage.”
Buckets of horse blood soon began showing up on Goldwasser’s doorstep. Although Goldwasser never extracted enough pure EPO from the blood to test its sporting efficacy, he, like the racing entrepreneur, saw the performance-enhancing potential in the blood-regulating hormone in the early 1950s. When Goldwasser’s lab finally isolated the EPO gene in the early 1980s, an infant biotech startup called Applied Molecular Genetics approached him, and Goldwasser began sharing his three decades of knowledge with the company that would later rename itself Amgen. The company was funded by Montgomery Securities, an investment bank founded by Lance Armstrong’s U.S. Postal Service team backer Thomas Weisel.
Amgen finally cloned EPO in November 1983, opening the door to industrial scale production of a synthetic version of the hormone under the name Epogen. It also licensed the patent to Johnson & Johnson, which sold its EPO as Procrit. The startup exploded into a pharmaceutical giant worth over $100 billion today. By 2006, annual EPO sales were $13 billion worldwide. After Amgen went public in 1983, the company generated a stock-market windfall that seed investor and dedicated cyclist Weisel would later use to fund pro bike racing teams and pay for his own personalized coaching by Eddie Borysewicz.
The spectacular rise of Amgen and its miracle drug coincided with what appeared to be a rash of mysterious deaths among endurance athletes. Echoing claims made in other general news and cycling-specific publications, a May 1991 New York Times article concluded that EPO’s development came too close to a glut of pro cyclist funerals to be mere coincidence. The piece described the mysterious death of Dutch pro Johannes Draaijer, who passed away in his sleep in 1990 at the age of 27. A caption beneath a photo of Draaijer read, “Mr. Draaijer’s widow believes that the drug recombinant erythropoietin was involved with his death.” A pull quote declared, “You just don’t get 18 deaths in 4 years, mysteriously.” The story left the impression that the new life-saving anemia drug played double duty as an indiscriminate athlete killer.
EPO deaths made for good news stories, even if there was no autopsy evidence that EPO was actually killing cyclists. However, the New York Times knew the connection between EPO and the apparent boomlet in dead cyclists was speculative, and admitted so a week later. Backtracking, the Times ran a correction: “A picture caption last Sunday with an article about a stamina-building drug linked to athletes’ deaths misstated what is known about the death of the Dutch cyclist Johannes Draaijer. An autopsy did not specify the cause, and it is not known conclusively whether he had used the drug.” Despite the correction, the rumor was already set: EPO was a new drug of athlete destruction.
If you take a lot of EPO without a doctor’s supervision, in theory you can kill yourself. As University of Oklahoma chief of hematology Dr. Randy Eichner explained in the Times piece, increasing red-blood-cell count can thicken blood. Take too much EPO and “pretty soon you have mud instead of blood; then you have trouble.” The results can be blood clotting, stroke, or heart failure. The Times also cited Ed Burke, the USCF physiologist who oversaw the 1984 Olympic cycling team’s blood boosting. “EPO can do wonders for your aerobic capacity,” Burke noted, before warning, “The problem is, it can also kill you.”
By sensationalizing the potentially deadly effects of EPO without reporting any evidence for a correlation with actual events, the New York Times seemed to be taking up the role of an anti-doping missionary whose conclusions are based on faith rather than evidence. Under a hematologist’s expert care, EPO is safe. The drug saves thousands of lives every year. Yet because this drama-killing statement of fact contradicted the sensationalist thrust of a story about a scary new athlete killer, that is not the story that snowballed in the press.
In a New England Journal of Medicine (NEJM) article on the therapeutic uses of EPO published on May 9, 1991, 10 days before the Times piece, hematologist Dr. Allan Erslev wrote that erythropoietin “appears to be almost nontoxic.” Born in Denmark, Erslev graduated from medical school in 1945 and then traveled to the United States to conduct postgraduate research at Yale and at New York’s Sloan Kettering Institute. Testing anemic rabbits in the early 1950s, Erslev was one of the first to identify the blood-regulating effect of EPO. In his 1991 NEJM piece, Erslev theorized that since EPO seemed to be nontoxic, it was viable for elective surgery patients who were concerned about contracting AIDS from donated blood. At a time when the blood-borne autoimmune-deficiency disease dominated headlines, surgery patents were afraid to use anonymously donated blood from blood banks. To eliminate the perceived risk, patients stored their own blood in advance of surgery. However, this blood banking created the problem of already sick or injured patients making themselves anemic in advance of surgery. Using America’s most esteemed medical journal to broadcast his message, Erslev told the surgical community that by using EPO, patients could safely extract and store more blood than was otherwise recommended without suffering a lower hematocrit level. With EPO therapies, “the number of donations could undoubtedly be increased,” he advised.
EPO deaths made for good news stories, even if there was no autopsy evidence that EPO was actually killing cyclists.
Erslev also wondered whether EPO could have a role as a rehabilitative therapy for endurance athletes. In 1991—the midst of the popular press’s EPO-kills-cyclists panic—Erslev asked if “athletes engaged in exhausting long-distance events such as swimming, running, bicycle racing, or cross-country skiing would benefit from a moderate rise in hematocrit and red-cell mass.” Since many world-class athletes were already anemic because their training regimes increased plasma volume and thereby diluted red-cell density, Erslev seemed to posit that the use of EPO as a sports medicine recovery therapy would merit further investigation.
As for EPO dangers, Erslev postulated that the combination of lower blood volume from dehydration and higher hematocrit from EPO “would increase blood viscosity and be not only detrimental to muscular action but also the cause of possible life-threatening thrombosis.” In other words, an athlete would be both slower and more likely to die from a blood clot in the brain. While Erslev did not have studies to prove it, in theory, it would seem that EPO would both decrease muscle performance and potentially thicken blood to the point that it might kill you. In spite of these theoretical complications, Erslev reported that the studies he had run indicated that the blood-clot problem was “quite sporadic” and in some clinical tests “nonexistent.”
Ten days after the publication of Erslev’s article, news sources were calling the sports world to EPO panic stations. On July 14, 1991, Britain’s Independent ran a piece with a stretched-out title worthy of its endurance topic: “Cyclists Don’t Die Like This; Cycle Racing Gets Tough—and Sometimes Racers Die: But on the Track, Not at Home, in Bed, in Their Prime. Not 18 of Them. So Were They Abusing a Billion-Dollar Wonder Drug?” The piece began with a vignette of Draaijer’s wife, Lisa, waking up to a gurgling sound—her husband’s death rattle. It then listed other cyclists who had passed away, including Dutch pro Ruud Brouwers who fell out of bed and died on May 3, 1989, and Dutch amateur Connie Meijer, dead after abandoning a criterium on August 17, 1988. Heart failure had killed 18 cyclists in all, the Independent claimed.
The Independent writer rang up retired 1970s Dutch pro Henk Vogels at his home in Australia. Vogels told the journalist, “Half the people I cycled with are now dead. They often die in their early forties after 15 years of taking stuff and going all out.” In the same piece, 1984 U.S. Olympic cycling team doctor Ed Burke warned UK readers that EPO abuse “raises the red-cell count to the point where it turns the blood into sludge.”
A decade later, Burke died of a sudden heart attack while cycling near his Colorado Springs home, a victim of sudden cardiac failure, the number-one killer of athletes. Burke was 53. While no one blamed his death on dope, in the early 1990s, both Burke and the journalists who quoted him were quick to pin the cardiac failure of 18 cyclists on EPO. These pieces came at such a fast pace that a supposition became received wisdom: EPO is a mass killer.
Even the Sporting News, a magazine that usually keeps its nose pointed firmly in the direction of stick-and-ball sports, got on the EPO-kills bandwagon, writing in a 2004 piece titled “Cycling’s Deadly Downward Spiral” that “death is yet the unseen rider in world-class cycling.” The story cited the death of nine riders due to heart failure between January 11, 2003, and June 30, 2004, including “one in a dentist’s chair.” The piece also referred its readers to the death of Italian superstar cyclist Marco Pantani in 2004. Though Pantani’s autopsy singled out a cocaine overdose as the cause of death, that did not stop the Sporting News from attaching its amplifier to the common speculation: “Some cyclists believe he died as the other eight did—of heart failure prompted by use of EPO.”
On January 29, 2004, the Sydney Morning Herald described soccer players who had mysteriously died on the pitch. Although none of the players’ autopsies indicated EPO as a cause of death, the Australian paper did not let medical records get in the way of a growing fiction. It promptly made the EPO connections that coroners did not. Citing a French investigation into doping by the Cofidis cycling team, the paper wrote, “Perhaps the soccer authorities should start an inquiry into these supposed unrelated deaths.”
Marathoners also got their moment in the EPO-kills glare. “Fear on the Marathon Starting Line,” blared an April 22, 2001, piece in Scotland’s Sunday Herald. It asserted that the top runners in that year’s London Marathon were wondering whether their days on Earth were so numbered that they would not have time to spend their appearance fees. The reason? EPO. Spanish marathoner Sergio García had died earlier that year at the age of 39, and coaches and runners were abuzz with speculation that his death was related to EPO. “Garcia’s spectre has been stalking the corridors of the London Marathon race headquarters this week,” the paper whispered. The connection between García’s death and EPO was hypothetical, and yet by 2001, the EPO-kills myth was so hardened that newspapers could get away with publishing gossip in the guise of reporting.
Unlike the press, EPO-using athletes separated the true risks of EPO from myth. U.S. Postal Service team rider Tyler Hamilton started using the synthetic hormone in 1997. In his 2012 book The Secret Race, the American compared the risk of taking EPO to the damages he suffered while racing—a catalogue of smashed bones from nose to back to ribs. “Bike racing is not a healthy sport in any sense of the word,” Hamilton wrote, “so when it comes to the risks of EPO, they tend to feel pretty small.” In light of the actual clinical facts available in the 1990s that EPO and hypertension were “not related” in healthy patients and that the drug’s causation of blood clots was “quite sporadic” if not “nonexistent,” Hamilton’s response to the public perception of EPO danger was rational. As Erslev and the European and American drug regulators who approved Epogen and its variants indicated, under a doctor’s supervision, EPO was safe. And as Hamilton pointed out, the risk of doctor-supervised EPO use was especially slight compared to the nearly 100 percent statistical chance that a rider would suffer multiple, and sometimes life-threatening, injuries while racing on Europe’s narrow roads.
Spanish scholar Bernat López researched how EPO was transformed from a life-saving miracle hormone into what he calls a “drug of mass destruction.” Although no evidence exists to support the claim that EPO caused any of the cyclists’ deaths in the early 1990s, López’s research led him to conclude that the rumor had ossified into received wisdom through media repetition. The fiction served as propaganda that made it professionally and personally suicidal to challenge the morality and righteousness of the antidrug movement.
As López sees it, the story of EPO killing loads of cyclists became a “flagship myth” for anti-doping interests. It was a story manufactured and spread by the press with the intent of scaring athletes. López, a professor at the Universitat Rovira i Virgili in Catalonia, also argues that because the general public is largely indifferent to the drug-regulating policies that are the bedrock of anti-doping organizations, anti-doping missionaries played up the deadly EPO myth as a way to gain sympathy from a public that has an otherwise insatiable appetite for legal and illegal performance- and lifestyle-enhancing drugs.
When López ran a meta-analysis of 36 academic texts that referenced the EPO deaths as evidence of the danger of EPO, he discovered a scholarly train wreck. All the articles either referred to no source for their EPO-deaths claims or noted secondary resources that cited no source. As a result of this evidence-free conclusion making, academics came up with a shambolic number of EPO deaths, ranging from 5 to 20. The victims’ nationalities were also wildly inconsistent. While newspapers like the New York Times reported that the dead riders were Dutch, the academic researchers indicated that they hailed from Spain, Holland, Belgium, and Scandinavia. The deaths also took place during variable time frames ranging from “the 1980s and early 1990s” to “between 1997 and 2000,” to “1987 to 1991.”
López also looked at 20 academic texts that offered evidence against the claim that EPO killed a bunch of cyclists in the late 1980s and early 1990s. The articles commonly pointed to genetic heart defects as the most likely cause of the deaths. None of these studies cited EPO as a potential or actual cause. If the researchers behind the 20 papers came up with any one Grim Reaper haunting bike races and marathons around the world, it was the damaging effect of extreme and prolonged training. In sum, López concluded, the 20 studies he investigated “suggest that EPO is extremely unlikely to have had the effects that have been claimed in the speculation of anti-doping sports doctors, academics, and journalists.”
When López performed the same analysis of coverage in the popular press, he found an even bigger mess of chronology and nationality. News reports put the number of EPO “victims” anywhere from 7 to 40, from countries including Spain, Holland, Belgium, Germany, and Poland as well as generic “Europe.” Moreover, the articles cited athletes dying from EPO beginning in 1970, even though EPO was not produced for clinical trials until 1986.
When López broadened the scope of his search to include newspapers, magazines, blogs, and cycling websites for mentions of sudden deaths among cyclists between 1987 and early 2010, he found 49 cyclist sudden-death stories. In the time frame most often mentioned as ground zero for EPO deaths, 1987 to 1992, López unearthed news reports of 17 sudden deaths in Belgium, Holland, France, and the UK. These numbers are in line with the expected number of deaths from naturally occurring heart failures in athletes and the general population.
According to López’s research from 1995 to 2006, 180 athlete sudden deaths were reported in Spain alone—about 15 per year. Of that total, 39 deaths were cyclists and 40 were soccer players. In other words, whether the number of cyclist deaths in Europe in the early 1990s was 15, 17, 18, or 20, those numbers do not reflect a spike, but rather a death rate entirely consistent with normal athlete sudden-death statistics in a single European country and low for all of Europe combined.
Compared to sudden cardiac deaths in both the athletic and larger population, the “explosion” of cyclist deaths that supposedly came at the hand of EPO does not seem like an anomaly; that number of deaths is normal. The anomaly was the arrival of a new, highly effective doping product. Blinded by a rising anti-doping fervor, journalists and medical researchers alike seemed to have superimposed EPO onto normal death rates and created a crisis where there was little, if any, postmortem evidence to suggest a correlation between EPO and fatalities. Yet the ghosts of the mythical 18 cyclists still haunt us today. As recently as 2012, an academic review of scientific studies on the effectiveness and safety of erythropoietin mentions the possible link between EPO and “18 European professional cyclists [who] have died.”
The narrative about crime, death, and drugs was believable because—three years after the 1988 approval of EPO use in Europe—the story sounded logical. Athletes eager to win plus a potentially dangerous new drug equaled death. When I called López at his home south of Barcelona, he told me he has yet to find a scrap of hard evidence linking EPO with any cyclist’s death in the early 1990s. With the weary sigh of a man who had discovered a truth no one wanted to hear, he told me, “Science has not produced so far—at least to my knowledge—any conclusive evidence linking EPO with sudden death.” While dozens of papers continue to speculate about a link between EPO and the rash of Belgian and Dutch deaths, “they are just reproducing the myth,” López explained.
As López sees it, the role of the EPO deaths in the war on drugs in sport is analogous to the role fictional weapons of mass destruction played in the justification of the United States’ invasion of Iraq in 2003. “There was a war to be waged, and the people waging that war needed justification, an excuse, a solid reason,” he observed. Turning back to the EPO fiction, he said, “The best reason for waging that war is that doping kills. ‘We honest men, we must stop athletes from taking drugs because we are interested in saving their lives.’” By exaggerating and distorting the EPO story, the anti-doping establishment was able to predict a dire future. And a bleak tomorrow creates incentives for stronger, better-funded anti-doping measures while also spinning far more compelling media narratives.
In 1906, Olympic founder Pierre de Coubertin described the Olympic Games as a “program of moral purification.” This mission carries on today as an anti-doping errand in a chemically polluted sporting wilderness. For López, there is a link between the foundation of Olympic sports as a morally purifying, soul-cleansing experience and Olympic sports’ ongoing efforts to preserve what the WADA code formally labels the “spirit of sport.” “Well, actually,” López clarified for me, “they are interested in saving their souls, but they pretended that they were interested in saving their lives.”
My own search of medical literature finds plenty of warnings about the dangers of too much EPO. And there are many examples of pharmaceutical companies paying physicians kickbacks to overdose patients, a process that inadvertently accelerates the growth of deadly tumors. However, I found no documented instances of EPO killing already healthy humans, athletes or otherwise.
In December 2006, Danish researchers reported that 10 percent of a clinical trial group of 516 head and neck cancer patients on heavy EPO doses experienced accelerating tumor growth, even while undergoing radiation treatment. This confirmed studies going back to 2003, which also showed that EPO could boost cancer growth. And 10 years earlier, a 1996 study of dialysis patients was halted because patients on high EPO dosages suffered more heart attacks than a control group on lower amounts of EPO.
The deaths were not related to something that was inherently destructive about EPO. Instead, they were caused by overdosing. In 2007, Johnson & Johnson’s annual EPO sales were $3.5 billion, while Amgen moved $5.6 billion worth of the product. To attain these astronomical numbers, Amgen and Johnson & Johnson built incentive programs that financially rewarded doctors who administered heavy “off-label” doses of EPO to cancer and anemia patients. One West Coast office of six oncologists pocketed $2.7 million in incentives from Amgen in 2006 alone. The nationwide priming of the EPO pump led to a well-documented rash of heart attacks and carcinoma deaths in cancer and renal failure patients—so many that in 2007, the FDA released a report suggesting the dollar-incentivized high doses were neither improving nor extending patient lives.
That said, even massive amounts of EPO don’t automatically lead to death. A 2006 paper described two hospitalized South Korean heart-attack patients who accidentally received nearly 10 times their prescribed dose of EPO—318,000 units instead of 33,000. Both patients were smokers, and one had a history of hypertension and diabetes. After discovering the overdose, the hospital closely monitored the patients for symptoms such as elevated blood pressure, nausea, vomiting, shock, and thrombosis (which had already put them in the hospital). Despite the overdose, doctors reported that the two patients experienced none of the negative expected side effects from toxic levels of EPO. While known reactions to EPO overdoses make for a long, serious list—headache, muscle and joint pain, allergic reactions, nausea, itching, seizures, enlarged spleen, elevated blood pressure, and overproduction of blood platelets—the doctors reported that “in the course of close observation, we found none of the specific symptoms we expected as side effects of erythropoietin, and no abnormal objective findings on physical examination.” The patients were soon discharged, and their EPO levels returned to normal.
However, I found no documented instances of EPO killing already healthy humans, athletes or otherwise.
In 1993, a wheezing, clammy-skinned man showed up at a New York emergency room complaining of shortness of breath and a cough. The frail 62-year-old repeatedly told the doctors that he needed a “transfusion to correct anemia” and that he was stricken by “chronically low hematocrit.” The ER doctors had a delusional hypochondriac on their hands with a history of self-medicating. The victim, a retired biomedical engineer, had a friend in the pharmaceutical industry who supplied him with Epogen. The arrivee had been injecting himself with EPO every day for several months (EPO is typically administered three times a week). He was also taking daily doses of a stew of other medicines, including penicillin.
When the patient checked into the ER, his hematocrit level was a through-the-roof 70.4 percent, a number that startled doctors used to finding a typical 42 to 54 percent hematocrit in adult males. While the fact that the patient was taking so many other drugs made it difficult to tie his symptoms to EPO alone, a report on the case in the American Journal of Emergency Medicine indicated that the months-long overdosing on EPO was causing the patient chest pain and hypertension, and it had worsened symptoms of his existing lung disease. The report pointed out that when a hematocrit level exceeds 70 percent, the amount of oxygen reaching the brain decreases, which in itself can be dangerous. In spite of his spectacular abuse of EPO, the patient recovered and was later released to a psychiatric hospital.
These vignettes are not meant to argue that EPO abuse is safe. It’s not. In their write-up of the case, the physicians took the opportunity to warn other doctors to be on the lookout for athletes who self-administer EPO: “It seems likely that an erythropoietin-induced increase in hematocrit, coupled with the dehydration that develops during prolonged exertion, would increase blood viscosity and cause impaired muscle perfusion and possible fatal thrombosis.” The point remains, however, that it is extremely difficult to find a case that backs up the press-supported notion that EPO was indiscriminately slaughtering cyclists in the early 1990s.
One reason European athletes may have quickly adopted EPO in Europe in the late 1980s is related to a difference in European and American patent law. Shortly after Amgen successfully cloned EPO in 1982, at least four other biotech firms and the University of Washington separately made the same breakthrough. A court battle handed the U.S. patent to Amgen. European patent law, however, is reluctant to grant patents on naturally occurring substances, and Amgen did not get an EPO monopoly on the other side of the Atlantic. As a result, Europeans had access to EPO from at least three manufacturers.
This pharmaceutical company competition, along with the buying power of Europe’s national health care systems, kept EPO prices much lower in Europe. The affordability put the drug within financial reach of struggling European athletes while the drug’s distribution from multiple chemical manufacturers may have created more opportunities for gray market product leakage. According to Alessandro Donati, an Italian sports professor and doping investigator, data from the sales of performance-enhancing drugs in Italy show that of 181 million prescriptions studied in 2000, the best-selling ones were erythropoietin and human growth hormone. The €158 million worth of EPO sold in Italy in 2000 did not include amounts brought in from Switzerland, nor the EPO distributed by the Mafia—much of it stolen from pharmacies or obtained from illicit distributors. Donati also cites a 1999 French study that indicated that only one-sixth of global EPO production went to patients with pathologies, with the rest being distributed through underground markets. Because there were more manufacturers of EPO in Europe than in the United States, Europe had more distribution nodes from which the drug could be bought or stolen, he says.
Interestingly, health care system differences ended up saving the lives of cancer victims in Europe compared to the United States. In 2001, Amgen released a new EPO called Aranesp. To spur product sales, the company offered $1,200 kickbacks to doctors for every prescription written. Amgen also ran a TV ad blitz that encouraged patients to ask for Aranesp as an antidote to fatigue. Prescriptions skyrocketed 340 percent in the United States, but increased only 52 percent in Europe. Across the pond, direct-to-consumer marketing is illegal, national health care systems use their buying clout to negotiate lower drug costs, and doctors in those same health care systems are immune to Big Pharma payola.
Five years after the Aranesp release, studies began to indicate that American cancer patients were dying 10 percent more frequently than European cancer sufferers. As it turned out, EPO was accelerating tumor growth; the American sales-and-marketing incentives that got more patients to take more EPO had the unintended effect of killing them off more quickly than in Europe, where patients were shielded from the pharmaceutical company’s aggressive sales-and-marketing efforts. While there is no evidence directly linking EPO to any competitive cyclist deaths in Europe, in the United States, there are ample data showing that heavy EPO use incentivized by the oddities of the American health care system was shortening cancer patient lives. This discovery lead to a sterner FDA-mandated “black box” warning on EPO packaging and a decline in American oncologists’ enthusiastic EPO prescription writing.36 The scandal also suggests how EPO’s black reputation in sports as a drug of mass destruction got an assist from drug makers’ efforts to expand product sales.
DURING A CONVERSATION with López over Skype, I mentioned Michele Ferrari’s infamous statement about EPO and orange juice. López said that Ferrari had dared to tell a truth that violated an anti-doping article of faith, one that firmly established itself after the IOC took its more aggressive anti-doping stance in the wake of the 1984 Los Angeles blood-doping episode: If it’s a performance-enhancing drug, it must be categorically destructive to health and the spirit of sport. In the severe catechism of anti-doping thought that was hardening after Los Angeles and the 1988 Ben Johnson scandal in Seoul, there was no room for a fact-based argument like Ferrari’s. Performance-enhancing drugs must be evil—end of story. For challenging the anti-doping missionaries’ creed by suggesting that the abuse of drugs is harmful, not drugs in and of themselves, Ferrari was immediately exiled.
“You cannot say Ferrari,” López observed. For his orange-juice comment, “he has been condemned. He is in hell and you cannot rehabilitate Ferrari’s image or respectability because received wisdom says that Ferrari is the devil.”
López was not justifying Ferrari’s acts. The Italian doctor repeatedly broke the laws of the land and sports, and he conspired to give certain athletes an illegal performance advantage that others did not share. He was banned for life by the U.S. Anti-Doping Agency for his involvement with Lance Armstrong’s doping and for administering and trafficking in performance-enhancing drugs. Even in 1994, he was up to no good. However, what interests López is how journalists who write about doping, and the agencies that create and enforce doping codes, can condemn Ferrari for speaking a truth about EPO when they have used the EPO-kills fabrication as a justification for a steadily growing anti-doping infrastructure.
López is not optimistic that journalists or anti-doping agencies will hold themselves accountable about the true health risks of doping any time soon. Doing so would be to spit in the soup that feeds them. It would also suggest that our responses to drugs are based more on personal bias than on hard data. “People are not interested in listening to other versions” of this colorful, body-strewn doping history, López told me. Excising the “doping kills” fable does no good for the anti-doping evangelists’ cause because the falsehood has self-justifying utility. As López put it, the EPO-kills story is useful as an anti-doping foundation myth. Like Knud Enemark Jensen’s “death by amphetamines,” the tale is factually ignorant but practically useful for the media and anti-doping bureaucracy’s “general condemnation and refusal of doping.”
As for the inherent ethical contradiction in the twisting of truth by anti-doping activists in order to return athletes to “true sport,” López does not think sinister motives are at play. Anti-doping agencies, scientists, and journalists are reluctant to discuss the fictional nature of drug-death stories because these tales serve a moral good that is a descendent of Coubertin’s quest for purity. The EPO-kills story “was useful for the anti-doping campaign,” López explained. “So it didn’t matter if the evidence was good enough or not because it was conducive” to the anti-doping missionaries’ goal of imposing a new purity on sports. In fact, López feels that anti-doping campaigners are acting in good faith, rather than willful hypocrisy. “I don’t think that they lied on purpose,” López told me. “But what they did was create a truth out of circumstantial and scattered evidence. And they believed in their own creation.”
Listen to our conversation with Mark Johnson on the VeloNews podcast: