The name Eero Mäntyranta is not one most readers will know. It’s probably not even a name that many will remember if you continue to read, but it is the name of a remarkable man whose story I hope you can’t forget.
Mäntyranta is a Finnish 7-time Olympic medalist (3-gold), and the subject of the final Chapter of David Epstein’s outstanding book, The Sports Gene. That’s because he is also a subject of a scientific research paper that showed the presence of a genetic mutation that made Mäntyranta hypersensitive to EPO. The result was an over-production of hemoglobin, and a predisposition to endurance that he was able to parlay into cross-country skiing dominance in the 1960s.
He also died yesterday, at the age of 76.
The obituary below was written by David Epstein, who met him 2-years ago while researching for his book. It explains Mäntyranta’s story, and acknowledges his place not only in Olympic folklore, but also that of sports science. Some comments from me follow the piece.
[ribbon toplink=true]Eero Mäntyranta, by David Epstein[/ribbon]
Yesterday morning, I learned that Eero Mäntyranta had died, at the age of 76. For whatever silly reason, my mind leapt straight to the first time I saw the paper—specifically, to the sentence that stopped my eyes and ultimately brought me to him.
“The proband, a 53-year-old male, whose Hb level has been 200 g/liter or greater since childhood (last measurement, 236 g/liter), has been one of the best cross-country skiers in the world, having won three Olympic gold medals and two world championships.”
I remember my first thought: holy shit that’s a lot of hemoglobin (Note: typical male range is 140-180g/L). And my second: that might be the most transparent anonymity cloak in scientific history. I figured there couldn’t be many Finnish guys with seven Olympic medals. I took a quick look through Olympic records and found only two Finnish skiers with seven medals. And only Eero Mäntyranta was the right age. I determined right then to learn his story.
At the 1964 Winter Olympics in Innsbruck, Austria, Eero earned the moniker “Mr. Seefeld,” a reference to the competition venue he dominated. He finished the 15K race forty seconds ahead of the next skier, a margin of victory never equaled in that event at the Olympics before or since. The next five finishers were within twenty seconds of one another. Eero won the 30K race by over a minute.
The paper, and subsequent associated journal articles, documented extraordinarily high levels of red blood cells and hemoglobin that were passed down to some members of the Mäntyranta family. Another passage from one of the papers, written by hematologist Eeva Juvonen, (and fleshed out for me in an interview with geneticist Albert de la Chapelle), will remain lodged in my science-writing cortex until it shrivels up.
Juvonen described lab-testing samples of Eero’s bone marrow cells, which produce red blood cells. The plan was to add EPO to the cells and track the creation of red blood cells. A typical human’s bone marrow cells won’t start making blood cells in the lab until EPO is added. But Eero’s bone marrow cells began the process of creating red blood cells before Juvonen could even stimulate them with EPO. Whatever tiny speck of EPO that was already in the sample was enough to keep the red cell factories humming. Eero’s body was hypersensitive to even trifling traces of EPO.
Subsequently, de la Chapelle pinpointed the cause: a genetic mutation that ran in the Mäntyranta family and affected the EPO receptor. The EPO receptor is like a lock for which the EPO hormone is a key. Put the lock in the key, and the production of red blood cells begins. (That is why, of course, injecting synthetic EPO makes for effective doping in endurance sports.) The Mäntyranta family mutation happened to truncate the receptor such that it lost the portion that served as the brakes for red cell production.
Of ninety-seven Mäntyrantas who were studied, twenty-nine were naturally doped. They were gifted with what Lance Armstrong and co. achieved through technology. After the release of my book, The Sports Gene, which told Eero’s story in detail, the question was raised—prominently—as to whether the Mäntyranta family EPOR mutation means that sports can never truly be fair.
In my opinion, sport was never about standardizing the genes in competition, but about standardizing the rules. The same case for relativism and inherent unfairness of sports could have been made using athletes who stand six-foot-ten through no hard work of their own. With Eero, the only difference is that the athlete happened to have a single gene mutation with a large effect—typically, as with height, any single gene only has a small effect—and intrepid scientists happened to find it. Essentially, the distinction is that Eero’s story makes for a blessedly tidy genetic tale for someone like me. (The fact that he was living in the Arctic as a reindeer farmer also didn’t hurt the narrative.)
Eero’s is the last chapter of The Sports Gene, and it was my favorite to write. There are the obvious narrative reasons: in a book whose main character was an idea, constructing a chapter that had a single main character and a single scientific mystery was literary manna. But that’s not why I was so eager to write the chapter that I started it by hand in a notebook on the frigid three-hour drive back to Luleå, Sweden, after I met Eero. (Last in the book, this was the first chapter I actually finished.)
There was just something magical about him and the day we spent together. As he aged, his condition showed on his face, literally. He had turned red. His cardinal mug made an incredible contrast with his blonde-haired, ice-blue eyed wife, Rakel. Sitting at lunch in their home, red-faced Eero wearing a red reindeer sweater, with reindeer gamboling in the backyard and pine trees bending under the weight of snow, I couldn’t help but feel that I had stepped into a Christmas snow globe.
At that lunch, Eero laughed when he picked up a fork, and started telling a story. His daughter Iiris translated, explaining that the fork had reminded her father of a stately dinner thrown in his honor after his victories at the 1964 Games. On that night, Eero had found three forks beside his plate—three times as many as the number his family had shared, growing up in a 170-square-foot-house in rural Lankojärvi, Finland. In lieu of cutlery, the children had used sharpened sticks to spear potatoes and bits of bread.
Eero was uncomfortable with the pomp and politesse of the ceremonial dinners his athletic success foisted upon him. At one such event, he was about to drink from a goblet on the table when a group of urbane guests began washing their hands in it.
When I asked Eero if he had ever visited New York City, where I had come from to meet him, he said yes, and gave his first impression with one word: “scary.”
Today’s Finland is a prosperous country. But when Eero was growing up, it was a poor, rural nation locked in debt from World War II. Eero started skiing almost as soon as he could walk, because it was the only way to get across the frozen lake to school. As a boy, he realized he could lay waste to his peers in racing, but only considered a racing career after working in the forest as a fifteen-year-old among criminals who fled north to evade the law. Skiing was the path to a better life. Trade the skis for feet and the Arctic forest for the Rift Valley, and Eero’s tale would fit neatly into the narrative template of a Kenyan marathoner.
Being born with talent is one thing; alchemizing it into Olympic gold entirely another. And though I drew attention to Eero’s startling biology, that’s worth remembering as well. I’ll remember Eero the way he was when I met him. A jovial and remarkable-looking man, with dark, slicked-back hair and prominent cheekbones that seemed to pull at the corners of his mouth, giving him a slightly inquisitive look. There was a thickness about him, a barrel chest and bulbous nose. I remember when he shook my hand, I felt as if he could’ve crushed my fingers, and I noticed that his middle finger was bent at a right angle from the top joint.
He spent the brief period of Arctic winter sunlight that day working in his reindeer yard. I thought he must have been the strongest seventy-three year old I had ever met. That’s how I’ll remember him.
[ribbon toplink=true]Some thoughts on complexity and multi-factorial pathways to success, Ross[/ribbon]
First, thank you to David for writing that and allowing me to publish it here. Mäntyranta’s story is remarkable, and he clearly made an impact on a writer who has seen more than a few remarkable things, so I felt it important to highlight his story and life. May he rest in peace.
Now, in terms of the actual content, David referred to Mäntyranta as a “blessedly tidy genetic tale”, which he certainly is, because it is incredibly rare that a single mutation confers such a large physiological effect which is also advantageous to endurance performance (unless one wants to deny this, which implies also that doping is ineffective).
The reason it’s tidy is because the effect of genes on performance is normally drowned out by the extra-ordinary complexity that underlies complex physiology and exercise performance. Consider for instance that height, one of the relatively “simple” hereditary traits, was only 80% accounted for by a staggering 294,831 gene variants, and you get some understanding of just how many pieces there are in the puzzle.
This is why any sensible person, in response to the questions: “Is there a genetic test for performance? Is there a performance gene?”, can only ever answer “No, it’s too complex to reduce to a single gene, and tests cannot assess this level of complexity. Yet”.
Mäntyranta is about as close as it gets to that. However, despite that, I want to point out that even with this mutation, one which saw his hemoglobin levels increase by around 50% compared to the typical male, he still didn’t wipe the floor with everyone, every time. Yes, he dominated his events in unmatched fashion in 1964, but he still got beaten, and that single mutation did not confer invincibility, only advantage. That’s again an illustration that performance is multi-factorial, and it suggests that many other factors are responsible.
[ribbon toplink=true]One gene does not a champion make[/ribbon]
That’s why David is at pains to point out that Mäntyranta’s life as a young boy, his commitment to training and his socio-economic situation, all contributed to his ultimate success. Every one of those factors, plus numerous others, physiological and otherwise, are all part of the mix, and a single gene, however physiologically relevant, is not the guaranteed shortcut to sporting success. That’s why others with the same mutation have not hoarded Olympic medals, and it’s also why so many men who stand 6 foot 10 are not playing in the NBA – it shortens the odds, it doesn’t guarantee the win.
Sporting success, to repeat, is multi-factorial, something we all (scientists and coachs) recognize, and it’s why the straw man premise of Bounce, Outliers and The Goldmine effect is so fallacious. Nobody ever guaranteed that sporting success was purely the result of genetics. Or talent, if you wish. It’s a PLUS model, not an EITHER/OR. Mäntyranta captured that.
For more reading on the complex interaction between environment and genetics, this review article I wrote for BJSM is a start.
And for more on the genetic basis for elite running, and why you’re chasing shadows if you think a unique gene explains it, there’s this more recent one I co-authored with colleagues earlier this year.
Thanks again to David for his piece.
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