By Matt Wood

In 2006, Dale Lloyd II, a 19-year-old freshman football player at Rice University, collapsed during a conditioning workout and died the next day. His death was linked to complications from sickle cell trait, or having one of the genes that causes sickle cell disease.

At least 20 deaths of football players with sickle cell trait have been reported since 1974. As part of a settlement with Lloyd’s family in 2009, the National Collegiate Athletic Association (NCAA) agreed to screen all athletes for sickle cell trait. But does this policy make good medical sense, or does it discriminate against athletes with sickle cell trait and unnecessarily exclude them from sports? Lainie Friedman Ross, MD, PhD, the Carolyn and Matthew Bucksbaum Professor of Clinical Medical Ethics, recently surveyed pediatricians and sports medicine providers about the NCAA policy and found conflicting responses to these questions.

Sickle cell trait is most common among African Americans but can affect Caucasians as well, particularly those of Mediterranean and Middle Eastern origin. It can cause red blood cells to change shape and clog blood vessels, which can lead to heat illness, dehydration, kidney failure and exertional rhabdomyolysis, or breakdown of muscle tissue. Athletes and military trainees with sickle cell trait are especially at risk during intense conditioning at high altitudes or in extreme heat and humidity.

The idea behind the NCAA policy is that coaches would be able to take precautions during practices and games for athletes with sickle cell trait, but Ross said anybody is at risk for heat illness under those conditions.

“People who have sickle cell are at increased risk, but anybody can die from heat exhaustion,” she said. “This isn’t just unique to sickle cell trait. The whole point is we should be protecting all of our athletes and military personnel.”

The United States military has long studied this issue, and found that modifying training on hot, humid days for all recruits — not just those with sickle cell trait — eliminated the excess risk of death from heat illness and exertional rhabdomyolysis for those with sickle cell trait. Under normal conditions, athletes with sickle cell trait can participate with no restrictions, so by singling them out instead of enforcing rules on practice conditions for all athletes, the NCAA may be discriminating against them.

“Even if sickle cell trait doesn’t affect their performance, it affects how they get measured for their performance,” Ross said. “If we’re going to discriminate against these kids in practice, we’re going to discriminate against them in games too.”

In two separate surveys published in Pediatrics and the Clinical Journal of Sports Medicine, Ross and her colleagues asked pediatricians and sports medicine providers about the NCAA policy.  More than 70 percent of both groups supported targeted screening for African American athletes in all NCAA divisions. At the same time, a majority of both groups also expressed concerns about discrimination against athletes with sickle cell trait. These answers seem to contradict each other. If providers were concerned about discrimination they wouldn’t support targeted screening versus screening all athletes, or they wouldn’t support the screening policy at all.

Although initially the NCAA recommended screening all athletes, when the policy was implemented in 2010, the NCAA required screening for only Division I athletes. The final policy also allowed athletes to opt-out of screening. Both pediatricians and sports medicine providers overwhelmingly supported the opt-out policy  (75 percent of pediatricians and 88 percent of sports medicine providers), which would also seem to contradict their support for screening in the first place.

Besides the potential for unfair treatment of athletes with sickle cell trait, Ross also has concerns with the NCAA’s testing method. The official policy recommends a test called “Sickledex” which tests only for the specific sickle cell hemoglobin. However, there are a number of variants of sickle cell disease that the Sickledex test doesn’t detect.  While these variants may not pose the risk of exertional heat illness, they do have implications for having a child with a sickle cell disease variant.  By using the Sickledex, athletes who test negative may misunderstand their risks in the reproductive context.

“You’re taking 18- to 25-year-old athletes and you’re telling them that they’re sickle negative,” Ross said. “So later they decide to get married and have a family, and they tell their partner they’re sickle negative, not knowing that they were using a really bad test.”

There is a more sophisticated test available that detects all the sickle cell variants, but it costs more than $100 to administer, versus $10 for the Sickledex test. Ross believes this is the main reason driving the NCAA’s recommendation. “It’s very problematic to use a really bad test,” she said. “If we’re going to do a test, let’s do the right test so we give kids the proper information about their sickle cell status.”

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by Rob Mitchum and Matt Wood

When superstar Derrick Rose crumpled to the ground late in the Chicago Bulls game Saturday, the playoff hopes of Chicago basketball fans followed suit. Experienced sports fans saw the point guard grabbing at the front of his left knee and thought immediately of three dreaded letters: A, C, and L. Sure enough a subsequent MRI confirmed that Rose had torn his anterior cruciate ligament, an injury that would knock him out of this year’s NBA playoffs, the Olympics, and a significant chunk of the next season.

Despite the long rehabilitation time, an ACL tear is a common injury for athletes playing sports that involve frequent cutting and pivoting. J. Martin Leland, assistant professor of surgery at the University of Chicago Medicine, performs 75 to 100 ACL reconstructions each year on recreational athletes who injured themselves during basketball, soccer, lacrosse, or skiing activities. On Monday, after repairing the ACL of a cricket player, Leland sat down with ScienceLife to discuss how ACLs are torn, how they are repaired, and “the perfect storm” of factors that may have led to Rose’s injury.

Q: First of all, what is the ACL?

The ACL is one of four major ligaments in the knee that stabilize the knee. You have one ligament on the inside of the knee called the MCL or medial collateral ligament, one ligament on the outside of the knee called the LCL, or lateral collateral ligament, then two ligaments in the center of the knee: the ACL, which is right in front of the PCL, or posterior cruciate ligament.

The ACL is most important for rotational stability of the knee, so if someone has an ACL rupture, once the knee comes down and the swelling goes away, they’ll find they can walk, jog, go up stairs, no problem. Then, if they get an MRI showing an ACL tear they’re very confused: “How can I possibly have an ACL tear if I can walk without difficulty with no pain?” But the ACL is not important for walking, it’s important for rotational stability.

Q: What happens to a person’s knee right after they tear the ligament? Are they in pain?

The ACL has an artery that runs right up the center of it. So the first thing that happens is the knee typically swells up like a balloon in a matter of an hour to two hours. Normally people have difficulty putting weight on it because it just feels weird. Some people will describe a pop, other people won’t, but you’ll feel like a sharp shooting pain in the knee, and then it will be gone, and it won’t really hurt. But the knee typically tends to get very swollen within 1 to 2 hours usually, and will stay swollen for up to a week, so people tend to say they have trouble putting weight on it for anywhere between immediately after the injury and four or five days. After that they can put weight on it, but the knee is very stiff, and it takes anywhere between a week and three weeks for that swelling to go down and the stiffness to go away so that you can get range of motion again.

Q: With Rose’s injury, Bulls trainers were doing knee exams right on the court after he collapsed. Can a doctor diagnose an ACL injury that quickly?

The Lachman exam is the name of the test that’s typically done to test the ACL. It’s done with the knee at 30 degrees of flexion. Basically, you stabilize the femur, and with your hand on the tibia, you just kind of pull up. If you feel increased laxity, or the tibia pulls forward on the femur more than what’s normal, you know right off the bat that they tore their ACL.

When I watched the video, I could tell that he had ruptured his ACL without even examining him. The sportscasters couldn’t tell the instant when he injured it, they said he jumped up and was complaining of pain, so maybe it was the jump. But it was when he planted, immediately before jumping. If you watch the clip very carefully, you can see he comes in, plants, and his left knee bows in, so that the knee comes towards the right knee as well as rotates, and then he comes out of that and jumps up. That’s why he dishes the ball off, because the second the knee went in that position, he felt it pop, and felt the pain, and you can see for a split second the classic valgus instability where the one knee moves towards the other knee and ruptures the ACL.

Q: Was it unusual that Rose injured his knee without being struck by another player or running into an object?

The most common way of tearing your ACL is non contact. It was the perfect storm for Derrick Rose to rupture his ACL. He’s missed much of the season because of his prior four injuries, and he’s only been back playing for three weeks, and it was in the last minute and a half of the game. He can’t possibly be at full strength because he missed so much time, so his muscles are more weak.

He went to make that sudden stop, and normally, if he was a little bit stronger, his muscles would have fired and kept his knee still. But his muscles were fatigued and they just gave out, and once they gave out, his knee started going into that position. Basically, he was coming in and stopped with such force that normally his muscles would have kicked in and stabilized his leg, but because his muscles were weak, his knee just kept going, and then ruptured the ACL. So it was really the fact that he wasn’t at 100 percent strength, and the fact that he was fatigued at the end of a game.

When you hear about skiers rupturing the ACL, it’s almost always in the afternoon, because someone like myself who is a recreational skier is not used to 8 hours of sports participation because we work all day. In the afternoon, my muscles are tired and fatigued, and that’s when my knee gets in that bad position.

Q: Is the ACL the most fragile knee ligament, or do sports fans just hear about those injuries more often?

The most commonly injured ligament in the knee is the MCL. But the MCL when injured in isolation, it heals very well non-operatively. So some people will be in a knee brace for six weeks and then get right back out there. Professional football, if it’s a mild injury, they might not even miss a game. People are injuring their MCLs all the time but we never hear about them, because it’s not nine months until you come back, it’s anywhere between two and six weeks.

Q: Is basketball one of the worst sports for causing ACL injuries? Who’s at highest risk for the injury?

There are some studies that have been done, and it’s been shown that women who play soccer and basketball have a much higher likelihood of developing ACL ruptures, versus men or women who play other sports. It hasn’t been shown in men’s sports that basketball is any more dangerous than say football or soccer.

It’s sometimes shown that women have an even higher risk of rupturing their ACL than men. There’s a 2 to 4 times higher rupture risk in women that play soccer or basketball in comparison to male counterparts, because of different reasons. Hormones tend to stretch out ligaments and estrogen can cause increase rupture of ligaments when there’s stretching at certain times of the menstrual cycle. Women also have proportionally smaller ACLs, even accounting for the fact that women are slightly smaller than men. But there haven’t been any research to show that men who play basketball are at a higher likelihood of injury than men who, say, play soccer.

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As another year comes to a close we’d like to look back at the fascinating research breakthroughs and inspiring patient stories from 2011. ScienceLife ran 168 posts this year, and while we wish we could highlight all of them, here are a handful of our favorites from each month.

January

Patrick Wilson found out that the H1N1 virus could end up helping us fight all types of flu. Stephen Pruett-Jones studied how some male birds mimic the sounds of predators to pick up the ladies (with an audio clip). We interviewed David Gozal about his study on the link between childhood obesity and lack of sleep, and took a look at NCAA regulations mandating sickle cell testing for athletes.

February

Harold Pollack gave a lecture on why violent crime in urban, minority communities should be considered a public health epidemic. Siri Atma Greeley studied the actual medical benefit of widespread genetic testing. Stacy Lindau wanted to know why so few women get help for sexual problems after surviving cancer. We talked to Bana Jabri about the causes of celiac disease, and Sliman Bensmaïa showed us how the brain processes the basic elements of touch very much like it handles visual information.

March

Sola Olopade educated women in Nigeria about using clean-burning stoves to prevent indoor pollution. Stefano Allesina and Jonathan Levine looked at how rock-paper-scissors helps explain evolution. Joshua Miller went to Yellowstone Park to see what stories the ghostly bones of animals can tell, and Scott Eggener questioned the wisdom of indiscriminate prostate cancer screening.

Photo by Gerald Waddell

Andrea King studied the wide range of responses to drinking alcohol, and why it can be fun for some people and a bummer for others. Cheryl Reed took a ride in a helicopter with our UCAN nurses. Kamal Sharma looked at the genes that control animals’ gait, and Ningqi Hou studied how urban environments can dictate how much exercise people get.

May

Daniel McGehee looked at the long-term effects of nicotine on the brain. Habibul Ahsan went to Bangladesh to study the health impacts of accidental exposure to arsenic in drinking water. The brain’s overlooked supporting cells got their due at a conference on neuroscience, and we remembered a landmark discovery about a once popular drug taken during pregnancy that we now know can cause cancer.

June

As we headed into summer, Diana Lauderdale used Google to track MRSA. We learned about an extraordinary transplant where a man received a new heart, liver AND kidney. Daniel Geynisman gave us the rundown on whether or not cell phones are killing us (they’re not, as long as you don’t use them in the car), and some UChicago undergrads studied what happens to gorillas on the birth control pill.

July

We spoke to Donald Jensen and Andrew Aronsohn about the new outlook for patients with hepatitis C. Igor Schneider made a time machine to find the genetic switch for limb development. Farr Curlin led a study about the benefits of addressing spiritual needs alongside medical care, and Adam Cifu looked at the phenomenon of scientific study reversals.

August

Stefano Allesina dug into the long, shady history of nepotism in academia in Italy. John Schneider talked about his work addressing sexual health and stigma in India. Michael Becker discovered a new treatment for the Royal Disease, and we had the rare chance to name check a Spiderman villain in a post.

September

Martha McClintock and Suzanne Conzen studied the connection between social isolation, stress and breast cancer. Gallego Romero traveled to India to search for the origins of lactose intolerance. Stephanie Dulawa developed a mouse model for OCD, and Paul Vezina looked at a different kind of obsession, compulsive gambling.

October

Arshiya Baig started a pilot project to help people learn about life with diabetes through pictures. Manyuan Long found that some of the youngest genes are in the brain. Jens Ludwig and Stacy Lindau published a landmark study about the connection between neighborhood poverty and health, and Issam Awad studied a rare brain disease that soon could be treated with a drug instead of surgery.

November

Cathy Pfister and Tim Wootton figured out how to use seashells to track climate change over the years. Lianne Kurina found a link between loneliness and sleep quality. Shantanu Nundy, Monica Peek and Marshall Chin developed a program to send text message reminders to people with diabetes, and Pan Chen looked at the links between childhood abuse and aggressive behavior in adults.

December

Inbal Ben-Ami Bartal, Jean Decety and Peggy Mason discovered that rats can show empathy for their fellow rats in distress. Maciej Lesniak performed a scary but amazing brain surgery on a patient who was awake. Cathryn Nagler searched for the source of food allergies within our bodies, while Stafano Guandalini uncovered the challenges in educating doctors about one of those allergies, celiac disease.

Whew. Hope you were able to click through at least a few of those. We look forward to another great year of research in 2012. We’re taking a break next week, but we’ll be back on January 5. Happy holidays!

Welcome to pilot episode 2 of our Medical Center research news podcast. We’re keeping the water wings on for now as we continue to refine the format and discover all the technical struggles inherent in podcasting, but please do listen and give us feedback on how we’re doing - and if you have good ideas for a name.

In this episode, we talk to J. Martin Leland about the Stay in the Game event and preventing injuries for baseball, golf, and tennis season. Dianna Douglas reports on the oldest patient to ever receive Whipple surgery at the University of Chicago Medical Center, talking with Kevin Roggin and William Dale about the procedure. And Rob Mitchum reports from a news conference held last weekend by Sen. Dick Durbin about the impact of potential cuts to the National Institutes of Health budget currently being debated in Congress. Thanks for listening!

University of Chicago Research Podcast Episode #0.2 by robmitchum

[If you missed episode 0.1, you can listen here.]

As the call for pitchers and catchers to report goes out in Arizona and Florida, amateur athletes are also getting the itch for warm weather and outdoor activity.  Whether you’re dusting off your baseball glove, your tennis racket, or your golf clubs, it’s not too early to start thinking about avoiding a sports injury that could keep you out of commission for most of this season. On Wednesday, March 2nd, at the Tinley Park Convention Center, the University of Chicago Medical Center will present a free seminar, Stay in the Game, featuring a panel of sports medicine specialists (and a buffet and iPad raffle, to boot).

Among the panelists will be J. Martin Leland, MD, assistant professor of surgery, and ScienceLife’s go-to expert on sports medicine topics. Leland has worked with professional baseball teams, college athletics programs, and youth athletes of all ages to diagnose and treat sports injuries such as torn labrums and ligament sprains, using physical therapy, non-surgical interventions, or surgical procedures whenever appropriate. But Leland also has an interest in preventing those injuries from happening in the first place, and will present tips on avoiding elbow and shoulder damage from various sports at the Tinley Park program.

“Prevention is very different. You’re thinking of very different things in terms of preventing injuries compared to if you’re trying to rehab one,” Leland said. “If you’re trying to rehab a specific injury, you’re going to have a very specific course. Prevention tends to be a broader strategy.”

As such, Leland identified four areas where injury prevention can be strengthened for athletes of all ages: conditioning, equipment, hydration, and mechanics. Though he’ll expand upon those topics at Wednesday’s event - and will, of course, answer attendee’s questions - here’s a sneak preview of his tips for avoiding the disabled list this year.

Conditioning

“I’ve worked with numerous professional baseball players, some of whom are incredibly flexible, to the point where grown men who are centerfielders in Major League Baseball can do a split at the drop of a hat,” Leland said.

That’s testimony to the importance of stretching and flexibility in avoiding sports injuries - a ritual you can personally observe if you ever show up early enough to watch the warm-ups before a baseball game. But amateur athletes should also be sure to stretch their muscles before any type of strenuous activity, even for a sport like golf that seems distinctly low-impact. People can loosen muscles with an activity as simple as jumping jacks, Leland said, but should make sure that all stretches are “slow, gradual, and progressive,” holding the stretch for at least 30 seconds, and avoiding stretches that could actually do more harm than good.

“You’ll see some people when they’re trying to stretch their hamstrings, they’ll bounce up and down,” Leland said. “That actually increases your risk of injury, and you can strain or tear a muscle doing those stretching exercises alone.”

Equipment

One of the most important precautions against injuries on the playing field is simply making sure the playing field is as safe as possible. Many youth baseball leagues have started to transition to new magnetic breakaway bases, Leland said, replacing the more common rigid, locked-in-place versions that can cause ankle and leg injuries during slides.

“When you slide into them really hard, the breakaway bases will move out of the way and it’s not like you’re basically sliding into a brick wall,” Leland said.

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A sickle cell (left) and a normal red blood cell (right). From carnegiescience.edu.

In 2006, Rice University football player Dale Lloyd II collapsed during a practice and later died. The cause of death was acute exertional rhabdomyolysis, a sudden breakdown of muscle tissue into the blood brought on by strenuous exercise. But the trigger for Lloyd’s death may have been sickle cell trait, the name for when a person carries one of the two genes required for full-blown sickle cell disease.

People with sickle cell disease form abnormal red blood cells that can lead to chronic pain, hypertension, stroke, and death, while people with sickle cell trait (approximately 2 million in the U.S.) are generally thought to be symptom-free. But Lloyd’s death drew attention to potentially fatal consequences for athletes with sickle cell trait, and a lawsuit filed by the player’s family led to the NCAA mandating testing for all Division I athletes in 2010.

But is screening for sickle cell trait the best preventive measure for college athletes? That was the topic on the table at the first Department of Pediatrics Grand Rounds of 2011 last week, where both the medical and ethical implications of the NCAA’s new policy were considered. Though mandatory sickle cell trait screening has previously been adopted by the military and the National Football League, the NCAA stance could cause a “trickle-down” effect to high schools and youth sports, leading to millions of tests that might cause more harm and expense than good.

At least fifteen NCAA athletes have died from sickle cell trait-related causes in the last 30 years. But given that there have been approximately 2 million total athletes over that time span, that’s only 1 death for every 400,000 people, said Holly Benjamin, associate professor of pediatrics and surgery. Compared to more common, harmful occurrences such as concussions and spinal cord injuries, that’s an exceedingly rare event.

Which is not to say that it shouldn’t be closely monitored. Sickling, the name for a sickle-cell-related attack, can develop after as little as 2 or 3 minutes of strenuous exercise, and can be exacerbated by heat, altitude, and dehydration, Benjamin said. Parents, coaches, and trainers should be vigilant about athletes who suddenly collapse, giving them fluids and oxygen and transporting them to the nearest emergency department.

But while screening athletes for sickle cell trait might improve the response to an athlete’s collapse, preventing that collapse in the first place would be even more beneficial. As a demonstration, Lainie Ross, professor of pediatrics, surgery, and medicine, used the history of sickle cell trait testing in the American military, which has faced similar tragedies and pressure to screen.

After 4 sickle cell trait-related deaths in 1970, a study found that African-American recruits with the gene were 30 times more likely to die during basic training. In response, the Armed Forces considered screening for carriers of the gene and restricting service in those with positive tests. Meanwhile, another study was started to test whether the danger could be reduced by using the wet-bulb globe temperature (WBGT) index, a measure incorporating temperature, humidity and other factors to determine how dangerous conditions are for physical activity. An intervention based around reducing exertion and increasing rest for basic training recruits on days with a high WGBT index was successful not only in completely eliminating deaths related to sickle cell trait, but reduced deaths in non-carriers as well.

“What this shows is that effective intervention does not require the identification of sickle cell trait,” Ross said.

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In recent weeks, stem cell research has once again been drawn into a battle over political, ethical, and legal questions. Given all the controversy, it’s easy to forget that there are still many scientific questions surrounding stem cells and their potential for medical use. The ability of such cells to grow into different types of organs and tissue is exciting, but harnessing that ability has remained a challenge for scientists. Much work remains to be done in finding the control panel for pushing stem cells in a particular direction - and some of that work continues despite recent court rulings.

Mesenchymal stem cells are less controversial than their embryonic cousins because they can be harvested from adult bone marrow. But they are also more restricted in their potential, with their future limited to three destinies: bone, fat, or cartilage. Of course, those three fates alone would be very useful in medicine, with applications for orthopedic surgery, arthritis, and wound healing. So scientists are looking for the best ways to manipulate mesenchymal stem cells (MSCs) toward one of those forms.

In the laboratory of Tong-Chuan He, associate professor of surgery at the University of Chicago Medical Center, the desired outcome for mesenchymal stem cells is bone.

“Our goal is try to develop an efficient way to promote cells to making bone,” He said. “Ideally, we can create a treatment where we don’t have to use protein, deliver genes or modify cells. It can be a form of cell-based therapy.”

He and colleagues tested different growth factors from the appropriately-named bone morphogenetic protein (BMP) family on the basis of their ability to drive stem cells to become bone. The majority of research and therapy development focused on two members of the family, BMP2 and BMP7. But a 2007 study by He’s lab found that a neglected underdog, BMP9, was the real heavy hitter in pushing stem cells into a career as a bone cell.

But identifying BMP9 only gave researchers the key to bone differentiation, and it was necessary to find the lock as well. A new paper published by He’s lab last month in the Journal of Biological Chemistry, in collaboration with a team of Chinese researchers, tested out different receptors for BMP9 to determine which were critical for bone differentiation. The team tested a series of type I receptors (ALK1 through ALK7) to see which ones helped BMP9 drive MSCs - harvested from adult and embryonic mice - to become bone.

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The link between sports-related concussions and severe brain injury has been percolating in the press for several years now, due mostly to the tireless reporting of Alan Schwarz at the New York Times. But until this week, the research was lacking a prominent face, with most of those found to have suffered from early dementia and even death after multiple concussions unknown to all but the biggest football fans. That changed Wednesday with an article by Schwarz with an impossible to ignore hook: what if Lou Gehrig didn’t have Lou Gehrig’s Disease? In the ensuing days, the story has gained traction around the world, but also generated some justifiable skepticism.

That speculation (based on particularly circumstantial evidence) was an extension of an article published this week by researchers with the Center for Study of Traumatic Encephalopathy, which has led the way on the link between concussion and brain disorders in athletes. Previously, the group had found that deceased football players who had suffered multiple concussions during their careers, such as Lou Creekmur and Mike Borich, had several physical markers of Alzheimer’s disease despite dying at a young age. The new study shifts the focus to ALS, or amyotrophic lateral sclerosis, which was diagnosed in Lou Gehrig, prompting one of the most famous speeches in sports history.

In three athletes diagnosed with chronic tramuatic encephalopathy (CTE), the Alzheimer’s-like condition reported earlier, the researchers also found symptoms that resembled ALS: muscle weakness, atrophy, and spasticity. Autopsies on the athletes also found extensive death of motor neurons - the cause of ALS - but test showed that the damage resembled the brain damage seen in CTE rather than typical ALS damage. That suggests that brain traumas suffered during athletic competition can produce damage that simulates not one, but two of the most frightening neurological disorders. With exquisite timing, Carl Zimmer had a story at Discover the same day on just how such traumas could irreversibly damage neurons by stretching and contorting their string-like axons.

But while the science is interesting (and frightening), the link to Gehrig is shakier. Though the baseball player does not appear in the scientific article, the authors use Gehrig as a prominent example in the New York Times article, and cite newspaper records of the famous Ironman suffering head injuries in games but returning to play again the next day. But since his remains were cremated and his medical records remain confidential, there’s no way to tell whether Gehrig truly had ALS or the CTE-related faux-ALS described in the new article. That’s one of many criticisms Gary Schwitzer raises in his critique of the NYT article, alongside a neurologist urging caution regarding a journal publication based on a mere three case studies.

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For the next month, the world’s attention (and mine) will be focused on South Africa for the 2010 World Cup. Though it’s just starting to break through the public consciousness in the States, the World Cup is such a massive cultural force in the rest of the world that its tremors are felt even in scientific circles. A recent psychology study on how to take the best penalty kick got a lot of media play this week, and at least two different economists developed models to predict the winner via a country’s GDP and other factors (both picked Brazil).

I jumped into PubMed to see what other World Cup-related research could be found, and it turned out the water there was very deep. Since the last World Cup in 1996, dozens of scientific and medical articles have been published, ranging from editorials advising fans about potential diseases they need to be immunized against in South Africa to surveys of injuries suffered by referees during the tournament. But one topic appeared to drive much of the World Cup-related scientific debate, and it explains just how seriously the competition is taken around the world: does watching important World Cup games cause heart attacks?

The controversy started with a 2008 New England Journal of Medicine article called “Cardiovascular Events During World Cup Soccer.” A team of German researchers looked at emergency medicine records from June 9 to July 9, 2006, when the last World Cup was taking place in Germany, and compared the period to two control months free from international tournaments. According to the authors, “six of the seven games in which the German team participated were associated with an increase in the number of cardiac emergencies,” averaging out to a 2.5-fold increase in heart attacks. People with a history of coronary artery disease had an even higher health risk of watching their countrymen on the pitch: a four times increase in events. Blog founding father Jeremy Manier wrote about the study for the Chicago Tribune, and related it to local stress about the Cubs and Bears.

But wait - a counter-attack was sprung this year by an Italian team of researchers, who focused upon their own population during not only the 2006 World Cup, but the 2002 event as well as the 2004 European Championships. Studying more than 25,000 hospital admissions, the authors failed to find any uptick in heart-related events, even when Italy’s national team defeated France in a tense penalty shootout to win the ‘06 Cup (there was, however, at least one Italian with a chest injury that day). The Italian authors claim that their negative results are more in line with previous literature, including an English study that found only a small (but significant) increase in heart attacks and strokes during club soccer matches.

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With baseball’s Opening Day celebrated across the country this week, fans will begin their daily rituals of checking the small type at the back of the sports section to see who on their hometown or fantasy team has picked up an injury. But while baseball fans have become comfortable with slinging around phrases such as “plantar fasciitis,” “ulnar collateral ligament tear,” and “torn labrum,” the medical details of these injuries are often glossed over by sportswriters. So I sat down with J. Martin Leland, MD, assistant professor of orthopedic surgery at the University of Chicago Medical Center, to talk about baseball injuries, from the severe cases that destine a player for the disabled list to the wear and tear accumulated over a long season.

“It’s a 162 game season in baseball…no other game compares to it,” said Leland, who spent part of two seasons as a member of the Philadelphia Phillies medical team. “While one game might not be too taxing to a professional athlete, 162 of them sure are. There’s not a single baseball player that’s not sore for a majority of the season.”

Leland and I discussed some of the most common injuries seen in the sports pages each day and how they’re treated, as well as some current trends in sports medicine. Clip and save this article for when you see the dreaded combination of your favorite player’s name and “DL” in the ESPN scroll.

Lower Body Injuries

Baseball players are often forced to play in less-than-ideal conditions early in the season - Opening Day in Chicago seems to alternate between beautiful, sunny spring afternoons and weather more suited to dogsled racing. These chilly games are more than just annoyances to baseball players, they can actually lead to more of the most frequent injuries to affect position players: lower-body muscle pulls. The unique pace of baseball with its flurries of activity between long stretches of stasis can be hazardous to players expected to suddenly burst into action, Leland said.

“You can stand in the outfield for three innings and not do a single thing, and then suddenly there’s a shot and you’re running full blast,” Leland said. “So you get calf and hamstring pulls probably in equal proportions with other running sports. It’s the stop and go of baseball that really causes a lot of those muscle sprains.”

Even in warmer months, such injuries can result from the strain picked up playing almost every day for six months or more or from pure bad luck - Leland recalled one game where two different players went down injured after stepping on a base awkwardly while running. Players can reduce their chance of muscle pulls with extensive stretching, Leland said, explaining the long sessions of on-field stretching exercises a fan sees if they show up early for a game. And quick treatment after muscle pulls occur, such as hyperflexion of the knee after a quadriceps pull, can be the difference between missing a few games and missing several weeks.

“If you can’t run, you’re done in the outfield and for baserunning,” Leland said.

Current Examples: Daniel Murphy, New York Mets; Endy Chavez, Texas Rangers

Abdominal Injuries

To the untrained eye, the type of injuries baseball players suffer seem to come and go in waves, almost like fashion trends. One frequently-spotted injury that may appear to have only arisen in the last few years is the ubiquitous “oblique strain,” a pull of the abdominal muscles that can put a player on the bench for weeks. Leland said that oblique injuries didn’t come out of nowhere, but probably appear more frequent to sports fans due to increased media coverage and better diagnostic capabilities.

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Please welcome Laurel Mylonas-Orwig, author of today’s post and a new contributor to the blog!

Every two years, the best athletes in the world gather to compete in the modern Olympic Games. Against a backdrop of sand or snow, these seemingly superhuman competitors push their bodies to perform feats that would be impossible for the average person. Yet in the past few decades, concerns have mounted over whether some participants have gone beyond what the human body is truly capable of, relying on performance enhancers to reach new heights. In the 2004 Summer Olympics, a record number of athletes tested positive for banned substances, leading to several disqualifications and stripped medals. But in the just-completed 2010 Winter Olympics in Vancouver, drug testing has only caught two athletes thus far.

Despite this low number, experts are skeptical that athletes have stopped looking for illegal ways to gain a competitive edge. Instead, officials suspect that those who want to cheat have found ways around the current doping tests. The biggest elephant currently in the drug-testing room is an enhancement that is not yet reliably detectable, or even proven to be scientifically possible: gene doping.

Gene doping is a new and dangerous frontier in performance enhancement. An offshoot of gene therapy, gene doping may someday allow athletes to produce extra copies of genes that provide a competitive advantage such as increased muscle mass or endurance. At present, however, both gene doping and gene therapy remain largely untested in humans. Although some animal studies have shown promising results, others have demonstrated deadly side effects, leaving the effects of such treatments questionable at best.

Natural Enhancement?

When research into gene therapy began, it was not intended to yield performance-enhancing technology. Gene therapy is designed to treat debilitating or deadly medical conditions via the insertion of corrective genes into the body’s cells. But the theory behind gene therapy indicates that if the right gene were to be spliced into a healthy person’s DNA, a competitive edge could be gained. One example is that of erythropoietin, more commonly known as “Epo.” First purified in the late 1960’s by University of Chicago researcher Eugene Goldwasser, Epo is a hormone that promotes the production of oxygen-carrying red blood cells.

In 1997, a group of University of Chicago scientists led by Dr. Jeffrey Leiden experimented with Epo gene therapy as a treatment for Epo-responsive anemia, a debilitating condition caused by chronic renal failure. The study focused on the safety and efficacy of injecting a virus carrying the gene into the muscles of mice and non-human primates. Overall, the experiments proved successful: researchers were able to establish a threshold dose required for long-term Epo expression, and the elevated hematocrit, or red blood cell volume, in the animals that underwent the treatment led to increased aerobic ability. More importantly, no adverse reactions to the treatment were observed.

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I’ve come down with a severe case of baseball fever this week, earlier than ever before. Could climate change be to blame? Regardless, I thought I’d put that condition to good use with a couple pieces of science news from the sports world.

The Touchy-Feely Strategy

To tide me over through the long, slow crawl of spring training, I’ll be paying extra attention to college basketball as March Madness gets into full swing. As I start to ponder my bracket, I might do some scouting of how the top-ranked teams perform in an unusual statistical category: high-fives. That’s based on an unusual paper, reported recently in the New York Times, that correlated “tactile communication” with better performance in NBA teams analyzed during the 2008-09 season. The vocabulary of such communication includes the following, according to the paper: “fist bumps, high fives, chest bumps, leaping shoulder bumps, head slaps, head grabs, low fives, high tens, full hugs, half hugs, and team huddles.” What, no Christian side hugs?

The authors, from the University of California, Berkeley, wanted to test their hypothesis that touch is an important way by which humans build “trust, cooperation, and group functioning” (The paper has not yet been published, but is available from lead author Michael Kraus’ website). The background section mentions that primates spend as much as a fifth of their time grooming each other, and that several psychology experiments have found that brief touches increase trust and bonding between two people. That benefit, they reasoned, would be especially useful in team sports, where working together presumably increases chances of success (don’t tell Allen Iverson).

Testing this hypothesis involved “scoring” a number of basketball games from early in the 08-09 season for the above list of hands-on celebrations, as well as less overt “expressions of cooperation and trust,” such as talking, gesturing, passing the ball and helping on defense. The researchers then correlated those touch scores to individual players’ and teams’ performances over the rest of the season, and found a positive correlation for both. In other words, the touchier a player was, the better season they had; the touchier a team was as a whole, the more successful they were over the course of a season.

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The risks of being ahead of the curve in reporting on an experimental therapy: you never know when new information is going to shake loose from the scientific community. Tuesday, our Dr. FAQ series focused on platelet-rich plasma therapy, a treatment gaining popularity over the last year for a variety of sports-related injuries. J. Martin Leland, an assistant professor of surgery with our orthopaedic sports medicine team, explained the idea behind PRP therapy and the injuries it is currently being used on at the University of Chicago Medical Center and other health centers.

Leland also warned that PRP therapy remained experimental, without the double-blind, placebo-controlled trials that are the gold standard for proving that a medical treatment is effective. The day after I posted the videos, just such a trial was published in one of the leading medical journals, JAMA. The news was less than encouraging for PRP therapy. In a trial of 54 patients with an Achilles tendon injury called chronic achilles tendinopathy, PRP therapy in combination with a physical therapy technique called eccentric exercise was no more effective at reducing pain and increasing activity than a combination of placebo and eccentric exercise. News coverage of the research described the therapy as “no more effective than saltwater.”

The study itself highlights the difficulty of translating basic research into clinical application. Review articles, like this one, recommended the procedure based on promising results from lab-bench and animal studies, experiments which don’t always make the jump to the clinic. The authors also point out that invasive therapies, such as injections, can induce a potent placebo effect (even the participants in this study who received placebo showed significant improvement in pain and activity).

However, before PRP therapy is written off completely, it’s important to note that this study only tested the treatment in one specific kind of injury. After reviewing the JAMA, paper, Dr. Leland wrote the following statement to me about the current status of PRP therapy.

A Dutch study published in the Jan. 13, 2010 issue of the Journal of the American Medical Association (JAMA) found that an injection of platelet-rich plasma (PRP) performed no better than saline for chronic Achilles tendinopathy patients who were treated with eccentric exercises. This is an important study because it is one of the first of its kind regarding the effectiveness of PRP when used for the treatment of different issues in humans. However, this is only one of the first studies to come out and rash decisions should not be made based upon its findings alone.

I feel that physicians and patients should remain “cautiously optimistic” regarding the use of PRP. Over time, more and more studies will be published regarding the effectiveness of PRP. This study is a perfect example that PRP is not the solution to every problem. However, this is only one study on one specific disorder in the human body. Much more research is needed to determine if this study can be reproduced in other studies as well as what the effectiveness is of PRP on other parts of the body. In my opinion, the risks of PRP use are low and the benefits, in certain situations, may warrant its use. However, only research in the future will be able to specifically determine when and where PRP is specifically effective.

As the New York Times article linked above notes, a study showing encouraging effects of PRP therapy in combination with steroids for tennis elbow is forthcoming, and much more research is currently underway. So the story of PRP therapy is still just beginning, and it will be worth tracking which way the research tips on the procedure in the months and years to come.