Hot Peppers

The peppers that were tested helped with a lot of different things, including concentration and energy. You’ll need both of those while playing online blackjack.

Recently, the wife and I were enjoying a pre-movie drink at Chicago Cajun restaurant Heaven on Seven, when we made a fateful decision to order an appetizer. Being connoisseurs of spicy food, we decided to try an item called “Hot as a Mutha,” a breaded habanero chile pepper filled with jalapeno Chihuahua cheese and covered in peach salsa. It sounded delicious, and we weren’t perturbed by the little pepper icon meant to convey warning; after all, we were spicy-food veterans, we eat authentic Thai food like Cheerios and mainline wasabi.

Five minutes later, we were both furiously sucking on ice cubes, eyes watering, unable to speak, sharing a pain that showed no signs of abating. Chalk up another victory for peppers over the naïve and unsuspecting taste buds of Western Hemisphere humans.

Scientifically, the pain inflicted by hot peppers is actually a pretty well-studied phenomenon. The active ingredient, capsaicin, was used to find a novel protein, the vanilloid or TRPV1 receptor, which can be activated by that chemical, as well as heat and physical abrasion. Normally, this receptor is used to sense increases in temperature, so exposure to the capsaicin in hot peppers is literally like tricking your sensory system into thinking the external environment – or, say, the inside of your mouth — just got a lot hotter.

So, it’s not too surprising that typing “hot peppers” into PubMed yields a healthy 99 results, while the more specific “capsaicin” yields 8111. Besides the expected links to papers about TRPV1 receptor structure and function, some interesting avenues pop up, such as the analgesic properties of capsaicin (it can be used to treat arthritis pain), the chemical’s ability to protect against experimentally-induced strokes in gerbils, and use of capsaicin as a growth substrate in certain strains of bacteria. There’s also one paper about something called a pepper maggot, which I’m pretty sure I don’t want to know about, lest I swear off spicy food forever.

But one article I couldn’t resist reading in full contained a title promising “A hot new twist to hair biology,” the kind of groaner pun scientists relish the chance to use. Hair biology is also a topic near and dear to my heart, given that baldness runs through basically every male branch of my family tree, producing a deep genetic dread about the future status of my own mop. This study, conducted by a team of scientists at the University of Debrecen in Hungary, sought to determine why the TRPV1 receptor isn’t by more than just sensory neurons, where they mediate the temperature responses discussed before. One particular TRPV1-expressing cell type that piqued their Hungarian curiosity was hair follicles, in part because (to paraphrase the article’s introduction) hair follicles are cheap and easy to run experiments on. Times must be tough for funding in Hungary.

Thankfully, these studies were conducted using cultured hair follicles, meaning the follicle cells were grown in a dish, rather than in human subjects; the abstract worried me that some poor volunteers were washing their hair with jalapeno-based shampoo, which would be, er, unpleasant. The researchers exposed these cell cultures to capsaicin for five days and found that the chemical reduced hair shaft elongation, increased cell death, and inhibited proliferation of the follicle cells. So, rather than being a cure for baldness, the spicy component of hot peppers is actually a promoter of baldness, a result that’s probably a lot less profitable for the researchers. They do, however, suggest a clinical application in treating “unwanted hair growth,” surely a pretty lucrative industry itself; they also suggest that antagonists to these receptors may disrupt hair loss, by blocking the action of endogenous activators of TRPV1 receptors. But long story short: don’t go rubbing hot peppers on your head.

A side visit to the Wikipedia page for capsaicin turned up the intriguing information that capsaicin is being considered as a potential deterrent for illicit use of pain medication like OxyContin, as reported by the Harvard Gazette in 2004. The idea is basically to put capsaicin into pills, so that if taken orally, there would be no effect, but if crushed in order to be snorted or injected, the substance would produce “intense pain,” the equivalent of “snorting an extract of 50 jalapeno peppers,” according to anesthesiologist Clifford Woolf. Woolf also goes on to describe the sensation: “… on a one to 10 scale, the pain is about a thousand … it feels like a mininuclear explosion in your mouth.” This dude has clearly thought a lot about negative reinforcement for drug users.

Finally, if only we’d had the Internet at Heaven on Seven, we could’ve learned that the most effective way to cool pepper burning is drinking milk; water is basically ineffective. I also learned that the habanero peppers we ate rate at least 350,000 units on the Scoville scale, the international measure of a pepper’s hotness; by comparison, your humble jalapeno rates a mere 2500-8000. Scoville ratings used to be established by the humble low-budget system of dilution and taste-testing, but nowadays pepper heat is determined via HPLC (High Performance Liquid Chromatography), the common lab procedure used to measure the concentration of any solution’s component chemicals. Our personal measure of Hot as a Mutha’s potency: it’s hair-recedingly, gerbil-stroke-preventingly, drug-abuse-discouragingly, burning, enough to cut anybody’s spicy food ego down to size.

Interview: Johnny Tonic, Science Comic

comicFor the past 20 years, Johnny Tonic has been turning the science world on its head with his unique brand of comedy. Tom Hummer caught up with one of the world’s only science comedians to see what makes him tick. Scientific comedy is pretty cool, as long as it doesn’t go over your head. If you need to relax your brain in between jokes, play some online casino blackjack.

Tom Hummer: OK, I have to admit, I hadn’t heard of this before. In your own words, what is it that you do?

Johnny Tonic: Who else’s words are they going to be? Sorry, too easy. I’m a science comic.

TH: And what exactly is that?

JT: Well, someone has to get these uptight scientists to loosen up, and I’m the stirbar that makes it happen. So I travel around to scientific conventions and meetings and do my thing. Do some official shows, some unofficial, depending on what my agent can get. It pays the bills.

TH: How do you think you’re received at these meetings?

JT: I think I provide a nice break from the tedium of some scientific meetings. Some of those talks are like element five: Booorr-on!

TH: So how’d you get started?

JT: Funny story, actually. I was in grad school at the time…couldn’t get any NIH funding. So my advisor tells me I had to work longer and harder to get the job done. Naturally, I blurt out “That’s what she said!” Two seconds later, I was out on my ass. I took it as a sign from Darwin.

TH: But isn’t that ever a problem…I mean, does the scientific community really like to laugh? I’d be worried about working a room with a bunch of stiffs.

JT: That’s what she—

TH: Let me rephrase. Do scientists have a sense of humor?

JT: It’s all about timing, really. And knowing the audience. Like, in front of a bunch of geneticists, our famous “What determines maleness?” routine killed. Any chromosome joke, really. But for particle physicists, not so much.

TH: Can’t say I’m not familiar with that routine.

JT: Oh c’mon, you know: [Imitating two voicesWhat determines maleness? ‘Y.’ I just want to know. ‘Y.’Because I’m curious. ‘Y.’ That brought down the house at Human Genetics every year.

TH: Yeah, that’s not bad.

JT: Not bad?! You’re obviously not in genetics. I swear Francis Crick peed his pants when he heard that.

TH: And when you say ‘our’ I assume you are referring to your history with Bill Nye, the Science Guy.

JT: Jesus, that hack? Yeah, Will and I used to be tight, but he changed. Back in the day, we were grinding it out together, working the Science Olympiad circuit. Had dreams of playing the Nobel afterparty. But he sold out, big time. Went corporate and cleaned up his act.

TH: Cleaned up his act? What do you mean?

JT: Will was one dirty comic. He dropped so many F-bombs at a 1995 mechanical engineering conference that he got kicked out. But he didn’t care—you should’ve seen how many MIT chicks he nailed that week.

TH: MIT is coed?

JT: Oh, you bet! And they were all over him. Some of those freaks are easier than igniting Hydrogen.

TH: I’ll take your word for it.

JT: But yeah, Will used to make a lot of cleavage references, uranus jokes, stuff like that.

TH: Uranus jokes? That seems kind of played out, doesn’t it?

JT: But he had a new take on it. He would talk about the rings.

TH: Wow. That’s disturbing, and I’m not even sure what it means. So you weren’t too happy when he became the Science Guy?

JT: First of all—“The Science Guy”? Where do you think he got that? I was Johnny Tonic, the Science Comic, and he was Chemical Spill Will.

TH: Chemical Spill Will? Really? That sounds like a Garbage Pail Kid.

JT: Ha! He wishes. Oh, and that bowtie? My idea, too. It was for this bit where he’d go out in his labcoat and bowtie and complain about being bullied, said they stuck his test tubes where the sun don’t shine. He’d ask for a volunteer to help retrieve them—of course, no one would—and then he’d reach behind him and pull out a picture of Mammoth Cave. Geologists love that one.

TH: I bet.

JT: I actually heard Carlos Mencia stole it, except he used bongs and the “Dark Side of the Moon.” Hey, great job, Carlos—you got Pink Floyd fans to laugh. Now, I’m not above borrowing jokes—I ripped this Gallagher bit where I smashed the periodic table with a giant hammer—but give a brother some credit, you know?

TH: It’s hard to see Bill going from that to his TV gig.

JT: Apparently some corporate stiff just saw the outfit, thought he’d be great for some kids show. Threw a mole of cash in his direction, and The Science Guy was born. You ask me, now he’s more like Billy Nooshbag, the Science—

TH: Still have a beef, huh?

JT: Eh, it’s H2O under the bridge, I guess.

TH: Yeah, sounds like it. So what are you up to now?

JT: I’m still touring. Just played a show outside the big aquatic sciences meeting in Santa Fe. I tell you, those limnologists are nuts! Let’s see, I have an album coming out: Live from the St. Petersburg Convention Center, and I guess I should also mention my old albums, I’m Naked Under My Labcoat andYou Call That A Hypothesis?.

TH: Have you ever been heckled on stage?

JT: Of course, it happens to the best of us. Meteorologists are especially rough, they think every joke should be perfect. I mean, of all people.

TH: Any heckling stories stand out in particular?

JT: Oh yeah, back in ’96 or ’97, I was at this astronomy convention. Had this joke about Mars having Venus envy. Some drunk NASA blowhard starts needling me: “Yeah, well you’re the gaseous one!” Keep in mind he’s slurring every other word. I get to Jupiter and he starts calling me the “Great Red Dope,” and I couldn’t even get to my joke about the IRS’s favorite moon. He ruined a great set.

TH: That’s rough.

JT: Well, it happens to all the great ones.

TH: I hate to bring this up, but I understand you were in a bit of controversy over the last year. How did that come about?

JT: Well, against my better judgment, I made a joke about the Hurricane Katrina response. The audience did not take it so well.

TH: For the record, you stated, “Don’t blame Bush, blame the butterfly that flapped its wings in South America.”

JT: Yeah, that’s correct. And scientists still won’t let me live that down.

TH: Probably not a good idea to joke about Katrina.

JT: Yeah, I learned my lesson. It was dumb.

TH: Or was it the “Don’t blame Bush” part?

JT: Either way.

TH: So do you consider yourself more of a scientist or a comedian?

JT: I don’t think I’m more of either one. That’s what makes me so great. I am a science guy, but I also have comedy, my art. So really, I guess you could call me a science artist—a sartist.

TH: You’re an existentialist, too?

JT: Ooh, philosophy humor. Not my cup of tea.

TH: Sorry. Well, thanks for talking to me, and good luck making it to that Nobel afterparty.

JT: You know, I just want a chance. I think those Nobel guys would really dig my stuff. Except the peace prizers. Those guys are pansies.

The Brain Research Lab – The First Decade


Dr. Robert White has published several hundred papers over the course of his scientific career, a mountain of publication that would take weeks to read in full. As a public service, we’ve compiled his greatest hits, a short guide to how to do your own total body monkey transplants at home (provided you have a couple million dollars and a full medical staff handy).

White RJ, Albin MS, Verdura J. 1963. Isolation of the monkey brain: in vitro preparation and maintenance. Science 141: 1060-1.

Synopsis: Michelangelo is supposed to have responded to a question about how he was able to create his masterful sculpture with the answer: “It’s simple, I simply remove all the marble which is not David.” The procedure described in this paper is very similar, except that it involves removing all the monkey which is not brain. The isolated brains of smaller animals were supported by the circulatory system of beefy “donor” monkeys via a shunt on the donor monkey’s femoral artery and vein. Venous and arterial oxygen and carbon dioxide ratios were measured in order to establish that the detached brain was metabolically active. EEG recordings on the parietal and occipital lobes of the isolated brain confirmed that electrical activity persisted – despite the obvious absence of sensory input. When perfusion was stopped after an hour or two, so did the electrical activity.

White RJ, Albin MS, Verdura J. 1964. Preservation of viability in the isolated monkey brain utilizing a mechanical extracorporeal circulation. Nature 202: 1082-3.

Synopsis: Very similar to the 1963 article, except that the large “donor monkey” was replaced with a small “disk oxygenator” to re-oxygenate the blood, and a pump was used to circulate it. Because there was no liver in the loop (unlike in the 1963 procedure), increasing lactate levels made the blood gradually more acidic, which after a few hours resulted in the cessation of electrical activity. Despite the short term nature of these experiments, the authors remained optimistic, concluding that “In spite of the self-limiting design of these experiments and the eventual development of reduced biological function, this investigation demonstrates for the first time the feasibility of the protracted survival of the sub-human primate brain as a totally isolated organ, solely supported by a mechanical circulation system.”

White RJ, Albin MS, Locke GE, Davidson E. 1965. Brain transplantation: prolonged survival of brain after carotid-jugular interposition. Science 150: 779-81.

Synopsis: Similar to the first procedure again, but with dogs instead of monkeys. After the brain from one animal was isolated, it was transplanted into the body of another animal. You’d think the natural place to put a transplanted brain would be in the head of the recipient, but since connecting the new brain to the old spinal cord is impossible anyway, the authors in this case found it more convenient to place the donor brain in the recipient’s neck. Of course, neither brain realized they were sharing the same circulatory system with the other. How embarrassing. Wait, what’s that lump in your neck?

The scientific community is looking to expand more, and they’ve been using the internet to do so. One place you can see these discussions is at an online casino.

White, RJ, Albin MS, Verdura J, Locke GE. 1966. Prolonged whole-brain refrigeration with electrical and metabolic recovery. Nature 209: 1320-2.

Synopsis: You’ve heard the stories about people drowning in ice-cold water and then being revived an hour later with no problems? This paper is kind of like that, except that maybe an artic shark is involved so that when you are revived you are somehow missing your body. Isolated dog heads were cooled slowly to approximately 2 degrees centigrade, kept on ice for a period of hours, and then slowly warmed in a microwave.

No, just kidding! They were actually warmed by connecting the decapitated head to the circulatory system of a donor animal. I can’t believe you actually thought they were warmed in a microwave, that’s crazy. Once again oxygen and carbon-dioxide levels were used to establish that the resuscitated brain was metabolically active, and EEG patterns and pupillary responses were found to be relatively normal – even after the brain had been stored without circulation for up to four hours. If you think this sounds like fun, you want to try it for a longer period of time (say until the year 2350), and you’re not deterred by the fact that these researchers were unable to revive their brains after more than four hours, feel free to click here. Or better yet, you can PayPal me, and I’ll make sure everything is taken care of when the time comes.

White RJ, Wolin LR, Massopust LC Jr., Taslitz N, Verdura J. 1971. Cephalic exchange transplantation in the monkey. Surgery, 70: 135-9.

Synopsis: Just what it sounds like. Despite the EEG evidence that the isolated brains in the earlier procedures were still active, the authors decided that transplanting the whole head was the only definitive way to prove that a brain could survive the process of being connected to a donor circulatory system. So they removed the heads of both monkeys and sewed the head of one onto the neck of the other. Of course, all the king’s horses and all the king’s men can’t put a severed spinal cord back together, so even though they were able to connect all the necessary piping, there was nothing they could do about the wiring, and the animal remained a paraplegic. The million dollar question, of course, is whether they gave that monkey a new head or a new body.

[Here is a link to the National Geographic video. Warning - it's pretty gory!]

A Pill to Take or Not to Take

For all the advances in medicine, doctoring is still a risky business. Dealing with complex problems in the most nuanced of systems, the human body, few things follow a pre-determined algorithm. While scientific evidence and clinical judgment certainly help steer the odds, diagnostic and treatment decisions often involve taking chances. And at times, like these, the stakes are high.

From across the dim hospital room, Nicola Marshall’s eyes were clearly glowing — and as the senior resident on that night, it was my job to try to figure out why.

So as the intern asked questions, I took notes. She said she hadn’t noticed them turning yellow. Generally she had been feeling pretty well, but was more tired than usual. She had been working two jobs and stayed home a few times the previous week. But otherwise she was doing fine, without any concerns. She merely went to her doctor for a routine check, to refill her medications, and was surprised to have him send her to the hospital.

It was clear from her eyes’ yellow shine that the bilirubin level in her blood was extremely high. Bilirubin is a pigment formed when a protein in red blood cells breaks down. It’s the same pigment that causes jaundice in babies and bruises to turn yellowish before they disappear. When it’s circulating in abundance in the blood, it deposits in various places and the whites of the eyes quickly and predictably turn yellow. There was no doubt that Nicola had extra bilirubin in her blood; why she did was not so clear.

One of the more common reasons for excess bilirubin is liver damage. The liver helps manage the elimination of bilirubin in the body by conjugating it – making it soluble in water. Conjugated bilirubin is stored in the gallbladder as bile, and eventually sent out through the intestines. If liver function is compromised or if the normal route of bile flow is blocked, bilirubin backs up and leaks uncontrollably into the blood.

However, when we questioned Nicola about symptoms of liver injury, she denied having any fevers or chills, abdominal pain, vomiting or diarrhea. We wondered about liver-damaging viral hepatitis, but she said that she hadn’t eaten any different or raw foods lately (Hepatitis A), was sexually abstinent (Hepatitis B), and had never injected drugs or received a blood transfusion (Hepatitis C). What about binging on other common substances that might cause liver damage? It turned out that Nicola hadn’t had a drink in over two months and she couldn’t remember the last time she took Tylenol. And no one in her family ever had liver problems. She acknowledged after we brought it up that her urine was darker than normal and her stools seemed light, but that was no surprise to us; excessive amounts of bilirubin can result in “tea-colored” urine and “clay-colored” stools.

Other than her eyes, her physical examination was relatively unrevealing. Her breathing was untroubled and her heart rate was regular. Her abdomen was soft and non-tender, without distention or the presence of fluid. (Intra-abdominal fluid can be a result of liver failure, or leakage caused by abdominal tumors or infection.) Her liver was of normal size, and she had no peripheral edema (swelling in her arms or legs), tremors, or asterixis (an abnormal flapping of the wrists as a result of elevated ammonia levels in the blood), all of which made chronic liver failure unlikely. She was alert, oriented and wanted to make sure we knew that she wasn’t staying in the hospital past Friday, which is probably the surest sign of a working neurological system.

It wasn’t until we started looking into her recent medical history that we found some clues. Two months ago, Nicola had a heart attack – a big one. One day before her 57th birthday, and for the first time in her life, she felt a strong pain in her chest that woke her up from sleep. She popped an aspirin, felt nauseated, and called 911. By the time she got to the ER, her ST segments had shot up on her electrocardiogram and her cardiac enzymes were leaking into her blood, signifying serious damage to cardiac muscle cells. Her heart was dying, and if not for the 24-hour cardiac catheterization lab in the hospital, she might have died as well. Instead, she left the hospital pain-free with her right coronary artery propped open by three medication-coated stents (pastic tubes) and a stern warning never to stop taking her Plavix.

I wager that once you have a piece of plastic placed in an artery wrapped around your heart, all bets are off. Yes, the new stents are great at restoring blood flow, and in the setting of an ongoing heart attack, they undoubtedly save many people’s lives, like Nicola’s. But unless drastic lifestyle changes are made, the same underlying processes that led to the first heart attack remain – and now there is the ever-present risk of sudden re-occlusion.

If the stents were in me: once bitten, twice shy. At any moment after it’s placed, a stent can clog right up again. Just like that. With nary a warning sign, clumps of cells and protein can work themselves into a bundle right inside the stent itself. One minute the artery is open and the next minute it’s not, shutting out all the oxygen with it. Although it’s pretty uncommon, this complication of coronary artery intervention doesn’t often give second chances, usually leading to death or massive heart attack. It is this frighteningly serious event that has stent-carriers everywhere clutching their Plavix tight. Patients who take aspirin alone have a significantly higher risk of heart attack, stroke, and death one-year post-stent than those who take both aspirin and Plavix. So as it would seem, that’s one pill to surely take.

We are trying to keep up with this particular story, because there is always new information coming out about it. Sometimes, you can learn more while chatting at an online casino.

However, with the benefits of every drug come the risks. One week after her heart attack, Nicola was back in the hospital with dark, tarry stools, a sign of bleeding in her intestinal tract. She was feeling fine, but her blood count had dropped, nearly necessitating a blood transfusion. The gastroenterologists and cardiologists were called from the Emergency Room, and after she had cameras steered down her throat and up into her colon (two separate times) without much result, aspirin and Plavix were deemed the culprits. Although they work in different ways, as inhibitors of platelets (tiny cells that help organize clots) they both independently increase the chance of bleeding. In preventing life-threatening clots in the brain and around the heart, they also “thin” the blood all throughout the body. Some people get nosebleeds, some ooze from their gums, and some have microscopic bleeding from their small intestine. Nevertheless, she wasn’t dying from it, so the cardiologist wrote: Do not stop the aspirin or Plavix!

But this time, when Nicola came to the hospital, I thought her liver might be dying. We weren’t sure of the cause, but the blood tests showed profound liver damage. Her liver cells were spilling all their contents, bilirubin and ammonia were building up, and the ability of her liver to make basic proteins was failing. To corroborate the answers that Nicola gave us, we checked her blood for toxins (including illicit drugs, alcohol, and Tylenol), bacteria, viruses, and signs of autoimmune hepatitis (one’s own immune system attacking the liver). We ordered an ultrasound to look for obstruction of blood or bile flow and a CT scan to look for masses. We ran tests to fish for rare etiologies like primary biliary cirrhosis, primary sclerosing cholangitis and Wilson’s disease (too much copper). And, of course, we stopped nearly all of her medications in case they were the cause – but we didn’t stop her aspirin or Plavix.

Two days later, Nicola was in no better shape, but we had learned a lot about what was not causing her liver failure. As we initially thought, she did not have Hepatitis A, B, or C, the architecture of her liver and gallbladder looked normal, she never showed any signs of infection and she had not taken any illicit drugs, alcohol, or Tylenol. Nevertheless, all the while, her liver function was worsening. The measured time it was taking her blood to clot was climbing unnaturally because her liver was not making proteins well. Her risk of serious bleeding was going up, up, up, and with it went her our level of concern. Her gastroenterologist wanted her transferred to another medical center for a possible liver transplant. And he wanted to stop the Plavix. Yes, the Plavix!

It was at this point that several worlds of medicine collided. The cardiologists, forever concerned for her heart, still warned against stopping the Plavix. The gastroenterologists and me, fearing complete liver failure that could lead to death, wanted it stopped. According to the Food and Drug Administration (FDA), there are reports from post-market surveillance data that Plavix rarely causes acute liver failure. Of possible adverse effects, it’s so far down the list in frequency that it’s not something we typically even think of. In fact, liver failure didn’t happen even once during the controlled experiments on tens of thousands of people that proved the worth of Plavix as an effective medication. But now that the medication is being prescribed to millions, we are learning more about its possible dangers. In the case of Nicola and her Plavix we had to make a decision. How much extra benefit (to her heart) was worth the additional risk (to her liver)?

Since our medical team was calling the final shots, we stopped the Plavix and prepared for her transport downtown. And in the 24 hours or so after her last dose, her liver function seemed to stabilize. Her ammonia levels were sky-high but they caused her to hallucinate. Her bleeding times were prolonged but she never lost a lot of blood. And although her liver was failing, we were able to get her the hyper-specialized care she needed – all on account of the Plavix. I hope her heart agreed with our decision.


Food and Drug Administration. Plavix: prescribing information. NDA20-839/S-035.

Sniffing Cork: Bench-Top Boozing and the Health Effects of Red Wine

We have been looking for ways to measure and rate different scientific processes. The good thing is, if you want casino ratings, you can go check out

wine“If wine is so good for you, why do I feel like shit this morning?” asked a visiting college friend.

“Because you drank a bottle and a half by yourself and then ate two chalupas,” I responded, “and I’m pretty sure that none of the studies evaluating the health benefits of red wine have ever included slamming three-buck-Chuck and Taco Bell, but I could be wrong.”

“Yeah… But wouldn’t it be great if you could get hammered and it was, like, good for you?” It was this sort of statement that made me understand why my wife is never all that enthused about my college friends coming to visit. Plus she caught him picking up every single slice of leftover Thanksgiving turkey with his sticky fingers, returning pieces to the Tupperware until he found one that best suited his needs. From that point on, she refused to eat any more leftover turkey.

But my friend got me thinking about this whole red wine ass-kiss that’s been going on for over a decade now. You know how every month or so we find Sanjay Gupta’s toothy mug on CNN reporting on the latest in a seemingly endless string of conditions for which red wine is supposed to be the magic elixir? Heart attack. Stroke. Dementia. Cancer. Obesity. Diabetes. Aging…and God knows what else – maybe scabies? In fact, just a few weeks ago the cable news channel ran a story called “Red wine wonder drug?” with the tagline: “The answer to losing weight and living longer may be in red wine.”

So is red wine really the first substance in history to go against that well-known rule of adulthood: Anything that’s delicious or that makes you feel good probably also makes you fat, stupid, and impotent? Or, does all this favorable evidence originate from someplace darker and self-serving? In fact, I have an unfounded suspicion that most red wine investigators are unhappy, aging men desperately trying to justify their alcoholism and/or bolster the wine-producing economies of the governments that fund their research. I have no proof of this, but it just seems too convenient that a vice as universal as wine should posses such extensive medicinal qualities. What’s next? That gambling or sleeping with prostitutes increases immune function and fights off infection? Why don’t we take a quick look at the evidence and see if we can detect any ulterior motives at work.

1992: The potential health benefits of wine garner their first wave of publicity thanks to Serge Renaud’s “French Paradox” paper, published in the revered English medical journal The Lancet. How can the French eat six pounds of butter a day followed by a course of fried sweetbreads and chocolate mousse and still have a lower incidence of heart disease than Americans? The answer: a shit-ton of red wine.

At the time, it was already known that alcohol in any form reduces the risk of heart disease, most likely by preventing atherosclerosis, the hardening and narrowing of the arteries in which cholesterol builds up along vessel walls. Renaud’s work suggested that red wine in particular was a “superior quality” alcohol, which had additional protective benefits over other forms of booze. While this sounds plausible, I’d like to point out one thing for all the freedom-lovers out there: This guy’s name is probably pronounced “Ren-oh,” not “Ren-aw-duh.” That’s right folks, Monsieur Renaud is most likely a wine-chugging Frenchman – and let’s not forget that France has an awful lot of vineyards that could benefit from increased wine sales.

1992-1993: Researchers out of UC Davis (mere hours from California’s wine-glutted Napa Valley) assert that it is wine’s antioxidant properties that explain its superiority in preventing heart disease. Antioxidants are all the rage these days because they prevent damage from extremely reactive molecules containing oxygen atoms with unpaired electrons (free radicals) that can damage cells and DNA through a chemical process called an “oxidation reaction.” Oxidation of low-density lipoprotein (LDL), or the so-called “bad cholesterol” is thought to be one of the processes that leads to cardiovascular disease, and the researchers reason that red wine might act like a Berkeley policeman in the 1960s, reducing the number of free radicals at large and thus preventing the dangerous oxidation of LDL. The research team further concludes that red wine should be particularly beneficial, since most antioxidants in wine come from the skin, which as any sommelier will tell you, is removed in the making of white wine.

Meanwhile, on the other side of the country, a group at Cornell University’s Department of Fruit and Vegetable Science finds that resveratrol, an antioxidant found in grape skins, significantly lowers lipid levels in the livers of rats and thus may be at least partially responsible for the health benefits of wine.

1997: An article published in Science by a group at the University of Illinois’s College of Pharmacy finds resveratrol to have chemotherapeutic properties, preventing the development of early stage breast and skin cancers in mice. Efficacy is seen at doses equivalent to those obtained from moderate red wine consumption, but results are much more dramatic at higher doses. Since every starving scientist dreams of eradicating cancer, these data help trigger a worldwide surge in resveratrol research.

2002: A group at the University of Missouri report for the first time that resveratrol can cross blood-brain barrier and protect against cerebral ischemic injury (i.e. stroke) in gerbils. Other work conducted around the same time shows that resveratrol protects against DNA damage in stroke-prone rats and may also inhibit cell death caused by oxidation. The only problem is, most of these studies are conducted using doses well out of the range realistically available through wine consumption, even for hardcore winos and guzzling alcoholics. In my mind you can almost hear wine sellers, drinkers, and researchers the world over swearing resoundingly together. Even though the evidence is strong that resveratrol is effective in preventing cardiovascular disease, such high doses must be delivered in a pill, not a glass. Now scientists were obligated to follow through with what appeared to be a promising new field of research, only they could no longer justify getting schnockered while doing so.

2004: A review article in Cardiovascular Drug Reviews concludes that resveratrol is a “highly promising” cardiovascular protective agent with the ability to “influence vascular cell function, inhibit LDL oxidation, suppress platelet aggregation and reduce myocardial damage during ischemic episodes.” In other words, resveratrol protects against cardiovascular diseases, such as stroke and heart attack, by preventing the narrowing and obstruction of blood vessels. They further posit that the compound is most likely effective at doses equivalent to those consumed in wine. “PHEW!” say the scientists. Everything’s back on track. Of course this study was conducted in Italy, which just happens to be the world’s leading exporter of wine.

2003-2006: Researchers around the world attempt to characterize the mechanism behind resveratrol’s influence on cardiovascular pathophysiology. Since there are way too many published works on the subject to review here, I’ll summarize by saying that many groups find the compound effective in preventing, and/or slowing the progression of cardiovascular disease, most likely by attenuating atherosclerosis through anti-oxidant activity. Resveratrol certainly looks promising, but again, many of the studies are conducted using unboozable doses.

2006-present: Researchers from Harvard Medical School and the National Institute on Aging report that resveratrol offsets the negative effects of a high-calorie diet in mice. The mice fed a high-fat diet develop diabetes, get fat and die, whereas those fed the same high-fat diet with a daily dose of resveratrol still get fat, but fail to develop diabetes. The resveratrol group also live considerably longer. This is like every American’s dream – eat all you want, get fat, drink heavily, and don’t suffer any negative health consequences. However, once again the doses used in this study were truly astronomical: equivalent to a human drinking 750-1500 bottles of wine a day!

A French study published in Cell reports that mice given resveratrol (at doses equivalent to slamming roughly 8000 bottles per day) become more athletic, as assessed using tiny mouse treadmills. Treated mice can run twice as far, and have reduced heart rates compared to controls. The article suggests that resveratrol activates certain enzymatic pathways, which lead to increased numbers of mitochondria in the muscles. (Often described as “the powerhouse of the cell,” mitochondria are the machinery in our cells responsible for producing useable energy from nutrients.) The Frenchies also demonstrate that resveratrol increases the clearance of free radicals generated by mitochondrial metabolism. In other words, resveratrol allows for increased endurance while eliminating the negative consequences that result from increased energy expenditure.

Another study out of Mt. Sinai involves feeding moderate amounts of Cabernet Sauvignon to what must have been the happiest mice in all of science. They conclude that red wine consumption in the amount of one glass a day for women and two for men is enough to reduce the risk of developing Alzheimer’s disease. Ah ha! Isn’t it suspect that a team of mostly men would conclude that the hairier sex needs twice as much wine to fight off dementia as women! Oh wait, these are the amounts recommended by the FDA health guidelines as being beneficial without doing any harm. Never mind.

In conclusion, it does seem that there is good evidence that resveratrol, and by extension red wine, offers some form of health benefit. So maybe my theory that all wine researchers are alcoholics isn’t true – it’s probably only more like half. More importantly, a lot of work still has to be done to elucidate the mechanism of action and figure out the appropriate doses. With regards to the former, all that can be said at this point is that resveratrol’s broad efficacy is most likely due to its potent antioxidant properties. This seems like a pretty reasonable conclusion since free radicals play such an important role in heart disease, cancer and aging. With regard to dosing, there are still major disagreements about how much of this magic molecule one must ingest to garner any benefit. The levels of resveratrol contained in grapes, grape juice, and various other resveratrol-rich foods (for example, mulberries, peanuts, dark ales, and aged whiskey) are far less than those found in both red and white wine. The process of converting grapes into wine appears to greatly increases levels of resveratrol, making red wine (and to a lesser degree white) the only realistic dietary source of the compound. That said, the body of hard, scientific evidence supporting the low-dose, “drinkable” efficacy of resveratrol is small, and vitamin supplement makers are already starting to market mega-doses of the compound. Five years from now, resveratrol may come in a chewable shaped like Fred Flintstone and be as common in kitchen cabinets as vitamin C. However, at the moment, large supplemental doses of resveratrol have not been adequately studied for the potential negative effects of long-term use.

More importantly, where’s the cultural and culinary romanticism in popping a pill? I think it’s important to remember that while scientists tinker away in their labs, some of the best evidence we have about the efficacy of small doses of resveratrol goes back to what started this whole thing in the first place: the fact that wine-drinking cultures like the French and Italians continue to eat massive amounts of unhealthy food loaded with saturated fat and cholesterol, but still manage to outlive us Americans. That’s really all the evidence I need to justify my nightly glass of red, regardless of whatever self-serving, booze-addled experiments-of-debauchery these crazy drunken scientists are cooking up next.


Renaud S, de Lorgeril M. 1992. Wine, alcohol, platelets, and the French paradox for coronary heart disease. Lancet. 339;(8808): 1523-26.

Siemann EH, Creasy LL. 1992. Concentration of the phytoalexin resveratrol in wine. Am J Enology Viticulture 43(1): 49-52.

Frankel EN, Waterhouse AL, Kinsella JE. 1993. Inhibition of human LDL oxidation by resveratrol. Lancet 341(8852): 1103-4.

Jang M, et al. 1997. Cancer chemopreventive activity of resveratrol, a natural product derived from grapes. Science 275(5297): 218-20.

Wang Q, et al. 2002. Resveratrol protects against global cerebral ischemic ischemic injury in gerbils. Brain Res. 958(2): 439-47.

Bradamante S, Barenghi L, Villa A. 2004. Cardiovascular protective effects of resveratrol. Cardiovasc Drug Rev. 22(3): 169-88.

Baur JA, Sinclair DA. 2006. Therapeutic potential of resveratrol: the in vivo evidence. Nat Rev Drug Discov. 5(6): 493-506.

Lagouge M, et al. 2006. Resveratrol improves mitochondrial function and protects against metabolic disease by activating SIRT1 and PGC-1a. Cell 127(6): 1109-22.

Wang J, et al. 2006. Moderate consumption of Cabernet Sauvignon attenuates Abeta neuropathology in a mouse model of Alzheimer’s disease. FASEB J. 20(13): 2313-2320.

To Catch a Cheat: Testing in the Steroid Era

whizOK, stop me if you’ve heard this one before. There’s no doubt that steroids are the worst thing to ever happen to sports, disrupting the sanctity of athletics for generations to come and (probably) leading to the inevitable fall of mankind. While we might all agree about this, even the fate of the world may not be enough to sway the potential doping athlete to stay clean. Instead, a simpler maxim may win out: “It ain’t cheating if you don’t get caught.”

In the case of performance-enhancing drugs, however, getting nailed is not as simple as just getting caught with your pants down – though usually that’s how the process starts. The decrees of sports organizations are only as strong as the scientific technology that’s available to enforce the rules, and athletes looking to get a substance-induced edge are in a continuous battle with the testers trying to catch them in the act.

This is a battle with high stakes – the most coveted athletic titles in the world – and one organization, the World Anti-Doping Agency (WADA), has positioned itself as the international authority on accurate and state-of-the art testing. The Olympic Games and le Tour de France are the biggest events that specifically subscribe to WADA’s guidelines, sanctimoniously referred to as the Code. In the U.S., Major League Baseball (MLB), the National Football League (NFL) and the National Basketball Association (NBA) don’t specifically follow WADA guidelines, but all have started to ramp up their rules to combat a perceived tidal wave of doping athletes.  As a result of the apparent urgency of this problem, in recent years athletes worldwide have been subject to a set of increasingly complex procedures and sophisticated analyses to determine if they’re clean.

Your Pee, Please

The easiest way to avoid a positive detection is to provide clean urine. While this would typically be done by, well, not using steroids, athletes in the past have also used false bladders like the whizzinator to provide unblemished pee. Let’s see the requirements in place to avoid the old switcheroo:

WADA: “Once in the toilet facility the Athlete must remove all clothing between the waist and mid-thigh, in order that the Witness has an unobstructed view of sample provision. Sleeves should be rolled up so that the Athlete’s arms and hands are also clearly visible…The Witness shall directly observe the Athlete provide the urine sample, adjusting his/her position so as to have a clear view of the sample leaving the Athlete’s body.”

If you want to be thorough, you have to provide detail. Graphic detail.

MLB: “As you accompany the player to and from the restroom facility, be sure to walk BESIDE him, not in front or behind him. This way, you always have a view of the collection cup…You must have a clear and unobstructed view of the passing of the specimen. [No observing from behind.]”

I’m guessing the bracketed sentence did not appear in the job description.

NFL: “Dress Code: The player’s dress code for NFL drug testing is BARE ABOVE THE KNEES. No shirts or other upper body garments are to be worn for a test and all lower body garments are to be lowered to the knees.”

That is actually the exact opposite dress code of my grade school.

NBA: “Under direct observation of the collector.”

Open to interpretation, just like the Framers intended.

The athlete’s sample is immediately separated into the “A” and “B” containers, the second of which is only used to confirm a positive result from A. Otherwise, the B jar remains untested. A small remainder of the sample may be tested to ensure the integrity of the sample, such as measuring specific gravity and pH before any drug testing. The samples are identified only by an ID number, and a strict “chain of custody” process is followed to diffuse the possibility of framing, as if scientists would ever be so dishonest. Samples are then sent to designated testing centers – here the supremely commercialized NFL even manages to get in a plug for official sponsor Federal Express in their testing protocol.

There are currently only two WADA-accredited labs in the U.S., one in Los Angeles and another in Salt Lake City. The pro sports leagues, however, are less stringent, requiring that facilities only be approved by the federal Substance Abuse and Mental Health Services Administration (SAMHSA), which number around fifty nationwide.

The requirements for constituting a positive test result vary depending on the nature of the prohibited substance. Essentially, there are three distinct manners in which illicit use of a substance can be determined: (1) Detection, in any amount, of a prohibited substance or its metabolites; (2) Detection of a naturally occurring substance in a quantity greater than the allowable limit; and (3) Detection of secondary markers of doping.

The majority of this testing involves using gas chromatography/mass spectrometry (GC/MS) and the technique so nice they named it twice, liquid chromatography tandem mass spectrometry (LC-MS/MS). These techniques uniquely identify molecular compounds based on retention times in a gas or liquid stream and the mass-to-charge ratio of its characteristic ions. When these attributes precisely match those of a prohibited substance, a positive detection has been made.

Urine Trouble with Steroids

Anabolic-androgenic steroids exist in exogenous (not typically present in human body) and endogenous (naturally present) forms. For known exogenous steroids, testing is a pretty straightforward process. If the compound is detected in the urine sample, then it is marked as a positive. For those endogenous compounds that are found naturally in the body, however, it is important to set a threshold for determining a positive. For instance, compounds such as clenbuterol and methandienone must be present at a quantity of 2 ng/mL or higher to be considered a violation.

An interesting case is the steroid nandrolone, a commonly abused compound that is detected in an average of 0.23% of all WADA urine samples each year. Recently, San Diego Charger Shawn Merriman tested positive for the substance, resulting in a four-game ban. A nandrolone positive actually indicates the presence of its urinary metabolites, usually 19-norandrosterone (19-NA) at a level greater than 2 ng/mL. Although nandrolone is an exogenous steroid, 19-NA can be naturally produced as part of the pathway from androgens to estrogen. Several studies have examined how natural levels of 19-NA can vary following exercise or throughout the menstrual cycle, but controlled study has yet to find natural levels above the positive cutoff. However, exceedingly high levels are present in pregnant women, so such a scenario must be ruled out before reporting an adverse event. Don’t worry, guys, a far more plausible excuse is available: high urinary concentrations of 19-NA could, in theory, result from eating large amounts of uncastrated boar, particularly the liver, kidney and testes (need a recipe?) within a day of testing.

The major problem with these current testing techniques is the necessity that a compound must be characterized by its ionic properties before a lab can look for it. If a lab does not know of a newly-developed performance enhancer, the steroid will escape detection. This loophole is a major battleground in the fight between dopers and testing scientists. “Designer steroids” are developed and circulated among athletic circles unbeknownst to labs and sport officials, and until the labs get their hands on the substance, athletes have free reign. Such was the case with the BALCO designer steroid tetrahydrogestrinone (THG; “the clear”), which was analytically invisible until a syringe containing the steroid was anonymously mailed to L.A.’s Olympic Analytical Laboratory in 2003 (the sender was later revealed to be U.S. track coach Trevor Graham). But BALCO chief Victor Conte (himself no bedrock of credibility) has claimed that he was dispensing THG since at least 2000.

So the two sides are essentially pitted in an arms race (or legs, as the case may be). The deep pockets behind the athletes give them a leg up (or…never mind) in the clash, and they are probably always a step ahead of testers. The federally-funded U.S. Anti-Doping Agency (USADA) tries to compete by committing $2 million per year towards research. That’s not to say the USADA budget should be too much higher. Despite the hype, sports doping falls well below childhood obesity on the list of serious medical issues facing the country, though still somewhere above shark attacks. There is some hope, though. Recent research is making advances towards a method that does not require previous characterization of anabolic substances for detection, which would be a huge chink in the armor for the designer steroid market.

The scientific community encourages people to bring forward their ideas for exploration. You can even see people discussing them at a netti kasino.

The T Factor

GC/MS and LC-MS/MS techniques are also not foolproof when it comes to testosterone, because the endogenous and pharmaceutical variants look identical in these tests. Due to this inconvenience, the approach is instead to monitor the ratio of testosterone to epitestosterone (T/E). A normal T/E ratio is approximately 1:1, and use of any compound that artificially raises testosterone levels will do so without increasing epitestosterone; most organizations consider 4:1 the level for indication of possible foul play. So why not just take epitestosterone, too? This is in fact was the idea behind BALCO’s “the cream,” a topical ointment that contained both compounds in order to maintain a relatively even T/E ratio (this is not to be confused with Falco’s Rock Me Amadeus, which is pure testosterone). But organizations have caught on – epitestosterone, which has no direct benefits, is now a prohibited substance as well.

Due to some natural variability of T/E ratio, it is not typically considered an absolute marker of doping. Instead, a second test can be performed to detect the carbon isotope ratio (13C/12C) in the urine, which can differentiate between endogenous and exogenous testosterone. WADA states that this test should be performed for anyone with a ratio over 4:1. The NFL policy is similar, but if the ratio is above 10:1 they don’t even bother: the athlete is “conclusively positive.” The carbon isotope ratio – well, it’s complicated – let’s just say it changes with your diet, and the 13C/12C value of testosterone or its metabolites should match that of the reference compounds that are altered with diet.

The complexity of testosterone testing is well-illustrated by the curious case of Floyd Landis, who overcame a degenerating hip and a wispy mustache to finish first at last year’s Tour de France. Landis was suspected of doping, and though the case has yet to be fully resolved, many Americans immediately came to the defense of Landis since he’s from the U.S. and he doesn’t play baseball. After a high T/E ratio was found in both the “A” and “B” samples, though, WADA reported that the carbon isotope test found that Landis had used synthetic testosterone. Landis has disputed the results on a variety of levels, primarily blaming failures to follow WADA’s own scientific protocol.

Note: A Landis defense can be seen here; I don’t recommend it unless you want to see a man with a lot of pins on his vest speak to a bunch of cyclists who have no idea what he’s talking about. Actually, scratch that – I recommend it for those same reasons. The woman who introduces him…well, just watch it. But don’t watch the whole thing.

The case does present an interesting point about the nature of testing and doping. The length of time over which a substance is detectable is typically related to the duration it actually benefits performance. For instance, stimulants assist the athlete for only a matter of hours, and can be discerned in the urine for only a few hours or days, so a positive result would most likely only be seen immediately after competition if an athlete is effectively cheating. Likewise, athletes may not appreciate the long-term effects of most anabolic steroids come testing time, as the compounds are detectable for several months following injection. (Sometimes, a specialized test is even necessary to ensure that an athlete has not injected again since a previous positive test.) In the Landis case, the high T/E ratio occurred between two days of testing with a T/E in the normal range. There would be no real advantage of taking testosterone for one day only; it is better suited for long-term muscle growth. So either Landis botched his masking technique (not inconceivable) or the French screwed up (no comment).

hGH: The Worst Form of Cheating?

Much recent firestorm have focused on the lack of testing for human growth hormone (hGH; the injected form is recombinant hGH, or rhGH) in the major American sports leagues. hGH is naturally released in pulses by the pituitary gland and, among other functions, promotes growth (particularly in childhood) and increases muscle mass. But here’s the funny thing about supplementing with rhGH (as I resist temptation to call this “the straight dope”): it might not even work. Controlled research of supraphysiologic use of hGH in normal adults has found that muscles may increase in size, but there is no change in strength (though it may help protect muscles or tendons from rupture).

So why might rhGH be attractive to athletes? Perhaps just the very fact that it is difficult to detect. It’s like cheating on your high school geometry test. When you copied your classmate’s acute answer, were you more concerned with its correctness or whether your wandering eyes would be spotted? If you didn’t get caught, at that point a right answer is a bonus. So it goes with rhGH: Other guys are doing it, and there aren’t any repercussions (professionally speaking), so why not?

Now, technically, we don’t really know how many athletes use rhGH. And, technically, it is possible to detect, via a blood test (urine concentrations are extremely low). At the 2004 Olympics in Athens and the 2006 Games in Torino, blood samples from athletes were tested for rhGH. Total positive tests: zero. You see, rhGH has a short half-life, so it can only be detected in the bloodstream within about 24-36 hours after injection. Such testing is thus better suited for randomly timed testing, but it would still be a logistical nightmare to implement testing that requires such immediate action.

Of course, another requirement is that the league actually tests for the hormone. No American professional leagues take blood samples, thus eliminating the possibility of detecting rhGH even though it is listed as a prohibited substance by MLB and the NFL. When NFL commissioner Roger Goodell recently explained, “There is no reliable test for hGH right now,” he wasn’t too far off. Reliable? Yes. Useful? Not really. Even if a better blood test is developed, it is unlikely to be implemented without a fight. NFL Player’s Association chief Gene Upshaw has stated that he is opposed to any type of blood testing for pro football players, who have a reputation for being squeamish.

In the end, this debate probably doesn’t matter too much. It is thought that rhGH is often taken in concert with steroidal compounds, which would do the real dirty work. Barry Bonds reportedly took rhGH with his supplements of THG (“the clear”) and testosterone (“the cream”). If reliable tests for these more potent compounds are in place, then the hGH problem is not so significant.

There are plenty of other doping techniques and new methods on the horizon, where new battle lines will be drawn. The next step may be gene doping, in which genetic alterations would be utilized to enhance muscle growth. WADA claims they will be able to test for gene doping. Now, if you read enough WADA press releases, you catch on that they don’t like to admit that they can be beat. It’s a good stance to have—they function best as a combination of impartial policing and fierce intimidation. And if its intimidation you want, having a chief named Dick Pound goes a long way.

So the quest continues, and the battle will likely never be truly and completely won. The never-ending struggle makes one long for the days before the steroid era, a time when sports were pure. Back then, you didn’t need a biochemistry degree to know whom to respect. Instead, the cheaters did it the right way: by stealing signs, sharpening spikes and corking bats. Now, that is how sports were meant to be played.


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Bidlingmaier M, Wu Z, Strasburger CJ. 2000. Test Method: GH. Baillieres Best Pract Res Clin Endocrinol Metab. 14(1): 99-109.

de Geus B, Delbeke F, Meeusen R, Van Eenoo P, De Meirleir K, Busschaert B. 2004. Norandrosterone and noretiocholanolone concentration before and after submaximal standardized exercise. Int J Sports Med. 25(7): 528-32.

De Wasch K, Le Bizec B, De Brabander H, Andre F, Impens S. 2001. Consequence of boar edible tissue consumption of nandrolone metabolites. II. Identification and quantification of 19-norsteroids responsible for 19-norandrosterone and 19-noretiocholanolone excretion in human urine. Rapid Commun Mass Spectrom. 15(16): 1442-47.

Dean H. 2002. Does exogenous growth hormone improve athletic performance? Clin J Sports Med. 12(4): 250-53.

Green GA. 2006. Doping control for the team physician: a review of drug testing procedures in sport. Am J Sports Med. 34(10): 1690-98.

Hemmersbach P, Hagensen Jetne AH, Lund HS. 2006. Determination of urinary norandrosterone excretion in females during one menstrual cycle by gas chromatography/mass spectometry. Biomed Chromatogr. 20(8): 710-17.

Nielen MW, Bovee TF, van Engelen MC, Rutgers P, Hamers AR, van Rhijn JH, Hoogenboom LR. 2006. Urine testing for designer steroids by liquid chromatography with androgen bioassay detection and electrospay quadropole time-of-flight mass spectrometry identification. Anal Chem. 78(2): 424-31.

Rosen T. 2006. Supraphysiological doses of growth hormone: effects on muscles and collagen in healthy active young adults. Horm Res. 66(Suppl 1): 98-104.

Bees, Cell Phones, and Human Extinction

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beeLike any technology ubiquitous enough to earn borderline essential status in modern society, cellular phones have accumulated a long list of urban legends, catching the blame for a whole slew of modern maladies. From reasonable and scientifically supported claims about cell phones increasing auto accidents and hearing damage to more specious scares over their ability to cause everything from brain cancer to plane crashes, cell phones are the current favorite villain of publicity-starved politicians and people who wear tinfoil hats. Now, cell phones are catching the blame for the mysterious bee disappearance that has hit the United States and Europe this summer, an ecological disruption that is beginning to cause Y2K-like media panic. Has our selfish desire to be phone-accessible to friends and family 24/7 inadvertently set in motion agriculture disaster and mass starvation?

First of all, you may have noticed the creepy X-Files like shortage of bees as a nature curiosity that’s slowly creeping up into the periphery of the media’s visual field. In fact, people hip to the world of bees (known as apiarists, if you were wondering) have been worried about this population decline for a while now, even coming up with not one but two scary acronyms: CCD, for Colony Collapse Disorder, and the much cooler VBS, Vanishing Bee Syndrome. As with a lot of animals, bee numbers have been declining for quite some time, due to a variety of ho-hum factors like urbanization and pesticides. But the sudden uptick in bee disappearances, and the widespread geography of the occurrence, have put the bee community on red alert and set researchers on desperate hunts for the missing factor behind the mystery.

Right now you’re likely thinking “why should I care about bees? Fuck bees!” It’s an understandable impulse, given that bees are best known by humans for their ability to ruin picnics, torment Winnie the Pooh (or Nick Cage), and threaten the life of that pale, sickly kid with all the allergies back in 2nd grade. Furthermore, you’d guess the most direct effect of a bee shortage would be a decline in honey production, which is kind of a bummer, but hardly a foodstuff that is essential to mankind’s continued existence. Ah, but don’t forget the bee’s important day job, pollination, which is not merely the creepy, sexually-deviant process you vaguely remember from biology class, but an essential component of the agricultural industry, playing a role in fertilizing crops such as apples, berries, almonds, cucumbers, and many more.

Hence, when the bees leave town, so too do a lot of our fruits and vegetables, and if the problem gets bad enough (some regions are already reporting a 60-70% decline in populations), one can easily imagine a slippery slope down to Biblical-strength famine conditions, especially if one is a Fox News copywriter. Researchers are therefore justified in urgently tracking down the cause of CCD, and have investigated possible culprits like insecticides, genetically-modified crops, climate change, malnutrition, and weird-sounding beekeeper practices like “bee rental.” But by far the sexiest explanation for the mass bee abductions is the electromagnetic radiation produced by cell phones, a story first publicized by a British paper – always good sources for crazy, erroneous shit – called The Independent.

You see, the weirdest thing about CCD is that you don’t just find an empty beehive with a bunch of dead bees on the ground around it, evidence of the kind of bee genocide you’d expect a nasty insecticide to cause. What is usually found is a colony with no adult bees, without the corresponding pile of dead bee bodies that logically should accompany such a shortage. The bee larvae remain present, and there’s plenty of food stored up, but no adults, as if they all just decided to skip town simultaneously. Thus, one explanation theorizes that the bees aren’t dying off, they’re merely getting lost on their way back home, due to some disruption of their navigational systems.

On April 15, The Independent waded into the scientific publication waters and came back with the most eye-catching explanation of all: cell phones were the true cause of the bee aberrations! They cited a 2007 paper, by the German Stefan Kimmel and colleagues that found (in The Independent’s words), that “bees refuse to return to their hives when mobile phones are placed nearby.” A quote from the study’s senior author, Jochen Kuhn, appeared to support the newspaper’s interpretation of his results, though astute journalistic observers may have noticed that the “quote” from Kuhn was only one word long: “hint.”

And … they’re off! The media, already starting to smell a good old-fashioned “fear culture” story with the bee disappearance, jumped all over this new connection as the next in a long line of stories exploiting our discomfort with complex modern technology. Throw the word “radiation” and “extinction” together with an electronic object we all hold up to our ears for minutes or hours per day, and you’ve got a crackin’ story, brother! A Google search of “bees AND cell phones” will tell you all you need to know about how fast the story spread around the internets, and the news portal Digg reports over 1300 hits for the original story, with an ensuing discussion that counter-proposes a “bee rapture” and bees’ ability to exist in six simultaneous dimensions as alternate CCD explanations.

There’s a less exciting rebuttal to the cell phone-bee relationship, however; The Independent just read the damn study wrong. A quick reading of Kimmel’s paper shows that 1) it was a small pilot study with very subtle results and 2) they didn’t even use freaking cellular phones in the study. What Kimmel and friends actually tested was the ability of cordless phone base stations that were actually placed inside beehives, to throw off the navigation of bees. Bees were marked as they were leaving their hives (not a fun job, I imagine), and then hives with implanted phone stations were compared to non-phoned-up hives to see how many bees came back. In the end, bees were less likely to return to the hives with the electromagnetic radiation-spouting cordless phone bases, but only by the slimmest of statistically significant margins: 63% for the control group vs. 55% in the experimental groups.

Obviously then, the jump from this short, humble little paper to “OH MY GOD CELL PHONES WILL KILL US ALL” requires a bit of creative license on the part of the newspaper. Caught in the middle were the researchers themselves, who were probably sitting around on April 14th muttering “nobody ever cares about our work” only to be wistfully recalling their long-lost obscurity by the 16th. As reported here and here and here, Kimmel and Kuhn were shocked by the distortion of their study, saying they never set out to study CCD, and bemoaning the media attention: “It’s not my fault if people misinterpret our data,” said an obviously flustered Kimmel to the International Herald Tribune. “Ever since The Independent wrote their article, for which they never called or wrote to us, none of us have been able to do any of our work because all our time has been spent in phone calls and e-mails trying to set things straight. This is a horror story for every researcher to have your study reduced to this. Now we are trying to force things back to normal.”

The link between manmade electromagnetic fields and bee navigational issues may not be total fantasy; as this page discusses, bees (and a lot of other insects) use some of the same frequencies as various electronics to orient themselves spatially. However, bees also really like to make hives underneath power lines, which suggests that they don’t really mind being around gigantic sources of electrical interference. The evidence for this interaction, at best, is flimsy, anecdotal, and insignificant compared to the accumulating negatives about how pesticides and genetically-engineered crops affect bees and ecosystems in general. Hell, it may not even be a human effect at all; a similar, but less dramatic, bee decline in 2004/05 was eventually attributed to a gross little parasite called the Vampire Mite. So don’t worry too much that texting your pals is contributing to the global bee disappearance … unless you are texting them from inside a beehive, that is.


Colony Collapse Dot Org

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H.E.S.E. Project. 2007. Decline of bees, UK and worldwide.

Kimmel S, Kuhn J, Harst W, Stever H. 2007. Electromagnetic radiation: influences on honeybees (Apis mellifera).

Johnson C. 2007. Researchers: Often-cited study doesn’t relate to bee colony collapse. Foster’s Online, April 22, 2007.

Lean G, Shawcross H. 2007. Are mobile phones wiping out our bees? The Independent, April 15, 2007.

Sylvers E. 2007. Wireless: Case of the disappearing bees creates a buzz about cellphones. International Herald Tribune, April 22, 2007.

Hydrofatality! – The Science and Culture of Excess Fluid Consumption

One of the best things that scientific technology has given to us is mobile devices, even though many people just use them to play games at

Ah, precious, nurturing water: so fundamental to our existence, so synonymous with life in all its forms. Our bodies are around 60% water; you may have heard higher figures, but the fact that this number is often inflated is evidence of the degree to which our culture is obsessed with hydration. To ensure our health, we are often told it is necessary to consume at least 8-10 glasses a day. We are even taught to mistrust our own thirst; thirsty or not, we are told, one should “push” water during exercise or when outside in the heat. Where convenience stores used to have one or two brands of bottled water, there are now shelves lined with dozens of different varieties; some advertise the purity of their contents: “Fiji Water never meets the compromised air of the 21st century!” while others advertise their embellishments: caffeine, vitamins, taurine, selenium. Of course, hydration is not just a fad – water is, in fact, crucial to our existence. But there are limits, however rarely breached, to water’s beneficial effects. Even venerable Hippocrates recognized that “everything in excess is opposed to nature,” and water is no exception.

If you’ve been paying attention to the news, you’ve probably heard about the recent death of Jessica Strange, a woman in California who died from drinking too much water in a “hold your wee for a Wii” contest sponsored by a local radio station. It may or may not have come as a surprise to you that too much water could be fatal, but it certainly wasn’t a surprise to everyone. Part of the insane tragedy of this story is that the DJs apparently ignored a number of people who called the radio station to tell them that this contest was no joke. It might be a stretch to blame the ignorance involved in this tragic event on our “if some is good, more is better” American culture, but at the very least it goes to show how hard it is for some people to get their mind around the idea that any quantity of something so necessary to life might be deadly.

On the other hand, many people have an intuitive sense of why drinking lots of water might be bad for you: because it dilutes your, you know…stuff. The fact is, if by “stuff” you mean sodium, that’s a pretty good start toward explaining how water can be deadly. Generally, American diets are high in sodium, and we often hear TV docs saying that it is good to cut down your sodium intake, that too much salty food is bad for you, and therefore as a rule, the less salt the better. But despite its bad rap in our culture, sodium is just as essential to life as water. If we’re talking canned soup, “30% less sodium” might mean that it’s good for you, but when we’re talking bodily fluids, a reduction in sodium concentration of just a couple percent can have devastating effects. This is especially true in the heart and brain, which rely on the maintenance of sodium concentrations for their normal functioning.

When the body is inundated with water, hyponatremia (abnormally low sodium) can result, and in extreme cases, the brain swells like a balloon inside the skull, producing confusion, dizziness, nausea, coma, and in extreme cases, death; a constellation of symptoms that together are known as “water intoxication.” To understand why this dangerous swelling occurs, it’s important to understand something about the salt and water economy in the body.

Under normal conditions, the body is as meticulous as a freshman designing a Myspace page about keeping the balance of salt and water just right. Water can move relatively freely between the insides and outsides of cells; typically about two thirds of the water in your body is located inside cells and the other third is located in the circulating fluids outside of the body’s tissues. Sodium, on the other hand, is highly concentrated in the extracellular fluid, ensuring that intracellular and extracellular fluids have about the same amount of “stuff” dissolved in them, and keeping the net movement of water across cell membranes to a minimum. In the case when you have, for example, maybe ingested a pound of rock salt or five gallons of tap water, it’s not hard to imagine this delicate balance being thrown entirely out of whack. In the latter case, the extracellular fluid can become more diluted than the intracellular fluid, causing the cells in organs like the brain to quickly soak up excess water like sponges, expanding in the process.

If identified quickly, even severe cases of acute water intoxication can be treated relatively easily. As you might expect, the condition can be rapidly reversed by the intravenous administration of hypertonic saline (basically just extra-salty water). For those of you do-it-yourselfers out there, it’s worth pointing out that just drinking a glass of saltwater is not recommended, because the absorption of sodium through the stomach is not terribly efficient. Plus, if the two gallons of water in your stomach haven’t made you nauseous already, drinking a cup of saltwater might. One of the little ironies of water intoxication is that nausea is an extremely potent inhibitor of urination, so urination is actually inhibited in one of the cases where you need it most. Substituting sports drinks for water won’t keep you out of trouble either, since sports drinks actually contain only about one tenth of the sodium concentration that you need. There is absolutely no evidence that Gatorade is better than water with regard to the risk of hyponatremia.

So how much fluid does it take to get into the danger zone? Jennifer Strange, the woman who died in the radio contest, drank an 8 or 16 ounce bottle of water every 10-15 minutes, totaling 224 ounces or almost two gallons of water in a couple hours, a number that’s probably at the low end of the potentially deadly range. In fact, given the large quantities of water involved, cases of fatal water intoxication are relatively rare. The first recognized human case wasn’t described until 1935, although the phenomenon was observed in animals a number of years earlier. Curiously enough, the 1935 fatality wasn’t due to excessive drinking, but was instead a consequence of (and I quote) “the administration of nine liters of tap water by rectum.”

Although excessive thirst and other disorders of water maintenance can occur in some forms of diabetes and other diseases, death by water often seems to involve the same peculiar mix of insanity, tragedy, and ignorance embodied in the case of Jessica Strange. Before the latter quarter century, cases of compulsive water-guzzling and the resulting mal effects were restricted almost exclusively to psychiatric wards. Patients attempting to “’wash out parasitic worms’, to ‘keep the body pure’, and to ‘cleanse the body of sins’” have been observed to ingest up to 10-20 liters of water in a day. In recent decades, however, there have been a number of fatal cases of hyponatremia in two other less obviously at-risk populations: endurance runners and U.S. Army recruits.

Conventional Science: A Field Report from SfN ‘06


Chapter 1: A Disappointing Lack of Baking Soda and Vinegar Volcanoes

Every profession or hobby has its ritual gathering: doctors have their conferences, Trekkies have their conventions, salespeople have their trade shows. Once a year, scientists are coaxed out of their lab holes for their own forced assembly, traveling with poster tube in tow to a (hopefully) warm location suitably outfitted with a large enough exhibition hall. Ask any random scientist, faculty member, or student whether they look forward to these events of concentrated data, and you’ll get a negative response or curse word 9 times out of 10, despite the fact that these meetings are, in theory, a chance to show off your work to a potential crowd of thousands, harvesting their criticism and advice by the bushel. The most obvious reason for this disconnect is that science, so often a solitary pursuit, is an awkward fit for the big-convention model of glad-handing, vendor-pimping, and nighttime debauchery.

This contradiction is magnified at the largest scientific conferences, foremost among them the Society for Neuroscience Annual Meeting, which landed this year in the Olympic ruins of downtown Atlanta. Attracting over 30,000 attendees per year, and able to squeeze into only the most cavernous of convention centers, SfN sets a standard for girth and breadth among the scientific disciplines, swelling to a pretty much impossible-to-navigate size. This obesity results largely from the diverse territory that falls under the umbrella term “neuroscience,” a field which has come to encompass everything from clinical neurology to human psychology to behavioral research to molecular biology to genetics, along with every line of study that falls into their gaps. Throw all of this research into one (albeit very, very large) room and you get a confusing mix: something like a peanut butter, sausage, and blueberry casserole.

If the variety of science on display doesn’t faze you, the layout will: imagine the kind of gargantuan rooms used for car shows, let’s say 5 football fields lined up horizontally, filled with row after row of 3’ X 6’ posters. Now imagine those posters being changed twice daily, replaced a total of 9 times over the course of the conference. Imagine further a small city of vendor displays nestled between the rows of posters, plus constant, overlapping talks, symposiums, slide presentations, mini-symposiums, continuing education classes for physicians, press conferences, informational sessions, socials, and seminars all orbiting around the central mass of the poster sessions. Oh yeah, and all the pre-conference meetings that occupy the surrounding ring of hotels for days before the meeting even officially begins. That’s a fucking avalanche of science right there.

Unless you’re one of the lucky few who a) knows someone on the organizing committee, b) discovered something really cool in the 1970s, or c) pestered someone into letting you chair a topical symposium, the typical pebble contributed to the mosaic of an SfN meeting is a poster. A glossy industrial-printed rectangle summarizing your past year of research, it’s the visual aid for your four hours of service at the conference, a vehicle for hollow praise, vicious criticism, and all the social courtesies in between. Yes, a large scientific conference is really not much different from a grade-school science fair, albeit with a disappointing lack of baking soda volcanoes and award ribbons.

This year’s setting, the triumphantly named World Congress Center, was no different than the other aircraft-hanger convention centers that have paid host to the SfN meeting, save for the unusual surroundings: the CNN headquarters building, the Atlanta Falcons-hosting Georgia Dome, the Olympics’ infamous Centennial Park. The interior was standard sky-high ceiling/industrial-carpet décor, with the one quirk being the remarkably subterranean location of the poster hall and largest lecture room, with four downward escalator rides required between front door and the epicenter of the meeting. This architectural decision ensured that no natural light would tempt us away from our business, while cattle-herd traffic jams filled the spaces between sessions as 30,000 people were gently shepherded through four tiers of single-file escalators by bored security guards. But hey, at least we weren’t running around the cruel 10-mile long corridor of the New Orleans convention center, where the meeting was originally scheduled before nature’s fury pre-empted science.

Chapter 2: Opening act: Am I boring you as much as you’re boring me?

Before the convention proper could begin, it was my duty to attend the official pre-meeting of the shady government operatives who write my paltry paycheck, the National Institute on Drug Abuse. This event was held not in the convention center, but in the stalk of Atlanta’s shiny, cylindrical Westin, ritzy digs to be sure, but the schedule was tauntingly devoid of any events in the revolving restaurant on the top floor. The meeting was focused on drug addiction, Frontiers in Addiction Research, to be exact, and was notable for its inclusion of the precious resources of coffee, snacks, and lunch in its $50 registration fee. With about 500 people in attendance, it was relatively intimate by the standards of SfN, yet the subject matter still reflected the difficulties in navigating such a conference, with four sessions (of four speakers each) all ostensibly about the same topic but utilizing far-flung methodology: satisfying everyone, pleasing nobody.

If anything, the over-stretched diversity of fields was a fascinating sociological demonstration of the different languages that scientists speak, far from the homogeneity assumed by people outside the field. Perhaps it’s my bias, but the electrophysiologists seemed the most balanced, presenting the interesting fact that narcoleptics are less likely to be addicted to drugs, and then detailing what the protein messenger implicated in narcolepsy (orexin) does to areas of the brain associated with reward. On the other hand, the social neuroscientists were by far the most entertaining group, because they rarely had anything resembling hard data to present, leaving them free to wildly speculate about abstract concepts like impulse control and stimuli reappraisal with Shakespeare quotes and Venn diagrams. Most fascinating was a talk on dominance hierarchies and addiction potential in monkeys, from which I learned that monkeys at the bottom of the social ladder exhibited changes in receptor function that are associated with increased drug reward in humans; a fairly political and socially relevant finding for a field (addiction research) that tends to shy away from such (gasp!) potentially useful applications.

However, the afternoon sessions killed the momentum of the morning, leading off with a quartet of genetics researchers that were all build up and no pay off. The quest for polymorphisms (genetic markers) that may predispose people to addiction or make them more responsive to the effects of abused drugs is a fascinating endeavor, which makes it even more astonishing that these people could give such dry talks, 29 minutes of buildup and methods with no payoff. The ultimate frustration was the explanation that the most highly significant correlations between polymorphisms and drug use are actually thrown out for being too significant, and they choose to focus on some arbitrary group of less significant correlations. WTF. I would maybe slightly understand the reasoning for this choice, but by the time they got to the talk that was pure statistical methods I had fled to the lobby Starbucks.

The only surprising tidbit from the genetics session was that these correlation studies are pointing to a lot of cell adhesion molecules (sort of the Lego prongs that enable specific cells to stick together) as being important for sensitivity to drugs. This confusing finding wasn’t made any more lucid by the scientists in the last session, who were all giving their standard talks about cell adhesion molecules without mentioning drug addiction once, despite supposedly being on the Frontiers of the field. Two talks into the final session, it was time to cut and run, to prepare for a night of studying drugs of abuse firsthand.

Chapter 3: Stadium Science

At a scientific meeting of this impressive size, the headliners make their appearances in the main auditorium hall, a cavernous room filled with enough chairs and high-tech audio/visual equipment to house a Pink Floyd reunion tour. It was in this room, tastefully down-lit to a light intensity that heightened Powerpoint clarity and facilitated hangover-naps, that the convention began in earnest. Yet strangely, the opening event of the Society for Neuroscience meeting had very, very little to do with neuroscience at all. Last year’s conference inaugurated the Science and Society Lecture, a construct apparently invented so that we could host a rare US speaking appearance by the Dalai Lama, who gave an endearingly awkward and unscripted chat about meditation and why neuroscientists and Buddhists should pay more attention to each other. Not the most scientific of talks, but a welcome recess from the claustrophobic flood of hard data and incremental findings, not to mention a good story to tell all the non-scientists back home when they hesitantly asked what we do at these things anyway.

This year’s Science and Society speaker couldn’t help but be a step down from one of the three most important religious figures alive, but architect du jour Frank Gehry wasn’t too shabby a follow-up stunt booking, and I held out hope that he’d give a more directly scientific lecture, perhaps on why his unusual shape and material choices are related to facets of human perception, or at least speculate on the neuroscience of creativity. Alas, that was not to be, as Gehry gave an off-the-cuff presentation that wasn’t quite as lovable as the Dalai Lama’s; it just looked like he hadn’t bothered to prepare anything. Most of the hour was taken up by a slide presentation where Gehry showed pictures of his buildings and used shockingly non-specific lingo, i.e. “See that silver thing by the blue thing? I designed that when…” Even the question and answer period, conducted by a neuroscientist/architect (such a thing exists? Why wasn’t he giving this talk?) yielded no scientific insights, other than hinting at the tortured psychology of Gehry’s assistants who have to translate his spontaneous scribbles into actual buildings.

(Aside: Gehry’s one attempt to confront issues of brain function was actually somewhat interesting, as he described his creative process as taking in a project’s specifications and then letting his hand automatically start to draw without over-thinking the details. This description of creating without “thinking” turns up again and again in artist’s discussions of how they work, from musicians to painters to writers. Because the neurobiology of creativity is such a loaded and abstract topic, I haven’t seen a lot of controlled lab work investigating these commonalities, though I suspect there are a lot of ambitious fMRI-wielders with thoughts on the topic. Frank Gehry either didn’t care about the details or didn’t want to know.)

However, other Presidential Lectures (i.e. the ones in the big room) that week made Gehry’s spontaneous ramble look better in retrospect. One particular all-star series of talks was focused upon long-term potentiation (LTP), the theory of neural memory storage that is always fashionable at SfN meetings, and was even more ubiquitous than usual at this year’s incarnation. After sitting through the opening act of Robert Malenka, an occasional rival of our lab, with white knuckles for fear of project overlap, we got to the main event(s): Roger Nicoll and Masao Ito, the discoverers of LTP and long-term depression (LTD), respectively. Receiving an award, impressive medals and all, from some rich benefactor or another, Nicoll and Ito proceeded to completely ignore the stories behind the findings that made them famous during their acceptance talks, choosing to focus on either more recent, more boring findings (Nicoll) or tedious circuit anatomy lessons (Ito).

Nevertheless, the fault may have been due to the medium more so than the message. Even though these massive lectures are intended to shine a spotlight on the most exciting avenues of current neuroscience research, the format couldn’t help but serve up dud performances. Scientists used to presenting their research in classrooms of maybe 100 people suddenly found themselves in front of thousands, with their non-photogenic visages projected on enormous screens and their Powerpoint slides awkwardly distant and difficult to laser-point. Faced with likely the largest crowd they’ll ever see, some speakers tried to cram every single research finding they’d ever accumulated into their hour, leading them to speak at the pace of the Micro Machine Man. Others focused only on research published years ago, afraid to present fresher material to a crowd full of unfamiliar and potentially unethical faces. The few talks that allowed time for questions produced no compelling dialogue, as audience members lobbed softball or comically irrelevant (“what do you think about the reported benefits of THC to prevention of Alzheimer ’s disease?”) from microphones positioned meters away from the podium. All these effects conspired to make what should be the most exciting opportunity of such a conference appear roughly as shallow as award-ceremony thank-you speeches.

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Chapter 4: …and on the smaller stages…

Having not been particularly fired up, then, by these large-scale presentations, I attempted to find excitement and motivation in more intimate settings…relatively speaking. Mini-symposiums are similar in format to the pre-meeting I had attended, though more focused on one particular narrow topic; four to six speakers give 20-30 minute mini-talks all based around a single concept, held in gigantic, bisected ballrooms. These sessions are notable for depersonalizing the speakers themselves, as movie-size screens project their Powerpointed data while the speaker his or herself is shrouded in darkness and surrounded by electronic equipment, anonymous like a rave DJ overshadowed by the light show.

Speaking of which, other ways how a scientific conference is like a large music festival:

- Schedule & Map Required: with about 20 different things going on at any one time, much of the time is spent running from place to place in the spacious conference center, missing the ends and beginnings of talks due to the sprawling layout.

- Celebrity Sightings: a crucial conference talent is to be able to surreptitiously read a person’s nametag, occasionally discovering that the guy subtly picking his nose down the row from you is actually a member of the National Academy of Sciences.

- The Press Gets Treated Like Shit: seriously, I peeked into one of their “hospitality areas,” it made the Lollapalooza press tent look like the Hilton.

- Huge Video Screens: with less attractive people on them, however.

- After the Party is the After-Party: more to come on this point.

- Long Lines for Overpriced & Disgusting Concessions: never have you seen a more overcrowded Starbucks, and the finest cuisine on-site was probably the lady selling cinnamon-roasted peanuts that made the entire building smell like a Cinnabon. Frustrating, since there was no Cinnabon.

Chapter 5: This is what I came for? The odyssey of the Poster Session

Presenting a poster is the research scientist’s marathon, a lengthy test of physical, psychological, and social resolve while surrounded by a sea of peers. It even takes about the same amount of time (four hours) and requires a similar amount of hydration and preparation; the only major difference is that poster presenters don’t have problems with nipple bleeding…at least in my experience. Should your poster have survived the travel to the conference location, avoided being left in the overhead compartment or in a bathroom stall, escaped the smears and rips of inappropriate handling, and managed to be relatively free of humiliating typos, it reaches its final destination, hung by pushpins amongst a few thousand counterparts. By this time, most people have taken advantage of departmental funds and equipment to print out their posters (in vivid color!) on one large sheet of glossy paper, but occasionally you still see adherents to more classical forms of poster-making: the 8×11 sheets mounted on colored cardboard backing, the taped-together dot-matrix matrix, and, very rarely, the guy who scrawled his text and figures on yellow notebook paper.

My own poster experience followed a pretty traditional arc:

1:00 – 2:00: no visitors aside from a handful of friends and co-workers you or your boss has begged/guilted into stopping by. Awkwardly start to pace around the poster, half-heartedly making small chat (“quiet so far, eh?”) with neighbors before eyeing them with envy once people start to accumulate at their posters. Any unknown person that happens to even so much as glance at the poster gets pounced upon with an overbearing greeting, i.e. “LET ME KNOW IF YOU HAVE ANY QUESTIONS?” before they awkwardly back away to the poster they were actually walking over to see.

2:00 – 4:00: miraculously, people who actually are interested in your work that you don’t know personally begin to appear, asking constructive questions (albeit the same three over and over again) and telling you “nice job, very interesting” in an almost believable manner. The “five-minute summary” talks begins to blur together, until you’re basically starting the next round over again as soon as the previous take is finished. Start to feel a bit like an audio-animatronic character on a Disney ride.

4:00 – 5:00: voice fading, your explanations start to get increasingly far-fetched and/or confessional. As visitors become more and more intermittent, time is free for cold coffee sips, stretching exercises, and awkward “glad we’re almost done, eh?” small talk with neighbors. At 4:55, three of the most important researchers in your field show up and start giving you actual interesting feedback just as the conference center, at the very stroke of 5:00, begins acting like a bar at last call: flicking the lights, making annoying loud announcements, launching the custodial fleet.

The post-poster feeling is one of the finest in science: rolling up the poster for the last time (resisting the urge to drop a match in the tube after it), feeling like people actually care about your project, pocket full of business cards from faculty that were maybe trolling for post-docs, your week’s major responsibility checked off and filed away.

Chapter 6: Hands-On Research

The occasion of a successful poster session calls for excessive imbibing of alcohol, some of which was courtesy of the boss himself at the usual ritzy lab dinner, the one night where us lowly students don’t have to be mindful of the $25 per diem. After that, such a luxurious night called for something special, something above the routine pleasures of going out in a strange city, surrounded by people from home. Something crazy, something outlandish, something like…the Mother. Fucking. MIT. Party.

Yes, that’s MIT as in Massachusetts Institute of Technology, the school whose primary social purpose is to make Harvard students look like raging frat boys by comparison. For this very good reason, we were understandably skeptical at the idea of traveling out to a social thrown by the MIT neuroscience department, as an alternative to drinking ourselves silly at yet another dark, random Atlanta bar. Add to the arguments-against list that this shindig was reportedly being held at a venue called The Compound; it sounded better than yet another hotel ballroom, but also sounded vaguely like some sort of convict bar.

Yet the fear of missing out on what could have been the party of the week compelled us to give it a shot, and soon enough we were packed into a cab that was taking us somewhere $25 away from downtown, into a labyrinth of warehouses and parking lots. Nestled within this industrial district was a true-to-life velvet-rope-sporting club, looking like the kind of place where Outkast might throw a record release party, or where the Hawks go to celebrate a 10-win season. But not tonight, for inside, beneath an MIT banner and spread out over a pretty ridiculous assemblage of enclosed gardens, modernist couch rooms, and club dance floors lurked nearly 1000 neuroscience graduate students.

Despite the fact that the free bar tab had already been depleted for the night, what ensued was a conference occurrence probably universal to all disciplines, that uneasy delirium of professional relationships dissolving into real social interaction, uninhibited and primal. Other than a few exceptions (I fuzzily remember discussing staining protocols with another student around 1am), the protective layer of scientific conversation was stripped away by alcohol, smoke inhalation, and the beat-heavy colored light trappings of the dance floor. However, the night never quite reached complete escapism, what with the venue’s usual flat-screen visuals replaced by 3D blueprints of MIT buildings and institute logos, but unless you were really paying attention between repeated playings of “SexyBack” and Fergie, you wouldn’t have noticed.

Spit back out into the eerie quiet of the post-party night, the cab ride was marked by the strangely giddy out-of-town camaraderie born of getting sloshed and candid in the company of co-workers in a strange place. But beneath all this fresh companionship was a haze of guilt at letting one’s guard down in front of people normally considered in professional, formal tones as “colleagues” back home in the real world. It’s a curious, transient thing: grad students, usually sequestered in their individual labs, too tired for post-work social interaction or consciously seeking separation between their school life and their free time, colliding for a brief period around a scientific meeting.


The MIT Party completely shattered the delicate balance of alcohol and caffeine that was fueling the week’s activities, and the rest of the meeting became little more than a blur, as I found myself sleepwalking through posters and talks and vendor freebies and whatever came afterwards. Fortunately, there were only two days left. One of the days was a total wash, as I expended all my energy just getting out of bed and to the conference center and had nothing less to take notes or admire posters. A night that started out as “let’s take it easy,” quickly descended from hotel room relaxation to yuppie-bar baseball-watching before ending up in a dive bar/strip club where more people watched the surprisingly competent karaoke than leered at the three world-weary strippers that took turns on the bar’s tiny platform.

The final day meant recovering our mental faculties just enough to put in a respectable appearance at the boss’ symposium, which occupied the no man’s land of the conference’s final session. Cruelly, the schedulers had placed the event in the largest of the symposium ballrooms, a room filled with probably 2500 seats that was, at the peak, maybe 10% full, and by the last of the four talks flirted with the 1% barrier. However, it wasn’t so bad from the front row, where anxieties over whether the boss’ jokes would flop and the queer sensation of seeing one’s data projected on a gigantic screen (alongside, you know, actual real data from other labs) were diminished by the intimate audience.

Then there was nothing left but the mad dash to the airport, living it up on one last department-subsidized cab ride, navigating through the cattle run of the Atlanta airport, finding out the flight was delayed for several hours, desperately trying to sneak peeks at Game 6 in the airport bar amongst the legitimate traveling businessmen, then trying to sleep through the flight back home.

And as the weather cooled in the harsh transition between muggy Atlanta and frigid Chicago, so too did the brief fire of scientific excitement lit by the meeting. The self-esteem boost provided by the poster session – the pleasant feeling that people really do care about your project – was soon to be engulfed by the day-to-day drudgery and technical headaches of laboratory life, and any nuggets of useful or stirring new research that had been accumulated quickly became little more than notebook scribbles and half-remembered details. Even so, we’ll all return next year, as we will every fall, to get our annual fix of fleeting self-esteem and free drinks.

Pupils Dilate to Pinpoint: The Contradiction in Requiem for a Dream

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When director Darren Aronofsky says Requiem for a Dream “is not a drug movie,” it doesn’t sound like an excuse. Yet considering the inaccurate portrayal of the main pharmacologic effect of heroin displayed in his film, a dilating pupil, perhaps we should consider it one.

Based on the 1978 Hubert Selby Jr. novel, Requiem for a Dream is a film about the biological, psychological, and social consequences of addiction. Released in 2000 to a flurry of MPAA scorn and critical acclaim, it interweaves the stories of four desperate Brooklynites who fall victim to the shackles of substance dependence. Although ultimately the film speaks to addictions of all varieties, including television, vanity, and prescription drugs, the film’s major visual motif relates to heroin.

Each time someone uses heroin we see a montage ending with a singular, striking image: a rapidly dilating pupil. While it could be debated ad nauseam what broader significance this image connotes, it is clear that this image is a central metaphor. An eye hovers unflinchingly above the characters on promotional posters. We see two pupils dilate right after the opening credits and dozens of times thereafter. Instead of seeing the characters use heroin, we only see the so-called physiologic effects of it. The dilating pupil is an icon for the film, and in many ways, heroin use itself.

Unfortunately, the image makes no pharmacologic sense. In fact, if they were indeed using heroin, the effect would be precisely the opposite. Heroin is an opioid, which are synthetic versions of naturally occurring derivatives of opium. When opioids enter the bloodstream, they quickly cross into the central nervous system and induce their wide-ranging effects. In addition to the obvious euphoria and pain relief, opioid intoxication classically causes nausea, clammy skin, and pupil constriction.

There are many mechanisms that lead to pupil constriction or dilation. Tethered by muscles that are under involuntary control, the pupil can change size in response to the amount of light, the proximity of an object, neurological damage, or drugs. When heroin enters the body it is rapidly converted to its active form (i.e. morphine), which binds to μ (mu) opioid receptors in the brain (μ is pretentious Greek shorthand for morphine). By cueing several chemicals including acetylcholine, GABA, and the creatively-named Substance P into action, this cascade of events results in an overall deceleration of cognition and upper-level motor processes. (Those of you who have ever taken an opioid, like Codeine, after a dental procedure may know this feeling well.) In coincidental fashion, the excitation of receptors in a nerve bundle called the ciliary ganglion predictably results in muscle contraction and nearly intractable pupil constriction.

As you might surmise, the converse also applies. When central nervous system stimulants, like cocaine or methamphetamine, enter the body they initiate an analogous but opposite chain of reactions that leads to pupil dilation. Similarly, if someone is experiencing physiologic withdrawal from opioids, their pupils will dilate. However, it is quite clear that when pupils dilate in Requiem for a Dream, the characters are not going through opioid withdrawal, which would be accompanied by a completely different set of physiologic signs.

So where exactly did Aronofsky err? Did he fail to research the effects of heroin? Considering the detailed precision of the rest of the film, that is not likely. Did he purposefully choose to show dilation despite the pharmacologic contradiction? If you exclude the effect of opioids, pupil dilation occurs in several emotional states, including fear, sadness, or general arousal. Studies have shown that pupils dilate in response to positive images such as nudity or food, and negative ones such as a disabled person or a crying baby. As “windows to the soul,” pupil reactions are thought to represent our overall cognitive load or level of arousal. The more we think, or the more excited we are, the bigger our pupils get, and vice versa. It is possible Aronofsky wanted to use the image of pupil dilation to show the level of complexity in his characters’ lives.

Yet as the plot moves forward, the characters seem to think less and less. Obtaining heroin consumes more and more of their life at the expense of other decisions, thoughts, and emotions. Perhaps showing their pupils dilating is an intentional contrast to paradoxically highlight the constricting worldview caused by their addiction. As it stands, the image remains a powerful metaphor.

Still, there is some evidence that suggests he merely inadvertently got caught in a contradiction. In the bonus feature interview “Anatomy of a Scene” on the DVD release of Requiem for a Dream, Aronofsky shows a glimpse of a revealing storyboard sketch. There is an image of a colorless eye next to the text “pupils dilate to pinpoint.” To put it simply, it is impossible for pupils to dilate to pinpoint. Pupils are measured according to their diameter in millimeters and the term “pinpoint” is used to refer to pupils that are severely constricted. Heroin intoxication causes pinpoint pupils, heroin withdrawal causes dilated pupils, and never can the two states occur together. At some point Aronofsky got his information crossed and never sorted it out.

Maybe he never realized his mistake; maybe he couldn’t capture pupil constriction on film; or maybe he liked the “eyes wide shut” metaphor a little too much. We will probably never know, but it does not excuse us from opening our own eyes to the real science behind the scenes.