By Angela Nitzke-Martin

I have no doubt that at some point after having my blood drawn, I have likened the experience to torture. Those minutes spent prospecting for gold in my evidently intractable veins is certainly unpleasant, and on occasion painful, but torturous — no. It is an attempt to add drama to a pretty boring story, and absurd to suggest that a medical professional would support suffering that wasn’t ultimately in the patient’s best interest. After all, they do have to take an oath.

Maybe that is why “Medical Complicity in Torture,” the title of a lecture given by New York University’s Allen Keller was a bit shocking. CIA physicians and psychologists seem out of place in military prisons, but they do play a role in interrogations and were present at Guantanamo Bay. Should medical professionals participate in torture or enhanced interrogation? “Moral and scientific reasons ultimately lead to the same conclusion: That, no, we shouldn’t be doing this,” said Keller, an associate professor of medicine and director of the Bellevue/NYU Program for Survivors of Torture.

Keller spoke at the University of Chicago on Wednesday as part of the MacLean Center for Clinical Medical Ethics seminar series. In his lecture, Keller drew from vast experience dealing with torture victims and the report he coauthored for Physicians for Human Rights titled, “Aiding Torture.” The paper cites the CIA Inspector General’s report released in 2004 that said psychologists not only monitored enhanced interrogation techniques like waterboarding, but also kept data on the prisoners’ reactions.

It is impossible to separate the physical, psychological and social dimensions of health, said Keller. “The consequences of torture are all interrelated.” Prisoners who are not mortally wounded may still experience intense psychiatric trauma with long lasting effects. Preventing death or severe injury does not preclude inflicting harm.

Although not as mind-boggling as what the definition of “is” is, there is still debate about what constitutes torture. We have the UN’s definition and the American Medical Association’s definition, but it boils down to something much simpler for Keller. “If it looks like torture, smells like torture, it’s probably torture,” said Keller.

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In the 1950s and ’60s, several villages in the Oceanic country of Papua New Guinea began to see an odd disease. Villagers of the Fore people in the Eastern Highlands - predominantly women and children - would show an array of frightening symptoms that rapidly worsened over about six months: muscle tremors, uncontrollable laughter, slurring of speech and finally an inability to move and swallow. In the 1960’s, European scientists began to study people with the disease, called kuru for the Fore word for “shiver,” and made two astonishing discoveries. First, that kuru represented a new kind of infectious disease that caused the brain and nervous system to degenerate. Second, that kuru probably resulted from people eating their dead relatives.

Yeah, that’s not a typo. Before the Fore people of Papua New Guinea were known for kuru, they were known for “mortuary feasts,” where villagers would mark the death of a family member by consuming him or her. And not just a nibble here or there - according to a 1979 book by anthropologist Shirley Lindenbaum, “meat, viscera, and brain were all eaten.” That’s a good way to spread a disease caused by prions - the mechanism for kuru eventually discovered by Daniel Carleton Gajdusek in research that won him the 1976 Nobel Prize in Physiology or Medicine. Now, kuru continues to fascinate the scientific community, as a new medical paper presents how the savage disease caused rapid natural selection in Papua New Guinea, selecting for a gene variant that may offer clues to how to treat prion diseases with no known cure.

Prions are also the culprit behind bovine spongiform encephalopathy, better known as Mad Cow Disease, which is thought to have broken out in Britain due to cannibalistic feeding practices in cattle. In short, prion diseases are caused by misshaped proteins that are a bad influence on native prion proteins present in all species, causing them to change shape, clump together, and eventually kill the cell. So when a prion disease enters a person’s nervous system - by, say, eating a person with a prion disease - it tends to wreak havoc in the brain, producing the odd symptoms of kuru or BSE.

At the height of kuru, 1 out of 50 people in some Fore villages succumbed to the untreatable, fatal disease. Women and children tended to die more often from kuru, likely because they usually were given the brains to eat while the men got the good, meaty parts. But what about those who participated in the mortuary feasts, but never contracted the disease? Was there something genetically different about them that made them resistant? Sounds like a case for…evolution!

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Disease screening is often a delicate balance. Catching a disease in its early stages almost always makes it more treatable, and can prevent permanent damage or even death. But it’s also cost-prohibitive to screen every person for every disease - even if you could convince everyone to show up for their regular doctor’s appointments - and so difficult decisions about benefit vs. cost and risk must be made.

Who actually makes those decisions is one of the key features of the U.S. health care debate. It’s nice to think that they are made by clinicians looking at the latest in medical research, but choices about what screens are affordable enough to be useful often boil down to which are considered acceptable for coverage by health insurance. In theory, insurance companies will follow the recommendations of scientific societies and expert task forces entrusted to analyze available data and make a decision. But what if those experts disagree?

That’s the battle being fought this week as new recommendations about mammograms for breast cancer screening are released by the U.S. Preventive Services Task Force. Published Tuesday in the Annals of Internal Medicine, the recommendations go against the grain of recent practice advising all women to start receiving mammograms at the age of 40, with yearly screening after the age of 50. Now, the task force says women who are not high-risk due to genetic factors or family history don’t need routine mammograms until age 50. Even then, screening every other year is sufficient until the age of 75, the task force concluded.

These new recommendations were not received quietly, as you may have discerned from the media covearge. University of Chicago professor of radiology Robert Schmidt told the Chicago Tribune that the recommendations were “arrogant and irresponsible.” My wife reports that one of the ladies of The View called the decision “gender genocide.”  Some medical societies have come out in favor of the new practice, while others said they will stick to the old guidelines. Ultimately, the decision on whether to be screened (if not the decision on how much screens will cost) lies with patients themselves. So here’s a quick primer on the support and opposition to the new recommendations.

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Until indoor smoking bans started popping up in cities across the country in recent years, smoke-filled bars were a fixture of American culture, smoking and drinking entwined like the peanut butter and jelly of vices. If you were a casual scientist of the street, you might have hypothesized that there was something meaningful behind the common sight of the barfly with a drink in one hand and a cigarette in the other. And laboratory research has mostly supported that anecdotal evidence, with study after study showing that alcohol does in fact promote smoking behavior, while larger surveys have found alcoholics more likely to be smokers and vice versa. But where do the effects of a beer and a cigarette meet in the brain, such that ordering up one raises a person’s desire to partake of the other?

That’s been one of the questions studied in the Clinical Addictions Research Laboratory at the University of Chicago Medical Center, where director Andrea King has examined the phenomenon of alcohol-induced smoking. The studies put the spotlight on an interesting population of smokers - not the pack-a-day regulars, but those who smoke “socially,” a few cigarettes on nights out on the town with friends. That’s a demographic that hasn’t received as much study as addicted smokers, King said, in part due to psychiatric guidelines that classified people as either smokers or non-smokers with no space for people in the gray areas.

“Older studies wouldn’t even ask how frequently subjects smoked; if they smoke, they must be addicted, daily smokers,” said King, an associate professor of psychiatry and behavioral neuroscience. “But we see this percent that seems to be increasing in subsequent surveys…about 20-30 percent would be non-daily smokers. Some of these people may continue and become vulnerable to being a chronic habitual user, or this may be a new subclass of smokers.”

King was drawn to social, alcohol-induced smoking behavior when she was attempting to recruit heavy drinkers who were not smokers for a control group, a task she found exceptionally difficult. With rates of smoking among alcoholics as high as 75 percent, the non-smoking drinker was a rare breed, so King decided to flip it around to study what causes the two behaviors to frequently co-exist.

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After a long layoff due to conference congestion, here’s a new installment of Linkage, our semi-regular round-up of science news from around the world and web.

The “Speech Gene” Gains a Function

One of the more intriguing genes discovered since the flood of genetic sequences began to arrive at the beginning of this decade is FOXP2. Encoding for a humble transcription factor (sort of a DNA light switch), FOXP2 nevertheless gained lofty status when it was found in the late 1990’s to be associated with human language - one of the most complex behaviors of all. Previously associated with speech and language disorders in humans, FOXP2 gained steam when a team of scientists (including University of Chicago professor of human genetics Molly Przeworski) compared our FOXP2 with our close primate relatives and found only two amino acids different between the human and chimpanzee versions of the gene. With only 715 amino acids total in the FOXP2 protein, that small difference suggests a recent evolution event, which that research group estimated at roughly 100,000 years ago - right around the time that “modern humans” appeared on the scene. This has led some to conclude that this fortuitous small change in the FOXP2 gene is one of the key moments in our evolutionary history that separated man from beast.

But what exactly does FOXP2 do, and how could such a minute change mean the difference between chimpanzee grunts and Shakespeare? One way to answer that question is to put the human version of the FOXP2 gene into another animal, an experiment that was published earlier this year by a very large team of German researchers. That mouse didn’t suddenly start reciting soliloquies, but it did show differences in “ultrasonic vocalizations,” as well as cellular changes in a part of the brain associated with movement - which makes sense given that FOXP2 is thought to mediate motions related to speaking. Still, changing just one gene to the “human version” in an animal and leaving all the other mouse genes intact would presumably limit the impact of the human FOXP2 gene in changing the mouse brain. (Jerry Coyne wrote about the media reaction to this paper here)

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A sleeping zebra finch (courtesy of Margoliash lab)

One of the repeated themes of the Darwin/Chicago 2009 meeting two weeks ago was the history of the anti-evolution movement, a resistance that has actually changed form, even *cough* evolved, quite a bit since The Origin of the Species. At the opening night event in Rockefeller Chapel, science historian Ronald Numbers talked about differences between the anti-Darwinists led by William Jennings Bryan in the 1920’s (immortalized in the Scopes Monkey Trial and Inherit the Wind) and today’s intelligent design supporters and creationists. Surprisingly, Bryan and his followers were considerably less extreme than today’s anti-evolutionists, as Numbers explained that most who railed against Darwinism in the early 20th century were fine with the evolution of animals over billions of years, they merely could not abide that humans also evolved.

The evolution vs. creation debate has obviously become a lot more complicated since then, but Bryan’s primary objection has lingered - the core of most people’s opposition to evolution is the idea that humans must be somehow separate and different from the rest of the natural world. One “proof” of this uniqueness is the complexity of human language, a form of communication that, to the casual observer, appears in an entirely different league from the songs, gestures, or simple noises that animals use to share information. The assumption that the more complex forms of human language are unique is even held by some in the field of linguistics and psychology, including the legendary Noam Chomsky, who argued as much in a 2002 Science paper with cognitive psychologist (and Darwin/Chicago speaker) Marc Hauser.

That assumption is a handicap to the study of language, argue University of Chicago’s Daniel Margoliash and Howard Nusbaum in a recent issue of the journal Trends in Cognitive Science. The idea that human language is biologically unique, and thus the kind of “hopeful monster” geneticist Richard Goldschmidt coined to describe the sudden appearance of a new feature in evolutionary history, walls off language from the world of biology. Perceiving human language in its proper evolutionary context, and thus exposing it to the tools of comparative biology, will allow scientists to fully understand how language works and where it originated, Margoliash and Nusbaum conclude.

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Calculating the carbon footprint of everything from U2 world tours to pet dogs and cats to presidential inaugurations has become a favorite pastime of the media, a measuring stick by which to label an entity’s environmental damage. But somehow in all of the footprint calculations, everyone forgot to run the greenhouse gas numbers on one of the biggest pieces of the American economy: health care. The U.S. health care sector, from hospitals to nursing homes to doctor’s and dentist’s clinics to pharmaceutical companies and insurance, makes up 16 percent of the country’s gross domestic product. And while many hospitals have launched efforts to help decrease their waste and energy appetites, nobody had taken the time to calculate the industry’s total carbon toll.

That is, until today, when University of Chicago researchers Jeanette Chung and David Meltzer published a letter in the Journal of the American Medical Association that measures the health care sector’s carbon footprint. By running the economic data about how health care spends its resources through a model, created at Carnegie-Mellon University’s Green Design Institute, that estimates the emissions of various greenhouse gases. Chung said she was surprised that nobody had run these numbers on health care effect, but thought it might have to do with the other priorities of the industry of late.

“In this country, the primary focus is on issues surrounding patient safety, health care quality, and cost containment at this current point in time. The health care sector, in general, may be a bit slower than other sectors to put this on their radar screen,” said Chung, a Research Associate in the Section of Hospital Medicine. “But given the focus on health care policy and environmental policy, it might be interesting - if not wise - to start accounting for environmental externalities in health care.”

In Chung and Meltzer’s analysis, health care accounted for 8% of the country’s total emission of carbon dioxide, methane, nitrous oxide and chlorofluorocarbons. That sounds pretty good - health care’s slice of the carbon pie only half the size of its slice of the economic pie - but Chung and Meltzer emphasize that such a huge contribution makes health care a ripe target for environmental improvement.

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I spent part of last week on vacation from science in Las Vegas, where I thankfully avoided financial ruin due to some fortunate combination of genes, math awareness and a wife that has no interest in gambling. Sure, I dabbled a bit in games of chance, but as soon as I got a little bit ahead on the blackjack tables I ran for my life, knowing that the probability would even out hard in the long run. For those concerned about the financial well-being of Sin City, they still managed to turn a profit on us, thanks to the low-return temptations of fine dining and French circus acts set to Beatles megamixes. But most of our time was spent on the free entertainment of people-watching and stuff-watching, observing row after row of people almost hypnotically at work on loud, noisy slot machines amid fake New York, Paris and Venice scenery.

It doesn’t take a PhD in neurobiology to conclude that slot machines are designed to lure people into a money-draining repetition, just as it doesn’t take expertise in the casino business to realize slots are absurdly profitable - there’s a reason why they outnumber table games 100-to-1. But I wanted to go back to the scientific literature to confirm a faint glimmer of information I retained from graduate school, specifically that slot machines are masterful manipulators of our brain’s natural reward system. Every feature - the incessant noise, the flashing lights, the position of the rolls and the sound of the coins hitting the dish - is designed to hijack the parts of our brain designed for the pursuit of food and sex and turn it into a river of quarters. Or so I remember.

Fortunately, there is a robust amount of research into why slot machines are so addictive, despite paying out only about 75% of what people put in. They are, some scientists have concluded, the most addictive of all the ways humans have designed to gamble, because pathological gambling appears faster in slots players and more money is spent on the machines than other forms of gambling. In Spain, where gambling is legal and slot machines can be found in most bars, more than 20.3 billion dollars was spent on slots in 2008 - 44% of the total money spent by Spaniards on gambling last year.

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The massive, long-term Diabetes Prevention Program study has now found (twice!) that altering one’s lifestyle in terms of diet and exercise is more effective than a common prescription drug in delaying the onset of the disease. To power this study and its recently published follow-up, dozens of medical centers conducted multiple examinations each year on thousands of patients - 3234 in the first 3-year study, and 2665 in the 10-year follow. It’s impressive - and more clinically useful - to look at the summary data accumulated from this very large population of patients. But what kind of impact does a huge study such as the DPP have on the individual participants?

With help from Margaret Matulik, the DPP program coordinator at the University of Chicago Medical Center, I connected with a couple of the study subjects to hear about the lives behind the data points. Both Katherine Seaberry, 80, and Robert Nolan, 61, are from Chicago, and enrolled in the study in the late 1990’s. Both were also motivated to join the DPP due to their respective families’ experience with diabetes - Nolan’s sister and mother suffered from the disease and died around the age of 60, and Seaberry said her “whole family” has been diagnosed with diabetes.

“It saved me,” Seaberry said of her involvement with the Diabetes Prevention Program. “It’s amazing that I’m the only one in my family that’s not diabetic. If I wasn’t in this study, I think I would be diabetic by now.”

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Pharmaceutical companies often make up trade names for new drugs that semi-subliminally evoke their purpose - some of my favorites are Boniva, for osteoporosis, or Ambien, the sleeping pill that sounds like it was named by Brian Eno.  It’s kind of a silly practice, motivated mostly by marketing reasons, because all of these drugs already have names - Ambien’s true name, Zolpidem, is even kind of fun to say. But the fact that these trade names are so widespread suggests they are effective at attracting consumers, so here’s my modest proposal: let’s give simple changes in diet and exercise that improve health a fancy trade name, Lifestyltrin.

This train of thought stems from a study published last week by medical journal The Lancet, in which one of the largest diabetes studies showed (again) that changes in lifestyle are more effective than a leading medication in preventing the disease. Originally published in 2001, the Diabetes Prevention Program (DPP) followed more than 3000 people at risk for diabetes at hospitals across the United States as they underwent either a lifestyle intervention, treatment with anti-diabetic drug metformin, or a placebo treatment. After nearly 3 years of study, the authors reported that lifestyle changes (meaning diet and exercise to reduce weight) reduced diabetes incidence by almost 60%. Metformin also reduced the disease, but only by about 31% - results so strong that the authors stopped the study and began offering both treatments to everyone in their study.

But the study didn’t end, and the medical centers involved continued to monitor as many patients as were willing to stay in contact. All told, 2766 of the original 3234 participants continued to be monitored, allowing the publication last week of a followup study examining how many of these at-risk patients had developed diabetes 10 years after the original study began. What they found was somewhat status quo - after 10 years, the lifestyle group still showed twice the decrease of new diabetes cases than the drug group, 34% vs 18% lower compared to placebo. But that also means there was no difference in the number of new diabetes cases between lifestyle and drug groups in the 7 years between the original study’s end and the followup study’s end, which authors attributed to the mixture of treatments - the group receiving lifestyle interventions was now allowed access to metformin, and vice versa.

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Daniel Dennett chatting with Robert Richards at the Darwin/Chicago 2009 conference. Credit: Jerry Coyne

The philosopher Daniel Dennett looked slightly puzzled as Robert Richards finished his Oct. 30 talk at the Darwin/Chicago 2009 meeting, on the subject of “Darwin’s Biology of Intelligent Design.” Dennett and Richards have spent years writing about Darwin and the historical significance of his ideas about evolution. But Richards’ talk challenged a central theme of Dennett’s influential book, “Darwin’s Dangerous Idea” - that Darwin revolutionized modern thought by showing that a mindless, mechanical process can give rise to complexity and minds capable of understanding their origins. In fact, Richards argued that Darwin did not always envision evolution as mindless or mechanical. Richards cited out passage after passage in Darwin’s notebooks and early published writing, showing that he thought of humanity as “the great object for which the world was brought into its present state.” He didn’t talk about an intelligence guiding evolution, but he was comfortable - at least before the 1860s - with the idea of an intelligence behind natural laws.

In other words, Darwin once believed that we are the ones evolution was waiting for.

I walked up to Dennett after Richards’ talk and briefly asked what he thought. Dennett shrugged and shook his head. “I don’t believe it,” he said.

He’s not alone. The question is, why should anyone care? What does it matter if a 19th-Century naturalist thought a higher intelligence might have planned out evolution in some vague way? Lots of Darwin’s other notions got jettisoned along the way (blending inheritance, anyone?), so why should this one be different?

In part it may be because of the unusual - and possibly unhealthy - role that Darwin has assumed in debates about biology and human nature. He is an especially potent figure for creationists and atheists alike, because in many ways he made modern atheism possible. It muddles the picture if, as Richards said, Darwin’s theory “was formulated under the idea that an intelligent cause formulated the laws of nature.”

But it’s also clear that Darwin believed in that “intelligent cause” less and less as he got older. He’s still an important author of modern materialism, though perhaps a mushier one than we often imagine. Dennett admitted the possibility in his talk - “It would be wonderfully ironic, Bob, if the person we honor for having the best idea ever didn’t understand his own idea,” Dennett said. “But I don’t think that’s the case.”

Darwin/Chicago 2009 was a bit like two conferences in one. In the movie theater of Ida Noyes Hall, evolutionary biologists sorted through the hard details of how evolution happens beneath wide-screen Powerpoint slides. Three floors above, in a long room with hand-painted walls, historians and philosophers of science synthesized decades of reading and scholarship into half-hour lessons. One session gazed forward at future promise, one session made sure the previous steps and missteps weren’t forgotten. After two days of running back and forth from one theater to the other, I felt I got a three-dimensional portrait of Charles Darwin and his elegant theory - the decades of thoughts, influences and experiences that went into the writing of On the Origin of Species, the multitude of new and exciting examples still being found that prove the truth of evolution.

Because my dispatches from the conference turned into two very long posts, here’s a menu to jump to the highlights of the conference.

Thursday

The conference kicked off in the Gothic setting of Rockefeller Chapel with a trio of talks (Richard Lewontin, Ronald Numbers, Marc Hauser) that set the tone for a gathering that would approach Darwin and his work from every possible angle.

Friday

Pietro Corsi reminded the room that Darwin (and Jean-Baptiste Lamarck) weren’t the only scientists pondering evolution in the 19th century.

The finches that bear Darwin’s name remain one of the best species for studying rapid natural selection in nature, as Peter and Rosemary Grant explained.

Robert Richards got provocative with his argument that Darwin believed in a purpose behind evolution when he was crafting his famous theory.

Famous fossil hunter Paul Sereno outlined his proposal for a common language of morphology while the second-oldest bird ever discovered lay beside him.

The University of Chicago’s Jerry Coyne threw down the gauntlet on the debate over how species have formed over Earth’s history.

Eric Lander, one of the leaders of the Human Genome Project, primed the audience on how that data and the sequences of other organisms have changed assumptions about genetics.

Perhaps Darwin’s most lasting metaphor, the Tree of Life has been dramatically altered by the flood of genetic data, and Philip Ward explained how that has changed biologists’ knowledge of how species are related.

Saturday

Thomas Schoener kicked us off with a discussion of how evolution and ecology are finally working together…and David Jablonski made a similar pitch for cooperation between evolutionary biologists and paleontologists.

The study of animal behavior helped Darwin craft his theory, but it took more than a century for it to gain steam as a scientific discipline, said Richard Burkhardt.

Neil Shubin used his discovery of Tiktaalik - and the ensuing lab experiments on the genetics of limb structure - to illustrate how evolution can build a bridge between two very different kinds of science.

To answer the question of whether being a “Darwinist” still has meaning in the modern world, Michael Ruse gave an inspiring and very funny explanation of how Darwin’s hypothesis was built to last.

How the oldfield mouse has adapted to beach living made for a perfect cap to the weekend, the research of Hopi Hoekstra an delightfully simple demonstration of natural selection at work.

Elsewhere

I was quite impressed with the instantaneous insight PZ Myers of Pharyngula posted all weekend from the front row of the conference; it was like reading over the shoulder of a truly excellent note-taker.

Skip Evans, of The Panda’s Thumb blog, was on hand representing Wisconsin Citizens for Science and photographing evolutionary biology superstars with his stuffed penguin, Flightless Frank.

As if conference organizer Robert Richards wasn’t busy enough, he also gave radio interviews to WMFT and WGN (the latter with science historian Ronald Numbers).

Jerry Coyne has posted some pictures from the conference to his blog, Why Evolution is True.

Finally: the entire conference was videotaped, and the organizers hope to have it online soon. Rest assured, when they are accessible, I’ll point you to them from here.

4:15 p.m. - Of Mice and Mammoths

The last talk of the day (for me, as I had to leave before the final, final talk) made for a great reminder of how far the field of evolutionary biology, wrapped in a relatively simple story told engagingly by Hopi Hoekstra of Harvard. Hoekstra described her research quest as “the hunt for genes that make a difference,” and she uses a really nice model system - the oldfield mice of the southern United States. These mice typically are brown in color, but they have migrated in the recent (meaning thousands) of years to the gulf and atlantic coasts and taken up residence, like a retired couple, on the beach. But a brown mouse on a beach is a target, and their predators, which include birds and coyotes, find it all to easy to locate their brown fur on white sand and make a beachside snack out of them.

Cue natural selection - soon you have brown oldfield mice inland, and predominantly white oldfield mice that live on the beach. Hoekstra tested whether the fur color really does construe an evolutionary advantage with a simple experiment - make a bunch of clay mice colored brown or white, and leave them out on the beach. Sure enough, the brown clay mice quickly showed divots and bitemarks left by attacks from (presumably very frustrated) predators.

That would have been a fine experiment for the 1959 conference, but Hoekstra’s next step was pure 2009 - she took examples of brown and white mice back to the lab, bred them, and searched for the genes that determined fur color. Her laboratory narrowed the gene candidates down to three genes, and in one of them - a receptor called Mc1r - the substitution of a single amino acid flipped the switch from brown fur to white fur. Amazingly, when another group of scientists sequenced the genome of extinct mammoths in 2006, they found the same amino-acid substitution in the same gene, implying that mammoths, like the oldfield mice, came in different color varieties.

After so much high theory and methodological complexity, Hoekstra’s experiment sent all of us (or at least me) home with a warm feeling - not only was her experiments a beautiful example of evolutionary biology that would have been impossible in 1959, it was a great example of teachable science, the kind of story that a 3rd-grader could wrap their head around and begin to see the truth of evolution. The cloud hanging over Darwin/Chicago 2009 was the uneasy feeling that all this scientific progress was still losing out in the arena of public opinion, but Hoekstra’s work and charismatic speaking style (on the heels of similar ambassador figures Neil Shubin and Michael Shue) chased away some of the pessimism, and left me confident that the more examples we find of Darwin’s elegant theory at work in nature, the easier it will be to convince the world that it is true.

And with that, we’re finished. Happy Halloween to those of you who have followed me this far, and thanks very much for reading and perhaps linking to the posts. I’ll be back Monday with a digest post to help navigate the coverage of the last few days, and Jeremy Manier will be here Tuesday with his own thoughts on the conference.

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5:00 p.m. - Biomedicine and Bracketology

Here’s the final report from today’s session, join us again tomorrow for a full Halloween day of evolutionary science and philosophy! Also, continue to follow PZ Myers of Pharyngula and Skip Evans of Wisconsin Citizens for Science for their reports on the conference.

Both talks in the final session of the day focused on how the incredible advances in gathering genetic information over the last decade have done much to shake up the worlds of genetics and evolutionary biology. As we’ve written about previously, the 1959 conference helped solidify what’s known as the modern synthesis of evolution that incorporated the then-new information about DNA, genes and molecular mechanisms of inheritance, an arrangement that forever married the two fields. Well, could the participants in that conference have predicted that 50 years later we would have a reasonably complete genome for humans, not to mention 43 other vertebrate species? And did they know how much trouble it would cause?

Eric Lander, who was one of the leaders of the Human Genome Project, said he felt slightly out of place at a conference about Darwin, but the modern synthesis marriage sometimes makes strange bedfellows! Regardless, Lander’s talk was a great primer on how the dogma of genetics has been forever altered by what we learned from the HGP and the genomes of other animals: that we have far fewer genes than we thought (~20,000 vs. previous estimates of 100,000), that much of what is handed down between generations is “non-coding” DNA that doesn’t make proteins, that those “non-coding” sections may create important regulatory elements that help organisms develop. Lander, who described himself as a biomedical scientist, said much of what has been found since the explosion of genetic data has been bad news for medical geneticists - many disease-associated alleles have been found, but most have very marginal effects on the probability of a person developing that disease. But Lander said it was a glass half-full/half-empty situation:

“Those people who want to do personal genomics - take your DNA and tell you your risk of diabetes - they’re in trouble. This is not going to be the best way to do that,” Lander said. “But if I want to understand what diabetes is about…I start to get clues to the pathways that matter to diabetes.”

The final talk of the day covered how genetics has caused a similar reshuffling in the field of phylogeny - the science of organizing life into “trees” that show the evolution and relationships of species. Philip Ward, from UC-Davis, talked about the durability of the “Tree of Life” simile, which Darwin readily used in Origin of Species - the only figure in the book is an early phylogenic tree. Modern phylogeny produces beautifully complex trees that look like 10,000-team basketball tournaments run in reverse, with the winner being life’s common ancestor. But as biologists have turned to genetics to build these trees, they’ve found that they lead to completely different trees than the ones built from morphology, the physical characteristics of organisms.

One reason for this is a tricky effect called convergence - two species that are not closely related and live continents apart could form a resemblance because they evolved in similar environments. Ward studies a type of ant that is found in both Asia and America, and morphology would suggest that they are closely related species despite being so far apart geographically. However, genetic data showed the ants were more distantly related than previously could have been estimated from their looks, suggesting they evolved to look similar due to their similar environments, without a recent common ancestor.

But the Tree of Life remains a strong structural model, Ward said. So strong, in fact, that it has been adopted by creationists, who describe an “orchard of life” of animals that evolved after Noah’s flood. As with most mentions of creation “science” at the meeting, Ward’s slides about these theories drew mostly giggles from an audience decidedly on the side of Darwin, even as genetics reveals a world more complex than he ever could have imagined.

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Many thanks to PZ Myers, author of the amazing evolution blog Pharyngula, who gave us a nod last night in his ongoing live-blogging of the Darwin/Chicago 2009 conference. PZ is doing a fantastic job covering the event in real time. For other coverage, check out WMFT’s interview with conference organizer Robert Richards, and Milt Rosenberg’s interview on WGN Extension 720 with Richards and conference speaker Ronald Numbers.