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.”

read more

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.

read more

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.

read more

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.

read more

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.

Darwin/Chicago 2009 is here! Here is the lineup for tonight, our live-blog will begin below around 6:00 p.m.

6:00 p.m. Welcome by Robert Zimmer, President of the University of Chicago

6:15 p.m. Richard Lewontin (Harvard University): “Genetic Determination and Adaptation: Two Bad Metaphors”

7:00 p.m. Ronald Numbers (U. of Wisconsin): “Anti-Evolutionism in America: Scientific Creationism to Intelligent Design”

7:45 p.m. Marc Hauser (Harvard University): “From Where do Morals Come? NOT Religion!”

We’re only a few hours away from the start of Darwin/Chicago 2009, 2+ days of the world’s leading evolutionary biologists discussing the past and future of the field. Come back to this space tonight at 6:00 pm Central time for live-blog coverage of the opening event at Rockefeller Chapel, and keep coming back all day Friday and Saturday for frequent updates from the conference.

Before things get into full swing, I wanted to play armchair Linnaeus and organize the conference’s 30-some talks into a few major themes. So much is packed into Friday and Saturday, with two simultaneous programs covering “biological sciences” and “history and philosophy,” I won’t be able to see everything, but the list also contains what I’m hoping to prioritize in order to get at least a representative sample of the event.

Evolution Goes to Church

Rockefeller Memorial Chapel, the looming gothic structure on the southeast side of campus where convocations and communion services are held, has been the site of Darwin discussion before - as mentioned yesterday, Sir Julian Huxley gave a speech predicting the end of religion at the 1959 conference. Thursday night’s trio of speakers both follows that agnostic tradition and nicely previews the main threads of the more tightly-packed Friday and Saturday schedules.

Addressing the renewed vigor of the evolution vs. religion debate, Ronald Numbers of the University of Wisconsin will recap the historic path of these conflicts, emphasizing that the “young earth” element of today’s creationists is a relatively new development. Harvard’s Marc Hauser, meanwhile, will pull the rug out from under one of the main creationist arguments - that morality could not have developed under natural selection and must have been given to humans by a supernatural power. But lest you think evolutionary biologists are too distracted by the external debate to do the hard work in their own field, legendary geneticist Richard Lewontin will open the night’s proceedings talking about the challenges of directly determining how genes contribute to an organism’s fitness.

read more

Sir Julian Huxley speaks in Rockefeller Chapel, 1959

As discussed yesterday, the Darwin/Chicago 2009 conference marks not just the anniversary of Darwin’s birth and most famous book (The Origin of Species) but also 50 years since a landmark evolution conference was held at the University of Chicago. Like this year’s gathering, the 1959 conference was meant to both look back at Darwin’s life and ideas and look forward to the future of the field his theory created: evolutionary biology.

To commemorate this historic conference, the University of Chicago’s Regenstein Library has put together a great web exhibit with video and audio from the Darwin Centennial conference in 1959. Encylopedia Brittanica Films produced a film of the conference, and you can watch several video clips from that film and listen to audio excerpts from three presentations - in addition to songs from the Darwin musical commissioned for the meeting.

From the film footage available on the website, you can see that the style of the conference in 1959 was very different from what will occur this weekend. Instead of individual talks and Powerpoints, the scientists participated in panel discussions on topics such as The Origin of Life and Man as an Organism - the latter of which was held on Thanksgiving Day. One clip shows overflow crowds that couldn’t get into Mandel Hall (where the panels were held) sitting in other University buildings and staring off into space as they listen to the audio of the conference. This weekend’’s overflow crowd will be able to stare at their computer and follow along right here on the blog, if you’ll forgive the plug.

Then again, some things weren’t so different between 1959 and 2009. Tension between evolution and religion was intact: Sir Julian Huxley, the renowned zoologist considered to be one of the main architects of the modern synthesis of evolutionary biology, gave a lecture in Rockefeller Chapel entitled The Evolutionary Vision which, according to Regenstein librarian David Pavelich, “proposed that religion, being subject to the laws of evolution, was fast becoming obsolete and would eventually evolve itself out of existence.” The religious opposition to Darwin’s theories was acknowledged by University of Chicago chancellor and professor of philosophy Lawrence Kimpton, who likened Darwin to John Stuart Mill as advocates of free thought and liberty:

“Darwin, in his own sphere and his own action, produced an independent defiance of the pressures of his day, challenging the rigidity of thought and temper with a naturalistic theory shocking to the entrenched supernatural explanation of biology. The outrage and the distortions that erupted immediately, persisting well into this century and even in this country, are measures of Darwin’s independence.”

Also in audio clips:

• Sir Charles Galton Darwin discussing his grandfather’s legendary voyage observing and collecting specimens on the H.M.S. Beagle, including a reading of what Darwin wrote in his journal the first time he ate a banana.
• Archaeologist Louis Leakey on the search for fossils of human ancestors - “You hear people say ‘what has Africa created to the human race?’ It contributed the human race.”

In lighter fare, check out the songs from the Darwin musical, Time Will Tell, premiered at the conference. They are very 1959, and are probably the only songs you will ever hear with lyrics such as “this gastropod has quite an odd phylogeny” and “Alas, to his sorrow, he generally finds/That pre-conceived notions of various kinds/Have already helped them to make up their minds/And the facts will only confuse them.” I could see that as the theme song for quite a few evolution blogs, actually.

There has certainly been no shortage of attention on Charles Darwin this year. With the dual landmarks of Darwin’s 200th birthday and the 150th anniversary of The Origin of Species, virtually every scientific publication, museum, conference and institution has taken the opportunity to pay tribute to the life and work of the man who gave us the theory of evolution. But now that the celebrations are (mostly) over, it’s time for the field of evolutionary biology to move forward, capitalizing on new technologies and discoveries that were only a dream when Darwin drew upon decades of observation and thought to craft his revolutionary book.

That same challenge faced evolutionary biologists in 1959, when they gathered at the University of Chicago to observe the 150th and 100th birthdays of Darwin and his book. Brought together were many of the 20th century’s greatest thinkers on the subject of evolution, including legendary biologists Julian Huxley, Theodosius Dobzhansky, and Ernst Mayr, Darwin’s grandson Charles Galton Darwin, and John Scopes of Scopes Monkey Trial fame. And according to Robert Richards, professor of the history of science and medicine at the University of Chicago, the discussions that took place at that conference helped solidify what we now think of as the “modern synthesis” of evolutionary theory, the merging of Darwin’s ideas about the gradual effects of natural selection with the then-new field of genetics.

Darwin/Chicago 2009, which begins Thursday night at the University of Chicago, will try to recapture that spirit and make a similar impact upon the path of evolutionary biology. Once again bringing the field’s brightest lights to Hyde Park for an exchange of ideas, Richards and the conference’s other organizers hope that the event will do more than merely acknowledge a triple anniversary, but will instead re-evaluate evolution science in light of a world much different from the 19th century environment that shaped Darwin’s thoughts. Here, with Richards’ assistance, are three reasons why now is a great time to talk about Charles Darwin and evolution.

1) New technologies

The 1959 conference took place only six years after James D. Watson and Francis Crick published their landmark paper on the double-helix structure of DNA. And it wasn’t until 1957 that the “central dogma” of biology - that DNA encodes for RNA which encodes for proteins - was enunciated by Crick. So the ‘59 conference took place at the dawning of the genetic age, when the biological substrate that Darwin’s natural selection acts upon was finally understood.

read more

Studies of human disease often work from the patient backwards - doctors and scientists take the common symptoms of a particular disorder and use them as clues to figure out what first went awry to spur the disease. For neurological diseases like Parkinson’s or amytrophic lateral sclerosis (aka Lou Gehrig’s Disease), symptoms and brain images have pointed the research at particular parts of the brain, which are then studied in animal models and on the genetic or cellular level. But disease research can also work from the other direction, where a particular cellular process is identified as a potential culprit in the disorder before a patient with that defect is even found.

That’s the case with a paper published this month by a team of University of Chicago researchers studying the cellular mechanisms that underlie diabetes. There are many types of diabetes mellitus, but all can be traced back to the hormone insulin - the body’s signal that cells should soak up sugar from the blood. Most cases of juvenile, or Type 1, diabetes result from the immune system erroneously attacking and killing the Beta-cells of the pancreas, which release insulin. Type 2 diabetes, which often develops in adulthood, results from a reduced sensitivity to insulin and/or a decreased release of the hormone.

But diabetes can also have a genetic origin, in some rare cases, when one of the genes involved in the secretion of insulin is disrupted. Previously on the blog, we’ve talked about the story of Lilly Jaffe, whose diabetes was found to be caused by a rare genetic mutation in a protein called a potassium channel, critical for the release of insulin. The mutated potassium channel seen in Lilly’s case interferes with the trigger of insulin release, causing lower amounts of the hormone to circulate through her blood. Thus, Lilly was treated by daily injections of insulin, until doctors at the University of Chicago detected the mutation and prescribed her a drug that directly targeted the potassium channel.

Now researchers at the University of Chicago have found another ion channel that must function properly for the right amount of insulin to be released. Only problem: there’s no patient.

read more

Over the course of four days covering the Neuroscience 2009 meeting in Chicago, I wrote nearly 7,000 words between Sunday, Monday, Tuesday and Wednesday. You might say I was excited to be there. But I know not everybody has an hour to devote to reading feverish recaps of the latest neuroscience research, so here’s a post summarizing some of my favorite parts, along with some excellent posts from other websites about the conference.

Best Talks

Eric Kandel - I was charmed by this 80-year-old Nobel laureate’s undiminished enthusiasm for scientific research; even though he’s already contributed more than perhaps anyone else to our understanding of how the brain learns and remembers, he’s still forging ahead with new, ambitious experiments.

Thomas Sudhof - There is no shortage of bad science about autism, so it was refreshing to hear some good science, even if the answers aren’t as easy and reassuring as those provided by the quacks. Sudhof, who used black widow spiders to discover two proteins that help neurons find each other and communicate, spoke eloquently about how defects in these proteins could underlie many of the symptoms of autism spectrum disorder.

Hot Tech

Optogenetics - Everyone at the conference seemed to be abuzz about this technique, developed by Karl Deisseroth of Stanford, for activating or de-activating specific neurons with light. Here’s an awesome video from Deisseroth’s lab of a mouse’s activity being controlled by a fiberoptic implant, and a talk by Deisseroth describing his method and its applications.

Wikipedia - Nothing new about this tech, of course, but two Wikipedian-scientists held a fascinating workshop on how neuroscientists can help improve public understanding of science by writing and editing for the open-source encylopedia…and circumvent the media in the mean time.

read more

And so Neuroscience 2009 comes to an end, and it’s time to put away my badge, rest my weary feet and note-taking hand and think about biology below the neck again. Here’s the final installment of our live coverage, but come back tomorrow for a roundup of the conference with highlights, loose observations and links to other people’s thoughts on the conference. Thanks for reading!

2:30 PM - The Final Talk

The schedule may say that Neuroscience 2009 runs through the end of the day today, but judging by how many suitcase-toting scientists were jumping in airport cabs this afternoon, a small portion of the 30,000+ attendance makes it to the very end. Indeed, even the main stage ends its conference early, shutting down after a talk by Mt. Sinai School of Medicine’s Eric Nestler, an expert in the field of molecular psychiatry.

Nestler’s research focuses on the gritty details of how drugs of abuse change the expression of a person’s genes - yes, it was another addiction talk, and the former addiction researcher that I am, it was great to see the topic getting so much attention this year. In the addiction press conference I attended yesterday, Nestler hinted at a bombshell idea - frequent users of addictive drugs such as cocaine, heroin or alcohol may change the mechanics of their genes so permanently, the modifications could be passed on to their children. This “inheritable addiction” has already been observed in lab rats, Nestler said, mirroring similar results seen with the offspring of obese rats (which I talked about on Monday).

But that data must be too fresh for mass consumption, despite Nestler telling a roomful of reporters about it the day before. His talk today focused on the steps leading up to that discovery, carefully examining how repeated cocaine increases or decreases the activity of hundreds of genes in the reward pathway of the brain. Those long-lasting changes, which can cause cells of the reward pathway to actually grow and change shape, help explain why addiction is such a difficult condition to treat - it may require a complete re-re-structuring of the brain.

Much of the addiction research I’ve talked about this week has taken place in animals, but before Nestler’s talk, I came across a rare experiment that looks at the behavioral effects of a commonly-used drug in humans. It might seem strange that we know a ton about the specific genes that are up or down-regulated by cocaine, but not so much about its effects upon humans, but that’s due to procedural reasons - it’s quite hard to get approval for a study that gives illegal drugs to humans.

Michael Ballard, from the University of Chicago laboratory of Harriet DeWit, was trying to fill in at least one of those gaps in the research by testing the effects of THC (the active ingredient in marijuana) to presumably eager volunteers. Ballard then tested the subjects’ ability to judge facial expressions and determine the emotional content of pictures and personality trait words while they were under the influence of the drug. Interestingly, higher doses of THC caused the subjects to misjudge the facial expressions they were shown, suggesting an effect of the drug on social perception. The other tests were normal during the drug effect, but when brought back to the laboratory a week later, the subjects showed a decreased ability to remember neutral and negative personality traits, possibly indicating that their memories of the drug effect were biased toward happier stimuli. Ballard hopes to continue that research into other drug types - he’s currently testing amphetamine - to give the field of addiction research much-needed, laboratory-controlled human data to make sense of the flood of animal experiments.

read more

6:45 PM - The Opposite of a History Lesson

Eric Kandel is 80 years old, was present at the first Society for Neuroscience meeting in 1969, is 9 years removed from winning the Nobel Prize for physiology and medicine. He’s also so well known at the Neuroscience meeting, he can go by one name, “like Bono,” said SfN president Tom Carew in his introduction to tonight’s Presidental Lecture. So you might have expected Kandel’s talk to be a history lesson, a retelling of how he uncovered the cellular chain of events that underlie learning and memory in sea slugs, fruit flies, mice and, by extension, you and me.

But Kandel, looking like The Sopranos’ Uncle Junior and speaking with Woody Allen’s Brooklyn accent, had very little interest in looking back. After 75 minutes of him excitedly flashing through graphs and figures explaining recent findings in his laboratory at Columbia University, he could only narrow his talk down to four conclusions. My thesis adviser, who was sitting next to me, leaning over and whispered in amazement, “these aren’t conclusions at all, he’s still forging ahead.”

That relentless drive in someone so late in his career was infectious. Kandel said the goal of his talk was to explain how a person remembers his first love for the rest of his life, as if that was a simple quest, but his lecture portrayed science as it should be: a never-ending story, with each answer giving birth to several more questions. While some researchers settle on a single technique and pass the torch to younger researchers when the limits of that technique are reached, Kandel proved that he has stayed on the cutting edge of science, bringing fresh talent into his lab to apply new tools to his endless questions about how neurons encode memory.

As a result, almost a decade after his Nobel victory, Kandel was excitedly telling 10,000 of his colleagues about a new cellular signal, called CRB-3 in mice, which he humbly described as “a new class of functional proteins” and “an entirely new model of synaptic plasticity.” The work was backed up with the latest in genetic, cellular biology and imaging evidence, testimony to both Kandel’s ability to keep up with the fast-moving world of science as well as the sprawling world of neuroscience itself.

“One of the wonderful things that has happened in my forty years in the society, is that neuroscience, which really was quite fragmented when I entered the field…has become a unified organism,” Kandel said.

read more