As if you don’t already feel guilty for double helpings of pie on Thanksgiving, Black Friday brought another reason to fret over an unhealthy diet: new diabetes projection numbers that suggest insulin injections could someday be a new shared family Thanksgiving ritual. In the journal Diabetes Care, Elbert Huang, assistant professor of internal medicine at the University of Chicago Medical Center, published the results of a new model that predicts more than 44 million Americans will suffer from Type 2 diabetes by the year 2034, a rate of disease that will cost the U.S. an estimated $336 billion each year.

Huang’s model, constructed with Anirban Basu, Michael O’Grady, and James Capretta, bases its projections on current prevalence of diabetes combined with projections about how demographics and diabetes care are expected to change in the coming 25 years. The near doubling of diabetes the paper predicts (currently, about 23.7 million Americans are diabetic) would result from the combination of more and more Baby Boomers entering age groups where diabetes is more common and people living longer with diabetes - an ironic byproduct of improved medical management of the disease. Surprisingly, Huang’s model does not predict much of a change in the rates of obesity, the largest risk factor for diabetes. That’s not entirely good news, though; Huang’s logic is that America has already reached a sort of flab ceiling where the proportion that is overweight or obese (currently holding steady at 65%) simply can’t get any higher.

Or as Huang told my colleague John Easton: “we anticipate that the population will reach an equilibrium in obesity levels, since we cannot all become obese.”

If Huang and his co-authors are wrong about that piece of their model, the diabetes rates could be even higher as we enter the 2030’s. And while that would mean Huang’s predictions were off, it wouldn’t be the first time diabetes researchers have underestimated America’s diabetes boom. As collected by Easton, scientists have regularly low-balled the numbers in their predictions about the diabetes epidemic, missing the mark by millions of cases.

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Picture a boxing match, Tao Pan said. A cell, facing viral or bacterial invasion, starts building new proteins, while the infection generates dangerous reactive oxygen species that rampage through the cell causing serious damage. When the new proteins meet the reactive oxygen species (ROS), they face off like welterweights circling each other in the ring - ROS dart in, trying to do damage to the protein’s most important sites, while the protein deflects attacks with an amino acid, called methionine, capable of absorbing those blows.

Cells can place protective methionines into proteins the old-fashioned way, by encoding for the amino acid in the DNA recipe. But in a paper published this week in the journal Nature, researchers from the University of Chicago and the National Institute of Allergy and Infectious Diseases describe a new, post-genetic way for cells to add methionine bodyguards to proteins when they are threatened: making purposeful mistakes.

To discover this useful fallibility, Pan - a professor of biochemistry and molecular biophysics at the University of Chicago - and graduate student Jeffrey Goodenbour developed a novel assay for measuring particular errors called misacylations. If you recall the central dogma of molecular biology, DNA is used to make protein via intermediaries called RNA. First, an RNA copy of the DNA gene for a particular protein is created, called messenger or mRNA. Then that mRNA moves to a cellular machine called a ribosome. Specific transfer RNAS - tRNAs - are then recruited to the ribosome, bringing along amino acids that are placed in order according to the mRNA recipe. After hundreds or downloadable software thousands of amino acids are arranged into a chain, you have a completed protein.

One would think it was a bad thing for mistakes to happen along this manufacturing process, and scientists have long believed that quality-control measures are in place to ensure that the proteins come out the way DNA says they should. One step that prevents mistakes is tRNA specificity - each of the 20 tRNA varieties can only bind to one type of amino acid. Occasionally, a tRNA grabs the wrong amino acid, an error called misacylation, but laboratory studies in artificial systems estimated that this mistake only happens about once every 10,000 times.

The keyword there is “artificial systems” - because when Goodenbour and Pan looked at the misacylation rate in live cells, it was much higher: 1 out of every 100 methionines was placed incorrectly, they found. And when the cell was stressed by a virus, bacteria, or a caustic chemical such as hydrogen peroxide, that methionine error rate went up even higher, with as many as 1 out of 10 off-recipe placements. That emergency measure would make new proteins more resistant to ROS damage when the cell needs them the most, Pan said.

“This mechanism allows every protein to get some protection,” Pan said. “The genetic code is considered untouchable, but this is a non-genetic strategy used in cells to create a bodyguard for proteins.”

The scientific question raised by this discovery is: why? Cells could more directly protect their proteins by loading them up with methionines through the DNA code, removing the need to rely on random “errors” imposed later in the translation process. But Pan proposes that very randomness as the secret weapon cells employ to make their proteins difficult targets for ROS attacks. By placing the protective methionines in different places in each protein, cells generate a diverse population of proteins each with their own unique set of armor - a strategy that would be impossible if translation of DNA into protein was perfect. Just like on the species level, diversity is one of the  best defense against attack.

“This sounds chaotic and doesn’t make a lot of sense according to the textbook,” Pan said. “But this way the cells can always ensure that a subset of these proteins is somewhat less sensitive to the extra hits. I think that’s the most important part of this - to make every protein molecule different - and you cannot do this genetically.”

Here at ScienceLife, we often focus on fresh laboratory findings that could be years away from being applied to patients in a clinic. Popular newspapers and magazines, meanwhile, sometimes get caught up in controversies surrounding health and medicine without focusing in on core questions that many patients have about common diseases and conditions. And with a tangle of information - reputable and otherwise - about common health topics available on the internet, it is often hard for people to navigate quickly to the reliable medical answers they seek.

So we’re launching a recurring feature here on the blog where a University of Chicago Medical Center physician will address - in a series of short Q&A-style videos - frequently asked questions about a popular medical topic. These videos are meant to be patient-focused and to offer clear, accurate information about common diseases and the accepted medical treatments currently available. If you have a medical topic you would like to see featured in future videos, or if you have questions you would like to have answered by a University of Chicago physician, please don’t hesitate to contact the editors.

There’s really no better subject to kick off this series than autism, the psychiatric disorder of communication and social behavior most commonly seen in children. Autism is in the news on an almost daily basis, and this week was no exception - Chicago Tribune reporters Trine Tsouderos and Patricia Callahan continued their excellent series Sunday and Monday on the proliferation of dangerous experimental treatments for autism that have little to no scientific basis. Last month, the journal Pediatrics published the results of a national survey that found that slightly more than 1 out of every 100 children have been diagnosed with an autism spectrum disorder, a higher figure than previously estimated - though experts have debated whether this reflects a rise in autism rates or an increase in diagnosis of the disease.

Sharon Hirsch, Section Chief for child & adolescent psychiatry at the University of Chicago Medical Center, treats many children with autism spectrum disorders each year through the Medical Center’s neurodevelopmental clinic. We interviewed her in her office last week about the latest autism numbers, how the disease is diagnosed by psychiatrists, how it is currently treated, and the types of challenges children with the disorder face at school and at home.

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There’s a strange new addiction sweeping across the heartland. Unsuspecting addicts are lured in by word-of-mouth promises of unbeatable prices, made to feel exclusive with a membership card, and turned loose upon shelves and shelves of merchandise. But while the initial high of savings may be thrilling, the addiction always spirals out of control, until the poor victims find themselves with 25 pounds of peanut butter and 300 boxes of Cheez-Its overflowing their pantry.

Warehouse club stores such as Costco or Sam’s Club have changed the way people shop for daily items like groceries and cosmetics, teaching them the financial joys and storage dangers of buying in bulk. But the savings associated with buying large quantities - so long as those 25 pounds of peanut butter are used up before they went bad - are undeniable. So it was only a matter of time before the bulk-buying strategy crossed over to another market where cost-cutting is sorely needed: health care.

One place where people feel the most pain from health care costs is prescription drugs. Even though the cost of pills only makes up about 10% of total medical costs, there’s something dispiriting about having to throw down $20 bills - or even hundreds of dollars - on a monthly basis at the pharmacy to fill one’s regular medications. As such, many experts have recommended buying prescriptions in 3-month quantities rather than 1-month installments, a switch that retailers such as Walgreen’s, Target, and yes, Costco have thrown their support behind.

But while buying three months of pills at a time instead of one made intuitive sense, nobody had bothered to actually quantify just how much individuals and their insurance companies could save from such a strategy. Atonu Rabbani and G. Caleb Alexander of the University of Chicago Medical Center stepped into that breach with a paper published this month in the journal Applied Health Economics and Health Policy, calculating that 3-month prescriptions can give both individuals and the health care system a little more pocket change in tight times.

Per person per month, the savings of receiving 3-month prescription supplies rather than the 1-month variety saved people the modest sum of $5.91. But in some places, that’s still a matinee movie, and over the course of a year, it’s about $70 - a nice dinner-for-two out, for sure. Total costs per month also drop by 18 percent ($7.81), which means both you and your insurance company will be happier on a monthly basis.

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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.”