Here’s a moral dilemma that seems tragically timely, given the chaos surrounding attempts to deliver aid to Burma’s cyclone victims. There are 60 orphans at the Canaan Children’s Home in Buziika, Uganda, and their meal allotment has to be cut. What do you want to do: take six meals away from each of two kids, or 10 meals away from one? You have eight seconds to decide.

In this and similar moral dilemmas, efficiency (the total number of meals lost) is pitted again against equity (how evenly the burden of lost meals is shared among the children). You have to take away a total of 12 meals if two children share the loss, but only 10 (which would seem better) if a single orphan bears the entire burden. You have to decide whether to sacrifice efficiency (losing fewer meals) to equity (spreading the loss over more children).

Here’s another way to think about it. You are driving a truck to the Burmese cyclone victims. It holds 1,000 pounds of rice. The time it will take to deliver the rice to everyone in the Irrawaddy Delta village you are headed for means that 200 pounds will spoil. If you deliver the rice to people you meet en route, you will be distributing it to only half the population of the village, but only 50 pounds will spoil. Do you deliver the rice to only half the number of victims, maximizing the total amount of food provided (efficiency), or do you sacrifice 150 pounds to distribute it to more people (equity), giving rice to more people but also causing more rice to go to waste?

In a study reported online today in the journal Science, researchers posed the orphan dilemma to people while scanning their brains with functional magnetic resonance imaging (fMRI). Unlike most studies of the brain basis of ethical decision making ("neuroethics"), this one was grounded in reality: the volunteers’ choices would determine how many meals the research team actually donated to the Ugandan orphans. The volunteers knew this, which made the dilemma painful in the extreme. “Quite a few came out saying: ‘This is the worst experiment I’ve ever been in. I never want to do anything like this again!’,” said study co-author Ming Hsu of the University of Illinois’s Beckman Institute for Advanced Science and Technology.

So, which is more critical to our sense of justice, equity or efficiency? And how does the brain decide?

In the experiment, the volunteers (26 men and women, ages 28 to 55) first read short bios of the orphans. Then they watched a video on a computer screen, showing a ball rolling toward a lever. By moving the lever, they could steer the ball toward either of two depictions of the moral choices: photographs of the actual orphans who would be affected by that choice, with numbers for the number of meals that would be lost to those children if that option were chosen.

By an overwhelming margin, people chose to preserve equity at the expense of efficiency—lose a few more meals, but spread the burden among as many children as possible, rather than making one hungry child—whose imploring little face stared back at them from the screen--shoulder the entire loss.

According to the fMRI, different brain regions became active at different points in the decision-making. The insula, which is involved in processing emotions and the awareness of bodily states as well as (in some studies) evaluating fairness, was active when the volunteers wrestled with questions of equity. The putamen, which is activated during learning that brings rewards, lit up when people thought about efficiency.

Since equity won, it suggests that decisions about fairness are rooted in emotion more than in cold-eyed cost-benefit analysis. “That the brain has such a robust response to unfairness suggests that sensing unfairness is a basic evolved capacity,” Steven Quartz of Caltech and co-author of the study said in a statement. “The emotional response to unfairness pushes people from extreme inequity and drives them to be fair,” suggesting that “our basic impulse to be fair isn’t a complicated thing that we learn,” but an instinctive one.

And whoever said scientists have no heart? After the experiment, and based on the volunteers’ decisions, the team donated $2,279 to the orphanage.

Bad enough that antidepressants fail to help an estimated one-third of people suffering from depression. Even worse is that it can take 6 to 8 weeks before that becomes clear: the patient dutifully swallows Zoloft after Zoloft or Paxil after Paxil, only to find after two months that she is no better off—at which point her doctor typically puts her on a different med, and the whole process of trial-and-error starts all over again. There’s got to be a better way—and now there may be.

Last September I wrote about a new use of EEGs—the decades-old technology that measures brain waves—in which psychiatrists compare the EEG of a patient to thousands of EEGs in a huge database that matches it to an effective treatment. (This is different from using EEGs to diagnose a mental illness, something that doesn’t seem to work, perhaps because there are many, many ways for a brain to have an underlying pattern of electrical activity that adds up to “depression” or “bipolar disorder” or other psychiatric disease.) CNS Response, the California company that runs the database, looks for matches between EEG and effective drug. In about 75% of cases, that produces surprising pairings—such as an anticonvulsive drug for a patient with depression—that the physician would never have thought of.

A new study being reported this afternoon at the annual meeting of the American Psychiatric Association finds another use for EEGs: predicting which patients will respond to the antidepressant they have just started. Rather than waiting for months, patients suffering from major depression—as nearly 15 million Americans do—take the drug for a week and then undergo an EEG (which is painless, noninvasive and relatively cheap, on the order of $150).

The study, led by Andrew Leuchter of UCLA and called BRITE (Biomarkers for Rapid Identification of Treatment Effectiveness), had 73 patients take the antidepressant escitalopram, which is sold as Lexapro and belongs to same category—selective serotonin reuptake inhibitors, or SSRIs—as Prozac and many others. That’s the quandary: all of the drugs supposedly work by targeting the brain’s serotonin system (which is actually a questionable claim, but that’s a story for another day), so which one will help a particular patient? Before starting the drug and again after taking it for 48 hours, for one week, and for two and seven weeks, the patients underwent EEGs. At the one-week visit, doctors assessed how well they were responding to the drug; the researchers also identified genetic markers that have been reported to predict how well patients will respond to SSRIs, and measured how much of the drug was in the patients’ blood, which is thought to be an indication of whether it is likely to work.

The bad news: the docs were terrible at predicting, based on how well the patients were doing after a week on Lexapro, whether the drug would alleviate their depression. The genetic markers fared no better. Neither did the blood levels.

But of the 38 patients who got a little better and the 28 who recovered completely by the end of the seven weeks, the EEG readings—measuring brain-wave changes after one week on the drug—did pretty well, predicting who would get a little better or even recover with 74% accuracy (compared to 51% accuracy for the docs’ evaluation).

“Early changes in frontal EEG signals carry important information about future clinical response,” Leuchter said in a statement, suggesting that EEGs have “the potential to help clinicians improve the care of patients suffering from depression.”

Caveats: the company that sells the EEG system, Aspect Medical Systems, funded the study, and Leuchter has been a paid consultant to Aspect, served on its board and received grant money from Aspect. (I have blogged before on how company-funded studies can be skewed.) And seven weeks is not exactly long-term. Still, anything that moves us beyond the current hit-and-miss approach to treating depression is to be welcomed.

If a stock market that swings 400 or more points in a single session has been making you queasy—not to mention too terrified to check your 401(k) balance—at least we now know who to blame: men and their raging hormones.

It’s a Wall Street cliché that the most successful traders are those with nerves of steel and you-know-whats the size of softballs. Scientists from the University of Cambridge therefore decided to measure what, exactly, is going on with traders’ testosterone (which is linked to the latter) and cortisol, the stress hormone. What they found, as they report in this week’s online edition of the Proceedings of the National Academy of Sciences], is that when male traders have high levels of testosterone in the morning, they make more profits than their daily average that day, and when market volatility is high their cortisol levels soar. Since both hormones are well-known to impair thinking, the scientists warn, high levels can make traders “display the irrational behavior often observed in real markets,” make traders take more risks, and exaggerate downturns in the market.

Sound familiar?

For their study, Cambridge’s John Coates and Joe Herbert recruited 17 traders, all men working for a financial firm in London. Most of the traders in the study, who were 18 (!; that’s not a typo) to 38 years old, focused on German interest-rate futures, making trades valued at £100,000 to £500 million, or about $196,000 to $980 million. For eight business days in a row, the traders gave the scientists saliva samples, from which the researchers measured levels of testosterone and cortisol.

Tons of studies on testosterone have shown that this “male” hormone (that’s in quotes because women have some, too) rises in athletes preparing for a competition, spikes even more in winning athletes and falls in losers. Testosterone seems to increase both confidence and risk taking. That can increase the chance of winning again.

That seemed to be what happens with the traders. Daily testosterone levels were significantly higher on days when they made especially high profits on their transactions, Coates and Herbert find. How? Because, according to other studies, high testosterone levels have been found to make men “increase search persistence” (that is, you keep looking for information of the wisdom of a trade), take greater risks (which can be a winning strategy if you usually make profitable trades) and display “fearlessness in the face of novelty,” such as when unexpected news hits the markets.

As for cortisol, it seemed to reflect how volatile the German market was: dizzying swings stressed out the traders. No surprise there.

But perhaps some red flags. Levels of both hormones were high enough to have cognitive and behavioral consequences, “specifically by shifting risk preferences or disturbing the neural basis for rational choice,” write the scientists. Exactly how this happens is the subject of intense research. But what neuroscientists know is that a handful of brain regions—the amygdala, anterior insula and nucleus accumbens—are the culprits behind irrational choices. If they’re overactivated, as can occur when they’re bathed in hormones, “then investors will display the irrational behavior often observed in real markets,” warn the scientists. “If testosterone continued to rise or became chronically elevated, it could begin to have the opposite effect on [profits and losses] . . . because testosterone has also been found to lead to impulsivity and sensation seeking [and] to harmful risk taking.”

The traders’ cortisol levels might also lie behind one of the U.S. stock market’s recent tendencies: once it starts to fall, especially at the end of the trading day, it often falls off the cliff. There you are, checking the Dow at 3:45, and see it’s down a couple dozen points—only to find when you check back after the close that it plummeted 200 points. Blame cortisol. It makes people more risk-averse, so in a slightly-down market men with soaring cortisol will “exaggerate the market’s downward movement,” the scientists warn, by selling like crazy.

There are also risks on the upside. Testosterone rises in a bubble. Since it also increases risk taking and irrationality, high levels in traders can exaggerate market rises. Hence the roller-coaster: every bit of news, good or bad, has an exaggerated effect on financial markets.

As Herbert puts it in a statement, “Our work suggests that [financial] decisions may be biased by emotional and hormonal factors.” And this, from Coates (an ex-trader himself): “If testosterone reaches physiological limits, as it might during a market bubble, it can turn risk-taking into a form of addiction, while extreme cortisol during a crash can make traders shun risk altogether. In the present credit crisis traders may feel the noxious effects of chronic cortisol exposure and end up in a psychological state known as ‘learned helplessness.’ If this happens central banks may lower interest rates only to find that traders still refuse to buy risky assets.” ”

Sound like any market conditions you know?

Scientists have not done a comparable study on female traders, who are rarer than hens’ teeth. But the implication is clear. Men are just too hormonal for the public to entrust them with something as crucial as the global financial system. Their raging hormones will be the ruin of us all.

Just for the record, reporters take no pleasure in questioning the power of drugs to treat depression. To the contrary: journalism is notorious for attracting curmudgeons, grumps and depressives—some of my best friends are one or more of the above—so we wish with all our hearts that antidepressants would work.

And that scientists wouldn't keep finding evidence that they do not.

In January I reported on the file-drawer effect in studies of antidepressants. The file-drawer effect refers to the fact that scientifically-sound studies on the efficacy of antidepressants are not published, as The New England Journal of Medicine article described. Most of those studies were negative—that is, the drugs did not help patients much more than a sugar pill (placebo) did, if they helped at all. That skews the perception of doctors, scientists and you and me about these drugs; basing our assessment of antidepressants on published studies alone is like evaluating the prowess of a baseball team when only its wins and not its losses are reported.

Now a team of scientists has examined many of those unpublished studies, obtained through a Freedom of Information Act request for the U.S. Food and Drug Administration. As many people feared, once you include the deep-sixed studies, antidepressants look hardly more effective than a placebo at lifting patients’ black cloud of despair.

For their analysis, scientists led by Irving Kirsch of Britain’s University of Hull started with the data dump they got from the FDA on fluoxetine (Prozac), venlafaxine (Effexor), nefazodone (Serzone), and paroxetine (Seroxat /Paxil). They zeroed in on differences between the improvement reported by patients receiving the drug and those receiving a placebo. As is standard in such clinical trials, neither the patients nor the scientists running the study knew which patients were receiving real drugs and which were receiving placebos.

In short, there was virtually no difference in the response to drug vs. placebo of patients who suffered moderate levels of depression, and a small difference for patients with very severe depression, they report in the study published this evening in the journal PLoS Medicine. That small difference was, however, clinically insignificant—that is, the difference was so small that government health authorities do not recognize it as a meaningful improvement: on a standard scale of depression, patients should improve by 3 points, but the spread between placebo and drug was only 1.8. The difference between drug and placebo was clinically meaningful only for patients at the upper end of the very severely depressed category.

The reason for the tiny, or nonexistent, differences? Patients respond so well to placebo—to the mere thought that something might be helping them—that there was little room for an actual drug to do more. Across all groups, response to placebo accounted for more than 80 percent of any improvement. (In contrast, the placebo response to pain drugs is estimated at about 50 percent.) That suggests that even when patients are taking and benefiting from, say, Zoloft, the vast majority of the improvement is due to what their minds are telling them—that is, the belief that they would be helped. Only the most depressed patients showed little placebo response.

The scientists conclude that there is little reason to prescribe the new antidepressants to any but the most severely depressed patients except as a last resort. Kirsch summarized the findings this way: “Although patients get better when they take antidepressants, they also get better when they take a placebo, and the difference in improvement is not very great. This means that depressed people can improve without chemical treatments.”

But it seems that there is a larger message here. The placebo response—the belief that treatment will make you better—is enormously powerful. Surely it’s time to investigate further how it works and how it can be harnessed.

Bringing Sexy Back: Leah and Partner. Photo:Thomas Breuer - WCS/MPI-EVA.

Scientists from the Wildlife Conservation Society and the Max Planck Institute for Evolutionary Anthropology were minding their own business recently while studying western lowland gorillas in Nouabalé-Ndoki National Park in the Republic of Congo when they saw what no one has ever recorded: Leah and her sweetheart trying to make baby gorillas through face-to-face copulation. Curiously, Leah was also the first wild gorilla to be observed using tools, scientists reported in 2005. (She used a stick to determine the depth of a pool of water before wading into it.) A true pioneer, indeed.

Face-to-face (or, technically, ventro-ventral) copulation is extremely rare in the animal kingdom. Before lowland gorillas joined the club, only people and bonobos (a chimp cousin known for really, really enjoying recreational sex) had been known to look at their partner while mating. From time to time, a scientist in the field reported seeing mountain gorillas mate face-to-face, but the sightings were like those of Bigfoot: no photo, no count. Captive western gorillas have also been known to mate face-to-face, but scientists always wondered if that was an artifact of living in a zoo, not natural.

Thomas Breuer of the Max Planck says, “we can’t say how common this manner of mating is, but it has never been observed with western gorillas in the forest. It is fascinating to see similarities between gorilla and human sexual behavior.” Let that serve as inspiration for the 14th.

Department of unintended consequences: with wild fish populations plummeting worldwide, aquaculture seemed like the best way to satisfy the world’s ever-growing appetite for fish. Oops: according to a new study in the journal PLoS Biology, Atlantic salmon, sea trout and pink, chum, and coho salmon that come into contact with salmon farming in Scotland, Ireland, Atlantic Canada and Pacific Canada are being decimated by the fish farms.

Salmon aquaculture now produces more than one million tons of fish per year. But that doesn’t mean wild salmon stocks are left alone to rebuild. Farm-raised salmon that escape from the open-net pens along coasts—which is how most salmon farms are set up—breed with wild populations, earlier studies showed, meaning the progeny are no longer truly wild. Also, the crowding in salmon farms breeds sea lice (which can be lethal to juvenile fish), as well as other parasites and disease-causing pathogens, which also escape—right into the coastal waters where wild salmon swim en route to and from the open sea. The effect of sea lice alone could be disastrous: according to a study published last December in Science, the parasites are so ravaging opulations of one species of salmon in British Columbia that the populations are projected to plummet 99 percent within eight years.

But while the detrimental effect of salmon farms on wild fish has been known generally, the quantitative impact of swimming past salmon farms has been murkier.

Enter this study, led by Jennifer Ford of the Ecology Action Center and the late Ransom Myers of Dalhousie University. In five regions around the world, they find that the number of wild salmon surviving and returning to spawn after swimming past salmon farms is less than half the survival rate of salmon that do not get anywhere near the farms. Combined with the earlier studies, the findings point to a grim future: salmon farming is so seriously compromising natural populations that scientists expect a 99 percent collapse of wild salmon stocks in four years, or two salmon generations.

Memo to Mitt Romney: do not—I repeat, do not—try to get over your disappointment over your failed campaign by going shopping. Or buying a company. Or even buying stocks. If you do, you are likely to overpay by at least 300 percent.

A few years ago scientists caught up with what many women who have had their heart broken knows: there’s nothing like new shoes, or new anything, to lift your mood. Called retail therapy, the idea is that “comfort items” distract you from your sadness, or at least counterbalance it a little. But in 2004 scientists led by Jennifer Lerner, who is now at the Kennedy School of Government at Harvard, reported a worrisome relationship between heart strings and purse strings: feeling blue makes you willing to pay more for stuff. That ran counter to the prevailing view in psychology, namely that feeling lousy makes you devalue things. That is, when you’re blue neither a good movie nor a great dinner are as appealing as when you’re in a good or even a neutral mood.

Now she and colleagues think they have figured out why unhappy people tend to overpay. In a study to be published in June in the journal Psychological Science and that she is presenting tomorrow, February 9, at the annual meeting of the Society for Social and Personality Psychology, Lerner and her team find that thinking intensely about yourself—what they call self-focus—explains the connection between sadness and overpaying.

In their new study, the scientists recruited smart, quantitatively-oriented volunteers (that is, lots of Harvard students). Each volunteer received $10 just for showing up. Then each settled into a cubicle and watched a short film clip, either from a tearjerker (“The Champ”) or a neutral film (on the Great Barrier Reef). The first was meant to make them feel sad, the second to have no emotional effect. Finally, each participant wrote an essay, on how the film made them feel or on their daily activities, that the scientists analyzed for how many times self-y words like “I,” “me” and “my” appeared.

Then came the test. Each volunteer was given the chance to buy a sporty, insulated water bottle, at prices from $10 to 50 cents in 50-cent increments. Those who were made a little sad by the film, and who wrote self-centered essays, were willing to pay an average of $2.11 for the bottle. Those in a neutral mood paid 56 cents, barely one-quarter as much. Yet the volunteers who felt a little blue insisted their mood had no effect on their spending decision.

Lerner explains this “misery is not miserly” effect by invoking people’s need to make themselves whole. Sadness leads people to devalue their self image; they try to repair that by buying stuff, and are willing to pay more because making the self whole again matters so much. Why people don’t try to restore their sense of self and lift their mood by, saying, helping little old ladies across the street remains a mystery, though certainly a welcome one for the nation’s retailers.

Lerner doubts people can avoid this effect by, say, realizing that sadness will make them overpay. “If anyone should be able to think themselves out of this, it was our volunteers, who were all smart and very quantitative,” she says. But the volunteers denied that their mood had any effect on their spending decision. Instead, says Lerner, “all you can do is change the situation. If you’re feeling sad put some time between that and your decision to spend money. If you’re negotiating a price, don’t do it when you’re in a down mood.” Or, she says, take the focus off yourself and your misery by helping others—even that little old lady.

Maybe there is yet hope for humanity: According to an analysis of 2.8 million variations in the human genome, we are still evolving.

People the world over differ by about one in a million of the nucleotides that make up our DNA, but what’s interesting is evidence that those differences are not random but, instead, the work of natural selection, report Lluís Quintana-Murci and colleagues of the Institut Pasteur in Paris, in the online edition of the journal Nature Genetics. That basic assertion is not surprising; the extent of the effect of natural selection's effects on our genes, in the recent past, is.

Geneticists have known for decades that traits such as resistance to malaria, and the ability to digest lactose in adulthood, confer a survival advantage and therefore have been under selective pressure—that is, individuals with mutations allowing them to be lactose tolerant had an edge over those who lacked the mutation, at least in certain environments (in this example, an environment where cows are raised for milk). In the case of malaria resistance, a mutation in the gene called CR1 is present in 85 percent of Africans, but absent in populations from other continents; this gene modulates the severity of malarial attacks, suggesting it has been positively selected for in Africans.

The Pasteur scientists find that genes showing the strongest signs of positive selection are involved in skin pigmentation and hair development, immune response to pathogens, the repair of DNA, sensory functions such as smell, insulin regulation in ways that affect obesity and diabetes, and metabolic pathways for, among other things, alcohol. (Yes, some people really can hold their liquor better, thanks to DNA.)

For example, the gene named EDAR regulates the density of hair follicles and the development of sweat glands and teeth; changes in the EDAR gene made hair denser in cold climates, and altered the regulation of body temperature so as to allow people to conquer the frozen north. And in the case of diabetes, the gene called ENPP1 harbors a mutation that has been shown to protect against obesity and type II diabetes; the mutation is present in about 90 percent of non-Africans but virtually absent in Africans.

In addition to showing that humans are still subject to the laws of evolution in terms of their physiology, the research challenges the claim that our minds are still stuck in the Stone Age. Evolutionary psychology argues that behavioral traits that stood our Paleolithic ancestors in good stead—male promiscuity, female coyness, stepfathers’ inclination to murder their stepchildren and other admirable qualities—still have our behavior in 2008 on a short leash. Many scholars have questioned that assertion, which even some diehard proponents are now wondering about. The new genetic research makes the very premise of Stone Age genes for anachronistic traits suspect.

If you’re still using polycarbonate baby bottles, sippy cups and juice bottles despite their propensity to leach the dangerous compound bisphenol A, as my colleague Anne Underwood explains in the Feb. 4 issue, at least don’t fill them with really hot water.

Bisphenol A is what’s called an environmental estrogen. That means it acts like a hormone, which may not be what you want for your fetus, baby or toddler. Hundreds of studies on lab animals find that exposure to even minute amounts of bisphenol A can trigger cancer of the breast or prostate years later, reproductive abnormalities and behavioral changes. There are no conclusive data on people, though there’s no doubt we’ve (almost) all become walking chemical cabinets: federal scientists find that 92 percent of us ages 6 and up harbor measurable amounts of bisphenol A. Anyone who wants to wait around for definitive human data, be my guest. For everyone else, some tips:

• Scrubbing or dish-washing polycarbonate baby bottles releases bisphenol A, tests have long shown.
• New data reveal that boiling-hot water increases that rate of release markedly. Even brief exposure to boiling water raises the rate of release by a factor of 15 to 55, scientists led by Scott Belcher of the University of Cincinnati report today in the journal Toxicology Letters. Before exposure to boiling water, the rate of release from individual bottles ranged from 0.2 to 0.8 nanograms per hour. After exposure, rates increased to 8 to 32 nanograms per hour.

There are more and more non-polycarbonate (and therefore bisphenol A-free) baby bottles on the market. That’s the only kind Whole Foods sells, for instance. But if you can’t or won’t buy those, at least wash yours gently in only lukewarm water. No child needs a dose of hormone with her apple juice.

Don’t say we didn’t warn you. Anyone, especially in the northeast and Midwest, who is surprised by the arctic express that moved in over the weekend and is still gripping most of us today wasn’t paying attention last month when climate scientist Judah Cohen issued his detailed winter forecast, the subject of my column in the December 17 issue of NEWSWEEK.

Unlike the official forecasters at the National Weather Service and elsewhere, Cohen, director of seasonal forecasting for Atmospheric and Environmental Research, Inc., doesn’t base his prognostications on crude indicators such as the status of El Nino. His research shows that something much subtler—the amount of snow cover in Siberia around the end of October—is the best crystal ball ever discovered when it comes to predicting winter weather in the U.S.

The connection, as I explained in the column, has several steps. But when Cohen ran the data through his forecasting model he came up with a prediction for cold for about the first three weeks in December, followed by milder weather especially during the first half of January (for which my heating bill thanks you) and a return to cold around Martin Luther King, Jr.’s birthday. Yesterday’s Giant-Packers playoff game was one of the coldest in NFL history. As Cohen writes me, “To predict swings in the weather almost to the day two months in advance should be impossible based on accepted climate theory. After all, chaos theory was invented to explain climate dynamics.”

Dumb luck? Doubtful. Will the rest of Cohen’s winter forecast, as well as those in coming years, prove as accurate? His track record is impressive, beating the official forecasts numerous times, but only time will tell. Will government forecasters acknowledge that Siberian snow cover can be a useful forecasting tool? When I spoke to them last month they were politely dismissive. But it’s tough to argue with success after success.

Although the Europeans got silver, gold, converts and tobacco out of their conquest of the New World in the 1500s, the Native Americans got nothing but genocide, as what UCLA biologist Jared Diamond called “guns, germs and steel” killed an estimated 90 to 95 percent of the Native Americans—a horrifying 20 million souls. Nothing was more one-sided than the direction that germs traveled. European conquistadors thoughtfully introduced smallpox, influenza and measles, against which the populations of the Americas had no immunity. Result: disease killed more of them than guns or steel.

Only one disease, scholars have long suspected, might have made the trip east to Europe: syphilis. Circumstantial evidence supported an America-to-Europe trajectory: the first recorded epidemic of syphilis occurred in Europe in 1495, upon Columbus’s return. Although some medical historians have argued that the syphilis pathogen (the bacterium Treponema pallidum) existed in Renaissance Europe long before Columbus returned from his voyage to the New World, the most sophisticated study to date, being published today in the journal PLoS Neglected Tropical Diseases, concludes otherwise: a genetic analysis of the treponeme bacteria supports the “Columbian theory” of syphilis’s origins in the Americas. Call it Montezuma’s revenge, squared.

To trace the origins of syphilis, scientists have mostly studied old bones, which preserve evidence of late-stage syphilis. But because it is tough to pinpoint the exact age of the bones, these studies have been inconclusive. Kristin Harper of Emory University and colleagues therefore studied 21 genetic regions in the genomes of 26 geographically disparate strains of treponemes. Based on how much the different strains had diverged from the basic genetic blueprint, the scientists were able to create a family tree for treponemes. It showed that the strains that cause venereal syphilis originated most recently. Their closest relatives were strains collected in South America that cause the disease yaws. Together, they say, the analyses supports the idea that syphilis originated in the Americas.

But wait. The syphilis that was present in the Americas when Columbus landed (there was a treponemal infection in the Dominican Republic when he arrived) might not have been venereal—that is, spread sexually. “Therefore, it is not clear whether venereal syphilis existed in the New World prior to Columbus’s arrival,” write the scientists. “While it is possible that Columbus and his crew imported venereal syphilis from the New World to Europe, it is also possible that the explorers imported a non-venereal progenitor that rapidly evolved into the pathogen we know today only after it was introduced into the Old World.” If so, then the Americas provided the ancestral germ, but that germ assumed its deadly venereal form only after it became ensconced in Europe.

Critics of the new study say the analysis compared too few DNA sites to reach the conclusions it did, arguing that “no evolutionary order” for the syphilis family of bacteria can be inferred, and urging “caution” in accepting Harper’s claim. Still, this study, combined with earlier work, presents the strongest evidence that the Native Americans got at least a modicum of revenge on their killers.

Despite the widespread myth that snakes (lacking outer ears, a tympanic membrane and other evidence organs of audition) cannot hear, it seems we have been too dismissive about these reptiles’ sensory abilities.

According to physicists Paul Friedel and J. Leo van Hemmen of the Technical University in Munich and Bruce Young of Washburn University in Kansas, however, not only can snakes hear. They can hear in stereo. Through their jaws.

Snakes’ jaws are connected to an inner ear with functional cochlea. Resting on the ground, a snake’s jaw can detect tiny vibrations that act like sound waves, the physicists will report in an upcoming issue of Physical Review Letters. As a result, the footsteps of, say, a mouse—to say nothing of the footsteps of a person—cause surface waves to propagate in the ground, which the snake detects as sound and “should be regarded as significant sensory input,” conclude the scientists.

They carried out a geometric study of the anatomy of desert horned vipers and the ground waves created by the footsteps of their prey. The jaw-to-cochlea system, it turns out, is attuned to the frequencies of the prey’s ground vibrations. Worse (for anyone or anything planning to tiptoe past a snake), snakes’ ability to unhinge their jaws and swallow their prey whole means the right and left jaws can receive vibrations independently. In other words, snakes hear in stereo, and so can use the auditory information to pinpoint the locations of passers-by.

I’ve never understood all those anti-evolution kooks who think that being related to apes and monkeys—sharing an ancestor with them—is an unspeakable insult. After all, chimps alone have been found to use tools, logic and semantics, and to demonstrate compassion and empathy greater than what some humans have shown themselves capable of. Now scientists have shown that rhesus monkeys can add.

Even a monkey can look at arrays of dots and determine which of two sets has more dots, which is not surprising: being able to take a quick scan of two bunches of bananas and decide which is worth climbing a tree for comes in handy in the jungle. But scientists didn’t know whether monkeys or other nonhuman animals can do mental arithmetic, although there had been hints. In 2005 scientists reported that when rhesus monkeys watched as two groups of four lemons were placed behind a screen, they looked longer when the screen was lowered to reveal an incorrect four lemons (“but wait!”, you could imagine them thinking; “4 + 4 = 8, not 4”) than when there were eight lemons. (Long looking time means the monkeys detected something amiss.) The most intriguing test of arithmetic in an animal was one conducted in 1989 on a chimpanzee who had been trained to recognize Arabic numerals; he could choose the right one when he had to add up sets of oranges, as long as the total was less than 4.

In the current study, Elizabeth Brannon of Duke University and graduate student Jessica F. Cantlon had two female rhesus monkeys (as well as 14 college students, which we’ll get to in a minute) look at two sets of dots on a touch screen monitor. The sets appeared half a second apart. Once the monkeys had had a good look at the sets, they saw two choices: an array with a number of dots equal to the sum of the sets and an array whose dots did not equal that sum. The arithmetic problems went up to sums of 16, and the questions used every permutation for that sum (for 8, for instance, the questions were 1 +7, 2 + 6, 3 + 5, 4 + 4, 5 + 3, 6 + 2 and 7 + 1).

As the scientists report tonight in the online journal PLoS Biology, “monkeys perform approximate mental addition in a manner comparable to college students tested on the same addition task.” To wit: the monkeys got about 76 percent of the questions right, compared to 94 percent for the students.

You may be sneering that this isn’t addition at all; it’s just memorizing the look of two arrays and mentally combining them. So to see whether the monkeys were not really adding but instead merging the spatial extent of the two sets of dots, the scientists varied that spatial extent. About one-quarter of the time, the area covered by the wrong answer more closely matched the total area of the dots in the two addends than the right answer did—that is, the dots were crowded together or spread apart in the right answer but had spacing comparable to that in the two addends in the wrong answer. The monkeys weren’t fooled, still answering correctly most of the time, “indicating that they based their choices on the numerical sum of the objects, not their surface area,” say the Duke scientists.

Okay, so it's not calculus. But as scientists probe for the evolutionary roots of human abilities, both cognitive and moral, expect more such discoveries that challenge many claims of human uniqueness.

If your favorite “Grand Theft Auto” fan has not yet turned into a raging violent madman, you may be tempted to dismiss the huge pile of evidence linking exposure to media violence to an increase in aggressive and violent behavior. Not so fast.

In a clever study tracking how the brain responds to violent film scenes, scientists at Columbia University found a very specific effect: diminished activity in the region of the brain that controls reactive aggression. In other words, watching gruesomely violent images might not incite violence in someone who lives peacefully in a Buddhist monastery. But in real life--where drivers cut you off, colleagues undermine you, friends tease you and countless other provocations ensue--the loss of control over a reflexively aggressive reaction can have dangerous consequences.

The scientists showed seven men and seven women, mostly in their 20s, two dozen movie clips. Among them: a teenager breaking a bottle over someone’s head in “The Basketball Diaries,” a man getting shot in the head in “The Patriot,” a man slashing another with a sword in “Pulp Fiction,” one man hitting another with a meat cleaver in “Gangs of New York,” and similar edifying footage. The 14 also saw some neutral clips, as well as those of people being frightened (though not meat-cleavered). During the mini-screenings, the volunteers’ brains were scanned by functional MRI, which observes which regions are more or less active during different activities.

The most striking change as the volunteers watched more and more slashings, shootings and stabbings was in what’s called the right lateral orbitofrontal cortex, the researchers report today in the journal PloS One. The right ltOFC is a cluster of neurons nestled just behind the right side of the forehead. A number of earlier studies have linked it to control over reactive aggression. And although the scientists did not see how aggressively their volunteers would react to someone cutting them off in line, they did ask them so engage in some introspection by, for instance, answering whether they agreed that, “given enough provocation, I may hit another person.” The lower the activity in the region controlling reactive aggression, the more likely the volunteers were to answer with the equivalent of “hell yes.”

No wonder the scientists conclude that “even short-term exposure to violent media can result in diminished responsiveness of a network associated with behaviors such as reactive aggression.” Be careful not to jostle a fellow audience member at “American Gangster,” or he might deck you.
More seriously, the work goes some way toward getting beyond the generalities of the effects of media violence--increasing aggression--to pinpointing what kind of aggression is increased. Watching beheadings and the like won’t send you into an unprovoked violent rampage, but it lowers the threshold of provocation needed to do so.