Before the month is out, I have to take note of a research article in the April issue of Psychological Science, which concludes that when it comes to reading women’s non-verbal signals—smiles, gaze, body language, tone of voice—men are complete and utter illiterates.

Especially when it comes to figuring out whether she is saying (in the family-friendly version): take me someplace where we can be horizontal and engage in activities that have been known to perpetuate the species. Or as scientists led by Coreen Farris and Richard McFall of Indiana University put it, “Men perceive more sexual intent in women’s behavior than women perceive or report intending to convey.”

I don’t mean to make light of this. Such misreading can lead to date rape, and telling the woman that she led the man on makes the victim feel complicit in her attack. Smiling, making eye contact, moving closer, or touching someone on the shoulder can indeed convey romantic interest—but all of these cues can also indicate “simple warmth, friendliness, or platonic interest,” the scientists note.

As is usual in questions like this, evolutionary psychologists have spun a theory to explain why men read “let’s have sex” into every nonverbal cue. If a man misses a signal to have sex, he loses out in the evolutionary sweepstakes. If he misreads an innocent signal as a sexual one, the worst that can happen (from the male reproductive point of view) is that he mates with a not-so-willing partner. In terms of evolution, erring on the side of “she wants sex” is a better, more adaptive strategy than erring in the other direction, missing such signals. As a result, goes this argument, men are programmed to read sex where no such message is intended.

No wonder “men consistently rate female targets as intending to convey a greater degree of sexual interest than do women who rate the same targets,” write the scientists. In a survey of university women, 67 percent said male acquaintance had misread friendliness as a sexual come-on.

According to the new study, however, it’s not just that men read sex where no sexual invitation is intended. Men can’t read any signals right. The scientists had 280 straight, undergraduate men and women look at a series of full-body photos of women, and categorize them as friendly, sexually interested, sad, or rejecting. The scientists selected the photos that were clearly one or another, then had a new group of 80 men and 80 women categorize the women in the photographs. A “correct” answer was one that agreed with the vast majority of raters in the first group, since only (seemingly) unambiguous photos were shown to this second, test group.

In every category, women categorized more images correctly than men did. Men were more likely than women to miscategorize a friendly-looking woman as indicating sexual interest, but—crucially—they also flunked out when it came to recognizing photos showing sexual interest: men were more likely than women to misidentify sexually interested targets as merely friendly, by 37.8% vs. 31.9%. In short, “men were more likely than women to misperceive friendliness as sexual interest, but they also were quite likely to misperceive sexual interest as friendliness,” the scientists found. “Men were significantly less sensitive to the distinction between friendliness and sexual interest”—in both directions, since they couldn’t tell when women were sad as opposed to rejecting, either. Men “oversexualized some women, but were quite likely to undersexualize other women.”

The take-home message is clear. Women can’t assume that men will understand anything they’re trying to convey.

All you connoisseurs who lament that new versions of old classics—the Corvette, Astroturf, metal bats—just do not measure up to the original can cross one example off your list: absinthe.

The bitter green liqueur made from wormwood was for decades the toast of Europe, imbibed by the likes of van Gogh, Degas, Toulouse-Lautrec and Picasso to, it was believed, spur their creativity. For absinthe was deemed more drug than drink: thujone, a natural essence found in common wormwood (Artemisia absinthium L.) and Roman wormwood (Artemisia pontica L.) that was widely believed to be its active ingredient, induces convulsions like those suffered by people with epilepsy, and was thought to account for absinthe’s supposedly mind-altering properties. Thujone was thought to explain absinthe’s reputation as a “green fairy” and a “green muse.” (The original absinthe also contained green anise, Pimpinella anisum L.; hyssop, Hyssopus officinalis L.; lemon balm, Melissa officinalis L. and Florence fennel, Foeniculum vulgare Mill.)

I couldn’t avoid all those “supposedly”s and “thought to”s in the paragraph above: it turns out that there had been only a single actual test of how much thujone classic absinthe contained.

When it comes to averting dangerous climate change, an awful lot of people seem to hold out hope that we can blast our way out of the mess we’re in. Nothing so boring as energy conservation, or even replacing coal, oil and natural gas with solar, wind and nuclear: Instead, let’s shoot sulfate particles into the atmosphere to reflect away sunlight! Let’s load up the oceans with iron so plankton will grow like dandelions on my lawn and suck up the heat-trapping carbon dioxide produced when we burn fossil fuels!

Hope springs eternal. This week brought a conference on weather modification, with the emphasis on getting clouds to drop their raindrops. My favorite paper was, alas, withdrawn: it proposed a machine—a ship, actually, with “four torpedo-shaped hulls”—that would “stop hurricanes from wrecking large parts of America.”

While the inventor goes back to the drawing board on that one, a new study suggests that geo-engineering proposals may well blow up in our faces. Injecting sulfate particles into the stratosphere would shred Earth’s protective ozone layer, conclude scientists led by Simone Tilmes of the National Center for Atmospheric Research, delaying the recovery of the Antarctic ozone hole by decades and triggering serious ozone loss over the arctic.

The problem, as she and colleagues explain in a paper published online in Science Express, is that although sulfur particles from volcanic eruptions do cool the planet’s surface, they also provide a surface on which chlorine gases—the chief culprits in ozone depletion—can cause chemical reactions that speed the destruction of ozone molecules. Sulfates themselves do not destroy ozone; they simply provide a convenient surface for chlorine to do so.

“Trying to artificially cool off the planet could have perilous side effects,” Tilmes said in a statement. “While climate change is a major threat, more research is required before society attempts global geoengineering solutions.”

Over the next few decades, the quantity of sulfates that geo-engineering schemes envision could destroy one-fourth to three-fourths of the ozone layer above the arctic, she calculates. Because of atmospheric mixing, this low-ozone mass would sometimes swing over inhabited regions of the northern hemisphere, leaving people and other living things without the protection from ultraviolet light that ozone provides. Injected sulfates would also postpone by 30 to 70 years the repair of the ozone hole over Antarctica, or until at least the 2090s.

More UV raises the risk of skin cancers, including deadly melanomas, and decimation of phytoplankton that anchor marine food chains. But hey, what’s a little (or a lot of) melanoma and fisheries crashes if we can avoid the hard steps needed to avert dangerous global warming?

In one of those “you can’t win for losing” things, another study concludes that if the ozone hole over Antarctica does return, as it is expected to now that the world has banned most ozone-destroying chemicals (and assuming we don’t mess it up with geo-engineering), the antarctic will finally start warming the way the rest of the world has.

It’s been a puzzle of climate-change models that the interior of Antarctica has not warmed as much as models project. Average global surface temperatures have been increasing, but the interior of the southern continent has actually been cooling during the austral summer and fall. That’s been traced to ozone depletion which, through a complicated mechanism, produces atmospheric circulation patterns—basically, intense westerly winds—that block warm air masses to the north from reaching Antarctica. In addition, with low levels of ozone the lower stratosphere over Antarctica doesn’t absorb as much ultraviolet radiation.

Once the ozone returns, calculate Judith Perlwitz of the University of Colorado at Boulder and colleagues, the warming trend will kick in as the westerlies fade and UV absorption causes air temperatures 6 to 12 miles up to rise by as much as 16 degrees F.

That might be good news for travelers who are waiting for Antarctica to warm up before they book a trip to the south pole, but it will be bad news to climate-change deniers. They have long pointed to Antarctica's cooling to question the basic predictions of global warming.

This is why millions of space fans erupted in fury when those fools at NASA announced in 2004 that the Hubble Space Telescope would be allowed to die. The images that Hubble has taken since its launch in 1990 (or, really, since its near-sightedness was corrected during a space shuttle mission in 1993) have revealed a universe wilder and more beautiful, mysterious and humbling than anyone suspected. This morning, the 18th anniversary of Hubble’s launch, NASA is unveiling a collection of photographs taken by the telescope—the most ever released at one time—showing that Hubble is far from running out of glorious targets.

Flip through them yourself and you’ll see why NASA calls these “galaxies gone wild.” Far from the static, staid islands of stars depicted in textbooks, galaxies are dynamic, antsy and even promiscuous, having what astronomers call “flirtatious close encounters that sometimes end in grand mergers and overflowing ‘maternity wards’ of new star birth as the colliding galaxies morph into wondrous new shapes.” Although only one in a million galaxies in the nearby universe is colliding, many more in the distant environs are: farther away equals longer ago, and longer ago galaxies were closer together because the expanding universe was smaller.

Among the standouts in the 59 images is Arp 148, the detritus of an encounter between two galaxies that produced a shockwave that first drew matter inward and then pushed it outward, creating a ring-shaped galaxy and a long-tailed hanger-on perpendicular to the ring. (Arp 148 is located in Ursa Major, the Great Bear, about 500 million light-years from Earth.)

Then there is Arp 256, two spiral galaxies in flagrante delicto: the merger has triggered blue knots of star formation that look like a 4th of July display. (Arp 256 is in the constellation of Cetus, the Whale, 350 million light-years away.)

Arp 220 is what happens when two spiral galaxies collide. This one is 250 million light-years away in the constellation of Serpens, the Serpent. The collision, 700 million years ago, ignited a fury of star formation, producing 200 huge star clusters in a packed, dusty region 5,000 light-years across (about 5 percent of the Milky Way’s diameter, it holds as much gas as the entire Milky Way).

ESO 148-2 looks like a flying owl, and is a pair of disk galaxies in the act of colliding. The centers of the two contain myriads of stars, while two enormous “wings” curving out from the center are actually the tidal tails of stars and gas that have been pulled from the disks.

I could go on, but it's much more fun to see the photos yourself.

It's a sad commentary on the current politicization of science that the latest example sounds like a dog-bites-man story----as in, what else is new? Still, the fact that 889 of 1,586 staff scientists at the Environmental Protection Agency say they've experienced political interference in their work over the last five years, as a study by the Union of Concerned Scientists being released today finds, is enough to make you despair for the state of policy-relevant science in this country.

In previous UCS investigations, scientists at the Food and Drug Administration, Fish and Wildlife Service, National Oceanic and Atmospheric Administration and climate scientists at seven federal agencies reported that Bush administration officials had manipulated the results of their research, such as by calling global warming a theory, playing down its potential impact and altering scientific reports concluding that particular species are endangered.

At EPA, there have been allegations (which Congress is investigating) that the administration overruled staff scientists on California's request to regulate vehicle emissions of greenhouse gases, and on scientific findings about the ground-level ozone pollution standard. Rep. Henry Waxman's Committee on Oversight and Government Reform has been documenting  the administration's manipulation of science for political ends since 2003. In a hearing today, he is getting testimony about abstinence-only sex education, an area where the administration has been less than forthright when it comes to measuring how well such programs work.

In the UCS report, 889 scientists said they had personally experienced at least one instance of political interference in their work over the last five years, 394 experienced "statements by EPA officials that misrepresent scientists' findings," and 285 experienced "selective or incomplete use of data to justify a specific regulatory outcome." That's when the scientists reach a conclusion, and the political appointees not only ignore it but twist it. Also, 224 scientists said they had been "directed to inappropriately exclude or alter technical information from an EPA scientific document." Why haven't the scientists spoken up more? 492 (31 percent) felt they could not speak candidly within the agency and 382 (24 percent) felt they could not do so outside the agency. Half said they couldn't talk to reporters.

Bill Hirzy, an EPA senior scientist and union official, put it this way: "Too many EPA scientists have had to fight interference from political or private sector interests and fear retaliation for speaking out."

Want to live longer? Move. Or make more money.

During the decades when life expectancy in the U.S. rose from 67 to 74 years for men and from 74 to 80 for women, the rising tide was lifting all boats: although death rates in poorer counties exceeded those in better-off counties, everyone experienced steady improvement. No more. From 1961 to 1983, the death rate in every county fell largely because deaths from cardiovascular disease (heart disease and stroke) did; the spread in death rates between poorer and wealthier counties also fell. “In the 1960s and 1970s the improvements seemed to reach everybody,” says Majid Ezzati of the Harvard School of Public Health, as people in poor as well as wealthy counties adopted such heart-healthy habits as controlling blood pressure and not smoking.

Since the early 1980s, however, the difference in death rates between counties has increased. Death rates in poorer ones have stagnated and, in some counties, have actually risen, Ezzati and colleagues report this evening in PLoS Medicine.

That means health inequality is rising. The spread between the counties with the greater life expectancy and the worst is now 18.2 years for men and 12.7 years for women. In 1983 it was nine years for men and 6.7 years for women.

The authors call the increased inequalities in mortality “particularly troubling because an oft-stated aim of the U.S. health system is the improvement of the health of all people, and especially those at greater risk of health disparities.” “There has always been a view in U.S. health policy that inequalities are more tolerable as long as everyone’s health is improving,” Ezzati said. “There is now evidence that there are large parts of the population . . . whose health has been getting worse for about two decades.”

Between 1961 and 1983, no county suffered a statistically-significant decline in life expectancy; not so in the years since. From 1983 to 1999 (the last year for which the National Center for Health Statistics would give the scientists the data it collects from counties--a story in and of itself), life expectancy actually fell in 11 counties for men and 180 counties for women, averaging a drop of 1.3 years. So much for "the best health care system in the world."

Most of the counties where mortality is rising—counties populous enough and numerous enough that 4 of men and 19 of women experienced either decline or stagnation in mortality beginning in the 1980s—are poor. They’re in the Deep South, along the Mississippi River and in Appalachia, extending into the southern portion of the Midwest and into Texas. Those are among the counties that experienced the greatest improvements in life expectancy in the 1960s and 1970s, because they had the most room for improvement. But progress there has come to a screeching halt since the 1980s.

You can see life expectancy at birth between 1961 and1999 for men here and for women here, and life expectancy in 1961, 1983 and 1999 here. The absolute change in life expectancy, also by country, in 1961–1983 and 1983–1999 is here.

It’s even sadder than those blue and red maps that show the country’s political divide. This one is literally a matter of life and death.

The thrill is gone.

Maybe voters are simply tired of the seemingly endless campaign for the Democratic nomination. Or maybe their excitement about the new (Barack Obama), the suddenly emoting (Hillary Clinton, in New Hampshire) or the coming-back-from the-politically-dead (John McCain) can’t last forever. But whatever the reason, voters are feeling much less excitement and fewer positive emotions about all three of the remaining presidential candidates than they once did, finds a poll that, uniquely, measures voters’ emotional reactions.

If the trend continues, that’s bad news for the candidates, because research keeps showing that voters base their decisions more on their hearts than their heads and are easily swayed by anxiety, fear and other negative emotions. Latest evidence: anyone who feels—the key word—that Obama doesn’t understand “people like me” because he said that voters embittered about their economic plight “cling to guns or religion or antipathy to people who aren’t like them.” If that loses him any votes, it will not be because of a rational analysis of his record and positions, but because of how it made people feel about him.

Anyway, a company called AdSam measures what it calls “Emotional Temperature,” which gauges people’s emotional engagement with a product, website or advertisement. Since, as we all know from Joe McGinniss’s 1969 book, “The Selling of the President, 1968,” candidates are marketed and sold just like detergent, the same technique should work with politicians.

In its latest study, AdSam measured how strongly voters feel about each candidate, and how engaging they find them. Since last September, Clinton’s “emotional temperature has been on a continual steep decline with voters,” says AdSam president Jon Morris, a professor at the University of Florida, dropping from 93 to 70 (where 173 is how emotionally positive voters say they would like to feel about a candidate). “Her emotional cool-off is a sign that she is not relevant and not making connections with voters. This is a significant barrier for her and will be very difficult for her to turn around.”

Clinton trails both McCain and Obama, whose emotional temperatures are very similar (85 and 88, respectively, this month) and have not fallen off a cliff the way Clinton’s has. Obama dropped 8 points from September to January (97 to 89), and has stayed at about that “temperature” since. McCain moved up 9 points from September to January (79 to 88), but is down 3 points since.

Obama generates the most positive emotional response among Democrats (beating Clinton 120 to 97) and beats McCain among Independents (97 to 81), with Clinton at 74 among Independents. McCain has finally excited and united Republicans, however, zooming from 101 last September to 145 now.

Clinton is leaving more voters cold, says Morris. Compared to last September or even January, fewer voters feel “interested/excited” by her, while more feel “reluctant,” “uninterested/unexcited” and even “disgusted.” The biggest reason for the turnaround, Morris finds, is that more voters perceive Clinton as dishonest.

Obama is making more Democrats “interested/excited” now than he did in January, but more are also feeling “ambivalent” about him. In follow-up interviews, voters use words such as “truthful,” “honest,” “trust” and “inspirational,” but more and more cite his scant experience on the national stage. The Illinois senator has further to go with Independents: 21 percent feel strong positive emotions about him, compared to 32 percent last September. Equally worrisome, 28 percent now feel “ambivalent,” the most of any emotion among Independents asked about Obama.

More Democrats (20 percent) were disgusted by Clinton’s dishonesty about coming under fire during a trip to Bosnia than by Obama’s links to his controversial pastor (10 percent). We'll see how this translates into votes in Pennsylvania next Tuesday.

Whooooooshshshshshsh. That sound you hear is Greenland lakes melting through the ice sheet they sit on and greasing the skids for ice to flow out to sea.

That, as everyone knows, raises sea levels. What no one knew is that a lake composed of meltwater and sitting on the Greenland ice sheet can drain as suddenly and completely as scientists have now documented. It adds an ominous twist to a key unknown about glaciers and ice sheets: as the world warms due to the greenhouse effect, will they flow out to sea slowly and gradually, or suddenly and catastrophically?

Every summer, thousands of lakes form atop Greenland’s ice, as sunlight melts the surface. Satellite observations have shown some of the lakes vanishing in a single day, but no one knew where the water went or how it affected the ice sheet’s plumbing— the network of channels and fractures through which meltwater travels.

Anyone contemplating which baby bottle to buy will find the new government report on bisphenol A sobering reading. Bisphenol A is used to make the ubiquitous plastic polycarbonate (you can tell if a bottle is polycarbonate because it has the number 7 in that recycling icon on the bottom), and there has long been concern that it can harm children because it acts like the hormone estrogen.

The draft report finds more to worry about from bisphenol A, concluding that there is "some concern for neural and behavioral effects in fetuses, infants and children at current human exposures,” and "some concern for bisphenol A exposure in these populations based on effects in the prostate gland, mammary gland and an earlier age for puberty in females." That belies a government report last year that expressed less concern for these effects, in large part because it did not consider a bunch of studies that found toxic effects in lab animals.

As usual, the chemical industry defends bisphenol A, ranting about the "myths" surrounding polycarbonate bottles. But what is particularly striking is the stark difference between what studies funded by industry conclude and what studies funded by the government or academic groups conclude about this chemical. As I wrote in this space almost exactly one year ago:

"Industry-paid studies conclude we shouldn't worry. Of the 13 studies of bisphenol A underwritten by chemical companies, none reported any adverse effects on the lab animals or tissue samples exposed to it, C&EN finds. But of the studies funded by government, 153 found such effects (including obesity, cancer and insulin resistance). . . .  There are all sorts of ways to stack the deck. One is to pick a lab animal that is insensitive to estrogen. Two large studies of bisphenol A that were funded by industry used a strain of rat called Sprague-Dawley, which is well-known to be insensitive even to powerful estrogens. No surprise, then, that the rats showed no ill effects of exposure to bisphenol A, a weaker estrogen."

One concern about bisphenol A is that it might mess up reproductive function. A friend of a friend writes from a meeting of the National Association of Pediatric Nurse Practitioners that "it is incredibly alarming what they report from the front lines in terms of possible BPA effects. They are seeing young girls, as young as 6, hitting puberty. Unbelievable. This from pediatric endocrinologists [BPA interferes with endocrine function]."

Fortunately for parents who don't want to take a chance, a few companies, such as Adiri, are now selling bisphenol-free baby bottles. Of course, parents who are perfectly content to wait until the final scientific word is in should go right ahead and use those old polycarbonate bottles. But you might want to get baby used to nice cold drinks: warm liquids cause more bisphenol A to leach out of the bottle, and more also comes out if the bottle is scratched up.

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.

Track-and-field star Marion Jones went to prison for it, pitcher Roger Clemens denied to a congressional committee that he did it, outfielder Barry Bonds was indicted last year for perjury and obstruction of justice related to an investigation into whether he did it. But while athletes get almost all the attention when it comes to performance-enhancing drugs, it turns out that another group is also juiced: scientists.

In an online survey that drew 1,400 people from 60 countries, the journal Nature asked scientists whether they had ever taken drugs reputed to boost brain power. The journal focused on three: the stimulant methylphenidate (Ritalin), which is prescribed for attention-deficit hyperactivity disorder but which students use to rev themselves up before tests or marathon study sessions; modafinil (Provigil), prescribed for sleep disorders but which has a street reputation for keeping you awake for all-nighters ("gotta finish this grant application!"); and beta blockers, prescribed for cardiac arrhythmia but well known among performers who use it to combat stage fright because of the drugs’ anti-anxiety effect.

One in five of those who answered the Nature survey copped to using one or more of these drugs to juice their concentration or memory. Ritalin was the most popular, with 62 percent of users saying they took it (and not because they have an ADHD diagnosis). Another 44 percent took Provigil, and 15 percent took beta blockers. Obviously, as you can tell by summing the numbers, some people are taking more than one.

The most frequent reason for mental doping was to improve concentration, though partying, house cleaning and “to actually see if there was any validity” to articles about the drugs were also up there. There was an even split between scientists who took the drugs daily, weekly, monthly or less often. My favorite reason? This one, from a scientist who described him- or herself as over 65: “As a professional, it is my duty to use my resources to the greatest benefit of humanity. If ‘enhancers’ can contribute to this humane service, it is my duty to do so.”

Just as the ethics of doping in sports is endlessly debated, so is brain doping. In the Nature survey, four-fifths “thought that healthy adults should be able to take the drugs if they want to.” And one-third said they would feel pressure to give brain-boosting drugs to their children if other kids were taking them. (As in, “but mom, all my friends are taking Ritalin before the SAT; do you really not want me to?”) You can see the full result on Nature’s site. Should scientists--or anyone--take drugs that purpotedly boost their mental powers? What would you do if you knew that your competitor down the hall was juiced?

A good friend has started telling her husband, “don’t let them take me.”

She’s not a drug dealer or a tax cheat terrified of the cops finding her, but someone who has seen both her parents enter hospitals for minor problems . . . and leave dead. The “they” she doesn’t want are EMTs who might load her into an ambulance and take her to the nearest ER (unless it’s after a car crash or other trauma; she’s not completely crazy).

So I’m not going to tell her that HealthGrades, a private company in Golden, Col., that rates hospitals, nursing homes and physicians found that from 2004 to 2006, medical errors at U.S. hospitals killed 270,491 people. And that’s just Medicare patients.

I’ll leave it to political reporters to explain why, of all the cringe-inducing business dealings that Mark Penn kept his hand in as chief executive of the PR titan Burson-Marsteller even as worked for Hillary Clinton’s presidential campaign, it was his work on behalf of Colombia to secure passage of a bilateral trade agreement with the U.S. that led to his downfall. Yesterday he quit as Clinton’s chief political strategist, though he’ll stay on as a pollster.

I have no idea whether a Colombian trade agreement would be good for the U.S. But I do know that Burson-Marsteller’s work on behalf of the high-mercury fish industry is an excellent way to get even more neurotoxins into babies’ developing brains. Burson-Marsteller has worked tirelessly to persuade people—especially pregnant women—that the mercury that tuna (especially albacore) is laced with is nothing to worry their pretty little heads about.

Last year, the New York Sun reported that it had obtained Penn’s internal blog entries, including one from Dec. 20, 2006, in which he brags about landing the U.S. Tuna Foundation’s PR business. His company pitched “ideas for how to act like a political campaign by neutralizing the negatives and bringing out the heart healthy benefits of tuna,” Penn wrote, according to The Sun.

The issue of mercury in tuna makes the industry apoplectic (as you can see from its response to an earlier blog item). But Clinton had, as a senator, stood with those trying to protect children, not the industry, when she signed a 2004 letter criticizing the Environmental Protection Agency for soft-pedaling its own advisory about mercury in fish (especially albacore tuna, since canned tuna is the fish Americans eat more of than anything other fish besides pollock), which “specifically informs women that they and their young children should limit consumption of tuna.”

If you think creationists and evolutionary biologists can’t stand one another, spend some time—about three minutes will do—with scientists who study the first Americans.

The old guard has for years defended the dogma that the so-called Clovis people, whose artifacts have been dated at 13,000 years old, are the rightful owners of that honor. Their challengers (who call their opponents the “Clovis police”) keep presenting evidence for older settlements, such as those at Meadowcroft in Pennsylvania, Topper in South Carolina and Monte Verde in southern Chile, which contains artifacts dated to 14,000 years ago. Now comes what some anthropologists are calling the most convincing evidence to date of an earlier settlement of America: ***.

Fossilized ***, to be exact. Called coprolites, they were discovered in caves in south-central Oregon in 2002 and 2003. The oldest of the droppings have been carbon-dated to about 14,340 years old, the scientists report in a paper published online this afternoon in Science—more than 1,000 to 1,400 years older than the generally-accepted age of the Clovis culture. And a genetic analysis finds that they contain mitochondrial DNA unique to present-day North American Indians—persuasive evidence that the legendary walk on a land bridge across the Bering Strait took place some 1,000 years earlier than the old school insists.

Assuming the report is right (there is some muttering that the *** are canine, and that the human DNA means the dogs ate people—but people would still have to have been in or near that cave to become dinner), it raises a question even more intriguing than when the first Americans arrived—namely, how. It has long been assumed that people from Siberia walked across to America and then continued inland and south only when the glaciers retreated. But “our findings show that there were people south of the ice cap several hundred years before the ice-free corridor developed. The first humans either had to walk or sail along the American west coast to get around the ice cap,” says Eske Willerslev of the University of Copenhagen, an expert in ancient DNA—that is, “unless they arrived so long before the last ice age that the land passage wasn’t yet blocked by ice.”

If they were indeed sailors, that would explain how they managed to reach points south, including Monte Verde, so quickly. And it paints a portrait of the first Americans as much more sophisticated than mere pedestrians.

How many scientists does it take to find a gene? If it’s a gene as important as one that raises your risk of lung cancer, at least 142—the number of researchers who conducted three separate studies being published today which all identify the same stretch of chromosome 15 as containing genes linked to lung cancer.

How many scientists does it take to figure out what the genes do and how important they are? More than 142, apparently, for the three groups have reached dramatically different conclusions about exactly how the genes function to make you more likely to develop lung cancer. Two conclude that the genes directly raise your risk of developing lung cancer whether or not you smoke, while one concludes that the genes make you more likely to smoke and only through that effect on behavior raise your risk of lung cancer.

The discrepancy gets to the heart of a longstanding debate about the value of genetic discoveries. Whenever scientists discover a gene “for” some disease or normal trait, it leads to the question of whether the gene causes that disease or trait directly, or is instead a bystander. (The classic here is the hypothetical chopsticks gene. Some genes are more common in Chinese people than in westerners, and Chinese use chopsticks more than Europeans do, but it would be a laughable mistake to conclude that the genes cause people to use chopsticks: the genes are merely markers for certain ethnic groups which, because of culture alone and not genetics, use chopsticks.) Now that debate has erupted in the clash of lung-cancer papers.

All three of the papers agree that the genes that increase the risk of lung cancer lie on chromosome 15, one of 23 (each part of a pair) in every human cell. The technique that each team used, called a genome-wide association study, cannot pinpoint which gene or genes on the chromosome is the culprit; all it can do is say the suspect gene lies in a certain region of the chromosome. Earlier studies have shown that among the five genes in the suspect region of chromosome 15 are three for parts of what is called the nicotinic acetylcholine receptor. All three groups agree that these nicotine-receptor genes are almost certainly the genes responsible for the elevated cancer risk. That is striking: it suggests that nicotine, long known to be what makes cigarettes addictive, might also cause lung cancer. And finally, all three groups agree that the dangerous gene variant is quite common: about half of people of European descent carry at least one copy, having inherited it from mom but not dad (or vice versa). About 10 percent to 15 percent carry two copies, inheriting it from both parents.

It is no surprise that there is a genetic component to lung cancer and smoking. Smoking causes an estimated 5 million deaths a year, but while many of those deaths are from lung cancer, not all of them are: only about 15 percent of smokers develop lung cancer, of which there are 1 million new cases worldwide every year. (In the United States, there are about 160,000 deaths from lung cancer every year.) The fact that relatively few smokers develop lung cancer strongly suggests that there is something inherently different between smokers who do and those who do not.

Two of the new papers conclude that the now-suspect nicotinic acetylcholine receptor gene is a large part of that difference. As its name suggests, this receptor acts as a docking port for nicotine molecules. In a study led by Paul Brennan of the International Agency for Research on Cancer and published today in Nature, the scientists conclude that the gene raises the risk of lung cancer directly: people who have this gene (to be precise, everyone has the nicotinic acetylcholine receptor gene; what matters is which variant, or chemical spelling, you inherited from mom and dad, since only some spellings raise the risk of lung cancer) have a greater risk of the disease even if they do not smoke.

So, too, concludes the study by Christopher Amos of the M.D. Anderson Cancer Center, published online in Nature Genetics. If you have ever smoked and have one or two copies of the gene variants, your risk of developing lung cancer is about 30 percent to 80 percent greater than if you do not have these variants, the researchers found. Putting actual numbers on that, the risk rises from about 15 percent to about 27 percent at the high end.

The extra risk of lung cancer conferred by these gene variants is unrelated to whether or how much you smoke, both the Amos and Brennan teams conclude. “What we do not understand is why some long-term smokers develop lung cancer and others don’t,” Amos said. “There are so many different cancer-causing compounds in tobacco smoke that it’s hard to separate them and we don’t fully understand the mechanisms that cause lung cancer.”

The third group reaches a strikingly different conclusion: that the genes affect how much you smoke, and only through that mechanism do they raise your risk of lung cancer—more cigarettes, more cancer. Each copy of the gene variant increases the risk of developing lung cancer 30 percent, they estimate. “This is a genetic predisposition to seek out a certain environment, to smoke,” said Kari Stefansson, CEO of the genomics company deCode who led the latter study, during a recent visit to Newsweek. “We know that complex diseases have both genetic and environmental components, and the challenge has always been to figure out their relative contributions. But if this gene causes you to seek out a ‘smoking environment,’ then it’s as if both gene and environment contribute 100 percent to the development of lung cancer.”

Scientists not connected to the new studies are scratching their heads over how the teams could come down on opposite sides of the question of whether the gene variants raise the risk of lung cancer directly (and therefore make you more likely to develop it whether or not you smoke) or indirectly (making it more likely that you will smoke). In the latter case, if you have these “lung cancer” genes and do not smoke, you’re fine—no extra risk of lung cancer. In the former, even non-smokers have cause for concern if they carry these gene variants.

“The extent of the disagreement in the conclusions of these studies is remarkable,” write Stephen Chanock of the National Cancer Institute and David Hunter of the Harvard School of Public Health in a commentary on the trio of studies. “They signal the need for greater methodological rigour in attempts to account for both the genetic and the environmental causes that we think underlie most diseases.”

Until that disagreement is resolved, don't rush to get tested for the nicotine-receptor genes. For one thing, even if you turn out to have the "good" gene variant and therefore to be resistant to developing lung cancer from smoking, you can't smoke with impunity: you’re unlikely to also be protected against emphysema, heart disease and other often-fatal consequences of lighting up. “I try to make a living by marketing genetic tests,” said Stefansson in a telephone briefing, “but I am not a proponent of this one.”

At least not yet. But if Stefansson’s interpretation turns out to be right, and the gene variants increase your risk of smoking but not of lung cancer otherwise, it will be one more piece of evidence that genes are not destiny: all you have to do to keep your risk of lung cancer near zero is to resist the urge to smoke. But you knew that already.

Although some steps that we take to save the planet entail sacrifice (personally, I am getting tired of seeing my breath in my ice-cold house as a result of turning down the thermostat on my gas-burning furnace all winter. But I digress.), more and more evidence is emerging that organic produce is a win-win.

Of course buying organic sends a market signal that leads growers to use fewer pesticides and other agricultural chemicals, not to mention keeps carcinogens and neurotoxins out of your diet. But according to the most comprehensive comparison to date of the nutrient content of organic vs. conventional fruits, vegetables and grains, organics contain higher levels of eight out of 11 important nutrients. Among them: polyphenols (linked to lower risk of lung cancer and heart disease, as well as to greater longevity) and antioxidants (ditto).

Since 2001 more than 40 studies comparing the nutrient content of organic and conventional foods have been published. From those and some earlier studies, the Organic Center identified 236 scientifically-valid head-to-head match ups between an organic food and a conventional one. The nutrients included antioxidants (total phenolics, total antioxidant capacity, quercetin and kaempferol), three precursors of key vitamins (Vitamins A, C, and E), two minerals (potassium and phosphorous) and total protein.

Results: the organic food trumped the conventional one in 145 match-ups, or 61 percent of the cases. Organics came out ahead in polyphenols and antioxidants in about three-quarters of the 59 match-ups of these compounds.