Mention “genes” and “race” in the same breath, and someone is likely to take offense. But while research on genetic differences that neatly track the three generally-recognized races has mostly come up empty—non-overlapping genetic differences track ethnic or population groups better than they do races, which are too large to be biologically meaningful—a new approach may yield more.

Or so believe scientists who will report next week that people of African and European ancestry differ in the levels of gene expression for 383 out of the 9,156 human genes they examined.

People are more than 99.9 percent identical at the level of their DNA, the Human Genome Project has found. But which genes you have isn’t the whole story. What also matters is how strongly those genes are expressed, or turned on. To use an analogy I’ve tried before, DNA is like your iPod downloads: what counts isn’t only what you’ve stored, but whether you play it. So what matters about DNA is not only which genes you have, but which ones are expressed and at what levels.

The finding that expression levels differ for hundreds of genes between people of African and European ancestry (the scientists studied 30 white families from Utah and 30 Yoruban families from Nigeria) links up with earlier observations. The researchers found differences among genes that help produce the antibodies that fight off bacterial invaders, and among genes that influence how you respond to certain drugs, they write in the American Journal of Human Genetics. Not coincidentally, perhaps, a 1980 study found that African Americans may be more susceptible to certain bacterial infections than are people of European ancestry. And a 2005 study found that individuals of European and African ancestry also differ in how they respond to anti-microbial drugs such as those used to treat gum disease.

The hope is that understanding the genetic basis for different responses to drugs could help direct treatment—the great hope (but still only a hope, for the most part) of personalized medicine.

But this work is interesting for another reason. It emphasizes again that what counts in genetics is not merely having a gene but expressing it. If your iPod never plays that Amy Winehouse you downloaded, then (in a tree-falling-in-an-empty-forest sense) you do not have the gene.

Patterns of expression—on in this person, off in that—likely lie behind such mysteries as why identical twins are not identical, especially in which supposedly “genetic” diseases they get. This field is called epigenetics. The Human Genome Project was all about determining the sequence of the 6 billion building blocks that constitute human DNA. But that sequence is only the start.

. . .would smell as sweet,” Juliet told Romeo. But the fate of the nation’s economy this year might depend on what we call those $300, $600 or $1,200 checks that some 100 million Americans are due as part of Washington’s plan to stave off recession.

Is the windfall a “tax rebate”? If that’s what officials and the media call it, expect most of the dough to get stashed in bank accounts or to be used to pay down credit card balances, not for new spending. The latter is what Congress and President Bush hope for, since boosting consumer spending, which makes up two-thirds of the economy, may help avoid an economic downturn. But if the money is labeled a “tax bonus,” then it might indeed be used for a few splurges.

The reason is that “decisions about whether checks from the government will be spent or saved depend very heavily on how people’s options are described,” Nicholas Epley, a professor of behavioral science at the University of Chicago business school tells the National Science Foundation, which funds his research. “If the goal is to increase consumer spending, the checks should have been pitched as ‘tax bonuses’ instead of ‘tax rebates.’ People are much more liberal about spending a bonus or a windfall than they are spending money thought of as part of their income. People consider a ‘tax bonus’ a windfall, but consider a ‘tax rebate’ more like their regular income.” They're more likely to put aside a rebate for a rainy day, especially in these uncertain times.

The size of this naming effect can be significant, Epley’s experiments show. He gave volunteers $25 in cash, described it as a rebate to some and a bonus to others. Recipients told they’d gotten a rebate spent $2.43 on items for sale in the lab “store,” while those told it was a bonus spent $11.16. That finding was borne out in the real world of the 2001 tax rebates, when Washington sent people $300 or $600 in an effort to prevent a 9/11-linked recession--and consumer spending hardly budged.

Warning to anyone planning a crime: don’t drink the water.

Scientists are reporting this evening that an analysis of hydrogen and oxygen isotopes in human hair reveals where a person drank water, which will allow investigators to figure out if a suspect was in the vicinity of a crime—and also to track past movements of unidentified murder victims.

The new technique analyzes isotopes of hydrogen and oxygen, forms of the elements that have an extra neutron in its atomic nucleus. The ratio of oxygen-18 to oxygen-16 in air is the same everywhere, and ratios of both hydrogen and oxygen ratios in food are also basically the same across the country because the American food supply is so uniform. But water is still like a microbrew, containing different constituents depending on where it comes from.

As a result, geochemist Thure Cerling and ecologist Jim Ehleringer of the University of Utah report in the journal Proceedings of the National Academy of Sciences, a single hair bears clues to where someone has been over the last few weeks or even years, depending on the length of the hair. “You are what you eat and drink—and that is recorded in your hair,” said Cerling in a statement from the university.

Salt Lake County Sheriff's Detective Todd Park is using the hair-isotope method to try to identify a murdered woman whose remains were found by hunters near Interstate-80 along the south end of the Great Salt Lake on October 8, 2000. Detectives recovered 26 bones, some hair, a T-shirt and a necklace. Despite creating a facial reconstruction and publicizing it nationally, the police have been unable to ID the woman, who stood about 5 feet tall and was 17 to 20 years old when she was killed. But when Park arranged with Ehleringer for an isotope analysis of the victim’s hair, it showed that for the last two years of her life she lived in the Northwest, mostly in the Idaho-Montana-Wyoming area, and maybe into Oregon and Washington. Park hopes that examining missing persons records from those areas will lead to an ID.

Ehleringer and Cerling are co-founders of IsoForensics, Inc., which sells isotopic analysis of forensic substances. A method Ehleringer developed to trace the origins of cocaine or heroin is now used by the a method now used by the U.S. Drug Enforcement Administration: variations in the amount of carbon, nitrogen, oxygen and hydrogen isotopes in soil and water show up in coca and poppy plants.

For the hair analysis, says Ehleringer, “You can tell the difference between Utah and Texas,” but probably not Chicago and Kansas City. In general, the amount of the heavy isotopes oxygen-18 and hydrogen-2 levels in drinking water decreases as you move inland from the West Coast: as rainstorms move off the Pacific Ocean, rain drops containing oxygen-18 and hydrogen-2 tends to fall first because it is heavier. But cloud temperatures and season also affect which isotopes rain drops contain, with the result that heavy isotopes are also relatively more common in water inland from the Gulf and southern Atlantic coasts. The lowest concentrations of hydrogen-2 and oxygen-18 are found in water in northern and western Montana, north-central Idaho and northwest Wyoming (because the heavy isotopes drop out of clouds before they reach these inland areas), while the highest amounts of hydrogen-2 and oxygen-18 in drinking water and hair are in southern Oklahoma, north-central Texas, Florida, south Georgia and southern South Carolina (in warm regions with more evaporation, lighter-isotope water evaporates from surface sources first, leaving heavier-isotope water behind to find its way into drinking water.

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.

Is this what tropical diseases look like in a greenhouse world?

Paraguay had not seen a case of yellow fever since 1974, so it’s no surprise that the current outbreak caught health authorities there short-handed: with only 100,000 does of vaccine available, according to the Associated Press, Paraguay got 50,000 doses from Brazil and is expecting 250,000 from Peru. But there have already been protests, with thousands of worried people blocking highways to demand that vaccine be made widely available.

With five confirmed cases in Paraguay, out of 46 reported, public health officials have their fingers crossed that that are not seeing the leading edge of a disease that spreads to more regions as a result of climate change, as some scientists have long warned.

Yellow fever is one of the tropical diseases (others include malaria and dengue fever) that might spread beyond their current infection zones if the world warms up and rainfall patterns change. The World Health Organization estimates that yellow fever kills 30,000 people worldwide every year, causing fever, vomiting, jaundice and bleeding from the mouth, nose, eyes and stomach. It is carried by at least 14 separate species of the mosquito genus Aedes.

In the past it struck cities as far north and south—that is, non-tropical—as Philadelphia, New York, Boston and Buenos Aires. Clearly, then, factors other than climate determine where and how seriously yellow fever strikes, and it is facile to attribute its appearance to changing climate alone. Still, the concern is that as freeze-free regions expand, disease-carrying mosquitoes will thrive in places they seldom did.

If you thought that electricity-generating knee brace thing announced last week in the journal Science by researchers at Simon Fraser University in British Columbia looked like too much work, take heart. With any luck, we may soon be able to get watts out of our waistcoats. Or sweaters. Or shirts, all without moving a muscle. It's the best thing to happen to textiles since wash-‘n-wear.

The knee-mounted generator captures energy from leg muscles. But you still have to walk to generate the five watts of electricity per leg that the scientists calculate as the device’s output, or 13 watts if your get a move on—enough for 30 minutes of talk time on a mobile phone. The inventors, led by Max Donelan, think the device could replace the 30-odd pounds of batteries that U.S. soldiers typically carry to operate their electronic gear. But as I say, you still gotta walk.

Now nanotechnology researchers are announcing fabrics that scavenge mechanical energy from sources as leisurely as heartbeats and ambient noise, and turn it into electricity. Call it the ultimate power suit.

It works like this: start with synthetic Kevlar fibers from DuPont and coat them with tetraethoxysilane and crystals of zinc oxide. Zinc oxide is what’s called piezoelectric: when stressed by moving, it produces a voltage. Zhong Lin Wang of the Georgia Institute of Technology and colleagues intertwine the fibers into yarn, so that when the fibers rub against one another charge, builds up on the bristles. “The two fibers scrub together just like two bottle brushes with their bristles touching, and the piezoelectric-semiconductor process converts the mechanical motion into electrical energy,” he explains. An output wire carries the resulting current to any device you like, including a battery if you want to store it.

Here’s the beauty part, as Wang and colleagues report today in the journal Nature. Because the fibers are so small (nano, after all), even the slightest oscillation moves them—a heartbeat, a light breeze, reaching out for a poolside drink. The whole thing can be scaled up into power tents or curtains. How much juice are we talking about? Wang estimates the output at up to 80 milliwatts per square meter of fabric, enough to run personal electronics off your shirt.

“The fiber-based nanogenerator would be a simple and economical way to harvest energy from physical movement,” said Wang. “If we can combine many of these fibers in double or triple layers in clothing, we could provide a flexible, foldable and wearable power source that, for example, would allow people to generate their own electrical current.” He added, “. . . while walking”—but clearly that much exertion is not necessary. Just position yourself poolside in a light breeze, and you’re good to go.

Biggest challenge LabNotes sees? Washing your power shirt. Zinc oxide doesn’t like to get wet, so the fabric would have to be dry-cleaned.

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.

Say 'Om': With the Beatles in 1968. Photo: Getty Images

The other legacy the Maharishi, who died on Tuesday, gave the West is more controversial. In 1971 he founded Maharishi International University, in Iowa (now called Maharishi University of Management), which has become the center for studies of Transcendental Meditation (TM). Almost immediately—research papers on the benefits of TM appeared as early as 1974—scientists there began researching how TM affects everything from job satisfaction to blood pressure to anxiety.

There was just one problem. “Those early studies were extremely tendentious and just not of high caliber scientifically,” B. Alan Wallace, president of the Santa Barbara Institute of Consciousness Studies, told me last fall.

In the early days, many studies compared people who meditate to those who do not. That made some of their conclusions suspect: if meditators have lower levels of stress than non-meditators, as studies found, that might be because only already-mellow people choose to meditate and stick with it, not because of the practice itself.

Still, it would be churlish to deny the numerous studies reporting benefits from TM. One found that learning TM reduced hypertension in older African-American men. Others reported that meditation can moderate the harmful effects of strenuous physical exercise on the immune system, that it can produce a feeling of euphoria akin to “runner’s high”, and that it reduced anxiety more than other relaxation techniques. Maharishi University regularly updates the list of research results.

But scientists are not fully convinced. It has been difficult to rule out an alternative explanation for apparent benefits such as reductions in stress, blood pressure and heart rate—namely, the placebo effect. If you expect an intervention, be it a pill or learning TM, to help you, it often does. If you are testing the benefits of a pill, you can give half your study subjects a dummy pill but not tell them, which can help control for the placebo effect. It’s pretty hard to hide from test subjects the fact that they are learning to meditate and then doing so for several hours a week. Perhaps it is the belief that TM will do wonderful things that produces benefits, not the actual meditation. That question remains very much up in the air.

Despite these concerns, the Maharishi and his American acolytes deserve credit for introducing the study of meditation to biology. Hospitals from Stanford and UCLA to Duke and NYU have instituted meditation programs to help patients cope with chronic pain and other ailments. Scientists unaffiliated with the TM movement have been emboldened to study the effects of other forms of meditation on diseases as different as depression, obsessive-compulsive disorder and psoriasis, all with impressive results. Whatever you think of the White Album, give the Maharishi credit for helping to launch what has become a legitimate new field of neuroscience.

If the band of showers stretching from the Midwest to New England dampens voter turnout today, we’ll know what to blame.

Cars. Factories, too.

Meteorologists have long known that particles “seed” rainclouds, a process in which water and ice in the clouds grab hold of the particles, forming additional (and larger) droplets that are more likely to fall as rain. That led to the suggestion that particulate pollution emitted by traffic, businesses and factories, all of which are greater during the workweek than on the weekend (traffic to malls notwithstanding), should make for greater rainfall Monday through Friday. A competing theory, however, held that the increased pollution might instead thwart rainfall, by dispersing the water in clouds over more seeds; that would prevent the droplets from growing large enough to fall as rain.

At least for summertime rainfall in the southeastern United States, the verdict is in: weekday pollution is causing more rainfall midweek than on weekends.

So conclude scientists analyzing data from NASA’s Tropical Rainfall Measuring Mission satellite, known as TRMM. As they report in the Journal of Geophysical Research-Atmospheres, those data show that midweek storms tend to be more intense than those during the weekend, dropping more rain, compared to calmer and drier weekends. Human-caused atmospheric pollution also peaks midweek, as the emissions from tailpipes and smokestacks build up before falling off as Friday approaches.

The scientists find that, on average, it rains more between Tuesday and Thursday than from Saturday through Monday. Tuesday has 1.8 times more rainfall than Saturday, which has the least amount of afternoon rain. Now I understand why, on this Super Tuesday, I am wringing out my drenched socks after venturing out into the storm to vote.

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.