As you might expect, my column pointing out the limits of cancer screening and early detection was not universally greeted with hosannas. Many people cling fiercely to the notion that screening will save their lives. When I wrote the column, I wasn't aware of a smart blog post  from March 18 by the American Cancer Society's "Dr. Len"--J. Leonard Lichtenfeld--who does a terrific job analyzing the two recent prostate-cancer-screening studies that were so disappointing.

He notes the two studies' methodological flaws (men in the non-screening group got screened, for instance), but then reaches a striking conclusion. Like many oncologists and cancer researchers, Lichtenfeld had eagerly awaited the results of the European and American prostate-cancer-screening studies, expecting (or at least hoping) they would once and for all answer the question of whether the PSA test saves men's lives. Unfortunately, he writes, "I don’t know that we now have any better idea whether or not prostate cancer screening actually works. . . .  At first blush, my reaction was that these studies don’t really give us the answer we were waiting for.  But on further reflection, maybe they did. . . Perhaps not getting a clear answer to the question as to the value of prostate cancer screening is in fact a clear answer." For if the mortality-reducing benefits of PSA screening are so small that they can be made to appear and disappear depending on a study's methodology, those benefits are falling way short of what we all hoped.

On one point, however, the cynical me has to disagree with Dr. Len. He writes, "I suspect the 'gung-ho go forward at any cost' attitude of those in the medical and advocacy communities who have promoted prostate cancer screening with a vengeance—absent evidence that it really saved lives—is going to calm down just a bit." That, I just don't see--not until oncologists come up with something else that will give men the illusion of control over their health and their life.

The idea that experience alters the adult brain in fundamental ways has finally become accepted, so the battle lines have formed around which aspects of brain function are too basic, too hard wired, for experience to change them. Whenever someone asserts that one or another function is fixed and beyond the reach of experience, I refer them to a study finding that the visual cortex—which you’d think is as hard-wired as hard-wired can be—can adapt to an environment of visual deprivation and segue into processing tactile and auditory sensations, as scientists reported last year.

It shouldn’t surprise anyone, then, that playing action video games can also alter the brain, especially circuits involved in vision, attention and other skills you bring to bear when you play games such as Halo or Call of Duty 2. But in a study being published online this afternoon in the journal Nature Neuroscience, scientists are reporting that playing action video games improves an aspect of vision that was thought to be pretty much fixed—namely, contrast sensitivity.

That’s the ability to detect tiny changes in shades of gray against a uniform background, and is something you need to deploy when driving at night or in poor-visibility conditions. You lose it with age, but amblyopia (“lazy eye”) can also impair contrast sensitivity. The only way to fix, supposedly, is with glasses or surgery.

But maybe not. Expert action-video-game players, Daphne Bavelier of the University of Rochester and colleagues find in the new study, have better contrast sensitivity than people who play non-action video games. To make sure that that correlation did not reflect a tendency for people with sharp contrast sensitivity to gravitate toward action games more than people with poor contrast sensitivity do, the scientists gave the non-players intensive daily practice in playing action games. After 50 hours of play spread over 9 weeks, these players’ contrast sensitivity improved. There was no such improvement after playing non-action video games such as Sims.

In 2003, Bavelier found that playing action video games can improve selective attention, as she and a colleague reported in Nature (gotta keep alert for the incoming missile!). But scientists have long suspected that selective attention is trainable. Contrast sensitivity, however, was thought to be something nature makes you good or bad at, something it took away as you aged, and something beyond the reach of training. Apparently, that’s not so. Even more intriguing, its deterioration may not be due solely to things happening in the eye. Improvements can come about by tapping the brain’s power of neuroplasticity, strongly suggesting that deterioration reflects events in the brain and not (just?) the eye.

If you want to immerse yourself in the power of video games to change the brain, Bavelier and two colleagues have written an excellent book chapter summarizing their and others’ findings, including how action video games improve players’ ability to read small print and—ironically, given the terrible reputation video games have among many educators—engage selective attention.

I’ve spent the last few days talking to cancer researchers about why early detection doesn’t reduce mortality from this disease much or at all, as recent studies of the PSA test for prostate cancer concluded (the New England Journal of Medicine has made the two papers available here and here). That conclusion, sadly, has been a frequent refrain, as I’ll discuss in next week’s magazine column.

An interesting paper in the April issue of Nature Reviews Cancer (part of a package of articles on cancer metastasis that Nature is making freely available for three month, here) suggests that in addition to whatever is going on with the primary tumor to thwart the value of early detection, the process of metastasis is also undermining the effectiveness of early detection. Cells might leave the primary tumor “much earlier in the course of disease than previously thought, even before the primary tumor is clinically detectable,” reports Nature.

The standard model of metastasis says that tumor cells migrate out of the primary tumor and head for far-flung parts of the body—often the bones, brain and liver—only when the primary tumor is fairly large. The idea is that a tumor's component cells need time to evolve characteristics that let them to invade other organs and grow there. But as Christoph Klein of the University of Regensburg in Germany argues, there is another possibility. Called the “parallel progression model,” it says that tumor cells head for distant sites when the primary tumor is still small. Only after they have landed in their new home do they develop the traits needed to survive and grow there.

Klein told me by email that “early dissemination is not identical to metastasis,” since tumor cells that head for the hills may fail to form a metastasis. “We frequently detect disseminated tumour cells (DTCs) in patients who will never develop metastasis,” he explained. “However, if we find DTCs, the risk for metastasis is higher.” The relevance of this to early detection is this: in many cases, malignant cells will migrate out of the primary tumor “before clinical detection,” he says. “Why tumor size is associated with metastasis is now open for discussion,” but the unhappy implication is that potentially metastatic cells will already be on the move before the primary tumor is detected or even detectable. In this case, “early” detection is still too late, since metastases account for some 90 percent of cancer deaths.

If you’re one of those people who read about the toxic effects of environmental pollutants or diet and say, bulls***: I know lots of people who breathed or drank or ate that so-called pollutant and are just fine, then toxicogenomics is for you. This young field examines interactions between genes and environment, identifying DNA variants that make one person develop asthma from air pollutants while another breathes free, for instance, or that make one person develop cancer from cigarettes while another smokes three packs a day for 70 years with nary a shadow on his lung x-ray. For a sense of what the field is doing, check out the “environmental genetics” group at the National Institute of Environmental Health Sciences (the site has a link to publications).

One of the most divisive issues when it comes to pollutants and health is second-hand smoke. Across the population, passive smoking (as it’s also called) raises the risk of heart disease, lung cancer and other things you really should avoid. But not everyone suffers ill effects. A new study suggests why. A variation within a single gene can determine how susceptible children will be to second-hand smoke, even in utero, conclude scientists led by Carrie Breton and Frank Gilliland of the University of Southern California

For the study, published in the April issue of the American Journal of Respiratory and Critical Care Medicine, the researchers examined a family of genes called glutathione-s transferase (GST) genes which defend cells against damage by free radicals, which are abundant in cigarette smoke. The genes come in several variants, three of which had a significant effect on lung function in the 2,100 fourth graders in the study.

One of the variants, present in 30 to 35 percent of the white population, is correlated with poorer lung function and more susceptibility to respiratory damage if mom smoked during pregnancy. Since the GST genes help detoxify free radicals, including those in cigarette smoke, says Breton, “we speculate that the patterns of genetic variation we investigated may alter this process, thereby reducing the lung’s ability to detoxify harmful agents and causing a cascade of other events that promote inflammation, bronchial constriction, airway hyper-responsiveness and asthma-like symptoms.”

For those of you with memories that go back to 1989, the news that cold fusion has not slinked off into the abyss might come as a bit of a surprise. After all, the claim 20 years ago that atomic nuclei could be induced to fuse at room temperatures (rather than the temperature of the Sun, as happens in fusion reactors) and to emit measurable quantities of heat was shown to be based on poor measurements, nonexistent controls and nutty theory. But off in the dim, dark corners of physics, the field—since renamed “low energy nuclear reactions”—continues apace, albeit without quite shaking the stigma attached to the original claims, especially now that the world’s need for carbon-free energy sources has become even more desperate than it was 20 years ago.

A brilliant 2004 story in The Washington Post by Sharon Weinberger chronicled cold-fusion progress (which I should probably call “progress”) up until that year, and now comes news from the American Chemical Society of “compelling new scientific evidence for the existence of low-energy nuclear reactions (LENR), the process once called ‘cold fusion’ that may promise a new source of energy.” At ACS’s annual meeting this week, no fewer than 30 papers are being presented in sessions on “New Energy Technology,” including here, here and here.

A number of the scientists in this field work for the federal government, which has quietly kept supporting cold fusion research (though not under that name). For instance, analytical chemist Pamela Mosier-Boss of the Navy’s Space and Naval Warfare Systems Center in San Diego is presenting what she calls “the first scientific report of the production of highly energetic neutrons from an LENR device.” Mosier-Boss is no novice in this field, having unveiled tantalizing results before. The neutrons, she and her team suggest, came from nuclear reactions, perhaps from the fusing of deuterium nuclei. “People have always asked ‘Where’s the neutrons?’” Mosier-Boss says. “If you have fusion going on, then you have to have neutrons. We now have evidence that there are neutrons present in these LENR reactions.”

Other teams make similar claims. Tadahiko Mizuno of Hokkaido University in Japan is reporting the production of excess heat and gamma ray emissions from his own LENR device, for instance, while Antonella De Ninno of New Technologies Energy and Environment claims she and her team got both excess heat and helium gas (both indications of nuclear reactions) from theirs.

If you play the Village People’s YMCA to natives of Borneo, will they feel energized and upbeat? If you play a dirge for people from deepest Amazonia, will they feel blue? If you play the thumping beat that announces the arrival of the killer in a slasher movie, will someone who has never heard it before feel scared?

Conveying emotions is one of the key qualities (and, indeed, purposes) of Western music, in contrast to music from cultures whose purpose is more to coordinate group activity. So it had been an open question whether people from non-Western cultures who had never heard its music would respond to it the way Westerners do. If the results from a new study published in Current Biology stand up, the answer is a resounding yes: Africans who had never even listened to a radio were able to identify various pieces of Western music as happy, sad, or fearful, report scientists led by Thomas Fritz and Stefan Koelsch of the Max-Planck-Institute for Human Cognitive and Brain Sciences. That, said Fritz, “could explain why Western music has been so successful . . . even in music cultures that do not as strongly emphasize the role of emotional expression in their music.”

For the study, Fritz sought out members of the Mafa ethnic group in the Mandara mountain range of Cameroon. (The region is so remote, he had to carry a solar collector to supply electricity for his laptop.) He found 21 Mafas who said they had never listened to a radio, attended a church (where they might have heard Western music), or heard Western music any other place. He played recorded piano pieces composed by two colleagues, Isabelle Peretz and Nathalie Gosselin of the University of Montréal, to sound happy, sad, or fearful, and then, back in Germany, played the same pieces for 20 Germans, and asked his volunteers which of the three emotions the music conveyed.

If the Mafas had been merely guessing, they would have gotten it right one-third of the time. But they were right 60% of the time when trying to classify “happy” music, and half the time with “sad” and “fearful” music. The Westerners scored 100% on happy music and just over 80% with sad or fearful. Two of the 21 Mafa did no better than chance, but the others did significantly better. “Both Mafa and Western listeners showed an ability to recognize the three basic emotional expressions tested in this study from Western music above chance level,” the scientists write. “This indicates that these emotional expressions conveyed by the Western musical excerpts can be universally recognized, similar to the largely universal recognition of human emotional facial expression and emotional prosody.”

The idea that “parents don’t matter”—shorthand for the view that how parents treat their children has no effect on the kids’ behavior, values, achievements and other outcomes—just won’t go away. I can hardly believe it’s been more than 10 years since I wrote about the controversial claim that only genes and peers shape children; once parents contribute an egg or sperm, asserted the book The Nurture Assumption (now out in a revised paperback edition), they have no effect on how their kids turn out.

So I was struck by what’s being called “the largest meta-analysis ever conducted on the association between parenting styles and delinquency.” The meta-analysis, in the Journal of Abnormal Child Psychology, looked at 161 published and unpublished studies on the question, and found that how well parents monitored their children, whether they expressed rejection or hostility, and a number of other factors indeed had an effect.

What’s particularly interesting is the size of the effect. An association can be statistically significant (unlikely to be due to chance) without being practically significant; that is, there can be true cause-and-effect, but a tiny effect. Not so in this case. Rewarding kids for good behavior had an effect size of .11, for instance; not huge, but not tiny (it means that 11% of the difference between kids’ levels of delinquency is due to whether their parents rewarded them for good behavior, something that reduces delinquency). Being authoritative also reduced delinquency, again with an effect size of .11, while being authoritarian increased delinquency, with an effect size of .12. Put the two together and being authoritarian (dictatorial, controlling) as opposed to authoritative (firm, consistent, setting limits, but with love and kindness) accounts for a swing of .23. Physical punishment and verbal aggression also were associated with more delinquency.

The “parents don’t matter” school might argue that little delinquents-to-be bring out the worst in parents, who turn authoritarian. It is the kids’ innate tendencies that cause later delinquency, according to this argument, not how parents behave. The problem with this claim is the many studies showing that whether you are an authoritarian or an authoritative parent “is most often determined before your first kid is even born, and is highly dependent upon your own experience of discipline . . . and your general political/personality orientation,” as clinical psychologist Nestor Lopez-Duran wrote.

With the opening round of March Madness (a.k.a. the NCAA Men’s basketball tournament) getting underway Thursday, the mathematicians are out in force. If you’re still looking for additional help with your bracketology, Lab Notes is here to help.

Among the more interesting picks is the computer ranking system devised by researchers at the Georgia Institute of Technology. Called LRMC (Logistic Regression Markov Chain), it was developed by Joel Sokol, Paul Kvam and George Nemhauser based on results during the season, which teams are competing, home court advantage and margin of victory. Last year, LRMC correctly predicted all of the Final Four and picked Kansas to defeat Memphis in the championship game.

And this year? The Georgia trio has University of North Carolina (number 1 in the South) vs. the University of Pittsburgh (number 1 in the East) and the University of Memphis (number 2 in the West) vs. the University of Louisville (number 1 in the Midwest) in the final four, North Carolina against Memphis in the championship game, and North Carolina coming away with the crown. Granted, the LRMC system deviates in only one place from the NCAA seedings, which have the University of Connecticut (number 1 in the West) rather than Memphis in the Final Four, but 1 in 4 is significant.

In earlier rounds, the LRMC system identifies Michigan State, Boston College and Utah State as potential upsets. You can find the LRMC rankings and analysis here.

If you prefer you pick your games one at a time, try to get whoever you’re betting against to re-open the wager at halftime. According to a new paper by Jonah Berger and Devin Pope of the Wharton School at the University of Pennsylvania, “being slightly behind can motivate people to work harder, and consequently, lead to increased success,” Berger tells me. Their analysis of 6,572 NCAA basketball games from 2005 to 2008 shows that being slightly behind at halftime increases a team’s chance of winning by 5.5 to 7.7 percentage points—half the home-court advantage. And compared to teams that are slightly ahead, teams that are slightly behind at halftime are more likely to win.

In general, if you’re ahead in a competition you are more likely to win, something that holds for sports or for groups of employees competing for a contract. “In hockey, the team behind after the first period wins fewer than 33 percent of the games,” Berger and Pope write in The New York Times. “In baseball, the team losing after three innings wins less than 20 percent of the time. Basketball is no different. N.C.A.A. teams across all divisions that fall behind in games tend to lose, and more so as the deficit increases. Teams down by 4 at halftime lose about 60 percent of games. Teams down by 8 lose about 80 percent of the time.”

With a record number of Americans now saying that press accounts of the impact of global warming are exaggerated—41 percent say that, according to a Gallup poll released last week—I can easily imagine the reaction to this study, but here goes anyway: sea level due to global warming will be almost twice as great along the northeastern U.S. coast as it is globally. As always, it’s not merely the average level of sea-level rise that’s the problem, but the synergistic effect of sea-level rise with hurricanes and winter storm surges. When winds hurl water onto coasts from a higher starting point, the damage is that much greater.

Of all the predicted impacts of global warming, sea-level rise is where models have most underestimated what we can expect, scientists told a climate change conference in Copenhagen last week. Now a new study, focused on the eastern seaboard of the United States, suggests that the models are really off for that part of the world.

Writing in the advance online edition of Nature Geoscience, the team of Jianjun Yin of the Center for Ocean-Atmospheric Prediction Studies (COAPS) at Florida State University, Michael Schlesinger of the University of Illinois at Urbana-Champaign and Ronald Stouffer of the Geophysical Fluid Dynamics Laboratory at Princeton University analyzed 10 of the climate models used by the Intergovernmental Panel on Climate Change (IPCC). All the models show that, in a warming world, water expands and land ice such as the Greenland ice sheet melts, raising sea levels. But the models did not account for the effect of changes in ocean circulation.

When those are incorporated, the scientists predict, there will be a sea-level rise in New York of 15 to 23 centimeters (about 6 to 9 inches) on top of the rise of 36 to 51 centimeters (14 to 20 inches) globally. “The northeast coast of the United States is among the most vulnerable regions to future changes in sea level and ocean circulation,” Yin said. Much of New York City is less than 16 feet above sea level, with some parts of lower Manhattan only about 5 feet above. That means that a rise of 6 to 9 inches on top of the 14 to 20, especially with a storm surge, poses a real risk of flooding, beach erosion, destruction of wetlands and increase in the salinity of estuaries.

One thing that’s been interesting to note about climate change research over the decades is what happens to the assessments when scientists realize they forgot something. The result is almost never that the predicted impacts or severity of climate change need to be dialed back. Instead, as researchers learn more about the climate system and feedback loops, the expected impacts keep getting worse. So it is in this case, in which the researchers took a look at the effect of the Atlantic meridional overturning circulation. This current is characterized by warm and salty seawater flowing north from the Gulf of Mexico in the ocean’s upper layers and cold water flowing south at depth. Global warming could reduce or prevent the sinking of the surface water, which would slow the AMOC and raise sea levels off the eastern seaboard. Or, as the scientists put it in their paper, “future changes in sea level and ocean circulation will have a greater effect on the heavily populated northeastern United States than estimated previously.”

Have you ever had the experience of smiling to be sociable at a party, even though you don’t feel especially chipper, and finding that the smile actually makes you feel happier? Or of making a frown, perhaps when you’re in a meeting where layoffs are announced (even though your job is safe), to show that you are in sync with others, and even though you did not feel angry before you frowned the facial expression makes you feel mad? The phenomenon was first noticed by Charles Darwin, giving rise to his “facial feedback hypothesis”—but Darwin didn’t know anyone who’d had Botox.

Scientists therefore ran a cool little study in which they compared people before and after they had Botox treatments that immobilized their frown muscles. One mystery that still surrounds the facial-feedback effect is whether the feeling of happiness or anger induced by smiling or frowning is due to the brain activity that causes the muscles to move, or to the actual muscle movement that, presumably, sends feedback to the brain. If only the brain activity sending the command “smile!” or “frown!” matters, then the fact that the immobilized muscles don’t move shouldn’t matter; people should still feel the emotion.

In a paper in the March issue of the journal Cerebral Cortex, scientists led by Andreas Hennenlotter and Bernhard Haslinger of the Tcchnische Universitat Munchen and the Max Planck Institut für Kognitions (Human Cognitive and Brain Sciences), both in Germany, note that when people imitate facial expressions, their brain’s emotion regions become more active. To tease apart whether the actual muscle movement is causing the effect, they studied 38 women who received Botox (botulinum toxin) injections to their frown muscles (to reduce lines in their forehead).

Before Botox, imitating pictures of sad or angry facial expressions caused a large increase in activity in the amygdala, a key emotion region for, especially, anger and anxiety. But after Botox, imitating the angry expressions caused a much lower level of activity in the left amygdala. (The British Psychological Society did a nice write-up of the study here.) This suggests that making an angry face affects the amygdala through feedback from the facial muscles and skin (the latter being absent for the botox-injected women). There was no difference in amygdala activation pre- and post-Botox when the women imitated sad expressions, reinforcing the idea that muscle movement is key to inducing the emotion; their Botox shots did not immobilize muscles that make a sad face.

The scientists conclude that “during imitation of angry facial expressions, reduced feedback due to [Botox] treatment attenuates activation of the left amygdala . . . . These findings demonstrate that facial feedback modulates neural activity within central circuitries of emotion during intentional imitation of facial expressions.” Any thoughts on whether immobilizing the smile muscles takes away the ability to feel happiness when you make yourself smile—or, in the case of Botoxers, try but fail to smile?

It’s always been a mystery to me why the fishing industry equates “some fish have mercury, so avoid high-mercury fish” with “don’t eat any fish at all, ever ever ever!!!” Yet it does, arguing that those irresponsible scientists who issue warnings about mercury in fish will make people miss out on the heart and (for fetuses) cognitive benefits of fish.

Rather than join with scientists and government agencies to maximize the benefits of eating fish and minimize the risks by guiding us to low-mercury seafood, the industry has taken the low road: Deny the existence of any risk at all, attack and discredit those who disagree, try to intimidate the press by challenging every report that mentions risk.

A particularly extreme example has been the continuing coverage of actor Jeremy Piven, who in December got sick (exhaustion, memory, loss balance problems) from the high levels of mercury he developed, apparently as a result of eating a lot of tuna sushi, and withdrew from the Broadway play Speed the Plow. His physician said Piven’s blood mercury level was 60 parts per billion (ppb), which is more than 10 times the EPA “reference level,” and his symptoms were similar to those in other people who eat a lot of the wrong kind of fish. His symptoms and his blood mercury level fit the diagnosis. Yet the press was full of credulous interviews with industry-friendly doctor who insisted, “It’s almost impossible to get mercury poisoning from eating fish.”

In fact it’s not hard at all. A 6-ounce swordfish steak contains about 130 µg of mercury, or 16 days’ worth of the Environmental Protection Agency’s reference dose for an adult man. A 5.5-ounce can of albacore tuna contains 55 µg, a full week’s dose for an adult man. Even canned light tuna, touted as a “low-mercury” fish by the industry (and the FDA, after intense industry lobbying), has 18 µg of mercury in a 5.5 ounce can. For someone like Piven, who eats fish twice a day, those µg’s can add up fast, and it’s easy to get a mercury dose far above the reference dose.

As a public service, let me then make the obvious point. If you eat a lot of fish—which in America, means more than twice a week—you should know what fish to choose to minimize your mercury exposure. The more fish you eat, the more often you should choose from the low-mercury list. Here’s a list of fish and seafood, sorted by mercury content, based on data from the U.S. Food and Drug Administration:

Low-Mercury: Contain less than 0.05 part per million (ppm) mercury. Can safely be eaten daily, or more often, without risk of exceeding reference dose: salmon, tilapia, ocean perch, whiting, pollock, hake, flounder, sole, , haddock, sardines, herring, anchovies, catfish, Atlantic mackerel, shrimp, clams, oysters, crayfish, scallops.

Medium-Mercury: Contain between 0.05 and 0.20 ppm mercury. Can be eaten once or twice a week as long as other choices are from the low-mercury group. American shad, cod, whitefish, Atlantic croaker, freshwater trout, Pacific mackerel, canned “light” tuna, skate, freshwater perch, monkfish, mahi-mahi, snapper, blue crab, king crab, snow crab, squid, spiny lobster.

Higher-Mercury: Contain between 0.21 and 0.50 ppm mercury. Should be eaten only in limited amounts (less than once a week) if you eat fish often: Canned albacore tuna, tuna steak, sea bass, Chilean sea bass, halibut, sablefish, sea trout, Pacific croaker, bluefish, Spanish mackerel, grouper, marlin, orange roughy, American lobster.

Very High Mercury: Contain more than 0.50 ppm mercury. Should be avoided by people who eat a lot of fish and by women of childbearing age: swordfish, shark, tilefish, king mackerel.

Devoted as I am to my job, I think I would draw the line at eating one can of albacore tuna day for 20 days, as reporter Sue Kwon of San Francisco’s KPIX did for a report broadcast last week. The idea was to see how high her blood levels of mercury rose, and rise they did: from 4 parts per billion (already well above the U.S. average of 1 ppb, suggesting that Kwon ate a lot of mercury-laden fish even before her experiment) to 8.9 ppb by day 10, and to 17.2 ppb on day 20. That's when, on her doctor’s advice, she stopped her experiment. Eating a can of tuna a day quadrupled her blood mercury level in just three weeks, which raises obvious questions about what happens to people who eat high-mercury fish for years.

But that's not the point of this post, for having her blood levels of a known neurotoxin rise wasn’t the only hit Kwon took. She also heard from the National Fisheries Institute, the industry trade association, which works very hard to keep you from realizing that it’s easy to get too much mercury, if you eat the wrong kind of fish, and that the resulting levels of mercury pose health risks.

The industry did not take kindly to Kwon’s reporting. NFI flack Gavin Gibbons fired off a letter (posted on the media blog part of NFI’s Website) to KPIX, attacking her. You can also get the gist of Gibbons’ letter in a YouTube video they posted.

It’s always interesting to see how a true artist works, and NFI is second-to-none in distorting science to suit its ends. The letter is a clone of attacks the industry has launched at other journalists who’ve dared to report about mercury risks. Just a few highlights:

• Gibbons, arguing that Kwon’s 17 ppb is nothing to worry about, refers to “the recognized EPA Reference Dose (RfD) of 58 micrograms per liter.” That’s false; the reference level, not dose, is 5.8 µg/l (1 µg/l = 1 ppb). It's the level judged to be free of appreciable risk for almost everyone.
• He raises the bar for falsifying facts by asserting (again to make Kwon’s 17 ppb seem insignificant), “The Environmental Protection Agency has deemed 580 micrograms per liter as the level of mercury that approaches risk.” How did they get from 5.8 to 580? Watch carefully. EPA got the 5.8 by starting with a blood mercury level that had adverse effect on brain development in a key human study—a level of 58 ppb. EPA then divided that by an uncertainty factor of 10, to get the reference level of 5.8 ppb.
• The industry likes to say the reference level has a 10-fold “safety factor” built in. No. EPA applied its 10-fold “uncertainty factor” to account for individual variability. Translation: People differ in their sensitivity to the toxic effects of mercury and everything else. If the average blood mercury level at which an effect is observed in a large group of people is 58 ppb, some people were affected only at higher levels, some at lower levels, and a few at much lower levels. The “uncertainty” is how wide the variability is; there are too few data to establish that. By using a factor of 10, EPA hopes its reference level protects even sensitive individuals. No one can prove that it does, or doesn’t; it’s an educated guess, and some experts have argued for applying a larger uncertainty factor. But in no way is it a "safety factor" with the implication that 58 is just fine.
• The fishing industry has long distorted this scientific process. They falsely call the uncertainty factor a “safety margin.” They claim that the actual “safe” level is 58 ppb, a clear falsehood, as I said. The industry assumes that most of us are too dumb or too busy to catch their misrepresentations. But having fooled us once, they now aim to fool us even more egregiously. If 58 ppb is the safe level, and there is a 10-fold “safety cushion” built in, the actual level where harm occurs must be 580 ppb!

A blood mercury level of 580 ppb would probably kill many people. Toxicity symptoms, like those actor Jeremy Piven suffered (according to his physician, who was interviewed on Good Morning America), have been seen at around 50 ppb. The claim that one merely “approaches risk” with a blood mercury level of 580 ppb is blatantly false and recklessly irresponsible.

Give the industry credit for using New Media to get their message out. Go to YouTube and search for “mercury in fish.” Five of the first six videos are NFI postings, rebuttals to media reports they don’t like. Sue Kwon’s report on KPIX is there, with industry responses that repeat the claim that 580 ppb is a safe level of mercury in blood and generally maul the truth.

Of course eating fish has health benefits, and no one should stop eating fish to avoid eating mercury. But people who eat a lot of fish should choose low-mercury fish (see my rundown of the good kinds, here). That’s just common sense. Why does the message, “Eat lots of low-mercury fish,” terrify the fishing industry? If public health officials concerned about mercury in fish think the battle is about science, they're sadly mistaken. NFI knows the battle is about propaganda, and they are kicking science’s butt.

Whenever a study claims a “first”—as in the first evidence for this or that phenomenon—my suspicious side emerges. A fascinating paper in the March 9 issue of Current Biology describes what it calls the first unambiguous evidence that a non-human animal (in this case, a male chimpanzee who lives in Sweden’s Furuvik Zoo) can plan for future contingencies: for the last 11 years Santino, who is 30, has been regularly collecting stones from his enclosure in the early morning hours before the zoo opened, stockpiling them in groups of three to eight, and then hurling them at visitors later in the day.

Planning, sure. But the first evidence of that? As coincidence would have it, the same journal published a study last month describing how capuchin monkeys in the wild intently check out stones of various weights and sizes, compare them to one another, and then choose those that will serve as the best anvils and hammers. Capuchins, like some other wild primates, use tools and, as this study shows, form a mental image of what that future tool should look like. (Current Biology has, on its home page today, a charming video of the capuchins doing this.)

But back to Santino. As Mathias Osvath of Lund University reports, Santino began hurling stones across a moat at visitors in 1997, in what zoo officials infer was a dominance display. Curators did some sleuthing, and found that he had cached dozens of stones in his activity area. The curators removed them, but Santino just collected and stashed away more—those he found in the enclosure as well as chunks of concrete he knocked off walls and broke into smaller, more throw-able pieces. Over the years, they found hundreds of caches. Santino would throw the rocks underhanded across his moat at visitors (luckily, he has lousy aim).

Planning, yes. As Osvath put it, “These observations convincingly show that our fellow apes do consider the future in a very complex way. It implies that they have a highly developed consciousness, including life-like mental simulations of potential events. They most probably have an ‘inner world’ like we have when reviewing past episodes of our lives or thinking of days to come. When wild chimps collect stones or go out to war, they probably plan this in advance. I would guess that they plan much of their everyday behavior.”

But the first evidence of planning? Orvath argues that inspecting and collecting stones in the wild, to use for cracking nuts, may not truly represent planning. Instead, it may meet what he calls an immediate or current need rather than a future one. Santino’s collecting, in contrast, is not based on his “current drive state,” Orvath argues, since while collecting and caching stones he was calm but when throwing them he was extremely agitated.

But surely that same criterion could be applied to using stones in the wild. The capuchins who carefully consider the merits of various stones for anvils and hammers are projecting forward in time to when they will need them to crack nuts, no? If you want to claim that the capuchins’ “immediate need” is acquiring good tools, but their future need is food, then surely that same argument goes for Santino: his immediate need is to acquire weapons, which he satisfies by stashing rocks, and his future need is throwing them.

Osvath himself admits that “wild chimpanzees might be even better at planning as they probably rely on it for their daily survival.  The environment in a zoo is far less complex than in a forest. Zoo chimps never have to encounter the dangers in the forest or live through periods of scarce food. Planning would prove its value in ‘real life’ much more than in a zoo.”

Anyway, it’s always a good idea to be cautious about claims of firsts.

There are all sorts of ways to get a sense of when an idea’s time has come, but I recommend looking at how many conferences are devoted to it. By that measure, carbon capture and sequestration is ready for its close-up. I just got back from a conference on this, and was struck by how little the message had changed since I began writing about it in 2003 (such as here, here and here).

The basic idea, as laid out by James Dooley of the Department of Energy’s Pacific Northwest National Lab, is this: all the talk about stabilizing emissions of carbon dioxide misses the point. What we need to do to avoid catastrophic climate change is to stabilize atmospheric concentrations of CO₂. As long as we send up more CO₂ than the oceans and other sinks can absorb, concentrations will rise and the associated climate changes will worsen.

Capturing the carbon in coal and other fossil fuels that are burned for electricity has the potential to get us partway to the goal of stabilizing the atmosphere, as Stanford’s Sally Benson said in her talk. (On Benson’s Website, scroll down to her presentation at Google on Oct. 23, 2008, for a good sense of what she spoke about this week.) Carbon capture and sequestration (CCS) can get us 20 percent of the way toward that goal, she argued, with the rest having to come from efficiency and substituting renewable energy for carbon-based sources.

One hopeful sign of the potential of CCS is that the technologies to capture CO₂ at power-plant smokestacks, to pipe it to rock formations suitable for underground storage, and to sink it deep into sedimentary basins (where sandstone whose pores can hold CO₂ alternates with layers of shale that serve as an impermeable barrier) all exist. Carbon sequestration is already being used off Norway (where the state oil company decided it was cheaper to sequester CO₂ produced in its natural-gas operations than to pay Norway’s carbon tax) and at three other sites, so we have the know-how. But it won’t be deployed in any significant way until and unless we price carbon. In other words, CCS’s time has come in terms of technology, but not in terms of public policy.

Among the many, many (really many) doctors who have written in to berate me for my column in this week’s magazine claiming that “doctors hate science” (which was shorthand and headline-speak for “why doctors are so reluctant to embrace evidence-based medicine and comparative-effectiveness research”), quite a few made a crucial point. Doctors may be paragons when it comes to using only treatments that have been proved to work. Patients are a whole ‘nother story.

Robert M. Kaplan of UCLA warned me about that when I spoke to him last week about his brilliant book, Disease, Diagnoses, and Dollars, in which he lays out proposals for using our health-care dollars a lot more intelligently than we do today. (He is particularly thought-provoking in explaining the dubious benefits we get from cancer screening.) I mentioned the 2004 study finding that something like 10 million women who had had total hysterectomies for a condition other than cancer were still getting regular Pap tests even though they did not have a cervix. Kaplan went me one better. After medical groups concluded that women who have had several clear Pap tests in a row (and met a few other criteria) can get the test every three years rather than annually, a California clinic began to implement that recommendation. But when it told its low-income patients that they could skip the Pap test this year, the women rose up in protest. How come those rich women going to private doctors get an annual Pap test, and you’re letting me have one only every third year?, they demanded.

Which brings me to some of the points the unhappy doctors have been making to me via email. What are they supposed to do when a patient demands antibiotics for a cold? for a child’s ear infection? when a patient demands an MRI for back pain or knee pain? If the y refuse, several doctors told me, they can expect a call from the patient’s lawyer that afternoon.

As my former colleague (at The Wall Street Journal) Tara Parker-Pope writes in today’s New York Times, as long as patients demand the most expensive, newest, high-tech pill, scan or treatment, we’ll never implement good medical practices. Doctors just can’t be expected to stand up to this onslaught themselves. Which is why evidence-based medicine needs to have teeth in it, and those teeth have to do with insurance coverage. Simply put, if Medicare and private insurers refuse to pay for things that are not needed or that do not work, then patients will stop demanding them and doctors can stop acquiescing in this insanity. Just to be clear, this is about more than saving money. It is also about giving patients the best treatment: prescribing something that doesn't work exposes a patient to side effects with no attendant benefit.

The American Medical Association issued a statement on Feb. 20 supporting comparative-effectiveness research but, curiously, insisted that whichever government entity conducts or disseminates that research “not have a role in making or recommending coverage or payment decisions. . . . Physician discretion in the treatment of individual patients remains central to the practice of medicine.” In other words, it’s fine to disseminate research showing that antibiotics for colds are a waste of money and an excellent way to spread antibiotic resistance, but for God’s sake don’t let insurers refuse to pay for the prescription.

As I said in the column, of course patients are individuals, and whatever works for the majority might not work for some; doctors must be free to customize treatment. But really—aren’t there some dumb practices we can agree should not be covered, especially since that will arm doctors against the ridiculous demands of their patients? (See Pap test example above.)

I hope Lab Notes readers got their votes in. As I blogged last month, NASA had invited people to weigh in on what additional target the Hubble Space Telescope should photograph during the International Year of Astronomy's “100 Hours of Astronomy,” taking place April 2 to 5. The winner is (sorry, planetary nebulae, spiral galaxy, star-forming region and edge-on galaxy): a pair of interacting galaxies.

Out of the 139,944 votes cast online since January 28, nearly 50 percent went to the interacting pair of spiral galaxies called Arp 274. (To find it yourself--or at least the general neighborhood, go here) It’s a good choice, since interacting galaxies “weave elegant twisted lanes of dust and stars, and brilliant blue clusters of newborn stars,” a NASA announcement says.

We’ll see what Hubble comes up with next month.