If work or play takes you to Houston between now and September 7, check out the Genghis Khan exhibit at the Houston Museum of Natural History and you’ll never again equate the conquering Mongol with “barbarian.”

The “conquering” part is definitely an understatement. During his reign Genghis Khan, who died in 1227, brought more land under his control than either Julius Caesar or Alexander the Great, but the 200-plus treasures (jewels, bows, arrows, armor, silk robes, imperial gold and other artifacts, many of which had never before left Mongolia) on exhibit paint a more nuanced portrait. Created and designed by Don Lessem, who is best known for the dinosaur exhibits he designs for museums, the Genghis Khan exhibit shows that “we have Genghis to thank for the post office, passports, paper money, diplomatic immunity, national parks, even hamburgers, pants, skis, baklava, and yelling ‘hooray,’” Lessem says. “No one ruled more of the Earth, no one influenced its future like Genghis,” who brought these innovations to the West. There’s also an IMAX film; the show moves to Denver, Dallas and other North American museums for two years after it closes in Houston.

The exhibit, the most comprehensive assembly of Genghis artifacts ever displayed, takes aim at the stereotype of Genghis as the barbarian leader of barbaric “Mongol hordes” who swooped in from the East and destroyed every civilization they encountered. “Although he was often referred to as a brutal killer, Genghis Khan achieved his victories through brilliant tactics, earning him the reputation as a military genius,” said Dirk Van Tuerenhout, Curator of Anthropology of the Houston Museum. “However, this special exhibition presents a new image of the legendary leader,” who not only created the nation of Mongolia and its written language but (with his descendants) established what became the borders of countries from India to Iran, Korea to China.

Born into poverty, Temujiin—the future Genghis Khan—built the greatest military machine the world had ever seen, but Lessem emphasizes what an accompanying book calls “the civilizing influence of a uniquely sophisticated ruler too long branded only as a barbarian.” Genghis established freedom of religion and cultural expression in the lands he conquered, promoted a meritocracy and created the first efficient mail system. He even popularized pants (much better for horseback riding). There is a more literal sense in which there is a little Genghis in all of us: geneticists estimate that one-quarter of the world’s population carries his genes.

As Lessen writes in his foreword to the book that accompanies the museum show, “Genghis Khan was one of the world’s most visionary geniuses. From an impoverished, illiterate and isolated youth, Genghis created a nation, a language, religious and political freedoms, a post office, Pony Express, diplomatic immunity, a network of international toll roads, and a host of other innovations in what was by far the largest empire in the history of the world. The greatest of civilizers never slept indoors and only once set food in a building. He dressed as a common man. . . . Raising his sons to become rulers, he insisted that the key to leadership was self-control, and he cautioned them against pursuing a ‘colorful’ life with material frivolities and wasteful pleasures.”

The exhibit includes a male mummy dated to a millennium ago and uncovered with two females in a Mongolian cave by local herdsmen in 1997. He appears to have been murdered when he was between 25 and 30, says Bruno Frohlich at the Smithsonian Institution, his neck twisted and broken, his head bashed in. Truth be told, the date makes him a little old to have been the victim of Genghis’s army, as the exhibit coyly implies, but hey, what museum can resist a mummy?

There is more than enough evidence that physical exercise is good for the brain, bringing benefits like lower cholesterol and blood pressure, but here’s more: it can increase the size of your hippocampus, the structure responsible for the formation and storage of new memories as well as for spatial navigation--finding your way around.

In a paper to be published in the journal Hippocampus, scientists report that elderly people who are physically fit generally have a larger hippocampus and better spatial memory than peers who are less fit. Previous studies have shown that challenging the hippocampus—exercising its spatial skills and its memory abilities—can increase its volume, too. London cabbies have bigger ones than your average Londoner, and experienced cabbies have larger ones than newbies, suggesting that making the hippocampus find its way through London’s labyrinth can boost its size. And exercising its memory-making skills seems to do the same thing: a study of German medical students found that the hippocampus got larger as they studied for finals. This is the first study, however, to show that plain old physical exercise, which does not engage the hippocampus to any real extent, can also give it a boost.

The scientists, led by Art Kramer of the University of Illinois and Kirk Erickson of the University of Pittsburgh, studied 165 adults, ages 59 to 81. They measured the volunteers’ hippocampus volume and gave them a test of spatial memory (recalling where three black dots on a computer screen had been a few seconds after they disappeared). Finally, they measured aerobic fitness by VO₂ max. They found what they call a “triple association”: higher fitness levels were associated with a larger hippocampus (taking into account age, sex and years of education), and a larger hippocampus due to higher fitness levels was correlated with better spatial memory. “The higher fit people have a bigger hippocampus, and the people that have more tissue in the hippocampus have a better spatial memory,” said Kramer

Depression, stress, hypertension, chronic heavy drinking and getting old all shrink the hippocampus, studies in humans as well as lab animals show. And in rodents, voluntarily running in an exercise wheel increases the volume of the hippocampus as well as the rate of neurogenesis, the production of new neurons. (It doesn’t work if the mice or rats are forced to run in the wheel—spouses hectoring your partner to exercise, take note.) Or as Erickson put it, the finding “supports the notion that your lifestyle choices and behaviors may influence brain shrinkage in old age. Basically, if you stay fit, you retain key regions of your brain involved in learning and memory.”

Importantly, however, there was no evidence that aerobic fitness slowed the rate at which the hippocampus shrinks in old age. Instead, it seems that fitness lets you enter your later adulthood with a larger hippocampus, giving yourself more of a cushion against the (probably inevitable) shrinkage. Targeted studies will need to be done to determine whether becoming more physically fit after age 60 or so can halt and even reverse the shrinking of the hippocampus.

Let me also mention an upcoming study showing that one commercial brain-training program, Brain Fitness from Posit Science, improved the ability to remember what you heard (auditory memory) and to focus attention. Funded by Posit (potential conflict-of-interest alert), the study of 487 healthy adults over 65 was conducted by the Mayo Clinic and University of Southern California and will appear in the April edition of The Journal of the American Geriatrics Society.

I blogged about this study when preliminary results came out in November, but now the scientists have dotted all the i’s and crossed all the t’s. Volunteers using Brain Fitness for 40 hours over the course of eight weeks improved their memory and attention by about 10 years--that is, 65-year-olds had the brains of 55-year-olds--and the benefits carried over from the lab into real life: people reported noticeable improvements in remembering names they heard spoken and understanding conversations in noisy settings.

Equally important is that the study did not compare Brain Fitness to doing nothing. Half the volunteers did the six Brain Fitness exercises, which involve listening for finer and finer auditory distinctions, and half watched an educational DVD. Only the first group showed the notable improvements, lending support to Posit’s belief that only exercises based on neuroplasticity (the brain’s power to alter its structure and function in response to certain inputs) can produce lasting mental benefits. Importantly, the volunteers improved on mental skills that the exercises did not specifically target, namely memory and attention.

So both aerobic fitness and brain training can reduce your mental age. What are you doing glued to a computer screen?

When I was reporting the story on vaccines and autism for the current issue of the magazine, everyone warned me that despite a sweeping decision by the “vaccine court” that neither thimerosal nor the MMR vaccine cause autism, the belief that either or both do was not going to fade away. Hard on the heels of that February 12 decision by the court, another case—decided in July 2007 but being released only now—went in favor of parents who believe the MMR vaccine caused their son’s Pervasive Developmental Delay (of which autism is one form).

In the case, the parents of Bailey Banks, now 10, argued that their son had a seizure 16 days after his first MMR, in 2000. That, they said, led to Acute Disseminated Encephalomyelitis (ADEM), a rare neurological disease, which in turn led to PDD.

The first question for the court, then, was whether Bailey had Acute Disseminated Encephalomyelitis, and its answer was yes, based on medical records. It then addressed the question of whether the MMR vaccine can cause ADEM, and here there was precedent: Two previous vaccine cases, in 1994 and 2001, had led to decisions that ADEM can be caused by natural measles, mumps, and rubella infections, as well as by measles, mumps, and rubella vaccines. In Bailey’s case, the court ruled, the MMR had indeed caused his Acute Disseminated Encephalomyelitis.

For the final step, the court wrestled with whether Acute Disseminated Encephalomyelitis can cause pervasive developmental delay, and whether it caused Bailey’s. (Just to reiterate, the issue was PDD, not autism. As the court said in its decision, Bailey “more likely than not suffers from PDD, and not from autism.”) Here, the medical literature leaves plaintiffs much more room than does the literature on classical autism. The government argued against the claim that ADEM can cause pervasive developmental delay, of course, acknowledging “that Bailey currently suffers from PDD, and that the MMR vaccine can cause ADEM" but disputing "the biologic plausibility [of] whether ADEM can lead to PDD.”

Here, the science is not so negative as it is in the case of vaccines and classical autism. As the court said in its decision, “Bailey’s ADEM was severe enough to cause lasting, residual damage, and retarded his developmental progress, which fits under the generalized heading of Pervasive Developmental Delay, or PDD. Additionally, this chain of causation was not too remote, but was rather a proximate sequence of cause and effect leading inexorably from vaccination to Pervasive Developmental Delay.”

The decision is being announced so long after the fact because, under the rules of the vaccine court, after a special master decides that a plaintiff is entitled to compensation the parties (Bailey’s parents and the U.S. government, the defendant) must negotiate a settlement, Michael McLaren, the Banks’s lawyer, told me Tuesday evening. That required determining what Bailey would need for his care for the rest of his life—less now, when he is living with his parents and attending a school for autistic children, but more later, when he is on his own. The government agreed to a lump sum of $750,000, and an annuity that will provide as much as $70,000 to $100,000 a year for Bailey once his parents are not able to care for him.

It was only in 2004 that scientists led by Michael Meaney of McGill University reported an intriguing study in which the on-off switches on the DNA of baby rats were set by their mother’s behavior. Specifically, they reported, when mother rats licked and groomed their pups, the gene that turns up production of the brain’s glucocorticoid receptor worked at full steam. But when the rat moms were neglectful, the promoter gene was silenced. Result: fewer receptors, and a hair-trigger response to stress. These neglected rats grew up to be fearful, neurotic messes because this gene had a silencer sitting on it.

Ever since that study, the obvious question has hung in the air: Are people like rats? Do childhood experiences re-set the genome, turning some genes on and others off, or turning some to “high production” and some to “low”?

Meany and his team are back with a fascinating new study, in the online edition of Nature Neuroscience, that answers yes. Early childhood abuse can change the expression of the same gene as in rats—the glucocorticoid receptor, which shapes how people respond to stress.

The scientists found that in the brains of people who committed suicide and who had been abused as children, the glucocorticoid receptor gene was dialed way down. It was producing fewer receptors (which are proteins) than was the same gene in suicide victims who had not been abused as children. Even more impressive, the scientists discovered the reason for the low rate of production: a stretch of DNA that acts as a rheostat on the receptor gene (in genetics parlance, the rheostat is a promoter region) had had a silencer slapped on it. The silencer is a methyl group, the exact same molecular entity that had silenced the receptor gene in the rats.

Such changes are called “epigenetic,” to distinguish them from changes that affect the sequence of nucleotides in DNA. Epigenetics is arguably the next frontier in genetic research, promising to show why people with identical DNA, such as monozygotic twins, have different traits, including traits known to be strongly affected by genes. The answer seems to be that the events of our lives, including parental behavior, turns some genes on and some genes off. In this case, parental care (or, specifically, abuse) changed the expression of the crucial glucocorticoid-receptor gene in the brain.

When I met Meaney at a 2004 conference that got neuroscientists together with the Dalai Lama, he was truly eloquent about the import of such research, as I tried to convey in my last book. For too long we have been in the grip of genetic determinism, the idea that the genes we enter the world with shape the lives we lead, that genes have behavior on a short leash. But as Meaney pointed out, that is not only defeatist—ceding responsibility for who we are and how we act to forces beyond our control—but scientifically wrong. The lives we lead reach into the very double helices of our cells.

Sometimes it takes an SOB to get anything accomplished, especially against steep odds, and the battle to protect children from lead was especially uphill. Anyone who cares about children’s brains—for lead is a potent neurotoxin—can therefore thank two men who were arrogant, abrasive, and uncharitable with colleagues who did not see things their way. One of them, geochemist Clair Patterson of Caltech, was well known for insisting he was right, and for pointing out to others in great detail all of the mistakes and limitations in their work. The other, psychiatrist/epidemiologist Herbert Needleman of the University of Pittsburgh, was impatient, passionate about his science and social justice, and inclined to divide the world into those who were with him and those who were not, and not to waste much effort trying to get along with the latter.

With protagonists like this, a new book by journalist (and my former Newsweek colleague) Lydia Denworth called Toxic Truth, reaching bookstores next week, manages to do something else that has steep odds against it: make the process of scientific research riveting. She chronicles the fight to prove that lead in the environment was poisoning children’s developing brains, and then the fight to reduce lead exposure. While the latter struggle still goes on, the former was won in the 1970s thanks to Patterson and Needleman. It’s sort of a dual biography, tracing the two men’s scientific careers and discoveries, and recounting the political skirmishes and controversies that embroiled them.

Patterson’s early research sought to determine the age of the earth, using lead isotope ratios in ancient rocks. (He is credited with discovering, in 1953, the age of Earth, 4.55 billion years.) His success was based on the ability to measure, very accurately, tiny differences in the amounts of different isotopes. When his initial efforts to do that produced clearly erroneous results, Patterson discovered that everything in his laboratory—glassware, reagents, tabletops, floors, walls—was contaminated with lead, brought in with the air, itself contaminated with the exhaust of millions of cars burning leaded gasoline. Within a decade, he had amassed enough evidence to conclude that most of the lead in plants and animals—and about 99 percent of the lead in the human body—came from pollution. Increasing human exposure to lead 100-fold above natural background levels, he argued in 1965, could not be good for health.

This was not a message the lead industry or mainstream toxicologists wanted to hear. Although lead poisoning had been known since ancient times (it was thought to have contributed to the fall of Rome, where the wealthy and powerful drank wine stored in lead-lined casks, and drew water through lead pipes), most scientists in the 1960s insisted that the amounts of lead in our bodies were far too low to have any adverse effects. Industry spokesmen described the amounts of lead in Americans’ bodies as “normal, natural background levels.” The petroleum industry, which funded some of Patterson’s research, cut him off as soon as he pointed the finger at leaded gasoline as a health hazard. And the establishment lead research community dismissed his work. It threatened to overturn most of their own accepted wisdom, and nobody could replicate his findings—his techniques gave him a unique capability to see things others could not see.

Patterson, however, never doubted that he was correct, and he persisted—amassing a mountain of evidence that began to convince doubters.  Ironically, when he died in 1995, Patterson, long ignored by many of researchers and reviled by others as a “troublemaker,” was convinced he had failed; he did not know that within a few years his work would be accepted as incontrovertible fact, and cited as a basis for aggressive lead-control policies.

Needleman, working at Children’s Hospital in Philadelphia, was often consulted on cases where a patient had behavioral problems or learning disabilities. After encountering a few cases of lead poisoning among the clinic’s low-income patients, he began testing children’s blood for lead. He was astonished at the number who had high lead levels, which he realized were associated with poverty: old, run-down inner-city housing was filled with deteriorating lead paint, lead in soils from industries and auto exhaust, and old lead plumbing.

A 1979 study by Needleman and colleagues compared children’s performance on a dozen indices of learning and classroom behavior with the amounts of lead in their baby teeth. The results were striking: For each increment of lead exposure, performance on intelligence and learning-behavior tasks decreased. These were not children who had lead poisoning; they were normal kids, with no overt symptoms, with lead levels typical of kids in any urban area. Published in the New England Journal of Medicine in 1979, it suggested that, just as Patterson had speculated 14 years earlier, we were all adversely affected by lead, at least when we were young, and even the “normal” levels of lead in our industrialized environment could damage the developing brain.

The lead industry and its friends reacted as you'd expect. They attacked the study on scientific grounds, questioning its methodology and demanding that it not be accepted as valid until replicated by others. (Sound familiar? See phthalates, bisphenol A, . . . ) But within a few years, the results were confirmed by different teams in other countries, and ultimately more than a dozen studies would support Needleman’s observations.

But controversy persisted. When the U.S. EPA cited Needleman’s work as a basis for its phase-out of lead in gasoline, in 1983, the lead industry and a scientist named Claire Ernhart challenged Needleman’s study, arguing that its data did not support its conclusions. The EPA sponsored an independent re-analysis of the data, which reaffirmed the original conclusions.

But still it didn’t stop. In 1992, Ernhart and a colleague accused Needleman of scientific misconduct, claiming he had manipulated data and falsified results in his 1979 paper. A hearing was held at the University of Pittsburgh (where Needleman worked at the time), and he was found not to have engaged in misconduct. Still, his critics would not let go. They filed a formal complaint with the federal Office of Research Integrity alleging scientific misconduct. Again, after an extensive investigation, Needleman was cleared.

It was a long battle, but lead was phased out of gasoline, lead-soldered food cans were replaced with lead-free containers, and steps were taken to reduce lead in drinking water. The use of lead in new paint was banned, although old lead paint still remains in place in millions of older homes. The average American’s exposure to lead is now at least 95 percent lower than the 1960s “normal,” and the number of children with elevated blood lead levels has been markedly reduced. The problem has not been totally solved, but it has been shrunken and contained, and Denworth’s fascinating historical, biographical, scientific and political saga shows how we got even this far. She suggests, too, that what happened with lead has happened again and again—initial scientific discoveries suggesting a hazard are challenged by industry or skeptical researchers. PR techniques are used to discredit their research, and denial dominates the official response until the evidence is overwhelming. Even then, action is taken only grudgingly, with great deference to avoid “unacceptable” economic impacts.

Pick your poison—phthalates in toys, methylmercury in fish, pesticide residues in foods, carbon dioxide and climate change, the list goes on—and the pattern looks familiar. The amazing thing is that industry gets away with it time and again. As Santayana said, those who forget the lessons of history are condemned to repeat it.

Full confession: after the concerns raised by scientists about brain imaging, which I’ve written about here before as well as in the paper magazine, I don’t think I’ll ever look at an fMRI study the same way again. I hope I was properly skeptical about such studies before MIT's Ed Vul and colleagues showed how many of these emperors have no clothes, but now whenever a neuroimaging study crosses my desk I wonder, does it fall into the same statistical trap that so many others have, rendering the results meaningless?

So it is with what would otherwise be a perfectly interesting little study being published tomorrow in Science. It’s about envy and schadenfreude, taking pleasure from someone else’s pain, that feeling of glee we get when someone we envy suffers a setback (cf. Bernie Madoff, Wall Street bankers . . . ). The study, described in paper called “When Your Gain Is My Pain and Your Pain Is My Gain: Neural Correlates of Envy and Schadenfreude,” was led by Hidehiko Takahashi of Japan’s National Institute of Radiological Sciences, who is one of the most prolific social neuroscience imagers around (for a sampling, see here and here. Like a 2003 study finding that the psychological pain of social rejection increases activity in the same brain regions that process physical pain, this one concludes that the social and the physical are closely related. In brief, brain regions that respond to feelings of envy and schadenfreude are also those that respond to, respectively, physical pain (envy hurts) and reward/pleasure (schadenfreude feels good).

Takahashi and colleagues ran two fMRI studies on 19 volunteers. Feelings of envy (triggered by reading about a peer's status, abilities and wealth), led to heightened activity in the dorsal anterior cingulate cortex (dACC), the same region associated with the distressing aspect of physical pain. Schadenfreude (triggered by reading about the downfall of the envied person) was linked to extra activity in the ventral striatum, which processes reward.

I can hear many of you saying “so what? why shouldn’t the brain use the same circuitry to process physical pain and social pain, and physical pleasure/reward and social pleasure/reward?” At least one eminent neuroscientist is in this camp. The fact that there is heightened activity in the dACC when people felt envy “seems utterly uninformative even if true,” she said by email. “The ACC activates for nearly everything. Presumably it would also activate for any other strong emotion, not to mention cognitive effort. So who cares that it activates when you experience envy? This tells us nothing about envy and nothing about the ACC.”

In an accompanying “Perspective” in Science, UCLA’s Matthew Lieberman and Naomi Eisenberger take the opposite view, praising the significance of the study. The finding that “emotional responses to these psychological events rely on much of the same neural circuitry that underlies the simplest physical pains and pleasures” is significant and surprising, they argue. (They themselves found, in the 2003 paper I cite above, that being socially excluded raises activity in the dACC and insula, with more activity associated with feelings of greater social pain.) “Such findings suggest that the brain may treat abstract social experiences and concrete physical experiences as more similar than is generally assumed,” they write.

They offer a provocative hypothesis for how that shared circuitry for the physical and the social might have evolved, or, as they phrase the question, “Given that physical needs intuitively seem more critical to survival than social needs, why would the brain have evolved to treat them as motivationally similar?” One possibility: since newborns are totally dependent on others, “for both caregiver and infant to feel pain upon separation ensures social connection and thus offspring survival. In a sense, for mammalian infants, social needs take precedence over physical needs because meeting the social needs is what allows the physical needs to be met as well.” And after childhood, they suggest, “Being fair, cooperative, or charitable may increase the survival of the group . . . Thus, evolutionary pressures may have created internal mechanisms that register being socially cooperative as pleasurable and being ostracized as painful in order to promote the maintenance of group bonds and ensure survival.”

That just-so story may well be correct, and so might the claim of the Takahashi paper. The point the critics of neuroimaging make is that one just cannot tell from its methodology and statistical analysis. I asked scientists who were not involved in the study to take a look at it and tell me whether they thought it fell into the same methodological traps that had tripped up other fMRI studies. One key step in the analysis of the raw fMRI data, said one neuroscientist, “is unambiguously and definitively bullshit. Many of the claims in the paper are statistically suspect. Remember, this does not mean that the conclusion of the paper is wrong, simply that the data don’t provide evidence for that conclusion.”

Science received the Takahashi paper last September 8, and accepted it (after the usual peer review) on December 10. That was about three weeks before the Vul et al. criticism was widely known. I wondered whether the editors took the new concerns into account when deciding whether or not to run the paper, perhaps asking for another round of peer review in light of it. Unfortunately, none of the editors who were involved in the review and acceptance process were willing to talk to me. Instead, the journal’s spokesperson sent me this email:

“On behalf of Science, the Science press office is unable to comment on the Editorial peer review process, which is confidential. However, in general we make sure that our peer reviewers are up to date on relevant current issues regarding the papers they evaluate for us. In this case, as for all Science papers, the peer review process was rigorous and the journal took seriously any questions raised about the validity of the conclusions in the paper.”

It’s too bad the editors are unwilling to address the criticism directly, because Vul et al. call out Science and Nature as among the worst actors in the publication of problematic neuroimaging papers. If those journals believe the criticism is bunk, they should say so. But to pretend it doesn’t exist, or that eminent neuroscientists and statisticians with no axe to grind are taking the criticisms seriously, is ignoring the elephant in the room.

Update: I was remiss in not factoring in the 14-hour time difference when I emailed Dr. Takahashi asking him to respond to the criticisms of his paper. But, in the better-late-than-never spirit, let me include his response here:

"We believe Vul’s paper is misleading and their assumption was wrong. These will be rebutted in peer-reviewed journal from many researchers. . . . Our Science paper is not the case with the points they criticized (false correlations, non-independent tests). I believe that Science editors might clearly understand the potential pitfalls Vul et al pointed out. In other words, the editors might understand our paper [does not make these errors]."

Before we get all excited about a potential urine test for prostate cancer, which is being reported tomorrow in the journal Nature, it’s worth remembering how littered the medical landscape is with promising early-detection tests that bombed. The biggest problem: if you want to do large-scale, population-wide screening, your test better be close to 100% specific (that is, not detect cancers that aren’t there). If you have even 1% false positives in a test that 25 million people take every year (25 million is how many men undergo PSA testing for prostate cancer), that’s 250,000 people you’re sending to have biopsies that will in most cases find nothing . . . and worrying those patients sick for no reason.

It’s way too early to tell if the test suggested by the new study would clear this hurdle. In the study, scientists led by Christopher Beecher and Arul Chinnaiyan of the University of Michigan describe how a molecule called sarcosine, which can be identified in urine, might act as an indicator of the progression and spread of prostate cancer (it doesn’t seem as promising as a tool to detect the simple presence of cancer as opposed to its invasiveness—that is, sarcosine seems to be better for prognosis, not diagnosis). The scientists compared molecules in the urine of 59 prostate cancer patients to those in the urine of 51 healthy men. They found that levels of sarcosine, a derivative of the amino acid glycine, were higher in the urine of patients with aggressive prostate cancer. And in healthy prostate cells growing in lab dishes, sarcosine made the cells extremely mobile (enough to push into a blob of gelatine), a trait characteristic of cancerous cells. That's strong evidence that the link between invasive prostate cancer and the presence of sarcosine is not just a coincidence.

The test obviously needs to be validated to determine its rate of false positives (yelling “prostate cancer” when none is present) and false negatives (failing to find prostate cancer when it is there). Still, the result is notable for being the first time a marker for prostate cancer has been detected in urine. As things now stand, prostate cancer can be detected by the PSA test or by biopsy, but the latter is invasive and sometimes painful, while the former is such a mess physicians hardly know what to make of readings any more. PSA tests do not even reduce mortality. Clearly, we need something better.

That's unlikely to be genetic tests, even though they hog the spotlight when it comes to early detection. Genetic tests give probabilistic answers. That is, except for single-gene disorders such as Huntington’s, which affect only 1 percent of the population, the answer to “does having this ‘disease gene’ mean I will get breast cancer/colon cancer/heart disease/schizophrenia . . . .” is: maybe. Carrying the mutated form of BRCA1, for instance, confers a risk of eventually developing breast cancer of 50 percent to 80 percent. A better solution would be a test that led to very early detection of disease, rather than one that shows your odds of getting something.

Enter biomarkers like sarcosine. These are, usually, proteins in the blood or urine whose presence means not that you have some probability of developing the disease but that you actually have it, now—but at a much earlier stage than x-rays or other tests can divine. I have written before about a company called Biophysical that offers a battery of tests to detect 250 such biomarkers in blood. The approach has yet to catch on, though some boutique providers offer the Biophysical test. Whether prostate cancer cells or any other kind of malignant cells betray their presence in urine or blood in a way that can--or should--find widespread clinical application remains to be seen.

If you are the kind of aquarium goer who can’t help touching the glass in hopes of petting a fish, then if you see Under the Sea 3D at an Imax Theatre you should definitely sit on your hands: thanks to the 3D effect, green sea turtles, cuttlefish, sea lions, leafy sea dragons and other denizens of the Coral Triangle (around Papua New Guinea and Indonesia) and the Great Barrier Reef seem to swim just inches in front of your hands. The children at the screening I attended this past weekend were grabbing for fish in the air more than they were reaching into their popcorn.

The 40-minute film, which opens this Friday at IMAX theatres around the country as well as overseas (click around here to find one near you), seems to bring coral reefs and the animals that call them home within arm’s reach and with a clarity you are unlikely to find without scuba gear. Giant cuttlefish hunt a crab and, later, mate face to face in a prim little waltz; garden eels sway from (and pop straight down into) the sandy sea floor; a crocodile fish lunges directly at you in pursuit of a blue chromis. Filmmaker Howard Hall’s production journal, describing five month-long shoots at five sites, is an epic in itself. I’m not sure how much of the environmental message comes through—the danger that global warming poses to coral reefs through bleaching and the acidification of the ocean—and listening to Jim Carrey’s narration kept me tensed for when he might let loose (he never did), but it’s a spectacular look at a world that may soon exist only on film and in aquariums.

Is your job to detect side-effects of a new experimental drug, scrutinize manufactured parts for defects or something else that requires close attention to detail? Then you might want to pick red chairs, curtains and carpet for your work space. Ditto if you're a student studying for a test: find a room with lots of red. Is your job to brainstorm new product designs, dream up ad campaigns and do something similarly creative? Paint the walls blue. And if you're a student who has to write a paper or poem for this weekend's homework, plan on doing it in a room with lots of blue.

That color affects the way we think is obvious to anyone who has been totally unproductive in a chartreuse room. But for a long time researchers came up with conflicting findings on the precise cognitive effects of being surrounded by particular colors, with some suggesting that red enhances cognitive task performance compared with blue or green, as this study and this one did; others have shown the opposite, finding that blue or green enhance thinking.

Ravi Mehta and Rui (Juliet) Zhu of the University of British Columbia had the bright idea that both sets of findings could be true—that is, either red or blue could boost thinking, but different forms of thinking. In a paper published today in Science, that’s what they report finding. Because of its associations with danger (alert levels), stopping (road signs), mistakes (wrong answers circled in red) and the like, red should induce what psychologists call “avoidance motivation,” meaning people become vigilant and try to avoid risks; that should make them excel on detail-oriented tasks that require careful, focused attention. But blue, associated with openness (the sky), peace, and tranquility (the sea), should induce “approach motivation,” which should make people feel freer to take more risks and explore more—perfect for creativity.

In six studies, the researchers indeed found that exposing people to red or blue (on the background of computer screens) affected different mental abilities differently. When volunteers did a memory exercise, trying to recall 36 words on a list they studied for 2 minutes, those who did it on a red background recalled more correct items than those who did the exercise on a blue background, supporting the idea that red makes people vigilant and detail-oriented. When volunteers were asked to think of as many creative uses for a brick as they could within 1 minute, the color of the screen background had no effect on the total number of uses they came up with, but volunteers who saw a blue background got higher creativity scores from judges (who didn’t know who had which background color). Other tests pointed to the same conclusion: “red led to superior performances on detail-oriented tasks and blue, on creative tasks,” the researchers write.

The findings have obvious implications for real life, such as what color to paint walls in a classroom or lab and what color to use in different business settings. “If the task on hand requires people’s vigilant attention (e.g. memorizing important information or understanding the side effects of a new drug), then red . . . might be particularly appropriate," the researchers write. "However, if the task calls for creativity and imagination (e.g., designing an art shop, or a new product idea brainstorming session), then blue . . . would be more beneficial.”

I'm spending the rest of today picking out paint swatches.

Jason Bourke/Nature Press Group

To support a cold-blooded body of that size, estimate scientists led by paleobotanist Carlos Jaramillo of the Smithsonian Tropical Research Institute and paleontologist Jason Head of the University of Toronto, its tropical home would have had to have a minimum mean annual temperature of 30 to 34 degrees Celsius (86 to 93 degrees Fahrenheit), way hotter than today’s tropics. That calls into question the longstanding belief that the planet has a thermostat that keeps tropical temps in check. As they describe in tomorrow’s issue of Nature, it has long been known that there is a rough correlation between an era’s temperature and the size of its cold-blooded animals: warmer temps, bigger beasts. But the average temperature at which the giant snake thrived was 5 degrees warmer than the maximum for tropical rainforests today.

If tropical temps 60 million years ago were really that high, it undercuts the idea that the planet has a thermostat that keeps a tight lid on them. That’s important for three reasons, climatologist Matthew Huber of Purdue University points out in an accompanying article. The tropics, from 30° N to 30° S, make up half of Earth’s surface area and therefore strongly influence the sensitivity of global temperatures to greenhouse-gas concentrations and other climate-altering forcing. Also, the tropics have long been considered “stable, safe havens for fauna and flora compared with the more variable high latitudes,” says Huber; if their temperature can soar, they might not be such safe arks in a greenhouse world after all. Finally, temperature gradients drive atmospheric circulation, so a super-hot tropics would alter the general circulation.

Using snake size to infer temperatures is novel, to say the least, and might be wrong. But if the claims are right, says Huber, “there is no tropical thermostat: although negative feedbacks may slow or inhibit tropical warming, they do not provide a hard limit, and theories that predict the existence of thermostats are invalid.”

Among the things that scientists don’t like is having their grant proposal denied, having their papers rejected by eminent journals, and not getting tenure. Among the things they really, really hate (based on the comments I got on my column last month on Lamarckian inheritance) is for a science writer to describe studies that show that the Modern Synthesis (the marriage of Mendelian genetics and Darwinian natural selection acting on random variation, which forms the basis of evolutionary biology) is not the last word. “Why is a creationist writing for Newsweek??!!” and “there is no evidence of Lamarckism!!!” were among the more polite comments.

So it pains me to have to take note of a new study that describes—and here I’ll just quote from the abstract—how “qualities acquired from experience can be transmitted to future offspring,” and documents “non-Mendelian transgenerational inheritance” and a “‘Lamarckian’-like phenomenon.” In short, what scientists led by Larry Feig of Tufts University are reporting today in The Journal of Neuroscience is that when adolescent mice are exposed to an environment that improves the ability of brain neurons to communicate with one another and, as a result, improves their ability to learn and remember, that enhancement is transmitted to unborn offspring—offspring that never experienced the brain-boosting environment, that were not even conceived at the time their mothers did, and that are not even raised by the learning-enhanced mothers.

Might a similar effect occur in people? No one knows. But if it does, conclude the scientists, “the effectiveness of one’s memory during adolescence . . . can be influenced by environmental stimulation experienced by one’s mother during her youth.”

This result is so remarkable that the usual caveat—the study must be replicated by an independent lab—needs to be underlined. You get a sense that the scientists themselves are astonished by what they found, for they sprinkle their paper with words like “remarkably” and “dramatically.” “When we first got the results I didn’t believe them,” Feig told me.

Here’s what he and his team did. They built on the well-established finding that when lab rodents are raised in an “enriched” environment, filled with toys and other animals and an opportunity to exercise, it enhances their learning and memory, promotes neuronal changes such as the dendritic branching and synapse formation that underlie cognition, and even stimulates neurogenesis. In 2006, Feig and colleagues showed that an enriched environment can overcome the effects of a genetic defect that otherwise impairs learning. What seems to happen, says Feig, is that a secondary pathway supporting neuronal communication is turned on, sort of like when surgeons bypass a blood vessel. Now he and his team have gone further.

They housed adolescent mice (15 days old) in an enriched environment (plastic play tubes, cardboard boxes, running wheel, toys, friends—all rearranged every other day to keep it interesting) for two weeks. In the mice with mutations that impair memory (the underlying deficit is in the cellular process called long-term potentiation), the experience repaired the defect that kept brain neurons from communicating well, as Feig and his colleagues had previously found. But when the mice grew up, mated and had pups, the pups of the mutant/memory-impaired mice (the pups also carried the mutation) seemed to have benefited from their mothers’ acquired trait: their brain neurons’ communication capacity was as good as that of normal mice. As a result, they learned and remembered better: after experiencing an electric shock delivered through the floor of their cage, next time they entered the cage they froze, recalling the unpleasant experience. (The pups of normal mice that experienced the enriched environment had improved levels of neuron communication as well, but showed no improvement in their memory capabilities, at least as measured by the shock test.)

Just to reiterate: the offspring still had the genetic defect that impairs memory. They never experienced the brain-boosting enriched environment. But their mothers’ experience of that environment—an experience the mothers had before the pups had even been conceived—repaired the biochemical glitch that the mutation causes and that impairs memory. “Transgenerational inheritance of the effect of enriched environment,” write the scientists, “occurs before birth. . . . Enrichment can restore . . . a genetically-induced memory defect in both mice directly exposed to an enriched environment and, more remarkably, in their future offspring.”

To be sure that the pups’ improved memory was not the result of better nurturing by mothers whose own brains had been improved by the enriched environment, the scientists had foster mothers raise the pups. The foster mothers had never experienced the enriched environment. Yet the pups still had improved brains. “The effect lasted until adolescence, when it waned, suggesting that this process is designed specifically to aid the young brain,” said co-author Shaomin Li, who is now at Brigham and Women’s Hospital.

And why do the scientists describe this as the inheritance of acquired traits, or Lamarckism? Because the mothers-to-be acquired a change in their genome as a result of an experience in the environment (a cage filled with goodies). That change was transmitted to—inherited by—their pups. The scientists don’t yet know what molecular mechanism achieve this magic, but Feig was willing to speculate about how it evolved: “We hypothesize that this evolved to let mothers pass on a signaling pathway that was turned on by the enriched environment, in case the pups were not themselves exposed to that environment.”

There’s an interesting historical footnote to all this. A 1985 paper reported that when pregnant rats are exposed to an enriched environment, their pups are better at learning mazes. And a 1987 paper found that rat pups of moms exposed to an enriched environment before pregnancy “inherit” mom’s exploratory behavior and learning ability. Those studies, while occasionally cited, were so far ahead of their time that they essentially were lost to science. “People thought, how could this possibly be so?” Feig said.

This study is the first to show that genetic defects in neuronal transmission and hence memory, caused by a mutation, can be at least partly reversed by an experience a mother has long before she is pregnant. Might this happen in people? Obviously it is way too soon to speculate, so let me leave it at this: the reflexive antipathy of many biologists to the possibility of Lamarckian inheritance reflects badly on the scientific community’s reputation for openness to new ideas and to data that challenge existing ones.

The science of cloning and stem cells has been somewhat of an unholy mess, what with fraudulent claims (by a South Korean biologist) of generating custom-made stem cells lines and, sigh, of producing a baby through cloning. (The little cloned boy should be 5 now; we wish him well in kindergarten.) The latest advance therefore shouldn’t inspire headlines about cloned babies being right around the corner, but here goes: scientists have transferred DNA from an adult human cell into a human egg, and gotten the egg to “reprogram” the donor DNA back to its embryonic state, producing a pattern of gene activation like that in normal IVF embryos--and therefore, it seems, the pattern necessary to create an embryo.

What this means, in a nutshell, is that if the study holds up, it will look increasingly likely that there are no known technical obstacles to reproductive cloning, the creation of human clones not for stem cells (in which case the clone never gets further than a days-old ball of cells) but for babies.

Scientists led by Robert Lanza, chief scientific officer of the biotech company Advanced Cell Technology, have no such goal in mind. They just wanted to see whether putting adult human DNA into (non-human) animal eggs would send the DNA back in time, so to speak, to its embryonic stage. Such “reprogramming” could, in theory, produce a days-old ball of cells from which scientists could extract stem cells that, with some coaxing, could be used to treat patients with diabetes, spinal cord injury, Parkinson’s disease and other ailments. If the DNA came from the patient himself, the stem cells would be perfect and personalized genetic matches, eliminating the risk that they would be rejected by the recipient's immune system.

The reason human DNA would be put into animal eggs rather than human eggs is that the latter are hard to get. Harvard’s Kevin Eggan, for one, has described “stomping around to different disease advocacy groups, tea circles, knitting circles, trying to find anyone and everyone who would donate their oocytes,” to little avail. The new study throws cold water on the hope of using animal ova.

The scientists used standard methods to transfer DNA from adult human cells into ova (human, cow and rabbit) whose own DNA had been sucked out. All three kinds of ova yielded about the same success rate in getting the ovum to divide like a fertilized egg  (39%, 36% and 36%, respectively, formed balls of 12 to 32 cells). But when the scientists tested these embryos to see which genes were active, they found a stark difference. The pattern “was dramatically different” in embryos created from human ova and from cow or rabbit ova, they report online ahead of print in the journal Cloning and Stem Cells. The human-human clones had gene activity patterns that matched those of normal embryos created at IVF clinics—that is, they seemed to follow the recipe for baby making in that the adult donor DNA had been reprogrammed back to an embryonic state. The human-animal hybrids had a different pattern, Lanza told me: “The donor DNA just wasn’t being reprogrammed.”

Several key genes were activated in the human-human clones but not the human-animal ones. Called Oct-4, Sox-2 and nanog, they seem to be the keys to directing the entire genome to revert to the embryonic state necessary to create both stem cells and babies. Called pluripotency genes, they had been “effectively silenced” in the human-animal hybrids, said Lanza, making it impossible for the hybrid to produce stem cells. “These data call into question the potential use of [animal ova] to generate patient-specific stem cells,” the scientists conclude.

Now about those human embryos. There have been several previous claims (such as one in 2001, by a team that included Lanza, and one last year by a company in California called Stemagen). But although some of the balls of cells looked normal (others did not), there was no molecular evidence that the donor DNA had been reprogrammed back to an embryonic state. In the new study, gene chips that test for DNA expression confirmed that the donor DNA had been reprogrammed to a state “very similar to normal IVF embryos,” said Lanza. “This is the first real evidence that the donor DNA is reprogrammed, and the first time anyone has furnished hard evidence that human cloning is indeed possible, at least in terms of proving that the donor human cell was actually reprogrammed.”

Ian Wilmut, who led the team that cloned Dolly the sheep in 1997, the first mammalian clone, is now director of the MRC Centre for Regenerative Medicine at the University of Edinburgh. He told me in an email that the study underlines “an important difference in gene expression from transferred human nuclei depending upon whether they were transferred into a human oocyte or a non-human oocyte.” Although it does not “absolutely rule out the use of animal oocytes, . . . the balance of probability is that transfer into human oocytes is more likely to work” for generating therapeutic stem cells.

I had no intention of revisiting the debate over the use of brain imaging in social neuroscience, which I blogged about last month. But that post brought such a tsumani of anger, dismay, invective and outrage that I felt an obligation to go back and dig more deeply into whether the charges in a paper by Ed Vul of MIT, Hal Pashler of UC San Diego and colleagues that is in press at Perspectives on Psychological Science were as meritless as many of the scientists I heard from claimed.

The basic criticism of Vul et al rests on statistics, so I sought out eminent statisticians who have no horse in this race. I had room to cite only two of them in my magazine column this week, but there were no dissenting voices: some studies that use fMRI to correlate patterns of brain activity with some measure of emotion, thought or other psychological trait/behavior of interest to social neuroscience are indeed problematic. For a good discussion, I recommend a post by Andrew Gelman, professor of statistics and of political science and director of the Applied Statistics Center at Columbia University.

But the targets of the criticism also make legitimate points. They're right that calling anyone’s science “voodoo” (in the title of the Vul et al paper) is not very nice or conducive to constructive dialogue. And as they say, social neuroscience is not the only field that uses functional neuroimaging in a way that has problematic stats.

Neither of these points gets to the heart of the criticism, however. Even a response prepared by Matthew Lieberman of UCLA and colleagues, while viewed as the best of the bunch by the statisticians and neuroscientists who were kind enough to read it for me, doesn’t answer all the concerns Vul et al. raised. As Lieberman told me, “What we’re fundamentally interested in is whether there are these relationships [between a pattern of brain activity and a psychological measure] at all. The initial test [looking for patterns that correlate with these measures] tells you there are regions of the brain worth interrogating.” Once scientists do that initial pass, he argues, those who know what they’re doing apply the proper controls and methods of statistical analysis to make sure their subsequent scans are independent of the first. The problem, say other scientists with extensive experience in neuroimaging (and in reading neuroimaging papers), is that “what he describes as good statistical practice doesn’t occur in a lot of these papers,” as one researcher (who doesn’t want to antagonize colleagues more than he already has) told me.

Failure to do the stats properly is the main problem identified by Vul et al. Alas, some experienced practitioners of neuroimaging concede that their field is indeed beset by the “circularity” the imaging critics identified, Nikolaus Kriegeskorte of NIMH told me. “In extreme cases, the effect [in which a pattern of brain activity is correlated with a behavior, feeling, etc.] doesn’t exist at all, and what you are reporting is just noise. Because we have so much data and selection is inevitable, neuroscience is faced with the challenge of avoiding the bias that can come with data selection.” That problem is not unique to imaging, I hasten to add: EEGs and invasive recording have it, too. “It is not a new problem, and there are techniques to avoid it,” Kriegeskorte said.

“Things can do wrong, but how wrong?” he continued. “Our sense is, a whole range of things can happen, from a slight distortion [in the strength of correlations] to entirely spurious results. Some papers do not deal with it well, and are based on incorrect statistics. Whether the central conclusions are wrong cannot be determined without redoing or at least reanalyzing the experiment. Vul et al. have the central point right, but they were unnecessarily inflammatory and their estimate of how much [reported correlations have been inflated] might be too high. But reported correlations are almost certainly higher than they should be.”

The reason that matters is that brain imaging is increasingly being usd not for pure discovery and hypothesis testing, as UCLA’s Lieberman rightly explains, but for real-world uses with potentially worrisome implications, as I explain in my column this week.

So how can laymen, not to mention science journalists, separate good studies from questionable ones? Not easily. Even when we play by the rules and report only studies that have been peer-reviewed and published, it turns out, we can't be assured that the study found what it claims to: some of the most problematic studies ID'd by Vul et al. are in eminent journals. But speaking for myself, when I write about neuroimaging studies in the future I will ask a lot more, and harder, questions about the method of analysis than I have in the past.