The unveiling of James Watson's complete genome came off as planned this morning. As I wrote in this week's issue of NEWSWEEK,  Watson, who with Francis Crick discovered in 1953 that DNA is shaped like a double helix, volunteered to have his DNA sequenced by the biotech company 454 Life Sciences. But more than that, he agreed to have the sequence posted in a government database for all to see--making him the first person to share his personal genome with the world.

Watson was quite eloquent at the press conference announcing the genome. He has been extremely reluctant in the past to talk about the mental illness that afflicts his son Rufus, who has a form of schizophrenia. But this morning Watson talked about how if he and his wife had known  about any genes related to mental illness that Rufus carries, they would have been better able to understand the travails and limitations he would encounter in his life. In my print story, I raised the concern that this kind of fatalism--if you carry a gene "for" some trait or disease you will definitely have that trait or disease and there's nothing you can do about it---is biologically misplaced. That's because geneticists are learning more and more about how simply having a gene does not mean you'll express the trait that the gene codes for. It's like having a tune on your iPod: just because you have it doesn't mean you'll play it. Similarly, just because you have a gene doesn't mean it will be expressed; some genes are silenced, others are modified by neighboring genes. If we all start believing that carrying a gene "for" cancer or heart disease or mental illness or some personality trait determines our fate, it seems to me, that's a recipe for giving up--on ourselves and our children.

There is no polite way to say this: people who resist scientific explanations for natural phenomena such as the age of the earth and the fact of evolution are guilty of childish thinking.

So argue two experts in cognitive and developmental psychology, the science of how thinking and other mental functions change as people grow up. “Resistance to certain scientific ideas,” Paul Bloom and Deena Skolnick Weisberg of Yale University argue in the May 18 issue of the journal Science, is largely a result of patterns of thinking that are characteristic of young children but which, in some people, “persist into adulthood.”

Scientists bemoan the huge numbers (42 percent, in a 2005 poll) of Americans—and this does seem to be more an American phenomenon than a European or east Asian one—who believe that humans and all other animals have existed in their current form since their first appearance on Earth, despite fossil and genetic evidence showing that, to the contrary, species change over time in the process of evolution. Tens of millions believe—again, contrary to scientific evidence—that unproved medical therapies work, that out-of-body experiences are real (rather than results of particular brain activity), and that astrology has merit, for instance. But if you look at what children think and how they learn, the resistance to science and the persistence of unscientific thinking doesn’t look so surprising.

We come into the world with preconceived ideas about how that world works; like a computer, we’re pre-loaded with some programs and knowledge. Babies know that objects fall unless held up, for instance (scientists test for this knowledge by noting what surprises babies, and an object defying the law of gravity definitely does). Little kids know that people act according to goals. They believe that actions and situations have purposes.

Are males necessary? Not if you’re an aquatic snail, a crayfish, a python or a host of other species of insects, crustaceans and reptiles. In every major group of vertebrates and many invertebrates, females occasionally or always manage to reproduce without an assist from males—every major group except, that is, mammals and so-called cartilaginous fish, which include sharks. Now the roster of animals able to produce offspring by virgin birth has a new addition. According to a genetic analysis released this week, a bonnethead (a small species of hammerhead shark) born in December 2001 at a Nebraska aquarium contained only female DNA. Her mother was her father, too, so to speak.

In 1861 Charles Darwin wrote, “We do not even in the least know the final cause of sexuality; why new beings should be produced by the union of the two sexual elements, instead of by a process of parthenogenesis.” Ever since, biologists have been asking, who needs sex, anyway?

The standard answer has been that sex is nearly ubiquitous in both the plant and animal kingdom because it creates genetic diversity. When DNA from two parents mix it up inside a fertilized egg, the resulting offspring are more likely to have novel genetic combinations that will stand them in good stead in a variety of conditions (it’s like packing for a trip with snow boots as well as sandals—you never know what you’ll find out there). But there is a competing argument. Evolution is all about getting your genes into the next generation—the “selfish gene,” as British biologist Richard Dawkins called it. And what better way to do that than to get all your genes into your offspring rather than half of them, which is what happens when you let a mate contribute 50 percent of the DNA to junior? Offspring that come from just an egg, or perhaps two eggs, would be all Mom.

We're not making this any easier for ourselves. Like an already-overweight person who just keeps packing on the pounds--making his weight-loss goal even harder to achieve should he ever go on a diet--we're heading in the wrong direction if we want to avert a climate crisis caused by loading the atmosphere with carbon dioxide.

To stabilize the amount of carbon dioxide, we have to throttle back emissions radically, not merely slow the rate of increase. But we can't manage even the latter. During the 1990s, worldwide emissions of carbon dioxide (mostly from burning fossil fuels such as coal, oil and natural gas) increased at a rate of 1.1 percent per year. In other words, in the years right after the climate pact reached at the Rio "earth summit," we didn't exactly cover ourselves with glory. But it gets worse! Between 2000 and 2004, the rate increased to 3.1 percent per year, finds a study published this evening in the online edition of the Proceedings of the National Academy of Sciences.

What's in a name? Drug makers agonize over what to call their products--"Viagra" carries that bit of virility at the front, for instance, while "Lunesta" evokes the moon. The idea is to associate drugs with positive attributes as well as make them memorable. Looks like the companies know what they're doing: in a disturbing study from Canada, scientists find that names can strongly influence decisions patients make about treatment.

To investigate what role a name plays, scientists at McMaster University started out by showing volunteer patients information on the benefits and harms of various treatment options. It's well known that many patients suffer from "health illiteracy" "and inability to understand what their doctor tells them or the meaning of printed information that comes with prescription drugs. The McMaster team therefore set out to see whether the format of the information would make any difference in patients' understanding and decisions.

They compared a graphic presentation called a decision board, a decision booklet plus audiotape, and an interactive computer program, all displaying benefits and risks of three treatments for blood clots on a pie graph or pictogram. The treatment options were labeled "treatment A," "treatment B" and "treatment C." Patients' understanding of whether their condition was one the treatment was good for, and of the risks and benefits, all improved significantly with the board, booklet and computer program, with pie chart or pictogram. Virtually all (96 percent) of the participants said the decision aid helped them choose among the three treatments.

Then the scientists replaced A, B and C with the treatment's true name "warfarin, acetylsalicylic acid (aspirin) and "no treatment." Under these conditions, 36 percent of the patients changed their initial choice, including 46 percent of those who initially chose warfarin and 78 percent who initially chose no treatment, the scientists are reporting this evening in the Canadian Medical Association Journal.

Although they grasped the risks and benefits, that rational decision was trumped by the pull of the name, or the belief that no treatment (which is actually the best option in some cases) must be the worst choice. No wonder drug advertising is so effective.

Do fruit flies have free will?

If you find it hard to imagine how any such thing could be packed into a brain (hardly more than a tangle of neurons) that small, you are not alone. Scientists have basically viewed insects "as complex robots which only respond to external stimuli," says Björn Brembs of the Free University Berlin. Of course, lots of scientists think this about humans, too, viewing our brains as input-output devices responding to external stimuli, neurochemicals and earlier brain activity in a deterministic way that leaves no room for free will.

Among the "just-so stories" popular with scientists who seek genetic explanations of human behavior, few are so odious as the idea that males are genetically predisposed to kill their stepchildren.

The idea is that such behavior would have been adaptive for our Stone Age ancestors. Males who carried genes pushing them to kill their stepchildren, goes the theory, would have left more kids themselves because the murder would have freed up their new mate for, well, mating (a female nursing a small child is much less likely to conceive). Also, a Stone Age man who cared for and supported only his biological children, rather than stepkids, would leave more descendants than a man who cared for his stepchildren. Such murderous males would have left more descendants than males who tolerated, let alone supported, their stepchildren; we, their descendants, would therefore also carry the stepchildren-killing gene.

Thanks to the Dalai Lama, lots of monks have lent Richard Davidson their brains. For almost 20 years Davidson, a neuropsychologist at the University of Wisconsin, Madison, and a long-time meditator himself, has been curious about how Buddhist meditation of the kind the monks practice might change their brains. He has lugged electronic equipment up into the hills above Dharamsala (the Dalai Lama's home in exile in northern India) to test the brains of yogis, lamas and monks living in primitive huts there, and persuaded other monks to visit his lab.

Over the years he has found that the brains of monks who are the most experienced meditators are indeed different from other brains. They have a much stronger "gamma" wave, a form of electrical activity in the brain that is associated with consciousness and pulling together information and perceptions from different regions of the brain. They also have much greater activity in the left than the right prefrontal cortex (just behind the forehead), a mark of well-being and happiness.

But all of these studies came with an asterisk. There was no way to tell if the monks' brains started out different. That is, maybe people with high gamma-wave activity and lopsided left-prefrontal activity were more likely to become Buddhist monks. If so, then their brain traits caused them to become expert meditators, rather than their years of meditation changing their brain.

Now Davidson has taken a big step toward showing that the causal arrow really does point from meditation to brain changes rather than from brain differences to a life of meditation. Specifically, meditation can change brain circuits linked to attention.

The old dogma that the adult human brain cannot generate new neurons was overthrown almost 10 years ago, but a question persists: do those new neurons do any good?

In 1998 scientists led by Fred (Rusty) Gage of the Salk Institute for Biological Sciences discovered that older adults "well into their 50s, 60s and even 70s "continue to produce new neurons in their brains. Last November, a study found that as little as three hours a week of brisk walking increases blood flow to the brain and increases production of new neurons, researchers reported in the Journal of Gerontology: Medical Sciences. The same team, led by Arthur Kramer of the University of Illinois, had earlier shown that older adults who engage in physical activity have better working memory, are more adept at switching between mental tasks (a skill that generally declines with age), and are better able to screen out distractions (ditto) compared to people of the same age who did not get exercise training. The obvious question arose: is the reason exercise improves cognitive function in older adults that it boosts "neurogenesis," the production of new brain neurons?

Mitt Romney was clearly primed for the inevitable question about human embryonic stem-cell research. So when it was his turn in Thursday's debate among Republican presidential hopefuls, he pounced like a grad student taking his orals. MSNBC's Chris Matthews said that "Mrs. Reagan wants to expand federal funding of embryonic stem-cell research. Will that progress under your administration?" To which Romney replied, "It certainly will. Altered nuclear transfer, I think, is perhaps the best course." Matthews apparently had no idea what he was talking about--he seemed to think it was a form of adult stem-cell research, since he fired back, "embryonic; embryonic"--but Romney was ready: "Altered nuclear transfer creates embryolike cells that can be used for stem-cell research. In my view, that's the most promising source."

Leaving aside the "most promising" part, Romney got the science right. Altered nuclear transfer is the latest darling of those in the pro-life camp who have decided that "pro-life" might strike a discordant note if it means that people suffering from Parkinson's disease, spinal-cord injury and other diseases and conditions that might be treated with embryonic stem cells or with drugs derived from stem-cell research are left to suffer and die. By "latest," however, we mean at least two years old. It was in the spring of 2005 that bioethicist William Hurlbut of Stanford University made the case for "Altered Nuclear Transfer as a Morally Acceptable Means for the Procurement of Human Embryonic Stem Cells" in a paper in the academic journal Perspectives in Biology and Medicine; he laid out the same case before the President's Council on Bioethics in December 2004. What makes this technique "morally acceptable" to Hurlbut and others who believe that human life begins at conception and that the 16-cell blastocyst is a human being is that the ball of cells you create in the lab can never develop into a fetus.

If you are a 45-year old woman who weighs 140 pounds and stands 5 feet, 9 inches tall (in other words, several layer cakes away from obesity), with a blood pressure of 130/80, then you have a 70 percent greater risk of having a heart attack than if your blood pressure were below 120/70. If you are a 50-year-old man who weighs 180 pounds and stands 6 feet tall, with a blood pressure of 160/90, then your risk of heart attack is 130 percent greater--that is, 2.3 times as much--than if your blood pressure and weight were lower.

I mention these facts (you can calculate your own risk of heart attack, heart failure and stroke based on your sex, weight and blood pressure at the American Heart Association's nifty site) because of two new studies on genetic factors that raise the risk of heart disease. Two competing teams of researchers writing in the online issue of the journal Science both found a genetic variant that raises the risk of heart disease 15 to 20 percent in people who carry one copy of it (that is, they inherited the variant form mom or dad, but not both) and 50 percent in those who carry two copies of it (both mom's egg and dad's sperm carried the variant). The variant lies on chromosome 9. Neither team knows what exactly it does. They've ruled out the possibility that it acts through mechanisms known to raise the risk of heart disease, such as increasing blood pressure or bad cholesterol, but promoting atherosclerosis remains a possibility.

Just to emphasize those numbers: factors we already know about raise the risk of heart attack significantly more than these (still mysterious) new heart-risk genes. So why the fuss?

Oh, those hysteria-prone environmentalists, always exaggerating how bad things are going to get as a result of global warming. Or so the deniers would have you believe. They may want to rethink that attack in light of the most recent evidence that models of future climate are underplaying the extent of the coming crisis: projections by the Intergovernmental Panel on Climate Change (IPCC), composed of hundreds of scientists from around the world, have been falling short of reality when it comes to how quickly Arctic sea ice is melting.

According to the IPCC, the Arctic might have no summer sea ice as early as 2050, something that has not happened for about a million years. While that's bad news for the polar bears that use the ice as a hunting platform, and who are going to be in big trouble as sea ice keeps shrinking, it also has dire implications for those of us living thousands of miles to the south: when sea ice is replaced with open water for even a few weeks in September (usually the month with the least sea ice), it changes atmospheric wind patterns in a way that could throw a huge wrench in our weather. Sea ice has been shrinking since the middle of the 20^th century "at a rate, new research finds, some three times faster than predicted by the 18 climate models the IPCC uses. That means Arctic sea ice could vanish by 2020, not 2050.

The difference between models and reality seems to lie in the fact that models capture large-scale changes--but the melting of sea ice is also driven by small fluctuations in the temperature of the ocean and the thickness of ice, for example. When climatologists led by Julienne Stroeve of the National Snow and Ice Data Center at the University of Colorado, Boulder, compared IPCC projections to observations of melting sea ice made by satellites, ships and aircraft, they found a significant gap. The models forecast ice losses of 2.5 percent per decade from 1953 to 2006, but real-world observations documented a loss of 7.8 percent per decade, on average, they report in the online edition of the journal Geophysical Research Letters. The discrepancy seems to come about because the models understate how much warmth from temperate regions of the Atlantic Ocean and Bering Sea is carried into the Arctic. Whatever the explanation for the gap, those models constantly being criticized by climate deniers as Cassandra-ish are, in other words, too conservative.

What other predictions "of rising sea levels, displaced agriculture zones, more extreme storms, more frequent deluges "are also going to be worse than forecast?