An old joke holds that the only people allowed to refer to themselves as “we” are royalty, editors and people with tapeworms. Yet as a 2007 NEWSWEEK cover story notes, we are all collections of thousands of species of bacteria, worms and other parasites—and losing some of them, it turns out, has dire consequences.

Helicobacter pylori, which lives in the acid environment of the stomach, can cause both gastric ulcers and stomach cancer. But it also seems to protect against esophageal reflux and cancer of the esophagus, and now that it is on the verge of extinction in the West, report Martin Blaser and Yu Chen of NYU in the Journal of Infectious Diseases, watch out for an explosion of asthma.  

H. pylori infected around 90 percent of children born at the turn of the 20th century but fewer than 10 percent now, mostly thanks to better hygiene and widespread use of antibiotics. But the bacteria had evolved the ability to calm the human immune system. Remove the bacteria and immune reactivity can overcompensate. One result may be that asthma, a hyper-reactive immune response in tissues lining the airways, has spread like a modern plague.

In their paper, Blaser and Chen review 12 studies on the relationship between infection with H. pylori and several immune-mediated diseases, including asthma, hay fever, eczema and other skin rashes. Message: the lower the infection rate with H. pylori, the higher the incidence of immune diseases. Blaser also found the same inverse relationship between H. pylori and asthma and skin rashes.

Worms, too, can damp down humans’ immune reactions—far enough that the parasites can live in the gut, but not so far that the host is defenseless against other threats. Without the calming effect induced by gut worms, the immune system becomes over-active, as a story in The New York Times magazine shows. To summarize, one result might be an increase in inflammatory bowel disease (IBD) and other disorders (like arthritis) caused by an over-active immune system that attacks the body’s own tissues.

When Joel Weinstock, an Iowa gastroenterologist, infected volunteers—patients with Crohn’s disease—with parasitic intestinal worms, 23 of 29 improved after 24 weeks; 21 were in complete remission. In a second study, 13 of 30 patients with ulcerative colitis who were infected with worms got better, while only 4 of 24 controls (given a placebo) improved.

All of which suggests that our never-ending quest to rid the world of microbes (that means you, anti-microbial soap user) will have unintended consequences--and not necessarily happy ones.

We’ve all been there (though some of us longer ago than others): the cruising bar, fraternity party or other gathering place where men vastly outnumber women. As the men trip all over themselves trying to make their competitors look like losers and themselves like desirable partners, women get the upper hand: they have their pick of partners, and can crush the already-sensitive egos of the men with the back of their manicured hand.

If you assumed that this kind of female-over-male dominance was a freak result of humans’ peculiar mating habits, biologists in Germany have some monkeys they’d like you to meet. The higher the percentage of males in troops of lemurs, macaques and other primates, they report in the journal PLoS ONE, the more dominant over males the females are.

That there are any circumstances in which female primates lord it over males in a social hierarchy may come as a surprise, but it's actually not that uncommon. Although in most species females rank below the males (which means most males win aggressive encounters), in the lemurs of Madagascar the females are dominant, in bonobos the males and females are roughly equal in dominance, and among macaques females are weakly dominant, with “the most dominant females rank[ing] above approximately a third of  the males,” says biologist Charlotte Hemelrijk of the University of Groningen, who led the new study.

There are two competing hypotheses for how this female dominance develops. One holds that dominance is inborn; you are more likely to be dominant if you are born big and strong, or if you inherit it from your mother, and that’s that. The alternative holds that there is a “winner-loser effect.” Primates have chance encounters, and if they win they are more likely to win again, while if they lose they are more likely to lose the next time; it's a snowball effect.

The reason is that the outcome alters an individual’s fighting ability. Winning raises, and losing lowers, self-confidence, which can be self-fulfilling (animals filled with swagger are more likely to win the next time, too). As Hemelrijk puts it, if an individual monkey wins an aggressive interaction, “the monkey’s self-confidence grows and it also wins other aggressive interactions. It’s a self-reinforcing effect.” Also, losing is so traumatic that it raises an animal’s levels of corticosteroids (stress hormones) and lowers its levels of testosterone; that makes for a wimpy monkey more likely to lose its next encounter.

So imagine what happens in troops with many more males than females. The males are always mixing it up, playing one-upmanship in the drive to be the alpha male. That provides many chances for males to lose and hence to feel bad about themselves and have a losing mix of testosterone and stress hormones. The females take advantage of this. “In groups with more males, males are more often defeated by other males,” says Hemelrijk. “Consequently, high-ranking females may be victorious over these losers. Furthermore, the presence of more males in the group leads to more interactions between males and females, causing more chance winnings by females. Through a self-reinforcing effect, these females will go on to win more frequently and grow more dominant.”

In other words, the large number of losing males in a group with a preponderance of males makes them more likely to lose a fight with another male, and therefore with a female; the female gains confidence (and higher testosterone levels), enabling her to go on to lord it over more males. As a result, say the scientists, “high ranking females may beat low ranking males and rank above them.” In contrast, in less-aggressive primate groups, such as the egalitarian societies of macaques, the presence of many more males than females does not lead to female dominance over males: the males don’t fight enough to produce enough losers for the females to lord it over.

The scientists were particularly struck by their finding that whether females dominate males has little to do with the difference in their sizes, or what’s called sexual dimorphism. That is “unexpected,” they say, because size seems to explain male dominance in species where males are way bigger than females, such as gorillas. But when it comes to whether females can be the top bananas, the relative sizes of males and females matters less than the percentage of each sex in the group.

Says Hemelrijk, “It would not surprise me if [similar mechanisms] play a role in the development of dominance between the sexes among human beings, too.” Keep it in mind next time you find yourself in a group where the sex ratio veers far from 50-50.

It’s a tough call, deciding which topics gets readers most incensed. Evolution always makes a strong run for the title, but I have to go with something else: readers get really, really upset when you tell them that early cancer detection is unlikely to save their life.

So apologies that I have to say it again. But the latest review of studies evaluating the value of monthly breast self-exams—a staple of college health centers, OB-GYN visits and women’s mags—comes to a dismal conclusion: there is no evidence that they actually reduce breast-cancer deaths, and instead may do more harm than good.

Before you roll your eyes and say, oh, just one little study, what does it know?, let me say this: there are actually a lot of studies casting doubt on what breast self-exams can do for you. In 2002, for instance, scientists at the Fred Hutchinson Cancer Research Center in Seattle concluded in the Journal of the National Cancer Institute that teaching women breast self-examination does not decrease the number of deaths in the group from breast cancer. And just as the study released this evening finds, teaching BSE increases the rate of benign breast biopsies, which are no fun. A JNCI editorial concluded that rather than spending time teaching breast self-exam, physicians should educate women about cancer symptoms and take more time performing the clinical breast exam. “Routinely teaching BSE may be dead,” they wrote, “but giving women information . . . should live on.”

Alas, six years later, BSE is not at all dead, and the myth of the value of self-exam persists. Lest you think this is all a vast conspiracy on the part of unfeeling male scientists to make more of us die from breast cancer, check out the Website of the National Breast Cancer Coalition, a women's research and advocacy group that has often taken unpopular positions. For years it has been telling women that “there is currently no scientific evidence from randomized trials that breast self-exam (BSE) saves lives or enables women to detect breast cancer at earlier stages. In addition, there are some data that show that BSE greatly increases the number of benign lumps detected, resulting in increased anxiety, physician visits, and unnecessary biopsies. Therefore, NBCC does not support efforts to promote and teach BSE on a population-wide level in any age group of women.” And the American Cancer Society stopped recommending monthly self-exams five years ago; there’s just no evidence it saves lives.

How can it be that self-exam doesn’t make you less likely to die of breast cancer, as the latest paper, from the Cochrane Library, concludes? (And that the PSA test for prostate cancer, mammograms, and X-ray screening for lung cancer also have little to no value in keeping you alive?)

For one thing, many tumors grow so slowly that they can be in you for years with no ill effects. So whether you find the tumor today or on July 15, 2014, makes no difference. For another, just because someone who found a tumor herself lives for 17 years, while someone whose tumor was found on a mammogram lived only 6, doesn’t mean the earlier detection improved survival: the ultimately fatal outcome might have been inevitable, and the only thing early detection bought was more years of living with cancer, not more years of life.

If you want to know who is really, really upset about natural disasters—ranking right after the victims, of course, but probably ahead of the environmental activists who point to the disasters and see the hand of climate change—look no further than the insurance industry and its re-insurers (those are the companies that insure the insurers). One of the biggest, Munich Re, is already saying that 2008 is likely to “go down in history as a year with one of the highest numbers of victims of natural catastrophes.”

As I wrote in a recent column, the world is suffering more and more extreme weather, and scientists are coming around to the view that global warming is contributing to the increase. According to Munich Re’s analysis, ofabout 400 natural catastrophes in the first half of the year, “300 were attributable to weather extremes.”

That’s been costly. Overall losses (excluding the China earthquake, which no one blames on climate change) come to $30 billion.

If you think there have been an unusual number of tornadoes among those "natural" catastrophes, give yourself a gold star. “There have never been so many tornadoes recorded [in the U.S.] in the first six months of a year,” Munich Re reports. In addition, heavy rain, hail and flooding inthe Midwest caused estimated losses of  $10 billion.

2008, said Munich Re’s Torsten Jeworrek, “is following the long-term trend toward more weather catastrophes, which is influenced by climate change.”

The goal adopted by the G-8 this week, of halving emissions of greenhouse gases by 2050 (from what baseline is not clear), will of course do almost nothing to mitigate the problem. Think of it this way: Your teenager throws dirty clothes and empty food containers on his floor every day. The junk never leaves, because you refuse to clean up after him and he doesn’t care if he lives in filth. But you prevail on him to add only half as much debris from now on. Guess what? The total mount of debris keeps on rising, just at a slower rate.

Here’s one of those phrases that The New Yorker would label as “sentences we never read past”:

"I was skimming the program for the annual meeting of the American Statistical Association . . ."

But really, where else can you find not only research on “Modeling Sparse Generalized Longitudinal Observations with Latent Gaussian Processes” but also on managerial strategies in baseball, parity in the NFL and the accuracy of sports predictions? It’s striking how many statisticians who study weighty matters—how to tell if a cancer drug works or a compound is dangerous—got their start studying sports statistics.

“A lot of us really enjoyed baseball statistics when we were growing up, and that’s how we got into the field,” biostatistician Michael Schell of the Moffitt Cancer Center in Tampa told me.

So I got in touch with Jack O’Gara, who wrote the book on using statistical techniques to spot chicanery in business (that would be the 2004 “Corporate Fraud: Case Studies in Detection and Analysis”). Now retired, O’Gara has put his statistical skills to use analyzing baseball, especially cheating.

In the business world, he focused on what he calls inflection points, a sudden discontinuity in data. That is what he saw, galore, when he analyzed the career stats of pitcher Roger Clemens.

Clemens, of course, was named in the Mitchell Report, which last December reported that an alarming number of baseball players had taken performance-enhancing drugs such as steroids. (Clemens' section starts on p. 215.) Clemens and his camp deny it. O’Gara decided to see if stats could tell us anything.

One of the most telling is ERA Margin, which compares a pitcher’s earned run average in a given year to the league average. It’s more informative than ERA alone because it controls for weird things like hitters league-wide being in a slump (which would reduce every pitcher’s ERA but not ERA Margin), or the use of a juiced ball that year, which would raise pitchers’ ERAs but, again, not the margin. The ERA Margin tells you how one hurler is doing compared to his peers.

O’Gara compared Clemens’ ERA Margins to those of the 20 post-World War II pitchers with the most wins, turned in by legends such as Warren Spahn, Tom Seaver and Bob Gibson. Through age 34, Clemens’ margin was 1.09, notably better than the others’ 0.6. Fine, the guy was an ace.

But from age 35 to 40, when most pitchers fade, Clemens’ margin was 1.18, compared to 0.43 for the other greats. Here's where it gets weird: from age 41 to 45, it was 1.30, while the others’ was a negative 0.01. That is, the other great pitchers’ margin shrank as they got older, falling more in line with the league average and normal aging patterns, but Clemens’ soared. As O’Gara put it, “Clemens is the only pitcher who gets progressively better as he ages into the post-40 category.”

When the ERA Margins for baseball’s top 10 or top 20 pitchers each year is graphed, Clemens is better than the rest when he was 29 and 30, then twice more—three performance peaks while none of the top 20 had more than two. “More significantly, the second two peaks were higher than the initial peak, which occurred in the presumed prime of his life, contrary to normal aging patterns,” O’Gara says. “At age 43, Clemens had the seventh-best season [measured by ERA Margin] since World War II.”

Of the 20 best ERA Margins since 1945, all came when the pitcher was 34 or younger (average age: 28), with the exception of Clemens, who did it when he was 35 and again when he was 43. The best two-year average ERA Margins cluster when pitchers were in their late 20s (Sandy Koufax: 29-30; Greg Maddux: 28-29), and again Clemens’ best coming when he was 43-44 stands out. Clemens’ ERA margin at age 43 was the best in the majors that year and the best-ever for a 43-year-old.

Testimony taken for the Mitchell Report and given to Congress this spring included accusations from a trainer that he injected Clemens, which the pitcher denies. As it happens, the three periods when the trainer said he administered shots “correspond to performance bursts by Clemens,” says O’Gara. “The ERA for these three periods totaled 1.92 over 183 innings, significantly better than his career average ERA of 3.12.”

As has been widely reported, in 1996 Clemens, then 34, was coming off a sub-par 1995 season and struggling through the first months of the '96 season, his last of 14 with Boston. “Then he suddenly went from being mired in the worst multiple year performance of his career (the preceding one and 2/3 years) to his best two-year-plus performance of his career,” says O’Gara. “He averaged a 2.91 ERA margin for the remainder of 1996, better than for any single calendar year.”

One baseball statistician I asked about this analysis warned me against “guilt by graph”—that is, concluding that someone was juiced based on stats alone. “Stats can tell you if someone’s performance is unusual, but by definition a great player has an unusual performance,” he said. See, for instance, this post by another stats guru.

So in Clemens’ case, do the stats lie—or expose a lie?

Not that anything about global warming is fair, but one of the most unjust things about it is that the nations that have spewed most of the greenhouse gases into the atmosphere tend to be in the north (the U.S., Europe and now China), while the nations that stand to suffer the most--as in having their entire island covered by the rising seas--tend to be in the south. If a German researcher is right, it looks like nations will reap what they sow.

According to a new paper by Detlaf Stammer of Hamburg University, once Greenland melts most of the water will hang around in the Atlantic Ocean rather than spreading through the world's seas. As New Scientist reported, most of the meltwater will add to the Atlantic for some 50 years, causing sea levels to rise--and rise more than if the water were evenly distributed around the globe, which it will not be. As Stammer told the magazine, a melting Greenland "is much less of a threat to tropical islands in the Pacific than it is for the coasts of North America and Europe."

Call it poetic justice, climatologically.

If you are diligently following the experts’ advice on mosquito control—getting rid of standing water in old tires, pots, gouges in your patio and other places where water pools—scientists have made a discovery that can reduce your labors: concentrate on the puddles where leaves are floating. That might be especially welcome news for Midwesterners who, after suffering the floods of June, are now dealing with plagues of mosquitoes that are in some cases 20 times the usual number.

Entomologists have long known that female mosquitoes—the ones that bite—are drawn to water to lay their eggs, but exactly what the draw was has been a mystery. Scientists at North Carolina State University therefore gave Aedes aegypti, the species that carries yellow fever, dengue fever and other diseases, a choice: lay eggs in plain water or in those where leaves have fallen. As they report this evening in Proceedings of the National Academy of Sciences, the females definitely prefer the latter, by something like 16-to-1.

What seems to happen is that bacteria find the leaves (the scientists tried both bamboo and white oak) and start decomposing them. Chemicals released by the bacteria are sensed by female mosquitoes, who then decide that the water is an acceptable nursery for junior, conclude NCSU’s Charles Apperson and colleagues. Specifically, carboxylic acids and methyl esters released by the bacteria scream “lay your eggs!” to mama mosquito.

How much do mosquitoes prefer leaf-infused water? When the female lands on water in a container, she senses the presence of various bacteria and the chemicals they release, using chemoreceptors on her antennae, mouthparts or ovipositor. Given a choice between pure water and the leaf-infused variety, Ae.aegypti laid 94 percent of their eggs in cups containing bacteria from bamboo infusions and 6.5 percent in plain water; in the next experiment, the insects laid 91 percent of their eggs in cups containing bacteria from white-oak leaf infusions and 9.8 percent in plain water.

“Some water-filled containers are rejected by the female mosquito,” Apperson says. “If we filter the bacteria out, the mosquitoes want no part of the water container. But put the filtered bacteria back in the water container, and the mosquitoes will be stimulated to lay eggs.” Once they hatch, the larvae will chow down on the microbes.

Knowing what stimulates disease-carrying mosquitoes to lay their eggs is getting more important now that once-tropical diseases are invading temperate latitudes. (The World Health Organization estimates that 51 million people are infected with dengue fever every year, that the disease occurs in 100 countries, that there has been a sharp rise in the number of cases in Asia and that it has made its way to Central and South America, on America’s doorstep.) Lesson: be extra vigilant about getting rid of standing water where leaves have fallen. Or have a large supply of calamine lotion on hand this summer.

RELATED: Why Some People Are Mosquito Magnets

Of all the columns I’ve written, no topic has brought more agonized, heartfelt and desperate-sounding emails than Alzheimer’s disease. Back in 2004, I wrote three columns (when I was at The Wall Street Journal) on how one particular theory of what causes this awful disease—and therefore the best approach for treating it—has had the field in a headlock, censoring competing theories. That closed-mindedness, I quoted scientists as saying, had a lot to do with why there is not only no cure or preventive for Alzheimer’s, but not even a treatment that slows down the inexorable cognitive decline.

The emails, as you might expect, told me about loved ones who had been lost to Alzheimer’s, and expressed frustration, anger and fury that part of the reason for the lack of progress might be that scientists were not open-minded about any but their pet hypothesis.

This all came rushing back to me this week when Myriad Genetics, Inc., reported that a Phase 3 clinical trial (the last one before a company seeks FDA approval for a new drug) it had been testing for an experimental Alzheimer’s drug had failed. The drug, Flurizan, is called a “selective amyloid lowering agent,” or SALA. Amyloid is a peptide (part of a protein). The amyloid known as Aβ42 is—according to the dogma—the “primary initiator of neurotoxicity and amyloid plaque development in the brains of Alzheimer’s disease patients,” as Myriad puts it. And indeed, in human cells growing in lab dishes as well as in lab animals, Flurizan reduces levels of Aβ42.

But when Myriad gave it to people with early-stage Alzheimer’s, it didn’t help them a bit. We don’t know why. Maybe Flurizan did not reduce Aβ42 in the patients. Or maybe—and this would be disastrous for the field—itdid reduce Aβ42 but that had no beneficial effect. If the latter, it is more proof that the amyloid dogma—Aβ42 causes Alzheimer’s, therefore get rid of Aβ42 and you’ll cure the disease—is wrong. I call it “disastrous” because a huge majority of the research and drug-development efforts in Alzheimer’s assumes that Aβ42 causes the disease and that getting rid of Aβ42 is the holy grail.

At the risk of being obnoxiously self-referential, let me re-cycle some of what I said about the amyloid dogma back in 2004:

“Beliefs about what causes this merciless disease have taken on such a religious fervor that one group is called tauists, after a protein called tau that forms 'neurofibrillary tangles' inside the neurons and, say these scientists, kills neurons responsible for memory and thought. Another is called baptists, after the [Aβ42] that forms plaques around brain neurons and, say its accusers, causes neuron-killing tau tangles or kills neurons directly, or both. Apostates think amyloid plaques sop up neurotoxic proteins along with poisonous metals such as zinc and copper, and that eliminating plaques could therefore harm patients. . . . [But] there are growing doubts that amyloid is guilty as charged. Autopsies of people with early-stage Alzheimer's show that the tangles form first, before plaques, in brain regions initially affected by the disease. 'If you look at the evidence, it's the tangles that cause neuronal degeneration, and they come first, before the amyloid,' says neurologist Patrick McGeer of the University of British Columbia. Another problem for the amyloid dogma, ... adds neurobiologist Nikolaos Robakis of Mount Sinai School of Medicine, New York City, is that autopsies of the brains of Alzheimer's victims show that 'plaques don’t correlate with neuronal death. The amyloid is here and the dead neurons are somewhere else.'. . .  'If amyloid were the answer,' says Dr. McGeer, 'the disease would have been solved by now.'

I’m afraid that’s still where things stand, four years after I wrote that. Now let me share a note I just got from a scientist who has long questioned the amyloid dogma:

“I couldn’t resist contacting you....not with glee [about the Myriad failure], instead sadness at how scientific narcissism [he means the focus on the amyloid hypothesis to the near-exclusion of everything else] fails every damn time. . . . As far as Flurizan is concerned, I am sure the amyloid contingent will make their excuses: blame the drug, the placebo group (for not falling fast enough!), the timing (clearly we need to start anti-amyloid therapy in utero!) and, ultimately, the species (humans simply are not as good responders as mice). However, at this stage, I sense that the heads are beginning to drop and the swagger has disappeared. . . . While my hope is that this will open the field to all manner of crazy hypotheses, my fear is that the excuses will be persuasive enough. At this point, everything that lowers amyloid in mice/cells has failed in human trials. Perhaps a coincidence? Maybe. However, the alternate is never really considered. All of this is not to say that I was right [that amyloid is not the cause of Alzheimer’s and therefore cannot be the target of drugs to treat it]. I still don't know exactly how amyloid fits into the puzzle. But betting the house on 00 in roulette is no way to conduct science. Trouble is, we mostly are not gambling with our own money or lives.”

No, they are gambling with the lives of patients now and in the future whose lives are being taken by Alzheimer's. On that depressing note, Happy 4th.

Yeah, I know that headline echoes yesterday's, but I can't help it: we have now moved beyond studies showing that mental training alters the structure and function of the brain to studies showing that it alters the structure and function of our genes.

Regular readers may have noticed that I’m not a big fan of the “my genes made me do it” school of life, whether “it” is acting in a certain way (as genes “for” shyness or neuroticism supposedly make you do) or developing a particular disease. As I’ve written, the genes in our cells don’t matter one iota if they’re not turned on, and there are many things in life that can turn off bad genes such as those that raise the risk of disease such as breast cancer. That’s why it seems to me that personal genome scans are just a couple of steps removed from palm reading. As it happens, last year New York started telling 31 private companies that they need licenses to take DNA samples from state residents, and in June California sent cease-and-desist letters to 13 of the companies with the same message.

Reading what genes a person has is so 20th century. Determining which genes are turned on is where the action is. A rat study I’ve mentioned before, for instance, showed in 2004 that the way a mother rat treats her pups determines whether genes related to neuroticism and fearfulness are on or off.Now comes a study that looks at something similar in people.

The variable wasn’t how mom treats you—though I’d bet a nickel that study is just around the corner—but the relaxation response. Back in the 1960s Herbert Benson of Harvard Medical School coined this term to refer to the opposite of the stress response, which floods the body with stress hormones, raises blood pressure and elevates heart rate. In contrast, the relaxation response is a state of deep rest that decreases metabolism, relaxes muscles, slows heart rate and lowers blood pressure. Over the years, Benson and colleagues developed a sure-fire way to elicit it.

Now they’ve figured out how it works to, among other things, treat hypertension (high blood pressure), alleviate pain, even help with infertility and rheumatoid arthritis. As they report in PLoS One this evening, the relaxation response alters which genes associated with the body’s response to stress are on and which are off. As Benson said in a statement, “we’ve found how changing the activity of the mind can alter the way basic genetic instructions are implemented.”

It’s being billed as “the first comprehensive study of how the mind can affect gene expression.” By “mind,” they mean mental practices such as meditation and prayer, which are among the techniques used by the 19 long-term practitioners of the relaxation response who were studied, along with 19 volunteers who had never engaged in such practices. After the latter went through eight weeks of training, the scientists compared before-and-after patterns of gene expression, finding that mental training alters the expression of genes involved in inflammation, in the form of cell suicide called apoptosis (which can keep damaged cells from forming cancers), and in how the body handles damaging free radicals.

It really is time to stop thinking of our DNA as immutable. Even thinking can change it.

Can you think your way out of addiction? Maybe not yet, but the latest results from the burgeoning field of research that examines how mental training can alter the brain—and therefore behavior—say the rest of the answer may be "but probably soon."

In a new study, just published online in Nature Neuroscience and scheduled for the print version later this year, Elizabeth Phelps of New York University and colleagues measured how volunteers responded physiologically (including through brain activity) to a cue that, they were told, meant they were about to win $4. Specifically, the volunteers were shown either a blue square or a yellow square for four seconds; the blue meant they'd win the $4.

As expected, seeing the blue square lit up a region in their brains called the striatum; activity there is linked to the expectation of reward. It's the part of your brain that sits up and pays attention when you think of the barista handing you your iced coffee on a sweltering day, your significant other walking through the door … or the thought of a hit of pot, cocaine or other illegal drug.

There is definitely something to be said for holding a science meeting in Las Vegas, especially when the subject of the meeting is skepticism about pseudoscience and the paranormal. When I took a break from listening to the scholarly papers on people’s gullibility and the psychological basis for the belief in weird stuff, I strolled through the ubiquitous casinos and saw, yup, people believe in things (like the possibility of beating the house) for which there is little to no basis in reality.

The (almost) annual "Amazing Meeting" is put on by the James Randi Educational Foundation. Randi, of course, is the magician who has put his expertise in and knowledge about illusion and fooling people to good use in debunking claims of the paranormal, most famously showing that Uri Geller was not bending spoons with his thoughts:

In that fine tradition, psychology researcher Richard Wiseman has posted YouTube videos of how “magic” card tricks work, and at the conference last weekend persuaded the magician Teller (the silent half of Penn & Teller) to explain how “mentalists” (appear to) bend spoons.

My small contribution was a talk arguing that skeptics should not count on the press to enlist in their debunking crusade, something that also extends to the fight between evolution and creationism. So as not to bore you with the whole 30-minute speech, let me just say that my basic argument was that people believe weird things because of emotion, something no number of magazine and newspaper stories on the solidity of the science behind evolution (or the lack of evidence for homeopathy, psychic phenomena et al, as I also discussed in a column last year), is going to change. Add to that the public’s antipathy toward the press, and there’s no way the press can help the skeptics’ cause.

I’ll write more about the meeting eventually, but for now I can’t get something out of my mind. Penn and Teller did a q&a with the audience the day before Teller alone spilled the beans on spoon bending, and one question yielded a surprising answer. Someone asked Penn whether he still believed that man-made climate change is bunk, as he has said more than once. Penn's basic answer was: I loathe everything about Al Gore, so since Gore has been crusading against climate change it must be garbage.

Now, Penn & Teller’s terrific “Bull****,” now beginning its sixth season on Showtime, has debunked psychics such as John Edward, feng shui, acupuncture and other forms of pseudoscience and the paranormal. But here was Penn, a great friend to the skeptic community, basically saying, don’t bother me with scientific evidence, I’m going to make up my mind about global warming based on my disdain for Al Gore. (Both Penn and Teller are well-known libertarians and supporters of the libertarian Cato Institute, which has been one of the leaders in spreading doubt about global warming.) Which just goes to show, not even the most hard-nosed empiricists and skeptics are immune from the power of emotion to make us believe stupid things.

Let me say this at the outset: I don’t expect the latest discovery of a “transitional fossil”—the kind of thing that was once called a missing link—to change anyone’s mind about evolution. I have gotten too many letters and emails from creationists and intelligent-design proponents to have any illusions that something as silly as, you know, data will persuade them that living things change through time as a result of random mutation and natural selection. (My favorite contained a sponge with a verse from the bible printed on it; the letter writer promised to pray for my immortal, if misguided, soul.)

With that preamble, it’s still worth noting what scientists are reporting in the journal Nature, for it’s a transitional fossil between transitional fossils. That is, the fish-like thing whose 365-year-old fossil was discovered by Per Ahlberg of Uppsala University in Sweden and colleagues in Latvia seems to lie half-way between the lobe-finned fish Tiktaalik (itself a transitional fossil between true fish and four-legged land animals) and primitive tetrapods such as Acanthostega and Ichthyostega.

The new fossil, of Ventastega curonica, is remarkably well preserved, allowing the scientists to scrutinize it from skull to pelvis. Its lower jaw resembles a tetrapod’s, while its fangs are more fish-like.

There was a time when those who rejected evolution asked where the transitional fossils were, but as more and more are discovered they’ve changed their tune (if my mail is any indication). According to one, he won’t believe in evolution until there are “billions” of transitional fossils. We’ll get back to you on that.

In Olympic track events, the difference between winning a medal and going home empty-handed is measured in hundredths of a second, so no edge is too small to dismiss—even the advantage you get from proximity to the starter’s pistol. Which, it turns out, is greater than anyone realized.

A few years ago Olympics officials tried to equalize things by delivering the sound of the pistol—which is fired on the infield, nearest to lane 1—to speakers positioned behind each runner. That way, the millisecond difference in the time it takes sound to travel to the different lanes would not give the inside lanes an edge. But according to new research, runners in the inside lanes still have an advantage: because they are closest to the gun they hear the sound more loudly than do runners in outside lanes, and louder sounds make runners react more quickly, leaving the starting blocks sooner than if they heard a quieter sound.

The rules say that the runner who posts the fastest time in preliminary heats gets lane 4 for the finals, with the second-faster prelim time earning lane 5 (followed by 3, 6, 2, 7, 1 and 8, the idea being that there is an advantage to being in the middle where you can more easily see the other runners in your peripheral vision). But when scientists led by Dave Collins of the University of Alberta in Edmonton analyzed reaction times for the 100 meter sprints and the 110 meter hurdles at the 2004 Olympics, they found that runners closest to the starter reacted significantly faster than those further away, they report in the June issue of Medicine & Science in Sports & Exercise.

For the Athens games the reaction times (in milliseconds) were:

lane 1: 160 ms

lane 2: 171 ms

lane 3: 172

lane 4: 173

lane 5: 177

lane 6: 175

lane 7: 185

lane 8: 175

Some of the reaction times reflect individual variation: the runner in lane 7 was notably slow to react, while lane 8 was notably quick. To control for that, the scientists had four trained sprinters and 12 untrained volunteers run sprints from starting blocks that had been engineered to measure how hard the runners were pushing off. The scientists also fired a (simulated) starter’s gun at various volumes, from 80 to 120 decibels. The louder the gunshot, the faster the runners, both trained and novice, reacted, replicating the actual results in Athens: at 80 decibels, the average reaction time was 138 milliseconds, while at 120 it was 120. How strongly the runners pushed out of the starting blocks did not vary with the loudness of the gunshot, however, though how long it took the runners to reach their peak push-off force was significantly lower at a loud 120 dB than at a quieter 80 dB.

Bottom line: the starting procedures at the Olympic sprint events “afford runners closer to the starter the advantage of hearing the ‘go’ signal louder; consequently, they react sooner,” write the scientists.

Collins told me that a fairer way to start a race is the way the world championships do it: “Use the speakers [behind each runner] and a silent gun.” That way, each runner hears the starter’s gun not only at the same time, but at the same volume.

A staple of science fiction is to change the laws of nature, especially by having interplanetary travelers land on a world where those laws differ from the ones on Earth. It is equally a staple of science fact that the laws here are the same as the laws anywhere. But really, that was more assumption than a firm observation.

Well, I’m sorry to say that those of us who think it’d be cool to get wind of a galaxy where quarks roam free or where the speed of light is variable will have to keep waiting. For at least one of the bedrock constants in physics, the value is the same in a galaxy 6 billion light years away as it is on Earth.

The number is the ratio of the mass of the proton to that of the electron, about 1,836.15. Scientists led by Christian Henkel of the Max Planck Institute for Radio Astronomy in Bonn and Michael Murphy of the Swinburne Centre for Astrophysics and Supercomputing in Melbourne, Australia, examined a distant quasar, called B0218+367. The quasar’s light began its journey toward Earth 7.5 billion years ago, and along the way was partly absorbed by ammonia gas in an intervening galaxy 6 billion light years away.

The colors of light that ammonia absorbs is a function of the proton-to-electron mass ratio. Lo and behold, the colors of the quasar light making it through the ammonia galaxy—and from which astronomers can infer the colors that were absorbed—yielded the answer: the proton-electron mass ratio in the ammonia galaxy is the same as it is on Earth. Oh well.

Call me an optimist, but I see some wiggle room here. Something 6 billion light years away is also 6 billion years ago. Maybe we can hope that even if the laws of physics were the same there as on Earth 6 billion years ago, they have since changed? (The idea that the speed of light and other “constants” of nature are not constant isn’t looking as possible as it did when Joao Magueijo got a boatload of money to write his 2003 book Faster Than the Speed of Light: The Story of a Scientific Speculation, but it hasn't been ruled out completely.) And maybe we can hope that this galaxy now has laws of nature that we wouldn't recognize?

The astronomers, who reported their findings in Science (if you cannot access the paper at Science (which charges for content), try the scientists’ Webpage, which also has cool photos and diagrams), plan to keep testing the laws of nature in as many different places and at as many different times in the universe and its lifetime as they can. They say they “hope to find a window into the extra dimensions of space that many theoretical physicists think may exist.”

Polar bears have enough people advocating for them and working to save them from the effects of global warming, so how about some sympathy for puffins?

A warmer world threatens polar bears because it melts the arctic sea ice they use as a hunting platform. It threatens puffins—the seabirds whose scientific name, Fratercula arctica, means “little brother of the north,” because their black and white plumage are reminiscent of a friar’s robes—because it alters o cean currents and salinity in a way that can decrease the plankton and fish that puffins eat. Such as:

• On Iceland’s western coast, ocean temperatures have risen 3.6°F in the last two decades, and as a result one of the puffins’ favorite fish dinners—sand lance—have disappeared. Replacing them are less nutritious fish.
• The absence of sand lance has also led to widespread starvation of chicks and breeding failures among puffins on Britain’s Shetland Islands. The situation is made worse by the kudzu-like growth of the tree mallow (Lavatera arborea), a plant native to the Mediterranean region that has made itself at home up north thanks to global warming and that has overgrown puffin nesting habitat.
• On Norway’s Rost Island, where puffins typically feed on small herring, the fish have followed the cold-water plankton farther north. “Herring have now moved beyond the feeding range of puffins, resulting in the death of most nestlings,” the National Audubon Society reports. “The timing of puffin breeding is [also] being influenced by climate change and food may not be available when needed by the puffin chicks.”

This is all that much sadder because of the Herculean efforts to save one particular colony of puffins, those on Seal Island, 18 miles off the coast of Rockland, Maine. Puffins there had been almost completely wiped out by centuries of hunting (for their eggs, meat and feathers). But 35 years ago the Audubon Society started Project Puffin, in which biologist Stephen Kress and colleagues hand-carried nearly 2,000 puffin chicks from Newfoundland, where puffins are abundant, to Seal Island by plane, truck, and boat. Kress and his team fed each chick small fish, and when the puffins fledged the scientists crossed their fingers in the hope that the birds would return to the island to establish a breeding colony. Actually, the scientists did more than cross their fingers: they set up wooden puffin decoys and mirrors to convince the puffins they had company.

It worked, and today about 90 pairs nest at Eastern Egg Rock and more than 330 pairs nest at Seal Island.

If you have RealPlayer, you can watch the puffins at http://www.projectpuffin.org/puffin-cam.html . Notice the body language. A puffin walking quickly with its head bowed is signaling that it is “just passing through and doesn’t mean any trouble” as it walks through a crowded colony and inevitably crosses another puffin’s territory. If you see a puffin gaping, it’s likely a prelude to aggression. T he wider the beak is opened the more upset the puffin; if he’s really ticked off he’ll stomp his foot. T he best times are morning and early afternoon; very relaxing.

But here, too, global warming threatens to flood key puffin colonies, says Kress, who doesn’t want to see his decades of work swallowed up by the rising seas.