Does anyone need more proof that stem cells are not going to serve as universal repair kits for Alzheimer’s disease, Parkinson’s disease, Lou Gehrig’s disease and spinal cord injury any time soon? Here is what counts as a big breakthrough in stem-cell research these days: producing cells that can then be studied for clues to what drugs will work against a particular disease.

I don’t mean to be cynical. Scientists today are announcing what is truly a milestone: they have taken skin cells from two elderly women—ages 82 and 89—who have Lou Gehrig’s disease, or amyotrophic lateral sclerosis (ALS), and used a technique that was announced less than a year ago to make the cells go backward in time, so to speak, and become embryonic stem cells. The researchers then made the stem cells morph into spinal motor neurons, the very ones that die in ALS. It’s a milestone because earlier studies had generated these induced stem cells from healthy donors, but no one knew if it would work on cells from elderly patients with a serious genetic disease.

So kudos all around. But the achievement is not, as the press release puts it, “an important step toward the goal of using induced pluripotent stem cells . . . to treat disease”—except if the step is small and the goal is decades away.

Just to recap what scientists led by Kevin Eggan of the Harvard Stem Cell Institute and Christopher Henderson of Columbia are reporting online today in Science. They started with skin cells from the two women, who had an inherited form of ALS in which one gene is mutated (this mutation is the cause of only about 2 to 5 percent of ALS cases, however, something to keep in mind). They then followed the recipe discovered last year, introducing four genes into the skin cells to “reprogram” them, essentially causing the cells to revert to embryonic stem-cell status. They then bathed the "pluripotent" cells in a stew of molecules that caused them to morph into motor neurons. Voila: motor neurons with the exact same genetic make-up as the women.

Not too long ago, that possibility was hailed as a technique for producing “patient-specific cells” that could then be returned to the patient to cure what ailed her. But think about it. The cells carry the same mutation that causes these women’s ALS in the first place. Transplanting them into the women would be like putting a cirrhotic liver into an alcoholic whose own liver was kaput.

Sure, maybe the cells could be used to generate genetically-matched healthy neurons to replace the diseased ones. But in a press conference, the scientists were quite clear about the more likely next step. “Because the cells contain the genes that produced the disease [in these women],” Eggan said, “you can study them in a Petri dish.” Henderson added, “we don’t understand the disease process, and that is preventing us from developing cures. But we now have in a culture dish cells with the same genetic make-up as the ALS patients in the very cells that are affected by the disease. We’ll see if they degenerate and die faster than normal cells, and will try to understand the mechanism of the degeneration process, since it is the mechanism that is the key to a cure, and will test chemical compounds that might stop the degeneration.”

That may sound like something that should have been done before, but in fact it has been impossible to isolate the diseased motor neurons from ALS patients, of which there areabout 30,000 in the United States. With a limitless supply of those neurons thanks to the iPS technique, scientists can both study the disease process and try everything they can think of to stop it.

Eggan had originally hoped to produce patient-specific stem cells using human eggs, in the process called therapeutic cloning, or somatic-cell nuclear transfer. In this technique, scientists remove all the genetic material from the ovum and replace it with the DNA from the skin cell of a patient. The fertilized ovum undergoes several cell divisions, yielding stem cells that the scientists then extract and induce to differentiate into the motor neurons they want to study.

But despite blanketing the Boston area with ads asking women to donate, he had no takers: women were eager to help, but when they learned that Massachusetts law prohibits the scientists from compensating them in any way—not for lost time at work, not for transportation—they had second thoughts. Women can, of course, be paid thousands of dollars for donating eggs to infertile couples. “Over the last two years we’ve done everything we could within the law to recruit women to donate ova,” Eggan said. “We were never able to recruit enough donors because we were legally prevented from providing the same sort of compensation that these women would receive for donating their ova for in vitro fertilization.”

Move over, steroids. Take a hike, human growth hormone. If scientists are right, a simple pill can enhance and even mimic the beneficial effects of exercise. At least in mice. But some people may not be waiting for research to show that the compounds work in people as well. The scientist who discovered the drugs, which are a cinch for chemists to synthesize, believes they may already be in athletes’ equipment bags—since anti-doping agencies had no idea they should even be on the lookout for them.

The drugs, called AICAR and GW1516, work by genetically reprogramming muscle fibers. The result is that the fibers use energy more efficiently, allowing them to contract repeatedly without tiring. Mice given the drugs ran faster and—this is where marathoners should prick up their ears—44 percent longer on the treadmill than un-drugged mice without flagging, Ronald Evans, a Howard Hughes Medical Institute investigator at the Salk Institute for Biological Studies in La Jolla, and colleagues are reporting today in an advance online publication in the journal Cell. The drugs also retool the muscles, with the result that there are more slow-twitch fibers (the kind used for endurance exercises) and fewer fast-twitch fibers (which let you put on bursts of speed, as in a sprint).

The drugs differ in just how much you—by which I mean a mouse, of course—can get away with. GW1516 had a dramatic impact on endurance, but to get the benefit the mice had to exercise. AICAR, on the other hand, really does seem like the proverbial exercise in a pill: no exertion required.

The work builds on research that Evans reported in 2004, when he created genetically-engineered “marathon mice” that had altered muscle composition and enough physical endurance to run twice as far as normal mice. The genetic engineering basically flipped a switch so that a gene called PPAR-delta was permanently “on.” PPAR-delta is more prevalent in slow-twitch muscle fibers than in fast-twitch ones, so keeping the gene turned on “increase[d] the amount of non-fatiguing muscle fibers,” Evans said. The result was a mouse able to run up to twice the distance of a normal littermate without training.

Despite whisperings that genetic engineering will be the next Olympic doping scandal, it’s obviously easier to get the benefits of the marathon mouse through a pill rather than gene splicing. But this genetic switch was flipped when the animals were still embryos. That raised the question, “what about reprogramming in an adult?” Evans said. “When all the muscles are in place, can you give a drug that washes over the muscle for a few hours at a time and reprograms existing muscle fibers? That’s a very different question.”

And it’s the question the new study answers with a resounding “yes.” GW1516 acts in concert with exercise: Evans had two groups of mice run on a treadmill for 30 minutes five days a week for a total of four weeks. All of the mice, as expected, became more fit, able to run longer and faster than when they were couch potatoes. But the animals that also got GW1516 ran 68 percent longer than un-drugged mice. “The dramatic effect of the drug was stunning,” Evans said.

The second drug, AICAR, wowed them even more: even in the absence of exercise, it activated many of the genes in muscle that are turned on by exercise. After four weeks of swallowing the drug, mice were able to run 44 percent longer than un-drugged mice—despite never having set paw into the treadmill. “The mice were behaving as if they’d exercised,” said Evans. Even better, actually: mice on the drug ran longer and farther than mice that had dutifully taken to the treadmill every day. Who said life was fair?

Both drugs trigger a suite of changes that underlie the improved endurance. They increase the number of mitochondria (structures that produce energy) in muscle cells, and increase blood flow. Evans suspects there were also beneficial changes to the heart and lungs. That suggests that the drugs could give even sedentary people the benefits of exercise. “Almost no one gets the recommended 40 minutes to an hour per day of exercise,” Evans says. “If there was a way to mimic exercise, it would make the quality of exercise that they do much more efficient.”

And for people who already walk, jog or run? “If you like exercise, you like the idea of getting more bang for your buck,” which GW1516 can provide, he says. “If you don’t like exercise, you love the idea of getting the benefits from a pill,” as with AICAR.

If only Vincent van Gogh (1853−1890) had been able to afford canvas, the world would have many more of the master’s paintings. But as scholars have long known, van Gogh re-used his canvasses, especially when he wasn’t happy with a painting, creating a new work on top of an old one. These hidden compositions have mostly eluded art historians because current museum-based imaging tools cannot properly visualize them.

But European researchers now say they have a way to reveal the covered-over paintings in unprecedented detail, finding the van Goghsunder the Van Goghs. In the first use of the technology, they report in the online issue of Analytical Chemistry, they have discovered a woman’s head hidden under van Gogh’s "Patch of Grass."

Since scholars estimate that one-third of van Gogh’s paintings were covered over, the technology—called synchrotron radiation-based X-ray fluorescence mapping—could reveal a whole new world of the master’s works that have remained invisible to earlier techniques, notably X-ray radiation transmission radiography. XRR mostly picks up heavy metals in paint pigments, such as lead in lead white or mercury in vermillion. Since van Gogh’s “do overs” usually started with a primer coat of lead white to cover up the original image, XRR often produces few recognizable details. Under"Patch of Grass," for instance, XRR revealed the vague outlines of a head, but no facial characteristics, making the person portrayed unidentifiable.

Scientists led by Joris Dik of Delft University of Technology in The Netherlands thought they could do better. They transported Patch of Grass to the synchrotron light source at the HASYLAB, part of the particle physics lab DESY in Hamburg, Germany. After bombarding the painting with the radiation, they write, “we succeeded in visualizing the hidden face with unprecedented detail."

The technique picked up and identified mercury and antimony in the red (vermillion) and light (Naples yellow) pigments, respectively, letting the scientists see the flesh tones, the brushstrokes and all the facial details—eyes, nose, mouth, and chin. They could even see “the reddish intensity of the flesh tones of the lips, cheek, and forehead,” they report:

“The hidden painting dovetails with an extensive series of heads from the artist’s period in Nuenen (The Netherlands). Between October 1884 and May 1885 he painted the heads of peasant models in the dark settings of their huts, in the neighborhood of the village of Nuenen. . . . The present head must belong to a smaller group of studies that Vincent gave to his brother Theo in Paris, as mentioned in his letters (Some of the heads I promised you are finished, but they are not quite dry yet; I should like to hear whether those rolled-up things arrived safely). After 2 1/2 years, Vincent went to join Theo in Paris and may very well have found the woman’s head hopelessly old-fashioned by then. This, together with his uncomfortable financial situation, can explain the presence of a colorful, Parisian style floral painting on top of a dark and sombre head of a provincial Dutch woman.”

Here she is:

CT scans have been done on mummies (showing that King Tut wasn’t murdered), dinosaurs (determining, for instance, what parasaurolophus sounded like) and other pieces of the past, and now scientists have put computed tomography (CT) technology to another nifty use: taking skull fragments of a rare extinct lemur which were found at sites thousands of miles apart and virtually assembling them to produce a nearly-complete skull.

The first fossil of the extinct lemur called Hadropithecus stenognathus, which last lived 2,000 years ago, was found in 1899 in Andrahomana Cave in Madagascar. Since then the jaw and partial skull have resided in Vienna, remaining annoyingly incomplete. But in 2003 scientists excavated new cranial fragments and limb bones of Hadropithecus. Alan Walker of Penn State, who happened to have CT scans of the Vienna skull in his lab for another project, realized that the new pieces might fit into the incomplete skull.

As Walker and colleagues describe in a paper in the early online edition of the Proceedings of the National Academy of Sciences Monday evening, they CT-scanned the new fragments and found that they fit into the Vienna skull perfectly.

That let them measure the lemur’s cranial capacity (115 ml.) and, using limb and trunk bones of the same guy, infer that it was as large as a large male baboon. Hadropithecus, it seems, had a relative brain size (as a fraction of body size) as large as some large monkeys, and one of the largest of any known prosimians (a group that includes lorises, lemurs and bushbabies). Hadropithecus, similar to today's sifaka, was one more piece of the stunning mosaic of biological diversity that Madagascar once supported, at least before the island was gripped by an extinction crisis.

The huge annual Alzheimer’s meeting starts tomorrow in Chicago, and it comes at an interesting time for the field. I mean “interesting” in, of course, the sense of the old curse, “may you live in interesting times.”

The last couple of weeks brought shocks from two different directions. One was the devastating failure of two drugs based on the leading theory of the disease: that Alzheimer’s is caused by an accumulation of sticky brain plaques made of the peptide (a part of a protein) called amyloid-beta, and that if you induce the body to make antibodies against this protein and/or administer a drug to dissolve the plaques, you will be well on your way to treating the disease. The other shock was the surprising success of an antihistamine drug (!) that came out of left field, by which I mean Russia.

Let’s start with the seemingly good news. A drug called dimebon, which years ago was sold in Russia as an antihistamine (manufacturers stopped selling it when a new generation of antihistamines became available) was given to 183 patients there with mild to moderate Alzheimer’s three times a day for six months, followed by another six months of getting the drug or a placebo. As scientists led by Rachelle Doody of Baylor College of Medicine reported in a special edition of The Lancet, the dimebon group showed significant improvements in ability to track dates, understand instructions, follow commands, memorize a list of words, and perform simple tasks such as copying drawings or addressing an envelope. The placebo group declined on these measures.

As the authors write, “patients given dimebon were significantly improved compared with baseline, and compared with those taking placebo.” Considering that there are currently “no approved therapies for mild-to-moderate Alzheimer’s disease [that] have shown increasing improvement over 12 months,” they write, that is no small feat.

In the same issue, scientists reported that although immunizing 80 Alzheimer’s patients against the amyloid-β peptide can clear amyloid plaques in their brains, it does not keep them from getting worse. Hopes that that approach would work were based on positive findings in mice (immunizing them with full-length amyloid-β both reduced plaques and improved brain function), but it doesn’t work in people, Clive Holmes and colleagues at Moorgreen Hospital, in Southampton, England, reported. “There is little evidence to suggest that there is any major effect on cognitive function,” they reported. “All but one of the individuals who died during the follow-up phase had clear end-stage dementia before death, including the two individuals with . . . almost complete elimination of plaques. These findings imply that progressive neurodegeneration can occur in Alzheimer’s disease despite removal of plaques.”

What’s going on? One scientist told me that dissolving plaques may be completely the wrong way to go: you melt these suckers and the gunk they’re made of is free to wash around the brain, somehow exerting mind-killing effects.

But the larger point is that we are more than 20 years into gene-based, rigorous basic research on this horrific disease. And pet hypotheses keep falling, while the totally unexpected keeps happening.

That's worth keeping in mind when the parade of announcements start coming out of the annual Alzheimer’s meeting this weekend and next week. You will be hearing lots of claims for successful therapies, some targeting amyloid-beta and others taking aim at tangles inside brain neurons made of a different protein, called tau. Just remember, we have been down this road before. Some questions to keep in mind:

• Nothing counts in science until it has been replicated.
• If a study says it cleared away plaques, did it also find cognitive improvement? If not, there is no cause for optimism. If so, how long did they follow the subjects, since although stabilizing grandma for a few weeks is not meaningless what really counts is turning back the disease for good.
• Likewise, if a study reports a therapy that destroys tau tangles, how much (if any) cognitive improvement occurred, and for how long?

 A Times Roman font walks into a bar. The bartender says, “Sorry, we don’t serve your type here.”

No, what I meant was, a guy walks into a bar with a duck on his head. The bartender says, “Can I help you?” The duck says, “yeah, you can get this guy off my butt!” Or maybe, two guys walk into a bar; the third one, not being an idiot, ducks (thank you, funny2).

But seriously, one guy walks into one bar, has a few, and then into another one down the street, and has a few more, faster. What’s the difference between the two bars? If scientists who study drinking behavior are right, it may be the loud music in the second one. That, researchers will report in the October issue of Alcoholism: Clinical & Experimental Research (it’s also available at the journal’s online “Early View” page), can make you drink more, in less time.

“Previous research had shown that fast music can cause fast drinking, and that music versus no music can cause a person to spend more time in a bar,” said Nicolas Guéguen, a professor of behavioral sciences at the Université de Bretagne-Sud in France, who led the study. But “this is the first time that an experimental approach in a real context found the effects of loud music on alcohol consumption.”

By “real context,” he means the two bars in the west of France that he and his colleagues visited—purely for research purposes!—on three Saturday evenings. They surreptitiously observed 40 men between the ages of 18 to 25 who had ordered a glass of draft beer. They also toggled the sound levels of the top 40 songs on the bars’ playlist between 72 decibels, which is normal, and 88 dB, considered loud. Result: the louder the music, the more the guys drank, and in less time than when the volume was turned down.

One reason may be that loud music causes higher physiological arousal—a faster heart rate, higher blood pressure and the like, which led the men “to drink faster and to order more drinks,” said Guéguen. Alternatively, loud music may make it so hard to hold a conversation that patrons drink more because they talk less.

The lesson he takes from this is that “we need to encourage bar owners to play music at more of a moderate level ... and make consumers aware that loud music can influence their alcohol consumption.” We won’t hold our breath while bars weigh the increased revenue from getting patrons to drink more, faster, against the social virtue of doing something as simple as turning down the volume in order to reduce how much booze they sell.

Sure, broccoli fights cancer. But tobacco?

When scientists at Stanford University looked around for a good way to grow a cancer vaccine, they realized they could do no better than the plant that has caused more cancers than you can count. They were not trying to develop a cancer vaccine such as Gardasil, which gives the body immunity against an infectious agent (in this case, the papillomavirus) that can trigger cancer (in this case, cervical). That's all well and good, but the true grail is a therapeutic vaccine, one that would prompt the body’s immune system to attack cancer cells and only cancer cells, or that would consist of antibodies that do so.

The theory rests on the fact that the surface of malignant cells are studded with molecules that can prime the immune system’s T cells, for instance, to attack the cancer cells, or act as homing signals that lure antibodies to munch up and destroy the cells.

A bunch of such cancer vaccines are in development, but they face a serious problem. Everyone is likely to need a different vaccine, because everyone's cancer cells are probably slightly different on the molecular level. Growing the antibodies according to the usual recipe means using animal cells, which is expensive (thousands of dollars per patient), time consuming (months) and possibly risky (they might contain viruses or other contaminants that are not exactly what you want to inject into cancer patients). So biologist Ronald Levy of Stanford University and colleagues decided to investigate plants as vaccine factories.

This evening, they are announcing in the advance online issue of the Proceedings of the National Academy of Sciences that they have grown an injectable cancer vaccine in genetically-engineered plants, tested it in 16 cancer patients and found it to be safe (tests of whether it works come next).

Fully aware of the irony here, Levy and his team used tobacco plants to grow the vaccine, which would act against follicular B-cell lymphoma. This chronic, incurable form of non-Hodgkin’s lymphoma strikes some 16,000 people in the United States each year. For all its horrors, however, follicular B-cell lymphoma just may be tailor-made for a cancer vaccine: all of the malignant cells are the descendants of a single bad actor and have an identical molecule on their surface. But the molecular signature of one patient’s cancer cells is slightly different from every other patient’s; hence the need for potentially expensive personalized vaccines.

The scientists therefore spliced the DNA for the molecular sequences of the antibodies from each of the 16 patients into tobacco cells. The DNA triggered production of antibodies in the tobacco plants’ leaves which were tailor-made for each patient’s lymphoma cells. The scientists ground up the leaves and isolated the antibodies, injecting them into each patient.

The patients’ immune systems got cracking: 70 percent of the patients developed an immune response to the plant-produced vaccine, and 47 percent produced a response specific to the antigen.

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.