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.

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?

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.

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 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.

The 1999 comedy Dogma opens with a disclaimer, exhorting the audience to remember that “even God has a sense of humor. Just look at the Platypus. Thank you and enjoy the show. P.S. We sincerely apologize to all Platypus enthusiasts out there who are offended by that thoughtless comment about Platypi. We at View Askew respect the noble Platypus, and it is not our intention to slight these stupid creatures in any way. Thank you again and enjoy the show.”

God expressed his sense of humor, of course, in assembling a creature that is a little bit mammal (the platypus, a native of Australia, produces milk and is furry), a little bit reptile (it lays eggs and has venom, released from spurs in the hind legs) and a little bit bird (eggs again, plus it has a bill like a duck as well as webbed feet). Its cognitive capacity and/or nobility we’ll leave to the guys at Dogma, but one particular platypus—Glennie, from New South Wales, Australia—has made scientists smarter: an international team of researchers from the U.S., Australia, England, Germany, Israel, Japan, New Zealand and Spain collected her DNA and from it sequenced the platypus genome, they’re announcing today in papers in Nature and Genome Research.

The platypus genome consists of roughly 2.2 billion pairs of chemical “letters,” those As, Ts, Cs and Gs that spell out a species’ genetic code. (Humans have about 3 billion.) Within those letters are some 18,500 genes, compared to maybe 24,000 in humans.

Not surprisingly, the platypus genome is an amalgam of mammal, reptile and bird DNA, too.

Like reptiles, the platypus (Ornithorhynchus anatinus) has genes for egg laying. Its venom comes from genes that are duplicates of genes that evolved in ancestral reptiles, which is also the source of venom in today’s reptiles. Like mammals, it has genes for lactation (though, lacking nipples, it nurses its young through the abdominal skin). Like birds, it has a weird way of determining sex: of its 52 chromosomes, 10 are sex chromosomes (in humans, the X and Y, of 23 chromosomes, are sex chromosomes), and the platypus X resembles the sex chromosome of birds, called Z. A female platypus has five pairs of X chromosomes, while males have five Xs and five Ys. The platypus genome contains both reptilian and mammalian genes involved in the fertilization of eggs. Unlike most mammals, which have a pretty good sense of smell, the platypus doesn’t—and its genome has about half as many odor receptors as the mouse and other mammals.

Just one request, please. In the PR avalanche preceding this announcement, one talked about the medical benefits that would surely come from this feat. ("What does this discovery mean for the public? The very real potential for advances in human disease prevention and a better understanding of mammalian evolution.") Aren't we beyond that yet? There have been virtually no medical benefits from sequencing the human genome (yet), for goodness sake; can't we, just occasionally, celebrate a feat of pure science without raising hopes that it will, you know, cure cancer or something? Sometimes a platypus genome is just a platypus genome.

This has been the enduring mystery: How do events in the outside world get inside your head? That is, how do things that affect whether a child grows up to be contented and well-adjusted or a neurotic mess—things like abuse and neglect—change the gray matter to produce the brain activity and circuitry that corresponds to these psychological states? By turning some genes on and other genes off, according to a study posted this evening in the May 6 edition of the online PLoS ONE.

One of my favorite studies ever done showed how this happens in rats. In the 1990s Michael Meaney of McGill University saw that when a Mother Rat rarely licks and grooms her pups, the pups grow up to be fearful, stressed-out, jumpy and neurotic. If a Mother Rat is attentive and grooms her pups a lot, they grow up to be less neurotic, less fearful, more curious, mellower. The reason isn’t genetic, at least not in the usual sense. That is, it isn’t that mellow moms have mellow pups and neglectful moms have neurotic pups because the pups inherited mom’s mellow or neurotic DNA. (Pups born to attentive moms but reared by neglectful ones grow up to be stressed out, while pups born to neglectful moms but reared by attentive ones grow up to be less fearful, less neurotic. That is, they resemble their adoptive mom, not their biological one.)

Instead, licking and grooming removes the silencer on a gene that makes stress-hormone receptors in the rats’ brains. The more such receptors the brain has in the hippocampus, the fewer stress hormones are released and the mellower the rat is. But in rats reared by neglectful mothers, the silencer stays firmly attached, the brain therefore has a small supply of stress-hormone receptors, and glands pump out a flood of the hormones, producing a rat that is constantly jumpy and on hair-trigger alert. There you have it: Maternal behavior alters whether a gene is on or off.

Now the same core team of scientists has found that something like this happens in people, too. They compared the brains of troubled individuals who committed suicide, and who had been abused or severely neglected when they were children, to a comparison group of people who had no history of childhood abuse and who died suddenly of other causes. What the scientists did not find was any significant differences in the two groups’ gene sequences—that is, the strings of As, Ts, Cs and Gs that make up the double helix were basically the same.

But there were stark differences in the on-off setting of genes that work in the brain’s hippocampus. In the suicides, the genes were turned off like lights during a blackout, the McGill scientists report. In particular, “ribosomal RNA genes,” which humans have about 400 copies of and which make a big chunk of the cellular machinery that produces proteins, were studded with “off” switches. (This was not so in the cerebellum, but only the hippocampus. The former is mostly involved in movement, while the hippocampus encodes memories—and is often shrunk in people who have experienced trauma.)

As you would expect, the suicides—because of the “off” genes—made fewer rRNAs in the hippocampus. That likely means they also made fewer proteins—the workhorses of cells, since they include enzymes.

The next question is what effect the turned-off genes have in the brain, and how that may explain the suicides. But for now, chalk up another advance in understanding how the experiences we have can reach into our very DNA.

My favorite story about the Dalai Lama doesn’t concern his activities on behalf of Tibet, which is one unrelieved tragedy, but is about his interest in neuroscience. A few years ago the Dalai Lama was visiting an American medical school and watched a brain operation. Afterwards, he chatted with the surgeon, telling him how his scientist friends had patiently explained to him that all of our thoughts, feelings, memories, dreams and other mental activities are the products of electrical and chemical activity in the brain. But he had always wondered something, the Dalai Lama told the surgeon. If electricity and chemistry can produce thoughts and all the rest, can thoughts act back on the physical stuff of the brain to change its chemical, electrical and other physical properties?

The surgeon dismissed the question with a polite but indulgent no. (The Dalai Lama's English translator, Thupten Jinpa, told me this story in 2005.) The brain produces and shapes mental activity, the brain surgeon said; mental activity does not alter the brain.

That wasn’t a stupid answer 10 years ago, before scientists had fully grasped the potential of the adult brain to change in structure and function—an ability called neuroplasticity. But now researchers have documented a long list of examples of how the brain, once thought to be basically unchangeable after the ripe old age of 3, can indeed change.

The first things that were found to change the brain were sensory inputs. If you spend a lot of years playing violin, say, then the regions of the motor and somatosensory cortexes that correspond to the fingering digits (the fingers on the left hand, if you're right-handed) expand.

But now neuroscientists have documented how “mere” thoughts can also sculpt the brain. Just thinking about playing a piano piece, over and over, can expand the region of motor cortex that controls those fingers; just thinking about depressive thoughts in new ways can dial down activity in one part of the brain that underlies depression and increase it in another, leading to clinical improvement.

The scientist who has worked most closely with the Dalai Lama is Richard Davidson of the University of Wisconsin, Madison. Davidson first met the Dalai Lama in 1992, and since about 2000 has been investigating a question dear to the heart of the leader of Tibetan Buddhism: can mental training such as meditations change the brain in an enduring way? That “enduring” is key: of course the brain “changes”—in the sense that some areas become more active—when you meditate, just as it changes when you think of pink elephants, watch Obama or try to remember your first kiss. Everything we think has a corresponding brain activity. But once the thought stops, so does the activity. Usually. What Davidson wanted to know was whether meditation left a long-lasting imprint on the brain, some change of function or structure.

Since 2004, Davidson and his colleagues have reported that meditation can alter the brain’s attention capabilities and that it can increase production of brainwaves called gamma, which are associated with consciousness. Now they have found another long-lasting brain change produced by Buddhist meditation: practicing compassion meditation (more on this below) alters regions of the brain that make us empathetic, Davidson and his colleagues are reporting this evening in PLoS ONE.

In compassion meditation, as the French-born Buddhist monk Matthieu Ricard explained it to me when we were both visiting the Dalai Lama in Dharamsala for a meeting of neuroscientists and Buddhist scholars, you focus on the wish that all sentient beings be free of suffering. You generate an intense feeling of love for all beings, not fixating on individuals but encompassing all of humanity. It takes practice, since the natural tendency is to focus on one or a few specific suffering people.

Davidson conducted his new study as he has his others on meditation, enlisting expert meditators (the Dalai Lama has asked Buddhist scholars to volunteer their brains to Davidson’s research). Antoine Lutz has the meditators (monks who have 10,000 hours or more of meditation under their belts—er, saffron robes) lie in a functional magnetic resonance imaging (fMRI) tube. The fMRI detects which regions of the brain are active during meditation and which are quiet. It also detects which are active during periods between meditations. The scientists compare these readings to those on non-meditators, who undergo a quickie course in compassion meditation. In this case, Davidson and Lutz enlisted 16 monks plus 16 age-matched controls, members of the UW-Madison community.

Each of the 32 subjects lay in the fMRI and turned compassion meditation on and off, on Lutz’s command. Throughout, Lutz piped in happy sounds (a baby laughing and cooing), distressed ones (a woman who sounded as if she were in pain) and neutral ones (restaurant noise). Two regions lit up with activity:

If you thought that electricity-generating knee brace thing announced last week in the journal Science by researchers at Simon Fraser University in British Columbia looked like too much work, take heart. With any luck, we may soon be able to get watts out of our waistcoats. Or sweaters. Or shirts, all without moving a muscle. It's the best thing to happen to textiles since wash-‘n-wear.

The knee-mounted generator captures energy from leg muscles. But you still have to walk to generate the five watts of electricity per leg that the scientists calculate as the device’s output, or 13 watts if your get a move on—enough for 30 minutes of talk time on a mobile phone. The inventors, led by Max Donelan, think the device could replace the 30-odd pounds of batteries that U.S. soldiers typically carry to operate their electronic gear. But as I say, you still gotta walk.

Now nanotechnology researchers are announcing fabrics that scavenge mechanical energy from sources as leisurely as heartbeats and ambient noise, and turn it into electricity. Call it the ultimate power suit.

It works like this: start with synthetic Kevlar fibers from DuPont and coat them with tetraethoxysilane and crystals of zinc oxide. Zinc oxide is what’s called piezoelectric: when stressed by moving, it produces a voltage. Zhong Lin Wang of the Georgia Institute of Technology and colleagues intertwine the fibers into yarn, so that when the fibers rub against one another charge, builds up on the bristles. “The two fibers scrub together just like two bottle brushes with their bristles touching, and the piezoelectric-semiconductor process converts the mechanical motion into electrical energy,” he explains. An output wire carries the resulting current to any device you like, including a battery if you want to store it.

Here’s the beauty part, as Wang and colleagues report today in the journal Nature. Because the fibers are so small (nano, after all), even the slightest oscillation moves them—a heartbeat, a light breeze, reaching out for a poolside drink. The whole thing can be scaled up into power tents or curtains. How much juice are we talking about? Wang estimates the output at up to 80 milliwatts per square meter of fabric, enough to run personal electronics off your shirt.

“The fiber-based nanogenerator would be a simple and economical way to harvest energy from physical movement,” said Wang. “If we can combine many of these fibers in double or triple layers in clothing, we could provide a flexible, foldable and wearable power source that, for example, would allow people to generate their own electrical current.” He added, “. . . while walking”—but clearly that much exertion is not necessary. Just position yourself poolside in a light breeze, and you’re good to go.

Biggest challenge LabNotes sees? Washing your power shirt. Zinc oxide doesn’t like to get wet, so the fabric would have to be dry-cleaned.

. . . if you want to get the most cancer-fighting nutrition out of your carrots, zucchini and broccoli. Despite the conventional culinary wisdom that raw is best in terms of preserving veggies’ nutritional value, scientists in Italy—where they know a little about food—find that the right kind of cooking actually preserves or even boosts their nutritional value, the researchers will report December 26 in the Journal of Agricultural and Food Chemistry.

In the new study, the researchers at the University of Parma measured how boiling, steaming, and frying affected the nutritional contents of carrots, zucchini and broccoli, especially such anti-cancer compounds as antioxidants and polyphenols. For those of you planning to serve any or all of these three during the holiday season, here’s the bottom line:

Can four little genes (or maybe six) really make the whole bitter debate about human embryonic stem cells go away?

Two separate tems of scientists are announcing this morning that they can create the precious cells, which have the potential to turn into any of the 200-plus kinds of cells in the human body, without producing, let alone destroying, human embryos, which until now have been the only source of embryonic stem cells. If they're right, and if the recipe works reliably, then stem cells could be created from cells no more ethically problematic than human skin.

Every cell of the human body contains the exact same DNA (sperm, eggs and red blood cells being the only exceptions)—that is, the complete human genome. But neither skin cells nor muscle cells nor liver cells nor any other specialized cell follows the whole program. Only fertilized eggs—the union of egg and sperm—do that, using all the genes to produce a complete individual. Because the vast majority of genes in adult cells are silent, no one has been able to take, say, skin cells and make them turn into any chosen kind of cell, such as neurons to treat patients with Parkinson’s disease. Only the cells in very early embryos—stem cells—can transform into whatever cell you want, and you all know the ethical problems that research on stem cells raises in some quarters.

If only it were possible to take one of those specialized, or differentiated, cells and roll back the clock, back to when that skin or kidney or liver or other cell was a stem cell and had that unlimited potential. According to this morning announcement, it is possible, and scientists in the U.S. and Japan have done it.

This morning the journal Nature, citing widespread speculation, confirmed that it will soon publish the first report that scientists have used cloning technology with a primate, producing custom-made stem cells. Scientists at Oregon Health & Science University describe injecting the nucleus, which contains a cell’s DNA, of an adult rhesus monkey’s fibroblast into an egg whose own nucleus was removed. They then manipulated the egg so that it developed into an early-stage embryo called a blastocyst, from which they teased out and grew, in lab dishes, embryonic stem cells.

Their success rate was less than stellar, but that’s not unusual in cloning: the Oregon team generated two embryonic stem cell lines from 304 eggs, a 0.7% efficiency. Still, even this level of success suggests the approach might work in humans, allowing scientists to finally generate stem cells that have the DNA of an individual patient. Those cells would develop into neurons and other cells that would be perfect genetic matches for that patient, eliminating the possibility that transplanting these cells—neurons to treat Parkinson’s disease, for instance—would trigger the immune system to reject them.

In a highly unusual step, and in reaction to the South Korean fraud, an independent team of scientists in Australia verified that the Oregon team had indeed produced stem cells through cloning. Their report is being published by Nature simultaneously with the Oregon paper.

Nature asked the scientist who cloned Dolly, Ian Wilmut, to discuss the potential of such cells. He and a colleague inject a much-needed dose of realism into the stem cell debate, which has led the public to expect these almost magical cells—able to develop into any kind of cell, from pancreatic to muscle to neuronal—to be primarily used for therapy, via transplants. But as Wilmut says, “In our haste to use patient-specific cells in therapy, however, we tend to overlook that they have great value for basic research and drug discovery. . . . Realistically, a careful examination of resources and the time required to produce differentiated cells for treatment purposes suggests that large-scale use of stem cells would be impractical.” It will be interesting to see whether a public torn by the ethics of stem-cell production will support research that is at least one step removed from directly yielding cures for terrible diseases.

If you envy the lab rats with paralyzing spinal-cord injuries that have walked again, the legions of lab mice whose tumors have melted away thanks to experimental drugs, and the mice whose rodent version of Alzheimer’s has been cured—while human Alzheimer’s, paralysis and many cancers remain incurable and sometimes untreatable—join the club. For at least four years even biomedical scientists have been saying what many used to dismiss as the whining of no-nothing laymen who failed to grasp the value of basic biomedical research. Namely, “patients have been too patient with basic research,” as immunologist Ralph Steinman of Rockefeller University put it in 2003.

He meant that the basic discoveries that fill medical journals, reflecting research that has been generously supported by U.S. taxpayers (the National Institutes of Health received just over $28 billion in each of the last three years), do not result in enough new treatments soon enough. After all, there is no cure for Parkinson’s disease, for many cancers, for multiple sclerosis, for cystic fibrosis—or even for baldness, for pete’s sake. That failure threatens to shred the implicit understanding that taxpayers spend billions of dollars on cellular and molecular biology—from the genetics of slime molds to the neurology of the giant squid—for one reason and one reason only: because some of the resulting basic knowledge will lead to medical treatments for human diseases.

Now some big guns are taking aim at what more and more critics see as a broken system. This afternoon Andy Grove, co-founder of computer-chip giant Intel and its former CEO and chairman, is unleashing a no-holds-barred critique of the nation’s biomedical establishment for falling woefully short in its search for disease treatments. Speaking at the annual meeting of the Society for Neuroscience, he issues a wake-up call that should be heeded by every congressman who votes for multi-billion-dollar NIH budgets, by every CEO of a big pharma company who hasn’t had an important new compound approved in ages, by every dean of a biomedical center who bases tenure and promotion and hiring decisions on a scientist’s number of published papers with no regard to whether the research is leading to something that can alleviate the suffering of humankind.

Just to elaborate on that last point. The culture of academic biology is part of the problem. There is little prestige in “translational research,” in which basic discoveries are turned into medical treatments. Look at the very name: who gets more prestige, the author writing a great novel in her native tongue or the translator who produced a version for other audiences? So it is in biology. The basic discoveries bring the glory. Translating them is—and I exaggerate only slightly—considered the work of drones. Also, it’s easier to get an NIH grant for a simple animal experiment that is likely to yield clean results, rather than a human one that’s probably going to be ambiguous because humans—who are genetically diverse—are more complicated than fruit flies.

As Rockefeller’s Steinman told me when I first asked him about his “patients have been too patient” declaration, “Most of our best people work in lab animals, not people. But this has not resulted in cures, or even significantly helped most patients.”

Drug companies are also in Andy Grove’s crosshairs. Drawing a comparison to the semiconductor industry he knows so well, and to high-tech in general, he argues that pharma could learn something from how tech industries learn from their successes and failures. As an example of the latter, Grove notes that when Intel started new production lines, invariably a large fraction of the chips it made were faulty. Rather than throwing them out, he said, engineers scrutinized the manufacturing process to determine the cause of the failure.

Drug companies, in contrast, tend to abandon compounds that fail in clinical trials. As a result, they lose potentially valuable information on, say, whether the drug works in certain patients (those with particular genetic variations, for instance). Those rare successes, which Grove calls "golden nuggets," are washed out by the averaging of results across the whole patient population.

To take just one sorry example of the slow pace of drug discovery, in the 1960s the mainstay of treatment for Parkinson’s disease, from which Grove suffers, was L-dopa. In the 2000s the mainstay of treatment for Parkinson’s disease is . . . L-dopa. Need we contrast to the gains that the computer industry has made in 45 years?

It will be interesting to see whether a shot across biomedicine’s bow by someone of Andy Grove’s stature will give the system the shaking up it needs.