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.”

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.

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.

Just for the record, reporters take no pleasure in questioning the power of drugs to treat depression. To the contrary: journalism is notorious for attracting curmudgeons, grumps and depressives—some of my best friends are one or more of the above—so we wish with all our hearts that antidepressants would work.

And that scientists wouldn't keep finding evidence that they do not.

In January I reported on the file-drawer effect in studies of antidepressants. The file-drawer effect refers to the fact that scientifically-sound studies on the efficacy of antidepressants are not published, as The New England Journal of Medicine article described. Most of those studies were negative—that is, the drugs did not help patients much more than a sugar pill (placebo) did, if they helped at all. That skews the perception of doctors, scientists and you and me about these drugs; basing our assessment of antidepressants on published studies alone is like evaluating the prowess of a baseball team when only its wins and not its losses are reported.

Now a team of scientists has examined many of those unpublished studies, obtained through a Freedom of Information Act request for the U.S. Food and Drug Administration. As many people feared, once you include the deep-sixed studies, antidepressants look hardly more effective than a placebo at lifting patients’ black cloud of despair.

For their analysis, scientists led by Irving Kirsch of Britain’s University of Hull started with the data dump they got from the FDA on fluoxetine (Prozac), venlafaxine (Effexor), nefazodone (Serzone), and paroxetine (Seroxat /Paxil). They zeroed in on differences between the improvement reported by patients receiving the drug and those receiving a placebo. As is standard in such clinical trials, neither the patients nor the scientists running the study knew which patients were receiving real drugs and which were receiving placebos.

In short, there was virtually no difference in the response to drug vs. placebo of patients who suffered moderate levels of depression, and a small difference for patients with very severe depression, they report in the study published this evening in the journal PLoS Medicine. That small difference was, however, clinically insignificant—that is, the difference was so small that government health authorities do not recognize it as a meaningful improvement: on a standard scale of depression, patients should improve by 3 points, but the spread between placebo and drug was only 1.8. The difference between drug and placebo was clinically meaningful only for patients at the upper end of the very severely depressed category.

The reason for the tiny, or nonexistent, differences? Patients respond so well to placebo—to the mere thought that something might be helping them—that there was little room for an actual drug to do more. Across all groups, response to placebo accounted for more than 80 percent of any improvement. (In contrast, the placebo response to pain drugs is estimated at about 50 percent.) That suggests that even when patients are taking and benefiting from, say, Zoloft, the vast majority of the improvement is due to what their minds are telling them—that is, the belief that they would be helped. Only the most depressed patients showed little placebo response.

The scientists conclude that there is little reason to prescribe the new antidepressants to any but the most severely depressed patients except as a last resort. Kirsch summarized the findings this way: “Although patients get better when they take antidepressants, they also get better when they take a placebo, and the difference in improvement is not very great. This means that depressed people can improve without chemical treatments.”

But it seems that there is a larger message here. The placebo response—the belief that treatment will make you better—is enormously powerful. Surely it’s time to investigate further how it works and how it can be harnessed.

I consider myself an open-minded person. So just because a group attacks drunk-driving laws and anti-smoking regulations, just because it opposes replacing the junk food in school cafeterias and vending machines with healthy snacks, just because it opposed reducing the blood-alcohol level that constitutes the legal definition of drunk, and just because it calls concerns about obesity “hype,” do I dismiss its defense of mercury in tuna fish?

Of course not.

So when the Center for Consumer Freedom sent me (and probably scores of other reporters) a press release slamming yesterday’s New York Times story chronicling the high mercury levels the newspaper found in tuna sushi served in New York City restaurants and sold in upscale stores, I didn’t reflexively think, “oh, this is the group jump-started with a pile of money from a tobacco giant.” I didn’t think, “this is the group whose leader promised said tobacco company, Philip Morris, ‘to unite the restaurant and hospitality industries in a campaign to defend their consumers and marketing programs against attacks from anti-smoking, anti-drinking, anti-meat, etc. activists.’” I didn’t automatically recall the Washington Post editorial citing “documents showing that Coca-Cola, Wendy's, Tyson Foods, Cargill and Outback Steakhouse are among [founder Rick] Berman's largest donors.” I didn’t automatically recall that Berman had, as the Post reported, “accused Mothers Against Drunk Driving a. . . of ‘junk science, intimidation tactics, and even threats of violence to push their radical agenda.’” (I found those references only later.)

Here in science-writing land, when it comes to biomedicine we try hard to stick to rigorous, vetted evidence. That means studies published in reputable journals by, ideally, scientists with no financial or ideological stakes in what they’re investigating. Testimonials and anecdotal reports of patients who swear by some new remedy don’t count (except when we need a “real person” to liven up a dry medicine story).

So you can almost hear science writers emitting a loud collective groan this evening. It turns out that doctors and other researchers have been a trifle, well, selective in which studies they publish on antidepressants.

This conclusion emerged when scientists led by Erick Turner of Oregon Health & Science University and the Portland Veterans Affairs Medical Center compared studies in medical journals to studies submitted to the Food and Drug Administration. The difference? When a manufacturer asks FDA to approve a new drug, it has to submit all studies on the drug's safety and efficacy. But no such law compels anyone to publish those studies where you and I can read them.

Lo and behold, when Turner and his colleagues compared the two batches of studies—the uncensored whole, in FDA’s files, vs. the selected-for-publication subset—on 12 widely-prescribed antidepressants approved between 1981 and 2004, involving 12,564 patients, the mismatch was jarring, they report this evening in the New England Journal of Medicine. In the published literature, 94 percent of the studies concluded that the antidepressant worked better than a sugar pill. In the FDA files, 51 percent of the studies were positive. Of 36 studies that were not positive, 33 either were not published or were spun in such a way as to seem positive.

Turner put it this way in a statement: “Selective publication can lead doctors and patients to believe drugs are more effective than they really are, which can influence prescribing decisions." Based on all the studies and not the cherry-picked ones, each antidepressant was less effective than the published literature made it seem—and that stories in Newsweek and everywhere else that rely on that published literature conveyed.

It isn’t clear, says Turner, whether negative studies get deep-sixed because of the file-drawer effect (authors and sponsors don’t bother to submit manuscripts, for reasons I’ll let you infer), or because journal editors and reviewers decline to publish the negative studies that they do receive. I think he’s being too kind. With the proliferation of journals, virtually anything can get published somewhere—maybe not in the NEJM, but in some third-tier rag, which would still count as “published.”

The result of this selective publication is no less than a distortion of science and—since these are studies that drive what doctors advise their patients to do and what patients ask for—a perversion of the biomedical system in which untainted results are supposed to benefit public health. As Turner said, “doctors and patients must have access to evidence that is complete and unbiased when they are weighing the risks and benefits of treatment.” As things now stand, they do not. So next time you read or hear a story in the media about the wonders of a new drug, stop a minute and ask which contrary evidence might be moldering in a file drawer somewhere.

Despite the widespread myth that snakes (lacking outer ears, a tympanic membrane and other evidence organs of audition) cannot hear, it seems we have been too dismissive about these reptiles’ sensory abilities.

According to physicists Paul Friedel and J. Leo van Hemmen of the Technical University in Munich and Bruce Young of Washburn University in Kansas, however, not only can snakes hear. They can hear in stereo. Through their jaws.

Snakes’ jaws are connected to an inner ear with functional cochlea. Resting on the ground, a snake’s jaw can detect tiny vibrations that act like sound waves, the physicists will report in an upcoming issue of Physical Review Letters. As a result, the footsteps of, say, a mouse—to say nothing of the footsteps of a person—cause surface waves to propagate in the ground, which the snake detects as sound and “should be regarded as significant sensory input,” conclude the scientists.

They carried out a geometric study of the anatomy of desert horned vipers and the ground waves created by the footsteps of their prey. The jaw-to-cochlea system, it turns out, is attuned to the frequencies of the prey’s ground vibrations. Worse (for anyone or anything planning to tiptoe past a snake), snakes’ ability to unhinge their jaws and swallow their prey whole means the right and left jaws can receive vibrations independently. In other words, snakes hear in stereo, and so can use the auditory information to pinpoint the locations of passers-by.

You can bet that the increase in the percent of newborns who are breastfed, from 68 percent in 1999 to 74 percent in 2004, didn’t happen because more mothers cared about strengthening their child’s immune system (one of many reported benefits of breast over bottle, according to the American Academy of Pediatrics). Instead, this period coincides with more reports that breastfeeding spurs a baby’s brain development, conferring an extra half-dozen or so IQ points by the time he or she enters school. Talk about feeding into the neuroses of middle-class parents.

But not all breastfed babies are little Einsteins, and some parents may well wonder why all the months of milk-stained blouses and balky breast pumps didn’t seem to boost Junior's cognitive development. A remarkable study unveiled Monday evening offers a clue. Researchers are reporting in the Proceedings of the National Academy of Sciences that only babies who carry a particular form of a gene derive an IQ benefit from being breastfed. Without this form of the gene, breastfeeding has no effect on later IQ.

The study, of more than 3,000 children in Britain and New Zealand, cuts through the stultifying debate about whether intelligence reflects nature or nurture. Of course it reflects both, which is not exactly a stop-the-presses statement. More interesting is the finding that intelligence reflects a specific interaction of genes and environment: in children with a particular version of a gene called FADS2, breastfeeding raises intelligence an average of nearly 7 IQ points, find scientists led by Terrie Moffitt and Avshalom Caspi of King's College London and Duke University.

James Watson has made a career out of being the enfant terrible of molecular biology, but a 79-year-old enfant is just downright icky. In the past, as I noted in a recent story, Watson has endorsed aborting fetuses if they are known to carry a gene for homosexuality, encouraged genetic engineering so we can "make all girls pretty," and posited that having a darker skin makes you more libidinous.

Now he has ventured into even stupider waters, telling The Sunday Times of London that he was "inherently gloomy about the prospect of Africa" because "all our social policies are based on the fact that their intelligence is the same as ours–whereas all the testing says not really." Although people of good will might hope that all humans are equal in intellectual potential, "people who have to deal with black employees find this not true."

Watson is in London to promote his latest book, "Avoid Boring People: Lessons from a Life in Science," with a sold-out speech scheduled for the Science Museum tomorrow. Last night the Museum canceled the appearance after Watson's remarks, but merely skimming the book would have given them advance warning of what Watson is thinking these days. He writes, “there is no firm reason to anticipate that the intellectual capacities of peoples geographically separated in their evolution should prove to have evolved identically. Our wanting to reserve equal powers of reason as some universal heritage of humanity will not be enough to make it so.”

We have been this way before. In 1990, Science magazine noted that "To many in the scientific community, Watson has long been something of a wild man, and his colleagues tend to hold their collective breath whenever he veers from the script.” Now colleagues are, predictably, condemning his remarks, with Cold Spring Harbor Laboratory in New York putting out a statement saying the board and faculty "vehemently disagree with these statements and are bewildered and saddened if he indeed made such comments.''

Watson, of course, shared the 1962 Nobel Prize in Medicine or Physiology for discovering, with the late Francis Crick, the double-helix structure of DNA, the master molecule of heredity. In his chronicle of that achievement, "The Double Helix," Watson cast himself as the swashbuckling genius fighting his way to the top, climbing over anyone who got in his way (including Rosalind Franklin, who took the x-ray images that formed the basis for Watson and Crick's inference about DNA's structure but whom Watson and Crick failed to credit at the time).

What is it about mercury and fish that spawns (sorry) such fishy science? For the second time in a year, industry has tried to undercut the government’s advice that mothers-to-be should avoid mercury-contaminated fish. Their tactics: publicize industry-funded research that touts the benefits—and makes light of the risks—of eating fish. The latest such statement, issued last week by a group calling itself the Healthy Mothers/Healthy Babies Coalition (HMHB), touched off a new round of debate over eating fish and over the impacts of one-sided science on public understanding.

Last year, the hoopla followed a study by the Harvard Center for Risk Analysis, sponsored in part by the tuna industry (tuna is a big source of mercury in the diet because Americans eat so much of it and predator fish like tuna tend to have high levels of mercury). When researchers made a worst-case assumption—that people are too stupid to understand the government’s advice to eat less mercury-laden fish but keep consuming cleaner species—they got an unsurprising result: people would lose the heart-healthy benefits of eating fish. Duh. But in the scenario where people have half a brain and follow the government’s advice to eat fish but avoid certain mercury-tainted species such as swordfish, tilefish, shark, king mackerel, and albacore tuna, both their hearts and their babies benefited (mercury can be toxic to developing brains). And yet, the press release, and contrarian media stories it spawned, focused on the first scenario, concluding that “fish warnings do more harm than good.”

There is no evidence that Americans are so worried about mercury in fish that they’ve cut back on fish consumption. Quite the contrary: per capita fish consumption has grown steadily, and is at its highest levels since records began decades ago. But few Americans are aware of the government’s advice. Only about one-third say they have heard the warnings, and most of those who have can’t name the fish they should avoid.

Also clear is that the fishing industry is deeply worried that these warnings will sink their market. The U.S. Tuna Foundation, an industry group, launched a national campaign urging women to eat more tuna, and asserting that there is no scientific basis for concern about mercury’s effects on a baby’s brain. In asserting that mercury should not be a health concern, the tuna industry disagreed with the U.S. Food and Drug Administration, the Environmental Protection Agency, the National Academy of Sciences, the World Health Organization, and numerous other expert bodies. Yet the fishing industry sponsors a web site, fishscam.com, which claims that the concern about mercury is simply “hype” and that pregnant women should simply eat more fish.

By now you will likely have heard that scientists have figured out what’s causing the honeybee crisis, formally known as Colony Collapse Disorder, in which these crucial pollinators have been dying off in droves. The stories—all over radio, online news sites and newspapers—may say more about journalism than about dead bees.

Some background. Since 2004, something has been killing worker bees that go out to gather nectar and, by the by, pollinate crops by carrying pollen from one plant to another. About one-quarter of commercial honeybee colonies in the U.S. have been affected, and the death toll is something on the order of tens of billions of bees. Commercial beekeepers are panicking and farmers are worried that their crops are at risk (or that they’ll have to pay more to beekeepers for pollination service). In the U.S., some $14.6 billion worth of crops—one-third of the nation’s food crops—is pollinated by honeybees. But no one knows what’s killing the bees. So: Big Problem. Big Mystery. Guaranteed headlines.

When the high-profile and well-respected journal Science therefore alerted reporters to its imminent online publication of a paper identifying a virus as a possible cause of Colony Collapse Disorder, and organized a teleconference on Wednesday, and every university and company involved in the research sent out hyperventilating press releases, you could almost hear scepticism falling by the wayside. No matter how solid the study, it was going to get a lot of ink. It did.

But during the press conference, the scientists practically tripped over themselves cautioning that they had not come close to proving that their suspect—a virus called the Israeli Acute Paralysis Virus—was guilty in the massive bee die-off. Yes, the scientists had found the virus in CCD-infected hives but not in healthy ones. But, they write, “We have not proven a causal relationship between any infectious agent and CCD.” All they can say is that the presence of IAPV in hives afflicted by CCD “indicate that IAPV is a significant marker for CCD.”

Note the use of the word “marker.” That means something is lying around with something else—like, say, gravestones are markers for corpses. But gravestones don’t cause corpses, and IAPV might not cause Colony Collapse Disorder. If it’s involved in a causal sense, it is almost surely not the only cause.

To be sure, many reports of the study emphasized this uncertainty. The question is whether the study deserved the attention it got. But the combination of a mystery that has intrigued the public, and the drumbeat of PR in advance of the study’s release, probably made that inevitable. And who knows—maybe IAPV will turn out to be guilty as suspected. On the other hand, the Los Angeles Times dug up this factlet: “researchers from the Army's Edgewood Chemical Biological Center in Maryland cautioned that they had unpublished results in which the Israeli virus had been found in colonies without the disorder.” And Science itself, in a news story accompanying the study, quoted one scientist this way: "This paper only adds further to the confusion surrounding CCD."

The next time some grumpy (and uninformed) curmudgeon tells you that the only way for the world to reduce its emissions of greenhouse gases is to drink warm beer (give up refrigeration), freeze in the dark (take electricity and heat conservation to an extreme) and drive dangerous little tin cans (have vehicles meet fuel-economy standards not through smart engineering but by downsizing cars), offer them two words: gas flaring.

When petroleum is pumped out of the ground, some natural gas comes with it. Typically, it’s burned at the wellhead, a process called gas flaring. Countries report how much flaring goes on within their borders, but the World Bank, taking a cue from Ronald Reagan, has gone the “trust but verify” route: it asked the U.S. National Oceanic and Atmospheric Administration to use the military weather satellites at its disposal to peer down at oil wells from 400 miles up in space to measure who is really burning how much. Two more words: Russia lies.

Just to double-check that all the glowing accounts of the sacrifices that the "greatest generation" made during World War II weren't just nostalgia-laced propaganda, I called my favorite 80-year old. Sure enough, she remembered the rationing of gasoline and butter, Victory Gardens and--this one is particularly hard to imagine--saving aluminum foil rather than tossing it after a use or two.

These thoughts came to mind after the Live Earth concerts and the MoveOn-sponsored candidates' debate on climate change, both last Saturday. At the concerts, performers urged us to . . . turn off the shower while we shaved our legs. Among the six "actions against the climate crisis" we were asked to pledge were changing four standard light bulbs in our home to compact fluorescents, buying energy-efficient appliances, shutting off energy-using equipment when not in use, and riding public transit or carpooling once a week.

Flicking off the light switch when I leave a room now counts as doing my part to avert a climate crisis? Isn't it great to live in a time when it's so easy to feel virtuous?

Of course the press whines when government scientists won’t talk to reporters. Now the government itself—well, at least the congressional branch—has noticed the same problem. The U.S. Government Accountability Office (GAO) has released a report concluding that three federal agencies that conduct scientific research, including NASA and the National Oceanic and Atmospheric Administration, the latter of which is the home of much of the nation’s climate research, do a darn good job of preventing government scientists from telling the public what they’ve discovered.

Since it’s the public that pays for the research, this is kind of like hiring a roofer to tell you what’s going on with your flashing and having him clam up on you.

The GAO, the investigative arm of Congress, surveyed 1,811 randomly-selected researchers at three agencies. It found that 102 at NASA and 76 at NOAA have been barred from publicizing their research results. (This did not include those who were shut down for valid reasons, such as that the study did not pass technical muster.)