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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

lane 1: 160 ms

lane 2: 171 ms

lane 3: 172

lane 4: 173

lane 5: 177

lane 6: 175

lane 7: 185

lane 8: 175

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 
Bob Rowan / Progressive Image-Corbis 

I used to think that the most dangerous thing about bumper stickers was that they make curious drivers inch ever closer to the car in front of them in order to read the things (“He Put the Duh in W,” perhaps, or “At Least the War on the Environment is Going Well,” or “49% ***, 51% Sweetheart; Don’t Push It,” or “If There Is a Tourist Season, Why Can’t We Shoot Them?”—for all of which I am indebted to http://www.bumperart.com). But no, bumper stickers pose another danger: drivers who plaster their vehicles with the things are more prone to road rage than drivers who leave their car or truck unadorned.

As scientists led by Paul Bell, Lucy Troup and Bell's student William Szlemko of Colorado State University report in the June issue of the Journal of Applied Social Psychology, it’s a simple matter of territoriality. Researchers have long known that drivers who have a strong sense of personal space while in their vehicle are more likely to be road-ragers, and the more someone plasters his vehicle with bumper stickers and decals the more territorial he feels about the space inside.

So why are you making that face? Because back when humans were evolving into what we are now, those specific contortions of eyes, nose, mouth and cheeks were adaptive—that is, useful for surviving.

Have you ever wondered why people the world over make essentially the same face when they’re afraid, whether they’re Maori tribesmen facing a stampede or Wall Street titans being handed a subpoena from the SEC? One explanation for that sameness has been that the expressions arose randomly, but got locked into human nature because other people could understand them: that is, if everyone made the same face for “I’m afraid,” then others in their group could read and understand it instantly—very useful for times before spoken language or when you can’t hear what the other guy might be shouting.

The same reasoning applies to facial expressions of disgust. If your dinner companion makes a face as he tears into his serving of roast boar, it’s helpful to understand it instantly before you, too, chow down on spoiled meat. The sameness of facial expressions is called cultural invariance, and it means that the Maori tribesman can read the hedge fund manager’s expression and the manager can read the tribesman’s.

This is probably not going to placate the fans of Pluto (the denizen of our solar system, not the Disney dog) who are still furious that the International Astronomical Union demoted it from a planet to a “dwarf planet” two years ago, as my colleague Jerry Adler chronicled. But the IAU, which decides these things, has now ruled at its meeting in Oslo that we can forget the whole sorry “dwarf planet” fiasco. Those little bodies that don’t qualify as planets will henceforth be called . . .  “plutoids.”

For those of you for whom the whole Pluto-demoting episode is too painful to recall, a brief recap. In 1992, astronomers David Jewitt and Jane Luu of the University of Hawaii discovered the first of what are now known to be more than 1,000 orbiting the sun beyond Neptune in the Kuiper Belt. Called “trans-Neptunian objects,” they were bound to include at least one larger than Pluto. Sure enough, in 2003 astronomers led by Mike Brown of Caltech found one: at 2,500 kilometers across, “2003 UB₃₁₃” was indeed larger and more massive than Pluto. If Pluto is a planet, this thing should be called one, too.

To head off a torrent of new “trans-Neptunian objects” demanding classification as planets, the IAU voted to define a planet as a celestial body orbiting the sun, massive enough that its own gravity pulls it into a roundish shape, and with enough gravity to have “cleared the neighbourhood around its orbit” of asteroids and other chunks left over from the formation of the solar system. It was the third requirement that doomed Pluto: “Pluto now falls into the dwarf planet category on account of its size and the fact that it resides within a zone of other similarly-sized objects known as the Kuiper Belt,” the International Astronomical Union explains on its website. It is just too wimpy to clear out its orbital neighborhood.

That left only Mercury, Venus, Earth, Mars, Jupiter, Saturn, Uranus and Neptune as planets. Joining Pluto as a dwarf planet was Eris—the original 2003 UB₃₁₃. Eris is, appropriately, the Greek god of discord and strife, which is exactly what followed Pluto’s demotion.

Will junking the disrespectful term “dwarf planet” in favor of “plutoid” appease Pluto fans? With only the two members so far, it’s not exactly an impressive group, but astronomers fully expect to discover more of them in the Kuiper Belt.

Related Link: The Girl Who Named a Planet

When you’re sitting in the dentist’s chair waiting to have a cavity filled, you don’t see the package the amalgam filling comes in. But if you did your eye might well be drawn to a couple of “contraindications,” med-speak for “situations in which the dentist should not use this product.” In addition to ho-hum warnings about not using the amalgam, which contains about as much mercury as a thermometer, in patients known to be allergic to amalgam (duh), the manufacturers say it should not be used in children age 6 and under, or in pregnant women.

The reason, of course, is that mercury is a known neurotoxin, especially dangerous to developing brains. For decades anti-mercury activists have pushed the industry to develop substitutes (so-called composites, or resins, are now available), and even to persuade people to have their fillings ripped out, but have made very little headway.

Now they have won a big one. In a legal settlement, the U.S. Food and Drug Administration has changed the information on its Web site about amalgam fillings to say that they “may have neurotoxic effects on the nervous systems of developing children and fetus,” and that pregnant women “should not avoid seeking dental care, but should discuss options with their health practitioner.” Previously, there was no such warning. The FDA also agreed to decide by next year whether mercury fillings need more regulation.

When I write about new science books in my On Science columns for the print magazine, I try to pick ones that are Important and Interesting--you know, those that expose how corporate scientists cook the books when it comes to studying the toxicity of their products, or that explore how the human brain evolved. Not exactly the kind of book you can read with one brain hemisphere tied behind your back.

So let me atone by recommending a pure potboiler, the kind of thing that will even make waiting half an eternity for a delayed plane flight bearable. "Final Theory," by Mark Alpert, is a "Da Vinci Code" lookalike (scientist gets killed in first chapter; mild-mannered scholarly hero swoops in to solve mystery and vanquish bad guys; thrills and more murders ensue) but with a physics theme: Einstein actually did discover a unified field theory (something he worked on--fruitlessly, in real life--until his death), but hid it away so that evil humans could not harness it to produce a weapon that would make atomic bombs look like BB guns.

Among those in pursuit of the theory: the FBI, the Pentagon, a crazed Russian hit-man fresh from assignment in Chechnya, a surprise villain whose identity is not revealed until more than halfway through, and our hero, Columbia University science historian Mark Swift, ex-grad-student of the physicist whose death by torture gets the ball rolling (and who was himself an assistant to Einstein during his last years). Well-plotted, well-written, the book even has sweet references to Scientific American, the magazine where author Alpert is an editor/writer. Extra points for loyalty.

 Only quibble: the climactic scene takes place at Fermilab, amid superconducting magnets and speeding antiparticles. I kept waiting for Alpert to somehow make use of the lab's famous herd of American bison--have them charge the bad guy? provide a hiding place for our heroes?--but no such luck. You'll love it anyway.

Two phrases that drug companies almost never want to see in the same sentence: “clinical trial” and “side effects.” Almost any time an experimental drug has an effect other than the intended one—treating heart disease, diabetes, whatever—it’s bad news, which is why the huge majority of drugs flame out in clinical trials and never reach the market (or get pulled from the market, as Vioxx was when it was found to raise patients’ risk of heart attacks).

But every once in a great while, a side effect offers new possible uses for a drug. The most famous example is minoxidil—better known as Rogaine—which opens up blood vessels and was initially developed to treat high blood pressure. But when men began developing an interesting side effect—growing hair—the manufacturer (Upjohn, whose remnants have since become part of Pfizer) saw whole new possibilities, and the rest is hirsute history.

Now Allergan, Inc., best known as the maker of Botox (though it also makes Lap-Band, placed around a patient’s stomach as a treatment for obesity), may be in the same happy position, and Maybelline might want to look over its shoulder: a glaucoma drug that Allergan sells under the name Lumigan turns out to grow eyelashes that a model would kill for. At a conference in New York this week, the company announced that it would seek approval for this use of Lumigan by the end of the third quarter of 2008.

The company suspected it might have a hit on its hands when “no one in the clinical trial” returned the unused portion of the drug, Allergan’s head of R&D, Scott Whitcup, told me when he dropped by this morning. The company expects approval for this use—the drug would be applied to the base of the lashes, with each application lasting maybe three or four weeks—by next year.

The pharmaceutical industry has good reason for taking such side effects seriously, rather than abandoning a drug that does unexpected things. Although pharma R&D spending has soared past $40 billion a year (inventing, developing and testing a new drug costs something north of $800 million, if you include all the busts), the number of new FDA approvals has stagnated. “More and more,” said Whitcup, “people are realizing that ‘side effects’ might be effects,” as in something a company can market a drug for.”

Lush eyelashes aren’t exactly a cure for cancer, but the principle is a sound one: these days, drug companies can't afford to let any biological effect of a compound go unexplored.