Ask someone on the street to name a particularly deadly disease, and there’s a good chance he’ll say “Ebola.” Yet of the diseases I wrote about, the biggest killer by far is meningitis, the bacterial form of which kills some 170,000 people every year, according to the World Health Organization. (And if you want even bigger killers, in sub-Saharan Africa alone tuberculosis kills some 5,000 people a day, and yearly in that region malaria kills 700,000 and simple diarrhea 900,000.)

Ebola has captured the public imagination, however, because unlike most diseases, it’s gotten a foothold in pop culture, through books like Richard Preston’s 1994 best-seller The Hot Zone and the 1995 movie Outbreak.

I admit it also captured my imagination as I wrote my own book, not least because Ebola (which, by the way, is named after a river near Yambuku, Democratic Republic of the Congo, site of the first recognized outbreak), begins with fever, weakness, muscle pain, headache and sore throat—in other words, “flu-like symptoms.” Which I experienced while I was writing the book, since I was, after all, writing in Saskatchewan in the winter. Oh, sure, I knew intellectually I didn’t have Ebola, but still…

The symptoms get a lot worse than that, of course. Eventually, vomiting, diarrhea and rash develop, the kidneys and liver may stop functioning, and, in fatal cases, uncontrollable internal and external bleeding begins, resulting in the vomiting of blood and bleeding from the eyes, ears, nose and other orifices. And the most deadly of three different strains of Ebola, Ebola-Zaire, is fatal in up to 90 percent of cases.

(Fortunately, human-to-human transmission is via direct contact with blood or other bodily secretions, or contact with contaminated objects: no airborne transmission of Ebola has been documented in humans, which makes breaking the chain of transmission relatively easy with proper isolation and sterilization procedures.)

Ebola is frightening not only because it’s an awful way to die, but because there has been no effective treatment. But that may be changing, and a B.C. biotech firm is involved.

In a proof-of-concept study just published in the medical journal The Lancet, scientists report that they used tiny particles of genetic material to interfere in the replication process of the Ebola virus, and by doing so successfully prevented monkeys exposed to that virus from dying of hemorrhagic fever.

The scientists used particles called small interfering RNAs (siRNAs) to target a protein essential for Ebola virus replication. The process is similar to a natural mechanism used by all cells to silence genes.

Three rhesus macaques were given anti-Ebola-Zaire siRNAs intravenously half an hour after they were exposed to the virus, and again on days one, three and five. A second group of four macaques was given the treatment after half an hour and then for six consecutive days. The technique used to deliver the siRNAs is called SNALP (for “stable nucleic acid-lipid particles”), and was developed by Tekmira Pharmaceuticals Corporation of Vancouver.

Two of the three animals in the first group survived, and all four of the second group survived. The treatment itself seemed to produce no complications.

The results were so encouraging that lead author Dr. Thomas W. Geisbert of the Boston University School of Medicine says the work “justifies the immediate development of Ebola SNALP as a countermeasure to treat Ebola-infected patients.”

Of course there’s further research to be done: further studies in monkeys are needed to figure out dosing, toxicology and other issues before the treatment can be licensed for human use.

Still, it’s wonderful to think there may actually be hope for an effective treatment for Ebola at last…and what’s even more exciting is the fact that this approach to treating Ebola could also be used to combat other deadly viral diseases.

Even if it does make my books obsolete.

Funny thing, though: once you break one, it’s hard to think about anything else.

When first I wrote about bones, back in a 1993 instalment of this column, I told the story of my own broken-bone experience, for which I blame my big brother, Dwight (mainly because it was his fault).

I was seven years old and he was 12. We were both inside a big cardboard box that had held a refrigerator. For some reason, we’d decided it was fun to roll down the back steps inside this box. And it was fun, right up until Dwight’s friend from down the street jumped on top of the box. Inside, my brother was on top of my arm, which was up against the steps, and I was suddenly the startled owner of an L-shaped wrist.

My indignant initial reaction (I tried to say, “Now look what you’ve done,” but it came out more like “Glubbleulp!”) gave way to an intensely personal curiosity about bones. “Someday,” I vowed, “I will write science columns about them!”

This particular vow-fulfillment column was prompted by the report of a new procedure to turn blocks of wood, of all things, into artificial bones.

Developed by scientists at the Instituto di Scienza e Technologia dei Materiali Ceramici in Faenza, near Bologna, Italy, the wood-derived bone substitute promises to allow live bones to heal faster and more securely after a break than the metal and ceramic implants that are currently used.

It makes sense, because if you’ve ever seen a cross-section of a bone—there’s one at the Saskatchewan Science Centre, if you’d like to run down and have a look—you will have noticed that, far from being solid, it’s quite porous.

As I noted in that original column all those years ago, “We think of bones as hard, dead matter, like hair or fingernails, but they’re actually organs consisting of living cells embedded in a matrix of calcium phosphate and other calcium minerals, held together by collagen, the tough fibrous protein we also use to make ligaments, tendons and skin. Bone tissue constantly renews itself…dissolving old tissue and…depositing new tissue.”

That’s why broken bones can heal themselves. But when titanium is used as a bone implant, bone can’t interact with it. Instead, the titanium is simply encapsulated in fibrous tissue. Nor is it practical to introduce pores into the titanium: that weakens it to the point where it could break, inflicting more damage.

Wood, however, like bone, is porous. Bone tissue can interact with the new wood-based substitute bone, growing right into it, along with blood vessels, nerves and more.

Titanium and ceramic implants can also damage bone simply because they’re so much harder than it. Whereas natural bone flexes slightly (and that stress actually strengthens the bone), the harder, less flexible implants can apply so much stress to a particular area that the bone snaps.

So how do you go about turning wood into something approximating bone?

The process begins with a block of wood (rattan works best). It’s heated until nothing remains of it but pure carbon (i.e., charcoal). The charcoal is then sprayed with calcium, which creates calcium carbide, then heated further under intense pressure and treated with a phosphate solution. After about 10 days, the wood has become a bone-like material.

The cost? About $850 per block, which provides enough material, on average, for one bone implant. Virtually any size or shape can be created.

Dr. Anna Tampiere, leader of the research team, says the new material is strong enough to take the heavy loads bodies place on it, and durable enough that, unlike existing bone substitutes, it will never need replacing.

The bone substitute has been implanted into a flock of sheep. X-rays show that, indeed, the sheep’s bones have migrated into the wood substitute. With time, says Tampiere, “you don’t even see the join.”

Human tests are probably still about five years away, but so far there has been no sign of the sheep’s bodies rejecting the new material, raising hope that this new process could give us a natural, cheap and effective replacement for bones.

Bonus: these implants won’t set off metal detectors at airports.

Here’s the blurb from the back:

Working from high-tech labs in Canada or remote villages in Africa, epedemiologists travel the world trying to keep us safe from deadly diseases. Learn how these “disease detectives” are coming up with new wayts to fight disease, and find out if you have what it takes to become an epidemiologist, too!

I’d seen that before. What I hadn’t seen, until the books arrived today, was this very nice cover quote from Jonathan M. Samet, MD, Professor and Flora L. Thornton Chair, Director, Institute for Global Health, University of Southern California, Los Angeles (quite the title!):

“This book captures the excitement and significance of epidemiology and the hard work of being an epidemiologist. It is a great starting point for those who want to benefit world health by becoming an epidemiologist.”

Very nice. And now that I have my author’s copies, I can get the book entered into the Saskatchewan Book Awards before the first deadline of July 31.

That’s because science progresses in fits and starts. Researchers put forward a possible explanation, a hypothesis, for the results of an experiment. Other researchers attempt to duplicate their results and refine the hypothesis. Sometimes the hypothesis is completely discarded, and a new hypothesis gains sway.

But in the media, this slow process is seldom reported. It’s much easier to pick up on the report of a single study—particularly if it has startling results—and present the hypotheses put forward by its authors as fact, rather than simply one possible interpretation.

I’m sure I’ve been guilty of that myself in this column, though I try to avoid it by using phrases which, if I could only charge a dollar to every reader for each use, would have long since made me rich: “One possible explanation…” “The researchers suggest…” and, of course, “More research is needed.”

By this time you’ve probably twigged to the fact that I’m about to tell you that something you may think is a fact is anything but—and you’re right.

Go to any gym, and you’re likely to see people engaging in the time-honored practice of static stretching, bending themselves into a pose that pulls muscles and tendons tight and holding it for a few seconds.

They do this because they’ve been told, at some point, that it’s important to “stretch out” before engaging in vigorous physical activity, in order to avoid injury.

Guess what?  In all likelihood, they’re wasting their time.

This isn’t exactly news, or shouldn’t be. As Cynthia Billhartz Gregorian points out in a story in the St. Louis Post-Dispatch, it’s been five years since the Centers for Disease Control and Prevention reviewed 361 research studies done by its epidemiology program office and found no evidence that stretching either before or after exercise prevents either injury or muscle soreness.

In fact, some sports medicine experts say static stretching actually inhibits performance, decreasing power and speed, and can cause micro-tears in tendons, ligaments and muscles. Nor is stretching going to help you work out a strain: stretching it makes it worse, not better. Strained muscles should be rested, and then the focus should be on rebuilding strength.

So should you give up stretching altogether? (You know, just like you gave up coffee and chocolate before you found out both are good for you?)

No; but you might want to think twice about static stretching. Modern thinking—you know, as opposed to that old pre-2004 thinking—holds that dynamic stretching is the way to go: moving through stretches without pausing or holding a position, walking forward while grabbing the knee toward the chest, that kind of thing. A little jogging in place or skipping while swinging your arms, or going through the required motions of a particular sport at half-speed might help.

Now, static stretching does have some benefits. If you do it every day for three months, it will make you more flexible, for instance. “Senior athletes” can benefit by doing traditional stretching after—but not before!–their main workout, because it helps minimize the effects of arthritis and joint degeneration. And any athlete can benefit from static stretching after prolonged exercise because it reduces lactic acid accumulation in heavily exercised muscles.

But beforehand? Not recommended.

When you think about it, our physically active ancestors didn’t worry about stretching. As California doctor-and-author Dr. William Meller points out, “Can you imagine a caveman engaging in a program of stretching before heading out to chase down prey?” And I doubt most farm hands carefully stretched before going out for a day of tossing hay bales onto a wagon.

So why have we been stretching all these years? Because at some point, researchers decided it was good for us. Scientists continued to study the issue, however, and our knowledge evolved.

Which gives me great hope, because personally, I’m hoping for a study that says the whole “exercise is good for you” thing is similarly misguided.

If I find one, you’ll hear it here first!

In the movie Outbreak, researchers from the U.S. Army Medical Research Institute for Infectious Diseases and the Centers for Disease Control and Prevention (CDC) have to figure out how to stop a kind of super-Ebola virus from ravaging the U.S.

In 1995, the same year Outbreak came out, Marta Guerra, who already had her Doctor of Veterinary Medicine degree and was finishing her master’s degree in public health. “I remember seeing that movie and thinking, ‘Wow, that’s what I want to do!’”

Five years later, Guerra, now with a Ph.D. in epidemiology and a brand-new officer of the Epidemic Intelligence Service (EIS) of the CDC, received orders to head out on her first international mission: to study and combat an outbreak in Uganda of Ebola virus.

She joined a team in Lacor, Uganda, working in a laboratory set up at St. Mary’s Hospital, a private hospital which had much more advanced equipment than the local government-run hospital-equipment that allowed them to diagnose people with Ebola in less than 24 hours.

Accurate, fast diagnosis was important not only to identify Ebola patients but also to allow those who didn’t have the disease to be sent home, minimizing their risk of exposure.

Guerra’s tasks included tracking the spread of the disease, identifying those who had been exposed, and educating the public.

Every day team members would go to the government-run hospital and get the list of people who were newly admitted and/or diagnosed. “Then we would go out to the person’s home and make a list of contacts. Those contacts would have to be visited for 21 days. If there was anyone that appeared to be unhealthy or developing any kind of symptoms, then we would call in to the hospital to bring an ambulance out.” The effort involved 150 trained volunteers.

Over the course of the outbreak, 5,600 people who had been in contact with infected patients were identified and observed.

Although the Ugandan government had done a “wonderful job” educating people about HIV, Guerra says, the lessons learned regarding HIV actually made it harder to deal with Ebola. Whereas people who test positive for HIV remain infected for life, people who recover from Ebola are no longer contagious and are also protected from the disease in the future.

Because of what they’d learned about HIV, people thought that anyone with antibodies to Ebola was contagious and was dangerous to have around. “We’d find [survivors] totally by themselves, without food, because nobody wanted to share their food with them, allow them to use any dishes, anything.”

To counteract that, “I would definitely go up and touch them, or try to show them that I was not scared to be around them. I always ended up giving them some money so they could get food at least for a week to be able to buy some pots and pans and some things to sleep on, because some of them were not being allowed to come back to their families.”

Most people in the area would first be cared for by family members when they became ill, Guerra explains. After that, they would probably turn to traditional healers rather than trying to get to a probably distant clinic. That led to tragedies like the death of all four sisters in one family.

Team members urged the locals to go to a clinic as soon as they felt ill. “If it was malaria, then good, you got your treatment early,” Guerra would tell them, while if it was Ebola, the patient could quickly be isolated and supportive care begun.

The researchers, who knew what precautions to take, weren’t particularly concerned about contracting the disease. They were more worried about the risk of violence.

 ”We were in the territory of the Lord’s Resistance Army in northern Uganda. A lot of people had been displaced up there, a lot of people kidnapped and killed.”

In the end, though, Guerra’s team saw nothing of the rebels. “I think they were also very scared of the Ebola outbreak,” she says, and with good reason: it killed 225 people before being brought under control

Despite the difficulties and dangers, Guerra calls the experience “just wonderful.”

“There are still chances to go out there and help people who are in a very disadvantaged state,” she says. “There are still chances to go out there and do investigations.”

The chapters are much longer than these science columns, but I thought in honour of the book’s release, I’d try over the next little while to boil down some of those chapters into columns.

Call it the Reader’s Digest Condensed Books Version—not just condensed, but extremely condensed!

One chapter focuses on Jonathan Epstein, a veterinarian epidemiologist with the Consortium for Conservation Medicine. In 2005, he led the first of five expeditions into China that eventually determined that bats were the “natural reservoir” of the virus that emerged into humans in 2003 as Sudden Acute Respiratory Syndrome (SARS).

The SARS outbreak began on November 16, 2002, when the first case of an unusual form of pneumonia was reported in Guangdong province in southern China. It soon spread to countries around the world, including Canada. A vigorous containment effort paid off, but by the time SARS burned itself out, 8,098 people had become ill and 774 had died.

Scientists soon realized that SARS was caused by a new strain of coronavirus, the same kind of virus that causes many other upper respiratory infections, including the common cold.

They suspected it had emerged in the live animal markets of Guangdong.

According to Epstein, those marketplaces are “a complete menagerie. There are animals of all species, of all types, alive and dead, being kept together in very unhygienic conditions. As soon as someone picks one out, they butcher it with bare hands right there on site, so there is plenty of opportunity for cross-infection to occur among different animals.”

A WHO team tentatively concluded that the virus had jumped to humans from civets. But had it originated with civets, or did it circulate naturally in some other species?

Epstein became involved when he contacted Hume Field, a veterinarian epidemiologist in Australia, in search of research partners interested in testing bats in China for Nipah virus, which he’d been researching in Malaysia, where it emerged in 1998, killing 100 people.

Field wondered if the SARS virus might also be circulating in bats, and that eventually gave rise to the expedition led by Epstein, and the four that followed.

“There were bat biologists with expertise on a lot of things related to bats, but no one had a lot of experience collecting diagnostic samples from wild animals,” Epstein explains.

The expedition worked in extensive cave systems as much as two kilometers long, with some caverns as large as airplane hangars. To catch bats, they strung “mist nets,” similar to a volleyball net but with a much finer mesh, between two twenty-foot-tall bamboo poles.

Viruses can be transmitted by bats in their feces. To minimize that risk, the researchers wore long clothes, face masks with filters, safety glasses–and, of course gloves, made of a tough material stronger than latex that allows good movement but is puncture-resistant; bats “have pretty sharp teeth,” Epstein notes.

As each bat was untangled, it was put into a small cloth bag in which the bats could hang. That calmed them. Then the scientists began collecting samples of blood, saliva and feces.

The lab results revealed four or five different viruses within the bats, all within the SARS coronavirus family.

Putting all the pieces together, scientists now presume that bats infected with a SARS-like coronavirus were brought into the marketplace, where they came in contact with civets. In the civets, the virus mutated. It then jumped from civets to people.

“What happened with SARS is what everyone fears might happen with avian influenza,” Epstein says. Part of the mandate of Epstein’s employer, the Consortium for Conservation Medicine, is to point out that problems such as the emergence of the SARS virus arise from human behavior, not from anything the animals have done.

“The knee-jerk reaction from the public may be, well, if these bats are carrying a disease that kills people, why not just get rid of the bats. Our job is to say, no, these animals serve a very important function ecologically.

“We need to recognize that human activities are what are causing these diseases to emerge. It’s not the fault of the animals.”

Modern immunization began in 1796 when a British physician, Edward Jenner, noting that people who had had the much-less-deadly cowpox did not catch smallpox, inserted material from cowpox sores into the arm of a healthy eight-year-old boy. The boy caught cowpox, but when he was exposed to smallpox eight weeks later, he did not contract the often-fatal disease.

Vaccines have since become a mainstay of public health. Their impact has been enormous. Consider measles: in 2007, according to the World Health Organization, 197,000 people died of measles worldwide. That’s 540 people a day, or 22 people an hour. That sounds awful, and it is: but it’s tremendously good news compared to just a few years ago. Thanks to a worldwide focus on measles vaccinations, measles deaths dropped 74 percent between 2000 and 2007, and a whopping 90 percent in the eastern Mediterranean and Africa regions.

Vaccines, as I’ve written before, work by tricking the body’s immune system into treating them as a full-fledged infection. Traditional vaccines consist of disease-causing organisms that have been either inactivated or killed, so they can’t cause disease. However, they still trigger the immune system’s normal response to the presence of foreign bacteria or viruses: the creation of antibodies specifically designed to attack them.

These antibodies remain in place after vaccination, so that if the full-strength bacteria or viruses of the same type enter the body in the future, the immune system has antibodies available to attack them immediately, destroying them before they can cause infection or disease.

But vaccines have one major drawback: it may take days or even weeks for them to build a person’s immunity. If you’re exposed to a fast-moving, deadly disease before that immunity is in place, your vaccination may do you no good. As well, vaccine development, particularly in the case of influenza, is sometimes a guessing game: scientists have to try to figure out which particular strain is most likely to strike a particular area, and they’re not always right.

Which is why the report of a new type of vaccine developed at the Scripps Research Institute in California is so exciting: it holds out the tantalizing promise of instant immunity.

A team led by Professor Carlos Barbas III injected mice inflicted with either melanoma or colon cancer with a vaccine designed to trigger a universal immune response–but not on its own. It remained inert until joined by a second injection of “adapter molecules”–small molecules tailor-made to recognize specific cancer cells. The adapter molecules essentially programmed the vaccine, telling it what it should generate an immune response to.

The result? Those mice–and only those mice–that received both the vaccine and the adapter compound generated an immediate immune attack on the cancer cells, which significantly inhibited the growth of their tumors.

This is the first time this kind of chemical-based, rather than biologically based, vaccine has been successfully designed and tested, and the possibilities are exciting. Barbas points to current vaccines against HIV, the virus that causes AIDS. Many antibodies are generated, but most aren’t able to target the active part of the virus. Using the new approach, it may be possible to hone in on the active part of HIV much more precisely and effectively.

“It opens up the possibility of having antibodies primed and ready to go in the time it takes to receive an injection or swallow a pill,” Barbas says. “This would apply whether the target is a cancer cell, flu virus, or a toxin like anthrax that soldiers or even civilian populations might have to face during a bioterrorism attack.”

Three clinical trials are already underway by the pharmaceutical giant Pfizer to test this new approach against cancer and diabetes. Babas plans to continue his own research with cancer, and explore the use of this approach against HIV and infectious diseases for which no vaccines currently exist, the goal being to create adapter molecules specific to those diseases.

Keep your fingers crossed!

There are many manifestations of the aging process, most of which are far too depressing to go into, especially on a morning in late February. Still, we must all face facts sooner or later, and for many of us, the “sooner” arrives when we look in a mirror and notice…a gray hair.

It’s the advance scout of an army of pale invaders to our scalp, and it’s been the focus of speculation and research for a long, long time.

Now a new paper has been published that claims to have solved the mystery of why we go gray. The culprit, it seems, is none other than hydrogen peroxide.

“But wait!” I hear you cry. “I’ve never bleached my hair. Why am I going gray?”

Ah, you misunderstand. The fault lies not in the hydrogen peroxide applied from without, but hydrogen peroxide that arises from within.

Or, as Gerald Weissman, editor-in-chief of the Federation of the American Societies for Experimental Biology (FASEB) Journal, which published the study, puts it succinctly, “All of our hair cells make a tiny bit of hydrogen peroxide, but as we get older, this little bit becomes a lot. We bleach our hair pigment from within, and our hair turns gray and then white.”

Normally, hair is pigmented as it’s produced by hair follicles. Your exact hair colour is determined by how much of two pigments, eumelanin and phomelanin, are present. Eumelanin determines the range from blonde to black. If you just have a little, you’ll have light hair; if you have a lot, you’ll have dark hair. Phomelanin determines how red your hair is. So if you have very little of either eumelanin or phomelanin, you’ll be blonde; if you have very little eumelanin but lots of phomelanin, you’ll be a red-head; if you have lots of eumelanin and lots of phomelanin, you’ll likely have dark brown hair, and so on.

But gray hair is something else: it’s an absence of pigment. As hair follicles age, they stop producing pigment, and no one has been entirely sure why, though there have been lots of theories.

In the new study, a group of European researchers examined cell cultures of human hair follicles to see exactly what happens to them as they age. The loss of pigmentation turned out to be a complicated process.

Normally, an enzyme called catalase breaks hydrogen peroxide into water and oxygen, but as the hair follicles aged, that enzyme decreased. As a result, hydrogen peroxide began to build up. Two other enzymes, MSR A and B, normally repair the damage caused by hydrogen peroxide–but their levels also decreased as the follicle aged.

Not only that, but high levels of hydrogen peroxide and low levels of MSR A and B disrupt the formation of yet another enzyme, called tyrosinase, that leads to the production of hair pigments.

So while it’s hydrogen peroxide that causes your hair to turn gray, it’s not like it’s bleaching it white after it’s grown, the way an external application of hydrogen peroxide does: rather, it prevents the hair from getting any colour to begin with.

Which is all very well, but is only of academic interest if it turns out that, like the weather, graying hair is something everyone talks about, but nobody can do anything about.

The researchers have hopes that their research might actually point the way to an effective treatment for graying hair, however.

They suggest that it might be possible to do something about the loss of MSR A and MSR B, enabling the hair follicle to continue to repair the damage caused by hydrogen peroxide, allowing it to continue proper pigmentation of the hair it produces. “A corrected repair offers certainly an interesting target for the graying hair,” is the concluding, if somewhat Yoda-like, sentence of their paper.

Or as the aforementioned Weissman puts it, “This research…is an important first step to get at the root of the problem, so to speak.”

In the meantime, do what I do: avoid brightly lit bathroom mirrors.

It’s amazing how easily one can learn to shave in the dark.

Just in time for Christmas, two doctors, Aaron Carroll and Rachel Vreeman, both associate professors of pediatrics at Indiana University and practicing pediatricians at Riley Hospital for Children, have published a study taking a hard scientific look at some of the things “everybody knows” about topics associated with the holidays…and finding once again that a lot of things “everybody knows” simply aren’t so.

At the top of their list? “Sugar makes kids hyperactive.”

I’m the father of a seven-year-old girl, and I’ve heard some variation of this belief more times than I can count. But in the words of Carroll and Vreeman, it is “without a doubt false.”

They write, “in at least 12 double-blinded, randomized, controlled trials, scientists have examined how children react to diets containing different levels of sugar. None of these studies, not even studies looking specifically at children with attention deficit-hyperactivity disorder, could detect any differences in behavior between the children who had sugar and those who did not.” Even when the focus of the studies was children considered especially sensitive to sugar, there was no difference in behavior between children who ate lots of sugar and those who ate none.

At this point any number of parents are probably sputtering, “But I’ve seen the effect of sugar with my own eyes!”

Sorry, but it’s all in your head. In studies in which parents think their children have eaten sugar, parents rate their children’s behavior as hyperactive even if, in fact, no sugar was consumed. The difference in behavior is entirely in the parents’ minds; the children aren’t doing anything differently at all.

The sugar/hyperactivity myth isn’t the only one the doctors tackle. They also looked at the widespread belief that the number of suicides increases over the holidays. In fact, studies from around the globe show no such holiday peak. In fact, suicides are more common when it’s warm and sunny.

You’ve probably heard at some point that poinsettias are poisonous…but they aren’t. Of 22,793 cases involving poinsettias reported to the American Association of Poison Control Centers, none revealed significant poisoning. No one died, and more than 96 percent didn’t even require any treatment. And in other tests, no one has ever been able to feed rats enough poinsettia leaves or sap to poison them.

Have you heard that eating late at night–which we tend to do in the holiday season–makes you fat? No, eating more calories than you expend makes you fat. The time of day or night when you eat those calories is irrelevant.

Some people not only eat late at night, they also drink alcoholic beverages (shocking, but true). Sometimes they drink more than they should, and wake with a hangover. There are many “cures” for hangovers. In the opinion of Vreeman andCarroll, none of them work. Don’t want a hangover? Don’t drink enough to bring one on.

I had little or no personal belief invested in any of these myths (not even the sugar one, which I knew long ago had been debunked). But I confess I, like Vreeman and Carroll, was surprised to learn that you do not, in fact, lose most of your body heat through your head, no matter what you mother told you.

Apparently there was an old military study in which scientists put subjects in hatless arctic survival suits and measured their heat loss in cold temperatures. Since their heads were the only thing exposed, naturally they lost most of their heat through their heads. But if they had done that experiment with subjects in swimsuits, only 10 percent of their body heat would have been lost through their heads. It turns out all parts of the body lose heat at the same rate: the head needs no special attention (except for the ease with which ears freeze!).

I know it can be upsetting at Christmas time to discover that long-held beliefs have no scientific validity.

But hey, there are still plenty of things you can believe in: friends, family, warmth, music, beauty, laughter and love.

I believe in them all. Merry Christmas!

Failing to resist that particular temptation is of little moment, of course. Failing to resist another temptation endemic to this time of year is not: the temptation to eat…and eat…and eat.

Why do we eat more food than we need to survive, with consequences that range from the annoying (clothes now too snug for comfort) to the serious (diabetes, heart disease, etc.)?

Because as a species, until the last century or so, we’ve been more likely to be short of food than not, and so we are hardwired to eat whatever is put before us–particularly fatty foods which, over the millennia, have been harder for us to come by.

Will power alone is not always–or even very often–enough to enable us to overcome this genetic programming, which is why even if we succeed in losing weight, we almost always put it back on again.

Which naturally has led researchers to look for ways to short-circuit that genetic programming.

We have learned a few things about appetite over the years. Just in 1999, scientists identified ghrelin, a hormone produced in the gut at the times we have trained ourselves to expect food, that produces that “empty” feeling we associate with hunger.

If ghrelin were the only thing at work, we’d probably eat ourselves to death. Fortunately, other body systems produce the opposite feeling. Nerves in the stomach and upper intestine detect the fact those organs are being distended, and tell the brain we’re getting full. As well, various signaling chemicals are released as food is eaten, among them hormones that not only tell your brain you’re full but also tell your stomach to stop passing food along to the intestine–which really makes you feel full.

Then there’s leptin, which is produced by body fat itself and which muffles appetite signals, so that the fatter you are, supposedly, the less you want to eat. Unfortunately, over time our bodies can grow resistant to that signal.

If that all seems fairly straightforward, it isn’t, because there are dozens of other chemicals involved, too, and their interactions with each other and with the brain are complex, to say the least.

And, in fact, a new messaging chemical has been identified, in research reported last week by a group led by Gerald Shulman at the Howard Hughes Medical Institute. It goes by the name N-acylphosphatidylethanolamine, but you’ll be glad to know it’s been abbreviated to NAPE.

Shulman’s group, in working to understand how insulin resistance develops and leads to diabetes, has developed a sensitive method for identifying and measuring fats in tissue samples. Knowing (as noted earlier) that high-fat foods are very satisfying, they set out to use their new fat-detection method to see if any “fat derivatives” that make their way into the bloodstream after a high-fat meal communicate directly with the brain…and they found NAPE.

Fasting rats had low levels of NAPE in the blood; it shot up 40 to 50 percent when the animals were fed high-fat food, and it didn’t increase in rodents served only protein or carbohydrates.

Not only that, but injecting synthetic NAPE into the rats’ abdominal cavities or blood reduced their appetites: at the highest doses, it kept the rats from eating for up to 12 hours. They even went into “siesta” mode, as if they really had eaten a big meal.

Smaller doses delivered directly to the brain had the same effect, suggesting NAPE does indeed communicate directly with the brain.

Next they outfitted 22 rats with vests that allowed them to move freely around their cages while receiving NAPE intravenously. NAPE-receiving rats ate less and lost 10 percent of their body weight, while otherwise appearing normal and healthy.

Shulman’s team is now monitoring NAPE levels in humans, and plans to test NAPE on non-human primates…which, if it pans out, could lead to clinical trials with NAPE or NAPE-like compounds in humans in the not-too-distant future.

None of which helps you this high-calorie holiday season, alas. For now, your–and my!–only hope is willpower.

Good luck. We’re both going to need it.