And best of all, just this week some research results were released that indicate popcorn is also a very healthy food!

I’ll get to that in a minute, but first, some background.

Nobody knows who first popped popcorn, which is thought to have originated in Mexico. Ears found in the Bat Cave of West Central New Mexico were dated to some 5,600 years ago, and 1,000-year-old grains of popcorn found in tombs along the east coast of Peru were so well-preserved they could still be popped.

By 1492, when Columbus sailed the ocean blue, popcorn was widespread in the Americas. English settlers were introduced to it at the famous first Thanksgiving feast in Plymouth, Massachusetts, to which Quadequina, brother of the Wampanoag chief Massasoit, reportedly brought a deerskin bag full of popped corn.

Popcorn kernels pop due to water stored inside a layer of soft starch beneath a hard outer casing. Heat the popcorn up to about 230 degrees Celsius and that water turns to steam, which creates so much pressure that the casing gives away. The kernel explodes, turning inside out, the starchy layer beneath the casing becoming the fluffy white confection we like to eat.

And perhaps we should be eating more of it. At the 243rd National Meeting & Exposition of the American Chemical Society, Joe Vinson of the University of Scranton in Pennsylvania and his colleagues reported on a new study that found that the healthy antioxidants known as polyphenols are actually more plentiful in popcorn than in fruits and vegetables.

That’s because, Vinson says, popcorn averages only four percent water, while fruits and vegetables are 90 percent water, which dilutes the polyphenols. (Dried fruits have more polyphenols per serving than fresh fruit for the same reason.) Popcorn provides levels of polyphenols similar to those in nuts.

The highest concentration of polyphenols and fiber is actually in the hull, which isn’t exactly everyone’s favorite part of the popcorn, but perhaps the fact they’re, as Vinson calls them, “nutritional gold nuggets,” will make you feel better about having them stuck in your teeth. Thanks to that hull, popcorn is also the only snack that is 100 percent unprocessed whole grain, far better than your typical “whole grain” cereal, which only has to be 51 percent whole grain to qualify for that title.

Specifically, the study found that popcorn contains up to 300 mg a serving of polyphenols compared to 114 mg for a serving of sweet corn and 160 mg for a serving of fruit. One serving of popcorn provides up to 13 percent of the average daily intake of polyphenols per person in the U.S, and more than 70 percent of the recommended daily intake of whole grain.

Now for the caveats! How healthy popcorn is depends a great deal on how it’s prepared. If it’s cooked in a pot of oil, slathered with butter (or worse, butter-flavored topping like that used in some movie theatres), covered with salt or cooked as “kettle corn” in oil and sugar, then obviously, though the polyphenols will still be there, there are other concerns with fat, salt and calories.

According to Vinson, the lowest-calorie form of popcorn you can eat is, as you’d expect, hot-air-popped. Microwave popcorn has twice as many calories. And fat-wise, microwave popcorn has even more than popcorn you pop in oil yourself: 43 percent of regular microwave popcorn is fat, compared to 28 percent if you pop it yourself (and zero percent if you pop it in hot air).

Does this nutritional good news mean you should eat popcorn instead of, say, oranges, apples and bananas? Well, no: fruits obviously contain many other valuable vitamins and nutrients that popcorn doesn’t have.

But it does mean, if you’re looking for a satisfying snack you can actually feel pretty good about eating, you can fire up the hot-air popper without guilt.

My personal tip: use a really good olive oil on it instead of butter. Healthier, and yummy, too!

Although my daughter swears by soy sauce. But, hey, to each his or her own.

(Photo: Unpopped popcorn cobs, from Wikimedia Commons.)

Well, you get the idea.

But, men (and let us not forget I number myself among your…um, number), science has come to the rescue, with a study, published in the medical journal Blood, that shows that in rodents, at least, there are fundamental differences between the immune systems of males and females, lending scientific credence to the whole idea of what is sometimes called “man flu.”

We’re talking really serious science here, too: you can tell by the article title, “Sex-difference in resident immune cell phenotype underlies more efficient acute inflammatory responses in female mice.” I mean, when you read that title to your wife, especially in a really stuffed-up and fatigued voice, she’ll have to believe you when you say science proves you’re sicker than she was when she had the same thing, won’t she?

And to top it all off, the lead author of the study is a woman: Ramona Scotland, an immunologist from the William Harvey Research Institute at Queen Mary, University of London.

For their experiment, the scientists exposed both male and female rats and mice to different types of infections, then observed the behavior of the two genders to see how they were affected. Within three hours, the males looked very sick, but the females carried on as normal, apparently not ill at all.

All the other variables were carefully controlled: the rodents had the same genetics, lived in the same environment, were the same age, were infected with the same amount of live bacteria on the same day at the same time—the only difference was the sex.

Now, my wife’s response to this data would have been, “Well, that’s because women are superior to men. Duh!,” but apparently that’s not enough of a response when one is conducting serious scientific research. So the scientists set out to discover the mechanism behind this difference. They measured the number of white blood cells in the body cavity and lungs of the rodents.

White blood cells, or leukocytes, come in various flavors. Two of those involved in fighting infections are neutrophils and macrophages. Macrophages gobble up invading bacteria. Neutrophils also attack infection, but in the process, they damage the infected tissue, which contributes to the run-down feeling of being sick.

The researchers found that the female rodents had twice as many macrophages, and that they were more effective at gobbling up bacteria than were the corresponding cells in the male rodents. That meant they produced less of the chemical signal that summons the neutrophils, which meant tissue underwent less damage…and hence, the females did not feel the effects of the illness as much as the males.

Or, as Phillip English wrote in his article in Cosmos Online, which is what drew this to my attention, “this all added up to a set of female rodents that were much better equipped to fight off infection than males, and felt better while doing it.”

Now, of course, all this comes with the usual caveat about this kind of research: namely, that mice are not men (even though John Steinbeck wrote about them both), and in fact the immunological balance might vary widely between different strains of mice, never mind between mice and men, yada yada yada.

But you have my permission to ignore such fine distinctions if you are male, you are sick, and you are getting too little sympathy from your wife.

Just repeat after me, “The fault is in our macrophages, not our minds, that we are wusses.”

Science proves it. ’Nuff said.

 (The photo: Regina General Hospital interior.)

(It’s interesting to note that “survival of the fittest” is only one letter away from “survival of the fattest,” and one reason we’re so fond of high-calorie foods is that when food is in short supply, it really is the fattest who are the fittest to survive. But I digress.)

I’m not very good about exercising. I periodically begin it, and periodically end it, and have never managed to make it an everyday habit on the scale of something that really matters to me, like blog-reading.

But when I do exercise, the one part I’ve always hated more than the exercise itself is the stretching we’ve long been told to precede it with. Stretching is boring and takes too long.

Which is why I take a certain perverse pleasure in pointing out that science keeps studying stretching, and keeps finding out that it doesn’t work as long advertised.

Several years ago, as I reported in a previous column on this topic—allow me to quote myself—“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,” I wrote, “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.”

Now another study has come out saying, basically, that pre-running stretching doesn’t do anything.

Presented at the 2011 Annual Meeting of the American Academy of Orthopaedic Surgeons (AAOS), the study included 2,729 runners who run ten or more miles per week. (Yuck!)

They randomly split these runners into 1,366 stretchers and 1,363 non-stretchers. The stretchers stretched their quadriceps, hamstrings, and gastrocnemius/soleus muscle groups (gastrocnemius/soleus sounds to me like a debilitating stomach virus, but never mind) for three to five minutes before running.

The result? Stretching before running neither prevented nor caused injury.

Daniel Pereles, an orthopedic surgeon from Montgomery Orthopedics near Washington, D.C., was the study author. He’s a runner himself, and he went into the study fully expecting that stretching would help prevent injury. Instead, the researchers found the risk factors were quite different: “The more mileage run or the heavier and older the runner was, the more likely he or she was likely to get injured, and previous injury within four months predisposed to even further injury,” Pereles said.

So, if you’re a runner who stretches, should you stop stretching? Probably not. The other group of people most likely to be injured were runners who typically stretch as part of their routine but, because they were placed into the non-stretch group, quit doing it for the purposes of the study.

Or, as Pereles put it, “An immediate shift in a regimen may be more important than the regimen itself.”

If you stretch before working out, then, by all means continue. But no need to look askance at those who don’t. It’s just as likely you’ll be limping as they will the next time you meet.

Honesty, alas, compels me to point out, as I did in my previous stretching column, that stretching does have other benefits than preventing injury: do it every day for three months, and you’ll gain flexibility. And stretching after exercise can be beneficial for seniors, because it helps minimize the effects of arthritis and joint degeneration, and athletes, because stretching after a strenuous workout reduces lactic acid accumulation in heavily exercised muscles.

But if someone chides you for not stretching before running, tell them science is on your side.

Just don’t tell them science said you shouldn’t exercise at all. I’m afraid that would be stretching the truth.

(The photo: Ouch!)

The first book was Meningitis. Stiff neck? You bet. Of course, I was sitting and typing for hours on end, but I’m sure that was just a coincidence. I also wrote Arthritis (my fingers are still stiff), Ebola Virus (Ebola starts with flu-like symptoms; gee, thanks, that’s specific!), Alzheimer’s Disease (which I can barely even remember writing) and Hemophilia, which at least had the advantage of being a genetic disorder that you’re born with, so it wasn’t anything I could catch.

But just because I’m not writing books about diseases any more doesn’t free me from the tendency to suspect that every minor symptom that crops up could be the sign of the fatal disease or debilitating condition I’m always sure is lurking around the next birthday. (And yes, I did turn 50 a couple of years ago…why do you ask?)

Headache? Brain tumor! Tingling sensation? Multiple sclerosis! Itch? Incurable skin infection!

What I’m really suffering from, of course is cyberchondria: hypochondria exacerbated by the plethora of medical information available, just a few keystrokes away, on the Internet.

This is so common a condition that there’s a Wikipedia entry for it, and where better to turn to information about an Internet-fueled problem than Wikipedia?

Hmm. On second thought, let’s turn to the New York Times.

In an article dated November 25, 2008, John Markoff wrote about the results of a study, conducted by Microsoft, of health-related Web searches on popular search engines, combined with a survey of the company’s employees. “The study,” Markoff wrote, “suggests that self-diagnosis by search engine frequently leads Web searchers to conclude the worst about what ails them.”

Well, duh. But why?

Which isn’t to say you should ignore symptoms, of course; but you shouldn’t jump to conclusions, either. Star Trek: Voyager may have featured a computer-generated doctor, but for the moment, you’re better off going to the real thing.

Oh, and avoid writing books about diseases. That’ll help, too.

The photo: December hoarfrost, Regina, Saskatchewan

Apparently the Canadian Broadcasting Corporation, not trusting us to do it ourselves, has decided to make our resolutions for us: it’s started 2011 with a series of stories lecturing Canadians on how unhealthy their lifestyle is, and started something called the “Live Right Now” initiative.

Yes, apparently determined to live up to its nickname as “The Mother Corp.,” CBC is telling us to eat our vegetables, quit watching TV and go outside and play, always wear clean underwear in case we’re hit by a truck (OK, I may have made that one up) and, most motherly of all, to “Go to bed, it’s past your bedtime!”

Apparently a CBC poll has revealed that six out of 10 Canadians get about one hour less than the six to eight hours of sleep recommended for most adults. (Ironically, since our clock radio is set to the CBC, I was actually awakened the other day by the CBC telling me I wasn’t getting enough sleep.)

Although I personally don’t think it’s the job of a national news organization to nag its listeners, I can’t argue with the fact that sleep deprivation is a growing problem.

Whether you blame the advent of electric light or the advent of the Internet, which keeps millions of people staying up late playing games, catching up on email, Twittering, Facebooking, or watching their 37th consecutive YouTube video of cats doing something cute, there’s no doubt we’re one sleepy bunch.

Lack of sleep does more than just make you grouchy, too. The CBC quotes Dr. Rachel Morehouse, medical director of the Atlantic Health Sciences Sleep Centre in Saint John, as saying lack of sleep can affect your metabolism, contributing to obesity and Type 2 diabetes; your immune system, making it harder for you to fight off general infections such as colds; and your mental health, contributing to clinical depression.

And, of course, lack of sleep decreases your ability to learn, focus and be alert, and has contributed to an unknown number of accidents and disasters worldwide, from individual car crashes to things on the scale of the Exxon Valdez oil spill.

Research into the physical cost of sleep deprivation is continuing. To give just one example, just this week the results were released of a study conducted by a team at the University of Colorado, led by Associate Professor Kenneth Wright, which quantified for the first time the energy expended by humans during sleep.

The finding? Missing one night of sleep drains as much energy from you as walking slightly less than two miles.

The study included seven young adult subjects, all of whom were required to stay in bed for the entire three days of the study. Their diets were carefully designed to meet their individual daily energy requirements, and they had exactly the same meals at the same times during each of the three days.

The first day consisted of 16 hours of wakefulness followed by eight hours of sleep. Days two and three included 40 hours of sleep deprivation (one sleepless night), followed by eight hours of recovery sleep.

The researchers found that the amount of energy expended by their subjects during 24 hours of sleep deprivation was about seven percent higher than during a typical night of sleep. (Interestingly, energy expenditure during the eight hours of recovery sleep was about five percent lower than normal, because they slept more soundly than usual.)

The metabolic cost of sleep deprivation would have been higher if the subjects hadn’t been confined to bed, Wright suspects, since typically people don’t spend sleepless nights lying down.

The research is of interest not only to scientists who are still trying to figure out exactly what sleep does for us, but also to those who are trying to figure out what lack of sleep does to us. And Wright is quick to point out that just because the metabolic cost of skipping a night’s sleep is equivalent to a long walk, skipping sleep is hardly a safe or suitable alternative to exercise, and in fact (as I noted earlier) has been linked with obesity.

Probably a good thing he clarified that. It’s all too easy to imagine the supermarket tabloid headlines: “I Didn’t Sleep For A Week and Lost Five Pounds!”

With the CBC currently nagging us to both lose weight AND get more sleep, the cognitive dissonance would be devastating.

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!

But that process is, indeed, imaginary. The truth is that our brains prefer to do as little actual thinking as possible. They like shortcuts—and sometimes those shortcuts can get us into trouble.

Take, for instance, what psychologists at the University of Pennsylvania call “Unit Bias,” which, they say, “causes people to ignore vital, obvious information in their decision-making process, points to a fundamental flaw in the modern, evolved mind, and may also play a role in the American population’s 30 years of weight gain.”

The researchers conducted several studies with college-age participants. In one, the participants were asked to estimate the weight of adult women, whose height they were told, by either looking at photographs or at the woman in person. Other students were asked to estimate the calories in one of two actual meals, both of which contained the same foods, but one of which had larger portion sizes.

The researchers found that the students estimating the women’s weight disregarded or ignored the height information they were provided and based their guesses solely on the women’s girth. Even when the researchers inflated the actual height of the woman by as much as 10 inches, it didn’t alter the participants’ weight estimates.

Similarly, participants simply assumed the portion sizes in the meals they were shown were typical, and guessed no caloric differences between small and large portions.

The study, published in the June issue of the Journal of Experimental Psychology-Applied, suggests that far from using logical thinking to deduce the weight of the women or the calorie content of the meal, the students simply devalued or ignored critical information.

According to the researchers, these results are an example of what they call “negative artifacts” from the brain’s evolution. Our brains, the psychologists say, have evolved to free up our conscious thinking for when it’s really needed—to face sudden danger, for instance. So, rather than taking up consciousness to cycle through a series of decisions for everything we do, our brains simply jump to the easiest conclusion without bothering to think at all.

The example the Pennsylvania researchers give is stopping at a stoplight. When the light turns green, we go, without thinking about it.

“We have heuristics in our brain—simple mechanistic shortcuts that have evolved over hundreds of thousands of years, which free up precious space in our consciousness,” is how Andrew Geier, lead author of the study, puts it. “In these atypical instances, however, it’s the shortcut that hurts us.”

Consider that green-light scenario. Most of the time, the go-means-green shortcut is fine, and at least keeps you from getting honked at by the guy in the rusted-out beater with the extra-loud stereo system behind you. But if you rely too much on that shortcut, and fail to look both ways before pulling into the intersection at the changing of the light, you may get smacked by some driver—probably the first cousin of that annoying guy behind you—whose own built-in shortcut is “yellow means drive really fast.”

These shortcuts may also be contributing to the growing girth of North Americans. For most of human existence, food has been scarce, and so whenever you had it, you ate it. As a result, we have a built-in cognitive shortcut that drives us, in the presence of abundance—say, the hotel breakfast buffet—to eat far more than we need, and even to see our laden plates as simply a normal-sized breakfast instead of enough calories to meet our energy needs for the entire day.

Worse, we see it that way even though we know, intellectually, the approximate calorie content of eight pieces of bacon, two pieces of French toast slathered in syrup, a mound of scrambled eggs, a Danish and a tall glass of orange juice (somewhere around 1,100, by my count).

Or, as Geir puts it, “The eating environment has morphed into an atypical scenario where our usually helpful mental mechanisms betray us.”

Food for thought…which reminds me; I can’t write on an empty stomach.

I wonder what’s in the fridge?

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.”

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!