A new pipeline for antibiotics

When I was hired at the Canadian Medical Association Journal in 1991, it was because there were so many ads for drugs that they needed people to edit copy to keep the ads from bumping into each other. I joked that Prozac was paying my salary.

It turns out that was the crest of a wave of innovative drug discovery. Releases of novel drugs are less common today. Many of the new drugs are “biologics” engineered from DNA or proteins, many of which are for chronic conditions and diseases. And a lot of new drugs are so-called “me too” drugs, similar to other recently released drugs so that the manufacturer can grab some of the market. In this picture, there has been little new for pathogenic illnesses since the protease inhibitors revolutionized HIV treatment. It’s as if everyone has figured all the antibiotics have been found.

I recently covered the discovery of a new antibiotic for CMAJ. Several other media outlets had the story as well — it had been published in Nature. But I quickly realized that the particular antibiotic wasn’t the story. There had been some excellent features recently on “antibiotic hunters” who were scuba-diving in Greenland to find new antibiotics. Literally going to the ends of the earth. The reason for the extreme measures is that sources of antibiotics nearer to the lab had been “overmined” in the words of several researchers. The real story is that several research teams have figured out new ways to find antibiotics from old sources. There are lots of antibiotics all around us: we just didn’t know how to “tame” them, as the researchers call it. Some of the newly discovered antibiotics are coming from people’s back yards!

A lot has been made of the use of these novel antibiotics to overcome resistance, as this is a major problem in infection control. Bacteria and viruses adapt genetically very quickly, doing a kind of DNA juggling that other organisms can’t even do, swapping genes with other bacteria and reorganizing their own DNA. How can lengthy drug development cycles keep up with these fleet pathogens?

Yes, resisting resistance is one benefit of novel antibiotics. However, I think the molecules and pathways now being studied will go much farther than addressing resistance. If researchers can find thousands of potential antibiotics, some of them may be active against viruses — for which we still have very little –, cancer, and many chronic diseases for which we do not know the cause but which may be pathogenic. In fact, in a generation or two we may think of drugs in an entirely new way, as capable of curing illnesses minor and grave that today are accepted as incurable. A century from now, medicine may be as far ahead from today as it is today from our grandparents’ day.

Good news: Ebola has peaked

Deep within the newspaper today, a spark of good news: new Ebola treatment centres in Liberia are sitting 80% empty. Because Ebola is declining. Hurray. Health officials caution there are still hotspots and there may be another rise, but the trend is in the right direction.

With the official death toll around 5000 but the real toll probably more like 10,000, this was the next epidemic everyone feared. But “fear” is the operative word here, because the hyperbolic reaction outstripped the reality. I read columns in which opinion leaders blamed the World Health Organization, blamed doctors, blamed Obama (for goodness’ sake). If you believed any of this nonsense, you would think that no one did anything they should have.

But the reality is precisely the opposite.

Before 2006, there was no real global public health system. The World Health Organization (WHO) tracked only a few developing-world diseases. But that all changed, and the thing that changed it was SARS. When SARS broke out in China, the Chinese public health system did not have the tools in place to cope with it. It then took the Chinese government much too long to admit that the country had an outbreak. By that time, SARS had reached Canada, and the WHO said people should stop travelling here. Conferences were cancelled and Toronto streets were empty, which was ridiculous given that very few people were exposed, and most of them were doctors and nurses treating the sick. Canada’s economy suffered a loss of billions of dollars unnecessarily.

In the wake of SARS, a lot of people around the world got together to put in place a functioning world early-warning and intervention system. The result was the International Health Regulations, which came into effect in 2006. All UN members agreed to abide by the regulations, which give the WHO new powers to monitor outbreaks and knock on government doors, asking, “What’s going on?” The regulations also require countries to have a public health system. If a serious situation arises, an emergency committee is formed of experts from around the world. They can declare an international emergency, which has important ramifications. It means that the host country has to get on top of the epidemic, or the UN will walk in. But — and this is key — it does not mean trade and travel stop. On the contrary, the WHO tries to keep supply lines open.

The regulations got their first work-out during the H1N1 epidemic, which was the first declared international emergency. My Mexican colleagues explain that Mexico welcomed the involvement of the WHO, which worked side-by-side with the Mexican government to get the outbreak under control there. The WHO has also worked closely with China during its avian influenza outbreak and with Saudi Arabia during its outbreak of a new SARS-like virus, MERS. Neither was declared an emergency, but the close monitoring by the WHO nudged and supported the Chinese and Saudi Arabian governments to handle the outbreaks properly. The next emergency declared was an outbreak of polio in war-torn Syria… who knows what is going on there.

After putting out these fires, WHO was hit with the conflagration: Ebola. This was the nightmare the regulations had been set up to face: an outbreak growing at a geometric rate in countries with poor public health infrastructure and few resources. The WHO was quickly overwhelmed, and the UN set up a special body to cope with the outbreak.

I get the WHO’s daily progress reports, and amid the skyrocketing death toll there was a lot of good news. Many countries committed money and health-care workers to fighting Ebola right on the ground. Several African countries contained small outbreaks and conducted careful contact tracing to find all those infected. They quickly eliminated the virus. Local education and safe burial practices were instituted and started working to contain new infections. Travel and trade were kept open, and countries like Canada that imposed ridiculous entry conditions had their wrists slapped. (If it had been Canada with an outbreak like SARS, we would have been singing a different tune.)

In fact, as some commentators have noted, this was the first real test of the International Health Regulations, and the WHO passed. Ebola has been turned around. It did not become a pandemic, and most of the world is safe. Sure, there will be some lessons learned, but the fundamental approach is sound.

We have a lot to thank the WHO for. And it behooves us to cooperate with the WHO and abide by the regulations against the day that an emergency is declared here and we need to keep things going while battling to save lives.

Another day older and deeper in cell senescence

I don’t know about you, but I’m getting older. It has even started to show: grey hair, thinner skin, “fine lines,” more muscle pains that take longer to get better.

But while more of us are older than at any other time in human history, we are in our infancy in understanding aging. In the mid-1990s, I attended a talk by Leonard Hayflick, author of How and Why We Age (1994). Work conducted over the 30 years before Hayflick’s book had established some of the mechanisms of aging. But before that, we had little idea why the body aged.

Hayflick is a folksy, easygoing talker, who walked a group of non-specialists through how cells – and we – age. At one point, he picked up a fireplace poker to point at his projected slides. He said cheery things like there’s no reason for us to be around after we reproduce and raise our children. That is, from an evolutionary point of view.

Hayflick explained that the reason we get old is that our cells get old. Here’s why: every time they divide, cells lose a few of the little repeated bits of DNA at the ends of the chromosomes. This is not good, because that DNA might have some genetic code that runs something in our body. So the chromosomes have caps at each end, called telomeres, that don’t do any protein coding and that shorten after each division. As well, telomeres prevent chromosomes from joining or rearranging, which could result in abnormal cells, which could lead to cancer. Eventually, those telomeres are all used up, at which point the cell stops dividing. This was one of Hayflick’s breakthroughs, and the finite number of divisions is called the “Hayflick limit.” At that point, the cell may enter the cell’s equivalent of old age (senescence), in which does not divide and barely functions, or self-destruct (apoptosis). As various cells stop growing or die, we age, losing functions of our body, until one day some vital function stops altogether.

It’s a good thing cells get old and die, because it turns out the only type of cells that don’t age and die are cancer cells. These cells are immortal; their telomeres don’t shorten; they keep on going. That’s why the cells taken from the cervical cancer suffered by Henrietta Lacks, an African-American woman, in 1951 are still alive today and used extensively in scientific research (HeLa cells).

It’s ironic that the search for eternal life is ultimately self-defeating: the only immortality to be found is in cancer, which can end your life. So stop complaining about getting old, because the only biological alternative is worse.


But the relationship between aging and cancer turns out to be more complicated than that. As a scientific editor, I work with a number of authors on papers for submission to journals (among other things I do). One of the authors I work with, Richard Richardson of AECL and McGill University, studies cancer and aging.

Cancer rates go up with age. Here’s a typical graph, from one of Richardson’s papers (data for all types of cancer from Statistics Canada, graph reproduced here under a Creative Commons licence; ASR stands for age-standardized rate):cc-12-2468-g1

You will notice that the cancer incidence rates also begin to fall after about age 80.

Richardson looks at why these rates change with age, rising quickly and then falling off. As he explains, “Aging and cancer are inextricably entwined and involve multifaceted mechanisms.”

One such mechanism is a gene called TP53, which other authors have called the “guardian of the genome.” It is involved in some of these end-of-life processes for cells, ensuring that cells go into either senescence or apoptosis once their telomeres are used up. In an article published in Cell Cycle (doi: 10.4161/cc.25494) in 2013, Richardson looked at TP53’s role in aging and cancer. TP53 is a gene that often mutates as we get older. Mutations can stop it from doing its job in keeping old and abnormal cells from becoming cancerous. As a result, these mutations have a significant role in cancer, and can make a tumour malignant or invasive. As well, the mutations are implicated in cancer affecting a wide range of organs and cells. Richardson looked at large global databases of cancer tumours to tease out the relationship between TP53 mutations in these tumours and patient age. One theory of why cancer rises quickly with aging is “genomic instability” – problems with the entire genetic code that develop as we age. Experiments have shown that TP53 mutations may be a cause of this genomic instability. Based on his study findings, Richardson estimates about one-quarter of the aging-related rise in cancer is probably due to mutations in this gene.

So, aging is what cells do normally, and the only cells that resist aging are cancer cells. But aging also raises the chance of cancer if the TP53 gene is no longer working the way it is supposed to.


That’s not all that is happening as we age. Cells are growing and dying, and our organs are changing as a result. Richardson’s research shows that some of these processes actually start early in adulthood, and may hold clues to cancer and age-related changes.

First, cells in the body are replaced on a cycle, and the “turnover” time to replace cells varies widely, depending on the type of cells. Some cells with a fast turnover (but, mysteriously, not all) are more prone to cancer. Epithelial cells, for example, have a far higher turnover and cancer incidence than any other type of cells. These cells make up our skin and the tissues lining the inside cavities of our bodies, as well as many glands.

We also know that most of the tissues and organs of the body lose mass as we age. We may not realize that they are getting smaller because the mass lost is “functional” mass of the organ tissue, which may be converted to fat (in case you hadn’t noticed) or fibrous tissue.

In a paper published in Experimental Gerontology (doi: 10.1016/j.exger.2014.03.015), Richardson and his colleagues found that the tissues and organs start to lose mass when their owners are 12 to 50 years of age, depending on the organ, with most organs starting to decline in a person’s 30s. As well, in many organs the mass loss accelerates as we age, although in some organs this is not a strong or consistent effect.

They also showed that cell turnover time and this mass loss are related. As we age, the cells enter their old-age state or self-destruct, there are fewer and fewer replacement cells, and the organ or tissue shrinks. This happens earlier in cells that turn over faster because of the Hayflick limit – the number of divisions that can happen before the cells stop dividing. There are other factors that could lead to mass loss, too, so it’s not entirely straightforward.

So far we’ve tied together cell turnover, mass loss, our old friend Leonard Hayflick, and aging. Now cancer comes in.

Prevailing theories of aging and death hold that we lose overall fitness (all our bodily functions, not just why I can’t do the tougher exercises at the gym anymore) and generally decline with advancing age for an evolutionary reason. Evolution has selected humans who are strong and bear and care for children when they are young, but the trade-off is that we age and decline. Basically, these theories say, when humans were evolving we never made it to old age because of accidents and diseases, so the fact that our bodies started breaking down when we were older (through DNA damage as well as “wear and tear”) wasn’t part of the equation. (Both Richardson and I dispute this view: there is evidence that even early Homo sapiens achieved old age.) But Richardson asks, if this theory were true, then why would our organs start to shrink when we’re young adults? It seems like there’s a reason why the aging process starts soon after we start to have children. Richardson’s research seems to contradict the longstanding theory that evolution just turned a blind eye to aging.

The mass loss seen even in young adults is linked to cell turnover, which leads cells to exhaust their divisions and attain the old-age state (senescence). If more cells are becoming senescent, and fewer are growing, this prevents cancer. In fact, Richardson theorizes, this mechanism may have evolved to prevent cancer in young people in their prime reproductive (and just plain productive) years. If so, it has done a good job, as cancer rates in young people are low (see graph).


Richardson thinks the patterns of cancer throughout the human lifecycle may also have to do with stem cells. Stem cells start the process to grow or replace tissues and organs. The stem cells produce progenitor cells, which can then “differentiate” into other types of cells, such as blood cells or bone cells, that are needed by the body. Stem cells can divide also into two stem cells (self-renewal).

Throughout life, the stem cell capacity slowly diminishes. While the body is growing, there are plenty of stem cells to supply the huge demand for cells for development. Growth tails off in the 20s, but then the demand for new cells starts to increase again as existing cells enter the old-age state (senescence) or self-destruct (apoptosis) and need to be replaced. In particular, the need for new cells to replace damaged cells increases throughout life. At a certain point, the demand for cells starts to outstrip supply. This is when the tissues and organs shrink. However, Richardson believes that, in some people, this demand-to-supply ratio becomes very high, either because of extremely high demand for new cells or “exhaustion” of stem cells. In this condition, some of the stem cells may become precancerous, and lead to cancer after a lag of a few years.

Richardson explored this hypothesis in a paper in Mechanisms in Ageing and Development (doi: 10.1016/j.mad.2014.06.001) by looking at age patterns and stem cell supply in relation to bone tumours; the demand-to-supply ratio fits the patterns seen in common ages when bone tumours are found.

And that drop-off in cancer rates in people over 80? Telomere length and cell senescence stabilize in elderly people, which means that the rising demand-to-supply ratio for stem cells peaks and then declines.



What I like about research – all research – is that it points us in a useful direction. For example, researchers have long wondered why women live longer than men, on average, and looked at estrogen, immune factors, oxygen usage and so on. Well, it turns out women’s telomeres are about 9% longer than men’s (according to evidence from peripheral blood cells), which is probably an important factor.

Understanding the relationship between aging and cancer may one day open doors in preventing and treating cancer. It is basic research like this that leads to the big health breakthroughs. But that can take time. I find that understanding how our bodies work can also help us accept the current reality of our human lives.

Predatory publishers in the crosshairs

At the Council of Science Editors’ meeting in San Antonio, Texas, this May, there was a lively session on predatory publishers. And an important step has been taken in turning the tables on these fraud artists.

Four major organizations are uniting to address the problem in a constructive way. The groups involved are the World Association of Medical Editors, the Committee on Publication Ethics, the Directory of Open Access Journals, and the Open Access Scholarly Publishers Association. They have agreed on a joint statement on The Principles of Transparency and Best Practice in Scholarly Publishing, available on the web sites of each of the organizations.

The statement sets out the expectations for a peer-reviewed journal, and the requirement that this information be fully available on the journal’s web site. The statement can be used by authors as a checklist to help ascertain that a journal is bona fide and not predatory.

More importantly, the organizations plan to ensure their members adhere to these requirements. While the first step will be to give the journal a chance to comply, if there are serious failures to meet these requirements, the journal is out.

I think the other step being planned is even more crucial: the organizations are going to put together a list of reputable publishers and journals. This is the reverse of Beall’s list: a list of the bona fide journals rather than the predatory ones. This will give authors a place to check on a journal they are planning to submit to — someone else has done the homework for them.

These are excellent moves in the right direction. But they stop short of what should happen: these so-called “publishers” should be shut down. That’s tricky to do when the “publisher” cannot be located, does not publish the names of its owners, and is in another jurisdiction from its victims. And what is the legal mechanism to stop them? These are all interesting problems, and they define the next steps in protecting the legitimate community of scholarly publishing.

Predators and prey

I would like to congratulate Ottawa Citizen science reporter Tom Spears on the latest exposure of what are being called “predatory publishers.” In his recent article, Spears put together a pseudo-scientific article that was complete gibberish to expose these fly-by-night “journals” that are actually scams to lure in beginning and foreign scientists looking for a publication credit.

In my career, I have had brushes with these modern-day confidence men (and possibly women!). Aside from my strong visceral reaction that anyone who would prey on young scientists is the lowest of the low, I find it hard to believe that anyone thinks “scientific publishing = easy money!”

Let me tell you about my experiences. Back in about 2009, I got a message from an engineer who was looking to publish an article in the Canadian Journal of Civil Engineering at NRC Research Press, where I worked. He had sent a manuscript to a website claiming to be CJCE; it was posted immediately and the “journal” then demanded money. He directed us to the website, which was an unknown publisher claiming to publish several journals called “the Canadian Journal of…,” including the Canadian Journal of Civil Engineering, which, in fact, we published. There was no editor listed, just an email address and a street address that was an apartment building in Toronto (no apartment number, no phone number). Long story short, there was a cease-and-desist letter and the CJCE name was taken off the website.

I teach scientists in Mexico (Universidad Nacional Autonoma de Mexico) to write articles for submission to English-language journals in English. From my first teaching experience in 2011, I became aware that several UNAM faculty were getting emails asking them to submit to journals they had never heard of. I investigated these journals, and many of them were suspect. I started warning Mexican scientists about these.

Several UNAM professors have told me that they get letters asking them to join the editorial board of a journal they have never heard of and promising them it won’t involve any work. Furthermore, the suspect journals ask immediately if they can use UNAM’s logo on their website.

One of my former students wrote an interesting interdisciplinary paper. She was understandably having difficulty finding a journal for it because it doesn’t fit into the scope of many journals. She was also hesitant to send the paper to solidly ranked journals. (I find that many beginning authors and those from developing or emerging countries lack the confidence to try an established journal.) Anyway, she had looked into journals that she had never cited and had found a journal that seemed to be in the right area for her paper.

Fortunately, she discussed her choice with one of my teaching colleagues, who was suspicious and asked me about it. The journal was with one of the most notorious predatory publishers. This so-called “publisher” had republished copyrighted articles without permission, didn’t seem to have a place of publication, put editors’ names on journals without their knowledge, etc. I did some research for my student and sent her several links to information about the predatory publisher. Fortunately, she decided against sending her paper to this journal.

This is a good example of how even intelligent researchers get pulled in.

Many editors and professors used to advise authors to try beginning or start-up journals for an early publication. Now, I tell my students not to send a paper to a journal that appears to be a start-up because of the very real possibility it is one of these predators. Instead, I show them how to research a journal, checking that the editors and publisher are well-known and reputable, and that the journal is indexed in standard indexes such as Web of Science, MEDLINE/PubMed, Chemical Abstracts, and other curated disciplinary indexes. (Google Scholar is not an index, it’s a search engine, and it crawls many predatory journals.) I tell them to submit to journals they actually read and cite.

As Spears’ article points out, the problem is completely out of hand.

The main person addressing this issue is Jeffrey Beall, a librarian at University of Colorado Denver. In his blog here on WordPress, Scholarly Open Access, Beall first started listing suspected predatory publishers and journals; I believe he coined the term “predatory” in this context as well. Beall has taken flak for his choice of predatory journals (some journals claim to be legitimate start-ups, and the usual anarchists claim that Elsevier is predatory ~sigh~), but at least he addressed the issue. He deserves our gratitude.

While journals and researchers have taken steps to expose these predatory publishers, to my knowledge there have been no moves to try to curtail them. I think it’s time that the legitimate editorial/publishing industry does something. Coming up on the first weekend of May, the Council of Science Editors annual meeting will include a session on predatory publishing, convened and moderated by my colleague Tamer El Bokl, a managing editor at Canadian Science Publishing (NRC Research Press). I am hopeful that this will raise awareness of this issue among editors and spur CSE on to some action on this front.

Citizen science and the loss of the loon

The sight of a painting-perfect loon on a lake this weekend reminded me that I covered the annual loon count on this blog three years ago. In that post, I discussed how Bird Studies Canada had turned the national summer pastime of watching loons into an exercise in “citizen science” — the involvement of non-scientists in scientific endeavours.

Now the Canadian Lakes Loon Survey has yielded important scientific evidence.

The common loon, with its characteristic silhouette and unearthly like-no-other-animal calls, stands out in another way. It is an “indicator” or “sentinel” species, defined as an organism that is sensitive to the environment and hence can provide an indication of the health of that environment. A canary in a coal mine, a distant-early-warning system.

In a study published this year in Avian Conservation and Ecology, authors Tozer, Falconer and Badzinski used the data from citizen observations to model the reproductive success of common loons in Canada. Loons are sensitive to changes in pH (acidity) and to methylmercury, making them an important indicator species for changes in these variables. Furthermore, methylmercury in combination with higher temperatures and acidity has a synergistic effect — more than the sum of its separate effects — on loon breeding success.

The analysis shows that loon reproduction has been going down at a worrying rate since 1992. Reproduction is more successful in western Canada than eastern. These findings are correlated with changes in acidification of lakes and methylmercury levels, but the authors caution that there may be unknown factors in addition. A correlation like this one is suggestive, but cannot prove cause-and-effect.

According to the model these authors developed, at a certain pH level in a lake, loons no longer reproduce enough to replace themselves. That is, the population no longer increases but starts to decline. In biology, this is called the “source-sink” threshold.

In lakes with a pH of 6.0, this threshold may have already been breached in 2001, according to the calculations. Other lakes with a current pH of 8.0 probably won’t hit this point until about 2034. Overall, the authors figure that the population is still increasing, but marginally, and if the declining trend continues, the total population will soon start to decline.

This is a different picture from the one painted by another study, the breeding bird survey, which showed increasing numbers over the same period. By contrast, while this new study indicates overall increase, it shows lower success rates, decelerating into the negative zone in some areas.

It’s an impressive achievement for citizen science, which has proven its worth, providing more data than possible in a limited scientific survey.

It’s also a red flag on environmental mercury and continuing acid rain. These problems have not gone away — far from it. The loon’s call is a warning not only about one of our iconic fauna but also about the future of our delicate lake ecosystems.

Where will the next pandemic come from?

You know how “pandemic” is just a word until you’re in bed delirious, feverish, shaking with chills, as one day blends into another? This was what happened to me in the fall of 2009. Unfortunately for me, I had been in hospital for routine surgery at the end of September. The nurse working closely over me a day or two after the surgery suddenly said, “Oh, I don’t feel good.” I told her to go home, and she vanished, but, sure enough, the next day I started feeling sick. The nurses figured I had caught a cold, and I was discharged. Once I was home, the fevers started. My husband took me to the hospital when I complained my chest felt weak. After many hours in an isolation room, I got a chest x-ray and a shot of toradol (which helped). The doctor told me they weren’t taking blood samples any more, as all influenza was coming back H1N1. She gently told me I had a mild case. I told her I had never been sicker from “just” influenza in my life. She told me cases were considered mild if the patient could breathe.

With this personal reason to take an interest, I became fascinated by the response to H1N1.

Remember, with avian influenza popping up occasionally and SARS a recent memory, there had been a huge amount of public health work on the possibility of a pandemic. But a lot of it was based on likely scenarios – a serious influenza, discovered in Asia, spreading rapidly around the world through person-to-person contact and international travel.

The big problem with epidemics is that they are unpredictable. They might be caused by any type of pathogen: bacteria, virus, prion, or something completely new. Existing pathogens might suddenly become deadly: SARS and the new coronavirus (which I recently wrote about in the Canadian Medical Association Journal) are from a virus family that normally causes “colds.” And pathogens can come from anywhere on the globe. While avian influenza (see my article on the new avian influenza virus in CMAJ)and SARS came from southeast Asia, H1N1 was first found in Mexico. The novel coronavirus is emerging in the Arabian peninsula.

Each pathogen has its own way to spread: food-borne, air-borne, water-borne. Some, like influenza, are incredibly contagious; SARS is less so. There is an inverse relationship with lethality and incubation: illnesses that strike quickly and kill many tend to disappear, for obvious reasons – the hosts don’t have time to spread them around. Instead, diseases with a 100% death rate (like HIV before recent drug regimens) tend to have a long period of incubation and illness; those that strike quickly like influenza have lower death rates.

Unlike H1N1, for most pathogens there are no vaccines. There is very good work being done on vaccines for certain pathogens. However, the development path for a vaccine is a long one, and often involves academic, public and private sectors.

Given this uncertainty, coupled with the unprecedented rate of international travel and the lack of strong public health systems in many countries, the chances of more pandemics during my lifetime are high. The worst-case scenario is an epidemic in a region that has remained off the international surveillance radar that simmers and flares up in the absence of a public health response. If it has a long incubation period (allowing travellers to take it around the world), a high death rate, and no vaccine, we’re in trouble.

From real research to misguided meme: the case of chocolate milk

One of my bugbears is the misinterpretation and misuse of research studies. An excellent PhD Comic illustrates how a researcher’s tentative, qualified conclusion is stripped of doubt and injected with pop power by the media. Soon, it’s on everyone’s lips. Biologist Richard Dawkins called these phenomena of rapid and wide cultural diffusion memes. While many science-based memes are simply byproducts of curiosity-driven research (everyone knows what a Higg’s boson is now, right?), others are either created or latched onto for purposes of selling something.

Nowhere is science more twisted to suit marketing than nutrition. I remember reading the original paper in Science about the discovery of a compound in several edible plants that shrinks cancer tumours in mice. Oh, boy, I thought. This will be big. As a result of that study, everyone knows about resveratrol today, and it is the number one rationalization for drinking wine (since resveratrol is found in grapes). But did you know it’s also in peanuts and mulberries? No, I didn’t think you did. I’ll have another peanut butter sandwich with mulberry jam, please.

Which brings me to chocolate milk. I’m a runner, and over the past few years I keep hearing runners telling other runners to drink chocolate milk. My latest iRun magazine lists chocolate milk as a super-food for runners.

But I was skeptical. This had all the hallmarks of scientific research going meme, with no complaints I’m sure from dairy companies.

I don’t know how you spend your day, but I look up original research papers. “Chocolate milk as a post-exercise recovery aid” was published in the peer-reviewed International Journal of Sport Nutrition and Exercise Metabolism in 2006.

The study involved 9 male, healthy, highly trained cyclists. They first cycled at intervals of 90% and 50% of perceived maximal exertion (2 min each), with the hard interval progressively stepped down. They kept going until they couldn’t maintain their cycling cadence because of glycogen depletion, about 40 min. They were given recovery drinks right after the exercise and 2 h later. After 4 h loafing around the lab, they got back on the bike and cycled at 70% of their VO2 max until exhaustion, an average of 40 min.

The drinks tested were low-fat chocolate milk, Gatorade and Endurox. What the researchers looked at was how long the athletes could exercise and how much work (in physics terms) they could do in the second cycling trial. That is, which drink worked best to restore their energy?

The results showed that the athletes who drank chocolate milk could do more work than athletes drinking Gatorade (relative numbers only given ~sigh~, but it looks from a graph like about 30 kJ difference) and much more than athletes drinking Endurox (200 kJ). The athletes who drank Gatorade cycled the longest before becoming exhausted, but on average just a few minutes more than those who drank chocolate milk. Both drinks added an average 13 minutes more to the time before exhaustion compared with the Endurox.

So, doesn’t that make chocolate milk good?

Sure, in highly trained athletes exercising to exhaustion, whose glycogen is depleted and needs to be restored to do the next tough bout. According to the authors, the reason chocolate milk works so well is that it restores fluid levels and glycogen, through carbohydrates. It should also be noted that milk contains plenty of protein and vitamins, which may help account for its value.

But here’s the catch: for most of us, chocolate milk has the same nutritional value as regular milk but with two added items – fat and sugar. These athletes drank low-fat chocolate milk to avoid the fat, and the carbohydrates they were getting were from sugar.

I went down to my local store and photographed the nutritional information for regular and chocolate milk. Of course, I hang out at a healthy food store with many organic and alternative products. They stocked the low-fat chocolate milk so, if you read closely, you’ll see the chocolate milk had the same fat content as regular milk. But it had lots of sugar. 29 g per 250 mL compared with 11 g per 250 mL for regular milk. Athletes usually drink about 500 mL to recover, so they would get 58 g sugar, rather than 22 g from regular milk. Multiply that by the number of times an athlete would drink a recovery beverage during the week, and it’s getting up there.

Regular 1% milk nutritional information
Regular 1% milk. Note sugar content

Chocolate milk nutritional information
Low-fat chocolate milk. Note sugar content

For the average recreational runner, who may be trying to eat healthy and watch his or her weight, it is really not good to consume extra fat and sugar. You don’t need the extra carbohydrates unless you are exercising again in a few hours; those are only for endurance athletes or athletes in high-performance training.
If you want a really good recovery drink, low-fat milk has protein and fluids.
The moral of the story: studies in one group (high-performance athletes) should not be generalized to other groups (recreational runners); studies in one situation (repeated bouts of exhausting exercise) should not be generalized to other situations (recreational exercise).
Oh, there is one use for chocolate milk: getting children who don’t like milk to drink it for the value of the other nutrients. But you’re all grown up now, aren’t you?

What will be the legacy of International Polar Year?

A selection of the Canadian contributions to International Polar Year appear in the November 2012 issue of the journal Climatic Change, available free online. Guest editor of this special issue, Tanuja Kulkarni, told me that the choice of journal reflects one of the main concerns of Canadian research during the year (really two years): how Canada’s arctic is changing and adapting (or not) to warming temperatures. (In the interests of full disclosure, Tanuja is a friend, and I’m proud of her role in this important publication.)

But the second main thrust for the IPY research was the health and well-being of northern communities. While there have been three other IPYs in history, they have focussed on hard sciences, whereas this one brought in the social aspects. As well, community knowledge played a role in many of the research projects, including those collecting scientific evidence.

As the authors point out in the introduction, past IPYs dating from the 1880s to the 1950s broke new scientific ground. From them, we learned about the jet stream and the ozone layer, among other discoveries. They also fostered international collaboration instead of competition, which allowed sharing of new knowledge that would not otherwise have been possible. They set the stage for the continuing international scientific exploration of Antarctica, as an example.

So what will come out of Canada’s work on the 2007-2008 IPY? A few years ago, I attended a symposium by IPY-funded researchers as part of the annual Canadian ecology and evolution conference. They were doing important research on the changing tree line, which in some places is moving northward year over year as the climate warms, with important effects on albedo and ecology. Others were studying what happens as permafrost melts, releasing additional greenhouse gases such as methane into the atmosphere, in a vicious circle that exacerbates climate change.

Climate, ecology, community — the interdependence of these systems is becoming increasingly apparent. A holistic view of our north is one of the positive legacies, certainly. Understanding the global effects of what happens in northern Canada is another. We will hear more in years to come about what is called the “cryosphere”: snow, permafrost and ice. These play a much more influential role in world climate and ecology than we ever imagined.

And, if we learn anything at all, we will learn that Canada has a challenge shared with only a few other arctic countries as guardian and steward of the north. There is a danger with the end of IPY funding that we will lose the momentum of this important research. We need to continue to explore the land — and sea — that are now less mysterious and more complex than previously thought.

End the staid academic journal: an appeal

This started with keywords. If you’ve ever even cracked open an academic journal, you’ve seen a few “keywords” at the end of an abstract. That is, you used to. Many journals have dropped these. Because, what are they used for any more?

Abstracting and indexing services such as PubMed/MEDLINE have professional indexers who assign terms, often from a controlled vocabulary such as medical subject headings. For Google, words are culled from titles, abstracts, text and so on (this is also true of site search engines). Users search using the keywords they think will pick up titles, abstracts and text. Many publishers ask authors to “optimize” their abstracts by including words that would be typed into search engines by researchers in the field.

So, those keywords? Way of the Dodo. Authors do a lousy job of choosing them, so it’s fortunate they don’t matter. If you edit or publish a journal, why not get rid of them now?

But the keywords are just the tip of the iceberg. With a recent class, I was exploring the “highlights” requested by many Elsevier journals. These are like the abstract in five tweets; they may represent the future of the abstract. The first time I saw them, I understood immediately how powerful they were. As I scanned an electronic table of contents, the whole article was there in a thumbnail. More than keywords, less than an abstract. They draw you in beyond the title, lead you to the abstract, and then to the article.

Because it’s all about communicating and getting eyeballs on papers.

I’m hooked on all the HTML bells and whistles too — suggestions of articles in the same area, by the same authors, and so on. I get zoned going from article to article, time slipping by unnoticed, so engrossed in learning that I could forget… no, I never forget to eat. (But I can bring snacks over to the screen.)

If you work at a journal, and you haven’t done so yet, review everything you’re doing, and ask why. Does it work? If not, throw it out like that stuff in your basement. If you need new ways to make your journal work, find them.

Don’t think that it’s not broken, so you don’t need to fix it. So many journals are losing subscriptions, readers, and then authors. It’s a vicious spiral, and it’s partly about communicating in this electronic age. Journals need to be living and breathing. Once you cut down a tree and pulp it, it’s dead.