What is the evidence for medical use of cannabis?

“Results reflect the … relative dearth of high-quality evidence related to cannabis for therapeutic purposes”

“The level of evidence for the use of medical marijuana among people with disabilities varies greatly and has a clear lack of methodologically sound studies”

“Evidence is gathering … but further research is required to declare cannabinoids a medicine”

“These studies suffered from multiple limitations, including selection bias, lack of standardized dose and route of administration, absence of blinding, recall bias and lack of a control population”

“The long-term safety profile of chronic cannabis use has not been well defined, mainly due to the heterogeneity of preparations, varying routes of administration, and the lack of controlled studies addressing safety”

“Evaluation of these low-quality trials … was challenged by methodological issues such as inadequate description of allocation concealment, blinding and underpowered sample size”

These are some of the things the experts are saying about the research into medical uses of cannabis to date. To prepare this article, I read 11 “review” articles — articles that pull together all of the research out there and reach conclusions.

The authors are unanimous in saying there is little research, and many of the studies that have been done are really small — less than two dozen patients. Some lack another treatment for comparison — either a placebo or another drug. Other studies can’t be blinded, because patients can tell whether they are getting cannabis, either because they are smoking it or they feel stoned. Others are “observational” studies (some patients are given cannabis and the researchers see what happens), considered the poorest type of evidence.

But there is some good research, and it shows that cannabis might be useful in a few health conditions:

  • Pain
  • Epilepsy
  • Inflammatory bowel disease (Crohn’s disease and ulcerative colitis)

These medical uses of cannabis are not just based on folklore (or, in this case, folk-singer lore). Science has shown that some of the chemicals in cannabis (cannabinoids) mimic natural chemicals in the human body that are important in the nervous system and the immune system. This is why its use is being taken seriously as a potential addition to the drugs we already have.

Pain

The toughest pain to control is cancer pain. A review of five randomized controlled trials looked at cannabis to treat this type of pain. Although one of the studies didn’t find any difference between cannabis preparations containing both THC and CBD (nabiximols) and placebo, there was definite effect in two larger studies with more than 150 patients each. Two earlier studies that had looked at short-term effects in small numbers of patients also found an effect. This review was funded by a Canadian medical cannabis company but was conducted with Sunnybrook Health Sciences Centre and the University of Toronto, so the oversight, ethics and evidence should be solid.

Epilepsy

I have known someone with very serious epilepsy who must cope with several seizures each day. This type of disability limits a person’s life and can even pose a danger. In some cases, the well-established drugs that control epilepsy in most people don’t work or cause serious side effects.

Four reviews of the research found evidence that cannabis preparations can reduce or even stop seizures in people with severe seizure disorders. But the effectiveness seems to vary from patient to patient.

A review that looked at cannabis research for many different disabilities found robust evidence only for epilepsy and pain. Another review that looked specifically at the non-intoxicating cannabinoid CBD for epilepsy showed that it was effective but also showed high rates of side effects, including sleepiness, loss of appetite and diarrhea. A third review found positive effects of CBD in the worst types of epilepsy: Dravet syndrome and Lennox-Gastaut syndrome.

Inflammatory bowel disease

There was a lot of hope that cannabis could help with IBD through its effects on the immune and gastrointestinal systems, but findings are mixed.

A review of five studies (only two of which were high-quality and all of which were small) found positive and remarkable effects on symptoms of IBD. However, two systematic reviews (one for Crohn’s disease and one for ulcerative colitis) by the Cochrane Collaboration — well known for its high-standard reviews — found that the effects were uncertain, the studies small, and conclusions unreachable. However, because of the positive findings of some studies, treatment of IBD needs to be tested in larger groups.

Why not more, better, larger studies?

That’s the question. When I attended a panel on medical cannabis earlier this year (2018), one of the panellists representing a cannabis company buttonholed me afterward about the difficulty in conducting studies. He pointed out that the best level of evidence is provided by randomized controlled trials involving hundreds or thousands of patients. But running those trials is incredibly expensive. He also argued that it is difficult to use placebos when testing cannabis, since those taking cannabis may be smoking it and it may be unethical to let patients go without some kind of treatment. This also means it might be impossible for the trials to be double-blinded — when neither patients nor researchers know who is getting the drug and who the placebo or comparison drug.

These are good points, but they sound like companies are throwing up barriers to running studies.

First, many randomized controlled trials compare the test drug with the standard treatment or best treatment (“gold standard”) rather than with a placebo. This is certainly the case for drugs for mental health problems, as it would be unethical to let a serious mental health problem go untreated. So, trials do not need to use a placebo.

Also, many trials are single-blinded rather than double-blinded. That is, the patients can figure out what they are getting, but the researchers don’t know who is getting what and aren’t influenced by that knowledge. In many trials, this is necessary, if not optimal.

The real issue is money. Running the kind of studies that you need to submit to Health Canada to have your drug recognized as a safe and effective treatment for a particular condition takes years and millions of dollars. Right now, cannabis companies are not that rich.

But in Canada the cannabis companies have formed a consortium that could fund trials. As well, disease foundations in Canada and other countries (like, the one to the south) are interested in the promise of cannabis, and they put money into research. With its open regime, Canada is a good place to carry out international studies of medical cannabis, which would not face the legal hurdles that exist in many other countries.

There are many conditions for which safe and effective drugs are needed. If cannabis can help, it should be prescribed and monitored by doctors to ensure it works for patients, and it should be covered by drug plans. It should not be bought at a dispensary for self-treatment, often by patients who can’t afford it.

As I mentioned to the cannabis company representative, doctors were burned on opioids. The manufacturers claimed opioids weren’t addictive, which wasn’t true. Studies would give doctors full information on cannabis’ effects and risks, so they could inform their patients. Doctors and patients deserve no less.

 

Medical cannabis use carries a risk of dependence and of lung cancer

I like to make my position clear from the outset: I support the legalization of cannabis (marijuana and hashish). I think criminalizing it makes criminals out of otherwise upstanding people who use it recreationally, either harmlessly or harmfully (of more, anon). And criminalizing it is a latter-day prohibition, often putting its sale in the hands of organized (and, frankly, disorganized) crime. The fact that cannabis has been illegal has never stopped anyone in Canada from using it and has probably stopped users from admitting their use to their doctor, social worker, parents, etc.

But does it have legitimate medical benefits? Should it be used to help with symptom control in pain, chronic neurodegenerative diseases and so on? Should it be prescribed and monitored, rather than just leaving patients to buy it at Shoppers Drug Mart and experiment with the dosage?

This spring, I attended a panel discussion by cannabis producers as part of the Science Writers and Communicators of Canada conference in Vancouver. Naturally, the producers were in favour of the medical use of cannabis, as this is a potential market for them. It also gives the leaf a patina of credibility and respectability.

I am all in favour of treating cannabis as a potential drug, including research into its safety and effectiveness and licensing for proven uses.

But I heard a few things said that were untrue, skirting serious issues in the medical use of cannabis. Sometimes I wondered whether the speakers had been smoking something.

I want to review a few things that were said.

  • Only 3% of cannabis users become dependent.
  • Cannabis doesn’t cause lung cancer, or does so at lower rates than tobacco.

Let’s look at these claims. The best study I have found on rates of cannabis dependence is a 2012 review of data to date [Degenhardt and Hall (2012). Extent of illicit drug use and dependence, and their contribution to the global burden of disease. The Lancet 379(9810): 55-70].

It found a 9% rate of dependence among users.

A later study by the same authors estimated the rate of cannabis dependence in Canada at 0.6% of the high-income population in 2010 [Degenhardt et al. (2013). The global epidemiology and contribution of cannabis use and dependence to the global burden of disease: results from the GBD 2010 study. PLoS One 8(10): e76635, Table S4]. The rate is undoubtedly higher for the low-income population, as the authors’ 2012 study found.

This is in line with the recent Statistics Canada survey that found that 14% of Canadians over 15 had used cannabis recently (previous three months), with 56% of that 14% saying they used cannabis daily or weekly.

I have seen people become dependent on cannabis, and my observations are in line with the higher estimates.

So, definitely more than 3% of users.

But whether it causes dependence shouldn’t matter anyway, because, evidently, smoking cannabis doesn’t cause lung cancer. Except that it certainly does.

In fact, it increases the overall risk by five times, according to a case–control study carried out in New Zealand and published in 2008 (Eur Respir J. 2008 Feb; 31(2): 280–286. doi: 10.1183/09031936.00065707. For each year of cannabis smoking, the risk increased 8%.

For every study, there is another that contradicts it. Some other studies have not found this association. One of the problems is that a lot of people who smoke cannabis also smoke tobacco, or smoke both together. The New Zealand study used statistical analysis to separate the effects of cannabis smoking from tobacco smoking, but some other studies have not found a separate effect.

An analysis that combined data from several studies had mixed conclusions [Int J Cancer. 2015 Feb 15; 136(4): 894–903]. On one hand, the authors found that having ever smoked cannabis did not alter the overall risk of lung cancer. On the other hand, risk was clearly higher when they looked at a particular kind of lung cancer – adenocarcinoma – especially if the patient smoked a joint or more per day, and especially if they had smoked for more than 10 years. The difference also showed up in people who had smoked cannabis for 20 years or more, for all types of lung cancer.

OK, the risk of lung cancer associated with cannabis smoking appears to be lower than the 23-fold higher risk linked to tobacco smoking (US estimate in men only). But yes, you could get lung cancer.

There is a growing body of evidence on medical use of cannabis, and more trials are needed. I’ll try to get to this in future blog posts.

But arguments for medical use are not helped by unsupported statements and claims. Risks of dependence and lung disease need to be addressed in medical use. Downplaying them or wishing them away doesn’t help anybody.

The anti-vaccination movement goes back more than 150 years: its history holds lessons for today

To be clear: when there’s a new vaccine, I’m the first in line, with my sleeve already rolled up. I’ve had a lot of diseases I wish I had been vaccinated for: measles, mumps, rubella (or German measles), chickenpox, influenza H1N1 (just before the vaccine was available), and pertussis (childhood vaccine must have worn off). So if you read the title and you’re looking for confirmation of anti-vaccination views, you’re in the wrong place.

Until recently, my view of vaccination was the standard one that I read in the Canadian Medical Association Journal when I was working there: humanity was plagued by terrible illnesses; Edward Jenner discovered vaccination in 1796; smallpox has been wiped out; we’re working on the other ones. The end.

IMG_0809But my view changed last month. It started with a book I found among my parents’ collection, called Man’s Redemption of Man by Sir William Osler, who basically invented modern medicine at McGill and Johns Hopkins universities. It was the text of an address he gave at the University of Edinburgh in 1910. He said, “A great deal of literature has been distributed, casting discredit upon the value of vaccination in the prevention of smallpox… Some months ago, I was twitted by the Editor of the Journal of the Anti-Vaccination League…” Whoa, whoa. There was an anti-vaccination movement in 1910? They had a journal?

I began to read about the history of the anti-vaccination movement. And I discovered the following, which I didn’t know and I bet many of you didn’t know either:

  • The anti-vaccination movement was born shortly after the discovery of cowpox-based vaccination for smallpox.
  • At the time, no one understood how vaccination worked, least of all its discoverer Edward Jenner, simply because doctors didn’t yet understand what caused diseases.
  • Compulsory vaccination was enforced in many countries on an unwilling populace.
  • Many children died as a result of vaccination, mainly, it seems, because of infection of the cowpox blisters with bacteria such as strep.

I started with Bodily Matters: The Anti-Vaccination Movement in England, 1853-1907 by Nadja Durbach (Duke University Press, 2005), an academic study of the birth of the movement. As Durbach shows, the early rollout of smallpox vaccination in its home country was a public policy disaster.

During this period, people tended to practise folk healing using herbs. Only well-off people had ever even had a physical exam by a doctor. Nobody really understood how illnesses happened, or that one illness was spread in a different way than another, so people blamed “filth” and “miasma” (bad smells from sewage and swamps). Some people thought that quarantine and isolation were a good way to prevent disease spread, but others experienced serious stigma from a disease “placard” posted on their house and tore the placards down. Medicine and physicians were just becoming a scientific, regulated practice and profession, and trying to stake out territory among a suspicious population. Civil liberties were a strongly held concept, and citizens defended their freedom to make their own choices. Working people had acquired a basic education and started to complain about how they were treated, at the same time as public health officials saw them as the source of “filth” and contagion. Into this morass came a smallpox epidemic, and the first compulsory vaccination law in 1853.

At a certain point in this story, I started seeing the situation from the parents’ point of view. They didn’t know what caused smallpox, or how this vaccine worked. Public health officials literally broke down their doors and attacked their children with a lancet, often causing wounds in several places. And a percentage of children died of after-effects. Other parents heard these stories. Talk in the streets was that the vaccine came from cows or the grease on horses’ hooves and would turn your baby into a cow-monster. While parents were used to a certain risk of child mortality, attributed to God’s will, they were afraid of an unproven, manmade “operation” that they couldn’t control. One man who was convicted said he would pay the fine rather than have a baby vaccinated, as a previous child had died as a result of vaccination.

I can see it. If you feel there is a risk of losing a child, you don’t care much about the greater good of society.

At the same time, middle-class protestors opposed vaccination on the grounds of civil liberties and often conflated it with opposition to vivisection. They felt the government was conducting a huge experiment on the population without consent.

Did the officials allay parents’ fears and provide them with reassurances? Somewhat in the public press, but not in the actual encounter, which looked like state oppression to the working people targeted by the law.

So the whole thing got mixed up in class perceptions, the role of the state and civil liberties.

Which brings me to the anti-vaccination riot in Montreal in 1885. Quebec was in the middle of smallpox epidemic that ultimately claimed around 3000 people in the city and around 2500 in the rest of the province. As Michael Bliss documented in his excellent book Plague: A Story of Smallpox in Montreal (HarperCollins 1991), the anti-vaccination movement had come to Montreal as well. Top doctors were divided on the effects of vaccination, and there was a rough division by ethnic group and class, with working-class francophone people targeted for vaccination and defended by francophone doctors who treated them. Newspapers and employers urged compulsory vaccination, but many Catholic priests and a few influential intelligentsia argued against it. On September 28, a crowd of men and boys pelted an East End health office with stones, breaking windows. They paraded around the city, breaking windows of pharmacies that handled vaccine. They also converged on the private homes of a member of the provincial board of health and an alderman who promoted vaccination. They called out “Down with vaccination!” The same day, 79 people died of smallpox.

Back in England, a royal commission on vaccination sat for seven years before recommending, in 1896, exemptions for “conscientious objectors.” Once this was introduced into law two years later, much of the wind slowly went out of the anti-vaccination movement. It had, in fact, won.

But the movement has flared up again with each new vaccination, as you can read more about on the History of Vaccines, a fascinating site created by the College of Physicians of Philadelphia.

Why does anti-vaccination keep coming back? Can this history teach us anything?

Most countries do not make vaccination compulsory or punish objectors, because governments have learned that that does not work. In fact, it backfires. But in Australia, the government has withheld social payments from parents who do not vaccinate their children since January 2016, fanning an anti-vaccination movement. The measure also targets people on welfare, repeating the mistake of treating the poor as a reservoir of disease.

What does work is education — about the causes of disease, about how vaccines work, about the real but rare risks involved in vaccination. And about the real risks of disease.

I think the cause might also be aided by admission that “mistakes were made” in the past and that today’s scientific and ethical oversight prevents the gross excesses of early vaccination.

In most communities, parents weigh the benefits against the risks of vaccination and opt for vaccination. There is also peer pressure to vaccinate children as the right thing to do for their health.

But I wonder how many people remember their parents or grandparents speaking against vaccination and are influenced by that history. How many are still fighting a 150-year-old fight for what they see as their liberty?

Why diseases matter

I was 25 when I got very, very sick. After six weeks of illness, four doctors who had no idea what was wrong, and two weeks in hospital, I was finally treated for giardia diarrhea I had caught in the countryside two months earlier. It took months to feel back to my old self, and I had post-traumatic stress symptoms for years.

Once I got back to something like everyday life, I began to notice that our society’s views of illness did not match the reality in many ways. As I started to work at the Canadian Medical Association Journal and learned much more about illness, this view was reinforced.

The reality is that most illness – in Canada and certainly elsewhere – is a matter of bad luck. You are in the wrong place at the wrong time and you catch something. Or something in your body misfires. Or a remote relative had a bad gene.

On a public-health level, society can make changes to prevent disease: vaccinations, good sanitation and water treatment, advisories to wash your hands, and surveillance and screening programs. But at the moment that those systems break down and a person gets a disease, there’s really not much that can be done.

At the same time, health classes in schools do not teach much about disease causation or medical care. Many Canadians come from cultures (and I’m talking about my own here) that see illness as a failing, either of morals or self-care or stoicism. Others see illness as someone’s – either the patient’s or the doctor’s — “fault.” Still others see illness in superstitious terms, even in this day and age. Many Canadians still think little of medical science and still say “I’ve never taken a day off work sick.” Well, either they were very lucky or they were going to work with viruses and infecting their colleagues.

Sometimes I prefer the views of those from other countries where diseases are more prevalent and acknowledged as a fundamental part of human existence. I believe from my own experience and my work that disease, disability and death are part of what makes us human.

Back in Canada, there’s an inaccurate view among people who have not had serious diseases that they happen only to people with poor lifestyles or people in other countries. That is manifestly not true. If you think about it, either you or your friends and family members have been profoundly affected by diseases: heart disease, cancer, rheumatoid arthritis, multiple sclerosis, ALS, SLE, diabetes, etc., etc.

There are a lot of things said in the street, in the media and even in medical literature about what causes these diseases, but biomedical researchers working on them are much more circumspect. In many cases, we do not really understand how these diseases start, or the things we have been saying are turning out to be incomplete — or even completely incorrect.

My feeling is that we are at the beginning of a coming explosion of knowledge on diseases, which will transform prevention and treatment. Because how can you prevent or treat a disease until you understand what is causing it?

That broken bone is osteoporosis

“The doctor said Mom has advanced osteoporosis,” said my sister. “How does he know that?”

The short answer is, because her hip broke spontaneously. At least the doctor mentioned why the fracture happened, even if he didn’t explain his reasoning. In the case of two friends who recently told me their mother had broken a hip, no one ever mentioned that the cause was osteoporosis, although that’s undoubtedly what it was.

In working on an article for Nature Outlook on current research into and treatment of osteoporosis, my eyes were opened to the widespread misunderstandings surrounding this common disease.

First, most people are unaware that a bone fracture in someone over 55 is usually due, at least partly, to loss of bone mass and density. In reading about the disease, I found the US guidelines are notably up front about the situation. The authors say:

“… most fractures in older adults are due at least in part to low bone mass, even when they result from considerable trauma. A recent fracture at any major skeletal site in an adult older than 50 years of age should be considered a significant event for the diagnosis of osteoporosis and provides a sense of urgency for further assessment and treatment.”

Yet they point out that in the US “many patients who have osteoporosis-related fractures are not being diagnosed with osteoporosis” and certainly not given lifestyle counselling and drug therapy to prevent the next, inevitable fracture. Anecdotally, I have seen this in Canada as well — many older people with osteoporosis are never diagnosed (or, more precisely, never told they have osteoporosis), even after a fracture.

It would help if people at risk of fractures and their families and friends understood osteoporosis, but most people know little or nothing about it, which becomes clear in the reactions and comments when their mother, father, aunt or uncle breaks a bone.

So let’s clear up some of these misunderstandings right here.

First, the broken bone is the end of a long process that has been going on for years. The bones have become progressively less dense, with larger holes in the sponge-like interior “trabecular” bone. By the time the bone breaks, it was hanging on by a thread. A fracture had become highly probable.

If you think about it, prime-age adults (25 to 60) rarely break a bone. If they do, it’s usually because of a major trauma such as a skiing or car accident. That’s because their bones are healthy. I’ve fallen down a few times during endurance sports such as skating, cross-country skiing or running — the worst thing I got was a bruise.

Second, about falls. If someone has osteoporosis, it’s advisable to prevent falls in a variety of ways. It takes very minor trauma to break a bone affected by advanced osteoporosis. However, as the US guidelines point out, sometimes the bone can break spontaneously if it is fragile enough, with no trauma at all. This is what happened to my mother. Elderly people can fall for a variety of reasons (many aging-related processes affect balance), and osteoporosis should be considered one of them. I have heard about many cases of frail elderly people with diminished cognition who had a fall and broke a bone, but it’s not clear whether the fall broke the bone or the broken bone caused the fall. Friends and families often wring their hands about why the person fell, often from a sense of responsibility for the person’s well-being. But they can let themselves off the hook:  the chances of a fracture were high, fall or no fall, and the fracture may have caused the fall.

Third, many people think that if you eat calcium and get vitamin D, you won’t get osteoporosis. In fact, three things give you your best shot at delaying or decreasing the effects of osteoporosis: calcium (better to eat calcium-rich foods than to take supplements, which can contribute to kidney and gall bladder stones), vitamin D (Canadians need supplementation in the winter), and exercise. Recent research shows that the chemical “crosstalk” between muscles and bones is very important — working your muscles strengthens your bones. As people age, they should get more exercise, not less. But these steps may not fully prevent osteoporosis. In fact, they probably won’t.

Why is this? The new research shows that not only do women lose a lot of their bone mass during menopause, then men and women are hit by a second, age-related bone mass loss after age 65. This one is caused by the bone cells becoming senescent and ceasing to function, as well as the stem cells producing fat cells rather than bone cells. There’s only so much that lifestyle can do to counteract these effects.

If you have a family history, talk to your doctor, and if the densitometry tests show you’re seriously losing bone mass, you may need medication.

Unless you have a strong family history of osteoporosis at a young age, you probably don’t need to worry about testing until you reach your 60s, when the second effect starts to kick in. In the meantime, calcium, vitamin D, exercise.

Yeah, aging sucks. But it’s better than the alternative.

 

Where has Beall’s List gone?

For many years now, Jeffrey Beall, an academic librarian and associate professor at the University of Colorado, has maintained a WordPress blog of “Potential, possible or probably predatory scholarly open-access journals.” It was a “grey” list of suspicious journals — with a sister list of suspicious-looking “publishers.” (Gosh, I’m using a lot of quotation marks.)

Suddenly, that list, and the archive of stored blogs, has disappeared. Retraction Watch here on WordPress has more information on the closure. There has also been a lot of chatter on Twitter.

The one person we haven’t heard from is Jeffrey Beall. Prof. Beall, wherever you are, we salute you. Beall coined the term “predatory journal” to describe the phenomenon. And it was apt argot, as “fraudulent” isn’t always strictly true or provable, but the journals are clearly not bona fide. These journals prey on unsophisticated authors who need to publish a paper, robbing them of their intellectual property and their money.

Many journals complained about being put on a public list, as some could make a claim to being start-ups. However, something like Beall’s list has to exist. We need to be able to distinguish between the real journals and the predatory ones. At the Council of Science Editors’ meetings, there has been talk of starting the reverse: a “white” list of journals. Journals I know are hurrying to be indexed in the Current Contents/Web of Science indexes that used to be run by Thomson Reuters or in Medline/PubMed. That, at least, is a good-housekeeping seal of approval. But I think we need another black list, so that authors can quickly discover what they’re dealing with.

In the meantime, I have saved the last published version of Beall’s list (available through the Wayback Machine), and I would be happy to check it for you if you contact me via this blog (Contact, above).

The cause of multiple sclerosis: we’re getting closer

My feature on the state of research into MS causes (published Dec. 1, 2016, in Nature Outlook) had a long and complex genesis, which is also true of the disease I wrote about.

I have long been interested in how diseases happen, from my days writing about research for my column in the Canadian Medical Association Journal (CMAJ). I covered a whole variety of health issues, of course, but the ones that were of most concern  the ones that could wipe out populations and cultures were diseases.

A few years ago at the Canadian Science Writers Association conference, Dr. Brian Goldman presented a news clip on an experimental treatment for MS touted by Paolo Zamboni, which he (suspiciously) called “liberation therapy” based on a theory that MS is caused by chronic cerebrospinal venous insufficiency. Or let’s just say veins blocked by metal buildup. Goldman was critical of the glowing media descriptions of the treatment, as they were not evidence-based.

I was sitting at the same table with Dr. Goldman at lunch, and our gang of science writers debated the ethics of this type of coverage. I recall I said, “Of course, we don’t know what causes MS.” Because that was the understanding at the time.

That discussion stuck with me, especially as I met more people with MS over the past few years. Then, in reporting for CMAJ, I covered two research stories on discoveries relevant to the cause of MS. I starting following the references in one of the articles to other research, and I soon learned that the evidence was mounting for several causal factors. Some researchers were looking into whether these factors were linked. In fact, right now there’s a new article every month on these factors.

But I had seen nothing (and I looked) in the media about the good, solid, research that had been slowly amassing over years about Epstein-Barr virus and vitamin D, in particular.

I pitched an idea for a feature on this research at this year’s Canadian Science Writers Association conference as part of a “Dragon’s Den” pitch session to a panel of four editors. And long story short I was eventually asked to write it for Nature Outlook.

Why I included the Elmvale Acres Ottawa cluster

I was in the midst of my research on MS causes, and I was particularly interested in the paper from Winnipeg researchers showing clusters of incident cases of MS in that city. As the authors of this paper told me, clusters are an important clue into causation. They can indicate genetic differences, especially in a multicultural city like Winnipeg, or environmental factors. I was fascinated because the clustering in Winnipeg (unfortunately, for copyright reasons, I couldn’t reproduce the study’s maps, which are worth a thousand words) looked like maps of disease outbreaks. That doesn’t mean they are it is just a possibility worth exploring.

I had wanted to get the human angle on this research, to show that this research is about real people, not just dots on a map. I was even thinking of calling the MS society in Winnipeg to contact patients in the affected neighbourhoods. At this point, several of my friends who knew I was working on the article called or emailed to say there was a CBC story on a cluster right in my city – Ottawa.

I contacted the man at the centre of the CBC story, Jacques Dutrisac. Now, I have some graduate courses in statistics and I’ve read plenty of biostatistics. I know that disease clusters often occur by chance alone. There’s also a well-known perceptual effect that once you have a problem you tend to see it all around you. Careful and complex statistical methods like those used in the Winnipeg paper are needed to determine “true” clustering.

So, to be honest, I called Dutrisac prepared for the possibility that the cluster in the Elmvale Acres neighbourhood of Ottawa might be by chance alone. Dutrisac is a wonderful raconteur and sleuth. Not only had he kept track of all of his former friends and neighbours with MS, he had their names, locations, schools, ages, and ethnic background. He was telling me about one after the other, and I was taking notes. After our chat, I made a table of all 14 people with MS (at that point another neighbour with MS has come to light as a result of the publicity around the cluster). The prevalence of MS in Canada (where it is highest in the world) is 291 per 100,000 or a little under 3 per 1000. In an area of less than 1000 people, the rate was at least five times higher than the national average. When I looked at the fact that the people affected not only lived in a kilometre-radius area, but were all about the same age in fact, most exactly the same age as Dutrisac –, went to the same schools and were two-thirds francophone… well… that can’t possibly be by chance.

So I feel that I’m being responsible as a journalist in covering a cluster that has not yet been studied, but should be.