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Sunday, November 16, 2014

Microbiomania, microbophobia, and getting excited about the microbiome

Jonathan Eisen at UC Davis famously polices news and academic articles that oversell the microbiome on his blog, The Tree of Life. He provides a valuable service to the field of microbiome research, since it benefits neither the researchers nor the public when writers convey wishful or wrong messages.

Recently on his blog, Eisen "rediscovered" two new words that I think capture some important concepts:

1) Microbiomania:
The overselling of the impact (beneficial or detrimental or otherwise) of microbiomes without the evidence to support such impact.


2) Microbophobia:
The overwhelming and unreasonable fear of microbes (of any kinds).

One example of microbiomania from Eisen's blog is this:

Gut bacteria health may be the key to living longer, disease-free lives, U.S. fruit fly study reveals

...because extending the life span of a fruit fly in a study is a loooooong way off from making humans live "longer, disease-free lives".

One of my favourite examples of microbophobia is the "healthing" campaign of a major cleaning products company (critically analyzed in this blog post) that equates zealous cleaning with being healthy.

The terms zero in on two common mistakes in writing about the microbiome. In both cases, the problem is not sticking to the facts. Microbiomania is going beyond the facts and building up microbiome research to be something it is not, while microbophobia is letting existing fears and preconceptions about bacteria act as a filter through which we see the facts. Neither makes for good science writing.

I want to make sure, however, that no one equates microbiomania with simply getting excited about the microbiome. They are not the same thing.

Say someone reports on a study that found jet-lagged mice have a different gut microbiota and messed-up metabolism compared with normal mice. In microbiomania, there's conjecture: saying that jet lag is the cause of obesity, or that probiotics can cure jet lag. Not okay.

But it is completely okay to just get excited about the jet-lagged mouse study because it's interesting and awesome.

By Douglas P. Perkins (Own work) [CC-BY-SA-3.0 (], via Wikimedia Commons

Please don't tell your friends, "There's less than a 0.01% chance that my feeling of inspiration after reading the jet-lagged mouse study was due to chance." If you are inspired by it, tell them straight up. Do show your passion for the topic, as long as you're sticking to the science. The field will advance best if the researchers see that people are enthusiastic about their research.

For more, see this post:

Hail the Gut: Why it’s okay to get excited about the microbiome

Tuesday, July 1, 2014

What's on the menu at your local long-term care facility?

I recently came across the work of Paul O'Toole, of University College Cork (in Ireland). He works with the Alimentary Pharmabiotic Centre, which focuses on developing "bench-to-bedside solutions focusing on gut health". O'Toole was interviewed about one of his recent presentations here.

Some of O'Toole's recent work has to do with the relationship between diet and gut microbiota in elderly people. I recently wrote an article about nutrition for seniors that piqued interest here in Canada, so O'Toole's major findings are really interesting to me:

- The setting where an elderly person lives appears to determine his/her gut microbiota: based on microbial species in fecal samples, scientists could predict which seniors lived in the community, a day-hospital, a rehab setting, or a long-term care facility

- The difference in gut microbiota in each setting could be because of different diets

- In general, seniors living in the community has diverse gut microbiota, and seniors in long-term care had less diverse microbiota

- Low-diversity gut microbiota correlated with poor health: sarcopenia (muscle loss), inflammation, and even lower cognitive function
Source: Wikimedia Commons (Siobhan from Upstate New York)

Like any human research, it's not easy to tease apart cause and effect here. This issue of causality has been controversial on at least one other paper that O'Toole co-authored. But the bottom line is that seniors in care facilities have a less diverse microbiota and poorer health.

It could be the case that by the time a person is ready to go into long-term residential care, he/she is already naturally in a state of declining health, regardless of diet. But we have converging evidence from other places that diet can indeed affect health through the microbiota. The other major possibility is more intriguing: what if the poor diet of a senior in a long-term care facility was the thing that caused poorer health from the day they entered? This isn't so far-fetched, as those who study geriatric populations (like Keller, below) will tell you.

I, for one, wouldn't be so keen to support an elderly parent going into a care facility if the menu was going to guarantee a health decline.

The problem would seem to have such a simple solution: change the menus in these care facilities. But I doubt it's as easy as it looks. There are all kinds of social and cultural factors to consider when creating menus, not to mention the pressure of keeping down costs. Dr. Heather Keller at University of Guelph is knowledgeable about some of these factors.

A word to the wise here, if you happen to be checking out the menu at your local long-term care facility: macaroni and cheese won't cut it. Elderly folks need protein, protein, and more protein.

Friday, May 9, 2014

Babies in the womb are not sterile after all

Previously I've written about how infants become colonized with microbes. I, like many others, took it as gospel that babies were sterile in the womb, and got their first (literal) taste of microbes on their way through the birth canal during labour. C-section babies, of course, picked up their initial microbes from whatever things touch them in the operating room.

Now, however, scientists are challenging the truth of the "sterile womb paradigm". Studies (reviewed here) are beginning to suggest that babies do indeed acquire a collection of microbes before birth. The birth process and breastfeeding are ways of "copious supplementation" afterward.

Imagine that: when I had my daughter two years ago, I went through the pregnancy thinking that she was more or less shrink-wrapped from the microbes inside of me. I only had to start consuming lots of probiotics when I got close to the "big day" when she'd finally emerge into the great microbial world. 

But when I had my son this year, the scientific picture had changed. I thought of him in more of a mesh bag inside of me: vulnerable to, and benefitting from, the microbes that I encountered throughout the pregnancy.

Take-home message of the day: the womb is more of a mesh bag. Exactly what that means for pregnant mothers is still to come. 

Wednesday, July 10, 2013

How the microbiome is (slowly) making its way into clinical practice

If you follow my Twitter feed (@bykriscampbell) or read this blog, it will be obvious to you that the microbiome impacts our day-to-day health. The research, granted, is in an early-ish phase where certainties are few and far between (as I mention in this podcast interview). But still, there are myriad studies that say things like "administer probiotics", "avoid prescribing antibiotics to kids", and "consider c-sections only in emergency situations".

What has me puzzled lately is this: if lots of good evidence is already out there, how come it's being incorporated so slowly into clinical practice?

Well, it's Good News Day on this blog. Because here are a few examples where health professionals are taking the information on the microbiome and using it to immediately help patients:

1) Fecal transplants are moving from the realm of weird voodoo cure, into a respectable treatment option. The most likely reason for this is that they work ridiculously well a lot of the time. In a recent NEJM study, for example, fecal transplants were used to treat recurrent C. difficile infection, and were so effective that the study had to be discontinued because it was unethical to withhold the treatment from the control group.

In the US, the FDA recently tried to put up a barrier for doctors wanting to use this treatment with their patients: requiring an Investigational New Drug application for fecal transplants. Recently, though, the requirement was thankfully overturned.

2) I was having another dinner-table conversation about feces the other day (wait, not all families do that??), when I heard from a Winnipeg doctor that the formulary in his hospital carries probiotics, and that he and his colleagues often administer probiotics when antibiotics are given to inpatients. Since then, I've heard that Quebec's Pierre-Le-Gardeur hospital does the same, as do several others in Quebec and Ontario. (And probably more that I haven't heard about.)

3) Should you be fortunate enough to have access to a clinic that does bacterial sequencing, the data can be used to personalize your treatment experience. As explained in the video below (with helpful hand gestures) by Nicholas Chia, Ph.D., at Mayo Clinic, a patient with refractory bacterial vaginosis could get a bacterial swab and have it sequenced. This would help the doctors know what antibiotics she is resistant to, and which bacterial takeovers she'd be susceptible to. Based on that, the doctor could find a treatment that would work better than the repeated rounds of antibiotics she might have had in the past. Here's the video with the full explanation:

Using "the firehose of information that comes down off of sequencers"

Those are three examples that make me happy. But the job is far from done. Anyone can do their part to advance "the cause" by bringing up the microbiome at their next doctor's appointment. Even if the doctor doesn't know much about it, she or he might go home and catch up on the topic by reading a few journal articles.

The microbiome is going to change healthcare, but it'll be one doc and one patient at a time.

Tuesday, May 28, 2013

Two tales of gastric bypass surgery

This story appeared today from The Canadian Press:

Mom's obesity surgery may help her children

It reports on a study that followed kids' risk factors for obesity. Children who were born to an obese mother before she had weight-loss surgery were heavier, and had higher risk factors for heart disease and diabetes, than children born to that same mother after surgery. Researchers say it was because obesity causes differences in the activity of certain genes. Not that obesity affects the genes themselves, but how the genes express themselves.

The story is fine by itself. Rather well written, in fact. (Bonus points for great quotability go to co-author Dr. John Kral, who said fetuses are "differently marinated" depending on the weight of the mother.) And everything would be hunky dory were it not for this item, which was covered by Reuters two months earlier:

After weight-loss surgery, new gut bacteria keep obesity away

This one explains exactly how gastric bypass surgery helps people slim down. Researchers found that it may not have to do with going under the knife, but rather, with how the surgery changes the patient's gut bacteria. (The study was done on mice, and as a result, controlled for nearly everything; control group mice were even given a "sham" surgery.) The study raised an important question: might it be possible to skip surgery, and achieve the same effect by altering gut bugs through diet or another means?

These stories were two separate entities, presented weeks apart. But taken together, here's what I gather:

1) A mother's gastric bypass surgery helps change a baby's gene expression and makes him or her healthier for life

2) Gastric bypass surgery might not be necessary because what matters is the change in bacteria that occurs after the surgery

So if you were a woman of a high body weight who planned to become pregnant, wouldn't you want someone to have raised the connection between these two studies? Maybe you read the news today and have become convinced that gastric bypass surgery is the best way forward, even with the risks it presents. And your appointment to discuss it with your doctor is tomorrow.

But maybe you could have had other options.


The fact that no one communicated the connection between these studies is a huge oversight. I'd even argue that it is bad for scientific progress. Science is about converging upon the truth with different studies conducted under different circumstances. So why are we still presenting science studies without context or analysis, as individually-wrapped peppermint candies?

Let's give everyone the benefit of the doubt in this case and say it's because the person assigned to cover the study wasn't aware of any other relevant studies. Sure, the scientists this person interviewed are supposed to have told him or her about the context. But it's not actually a scientist's job to be aware of the news coming out of other labs at any given moment. It's the journalist's job to be informed in real time.

This is a strong argument for assigning health and science stories to those who make it their full-time mission to keep abreast of a certain area of health and science. That is to say, specialist journalists. (Luckily there are several great people, including Rob Steiner at U of T, who are working to create a new generation of specialist journos that will provide content to newsrooms that are operating on a skeleton staff of generalists.)

These two studies are just one example of something I notice all the time. Other specialists could probably cite examples from their own fields. The point is, news is set up for these obvious failures to connect the dots. But we need to work toward changing that. It's only fair to that woman - a future mother - signing the surgery release form at this very moment.

Thursday, May 2, 2013

Autism and gut bacteria: The vax. Er, the facts.

When you do an internet search for "autism" and "vaccine", you open the can of worms that was the claim that MMR vaccines caused autism. That fraudulent research and the conniving scientist behind it, Andrew Wakefield, have now been discredited. (For more on that, see the dedicated chapter in the book "Bad Science" by M.D. and writer Ben Goldacre.)

But lately in the news, we came across the words "autism" and "vaccine" in the same sentence again. As in these headlines:

Vaccine developed at U of G could help in battle against autism

Vaccine developed to fight gut bacteria and autism symptoms

First vaccine against autism-associated bacterium Clostridium bolteae

Just how did those two words end up together again? It piqued my interest.

The word vaccine is particularly suggestive. Because what we do know about the cause of autism is this:

(1) There is definitely a genetic component
(2) There may be an environmental component, but scientists don't agree on what it is

A vaccine would not address genes, of course. It would address one of the environmental components thought to cause the condition. But... hold on, if we're not sure what the environmental causes are, how can we take a vaccine and say it addresses that environmental cause?

With that question in mind, I approached this research, which came from the chemistry lab of Dr. Mario Monteiro at the University of Guelph.

I took the step (as always) of reading through the original research paper in the journal Vaccine (in press as of early May, 2013).  Ahem... that was clearly one more step than most of the reporters who produced articles on the topic (bless their time-strapped hearts). See, anyone who said there was a vaccine obviously didn't read or understand the paper. Because in the article, there is no vaccine.

Here are the facts:

A team of chemists has examined the cell walls of a kind of bacteria (Clostridium bolteae), and have determined that the bacteria can provoke an immune reaction in rabbits.

That is all.

The researchers say their knowledge could be used to develop a vaccine for human use (i.e. they now have a vaccine target), but they did not yet create the vaccine themselves. Contrary to what  pretty well every mainstream news article has reported.

Moreover, the facts in this article are padded with the stuff about autism that, given the context, seems absurdly off topic. They took their discovery of making the immune system of rabbits react to a bacteria, and they said, "Hey, some children with autism also have this bacteria in their guts. Maybe we could develop a vaccine against this bacteria and give it to them. And the bacteria would go away. And maybe so would their autistic behaviours."

Do I need to say it? That is not sound scientific reasoning. It's like saying:

"Hey, some children with blonde hair also have this bacteria in their guts. Maybe we could develop a vaccine against this bacteria and give it to them. And the bacteria would go away. And maybe so would their blonde hair."

To me, the paper is about developing a knowledge about a species of bacteria. At most, the discussion section should have mentioned that this particular bacteria may be found in the digestive tracts of some children with autism.

I'm not really sure why they picked on this species of bacteria, in fact. There is no scientific consensus that C. bolteae is special to the guts of children with autism. Some studies have been done comparing the bacteria in the guts of children with autism to that in non-autistic children, and even though some patterns are emerging, there are no bacteria that reliably distinguish one group from the other. This species of bacteria alone is surely not the "environmental cause of autism" that has been eluding scientists for decades. The researchers do make a case for why they chose C. bolteae, but to me their choice seems questionable, given the conclusions of the papers they cite.

Now, I do think that the connection between autism and gut bacteria warrants more research. (See this episode of David Suzuki's TV show, The Nature of Things.) I'm not dismissing it wholesale. It's just that this paper goes beyond what the empirical evidence shows - both in the peer-reviewed journal and in the media.

The upshot (yep, pun intended): the word "autism" should not be appearing with the word "vaccine" here at all. That's because the word "autism" should not appear at all, and the vaccine is still a dream. The headlines should read something like:

"Scientists may develop vaccine against species of bacteria with unknown importance".

Only, then they wouldn't be headlines. Hmm, see?? Pequegnat, B., Sagermann, M., Valliani, M., Toh, M., Chow, H., Allen-Vercoe, E., & Monteiro, M. (2013). A vaccine and diagnostic target for Clostridium bolteae, an autism-associated bacterium Vaccine DOI: 10.1016/j.vaccine.2013.04.018

Monday, April 8, 2013

Red meat and gut bacteria: partners in heart crime

We're used to thinking of nutrition the way we think about computers - input and output. For example, you eat carrots, you get lots of vitamin A. You eat strawberries, you get vitamin C. If you're deficient in a vitamin, take a supplement... or eat more foods containing that vitamin.

So far so good. Only, now science is teaching us it's more complicated.

For one thing, the exact nutrients you need may depend on your genes: see this article, "The nutrigenomics frontier". Which makes the ubiquitous "recommended daily intake" (RDI) nothing more than a ballpark estimate.

But there's another emerging facet of nutrition. There's increasing evidence that if we're going to make use of the nutrients we ingest through asparagus or chick peas or any other food, the body has to act on those nutrients. Sometimes the body's actions make things better for us, and sometimes they produce a bad result.

Hamburger (source: Wikimedia Commons,

Let's take red meat. Recently in Nature Medicine, a study found that omnivores who took a compound (found in red meat) called L-carnitine had higher markers of arterial plaque buildup than vegans or vegetarians who also took the compound. It also happened that the omnivores had very different gut bacteria, as measured through fecal samples, than the vegans/vegetarians. That would be correlation, not causation.

Enter the mouse part of the study. Here, the researchers found that arterial plaques increased in mice with normal gut bacteria when they were given L-carnitine. The red meat compound and the gut bacteria appeared to be partners in contributing to heart disease.

As a point of comparison, other L-carnitine-eating mice were given antibiotics that cleared their gut bacteria. Arterial plaques did not increase in these mice.

What are we left with? Certainly NOT that we should pop antibiotics alongside our red meat in order to prevent heart disease. Yikes. (For reasons why antibiotics are not the answer, check out this article by the excellent science writer, Carl Zimmer.)

We're left with a caution against red meat, I guess. An explanation of why vegans and vegetarians might have a lower risk of heart disease. But the research is preliminary, so personally I'm not going to swear off burgers forever. 

Most importantly, I think we're left with a picture of nutrition that's about more than just input. It's a picture of an ecosystem, where each thing interacts with other things to produce an output - in this case, heart disease. Gut bacteria seems to be a big player in these actions. In this article, Stanley Hazen, head of cardiovascular medicine at the Cleveland Clinic, says: "Bacteria make a whole slew of molecules from food... and those molecules can have a huge effect on our metabolic processes."

One more thing: after reading this study, I wouldn't be too quick to take L-carnitine supplements. Certain gut flora might love them... but it's possible that could have dangerous results. Koeth, R., Wang, Z., Levison, B., Buffa, J., Org, E., Sheehy, B., Britt, E., Fu, X., Wu, Y., Li, L., Smith, J., DiDonato, J., Chen, J., Li, H., Wu, G., Lewis, J., Warrier, M., Brown, J., Krauss, R., Tang, W., Bushman, F., Lusis, A., & Hazen, S. (2013). Intestinal microbiota metabolism of l-carnitine, a nutrient in red meat, promotes atherosclerosis Nature Medicine DOI: 10.1038/nm.3145