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Wednesday, December 23, 2015

Recipe hacks for good gut microbes

My time is devoted to learning and writing about the science of gut microbiota. As fascinating as it is to go deep into the mechanisms of gut-brain communication or how human versus bacterial genes contribute to obesity, I've been thinking a lot about the practical side of the science: how can I build what I know into my own life? What are the actionable items from this science?

Diet is a powerful way to affect the microbiota -- this much is clear. So when I've been making meals, I've been trying to hack them in ways that are good for my gut microbes. Here are three recent recipes:

Three-day salsa
Fermented foods deliver live bacteria to your gut, with possible beneficial effects on health.

Cauliflower 'rice' with ham
We still don't know the effects of processed meat on the gut bacteria specifically, but the best available evidence supports bulking up on fibre and eating processed meat in small quantities.

Easy gingerbread cake
You're going to eat something sweet from time to time, especially around the holidays. Spelt flour and prunes boost the fibre content of this cake, giving your gut bacteria something to chew on.

Merry Christmas!

Monday, April 20, 2015

A Microbiome Three-Conference Summary

During the month of March, I've been pleased to cover three great microbiome-related conferences for the Gut Microbiota for Health website. I heard about interesting things happening in the field -- research both deep and broad -- and talked to scientists and clinicians from around the world.

Here are the conferences I attended:

Keystone Symposium - Gut Microbiota Modulation of Host Physiology: The Search for Mechanism

Gut Microbiota for Health World Summit 2015

Experimental Biology 2015

It's hard to summarize the mass of information from these conferences, but here are some of the important messages I heard about gut microbiota:

"Lactobacillus spp Sauerkraut 1" by A doubt - Own work.
Licensed under CC BY-SA 3.0 via Wikimedia Commons -

The gut microbiota are constantly changing; in a single person, composition varies from day to day and over the course of the day.

Diet has a huge impact on (a subset of) the microbiota, with effects on long-term health; the impact of fibre is among the hottest areas of investigation.

Bacterial viruses (bacteriophages) are an important part of the gut community, and may have a role in diseases like Crohn's and AIDS.

Bacterial species are often interesting to note, but it's the metabolites they produce that may be doing the key work in the body.

The immune system is extremely sensitive, responding to slight shifts in the gut community and maybe even suffering long-term 'scarring' from environmental factors.

Clinical trials with therapies (e.g. fecal microbiota transplantation or probiotics) are useful, but it's even more important to investigate mechanisms that are making them work, so we can match therapies to patients with perfect precision.

So far, the established, concrete clinical applications of microbiota research are few (for example, fecal microbiota transplantation for C. difficile), but the intangible clinical applications are many!

I also talk about these three conferences in this podcast interview with the great guys at the American Microbiome Institute.

You can find Storify summaries of the live tweets from Keystone and Experimental Biology here:

Keystone Day 1
Keystone Day 2
Keystone Day 3
Keystone Day 4

Experimental Biology Day 1
Experimental Biology Day 2
Experimental Biology Day 3
Experimental Biology Day 4

Get in touch if you want to know more details about the science!

Sunday, March 29, 2015

"Speaking of Microbiota" - Important ideas in gut microbiota research - Mark Smith of OpenBiome

Currently, science shows that fecal microbiota transplantation (FMT) is clearly effective only in the case of recurrent C. difficile infection. OpenBiome, which supplies donor stool to hospitals all over the United States, is positioned to expand FMT access to other types of patients, but only if the science justifies it. By email, OpenBiome co-founder Mark Smith told me:

"There is an enthusiasm for projecting the success of [fecal microbiota transplation] in [C. difficile infection] onto other indications, but the mechanism is likely quite different and the efficacy is very unlikely to be as high."

- Mark Smith, co-founder of OpenBiome stool bank

See the original article here.

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. The field will advance best if the researchers see that people are enthusiastic about their research.

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

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.

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