Search This Blog

Saturday, September 17, 2016

The Intestinal Gardener is Moving

Hey intestinal gardener blog readers!


After a fair number of hits (...and a few misses, too...) I've decided to pack up and move this blog.

From now on I'll be posting on a new website, found here:

I'll be posting more regularly on the new site and keeping you up to date on the field of gut microbiota science. Watch for posts about new articles and projects and important developments in the field.

And sometimes, what I had for dinner.

Catch you there.

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 many different places.

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 possible 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 composition is often interesting to note, but it's the metabolites the bacteria 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 eventually 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

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 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).  That was clearly one more step than some 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's what's in the paper:

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.

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."

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.

There is no scientific consensus that C. bolteae is unique 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 evidence shows - both in the peer-reviewed journal and in the media.

The upshot (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

Saturday, December 29, 2012

Book Review: Wheat Belly is a bestseller, but what's the science behind it?

If a doctor writes a book in the forest...
Wait a minute, that's not right.

If a doctor writes a book about health... is it science?

This is the question I had in mind while reading Wheat Belly. When a physician like William Davis, MD, takes time out of his (no doubt) busy schedule to write a health-related book, ideally he has taken the time to  get familiar with all the scientific literature on the topic. This may be easier for doctors than for some other writers, as Davis may have had the benefit of hearing research summaries at conferences, or having literature reviews arrive on his desk with the daily mail. Add that to years of clinical experience, and you have the potential for a pretty compelling argument on a health issue.

But what if, instead, a doctor seems to have spent years giving a certain piece of unusual clinical advice about a dietary change. And he has had such great success with patients who follow that advice that he goes looking for science to explain why it works. He scraps together a few studies that he thinks are relevant, connects some dots, and writes a book. What then?

Interesting, but not necessarily science.

So here's the heads up: Wheat Belly is an example of the latter. Though Davis, a cardiologist, has written a very interesting book with a timely message, you should know that it is not strictly based on science. Meaning: there is little or no evidence for his claims about the ill health effects of wheat.

Case in point: the glycemic index stats he cites are from an article published in 1981 - and he repeats again and again that the study found a greater blood sugar rise with "whole-meal" bread than with white bread, even though - ahem - a fair amount of glycemic index research has been done since, and a quick visit to almost any diabetes association website will confirm that whole wheat breads (for the most part) have lower glycemic indices than white breads. Davis gives a few nods to how his claims fit in, or don't fit in, with the advice of professional bodies. But he doesn't present a complete picture of why and how science shows that eliminating wheat from one's diet is a good idea, because the scientific evidence doesn't exist at present.

The point of the book is that it's bad to eat things that spike your blood sugar - i.e. things with a high glycemic index (GI). Apparently wheat spikes the blood sugar more than you'd expect - the oft-cited study found whole grain bread had a GI of 72, while a Mars bar had a GI of only 68 - and therefore we should eliminate wheat.

It follows that we should eliminate all things that spike blood sugar. Davis advocates this. So properly, the book should be called "Carb Belly". (Of course, the arguments against carbs have been well-explored in books that promote the Atkins diet, Paleo diet, Specific Carbohydrate diet, etc.) But Davis says the one carbohydrate that people have the most trouble eliminating is wheat. Hence, the name Wheat Belly.

Here's what's in the book:

Part 1:
Davis explains how wheat strains have changed with hybridization and how modern types of wheat affect us in unprecedented ways.

Part 2:
Davis describes wheat's "head-to-toe destruction of health": (1) the addictive properties of wheat that can influence behaviour and mood, (2) the way wheat triggers blood sugar and insulin extremes, which lead to visceral fat accumulation, (3) how intestinal permeability triggered by a protein in gluten may be responsible for the rise of autoimmune disorders and digestive disorders, (4) an argument that wheat may cause type 2 diabetes, (5) an explanation of how wheat affects the body's pH, resulting in an "acid-rich situation" and that promotes osteoporosis, (6) wheat's promotion of AGEs, which signal aging, (7) how wheat leads to heart disease by increasing triglycerides that turn into atherosclerotic plaque, (8) how the immune system's attack on nerve cells results in cerebellar ataxia and brain fog, and (9) how increased levels of insulin, and an immune reaction to gluten, can show up as acne or skin rash.

Note that for most of these claims, Davis's evidence is in the realm of the "theoretically possible." As far as I can tell, the science actually addressing these claims is weak. The studies conducted on humans where all else is equal, except the inclusion of wheat in the diet, are rare. Making his claims premature at best.

Part 3:
He talks about the "how to" of eliminating wheat and other carbohydrates. The book includes menus and recipes for low-carb eating.

So now the question, can we really knock Dr. Davis for proposing a low-risk treatment that seems to work like magic clinically for a host of health problems? Can we truly fault a compelling book that's convinced a lot of people to do something that seems to improve their health? It doesn't escape me that it took a lot of bravery for him to so emphatically convey this message in a world that is very wheat-centred.

So yes, Davis has perhaps inspired many people to initiate a positive change for their health by penning a bestselling book with lots of media coverage. But by putting together a misleading scientific grab-bag for convincing people to make this change, he is ensuring they never fully understand what caused their complex health problems in the first place.


...mainly tell the same story as these:

Saturday, July 23, 2011

Living in symbiosis

Anyone who's ever managed a multi-person project - or managed a kids' art project, for that matter - knows how hard it is to keep everyone working together in harmony. In the best case scenario, everyone's efforts benefit everyone else. But more likely, something will offset the balance and leave at least one person feeling alienated and bitter.

Maybe we should take a lesson from our microbes: in the majority of cases, the intestinal bacteria manage to exist in a nice symbiotic relationship with the human body that houses them. It can't be an easy task for all those cells (and we're talking trillions of bacterial cells) to operate in such close contact with their (comparatively) giant host. Yet they do - their project of "living in symbiosis" usually goes off without a hitch.

"Symbiosis". Photobucket image by GlynGPKSS 

How do the microbes achieve that symbiosis so successfully?

This was the question explored by a team of Harvard researchers under the direction of Dr. Wendy Garrett, an immunology professor and oncologist. Their 2011 paper is entitled Host and gut microbiota symbiotic factors: lessons from inflammatory bowel disease and successful symbionts.

The researchers at the Garrett lab happen to know a lot about Inflammatory Bowel Diseases (IBDs) possible examples of what can happen when a host and its bacteria fail to maintain symbiosis. So, more than anyone, these researchers know about the challenges faced by the host-bacteria relationship: the foods that enter the body (since fried beef takes a different toll on the microbes than lentil soup), the functioning of the immune system, and the number of pathogenic bacteria that are competing for space in the gut. All these things have the capacity to work against symbiosis.

The study reads like one of those workplace "let's identify our strengths" exercises. First, it explored what features of the host (i.e. the human body) contribute to symbiosis. Then, it covered the contributions of the bacteria themselves.

When it came to the body, the researchers picked out several genes that they felt were necessary for coexistence with gut bacteria. According to previous experiments, these genes affect the immune system and thus affect what bacteria colonize the gut. Meanwhile, the researchers identified three genera of bacteria that seemed especially good at living in symbiosis: Bacteroides, Helicobacter and Lactobacillus. The bacteria's list of workplace strengths included the ability to stick to mucosal surfaces inside the intestine, a tolerance for extreme pH shifts in the gut, and a propensity for lowering inflammatory processes in the body.

This makes for a nice, tidy presentation of what it takes to live in symbiosis: the right genes and the right environment. Possessing certain genes may make it easier for bacteria to get along with you. And the specific bacteria that you have encountered in your daily comings and goings may do their part to keep the relationship in harmony.

This is part of an exciting new research path - and it's about more than just IBD prevention. The Garrett lab is exploring the overall relationship between gut bacteria and the immune system - how disruptions in the community of gut bacteria may contribute to the body's inflammation responses, and how that inflammation might lead to disease or cancer.
Ballal SA, Gallini CA, Segata N, Huttenhower C, & Garrett WS (2011). Host and gut microbiota symbiotic factors: lessons from inflammatory bowel disease and successful symbionts. Cellular microbiology, 13 (4), 508-17 PMID: 21314883

Monday, June 27, 2011

The connection between gut bacteria and restless legs syndrome

Some people's legs have a mind of their own. Their legs decide that they need to pace the room constantly instead of sitting. Their legs are responsible for the twisted knot of sheets at the end of the bed every morning. Their legs burn or tingle or get creepy-crawly sensations, especially when they try to sit down and relax.

Legs picture by Pedro Simões, via Flickr

Restless legs syndrome (RLS) is associated with an irresistible urge to move the legs. As you can imagine, this brings its own set of problems. A lot of the time, people with RLS have trouble getting to sleep or staying asleep - making them grouchy and unfocused in the daytime. The sensory and motor abnormalities in this syndrome have a neurological connection, but so far there is no clear answer about how to make restless legs go away.

According to one intriguing new study in Sleep Medicine, restless legs syndrome may be another thing connected to gut bacteria gone haywire.

The study came about because its investigators, Weinstock and Walters, had previously noticed that many people with celiac disease and Crohn's disease happened to have a diagnosis of restless legs syndrome.

They wondered: Does the reverse relationship hold between gastrointestinal problems and restless legs? That is, if we take a group of people with known RLS, would we find that they have more gastrointestinal problems than people with normal leg movement?

The gastrointestinal problems they were interested in studying were irritable bowel syndrome (IBS) and small intestinal bacterial overgrowth (SIBO).

Importantly, IBS is a "functional syndrome". That means doctors diagnose it based on reported symptoms rather than a specific test that confirms or disconfirms it. So to be fair, there's no guarantee that people with IBS have anything wrong with their gut bacteria. But in recent years IBS has been linked to SIBO, a condition that is definitely associated with too many bacteria hanging out in a neighborhood where they don't belong: the small intestine.

SIBO itself is diagnosed via an indirect method called the "lactulose breath test". The attraction of this method is that it involves nothing more invasive than drinking a cup of sugar solution and blowing into a plastic tube.

The researchers wanted to investigate both IBS and SIBO because each one indicates that something is going wrong with digestion; some patients have both problems, but others have just one or the other. They ended up with one measure of gastrointestinal distress that was based on reported criteria (i.e. IBS), and one that was based on measurable biology (i.e. SIBO).

People with restless legs syndrome discovered the study through ads that made no mention of gastrointestinal symptoms. Their diagnoses of RLS were confirmed by the investigators, and then each subject was assessed for both IBS and SIBO.

It turned out that IBS was diagnosed in 28% of subjects with restless legs syndrome, compared to 4% of the controls. In some of the cases, the IBS symptoms had appeared before the onset of the RLS symptoms. In others, the two problems started around the same time.

As for SIBO, the breath test showed it was present in 69% of the people with restless legs syndrome, compared to 28% of the controls.

The conclusion? People with restless legs syndrome have a greater incidence of IBS and SIBO - that is, a greater incidence of problems in the digestive system - than people without it. And in at least some people with restless legs syndrome, the associated gastrointestinal problem was related to bacterial overgrowth in the small intestine.

The research is far from concluding that gastrointestinal problems CAUSE restless legs or vice versa. But the researchers did confirm co-occurrence, and they also put forward the idea that there may be a common mechanism that leads to both: maybe some kind of inflammatory process in the body that leads to central or peripheral nerve damage, or a change in micronutrient absorption, resulting in restless legs.

In support of this, the researchers did an informal review of conditions that tended to co-occur with RLS; 89% of these disorders had been associated with inflammation or immune system activation.

In turn, the connection between inflammation and alterations in gut microbiota has strong support in the literature. But that's a topic for another day.

Lots of questions remain about restless legs syndrome, but the connection that this study made between restless legs and gut troubles seems to confirm certain clinical observations. We need more information though - let's hope this area of research stays alive and... kicking.
Weinstock LB, & Walters AS (2011). Restless legs syndrome is associated with irritable bowel syndrome and small intestinal bacterial overgrowth. Sleep medicine, 12 (6), 610-3 PMID: 21570907