Gut Microbiome Conference 2015

When someone asks if you would like to attend a conference in Huntington Beach, California…you say, YES, just because it is a VERY beautiful place to visit!

When the conference entails discussions about the latest research about the relationship between the intestinal microbiota and gastrointestinal disorders…it’s a double win. 🙂

This past weekend, I was fortunate to attend the Gut Microbiome Conference 2015, an exciting 1 1/2 days of learning about one of my favorite topics presented by some of the world experts in the field of gut microbiome research including: Peter Turnbaugh, PhD; Gary Wu, MD; Mark Riddle, MD, drPH; R. Balfour Sartor, MD, Sarkis Mazmanian, PhD; Mark Pimentel, MD and many other esteemed researchers.gut_img-1

Gut Microbiome 2015 was an educational conference geared toward health professionals. The conference was presented by the GI Health Foundation, a  non-profit educational organization dedicated to increasing awareness of the effect of gastrointestinal disorders in the US. The foundation’s goal is to provide health professionals with the most current education and information on gastrointestinal health.

So here is a little recap for you with a little extra details added in an attempt to pull it all together for you:

The human body contains trillions of microorganisms — outnumbering human cells by 10 to 1. The microorganisms are so small but are estimated to make up about 1-3 percent of your body weight. For a 150 pound person that would equate to about 4 pounds of microbes! Yowza!  The more I learn about these little ‘bugs’ the more I realize how their capabilities are truly quite complex. They have been on Earth and evolved a lot longer than humans.

The intestinal microbiota is a complex community of bacteria, archaea, yeast (fungi) and viruses that live in our GI tract. There are 300-1000 different species.  David Underhill PhD spoke about the fungal microbiome and emphasized how little we know about the fungi that reside in our gut.  Fungal DNA is harder to extract as it is encased in a cell wall that is more difficult to degrade. This makes categorizing fungi a bit more challenging.  Fungi are large compared to bacteria… about 50 times bigger! It is estimated that 50-69% of individuals with Crohn’s disease have circulating antibodies to yeast. A similar finding is found with individuals with celiac disease suggesting that immune related small bowel inflammation may correlate somehow with the fungal antibodies.

The intestinal microbiome are the cumulative genomes of the intestinal microbiota.

When it comes to our gut microbes, its all about balance. We all harbor some pathogenic microbes in our intestine and it’s believed that they keep the good microbes in check.  But it is not just about what kind and how many microbes reside in our intestine, research is leading us to look more at what these microbes are doing.  Looking at the numbers and types of bacteria can provide some answers, researchers do this with by sequencing the bacteria in the gut via 16S rRNA profiling, this technique is used as a biomarker and is also known as 16S ribosomal RNA (genes found in all bacteria and are necessary for life.)  The 16S rRNA testing helps identify the community BUT not about their functionality. To see what the microbes are doing or what metabolites they are producing, researchers look at the metabolome (the full complement of metabolites present in an organism in a particular physiological or developmental state.)

Some interesting points made at this conference:

Microbes are chemists!

  • They produce essential vitamins and amino acids
  • Synthesize drugs -compelling evidence that shows drugs can be changed by microbes
  • Digest fiber–that our body is unable to digest on its own.
  • Help circulate hormones and bile acids
  • Detoxify foreign compounds

Many researchers that presented had a particular interest or expertise in inflammatory bowel disease (IBD). There was a fair amount of discussion on the potential relationship with our gut microbes and their role in the advent of this condition.  A few topics reviewed about the IBD and microbial connection:

  • We know that antibiotics improve symptoms for many with IBD.
  • We also know that germ-free animals (in research) do not develop IBD
  • We know that there are alterations in the gut microbiota of IBD patients.

IBD is presumed to occur like a perfect storm: if you are genetically susceptible for IBD, acquire some gut microbial alterations that may trigger an altered immune response, and/or have an environmental trigger (poor diet, stress) you can develop this inflammatory condition. A similar stage of events can lead to the onset of celiac disease too.

The other important point discussed was do the microbes cause the inflammation seen in IBD or does the inflammation itself change the microbiome? More research is needed to tease this out.

Dr. Mazmanian discussed the role of Bacteroides fragilis in IBD. B. fragilis can produce at least eight structurally distinct capsular polysaccharides including Polysaccharide A,(PSA), a novel cell surface molecule that promotes potent anti-inflammatory response. 

A distinctive feature of B. fragilis is the large proportion of the genome is devoted to carbohydrate metabolism, including the degradation of dietary polysaccharides (long chain carbohydrates) and the production of surface capsular polysaccharides.  Research has shown that B. fragilis can protect animals from experimental colitis induced by Helicobacter hepaticus, a commensal bacterium with pathogenic (disease causing) potential. This beneficial activity requires the single microbial molecule (polysaccharide A, PSA). In animal studies, animals that harbour B. fragilis that do NOT express PSA, H. hepaticus colonization leads to disease and pro-inflammatory cytokine production in colonic tissues. This study can be accessed here.  PSA has been shown to reduce inflammation in the central nervous system, as well and may lower risk of colon cancer, multiple sclerosis and colitis. We know inflammation is a hallmark of many diseases. So as you can see by this example it is important to look beyond the simple presence of a microbe in our gut but rather understanding its activity, function or capabilities.

SIBO was discussed in brief.  Mark Pimentel’s group is working on a new medication gear toward methane + SIBO patients. This new drug will not reduce methane producing microbes but rather target their ability to produce methane.  With a decrease in methane production, symptoms of methane + SIBO are reduced.

Mark Riddle reviewed an interesting study found here about use of green bananas which are rich in resistant starch in children with severe diarrhea and Shigella infections. The green banana improved symptoms. Resistant starch is a prebiotic, food for our gut microbes.

Another key point from the conference was that microbial composition differs in association with disease states such as IBS, IBD, fatty liver, obesity and diabetes and the mucosal microbes appear to be more related to the disease state that the microbes found in stool. Microbes find niches in the GI tract in crypts in the colon and or in biofilms and these bacteria might not even be present in stool studies.

Different events and or conditions can alter our gut microbiota as seen during pregnancy particularly in the last trimester, illness, antibiotic use, bout of food borne illness, detrimental lifestyle (stress, poor diet.)  We are seeded by different bacteria depending on whether we were born by c-section or vaginal birth and these differences can impact health later in life.  If we over sanitize (the hygiene hypothesis) this might be detrimental to our gut microbiata and if we live on a farm or have pets it might be beneficial to our gut microbial populations and future allergy risks.

Imbalance of our gut microbiota is called dysbiosis and some consequences are:

  • Local gut inflammation
  • Systemic (throughout the body) inflammation
  • Increased oxidative stress
  • Altered production of neurotransmitters
  • Increased production of endotoxins such as LPS (bacterial lipopolysaccharide) which has been shown to disrupts mucosal integrity.
  • Chronic infections
  • Impaired detoxification or regulation of oxidative stress
  • Impaired energy metabolism (obesity associated with methane producing microbes)
  • Autoimmune disease

One mice study revealed consumption of raw tubers had an antimicrobial effect. And other research has shown honey to have anti-bacteria properties.

What should you eat to better your microbiome? The reality is, this science and these microbes are very complicated. And the truth is, we can’t say with certainty what is the best diet to boost the health of you and your microbiome.  I believe that the future will combine genetic testing with those of our gut flora and have targeted diets, especially for those who suffer with GI issues. I don’t think there is a one size fits all approach to this.  I am sure there will be some general recommendations for a healthy microbiome diet including eating adequate fiber, modifying animal fats and eating a diet that is anti-inflammatory (anti-oxidant rich, monounsaturated and omega-3 fats such as olive oil,nuts, seeds and fish) perhaps even a personalized prebiotic and probiotic mixture?! Eating more whole foods vs. products is key too. Perhaps even greater use of fecal transplants for those challenged with GI disorders.  Fecal transplants have been used very successfully for individuals that suffer with C. diff infections.  For more on this topic, check out my Harvard Medical School Probiotic Gut Microbiome conference post here.



13 replies on “Gut Microbiome Conference 2015

    • katescarlata

      Thanks, Deirdre. It is very complex and relatively speaking a very new area of research. The problem is we all want answers now…and some individuals are promoting information about our gut microbiota needs well ahead of the science.

  • Whitney Stewart

    Thanks, Kate, for keeping us updated. I follow this research closely and am eager to read your conference summaries.
    I wish we were already at the stage of tailoring personal diets and supplementation (prebiotics and probiotics). Those of us who have long lived with GI complications will celebrate new medical approaches when they work.

  • Christy

    Thank you for this update! I am encouraged to know there is so much new research being done in the field. I have struggled to find a Dr who is literate in this and am curious to find someone who can help with extreme dysbiosis. Would you have any recommendations on this or be aware of any clinical studies that are recruiting for this? I too look forward to your updates from conferences.

  • Terry

    Thank you for posting this summary so quickly after your meeting! I have a question about the PUFA in some oils, nuts and seeds – are they more harmful than helpful? I have thyroid disease and have heard they can suppress thyroid function even more. Thank you!

  • Trish

    Thanks, Kate, for your synopsis so quickly! Though not a scientist by any means, I am interested in this topic. Right now it seems what I can do is watch my diet and reduce stress as much as possible. Interesting about the green bananas.

    • katescarlata

      No discussions about Enteragam at the conference–but there is some research to support its use in some patients with diarrhea. Will be interested in seeming more research.

  • Divya

    Excellent post Kate and thank you for the valuable information. It’d be interesting to see what the role of B. fragilis is in other gut disorders/immune dysfunction that we don’t automatically think “IBD” but there is an inflammatory component. For instance, in the UK, there’s been a lot of publicity of late around endometriosis and the conditions that tag along for the ride, including thryoid dysfunction, allergies/atopy and surprise surprise, IBS. I and a few other people I know have endometriosis and complain of terrible IBS/SIBO/immune dysfunction… The potential for cross over is fascinating!

  • Linda Tucker

    I am curious your thoughts on neomycin. I have IBS-C and have been following a low FODMAP diet with some success. I have finally decided I need to go to the next step and conquer the underlying SIBO causing the FODMAP sensitivity. After TONS of research I wanted to take the plunge into a 14 day Rifaximin and Neomycin protocol. My doctor doesn’t feel comfortable prescribe an oral form of neomycin.. says there is a black box warning about possible hearing loss. Thoughts?

    • katescarlata

      Hi Linda, the neomycin makes me a bit nervous too–and have more recently heard of this black box warning. Rifaximin will address some of the methane microbes–maybe not as well as the dual rifaximin/neomycin combo–but for some, the rifaximin alone works.

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