'Managing Gut Autoimmunity Advanced Microbiome Strategies for Inflammatory Bowel Disease' - IHCAN Summit Webinar

Which countries can have an access to the microbiome test?
Currently Microba’s testing range is available in Australia and mainland UK. We are working hard to bring the test to other regions, so please do keep an eye out for announcements.  

Are there additional genetic factors that should be considered for monitoring patients (i.e. Human Leukocyte Antigens, HLA antibody or typing).
There are two broad categories of genetics to consider:

1. Disease susceptibility genetics – IBD is polygenic, with more than 240 susceptibility loci identified. While these variants contribute to disease risk, none are currently used routinely for monitoring disease activity or guiding management of individual patients.

2. Pharmacogenetics – Several genetic markers may inform treatment selection or safety:

• HLA-DQA1*05 is associated with an increased risk of developing anti-drug antibodies to anti-TNF therapies (particularly infliximab and adalimumab). Carriers have approximately twice the risk of immunogenicity, which may support decisions regarding combination therapy and biologic selection.

• TPMT and NUDT15 testing before thiopurine therapy (azathioprine or mercaptopurine) identifies patients at increased risk of severe myelosuppression and is recommended before treatment initiation.
• Emerging evidence also links specific HLA-DQA1/HLA-DRB1 haplotypes with thiopurine-induced pancreatitis, although routine clinical implementation is not yet widespread.

These genetic tests are typically performed once before treatment initiation and are not used as serial monitoring biomarkers.

Routine HLA antibody testing is not generally recommended in IBD management.

Re Oral bacteria being in the gut, is there any link to low stomach acid? which is not killing them effectively before they pass on?

High levels of oral species in the gut can arise in several situations. One is intestinal inflammation, which I discussed during the presentation. Another is reduced gastric acid exposure. For example, individuals taking proton pump inhibitors (PPIs) often show increased oralisation of the gut microbiome, likely because fewer oral bacteria are eliminated in the stomach before reaching the intestine.

Other factors associated with increased oralisation include disruption of the resident gut microbiome (for example following antibiotic use, where there is a reduction in microbial load) and periodontal disease.

 I have had Crohn’s Disease for 35yrs and only 5yrs ago, after requesting testing with my IBD Nurse, have Bile Salt Malapsorption. As the management of BSM is easy, curious to know why this wasn’t considered alongside my Crohn’s diagnosis – any thoughts?

Bile acid malabsorption (BAM) is relatively common in Crohn’s disease, particularly when the terminal ileum is affected or has been surgically resected. The terminal ileum is responsible for reabsorbing bile acids, so inflammation or damage in this region can allow excess bile acids to reach the colon, where they stimulate water secretion and motility, leading to bile acid diarrhoea.

Bile acids also play an important role in regulating inflammation. In IBD, changes in the gut microbiome can reduce the bacteria responsible for converting primary bile acids into anti-inflammatory secondary bile acids. This may reduce signalling through pathways such as FXR and TGR5, which normally help maintain intestinal barrier function and immune balance.

In terms of why BAM may not have been investigated earlier, it’s difficult to comment on an individual case. Historically, awareness and testing for bile acid diarrhoea may have been less widespread than they are today, and symptoms can overlap considerably with those of Crohn’s disease itself. In some patients, diarrhoea may be attributed to active inflammation, previous surgery, functional bowel symptoms, or other complications, meaning BAM is not always considered immediately. I’m glad you did eventually get a diagnosis.

I have found minimal Crohn’s health problems after adopting a vegetarian diet. Is there is reason for promoting animal proteins when they are also inflammatory?

That’s great that you have been able to manage your Crohn’s so successfully through dietary intervention.

In general, it’s not a case of promoting animal protein as inherently beneficial in Crohn’s disease. Rather, some structured dietary approaches used in Crohn’s, such as CDED or low-residue diets, include protein for nutritional adequacy and often recommend choosing leaner, less processed sources where an omnivorous diet is being followed.

The evidence around red and processed meat is nuanced. A diet lower in red and processed meat may help reduce flares in ulcerative colitis, but this has not been shown to reduce relapse rates in Crohn’s disease.

That said, there are good microbiome reasons why a more plant-forward, fibre-rich diet may benefit many people. When the microbiome has more fermentable fibre available, fermentation tends to shift toward short-chain fatty acid production, including butyrate, which supports gut barrier and immune regulation. By contrast, higher levels of protein fermentation can increase production of metabolites such as ammonia, hydrogen sulfide, phenols, indoles and branched-chain fatty acids, which may be less favourable in excess.

Should we wait for patients to be in remission before we look to advise on CDE Diet?

Not necessarily. In fact, the Crohn’s Disease Exclusion Diet (CDED) was originally developed as an induction therapy and has been studied in patients with active mild-to-moderate Crohn’s disease, often in combination with partial enteral nutrition (PEN).

However, because the strict induction phase of CDED involves PEN, nutritional therapists should only support this approach when it has been prescribed and overseen by the patient’s gastroenterology team. BANT’s Scope of Practice guidelines specifically state that nutritional therapists should not prescribe enteral or elemental diets independently.

If a patient’s medical team has recommended CDED and PEN, a nutritional therapist can play an important role in supporting implementation, adherence, nutritional adequacy and the practical aspects of the diet. Once remission has been achieved, the maintenance phases of CDED involve a wider range of foods and may be more appropriate for ongoing dietary support.

For clients who’ve had a history of cancer diagnosis, what would you suggest to replace glutamine for gut barrier repair?

The NHMRC graded insights for intestinal permeability included in the Microba test (approved via our Science review process) are: Glutamine, Colostrum, Zinc carnosine  and Saccharomyces boulardii.

If glutamine (which has the strongest evidence) is not suitable for use, then colostrum and zinc carnosine are good potential alternatives. However, both have a lower evidence grade (C versus B). S. boulardii also has some grade D evidence, which comes from use in patients with Crohn’s disease specifically. 

Is the technology use in Microba tests, comparible to a new technology called Titan-1 Technology which is being promoted (eg. GUT ID testing)?

Titan-1 is a sophisticated long-read amplicon technology (Long read 16S-ITS-23S rRNA) and likely represents an improvement over conventional 16S testing. However, it is not directly comparable to shotgun metagenomics because it does not capture the whole microbiome or assess microbial functional capacity. See slide 38 of the presentation deck for a comparison of the two technologies.

If a person has PSC (primary sclerosing cholangitis) besides ulcarative colitis, what do you think, is microbiome analysis suitable? If any infection is present, is antimicrobial protocol suitable due to PSC diagnosis?

Yes, I think microbiome analysis can still be useful in individuals with both ulcerative colitis and primary sclerosing cholangitis (PSC). In fact, PSC is quite strongly associated with alterations in the gut microbiome, and there is growing evidence that interactions along the gut-liver axis may contribute to disease progression.

Regarding antimicrobial protocols, the presence of a microorganism on a microbiome test does not necessarily mean it should be treated. Many organisms can be present without causing disease, and antimicrobial interventions can further disrupt the microbiome. In PSC specifically, caution is warranted because patients may already have significant dysbiosis and altered bile acid metabolism.

If a recognised gastrointestinal pathogen is identified, treatment decisions should be made in conjunction with the patient’s gastroenterologist and hepatology team. The appropriateness of any antimicrobial protocol will depend on the organism identified, the severity of symptoms, liver function and the patient’s overall medical management.

More generally, in PSC the greatest value of microbiome analysis may lie in understanding broader ecosystem patterns, such as microbial diversity, short-chain fatty acid production and inflammatory signatures, in order to support the wider gut ecosystem, rather than simply identifying organisms to target with antimicrobials.

 I am seeing a UC client on a pro-bono basis as they have only just returned to work after 6 months off sick.  At the very minimum, would optimising their omega 3 levels, Vit D and other basic nutrients be helpful as a starting point to improve their energy and absorption levels? They just don’t have the funds but desperate not to have a flare/relapse.  Thanks for such a great webinar.

That’s very generous of you to support them pro-bono. I think focusing on the foundations is a good strategy, particularly when resources are limited. Optimising nutritional status is certainly important for supporting recovery, energy levels and overall resilience.

If budget is a concern, I would encourage them to discuss testing with their GP or IBD team, as they may be able to access relevant investigations through routine care, for example, vitamin D, iron markers, vitamin B12 and folate. 

It may also be worth asking whether their gastroenterology team monitors faecal calprotectin, as this can provide an objective measure of intestinal inflammation. Where raised, omega 3, curcumin and inulin all have evidence for helping to reduce levels (as discussed in my presentation). However, these approaches should be viewed as complementary to, rather than replacements for, their prescribed medical treatment.

From a practical perspective, if budget is a concern, I would focus on:

1. Maintaining medical therapy and regular follow-up with their IBD team.
2. Assessing and correcting any nutrient deficiencies where possible.
3. Supporting as diverse and nutrient-dense a diet as can be tolerated.
4. Addressing lifestyle factors such as sleep, stress, physical activity, alcohol, and environmental pollutants.

While we can’t ever guarantee prevention of a flare, ensuring nutritional adequacy and addressing modifiable risk factors is a good foundation on which to build further support if she does have more funds for further testing in the future.

Is there any specific test for Diverticulitis? Or would the microbiome test be a good choice?

Acute diverticulitis is typically diagnosed based on symptoms (such as left-sided abdominal pain, fever and changes in bowel habit), blood markers of inflammation, and when needed, imaging such as a CT scan. A microbiome test would therefore not be considered a diagnostic test for diverticulitis itself.

Where microbiome analysis may be helpful however is in understanding factors that could contribute to recurrent symptoms or future risk. For example, people with diverticular disease often show reduced microbial diversity and lower levels of beneficial short-chain fatty acid producers. These insights may help inform dietary and lifestyle strategies aimed at supporting long-term gut health.