If you live with an autoimmune condition, you already know the pattern: good weeks, then a flare that seems to come from nowhere. Fatigue, sore joints, gut upset, brain fog. Different diagnoses, but the same underlying cause: chronic inflammation, often rooted in the gut microbiome. Research has found gut dysbiosis, an imbalance in your gut bacteria, across most autoimmune conditions studied. It weakens the gut lining, making it more permeable or “leaky” and letting bacterial fragments into your bloodstream that keep your immune system on constant alert.

I know this one personally. I was diagnosed with an inflammatory bowel disease in my 20s and spent decades managing symptoms when medication alone wasn’t enough. What finally changed things was testing. Microbiome stool testing and SIBO breath testing showed me that dysbiosis was actually driving my inflammation.

Then I could treat it, rather than guess.

Here’s what I’ve learned, clinically and personally: in autoimmune disease, the gut microbiome is often where inflammation starts — and where we have the most leverage to calm it.

First, not all inflammation is bad

Inflammation is your immune system’s way of protecting you. Cut your finger, catch a virus or get stung by a bee, and your body sends in a rapid-response team to contain the damage and start repairs.

Acute inflammation is short and protective. You’ll notice redness, heat, swelling, pain or loss of function, and it resolves within days to a couple of weeks. The outcome is healing.

Chronic inflammation is low-grade and never fully switches off. It’s often subtle: fatigue, aches, gut symptoms, brain fog, recurring flares that can persist for months or years, causing ongoing damage to cells, tissues and organs.

Over time, chronic inflammation stops being a response to disease and becomes part of what drives it.

What keeps chronic inflammation switched on?

In autoimmune disease, the immune system mistakenly targets the body’s own healthy tissue — the thyroid in Hashimoto’s, the joints in rheumatoid arthritis, the gut lining in Crohn’s and ulcerative colitis. Each condition looks different, but chronic inflammation is the common driver of symptom severity. Common contributors include:

• An unresolved trigger — an infection or injury that never fully settled
• Gut dysbiosis and increased intestinal permeability (“leaky gut”) — more on this below
• A diet heavy in ultra-processed food, added sugar and refined flour, and low in fibre and plants
• Ongoing stress and poor sleep, which shift the immune system into an overactive state
• Movement extremes — inactivity promotes inflammatory visceral fat, while chronic over-training can add to the load
• Environmental exposures — pollution, chemicals, smoking

Whether it’s the cause or the consequence, bringing down inflammation is central to managing chronic illness.

The gut microbiome and autoimmune disease: where it often starts

If there’s one place to look when you want to reduce inflammation in autoimmune disease, it’s your gut. Most of your immune tissue sits just beneath your gut lining, separated from trillions of microbes by a barrier only one cell thick.

That proximity is deliberate. From birth, your gut microbes train your immune system to tell friend from foe — what to tolerate (food, beneficial bacteria, your own tissues) and what to attack (genuine pathogens). Autoimmunity is, at its core, a breakdown in that tolerance.

Genes load the gun, but they don’t fully explain who develops autoimmune disease. In animal studies, mice that are genetically prone to arthritis stay healthy when raised germ free and develop joint inflammation once specific gut bacteria are introduced. Your microbiome is one of the most important environmental triggers, and unlike your genes, it’s something you can change.

4 ways an imbalanced microbiome fuels autoimmunity

1. A leaky gut barrier. Dysbiosis weakens the tight junctions between gut lining cells. Bacterial fragments such as lipopolysaccharide (LPS) and partially digested food proteins then slip into circulation, keeping the immune system on constant high alert.

2. Losing your anti-inflammatory bacteria. Beneficial species ferment fibre into short-chain fatty acids, especially butyrate. Butyrate feeds your gut lining and supports regulatory T cells (Tregs) — the immune system’s peacekeepers. Lose those bacteria and the balance tips toward inflammatory Th17 cells, which drive tissue damage in many autoimmune conditions.

3. Mistaken identity. Some bacterial proteins closely resemble human ones. When the immune system mounts a response against a microbe, it can cross-react with similar-looking proteins in your own tissues — a process called molecular mimicry.

4. Bacteria in the wrong place. In a 2018 study published in Science, a gut bacterium called Enterococcus gallinarum crossed a damaged gut barrier into the liver and lymph nodes of autoimmune-prone mice and triggered autoantibodies. Researchers then found the same microbe in liver biopsies from people with lupus and autoimmune liver disease.

What a microbiome test can show you

This is why I don’t start with a generic anti-inflammatory list. Two people with the same diagnosis can have completely different gut drivers. A comprehensive stool test can show:

• Diversity — how resilient your gut ecosystem is
• Your butyrate producers — whether species like Faecalibacteria prausnitzii and Roseburia are present in healthy numbers
• Inflammatory and opportunistic species — overgrowths linked with immune activation
• Gut barrier and inflammation markers — such as zonulin, calprotectin and secretory IgA, depending on the test
• Fungal and parasitic overgrowth

Where the Autoimmune Protocol (AIP) fits

The Autoimmune Protocol is an elimination-and-reintroduction diet. It temporarily removes foods that commonly aggravate the immune system or gut: grains, gluten, dairy, eggs, legumes, nightshades, nuts, seeds, refined sugar, alcohol and processed foods while doubling down on nutrient-dense vegetables, quality protein and healthy fats. Foods are then reintroduced one at a time to see what you actually tolerate.

The research is still small, but encouraging:

• IBD: In a pilot study of 15 people with active Crohn’s or ulcerative colitis, 73% reached clinical remission by week 6, and all maintained it through the maintenance phase. Quality-of-life scores also improved.
• Hashimoto’s: A 10 weeks study in 17 women found significant improvements in quality of life and symptom burden, with signs of reduced systemic inflammation (measured by CRP). Thyroid antibodies didn’t shift in that timeframe, but I have seen them shift over time.

AIP is a short-term tool, not a forever diet and the reintroduction phase is key. Staying restricted long-term can narrow your microbiome and risk nutrient gaps. Microbiome testing alongside can show whether your priority is restoring fibre-loving bacteria, addressing overgrowth or repairing the gut barrier.

6 gut-first ways to reduce inflammation in autoimmune disease

1. Feed your anti-inflammatory gut bacteria

This is the foundation everything else builds on. Your butyrate-producing bacteria need fermentable fibre to thrive, and in return they calm your immune system and strengthen your gut barrier.

• Prebiotic fibres: cooked-then-cooled potato or rice, green banana, oats, ground flaxseed, leeks, onions and asparagus (if tolerated)
• Polyphenols: berries, extra virgin olive oil, green tea, cacao and pomegranate help feed beneficial species such as Akkermansia
• Fermented foods: sauerkraut, kimchi, kefir or coconut yoghurt — start with a teaspoon and build up
• Go slowly: if fibre makes you bloat, that’s a clue, not a failure. It can point to SIBO or slow motility, and it’s worth testing before you push through.

A note on probiotics: benefits are strain-specific, and a generic supermarket product may do little for your gut. Your test results show which bacteria actually need support.

2. Eat the rainbow — your microbes love variety

Colourful plants are packed with phytonutrients: the compounds that give food its colour, flavour and aroma, and act as antioxidants that help quieten inflammation. Variety matters as much as volume — different plant fibres feed different gut bacteria. Aim for 30 different plants a week, counting vegetables, fruit, herbs and spices, and lean on dark leafy greens.

3. Cook with anti-inflammatory spices

Turmeric, ginger, garlic, cinnamon and cloves all have antioxidant and anti-inflammatory properties — and they count toward your plant total.

4. Check your vitamin D

Vitamin D helps regulate immune function, and low levels are common in people with autoimmune conditions. Unless you send enough time outdoors without sunscreen in the mornings before the heat of the day, supplementation may be the better option. Food sources include salmon, sardines and eggs.

5. Protect your sleep

Sleep is when your body repairs and recalibrates its immune response — even one bad night raises inflammatory markers. Aim for 7–9 hours with a consistent bed and wake time. Switch off screens an hour before bed, keep the room cool and dark, and use whatever helps you wind down: breathwork, a bath, music, a book.

6. Lower your stress load

Chronic stress keeps cortisol and inflammatory signalling elevated and directly affects your gut via the gut–brain axis. Mindfulness meditation, yoga and tai chi have all been shown to improve stress resilience, and research suggests mindfulness practices may reduce inflammation in chronic inflammatory disease. Start with five minutes a day.

Bonus: move most days. Regular moderate movement such as walking, swimming or strength work lowers inflammatory markers. Match intensity to your energy — in a flare, gentle beats intense.

Test, don’t guess

Symptoms tell you something is wrong. They don’t always tell you why.

I combine microbiome testing, SIBO breath testing (when indicated) and a review of your pathology with a detailed health history. That shows me what’s driving your inflammation, so your food, supplement and lifestyle plan is built around you.

Struggling with autoimmune or gut symptoms? Book a discovery call here.

If you’re ready to understand your gut health a little better, follow along on Instagram. 💚

In clinic, I often see women who are on thyroid medication, whose blood tests look “normal”, and who still feel tired, bloated, foggy and constipated. Medication replaces the hormone. It doesn’t address why the immune system is attacking the thyroid in the first place, and that is where the gut comes in.

How does the thyroid work?

Your thyroid is a small, butterfly-shaped gland at the front of your neck, just below your Adam’s apple. Its hormones help regulate almost every system in your body, including metabolism, energy, body temperature, heart rate, digestion, mood, brain function and bone health.

The thyroid uses iodine and the amino acid tyrosine from your diet to make two main hormones:

• T4 (thyroxine): about 80% of what the thyroid releases. T4 is a storage form that needs to be converted into T3 before your cells can use it.
• T3 (triiodothyronine): the active hormone. The thyroid makes a small amount directly, and most of your T3 is made from T4 in tissues like the liver, kidneys and gut.

Your brain controls how much hormone the thyroid makes. The hypothalamus releases thyrotropin-releasing hormone (TRH), which tells the pituitary gland to release thyroid stimulating hormone (TSH). TSH then tells the thyroid to produce more T4 and T3. This feedback loop is called the hypothalamic-pituitary-thyroid (HPT) axis.

This system can be thrown off by nutrient deficiencies, chronic stress, infections, environmental toxins, inflammation, gut dysbiosis and autoimmunity.

Hashimoto’s and Graves’ disease

There are two main types of autoimmune thyroid disease.

Hashimoto’s thyroiditis is the most common. The immune system attacks the thyroid, causing inflammation and gradual damage to thyroid cells, so over time the thyroid makes less hormone (hypothyroidism). Symptoms can include fatigue, weight gain, constipation, feeling cold, dry skin, thinning hair, joint and muscle aches, low mood and heavy periods. It is far more common in women.

Graves’ disease happens when antibodies switch the thyroid on, so it makes too much hormone (hyperthyroidism). Symptoms can include weight loss, a racing heart, loose bowels, sweating, anxiety, poor sleep, shaky hands and lighter periods.

Once you have one autoimmune condition, you’re more likely to develop another. Hashimoto’s often occurs alongside coeliac disease, rheumatoid arthritis, lupus and Sjögren’s syndrome.

The gut and thyroid connection

Researchers now talk about a “gut-thyroid axis”. Your gut and your thyroid affect each other in both directions, and when one is out of balance, the other usually is too.

Dysbiosis and leaky gut. People with Hashimoto’s and Graves’ tend to have different gut bacteria to people without thyroid disease. When the microbiome is out of balance, the gut lining becomes more permeable and lets bacterial fragments into the bloodstream. This keeps the immune system on alert and can make thyroid autoimmunity worse. I explain this in more detail in How Your Gut Microbiome Drives Inflammation in Autoimmune Disease.

Nutrient absorption. Your thyroid depends on selenium, zinc, iron and iodine, and your gut bacteria play a key role in absorbing them. You can eat well and still be low if your gut isn’t absorbing properly.

Hormone recycling. Gut bacteria help reactivate thyroid hormone that the liver has packaged up for removal, so more of it goes back into circulation.

Medication absorption. Thyroid medication is absorbed in the small intestine. Coeliac disease, H. pylori infection, low stomach acid and inflammatory bowel conditions can all reduce how much you absorb. If your dose keeps creeping up, your gut is worth checking.

SIBO. A slow thyroid slows the gut, and a sluggish gut is a set-up for small intestinal bacterial overgrowth. A 2025 study found people with hypothyroidism were about twice as likely to develop SIBO, and the risk was higher again with autoimmune thyroiditis. This is one reason bloating and constipation are so common with Hashimoto’s.

Coeliac disease. Coeliac disease is more common in people with autoimmune thyroid disease. It damages the gut lining, affects nutrient and medication absorption, and is easy to miss because the symptoms can be subtle.

Testing: look at the thyroid and the gut

Thyroid symptoms overlap with so many other conditions that they’re easy to miss. A detailed personal and family history is often the first clue that the thyroid needs testing.

A full thyroid panel, not just TSH, should include:

• TSH: high usually means an underactive thyroid, low usually means an overactive one
• Free T4 and free T3: how much hormone is available, and how well you’re converting T4 into active T3
• Thyroid peroxidase antibodies (TPO Ab) and thyroglobulin antibodies (TgAb): raised in Hashimoto’s
• TSH receptor antibodies (TRAb): raised in Graves’ disease

Your doctor may also order a thyroid ultrasound to check for nodules or enlargement.

Gut testing is where we find out what’s driving the immune response:

• Microbiome stool testing to look at diversity, beneficial bacteria, inflammatory species and gut barrier markers
• SIBO breath testing if you have bloating, gas, constipation or reflux
• Coeliac screening through your GP, before removing gluten, because the blood test needs gluten in your diet to be accurate
• Nutrient levels such as iron studies, vitamin D and zinc

Test don’t guess. Two people with the same antibody levels can have very different things going on in their gut microbiome.

Where does AIP fit?

The Autoimmune Protocol (AIP) is an elimination and reintroduction diet. For a period of time, it removes foods that can trigger an immune response in some people (gluten and other grains, dairy, eggs, legumes, nightshades, nuts, seeds, refined sugar, alcohol and processed foods). The focus is on vegetables, quality protein and healthy fats. Foods are then brought back one at a time so you can see what you actually react to.

In a 10-week study of 17 women with Hashimoto’s, AIP significantly improved quality of life and symptoms, and lowered a marker of inflammation (hs-CRP). Thyroid antibodies didn’t change in that time. It’s a small study, but it supports what I see in practice. People often feel much better even when their medication dose stays the same.

AIP is a short-term tool, and the reintroduction phase is the most important part. Microbiome testing shows which beneficial bacteria are missing or low, which helps me prioritise the foods to bring back first. Fibre is usually the most important, because it feeds the bacteria that produce anti-inflammatory compounds like butyrate. Staying restricted for too long starves these bacteria, so a guided reintroduction is important.

Nutrients that support the thyroid

• Selenium: an analysis of 35 studies found selenium lowered TPO antibodies in people with Hashimoto’s. Brazil nuts are a rich source, but the amount varies a lot between nuts, so supplements should be dosed carefully.
• Zinc: needed to make thyroid hormone and convert T4 to T3.
• Vitamin D: helps regulate the immune system, and low levels are common in autoimmune disease.
• Iron: low iron stores can slow thyroid hormone production.
• Iodine, with care: the thyroid needs iodine, but too much can trigger or worsen Hashimoto’s. Don’t take iodine supplements or kelp without professional advice.

Stress, sleep and regular movement all matter too. Chronic stress affects both your thyroid and your gut, so it’s part of any plan I put together.

Ready to look deeper?

If you’ve been diagnosed with Hashimoto’s or Graves’ and you’re still struggling with fatigue, bloating, constipation or brain fog, your gut is a good place to start. I combine microbiome testing, SIBO breath testing (when needed) and a review of your pathology, then build a plan around what’s actually going on for you.

Book a discovery call here.

If you’re ready to understand your gut health a little better, follow along on Instagram. 💚

REFERENCES

Abbott RD, Sadowski A, Alt AG. Efficacy of the autoimmune protocol diet as part of a multi-disciplinary, supported lifestyle intervention for Hashimoto’s thyroiditis. Cureus. 2019;11(4):e4556. doi:10.7759/cureus.4556. https://doi.org/10.7759/cureus.4556

Busto Silva I, Puig-Domingo M. The impact of thyroid disorders on the gut microbiome: emerging mechanisms and clinical relevance. Arch Endocrinol Metab. 2026;70(spec issue 1):e250075. https://pmc.ncbi.nlm.nih.gov/articles/12679698

Hughes K, Eastman CJ. Hashimoto’s thyroiditis: how to spot the diagnosis and how to manage it. Med Today. 2017;18(9):27-32. https://medicinetoday.com.au/mt/2017/september/feature-article/hashimotos-thyroiditis-how-spot-diagnosis-and-how-manage-it

Huwiler VV, Maissen-Abgottspon S, Stanga Z, et al. Selenium supplementation in patients with Hashimoto thyroiditis: a systematic review and meta-analysis of randomized clinical trials. Thyroid. 2024;34(3):295-313. doi:10.1089/thy.2023.0556. https://pmc.ncbi.nlm.nih.gov/articles/PMC10951571/

IBD is an immune-mediated condition that causes chronic inflammation in the digestive tract. The two main types are ulcerative colitis (UC) and Crohn’s disease (CD). There’s no single cause. Genetics, immune dysregulation, gut dysbiosis, a Western-style diet low in fibre and high in ultra-processed food, antibiotic use, smoking (for Crohn’s), stress and poor sleep can all play a part.

Research is also showing that UC may have a true autoimmune component. People who go on to develop UC can carry antibodies against integrin αvβ6, a protein that helps hold the gut barrier together, and these antibodies can appear up to 10 years before diagnosis. It’s another sign of how central the gut barrier is in IBD.

Ulcerative colitis and Crohn’s disease

UC and Crohn’s share many symptoms, including abdominal pain and cramping, diarrhoea, urgency, a feeling of incomplete emptying, blood or mucus in the stool, fatigue, poor appetite, weight loss and sometimes fever. Both follow a pattern of flares and remission, and both can range from mild to severe. They are still quite different conditions.

Ulcerative colitis affects the inner lining of the large intestine. It starts in the rectum and spreads upwards in one continuous stretch. The ulcers can bleed and produce mucus or pus, and ongoing blood loss can lead to iron deficiency anaemia.

Crohn’s disease can affect any part of the digestive tract, from the mouth to the anus, but most often involves the end of the small intestine (the ileum) and the colon. Inflammation can go through the full thickness of the bowel wall and appears in patches, with healthy sections in between. When the small intestine is affected, it can interfere with absorbing nutrients such as iron, vitamin B12, vitamin D and fats.

The gut microbiome in IBD

The gut microbiome is one of the most studied areas in IBD research, and the patterns are consistent. People with Crohn’s and UC tend to have:

• Lower diversity. Fewer different types of bacteria, which makes the gut ecosystem less resilient.
• Fewer butyrate producers. Bacteria like Faecalibacterium prausnitzii turn fibre into butyrate, which feeds the cells lining the bowel and helps calm the immune system. F. prausnitzii is often low in Crohn’s, and lower levels have been linked with a higher risk of the disease coming back after surgery.
• More inflammatory bacteria. Some species thrive in an inflamed gut and keep the immune system switched on.
• A weaker gut barrier. The protective mucus layer thins and the gut lining becomes more permeable, so bacteria come into closer contact with immune cells.

It becomes a cycle. Dysbiosis drives inflammation, and inflammation changes the environment in a way that favours more dysbiosis. I explain this process in more detail in How Your Gut Microbiome Drives Inflammation in Autoimmune Disease.

SIBO is common too. A 2025 analysis found around 31% of people with IBD had small intestinal bacterial overgrowth, much higher than in healthy people. The risk was higher after bowel surgery and in stricturing Crohn’s. SIBO can cause bloating, gas and diarrhoea that look a lot like a flare, so it’s worth testing when symptoms don’t match your inflammation markers.

Is IBD different from IBS?

Yes. The symptoms can look similar, but they are very different conditions.

IBD is driven by the immune system. It causes inflammation and damage to the gut lining that can be seen on colonoscopy and biopsy, and inflammation markers in the blood and stool are usually raised.

IBS is a disorder of gut-brain interaction. There’s no visible damage on colonoscopy and inflammation markers are usually normal. Gut sensitivity, motility changes, dysbiosis, SIBO, food triggers, stress and past gut infections can all play a part.

It’s possible to have both. Some people with IBD in remission still have IBS-type symptoms, which is why Microbiome testing is so important. Microbiome testing shows where the imbalance of bacteria is and we can then use selective prebiotics and probiotics to favourably change the composition of the gut microbiota.

How is IBD diagnosed and what happens next?

Diagnosis is done by your gastroenterologist who will use a combination of tests:

• Blood tests to check for inflammation (such as CRP), anaemia and nutrient deficiencies like iron, vitamin B12 and vitamin D
• Faecal calprotectin, a stool test that measures inflammation in the bowel and helps tell IBD apart from IBS
• PCR Stool tests to rule out infection
• Colonoscopy with biopsy, the main test for confirming IBD and telling UC and Crohn’s apart
• Gastroscopy if Crohn’s may be affecting the upper digestive tract
• MRI, CT, bowel ultrasound or capsule endoscopy to look at the small intestine, which a colonoscopy can’t fully reach

Gut testing

Once IBD is diagnosed, the next question is what’s driving the inflammation in your gut. This is what I look at starting with a detailed history: when your symptoms began, how severe they are, and what makes them better or worse. I then use:

• Microbiome stool testing to see your diversity, which beneficial bacteria are missing or low, which inflammatory species are overgrown, and markers of gut barrier health
• SIBO breath testing if bloating, gas or diarrhoea don’t match your inflammation markers
• A review of your pathology, especially iron, B12, vitamin D and zinc

Managing IBD with AIP

There’s no cure for IBD, but diet, targeted supplements and lifestyle changes can ease symptoms, reduce the severity of flares and help you stay in remission for longer. This works alongside your medical treatment, not instead of it.

The Autoimmune Protocol (AIP) is an elimination and reintroduction diet that can be very effective at reducing inflammation. Foods that can trigger an immune response in some people (gluten and other grains, dairy, eggs, legumes, nightshades, nuts, seeds, refined sugar, alcohol and processed foods) are removed for a short period of time. The focus is on nutrient-dense fruit and vegetables, quality protein and healthy fats. Foods are then brought back one at a time to see what you actually react to. Stress management, sleep and movement are part of the protocol too.

IBD was the first condition AIP was studied in. In a pilot study of 15 people with active Crohn’s or UC, 73% were in clinical remission by week 6, and they stayed in remission through the rest of the study. Most participants were still on their usual medication, so AIP was used as an add-on.

Reintroduction and fibre

AIP is a short-term tool, and the reintroduction phase is the most important part. Your microbiome results show which beneficial bacteria are missing or low, which helps me prioritise the foods to bring back first. Fibre is usually the most important, because it feeds the bacteria that make butyrate, and butyrate is one of the main things that helps settle inflammation in the bowel. We start with gentle, cooked and soluble fibres and build up slowly.

A note on strictures. If you have Crohn’s with a narrowed section of bowel, high amounts of insoluble fibre (raw vegetables, skins, seeds, nuts and tough fibrous foods) can raise the risk of a blockage. International IBD dietary guidance recommends limiting insoluble fibre in this situation, so your plan needs to be adjusted around it.

Other things that help

International dietary guidance for IBD also suggests:

• Eating more oily fish such as salmon and sardines for omega-3s
• Eating plenty of fruit and vegetables
• Cutting back on ultra-processed foods, especially those containing emulsifiers like carrageenan, carboxymethylcellulose and polysorbate-80
• Reducing red and processed meat

It’s also important to correct nutrient deficiencies, especially iron, vitamin B12, selenium, vitamin D and zinc, which are common in IBD.

Ready to look deeper?

If you’ve been diagnosed with Crohn’s or ulcerative colitis and you’re still dealing with flares, bloating, fatigue or unpredictable bowels, your microbiome is a good place to start. In my Gut Program, we combine microbiome testing, SIBO breath testing when needed and a review of your pathology, then build a plan around what your gut actually needs.

Living with IBD and want support? Book a consultation with me here: https://dashboard.healthbank.io/practitioner/vicky-ellenport

References

Feng X, Hu J, Zhang X. Prevalence and predictors of small intestinal bacterial overgrowth in inflammatory bowel disease: a meta-analysis. Front Med (Lausanne). 2025;11:1490506. doi:10.3389/fmed.2024.1490506. https://www.frontiersin.org/journals/medicine/articles/10.3389/fmed.2024.1490506/full

Konijeti GG, Kim N, Lewis JD, et al. Efficacy of the autoimmune protocol diet for inflammatory bowel disease. Inflamm Bowel Dis. 2017;23(11):2054-2060. doi:10.1097/MIB.0000000000001221. https://doi.org/10.1097/MIB.0000000000001221

Levine A, Rhodes JM, Lindsay JO, et al. Dietary guidance from the International Organization for the Study of Inflammatory Bowel Diseases. Clin Gastroenterol Hepatol. 2020;18(6):1381-1392. doi:10.1016/j.cgh.2020.01.046. https://doi.org/10.1016/j.cgh.2020.01.046

Livanos AE, Dunn A, Fischer J, et al. Anti-integrin αvβ6 autoantibodies are a novel biomarker that antedate ulcerative colitis. Gastroenterology. 2023;164(4):619-629. doi:10.1053/j.gastro.2022.12.042. https://pubmed.ncbi.nlm.nih.gov/36634824/

Sokol H, Pigneur B, Watterlot L, et al. Faecalibacterium prausnitzii is an anti-inflammatory commensal bacterium identified by gut microbiota analysis of Crohn disease patients. Proc Natl Acad Sci U S A. 2008;105(43):16731-16736. doi:10.1073/pnas.0804812105

#Inflammatoryboweldisease #Crohnsdisease #ulcerativecolitis #AIP #IBD #gutmicrobiome #clinicalnutritionist #personalisednutrition

What is constipation?

Constipation occurs when stool is moving too slowly through the digestive tract, becoming dry and hard, or when the pelvic floor doesn’t coordinate properly to let stool out. Bowel motions can become infrequent, difficult to pass, or leave you feeling like you haven’t fully emptied.

Common symptoms include:

• Infrequent, hard or lumpy stools
• Straining or painful bowel motions
• A feeling of incomplete emptying
• Bloating, excess gas and distension

Many people also report fatigue and brain fog alongside their constipation.

How often should you go?

Healthy bowel movements should happen at least once a day and be well formed and easy to pass.

Frequency alone doesn’t tell the whole story. It’s common to go every day and still be constipated if your stools are hard, small, or you never feel fully empty.

Occasional constipation is normal. Chronic constipation, however, can significantly affect your quality of life, and it’s worth investigating rather than putting up with.

What causes constipation?

The most common causes are the everyday ones:

• Dehydration
• A low-fibre diet
• Lack of movement
• Stress
• Certain medications and supplements, such as iron, opioid pain relief and some antidepressants

Other contributors are often missed:

• Low thyroid function, including subclinical hypothyroidism
• Pelvic floor dysfunction
• SIBO (small intestinal bacterial overgrowth) or methane overgrowth
• Microbiome imbalance (dysbiosis)

For most people, improving fibre, hydration and movement is enough to get things moving. But what if it isn’t? That’s when it’s time to look deeper, and the gut microbiome is one of the first places I look.

How your gut microbiome affects your bowels

The trillions of microbes in your large intestine don’t just sit there, they actively help regulate how quickly things move through. Research suggests they influence motility in four key ways.

1. Short-chain fatty acids (SCFAs). When your gut bacteria ferment fibre, they produce SCFAs such as butyrate. These fuel the cells lining your colon and help stimulate the muscle contractions that move stool along. Lower numbers of SCFA-producing bacteria may be linked to slower transit.

2. Bile acids. Gut microbes transform the bile acids your liver releases. Some of these microbial bile acids help stimulate bowel movement and draw water into the colon. When this process is disrupted, transit can slow.

3. Serotonin. Around 90% of your body’s serotonin is made in the gut, and your microbes help regulate how much is produced. In the gut, serotonin is a key signal for peristalsis — the wave-like contractions that keep things moving.

4. Methane. Some gut microbes, called methanogenic archaea (mainly Methanobrevibacter smithii), produce methane gas. Methane is strongly associated with slower transit and constipation.

This is why two people eating the same diet can have very different bowel habits — and why more fibre and water alone doesn’t always solve the problem.

What I look for in clinic

When a client comes to me with constipation, these are the three things I consider first.

1. Are the basics in place? Enough fibre, water and movement. If not, these are the easiest and quickest things to fix.
2. What is their gut transit time? A simple at-home test using sweetcorn or beetroot shows how long food takes to travel from plate to toilet. Conventional ranges extend up to around 72 hours, but in practice I like to see transit closer to 14–24 hours. Slow transit is a common reason people go daily and still feel constipated.
3. Is there a methane or microbial imbalance? Methane-producing microbes can overgrow in the small or large intestine (called Intestinal methane overgrowth – IMO) and slow everything down. Hydrogen-dominant SIBO, on the other hand, more often shows up as bloating and looser stools.

Testing, not guessing

To find out what’s driving a client’s constipation, I use:

• Gut microbiome stool testing — this shows not just which microbes are present, but what they’re doing: levels of methane-producing archaea and the capacity of your SCFA-producing bacteria.
• SIBO breath testing — this measures hydrogen and methane gas to identify overgrowth and its type.

From there, I build an individual treatment protocol focused on food, probiotics, prebiotics and, where needed, herbal support.

My top tips for stubborn constipation

1. Eat 2 green kiwifruit a day. Green kiwifruit has the strongest research behind it for constipation, and gold kiwifruit can help too. Eating the skin adds extra fibre. Give it around four weeks to see the full effect.
2. Add prunes or mango. Prunes contain sorbitol, which draws water into the bowel, plus polyphenols that feed beneficial gut bacteria. Mango has also been shown to ease constipation. Note that both are high FODMAP, so if you have SIBO or IBS they may increase bloating.
3. Feed your fibre fermenters. Aim for a wide variety of plant foods across the week — vegetables, fruit, legumes, wholegrains, nuts and seeds. Polyphenol-rich foods such as berries, extra virgin olive oil, cacao and green tea help support SCFA-producing bacteria.
4. Consider magnesium. Magnesium citrate, around 400mg in the evening, draws water into the bowel. Check with your practitioner first, particularly if you have kidney issues or take other medications.
5. Fix your toilet posture. Use a footstool so your knees sit above your hips. A pelvic floor physiotherapist can make a big difference if emptying is difficult.
6. Don’t ignore the urge. Go as soon as you feel the need. Putting it off can teach the bowel to ignore its own signals. The 20–30 minutes after breakfast is often the most productive window.
7. Move every day. A 10–15 minute walk after meals helps stimulate gut motility.

Get help from a professional

If you’re struggling with constipation and want to understand what’s really driving it, book in for a discovery call with me. Together we can find the root cause and build a long-term plan.

This article is general information only and is not a substitute for individual medical or nutrition advice.

REFERENCES:

Bin Waqar et al. (2019). Methane and Constipation-predominant Irritable Bowel Syndrome: Entwining Pillars of Emerging Neurogastroenterology. Cureus, 11(5), e4764. https://doi.org/10.7759/cureus.4764

Chan et al. (2007). Increasing dietary fiber intake in terms of kiwifruit improves constipation in Chinese patients. World journal of gastroenterology, 13(35), 4771–4775. DOI: 10.3748/wjg.v13.i35.4771

Chey SW, Chey WD, Jackson K, Eswaran S. (2021). Exploratory comparative effectiveness trial of green kiwifruit, psyllium, or prunes in US patients with chronic constipation. American Journal of Gastroenterology, 116(6), 1304–1312.
DOI: 10.14309/ajg.0000000000001149

Gao et al. (2019). Exercise therapy in patients with constipation: a systematic review and meta analysis of randomized controlled trials. Scandinavian journal of gastroenterology, 54(2), 169–177.
DOI: 10.1080/00365521.2019.1568544

Pimentel M, Saad RJ, Long MD, Rao SSC. (2020). ACG clinical guideline: small intestinal bacterial overgrowth. American Journal of Gastroenterology, 115(2), 165–178.
DOI:10.14309/ajg.0000000000000501

Soltanian et al. (2019). Effect of flaxseed or psyllium vs. placebo on management of constipation, weight, glycemia, and lipids: A randomized trial in constipated patients with type 2 diabetes. Clinical Nutrition ESPEN,  29, 41-48. https://doi.org/10.1016/j.clnesp.2018.11.002

Research suggests that increased intestinal permeability, often called “leaky gut”, may play a role in how some autoimmune conditions develop and progress.

The link between the gut and conditions like coeliac disease, Crohn’s disease and ulcerative colitis is easy to see. The connection to autoimmune conditions elsewhere in the body, such as type 1 diabetes, multiple sclerosis or rheumatoid arthritis, can be harder to picture.

So, let’s break it down.

What is the gut? Your digestive system and gut microbiome explained

“Gut” is another word for your gastrointestinal tract, or digestive system. Digestion begins in the mouth and continues in the stomach, but most food is broken down and absorbed in the small intestine. The large intestine absorbs water and electrolytes, and it is where gut bacteria ferment fibre into beneficial compounds called short-chain fatty acids. Waste is then expelled via the rectum.

The inner lining of the gut forms the intestinal barrier. It has several layers working together: a protective mucus layer, a single layer of cells joined by “tight junctions”, and immune cells sitting just beneath. The barrier is semipermeable. It lets nutrients, water and electrolytes through while keeping bacteria, toxins and other unwanted substances inside the gut to be excreted.

What is leaky gut? How intestinal permeability develops

The tight junctions between gut cells open and close in a regulated way. When the barrier is disrupted, these junctions loosen and the mucus layer can thin. This allows more to pass between the cells than should. This is known as increased intestinal permeability, or leaky gut. It can occur in both the small and large intestine.

What crosses is mostly bacterial products, such as lipopolysaccharide (LPS) from bacterial cell walls, along with toxins and fragments of food proteins. Immune cells beneath the lining recognise these as potential threats and respond, which creates inflammation.

Short-term, this is a normal protective response. However, when barrier disruption is ongoing, low-grade inflammation can persist and may contribute to wider health issues, including autoimmune disease.

What causes leaky gut? The main triggers that disrupt the intestinal barrier

1. Gluten. Gliadin, a protein found in gluten, can trigger the release of zonulin, a protein that temporarily loosens the tight junctions between gut cells. This response is strongest and most persistent in people with coeliac disease. Research suggests a smaller, short-lived effect may also occur in people without coeliac disease, including those with non-coeliac wheat sensitivity.
2. Dysbiosis. The gut microbiome plays a key role in keeping the barrier intact. Beneficial bacteria produce short-chain fatty acids such as butyrate, which fuel the cells of the gut lining and support tight junction integrity. When the microbiome is out of balance, these protective functions decline. A low-fibre diet can also shift bacteria towards feeding on the protective mucus layer, thinning the gut’s first line of defence. Bacterial overgrowth in the small intestine (SIBO) is another known trigger for zonulin release.
3. Elevated blood sugar. Persistently high blood glucose can reprogram the cells of the gut lining, weakening the junctions between them and allowing microbial products into circulation. In humans, poorer long-term glucose control (HbA1c) has been linked to greater leakage of microbial products. Diets high in sugar and fructose may also affect the barrier indirectly by altering the gut microbiome.
4. Stress. Psychological stress can increase gut permeability directly. Stress hormones such as corticotropin-releasing hormone (CRH) activate immune cells called mast cells in the gut wall, which loosens the barrier. Stress can also alter the gut microbiome over time. The effect appears to vary between individuals, and human research is still developing.
5. Alcohol. Alcohol and its by-product acetaldehyde directly disrupt the tight junctions between gut cells. Regular or heavy intake also promotes dysbiosis and bacterial overgrowth, which further weaken the barrier.
6. NSAIDs. Non-steroidal anti-inflammatory drugs such as ibuprofen, naproxen, diclofenac and aspirin are among the best-documented causes of increased gut permeability. They reduce protective prostaglandins in the gut lining and directly damage the energy-producing mitochondria in gut cells. Permeability can rise within hours of a single dose, and regular use commonly causes inflammation and injury in the small intestine

Leaky gut and autoimmune disease: how are they connected?

Autoimmune disease develops when the immune system loses “tolerance”, its ability to tell the body’s own tissues apart from genuine threats. Researchers think three factors often come together: a genetic predisposition, an environmental trigger, and a gut barrier that lets more through than it should.

When bacterial products and food proteins cross a disrupted barrier, the immune system is repeatedly activated. In someone who is genetically susceptible, this ongoing activation and inflammation may help tip the immune system towards attacking the body’s own tissues.

The outcome depends on the condition. In coeliac disease, gluten drives an immune response that damages the small intestine. In other autoimmune conditions, the immune response targets joints, the thyroid, the pancreas or the nervous system.

This model is well supported in coeliac disease. For many other autoimmune conditions, increased permeability is a likely contributor rather than a proven cause, and research is ongoing.

Can leaky gut improve? How gut microbiome testing helps

The gut lining renews itself every few days, so barrier function can improve when the factors disrupting it are addressed. For many people with autoimmune conditions, supporting gut health can help reduce inflammation, ease symptoms and improve quality of life, alongside their medical care.

Microbiome stool testing shows us what is actually happening in your gut: which bacteria are overgrown, which beneficial species are missing, and how that may connect to your symptoms. SIBO breath testing and a review of your pathology can add to the picture. From there, we build a targeted plan rather than guessing.

That plan may include microbiome-focused nutrition and supplements, stress and lifestyle support, and, where appropriate, a structured elimination and reintroduction approach such as the Autoimmune Protocol (AIP). Small studies of AIP in inflammatory bowel disease and Hashimoto’s thyroiditis have reported improvements in symptoms and quality of life.

5 natural ways to support leaky gut healing

1. Anti-inflammatory foods. Inflammation is a key driver of both leaky gut and autoimmune disease. Colourful fruit and vegetables, herbs and spices such as turmeric, and omega-3-rich oily fish (salmon, sardines, mackerel, anchovies, herring) all help. Plant foods contain polyphenols, which have anti-inflammatory properties and also feed beneficial gut bacteria.
2. Fermented foods. Fermented foods such as yoghurt, kefir, sauerkraut, kimchi and kombucha introduce live microbes and beneficial compounds. In one study, a diet high in fermented foods increased microbiome diversity and reduced markers of inflammation.
3. Prebiotic fibre. Prebiotics are fibres that feed beneficial bacteria, helping them produce barrier-supporting short-chain fatty acids. Good sources include onion, garlic, leek, asparagus, artichoke and green bananas. Many of these foods are high-FODMAP, so if you have IBS or SIBO, introduce them slowly or with guidance. Targeted prebiotic supplements can help if a high-fibre diet causes discomfort.
4. Glutamine. Glutamine is an amino acid that fuels the cells of the gut lining and supports tight junction integrity. In a clinical trial in people with post-infectious IBS, glutamine supplementation reduced symptoms and improved gut permeability. Food sources include meat, fish, eggs, dairy, tofu and legumes.
5. Reduce stress. Because stress directly affects the gut barrier, calming the nervous system is part of gut healing. Daily practices such as meditation, slow breathing or mindfulness can reduce stress, support sleep and help regulate immune function.

Gut health support for autoimmune conditions

If you’re living with an autoimmune condition or ongoing gut symptoms and want to understand what’s driving them, book a consultation. Together we’ll look at your gut microbiome, history and symptoms, and build a plan based on what your gut actually needs.

This article is general educational information and is not a substitute for individual medical advice. Please continue working with your GP or specialist for the management of any autoimmune condition.

References

Abbott et al. (2019) Efficacy of the autoimmune protocol diet as part of a multi-disciplinary, supported lifestyle intervention for Hashimoto’s thyroiditis. Cureus.11(4): e4556.

Bjarnason et al. (2018) Mechanisms of damage to the gastrointestinal tract from nonsteroidal anti-inflammatory drugs. Gastroenterology. 154(3):500–514.

Camilleri M. (2019) Leaky gut: mechanisms, measurement and clinical implications in humans. Gut. 68(8):1516–1526.

Chelakkot et al. (2018) Mechanisms regulating intestinal barrier integrity and its pathological implications. Exp Mol Med. 50(8):1–9.

Desai et al. (2016)A dietary fiber-deprived gut microbiota degrades the colonic mucus barrier and enhances pathogen susceptibility. Cell. 167(5):1339–1353.

Fasano A. (2020) All disease begins in the (leaky) gut: role of zonulin-mediated gut permeability in the pathogenesis of some chronic inflammatory diseases. F1000Res; 9:F1000 Faculty Rev-69.

Konijeti et al.(2017) Efficacy of the autoimmune protocol diet for inflammatory bowel disease. Inflamm Bowel Dis. 23(11):2054–2060.

Kreimeyer et al. (2025) Influence of alcohol on the intestinal immune system. Alcohol Res. 45(1).

Maccioni et al. (2023) Alcohol-associated bowel disease: new insights into pathogenesis. eGastroenterology. 1(1):e100013.

Thaiss C et al. (2018) Hyperglycemia drives intestinal barrier dysfunction and risk for enteric infection. Science. 2018;359(6382):1376–1383.

Uhde et al.(2016) Intestinal cell damage and systemic immune activation in individuals reporting sensitivity to wheat in the absence of coeliac disease. Gut. 65(12):1930–1937.

Valitutti et al. (2019) Breaching the gut barrier: celiac disease as a paradigm of chronic inflammatory diseases. Dig Dis Sci. 64(7):1748–1758.

Vanuytsel  et al. (2014) Psychological stress and corticotropin-releasing hormone increase intestinal permeability in humans by a mast cell-dependent mechanism. Gut. 63(8):1293–1299.

Wastyk et al. (2021) Gut-microbiota-targeted diets modulate human immune status. Cell. 184(16):4137–4153.

A new study has found distinct differences in the gut microbiome of people newly diagnosed with multiple sclerosis (MS) compared with healthy individuals.

MS is an inflammatory, neurodegenerative autoimmune disease affecting the central nervous system. The immune cells mistakenly attack the myelin sheath surrounding nerve fibres, damaging nerves and disrupting nerve signaling.

About the study

Italian researchers used shotgun metagenomic sequencing to analyse stool samples from 53 adults with MS, recruited across four centres between 2017 and 2023, and 55 healthy controls. Patients were newly diagnosed, had not yet started disease-modifying therapies, and anyone who had used antibiotics in the previous three months was excluded. Almost half had received a short course of steroids at diagnosis, which the researchers accounted for in their analysis.

Which gut bacteria were linked to MS?

The gut microbiome differed significantly between people with MS and healthy controls:

• Barnesiella sp. An22 and Romboutsia ilealis were more abundant in MS and associated with a higher lesion burden.
• Clostridium innocuum and Ruminococcus sp. JL13D9 were more abundant in MS and associated with spinal cord lesions.
• Bacteroides species (B. ovatus, B. cellulosilyticus) were depleted, which may reflect reduced anti-inflammatory capacity. The MS microbiome also showed a reduced capacity to produce butyrate, an anti-inflammatory short-chain fatty acid.

Could microbiome testing help predict MS progression?

The researchers suggest that gut microbiome profiling at diagnosis may help identify patients at higher risk of faster disease progression and could offer new targets for microbiome-based interventions, though larger studies are needed to confirm this. They concluded that “incorporating microbiome analysis into clinical practice could contribute to more personalised management of MS.”

What this means for autoimmune gut health

In clinic, we often see that targeted microbiome modulation can help shift the gut ecosystem towards a more anti-inflammatory profile.

If you live with an autoimmune condition and want to understand how microbiome testing could inform your overall treatment, book a consultation with me in my Melbourne clinic or online.

References:
Maglione A, et al. (2026) Gut microbiome profiling at multiple sclerosis onset as a potential early prognostic marker of disease course: evidence from an observational cohort study, eBioMedicine,132:106470. doi.org/10.1016/j.ebiom.2026.106470

How antibiotics affect the microbiome

Antibiotics impact the gut microbiome by causing rapid reductions in microbial diversity and shifting the balance of bacterial populations in the gut away from health-promoting species. The longer the course of treatment, the more species are affected and the longer the microbiome takes to recover. Taking a combination of different antibiotics is also more disruptive to the gut microbiome, as is repeated course of antibiotics.

After antibiotic treatment, gut bacterial populations can recover within a few weeks. However, some studies show it can take months to rebuild and occasionally a course of antibiotics can lead to the extinction of certain species (Palleja et al 2018).

Antibiotics commonly reduce key beneficial bacteria such as Bifidobacterium and Faecalibacterium, while allowing populations of opportunistic, inflammatory species such as Escherichia and Klebsiella to expand. This is why some people experience diarrhoea, which is a common complaint when on antibiotics.

Microbiome recovery is highly individual, and your baseline composition strongly influences outcomes. Some people recover quickly, while others experience lingering digestive issues and other systemic symptoms.

Gut microbiome repair

As practitioners looking to support you to restore your microbiome, we focus on three things: diet, probiotics and prebiotics.

Diet

The most important factor in restoring the gut ecosystem and maintaining microbiome health in the long term, is ensuring your diet has plenty of plant foods. These are rich in fibre, including prebiotics, and contain different polyphenols that feed our beneficial bacteria.

Poor diets, lacking in prebiotics and polyphenols, can increase vulnerability to infection after antibiotic use, while conversely, plant-rich diets increase microbiome resilience to antibiotic treatment (Kennedy et al 2024).

Probiotics

Research has shown that using probiotics alongside antibiotic treatment leads to a faster recovery of beneficial species (John et al. 2024). Probiotics do not re-seed, rather they support and communicate with other organisms in the gut, influencing bacterial behaviour, gene expression and immune responses.

We refer to clinical trial data to see what probiotic strains would be most supportive, including whether the antibiotics are targeting a respiratory infection or a gut infection.  We commonly prescribe Saccharomyces boulardii CNCM I-745 (SB) and Lacticaseibacillus rhamnosus GG (LGG). Clinical trials have shown SB is very effective at reducing antibiotic-associated diarrhoea. SB is a yeast, so antibiotics (that only target bacteria) don’t decrease its efficacy. SB doesn’t decrease the effectiveness of antibiotics either. For safety reasons, there are some cases where we wouldn’t recommend SB, including where someone’s health is very frail or where there are deep puncture wounds or cannulas in use.

Clinical trials show LGG protects against antibiotic-induced changes in the microbiome, reduces inflammation markers and positively influences microbiome balance. However, LGG is also impacted by antibiotics, so this requires frequent, high doses and timing carefully within the antibiotic regimen. Depending on the nature of the infection and your health needs we may prescribe better-targeted probiotics.

Prebiotics

Prebiotic fibres selectively feed beneficial gut bacteria, helping support microbial regrowth after antibiotic exposure. Prebiotics have been shown in human studies to increase populations of beneficial bacteria and to promote the production of health-promoting short-chain fatty acids, particularly butyrate.

Prebiotics are found naturally in certain plant foods, but for protecting the gut microbiome from antibiotic-induced changes and for encouraging large-scale and long-term shifts in the gut ecosystem, we recommend prebiotic supplements (usually powders that can be mixed into drinks or food).

We most commonly recommend partially hydrolysed guar gum (PHGG), lactulose, galactooligosaccharides (GOS), or inulin/FOS. Each different prebiotic has different properties and targets different groups of beneficial bacteria. For example, PHGG is the most gentle on the stomach and can normalise stools and help prevent antibiotic-related diarrhea. Inulin/FOS feeds up a broader range of beneficial bacteria but can cause digestive symptoms especially if used in large quantities.

In our practice, we personalise all our treatment plans, and so we consider an individual’s microbiome profile, health history, diet, lifestyle, symptoms and other needs in order to choose which prebiotic to recommend and at what dose. It’s always helpful to have baseline microbiome data gathered prior to antibiotic use to guide our treatment plans. However, if someone hasn’t done a microbiome stool test before commencing treatment, we can still make recommendations for prebiotics to take alongside and immediately after antibiotic treatment to help protect microbiome health, but our recommendations may not be so well targeted.

Tracking progress

Gut bacterial populations can fluctuate rapidly for several weeks after the course of antibiotics is completed. We usually advise stool testing after a few weeks of microbiome support to check the impact of treatment, ensure the most accurate advice and inform any treatment plans going forward.

If you are about to take a course of antibiotics, or have recently completed a course, please get in contact for microbiome support.

REFERENCES

Elvers KT, et al. (2020) Antibiotic induced changes in the human gut microbiota for the most commonly prescribed antibiotics in primary care in the UK: a systematic review. BMJ Open. 10.1136/bmjopen-2019-035677

John D, et al. (2024). A double-blind, randomized, placebo-controlled study assessing the impact of probiotic supplementation on antibiotic induced changes in the gut microbiome. Frontiers in Microbiomes, 3.

https://doi.org/10.3389/frmbi.2024.1359580

Kennedy, M.S. et al. (2025) Diet outperforms microbial transplant to drive microbiome recovery in mice. Nature.

https://doi.org/10.1038/s41586-025-08937-9

Palleja, A. et al. (2018) Recovery of gut microbiota of healthy adults following antibiotic exposure. Nat Microbiol 3.

https://doi.org/10.1038/s41564-018-0257-9

While many bacteria play a role in supporting gut health, Bifidobacterium has been shown to regulate immune responses, positively impact mood and anxiety, reduce inflammation and protect the gut lining.

Furthermore, many different species of Bifidobacterium show positive correlations with improvement in fatigue, gastrointestinal upset and memory loss, all hallmarks of LC.

A recent study has shown that having a gut microbiome low in Bifidobacterium and overall diversity was more likely to result in a higher disease severity of Covid and/or LC. Other research that tested the gut and nasal microbiome in an active Covid infection showed a decrease in the abundance of Bifidobacterium.

Another study using probiotics in Covid patients showed that supplementing with Bifidobacterium may offer protection against Covid symptoms through its ability to modulate the immune response, reduce inflammation, and maintain gut barrier function. The findings highlighted the potential of microbiome modulation in the treatment of LC.

Increasing levels of Bifidobacteria, using a mix of prebiotics, probiotics and a healthy plant-based Mediterranean diet is what I try to achieve for my clients. Some of the best prebiotics are GOS (Galactooligosaccharides) and Lactulose but there are many others, especially as all clients respond differently to prebiotics. Some people find prebiotics can cause loose stools or even constipation, so I always start low and increase slowly. If clients can tolerate dairy and their microbiome is not overgrown with bile loving species then I also recommend Greek yoghurt with live cultures or kefir, a fermented yoghurt.

Testing your microbiome is very important and I don’t like to prescribe supplements without having those results. Gut microbiome stool testing allows me to individualise your treatment plan according to your specific symptoms and unique microbiome profile.

REFERENCES:

Hazen et al. (2022) Lost microbes of COVID-19: Bifidobacterium, Faecalibacterium depletion and decreased microbiome diversity associated with SARS-CoV-2 infection severity. BMJ Open Gastroenterol 9(1)

https://pubmed.ncbi.nlm.nih.gov/35483736/

Taufer CR, Rampelotto PH. (2023) The Role of Bifidobacterium in COVID-19: A Systematic Review. Life (Basel). 13(9):1847

https://pmc.ncbi.nlm.nih.gov/articles/PMC10532519/

]]> https://thenutritionfactor.com.au/reflux2416-2/ Wed, 05 Jun 2024 09:18:02 +0000 https://thenutritionfactor.com.au/?p=2416 How to Manage Reflux Naturally

Reflux, or Gastroesophageal reflux disease (GORD) is a chronic condition where stomach acid frequently flows back into the oesophagus, leading to mucosal damage and symptoms such as heartburn, regurgitation of food or acid, chest pain, chronic cough, difficulty swallowing and dental erosion.

There are many factors that contribute to the onset of GORD, the most common being reduced tone in the lower oesophageal sphincter (LOS). This can be caused by certain medications, such as NSAIDs, calcium channel blockers, barbiturates, and anticholinergics. Decreased saliva production and delayed stomach emptying are also contributing factors, as are lifestyle factors such as smoking, obesity, a diet high in fatty and processed foods, and alcohol consumption.

Gut dysbiosis contributes to both reflux and GORD symptoms and slow transit time and methane overgrowth can increase symptoms. Gut dysbiosis occurs when there is an imbalance between beneficial bacteria and harmful bacteria in the gut microbiome. Certain species of Proteobacteria and Fusobacteria produce lipopolysaccharides (LPS) which contribute to systemic inflammation and are thought to promote reflux by oesophageal sphincter relaxation. Research shows that high levels of Proteobacteria and Fusobacteria are more evident in people with GORD.

Conventional medicine includes proton pump inhibitors (PPI), H2 Receptor Antagonists (H2RAs) and other antacids which reduce stomach acid and can help with symptom management. However, they fail to address the cause of the reflux and are associated with many side effects such as diarrhoea, nausea, and abdominal pain. They also increase the risk of Small Intestine Bacteria Overgrowth (SIBO), Colonic Methane Overgrowth (CMO), nutrient malabsorption, and gut dysbiosis.

We use Microbiome testing to identify and treat any underlying drivers of reflux. We develop individual treatment plans based on your unique microbiome profile and your symptoms. Our holistic approach includes dietary and lifestyle recommendations and targeted supplements where necessary.

Here are a few of my recommendations.

Dietary modifications:

1. Eat a fibre-rich, plant-based, Mediterranean style diet.
2. Avoid trigger foods such as chocolate, fatty foods, and processed foods.
3. Avoid alcohol, sugar, and minimise coffee.
4. Have a 3-hour window between dinner and bedtime.
5. Do not consume fluid with meals or immediately after meals.

Lifestyle changes:

1. Elevating the head of the bed by 20-30 cm can reduce night-time reflux.
2. Stop smoking or vaping.
3. Reducing weight can alleviate symptoms.
4. Managing stress through breathing and nervous system support.

If you want to know more, please make an appointment or book in a discovery call.

REFERENCES:

De Bastiani et al. (2023) Assessment of small intestinal bacterial overgrowth and methane production in patients on chronic proton-pump inhibitor treatment: prevalence and role of rifaximin in its management in primary care. Minerva Gastroenterol 2023;69:523-8.
DOI: 10.23736/S2724-5985.21.03118-1

Baumeister et al. (2019) Gut microbiota and oesophageal disease – an update Microbiota Health Dis 1: e207 1 II.
DOI: 10.26355/mhd_20201_207