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

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.

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

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

Cinnamon is known for its warm and sweet flavour, but it has a lot more to offer than its culinary applications. Cinnamon has been valued for centuries for its medicinal properties, and research shows it can be effective in reducing high blood pressure, regulating glucose levels, reducing inflammation, and improving cognition.

Cinnamon is rich in polyphenols, which are plant compounds known for their antioxidant properties. These polyphenols, including procyanidins and cinnamaldehyde, exhibit strong antioxidant activity, protecting cells from oxidative stress and damage caused by free radicals. Cinnamaldehyde has been shown to inhibit the release of pro-inflammatory cytokines in the gut, thus aiding in the reduction of gut inflammation and promoting gut health.

Cinnamon also exhibits prebiotic-like activity, supporting the growth of beneficial gut bacteria and suppressing the growth of pathogenic bacteria, positively impacting the balance of the gut microbiome. Several studies in healthy adults have demonstrated that cinnamon extract significantly increased the abundance of Bifidobacteria, Akkermansia and Lactobacillus, all known for their beneficial effects on gut health.

Studies have also shown that cinnamon oil can improve the oral microbiome by exhibiting a broad range of antimicrobial activity against the microbes causing dental caries. This is significant as dental caries is a risk factor for heart disease and Metabolic Syndrome.

Cinnamon also has many nutritional benefits. Adding one teaspoon (2-4 grams) of cinnamon powder a day provides calcium, potassium, vitamin A as well as small quantities of fibre and trace amounts of many other vitamins and nutrients.

So be bold and start adding cinnamon to your food and reap the benefits of its exotic taste whilst also supporting your gut microbiome and promoting optimal health.

REFERENCES

Jeong. et al. (2021). Antibacterial and antibiofilm activities of cinnamon essential oil nanoemulsion against multi-species oral biofilms. Sci Rep 11, 5911. DOI: 10.1038/s41598-021-85375-3

Kim et al. (2019). “Severity of dental caries and risk of coronary heart disease in middle-aged men and women: a population-based cohort study of Korean adults, 2002–2013.” Scientific Reports 9:10491 DOI: 10.1038/s41598-019-47029-3

Lu et al. (2019). “Mixed Spices at Culinary Doses Have Prebiotic Effects in Healthy Adults: A Pilot Study” Nutrients 11, no. 6: 1425. DOI: 10.3390/nu11061425

Lu et al. (2017). “Prebiotic Potential and Chemical Composition of Seven Culinary Spice Extract” Journal of Food Science Aug; 82(8): 1807–1813 DOI: 10.1111/1750-3841.13792

Mollazadeh et al. (2016). “Cinnamon effects on metabolic syndrome: a review based on its mechanisms.” Iran J Basic Med Sci. Dec; 19(12):1258-1270. DOI: 10.22038/ijbms.2016.7906.

Rao PV, Gan SH. (2014). “Cinnamon: a multifaceted medicinal plant.” Evid Based Complement Alternat Med. 642942. DOI: 10.1155/2014/642942

Vicky Ellenport BHSc NUT is a registered Nutritionist and Microbiome Analyst who uses a food first approach in her treatment protocols.