Causes of SIBO: What Triggers Small Intestinal Bacterial Overgrowth?

Causes of SIBO: What Triggers Small Intestinal Bacterial Overgrowth?

The causes of SIBO are more varied than many people realise, and it rarely appears out of nowhere. In most cases, something has changed or gone wrong with one of the body’s natural defence mechanisms, those systems that ordinarily keep bacterial populations in the small intestine in check. Understanding what that something is matters enormously, because treating the overgrowth without addressing its underlying cause is one of the main reasons SIBO keeps coming back. This piece walks through the most clinically significant causes of SIBO.

What is the migrating motor complex (MMC) and why does it matter?

The migrating motor complex, or MMC, is one of the gut’s most important but least talked-about functions. A coordinated series of muscular contractions that sweep through the small intestine in cycles during periods of fasting. Its job is to act as a ‘housekeeping wave’, moving residual food, debris, and bacteria along and out of the small intestine into the large intestine, where higher bacterial populations are normal and expected.

When the MMC functions well, it creates a self-cleaning mechanism that prevents bacterial accumulation in the small bowel. When it is impaired, bacteria have the opportunity to accumulate and proliferate — the fundamental process underlying SIBO.

MMC dysfunction is considered one of the most common underlying drivers of SIBO (Capuano et al. 2026). A number of factors can impair MMC activity, including:

• Post-infectious damage following food poisoning (discussed further below)
• Chronic stress, which governs gut motility
• Underactive thyroid and other hormonal conditions that slow gut transit
• Diabetes, particularly where nerve damage has developed
• Frequent eating or grazing patterns — the MMC only activates during fasting, so constant eating disrupts it
• Certain medications, including opioids, which suppress gut motility

This is why motility support (approaches that actively promote MMC function) forms an important part of SIBO treatment and prevention plan. Treating the overgrowth without restoring motility leaves the underlying vulnerability in place.

Food poisoning and SIBO — the research

Food poisoning is one of the most well-documented triggers of SIBO, and for many people it marks a clear ‘before and after’ in their digestive health. The mechanism by which it causes SIBO is now reasonably well understood, and it involves an immune response that inadvertently damages the very nerve cells responsible for MMC function.

During an acute gastrointestinal infection, most commonly caused by bacteria such as Campylobacter, Salmonella, or E. coli, the body produces antibodies to fight the infection. In some individuals, these antibodies ‘cross-react’ with a protein called vinculin, which is involved in the pacemaker cells in the gut that coordinate motility. This essentially damages the gut’s own motility system, impairing the MMC and creating conditions favourable to bacterial overgrowth.

Research by Pimentel and colleagues (2015) has been particularly significant in establishing this connection, identifying anti-vinculin and anti-CdtB antibodies as markers of post-infectious IBS and SIBO. The degree of immune response, and therefore the extent of MMC damage, appears to vary between individuals, which may partly explain why some people develop post-infectious SIBO after a bout of food poisoning while others do not.

For people whose SIBO has a clear post-infectious origin, addressing the resulting motility impairment, and not just the overgrowth, is essential to achieving lasting resolution.

Low stomach acid and SIBO

Stomach acid (hydrochloric acid (HCl) performs a critical antimicrobial function that is often underappreciated (Busheyhead & Quigley, 2022). The highly acidic environment of the stomach acts as a barrier, destroying a large proportion of the bacteria we ingest through food and water before they have the opportunity to reach the small intestine. When stomach acid production is insufficient, this barrier weakens, and more bacteria can make passage through to the small bowel.

Hypochlorhydria (low stomach acid) is more common than widely recognised and can result from:

• The natural decline in stomach acid secretion that occurs with ageing
• Chronic stress, which literally halts digestive function and acid secretion
• Helicobacter pylori infection, which directly damages acid-secreting cells
• Nutrient insufficiencies, particularly zinc and B vitamins, which are essential for stomach acid production
• Proton pump inhibitor (PPI) use — covered in more detail below

It is worth noting that the symptoms of low stomach acid — bloating, belching, reflux, and a sensation of food sitting heavily — are often mistaken for excess acid, leading to unnecessary acid-suppressing treatment that can compound the underlying problem. This is an area where accurate assessment matters considerably.

Medications that can contribute to SIBO: PPIs and antibiotics

Proton pump inhibitors (PPIs)

Proton pump inhibitors — commonly prescribed for acid reflux, gastro-oesophageal reflux disease (GORD), and ulcer protection — are among the most widely used medications in the UK. They work by suppressing gastric acid production, which is effective at managing reflux symptoms but comes with a consequence relevant to SIBO: by reducing the acidity of the stomach, they diminish its antimicrobial barrier function.

Multiple studies have found an association between long-term PPI use and increased risk of SIBO. A 2013 meta-analysis by Lo and Chan found PPI users to have significantly higher odds of developing SIBO compared to non-users. The relationship appears particularly relevant in people taking PPIs long-term rather than as a short course, and the risk may be further increased in those with other predisposing factors. However, this does not mean that everyone taking PPIs will develop SIBO, nor that PPIs should be discontinued without medical guidance. It does mean that PPI use represents a clinically relevant risk factor that warrants consideration — particularly in someone presenting with SIBO who has been on long-term acid suppression.

Antibiotics

Antibiotics disrupt the delicate gut ecology (microbiome) by eliminating not only the target ‘bad’ bacteria, but also significant populations of beneficial ‘friendly’ bacteria (Kesavelu & Jog 2023). This disruption can alter the ecological balance of the gut in ways that may favour bacterial overgrowth in the small intestine, particularly in the period immediately following a course of treatment.

Repeated or prolonged antibiotic use carries a higher risk in this regard. Some individuals report a clear connection between antibiotic use and the onset of digestive symptoms consistent with SIBO, and it is a question we routinely explore in clinical history-taking. Research here is inconsistent, but chronic systemic antibiotic use may increase the susceptibility to developing SIBO especially if other risk factors are present.

A certain irony exists here: antibiotics are also among the primary treatments for SIBO. The key distinction lies in targeted, time-limited use with appropriate support, versus broad-spectrum or repeated use that repeatedly disrupts the intestinal environment.

Structural causes: adhesions, the ileocecal valve, and surgery

The physical architecture of the gastrointestinal tract plays an important role in preventing bacterial overgrowth. When structural abnormalities are present they can create conditions that allow bacteria to accumulate (Wilk et al. 2025)

Adhesions

Adhesions are bands of scar tissue that form following abdominal surgery, infection, or inflammation. They can cause partial obstructions or altered motility in sections of the small intestine, creating areas of stagnation where bacteria can accumulate. People with a history of abdominal or pelvic surgery — including appendectomy, gynaecological procedures, or bowel surgery — carry a higher structural risk for SIBO (Wilk et al. 2025).

The ileocecal valve

At the junction between the small and large intestine sits the ileo-caecal valve (ICV), serving as a one-way system preventing bacteria-rich colonic contents from flowing backwards. When this valve fails to close properly, colonic bacteria can migrate into the small intestine, directly seeding the overgrowth.

ICV dysfunction is an under-recognised contributor to SIBO and recurrent SIBO in particular. It has been associated with conditions including hypermobility disorders and connective tissue disorders.

Bowel surgery and anatomical changes

Surgical procedures that alters the normal anatomy of the gastrointestinal tract — including gastric bypass, bowel resection, or procedures that create ‘blind loops’ — can create areas where bacterial populations accumulate unchecked. This is sometimes referred to as ‘blind loop syndrome’ and represents one of the more classic and well-established structural causes of bacterial overgrowth (Wilk et al. 2025).

Thyroid conditions, diabetes, and motility disorders

A number of systemic health conditions predispose individuals to SIBO through their effect on gut motility and the autonomic nervous system. These are frequently overlooked as contributing factors, particularly when SIBO is treated as a standalone digestive problem rather than within the context of a person’s broader health picture.

Hypothyroidism

Thyroid hormones play a significant role in regulating gut motility. In hypothyroidism — where thyroid hormone production is insufficient — gut transit slows, often considerably. This slowed transit reduces MMC activity and creates a stagnant environment in the small intestine that is conducive to bacterial overgrowth. Constipation is a well-recognised symptom of hypothyroidism, and SIBO is increasingly recognised as a complication in people with undertreated or undiagnosed thyroid dysfunction (Wei et al. 2025).

It is therefore important that thyroid function is assessed and optimised as part of a comprehensive approach to SIBO — not as an afterthought, but as a potential root cause that, if left unaddressed, will continue to drive recurrence.

Diabetes and diabetic gastroparesis

Both type 1 and type 2 diabetes are associated with an increased risk of SIBO, through several interconnected mechanisms (Ahmed et al. 2022). Chronically elevated blood glucose can damage the vagus nerve and the autonomic nervous system — a complication known as ‘autonomic neuropathy’ — impairing the nerve signals that coordinate gut motility and MMC function. Diabetic gastroparesis, a condition characterised by delayed stomach emptying, further compounds this by slowing the transit of food and bacteria through the upper gut.

SIBO in the context of diabetes is a clinically significant finding, as unresolved bacterial overgrowth can itself worsen blood sugar control — creating a bi-directional relationship that requires integrated management.

Other motility disorders

A range of other conditions that impair gut motility carry an elevated SIBO risk, including (Ahmed et al. 2022):

• Scleroderma and other connective tissue disorders, which can cause fibrosis of the gut wall
• Coeliac disease, particularly in those with ongoing mucosal damage
• Crohn’s disease, especially where strictures or surgical resection have altered gut anatomy
• Hypermobility spectrum disorders (hEDS/HSD), which are increasingly recognised in SIBO clinical populations
• Parkinson’s disease and other neurological conditions affecting autonomic function

Why identifying the cause of your SIBO matters

The causes of SIBO are not merely academic. They are clinically decisive — because the cause determines what needs to be addressed alongside any antimicrobial treatment for resolution to be lasting rather than temporary. Treating the overgrowth without addressing the predisposing factor is one of the most common reasons SIBO keeps coming back.

At IBS & SIBO Clinics, a thorough investigation of the likely causes of your SIBO is the starting point of everything we do. We don’t begin with the antimicrobials — we begin with the question of why the overgrowth developed in the first place.

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