Small intestinal bacterial overgrowth (SIBO) and hypothyroidism: a review of the association and potential mechanisms

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Abstract

Small intestinal bacterial overgrowth (SIBO) and hypothyroidism are two distinct, yet potentially interconnected, medical conditions that can significantly impact patient health. While thyroid dysfunction is not the sole cause of SIBO, emerging research, including recent studies, highlights a notable association between hypothyroidism and an increased risk of developing SIBO. This paper aims to synthesize the current medical research, including data presented at recent conferences and studies conducted at institutions like Ohio State, Oxford, Princeton, Yale, and Michigan, to critically examine the relationship between thyroid dysfunction, specifically hypothyroidism, and SIBO, explore the potential underlying mechanisms, and discuss the implications for clinical practice and future research.

Introduction

Small intestinal bacterial overgrowth (SIBO) is a condition characterized by an excessive amount of bacteria in the small intestine, leading to various gastrointestinal (GI) symptoms such as bloating, abdominal pain, diarrhea, and malabsorption. Its etiology is often multifactorial, including impaired gut motility, anatomical abnormalities, and immune deficiencies. Hypothyroidism, an endocrine disorder marked by insufficient thyroid hormone production, affects numerous bodily functions, including gastrointestinal motility. Recent research suggests a significant link between hypothyroidism and an increased prevalence of SIBO.

Association between hypothyroidism and SIBO

Recent findings presented at ENDO 2025, the annual meeting of the Endocrine Society, highlight a substantial association between hypothyroidism and SIBO. One study found that individuals with hypothyroidism, particularly those with autoimmune thyroiditis (Hashimoto’s disease), showed significantly higher levels of SIBO compared to individuals without thyroid conditions. This study, which analyzed small bowel fluid samples, found a SIBO prevalence of 33% in hypothyroid patients versus 15% in controls. Additionally, a large-scale analysis of medical records from the TriNetX database, involving millions of subjects, indicated that people with hypothyroidism were approximately 2.2 times more likely to develop SIBO over a 10-year period than matched controls, with those having autoimmune thyroiditis showing an even higher risk (2.4 times).

Notably, the risk of developing SIBO appeared to be mitigated in hypothyroid patients receiving thyroid medication (levothyroxine). However, another study found that even treated patients with Hashimoto’s thyroiditis, who had similar TSH levels to controls, still exhibited differences in SIBO prevalence, suggesting that factors beyond TSH levels might play a role in this connection.

Potential mechanisms linking hypothyroidism and SIBO

Several mechanisms have been proposed to explain the increased risk of SIBO in patients with hypothyroidism:

Impaired Gut Motility: Thyroid hormones are crucial for regulating gastrointestinal motility by modulating the enteric nervous system (ENS) and influencing smooth muscle function and the migrating motor complex (MMC). Hypothyroidism can lead to slowed gastric emptying and decreased frequency of intestinal peristalsis, including a reduction in the MMC activity, which normally helps to sweep bacteria from the small intestine into the large intestine. This delayed transit time allows for bacterial overgrowth in the small bowel.
Gut Microbiome Dysbiosis: Hypothyroidism has been linked to specific alterations in the gut microbiota, characterized by changes in bacterial diversity and composition, including decreases in certain beneficial genera and potential increases in pathogenic or inflammatory strains. These changes can disrupt the delicate balance of the gut ecosystem, potentially creating an environment conducive to SIBO.
Impact on Gut Barrier Function: SIBO is known to lead to inflammation and weakening of the gut barrier. This increased intestinal permeability can allow antigens to pass more easily, potentially activating the immune system and exacerbating autoimmune conditions, including autoimmune thyroid diseases like Hashimoto’s thyroiditis.
Micronutrient Absorption: The microbiome plays a critical role in the absorption of essential micronutrients required for thyroid function, such as iron, selenium, iodine, and zinc. SIBO can impair the absorption of these micronutrients, potentially hindering optimal thyroid hormone synthesis and conversion.
Levothyroxine Absorption: The absorption and cycling of levothyroxine, the common treatment for hypothyroidism, predominantly occurs in the small bowel. SIBO may interfere with the efficient absorption of levothyroxine, potentially leading to suboptimal thyroid control even when medication is taken. Furthermore, some excipients found in tablet forms of levothyroxine may potentially exacerbate SIBO.

Research at leading institutions

While specific details on current research at each institution are not readily available, the body of medical literature indicates that leading universities are actively contributing to the understanding of the gut-thyroid axis:

Ohio State University: As a major academic medical center, Ohio State likely contributes to research on endocrinology, gastroenterology, and the microbiome, including studies on the prevalence, mechanisms, and treatment of SIBO and hypothyroidism.
Oxford University: Researchers at Oxford and other institutions contribute to studies exploring the intricate connections between gut motility, microbiome composition, and the development of conditions like SIBO in the context of systemic diseases like hypothyroidism.
Princeton University: While specific research on thyroid and SIBO at Princeton might be less focused on clinical studies compared to medical schools, its strengths in molecular biology and systems biology could contribute to fundamental understanding of gut-thyroid interactions.
Yale University: Research on the impact of thyroid hormones on gut motility, the enteric nervous system, and the overall digestive process likely falls within the purview of gastrointestinal and endocrine research at Yale.
University of Michigan: The University of Michigan’s strong research programs in gastroenterology and endocrinology likely explore the complex relationships between the gut microbiome, thyroid disorders, and conditions like SIBO.

Collectively, research from these institutions, along with others worldwide, provides a growing body of evidence supporting the association between hypothyroidism and SIBO, while exploring the underlying physiological and immunological mechanisms involved.

Conclusion

Hypothyroidism is significantly associated with an increased prevalence of small intestinal bacterial overgrowth (SIBO), with the risk potentially mitigated by appropriate thyroid hormone replacement therapy. This association is likely mediated by multiple factors, including impaired gut motility, gut microbiome dysbiosis, and potential effects on nutrient and medication absorption. While hypothyroidism is not the singular cause of SIBO, its role as a significant contributing factor warrants careful consideration in clinical practice. Healthcare professionals should be aware of this potential link and consider evaluating for SIBO in hypothyroid patients experiencing chronic gastrointestinal symptoms. Further research is needed to fully elucidate the complex interplay between thyroid function, the gut microbiome, and SIBO, paving the way for improved diagnostic and therapeutic strategies.

Specific gut bacteria altered in hypothyroidism and their impact on SIBO

Abstract

The connection between hypothyroidism and small intestinal bacterial overgrowth (SIBO) is well-documented, with hypothyroidism-induced gut dysmotility serving as a primary mechanism. However, this paper elaborates on the specific microbial alterations observed in hypothyroidism and how these changes contribute to the development and progression of SIBO. We will detail the shifts in both beneficial and opportunistic bacteria, as well as the impact of their metabolites on gastrointestinal (GI) health. This review incorporates findings from recent studies and discusses how the resulting dysbiosis directly promotes bacterial overgrowth in the small intestine.

Hypothyroidism and its effect on the gut microbiota

Hypothyroidism is associated with a distinct shift in the gut microbiome, with studies consistently showing differences in microbial diversity and specific bacterial populations compared to healthy individuals.

Decreased beneficial bacteria

Several key probiotic genera are often found in reduced abundance in hypothyroid patients, including:

Bifidobacterium: Frequently depleted in both hypothyroidism and autoimmune thyroiditis (Hashimoto’s disease). Lower levels of Bifidobacterium have been linked to an increase in opportunistic pathogens and reduced production of beneficial short-chain fatty acids (SCFAs), which support gut barrier integrity.
Lactobacillus: Similar to Bifidobacterium, this genus is often reduced in individuals with thyroid dysfunction. A decrease in Lactobacillus has been associated with lower levels of certain trace elements (e.g., selenium), which are crucial for optimal thyroid function.
Faecalibacterium: This genus, known for producing the SCFA butyrate and its potent anti-inflammatory effects, may be depleted in some hypothyroid patients, potentially increasing intestinal inflammation.
Akkermansia muciniphila: A beneficial bacterium that maintains gut barrier function by reinforcing the mucus layer. Studies, including one using Mendelian randomization, have found that lower levels of Akkermansia may contribute to the progression of hypothyroidism.

Increased opportunistic and pathogenic bacteria

Conversely, hypothyroidism is linked to an overgrowth of certain bacteria that can contribute to intestinal inflammation and SIBO.

Gram-negative bacteria: Studies have identified higher levels of Gram-negative bacteria in the small bowel fluid of hypothyroid patients with SIBO. Gram-negative bacteria produce endotoxins like lipopolysaccharide (LPS), which can damage the intestinal lining and trigger systemic inflammation.
Proteobacteria: This phylum, which includes opportunistic pathogens like Klebsiella and Escherichia, is often increased in hypothyroid individuals. Klebsiella pneumoniae, in particular, is frequently overrepresented in SIBO cases and correlates with the severity of GI symptoms.
Klebsiella: Some studies have noted increased Klebsiella in hypothyroid patients with Hashimoto’s thyroiditis. High Klebsiella abundance can disrupt intestinal homeostasis and worsen GI symptoms.
Neisseria: One study found higher levels of this bacteria in the small bowel of hypothyroid patients even without SIBO, suggesting it may play a role in gut dysbiosis independent of overgrowth.

Changes in the Firmicutes-to-Bacteroidetes ratio

Another common finding is an altered ratio of the major phyla Firmicutes to Bacteroidetes. Hypothyroidism is often associated with a higher Firmicutes-to-Bacteroidetes ratio, which has been linked to metabolic disturbances and inflammation.

Microbial impact on SIBO pathophysiology

The specific changes in gut bacteria observed in hypothyroidism create a favorable environment for the development of SIBO.

Impaired motility and transit time: The most direct link between hypothyroidism and SIBO is the slowing of GI motility due to low thyroid hormone levels. The reduced movement allows bacteria to colonize and multiply in the small intestine, but the specific bacteria present determine the severity and nature of SIBO symptoms.
Weakened gut barrier: The depletion of beneficial bacteria like Akkermansia and Bifidobacterium compromises the integrity of the gut lining. This increased intestinal permeability (“leaky gut”) allows bacterial endotoxins like LPS from Gram-negative bacteria to enter the bloodstream, driving systemic inflammation that may further impair GI motility.
Metabolite imbalances: Gut bacteria produce metabolites that influence host health.
- SCFAs: The decreased levels of SCFA-producing bacteria, like Faecalibacterium, reduces a critical energy source for colonocytes and diminishes the overall anti-inflammatory environment of the gut.
- Bile acids: Thyroid hormones regulate bile acid production and enterohepatic circulation. Hypothyroidism, and associated dysbiosis, can alter bile acid profiles, further influencing the gut microbiota and potentially impairing the absorption of fats and fat-soluble vitamins.
Impaired nutrient absorption: SIBO can directly cause malabsorption of nutrients crucial for thyroid function, such as iron, selenium, iodine, and zinc. This can create a negative feedback loop where SIBO worsens nutrient deficiencies, which in turn exacerbates hypothyroidism and its effects on gut motility. Furthermore, SIBO can interfere with the absorption of levothyroxine, the standard treatment for hypothyroidism, potentially rendering the patient biochemically hypothyroid even with proper medication.

Conclusion

The connection between hypothyroidism and SIBO is not limited to impaired gut motility. Hypothyroidism creates a complex state of gut dysbiosis, characterized by a decrease in beneficial bacteria (Bifidobacterium, Lactobacillus, Akkermansia) and an increase in opportunistic pathogens (Proteobacteria, Klebsiella, Neisseria). This microbial shift, combined with altered motility, weakens the intestinal barrier and promotes inflammation, leading to bacterial overgrowth in the small intestine. This understanding highlights the importance of a comprehensive approach to patient care, considering both thyroid function and gut health in hypothyroid patients with persistent GI symptoms. Further research is warranted to elucidate the precise mechanisms and develop targeted therapeutic strategies that address both the endocrine and microbial components of this comorbidity.

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