Do you see a lot of patients with small intestinal bacterial overgrowth? While the underlying causes of SIBO are diverse, one that has received more attention in the literature lately is low thyroid function. Read on to learn how hypothyroidism can impair gut motility and contribute to the pathophysiology of SIBO.
A healthy small intestine contains relatively few microbes. Antimicrobial peptides, the acidity of incoming chyme from the stomach, and gastrointestinal motility all help maintain this relatively low bacterial load (1). However, if these systems break down, small intestinal bacterial overgrowth (SIBO) can develop.
I’ve written extensively about the pathophysiology of SIBO and why it’s so difficult to treat. Treatment not only involves addressing the overgrowth with antibiotics or herbal antimicrobials, but also restoring the mechanisms that prevent overgrowth from recurring. This includes proper thyroid function. In this article, I’ll discuss why thyroid function impairs gut motility, the association between hypothyroidism and SIBO, and why thyroid panels are a must in patients with SIBO and irritable bowel syndrome (IBS).
Meet the Migrating Motor Complex
The gut has a dense, mesh-like network of more than 500 million neurons that, along with other nerve cells, form the enteric nervous system (ENS). The ENS innervates the smooth muscle cells that line the intestine and governs intestinal mixing and peristaltic contractions.
Thyroid function impairs gut motility, so if you’re suffering from IBS or SIBO, a thyroid panel is a must
During times of fasting, the ENS sends waves of electrical activity through the small intestine, moving the contents along the gastrointestinal tract to the colon. This is called the migrating motor complex (MMC). The MMC is crucial for keeping bacteria out of the small intestine and in the colon, where they belong. In animal models, drugs that disrupt MMC function have been shown to cause SIBO, while restoring MMC function reduces the density of small intestinal bacteria to normal levels (2, 3).
The MMC is affected by numerous conditions, including anatomical abnormalities such as gastrointestinal surgery, intestinal diverticula or fistulas, and diseases of neuropathic, autoimmune, inflammatory, or metabolic nature (4). It’s also influenced by endocrine disease, including thyroid function. In the next section, I’ll discuss how poor thyroid function can impair MMC function and motility.
The Thyroid and Motility
Thyroid hormones influence gut motility by modulating the ENS and altering smooth muscle function and the MMC (5, 6). Studies in both animals and humans have shown that hypothyroidism is associated with delayed gastric emptying, decreased frequency of intestinal peristalsis, and slower orocecal transit time (7, 8). This slower transit time from the oral cavity to the end of the small intestine often results in constipation, which is the most frequent gastrointestinal complaint in patients with hypothyroidism (9).
However, some patients may have slow orocecal transit time followed by rapid colonic transit time, resulting in diarrhea. This is thought to be due to carbohydrate malabsorption and fermentation in the distal ileum, which then leads to high osmolality in the colon. A study published in January 2017 found that 29 percent of patients with IBS had delayed orocecal transit time, but there was no difference in the presence of delayed transit between subtypes (diarrhea, mixed, or constipation) (10).
The Association between Hypothyroidism and SIBO
Now that we understand why thyroid would impact gut motility, let’s look at a few studies that have assessed hypothyroidism and SIBO in humans:
Study 1: A group of researchers in Italy wanted to determine whether a history of overt hypothyroidism due to autoimmune thyroiditis was associated with SIBO. They recruited 50 patients with hypothyroidism and 40 healthy controls (11). Patients with hypothyroidism were given synthetic T4 and achieved normal thyroid levels prior to performing glucose breath tests (GBT). Astoundingly, they found that 27 out of the 50 patients with a history of hypothyroidism (54 percent) were positive for SIBO, compared to 5 percent of controls (two of 40).
They further found that abdominal discomfort, flatulence, and bloating were all common in the hypothyroid patients with SIBO, but there was no significant correlation between hypothyroidism and bowel frequency (constipation or diarrhea). After a one-week course of rifaximin, 19 of the 27 patients (70.4 percent) were negative for SIBO according to a repeat glucose breath test and had significantly improved self-reported abdominal discomfort, flatulence, and bloating.
Overall, this study identifies prior hypothyroidism as a risk factor for SIBO, suggesting that once SIBO develops in a hypothyroid state, restoring normal thyroid status may not be enough to clear bacterial overgrowth. It’s unfortunate that no breath tests were performed before thyroid medication was begun—it would have been interesting to see if any patients successfully eradicated their SIBO simply from restoring thyroid hormone levels. We’ll have to hold out for future studies!
Study 2: In this study, researchers in Poland recruited 34 patients with diarrhea-predominant SIBO (SIBO-D), 30 patients with constipation-predominant SIBO (SIBO-C), and 30 healthy controls. Thyroid hormone levels were similar in controls and patients with SIBO-D, but patients with SIBO-C often had thyroid panels that were characteristic of hypothyroidism. Both SIBO groups had elevated anti-thyroid peroxidase (ATPO), with SIBO-C patients having the highest levels (12).
Study 3: Researchers in Germany performed a retrospective cohort study of 1,809 patients to assess various risk factors for SIBO. They found that hypothyroidism and T4 therapy were associated with a 2.6 and 3.0 times increased risk of SIBO, respectively (13). While the authors suggested that T4 medication itself might somehow be contributing to SIBO, I think it’s more likely that those on T4 therapy had more severe hypothyroidism in the first place, which required more aggressive intervention.
Treating SIBO in Cases of Hypothyroidism
There’s certainly still a lot we don’t know, but hopefully this article helps illuminate the connection between hypothyroidism and SIBO. Here are some practical takeaways that you can put into practice in your clinic:
Perform a Full Thyroid Workup on all Patients with SIBO or IBS
All patients with SIBO or IBS should receive a full thyroid panel, including thyroid antibodies, as part of their routine lab work. Thyroid conditions are quite common, and an estimated 60 percent of people with thyroid disease are unaware of their condition (14). While no studies to date have been done on subclinical hypothyroidism (SH) and SIBO, I would venture to guess that SH contributes to SIBO as well, just to a lesser degree.
Support Thyroid Function with Diet and Lifestyle Changes
I’ve written several articles on how to improve thyroid function by correcting nutrient deficiencies, rebalancing the immune system, and making simple diet and lifestyle changes. In many patients, reducing inflammation and eating a nutrient-dense diet can help restore thyroid function and proper gut motility.
Consider Thyroid Medication to Support Motility
While diet and lifestyle changes will improve thyroid function over time, many patients, particularly those with constipation, will benefit from acute thyroid support to help with motility.
Consider other Motility Enhancers
If thyroid support does not restore normal bowel function in patients with constipation, motility enhancers like low-dose naltrexone (LDN), low-dose erythromycin, Iberogast, 5-HTP, or MotilPro can also be considered. Motility enhancers have been shown to delay the recurrence of SIBO (15).
Treat the Overgrowth
While slow transit is often what allows SIBO to occur in the first place, speeding up transit will not necessarily be enough to clear the overgrowth once the microbes have set up camp. However, it’s important to remember that treating the overgrowth will only be successful in the long term if we simultaneously address the underlying cause of low motility.