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Written by Chris Kresser
While there are many factors that influence thyroid function, recent research suggests that gut health may be a key player. The trillions of microbes that reside in your gut have a profound influence on the production of hormones in the body—including thyroid hormones. Read on to find out if a disrupted gut microbiota might be contributing to your thyroid problem, and learn how healing your gut could improve your thyroid function.
A central principle of functional medicine is addressing the underlying cause of a disease, as opposed to just treating symptoms. In a previous article on the blog, I discussed the connection between overall gut health and the thyroid. In this article, we’ll focus on the microbes themselves and the many ways in which they are connected to thyroid function.
In recent years, the microbiota has been implicated in numerous chronic diseases, from obesity to inflammatory bowel disease to multiple sclerosis (1). It really should be no surprise that it also has a profound impact on endocrine organs like the thyroid. Disruption of the intestinal flora and subsequent impaired thyroid function was first hypothesized back in the early 1900s, long before the terms “microbiota” and “microbiome” were even coined (2).
Today, microbial sequencing of human fecal samples allows us to measure compositional differences in the microbiota. A 2014 study found that individuals with hyperthyroidism had significantly lower numbers of Bifidobacteria and Lactobacilli and significant higher levels of Enterococcus species compared to healthy controls (3). No equivalent study has yet been done in individuals with hypothyroidism, but given that 90 percent of hypothyroid cases are autoimmune in nature (4) and the fact that an altered microbiota has been implicated in countless other autoimmune diseases, it’s quite likely that dysbiosis plays a significant role (5).
Microbes recognize a number of different host endocrine molecules, including adrenaline, noradrenaline, sex hormones, and thyroid hormones, and can even change aspects of their metabolism and virulence in response to these signals (6). Moreover, germ-free rats, which are raised in sterile conditions and lack gut bacteria altogether, have smaller thyroid glands than conventionally raised rats, suggesting a crucial role for these microbes in thyroid health (7).
The epithelial cells that form the lining of the gut have fingerlike projections called villi, which increase the surface area for transporting nutrients into the body. When the gut is inflamed, as is often the case with microbial dysbiosis, these villi can become truncated, resulting in impaired nutrient absorption. This includes nutrients like iodine and selenium, which are vital for thyroid health.
While the microbiota provides many benefits to the host, it also competes with the host for nutrients. The nutrients that are essential for our cells to function properly are also important nutrients for our microbes! The composition of the microbiota may therefore influence a person’s requirement for various nutrients. In fact, a 2009 study in mice suggested that the microbiota competes with the host for selenium when selenium is scarce, impairing synthesis of selenoproteins, which are necessary for proper thyroid function. In another study, rats fed kanamycin, a broad-spectrum antibiotic, had significantly lower iodine uptake by the thyroid.
Lipopolysaccharide, or LPS, is a component of bacterial cell walls. When intestinal permeability is increased, often as a result of gut dysbiosis, LPS can “leak” into the bloodstream. This can wreak havoc on the thyroid in a number of ways.
Thyroid-stimulating hormone (TSH) induces the thyroid to produce T4. T4 is the inactive form of thyroid hormone and must first be converted to T3, the active form. Our bodies produce an enzyme called iodothyronine deiodinase that is responsible for making this conversion. LPS has been shown to inhibit this enzyme, decreasing the amount of active T3 in circulation (9).
Not only do you need active thyroid hormone, but you also need receptors for thyroid hormone on cells throughout the body. Even someone whose thyroid hormone panel looks perfect could suffer from symptoms of hypothyroidism if their body does not produce enough receptors to receive signals from the thyroid. LPS has been shown to decrease expression of thyroid receptors, specifically in the liver (10).
LPS also induces expression of the sodium-iodine symporter (NIS) in thyroid cells, increasing iodine uptake in the thyroid (11). Since iodine is important for thyroid health, this might sound like a good thing, but excess iodine (especially with concurrent selenium deficiency) has been found to contribute to the development of Hashimoto’s, the autoimmune form of hypothyroidism (12).
Remember in the last section how we said that inactive T4 must be converted to active T3? Well, about 20 percent of this conversion takes place in the GI tract! Commensal gut microbes can convert inactive T4 into T3 sulfate, which can then be recovered as active T3 by an enzyme called intestinal sulfatase (13).
Bile acids present another interesting connection between gut bacteria and thyroid function. Primary bile acids are produced in the gallbladder and secreted into the small intestine following the consumption of fats. Metabolism of primary bile acids by the gut bacteria results in the formation of secondary bile acids. These secondary bile acids increase activity of iodothyronine deiodinase (the main enzyme that converts T4 into T3) (14).
We’ll see one more way that gut bacterial metabolites influence thyroid health later when we talk about prebiotics.
Thyroid function is also closely related to small intestinal bacterial overgrowth (SIBO). In a healthy individual, the majority of microbes are concentrated in the large intestine. In SIBO, certain bacteria and archaea are able to colonize the small intestine and proliferate, causing bloating, gas, and distention, among other unpleasant symptoms.
The connection between SIBO and the thyroid is underappreciated. A 2007 study found that among people with a history of autoimmune hypothyroidism, 54 percent had a positive breath test for SIBO compared to 5 percent of controls (15). It is currently unknown whether the relationship is causal. Since thyroid hormones help stimulate gut motility, it is also possible that low motility and constipation provide an environment in the small intestine that is conducive to bacterial overgrowth. This may be one of many examples of bidirectional interaction between the host and its resident microbes.
So how can we apply this information? Here are four ways that you can improve your thyroid function:
Bone broth can heal your leaky gut. Start the healing immediately!