When I talk about thyroid disease I often talk about also improving digestive health. But what is the connection between the two? Why do we need good gut health when treating conditions like hypothyroidism or Hashimoto's hypothyroidism?
The truth is they go hand in hand. You can't have good gut health without good thyroid health and vice versa. If you have hypothyroidism or autoimmune thyroiditis continue reading to learn more about the thyroid-gut connection and how the two systems are interconnected.
The Thyroid-Gut Connection
Because most of our immune system is in our digestive tract it also plays a role in the thyroid-gut connection. Thyroid and reproductive hormones are activated, regulated, eliminated, and metabolized through processes that occur in the gut. Autoimmunity, which can affect more than just the thyroid, can be initiated by poor digestive health and leaky gut.
Thyroid hormone activation - The thyroid secretes inactive thyroxine (T4) that needs to be converted into active triiodothyronine (T3). This conversion happens in the gut with the help of an enzyme made by our gut bacteria. This is yet another reason to have a healthy microbiome populated with beneficial bacteria!
Inflammation in the gut decreases thyroid hormones - The gut is home to about 70% of our immune system as part of the gut-associated lymphoid tissue or GALT. When there is inflammation from conditions like food allergies or Celiac disease this increases the stress hormone cortisol. Cortisol can weaken the gut wall leading to leaky gut and autoimmunity. It can also increase the amount of T3 that's bound to carrier proteins, making it unusable by the body. The T3 that is available is more likely to be pushed into inactive reverse T3. This is one way the adrenals are involved in thyroid health, making stress reduction an important factor in treating thyroid conditions, too.
Metabolism and elimination of hormones - Digestive function can affect the thyroid, but thyroid function can also influence gut function. In hypothyroidism, the whole digestive system slows down leading to constipation and bloating. One way the body gets rid of hormones is by attaching them to bile and excreting them through bowel movements. Low levels of T4, seen in hypothyroidism, may reduce bile flow. If hormones aren't being eliminated they can be reabsorbed and recirculate in the body. Estrogen is a hormone that's affected by slow digestion and when it's reabsorbed it can lead to menstrual issues and PMS. Constipation can increase circulating estrogen as well as a protein that binds thyroid hormones, making them less available.
The gut absorbs, converts and produces thyroid hormones - The thyroid secretes T4 but most of our body's T3 is produced elsewhere in other organs such as the liver and intestinal tract. The liver is an important organ when it comes to regulating thyroid hormones. T4 is stored and converted to T3 here. Both T3 and T4 are absorbed well in the gut, but less so if there are digestive issues that interfere with absorption. If you're taking thyroid hormone supplementation you want to make sure that you have a healthy gut to improve absorption of your medication.
The gut plays a role in autoimmunity - If you have an autoimmune disease like Hashimoto's thyroiditis, a healthy gut is a way to decrease the inflammatory response. In this situation, inflammation caused by chronic digestive diseases or food allergies lead to a breakdown of the cells that line the digestive tract. They are usually good at controlling what substances are allowed through, but in the case of leaky gut, toxins, bacteria, and undigested food are able to pass through into the rest of our body. The immune system mounts an attack to protect us, but that can also initiate body-wide inflammation and autoimmune disease. T4 from the thyroid can act like an anti-inflammatory in the gut by influencing the activity of a group of immune cells called T-cells. When there are low levels of T4, as seen in hypothyroidism, inflammation can remain elevated.
Summary
Treatment strategies for thyroid diseases like hypothyroidism and Hashimoto's thyroiditis often include working on good gut health. These two body systems influence the function of each other, along with the immune system and adrenals. Thyroid hormone, T4, is produced in the thyroid and is converted into active T3 in the gut. Inflammation in the gut can lead to higher levels of cortisol, which can lower levels of T3 by pushing its conversion towards inactive rT3 and increase the amount of T3 that becomes bound to proteins, making T3 less available. Constipation and bile flow affects elimination and reabsorption of hormones, including estrogen, that can increase bound thyroid hormones, making them unavailable. The gut secretes and absorbs thyroid hormones, making a healthy gut necessary for absorbing thyroid hormone medications. Improving leaky gut and controlling autoimmune reactions is important when dealing with autoimmune thyroiditis.
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Dr. Jamie
This website is not intended for the purpose of providing medical advice. All information, content, and material of this website is for informational purposes only and are not intended to serve as a substitute for the consultation, diagnosis, and/or medical treatment of a qualified physician or healthcare provider.
Resources
Kresser, Chris. “The Thyroid-Gut Connection.” Chris Kresser, 18 Feb. 2019, chriskresser.com/the-thyroid-gut-connection.
Miller, Laurence, et al. “Gut Thyroid Interrelationships.” AGA Journals, Nov. 1978, www.gastrojournal.org/article/0016-5085(78)90478-X/fulltext.
Mu, Qinghui, et al. “Leaky Gut As a Danger Signal for Autoimmune Diseases.” Frontiers in Immunology, Frontiers Media S.A., 23 May 2017, www.ncbi.nlm.nih.gov/pmc/articles/PMC5440529/.
Vighi, G, et al. “Allergy and the Gastrointestinal System.” Clinical and Experimental Immunology, Blackwell Science Inc, Sept. 2008, www.ncbi.nlm.nih.gov/pmc/articles/PMC2515351/.
Wang, Jin, and John Klein. “Hormone Regulation of Murine T Cells: Potent Tissue-Specific Immunosuppressive Effects of Thyroxine Targeted to Gut T Cells.” OUP Academic, Oxford University Press, 1 Feb. 1996, academic.oup.com/intimm/article/8/2/231/671078.