Hashimoto’s disease is the most common autoimmune condition globally.[1] It entangles both the gut and the brain symptomatically. Common examples of these symptoms are constipation and brain fog.
But what about the gut when it comes to the triggers of Hashimoto’s disease?
In this article, we will look at the gut’s contribution in sustaining and perhaps even triggering Hashimoto’s disease and some possible things to look into if you haven’t already.
Starting with the digestive system.
Let’s define what autoimmunity, Hashimoto’s disease and the microbiome are so it’s easier to understand the connection.
Auto-immunity occurs when the component of the immune system that defends us from specific infections begins to attack the body’s cells.[2] An easy and essential way of understanding how this happens is as a “loss of immune tolerance.”
When the immune system defends the body from a specific invader, the immune cells can recognise the pathogen if it arrives again. This level of recognition allows the immune system to differentiate between cells usually found in the body and antigens not part of the body.
Immune tolerance occurs when the immune system recognises the cell or molecule as part of the body and doesn’t mount an immune response.[3]
One way I tend to explain it to my patients is to analogise this process with how people get into nightclubs.
Just bear with me, ok?
The immune system encounters a variety of different potential invaders all the time. It’s the hope that the components of the barrier immune system, like your skin, for example, do the bulk of the work when it comes to keeping things out.
If this doesn’t happen, then it’s the immune system’s job to provide the extra layer of security, just like bouncers at a nightclub. Most of the time, the bouncers ensure that the patrons entering the club fulfil the terms of entry, for example, the legal drinking age.
Imagine you work in the said nightclub as one of the bar staff. A loss of tolerance would be when one of the bouncers decides that you shouldn’t be in the club and tries to throw you out.
“But I work here!”
“Doesn’t matter. You’re out!”
When this tolerance fails, we start to see the immune system misfire and autoimmunity develop.
With that said, Hashimoto’s disease occurs when the immune system loses its tolerance to molecules involved in thyroid function.[4]
These molecules are either proteins or enzymes and are naturally occurring cogs in the function of the thyroid. When the immune system essentially destroys these cells, the function of the thyroid is directly affected. This effect on the thyroid then brings about hypothyroid symptoms or low thyroid function as a consequence.
Hypothyroidism symptoms include fatigue, cold intolerance, unexplained weight gain, dry skin and constipation.[5] Often symptoms of Hashimoto’s disease overlap with hypothyroidism but will only be diagnosed with the help of blood tests to check on the autoimmune antibodies.[6]
An easy way to think about what happens when the thyroid slows down is to understand thyroid hormones’ role in the body. I’ll make it easy. Nearly every organ of the body is activated by thyroid hormone, including your heart, blood sugar control, brain and reproductive health, particularly in women.[7]
Things just seem to slow down.
No more than what we see in the gut and the brain. How, though, do the microbiome and the bacterial environment in the gut play a role in Hashimoto’s disease?
If you are new to what the microbiome is, then an updated definition not only includes the collection of all the microbes that live in or on the human body but the associated genes they carry along with the molecules they give off as well.[8]
Trillions of microbes live in different colonies in different parts of your body.
All the different species contribute to the body’s function uniquely, similar to the ecosystem of a rainforest.
What’s most interesting about this community’s contribution to Hashimoto’s disease and other illnesses is that each microbiome is highly personal and unique to each individual. One researcher said that the “microbiome is as unique as our fingerprint.[9]”
This unique nature means that each microbiome’s contribution to illness could be just as unique as the presentation itself. Still, researchers have found common traits within the microbiomes of people living with Hashimoto’s disease.
The gut microbiome is involved in how available essential minerals are for your thyroid function.
The first way the microbiome in the gut may cause symptoms of Hashimoto’s disease and low thyroid function is via its influence on the uptake of iodine, selenium, zinc and iron. Four of the critical forms of currency the thyroid uses to drive its function.[10]
In the case of iodine, most people in developed regions get enough iodine. Still, a deficiency is known to cause thyroid symptoms along with a more commonly deficient mineral, selenium.[11]
An excellent example of the relationship between probiotics and our minerals is between a popular probiotic, Lactobacillus and selenium. Lactobacillus converts a sodium-based form of selenium into a different, more active form so it can absorb into the body.[12]
The byproducts created by the microbiome work with thyroid hormones to protect your digestive lining from becoming leaky.
A key healthy microbiome characteristic is the level of diversity of different probiotic species. An easy way to understand this is that we don’t want too many or few of a particular species.
Just like we would if we were cooking a recipe in the kitchen.
In contrast, research now points to various illnesses associated with the low diversity of microbes in the microbiome.[13]
This association also seems to be the case with the gut and Hashimoto’s disease. A few studies have now looked into “impaired” diversity of the microbiome and Hashimoto’s disease.[14] An important note to remember is that these studies are correlative, requiring further confirmation.
One interesting theme that carried through the more prominent studies was the reduced presence of a species of bacteria called Prevotella. Now the presence of this species doesn’t represent an infection that leads to Hashimoto’s disease. It means something that Prevotella doesn’t do just by existing in lower levels than desired.
In the case of Hashimoto’s disease, Prevotella upregulates the immune system’s ability to regulate the inflammatory T-helper cells believed to cause autoimmune responses.[15] Without reasonable amounts of this bacteria, the immune system finds it hard to contain an autoimmune fire when it starts.
When the thyroid slows down, so does the conveyor belt that carries your food through the digestive system.
This slowdown leads to a different type of imbalance within the microbiome: one we’ve discussed on this website before – small intestinal bacterial overgrowth or SIBO. If you haven’t heard of SIBO before, it is the presence of excessive amounts of bacteria from the colon in the small intestine.[16]
SIBO can cause bloating, food sensitivities, and changes in bowel patterns with either loose diarrhoea-like stool or a more constipation-like challenging bowel experience. A small study looking at the link between SIBO, Hashimoto’s disease and low thyroid function found that out of the ninety subjects, around fifty-four per cent of participants who had hypothyroidism tested positive for SIBO.[17]
There is a crucial point to look at regarding the gut and Hashimoto’s disease.
When looking at associative studies to assess the link between two things, we must always remember the possibility of a bi-directional relationship. For example, we know that SIBO changes the bacterial diversity of the microbiome, which as a consequence, affects thyroid function and Hashimoto’s disease. Second to this, we also know that hypothyroidism caused by Hashimoto’s disease slows down the motility in the digestive system.
Something that causes and sustains SIBO.
Another highlight here is how easy it is to miss testing the thyroid when it comes to having irritable bowel syndrome or IBS symptoms. I remember a patient who I treated for IBS successfully coming back with the same symptoms again in six months, perplexed about why. It wasn’t until we rechecked her thyroid that her antibodies were up, and her thyroid-stimulating hormone was through the roof. Interestingly, in this case, her levels had returned normal when we had checked previously.
Building on this a little further, certain types of bacteria, called gram-negative bacteria, colonise themselves in the small intestine and other regions of the digestive system.
If you are new to gram-negative bacteria, they are named this way because they don’t have a cell wall. Not because they are necessarily negative.
One of the issues with not having a cell wall is that toxic byproducts called lipopolysaccharides can “leak” out of the bacterial colonies into the bloodstream. This leak of toxic byproducts, or LPS, causes the immune system to flare up, increasing pro-inflammatory chemicals in the body. The pro-inflammatory chemicals then influence both thyroid function and autoimmunity in the thyroid.
Some initial evidence shows that improving these conditions can profoundly affect some people with Hashimoto’s disease in general but also in a pretty unexpected way.
It’s possible that your microbiome may even affect how successful your medication for Hashimoto’s disease is.
One particular study even found that a high-dose multi-strain probiotic formula reduced the number of L-thyroxine dose adjustments compared to control groups. Even though it was small, with thirty or so participants, the study concluded a role for probiotics in managing thyroid hormone levels in the blood.[18]
Initial studies have also found a role in synbiotics or combinations of probiotics and prebiotics.
This randomised, double-blind, placebo-controlled trial looked at the combination of pre-and probiotics in sixty people with hypothyroid over eight weeks. The study showed that thyroid-stimulating hormone (TSH) levels, often a vital indicator of thyroid function, were decreased along with fatigue levels and, as we looked at above, doses of L-thyroxine.[19] Indeed, an interesting study and the more extensive studies that follow this one will hopefully shed more light on why this happened and whether we can apply it to a more significant population.
So, what do you think?
I’m finishing this article after seeing my morning round of patients. One of my conversations was about how surprised my patient was about how her digestive changes had rippled out to other health areas and the condition we now have under control.
The connection between the gut and Hashimoto’s disease is an intimate one. I hope this article helped.
Would you believe we have only touched the basics in an article this length?
That said, the potential for change by mediating the relationship between the gut and Hashimoto’s disease is definitely there!
Hope this helps xx
References
[1] McLachlan SM, Rapoport B. Breaking tolerance to thyroid antigens: changing concepts in thyroid autoimmunity. Endocr Rev. 2014;35(1):59-105. doi:10.1210/er.2013-1055
[2] Kurup S, Pozun A. Biochemistry, Autoimmunity. [Updated 2021 Dec 29]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK576418/
[3] Romagnani S. Immunological tolerance and autoimmunity. Intern Emerg Med. 2006;1(3):187-196. doi:10.1007/BF02934736
[4] McLachlan SM, Rapoport B. Breaking tolerance to thyroid antigens: changing concepts in thyroid autoimmunity. Endocr Rev. 2014;35(1):59-105. doi:10.1210/er.2013-1055
[5] Chaker L, Bianco AC, Jonklaas J, Peeters RP. Hypothyroidism. Lancet. 2017;390(10101):1550-1562. doi:10.1016/S0140-6736(17)30703-1
[6] Mincer DL, Jialal I. Hashimoto Thyroiditis. [Updated 2022 Jun 21]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459262/
[7] Armstrong M, Asuka E, Fingeret A. Physiology, Thyroid Function. [Updated 2022 Mar 18]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537039/
[8] Mousa WK, Chehadeh F, Husband S. Recent Advances in Understanding the Structure and Function of the Human Microbiome. Front Microbiol. 2022;13:825338. Published 2022 Feb 3. doi:10.3389/fmicb.2022.825338
[9] Dekaboruah E, Suryavanshi MV, Chettri D, Verma AK. Human microbiome: an academic update on human body site specific surveillance and its possible role. Arch Microbiol. 2020;202(8):2147-2167. doi:10.1007/s00203-020-01931-x
[10] Fröhlich E, Wahl R. Microbiota and Thyroid Interaction in Health and Disease. Trends Endocrinol Metab. 2019;30(8):479-490. doi:10.1016/j.tem.2019.05.008
More References!
[11] Guastamacchia E, Giagulli VA, Licchelli B, Triggiani V. Selenium and Iodine in Autoimmune Thyroiditis. Endocr Metab Immune Disord Drug Targets. 2015;15(4):288-292. doi:10.2174/1871530315666150619094242
[12] Calomme M, Hu J, Van den Branden K, Vanden Berghe DA. Seleno-lactobacillus. An organic selenium source. Biol Trace Elem Res. 1995;47(1-3):379-383. doi:10.1007/BF02790140
[13] Kriss M, Hazleton KZ, Nusbacher NM, Martin CG, Lozupone CA. Low diversity gut microbiota dysbiosis: drivers, functional implications and recovery. Curr Opin Microbiol. 2018;44:34-40. doi:10.1016/j.mib.2018.07.003
[14] Ishaq HM, Mohammad IS, Guo H, et al. Molecular estimation of alteration in intestinal microbial composition in Hashimoto’s thyroiditis patients. Biomed Pharmacother. 2017;95:865-874. doi:10.1016/j.biopha.2017.08.101
[15] Li J, Sung CY, Lee N, et al. Probiotics modulated gut microbiota suppresses hepatocellular carcinoma growth in mice. Proc Natl Acad Sci U S A. 2016;113(9):E1306-E1315. doi:10.1073/pnas.1518189113
[16] Sorathia SJ, Chippa V, Rivas JM. Small Intestinal Bacterial Overgrowth. [Updated 2022 Oct 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK546634/
[17] Lauritano EC, Bilotta AL, Gabrielli M, et al. Association between hypothyroidism and small intestinal bacterial overgrowth. J Clin Endocrinol Metab. 2007;92(11):4180-4184. doi:10.1210/jc.2007-0606
[18] Spaggiari G, Brigante G, De Vincentis S, et al. Probiotics Ingestion Does Not Directly Affect Thyroid Hormonal Parameters in Hypothyroid Patients on Levothyroxine Treatment. Front Endocrinol (Lausanne). 2017;8:316. Published 2017 Nov 14. doi:10.3389/fendo.2017.00316
[19] Talebi S, Karimifar M, Heidari Z, Mohammadi H, Askari G. The effects of synbiotic supplementation on thyroid function and inflammation in hypothyroid patients: A randomized, double‑blind, placebo‑controlled trial. Complement Ther Med. 2020;48:102234. doi:10.1016/j.ctim.2019.102234
