Thyroid and gut: how they influence each other

Your values are adjusted. The TSH is where it should be. And still your belly is not calm.

Maybe it is the constipation that has been part of your life for years. Maybe bloating that comes every afternoon. Maybe a dose that creeps upward in small steps, without anyone being able to say why.

Many people with Hashimoto's know this pattern. And many have already heard two sentences about it, neither of which gets them any further. One goes: that has nothing to do with the thyroid. The other: it's your gut, do a gut restoration program.

I would like to show you a third view here. It is less exciting than the second. But it can be measured, and it often leads to questions nobody has asked in your case yet.

Two organs, one conversation in both directions

Imagine your digestive tract as a long postal route. The thyroid is the pacemaker that decides how fast the parcels move. The gut is the post office that decides what gets delivered. If the pace is off, the parcels pile up or rush through. If the post office is not working, nothing arrives despite a perfect pace.

Direction one runs from hormone to gut. Thyroid hormones can influence the pace of the smooth muscle and the nerve network in the gut wall and influence mucosal secretion and sensation in the rectum. Direction two runs from gut to hormone: via absorption, via the cycle between liver, bile and gut, and via the immune system.

From the perspective of Clinical Psychoneuroimmunology, these are four lenses on the same process. The hormonal lens sees transit time. The nervous lens sees the enteric nervous system, the gut brain, which can work more sluggishly with too little hormone. The immune lens sees that an autoimmune disease rarely comes alone. And the metabolic lens sees the question of what from the tablet and from the plate actually arrives in the blood.

Two reviews describe the basic pattern. With hypothyroidism, reduced motility can lead to constipation, up to ileus, megacolon or, rarely, pseudo-obstruction, and according to Ebert symptoms usually improve when the thyroid disease is treated (Ebert 2010). Daher and colleagues emphasize that both hormone excess and hormone deficiency can cause diarrhea, through different mechanisms, and that celiac disease is among the most common accompanying digestive diseases (Daher 2009). Reviews Diarrhea alone therefore does not reveal in which direction the thyroid has gone off track.

So you do not read things twice: why the immune system attacks the thyroid in Hashimoto's is covered in Understanding Hashimoto's thyroiditis. Which lab values matter is covered in Reading thyroid values correctly. If your values are good and you still do not feel that way, normal values, still symptoms takes it further.

And now you know why this article does not start with the microbiome, but with a map.

Direction one: when the thyroid sets the pace in the gut

Three days without a bowel movement, and that for years. Or the opposite: for a few weeks five times a day, along with palpitations and a weight that drops for no reason.

Both can have to do with the thyroid. Thyroid hormones can help determine the metabolic rate of the muscle cells in the gut wall and their nerve network. Too little hormone is like a conveyor belt at half power, too much like one at the highest setting.

Hypothyroidism: when everything takes longer

Even subclinical hypothyroidism, visible only in the TSH, can change the gastric rhythm. In 20 women with subclinical hypothyroidism, a symptom score and two parameters of disturbed gastric rhythm were higher than in 20 healthy women. After six months on levothyroxine, all three improved and reached values similar to those of the healthy women (Canpolat 2013). Controlled prospective study, n=40

Salt and water transport in the mucosa also plays a part. Rat Rats with induced hypothyroidism showed a longer transit time and more chloride absorption in the small intestine, and serum T4 correlated with net chloride transport at minus 0.74 (Tenore 1996). This has not been shown directly in humans.

Hyperthyroidism: when the belt runs too fast

With hyperthyroidism, passage from the mouth to the beginning of the large intestine can be accelerated, leaving the gut less time to absorb water and fat. According to Ebert, increased appetite and an activated sympathetic nervous system come on top, which can favor fatty stools. The most common cause of hyperthyroidism is Graves' disease, according to the same review 60 to 80 percent of cases, more on this in Graves' disease and hyperthyroidism. The often quoted figure that up to a quarter have diarrhea I leave out, because no primary source could be found.

If constipation has been with you for a long time, the broader view in Constipation from a holistic perspective is worthwhile. If it is mainly the stomach that is sluggish, delayed gastric emptying takes it further.

When the values are right and the diarrhea stays

SIBO and hypothyroidism: three studies, three stories

A belly that rises after eating like yeast dough is familiar to many people with Hashimoto's. One possible lead is small intestinal bacterial overgrowth, SIBO for short. That is plausible, because the cleansing waves that sweep the small intestine between meals depend on pace. Still, the studies do not tell a consistent story.

Story two. Brechmann and colleagues analyzed 1,809 hydrogen breath tests from one center. Among the factors linked to overgrowth were hypothyroidism with an odds ratio of 2.6 and levothyroxine treatment with 3.0, in a simplified model the strongest single factor. The authors themselves state that the factors they found do not sufficiently explain the development of overgrowth (Brechmann 2017). Retrospective cohort, n=1,809 This is an association and explicitly no reason to question the tablet.

Story three. Wei and colleagues found overgrowth in duodenal samples in 32.65 percent of people with hypothyroidism versus 15.17 percent of controls. In a large database, the ten year risk was increased in two hypothyroidism groups, with relative risks of 2.20 and, in autoimmune thyroiditis, 2.40. On levothyroxine this risk appeared reduced, with values of 0.33 and 0.78 (Wei 2026). Cross-sectional plus registry cohort This points in the opposite direction to story two.

A fourth, often cited study without a control group found overgrowth in 65.3 percent of 75 people with hypothyroidism and irritable bowel syndrome, and after switching to liquid levothyroxine the TSH was more often in the target range, at 77.55 versus 57.14 percent (Henderson 2024). This is a hypothesis and not proof, and a change of formulation is a medical decision.

How overgrowth is diagnosed and treated is covered in SIBO in the small intestine, why it can come back in SIBO relapse and motility, and for constipation with methane, methane producing gut bacteria takes it further.

And now you know why constipation with hypothyroidism is a clue and not a verdict.

Direction two, first station: the building blocks have to arrive first

You have been taking iron for months. Your ferritin barely moves. At some point you ask yourself where it is all going.

The thyroid has a short list of ingredients: iodine as the material of the hormone, selenium in the conversion and protective enzymes, iron at the center of thyroid peroxidase, zinc at the hormone receptor. What each building block does is covered in Selenium, zinc, iron and vitamin D. Here it is about the question before that. The best delivery is of no use if the gate is stuck, and every station in the digestive tract has its own way of sticking.

The stomach: when acid is lacking

The parietal cells of the stomach lining produce hydrochloric acid and the intrinsic factor for vitamin B12. In autoimmune gastritis, the immune system attacks exactly these cells. Iron needs acid to reach its readily absorbable form, which is why such gastritis can show up first as iron deficiency and only later as B12 deficiency.

How common the marker for this is was shown by a cohort of 2,016 women and 258 men with autoimmune thyroiditis. Antibodies against parietal cells were found in 29.7 percent of the women, rising from 13 percent in the first and second to 42 percent in the ninth decade of life, and in 29.8 percent of the men (Checchi 2010). Cohort, n=2,274 Antibodies, however, are not the same as gastritis. The often quoted claim that up to 30 percent of people with Hashimoto's have autoimmune gastritis confuses exactly these two things. A meta-analysis of 56 studies found a second overt autoimmune disease in 13.46 percent of people with autoimmune thyroid disease, above all type 1 diabetes and autoimmune gastritis (Botello 2020). Meta-analysis, 56 studies

Helicobacter: two meta-analyses, two statements

In 2013, Shi and colleagues found in seven studies a clear association between Helicobacter and Graves' disease, odds ratio 4.35, but no significant one for Hashimoto's, 1.45 with a confidence interval of 0.92 to 2.26. In 2017, Hou and colleagues found with fifteen papers an odds ratio of 2.16 for Hashimoto's and 2.78 for Graves' disease. Meta-analyses Hou concludes from this that eradication could lower thyroid antibodies. I do not adopt this conclusion, because the data show associations and not treatment effects. Whether a detected germ should be treated is a separate weighing of pros and cons, described in Helicobacter pylori: treat it or leave it?

Iron as a shared final pathway

A meta-analysis of 18 studies found biopsy-confirmed celiac disease in 3.2 percent of people with iron deficiency anemia, roughly one in every thirty-one (Mahadev 2018). Meta-analysis, 18 studies More on this in Iron deficiency due to malabsorption, in Iron, inflammation and hepcidin and in Acid blockers and iron absorption.

The small intestine in inflammatory bowel disease

In Crohn's disease and ulcerative colitis, the mucosa itself is altered. A meta-analysis found zinc deficiency in 54 percent of people with Crohn's disease and in 41 percent with ulcerative colitis, with the overall estimate showing very high heterogeneity, I² = 96 percent (Zupo 2022). Meta-analysis, 9 studies On top of that comes a general principle that this study does not quantify: inflammation can lower serum zinc, even without empty stores. Selenium and zinc can also be low in Crohn's disease in remission, but the data are too inconsistent for practical rules (McDonnell 2023). Systematic review A genetic analysis found no causal relationship between inflammatory bowel disease and Hashimoto's, in either direction (Ding 2025). The two share absorption routes rather than a cause. An integrative view is given in Crohn's disease and ulcerative colitis, integrative.

Iodine: an honest short paragraph

This research found no human study that quantifies a gut-related impairment of iodine absorption. Two reviews describe that gut bacteria can influence the uptake and cycling of iodine (Fröhlich 2019, Knezevic 2020). This is mechanistically plausible and thin in humans. How much iodine the thyroid needs is covered in Putting iodine in perspective.

And now you know why a ferritin that does not budge can also tell you something about your thyroid tablet.

Direction two, second station: why the tablet depends on the stomach

The dose fit for years. Then the TSH rises without you having changed anything. The dose is increased, and half a year later again.

That coffee, calcium, iron, fiber and some medications can interfere with absorption is well known, and these interfering factors with their time gaps are covered in Symptoms despite levothyroxine. Here it is about the view that is only touched on there: the stomach and the gut themselves. Because there is a paradox. Levothyroxine is absorbed in the small intestine, and yet its absorption depends on the stomach.

The why: a tablet first has to dissolve

Think of sugar. In hot tea it disappears in seconds, in cold water it stays on the bottom for a long time. For the levothyroxine tablet, stomach acid is the hot water. Only what has dissolved in the stomach can be absorbed by the small intestine afterwards. In vitro In laboratory testing of three levothyroxine products, dissolution decreased markedly as pH rose, while the soft gel capsule barely reacted (Pabla 2009). This explains the mechanism, not the size of the effect in humans.

How low stomach acid can show itself, even when it looks like heartburn, is covered in Hypochlorhydria and in Low stomach acid. I deliberately give no advice on betaine HCl in connection with levothyroxine. There is no study on it, and any change that affects absorption would need a TSH check anyway.

Helicobacter, lactose, colitis, celiac disease: the same pattern in different places

The foundational 2006 study on the stomach and the tablet examined 248 people with nodular goiter, not with Hashimoto's, which is easy to overlook. With Helicobacter gastritis, atrophic gastritis or both, the daily requirement was 22 to 34 percent higher, and on omeprazole the TSH rose in all ten people examined (Centanni 2006). Cohort, n=248

Lactose intolerance. Of 34 people with Hashimoto's hypothyroidism and lactose intolerance who were not on a lactose free diet, only five reached their target TSH with a dose similar to that in Hashimoto's alone. The rest needed a median of 38 percent more, 31 percent with isolated lactose intolerance and 55 percent more with additional gastrointestinal disorders (Cellini 2014). Cohort, n=34 The ETA guideline names lactose malabsorption as the most common disorder affecting the availability of levothyroxine. How intolerances are tested is covered in Lactose, fructose, sorbitol.

Ulcerative colitis. In 12 of 13 people with hypothyroidism and ulcerative colitis in remission, the dose had to be increased, by a median of 26 percent compared with matched controls (Virili 2019). Case-control, n=64 The group is small, but the finding still fits the picture.

Celiac disease. In Hashimoto's with atypical celiac disease, 21 people on a gluten free diet reached their target TSH after about eleven months without a dose increase, while those who did not stick to the diet needed a median of 49 percent more (Virili 2012). Cohort, n=103 The authors emphasize: impaired T4 absorption can be an opportunity to discover a previously overlooked celiac disease.

A review by the same research group calls impaired T4 absorption in the gastrointestinal tract an increasingly recognized cause of hypothyroidism that is difficult to adjust, which could be more common than assumed (Virili 2019, Endocrine Reviews). Review

Acid blockers, liquid formulations and the time of intake

A systematic review found a rise in TSH in each of seven studies with concurrent use of levothyroxine and proton pump inhibitors, significant in most, although the overall data base is small (Guzman-Prado 2021). Systematic review, 7 studies This sentence matters to me: acid blockers are not prescribed without reason. For reflux disease, a stomach ulcer or as stomach protection, they have their place. Do not stop them on your own. At your next check-up, mention since when you have been taking them, so the TSH can be interpreted correctly.

The 2025 guideline of the European Thyroid Association says that with a TSH repeatedly above the reference range, after counseling on correct intake, switching to a liquid solution or soft gel capsule at an unchanged dose may be considered (recommendation 16a, strong recommendation with low quality of evidence). Guideline The data behind it are mixed. In 204 people with gastric diseases, the most recent TSH was above 3.5 in 18 percent on tablets and in 5 percent on the liquid formulation, collected retrospectively (Fallahi 2024). Cohort, retrospective, n=204 On omeprazole, a liquid formulation was absorbed bioequivalently, though in 36 healthy people after a single dose (Seng Yue 2024). RCT, crossover, n=36 A systematic review describes that solutions and soft gel capsules can bypass problems caused by binding and lack of acid, with mostly moderate study quality (Liu 2023). Systematic review A change of formulation also changes how much arrives, and it is a medical decision.

On timing, the same guideline recommends choosing it to fit the person's daily life and, for optimal efficacy, taking it consistently 60 minutes before breakfast or at bedtime, then at least three hours after the evening meal, and never with a gap of less than 30 minutes to food or drink (recommendation 4, strong recommendation). Guideline The reason is location. In small absorption tests, coffee lowered absorption by 36 and 27 percent, but not when drunk 60 minutes later (Benvenga 2008). Case Series, n=8 On calcium carbonate, mean TSH rose from 1.6 to 2.7 and fell to 1.4 after the calcium phase ended (Singh 2000). Cohort, n=20 Wheat bran bound levothyroxine nonspecifically in laboratory testing (Liel 1996). In vitro According to the review by Liu and colleagues, iron forms complexes with the hormone. All four can act in the stomach and upper small intestine. Do not change the time you take it on your own. Even a different gap to your coffee can change the amount absorbed, which is why TSH is measured again after every change.

And now you know why, when a dose does not fit the person, the stomach is one of the first questions.

Direction two, third station: microbiome and hormone metabolism, plausible and thin

Mechanistically plausible, human studies thin

You have read that a fifth of your T3 is produced in the gut. That sounds like a big lever. According to the evidence it is not that simple, but the idea has a genuine core.

The cycle between liver, bile and gut

The liver attaches part of the thyroid hormones to sulfate or glucuronic acid. That is something like a label reading: for disposal. With the bile, the labeled hormones reach the gut. And there, bacterial enzymes, sulfatases and glucuronidases, can unscrew the label again. The freed hormone can be absorbed again.

A review by Fenneman and colleagues describes exactly this route, and also that thyroid hormone can act directly on the cells of the intestinal mucosa via the TRα1 receptor. But it also states that the cause and effect mechanisms have yet to be proven (Fenneman 2023). Review In their review, Virili and Centanni call the influence of the gut flora on hormone balance a fascinating question, and that is exactly what it is: open (Virili and Centanni 2017). Review

Two further reviews describe that microbes have a say in iodine uptake, breakdown and the cycle via the bile, and that selenium, iron and zinc shape the relationship with the flora. Which bacteria matter and whether therapies targeting the flora achieve anything is less clear, they say, and sufficiently large human studies are needed (Fröhlich 2019, Knezevic 2020). Reviews

At this point the permeable gut wall, leaky gut, is often mentioned too. What is documented about it and where the limits lie is covered in Leaky gut and intestinal permeability.

And now you know why I find the microbiome fascinating and still do not ask about it first.

Direction two, fourth station: Hashimoto's and celiac disease

Someone recommends that you eat gluten free. It sounds sensible, like something you have in your own hands, and you would like to start tomorrow.

Why this matters so much here is shown by the numbers: Hashimoto's and celiac disease frequently occur together.

Conversely, according to the German guideline: autoimmune thyroiditis is found in about 4 to 10 percent of people with celiac disease, which is why an initial TSH measurement makes sense for them.

The guideline of the European Society for the Study of Coeliac Disease also lists Hashimoto's thyroiditis and Graves' disease among the groups in which serology is indicated, with biopsy only if the result is positive. The exception: for gastrointestinal symptoms together with an autoimmune disease and for iron deficiency anemia without another cause, its table lists endoscopy and small bowel biopsy even with negative serology (Al-Toma 2019). Guideline

With Hashimoto's and abdominal symptoms, a negative blood test is therefore not always enough. How testing works is covered in Recognizing celiac disease: diagnosis, testing and common mistakes.

Gluten free without celiac disease: what the data support

Whether people with Hashimoto's should eat gluten free even without celiac disease is covered in detail in Hashimoto's and nutrition. Here, just two pieces of work that are connected.

The often cited pilot study by Krysiak and colleagues followed 34 untreated women with Hashimoto's over six months, 16 ate gluten free, 18 did not. On the gluten free diet, thyroid antibodies fell. However, all 34 participants had incidentally detected positive tissue transglutaminase antibodies, that is, a sign of celiac disease, and the study was not randomized (Krysiak 2019). Controlled pilot study, n=34 It is therefore not a study of Hashimoto's without celiac disease. A meta-analysis by Piticchio and colleagues with four non randomized studies and 87 people without symptoms or findings of celiac disease found no significant reduction in antibodies, with p values of 0.06 for thyroglobulin and 0.07 for TPO antibodies. Important for context: it includes the Krysiak study, and 47 of the 87 people had a gluten related finding. The authors see a possible benefit mainly in this group, but do not consider the data sufficient to recommend this diet to all people with Hashimoto's without celiac disease (Piticchio 2023). Meta-analysis, 4 studies, n=87

Anyone who reacts to gluten without celiac disease still experiences that as real. What gliadin, wheat sensitivity and the gut wall have to do with it is covered in Gluten and gliadin without celiac disease.

The bridge: why celiac disease changes three things at once

Undetected celiac disease can alter the small intestine and thereby touch three things at once: the absorption of iron and other building blocks, the absorption of the tablet, as the 49 percent higher requirement without dietary adherence suggests, and it is a second autoimmune disease that needs attention of its own.

This also leads to a safety consideration. If celiac disease is found and the diet is changed, absorption can improve. In the study by Virili and colleagues, the target TSH was reached on a gluten free diet without a dose increase. A previously suitable dose can then become too high. That is why a TSH check belongs after such a change.

And now you know why, with gluten, the order matters more than the decision itself.

The microbiome studies in Hashimoto's and Graves' disease: findings and contradictions

You read that something is missing from your gut flora. Shortly afterwards you get an offer for a stool test, then a package of capsules. Before that, it is worth looking at what the studies found. The short answer: there are differences, but they do not point in the same direction.

Zhao and colleagues compared the stool flora of 28 people with Hashimoto's and 16 healthy people, with a second validation group. Diversity was similar, composition was not: Blautia, Roseburia and Dorea were increased, Faecalibacterium, Bacteroides and Prevotella_9 reduced. Cross-sectional, n=44 The meta-analysis by Gong with eight studies found increased diversity in Hashimoto's and reduced diversity in Graves' disease. Meta-analysis, 8 studies The meta-analysis by Alkader with 16 studies came to a different picture: in Graves' disease only the Simpson index was clearly lower, in Hashimoto's all other indices were significantly higher, with more Prevotella and bifidobacteria. Meta-analysis, 16 studies

The picture is most consistent for Graves' disease. A meta-analysis of ten studies found reduced diversity in three indices, with standardized mean differences of minus 0.58 for Chao1, minus 0.64 for ACE and minus 0.71 for Shannon, with high heterogeneity (Zufry 2024). Meta-analysis, 10 studies A Mendelian randomization found individual protective and harmful bacterial groups for Hashimoto's, for example the order Lactobacillales with an odds ratio of 0.759, but many p values lie just below 0.05, and a correction for multiple testing is not evident in the abstract (Zheng 2025). Mendelian randomization This generates hypotheses, not certainty.

Probiotics and gut restoration: what randomized trials have shown

And then the question that is often asked online: gut restoration for Hashimoto's. No study that tested a gut restoration program as a treatment for Hashimoto's could be found. The available data allow neither the conclusion that gut restoration reliably lowers antibodies nor that it halts the course of the disease. Such a promise goes beyond any existing study.

That does not mean the flora does not matter. Constipation can improve on synbiotics, and a gut that works well can make everyday life easier. More on fiber and resistant starch is covered in Prebiotics and resistant starch. Because fiber can affect absorption of the tablet, a larger dietary change should be discussed and the TSH checked afterwards. What is documented about thyroid antibodies themselves is covered in Lowering Hashimoto's antibodies.

And now you know why, when offered a stool test, I first ask which decision its result would change.

What this means in practice when levothyroxine does not work as expected

Maybe you are at the point where the next dose increase is due. And you are wondering whether it will always go on like this.

This is where the threads come together, as directions and not as a recipe. What makes sense for you depends on your findings.

The word adherence sounds like an accusation and is not one. A tablet every morning on an empty stomach, with a gap to your coffee, over years, is hard, and everyday life gets in the way. Answering this question honestly sometimes spares a whole chain of tests.

Three doors along the same corridor

Once this question is settled, there are three doors along the corridor that I would open first. They have three things in common: they are common, they are measurable, and each can affect absorption of the tablet and the building blocks at the same time.

Why these three in particular? Because they come up again and again in the data: the stomach in Virili 2022, Checchi 2008 and Centanni 2006, celiac disease in the guideline, in Virili 2012 and Mahadev 2018, iron in Hershko 2014 and Cellini 2017. And because each door can lead to a condition that deserves its own treatment, independent of the thyroid.

If you would like not just to read this, but to sort it out with a view to your own findings: below this article you will find the option to book an appointment.

And now you know why, when a dose does not fit, I ask about the stomach first and only then about the gut flora.

Frequently asked questions about the thyroid and the gut

Where this topic leads next

The thyroid and the gut touch many other topics. From here, these paths lead further.