Gut-Thyroid connection: How to fix your thyroid through your gut

Thyroid medication is one of the most over-prescribed medication as of yet.

Not that it’s a bad thing, such as SSRIs or other harmful meds, but it’s not always useful.

How many people do you know that are using thyroid and not improving?

I sure know of quite a few.

It’s not that I’m against thyroid, I think it can be very helpful if used correctly, however, using it wrongly can actually make things worse.

And what I want to talk about is the gut-thyroid connection.

The gut-thyroid connection

Nothing is the body works in isolation and with that being said; whatever is negatively influencing the gut, can have a negative effect on the thyroid.

Thus if you have inflammation in the body which originates from the gut, taking thyroid because of hypothyroid symptoms might not do the trick.

The gut influences thyroid hormone production and functions in a few ways.

Gut inflammation

Hashimoto’s thyroiditis (HT) is the most common thyroid disorder worldwide with a general prevalence of around 10–12% and is characterized by chronic inflammation, autoantibodies against thyroid peroxidase (TPO) and thyroglobulin (TG), leading to hypothyroidism, and often, destruction of the thyroid gland.

Graves’ disease (GD) has a prevalence of 1–1.5% and is marked by autoantibodies against the thyroid stimulating receptors (TSHR), causing hyperactivity of the thyroid.

I’m pointing out these two conditions because they’re both linked to gut dysbiosis and chronic gut inflammation.

Inflammation in the gut causes quite a few issues. It can cause inadequate digestion (and these undigested particles can then absorbed through a leaky gut), stomach ulcers, leaky gut, the proliferation of pathogenic bacteria, such as H. pylori, E. Coli, etc., damage to the small intestine (thus reducing the absorption of micros), immune responses (which cause inflammation and damage the thyroid gland), etc.

Gut inflammation is one of the last things you want on your journey to optimizing thyroid function.

Thyroid and intestinal diseases prevalently coexist—Hashimoto’s thyroiditis (HT) and Graves’ disease (GD) are the most common autoimmune thyroid diseases (AITD) and often co-occur with Celiac Disease (CD) and Non-celiac wheat sensitivity (NCWS).

Patients with Hashimoto’s thyroiditis showed significantly higher inflammatory markers, such as serum IL-17 compared with controls (R).

Gut dysbiosis in thyroid disorders

Gut dysbiosis is a condition where there is an increase in gut inflammation, a decrease in the “beneficial” gut bacteria and an increase in harmful, inflammation and carcinogenic gut bacteria.

Here are a few studies that looked at the composition of gut bacteria in people with thyroid issues.

Zhao et al. and Ishaq et al. investigated the microbial composition in euthyroid and hypothyroid HT patients and found dysbiosis as well as bacterial overgrowth in the hypothyroid patient group (R).

Patients with Hashimoto’s thyroiditis showed a significantly higher serum IL-17 compared with controls, and those infected with Blastocystis hominis had the highest levels of IL-17 (R). Treating BH (Blastocystis hominis (BH) – the most common intestinal protozoan isolated in humans) infection using 500 mg nanazoxid 3 tablets/day for 3 days, showed that IL-17 was significantly negatively correlated with fT3 and significantly positively correlated with anti-TPO.

Here is their conclusion:

Treatment of BH infection ameliorates HT through reduction in IL-17, anti-TPO, and TSH.

Furthermore, dysbiosis has not only been found in autoimmune thyroid diseases, but has also been reported in thyroid carcinoma, in which an increased number of carcinogenic and inflammatory bacterial strains were observed (R).

Hypothyroid patients are most often constipated (longer gastrointestinal (GI) transit time) and this causes microbiota species diversity to increase and the risk of overgrowth of a pathogenic bacteria (R). One of the best ways to improve intestinal health is to speed up transit time, with something like cardamoms, rhubarb, senna, magnesium, aloe vera, etc.

Another three examples include:

For example, some phylotypes belonging to the class Bacteriodales showed increases in response to Se (e.g., Porphyromonadaceae phylotypes 1 and 3, Tanerella phylotype 2), whereas others, such as Alistipes phylotype 1 and Parabacteroides phylotype 3 (of the phylum Bacteriodetes) declined. Relative to absolute abundance, the decline in Parabacteroides in response to Se in the diet was by far the most significant effect on the microbiota.


A detailed fecal microbiota Mann-Whitney U-test (Q value <0.05) revealed that the abundance levels of Blautia, Roseburia [Roseburia is significantly related to total grain], Ruminococcus_torques_group, Romboutsia, Dorea, Fusicatenibacter, and Eubacterium_hallii_group genera were increased in HT patients, whereas the abundance levels of Fecalibacterium, Bacteroides, Prevotella_9, and Lachnoclostridium genera were decreased. 


We observed the declined abundance of Prevotella_9 and Dialister, while elevated genera of the diseased group included Escherichia-Shigella and Parasutterella. The alteration in gut microbial configuration was also monitored at the species level, which showed an increased abundance of E. coli in HT.


Instead of thinking one bacteria is bad and another good and how do we modulate it, we must realize that these alterations are a result of their current diet or of their diet at the time of the test.

These microbial profiles above are a result of eating a lot of junk food, such as cereals, baked goodies, high PUFA foods, lots of refined flours and sugars, food with fortified iron, high fat diet, micronutrient devoid food, etc.

These people with these microbial changes just have to change their current inflammatory diet to a healthier non-reactive diet and their gut bacteria will re-modulate and inflammation will drop.

Harmful inflammatory food can:

  • Slow transit time
  • Irritate the gut lining, which will create an excess of serotonin, which is implicated in many inflammatory conditions.
  • Create gut permeability
  • Lower the “beneficial” gut bacteria
  • Increase the harmful bacteria
  • Cause an immune response and subsequent inflammation
  • etc.

Just by eliminating the problematic foods can dramatically resolve the inflammation and in most cases, additional treatment isn’t even needed.

Fix the diet and gut inflammation will drop and thyroid function will improve.

Interestingly, in this study, taking a probiotic with the “beneficial” bacteria, namely Bifidobacterium spp. and Lactobacillus spp., didn’t change susceptibility or improve hypothyroidism in HT patients (R).

However, this study found that synbiotic supplementation (a combination of pro- and pre-biotics) showed beneficial effects on patients with hypothyroidism by significantly reducing TSH, levothyroxine dose and fatigue, and increasing fT3 (R).

So there might be some validity to probiotic supplementation, however, rather rely on diet than trying to patch things with probiotics.

Leaky gut-thyroid connection

A very high percentage of people with Hashimoto’s thyroiditis or just hypothyroidism in general have leaky gut. This can be caused by gluten, lectins, SIBO, nutrient deficiencies, etc.

Leaky gut is when the intestine allows undigested food particles, toxic waste products, bacteria and bacterial products, etc., to “leak” through the intestines and flood the bloodstream. Then the immune system reacts with it and causes an immune response and massive inflammation or cross-react with extraintestinal tissues, such as the thyroid gland.

Either way, this damages the thyroid gland and reduces its function.

Resolving gut inflammatory and restoring the gut lining is one way to improve thyroid function.

Endotoxin-thyroid connection

Endotoxins, also known as Lipopolysaccharides, are found in the outer membrane of Gram-negative bacteria. They are large molecules consisting of a lipid and a polysaccharide composed of O-antigen, outer core and inner core joined by a covalent bond. Different bacteria can create different kinds of endotoxins, some being much more inflammatory than others.

Endotoxins can antagonize thyroid function through a variety of way.

#1 By increasing inflammation (through activation of the endotoxin receptor TLR4). Endotoxins suppress thyroid hormone production and can result in hypothyroid symptoms, such as fatigue, water retention, low androgen symptoms, etc (R). TLR4 activation by LPS triggers thyroiditis development in mice (R).

Endotoxins also induces expression of the sodium-iodine symporter (NIS) in thyroid cells, which increases iodine uptake in the thyroid (R). 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 (R).

#2 Endotoxins inhibit the conversion of T4 into T3, by suppressing the enzyme, type 1 iodothyronine deiodinase (D1) (R).

#3 Endotoxins increase type 3 iodothyronine deiodinase (D3), which increases reverse T3 (rT3). rT3 directly blocks the effect of T3. So you might have enough T3 on your blood test, but if you don’t look at rT3, then you won’t know why you’re still experiencing hypothyroid symptoms.

#4 Endotoxins have been shown to decrease the expression of thyroid receptors, specifically in the liver (R, R).

As you can see, endotoxins are bad news. So the best way to lower endotoxins is to lower gram-negative bacteria (specifically the Enterobacteriaceae family) and you can do this by increasing transit time, lowering gut inflammation and using a few anti-microbial herbs such as cinnamon, turmeric, thyme, oregano, coconut oil, etc., combined with activated charcoal.

Gut-micronutrient-thyroid problem

The thyroid requires various micronutrients in order to work properly and produce adequate thyroid hormones. Micronutrients are also needed for the proper conversion of thyroid hormone T4 to T3, which is the active form.

Last by not least, micronutrients are needed for the cells in the body to function properly to execute the effects of thyroid hormones.

Micronutrients are vitamins and minerals. It’s micro, because it’s present in small amounts in foods. From micro to mg amounts. If you eat enough of a certain food, you might get several grams of certain micronutrients, such as calcium, potassium, phosphorus, etc.

A few micronutrients needed for proper thyroid function include:

  • Iodine
  • Iron
  • Copper
  • Zinc
  • Selenium
  • Vitamins A, B1, B2
  • Magnesium
  • Manganese
  • Potassium

As the bare minimum, focus on iron and copper (which are crucial for thyroid hormone synthesis), selenium and zinc (which are needed for converting T4 to T3), and vitamin A and D (which assists in regulating the immune response).

So if you have too little of these, then thyroid function will be compromised.

So what does the gut have to do with it?

If there is inflammation in the gut, then the absorption of these micros is reduced, because the villi in the gut (which is responsible for absorption), is small, damaged and reduced. Some bacteria in the gut can also use these micronutrients for themselves, which further lower the availability for you.

Thus we want to lower gut inflammation to restore proper gut function to absorb these essential micronutrients.

Many of these micronutrients also have an effect on the gut

For example, zinc, copper, selenium and iron can modulate the gut bacteria.

So the question comes in, are we hypothyroid because of gut dysbiosis or is the lack of micronutrient consumption together with harmful foods causing the gut dysbiosis and inflammation and is thus resulting in hypothyroid symptoms.

If we continue to eat junk or inflammatory foods, we’ll continue to have gut inflammation and micronutrient deficiencies despite the fact that we might be consuming enough of them.

So we need to eliminate the inflammatory foods, such as gluten, lectins, refined grains, high PUFA oil foods, etc., restore gut integrity and function (such as the villi) and then load up on micronutrients.

Zinc’s effect on the gut and thyroid

Zinc is an essential mineral that is highly abundant in animal foods, such as red meat, organ meat and oysters. Who do you know that is eating enough of these foods?

Not nearly enough since we’ve been brainwashed for so long to believe that red meat is bad and we should stick to one small portion per day. Now we all border on zinc deficiency.

Zinc is essential, because:

  • Intracellular zinc regulates intestinal permeability through occludin proteolysis and occludin transcription and is an essential promoter of normal intestinal barrier functions and the regeneration of impaired epithelium. Meaning, low zinc intake can cause leaky gut and poor gut integrity (R).
  • Under zinc-deficient states, the intestinal tight junction and membrane function is impaired which allows the migration of large number of neutrophils that leads to mucosal inflammation (R).
  • Zinc reduces the inflammation of intestinal mucosa (R).
  • Zinc has antibacterial effects and modulating properties.
    • It’s been seen that beneficial bacteria e.g. Lactobacillus and Streptococcus in the gut are increased with zinc supplementation (R).
    • Zinc supplementation in humans inhibits the growth of pathogenic Escherichia coli (R)
  • It enhances the immune system (R).
  • The enzymes the convert T4 into T3 uses zinc as a cofactor.
    • Low zinc can lead to low T4, low T3 and elevated rT3 (R, R, R, R).
    • Zinc deficiency impairs TRH synthesis and the release of TSH, T3, and T4.
    • Zinc influences T3 binding to nuclear receptors and binding of this receptor to DNA.

We need a good amount of zinc daily and plant sources are out of the question. Eat meat!

Copper’s effect on the gut and thyroid

Copper is also a very important mineral, not only for the gut, but also for anti-oxidant enzymes in the body, iron mobilization, energy production, neurotransmitter synthesis, thyroid hormone synthesis, etc.

Copper and thyroid hormones showed a strong positive correlation in early life (R), however, an excess can also lower T3 production (R).

If T3 is high, but serum copper is low, then someone might have thyroid hormone resistance (R).

Dietary copper plays an important role in maintaining intestinal barrier integrity and lowering oxidative stress (R).

Iron’s effect on the gut and thyroid

People with hypothyroidism might be prone to iron overload (high ferritin and low transferrin saturation), despite anemia (R, R). This can be due to low copper/ceruloplasmin and inflammation since inflammation increases ferritin and ceruloplasmin transports iron out of tissue (R, R).

Having enough copper available will help transport the iron to the right places such as the thyroid to aid in thyroid hormone production.

This study found that there was a significant correlation between T4, TSH and ferritin. Subjects with low serum ferritin (due to lower inflammation) had a higher ratio of T3/T4. Also, only (elevated) ferritin contributed significantly to rT3 concentration (R).

On the other hand, fortified iron or supplemental iron, which isn’t very well absorbed, can also negatively modulate the gut, allow the growth of pathogenic bacteria and contribute to gut inflammation.

Selenium’s effect on the gut and thyroid

Most people already know that selenium is needed for the conversion of T4 to T3.

But did you also know that:

  • Selenium is needed for glutathione peroxidase, deiodinase isoenzymes, and thioredoxin reductase—which protect the thyroid gland from free radicals.
  • The thyroid gland contains the highest amount of selenium in the body and under conditions of deficiency, it is able to retain selenium.
  • Selenium can modulate gut bacteria (R).
    • Epidemiological studies have suggested an inverse association between selenium levels and inflammatory bowel disease (R).

In patients with autoimmune thyroid diseases, selenium supplementation may reduce levels of antithyroid antibodies, improve thyroid structure, improve thyroid metabolism, and improve clinical symptoms (R).

Beef and lamb kidney, liver, red meat and seafood are fantastic sources of selenium. Now you know why people have thyroid issues. They don’t eat their meat!

Iodine’s effect on the gut and thyroid

Iodine is essential for the synthesis of thyroid hormones, however, our requirements aren’t high at all. Just 200-500mcg daily is enough unless our diet is high in halogens, such as fluoride, chlorine and bromine and other anti-thyroid compounds such as those found in some vegetables.

Excess intake of iodine triggers the Wolff-Chaikoff effect, a transient reduction of thyroid hormone synthesis for around 24 h after the ingestion of a high iodine load (R). High iodine intake additionally can either induce hypothyroidism in susceptible patients, such as those with autoimmune thyroid disease, antithyroid drug therapy, or patients with higher intake of goitrogens, but it can also cause hyperthyroidism in patients at risk, e.g., with diffuse nodular goiter or latent Grave’s disease (R).

As mentioned above, excess iodine intake together with elevated endotoxins and low selenium can contribute to Hashimoto’s.

If you eat high iodine food sources, such as milk, eggs and seafood (fish, shellfish, etc.), then you should be getting enough iodine through your diet.


There you have it, the gut-thyroid connection.

Don’t try to look at other methods to optimize thyroid if you don’t have a good strategy in place to sort out your gut.

To learn how to look after your gut, download this PDF that I’ve created with the top 6 tips on how to improve thyroid function naturally.


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