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The thyroid-gut connection

http://thehealthyskeptic.org/

Hippocrates said: " All disease begins in the gut. " 2,500 years later we're just

beginning to understand how right he was. And, as I'll explain in this article,

hypothyroidism is no exception. Poor gut health can suppress thyroid function

and trigger Hashimoto's disease, and low thyroid function can lead to an

inflamed and leaky gut – as illustrated in the following diagram:

The gut-thyroid-immune connection

Have you ever considered the fact that the contents of the gut are outside the

body? The gut is a hollow tube that passes from the mouth to the anus. Anything

that goes in the mouth and isn't digested will pass right out the other end.

This is, in fact, one of the most important functions of the gut: to prevent

foreign substances from entering the body.

Another important function of the gut is to host 70% of the immune tissue in the

body. This portion of the immune system is collectively referred to as GALT, or

gut-associated lymphoid tissue. The GALT comprises several types of lymphoid

tissues that store immune cells, such as T & B lymphocytes, that carry out

attacks and produce antibodies against antigens, molecules recognized by the

immune system as potential threats.

Problems occur when either of these protective functions of the gut are

compromised. When the intestinal barrier becomes permeable (i.e. " leaky gut

syndrome " ), large protein molecules escape into the bloodstream. Since these

proteins don't belong outside of the gut, the body mounts an immune response and

attacks them. Studies show that these attacks play a role in the development of

autoimmune diseases like Hashimoto's.

We also know that thyroid hormones strongly influence the tight junctions in the

stomach and small intestine. These tight junctions are closely associated areas

of two cells whose membranes join together to form the impermeable barrier of

the gut. T3 and T4 have been shown to protect gut mucosal lining from stress

induced ulcer formation. In another study, endoscopic examination of gastric

ulcers found low T3, low T4 and abnormal levels of reverse T3.

Likewise, thyrotropin releasing hormone (TRH) and thyroid stimulating hormone

(TSH) both influence the development of the GALT. T4 prevents over-expression of

intestinal intraepithelial lymphocytes (IEL), which in turn causes inflammation

in the gut.

The gut-bacteria-thyroid connection

One little known role of the gut bacteria is to assist in converting inactive T4

into the active form of thyroid hormone, T3. About 20 percent of T4 is converted

to T3 in the GI tract, in the forms of T3 sulfate (T3S) and triidothyroacetic

acid (T3AC). The conversion of T3S and T3AC into active T3 requires an enzyme

called intestinal sulfatase.

Where does intestinal sulfatase come from? You guessed it: healthy gut bacteria.

Intestinal dysbiosis, an imbalance between pathogenic and beneficial bacteria in

the gut, significantly reduces the conversion of T3S and T3AC to T3. This is one

reason why people with poor gut function may have thyroid symptoms but normal

lab results.

Inflammation in the gut also reduces T3 by raising cortisol. Cortisol decreases

active T3 levels while increasing levels of inactive T3. 1

Studies have also shown that cell walls of intestinal bacteria, called

lipopolysaccharides (LPS), negatively effect thyroid metabolism in several ways.

LPS:

reduce thyroid hormone levels;

dull thyroid hormone receptor sites;

increase amounts of inactive T3;

decrease TSH; and

promote autoimmune thyroid disease (AITD).

Other gut-thyroid connections

Hypochlorhydria, or low stomach acid, increases intestinal permeability,

inflammation and infection (for more on this, see my series on acid reflux &

GERD). Studies have shown a strong association between atrophic body gastritis,

a condition related to hypochlorhydria, and autoimmune thyroid disease.

Constipation can impair hormone clearance and cause elevations in estrogen,

which in turn raises thyroid-binding globulin (TBG) levels and decreases the

amount of free thyroid hormones available to the body. On the other hand, low

thyroid function slows transit time, causing constipation and increasing

inflammation, infections and malabsorption.

Finally, a sluggish gall bladder interferes with proper liver detoxification and

prevents hormones from being cleared from the body, and hypothyroidism impairs

GB function by reducing bile flow.

Healing the gut-thyroid axis

All of these connections make it clear that you can't have a healthy gut without

a healthy thyroid, and you can't have a healthy thyroid without a healthy gut.

To restore proper function of the gut-thyroid axis, both must be addressed

simultaneously.

Healing the gut is a huge topic that can't be covered adequately in a few short

sentences. But I will say this: the first step is always to figure out what's

causing the gut dysfunction. As we've reviewed in this article, low thyroid is

one possible cause, but often hypochlorhydria, infections, dysbiosis, food

intolerances (especially gluten), stress and other factors play an even more

significant role. The second step is to address these factors and remove any

potential triggers. The third step is to restore the integrity of the gut

barrier. My preferred approach for this last step is the GAPS diet.

The influence of thyroid hormones on the gut is one of many reasons why I

recommend that people with persistently high TSH and low T4 and T3 take

replacement hormones. Low thyroid hormones make it difficult to heal the gut,

and an inflamed and leaky gut contributes to just about every disease there is,

including hypothyroidism. Fixing the gut is often the first – and most important

– step I take with my patients.

Stockigt, JR and Baverman LE. Update on the Sick Euthyroid Syndrome. Diseases of

the Thyroid. Humana Press, Totowa, NJ, 1997, pp.49-68 & #8617;

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I think this is also discussed in this book:

http://www.amazon.co.uk/Still-Thyroid-Symptoms-Tests-Normal/dp/1600376703/ref=sr\

_1_1?ie=UTF8 & s=books & qid=1291289943 & sr=8-1

i think it was that book, i can't be 100% sure tho, memory's not so good

chris

>

> The thyroid-gut connection

>> The gut-bacteria-thyroid connection

> One little known role of the gut bacteria is to assist in converting inactive

T4 into the active form of thyroid hormone, T3. About 20 percent of T4 is

converted to T3 in the GI tract, in the forms of T3 sulfate (T3S) and

triidothyroacetic acid (T3AC). The conversion of T3S and T3AC into active T3

requires an enzyme called intestinal sulfatase.

>

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