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This is a post I’ve been meaning to get to for a while now. Thyroid hormone impacts many areas of the body, including the GI tract, and in many cases the first symptoms of thyroid dysfunction are manifested here.


Courtesy Wikipedia

Courtesy: Wikipedia


To save myself a bit a typing, here is how I described the thyroid system in a previous post on stress and metabolism:

“The hypothalamus is the primary regulator of metabolic rate and does so through the hypothalamic-pituitary-thyroid axis. The hypothalamus secretes thyrotropin-releasing hormone (TRH) in a pulsatile fashion throughout the day. TRH, in turn, signals the pituitary gland to release thyroid-stimulating hormone (TSH). TSH causes the thyroid gland to release two forms of hormone, thyroxine, known more commonly as T4, and triiodothyronine, known as T3. Of the two types, T3 is from three to four times more metabolically active than T4.

Both types of thyroid hormone require iodine derived from diet for their production. Therefore, not getting enough iodine from your diet can impair synthesis of these vital hormones as can malabsorption caused by small gut dysbiosis. The enzyme responsible for converting T4 to T3 requires selenium, so low levels of this element due to low dietary intake or malabsorption will also interfere with thyroid hormone synthesis. Other elements like bromine can interfere with this system, but I’ll forgo discussing this for now.

The thyroid produces anywhere from 70% to 80% of T4 and 20% to 30% of T3. As previously mentioned, a certain quantity of T4 is converted in various peripheral tissues and organs to the more metabolically active T3 in a process known as deiodination. Of the organs responsible for this conversion, the liver and kidneys rank first and second. Note that both these organs are also responsible for the majority of detoxification functions in the body, and would be most vulnerable to damage caused by translocating gram-negative bacteria and their cell-wall remnants, lipopolysaccharides (LPSs).

Thyroid hormone increases metabolic rate, secretion of growth hormone and catecholamines. The catecholamines include dopamine, norephinephrine, and adrenaline.

Now this is an admittedly simplified overview of thyroid hormone synthesis and function. For example, there are differences between the amount of free or bound thyroid hormone in blood serum, the production of transport proteins by the liver, the level of metabolically inactive reverse T3, the extent and health of various thyroid receptors throughout the body, and the rate thyroid hormone is degraded and excreted.”

Now as I mentioned in that post, a lot can go wrong with this system, but for today’s purposes I’ll be focusing on three major disease states: hyperthyroidism, hypothyroidism and euthyroid sick syndrome (ESS).


Simply stated, hyperthyroidism is a condition of excessive thyroid hormone in the body. In general, metabolic processes are accelerated. In the majority of cases, elevated levels of thyroid hormone are caused by hyperactivity of the thyroid gland.

Other causes of hyperthyroidism include immoderate ingestion of thyroid hormone. In rare instances, excessive thyroid hormone secretion can come from ovarian tumors.

Graves’ disease is by far the most common form of hyperthyroidism. Females are five times more likely to suffer from Graves’ disease than men.

Graves’ disease is an autoimmune disorder with a strong family predisposition. 15% of patients with this disease have a close relative who also has the disorder. 50% of relatives of Graves’ patients also carry thyroid auto-antibodies.

In this disease, the immune system attacks the TSH receptors of the thyroid gland, which in turn causes growth of this gland and excess secretion of thyroid hormone. While there is clearly a genetic component to the disease, there are also environmental triggers. Some of these include:

  • pregnancy, especially in the period immediately after giving birth
  • iodine excess
  • elevated interferon alpha, an immune cytokine
  • viral or bacterial infection
  • stress

With the exception of iodine excess, these factors may impact or be affected by increased intestinal permeability or endotoxemia.

Some symptoms of this disorder include:

  • marked weight loss without loss of appetite
  • thyroid enlargement
  • eye and vision abnormalities
  • muscle weakness and loss of muscle mass
  • heart palpitations
  • nervousness
  • being easily fatigued
  • excessive muscle movement
  • excessive sweating
  • intolerance to heat

There are several digestive complaints common in this group of sufferers. Some complain of pain in the upper abdomen, usually while eating or right after. This is no doubt partly due to increased contractions in the esophagus. Many also complain of stomach fullness as well as excessive belching.

In the small intestine fat malabsorption is not uncommon as contractions here are accelerated, which reduces the time necessary for proper digestion. This in turn can lead to deficiencies in fat-soluble vitamins, as well as fat in stool (steatorrhea) akin to what is seen in small intestinal bacterial overgrowth (SIBO).

Up to 25% of those with hyperthyroidism have mild-to-moderate diarrhea and frequent bowel movements. As thyroid hormone regulates intestinal motility, this isn’t too surprising. The more frequent intestinal contractions, the faster chyme will move through the digestive tract and the less water will be reabsorbed by the body.

Gastrointestinal symptoms are further complicated by the fact that Graves’ patients are at a higher risk of developing autoimmune celiac disease. (1) In fact, given the also high prevalence of celiac in those who suffer from low thyroid function, I strongly suspect that gluten is a very strong environmental trigger for autoimmune thyroid disorders. This makes perfect sense given its role in increasing leaky gut via zonulin signaling, especially in those born with a genetic predisposition for celiac disease.

Graves’ disease sufferers are also at higher risk for developing ulcerative colitis. (2) Less prevalent associations with Crohn’s disease have also been noted. (3)


Whereas hyperthyroidism is characterized by too much thyroid hormone, those with hypothyroidism suffer from too little. As a result, these folks have metabolic processes that are too slow.

Hypothyroidism can be classified into four categories.

The first is known as primary hypothyroidism and is the most common. This is due to failure of the thyroid gland to produce enough thyroid hormone.

Secondary hypothyroidism is due to a deficiency of thyroid stimulating hormone (TSH) from the pituitary gland. Tertiary hypothyroidism is caused by deficiency of thyrotropin releasing hormone (TRH) from the hypothalamus. Finally, low-thyroid function may be caused by resistance to thyroid hormone in peripheral tissue.

Hypothyroidism has many causes. The autoimmune disorder known as Hashimoto’s thyroiditis is by far the most common cause in the developed world. In this disorder, the immune system attacks and destroys the thyroid gland.

Gluten intolerance is highly correlated with autoimmune thyroid disorders. About 43% of patients with Hashimoto’s carry genetic markers for celiac disease. (4)

In younger patients, Hashimoto’s is associated with a goiter, but not typically in adults. The end stage of Graves’ disease may also result in Hashimoto’s.

Outright iodine deficiency is not a typical cause of hypothyroidism in the developed world, but is still unfortunately common in poorer countries. There are those who claim that many in the developed world are suffering from sub-deficient iodine intake, but that it is masked by the lack of a goiter. I’ll leave that debate for others to engage in. That said, excessive iodine supplementation can itself cause hypothyroidism in those with preexisting autoimmune thyroid antibodies so caution must be exercised when supplementing with iodine.

Other causes of primary hypothyroidism include:

  • radioactive iodine therapy for Graves’ disease
  • partial or full removal of the thyroid gland (thyroidectomy)
  • genetic abnormalities in thyroid hormone synthesis
  • drugs: lithium, interferon-alpha, amiodarone (Nexterone)

Common causes of secondary hypothyroidism are benign tumor in the pituitary gland and full or partial pituitary destruction. Tertiary hypothyroidism is caused by dysfunction in the hypothalamus.

As thyroid hormone affects nearly every tissue in the human body, symptoms can be quite varied. In children and adolescents, hypothyroidism is characterized by retarded growth and short stature and many suffer from the following adult symptoms:

  • heart rate under 60 beats per minute (bradycardia)
  • higher total cholesterol, lipoprotein A and homocysteine levels
  • shallow, slow breathing
  • impaired kidney function
  • metabolic acidosis
  • anemia
  • severe muscle cramps and muscle weakness
  • low energy, feeling tired
  • inability to concentrate
  • insomnia
  • depression
  • dry skin
  • hypothermia or feeling cold, especially in the extremities
  • extreme agitation
  • infertility in women of child-bearing age
  • heavy and prolonged menstrual periods
  • decreased libido and erectile dysfunction in men
  • difficulty losing weight

Low thyroid function also results in a variety of digestive complaints. In the throat, it commonly causes oropharyngeal dysphagia, the medical term for difficulty in swallowing. It can also contribute to hiatal hernias.

It can cause heartburn or gastroesophageal reflux disease (GERD). This shouldn’t be too surprising as low thyroid function will result in delayed stomach emptying. (5) Couple this with too much dietary fiber that swells when in contact with gastric juices or general overeating, and the result can lead to GERD.

Low stomach acid production is another symptom of depressed thyroid function. (6) Low stomach acid will cause incomplete breakdown of protein increasing the risk of protein deficiency disorders. Persons with low stomach acid often complain of problems digesting protein-heavy meals.

As I explained in this post, stomach acid serves not only to break down protein, it also kills potentially harmful swallowed bacteria. Therefore, low stomach acid will predispose to small intestinal bacterial overgrowth.

Appetite is usually reduced in those with hypothyroidism, but weight gain is common due to fluid retention, and if untreated over a long period to lowered resting metabolism. Complaints of abdominal discomfort and bloating are also common.

Of major concern is the decrease in peristalsis or intestinal motility. Constipation is the major gastrointestinal complaint in this population. Up to 15% of those with hypothyroidism have fewer than three bowel movements weekly. (7) While relatively rare, it is not unheard of for constipation to become so bad that feces becomes impacted, requiring a visit to a doctor or the emergency room.

As I wrote in my SIBO series, the number-one cause of SIBO is impaired peristalsis. Just as thyroid hormone dysfunction impairs gastric barrier function increasing the risk of SIBO, reductions in intestinal motility will also predispose someone to developing SIBO, but from gram-negative bacteria migrating up from the colon.

This was the case with a woman who contacted me over a period of months. She told me that she had been successfully treated for SIBO by her physician. Nevertheless, she still experienced chronic constipation.

After making a number of suggestions, I didn’t hear from her for a while. Then she contacted me again in distress after once again being diagnosed with SIBO. I suggested she get her thyroid checked. She was later diagnosed with Hashimoto’s. She’s now on thyroid medication and luckily for her, the SIBO and her constipation have not returned.

Euthyroid Sick Syndrome

Euthyroid sick syndrome (ESS) is a form of hypothyroidism, but one not caused by lack of iodine in the diet, glandular tumors or autoimmune disease. Those suffering from this form of low thyroid function can also experience many of the same symptoms as those with Hashimoto’s.

As I previously wrote:

“In this syndrome, levels of both TRH and TSH are normal, as are production of both T3 and T4 by the thyroid gland. In fact, clinical tests that fail to directly measure levels of serum T3 or reverse T3 will typically show no abnormalities in someone experiencing ESS.

The mechanism for metabolic derangement in euthyroid sick syndrome appears to be two-fold. First, translocating LPSs will directly down-regulate thyroid receptor activity. All hormones require properly functioning receptors to affect biological processes. By interfering with receptor activity in the liver, lipopolysaccharides prevent these thyroid hormones from carrying out their functions even when their levels are in the normal range.

Secondly, stress hormones directly reduce the conversion of T4 to T3 in the liver, kidneys, and other peripheral organs. They do so because one of the functions of glucocorticoids is to shuttle energy to the brain and the heart in emergencies. Chronic stress, however, is a never-ending “emergency” that causes chronic stimulation of the HPA axis and cortisol release.

Another cause of euthyroid sick syndrome is malnutrition brought about by starvation, fasting, or as I described here, malabsorption. If you are not properly digesting and absorbing nutrients from food because of small gut dysbiosis, your body is under stress, and stress will cause depression of metabolic rate. Add in endotoxemia and the stress response is further amplified.”

I also need to emphasize that very low-carb or ketogenic diets are also known to consistently cause euthyroid sick syndrome.

In severe carbohydrate restriction, these thyroid hormone abnormalities can approach those seen in outright starvation. And what do I mean by severe carbohydrate restriction? Well, probably anything below 100 grams a day in a sedentary person, although that level may still be too low for many. Add in any amount of exercise, and dietary glucose requirements to avoid ESS rise dramatically.

In one study published in the literature in the 1980s, four healthy volunteers were instructed to consume four different isocaloric diets for 72-hours on four separate occasions. (8) This type of crossover study does a great job of controlling for confounding variables as each person undergoes the same dietary regimen.

Diet composition of the four diets was as follows: 100% fat, 50% fat and 50% protein, 50% fat and 50% carbohydrate and finally a mixed diet of 25% fat, 27% protein, and 48% carbohydrate.

During both the 100% fat and the 50% fat with 50% protein diet, serum levels of T3 plummeted while levels of reverse T3 rose. Levels of T3 fell significantly by 50% and 41% respectively. Serum reverse T3 rose 123% in the 100% fat diet.

These observations have been seen repeatedly in other studies. (9) (10) (11) For more in-depth coverage on the role of very low-carb dieting in inducing euthyroid sick syndrome, I refer you to two blog posts by Anthony Colpo. You can find them here and here. As always, Anthony doesn’t mince words, but he’s spot on with the science.

This is the major reason I warn against reliance on ketogenic dieting for weight loss. Lowered thyroid function, including that caused by ESS, will always impair intestinal peristalsis, which in turn will increase the chances of developing SIBO. As low thyroid hormone function can also lower stomach acid, the risk of SIBO increases. Sadly for many, the cause of their SIBO and/or constipation is staring back at them in the mirror.

Does this mean that everyone on these types of very low-carb diets comes down with SIBO? I honestly don’t know, but I certainly have received my fair share of emails from people who have experienced numerous digestive complaints while on them.

If you are on one of these regimens and experience constipation, cold hands and feet, insomnia and dry mouth or nasal passages, I strongly suggest you increase your intake of starchy carbohydrates, preferably from non-gluten sources like rice, corn and tubers.

Given the high-fiber content of many vegetables (remember that fiber is not digested, but fermented in the colon), increasing your intake of these will likely prove inadequate.

One last thing before I wrap this post up. The diagnosis of thyroid disorders is not to be taken lightly. Unless you are on a ketogenic or starvation diet where merely increasing carbohydrate or caloric intake resolves your problem, a visit to a qualified doctor is an absolute necessity.

I realize that many of you who read this blog visit alternative practitioners. It’s not my intention to tell you who to see for your health care needs or how to spend your money.

However, there are many charlatans out there who are more than happy to take your cash by selling you bogus hormone testing and useless quack remedies. My humble advice is to seek out an endocrinologist to accurately assess thyroid function if you suspect non-euthyroid sick syndrome thyroid disease.

Remember, the link between increased intestinal permeability and autoimmune disorders is a strong one. Maintaining gut-wall integrity is absolutely vital for maintaining health. That requires an intact intestinal mucus layer, a gut-associated immune complex, tight junction proteins and healthy epithelial cells. And the proper functioning of these intestinal components is ultimately reliant on healthy populations of beneficial gut flora.



Gardner, D. G., & Shoback, D. (2011). Greenspan’s Basic and Clinical Endocrinology, Ninth Edition (LANGE Clinical Medicine) New York: McGraw Hill Medical.

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