Welcome to our Thyroid Series of blog articles. This article covers Hashimoto’s and its many root causes. Some causes might be unexpected but are definitely worth considering and addressing if you are wanting to improve your thyroid health. Next week we will discuss Functional Medicine solutions to Hashimoto’s. We hope you have followed our previous articles on the thyroid; introduction to the thyroid, hypothyroidism and hyperthyroidism. In future articles in this series, we will look at other conditions of the thyroid and how to address each one.
** Please note: If you want the short summary version of this article with a video, then please click here **
Hashimoto’s: What is it?
Hashimoto's disease, or Hashimoto's thyroiditis, is an autoimmune disease that damages the thyroid gland. It is the most common cause of hypothyroidism (underactive thyroid). The thyroid, a small gland at the base of your neck (see our intro to thyroid here) makes thyroid hormones that control many activities in the body. In Hashimoto's disease, the immune system makes antibodies that attack the thyroid gland. This damages the thyroid gland, so it does not make enough thyroid hormone. Hashimoto's disease often leads to hypothyroidism and the symptoms of low thyroid.
- Hashimoto’s is the main cause of hypothyroidism (Fröhlich E, 2019).
- Hashimoto thyroiditis affects 1 to 2% of the population in the US (NIH US National Library of Medicine, 2020).
- Hashimoto’s, and autoimmune diseases generally, are more common in women than in men, which is thought to be related to hormonal factors (Fröhlich E, 2019).
- The risk of getting Hashimoto's disease is higher if you already have another autoimmune disease, such as rheumatoid arthritis, celiac disease, type 1 diabetes, lupus, etc.
- Hashimoto’s, as an autoimmune disease, is very much linked to gut health and leaky gut (see our article on that topic here).
- In Hashimoto’s, antibodies against thyroperoxidase (TPO) and thyroglobulin lead to destruction of the thyroid gland (Fröhlich E, 2019). Thyroperoxidase is an enzyme that adds iodine to thyroglobulin for the production of thyroid hormones (ScienceDirect, 2020). It is essential to making T4 and T3 (ScienceDirect, 2020). Thyroglobulin is a protein involved in making T4 and T3 (ScienceDirect, 2020).
What are the Symptoms of Hashi’s?
Hashimoto's disease typically leads to low thyroid function or hypothyroidism. Similar to hypothyroidism, symptoms are:
- Fatigue and sluggishness
- Increased sensitivity to cold
- Pale, dry skin
- A puffy face
- Brittle nails
- Hair loss
- Unexplained weight gain
- Muscle aches, muscle weakness, joint pain and stiffness
- Excessive or prolonged menstrual bleeding
- Memory lapses
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All Health Begins in the Gut
- Genetic tendency
- Environmental trigger
- Intestinal Permeability (leaky gut)
We cannot change a genetic disposition. We can aim to identify the environmental trigger or triggers. We can most certainly work on and improve gut health.
GUT HEALTH: As an autoimmune disease, Hashi’s is linked to poor gut health. Leaky gut, or intestinal permeability, is involved, as well as other possible GI problems. Our article here shows how leaky gut can lead to an overactivated immune system that can attack the thyroid gland.
These are the types of GI issues to look into:
Intestinal permeability or leaky gut: Tight junctions regulate the permeability of the gut, which is meant to remain ‘closed’ to the rest of the body. What you eat is digested, nutrients are absorbed through the gut lining and then the waste is excreted through the anus. What you put into your mouth is not meant to go directly into the bloodstream to circulate. If this happens and molecules, proteins and toxins can get into the blood circulation, then leaky gut exists. The immune system sees these unexpected molecules leaking through the gut lining as foreign invaders and mounts an immune response attack. Because the gut is leaky, this will happen over and over multiple times. The immune system eventually goes into high alert from so many invaders and becomes overactivated. It then starts to attack own tissue and the auto-attack of autoimmunity has begun. In the case of Hashi’s, the immune system is attacking thyroid tissue. We must heal the gut to ‘close’ the leaky gut in order to stop the autoimmune attack.
Dysbiosis: Imbalanced gut flora is also a risk factor for Hashi’s. Thyroid disorders are linked to the composition of the microbiota and an altered microbiota specifically increases the prevalence of Hashimoto’s (Fröhlich E, 2019). Gut bacteria influence thyroid hormone levels by regulating iodine uptake (Fröhlich E, 2019). Gut bacteria affect important minerals like selenium, iron and zinc. This can lead to sub-clinical nutrient deficiencies.
Absorption issues: In addition to potential poor absorption of important nutrients, dysbiosis of gut microbiota can impact the uptake of thyroid medication (Fröhlich E, 2019). The microbiota may alter the uptake, absorption and availability of the thyroid medication L-thyroxine used to synthetically increase levels of the thyroid hormone T4 (Fröhlich E, 2019).
Constipation, SIBO, SIFO and acid reflux: Decreased motility occurs when the MMC or migrating motor complex is not functioning well. This motility is what pushes the digested food through the GI tract and is important for the digestion process. One reason for decreased motility is a lack of thyroid hormone (Fröhlich E, 2019). Thyroid hormone helps to increase intestinal motility which breaks down food and nutrients and promotes normal levels of bacteria in the small intestines. People with Hashimoto's are at increased risk for developing GI related issues due to slower motility (Fröhlich E, 2019). It has been reported that SIBO may be present in more than half of patients with hypothyroidism which is primarily caused by Hashimoto’s (Patil, 2014). One study found that significantly higher numbers of patients (54%) with hypothyroidism have SIBO compared with the control group (Patil, 2014).
T4 => T3 conversion: The gut bacteria convert inactive T4 into the active form of thyroid hormone, T3. About 20% of T4 is converted to T3 in the GI tract (Kharrazian D, 2018). If there are not enough healthy bacteria, as in the case of dysbiosis for example, then T4 => T3 conversion in the gut is impaired.
Celiac disease: There is an association between Hashimoto’s and celiac disease (Krysiak R, 2019). In fact, autoimmune thyroiditis is the most prevalent co-existing autoimmune disorder in patients with celiac disease (Krysiak R, 2019). One study investigated how a gluten-free diet might affect thyroid autoimmunity and function (Krysiak R, 2019). The major finding of the study is that the gluten-free diet reduced thyroid autoimmunity and slightly increased thyroid hormone output in women with Hashimoto’s (Krysiak R, 2019). In 62% of these patients, the decrease in thyroid antibodies and changes in thyroid function tests were accompanied by the disappearance of anti-tissue transglutaminase antibodies. Anti-tissue transglutaminase antibodies are the marker for celiac disease so seeing these disappear means that the celiac disease also improved on the gluten-free diet. In addition, both vitamin D and selenium levels increased in people on a gluten-free diet. Both D and selenium play an important role in thyroid function and the rise in both is one reason why thyroid AI decreased in these study subjects. It was also found that the gluten-free diet reduced inflammation (Krysiak R, 2019). It has been found that Hashi’s patients often produce anti-gliadin and anti-transglutaminase antibodies, which would indicate some degree of celiac disease (Fröhlich E, 2019).
Gluten & molecular mimicry: Even if a Hashi’s patient does not have celiac, gluten is still problematic for people with thyroid conditions. This is due to the concept of molecular mimicry. Molecular mimicry is when the molecules of two substances in the body look extremely similar. The body can get confused and attack the wrong molecule, which is what happens in autoimmunity. Gluten is an issue in Hashimoto’s and other thyroid conditions. This is because the gluten molecule looks like thyroid hormone producing cells, on a molecular level. When the gut is leaky, gluten molecules can escape from the GI tract and get into circulation in the body. The body sees the gluten and attacks it as a foreign invader. Because gluten looks like thyroid cells, the body may mistake thyroid tissue for gluten and attack thyroid cells. This is partially why thyroid antibodies decrease on a gluten-free diet. In addition, we know that gluten is a large contributing factor to developing leaky gut in the first place (read here for an explanation).
Helicobacter pylori (H. pylori): H. Pylori is a common and contagious type of bacteria that infects the gut. Over time, it causes sores and ulcers in the lining of the stomach or the upper part of the small intestine. For some people, an infection can lead to stomach cancer. There may be a link with thyroid disease but there is not full consensus on the possible association between H. pylori infection and autoimmune thyroid diseases (Figura N, 2019). Different reports of an association between Helicobacter pylori and Hashimoto’s have been published (Fröhlich E, 2019). H. pylori infection was associated with Hashimoto’s, through an increased inflammatory status and molecular mimicry (Figura N, 2019). In fact, H. pylori infection prevalence was significantly increased in 64.4% of the Hashimotos patients in one study (Figura N, 2019). There appears to be a relationship between H pylori infection and the presence of thyroid auto-antibodies, such as thyroglobulin antibodies (Tg Ab) and thyroperoxidase antibodies (TPO Ab) (Papamichael KX, 2009). Another study showed a significant decrease in Free T3 and Free T4 in people with H pylori compared to people who tested negative for H pylori (Papamichael KX, 2009). Low FT3 and FT4 are part of hypothyroidism and Hashimoto’s. But another study concluded that no association was found between H pylori infection and Hashimoto’s in women (Shmuely H, 2016).
Food intolerances: As a result of the leaky gut associated with AI and Hashi’s, food intolerances can exist. This causes inflammation and over-activates the immune system response. Food intolerances are essentially a gut issue and can dramatically improve once leaky gut is healed. In research, it has been found that testing for food intolerances is very important for patients with AI disease (Coucke, 2018). Eliminating food intolerances from the diet could decrease symptoms and “probably stop or slow the progression of the autoimmune disease” (Coucke, 2018). The study concludes that food is probably an important trigger for autoimmunity in vulnerable patients (Coucke, 2018). You can read more about food intolerances here.
In addition to gut issues, other potential causes and triggers of Hashimoto’s are:
INFECTIONS: Many types of infections can trigger Hashi’s (and other AI conditions) but the most common include both viruses and bacterial infections. There is evidence that hepatitis C virus may contribute to Hashi’s (Ajjan RA, 2015). Epstein-Barr Virus (EBV), more commonly known as mono or “the kissing disease”, is a virus that can live dormant in a person for years. EBV can re-activate or flare and recur later in life in some individuals. EBV has been found to either cause or be linked to multiple autoimmune diseases, including Hashimoto’s (Dittfeld A, 2016).
TOXINS: Environmental toxic chemicals are damaging to the thyroid. Endocrine disrupting chemicals, such as Bisphenol A (BPA), polychlorinated biphenyls PCBs, phthalates, phenol, plastics, lead, cadmium, DDT, and some other pesticides, are a particular issue. These chemicals disrupt iodine transport and TPO enzyme action to make thyroid hormones (Calsolaro V, 2017). They can contribute to Hashi’s or exacerbate existing conditions by interfering with hormones and immune function. Various types of agricultural chemicals (pesticides, insecticides, fungicides) have been found to be strongly associated with Hashi’s (Goldner WS, 2010). One study looked at women living on farms in the Mid-West and found that these chemicals appear to be the cause for a higher incidence of thyroid disease including both Hashi’s and hypothyroidism (Goldner WS, 2010). Another study looked at people of both sexes living near a petrochemical plant and discovered an increased incidence of both Hashi’s and thyroid antibodies in these people (de Freitas CU, 2010). There was both a higher prevalence and a higher risk of Hashimoto's and thyroid antibodies (de Freitas CU, 2010). Glyphosate, the active ingredient in the herbicide Roundup, can lead to a depletion of selenium, an important nutrient in thyroid health. Selenium is important for making thyroid hormone and helps to lower thyroid antibodies (Drutel A, 2013). Glyphosate harms gut health as it can cause intestinal dysbiosis (Ackermann W, 2015). Furthermore, glyphosate can disrupt the barrier properties of intestinal cells and might cause a leaky gut, increasing the risk of developing an autoimmune condition such as Hashimoto’s (Vasiluk L, 2005).
MERCURY: The heavy metal, mercury, is found in many items including cosmetics, pesticides, fish and dental fillings. Mercury is released into the air through coal burning or other polluting activities and accumulates in the water supply. The mercury molecule looks very similar to iodine (The National Academy of Hypothyroidism, 2020). Due to molecular mimicry, the body can get confused and deposit mercury, instead of iodine, in the thyroid. This accumulated mercury can disrupt the conversion of T4 to T3, which can contribute to Hashimoto’s (The National Academy of Hypothyroidism, 2020). Mercury depletes selenium, an important nutrient used in making thyroid hormone (The National Academy of Hypothyroidism, 2020). There is a correlation between high mercury levels in the bloodstream and thyroid antibodies levels (The National Academy of Hypothyroidism, 2020). Increased thyroid antibodies is a key factor in developing Hashimoto’s. Finally, cell damage caused by mercury may encourage autoimmune activity (The National Academy of Hypothyroidism, 2020).
NUTRITION: Certain minerals and vitamins, selenium, zinc, iron and vitamin D, are important for thyroid health. Thyroid problems are linked to abnormal levels of these minerals (Fröhlich E, 2019) For example, the thyroid gland contains the highest amount of selenium per mg tissue in the body (Fröhlich E, 2019). Sufficient selenium levels are a prerequisite to prevent thyroid disease (Ventura M, 2017). Selenium is needed as an antioxidant and to produce thyroid hormones (Ventura M, 2017). Zinc is critical for the conversion of T4 to T3 and the production of TSH. It also helps to tighten the intestinal junctions of those with intestinal permeability (Fröhlich E, 2019). Iron deficiency decreases T4 and T3 levels, reduces T4 to T3 conversion and decreases T3 metabolism (Ashraf TS, 2017). Studies have found that vitamin D can reduce thyroid antibodies, especially TPO Ab (Chao G, 2020). It is thought that vitamin D may influence the effect of T4 on autoimmune diseases (Chao G, 2020). People with Hashimoto’s typically have a reduced vitamin D level and higher TSH (Chao G, 2020).
IODINE: Excess iodine consumption is a key risk factor of Hashimoto’s. Studies report excess iodine intake leads to an increase in both the incidence and prevalence of Hashi’s (Liu J, 2019). The specific mechanism linking excess iodine intake and Hashimoto’s is unclear (Liu J, 2019).
Iodine is required to make thyroid hormone. It is also a component of the thyroid hormones T4 and T3. We need just the right amount of iodine, either too low or too high iodine intake can lead to thyroid diseases, such as hypothyroidism and Hashimoto’s. Excess iodine is associated with the production of antibodies specific to thyroid hormones, which indicates an immune attack on the thyroid tissue is happening (Liu J, 2019). It is important to perform a urine test for iodine levels to be sure if this is an issue for a particular case of Hashi’s.
** Please check our blog next week to read our next article in the Thyroid Series on **
Solutions to Hashimoto’s
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