Hashimoto’s thyroiditis is the most common autoimmune disease and the main cause of thyroid disorders in the United States. While the specific causes of Hashimoto’s thyroiditis are not known, researchers have established that there are a number of factors that contribute to the development of Hashimoto’s, including:
Researchers reporting in the journal Thyroid looked at the effects of specific nutritional factors and their relationship to Hashimoto’s thyroiditis. The nutrients evaluated included:
The researchers had interesting findings that may expand the role of nutritional testing and supplementation in Hashimoto’s thyroiditis treatment.
Iodine is the main ingredient of thyroid hormone. Iodine intake comes primarily through ingestion of iodine-rich foods, eating produce grown in iodine-rich soil, iodized salt, and iodine supplements. The iodine in the bloodstream is taken up by the thyroid, where it is used to form the thyroid hormones triiodothyronine (T3) and thyroxine (T4).
Iodine levels have a major impact on thyroid disorders. Specifically, a severe deficiency of iodine can cause an enlarged thyroid (goiter), trigger hypothyroidism, and in pregnant women, can cause cretinism and mental retardation in their children.
Milder iodine deficiency can cause toxic nodular goiter and hyperthyroidism. Excessive levels of iodine can increase the risk of mild or subclinical hypothyroidism and autoimmune Hashimoto’s disease. A higher intake of iodine is associated with higher rates of Hashimoto’s thyroiditis, as well as worsening severity of the disease.
The researchers recommended:
To avoid an increased risk of Hashimoto’s thyroiditis, it is therefore important to ensure, as far as possible, that iodine intake falls within the relatively narrow range of the recommended levels. On a population basis, this would be represented by a median urinary iodine concentration in adults of 100–200 lg/L. Authorities introducing iodine fortification of the food supply in a country (e.g., universal salt iodization) need to ensure that such fortification is introduced very cautiously.
Here is a summary of iodine requirements by age:
Birth to age 10: 90 μg/L
Age 11-17: 120-150 μg/L
Age 15+: 150 μg/L
Pregnancy: 200-250 μg/L
Lactation 200-290 μg/L
The mineral selenium is essential to the production of thyroid hormone. Selenium deficiency has been associated with a number of thyroid conditions, including hypothyroidism, subclinical hypothyroidism, Hashimoto’s thyroiditis, goiter, thyroid cancer, and Graves’ disease. A number of studies have shown that thyroid conditions are more prevalent in areas with low selenium and that higher selenium levels are associated with a lowered risk of Hashimoto’s thyroiditis, hypothyroidism, subclinical hypothyroidism, and goiter.
Selenium supplementation has also been shown to trigger a significant improvement in Graves’ disease patients with mild thyroid eye disease.
Research has also shown that women who are pregnant and who have elevated thyroid peroxidase antibodies (TPOAb) are more likely to develop thyroid conditions during and after pregnancy if they are deficient in selenium. Supplementing with selenium lowered antibody levels significantly in pregnant women with elevated TPOAb. In one study, after the postpartum period, more than 44 percent of the TPOAb-positive women not taking selenium developed thyroiditis, compared to slightly more than 27 percent of the women taking selenium.
Intake of selenium tends to vary with geography based on the selenium content of the soil, as well as selenium levels in food. The key source of selenium is the Brazil nut, but their selenium content is variable, making it an unreliable way to ensure adequate selenium intake. Other good sources of selenium include organ meats, seafood, cereals, and grains.
The researchers concluded:
It makes sense to ensure that selenium intake is adequate, given the roles played by selenium in human health and particularly in the thyroid. Clinicians need to be especially vigilant to ensure that selenium intake/status is adequate. Women are at greater risk of thyroid disorders and may thus have a higher requirement for additional selenium, particularly in pregnancy. If there appear to be few or no selenium-rich sources in a patient’s diet, low-dose supplementation (50–100 mcg/day) is suggested. Even if a patient with HT is being treated with levothyroxine, one needs to be aware that some studies found that giving selenium as well as levothyroxine resulted in a greater reduction in TPOAbs. It is also important to bear in mind that though selenium is essential, excessive intake of selenium is toxic, and supplements of selenium of 200 lg/day, generally considered to be quite safe, have been associated with toxic effects.
Iron is a mineral essential to many physical processes, including the production of thyroid hormones. Studies have shown that lower iron levels are linked to an increased prevalence of subclinical hypothyroidism and lower levels of T4 and T3. Because Hashimoto’s thyroiditis is an autoimmune disease, patients are also at higher risk of other autoimmune conditions, including celiac disease and autoimmune gastritis, both of which can impair iron absorption.
Low iron levels are associated with persistent symptoms in patients treated with hypothyroidism, and several studies have shown that adding iron supplementation to levothyroxine treatment can more effectively help relieve symptoms.
The researchers concluded that when iron levels are low, “supplementation to restore iron sufficiency should be instituted and will help to prevent the deleterious effects of iron deficiency on thyroid function.”
Vitamin D is both a vitamin and a hormone precursor. One form, vitamin D2, comes from dietary intake, and the other form, vitamin D3, is dependent on sunlight exposure. While vitamin D has not been proven to have a direct effect on the thyroid gland, it does appear to have a role in immune function and is thought to have a role in protecting against autoimmune reactions. Several studies have shown a correlation between lower levels of vitamin D with a higher risk for and rates of Hashimoto’s thyroiditis. There are also studies that show that TSH drops and T3 levels rise as vitamin D levels increase.
Deficiency in vitamin D is common across the globe. In studies that have evaluated the link between vitamin D and Hashimoto’s disease, vitamin D deficiency is defined as a vitamin D-25 level of less than <50 nmol/L.
The researchers concluded that while the research does not show that vitamin D deficiency is a cause of Hashimoto’s thyroiditis, “it would be wise to ensure that patients avoid overt vitamin D deficiency.”
Ultimately, the researchers concluded that:
Chronic, long-term exposure to excessive levels of iodine can trigger Hashimoto’s thyroiditis.
Sufficient selenium is essential to thyroid function and selenium supplementation can reduce thyroid peroxidase antibodies (TPOAb), and can improve both hypothyroidism and postpartum thyroiditis.
A deficiency of iron can impair the production of thyroid hormone.
People with Hashimoto’s thyroiditis are frequently deficient in iron because many of these patients also have autoimmune gastritis, which interferes with iron absorption.
Low levels of vitamin D are seen in Hashimoto’s thyroiditis patients, as compared to people with normal thyroid function.
Practitioners should check iron levels in their Hashimoto’s patients, especially in women who are still menstruating, and correct any deficiencies.
Practitioners should check vitamin D levels in their Hashimoto’s patients, and correct any deficiencies.
Selenium should be evaluated, especially in areas where there is iodine deficiency or excess, and if selenium levels are low, or if the patient is geographically located in an area with low selenium intake, patients should supplement with 50 to 100 mcg/day of selenium.
Given what we know about the important role of these nutrients, as part of your treatment for Hashimoto’s thyroiditis you may want to work with your practitioner to evaluate your levels of iodine, selenium, iron, and vitamin D, and correct any deficiencies.