Autoimmune diseases are a group of disorders in which the immune system dysfunctions and attacks host tissues. Although the pathogenesis of autoimmune thyroid disease has not been elucidated, there are several factors that have been associated with the disorder. Factors include genetic predisposition, nutrient deficiencies, use of certain medications affecting thyroid function, and environmental factors including exposure to radiation, heavy metals, and chemical contaminants.

Thyroid disorders are often treated with drug therapy, which often have serious side effects and do not necessarily treat the underlying condition leading to the thyroid dysfunction. In recent years there has been increased interest in herbs and supplements as individuals take more interest in their health and well-being. For autoimmune disease, vitamin D supplementation is recommended as deficiency in this nutrient has been associated with the disorder. Additionally, it also modulates T cell response and inhibits Th1 cytokines.

In cases of autoimmune hyperthyroid disorder, rosmarinic acid, selenium and iodide supplementation are recommended. For autoimmune hypothyroid disorder, blue flag (Iris versicolor) and guggul (Commiphora mukul), selenium and iodide supplementation are indicated. Each of these supplements plays a specific role in restoring normal thyroid function.

Further, rosmarinic acid found in plants such as rosemary (Rosmarinus officinalis), bugleweed (Lycopus virginicus), and lemon balm (Melissa officinalis) also calms excess T cell activity and pro inflammatory cytokine release. The use of these combinations of supplements should restore thyroid hormone homeostasis in autoimmune thyroid disorders. Proper medical supervision is required to ensure these herbs and nutrients are used safely and potential adverse effects are avoided.

ENVIRONMENTAL FACTORS
Autoimmune thyroiditis is mediated by  lymphocytes and cytokines, which destroy the thyroid gland. Thyroid antigens are influenced by  a host of environmental factors, including toxins, halogens, pesticides, heavy metals and nutrient deficiencies among others.

Although it is reported that there is a genetic predisposition, onset of the disease can be triggered by environmental factors, including iodine intake and the proliferation of lymphocytes. The production of antibodies is stimulated by the iodination of thyroglobulin.

Heavy metals
Heavy metals (cadmium, lead and mercury) have  been linked to alterations in thyroid function. The association of mercury with thyroglobulin antibody positivity, but not thyroid peroxidase antibody positivity, indicates a relationship between mercury and autoimmunity.

Preclinical evidence suggests that thyroid peroxidase enzyme is inhibited by inorganic mercury but not organic mercury. Both organic and inorganic mercury inhibit the iodination of thyroglobulin. Further, it has been hypothesized that mercury induces protein alterations which result in cell-specific 
antigenicity as well as a theory that formation of polyclonal B lymphocytes and autoantibodies result from mercury induced T lymphocyte stimulation.

Mercury exposure typically reflects the consumption of fish in the general population.Cadmium exposure leads to lipid peroxidation in the thyroid, which can be protected against by ascorbic acid supplementation. Alterations in antioxidant enzyme systems and lipid peroxidation in response to heavy metals are hypothesized to lead to membrane integrity dysfunction and suboptimal 5′-deiodinase activity. In order for the body to remove cadmium, selenium becomes bound to the cadmium and is expelled from the body via the bile system. Selenium is an essential component of deiodinase enzymes responsible for conversion of T4 to T3, and reduced selenium also leads to an increase in rT3 which in turn can result in hypothyroidism. Selenium is also an essential component of the antioxidant, glutathione peroxidase. Reduction in selenium reduces the formation of glutathione peroxidase, resulting in increased levels of reactive oxygen species and hydrogen peroxide which can damage the thyroid.

Halogens and pesticides

Iodination of thyroglobulin and the sodium iodide symporter are affected by halogens including perchlorate, chlorine, fluorine and bromine. Each of these chemicals have differing effects on the thyroid and vary in their mechanisms of action.

Perchlorate (ClO4 ) competitively inhibits iodide uptake by the NIS and displaces T4 from serum. Chlorine inhibits iodide trapping and decreases serum T4.25 Fluoride decreases T3 and T4 and increases TSH in the blood; however, the mechanism by which this occurs remains unclear.

Bromine displaces iodine, increases plasma TSH and has an inhibitory effect on thyroid activity. 

I find these individual chemicals in our environment and often in household products including beverages, drinking water, toothpastes and cleaning agents; however, adverse effects on the thyroid are generally seen only with exposure to high amounts of these compounds. Organochlorine pesticides, which contain the chlorine molecule, have also been associated with increased incidence of euthyroid goiter or hypothyroidism. Usually the thyroid hormone concentration change occurs in response to a mixture of chemicals, but not to individual chemicals. Polyhalogenated biphenyls Polyhalogenated biphenyls such as polybrominated biphenyls and polychlorinated biphenyls are commonly used compounds with many industrial applications including flame retardants, foams, building materials, lubricants, adhesives, inks and plasticizers. They have been known to accumulate in water ways and are incorporated into the adipose tissue of fish and humans.

Toxins such as polychlorinated biphenyls (PCBs), polybrominated diphenyl ether (PBDE) and bisphenyl A (BPA) have been linked to modulation of thyroid hormones. PCBs resemble thyroid hormone structurally and have been shown to disrupt thyroid function in vivo.  Blood concentrations of PCBs negatively correlate with circulating thyroid hormone levels. Immunomodulatory effects of PCBs may be responsible for increases in thyroid peroxidase antibodies and subsequent interference with iodide transport seen in populations with long-term exposure to PCBs.

One study has reported that as PBDE increases, increased sub-clinical hyperthyroidism was seen in pregnant women. The structure of PBDE is similar to thyroid hormone and can displace T4 from serum thyroid binding protein transthyretin (TTR). BPA, commonly found in plastic and metal food packaging, is believed to disrupt T3 signaling pathways. It has been suggested that BPA may displace T3 from thyroid receptors and result in gene suppression.

References:

McLeod DS, Cooper DS. The incidence and prevalence of thyroid autoimmunity. Endocrine. 2012;42:252–65.

Ishii H, Inada M, Tanaka K, et al. Sequential deiodination of thyroxine in human thyroid gland. J Clin Endocrinol Metab. 1982;55:890–6.

McGrogan A, Seaman HE, Wright JW, de Vries CS. The incidence of autoimmune thyroid disease: a systematic review of the literature. Clin Endocrinol (Oxf). 2008;69:687–96. 4. Canaris GJ, Manowitz NR, Mayor G, Ridgway EC. The Colorado thyroid disease prevalence study. Arch Intern Med. 2000;160:526–34