90% of all hypothyroid conditions are autoimmune in nature. In other words, most people with hypothyroidism have the condition Hashimoto’s Thyroiditis. But what causes this condition? Numerous factors can trigger an autoimmune response and result in the elevated thyroid peroxidase (TPO) and/or thyroglobulin antibodies you see with Hashimoto’s Thyroiditis. These antibodies will damage the thyroid gland, which is what leads to the decreased production of thyroid hormone. And while taking synthetic or natural thyroid hormone might be necessary for someone who has low or depressed thyroid hormone levels, this won’t do anything to improve the health of the immune system. So the goal is to detect and then remove the trigger which is causing the autoimmune response, get rid of the inflammation, and suppress the autoimmune component of the condition.
Thyroid hormone replacement has been used for more than a century to treat hypothyroidism. Natural thyroid preparations (thyroid extract, desiccated thyroid, or thyroglobulin), which contain both thyroxine (T4) and triiodothyronine (T3), were the first pharmacologic treatments available and dominated the market for the better part of the 20th century. Dosages were adjusted to resolve symptoms and to normalize the basal metabolic rate and/or serum protein-bound iodine level, but thyrotoxic adverse effects were not uncommon. Two major developments in the 1970s led to a transition in clinical practice: 1) The development of the serum thyroid-stimulating hormone (TSH) radioimmunoassay led to the discovery that many patients were overtreated, resulting in a dramatic reduction in thyroid hormone replacement dosage, and 2) the identification of peripheral deiodinase-mediated T4-to-T3 conversion provided a physiologic means to justify l-thyroxine monotherapy, obviating concerns about inconsistencies with desiccated thyroid. Thereafter, l-thyroxine mono-therapy at doses to normalize the serum TSH became the standard of care. Since then, a subgroup of thyroid hormone–treated patients with residual symptoms of hypothyroidism despite normalization of the serum TSH has been identified. This has brought into question the inability of l-thyroxine monotherapy to universally normalize serum T3 levels. New research suggests mechanisms for the inadequacies of l-thyroxine monotherapy and highlights the possible role for personalized medicine based on deiodinase polymorphisms. Understanding the historical events that affected clinical practice trends provides invaluable insight into formulation of an approach to help all patients achieve clinical and biochemical euthyroidism.
The diagnosis of “subclinical” hypothyroidism that I discussed last week depends on having a TSH level higher than 5 m IU/ml and lower than 10 m IU/ml. As I mentioned above, new guidelines suggest anything over 3 is abnormal. While an improvement, practitioners following these guidelines may still miss many people who have normal test results and a malfunctioning thyroid system.
Supplement Intake: Another simple method to treat hypothyroidism naturally, is by taking supplements. Iodine plays a crucial role in the production of thyroid hormone and zinc and selenium also aid in the hormone production process. Vitamin D is seen to act as a binding agent in the initial stages of thyroid hormone. Vitamin E plays the role of a sustaining device by converting T4 into T4 hormones (deiodinase enzymes). Thus, taking iodine, selenium, zinc and vitamin E supplements are quite helpful in treating hypothyroidism.
Although the implementation of sensitive TSH assays resulted in dose reduction, it also fueled the discovery of subclinical states of hypothyroidism (i.e., serum TSH <10 mIU/L and normal serum free T4); this state is 20 times more prevalent than overt hypothyroidism (64). Hence, many patients with vague symptoms, such as depressed mood and fatigue, are commonly screened and found to have subclinical hypothyroidism. In many cases, this finding prompts the conclusion that the subclinical hypothyroidism is the cause of the nonspecific symptoms, and thyroid hormone therapy is initiated. The patients in whom the cause–effect relationship was incorrect contribute to the increasing number of euthyroid but symptomatic patients (57). The marked increase in prescribing of thyroid hormone with decreasing TSH thresholds amplifies this problem (47).
Megan Casper, RDN, a dietitian based in New York City and the founder of Nourished Bite, points out that iodine deficiency is the leading cause of hypothyroidism worldwide. This mineral can’t be made by the body, so dietary sources like iodized salt, dairy products, seafood, seaweed, and fortified cereals are important. “Iodine is an essential nutrient in the body, and thyroid hormones are composed of iodine,” explains Rizzo. “Those lacking thyroid hormones may also be lacking iodine.”
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