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.
Hypothyroidism can be easily treated with thyroid hormone replacement. The preferred treatment for most people with an underactive thyroid is levothyroxine sodium (Levoxyl, Synthroid). This is a more stable form of thyroid hormone and requires once a day dosing.Liothyronine sodium (Cytomel) also may be prescribed to treat hypothyroidism under certain conditions.
Goitrogens are naturally occurring substances in certain foods that interfere with the production of thyroid hormones (the hormones that people with hypothyroidism lack). They include some of the most commonly consumed foods of the health-conscious community: broccoli, cauliflower, kale, spinach, radishes, soybeans, peanuts, pine nuts, peaches and millet. The good news is that many health professionals believe that cooking may inactivate goitrogens.
Chromium picolinate, which is marketed for blood sugar control and weight loss, also impairs the absorption of thyroid medications. If clients decide to take chromium picolinate, they should take it three to four hours apart from thyroid medications.23 Flavonoids in fruits, vegetables, and tea have been shown to have potential cardiovascular benefits. However, high-dose flavonoid supplements may suppress thyroid function.24 The Natural Standards Database provides an extensive list of supplements that have a potential impact on thyroid function, so taking precautions and coordinating patient care with a knowledgeable practitioner is prudent.
In areas of the world where there is an iodine deficiency in the diet, severe hypothyroidism occurs in about 5% to 15% of the population. Examples of these areas include Zaire, Ecuador, India, and Chile. Severe iodine deficiency occurs in remote mountain areas such as the Andes and the Himalayas. Since the addition of iodine to table salt and to bread, iodine deficiency is rare in the United States.
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An article published in May 2017 in the journal Endocrine Connections noted that hypothyroidism and celiac disease are often present together, and while no research has demonstrated that a gluten-free diet can treat thyroid conditions, you may still want to talk to a doctor about whether it would be worth eliminating gluten, or getting tested for celiac disease.
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