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 effects of fluoride on various aspects of endocrine function should be examined, particularly with respect to a possible role in the development of several diseases or mental states in the United States. Major areas of investigation include . . . thyroid disease (especially in light of decreasing iodine intake by the U.S. population).” (National Research Council, 2006)
Sorry to hear this! It is usually related to autoimmune activity and/or excess hydrogen peroxide burning the thyroid leading to abnormal/mutated cells – like a callus on your hand when you are rough with your hands. I would recommend following the principles in this article. Not sure if it can be fully reversed, but you must STOP THE CAUSE and help the body to heal itself.
Most patients report improvement with a thyroid supplement too, but if you consistently eat a healthy and wholesome diet they are unnecessary. If you still want to try one however (under the supervision of your doctor), see this Thyroid Support Supplement (disclosure: this is an affiliate link). It contains both selenium and iodine for thyroid health, as well as vitamin B12 for improved energy levels. Additionally, it is one of the few available that is 100% vegetarian.

If you have been diagnosed with both hypothyroidism and iodine deficiency, there are some things you can do to make these vegetables less harmful. Cooking them can reduce the effect that cruciferous vegetables have on the thyroid gland, and limiting your intake of these (cooked) vegetables to 5 ounces a day may help as well, since that amount appears to have no adverse effect on thyroid function.

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