Treatment for hyperthyroidism - Hyperthyroidism is the opposite of hypothyroidism; it is a condition in which the thyroid gland is over-producing the thyroid hormones thus causing a hormone imbalance in the body. Hyperthyroidism can be treated with radioactive iodine and/or anti-thyroid medications, both of which are meant to reduce and normalize the thyroid function. In some cases, these treatments can cause permanent hypothyroidism if too much medication is administered.
Giving appropriate doses of T3 is trickier than appropriately dosing T4. T4 is inactive, so if you give too much there is no immediate, direct tissue effect. T3 is a different story, though, as it is the active thyroid hormone. So if you give too much T3, you can produce hyperthyroid effects directly—a risk, for instance, to people with cardiac disease.
l-Thyroxine was the first synthetic molecule used to treat hypothyroidism (23) and was shown to be efficacious as monotherapy for myxedema (24). Around that time, serum protein-bound iodine (PBI) emerged as a diagnostic test and therapeutic marker; serum PBI quantitation was the only valid way to biochemically assess thyroid hormone status (25). This tool was limited in terms of treatment monitoring because the effect on serum PBI varied by agent (26). For example, l-triiodothyronine corrected BMR without much increase in serum PBI, l-thyroxine increased serum PBI sometimes to above normal, and combination l-thyroxine and l-triiodothyronine and desiccated thyroid had the advantage of normalizing serum PBI (27). In addition to BMR and serum PBI, other surrogates for treatment response included cholesterol levels, symptoms, and deep tendon reflexes, but their lack of sensitivity was always recognized (28).
In humans, a factor associated with response to combination therapy in a large clinical trial is the Thr92Ala polymorphism in the type 2 deiodinase gene (DIO2), wherein the subpopulation of patients with this genetic alteration had improved well-being and preference for combination therapy (7). This has led investigators to consider whether this polymorphism could confer a defect in the D2 pathway, but normal Thr92AlaD2 enzyme kinetics have been demonstrated (73). Only recently has the Thr92AlaD2 protein been found to have a longer half-life, ectopically localize in the Golgi apparatus, and significantly alter the genetic fingerprint in cultured cells and in the temporal pole of the human brain without evidence of reduced thyroid hormone signaling (74). The significance of these studies transcends the thyroid field—this polymorphism has now been associated with a constellation of diseases, including mental retardation, bipolar disorder, and low IQ (75). If hypothyroid carriers of Thr92AlaD2 benefit from alternate therapeutic strategies in replicate studies, then personalized medicine—based on genotype— may have a role.
Much of the iodine in the average American diet comes from dairy products, according to a 2008 study by researchers from the Food and Drug Administration. But our consumption of dairy has been on the decline for decades: During the years between 1970 and 2012, there's been a 60-gallon drop, largely because we're drinking milk less often, say the researchers.
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.
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.
To offer some perspective: up to 95% of the thyroid hypothyroidism in the US is caused not by an iodine deficiency, but occurs as the result of an autoimmune disease so avoiding cruciferous vegetables will do little to fix your underactive thyroid, and may deprive you of valuable healthy benefits such as dietary fiber, and anti-inflammatory, cancer-fighting antioxidants.5
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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