A discussion on thyroid disease and good health isn’t complete without stressing the importance of physical activity. Lisa Lilienfield, MD, a thyroid disease specialist at the Kaplan Center for Integrative Medicine in McLean, Virginia, and a certified yoga instructor, is a firm believer in the importance of exercise, particularly for clients with a thyroid disorder. “With hypothyroid patients, certainly exercise can help with weight gain, fatigue, and depression. With hyperthyroidism, anxiety and sleep disturbances are so common, and exercise can help regulate both.”
In developing countries, insufficient amounts of iodine in the diet account for most cases of hypothyroidism. Iodine is necessary for the production of the two main thyroid hormones, thyroxine (T-4) and triiodothyronine (T-3). In the U.S. – where salt is iodized, and most Americans get plenty of iodine from table salt – an autoimmune condition known as Hashimoto’s thyroiditis is the most common cause. Hashimoto’s is more common in women and in those with a family history of autoimmune diseases. It involves immune-related inflammation and destruction of the thyroid gland, which reduces proper functioning and production of thyroid hormone. The exact cause and triggers of Hashimoto’s still remains unknown.
The most common treatment I use is Armour thyroid, (9) a prescription drug made from desiccated (dried) porcine thyroid. It contains the full spectrum of thyroid hormones, including T4, T3, and T2 (10). That last one – T2 – is a little-known product of thyroid metabolism that actually may be very important. The right dose ranges from 15 to 180 milligrams, depending on the person.
Goitrogenic foods can act like an antithyroid drug in disabling the thyroid function. They prevent the thyroid from using available iodine. It is made worse if you use a lot of salt because that causes the thyroid to swell. Do not eat these in large amounts if you are taking thyroid hormone replacement. It is thought that the enzymes involved in the formation of goitrogenic materials in plants can be destroyed by cooking, so cook these foods thoroughly if you want to eat them.
It is absolutely critical for any physician who is treating someone with a thyroid disorder to test for thyroid antibodies. Unfortunately, few mainstream medical doctors test for thyroid anti-bodies and so most do not ever get the proper diagnosis. In the medical system, an auto-immune condition, a sluggish thyroid, a burned out pituitary gland and a T4-T3 conversion problem are all treated the same way, with synthetic T4 such as synthroid or a T3 medication like levothyroxin.
As hypothyroidism becomes more severe, signs and symptoms may include puffiness around the eyes, the heart rate slows, body temperature drops, and heart failure. Severe hypothyroidism may lead to a life-threatening coma (myxedema coma). In a person with severe hypothyroidism, a myxedema coma tends to be triggered by severe illness, surgery, stress, or traumatic injury. Myxedema coma requires hospitalization and immediate treatment with thyroid hormones given by injection.
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.
Those with hypothyroidism may want to consider minimizing their intake of gluten, a protein found in foods processed from wheat, barley, rye, and other grains, says Ruth Frechman, RDN, a dietitian in the Los Angeles area and a spokesperson for the Academy of Nutrition and Dietetics. And if you have been diagnosed with celiac disease, gluten can irritate the small intestine, and may hamper absorption of thyroid hormone replacement medication.
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