Certainly, many of the foods listed above are an important part of a healthy diet. Try to eat a varied diet so that you avoid eating large amounts of goitrogenic foods on any one day. Be especially careful about raw juicing, which can concentrate these foods. Cooking, steaming, and even blanching (such as with kale) reduce goitrogen content and are good options when you wish to consume these foods.
Correcting these problems requires an integrative approach. It involves more than simply taking a thyroid pill. As you’ll see, it involves nutritional support, exercise, stress reduction, supplements, reducing inflammation, and sometimes eliminating certain foods and detoxification from heavy metals (such as mercury and lead) and petrochemical toxins (such as pesticides and PCBs).
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.
1. Jonklaas J, Bianco AC, Bauer AJ, Burman KD, Cappola AR, Celi FS, et al. American Thyroid Association Task Force on Thyroid Hormone Replacement. Guidelines for the treatment of hypothyroidism: prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement. Thyroid. 2014;24:1670–1751. [PMID: 25266247] [PMC free article] [PubMed]
“Excess iodine is generally well tolerated, but individuals with underlying thyroid disease or other risk factors may be susceptible to iodine-induced thyroid dysfunction following acute or chronic exposure. Sources of increased iodine exposure include the global public health efforts of iodine supplementation, the escalating use of iodinated contrast radiologic studies, amiodarone administration in vulnerable patients [amiodarone is a drug used to treat heart rhythm problems], excess seaweed consumption, and various miscellaneous sources.” [Leung]
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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Please Note: The material on this site is provided for informational purposes only and is not medical advice. Always consult your physician before beginning any diet or exercise program.
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