To document that this was a result of trends toward lower doses, an unblinded study tracked well-being according to various doses and found that the highest well-being was achieved at supraoptimal doses, resulting in a suppressed TSH (65). However, a blinded trial did not reproduce this finding (66). In a call to the public, a 1997 British Thyroid Foundation newsletter asked readers to recount personal history of residual hypothyroid symptoms. More than 200 patients responded, 54 of whom specifically mentioned that they did not feel well despite normal serum markers of thyroid function (67, 68). Because of this surge in symptomatic patients, some clinicians advocated titrating dose by symptoms rather than serum TSH, reminiscent of the period before the 1970s (69).
l-Thyroxine monotherapy, the novel and physiologically savvy method for treatment of hypothyroidism, contrasted with the traditional approach of natural thyroid preparations that was marred by potency concerns. In less than a decade, there was a major shift in treatment of hypothyroidism such that normalization of TSH with l-thyroxine monotherapy became the new standard of care (Appendix Table) (52). Many clinicians advocated for this to be first-line therapy and for patients previously treated with desiccated thyroid to be transitioned to l-thyroxine monotherapy (50).
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.

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.


Characteristic symptoms and physical signs, which can be detected by a physician, can signal hypothyroidism. However, the condition may develop so slowly that many patients do not realize that their body has changed, so it is critically important to perform diagnostic laboratory tests to confirm the diagnosis and to determine the cause of hypothyroidism. A primary care physician may make the diagnosis of hypothyroidism, but assistance is often needed from an endocrinologist, a physician who is a specialist in thyroid diseases.
Trisha Gilkerson is a homeschooling mom to four crazy boys. She blogs with her awesome hubby Luke at Intoxicated on Life where they talk about faith, homeschooling, and health. They’ve authored the Write Through the Bible curriculum and family Bible Studies and have recently released their first healthy living book – Weeding Out Wheat: A Simple Faith Based Guide. They love connecting with their readers, so be sure to follow them on their blog, Facebook, Twitter, Google+, and Pinterest.
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.
Also available on the market are combination medications that contain both synthetic T4 and T3 hormones, but such medications aren’t usually recommended. For one thing, most patients see their condition improve with synthetic T4 alone because of the ability of the thyroid to convert these hormones to T3 when needed. Also, synthetic T3-T4 combination drugs can cause anxiety — if you have a preexisting mental health disability, such side effects may be even greater. (3)

Short of eating a few kelp salads, you probably don't have to worry about getting too much iodine from any other foods. In particular, dairy products are full of this nutrient (and in more manageable amounts), according to a 2012 research in the journal Nutrition Reviews. Part of the reason is because livestock are given iodine supplements and the milking process involves iodine-based cleaners. Plain, low-fat yogurt, or Greek yogurt is a good source—it can make up about 50% of your daily intake of iodine.
But determining the correct dosage isn’t a quick process — you will need a blood test between six and eight weeks after you first start taking your medicine to see if your hormone levels are normalizing. If your doctor thinks you need a dosage adjustment, he or she will do so and recheck your hormone levels after another six to eight weeks. Once your thyroid hormone levels stabilize, you won’t need another thyroid check for six months. (5) Controlled hypothyroidism requires only an annual checkup. (3)
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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