Clinicians noted several differences in the ability of l-thyroxine monotherapy to normalize markers of hypothyroidism at doses that normalized serum TSH (45). For instance, in many l-thyroxine-treated patients with a normal serum TSH, the BMR remained at about 10% less than that of normal controls even after 3 months of therapy (53). At the same time, doses of l-thyroxine that normalize the BMR can suppress serum TSH and cause iatrogenic thyrotoxicosis (28, 45, 46). The clinical significance of this was not fully understood because many patients appeared clinically euthyroid with a BMR between −20% and −10% (36, 37).


There is little mention of patients who did not respond symptomatically to treatment despite having normalization of their other measured variables, such as BMR or serum PBI, in the early clinical trials in the 1940s through 1960s. After the 1970s (38, 52), a new category of hypothyroid patient was recognized: the patient who received thyroid hormone replacement therapy, had normal serum TSH, and exhibited residual symptoms of hypothyroidism. Initially, such symptoms were largely dismissed as unrelated to the thyroid condition (62). Indeed, hypothyroidism is prevalent, and symptoms overlap with those of other common conditions, including menopause, depression, and chronic fatigue syndrome. Likewise, thyroid hormone had been administered for nonthyroid disorders, including obesity and psychiatric disease, for decades. Thus, it was difficult to assess whether patients with residual symptoms had been misdiagnosed. Residual symptoms were even attributed to nonadherence (63).

The problematic compound in soy (for your thyroid) are the isoflavones. In fact, a study in the Journal of Clinical Endocrinology and Metabolism reported that researchers fed some subjects 16 mg of soy isoflavones, which is the amount found in the typical vegetarian's diet,  and others 2 mg soy isoflavones, which is the amount found in most omnivore's diets.


The development of TSH radioimmunoassay (43) provided the first sensitive and specific marker of systemic thyroid hormone status (Figure). Clinicians could now titrate therapy to achieve a serum TSH within the normal range as a specific marker of replacement adequacy (44). For patients who were once treated with doses that normalized their symptoms, BMR, or serum PBI, the use of serum TSH revealed such doses to be typically supratherapeutic (45, 46). Maintenance doses of l-thyroxine ranged from 200 to 500 mcg/d before the institution of the TSH assay and then became typically closer to 100 to 150 mcg/d (Appendix Table). Implementation of the TSH radioimmunoassay also provided a means to diagnose much milder, or even subclinical, cases of hypothyroidism that may have been undiagnosed with earlier, less sensitive, diagnostic methods (47).
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)
“For women who may become pregnant, during pregnancy, or lactating, the American Thyroid Association recommends taking a daily supplement containing 150 mcg of iodine,”8 says Elizabeth Pearce, MD, MSc, professor of medicine at Boston University School of Medicine in Massachusetts, and the ATA also recommends against taking added selenium during pregnancy given some concern that there is an increased risk of developing gestational diabetes.

Autoimmune disease - Autoimmune disorders occur when the body’s immune system produces antibodies that attack its own tissues. Scientists aren’t sure why the body produces these antibodies and why it would attack itself. Some think that a virus or bacterium might trigger this, while others believe that genetic factors cause autoimmune disorders. It could also be a combination of the two factors. Regardless of the cause of autoimmune diseases they are thought to be a cause of hyperthyroidism. When the immune system attacks the body, it often targets the thyroid. This limits the thyroid’s ability to produce hormones and results in hyperthyroidism.
Dry skin (xeroderma) may be caused by external factors, like cold temperatures, low humidity, harsh soaps, and certain medications, or internal factors, such as thyroid disease, diabetes, psoriasis, or Sjogren's syndrome. Symptoms and signs of dry skin include itching and red, cracked or flaky skin. The main treatment for dry skin is frequent, daily lubrication of the skin.
The development of TSH radioimmunoassay (43) provided the first sensitive and specific marker of systemic thyroid hormone status (Figure). Clinicians could now titrate therapy to achieve a serum TSH within the normal range as a specific marker of replacement adequacy (44). For patients who were once treated with doses that normalized their symptoms, BMR, or serum PBI, the use of serum TSH revealed such doses to be typically supratherapeutic (45, 46). Maintenance doses of l-thyroxine ranged from 200 to 500 mcg/d before the institution of the TSH assay and then became typically closer to 100 to 150 mcg/d (Appendix Table). Implementation of the TSH radioimmunoassay also provided a means to diagnose much milder, or even subclinical, cases of hypothyroidism that may have been undiagnosed with earlier, less sensitive, diagnostic methods (47).
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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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