Although it’s not very common, newborns are sometimes born with a dysfunction of the thyroid gland, a genetic condition called congenital hypothyroidism. Some evidence shows that people are more likely to develop hypothyroidism if they have a close family member with an autoimmune disease. But according to the National Institute of Health (NIH), the likelihood of congenital hypothyroidism is very low and only about 1 out of every 4,000 newborns is born with a thyroid disorder. (8b)


These clinical trials also began to define the adverse-effect profiles associated with these agents; thyrotoxicosis was frequently encountered. Patients treated with l-triiodothyronine3 (100 to 175 mcg/d) normalized BMR faster than did those receiving desiccated thyroid (120 to 210 mg/d) or l-thyroxine (200 to 350 mcg/d) but were more likely to experience angina (32). Desiccated thyroid was also associated with adverse symptoms in other studies; muscle stiffness, psychosis, and angina all occurred (33). In a crossover study of l-triiodothyronine monotherapy (75 to 100 mcg/d), l-thyroxine monotherapy (200 to 300 mcg/d), and desiccated thyroid (1.5 to 3 grains/d), all of these therapies restored BMR and serum PBI; with l-triiodothyronine, however, angina and heart failure occurred. Dose reduction corrected these adverse effects, but authors concluded that l-thyroxine monotherapy or thyroid extract was preferred (34). In a trial of l-thyroxine monotherapy at doses of 200 to 300 mcg/d versus l-thyroxine (80 mcg) plus l-triiodothyronine (20 mcg) daily, patients receiving the combination had such symptoms as palpitations, nervousness, tremor, and perspiration (35). Some early proponents of l-thyroxine monotherapy emerged because of less frequent thyrotoxic effects (24), but it is difficult to determine whether such adverse effects were related to the agent used or its high dosage. Thyrotoxic adverse effects were typically remediable by simple dose reduction (36), so desiccated thyroid remained the preparation of choice (37).
Some findings suggest that many people with Hashimoto’s disease (the most common type of hypothyroidism) have lower levels of vitamin D compared to the general population . That’s bad news, since low D is tied to higher levels of thyroid antibodies. “The antibodies activate the immune system to attack the thyroid tissue, which creates inflammation and makes it harder for the thyroid to do its job,” explains Lisa Markley, RDN, co-author of The Essential Thyroid Cookbook.
Hypothyroidism Medication: Conventional doctors almost always put their patients on either Synthroid® (a synthetic thyroid hormone pill that contains only T4; sometimes called Levothyroxine, Levothroid, Unithroid, and Tirosint) or Armour (Natural Desiccated Thyroid derived from the thyroid glands of pigs). Both are tablets that patients will have to take daily for the rest of their lives. In some cases, these medications might help, but there are all kinds of side effects and issues that arise. So I recommend two other medications over these two instead.
Megan Casper, RDN, a dietitian based in New York City and the founder of Nourished Bite, points out that iodine deficiency is the leading cause of hypothyroidism worldwide. This mineral can’t be made by the body, so dietary sources like iodized salt, dairy products, seafood, seaweed, and fortified cereals are important. “Iodine is an essential nutrient in the body, and thyroid hormones are composed of iodine,” explains Rizzo. “Those lacking thyroid hormones may also be lacking iodine.”

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