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.
Although it’s not a very common cause, sometimes newborns are 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 genetic hypothyroidism is very low and only about one out of every 4,000 newborns is born with a thyroid disorder.
The thyroid uses iodine to convert T4 into freeT3. If you have hypothyroidism, you may not have an iodine deficiency per se, but your thyroid is almost certainly struggling in some way to get ahold of the iodine available to it and do what it needs to do with it. If the root cause is left unaddressed, simply increasing iodine is not always useful and at worst can be dangerous depending on how high you’re increasing your supplementation thinking if a little is good, then more will “solve” your problem.
Hypothyroidism Supplements: Your thyroid is impacted greatly by specific nutrients, like Iodine, Selenium, Zinc, Copper, Vitamin B, Vitamin D3, Vitamin A, Iron, and Omega-3 fatty acids. Instead of taking a dozen separate vitamins every day, I recommend finding a thyroid-specific multi-vitamin that already contains optimal levels of these nutrients. Dr. Meyer’s makes my favorite thyroid multi-vitamin, and it contains methylated vitamins to help with absorption and efficacy. Adaptogenic herbs like ashwaghanda and reishi are also really helpful for managing stress and anxiety, which are linked with your thyroid. 

You may have read that green, leafy veggies like kale, bok choy, broccoli, and Brussels sprouts can make hypothyroidism worse. But before you keep reading, ask yourself a question: Do you live in the United States? That’s key — because if you do, you likely don’t need to worry about these cancer-fighting veggies messing with your hypothyroidism management. (7)

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