“A teaspoon of iodine is all a person requires in a lifetime, but because iodine cannot be stored for long periods by the body, tiny amounts are needed regularly. In areas of endemic iodine deficiency, where soil and therefore crops and grazing animals do not provide sufficient dietary iodine to the populace, food fortification and supplementation have proven highly successful and sustainable interventions.” [Brahmbhatt 2001].
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.
DISCLAIMER: The information provided on Root + Revel is not a substitute for professional medical advice or treatment for specific medical conditions. You should not use this information to diagnose or treat a health problem without consulting a qualified healthcare provider. Root + Revel is not liable for how the information is used and cannot be held responsible or guarantee any results. You alone are solely and personally responsible for the results, and your success depends primarily on your own effort, motivation, commitment, and follow-through. Root + Revel is simply serving as a coach, mentor, and guide to help you reach your own health and wellness goals through simple holistic remedies and healthy lifestyle changes.

According to some estimates, 40 percent of the population suffers with some form of low thyroid function. Women, especially older women, are the most susceptible group for developing hypothyroidism. People who are elderly or who have other existing autoimmune diseases – like type 1 diabetes, rheumatoid arthritis and celiac disease, for example – are also at a higher risk.


Over my several decades working as a Functional Medicine doctor, I can assure you that even in the toughest cases, you can heal your thyroid. With some patients, I can do this through the dietary, nutrient, and lifestyle factors I’ve discussed here. For others, that healing requires trial and error using several medications and working closely with a physician.

Having a thyroid condition is no picnic, but you're not alone with this health issue. According to the American Thyroid Association, more than 12 percent of the population may end up dealing with a thyroid condition at some point in their lives. And thyroid issues can be sneaky: Of the nearly 20 million Americans living with the disease, as many as 60 percent don't even realize they have it.

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