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.
Vitamin D is important for immune system health and is made in the skin from exposure to the sun's ultraviolet rays. Vitamin D is also found in foods like fatty fish, cod liver oil, and fortified cereals. Research suggests that vitamin D deficiency may be linked to the development of Hashimoto's thyroiditis (autoimmune hypothyroid disease), and that vitamin D supplementation may help with the treatment of thyroid disease.
The vast majority of individuals—one in seven are women—with hypothyroidism in the US have Hashimoto’s thyroiditis, an autoimmune disease in which your body doesn’t produce enough thyroid hormone, but this isn’t caused by iodine levels in the diet.2 Other less common causes of hypothyroidism include a deficiency of iodine in the diet, taking certain medications that interfere with thyroid absorption, surgical removal of the thyroid, and a genetic disorder.
There are medications commonly prescribed to limit the activity of the thyroid. Surgery may also be recommended as a last resort to remove all or part of the thyroid. It’s worth researching ways to treat hyperthyroidism naturally, as removing sources of inflammation from your diet and taking advantage of thyroid-supporting supplements and essential oils can help to make a big difference.
– Gluten. Gluten is compound of glutein and gliadin proteins. Gliadin’s molecular structure is similar to the thyroid gland, so when the inmune system tags it for destruction not only destroys the protein gliadin but also attacks the thyroid tissue affecting the secretion of the thyroid hormone. The gluten from refined flour is much worse than gluten coming from natural sources as whole barley or oats.
“More than 70 countries, including the United States and Canada, have salt iodization programs. As a result, approximately 70% of households worldwide use iodized salt, ranging from almost 90% of households in North and South America to less than 50% in Europe and the Eastern Mediterranean regions. In the United States, salt manufacturers have been adding iodine to table salt since the 1920s, although it is still a voluntary program.” [http://ods.od.nih.gov/factsheets/Iodine-HealthProfessional/#h3]
The normal values for the serum T4:T3 ratio are seldom discussed in the literature because measurement of serum T3 levels is not a recommended outcome in hypothyroidism (1). In a large study of approximately 3800 healthy individuals (4), the serum free T4:free T3 ratio was around 3, as opposed to a ratio of 4 in more than 1800 patients who had undergone thyroidectomy and were receiving l-thyroxine monotherapy. The corresponding serum free T4:free T3 ratio in patients continuing to receive desiccated thyroid is not well-defined, but the serum total T4:T3 ratio is known to be low (28, 50). In one study, the serum total T4:total T3 was about 40 in patients receiving desiccated thyroid and about 100 in those taking l-thyroxine monotherapy (60). Of course, this is affected by the timing of blood collection in relation to the timing of l-triiodothyronine administration, which is not commonly reported. Other key factors are the well-known poor reproducibility of the serum total T3 assay (61) and the interferences with direct measurement of free T3 (5).
“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].
Hi, Dawn: Yes, there’s definitely a TON of conflicting information out there. When it comes to cruciferous vegetables and the thyroid, it’s all about raw veggies, not cooked. Raw cruciferous veg contains a compound called goitrogens, which might impact thyroid function by impairing thyroid peroxidase, an enzyme normally found in the thyroid gland. I don’t think this means that you should NEVER eat a single serving of raw cruciferous veggies if you have thyroid issues. But just that you shouldn’t overdo it and eat raw daily. Hope that helps!
Iodine: Iodine is critical for thyroid hormone production in the body. A true iodine deficiency will cause hypothyroidism (43). In western culture we often see subclinical iodine deficiencies which contribute to hypothyroidism (44). I typically don’t recommend high doses of iodine as it could be problematic with individuals with Hashimoto’s – especially with TPO anti-bodies.
For starters, consider the effect that hypothyroidism can have on weight. Hypothyroidism (also called low thyroid or underactive thyroid) is marked by insufficient hormone production in the thyroid — the butterfly-shaped gland located at the bottom-front of your neck. This gland affects the body’s metabolic processes, and often, sudden weight gain is an early sign of low thyroid.
Affiliate Disclosure: There are links on this site that can be defined as affiliate links. This means that I may receive a small commission (at no cost to you) if you purchase something when clicking on the links that take you through to a different website. By clicking on the links, you are in no way obligated to buy.
Please Note: The material on this site is provided for informational purposes only and is not medical advice. Always consult your physician before beginning any diet or exercise program.
Copyright © livehopelupus.org