In humans, a factor associated with response to combination therapy in a large clinical trial is the Thr92Ala polymorphism in the type 2 deiodinase gene (DIO2), wherein the subpopulation of patients with this genetic alteration had improved well-being and preference for combination therapy (7). This has led investigators to consider whether this polymorphism could confer a defect in the D2 pathway, but normal Thr92AlaD2 enzyme kinetics have been demonstrated (73). Only recently has the Thr92AlaD2 protein been found to have a longer half-life, ectopically localize in the Golgi apparatus, and significantly alter the genetic fingerprint in cultured cells and in the temporal pole of the human brain without evidence of reduced thyroid hormone signaling (74). The significance of these studies transcends the thyroid field—this polymorphism has now been associated with a constellation of diseases, including mental retardation, bipolar disorder, and low IQ (75). If hypothyroid carriers of Thr92AlaD2 benefit from alternate therapeutic strategies in replicate studies, then personalized medicine—based on genotype— may have a role.
Other causes of hypothyroidism include surgical removal of the thyroid (usually for cancer), radiation therapy of the head and neck, or complications of medical therapies for hyperthyroidism. (Patients with overactive thyroids are often treated with radioactive iodine or anti-thyroid medications that reduce thyroid functioning. These effects can be extensive and permanent, and thyroid supplementation is often required flowing these interventions.) Certain medications can worsen or promote hypothyroidism or interfere with thyroid replacement therapy. One such drug is lithium, used for treating psychiatric conditions such as bipolar disorder.
A complete thyroid diet solution includes more than just food. I cannot emphasise how important these are for managing stress and emotions, especially for people with hyperthyroidism. We underestimate what stress and emotions do to us; each flare-up of anger, feelings of guilt, fear, hostility, jealousy, etc. fires up the adrenals which release cortisol, and cortisol has a detrimental impact on the thyroid.
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.
Thyroid hormones regulate cholesterol synthesis, cholesterol receptors, and the rate of cholesterol degradation. Hypothyroidism increases LDL levels, and increased cholesterol levels have been shown to induce hypothyroidism in animal models. Normalization of thyroid hormone levels has a beneficial effect on cholesterol, which may be worth noting especially for clients who choose not to take prescribed thyroid medications.7
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.
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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.
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