Thyroid Disease : Hashimoto's Thyroiditis (Chronic Lymphocytic Thyroiditis) Prevention - The Diet

Home of Kyle J. Norton for The Better of Living & Living Health Thyroid is one of the largest endocrine glands found in the neck, below the Adam’s Apple with the function of regulating the body use of energy, make of proteins by producing its hormones as a result of the stimulation of thyroid-stimulating hormone (TSH) produced by the anterior pituitary.
Thyroid disease is defined as a condition of malfunction of thyroid. Hyperthyroidism is a condition in which the thyroid gland is over active and produces too much thyroid hormones. Hypothyroidism is a condition in which the thyroid gland is under active and produces very little thyroid hormones. Thyroid cancer is defined as condition in which the cells in the thyroid gland have become cancerous.
Hashimoto’s thyroiditis (chronic lymphocytic thyroiditis)
Hashimoto’s thyroiditis is an autoimmune disease in which the immune system attacks the thyroid gland of that mostly often leads an underactive thyroid gland (hypothyroidism). According to the study by the University of Pisa, Women with Hashimoto’s thyroiditis (HT)  suffer from a high symptom load independently from hypothyroidism, which results just a contributing factor to the development of the clinical syndrome. In agreement with these results, we recently reported on the presence of symptoms and signs consistent with fibromyalgia (FM) in patients with HT regardless thyroid dysfunction, focusing to the weight of anti-thyroid autoimmunity in the HT-associated clinical syndrome(a).
E. Preventions
E.1. Diet to prevent Hashimoto’s thyroiditis 
1.  Brazil Nuts and Sunflower Seeds
In the study to investigate Selenium and thyroidal function; the role of immunoassays, showed that that dietary intake of about 300 micro g of selenium daily may have a toxic effect on growth hormone and insulin like growth factor-1 metabolism, as well as in the synthesis of thyroid hormones. Main adverse effects may be anorexia, diarrhea, depression, hemorrhage, liver and kidney necrosis, blindness, ataxia and respiratory disturbances. Dermatitis and CNS deficiency have also been described. It is concluded that selenium plays an important role in regulating thyroid function, as well as in the homeostasis of thyroid hormones through the action of selenoproteins, in which it incorporates as selenocystein(1). Others suggested that a different pattern of response to Se supplementation in HT relative to baseline TPOab titers, and this, if confirmed, could be used to identify which patients would benefit most from treatment. An improvement in thyroid function and morphology should be demonstrated before Se routine supplementation can be recommended in the treatment of HT(25).

2.  Sea buckthorn 
Sea buckthorn (Hippophae rhamnoides L.) constitutes thorny nitrogen fixing deciduous shrub. Sea buckthorn(SBT) is primarily valued for its very rich vitamins A, B(1), B(12), C, E, K, and P; flavonoids, lycopene, carotenoids, and phytosterols. and therapeutically important since it is rich with potent antioxidants. Scientifically evaluated pharmacological actions of SBT are like inflammation inhibited by reduced permeability, loss of follicular aggregation of lymphocytes from the inflamed synovium and suppress lymphocyte proliferation(26).

3. Balanced diet
Several minerals and trace elements are essential for normal thyroid hormone metabolism, e.g., iodine, iron, selenium, and zinc. Coexisting deficiencies of these elements can impair thyroid function. Iron deficiency impairs thyroid hormone synthesis by reducing activity of heme-dependent thyroid peroxidase. Iron-deficiency anemia blunts and iron supplementation improves the efficacy of iodine supplementation. Combined selenium and iodine deficiency leads to myxedematous cretinism. The normal thyroid gland retains high selenium concentrations even under conditions of inadequate selenium supply and expresses many of the known selenocysteine-containing proteins. Among these selenoproteins are the glutathione peroxidase, deiodinase, and thioredoxine reductase families of enzymes(27).

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Sources
(a) http://www.ncbi.nlm.nih.gov/pubmed/22147633
(25) http://www.ncbi.nlm.nih.gov/pubmed/20883174
(26) http://www.ncbi.nlm.nih.gov/pubmed/22530142
(27) http://www.ncbi.nlm.nih.gov/pubmed/12487769   http://medicaladvisorjournals.blogspot.com