| Thyroid Balance |
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The thyroid gland, located at the front of the neck, is one of the body’s main energy regulators. It functions partly like a thermostat and partly like a throttle, controlling the rate at which we “burn” food molecules to produce useful energy and body heat. Like all of the endocrine glands, the thyroid itself is controlled by a series of other structures including the hypothalamus deep in the brain, and the pituitary gland (sometimes called the “master gland”). When it’s working (which is most of the time), this complex system manages to keep us in such a steady state that we’re not even aware of its functioning. But when something goes wrong anywhere in this intricate system with its multiple feedback loops, the result can be chaotic and potentially devastating. The thyroid gland produces thyroid hormone, which occurs in several different forms with different degrees of activity. All thyroid hormone molecules contain iodine, an essential nutrient. Most people are familiar with goiter, an abnormal swelling of the thyroid gland that can result from iodine deficiency, among other causes. Fort unately, iodine deficiency is now rare in the industrialized world by the simple expedient of adding minute amounts of iodine to our salt supply. But thyroid disease still occurs – in fact many nutrition experts argue that it’s much more common than we realize. In particular, so-called subclinical hypothyroidism may affect millions of people who remain unaware that they have the condition, especially among women and older adults1. This term refers to a state in which thyroid hormone levels are “normal” or nearly so – but new research has shown that these levels may in fact still be too low for normal function, particularly with advancing age. Subclinical hypothyroidism has been associated with obesity, depression, cardiac rhythm disturbances, and cognitive decline, and may be a factor in other conditions as well 2-5. Overt, or obvious thyroid deficiencies also occur, as the result of autoimmune diseases, cancers, and other chronic conditions6. The opposite situation, hyperthyroidism, is less common but is potentially even more dangerous. Some forms of hyperthyroidism are also the result of autoimmune attack on the thyroid gland, which stimulates it to exceptionally high output7-10. During severe episodes, people can even experience so-called thyroid storm in which massive outpourings of thyroid hormone can produce deadly hypertension, increased heart rate, and ultimately death 11,12. In most cases of hyperthyroidism the overactive gland eventually “burns out,” leaving the person in a hypothyroid state. Both hyper- and hypothyroidism require a high level of suspicion on the part of the physician in order to diagnose correctly – and both require diligent adherence to medication, diet, and lifestyle changes in order to maintain proper balance. Some nutritional supplements are also helpful, most notably L-carnitine in hyperthyroid states13. Read more about the fascinating progress medical science has made in the diagnosis, management, and (most importantly) prevention of thyroid imbalance in Life Extension Foundation’s Health Concerns Textbook on-line at http://www.lef.org/protocols/metabolic_health/thyroid_regulation_01.htm. References(1) Papi G, Uberti ED, Betterle C et al. Subclinical hypothyroidism. Curr Opin Endocrinol Diabetes Obes. 2007;14:197-208. (2) Verma A, Jayaraman M, Kumar HK, Modi KD. Hypothyroidism and obesity. Cause or Effect? Saudi Med J. 2008;29:1135-1138. (3) van Harten AC, Leue C, Verhey FR. [Should depressive symptoms in patients with subclinical hypothyroidism be treated with thyroid hormone?]. Tijdschr Psychiatr. 2008;50:539-543. (4) Bakiner O, Ertorer ME, Haydardedeoglu FE, Bozkirli E, Tutuncu NB, Demirag NG. Subclinical hypothyroidism is characterized by increased QT interval dispersion among women. Med Princ Pract. 2008;17:390-394. (5) Hogervorst E, Huppert F, Matthews FE, Brayne C. Thyroid function and cognitive decline in the MRC Cognitive Function and Ageing Study. Psychoneuroendocrinology. 2008;33:1013-1022. (6) Staykova ND. Rheumatoid arthritis and thyroid abnormalities. Folia Med (Plovdiv ). 2007;49:5-12. (7) Balazs C. [Hashimoto's thyroiditis, the model of organ-specific autoimmune disorders]. Orv Hetil. 2007;148 Suppl 1:31-3.:31-33. (8) Bagnasco M, Bossert I, Pesce G. Stress and autoimmune thyroid diseases. Neuroimmunomodulation. 2006;13:309-317. (9) Bunevicius R, Prange AJ, Jr. Psychiatric manifestations of Graves' hyperthyroidism: pathophysiology and treatment options. CNS Drugs. 2006;20:897-909. (10) Mezosi E. [Hyperthyroidism]. Orv Hetil. 2006;147:1309-1314. (11) Karger S, Fuhrer D. [Thyroid storm--thyrotoxic crisis: an update]. Dtsch Med Wochenschr. 2008;133:479-484. (12) Kearney T, Dang C. Diabetic and endocrine emergencies. Postgrad Med J. 2007;83:79-86. (13) Benvenga S, Amato A, Calvani M, Trimarchi F. Effects of carnitine on thyroid hormone action. Ann N Y Acad Sci. 2004;1033:158-67.:158-167. |

