Medicine

The thyroid hormones, thyroxine (T4) and triiodothyronine (T3), are tyrosine-based hormones produced by the thyroid gland. An important component in the synthesis of thyroid hormones is iodine. The major form of thyroid hormone in the blood is thyroxine (T4), which has a longer half life than T3. The ratio of T4 to T3 released in the blood is roughly 20 to 1. Thyroxine is converted to the active T3 (three to four times more potent than T4) within cells by deiodinases (5'-iodinase). These are further processed by decarboxylation and deiodination to produce iodothyronamine (T1a) and thyronamine (T0a).

Triiodothyronine, C15H12I3NO4, also known as T3, is a thyroid hormone. Thyroid-stimulating hormone (TSH) activates the production of thyroxine (T4) and T3. This process is under regulation. In the thyroid, T4 is converted to T3. TSH is inhibited mainly by T3. The thyroid gland releases greater amounts of T4 than T3, so plasma concentrations of T4 are 40-fold higher than those of T3. Most of the circulating T3 is formed peripherally by deiodination of T4 (85%), a process that involves the removal of iodine from carbon 5 on the outer ring of T4. Thus, T4 acts as prohormone for T3. This thyroid hormone

A low amount of triiodiothyronine (T3, one of the two thyroid hormones) in the blood, due to lack of dietary iodine to make it, gives rise to high levels of thyroid stimulating hormone TSH, which stimulates the thyroid gland to increase many biochemical processes; the cellular growth and proliferation can result in the characteristic swelling or hyperplasia of the thyroid gland, or goiter. The introduction of iodized salt since the early 1900s has eliminated this condition in many affluent countries; however, in Australia, New Zealand, and several European countries, iodine deficiency is a significant public health problem.[4] It is more

Iodine uptake against a concentration gradient is mediated by a sodium-iodine symporter and is linked to a sodium-potassium ATPase. Perchlorate and thiocyanate are drugs that can compete with iodine at this point. Compounds such as goitrin can reduce thyroid hormone production by interfering with iodine oxidation.[3]

Due to the iodine content of the agent (37.3% by weight), abnormalities in thyroid function are common. Amiodarone is structurally similar to thyroxine (a thyroid hormone), which contributes to the effects of amiodarone on thyroid function. Both under- and overactivity of the thyroid may occur on amiodarone treatment. Measurement of free thyroxine (FT4) alone may be unreliable in detecting these problems and thyroid-stimulating hormone (TSH) should therefore also be checked every 6 months.[12] Hypothyroidism (slowing of the thyroid, called the Wolff-Chaikoff effect) occurs frequently; in the SAFE trial, which compared amiodarone with other medications for the treatment of atrial fibrillation, biochemical

The thyronines act on nearly every cell in the body. They act to increase the basal metabolic rate, affect protein synthesis, help regulate long bone growth (synergy with growth hormone), neuronal maturation and increase the body's sensitivity to catecholamines (such as adrenaline) by permissiveness. The thyroid hormones are essential to proper development and differentiation of all cells of the human body. These hormones also regulate protein, fat, and carbohydrate metabolism, affecting how human cells use energetic compounds. They also stimulate vitamin metabolism. Numerous physiological and pathological stimuli influence thyroid hormone synthesis. Thyroid hormone leads to heat generation in humans. However, the

Wolff–Chaikoff effect is used to describe hypothyroidism caused by ingestion of a large amount of iodine.[1] It is an autoregulatory phenomenon which inhibits formation of thyroid hormones inside of the thyroid follicle. This becomes evident secondary to elevated levels of circulating iodide. Wolff-Chaikoff effect lasts several days (around 10 days), after which it is followed by an "escape phenomenon",[2] which is described by resumption of normal organification of iodine and normal thyroid peroxidase function. "Escape phenomenon" was previously believed to occur because of decreased inorganic iodine concentration secondary to down-regulation of sodium-iodide symporter on the basolateral membrane of the thyroid follicular

Iodine is an essential trace element for life, the heaviest element commonly needed by living organisms, and the second-heaviest known to be used by any form of life (only tungsten, a component of a few bacterial enzymes, has a higher atomic number and atomic weight). Iodine's main role in animal biology is as constituents of the thyroid hormones, thyroxine (T4) and triiodothyronine (T3). These are made from addition condensation products of the amino acid tyrosine, and are stored prior to release in an iodine-containing protein called thyroglobulin. T4 and T3 contain four and three atoms of iodine per molecule, respectively.

There are no herbs (plant chemicals) that contain thyroid hormone[7][14]. Therefore, while there are some herbs that may provide some help for a sluggish thyroid (i.e. if the thyroid is producing a low amount of thyroid hormone, but has not stopped completely)[15], myxedema requires treatment with synthetic or desiccated natural thyroid hormones[16][14].

The United States Recommended Daily Allowance (RDA) is 150 micrograms per day (μg/day) for both men and women, with a Tolerable Upper Intake Level (UL) for adults is 1,100 μg/day (1.1 mg/day).[33] The tolerable upper limit was assessed by analyzing the effect of supplementation on thyroid-stimulating hormone.[24] Natural sources of iodine include sea life, such as kelp and certain seafood, as well as plants grown on iodine-rich soil.[34][35] Iodized salt is fortified with iodine.[35] As of 2000, the median intake of iodine from food in the United States was 240 to 300 μg/day for men and 190 to 210 μg/day for women.[33]

Leave a Reply

Name (required)

Mail (will not be published) (required)

Website