What hormones does the thyroid produce?
Thyroid hormones
Thyroid hormones are two hormones produced and released by the thyroid gland, namely triiodothyronine (T) and thyroxine (T). They are tyrosine-based hormones that are primarily responsible for regulation of metabolism. T and T are partially composed of iodine. A deficiency of iodine leads to decreased production of T and T, enlarges the thyroid tissue and will cause the disease known as simple goitre. The major form of thyroid hormone in the blood is thyroxine (T), which has a longer half-life than T. In humans, the ratio of T to T released into the blood is approximately 14:1. T is converted to the active T (three to four times more potent than T) within cells by deiodinases (5'-iodinase). These are further processed by decarboxylation and deiodination to produce iodothyronamine (Ta) and thyronamine (Ta). All three isoforms of the deiodinases are selenium-containing enzymes, thus dietary selenium is essential for T production. Edward Calvin Kendall was responsible for the isolation of thyroxine in 1915.
Thyrotropic cell
Thyrotropes (also called thyrotrophs) are endocrine cells in the anterior pituitary which produce thyroid stimulating hormone (TSH) in response to thyrotropin releasing hormone (TRH). Thyrotropes consist around 5% of the anterior pituitary lobe cells.
Thyroid (journal)
Thyroid is a medical journal in the field of endocrinology, covering research on diseases of the thyroid. It is the official journal of the American Thyroid Association and published by Mary Ann Liebert, Inc..
Thermogenesis
Non-shivering thermogenesis is regulated mainly by thyroid hormone and the sympathetic nervous system. Some hormones, such as norepinephrine and leptin, may stimulate thermogenesis by activating the sympathetic nervous system. Rising insulin levels after eating may be responsible for diet-induced thermogenesis (thermic effect of food).
Progesterone also increases body temperature.
Thyroid hormones
Thyroid hormones (T and T) are produced by the follicular cells of the thyroid gland and are regulated by TSH made by the thyrotropes of the anterior pituitary gland. The effects of T in vivo are mediated via T (T is converted to T in target tissues). T is 3- to 5- fold more active than T.
Tropic hormone
Tropic hormones are hormones that have other endocrine glands as their target. Most tropic hormones are produced and secreted by the anterior pituitary. The hypothalamus secretes tropic hormones that target the anterior pituitary, and the thyroid gland secretes thyroxine, which targets the hypothalamus and therefore can be considered a tropic hormone.
Thyroid disease
Hyperthyroidism is a state in which the body is producing too much thyroid hormone. The main hyperthyroid conditions are:
Certain medications can have the unintended side effect of affecting thyroid function. While some medications can lead to significant hypothyroidism or hyperthyroidism and those at risk will need to be carefully monitored, some medications may affect thyroid hormone lab tests without causing any symptoms or clinical changes, and may not require treatment. The following medications have been linked to various forms of thyroid disease:
Thyroid
About 20,000 protein coding genes are expressed in human cells and 70% of these genes are expressed in the normal thyroid. Some 250 of these genes are more specifically expressed in the thyroid with about 20 genes being highly thyroid specific. The corresponding specific proteins are mainly involved in thyroid hormone synthesis, such as thyroglobulin, TPO and IYD, and expressed in follicular cells. Other proteins elevated in the thyroid are calcitonin related proteins such as CALCA and CALCB, expressed in the parafollicular c-cells.
Thyroid-stimulating hormone
The concentration of thyroid hormones (T and T) in the blood regulates the pituitary release of TSH; when T and T concentrations are low, the production of TSH is increased, and, conversely, when T and T concentrations are high, TSH production is decreased. This is an example of a negative feedback loop. Any inappropriateness of measured values, for instance a low-normal TSH together with a low-normal T may signal tertiary (central) disease and a TSH to TRH pathology. Elevated reverse T (RT) together with low-normal TSH and low-normal T, T values, which is regarded as indicative for euthyroid sick syndrome, may also have to be investigated for chronic subacute thyroiditis (SAT) with output of subpotent hormones. Absence of antibodies in patients with diagnoses of an autoimmune thyroid in their past would always be suspicious for development to SAT even in the presence of a normal TSH because there is no known recovery from autoimmunity.
Thyroid-stimulating hormone
TSH (with a half life of about an hour) stimulates the thyroid gland to secrete the hormone thyroxine (T), which has only a slight effect on metabolism. T is converted to triiodothyronine (T), which is the active hormone that stimulates metabolism. About 80% of this conversion is in the liver and other organs, and 20% in the thyroid itself.
Hypothyroidism
In 1971, the thyroid stimulating hormone (TSH) radioimmunoassay was developed, which was the most specific marker for assessing thyroid status in patients. Many people who were being treated based on basal metabolic rate, minimizing hypothyroid symptoms, or based on serum protein-bound iodine, were found to have excessive thyroid hormone. The following year, in 1972, a T3 radioimmunoassay was developed, and in 1974, a T4 radioimmunoassay was developed.
Hypothyroidism
The thyroid gland is the only source of thyroid hormone in the body; the process requires iodine and the amino acid tyrosine. Iodine in the bloodstream is taken up by the gland and incorporated into thyroglobulin molecules. The process is controlled by the thyroid-stimulating hormone (TSH, thyrotropin), which is secreted by the pituitary. Not enough iodine, or not enough TSH, can result in decreased production of thyroid hormones.
Thyroid function tests
A TFT panel typically includes thyroid hormones such as thyroid-stimulating hormone (TSH, thyrotropin) and thyroxine (T4), and triiodothyronine (T3) depending on local laboratory policy.
Thyroglobulin
The protein is a precursor of the thyroid hormones; these are produced when thyroglobulin's tyrosine residues are combined with iodine and the protein is subsequently cleaved. Each thyroglobulin molecule contains approximately 100-120 tyrosine residues, but only a small number (20) of these are subject to iodination by thyroperoxidase in the follicular colloid. Therefore, each Tg molecule forms only approximately 10 thyroid hormone molecules.
Thyroid function tests
TSH is produced in the pituitary gland. The production of TSH is controlled by thyrotropin-releasing hormone (TRH), which is produced in the hypothalamus. TSH levels may be suppressed by excess free T3 (fT3) or free T4 (fT4) in the blood.
Thyroid disease
The parathyroid glands produce parathyroid hormone (PTH), a hormone needed to maintain adequate amounts of calcium in the blood. Removal results in hypoparathyroidism and a need for supplemental calcium and vitamin D each day. In the event that the blood supply to any one of the parathyroid glands is endangered through surgery, the parathyroid gland(s) involved may be re-implanted in surrounding muscle tissue.
Thyroid disease
Autoimmune thyroid disease is a general category of disease that occurs due to the immune system targeting its own body. It is not fully understood why this occurs, but it is thought to be partially genetic as these diseases tend to run in families. In one of the most common types, Grave's Disease, the body produces antibodies against the TSH receptor on thyroid cells. This causes the receptor to activate even without TSH being present and causes the thyroid to produce and release excess thyroid hormone (hyperthyroidism). Another common form of autoimmune thyroid disease is Hashimoto thyroiditis where the body produces antibodies against different normal components of the thyroid gland, most commonly thyroglobulin, thyroid peroxidase, and the TSH receptor. These antibodies cause the immune system to attack the thyroid cells and cause inflammation (lymphocytic infiltration) and destruction (fibrosis) of the gland.
Levothyroxine
The primary pathway of thyroid hormone metabolism is through sequential deiodination. The liver is the main site of T4 deiodination, and along with the kidneys are responsible for about 80% of circulating T3. In addition to deiodination, thyroid hormones are also excreted through the kidneys and metabolized through conjugation and glucuronidation and excreted directly into the bile and the gut where they undergo enterohepatic recirculation.
Thyroid
The core of a follicle is surrounded by a single layer of follicular cells. When stimulated by thyroid stimulating hormone (TSH), these secrete the thyroid hormones T3 and T4. They do this by transporting and metabolising the thyroglobulin contained in the colloid. Follicular cells vary in shape from flat to cuboid to columnar, depending on how active they are.
Hypothalamic–pituitary–thyroid axis
Both peripheral thyroid hormones (iodothyronines) inhibit thyrotropin secretion from the pituitary (negative feedback). Consequently, equilibrium concentrations for all hormones are attained.
Transgender hormone therapy (female-to-male)
In all people, the hypothalamus releases GnRH (gonadotropin-releasing hormone) to stimulate the pituitary to produce LH (luteinizing hormone) and FSH (follicle-stimulating hormone) which in turn cause the gonads to produce sex steroids. In adolescents of either sex with relevant indicators, GnRH analogues, such as leuprorelin can be used to suspend the advance of sex steroid induced, inappropriate pubertal changes for a period without inducing any changes in the gender-appropriate direction. GnRH analogues work by initially over stimulating the pituitary then rapidly desensitizing it to the effects of GnRH. Over a period of weeks, gonadal androgen production is greatly reduced. There is considerable controversy over the earliest age, and for how long it is clinically, morally and legally safe to do this. The Harry Benjamin International Gender Dysphoria Association Standards of Care permit from Tanner Stage 2, but do not allow the addition of gender-appropriate hormones until 16, which could be five or more years. The sex steroids do have important other functions. The high cost of GnRH analogues is often a significant factor.
Liothyronine
Liothyronine is a synthetic form of triiodothyronine (T3), a thyroid hormone used to treat hypothyroidism and myxedema coma. T3 is the metabolically active thyroid hormone, which causes feedback inhibition, and lowers elevated TSH levels. It increases metabolism in peripheral tissues and is indicated when there is an impaired conversion of T4 to T3 in peripheral tissues. It is also used as an augmentation strategy in treating major depressive disorder when used in combination with antidepressants. It is marketed as the sodium salt under the brand name Cytomel (or Tertroxin in Australia).
Thyroid
The thyroid is supplied with arterial blood from the superior thyroid artery, a branch of the external carotid artery, and the inferior thyroid artery, a branch of the thyrocervical trunk, and sometimes by an anatomical variant the thyroid ima artery, which has a variable origin. The superior thyroid artery splits into anterior and posterior branches supplying the thyroid, and the inferior thyroid artery splits into superior and inferior branches. The superior and inferior thyroid arteries join together behind the outer part of the thyroid lobes. The venous blood is drained via superior and middle thyroid veins, which drain to the internal jugular vein, and via the inferior thyroid veins. The inferior thyroid veins originate in a network of veins and drain into the left and right brachiocephalic veins. Both arteries and veins form a plexus between the two layers of the capsule of the thyroid gland.
Thyroid
The primary function of the thyroid is the production of the iodine-containing thyroid hormones, triiodothyronine (T) and thyroxine (T) and the peptide hormone calcitonin. T is so named because it contains three atoms of iodine per molecule and T contains four atoms of iodine per molecule. The thyroid hormones have a wide range of effects on the human body. These include:
Thyroid hormones
Thyroxine is believed to be a prohormone and a reservoir for the most active and main thyroid hormone T. T is converted as required in the tissues by iodothyronine deiodinase. Deficiency of deiodinase can mimic hypothyroidism due to iodine deficiency. T is more active than T, though it is present in less quantity than T.
Thyroid storm
The precise mechanism for the development of thyroid storm is poorly understood. In the human body, thyroid hormone may be free (biologically active T3/T4) or bound to thyroid binding hormone (biologically inactive) to be transported. The release of thyroid hormone is tightly regulated by a feedback system involving the hypothalamus, pituitary gland, and thyroid gland. Hyperthyroidism results from a dysregulation of this system that eventually leads to increases in levels of free T3/T4. The transition from simple hyperthyroidism to the medical emergency of thyroid storm may be triggered by conditions (see Causes) that lead to the following:
Hyperthyroidism
Thyroid hormone is critical to normal function of cells. In excess, it both overstimulates metabolism and exacerbates the effect of the sympathetic nervous system, causing "speeding up" of various body systems and symptoms resembling an overdose of epinephrine (adrenaline). These include fast heart beat and symptoms of palpitations, nervous system tremor such as of the hands and anxiety symptoms, digestive system hypermotility, unintended weight loss, and (in "lipid panel" blood tests) a lower and sometimes unusually low serum cholesterol.
Hormone
One special group of hormones is the tropic hormones that stimulate the hormone production of other endocrine glands. For example, thyroid-stimulating hormone (TSH) causes growth and increased activity of another endocrine gland, the thyroid, which increases output of thyroid hormones.
Thyroid
The thyroid gland also produces the hormone calcitonin, which helps regulate blood calcium levels. Parafollicular cells produce calcitonin in response to high blood calcium. Calcitonin decreases the release of calcium from bone, by decreasing the activity of osteoclasts, cells which break down bone. Bone is constantly reabsorbed by osteoclasts and created by osteoblasts, so calcitonin effectively stimulates movement of calcium into bone. The effects of calcitonin are opposite those of the parathyroid hormone (PTH) produced in the parathyroid glands. However, calcitonin seems far less essential than PTH, as calcium metabolism remains clinically normal after removal of the thyroid (thyroidectomy), but not the parathyroid glands.
Thyroid disease in women
Untreated or poorly treated underactive thyroid can lead to problems for the mother, such as:
It also can cause serious problems for the baby, such as:During pregnancy, women may want to see both an OB/GYN and an endocrinologist, a doctor who treats people with hormone problems. Levothyroxine is safe to use during pregnancy and necessary for the health of the baby. Women with Hashimoto's disease or an underactive thyroid who are taking levothyroxine before pregnancy may need a higher dose to maintain normal thyroid function. Clinicians may check thyroid function every 6 to 8 weeks during pregnancy. After delivery, hormone levels usually go back to the pre-pregnancy level.
Thyroid hormone resistance
The syndrome can present with variable symptoms, even between members of the same family harboring the same mutation. Typically most or all tissues are resistant to thyroid hormone, so despite raised measures of serum thyroid hormone the individual may appear euthyroid (have no symptoms of over- or underactivity of the thyroid gland). The most common symptoms are goiter and tachycardia. It has also been linked to some cases of attention deficit hyperactivity disorder (ADHD), although the majority of people with that diagnosis have no thyroid problems.
Thyroid storm
The primary treatment of thyroid storm is with inorganic iodine and antithyroid drugs (propylthiouracil or methimazole) to reduce synthesis and release of thyroid hormone. Temperature control and intravenous fluids are also mainstays of management. Beta blockers are often used to reduce the effects of thyroid hormone. Patients often require admission to the intensive care unit.
Kenneth Sterling
Sterling was one of the first researchers to use radioactive iodine to treat thyroid diseases. He used radioisotopic labels to study the metabolism of human serum proteins and red blood cells. He discovered that the body converts the pro-hormone thyroxine into triiodothyronine, the primary active form of thyroid hormone. This breakthrough led to a new field of thyroid hormone research and led to the first early studies on the mechanism of action of thyroid hormones. Sterling developed the equilibrium dialysis method for measuring free thyroxine, which remains the gold standard for evaluating free hormone levels in blood today. Sterling was a pioneering investigator identifying mitochondrial thyroid hormone receptors, shortened isoforms of the full-length, nuclear receptors. He wrote a chapter on thyroid hormone receptors in the fifth edition of "Werner's The Thyroid: A Fundamental and Clinical Text", which is known as "the bible of modern thyroidology."
Steroid hormone
Steroid hormones help control metabolism, inflammation, immune functions, salt and water balance, development of sexual characteristics, and the ability to withstand illness and injury. The term steroid describes both hormones produced by the body and artificially produced medications that duplicate the action for the naturally occurring steroids.
Thyroid-stimulating hormone
The TSH receptor is found mainly on thyroid follicular cells. Stimulation of the receptor increases T and T production and secretion. This occurs through stimulation of six steps in thyroid hormone synthesis: (1) Up-regulating the activity of the sodium-iodide symporter (NIS) on the basolateral membrane of follicular cells, thereby increasing intracellular concentrations of iodine (iodine trapping). (2) Stimulating iodination of thyroglobulin in the follicular lumen, a precursor protein of thyroid hormone. (3) Stimulating the conjugation of iodinated tyrosine residues. This leads to the formation of thyroxine (T) and triiodothyronine (T) that remain attached to the thyroglobulin protein. (4) Increased endocytocis of the iodinated thyroglobulin protein across the apical membrane back into the follicular cell. (5) Stimulation of proteolysis of iodinated thyroglobulin to form free thyroxine (T) and triiodothyronine (T). (6) Secretion of thyroxine (T) and triiodothyronine (T) across the basolateral membrane of follicular cells to enter the circulation. This occurs by an unknown mechanism.
Breast development
Insulin, glucocorticoids such as cortisol (and by extension adrenocorticotropic hormone (ACTH)), and thyroid hormones such as thyroxine (and by extension thyroid-stimulating hormone (TSH) and thyrotropin-releasing hormone (TRH)) also play permissive but less well-understood/poorly-characterized roles in breast development during both puberty and pregnancy, and are required for full functional development. Leptin has also been found to be an important factor in mammary gland development, and has been found to promote mammary epithelial cell proliferation.
Hypothyroidism
Thyroid hormone is required for the normal functioning of numerous tissues in the body. In healthy individuals, the thyroid gland predominantly secretes thyroxine (T), which is converted into triiodothyronine (T) in other organs by the selenium-dependent enzyme iodothyronine deiodinase. Triiodothyronine binds to the thyroid hormone receptor in the nucleus of cells, where it stimulates the turning on of particular genes and the production of specific proteins. Additionally, the hormone binds to integrin αvβ3 on the cell membrane, thereby stimulating the sodium–hydrogen antiporter and processes such as formation of blood vessels and cell growth. In blood, almost all thyroid hormone (99.97%) is bound to plasma proteins such as thyroxine-binding globulin; only the free unbound thyroid hormone is biologically active. Overexpression of deiodinase can thus lead to consumptive hypothyroidism.
Thyroid peroxidase
Thyroid peroxidase, also called thyroperoxidase (TPO) or iodide peroxidase, is an enzyme expressed mainly in the thyroid where it is secreted into colloid. Thyroid peroxidase oxidizes iodide ions to form iodine atoms for addition onto tyrosine residues on thyroglobulin for the production of thyroxine (T) or triiodothyronine (T), the thyroid hormones. In humans, thyroperoxidase is encoded by the "TPO" gene.
Adrenal tumor
The adrenal cortex is composed of three distinct layers of endocrine cells which produce critical steroid hormones. These include the glucocorticoids which are critical for regulation of blood sugar and the immune system, as well as response to physiological stress, the mineralcorticoid aldosterone, which regulates blood pressure and kidney function, and certain sex hormones. Both benign and malignant tumors of the adrenal cortex may produce steroid hormones, with important clinical consequences.
Thyroid hormones
Thyroid hormone leads to heat generation in humans. However, the thyronamines function via some unknown mechanism to inhibit neuronal activity; this plays an important role in the hibernation cycles of mammals and the moulting behaviour of birds. One effect of administering the thyronamines is a severe drop in body temperature.
Neuroendocrinology
The first of these factors to be identified are thyrotropin-releasing hormone (TRH) and gonadotropin-releasing hormone (GnRH). TRH is a small peptide that stimulates the secretion of thyroid-stimulating hormone; GnRH (also called luteinizing hormone-releasing hormone) stimulates the secretion of luteinizing hormone and follicle-stimulating hormone.
Hormone
Many hormones and their structural and functional analogs are used as medication. The most commonly prescribed hormones are estrogens and progestogens (as methods of hormonal contraception and as HRT), thyroxine (as levothyroxine, for hypothyroidism) and steroids (for autoimmune diseases and several respiratory disorders). Insulin is used by many diabetics. Local preparations for use in otolaryngology often contain pharmacologic equivalents of adrenaline, while steroid and vitamin D creams are used extensively in dermatological practice.
Thyroid hormones
Thyroxine (3,5,3',5'-tetraiodothyronine) is produced by follicular cells of the thyroid gland. It is produced as the precursor thyroglobulin (this is "not" the same as thyroxine-binding globulin (TBG)), which is cleaved by enzymes to produce active T.
Thyroid hormones
The thyroid hormones 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) and neural 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 storm
High levels of thyroid hormone result in a hypermetabolic state, which can result in increased breakdown of cortisol, a hormone produced by the adrenal gland. This results in a state of relative adrenal insufficiency, in which the amount of cortisol is not sufficient. Guidelines recommend that corticosteroids (hydrocortisone and dexamethasone are preferred over prednisolone or methylprednisolone) be administered to all patients with thyroid storm. However, doses should be altered for each individual patient to ensure that the relative adrenal insufficiency is adequately treated while minimizing the risk of side effects.
Heart rate
In general, increased levels of the thyroid hormones (thyroxine(T4) and triiodothyronine (T3)), increase the heart rate; excessive levels can trigger tachycardia. The impact of thyroid hormones is typically of a much longer duration than that of the catecholamines. The physiologically active form of triiodothyronine, has been shown to directly enter cardiomyocytes and alter activity at the level of the genome. It also impacts the beta adrenergic response similar to epinephrine and norepinephrine.
Hashimoto's thyroiditis
Given the relatively non-specific symptoms of initial hypothyroidism, Hashimoto's thyroiditis is often misdiagnosed as depression, cyclothymia, PMS, chronic fatigue syndrome, fibromyalgia and, less frequently, as erectile dysfunction or an anxiety disorder. On gross examination, there is often presentation of a hard goiter that is not painful to the touch; other symptoms seen with hypothyroidism, such as periorbital myxedema, depend on the current state of progression of the response, especially given the usually gradual development of clinically relevant hypothyroidism. Testing for thyroid-stimulating hormone (TSH), free T3, free T4, and the anti-thyroglobulin antibodies (anti-Tg), anti-thyroid peroxidase antibodies (anti-TPO, or TPOAb) and anti-microsomal antibodies can help obtain an accurate diagnosis. Earlier assessment of the person may present with elevated levels of thyroglobulin owing to transient thyrotoxicosis, as inflammation within the thyroid causes damage to the integrity of thyroid follicle storage of thyroglobulin; TSH secretion from the anterior pituitary increases in response to a decrease in negative feedback inhibition secondary to decreased serum thyroid hormones. Typically T4 is the preferred thyroid hormone test for hypothyroidism. This exposure of the body to substantial amounts of previously isolated thyroid enzymes is thought to contribute to the exacerbation of tolerance breakdown, giving rise to the more pronounced symptoms seen later in the disease. Lymphocytic infiltration of the thyrocyte-associated tissues often leads to the histologically significant finding of germinal center development within the thyroid gland.
Thyroxine-binding globulin
Thyroxine-binding globulin (TBG) is a globulin that binds thyroid hormones in circulation. It is one of three transport proteins (along with transthyretin and serum albumin) responsible for carrying the thyroid hormones thyroxine (T) and triiodothyronine (T) in the bloodstream. Of these three proteins, TBG has the highest affinity for T and T but is present in the lowest concentration. Despite its low concentration, TBG carries the majority of T in the blood plasma. Due to the very low concentration of T and T in the blood, TBG is rarely more than 25% saturated with its ligand. Unlike transthyretin and albumin, TBG has a single binding site for T/T. TBG is synthesized primarily in the liver as a 54-kDa protein. In terms of genomics, TBG is a serpin; however, it has no inhibitory function like many other members of this class of proteins.
Thyroid
An underactive thyroid gland results in hypothyroidism. Typical symptoms are abnormal weight gain, tiredness, constipation, heavy menstrual bleeding, hair loss, cold intolerance, and a slow heart rate. Iodine deficiency is the most common cause of hypothyroidism worldwide, and the autoimmune disease Hashimoto's thyroiditis is the most common cause in the developed world. Other causes include congenital abnormalities, diseases causing transient inflammation, surgical removal or radioablation of the thyroid, the drugs amiodarone and lithium, amyloidosis, and sarcoidosis. Some forms of hypothyroidism can result in myxedema and severe cases can result in myxedema coma.
Iodine in biology
In vertebrate biology, iodine's primary function is as a constituent of the thyroid hormones, thyroxine (T4) and triiodothyronine (T3). These molecules 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; iodine accounts for 65% of the molecular weight of T4 and 59% of T3. The thyroid gland actively absorbs iodine from the blood to produce and release these hormones into the blood, actions which are regulated by a second hormone, called thyroid-stimulating hormone (TSH), which is produced by the pituitary gland. Thyroid hormones are phylogenetically very old molecules which are synthesized by most multicellular organisms, and which even have some effect on unicellular organisms.
Desiccated thyroid extract
Brands include NP Thyroid , Nature-Throid, and Armour . All brands consist of desiccated porcine thyroid powder, differing only in binders and fillers. They contain a mixture of thyroid hormones: T4 (thyroxine) & T3 (triiodothyronine), in the proportions usually present in pig thyroids (approximately 80% T4 and 20% T3).
Thyroid hormones
Today most patients are treated with levothyroxine, or a similar synthetic thyroid hormone. Different polymorphs of the compound have different solubilities and potencies. Additionally, natural thyroid hormone supplements from the dried thyroids of animals are still available. Levothyroxine contains T4 only and is therefore largely ineffective for patients unable to convert T4 to T3. These patients may choose to take natural thyroid hormone, as it contains a mixture of T4 and T3, or alternatively supplement with a synthetic T3 treatment. In these cases, synthetic liothyronine is preferred due to the potential differences between the natural thyroid products. Some studies show that the mixed therapy is beneficial to all patients, but the addition of lyothyronine contains additional side effects and the medication should be evaluated on an individual basis. Some natural thyroid hormone brands are FDA approved, but some are not. Thyroid hormones are generally well tolerated. Thyroid hormones are usually not dangerous for pregnant women or nursing mothers, but should be given under a doctor's supervision. In fact, if a woman who is hypothyroid is left untreated, her baby is at a higher risk for birth defects. When pregnant, a woman with a low-functioning thyroid will also need to increase her dosage of thyroid hormone. One exception is that thyroid hormones may aggravate heart conditions, especially in older patients; therefore, doctors may start these patients on a lower dose and work up to a larger one to avoid risk of heart attack.
Thyroid hormones
Both T and T are used to treat thyroid hormone deficiency (hypothyroidism). They are both absorbed well by the gut, so can be given orally. Levothyroxine is the pharmaceutical name of the manufactured version of T, which is metabolised more slowly than T and hence usually only needs once-daily administration. Natural desiccated thyroid hormones are derived from pig thyroid glands, and are a "natural" hypothyroid treatment containing 20% T and traces of T, T and calcitonin.
Also available are synthetic combinations of T/T in different ratios (such as liotrix) and pure-T medications (INN: liothyronine).
Levothyroxine Sodium is usually the first course of treatment tried. Some patients feel they do better on desiccated thyroid hormones; however, this is based on anecdotal evidence and clinical trials have not shown any benefit over the biosynthetic forms. Thyroid tablets are reported to have different effects, which can be attributed to the difference in torsional angles surrounding the reactive site of the molecule.
Wolff–Chaikoff effect
The Wolff–Chaikoff effect is known as an autoregulatory phenomenon that inhibits organification in the thyroid gland, the formation of thyroid hormones inside the thyroid follicle, and the release of thyroid hormones into the bloodstream. This becomes evident secondary to elevated levels of circulating iodide. The Wolff–Chaikoff effect is an effective means of rejecting a large quantity of imbibed iodide, and therefore preventing the thyroid from synthesizing large quantities of thyroid hormone. Excess iodide transiently inhibits thyroid iodide organification. In individuals with a normal thyroid, the gland eventually escapes from this inhibitory effect and iodide organification resumes; however, in patients with underlying autoimmune thyroid disease, the suppressive action of high iodide may persist. 
The Wolff–Chaikoff effect lasts several days (around 10 days), after which it is followed by an "escape phenomenon," which is described by resumption of normal organification of iodine and normal thyroid peroxidase function. "Escape phenomenon" is believed to occur because of decreased inorganic iodine concentration inside the thyroid follicle below a critical threshold secondary to down-regulation of sodium-iodide symporter (NIS) on the basolateral membrane of the thyroid follicular cell.
Hypothyroidism
Pregnancy leads to marked changes in thyroid hormone physiology. The gland is increased in size by 10%, thyroxine production is increased by 50%, and iodine requirements are increased. Many women have normal thyroid function but have immunological evidence of thyroid autoimmunity (as evidenced by autoantibodies) or are iodine deficient, and develop evidence of hypothyroidism before or after giving birth.
Hormone
Hormone secretion may occur in many tissues. Endocrine glands are the cardinal example, but specialized cells in various other organs also secrete hormones. Hormone secretion occurs in response to specific biochemical signals from a wide range of regulatory systems. For instance, serum calcium concentration affects parathyroid hormone synthesis; blood sugar (serum glucose concentration) affects insulin synthesis; and because the outputs of the stomach and exocrine pancreas (the amounts of gastric juice and pancreatic juice) become the input of the small intestine, the small intestine secretes hormones to stimulate or inhibit the stomach and pancreas based on how busy it is. Regulation of hormone synthesis of gonadal hormones, adrenocortical hormones, and thyroid hormones is often dependent on complex sets of direct influence and feedback interactions involving the hypothalamic-pituitary-adrenal (HPA), -gonadal (HPG), and -thyroid (HPT) axes.
Thyroid function tests
Accurate interpretation takes a variety of factors into account, such as the thyroid hormones i.e. thyroxine (T) and triiodothyronine (T), current medical status (such as pregnancy), certain medications like propylthiouracil, temporal effects including circadian rhythm and hysteresis, and other past medical history.
Kent Holtorf
Holtorf states that the standard thyroid tests which are typically relied upon by primary care and specialist physicians to diagnosis hypothyroidism (low thyroid) and determine dosage are insufficient because they focus on TSH levels as an indicator of thyroid function and miss a large percentage of people with low thyroid. This is discussed extensively on the website of his nonprofit organization the National Academy of Hypothyroidism. Instead, Holtorf advocates labs and diagnostics which look at all thyroid hormone levels, with a particular emphasis on free T3, triodothyronine, the active hormone both produced by the thyroid and converted from T4, levothyroxine, and reverse T3, a metabolite of T4 conversion usually created during times of stress or trauma. This is contrary to position statements by societies such as the American Thyroid Association and American Association of Clinical Endocrinologist. Holtorf condones treating hypothyroidism with compounded combinations of bioidentical thyroid hormones.
Thyroid
Thyroid follicles are small spherical groupings of cells 0.02–0.9mm in diameter that play the main role in thyroid function. They consist of a rim that has a rich blood supply, nerve and lymphatic presence, that surrounds a core of colloid that consists mostly of thyroid hormone precursor proteins called thyroglobulin, an iodinated glycoprotein.
Maternal hypothyroidism
Maternal hypothyroidism is hypothyroidism in pregnant mothers. Even with appropriate treatment, it may pose risks not only to the mother, but also to the fetus. Thyroid hormones, T4 and TSH, diffuse across the placenta traveling from the mother to fetus for 10–12 weeks before the fetus’s own thyroid gland can begin synthesizing its own thyroid hormones. The mother continues to supply some T4 to the fetus even after he/she is able to synthesize his/her own. Infants with sporadic congenital hypothyroidism show T4 concentrations in the umbilical cord suggesting the mother is still providing 25-50 percent of T4. If these infants are not screened soon after birth for their hypothyroidism and treated, the infants can become permanently intellectually disabled, since they can’t meet their bodies demand for T4.
Hypothalamic–pituitary–gonadal axis
These two hormones play an important role in communicating to the gonads. In females FSH and LH act primarily to activate the ovaries to produce estrogen and inhibin and to regulate the menstrual cycle and ovarian cycle. Estrogen forms a negative feedback loop by inhibiting the production of GnRH in the hypothalamus. Inhibin acts to inhibit activin, which is a peripherally produced hormone that positively stimulates GnRH-producing cells. Follistatin, which is also produced in all body tissue, inhibits activin and gives the rest of the body more control over the axis. In males LH stimulates the interstitial cells located in the testes to produce testosterone, and FSH plays a role in spermatogenesis. Only small amounts of estrogen are secreted in males. Recent research has shown that a neurosteroid axis exists, which helps the cortex to regulate the hypothalamus’s production of GnRH.
Iodine in biology
Selenium also plays a very important role in the production of glutathione, the body's most powerful antioxidant. During the production of the thyroid hormones, hydrogen peroxide is produced in large quantities, and therefore high iodine in the absence of selenium can destroy the thyroid gland (often described as a sore throat feeling); the peroxides are neutralized through the production of glutathione from selenium. In turn, an excess of selenium increases demand for iodine, and deficiency will result when a diet is high in selenium and low in iodine.
Endocrine gland
The thyroid hormones increase the rate of cellular metabolism, and include thyroxine (T4) and triiodothyronine (T3). Secretion is stimulated by the hormone TSH, secreted by the anterior pituitary. When thyroid levels are high, there is negative feedback that decreases the amount of TSH secreted. Most T4 is converted to T3 (a more active form) in the target tissues.
Thyroiditis
Thyroiditis is the inflammation of the thyroid gland. The thyroid gland is located on the front of the neck below the laryngeal prominence, and makes hormones that control metabolism.
Thyroidectomy
The thyroid produces several hormones, such as thyroxine (T4), triiodothyronine (T3), and calcitonin.
Goitrogen
Goitrogens are substances that disrupt the production of thyroid hormones by interfering with iodine uptake in the thyroid gland. This triggers the pituitary to release thyroid-stimulating hormone (TSH), which then promotes the growth of thyroid tissue, eventually leading to goiter.
Releasing and inhibiting hormones
For example, thyrotropin-releasing hormone (TRH) is released from the hypothalamus in response to low levels of secretion of thyroid-stimulating hormone (TSH) from the pituitary gland. The TSH in turn is under feedback control by the thyroid hormones T4 and T3. When the level of TSH is too high, they feed back on the brain to shut down the secretion of TRH. Synthetic TRH is also used by physicians as a test of TSH reserve in the pituitary gland as it should stimulate the release of TSH and prolactin from this gland.
Thyroid hormones
Thyronamines have no medical usages yet, though their use has been proposed for controlled induction of hypothermia, which causes the brain to enter a protective cycle, useful in preventing damage during ischemic shock.
Antithyroid autoantibodies
Anti-thyroid peroxidase (anti-TPO) antibodies are specific for the autoantigen TPO, a 105kDa glycoprotein that catalyses iodine oxidation and thyroglobulin tyrosyl iodination reactions in the thyroid gland. Most antibodies produced are directed to conformational epitopes of the immunogenic carboxyl-terminal region of the TPO protein, although antibodies to linear epitopes have been seen. Anti-TPO antibodies are the most common anti-thyroid autoantibody, present in approximately 90% of Hashimoto's thyroiditis, 75% of Graves' disease and 10-20% of nodular goitre or thyroid carcinoma. Also, 10-15% of normal individuals can have high level anti-TPO antibody titres. High serum antibodies are found in active phase chronic autoimmune thyroiditis. Thus, an antibody titer can be used to assess disease activity in patients that have developed such antibodies. The majority of anti-TPO antibodies are produced by thyroid infiltrating lymphocytes, with minor contributions from lymph nodes and the bone marrow. They cause thyroid cell damage by complement activation and antibody dependent cell cytotoxicity. However, anti-TPO antibodies are not believed to contribute to the destruction of the thyroid.
Thyroid
Iodine is essential for the production of the thyroid hormones. Iodine (I) travels in the blood as iodide (I), which is taken up into the follicular cells by a sodium-iodide symporter. This is an ion channel on the cell membrane which in the same action transports two sodium ions and an iodide ion into the cell. Iodide then travels from within the cell into the follicular space, through the action of pendrin, an iodide-chloride antiporter. In the follicular space, the iodide is then oxidized to iodine. This makes it more reactive, and the iodine is attached to the active tyrosine units in thyroglobulin by the enzyme thyroid peroxidase. This forms the precursors of thyroid hormones monoiodotyrosine (MIT), and diiodotyrosine (DIT).
Thyroid disease
Thyroid disease is a medical condition that affects the function of the thyroid gland. The thyroid gland is located at the front of the neck and produces thyroid hormones that travel through the blood to help regulate many other organs, meaning that it is an endocrine organ. These hormones normally act in the body to regulate energy use, infant development, and childhood development.
Thyroid-stimulating hormone
TSH is secreted throughout life but particularly reaches high levels during the periods of rapid growth and development, as well as in response to stress.
Hürthle cell adenoma
There are three main treatments for Hürthle cell adenomas. Once the adenoma is detected most often the nodules removed to prevent the cells from later metastisizing. A total thyroidectomy is often performed, this results in a complete removal of the thyroid. Some patients may only have half of their thyroid removed, this is known as a thyroid lobectomy. Another treatment option includes pharmacological suppression of thyroid hormone. The thyroid gland is responsible for producing the thyroid hormones triiodothyronine (T3) and thyroxine (T4). Patients with suppressed thyroid function often require oral thyroid replacement (e.g. levothyroxine) in order to maintain normal thyroid hormone levels. The final treatment option is RAI ablation (radioactive iodine ablation). This treatment option is used to destroy infected thyroid cells after total thyroidectomy. This treatment does not change prognosis of disease, but will diminish the recurrence rate. Also, Hürthle cells do not respond well to RAI. However, often doctors suggest this treatment to patients with Hürthle cell adenoma and Hürthle cell carcinoma because some Hürthle cells will respond and it will kill remaining tissue.
Hypothalamic–pituitary hormone
Hypothalamic–pituitary hormones are hormones that are produced by the hypothalamus and pituitary gland. Although the organs in which they are produced are relatively small, the effects of these hormones cascade throughout the body. They can be classified as a hypothalamic–pituitary axis (HP axis) of which the adrenal (), gonadal (), thyroid (), somatotropic (), and prolactin () axes are branches.
Thyroid hormones
Ta and Ta are positively charged and do not cross the membrane; they are believed to function via the trace amine-associated receptor (TAR1, TA1), a G-protein-coupled receptor located in the cell membrane.
Endocrinology
Amines, such as norepinephrine, epinephrine, and dopamine (catecholamines), are derived from single amino acids, in this case tyrosine. Thyroid hormones such as 3,5,3’-triiodothyronine (T3) and 3,5,3’,5’-tetraiodothyronine (thyroxine, T4) make up a subset of this class because they derive from the combination of two iodinated tyrosine amino acid residues.
Derek George Smyth
54. Bilek, R., Gkonos, P.J., Tavianini, M., Smyth, D.G. and Roos, B.A. (1992) The thyrotropin releasing hormone (TRH)-like peptides in rat prostate are not formed by expression of the TRH gene but are suppressed by thyroid hormone. J. Endocrinol., 132, 177-184.
Thyroid
Excessive production of the thyroid hormones is called hyperthyroidism, which is most commonly a result of Graves' disease, a toxic multinodular goitre, a solitary thyroid adenoma, or inflammation. Other causes include drug-induced excess of iodine, particularly from amiodarone, an antiarrhythmic medication; an excess caused by the preferential uptake of iodine by the thyroid following iodinated contrast imaging; or from pituitary adenomas which may cause an overproduction of thyroid stimulating hormone. Hyperthyroidism often causes a variety of non-specific symptoms including weight loss, increased appetite, insomnia, decreased tolerance of heat, tremor, palpitations, anxiety and nervousness. In some cases it can cause chest pain, diarrhoea, hair loss and muscle weakness. Such symptoms may be managed temporarily with drugs such as beta blockers.
Thyroid hormone resistance
Hypothalamus secretes a hormone called thyrotropin releasing hormone (TRH) which in turn release thyroid stimulating hormone (TSH). TSH signals thyroid to secrete thyroid hormones thyroxine (T4) and triiodothyronine (T3). T4 gets converted to active T3 in peripheral tissues with the help of deiodinase enzymes. T3 negatively feedback on the pituitary and decreases TSH secretion.
Thyroid function tests
Drugs can profoundly affect thyroid function tests. Listed below is a selection of important effects.
↓: reduced serum concentration or structure parameter; ↑: increased serum concentration or structure parameter; ↔: no change; TSH: Thyroid-stimulating hormone; T: Total triiodothyronine; T: Total thyroxine; fT: Free thyroxine; fT: Free triiodothyronine; rT: Reverse triiodothyronineThe Centers for Disease Control and Prevention has published the following laboratory procedure manuals for measuring thyroid-stimulating hormone:
Thyroid hormones
Little is known about intracellular kinetics of thyroid hormones. However, recently it could be demonstrated that the crystallin CRYM binds 3,5,3′-triiodothyronine in vivo.
Fetal programming
Thyroid hormones play an instrumental role during the early development of the fetus's brain. Therefore, mothers suffering from thyroid-related issues and altered thyroid hormone levels may inadvertently trigger structural and functional changes in the fetal brain. The fetus is able to produce its own thyroid hormones from the onset of the second trimester; however, maternal thyroid hormones are important for brain development before and after the baby is able to synthesize the hormones while still in the uterus. Due to this, the baby may experience an increased risk of neurological or psychiatric diseases later in life.
Thyroglobulin
Thyroglobulin (Tg) is a 660 kDa, dimeric protein produced by the follicular cells of the thyroid and used entirely within the thyroid gland. Thyroglobulin protein accounts for approximately half of the protein content of the thyroid gland. Human TG (HTG) is a homodimer of subunits each containing 2768 amino acids as synthesized (a short signal peptide may be removed from the N-terminus in the mature protein).
Plastic pollution
Bisphenol A affects gene expression related to the thyroid hormone axis, which affects biological functions such as metabolism and development. BPA can decrease thyroid hormone receptor (TR) activity by increasing TR transcriptional corepressor activity. This then decreases the level of thyroid hormone binding proteins that bind to triiodothyronine. By affecting the thyroid hormone axis, BPA expoure can lead to hypothyroidism.
Parathyroid hormone
PTH is secreted by the chief cells of the parathyroid glands as a polypeptide containing 84 amino acids, which is a prohormone; effective hormone-receptor interaction requires solely the 34-N-terminal amino acids. (Data indicate that PTH is also possibly secreted in small amounts from the brain and the thymus.) While PTH acts to increase the concentration of ionic calcium (Ca) in the blood, calcitonin, a hormone produced by the parafollicular cells (C cells) of the thyroid gland, acts to decrease ionic calcium concentration. PTH essentially acts to increase the concentration of calcium in the blood by acting upon the parathyroid hormone 1 receptor, which is present at high levels in bone and kidney, and the parathyroid hormone 2 receptor, which is present at high levels in the central nervous system, pancreas, testes, and placenta. PTH half-life is about 4 minutes. It has a molecular mass around 9500 Da.
Triiodothyronine
Triiodothyronine, also known as T, is a thyroid hormone. It affects almost every physiological process in the body, including growth and development, metabolism, body temperature, and heart rate.
Thyroid disease in women
Thyroid hormone is vital during pregnancy. The unborn baby's brain and nervous system need thyroid hormone to develop. During the first trimester, the baby depends on the mother's supply of thyroid hormone. At 10 to 12 weeks of pregnancy, the baby's thyroid begins to work on its own. But the baby still depends on the mother for iodine, which the thyroid uses to make thyroid hormone. Pregnant women need about 250 micrograms (mcg) of iodine a day. Some women might not get all the iodine they need through the foods they eat or prenatal vitamins. Using iodized salt — salt that has had iodine added to it over plain table salt is recommended. Prenatal vitamins that contain iodine are also recommended.
Hypothyroidism
Desiccated thyroid extract is an animal-based thyroid gland extract, most commonly from pigs. It is a combination therapy, containing forms of T and T. It also contains calcitonin (a hormone produced in the thyroid gland involved in the regulation of calcium levels), T and T; these are not present in synthetic hormone medication. This extract was once a mainstream hypothyroidism treatment, but its use today is unsupported by evidence; British Thyroid Association and American professional guidelines discourage its use.
Thyroid
The production of thyroxine and triiodothyronine is primarily regulated by thyroid-stimulating hormone (TSH), released by the anterior pituitary gland. TSH release in turn is stimulated by thyrotropin releasing hormone (TRH), released in a pulsatile manner from the hypothalamus. The thyroid hormones provide negative feedback to the thyrotropes TSH and TRH: when the thyroid hormones are high, TSH production is suppressed. This negative feedback also occurs when levels of TSH are high, causing TRH production to be suppressed.
SOX2
There are three thyroid hormone response elements (TREs) in the region upstream of the Sox2 promoter. This region is known as the enhancer region. Studies have suggested that thyroid hormone (T3) controls Sox2 expression via the enhancer region. The expression of TRα1 (thyroid hormone receptor) is increased in proliferating and migrating neural stem cells. It has therefore been suggested that transcriptional repression of Sox2, mediated by the thyroid hormone signaling axis, allows for neural stem cell commitment and migration from the sub-ventricular zone. A deficiency of thyroid hormone, particularly during the first trimester, will lead to abnormal central nervous system development.
Further supporting this conclusion is the fact that hypothyroidism during fetal development can result in a variety of neurological deficiencies, including cretinism, characterized by stunted physical development and mental retardation.
Thyroid
The thyroid gland, or simply the thyroid, is an endocrine gland in the neck, consisting of two lobes connected by an . It is found at the front of the neck, below the Adam's apple. The thyroid gland secretes three hormones, namely the thyroid hormones (thyroxine/T and triiodothyronine/T) and calcitonin. The thyroid hormones primarily influence the metabolic rate and protein synthesis, but they also have many other effects including on development. The thyroid hormones are created from iodine and tyrosine. Calcitonin plays a role in calcium homeostasis.
Autoimmune thyroiditis
Thyroid autoantibodies appear mostly with the presence of lymphocytes in the targeted organ. Lymphocytes produce antibodies targeting three different thyroid proteins: Thyroid peroxidase Antibodies (TPOAb), Thyroglobulin Antibodies (TgAb), and Thyroid stimulating hormone receptor Antibodies (TRAb). Some patients who are healthy may be positive for more than one of these antibodies. Doctors who attend to such patients will most likely do routine follow-ups on the patient’s health since, even though it is highly unlikely that they will present any thyroid problems, there is still a chance that they will develop some type of dysfunction with time.
Thyroid storm
Sympathetic nervous system activation during times of stress may also play a significant role in thyroid storm. Sympathetic activation increases production of thyroid hormone by the thyroid gland. In the setting of elevated thyroid hormone, the density of thyroid hormone receptors (esp. beta-receptors) also increases, which enhances the response to catecholamines. This is likely responsible for several of the cardiovascular symptoms (increased cardiac output, heart rate, stroke volume) seen in thyroid storm.
Parathyroid gland
Parathyroid glands are small endocrine glands in the neck of humans and other tetrapods that produce parathyroid hormone. Humans usually have four parathyroid glands, variably located on the back of the thyroid gland. Parathyroid hormone and calcitonin (one of the hormones made by the thyroid gland) have key roles in regulating the amount of calcium in the blood and within the bones.
Thyroid hormone receptor beta
The protein encoded by this gene is a nuclear hormone receptor for triiodothyronine. It is one of the several receptors for thyroid hormone, and has been shown to mediate the biological activities of thyroid hormone. Knockout studies in mice suggest that the different receptors, while having certain extent of redundancy, may mediate different functions of thyroid hormone. Defects in this gene are known to be a cause of generalized thyroid hormone resistance (GTHR), a syndrome characterized by goiter and high levels of circulating thyroid hormone (T-T), with normal or slightly elevated thyroid stimulating hormone (TSH). Several transcript variants have been observed for this gene, but the full-length nature of only one has been observed so far.
Hypothalamus
Findings have suggested that thyroid hormone (T4) is taken up by the hypothalamic glial cells in the infundibular nucleus/ median eminence, and that it is here converted into T3 by the type 2 deiodinase (D2). Subsequent to this, T3 is transported into the thyrotropin-releasing hormone (TRH)-producing neurons in the paraventricular nucleus. Thyroid hormone receptors have been found in these neurons, indicating that they are indeed sensitive to T3 stimuli. In addition, these neurons expressed MCT8, a thyroid hormone transporter, supporting the theory that T3 is transported into them. T3 could then bind to the thyroid hormone receptor in these neurons and affect the production of thyrotropin-releasing hormone, thereby regulating thyroid hormone production.
Flame retardant
Many halogenated flame retardants with aromatic rings, including most brominated flame retardants, are likely thyroid hormone disruptors. The thyroid hormones triiodothyronine (T3) and thyroxine (T4) carry iodine atoms, another halogen, and are structurally similar to many aromatic halogenated flame retardants, including PCBs, TBBPA, and PBDEs. Such flame retardants therefore appear to compete for binding sites in the thyroid system, interfering with normal function of thyroid transport proteins (such as transthyretin) in vitro and thyroid hormone receptors. A 2009 "in vivo" animal study conducted by the US Environmental Protection Agency (EPA) demonstrated that deiodination, active transport, sulfation, and glucuronidation may be involved in disruption of thyroid homeostasis after perinatal exposure to PBDEs during critical developmental time points in utero and shortly after birth. Disruption of deiodinase as reported in the Szabo et al., 2009 "in vivo" study was supported in a follow-up "in vitro" study. The adverse effects on hepatic mechanism of thyroid hormone disruption during development have been shown to persist into adulthood. The EPA noted that PBDEs are particularly toxic to the developing brains of animals. Peer-reviewed studies have shown that even a single dose administered to mice during development of the brain can cause permanent changes in behavior, including hyperactivity.
Thyroid
The thyroid hormones are created from thyroglobulin. This is a protein within the follicular space that is originally created within the rough endoplasmic reticulum of follicular cells and then transported into the follicular space. Thyroglobulin contains 123 units of tyrosine, which reacts with iodine within the follicular space.
Thyroid hormones
If there is a deficiency of dietary iodine, the thyroid will not be able to make thyroid hormone. The lack of thyroid hormone will lead to decreased negative feedback on the pituitary, leading to increased production of thyroid-stimulating hormone, which causes the thyroid to enlarge (the resulting medical condition is called "endemic colloid goitre"; see goitre). This has the effect of increasing the thyroid's ability to trap more iodide, compensating for the iodine deficiency and allowing it to produce adequate amounts of thyroid hormone.
Reverse triiodothyronine
The production of hormone by the thyroid gland is controlled by the hypothalamus and pituitary gland. The physiological activity of thyroid hormone is regulated by a system of enzymes that activate, inactivate or simply discard the prohormone T and in turn functionally modify T and rT. These enzymes operate under complex direction of systems including neurotransmitters, hormones, markers of metabolism and immunological signals.
Thyroid disease in pregnancy
Thyroid disease in pregnancy can affect the health of the mother as well as the child before and after delivery. Thyroid disorders are prevalent in women of child-bearing age and for this reason commonly present as an intercurrent disease in pregnancy and the puerperium. Uncorrected thyroid dysfunction in pregnancy has adverse effects on fetal and maternal well-being. The deleterious effects of thyroid dysfunction can also extend beyond pregnancy and delivery to affect neurointellectual development in the early life of the child. Due to an increase in thyroxine binding globulin, an increase in placental type 3 deioidinase and the placental transfer of maternal thyroxine to the fetus, the demand for thyroid hormones is increased during pregnancy. The necessary increase in thyroid hormone production is facilitated by high human chorionic gonadotropin (hCG) concentrations, which bind the TSH receptor and stimulate the maternal thyroid to increase maternal thyroid hormone concentrations by roughly 50%. If the necessary increase in thyroid function cannot be met, this may cause a previously unnoticed (mild) thyroid disorder to worsen and become evident as gestational thyroid disease. Currently, there is not enough evidence to suggest that screening for thyroid dysfunction is beneficial, especially since treatment thyroid hormone supplementation may come with a risk of overtreatment. After women give birth, about 5% develop postpartum thyroiditis which can occur up to nine months afterwards.This is characterized by a short period of hyperthyroidism followed by a period of hypothyroidism; 20–40% remain permanently hypothyroid.