hypothyroidhypo-underactive thyroid
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. 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.

Hashimoto's thyroiditis

Hashimoto's diseasehashimoto diseaseHashimotos's disease
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.

Iodine in biology

Protective effects of iodine on breast cancertrace iodines
A family of non-selenium-dependent enzymes then further deiodinates the products of these reactions. 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.

Graves' disease

gravegraves diseaseGraves
The TSHr is expressed on the follicular cells of the thyroid gland (the cells that produce thyroid hormone), and the result of chronic stimulation is an abnormally high production of T3 and T4. This, in turn, causes the clinical symptoms of hyperthyroidism, and the enlargement of the thyroid gland visible as goiter. The infiltrative exophthalmos frequently encountered has been explained by postulating that the thyroid gland and the extraocular muscles share a common antigen which is recognized by the antibodies. Antibodies binding to the extraocular muscles would cause swelling behind the eyeball.

Thyroid-stimulating hormone

TSHthyroid stimulating hormonethyrotropin
The TSH receptor is found mainly on thyroid follicular cells. Stimulation of the receptor increases T 3 and T 4 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.

Iodised salt

iodized saltsalt iodizationiodized
Iodised salt ([[American and British English spelling differences#-ise.2C -ize .28-isation.2C -ization.29|also spelled]] iodized salt) is table salt mixed with a minute amount of various salts of the element iodine. The ingestion of iodine prevents iodine deficiency. Worldwide, iodine deficiency affects about two billion people and is the leading preventable cause of intellectual and developmental disabilities. Deficiency also causes thyroid gland problems, including "endemic goitre". In many countries, iodine deficiency is a major public health problem that can be cheaply addressed by purposely adding small amounts of iodine to the sodium chloride salt.

Follicular cell

follicular cellsthyroid follicular cellthyrocyte
The thyroid epithelial cells take up iodine and amino acids from the blood circulation on the basolateral side, synthesize thyroglobulin and thyroperoxidase from amino acids and secrete these into the thyroid follicles together with iodine. The thyroid epithelial cells can subsequently take up iodinated thyroglobulin from the follicles by endocytosis, extract thyroid hormones from it with the help of proteases and subsequently release thyroid hormones to the blood. These thyroid hormones are transported throughout the body where they control metabolism (which is the conversion of oxygen and carbohydrates to energy).


endocrinologistendocrinologistsEndocrinology & Metabolism
Examples include thyroid hormone, growth hormone, and insulin. The endocrine system involves a number of feedback mechanisms, so that often one hormone (such as thyroid stimulating hormone) will control the action or release of another secondary hormone (such as thyroid hormone). If there is too much of the secondary hormone, it may provide negative feedback to the primary hormone, maintaining homeostasis.

Thyroid adenoma

toxic adenomafollicular adenomasolitary toxic adenoma
A thyroid adenoma is distinguished from a multinodular goiter of the thyroid in that an adenoma is typically solitary, and is a neoplasm resulting from a genetic mutation (or other genetic abnormality) in a single precursor cell. In contrast, a multinodular goiter is usually thought to result from a hyperplastic response of the entire thyroid gland to a stimulus, such as iodine deficiency. Careful pathological examination may be necessary to distinguish a thyroid adenoma from a minimally invasive follicular thyroid carcinoma. A thyroid adenoma may be clinically silent ("cold" or "warm" adenoma), or it may be a functional tumor, producing excessive thyroid hormone ("hot" adenoma).


Many scientists observed that enzymatic activity was associated with proteins, but others (such as Nobel laureate Richard Willstätter) argued that proteins were merely carriers for the true enzymes and that proteins per se were incapable of catalysis. In 1926, James B. Sumner showed that the enzyme urease was a pure protein and crystallized it; he did likewise for the enzyme catalase in 1937. The conclusion that pure proteins can be enzymes was definitively demonstrated by John Howard Northrop and Wendell Meredith Stanley, who worked on the digestive enzymes pepsin (1930), trypsin and chymotrypsin. These three scientists were awarded the 1946 Nobel Prize in Chemistry.


In geology, redox is important to both the formation of minerals and the mobilization of minerals, and is also important in some depositional environments. In general, the redox state of most rocks can be seen in the color of the rock. The rock forms in oxidizing conditions, giving it a red color. It is then "bleached" to a green—or sometimes white—form when a reducing fluid passes through the rock. The reduced fluid can also carry uranium-bearing minerals. Famous examples of redox conditions affecting geological processes include uranium deposits and Moqui marbles.

Selenium deficiency

dietary deficiency of seleniumseleniumselenium deficiencies
Selenium is also necessary for the conversion of the thyroid hormone thyroxine (T4) into its more active counterpart, triiodothyronine, and as such a deficiency can cause symptoms of hypothyroidism, including extreme fatigue, mental slowing, goiter, cretinism, and recurrent miscarriage. It can occur in patients with severely compromised intestinal function, those undergoing total parenteral nutrition, those who have had gastrointestinal bypass surgery, and also in persons of advanced age (i.e., over 90). People dependent on food grown from selenium-deficient soil may be at risk for deficiency.


goitrogensgoitrogenicinterfere with iodine uptake
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.

Euthyroid sick syndrome

non-thyroidal illness syndromenonthyroidal illness syndromeLow-T3 syndrome
Prescribing thyroxine to treat this may lead to lifelong thyroid overtreatment. Hyperthyroidism may be assumed due to decreased TSH and a transient fT4 increase. This can be distinguished from NTIS via a thyroid ultrasound, which is commonly available in the hospital intensive care unit. NTIS looks similar to central hypopituitarism; both frequently have reduced TSH and thyroid hormone levels. There is an ongoing debate as to whether NTIS is an adaptive or maladaptive mechanism in response to physiological stress. Some sources indicate that NTIS is beneficial as an acute phase response, but detrimental during the chronic phase of illness.

Thyroid disease in pregnancy

Women are affected by hypothyroidism
As thyroxine is essential for fetal neurodevelopment it is critical that maternal delivery of thyroxine to the fetus is ensured early in gestation. In pregnancy, iodide losses through the urine and the feto-placental unit contribute to a state of relative iodine deficiency. Thus, pregnant women require additional iodine intake. A daily iodine intake of 250 µg is recommended in pregnancy but this is not always achieved even in iodine sufficient parts of the world. Thyroid hormone concentrations in blood are increased in pregnancy, partly due to the high levels of estrogen and due to the weak thyroid stimulating effects of human chorionic gonadotropin (hCG) that acts like TSH.

Potassium iodide

KIPotassium iodide (KI)potassium iodine
*Elephant toothpaste * World Health Organization's guidelines for iodine prophylaxis following a nuclear accident Saturated solutions of potassium iodide can be an emergency treatment for hyperthyroidism (so-called thyroid storm), as high amounts of iodide temporarily suppress secretion of thyroxine from the thyroid gland. The dose typically begins with a loading dose, then 1⁄3 mL SSKI (5 drops or 250 mg iodine as iodide), three times per day. Iodide solutions made from a few drops of SSKI added to drinks have also been used as expectorants to increase the water content of respiratory secretions and encourage effective coughing.


It works by decreasing the amount of thyroid hormone produced by the thyroid gland and blocking the conversion of thyroxine (T4) to triiodothyronine (T3). Propylthiouracil came into medical use in the 1940s. It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system. The wholesale cost in the developing world is about 3.62 USD a month. In the United Kingdom a month costs the NHS about 52.51 pounds. In the United States the wholesale price is 38.34 USD per month. Propylthiouracil is generally well tolerated, with side effects occurring in one of every 100 patients.

Wolff–Chaikoff effect

"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. The Wolff–Chaikoff effect has been used as a treatment principle against hyperthyroidism (especially thyroid storm) by infusion of a large amount of iodine to suppress the thyroid gland. Iodide was used to treat hyperthyroidism before antithyroid drugs such as propylthiouracil and methimazole were developed.

Selenium in biology

SeleniumSelenium compounds
A related selenium-containing enzyme in some plants and in animals (thioredoxin reductase) generates reduced thioredoxin, a dithiol that serves as an electron source for peroxidases and also the important reducing enzyme ribonucleotide reductase that makes DNA precursors from RNA precursors. Selenium also plays a role in the functioning of the thyroid gland. It participates as a cofactor for the three thyroid hormone deiodinases. These enzymes activate and then deactivate various thyroid hormones and their metabolites. It may inhibit Hashimotos's disease, an auto-immune disease in which the body's own thyroid cells are attacked by the immune system.

Human nutrition

nutritionhuman diethealthy eating
Estimates say that 28.5% of the global population is iodine deficient, representing 1.88 billion individuals. Although salt iodization programs have reduced the prevalence of iodine deficiency, this is still a public health concern in 32 nations. Moderate deficiencies are common in Europe and Africa, and over consumption is common in the Americas. Iodine-deficient diets can interfere with adequate thyroid hormone production, which is responsible for normal growth in the brain and nervous system. This ultimately leads to poor school performance and impaired intellectual capabilities.