A coenzyme in the metabolism of carbohydrates and branched-chain amino acids
An important neurological switch
An essential coenzyme (vitamin) necessary for the proper metabolism of sugar and starch to provide energy in the body. It also acts to help the body's memory and heart functions, digestive and nervous systems, and is important for the maintenance of healthy, clear, luminous eyes, hair and skin. •
Maintains a healthy nervous system as well as aiding proper function of the heart and other muscles. Stress increases the need for B-1 and all B vitamins. May promote growth, aids in digestion on carbohydrates, improve mental attitude, relieve dental postoperative pain, essential for normal functioning of nerve tissue, muscles and heart.
Lack of thiamine causes the deficiency disease called beriberi, which has been known since antiquity. Also found in association with chronic alcoholism presented as the Wernicke-Korsakoff syndrome.
The highest concentration is found in brewers yeast, followed by baker's yeast, pork (particularly the liver), cereal germs, whole grain and derivatives, nuts, and dried legumes.
In grain it is unevenly distributed, low in the starch of the grain, higher in the germ, and most of it occurs in the thin layer around the starch. This is why polished rice is almost completely deprived of it.
History: Thiamin was the first B vitamin identifiedit all began with investigations into the cause of the disease beri-beri. The first insight to the real cause of beri-beri came in the 1880s when Dr. K. Takaki, at the time Director General of the Japanese Naval Medical Services, noticed a correlation between the diet of sailors and beri-beri. Takaki discovered "...that the nitrogenous substances contained in the food were not sufficient to maintain nitrogen metabolism...". Takaki ordered an increase of vegetables, barley, fish and meat at the expense of rice in daily rations. The incidence of beri-beri in the Japanese Navy dropped from 40% to 0% in six years. These results were so convincing that the Japanese Army adopted the diet and by 1890 Takaki's diet was written into law.
While Dr. Takaki's findings did much to improve the health of the Japanese military, they did little to eradicate beri-beri in the rest of Asia. Due to Louis Pasteur's recent successes with the microbial causes of diseases, most of the medical community thought beri-beri was the result of a microbial infection or a toxin produced by a microorganism. The Dutch medical officer Dr. Christian Eijkman held this view as he began investigating beri-beri at a military hospital Batavia, Java in the Dutch East Indies (now Jakarta, Indonesia) in 1886. After months of searching for a toxic or microbial link to beri-beri he noticed certain chickens outside his laboratory were inflicted with a beri-beri like aliment. He named the disease polyneuritis gallinarum, and from pathological studies of myelin sheath degeneration of both human and fowl victims he concluded that polyneuritis gallinarum was an animal model for beri-beri. After consulting the hospital records and conducting experiments Eijkman discovered that chickens fed white (polished or milled) rice developed polyneuritis whereas red (partially polished) rice, unhusked rice (padi) and rice hulls prevented and even cured the disease. Eijkman and his colleague, Dr. Gerrit Grijns, showed that an "anti-polyneuritis factor" could be extracted from rice hulls with water or ethanol. Eijkman believed that this water soluble anti-polyneuritis factor was a "pharmacological antidote" to the "beri-beri microbe" present in the rice endosperm (white part of rice). Grijns, however, leaned toward the theory that white rice "lacked a certain substance of importance in the metabolism of the central nervous system".
In 1911 Dr. Casimir Funk, a young chemist at the Lister Institute in London crystallized an amine substance from rice bran. He was sure this was the anti-beri-beri factor and dubbed it "vitamine" for "vital amine". Though these crystals soon proved to have little antineuritic activity (it is now believed Funk crystallized nicotinic acid), the name stuck. About the same time U.S. Army Medical Officer Captain Edward B. Vedder became convinced by the work of Eijkman and Grijns and others that beri-beri was indeed caused by a nutritional deficiency. Vedder enlisted the help of Dr. Robert R. Williams of the Bureau of Science in Manila in isolating the anti-beri-beri factor. Though Williams worked diligently for over 25 years, often using his own money to fund the research, it was two Dutch chemists, Dr. B. C. P. Jansen and Dr. W. Donath, working in Eijkman's old laboratory, who finally crystallized vitamin B1 from rice bran in 1926. They named it aneurin for antineuritic vitamin. Unfortunately Jansen and Donath missed the sulfur atom, and their published incorrect formula for aneurin caused confusion for several years. It was Williams who published the first correct formula and synthesis for the vitamin in 1936. The American Medical Association did not accept any of the names by which it was known (anti-beriberi factor, anti-beri-beri vitamin, antineuritic vitamin, vitamin B, vitamin B1, etc.) for inclusion in their New and Non-Official Remedies list. Without inclusion in the list Williams' compound could not be advertised in reputable medical journals. The AMA demanded that Dr. Williams to choose a new name and he choose "thiamin". To reflect the vitamin's amine nature the American Chemical Society added an "e" and the name "thiamine" is now accepted.
Technicals: Chemically, it consists of substituted pyrimidine and thiazole rings linked by a methylene bridge. It exists mainly in various interconvertible phosphorylated forms, chiefly thiamin pyrophosphate.
The absorption of Thiamine occurs in the bowel by diffusion and with a specialized carrier only if the concentration of Thiamine is very low in the intestine. Vegetable sources of it must be processed by our metabolism before use.
Neurological Functions Thiamine has a vital neurological function in the nervous system independent of its coenzyme role.
An active form of thiamine in the body is thiamine pyrophosphate (AKA thiamine diphosphate or cocarboxylase). Stimulation of nerves results in the release of thiamine monophosphate and free thiamine into the associated medium with accompanying decrease of cellular thiamine pyrophosphate and thiamine triphosphate.
The concentration of thiamine in the brain seems to be resistant to changes dietary concentration.
In the brain the concentration of thiamine is quick to release, but slow to replemish.
Thiamine triphosphate (another internal form) is involved with nerve impulses via the Na+ and K+ gradient.
Deficiencies Caused by: A lack of thiamine can be caused by malnutrition, alcoholism, a diet high in thiaminase-rich foods.
Alcohol inhibits the intestinal absorption of Thiamine.
Natural thiaminase (thiamine's enzyme) substances and other antithiamines destroy Thiamine. Foods high in these anti-thiamine factors are; coffee, tea, betel nuts and other plants, raw freshwater fish, raw shellfish and ferns.
Signs or Symptoms of a Deficiency: Initial deficiency signs include fatigue, sleep disturbances, poor appetite. CV (wet) beriberi: edema, heart failure. Neurologic (dry) berberi: Wernicke’s encephalopathy, peripheral neuropathies, lactic acidosis with carbohydrate loading, depression, irritability, anxiety, memory problems, insomnia, and gastrointestinal disorders.
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