Question:

If you drink baking soda and water will weed come out of your system in two days?

Answer:

There is no way to get THC out of your system. It stays in your fatty cells from 30 to 90 days no matter what you take but taking acidic substances like niacin, baking soda, golden seal, and others can make your urine give the test problems. '

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Sodium bicarbonate
Sodium hydrogen carbonate Baking soda, bicarbonate of soda, nahcolite, sodium bicarbonate, sodium hydrogencarbonate [Na+].OC([O-])=O InChI=1S/CH2O3.Na/c2-1(3)4;/h(H2,2,3,4);/q;+1/p-1Yes 
Key: UIIMBOGNXHQVGW-UHFFFAOYSA-MYes  InChI=1/CH2O3.Na/c2-1(3)4;/h(H2,2,3,4);/q;+1/p-1
Key: UIIMBOGNXHQVGW-REWHXWOFAQ 50 °C, 323 K, 122 °F (decomposes to sodium carbonate) 69 g/L (0 °C)
96 g/L (20 °C)
165 g/L (60 °C)
236 g/L (100 °C) 6.351 (carbonic acid) Potassium bicarbonate Sodium hydrogen phosphate Sodium bicarbonate or sodium hydrogen carbonate is the chemical compound with the formula Na3HCO. Sodium bicarbonate is a white solid that is crystalline but often appears as a fine powder. It has a slightly salty, alkaline taste resembling that of washing soda (sodium carbonate). The natural mineral form is nahcolite. It is a component of the mineral natron and is found dissolved in many mineral springs. It is among the food additives encoded by European Union, identified by the initials E 500. Since it has long been known and is widely used, the salt has many related names such as baking soda, bread soda, cooking soda, and bicarbonate of soda. In colloquial usage, its name is shortened to sodium bicarb, bicarb soda, or simply bicarb. The word saleratus, from Latin sal æratus meaning aerated salt, was widely used in the 19th century for both sodium bicarbonate and potassium bicarbonate. The term has now fallen out of common usage. The ancient Egyptians used natural deposits of natron, a mixture consisting mostly of sodium carbonate decahydrate, and sodium bicarbonate. The natron was used as a cleansing agent like soap. In 1791, a French chemist, Nicolas Leblanc, produced sodium carbonate, also known as soda ash. In 1846, two New York bakers, John Dwight and Austin Church, established the first factory to develop baking soda from sodium carbonate and carbon dioxide. This compound, referred to as saleratus, is mentioned in the famous novel Captains Courageous by Rudyard Kipling as being used extensively in the 1800s in commercial fishing to prevent freshly-caught fish from spoiling. NaHCO3 is mainly prepared by the Solvay process, which is the reaction of sodium chloride, ammonia, and carbon dioxide in water. Calcium carbonate is used as the source of CO2 and the resultant calcium oxide is used to recover the ammonia from the ammonium chloride. The product shows a low purity (75 %). Pure product is obtained from sodium carbonate, water and carbon dioxide as reported in one of the following reactions. It is produced on the scale of about 100,000 tonnes/year (as of 2001). NaHCO3 may be obtained by the reaction of carbon dioxide with an aqueous solution of sodium hydroxide. The initial reaction produces sodium carbonate: Further addition of carbon dioxide produces sodium bicarbonate, which at sufficiently high concentration will precipitate out of solution: Commercial quantities of baking soda are also produced by a similar method: soda ash, mined in the form of the ore trona, is dissolved in water and treated with carbon dioxide. Sodium bicarbonate precipitates as a solid from this method: Naturally occurring deposits of nahcolite (NaHCO3) are found in the Eocene-age (55.8–33.9 Ma) Green River Formation, Piceance Basin in Colorado. Nahcolite was deposited as beds during periods of high evaporation in the basin. It is commercially mined using in-situ leach techniques involving dissolution of the nahcolite by heated water that is pumped through the nahcolite beds and reconstituted through a natural cooling crystallization process. Sodium bicarbonate is an amphoteric compound. Aqueous solutions are mildly alkaline due to the formation of carbonic acid and hydroxide ion: Sodium bicarbonate can be used as a wash to remove any acidic impurities from a "crude" liquid, producing a purer sample. Reaction of sodium bicarbonate and an acid produce a salt and carbonic acid, which readily decomposes to carbon dioxide and water: Sodium bicarbonate reacts with acetic acid (found in vinegar), producing sodium acetate, water, and carbon dioxide: Sodium bicarbonate reacts with bases such as sodium hydroxide to form carbonates: Sodium bicarbonate reacts with carboxyl groups in proteins to give a brisk effervescence from the formation of . This reaction is used to test for the presence of carboxylic groups in protein.][ Above 50 °C, sodium bicarbonate gradually decomposes into sodium carbonate, water and carbon dioxide. The conversion is fast at 200 °C: Most bicarbonates undergo this dehydration reaction. Further heating converts the carbonate into the oxide (at over 850°C): These conversions are relevant to the use of NaHCO3 as a fire-suppression agent ("BC powder") in some dry powder fire extinguishers. It is used along with Sulphuric acid in some fire extinguishers since they react to form Carbon di oxide which extinguishes flames. Sodium bicarbonate, referred to as "baking soda" is primarily used in cooking (baking), as a leavening agent. It reacts with acidic components in batters, releasing carbon dioxide, which causes expansion of the batter and forms the characteristic texture and grain in pancakes, cakes, quick breads, soda bread, and other baked and fried foods. Acidic compounds that induce this reaction include phosphates, cream of tartar, lemon juice, yogurt, buttermilk, cocoa, vinegar, etc. Sodium bicarbonate can be substituted for baking powder provided sufficient acid reagent is also added to the recipe. Many forms of baking powder contain sodium bicarbonate combined with one or more acidic phosphates][ or cream of tartar. Sodium bicarbonate was sometimes used in cooking vegetables, to make them softer, although this has gone out of fashion, as most people now prefer firmer vegetables. However, it is still used in Asian cuisine to tenderise meats. Baking soda may react with acids in food, including Vitamin C (L-ascorbic acid). It is also used in breadings such as for fried foods to enhance crispness. Heat causes sodium bicarbonate to act as a raising agent by releasing carbon dioxide when used in baking. The carbon dioxide production starts at temperatures above 80 °C. Since the reaction does not occur at room temperature, mixtures (cake batter, etc.) can be allowed to stand without rising until they are heated in the oven. Many laboratories keep a bottle of sodium bicarbonate powder within easy reach, because sodium bicarbonate is amphoteric, reacting with acids and bases. Furthermore, as it is relatively innocuous in most situations, there is no harm in using excess sodium bicarbonate. Also, sodium bicarbonate powder may be used to smother a small fire, as heating of sodium bicarbonate releases carbon dioxide. A wide variety of applications follows from its neutralization properties, including reducing the spread of white phosphorus from incendiary bullets inside an afflicted soldier's wounds.][ Sodium bicarbonate mixed with water can be used as an antacid to treat acid indigestion and heartburn. It is used as the medicinal ingredient in gripe water for infants. Sodium bicarbonate has been known to be used in first aid, in treating scalding, to prevent blistering and scarring with instructions to cover the scalded area with a liberal layer of sodium bicarbonate and water paste and seek medical assistance. This is due to the endothermic reaction that occurs between sodium bicarbonate and water and sodium bicarbonate's mild antiseptic properties][ Intravenous sodium bicarbonate is an aqueous solution that is sometimes used for cases of acidosis, or when there are insufficient sodium or bicarbonate ions in the blood. In cases of respiratory acidosis, the infused bicarbonate ion drives the carbonic acid/bicarbonate buffer of plasma to the left and, thus, raises the pH. It is for this reason that sodium bicarbonate is used in medically supervised cardiopulmonary resuscitation. Infusion of bicarbonate is indicated only when the blood pH is markedly (<7.1–7.0) low. Oral sodium bicarbonate has been shown to slow progression to end stage renal disease in individuals with stage 4 chronic kidney disease and metabolic acidosis (plasma sodium bicarbonate levels 16-20meq/L). It is used as well for treatment of hyperkalemia. Since sodium bicarbonate can cause alkalosis, it is sometimes used to treat aspirin overdoses. Aspirin requires an acidic environment for proper absorption, and the basic environment diminishes aspirin absorption in the case of an overdose. Sodium bicarbonate has also been used in the treatment of tricyclic antidepressant overdose. It can also be applied topically as a paste, with three parts baking soda to one part water, to relieve some kinds of insect bites and stings (as well as accompanying swelling). Adverse reactions to the administration of sodium bicarbonate can include metabolic alkalosis, edema due to sodium overload, congestive heart failure, hyperosmolar syndrome, hypervolemic hypernatremia, and hypertension due to increased sodium. In patients consuming a high-calcium or dairy-rich diet, calcium supplements, or calcium-containing antacids such as calcium carbonate (e.g., Tums), the use of sodium bicarbonate can cause milk-alkali syndrome, which can result in metastatic calcification, kidney stones, and kidney failure. Sodium bicarbonate can be used to treat an allergic reaction to plants such as poison -ivy -oak or -sumac to relieve some of the associated itching. Bicarbonate of soda can also be useful in removing splinters from the skin. Toothpaste containing sodium bicarbonate has in several studies shown to have a better whitening and plaque removal effect than toothpastes without it. Sodium bicarbonate is also used as an ingredient in some mouthwashes. It works as a mechanical cleanser on the teeth and gums, neutralizes the production of acid in the mouth and also acts as an antiseptic to help prevent infections.][ Sodium bicarbonate in combination with other ingredients can be used to make a dry or wet deodorant. It may also be used as a shampoo. Sodium bicarbonate may be used as a buffering agent, combined with table salt, when creating a solution for nasal irrigation. Small amounts of sodium bicarbonate have been shown to be useful as a supplement for athletes in speed-based events, like middle distance running, lasting from about one to seven minutes. But overdose is a serious risk because sodium bicarbonate is slightly toxic and in particular gastrointestinal irritation is of concern. Additionally this practice causes a significant increase in dietary sodium. A paste from baking soda can be very effective when used in cleaning and scrubbing. For cleaning aluminium objects, the use of sodium bicarbonate is discouraged as it attacks the thin unreactive protective oxide layer of this otherwise very reactive metal. A solution in warm water will remove the tarnish from silver when the silver is in contact with a piece of aluminium foil A paste of sodium bicarbonate and water is useful in removing surface rust as the rust forms a water soluble compound when in a concentrated alkaline solution. Cold water should be used as hot water solutions can corrode steel. Baking soda is commonly added to washing machines as a replacement for softener and to remove odors from clothes. Sodium bicarbonate is also effective in removing heavy tea and coffee stains from cups when diluted with warm water. During the Manhattan Project to develop the atomic bomb in the early 1940s, many scientists investigated the toxic properties of uranium. They found that uranium oxides stick very well to cotton cloth, but did not wash out with soap or laundry detergent. The uranium would wash out with a 2% solution of sodium bicarbonate (baking soda). Clothing can become contaminated with depleted uranium (DU) dust and normal laundering will not remove it. Those at risk of DU dust exposure should have their clothing washed with baking soda (about 6 ounces (170g) of baking soda in 2 gallons (7.5l) of water). Sodium bicarbonate can be an effective way of controlling fungus growth, and in the United States is registered by the Environmental Protection Agency as a biopesticide. Sodium bicarbonate is sold as a cattle feed supplement, in particular as a buffering agent for the rumen. Sodium bicarbonate can be used to extinguish small grease or electrical fires by being thrown over the fire. However, it should not be applied to fires in deep fryers, as it may cause the grease to splatter. Sodium bicarbonate is used in BC dry chemical fire extinguishers as an alternative to the more corrosive ammonium phosphate in ABC extinguishers. The alkali nature of sodium bicarbonate makes it the only dry chemical agent, besides Purple-K, that was used in large-scale fire suppression systems installed in commercial kitchens. Because it can act as an alkali, the agent has a mild saponification effect on hot grease, which forms a smothering soapy foam. Dry chemicals have since fallen out of favor for kitchen fires, as they have no cooling effect compared to the extremely effective wet chemical agents specifically designed for such hazards.][ Sodium bicarbonate is used in a process for removing paint and corrosion called sodablasting; the process is particularly suitable for cleaning aluminium panels which can be distorted by other types of abrasive. It can be administered to pools, spas, and garden ponds to raise pH levels. It has weak disinfectant properties, and it may be an effective fungicide against some organisms. Since it acts as a neutralizing agent, it can be used to absorb odors that are caused by strong acids.][ Because baking soda will absorb musty smells, it has become a reliable method for used-book sellers when making books less malodorous. Sodium bicarbonate is also used as required to increase Total Alkinity level in swimming pools and aquarium freshwater fish tanks. Sodium bicarbonate, as 'bicarbonate of soda', was a frequent source of punch lines for Groucho Marx in Marx brothers movies. In Duck Soup, Marx plays the leader of a nation at war. In one scene, he receives a message from the battlefield that his general is reporting a gas attack, and Groucho tells his aide, "Tell him to take a teaspoonful of bicarbonate of soda and a half a glass of water." In A Night at the Opera, Groucho's character addresses the opening night crowd at an opera by saying of the lead tenor, "Signor Lassparri comes from a very famous family. His mother was a well-known bass singer. His father was the first man to stuff spaghetti with bicarbonate of soda, thus causing and curing indigestion at the same time." M: DIG anat (t, g, p)/phys/devp/enzy noco/cong/tumr, sysi/epon proc, drug (A2A/2B/3/4/5/6/7/14/16), blte

Niacin
pyridine-3-carboxylic acid Pyridine-3-carboxylic acid Bionic
Vitamin B3 Oc(:o):c1cccnc1 OC(=O)C1=CN=CC=C1 InChI=1S/C6H5NO2/c8-6(9)5-2-1-3-7-4-5/h1-4H,(H,8,9)Yes 
Key: PVNIIMVLHYAWGP-UHFFFAOYSA-NYes  InChI=1/C6H5NO2/c8-6(9)5-2-1-3-7-4-5/h1-4H,(H,8,9)
Key: PVNIIMVLHYAWGP-UHFFFAOYAA 237 °C, 510 K, 458 °F Niacin (also known as vitamin B3, nicotinic acid, or less commonly vitamin PP; archaic terms include pellagra-preventive and anti-dermatitis factor) is an organic compound with the formula and, depending on the definition used, one of the 40 to 80 essential human nutrients. Niacin is one of five vitamins (when lacking in human diet) associated with a pandemic deficiency disease: niacin deficiency (pellagra), vitamin C deficiency (scurvy), thiamin deficiency (beriberi), vitamin D deficiency (rickets and osteomalacia), vitamin A deficiency (night blindness and other symptoms). Niacin has been used for over 50 years to increase levels of HDL in the blood and has been found to modestly decrease the risk of cardiovascular events in a number of controlled human trials. This colorless, water-soluble solid is a derivative of pyridine, with a carboxyl group (COOH) at the 3-position. Other forms of vitamin B3 include the corresponding amide, nicotinamide ("niacinamide"), where the carboxyl group has been replaced by a carboxamide group (), as well as more complex amides and a variety of esters. Nicotinic acid and niacinamide are convertible to each other with steady world demand rising from 8500 tonnes per year in 1980s to 40,000 in recent years. Niacin cannot be directly converted to nicotinamide, but both compounds could be converted to and are precursors of NAD and NADP in vivo. Nicotinic acid, nicotinamide, and tryptophan (via quinoline acid) are co-factors for nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). NAD converts to NADP by phosphorylation in the presence of the enzyme NAD+ kinase. NADP and NAD are coenzyme for many dehydrogenases, participating in many hydrogen transfer processes. NAD is important in catabolism of fat, carbohydrate, protein, and alcohol, as well as cell signaling and DNA repair, and NADP mostly in anabolism reactions such as fatty acid and cholesterol synthesis. High energy requirements (brain) or high turnover rate (gut, skin) organs are usually the most susceptible to their deficiency. Although the two are identical in their vitamin activity, nicotinamide does not have the same pharmacological effects (lipid modifying effects) as niacin. Nicotinamide does not reduce cholesterol or cause flushing. Nicotinamide may be toxic to the liver at doses exceeding 3 g/day for adults. Niacin is involved in both DNA repair, and the production of steroid hormones in the adrenal gland. One recommended daily allowance of niacin is 2–12 mg/day for children, 14 mg/day for women, 16 mg/day for men, and 18 mg/day for pregnant or breast-feeding women. Tolerable upper intake levels (UL) for adult men and women is considered to be 35 mg/day by the Dietary Reference Intake system to avoid flushing. In general, niacin status is tested through urinary biomarkers, which are believed to be more reliable than plasma levels. At present, niacin deficiency is sometimes seen in developed countries, and it is usually apparent in conditions of poverty, malnutrition, and chronic alcoholism. It also tends to occur in areas where people eat maize (corn, the only grain low in digestible niacin) as a staple food. A special cooking technique called nixtamalization is needed to increase the bioavailability of niacin during maize meal/flour production. Mild niacin deficiency has been shown to slow metabolism, causing decreased tolerance to cold. Severe deficiency of niacin in the diet causes the disease pellagra, which is characterized by diarrhea, dermatitis, and dementia, as well as “Casal's necklace” lesions on the lower neck, hyperpigmentation, thickening of the skin, inflammation of the mouth and tongue, digestive disturbances, amnesia, delirium, and eventually death, if left untreated. Common psychiatric symptoms of niacin deficiency include irritability, poor concentration, anxiety, fatigue, restlessness, apathy, and depression. Studies have indicated that, in patients with alcoholic pellagra, niacin deficiency may be an important factor influencing both the onset and severity of this condition. Patients with alcoholism typically experience increased intestinal permeability, leading to negative health outcomes. Hartnup’s disease is a hereditary nutritional disorder resulting in niacin deficiency. This condition was first identified in the 1950s by the Hartnup family in London. It is due to a deficit in the intestines and kidneys, making it difficult for the body to break down and absorb dietary tryptophan. The resulting condition is similar to pellagra, including symptoms of red, scaly rash, and sensitivity to sunlight. Oral niacin is given as a treatment for this condition in doses ranging from 40–200 mg, with a good prognosis if identified and treated early. Niacin synthesis is also deficient in carcinoid syndrome, because of metabolic diversion of its precursor tryptophan to form serotonin. In 1955, Altschul et al. (1955) described niacin as lipid lowering property for the first time that followed by subsequent studies. Niacin is the oldest lipid lowering drug with unique anti atherosclerotic property. It reduces traditional parameters such as low density lipoprotein cholesterol (LDL), very low-density lipoprotein cholesterol (VLDL-C) and triglycerides (TG) but effectively increases high density lipoprotein cholesterol (HDL). Despite the importance of other cardiovascular risk factors, high HDL correlated to lower cardiovascular event independent of LDL reduction Other effects include anti-thrombotic and vascular inflammation, improving endothelial function and plaque stability. Niacin alone or in combination with other lipid lowering agents such as statin or ezetimibe significantly reduces risk of cardiovascular disease and arthrosclerosis progression. Niacin therapeutic effect is mostly through its specific G protein coupled receptor (GPR109A and GPR109B) recently named as hydroxyl carboxylic acid (HCA) receptor 2 that highly expressed in adipose tissue, spleen, immune cells and keratinocytes but not in other expected organs such as liver, kidney, heart or intestine. GPR109A inhibits cyclic adenosine monophosphate production and thus lipolysis and free fatty acids available for liver to produce TG and VLDL and consequently LDL. Decrease in free fatty acids also suppress hepatic expression of apolipoprotein C3 (APOC3) and PPARg coactivator-1b (PGC-1b) thus increase VLDL turn over and reduce its production. It also inhibits diacylglycerol acyltransferase-2 (important hepatic TG synthesis). The mechanism behind increasing HDL is not totally understood but it seems to be done in various ways. Niacin increase apolipoprotein A1 levels due to anti catabolic effects resulting in higher reverse cholesterol transport. It also inhibits HDL hepatic uptake, down regulating production of cholesterol ester transfer protein (CETP) gene. Finally, it stimulates ABCA1 transporter in monocytes and macrophages and up regulates peroxisome proliferator-activated receptor γ results in reverse cholesterol transport. Improving vascular endothelial function has been reported in few experiments using niacin. In an experiment on type 2 diabetes, nicotinic acid improved endothelial function comparing with control. Daily dose of 1 g niacin shows significant lipid modifying properties and reach the plateau using 2 grams. GPR109A in immune cells such as monocytes, macrophages, and dendritic cells is responsible for atherosclerosis effects of niacin by reducing the immune cells’ infiltration of vessel wall It also down regulates endothelial adhesion molecules such as vascular cell adhesion molecule 1 (VCAM-1) or of chemokines such as monocyte chemotactic protein 1 (MCP-1) and inflammatory proteins which results in atherosclerotic stabilization and antithrombotic effects. The changes in adhesion molecules and chemokines might be through activation of receptor GPR109A on immune cells. Adipokines are the adipocytes’ produced mediators. Some adipokines such as tumor necrosis factor (TNF)-a, interleukins and chemokines, have pro-inflammatory effect and some others such as adiponectin have anti-inflammatory effect that regulates inflammatory process, decrease vascular progression and atherosclerosis. Nicotinic acid increase adiponectin plasma levels in humans and mice but inhibits pro-inflammatory chemokines such as MCP-1 and fractalkin. Other recently explored therapeutic effect of nicotinic acid are neuroprotective and anti-inflammatory effects, beneficial in animal models of arthritis, chronic renal failure or sepsis however more work needed in this area. Following Coronary Drug Project (CDP) as one of the first experiments being done to study long term clinical lipid lowering effect of niacin in 1960’s to early 1970’s, (JAMA, 1975) many other experiments been done. Their result been summarized in two most recent meta analysis concluded that therapeutic doses of niacin alone or in combination with other lipid modifying agents such as statin reduce cardiovascular event and arthrosclerosis progression significantly. This agrees with current Nation Cholesterol Education Program (NCEP) on high cholesterol treatment. NCEP recommends niacin alone for cardiovascular and atherogenic dyslipidemia in mild or normal LDL levels or in combination for higher LDL levels (NCEP, 2002). 1500 mg Immediate release niacin daily results in 13% LDL, 20% LP, 10% TG reduction and 19% HDL increase comparing to placebo. Extended release niacin alone or with anti-flushing agent (laropiprant) shows similar effects. Niacin binds to and stimulates a G-protein-coupled receptor, GPR109A, which causes the inhibition of fat breakdown in adipose tissue. Nicotinamide does not bind this receptor which explains why it does not affect blood lipid levels. Lipids that are liberated from adipose tissue are normally used to build very-low-density lipoproteins (VLDL) in the liver, which are precursors of low-density lipoprotein (LDL) or "bad" cholesterol. Because niacin blocks the breakdown of fats, it causes a decrease in free fatty acids in the blood and, as a consequence, decreases the secretion of VLDL and cholesterol by the liver. By lowering VLDL levels, niacin also increases the level of high-density lipoprotein (HDL) or "good" cholesterol in blood, and therefore it is sometimes prescribed for people with low HDL, who are also at high risk of a heart attack. The ARBITER 6-HALTS study, reported at the 2009 annual meeting of the American Heart Association and in the New England Journal of Medicine concluded that, when added to statins, 2000 mg/day of extended-release niacin was more effective than ezetimibe (Zetia) in reducing carotid intima-media thickness, a marker of atherosclerosis. Additionally, a recent meta-analysis covering 11 randomized controlled clinical trials found positive effects of niacin alone or in combination on all cardiovascular events and on atherosclerosis evolution. However, a 2011 study (AIM-HIGH) was halted early because patients showed no decrease in cardiovascular events, but did experience an increase in the risk of stroke. These patients already had LDL levels well controlled by a statin drug, and the aim of the study was to evaluate extended-release niacin (2000 mg per day) to see if raising HDL levels had an additional positive effect on risk. In this study, it did not have such an effect, and appeared to increase stroke risk. The role of niacin in patients whose LDL is not well-controlled (as in the majority of previous studies with niacin) is still under study and debate. However, it does not seem to offer benefits via raising HDL, in patients already lowering LDL by taking a statin. Many preparations of niacin are available over-the-counter, without prescription, as they are sold as dietary supplements. Immediate release niacin is effective at lowering cholesterol levels, and has minimal hepatotoxic side effects due to its rapid elimination from the body. However, it has the main drawback of causing strong vasodilation side effects with sensations of flushing and skin tingling that can be unpleasant to many patients. Non-prescription extended release niacin, such as Endur-acin, which uses a wax matrix to delay release are available as well. A prescription extended release niacin, Niaspan, has a film coating that delays release of the niacin, resulting in an absorbtion over a period of 8–12 hours. The extended release formulations generally reduce vasodilation and flushing side effects, but increase the risk of hepatotoxicity compared to the immediate release forms. A formulation of Laropiprant (Merck & Co., Inc.) and niacin had previously been approved for use in Europe and marketed as Tredaptive. Laropiprant is a prostaglandin D2 binding drug shown to reduce vasodilatation and flushing up to 73% The HPS2-THRIVE study, a study sponsored by Merck, showed no additional efficacy of Tredaptive in lowering cholesterol when used together with other statin drugs, but did show an increase in other side effects. The study resulted in the complete withdrawal of Tredaptive from the international market. Over-the counter niacin dietary supplements generally lack the safety and efficacy data required for FDA regulatory approval. Some “no flush” types, such as inositol hexanicotinate contain convertible niacin compounds, but have with little clinical efficacy in reducing cholesterol levels or “slow release” has higher hepatotoxic activity hence non-prescription niacin is not recommended due to potential harm. Pharmacological doses of niacin (1.5 - 6 g per day) lead to side effects that can include dermatological conditions such as skin flushing and itching, dry skin, and skin rashes including eczema exacerbation and acanthosis nigricans. Some of these symptoms are generally related to niacin's role as the rate limiting cofactor in the histidine decarboxylase enzyme which converts l-histidine into histamine.][ H1 and H2 receptor mediated histamine is metabolized via a sequence of mono (or di-) amine oxidase and COMT into methylhistamine which is then conjugated through the liver's CYP450 pathways. Persistent flushing and other symptoms may indicate deficiencies in one or more of the cofactors responsible for this enzymatic cascade. Gastrointestinal complaints, such as dyspepsia (indigestion), nausea and liver toxicity fulminant hepatic failure, have also been reported. Side effects of hyperglycemia, cardiac arrhythmias and "birth defects in experimental animals" have also been reported. Flushing usually lasts for about 15 to 30 minutes, though it can sometimes last up to two hours. It is sometimes accompanied by a prickly or itching sensation, in particular, in areas covered by clothing. Flushing is mediated by prostaglandin E2 and D2 due to GPR109A activation of epidermal langerhans’ cells and keratinocytes. Langerhans use cyclooxygenase type 1 (COX-1) for PGE2 production and are more responsible for acute flushing while keratinocutes are COX-2 dependent and are in active continued vaso-dilation. To reduce flushing many studies focused on altering or blocking the prostaglandin mediated pathway. This effect is mediated by GPR109A-mediated prostaglandin release from the Langerhans cells of the skin and can be blocked by taking 300 mg of aspirin half an hour before taking niacin, by taking one tablet of ibuprofen per day or by co-administering the prostaglandin receptor antagonist laropiprant. Taking the niacin with meals also helps reduce this side effect. After several weeks of a consistent dose, most patients no longer flush. Slow- or "sustained"-release forms of niacin have been developed to lessen these side effects. One study showed the incidence of flushing was significantly lower with a sustained release formulation though doses above 2 g per day have been associated with liver damage, in particular, with slow-release formulations. Flushing is often thought to involve histamine, but histamine has been shown not to be involved in the reaction. Prostaglandin (2PGD) is the primary cause of the flushing reaction, with serotonin appearing to have a secondary role in this reaction. Hepatotoxicity is another side effect of niacin. Metabolizing niacin occurs in liver in 2 ways one through conjugation pathway producing nicotinuric acid metabolite related to flushing the other is amidation resulting in NAD production related to hepatotoxicity. Although high doses of niacin may elevate blood sugar, thereby worsening diabetes mellitus, recent studies show the actual effect on blood sugar to be only 5–10%. Patients with diabetes who continued to take anti-diabetes drugs containing niacin did not experience major blood glucose changes. Thus looking at the big picture, niacin continues to be recommended as a drug for preventing cardiovascular disease in patients with diabetes. Hyperuricemia is another side effect of taking high-dose niacin, and may exacerbate gout. Niacin in doses used to lower cholesterol levels has been associated with birth defects in laboratory animals, with possible consequences for infant development in pregnant women. Niacin, particularly the time-release variety, at extremely high doses can cause acute toxic reactions. Extremely high doses of niacin can also cause niacin maculopathy, a thickening of the macula and retina, which leads to blurred vision and blindness. This maculopathy is reversible after niacin intake ceases. Nicotinamide may be obtained from the diet where it is present primarily as NAD+ and NADP+. These are hydrolysed in the intestine and the resulting nicotinamide is absorbed either as such, or following its hydrolysis to nicotinic acid. Nicotinamide is present in nature in only small amounts. In unprepared foods, niacin is present mainly in the form of the cellular pyridine nucleotides NAD and NADP. Enzymatic hydrolysis of the co-enzymes can occur during the course of food preparation. Boiling releases most of the total niacin present in sweet corn as nicotinamide (up to 55 mg/kg). One form of dietary supplement is inositol hexanicotinate (IHN), which is inositol that has been esterified with niacin on all six of inositol's alcohol groups. IHN is usually sold as "flush-free" or "no-flush" niacin in units of 250, 500, or 1000 mg/tablets or capsules. It is sold as an over-the-counter formulation, and often is marketed and labeled as niacin, thus misleading consumers into thinking they are getting the active form of the medication. While this form of niacin does not cause the flushing associated with the immediate-release products, the evidence that it has lipid-modifying functions is contradictory, at best. As the clinical trials date from the early 1960s (Dorner, Welsh) or the late 1970s (Ziliotto, Kruse, Agusti), it is difficult to assess them by today's standards. One of the last of those studies affirmed the superiority of inositol and xantinol esters of nicotinic acid for reducing serum free fatty acid, but other studies conducted during the same period found no benefit. Studies explain that this is primarily because "flush-free" preparations do not contain any free nicotinic acid. A more recent placebo-controlled trial was small (n=11/group), but results after three months at 1500 mg/day showed no trend for improvements in total cholesterol, LDL-C, HDL-C or triglycerides. Thus, so far there is not enough evidence to recommend IHN to treat dyslipidemia. Furthermore, the American Heart Association and the National Cholesterol Education Program both take the position that only prescription niacin should be used to treat dyslipidemias, and only under the management of a physician. The reason given is that niacin at effective intakes of 1500–3000 mg/day can also potentially have severe adverse effects. Thus liver function tests to monitor liver enzymes are necessary when taking therapeutic doses of niacin, including alkaline phosphatase (ALP), aspartate transaminase (AST), and alanine transaminase (ALT). The liver can synthesize niacin from the essential amino acid tryptophan, requiring 60 mg of tryptophan to make one mg of niacin. The 5-membered aromatic heterocycle of tryptophan is cleaved and rearranged with the alpha amino group of tryptophan into the 6-membered aromatic heterocycle of niacin. Riboflavin, 6vitamin B and iron are required in some of the reactions involved in the conversion of tryptophan to NAD. Several million kilograms of niacin are manufactured each year, starting from 3-methylpyridine. In addition to its effects as NAD and NADP, niacin may have additional effects by receptor activation. The receptor for niacin is a G protein-coupled receptor called HM74A. It couples to the Gi alpha subunit. Niacin is found in variety of foods, including liver, chicken, beef, fish, cereal, peanuts and legumes, and is also synthesized from tryptophan, an essential amino acid found in most forms of protein. Animal products: Fruits and vegetables: Seeds: Fungi: Other: Niacin was first described by chemist Hugo Weidel in 1873 in his studies of nicotine. The original preparation remains useful: The oxidation of nicotine using nitric acid. Niacin was extracted from livers by biochemist Conrad Elvehjem in 1937, who later identified the active ingredient, then referred to as the "pellagra-preventing factor" and the "anti-blacktongue factor." Soon after, in studies conducted in Alabama and Cincinnati, Dr. Tom Spies found that nicotinic acid cured the sufferers of pellagra. When the biological significance of nicotinic acid was realized, it was thought appropriate to choose a name to dissociate it from nicotine, to avoid the perception that vitamins or niacin-rich food contains nicotine, or that cigarettes contain vitamins. The resulting name 'niacin' was derived from nicotinic acid + vitamin. Carpenter found in 1951 that niacin in corn is biologically unavailable, and can be released only in very alkaline lime water of pH 11. This process, known as nixtamalization, was discovered by the prehistoric civilizations of Mesoamerica. Niacin is referred to as vitamin B3 because it was the third of the B vitamins to be discovered. It has historically been referred to as "vitamin PP" or "vitamin P-P," both of which are derived from the term "pellagra-preventive factor." As of August 2008[update], a combination of niacin with laropiprant is being tested in a clinical trial. Laropiprant reduces facial flushes induced by niacin. M: NUT cof, enz, met noco, nuvi, sysi/epon, met drug (A8/11/12) M: VAS anat (a:h/u/t/a/l,v:h/u/t/a/l)/phys/devp/cell/prot noco/syva/cong/lyvd/tumr, sysi/epon, injr proc, drug (C2s+n/3/4/5/7/8/9) M: MET mt, k, c/g/r/p/y/i, f/h/s/l/o/e, a/u, n, m k, cgrp/y/i, f/h/s/l/o/e, au, n, m, epon m (A16/C10), i (k, c/g/r/p/y/i, f/h/s/o/e, a/u, n, m)

Fat
Fats consist of a wide group of compounds that are generally soluble in organic solvents and generally insoluble in water. Chemically, fats are triglycerides: triesters of glycerol and any of several fatty acids. Fats may be either solid or liquid at room temperature, depending on their structure and composition. Although the words "oils", "fats", and "lipids" are all used to refer to fats, in reality, fat is a subset of lipid. "Oils" is usually used to refer to fats that are liquids at normal room temperature, while "fats" is usually used to refer to fats that are solids at normal room temperature. "Lipids" is used to refer to both liquid and solid fats, along with other related substances, usually in a medical or biochemical context. The word "oil" is also used for any substance that does not mix with water and has a greasy feel, such as petroleum (or crude oil), heating oil, and essential oils, regardless of its chemical structure. Fats form a category of lipid, distinguished from other lipids by their chemical structure and physical properties. This category of molecules is important for many forms of life, serving both structural and metabolic functions. They are an important part of the diet of most heterotrophs (including humans). Fats or lipids are broken down in the body by enzymes called lipases produced in the pancreas. Examples of edible animal fats are lard, fish oil, butter/ghee and whale blubber. They are obtained from fats in the milk and meat, as well as from under the skin, of an animal. Examples of edible plant fats include peanut, soya bean, sunflower, sesame, coconut and olive oils, and cocoa butter. Vegetable shortening, used mainly for baking, and margarine, used in baking and as a spread, can be derived from the above oils by hydrogenation. These examples of fats can be categorized into saturated fats and unsaturated fats. Unsaturated fats can be further divided into cis fats, which are the most common in nature, and trans fats, which are rare in nature but present in partially hydrogenated vegetable oils. There are many different kinds of fats, but each is a variation on the same chemical structure. All fats are derivatives of fatty acids and glycerol. The molecules are called triglycerides, which are triesters of glycerol (an ester being the molecule formed from the reaction of the carboxylic acid and an organic alcohol). As a simple visual illustration, if the kinks and angles of these chains were straightened out, the molecule would have the shape of a capital letter E. The fatty acids would each be a horizontal line; the glycerol "backbone" would be the vertical line that joins the horizontal lines. Fats therefore have "ester" bonds. The properties of any specific fat molecule depend on the particular fatty acids that constitute it. Different fatty acids are composed of different numbers of carbon and hydrogen atoms. The carbon atoms, each bonded to two neighboring carbon atoms, form a zigzagging chain; the more carbon atoms there are in any fatty acid, the longer its chain will be. Fatty acids with long chains are more susceptible to intermolecular forces of attraction (in this case, van der Waals forces), raising its melting point. Long chains also yield more energy per molecule when metabolized. A fat's constituent fatty acids may also differ in the C/H ratio. When all three fatty acids have the formula CnH(2n+1)CO2H, the resulting fat is called "saturated". Values of n usually range from 13 to 17. Each carbon atom in the chain is saturated with hydrogen, meaning they are bonded to as many hydrogens as possible. Unsaturated fats are derived from fatty acids with the formula CnH(2n-1)CO2H. These fatty acids contain double bonds within carbon chain. This results in an "unsaturated" fatty acid. More specifically, it would be a monounsaturated fatty acid. Polyunsaturated fatty acids would be fatty acids with more than one double bond; they have the formula, CnH(2n-3)CO2H and CnH(2n-5)CO2H. Unsaturated fats can be converted to saturated ones by the process of hydrogenation. This technology underpinned the development of margarine. Saturated and unsaturated fats differ in their energy content and melting point. Since unsaturated fats contain fewer carbon-hydrogen bonds than saturated fats with the same number of carbon atoms, unsaturated fats will yield slightly less energy during metabolism than saturated fats with the same number of carbon atoms. Saturated fats can stack themselves in a closely packed arrangement, so they can freeze easily and are typically solid at room temperature. For example, animal fats tallow and lard are high in saturated fatty acid content and are solids. Olive and linseed oils on the other hand are highly unsaturated and are oily. There are two ways the double bond may be arranged: the isomer with both parts of the chain on the same side of the double bond (the cis-isomer), or the isomer with the parts of the chain on opposite sides of the double bond (the trans-isomer). Most trans-isomer fats (commonly called trans fats) are commercially produced. Trans fatty acids are rare in nature. The cis-isomer introduces a kink into the molecule that prevents the fats from stacking efficiently as in the case of fats with saturated chains. This decreases intermolecular forces between the fat molecules, making it more difficult for unsaturated cis-fats to freeze; they are typically liquid at room temperature. Trans fats may still stack like saturated fats, and are not as susceptible to metabolization as other fats. Trans fats may significantly increase the risk of coronary heart disease. Vitamins A, D, E, and K are fat-soluble, meaning they can only be digested, absorbed, and transported in conjunction with fats. Fats are also sources of essential fatty acids, an important dietary requirement. Fats play a vital role in maintaining healthy skin and hair, insulating body organs against shock, maintaining body temperature, and promoting healthy cell function. Fats also serve as energy stores for the body, containing about 37.8 kilojoules (9 Calories) per gram of fat. They are broken down in the body to release glycerol and free fatty acids. The glycerol can be converted to glucose by the liver and thus used as a source of energy. Fat also serves as a useful buffer towards a host of diseases. When a particular substance, whether chemical or biotic—reaches unsafe levels in the bloodstream, the body can effectively dilute—or at least maintain equilibrium of—the offending substances by storing it in new fat tissue. This helps to protect vital organs, until such time as the offending substances can be metabolized and/or removed from the body by such means as excretion, urination, accidental or intentional bloodletting, sebum excretion, and hair growth. While it is nearly impossible to remove fat completely from the diet, it would also be unhealthy to do so. Some fatty acids are essential nutrients, meaning that they can't be produced in the body from other compounds and need to be consumed in small amounts. All other fats required by the body are non-essential and can be produced in the body from other compounds. In animals, adipose, or fatty tissue is the body's means of storing metabolic energy over extended periods of time. Depending on current physiological conditions, adipocytes store fat derived from the diet and liver metabolism or degrade stored fat to supply fatty acids and also glycerol to the circulation. These metabolic activities are regulated by several hormones (i.e., insulin, glucagon and epinephrine). The location of the tissue determines its metabolic profile: "visceral fat" is located within the abdominal wall (i.e., beneath the wall of abdominal muscle) whereas "subcutaneous fat" is located beneath the skin (and includes fat that is located in the abdominal area beneath the skin but above the abdominal muscle wall). Visceral fat was recently discovered to be a significant producer of signaling chemicals (i.e., hormones), among which several are involved in inflammatory tissue responses. One of these is resistin which has been linked to obesity, insulin resistance, and Type 2 diabetes. This latter result is currently controversial, and there have been reputable studies supporting all sides on the issue.

Urine
Urine (from Latin Urina, ae, f.) is a typically sterile liquid by-product of the body secreted by the kidneys through a process called urination and excreted through the urethra. Cellular metabolism generates numerous by-products, many rich in nitrogen, that require elimination from the bloodstream. These by-products are eventually expelled from the body during urination, the primary method for excreting water-soluble chemicals from the body. These chemicals can be detected and analyzed by urinalysis. Certain disease conditions can result in pathogen-contaminated urine. Most animals have excretory systems for elimination of soluble toxic wastes. In humans, soluble wastes are excreted primarily by the urinary system and, to a lesser extent in terms of urea removed, by perspiration. The urinary system consists of the kidneys, ureters, urinary bladder, and urethra. The system produces urine by a process of filtration, reabsorption, and tubular secretion. The kidneys extract the soluble wastes from the bloodstream, as well as excess water, sugars, and a variety of other compounds. The resulting urine contains high concentrations of urea and other substances, including toxins. Urine flows from the kidney through the ureter, bladder, and finally the urethra before passing from the body. Exhaustive detailed description of the composition of human urine can be found in NASA Contractor Report No. NASA CR-1802, D. F. Putnam, July 1971. That report provided detailed chemical analyses for inorganic and organic constituents, methods of analysis, chemical and physical properties and its behavior during concentrative processes such as evaporation, distillation and other physiochemical operations. Urine is an aqueous solution of greater than 95% water, with the remaining constituents, in order of decreasing concentration urea 9.3 g/L, chloride 1.87 g/L, sodium 1.17 g/L, potassium 0.750 g/L, creatinine 0.670 g/L and other dissolved ions, inorganic and organic compounds. Urine is sterile until it reaches the urethra, where epithelial cells lining the urethra are colonized by facultatively anaerobic Gram negative rods and cocci. Subsequent to elimination from the body, urine can acquire strong odors due to bacterial action,][ and in particular the release of ammonia from the breakdown of urea. Some diseases alter the quantity and consistency of urine, such as diabetes introducing sugar. Consuming beets can result in beeturia (pink/red urine containing betanin) for some 10–14% of the population. Healthy urine is not toxic. However, it contains compounds eliminated by the body as undesirable, and can be irritating to skin and eyes. After suitable processing it is possible to extract potable water from urine. Urine is principally water. It also contains an assortment of inorganic salts and organic compounds, including proteins, hormones, and a wide range of metabolites, varying by what is introduced into the body. Urine varies in appearance, depending principally upon a body's level of hydration, as well as other factors. Normal urine is a transparent solution ranging from colorless to amber but is usually a pale yellow. In the urine of a healthy individual the color comes primarily from the presence of urobilin. Urobilin in turn is a final waste product resulting from the breakdown of heme from hemoglobin during the destruction of aging blood cells. Colorless urine indicates over-hydration, generally preferable to dehydration (though it can remove essential salts from the body). Colorless urine in drug tests can suggest an attempt to avoid detection of illicit drugs in the bloodstream through over-hydration. The odor of normal human urine can reflect what has been consumed or specific diseases. For example, an individual with diabetes mellitus may present a sweetened urine odor. This can be due to kidney diseases as well, such as kidney stones. Eating asparagus can cause a strong odor reminiscent of the vegetable caused by the body's breakdown of asparagusic acid. Likewise consumption of saffron, alcohol, coffee, tuna fish, and onion can result in telltale scents.][ Particularly spicy foods can have a similar effect, as their compounds pass through the kidneys without being fully broken down before exiting the body. Turbid (cloudy) urine may be a symptom of a bacterial infection, but can also be caused by crystallization of salts such as calcium phosphate.][ The pH of urine can vary between 4.6 and 8, with neutral (7) being norm. In persons with hyperuricosuria, acidic urine can contribute to the formation of stones of uric acid in the kidneys, ureters, or bladder. Urine pH can be monitored by a physician or at home. A diet high in citrus, vegetables, or dairy can increase urine pH (more basic). Some drugs also can increase urine pH, including acetazolamide, potassium citrate, and sodium bicarbonate.][ A diet high in meat can decrease urine pH (more acidic).][ Cranberries, popularly thought to decrease the pH of urine, have actually been shown not to acidify urine. Drugs that can decrease urine pH include ammonium chloride, chlorothiazide diuretics, and methenamine mandelate. Average urine production in adult humans is about 1 – 2 L per day, depending on state of hydration, activity level, environmental factors, weight, and the individual's health. Producing too much or too little urine needs medical attention. Polyuria is a condition of excessive production of urine (> 2.5 L/day), oliguria when < 400 mL are produced, and anuria one of < 100 mL per day. Normal urine density or specific gravity values vary between 1.003–1.035 (g·cm−3), and any deviations may be associated with urinary disorders. Many physicians in ancient history have resorted to the inspection and examination of the urine of their patients. Hermogenes wrote about the color and other attributes of urine as indicators of certain diseases. Abdul Malik Ibn Habib of Andalusia d.862 AD, mentions numerous reports of urine examination throughout the Umayyad empire. Diabetes mellitus got its name because the urine is plentiful and sweet. A urinalysis is a medical examination of the urine and part of routine examinations. A culture of the urine is performed when a urinary tract infection is suspected. A microscopic examination of the urine may be helpful to identify organic or inorganic substrates and help in the diagnosis. The color and volume of urine can be reliable indicators of hydration level. Clear and copious urine is generally a sign of adequate hydration. Dark urine is a sign of dehydration. The exception occurs when diuretics or excessive amounts of alcohol][ or caffeine][ are consumed, in which case urine can be clear and copious and the person still be dehydrated. Urine contains proteins and other substances that are useful for medical therapy and are ingredients in many prescription drugs (e.g., Ureacin, Urecholine, Urowave).][ Urine from postmenopausal women is rich in gonadotropins that can yield follicle stimulating hormone and luteinizing hormone for fertility therapy. One such commercial product is Pergonal. Urine from pregnant women contains enough human chorionic gonadotropins for commercial extraction and purification to produce hCG medication. Pregnant mare urine is the source of estrogens, namely Premarin. Urine also contains antibodies, which can be used in diagnostic antibody tests for a range of pathogens, including HIV-1. Urine contains large quantities of nitrogen (mostly as urea), as well as significant quantities of dissolved phosphates and potassium, the main macronutrients required by plants, with urine having plant macronutrient percentages (i.e. NPK) of approximately 11-1-2 by one study or 15-1-2 by another report, illustrating that exact composition varies with diet. Undiluted, it can chemically burn the roots of some plants, but it can be used safely as a source of complementary nitrogen in carbon-rich compost. When diluted with water (at a 1:5 ratio for container-grown annual crops with fresh growing medium each season, or a 1:8 ratio for more general use), it can be applied directly to soil as a fertilizer. The fertilization effect of urine has been found to be comparable to that of commercial fertilizers with an equivalent NPK rating. Urine contains most (94% according to Wolgast) of the NPK nutrients excreted by the human body. Conversely, concentrations of heavy metals such as lead, mercury, and cadmium, commonly found in solid human waste, are much lower in urine (though not low enough to qualify for use in organic agriculture under current EU rules). The more general limitations to using urine as fertilizer then depend mainly on the potential for buildup of excess nitrogen (due to the high ratio of that macronutrient), and inorganic salts such as sodium chloride, which are also part of the wastes excreted by the renal system. The degree to which these factors impact the effectiveness depends on the term of use, salinity tolerance of the plant, soil composition, addition of other fertilizing compounds, and quantity of rainfall or other irrigation. Urine typically contains 70% of the nitrogen and more than half the phosphorus and potassium found in urban waste water flows, while making up less than 1% of the overall volume. Thus far, source separation, or urine diversion and on-site treatment has been implemented in South Africa, China, and Sweden among other countries with the Bill and Melinda Gates Foundation provided some of the funding implemenations. China reportedly had 685,000 operating source separation toilets spread out among 17 provinces in 2003. "Urine management" is a relatively new way to view closing the cycle of agricultural nutrient flows and reducing sewage treatment costs and ecological consequences such as eutrophication resulting from the influx of nutrient rich effluent into aquatic or marine ecosystems. Proponents of urine as a natural source of agricultural fertilizer claim the risks to be negligible or acceptable. Their views seem to be backed by research showing there are more environmental problems when it is treated and disposed of compared with when it is used as a resource. It is unclear whether source separation, urine diversion, and on-site urine treatment can be made cost effective; nor whether required behavioral changes would be regarded as socially acceptable, as the largely successful trials performed in Sweden may not readily generalize to other industrialized societies. In developing countries the use of whole raw sewage (night soil) has been common throughout history, yet the application of pure urine to crops is rare. Increasingly there are calls for urine's use as a fertilizer, such as a Scientific American article "Human urine is an effective fertilizer". In pre-industrial times urine, being rich in ammonia, was used – in the form of lant – as a cleaning fluid. Urine was was also used for whitening teeth in Ancient Rome. Urine was used before the development of a chemical industry in the manufacture of gunpowder. Urine, a nitrogen source, was used to moisten straw or other organic material, which was kept moist and allowed to rot for several months to over a year. The resulting salts were washed from the heap with water, which was evaporated to allow collection of crude saltpeter crystals, that were usually refined before being used in making gunpowder. The US Army Field Manual, advise against drinking urine for survival. These guides explain that drinking urine tends to worsen, rather than relieve dehydration due to the salts in it, and that urine should not be consumed in a survival situation, even when there is no other fluid available. In hot weather survival situations where other sources of water are not available, soaking cloth (a shirt for example) in urine and putting it on the head can help cool the body. During World War I the Germans experimented with numerous poisonous gases for use during war. After the first German chlorine gas attacks, Allied troops were supplied with masks of cotton pads that had been soaked in urine. It was believed that the ammonia in the pad neutralized the chlorine. These pads were held over the face until the soldiers could escape from the poisonous fumes, although it is now known that chlorine gas reacts with urine to produce toxic fumes (see chlorine and use of poison gas in World War I).][ The Vickers machine gun, used by the British Army during World War 1, required water for cooling when fired so soldiers would resort to urine if water was unavailable. Urban myth states that urine works well against jellyfish stings, and this scenario was demonstrated on a Season 4 episode of the NBC-TV show Friends, "The One With the Jellyfish", an early episode of the CBS-TV show Survivor and the documentary film The Real Cancun. At best, it is ineffective and in some cases this treatment may make the injury worse. Tanners soaked animal skins in urine to remove hair fibers—a necessary step in the preparation of leather.][ Urine has often been used as a mordant to help prepare textiles, especially wool, for dyeing. In Scotland, the process of "walking" (stretching) tweed cloth is preceded by soaking in urine. Prior to the acquisition of soap from the Germanic peoples during the first century AD, Ancient Romans used fermented human urine (in the form of lant) to cleanse grease stains from clothing. The emperor Nero instituted a tax (Latin: ) on the urine industry, continued by his successor, Vespasian. It is Vespasian to whom the Latin saying Pecunia non olet (money doesn't smell) is attributed – said to have been the emperor's reply to a complaint from his son about the unpleasant nature of the tax. Vespasian's name is still attached to public urinals in France (vespasiennes), Italy (vespasiani), and Romania (vespasiene). Alchemists spent much time trying to extract gold from urine, which led to discoveries such as white phosphorus by German alchemist Hennig Brand when distilling fermented urine in 1669. In 1773 the French chemist Hilaire Rouelle discovered the organic compound urea by boiling urine dry. The onomatopoetic term "piss" was the usual word for urination prior to the 14th century. "Urinate" was at first used mostly in medical contexts. "Piss" continues to be used, but is considered vulgar; it is also used in such colloquialisms as "to piss off" and "piss poor". Euphemisms and expressions used between parents and children such as "wee", "pee", and many others, arose. Notes Further reading
Body water: Intracellular fluid/Cytosol M: URI anat/phys/devp/cell noco/acba/cong/tumr, sysi/epon, urte proc/itvp, drug (G4B), blte, urte

Lactic acid
2-Hydroxypropanoic acid Milk acid CC(O)C(=O)O InChI=1S/C3H6O3/c1-2(4)3(5)6/h2,4H,1H3,(H,5,6)/t2-/m0/s1Yes 
Key: JVTAAEKCZFNVCJ-REOHCLBHSA-NYes  L: 53 °C
D: 53 °C
D/L: 16.8 °C 122 °C @ 12 mmHg Lactic acid, also known as milk acid, is a chemical compound that plays a role in various biochemical processes and was first isolated in 1780 by the Swedish chemist Carl Wilhelm Scheele. Lactic acid is a carboxylic acid with the chemical formula C3H6O3. It has a hydroxyl group adjacent to the carboxyl group, making it an alpha hydroxy acid (AHA). In solution, it can lose a proton from the acidic group, producing the lactate ion (to be specific, an anion due to being negatively charged with an extra electron) CH3CH(OH)COO−. Compared to acetic acid, its apK is 1 unit less, meaning lactic acid deprotonates ten times as easily as acetic acid does. This higher acidity is the consequence of the intramolecular hydrogen bridge between the α-hydroxyl and the carboxylate group, making the latter less capable of strongly attracting its proton. Lactic acid is miscible with water or ethanol, and is hygroscopic. Lactic acid is chiral and has two optical isomers. One is known as L-(+)-lactic acid or (S)-lactic acid and the other, its mirror image, is D-(−)-lactic acid or (R)-lactic acid. In animals, L-lactate is constantly produced from pyruvate via the enzyme lactate dehydrogenase (LDH) in a process of fermentation during normal metabolism and exercise. It does not increase in concentration until the rate of lactate production exceeds the rate of lactate removal, which is governed by a number of factors, including monocarboxylate transporters, concentration and isoform of LDH, and oxidative capacity of tissues. The concentration of blood lactate is usually at rest, but can rise to over 20 mmol/L during intense exertion.][ In industry, lactic acid fermentation is performed by lactic acid bacteria. These bacteria can also grow in the mouth; the acid they produce is responsible for the tooth decay known as caries. In medicine, lactate is one of the main components of lactated Ringer's solution and Hartmann's solution. These intravenous fluids consist of sodium and potassium cations along with lactate and chloride anions in solution with distilled water, generally in concentrations isotonic with human blood. It is most commonly used for fluid resuscitation after blood loss due to trauma, surgery, or burn injury. Lactic acid was refined for the first time by the Swedish chemist Carl Wilhelm Scheele in 1780 from sour milk. In 1808 Jöns Jacob Berzelius discovered that lactic acid (actually L-lactate) also is produced in muscles during exertion. Its structure was established by Johannes Wislicenus in 1873. In 1856, Louis Pasteur discovered Lactobacillus and its role in the making of lactic acid. Lactic acid started to be produced commercially by the German pharmacy Boehringer Ingelheim in 1895. In 2006, global production of lactic acid reached 275,000 tonnes with an average annual growth of 10%. During power exercises such as sprinting, when the rate of demand for energy is high, glucose is broken down and oxidized to pyruvate, and lactate is produced from the pyruvate faster than the tissues can remove it, so lactate concentration begins to rise. The production of lactate is a beneficial process because it regenerates +NAD which is used up in the creation of pyruvate from glucose, and this ensures that energy production is maintained and exercise can continue. The increased lactate produced can be removed in two ways: Strenuous anaerobic exercise causes a lowering of pH and pain, called acidosis. The effect of lactate production on acidosis has been the topic of many recent conferences in the field of exercise physiology. Robergs et al. have discussed the creation of H+ ions that occurs during glycolysis. and claim that the idea that acidosis is caused by the production of lactic acid is a "construct" or myth, pointing out that part of the lowering of pH is due to the reaction ATP−4+H2O=ADP−3+HPO4−2+H+, and that reducing pyruvate to lactate (pyruvate+NADH+H+=lactate+NAD+) actually consumes H+. However, a response by Lindinger et al. has been written claiming that Robergs et al. ignored the causative factors of the increase in concentration of hydrogen ions (denoted [H+]). Specifically, lactate is an anion, and its production causes a reduction in the amount of cations such as Na+ minus anions, and thus causes an increase in [H+] to maintain electroneutrality. Increasing partial pressure of CO2, PCO2, also causes an increase in [H+]. During exercise, the intramuscular lactate concentration and PCO2 increase, causing an increase in [H+], and thus a decrease in pH (see Le Chatelier's principle). During intense exercise, the respiratory chain cannot keep up with the amount of hydrogen atoms that join to form NADH. NAD+ is required to oxidize 3-phosphoglyceraldehyde in order to maintain the production of anaerobic energy during glycolysis. During anaerobic glycolysis, NAD+ is “freed up” when NADH combines with pyruvate to form lactate (as mentioned above). If this did not occur, glycolysis would come to a stop. However, lactate is continually formed even at rest and during moderate exercise. This occurs due to metabolism in red blood cells that lack mitochondria, and limitations resulting from the enzyme activity that occurs in muscle fibers having a high glycolytic capacity. Contrary to common belief, lactate or lactic acid buildup is not responsible for the muscle soreness felt in the days following strenuous exercise. The production of lactate and other metabolites during extreme exertion results in a burning sensation felt in active muscles. This painful sensation encourages one to stop overworking the body, thus forcing a recovery period in which the body clears the lactate and other metabolites. Researchers who have examined lactate levels immediately following exercise found little correlation with the level of muscle soreness felt a few days later. This delayed onset muscle soreness (DOMS) is characterized by sometimes severe muscle tenderness as well as loss of strength and range of motion, usually reaching a peak 24 to 72 hours after the extreme exercise event. The precise cause of DOMS is still unknown, though most research points to actual muscle cell damage and an elevated release of various metabolites into the tissue surrounding the muscle cells. These responses to extreme exercise result in an inflammatory-repair response, leading to swelling and soreness peaking a day or two after the event and resolves a few days later, depending on the severity of the damage. The type of muscle contraction is a key factor in the development of DOMS. When a muscle lengthens against a load the muscle contraction is said to be eccentric. The muscle is actively contracting, attempting to shorten its length, while failing. These eccentric contractions have been shown to result in more muscle cell damage than is seen with typical concentric contractions, in which a muscle successfully shortens during contraction against a load. Exercises that involve many eccentric contractions result in the most severe DOMS, even without any noticeable burning sensations in the muscles during the event. Although glucose is usually assumed to be the main energy source for living tissues, there are some indications that it is lactate, and not glucose, that is preferentially metabolized by neurons in the brain of several mammals species (the notable ones being mice, rats, and humans). According to the lactate-shuttling hypothesis, glial cells are responsible for transforming glucose into lactate, and for providing lactate to the neurons. Because of this local metabolic activity of glial cells, the extracellular fluid immediately surrounding neurons strongly differs in composition from the blood or cerebro-spinal fluid, being much richer with lactate, as it was found in microdialysis studies. The role of lactate for brain metabolism seems to be even more important at early stages of development (prenatal and early postnatal), with lactate at these stages having higher concentrations in body liquids, and being utilized by the brain even more preferentially over glucose. It was also hypothesized that lactate may exert a strong action over GABAergic networks in the developing brain, making them more inhibitory than it was previously assumed, acting either through better support of metabolites, or alterations in base intracellular pH levels, or both. A more recent paper by Zilberter's group looked directly at the energy metabolism features in brain slices of mice and showed that beta-hydroxybutyrate, lactate and pyruvate acted as oxidative energy substrates causing an increase in the NAD(P)H oxidation phase, that glucose was insufficient as an energy carrier during intense synaptic activity and finally, that lactate can be an efficient energy substrate capable of sustaining and enhancing brain aerobic energy metabolism in vitro. The paper was positively commented by Kasischke: "The study by Ivanov et al. (2011) also provides novel data on biphasic NAD(P)H fluorescence transients, an important physiological response to neural activation that has been reproduced in many studies and that is believed to originate predominately from activity-induced concentration changes to the cellular NADH pools." Blood tests for lactate are performed to determine the status of the acid base homeostasis in the body. Blood sampling for this purpose is often by arterial blood sampling (even if it is more difficult than venipuncture), because lactate differs substantially between arterial and venous levels, and the arterial level is more representative for this purpose. During childbirth, lactate levels in the fetus can be quantified by fetal scalp blood testing. Two molecules of lactic acid can be dehydrated to lactide, a cyclic lactone. A variety of catalysts can polymerize lactide to either heterotactic or syndiotactic polylactide, which as biodegradable polyesters with valuable (inter alia) medical properties are currently attracting much attention. Lactic acid is used also as a monomer for producing polylactic acid (PLA), which later has developed application as biodegradable plastic. This kind of plastic is a good option for substituting conventional plastic produced from petroleum oil because of low emission of carbon dioxide. The commonly used process in producing lactic acid is via fermentation, and, later, to obtain the polylactic acid, the polymerization process follows. Lactic acid is also employed in pharmaceutical technology to produce water-soluble lactates from otherwise insoluble active ingredients. It finds further use in topical preparations and cosmetics to adjust acidity and for its disinfectant and keratolytic properties. Lactic acid is found primarily in sour milk products, such as koumiss, laban, yogurt, kefir, and some cottage cheeses. The casein in fermented milk is coagulated (curdled) by lactic acid. Lactic acid is also responsible for the sour flavor of sourdough breads. This acid is used in beer brewing to lower the wort pH in order to reduce some undesirable substances such as tannins without giving off-flavors such as citric acid and increase the body of the beer.][ Some brewers and breweries will use food grade lactic acid to lower the pH in finished beers.][ In winemaking, a bacterial process, natural or controlled, is often used to convert the naturally present malic acid to lactic acid, to reduce the sharpness and for other flavor-related reasons. This malolactic fermentation is undertaken by the family of lactic acid bacteria. As a food additive it is approved for use in the EU, USA and Australia and New Zealand; it is listed by its INS number 270 or as E number E270. Lactic acid is used as a food preservative, curing agent, and flavoring agent. It is an ingredient in processed foods and is used as a decontaminant during meat processing. Lactic acid is produced commercially by fermentation of carbohydrates such as glucose, sucrose, or lactose, or by chemical synthesis. Carbohydrate sources include corn, beets, and cane sugar. Lactic acid has gained importance in the detergent industry the last decade. It is a good descaler, soap-scum remover, and a registered anti-bacterial agent. It is also economically beneficial as well as part of a trend toward environmentally safer and natural ingredients. M: ♀ FRS anat/phys/devp noco/cong/npls, sysi/epon proc/asst, drug (G1/G2B/G3CD)

Ascorbic acid
(5R)-[(1S)-1,2-dihydroxyethyl]-3,4-dihydroxyfuran-2(5H)-one Vitamin C OC=1C(OC(=O)C=1O)[C@@H](O)CO C([C@@H]([C@@H]1C(=C(C(=O)O1)O)O)O)O InChI=1S/C6H8O6/c7-1-2(8)5-3(9)4(10)6(11)12-5/h2,5,7-10H,1H2/t2-,5+/m0/s1 
Key: CIWBSHSKHKDKBQ-JLAZNSOCSA-N  190-192 °C, 463-465 K, 374-378 °F (decomposes) Ascorbic acid is a naturally occurring organic compound with antioxidant properties. It is a white solid, but impure samples can appear yellowish. It dissolves well in water to give mildly acidic solutions. Ascorbic acid is one form ("vitamer") of vitamin C. It was originally called L-hexuronic acid, but when it was found to have vitamin C activity in animals ("vitamin C" being defined as a vitamin activity, not then a specific substance), the suggestion was made to rename L-hexuronic acid. The new name for L-hexuronic acid is derived from a- (meaning "no") and scorbutus (scurvy), the disease caused by a deficiency of vitamin C. Because it is derived from glucose, many animals are able to produce it, but humans require it as part of their nutrition. Other vertebrates lacking the ability to produce ascorbic acid include other primates, guinea pigs, teleost fishes, bats, and birds, all of which require it as a dietary micronutrient (that is, a vitamin). Chemically, there exists a D-ascorbic acid which does not occur in nature. It may be synthesized artificially. It has identical antioxidant properties to L-ascorbic acid, yet has far less vitamin C activity (although not quite zero). This fact is taken as evidence that the antioxidant properties of ascorbic acid are only a small part of its effective vitamin activity. Specifically, L-ascorbate is known to participate in many specific enzyme reactions which require the correct epimer (L-ascorbate and not D-ascorbate). From the middle of the 18th century, it was noted that lemon juice could prevent sailors from getting scurvy. At first, it was supposed that the acid properties were responsible for this benefit; however, it soon became clear that other dietary acids, such as vinegar, had no such benefits. In 1907, two Norwegian physicians reported an essential disease-preventing compound in foods that was distinct from the one that prevented beriberi. These physicians were investigating dietary deficiency diseases using the new animal model of guinea pigs, which are susceptible to scurvy. The newly discovered food-factor was eventually called vitamin C. From 1928 to 1932, the Hungarian research team led by Albert Szent-Györgyi, as well as that of the American researcher Charles Glen King, identified the antiscorbutic factor as a particular single chemical substance. At the Mayo clinic, Szent-Györgyi had isolated the chemical hexuronic acid from animal adrenal glands. He suspected it to be the antiscorbutic factor, but could not prove it without a biological assay. This assay was finally conducted at the University of Pittsburgh in the laboratory of King, which had been working on the problem for years, using guinea pigs. In late 1931, King's lab obtained adrenal hexuronic acid indirectly from Szent-Györgyi and using their animal model, proved that it is vitamin C, by early 1932. This was the last of the compound from animal sources, but, later that year, Szent-Györgyi's group discovered that paprika pepper, a common spice in the Hungarian diet, is a rich source of hexuronic acid. He sent some of the now-more-available chemical to Walter Norman Haworth, a British sugar chemist. In 1933, working with the then-Assistant Director of Research (later Sir) Edmund Hirst and their research teams, Haworth deduced the correct structure and optical-isomeric nature of vitamin C, and in 1934 reported the first synthesis of the vitamin. In honor of the compound's antiscorbutic properties, Haworth and Szent-Györgyi now proposed the new name of "a-scorbic acid" for the compound. It was named L-ascorbic acid by Haworth and Szent-Györgyi when its structure was finally proven by synthesis. In 1937, the Nobel Prize for chemistry was awarded to Norman Haworth for his work in determining the structure of ascorbic acid (shared with Paul Karrer, who received his award for work on vitamins), and the prize for Physiology or Medicine that year went to Albert Szent-Györgyi for his studies of the biological functions of L-ascorbic acid. The American physician Fred R. Klenner M.D. promoted vitamin C as a cure for many diseases in the 1950s by elevating the dosages greatly to as much as tens of grams vitamin C daily by injection. From 1967 on, Nobel prize winner Linus Pauling recommended high doses of ascorbic acid (he himself took 18 grams daily) as a prevention against cold and cancer. The results of Klenner have been controversial as yet, since his investigations do not meet the modern methodologic standards. Ascorbic acid resembles the sugar from which it is derived, being a ring with many oxygen-containing functional groups. The molecule exists in equilibrium with two ketone tautomers, which are less stable than the enol form.][ In solutions, these forms of ascorbic acid rapidly interconvert. As a mild reducing agent, ascorbic acid degrades upon exposure to air, converting the oxygen to water. The redox reaction is accelerated by the presence of metal ions and light. It can be oxidized by one electron to a radical state or doubly oxidized to the stable form called dehydroascorbic acid. Ascorbate usually acts as an antioxidant. It typically reacts with oxidants of the reactive oxygen species, such as the hydroxyl radical formed from hydrogen peroxide. Such radicals are damaging to animals and plants at the molecular level due to their possible interaction with nucleic acids, proteins, and lipids. Sometimes these radicals initiate chain reactions. Ascorbate can terminate these chain radical reactions by electron transfer. Ascorbic acid is special because it can transfer a single electron, owing to the stability of its own radical ion called "semidehydroascorbate", dehydroascorbate. The net reaction is: The oxidized forms of ascorbate are relatively unreactive, and do not cause cellular damage. However, being a good electron donor, excess ascorbate in the presence of free metal ions can not only promote but also initiate free radical reactions, thus making it a potentially dangerous pro-oxidative compound in certain metabolic contexts. Ascorbic acid, a reductone, behaves as a vinylogous carboxylic acid wherein the electrons in the double bond, hydroxyl group lone pair, and the carbonyl double bond form a conjugated system. Because the two major resonance structures stabilize the deprotonated conjugate base of ascorbic acid, the hydroxyl group in ascorbic acid is much more acidic than typical hydroxyl groups. In other words, ascorbic acid can be considered an enol in which the deprotonated form is a stabilized enolate. Ascorbic acid and its sodium, potassium, and calcium salts are commonly used as antioxidant food additives. These compounds are water-soluble and thus cannot protect fats from oxidation: For this purpose, the fat-soluble esters of ascorbic acid with long-chain fatty acids (ascorbyl palmitate or ascorbyl stearate) can be used as food antioxidants. Eighty percent of the world's supply of ascorbic acid is produced in China. The relevant European food additive E numbers are It creates volatile compounds when mixed with glucose and amino acids in 90 °C. It is a cofactor in tyrosine oxidation. Ascorbic acid is found in plants and animals where it is produced from glucose. Animals must either produce it or digest it, otherwise a lack of vitamin C may cause scurvy which may eventually lead to death. Reptiles and older orders of birds make ascorbic acid in their kidneys. Recent orders of birds and most mammals make ascorbic acid in their liver where the enzyme L-gulonolactone oxidase is required to convert glucose to ascorbic acid. Humans, some other primates, and guinea pigs are not able to make L-gulonolactone oxidase because of a genetic mutation and are therefore unable to make ascorbic acid. Synthesis and signalling properties are still under investigation. The biosynthesis of ascorbic acid starts with the formation of UDP-glucuronic acid. UDP-glucuronic acid is formed when UDP-glucose undergoes two oxidations catalyzed by the enzyme UDP-glucose 6-dehydrogenase. UDP-glucose 6-dehydrogenase uses the co-factor NAD+ as the electron acceptor. The transferase UDP-glucuronate pyrophosphorylase removes a UMP and glucuronokinase, with the cofactor ADP, removes the final phosphate leading to D-glucuronic acid. The aldehyde group of this is reduced to a primary alcohol using the enzyme glucuronate reductase and the cofactor NADPH yielding L-gulonic acid. This is followed by lactone formation with the hydrolase gluconolactonase between the carbonyl on C1 and hydroxyl group on the C4. L-gulonolactone then reacts with oxygen, catalyzed by the enzyme L-gulonolactone oxidase (which is nonfunctional in humans and other primates) and the cofactor FAD+. This reaction produces 2-oxogulonolactone which spontaneously undergoes enolization to form ascorbic acid. There are many different biosynthesis pathways for ascorbic acid in plants. Most of these pathways are derived from products found in glycolysis and other pathways. For example, one pathway goes through the plant cell wall polymers. The Plant Ascorbic Acid Biosynthesis Pathway most principal seems to be L-galactose. L-galactose reacts with the enzyme L-galactose dehydrogenase where the lactone ring opens and forms again but with between the carbonyl on C1 and hydroxyl group on the C4 resulting in L-galactonolactone. L-galactonolactone then reacts with the mitochondrial flavoenzyme L-galactonolactone dehydrogenase. to produce ascorbic acid. An interesting fact about L-ascorbic acid is that it has shown to have a negative feedback on L-galactose dehydrogenase in spinach. Ascorbic acid is prepared industrially from glucose in a method based on the historical Reichstein process. In the first of a five-step process, glucose is catalytically hydrogenated to sorbitol, which is then oxidized by the microorganism Acetobacter suboxydans to sorbose. Only one of the six hydroxy groups is oxidized by this enzymatic reaction. From this point, two routes are available. Treatment of the product with acetone in the presence of an acid catalyst converts four of the remaining hydroxyl groups to acetals. The unprotected hydroxyl group is oxidized to the carboxylic acid by reaction with the catalytic oxidant TEMPO (regenerated by sodium hypochlorite — bleaching solution). (Historically, industrial preparation via the Reichstein process used potassium permanganate.) Acid-catalyzed hydrolysis of this product performs the dual function of removing the two acetal groups and ring-closing lactonization. This step yields ascorbic acid. Each of the five steps has a yield larger than 90%. A more biotechnological process, first developed in China in the 1960s but further developed in the 1990s, bypasses the use of acetone protecting groups. A second genetically-modified microbe species (such as mutant Erwinia, among others) oxidises sorbose into 2-ketogluconic acid (2-KGA), which can then undergo ring-closing lactonization via dehydration. This method is used in the predominant process used by the ascorbic acid industry in China, which supplies 80% of world's ascorbic acid. American and Chinese researchers are competing to engineer a mutant which can carry out a one-pot fermentation directly from glucose to 2-KGA, bypassing both the need for a second fermentation and the need to reduce glucose to sorbitol. The traditional way to analyze the ascorbic acid content is titration with an oxidizing agent, and several procedures have been developed, mainly relying on iodometry. Iodine is used in the presence of a starch indicator. Iodine is reduced by ascorbic acid, and, when all the ascorbic acid has reacted, the iodine is then in excess, forming a blue-black complex with the starch indicator. This indicates the end-point of the titration. As an alternative, ascorbic acid can be treated with iodine in excess, followed by back titration with sodium thiosulfate using starch as an indicator. The preceding iodometric method has been revised to exploit reaction of ascorbic acid with iodate and iodide in acid solution. Electrolyzing the solution of potassium iodide produces iodine, which reacts with ascorbic acid. The end of process is determined by potentiometric titration in a manner similar to Karl Fischer titration. The amount of ascorbic acid can be calculated by Faraday's law. An uncommon oxidising agent is -bromosuccinimideN, (NBS). In this titration, the NBS oxidizes the ascorbic acid in the presence of potassium iodide and starch. When the NBS is in excess (i.e., the reaction is complete), the NBS liberates the iodine from the potassium iodide, which then forms the blue-black complex with starch, indicating the end-point of the titration. M: NUT cof, enz, met noco, nuvi, sysi/epon, met drug (A8/11/12) M: NUT cof, enz, met noco, nuvi, sysi/epon, met drug (A8/11/12)

Alkali
In chemistry, an alkali (; from Arabic: al-qaly القلي, القالي ) is a basic, ionic salt of an alkali metal or alkaline earth metal chemical element. Some authors also define an alkali as a base that dissolves in water. A solution of a soluble base has a pH greater than 7.0. The adjective alkaline is commonly used in English as a synonym for base, especially for soluble bases. This broad use of the term is likely to have come about because alkalis were the first bases known to obey the Arrhenius definition of a base, and they are still among the most common bases. The word "alkali" is derived from Arabic al qalīy (or alkali), meaning the calcined ashes (see calcination), referring to the original source of alkaline substances. A water-extract of burned plant ashes, called potash and composed mostly of potassium carbonate, was mildly basic. After heating this substance with calcium hydroxide (slaked lime), a far more strongly basic substance known as caustic potash (potassium hydroxide) was produced. Caustic potash was traditionally used in conjunction with animal fats to produce soft soaps, one of the caustic processes that rendered soaps from fats in the process of saponification, one known since antiquity. Plant potash lent the name to the element potassium, which was first derived from caustic potash, and also gave potassium its chemical symbol K (from the German name Kalium), which ultimately derived from alkali. Alkalis are all Arrhenius bases, ones which form hydroxide ions (OH-) when dissolved in water. Common properties of alkaline aqueous solutions include: The terms "base" and "alkali" are often used interchangeably, particularly outside of the context of chemistry and chemical engineering. There are various definitions for the concept of an alkali. Alkalis are sometimes defined as a subset of the bases. However, two subsets are commonly chosen. The second subset of bases is also called an "Arrhenius base". Alkali salts are soluble hydroxides of alkali metals and alkaline earth metals, of which common examples are: Soils with pH values higher than 7.3 are usually defined as being alkaline. These soils can occur naturally, due to the presence of alkali salts. Although some plants do prefer slightly basic soil (including vegetables like cabbage and fodder like buffalograss), most plants prefer a mildly acidic soil (with pHs between 6.0 and 6.8), and alkaline soils can cause problems. In alkali lakes (or soda lakes), evaporation concentrates the naturally occurring carbonate salts, giving rise to an alkalic and often saline lake. Examples of alkali lakes:
Entheogens Cannabinoids Phenols Antiemetics Tetrahydrocannabinol Soft drink Sodium bicarbonate Properties of water Niacin Chemistry Matter Euphoriants
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