A banana plantation is a commercial agricultural facility found in tropical climates where bananas are grown.

Geographic distribution

Banana plants may grow with varying degrees of success in diverse climatic conditions, but commercial banana plantations are primarily found in equatorial regions, in banana exporting countries. The four leading banana export countries worldwide are Ecuador, Costa Rica, Philippines, and Colombia. Ecuador provides more than 33% of the global banana export. In 2004, banana producing countries totaled 130. Production, as well as exports and imports of bananas, are nonetheless concentrated in a few equatorial countries. 75% of total banana production in 2004 was generated in 10 counties. India, Ecuador, Brazil and China produced half of total bananas. Latin American and Caribbean countries lead banana production up to the 1980s, and Asian nations took the lead in banana production during the 1990s. African production levels have remained mostly unchanged.

Elements

Banana plantations, as well as growing the fruit, may also package, process, and ship their product directly from the plantation to worldwide markets. Depending on the scope of the operation, a plantation's size may vary from a small family farm operation to a corporate facility encompassing large tracts of land, multiple physical plants, and many employees.

Production-related activities on a plantation may include cultivating and harvesting the fruit, transporting the picked bunches to a packing shed, hanging to ripen in large bunches, dividing large bunches into smaller market-friendly bunches, sorting, labeling, washing, drying, packing, boxing, storing, refrigeration, shipping, and marketing. Depending on the scope of the operation, other activities may include drying, food preparation, tourism, and market research.

Soil

Bananas will grow and fruit under poor soil conditions but will be less productive without deep, well-drained soil; forest loam, rocky sand, marl, red laterite, volcanic ash, sandy clay, or even heavy clay. The key element in soil type for successful banana plant growth is good drainage. Alluvial soils of river valleys are ideal for banana growing. Bananas prefer an acid soil.

Physical plant

Physical plants on banana plantations, aside from growing fields, may include facilities or machinery for plant propagation, cultivation, labor housing, fertilization and pest mitigation, harvesting assists such as tractors or overhead cable systems, washing tanks, storage buildings, boxing or bagging, shipping docks, offices, public relations/tourism, and general maintenance.

Cultivation techniques specific to the type of banana produced may dictate the specific physical plant makeup. Much of banana cultivation since the mid-1950s has centered around a single monoculture: The Cavendish banana. The ravages of Panama Disease in that particular cultivar may cause a shift in variety selection, subsequently causing a major change in the physical plant structure of banana plantations.

Economy

Banana growing is a significant economic engine in many banana exporting countries because it is labor-intensive, delivers a relatively quick return on effort and investment, provides a weekly income year round, and the crop recovers quickly from hurricanes and other natural disasters. Banana industry exports worldwide total over 100 million tons in a market which generates over US$5 Billion per year and employs millions of workers.

Farming techniques

Banana plantations generally follow one of four major agricultural techniques: Intensive farming, sustainable farming, organic farming, and fair trade farming.

An intensive agricultural technique which requires clearing most if not all native vegetation from tracts of land, then densely planting and fertilizing the crop may produce the highest yield of fruit per acre, but it is viewed by environmental scientists as a technique which involves a history of high risk for damage to the local environment, and health risk to the agricultural workers.

Sustainable farming

As with broader sustainable agriculture, sustainable banana production aims to integrate three main goals: environmental stewardship, farm profitability, and prosperous farming communities. Producing goods without depleting an ecosystem's natural resources is a key goal of sustainable banana farming. The further goals of farm profitability and prosperous farming communities address free market viability issues which might threaten the viability of the business, rendering the ecological sustainability efforts moot. Because of the lower per-acre crop yield and higher wage cost intrinsic to this type of farming, profitability is addressed by the introduction of a price premium charged for the product at market. Such premiums are readily paid by a segment of the consumer market which places a value on the benefits of sustainable farming.

Organic farming

According to the United Nations, "no information is available regarding how many hectares are currently under conversion or how many producers are planning to convert to organic production methods." However major banana producers indicate they are responding to demands for organic bananas with new facilities tailored to that market.

Fair Trade farming

Some consumers are willing to pay a premium price for a product, including bananas, if the means of production are consistent with the philosophies of Fair Trade. The United Nations has published a description of fair trade banana production which states, "for banana producers this means they obtain a price which covers the cost of production and an additional price premium to be invested in social, environmental or quality improvements."

Social aspects

Early benefits in tribal/clanship culture

Certain aboriginal clanships benefited from early development of intensive banana cultivation by expanding previously territorial land views into concepts of cooperative inter-clan trading relationships.

Labor conditions

Labor conditions in the banana industry have historically drawn attention both in criticism of the traditionally poor industry working conditions, and more recently in attempts by labor advocacy groups and some producers to improve labor conditions.

Workers on banana plantations in Central America have been exposed to pesticides which have been found to cause various health conditions including sterility. Banana industry advocates maintain that exposure levels were too low to produce health issues, but juries in the United States found Dole Food Company guilty of specific cases of worker sterility related to pesticide exposure in the late 1970s. One successful lawsuit presented evidence that Dole continued to use the pesticide DBCP on banana plantations in Nicaragua after the agent was found by the manufacturer to cause health problems and was banned in California in 1977. The jury found the chemical manufacturer, Dow Chemical, 20% liable and Dole 80% liable because Dow had warned Dole of the dangers of aerial spraying in the presence of workers, yet evidence presented in court indicated Dole continued using the agent in close proximity to workers on its Nicaraguan banana plantations. Financial liability in the case was later stricken because of international jurisdiction issues, however the finding of culpability by the jury was left intact.

Child labor on banana plantations has also historically been a heated labor issue Labor unions, UNICEF, and others have resisted the use of child labor as young as 8 on banana plantations, and have won concessions in some countries such as Ecuador, which instituted a minimum worker age of 15 years. In Sub-Saharan Africa, banana plantations have had a tradition of utilizing child labor that dates to the 19th century and thrives in modern times.

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Vitamin B₁₂, vitamin B12 or vitamin B-12, also called cobalamin, is a water-soluble vitamin with a key role in the normal functioning of the brain and nervous system, and for the formation of blood. It is one of the eight B vitamins. It is normally involved in the metabolism of every cell of the human body, especially affecting DNA synthesis and regulation, but also fatty acid metabolism and amino acid metabolism. Neither fungi, plants, nor animals are capable of producing vitamin B₁₂. Only bacteria and archaea have the enzymes required for its synthesis, although many foods are a natural source of B₁₂ because of bacterial symbiosis. The vitamin is the largest and most structurally complicated vitamin and can be produced industrially only through bacterial fermentation-synthesis.

Vitamin B₁₂ consists of a class of chemically related compounds (vitamers), all of which have vitamin activity. It contains the biochemically rare element cobalt sitting in the center of a planar tetra-pyrrole ring called a corrin ring. Biosynthesis of the basic structure of the vitamin is accomplished only by bacteria and archaea (which usually produce hydroxocobalamin), but conversion between different forms of the vitamin can be accomplished in the human body. A common semi-synthetic form of the vitamin is cyanocobalamin, which does not occur in nature but is produced from bacterial hydroxocobalamin. Because of its stability and lower production cost, this form is then used in many pharmaceuticals and supplements as well as a food additive. In the body it is converted to the human physiological forms methylcobalamin and 5'-deoxyadenosylcobalamin, leaving behind the cyanide ion, albeit in a minimal concentration. More recently, hydroxocobalamin, methylcobalamin, and adenosylcobalamin can be found in more expensive pharmacological products and food supplements. Their extra utility is currently debated.

Vitamin B₁₂ was discovered from its relationship to disease pernicious anemia, which is an autoimmune disease in which parietal cells of the stomach responsible for secreting intrinsic factor are destroyed (these cells are also responsible for secreting acid in the stomach). Because intrinsic factor is crucial for the normal absorption of B₁₂, its lack in pernicious anemia causes a vitamin B₁₂ deficiency. Many other subtler kinds of vitamin B₁₂ deficiency and their biochemical effects have since been elucidated.

Terminology

The names vitamin B₁₂, vitamin B12, or vitamin B-12, and the alternative name cobalamin, generally refer to all forms of the vitamin. Some medical practitioners have suggested that its use be split into two categories.

• In a broad sense, B₁₂ refers to a group of cobalt-containing vitamer compounds known as cobalamins: these include cyanocobalamin (an artifact formed from using activated charcoal, which always contains trace cyanide, to purify hydroxycobalamin), hydroxocobalamin (another medicinal form, produced by bacteria), and finally, the two naturally occurring cofactor forms of B₁₂ in the human body: 5'-deoxyadenosylcobalamin (adenosylcobalamin--AdoB12), the cofactor of Methylmalonyl Coenzyme A mutase (MUT), and methylcobalamin (MeB₁₂), the cofactor of enzyme Methionine synthase, which is responsible for conversion of homocysteine to methionine and of 5-methyltetrahydrofolate to tetrahydrofolate.
• The term B₁₂ may be properly used to refer to cyanocobalamin, the principal B₁₂ form used for foods and in nutritional supplements. This ordinarily creates no problem, except perhaps in rare cases of eye nerve damage, where the body is only marginally able to use this form due to high cyanide levels in the blood due to cigarette smoking; it thus requires cessation of smoking or B₁₂ given in another form, for the optic symptoms to abate. However, tobacco amblyopia is a rare condition, and it is yet unclear whether it represents a peculiar B₁₂ deficiency that is resistant to treatment with cyanocobalamin.

Finally, so-called pseudovitamin-B₁₂ refers to B₁₂-like analogues that are biologically inactive in humans and yet found to be present alongside B₁₂ in humans, many food sources (including animals), and possibly supplements and fortified foods. In most cyanobacteria, including Spirulina, and some algae, such as dried Asakusa-nori (Porphyra tenera), pseudovitamin-B₁₂ is found to predominate.

Medical uses

Vitamin B₁₂ is used to treat vitamin B₁₂ deficiency, cyanide poisoning, and hereditary deficiency of transcobalamin II. It is given as part of the Schilling test for detecting pernicious anemia.

For cyanide poisoning, a large amount of hydroxocobalamin may be given intravenously and sometimes in combination with sodium thiosulfate. The mechanism of action is straightforward: the hydroxycobalamin hydroxide ligand is displaced by the toxic cyanide ion, and the resulting harmless B₁₂ complex is excreted in urine. In the United States, the Food and Drug Administration approved (in 2006) the use of hydroxocobalamin for acute treatment of cyanide poisoning.

High vitamin B₁₂ level in elderly individuals may protect against brain atrophy or shrinkage associated with Alzheimer's disease and impaired cognitive function.

Recommended intake

The dietary reference intake for an adult ranges from 2 to 3 µg per day (US), and 1.5 µg per day (UK). But according to a new study, the DRI should be 4 to 7 µg per day. The Center for Food Safety and Applied Nutrition recommends 6 µg per day, based on a caloric intake of 2,000 calories, for adults and children four or more years of age.

Vitamin B₁₂ is believed to be safe when used orally in amounts that do not exceed the recommended dietary allowance (RDA). There have been studies that showed no adverse consequences of doses above the RDA. The RDA for vitamin B₁₂ in pregnant women is 2.6 µg per day and 2.8 µg during lactation periods. There is insufficient reliable information available about the safety of consuming greater amounts of vitamin B₁₂ during pregnancy.

The Institute of Medicine states that because 10 to 30% of older people may be unable to absorb naturally occurring vitamin B₁₂ in foods, it is advisable for those 51 years old and older to consume B₁₂-fortified foods or B₁₂ supplements to meet the recommended intake.

Controversial sources in algae

The UK Vegan Society, the Vegetarian Resource Group, and the Physicians Committee for Responsible Medicine, among others, recommend that vegans either consistently eat B₁₂-fortified foods or take a daily or weekly B₁₂ supplement to meet the recommended intake.

It is important for vegans, whose food provides few sources of B₁₂, and anyone else wishing to obtain B₁₂ from food sources other than animals, to consume foods that contain little or no pseudovitamin-B₁₂ and are high in biologically active B₁₂. However, there have been no significant human trials of sufficient size to demonstrate enzymatic activity of B₁₂ from nonbacterial sources, such as Chlorella and edible sea algae (seaweeds, such as lavers), although chemically some of these sources have been reported to contain B₁₂ that seems chemically similar to active vitamin. However, among these sources, only fresh sea algae such as Susabi-nori (Porphyra yezoensis) have been reported to demonstrate vitamin B₁₂ activity in B₁₂ deficient rats. This has yet to be demonstrated for Chlorella, and no study in rats of any algal B₁₂ source has yet to be confirmed by a second independent study. The possibility of algae-derived active forms of B₁₂ presently remains an active topic of research, with no results that have yet reached consensus in the nutritional community.

Deficiency

Vitamin B₁₂ deficiency can potentially cause severe and irreversible damage, especially to the brain and nervous system. At levels only slightly lower than normal, a range of symptoms such as fatigue, depression, and poor memory may be experienced.

Vitamin B₁₂ deficiency can also cause symptoms of mania and psychosis. Vitamin B₁₂ deficiency is most commonly caused by low intakes, but can also result from malabsorption, certain intestinal disorders, low presence of binding proteins, and using of certain medications. Vitamin B₁₂ is rare from plant sources, so vegetarians will be the vulnerable populations most likely to suffer from vitamin B₁₂ deficiency. Infants are at a higher risk of vitamin B₁₂ deficiency if they were born to vegetarian mothers. The elderly who have diets with limited meat or animal products are vulnerable populations as well. Vitamin B₁₂ deficiency can manifest itself as anemia and in some cases cause permanent neurological damage. Recent studies showed depression is associated with vitamin B₁₂ deficiency; sufficient vitamin B₁₂ level was independently associated with a decreased risk of depression and better cognitive performance adjusted for confounders. Vitamin B₁₂ is a co-substrate of various cell reactions involved in methylation synthesis of nucleic acid and neurotransmitters. Synthesis of the trimonoamine neurotransmitters can enhance the effects of a traditional antidepressant. The intracellular concentrations of vitamin B₁₂ can be inferred through the total plasma concentration of homocysteine, which can be converted to methionine through an enzymatic reaction that uses 5-methyletetrahydrofolate as the methyl donor group. Consequently, the plasma concentration of homocysteine falls as the intracellular concentration of vitamin B₁₂ rises. The active metabolite of vitamin B₁₂ is required for the methylation of homocysteine in the production of methionine, which is involved in a number of biochemical processes including the monoamine neurotransmitters. Thus, a deficiency in vitamin B₁₂ may impact the production and function of those neurotransmitters.

Imerslund-Gräsbeck syndrome is a rare disease where there is selective malabsorption of cobalamine with proteinuria caused due to defect in ileal receptor.

Sources

Foods

Ultimately, animals must obtain vitamin B₁₂ directly or indirectly from bacteria, and these bacteria may inhabit a section of the gut that is distal to the section where B₁₂ is absorbed. Thus, herbivorous animals must either obtain B₁₂ from bacteria in their rumens or (if fermenting plant material in the hindgut) by reingestion of cecotrope feces.

Vitamin B₁₂ is found in most animal derived foods, including fish and shellfish, meat (especially liver), poultry, eggs, milk, and milk products. However, the binding capacity of egg yolks and egg whites is markedly diminished after heat treatment. An NIH fact sheet lists a variety of animal food sources of B₁₂.

Besides certain fermented foods, there are currently only a few non-animal food sources of biologically active B₁₂ suggested, and none of these have been subjected to human trials.

A Japanese fermented black tea known as Batabata-cha has been found to contain biologically active B₁₂. Unlike kombucha, which is made by fermenting already prepared tea, Batabata-cha is fermented while still in the tea leaf state.

Chlorella, a fresh-water single cell green algae, has been suggested as a vitamin B₁₂ source but not proven by any live animal assay. Algae are thought to acquire B₁₂ through a symbiotic relationship with heterotrophic bacteria, in which the bacteria supply B₁₂ in exchange for fixed carbon. Spirulina and dried Asakusa-nori (Porphyra tenera) have been found to contain mostly pseudovitamin-B₁₂ (see Terminology) instead of biologically active B₁₂. While Asakusa-nori (Porphyra tenera) contains mostly pseudovitamin-B₁₂ in the dry state, it has been reported to contain mostly biologically active B₁₂ in the fresh state, but even its fresh state vitamin activity has not been verified by animal enzyme assay.

One group of researchers has reported that the purple laver seaweed known as Susabi-nori (Pyropia yezoensis) in its fresh state contains B₁₂ activity in the rat model, which implies that source would be active in humans. These results have not been confirmed.

A single commensal bacteria present in the gut of many mammals has demonstrated an ability to perform all steps necessary to synthesize B₁₂ from common metabolically available products.

Foods fortified with B₁₂ are also sources of the vitamin, although they cannot be regarded as true food sources of B₁₂ since the vitamin is added in supplement form, from commercial bacterial production sources, such as cyanocobalamin. Examples of B₁₂-fortified foods include fortified breakfast cereals, fortified soy products, fortified energy bars, and fortified nutritional yeast. The UK Vegan Society, the Vegetarian Resource Group, and the Physicians Committee for Responsible Medicine, among others, recommend that every vegan who is not consuming B₁₂ foods fortify with supplements. Not all of these may contain labeled amounts of vitamin activity. Supplemental B₁₂ added to beverages in one study was found to degrade to contain varying levels of pseudovitamin-B₁₂. One report has found B₁₂ analogues present in varying amounts in some multivitamins.

Unconventional natural sources of B₁₂ also exist, but their utility as food sources of B₁₂ are doubtful. For example, plants pulled from the ground and not washed may contain remnants of B₁₂ from the bacteria present in the surrounding soil. B₁₂ is also found in lakes if the water has not been sanitized. Certain insects such as termites contain B₁₂ produced by their gut bacteria, in a way analogous to ruminant animals. The human intestinal tract itself may contain B₁₂-producing bacteria in the small intestine, but it is unclear whether sufficient amounts of the vitamin could be produced to meet nutritional needs.

Supplements

Vitamin B₁₂ is provided as a supplement in many processed foods, and is also available in vitamin pill form, including multi-vitamins. Vitamin B₁₂ can be supplemented in healthy subjects also by liquid, transdermal patch, nasal spray, or injection and is available singly or in combination with other supplements. It is a common ingredient in energy drinks and energy shots, usually at many times the minimum recommended daily allowance of B₁₂. Vitamin B₁₂ supplements are effective for preventing deficiencies, especially in vegetarians, and are often marketed as weight loss supplements. However, no scientific studies have shown that B₁₂ is effective for weight loss.

Cyanocobalamin is converted to its active forms, first hydroxocobalamin and then methylcobalamin and adenosylcobalamin in the liver.

The sublingual route, in which B₁₂ is presumably or supposedly taken in more directly under the tongue, has not proven to be necessary or helpful, even though a number of lozenges, pills, and even a lollipop designed for sublingual absorption are being marketed. A 2003 study found no significant difference in absorption for serum levels from oral versus sublingual delivery of 0.5 mg of cobalamin. Sublingual methods of replacement are effective only because of the typically high doses (0.5 mg), which are swallowed, not because of placement of the tablet. As noted below, such very high doses of oral B₁₂ may be effective as treatments, even if gastro-intestinal tract absorption is impaired by gastric atrophy (pernicious anemia).

Injection and patches are sometimes used if digestive absorption is impaired, but there is evidence that this course of action may not be necessary with modern high potency oral supplements (such as 0.5 to 1 mg or more). Even pernicious anemia can be treated entirely by the oral route. These supplements carry such large doses of the vitamin that 1% to 5% of high oral doses of free crystalline B₁₂ is absorbed along the entire intestine by passive diffusion.

However, if the patient has inborn errors in the methyltransfer pathway (cobalamin C disease, combined methylmalonic aciduria and homocystinuria), treatment with intravenous, intramuscular hydroxocobalamin or transdermal B₁₂ is needed.

Non-cyano forms as supplements

Recently sublingual methylcobalamin has become available in 5 mg tablets. The metabolic fate and biological distribution of methylcobalamin are expected to be similar to that of other sources of vitamin B12 in the diet. No cyanide is released with methylcobalamin, although the amount of cyanide (2% of the weight, or 20 micrograms cyanide in a 1 mg cyanocobalamin tab) is far less than ingested in many natural foods. Although the safety of cyanocobalamin has long been proven, the safety of the other types is also well established.

Adverse effects

• Hematologic: Peripheral vascular thrombosis has been reported. Treatment of vitamin B₁₂ deficiency can unmask polycythemia vera, which is characterized by an increase in blood volume and the number of red blood cells. The correction of megaloblastic anemia with vitamin B₁₂ can result in fatal hypokalemia and gout in susceptible individuals, and it can obscure folate deficiency in megaloblastic anemia.
• Leber's disease: Vitamin B₁₂ in the form of cyanocobalamin is contraindicated in early Leber's disease, which is hereditary optic nerve atrophy. Cyanocobalamin can cause severe and swift optic atrophy, but other forms of vitamin B₁₂ are available. However, the sources of this statement are not clear, while an opposing view concludes: "The clinical picture of optic neuropathy associated with vitamin B₁₂ deficiency shows similarity to that of Leber's disease optic neuropathy. Both involve the nerve fibers of the papillomacular bundle. The present case reports suggest that optic neuropathy in patients carrying a primary LHON mtDNA mutation may be precipitated by vitamin B₁₂ deficiency. Therefore, known carriers should take care to have an adequate dietary intake of vitamin B₁₂ and malabsorption syndromes like those occurring in familial pernicious anaemia or after gastric surgery should be excluded."

Allergies

Vitamin B₁₂ supplements in theory should be avoided in people sensitive or allergic to cobalamin, cobalt, or any other product ingredients. However, direct allergy to a vitamin or nutrient is extremely rare, and if reported, other causes should be sought.

Interactions

• Alcohol (ethanol): Excessive alcohol intake lasting longer than two weeks can decrease vitamin B₁₂ absorption from the gastrointestinal tract.
• Aminosalicylic acid (para-aminosalicylic acid, PAS, Paser): Aminosalicylic acid can reduce oral vitamin B₁₂ absorption, possibly by as much as 55%, as part of a general malabsorption syndrome. Megaloblastic changes, and occasional cases of symptomatic anemia have occurred, usually after doses of 8 to 12 g/day for several months. Vitamin B₁₂ levels should be monitored in people taking aminosalicylic acid for more than one month.
• Antibiotics: An increased bacterial load can bind significant amounts of vitamin B₁₂ in the gut, preventing its absorption. In people with bacterial overgrowth of the small bowel, antibiotics such as metronidazole (Flagyl) can actually improve vitamin B₁₂ status. The effects of most antibiotics on gastrointestinal bacteria are unlikely to have clinically significant effects on vitamin B₁₂ levels.
• Hormonal contraception: The data regarding the effects of oral contraceptives on vitamin B₁₂ serum levels are conflicting. Some studies have found reduced serum levels in oral contraceptive users, but others have found no effect despite use of oral contraceptives for up to 6 months. When oral contraceptive use is stopped, normalization of vitamin B₁₂ levels usually occurs. Lower vitamin B₁₂ serum levels seen with oral contraceptives probably are not clinically significant.
• Chloramphenicol (Chloromycetin): Limited case reports suggest that chloramphenicol can delay or interrupt the reticulocyte response to supplemental vitamin B₁₂ in some patients. Blood counts should be monitored closely if this combination cannot be avoided.
• Cobalt irradiation: Cobalt irradiation of the small bowel can decrease gastrointestinal (GI) absorption of vitamin B₁₂.
• Colchicine: Colchicine in doses of 1.9 to 3.9 mg/day can disrupt normal intestinal mucosal function, leading to malabsorption of several nutrients, including vitamin B₁₂. Lower doses do not seem to have a significant effect on vitamin B₁₂ absorption after 3 years of colchicine therapy. The significance of this interaction is unclear. Vitamin B₁₂ levels should be monitored in people taking large doses of colchicine for prolonged periods.
• Colestipol (Colestid), cholestyramine (Questran): These resins used for sequestering bile acids to decrease cholesterol, can decrease gastrointestinal (GI) absorption of vitamin B₁₂. It is unlikely this interaction will deplete body stores of vitamin B₁₂ unless there are other factors contributing to deficiency. In a group of children treated with cholestyramine for up to 2.5 years, there was not any change in serum vitamin B₁₂ levels. Routine supplements are not necessary.
• H₂-receptor antagonists: include cimetidine (Tagamet), famotidine (Pepcid), nizatidine (Axid), and ranitidine (Zantac). Reduced secretion of gastric acid and pepsin produced by H₂ blockers can reduce absorption of protein-bound (dietary) vitamin B₁₂, but not of supplemental vitamin B₁₂. Gastric acid is needed to release vitamin B₁₂ from protein for absorption. Clinically significant vitamin B₁₂ deficiency and megaloblastic anemia are unlikely, unless H₂ blocker therapy is prolonged (2 years or more), or the person's diet is poor. It is also more likely if the person is rendered achlorhydric(with complete absence of gastric acid secretion), which occurs more frequently with proton pump inhibitors than H₂ blockers. Vitamin B₁₂ levels should be monitored in people taking high doses of H₂ blockers for prolonged periods.
• Metformin (Glucophage): Metformin may reduce serum folic acid and vitamin B₁₂ levels. Long-term use of metformin substantially increases the risk of B₁₂ deficiency and (in those patients who become deficient) hyperhomocysteinemia, which is "an independent risk factor for cardiovascular disease, especially among individuals with type 2 diabetes." There are also rare reports of megaloblastic anemia in people who have taken metformin for five years or more. Reduced serum levels of vitamin B₁₂ occur in up to 30% of people taking metformin chronically. However, clinically significant deficiency is not likely to develop if dietary intake of vitamin B₁₂ is adequate. Deficiency can be corrected with vitamin B₁₂ supplements even if metformin is continued. The metformin-induced malabsorption of vitamin B₁₂ is reversible by oral calcium supplementation. The general clinical significance of metformin upon B₁₂ levels is as yet unknown.
• Neomycin: Absorption of vitamin B₁₂ can be reduced by neomycin, but prolonged use of large doses is needed to induce pernicious anemia. Supplements are not usually needed with normal doses.
• Nicotine: Nicotine can reduce serum vitamin B₁₂ levels. The need for vitamin B₁₂ supplementation in smokers has not been adequately studied.
• Nitrous oxide: Nitrous oxide inactivates the cobalamin form of vitamin B₁₂ by oxidation. Symptoms of vitamin B₁₂ deficiency, including sensory neuropathy, myelopathy, and encephalopathy, can occur within days or weeks of exposure to nitrous oxide anesthesia in people with subclinical vitamin B₁₂ deficiency. Symptoms are treated with high doses of vitamin B₁₂, but recovery can be slow and incomplete. People with normal vitamin B₁₂ levels have sufficient vitamin B₁₂ stores to make the effects of nitrous oxide insignificant, unless exposure is repeated and prolonged (such as recreational use). Vitamin B₁₂ levels should be checked in people with risk factors for vitamin B₁₂ deficiency prior to using nitrous oxide anesthesia. Chronic nitrous oxide B₁₂ poisoning (usually from use of nitrous oxide as a recreational drug), however, may result in B₁₂ functional deficiency even with normal measured blood levels of B₁₂.
• Phenytoin (Dilantin), phenobarbital, primidone (Mysoline): These anticonvulsants have been associated with reduced vitamin B₁₂ absorption, and reduced serum and cerebrospinal fluidlevels in some patients. This may contribute to the megaloblastic anemia, primarily caused by folate deficiency, associated with these drugs. It is also suggested that reduced vitamin B₁₂ levels may contribute to the neuropsychiatric side effects of these drugs. Patients should be encouraged to maintain adequate dietary vitamin B₁₂ intake. Folate and vitamin B₁₂ status should be checked if symptoms of anemia develop.
• Proton pump inhibitors (PPIs): The PPIs include omeprazole (Prilosec, Losec), lansoprazole (Prevacid), rabeprazole (Aciphex), pantoprazole (Protonix, Pantoloc), and esomeprazole (Nexium). The reduced secretion of gastric acid and pepsin produced by PPIs can reduce absorption of protein-bound (dietary) vitamin B₁₂, but not supplemental vitamin B₁₂. Gastric acid is needed to release vitamin B₁₂ from protein for absorption. Reduced vitamin B₁₂ levels may be more common with PPIs than with H2-blockers, because they are more likely to produce achlorhydria (complete absence of gastric acid secretion). However, clinically significant vitamin B₁₂ deficiency is unlikely, unless PPI therapy is prolonged (2 years or more) or dietary vitamin intake is low. Vitamin B₁₂ levels should be monitored in people taking high doses of PPIs for prolonged periods.
• Zidovudine (AZT, Combivir, Retrovir): Reduced serum vitamin B₁₂ levels may occur when zidovudine therapy is started. This adds to other factors that cause low vitamin B₁₂ levels in people with HIV, and might contribute to the hematological toxicity associated with zidovudine. However, the data suggest vitamin B₁₂ supplements are not helpful for people taking zidovudine.
• Folic acid: Folic acid, particularly in large doses, can mask vitamin B₁₂ deficiency by completely correcting hematological abnormalities. In vitamin B₁₂ deficiency, folic acid can produce complete resolution of the characteristic megaloblastic anemia, while allowing potentially irreversible neurological damage (from continued inactivity of methylmalonyl mutase) to progress. Thus, vitamin B₁₂ status should be determined before folic acid is given as monotherapy.
• Potassium: Potassium supplements can reduce absorption of vitamin B₁₂ in some people. This effect has been reported with potassium chloride and, to a lesser extent, with potassium citrate. Potassium might contribute to vitamin B₁₂ deficiency in some people with other risk factors, but routine supplements are not necessary.

Structure

B₁₂ is the most chemically complex of all the vitamins. The structure of B₁₂ is based on a corrin ring, which is similar to the porphyrin ring found in heme, chlorophyll, and cytochrome. The central metal ion is cobalt. Four of the six coordination sites are provided by the corrin ring, and a fifth by a dimethylbenzimidazole group. The sixth coordination site, the center of reactivity, is variable, being a cyano group (-CN), a hydroxyl group (-OH), a methyl group (-CH₃) or a 5'-deoxyadenosyl group (here the C5' atom of the deoxyribose forms the covalent bond with Co), respectively, to yield the four B₁₂ forms mentioned below. Historically, the covalent C-Co bond is one of first examples of carbon-metal bonds to be discovered in biology. The hydrogenases and, by necessity, enzymes associated with cobalt utilization, involve metal-carbon bonds.

Vitamin B₁₂ is a generic descriptor name referring to a collection of cobalt and corrin ring molecules which are defined by their particular vitamin function in the body. All of the substrate cobalt-corrin molecules from which B₁₂ is made, must be synthesized by bacteria. However, after this synthesis is complete, except in rare cases, the human body has the ability to convert any form of B₁₂ to an active form, by means of enzymatically removing certain prosthetic chemical groups from the cobalt atom, and replacing them with others.

The four forms (vitamers) of B₁₂ are all deeply red colored crystals and water solutions, due to the color of the cobalt-corrin complex.

Cyanocobalamin is one such form, i.e. "vitamer", of B₁₂ because it can be metabolized in the body to an active co-enzyme form. However, the cyanocobalamin form of B₁₂ does not occur in nature normally, but is a byproduct of the fact that other forms of B₁₂ are avid binders of cyanide (-CN) which they pick up in the process of activated charcoal purification of the vitamin after it is made by bacteria in the commercial process. Since the cyanocobalamin form of B₁₂ is easy to crystallize and is not sensitive to air-oxidation, it is typically used as a form of B₁₂ for food additives and in many common multivitamins. Pure cyanocobalamin possesses the deep pink color associated with most octahedral cobalt(II) complexes and the crystals are well formed and easily grown up to millimeter size.

Hydroxocobalamin is another form of B₁₂ commonly encountered in pharmacology, but which is not normally present in the human body. Hydroxocobalamin is sometimes denoted B_12a. This form of B₁₂ is the form produced by bacteria, and is what is converted to cyanocobalmin in the commercial charcoal filtration step of production. Hydroxocobalamin has an avid affinity for cyanide ions and has been used as an antidote to cyanide poisoning. It is supplied typically in water solution for injection. Hydroxocobalamin is thought to be converted to the active enzymic forms of B₁₂ more easily than cyanocobalamin, and since it is little more expensive than cyanocobalamin, and has longer retention times in the body, has been used for vitamin replacement in situations where added reassurance of activity is desired. Intramuscular administration of hydroxocobalamin is also the preferred treatment for pediatric patients with intrinsic cobalamin metabolic diseases, for vitamin B₁₂ deficient patients with tobacco amblyopia (which is thought to perhaps have a component of cyanide poisoning from cyanide in cigarette smoke); and for treatment of patients with pernicious anemia who have optic neuropathy.

Adenosylcobalamin (adoB₁₂) and methylcobalamin (MeB₁₂) are the two enzymatically active cofactor forms of B₁₂ that naturally occur in the body. Most of the body's reserves are stored as adoB₁₂ in the liver. These are converted to the other methylcobalamin form as needed.

Synthesis and industrial production

Neither plants nor animals are independently capable of constructing vitamin B₁₂. Only bacteria and archaea have the enzymes required for its biosynthesis. The total synthesis of B₁₂ was reported by Robert Burns Woodward and Albert Eschenmoser in 1972, and remains one of the classic feats of organic synthesis. Species from the following genera are known to synthesize B₁₂: Acetobacterium, Aerobacter, Agrobacterium, Alcaligenes, Azotobacter, Bacillus, Clostridium, Corynebacterium, Flavobacterium, Lactobacillus, Micromonospora, Mycobacterium, Nocardia, Propionibacterium, Protaminobacter, Proteus, Pseudomonas, Rhizobium, Salmonella, Serratia, Streptomyces, Streptococcus and Xanthomonas.

Industrial production of B₁₂ is achieved through fermentation of selected microorganisms. Streptomyces griseus, a bacterium once thought to be a yeast, was the commercial source of vitamin B₁₂ for many years. The species Pseudomonas denitrificans and Propionibacterium freudenreichii subsp. shermanii are more commonly used today. These are frequently grown under special conditions to enhance yield, and at least one company, Rhône-Poulenc of France, which has merged into Sanofi-Aventis, used genetically engineered versions of one or both of these species. Since a number of species of Propionibacterium produce no exotoxins or endotoxins and are generally regarded as safe (have been granted GRAS status) by the Food and Drug Administration of the United States, they are presently the FDA-preferred bacterial fermentation organisms for vitamin B₁₂ production.

The total world production of vitamin B₁₂, by four companies (the French Sanofi-Aventis and three Chinese companies) is said to have been 35 tonnes in 2008.

See cyanocobalamin for discussion of the chemical preparation of reduced-cobalt vitamin analogs and preparation of physiological forms of the vitamin such as adenosylcobalamin and methylcobalamin.

Mechanism of action

Coenzyme B₁₂'s reactive C-Co bond participates in three main types of enzyme-catalyzed reactions.

1. Isomerases
2. Methyltransferases
3. Dehalogenases

In humans, two major coenzyme B₁₂-dependent enzyme families corresponding to the first two reaction types, are known. These are typified by the following two enzymes:

1. MUT is an isomerase which uses the AdoB₁₂ form and reaction type 1 to catalyze a carbon skeleton rearrangement (the X group is -COSCoA). MUT's reaction converts MMl-CoA to Su-CoA, an important step in the extraction of energy from proteins and fats (for more see MUT's reaction mechanism). This functionality is lost in vitamin B₁₂ deficiency, and can be measured clinically as an increased methylmalonic acid (MMA) level. Unfortunately, an elevated MMA, though sensitive to B₁₂ deficiency, is probably overly sensitive, and not all who have it actually have B₁₂ deficiency. For example, MMA is elevated in 90-98% of patients with B₁₂ deficiency; however 20-25% of patients over the age of 70 have elevated levels of MMA, yet 25-33% of them do not have B₁₂ deficiency. For this reason, assessment of MMA levels is not routinely recommended in the elderly. There is no "gold standard" test for B₁₂ deficiency because as a B₁₂ deficiency occurs, serum values may be maintained while tissue B₁₂ stores become depleted. Therefore, serum B₁₂ values above the cut-off point of deficiency do not necessarily indicate adequate B₁₂ status The MUT function is necessary for proper myelin synthesis (see mechanism below) and is not affected by folate supplementation.
2. MTR, also known as methionine synthase, is a methyltransferase enzyme, which uses the MeB₁₂ and reaction type 2 to transfer a methyl group from 5-methyltetrahydrofolate to homocysteine, thereby generating tetrahydrofolate (THF) and methionine (for more see MTR's reaction mechanism). This functionality is lost in vitamin B₁₂ deficiency, resulting in an increased homocysteine level and the trapping of folate as 5-methyl-tetrahydrofolate, from which THF (the active form of folate) cannot be recovered. THF plays an important role in DNA synthesis so reduced availability of THF results in ineffective production of cells with rapid turnover, in particular red blood cells, and also intestinal wall cells which are responsible for absorption. THF may be regenerated via MTR or may be obtained from fresh folate in the diet. Thus all of the DNA synthetic effects of B12 deficiency, including the megaloblastic anemia of pernicious anemia, resolve if sufficient dietary folate is present. Thus the best-known "function" of B₁₂ (that which is involved with DNA synthesis, cell-division, and anemia) is actually a facultative function which is mediated by B₁₂-conservation of an active form of folate which is needed for efficient DNA production. Other cobalamin-requiring methyltransferase enzymes are also known in bacteria, such as Me-H4-MPT, coenzyme M methyl transferase.

Enzyme function

If folate is present in quantity, then of the two absolutely vitamin B₁₂-dependent enzyme-family reactions in humans, the MUT-family reactions show the most direct and characteristic secondary effects, focusing on the nervous system (see below). This is because the MTR (methyltransferase-type) reactions are involved in regenerating folate, and thus are less evident when folate is in good supply.

Since the late 1990s, folic acid has begun to be added to fortify flour in many countries, so folate deficiency is now more rare. At the same time, since DNA synthetic-sensitive tests for anemia and erythrocyte size are routinely done in even simple medical test clinics (so that these folate-mediated biochemical effects are more often directly detected), the MTR-dependent effects of B₁₂ deficiency are becoming apparent not as anemia due to DNA-synthetic problems (as they were classically), but now mainly as a simple and less obvious elevation of homocysteine in the blood and urine (homocysteinuria). This condition may result in long term damage to arteries and in clotting (stroke and heart attack), but this effect is difficult to separate from other common processes associated with atherosclerosis and aging.

The specific myelin damage resulting from B₁₂ deficiency, even in the presence of adequate folate and methionine, is more specifically and clearly a vitamin deficiency problem. It has been connected to B₁₂ most directly by reactions related to MUT, which is absolutely required to convert methylmalonyl coenzyme A into succinyl coenzyme A. Failure of this second reaction to occur results in elevated levels of MMA, a myelin destabilizer. Excessive MMA will prevent normal fatty acid synthesis, or it will be incorporated into fatty acid itself rather than normal malonic acid. If this abnormal fatty acid subsequently is incorporated into myelin, the resulting myelin will be too fragile, and demyelination will occur. Although the precise mechanism(s) are not known with certainty, the result is subacute combined degeneration of central nervous system and spinal cord. Whatever the cause, it is known that B₁₂ deficiency causes neuropathies, even if folic acid is present in good supply, and therefore anemia is not present.

Vitamin B₁₂-dependent MTR reactions may also have neurological effects, through an indirect mechanism. Adequate methionine (which, like folate, must otherwise be obtained in the diet, if it is not regenerated from homocysteine by a B₁₂ dependent reaction) is needed to make S-adenosyl-methionine (SAMe), which is in turn necessary for methylation of myelin sheath phospholipids. Although production of SAMe is not B₁₂ dependent, help in recycling for provision of one adequate substrate for it (the essential amino acid methionine) is assisted by B₁₂. In addition, SAMe is involved in the manufacture of certain neurotransmitters, catecholamines and in brain metabolism. These neurotransmitters are important for maintaining mood, possibly explaining why depression is associated with B₁₂ deficiency. Methylation of the myelin sheath phospholipids may also depend on adequate folate, which in turn is dependent on MTR recycling, unless ingested in relatively high amounts.

Absorption and distribution

Methyl-B₁₂ is absorbed by an intestinal mechanism using intrinsic factor and by a diffusion process in which approximately 1% of the oral dose is absorbed. The human physiology of vitamin B₁₂ is complex, and therefore is prone to mishaps leading to vitamin B₁₂ deficiency. Protein-bound vitamin B₁₂ must be released from the proteins by the action of digestive proteases in both the stomach and small intestine. Gastric acid releases the vitamin from food particles; therefore antacid and acid-blocking medications (especially proton-pump inhibitors) may inhibit absorption of B₁₂. In addition some elderly people produce less stomach acid as they age thereby increasing their probability of B₁₂ deficiencies.

B₁₂ taken in a low-solubility, non-chewable supplement pill form may bypass the mouth and stomach and not mix with gastric acids, but these are not necessary for the absorption of free B₁₂ not bound to protein.

R-protein (also known as haptocorrin and cobalophilin) is B₁₂ binding protein that are produced in the salivary glands. It must wait until B₁₂ has been freed from proteins in food by pepsin in the stomach. B₁₂ then binds to the R-protein to avoid degradation of it in the acidic environment of the stomach.

This pattern of secretion of a binding protein secreted in a previous digestive step is repeated once more before absorption. The next binding protein is intrinsic factor (IF), a protein synthesized by gastric parietal cells that is secreted in response to histamine, gastrin and pentagastrin, as well as the presence of food. In the duodenum, proteases digest R-proteins and release B₁₂, which then binds to IF, to form a complex (IF/B₁₂). B₁₂ must be attached to IF for it to be absorbed, as receptors on the enterocytes in the terminal ileum of the small bowel only recognize the B₁₂-IF complex; in addition, intrinsic factor protects the vitamin from catabolism by intestinal bacteria.

Absorption of food vitamin B₁₂ thus requires an intact and functioning stomach, exocrine pancreas, intrinsic factor, and small bowel. Problems with any one of these organs makes a vitamin B₁₂ deficiency possible. Individuals who lack intrinsic factor have a decreased ability to absorb B₁₂. In pernicious anemia, there is a lack of IF due to autoimmune atrophic gastritis, in which antibodies form against parietal cells. Antibodies may alternately form against and bind to IF, inhibiting it from carrying out its B₁₂ protective function. Due to the complexity of B₁₂ absorption, geriatric patients, many of whom are hypoacidic due to reduced parietal cell function, have an increased risk of B₁₂ deficiency. This results in 80-100% excretion of oral doses in the feces versus 30-60% excretion in feces as seen in individuals with adequate IF.

Once the IF/B₁₂ complex is recognized by specialized ileal receptors, it is transported into the portal circulation. The vitamin is then transferred to transcobalamin II (TC-II/B₁₂), which serves as the plasma transporter. Hereditary defects in production of the transcobalamins and their receptors may produce functional deficiencies in B₁₂ and infantile megaloblastic anemia, and abnormal B₁₂ related biochemistry, even in some cases with normal blood B₁₂ levels. For the vitamin to serve inside cells, the TC-II/B₁₂ complex must bind to a cell receptor, and be endocytosed. The transcobalamin-II is degraded within a lysosome, and free B₁₂ is finally released into the cytoplasm, where it may be transformed into the proper coenzyme, by certain cellular enzymes (see above).

It's important to note that investigations into the intestinal absorption of B₁₂ point out that the upper limit per single dose, under normal conditions, is about 1.5 µg: "Studies in normal persons indicated that about 1.5 µg is assimilated when a single dose varying from 5 to 50 µg is administered by mouth. In a similar study Swendseid et al. stated that the average maximum absorption was 1.6 µg [...]"

The total amount of vitamin B₁₂ stored in body is about 2-5 mg in adults. Around 50% of this is stored in the liver. Approximately 0.1% of this is lost per day by secretions into the gut, as not all these secretions are reabsorbed. Bile is the main form of B₁₂ excretion; however, most of the B₁₂ secreted in the bile is recycled via enterohepatic circulation. Excess B₁₂ beyond the blood's binding capacity is typically excreted in urine. Owing to the extremely efficient enterohepatic circulation of B₁₂, the liver can store several years' worth of vitamin B₁₂; therefore, nutritional deficiency of this vitamin is rare. How fast B₁₂ levels change depends on the balance between how much B₁₂ is obtained from the diet, how much is secreted and how much is absorbed. B₁₂ deficiency may arise in a year if initial stores are low and genetic factors unfavourable, or may not appear for decades. In infants, B₁₂ deficiency can appear much more quickly.

History

B₁₂ deficiency is the cause of pernicious anemia, an anemic disease that was usually fatal and had unknown etiology when it was first described in medicine. The cure, and B₁₂, were discovered by accident. George Whipple had been doing experiments in which he induced anemia in dogs by bleeding them, and then fed them various foods to observe which diets allowed them fastest recovery from the anemia produced. In the process, he discovered that ingesting large amounts of liver seemed to most rapidly cure the anemia of blood loss. Thus, he hypothesized that liver ingestion might treat pernicious anemia. He tried this and reported some signs of success in 1920.

After a series of careful clinical studies, George Richards Minot and William Murphy set out to partly isolate the substance in liver which cured anemia in dogs, and found that it was iron. They also found that an entirely different liver substance cured pernicious anemia in humans, that had no effect on dogs under the conditions used. The specific factor treatment for pernicious anemia, found in liver juice, had been found by this coincidence. Minot and Murphy reported these experiments in 1926. This was the first real progress with this disease. Despite this discovery, for several years patients were still required to eat large amounts of raw liver or to drink considerable amounts of liver juice.

In 1928, the chemist Edwin Cohn prepared a liver extract that was 50 to 100 times more potent than the natural liver products. The extract was the first workable treatment for the disease. For their initial work in pointing the way to a working treatment, Whipple, Minot, and Murphy shared the 1934 Nobel Prize in Physiology or Medicine.

These events in turn eventually led to discovery of the soluble vitamin, called vitamin B₁₂, from bacterial broths. In 1947, while working for the Poultry Science Department at the University of Maryland, Mary Shaw Shorb (in a collaborative project with Folkers and Merck) was provided with a $400 grant to develop the so-called "LLD assay" for B₁₂. LLD stood for Lactobacilis lactis Dorner, a strain of bacterium which required "LLD factor" for growth, which was eventually identified as B₁₂. Shorb and colleagues used the LLD assay to rapidly extract the anti-pernicious anemia factor from liver extracts, and pure B₁₂ was isolated in this way by 1948, with the contributions of chemists Shorb, Karl A. Folkers of the United States and Alexander R. Todd of Great Britain. For this discovery, in 1949 Mary Shorb and Karl Folkers received the Mead Johnson Award from the American Society of Nutritional Sciences.

The chemical structure of the molecule was determined by Dorothy Crowfoot Hodgkin and her team in 1956, based on crystallographic data. Eventually, methods of producing the vitamin in large quantities from bacteria cultures were developed in the 1950s, and these led to the modern form of treatment for the disease.

See also

• Cobamamide
• Cyanocobalamin includes discussion of chemistry of preparation of reduced-cobalt B₁₂ analogs
• Hydroxocobalamin
• Methylcobalamin

References

External links

• Vitamin B12 Fact Sheet from the U.S. National Institutes of Health
• Jane Higdon, "Vitamin B12", Micronutrient Information Center, Linus Pauling Institute, Oregon State University
• Vitamin B12 deficiency article in American Family Physician journal
• Vitamin B12 and Folate at Lab Tests Online
• Cyanocobalamin at the US National Library of Medicine Medical Subject Headings (MeSH)

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The apparent weight loss effects of water have been subject to some scientific research.

This evidence has been used by some of the scientists who worked on this research, and by others, to bolster suggestions that people who are trying to lose weight can benefit from augmenting - but not replacing - their dietary programs by drinking water, either before meals or at any time. Such advice had previously been given by dieticians even before the most recent research was published.

Energy impact

Energy regulation

There is some evidence drinking water before or during a meal may help aid weight loss when used in conjunction with a calorie-controlled diet.

Drinking water prior to each meal may help in appetite suppression. A promising approach to reducing appetite which does not involve taking any drugs, and is very safe, is to drink a moderate amount of water before a meal. Though this had been a folk remedy for overeating for many years, and is recommended by some dieticians and stipulated in some scientific studies, it was only recently that the approach was subjected to a scientific randomised controlled trial to see how much effect it had:

• A 2008 study concluded that drinking water is associated with weight loss in overweight dieting women independent of diet and activity.
• A 2010 study concluded that people that consumed two cups (500 mL) of water right before eating a meal ate between 75 and 90 fewer calories during that meal.
• A 2011 study conducted on obese children concluded that water drinking on resting energy expenditure was significant. Pediatricians agree that hydration in children may be optimal only in breastfed infants.
• A 2011 study conducted on middle-aged and older adults (aged >=40 years) given 500 mL 30 minutes before meal 3 times daily for 12 weeks found that the individuals lost 2 kg body weight compared to the control group.
• A 2013 study conducted on adults 18-23 concluded that when they were given 500 mL given 3 times daily for 8 weeks they lost body weight.
• A 2013 study concluded reviewed that Studies of individuals dieting for weight loss or maintenance suggest a weight-reducing effect of increased water consumption.

Thermoregulation

One study found that drinking 500 ml of water increased metabolic rate by 30% after 30-40 min with a total thermogenic response of 100 kJ (24 kcal). About 40% of the thermogenic effect originated from warming the water from 22 to 37 °C. However, a later study in 2006 states that approximately 500 mL 3 °C cold water caused only increase in energy expenditure by 4.5% for 60 minutes.

Dietary changes

Research by Barry Popkin et al. has shown that people who drink lots of water eat more vegetables and fruits, drink fewer sugary beverages, and consume fewer total calories. The reason for drinking less sugary beverages would likely be that the increased water substitutes for them in the diet, quenching the thirst so that the person does not feel as much need to drink sugary beverages.

Increased water consumption, or replacement of energy-containing beverages with energy-free beverages, or consumption of water-rich foods such as fruits and vegetables with a lower energy density, may help in weight management.

Motivation for higher water intake

Carbonated water

One study states that consumers of carbonated water prepared at home had significantly higher mean drinking water intake (tap + bottled + carbonated water) in percentage of total water intake than non-consumers, and lower mean intakes of milk, bottled water and tap water, respectively;

See also

• Anti-obesity medication
• Water intoxication (dilutional hyponatremia)

Further reading

• Daniels MC, Popkin BM (September 2010). "Impact of water intake on energy intake and weight status: a systematic review". Nutrition Reviews 68 (9): 505-21. doi:10.1111/j.1753-4887.2010.00311.x. PMC 2929932. PMID 20796216. 

References

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Very low calorie diet (VLCD) is a diet with very or extremely low daily food energy consumption. It is defined as a diet of 800 kilocalories (3,300 kJ) per day or less. VLCDs are formulated, nutritionally complete, liquid meals containing 800 kilocalories or less per day. VLCDs also contain the recommended daily requirements for vitamins, minerals, trace elements, fatty acids and protein. Carbohydrate may be entirely absent, or substituted for a portion of the protein; this choice has important metabolic effects. The VLCD products are usually a powder which is mixed with water or another low-food-energy liquid. The VLCD is prescribed on a case to case basis for rapid weight loss (about 1.5 to 2.5 kilograms or 3 to 5 pounds per week) in people with Body Mass Index of 30 and above. The health care provider can recommend the diet to a patient with a BMI between 27 and 30 if the medical complications the patient has due to being overweight present serious health risks. It results in 4% more weight loss over the short term as compared to control.

Health effects

Health benefits

A 1997 study concludes that the short-term use of a VLCD is very effective in rapidly improving glycaemic control and promoting substantial weight loss in obese patients with Type 2 diabetes. Moreover, a VLCD increases insulin sensitivity and reduces the substrate for gluconeogenesis. Thus VLCD treatment may improve glycaemic control more than calorie restriction alone. A VLCD is typically undertaken by an obese patient who wishes to lose a lot of weight quickly, as the risk to health that obesity presents is considered much greater than any risks of the diet itself, so long as it is undertaken with medical supervision.

Adverse effects

Studies have shown that in about one in four individuals following a VLCD for a few months, gallstones develop. However, these gallstones may be small enough to not cause discomfort, and often disappear when a normal eating pattern is resumed. Gallstone formation is facilitated by the more concentrated bile fluid and reduced flow as a result of a VLCD. Another potential side effect is constipation (depending on the fiber content of the diet). Unmonitored VLCDs with insufficient macronutrient and mineral intake have the potential to cause sudden death via ventricular tachycardia.

See also

• Obesity
• Weight loss
• Calorie restriction
• Negative calorie food
• Ketosis

References

External links

• Diet & VLCD - summary of studies

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Bodybuilding supplements are dietary supplements commonly used by those involved in bodybuilding and athletics. Bodybuilding supplements may be used to replace meals, enhance weight gain, promote weight loss or improve athletic performance. Among the most widely used are vitamin supplements, protein, branched-chain amino acids (BCAA), glutamine, essential fatty acids, meal replacement products, creatine, weight loss products and testosterone boosters. Supplements are sold either as single ingredient preparations or in the form of "stacks" - proprietary blends of various supplements marketed as offering synergistic advantages. While many bodybuilding supplements are also consumed by the general public, their salience and frequency of use may differ when used specifically by bodybuilders.

Annual sales of sport nutrition products in the US is over $2.7 billion (US) according to Consumer Reports.

History

Athletes in ancient Greece were advised to consume large quantities of meat and wine. A number of herbal concoctions and tonics have been used by strongmen and athletes since ancient times across cultures for the enhancement of strength, vigour, prowess and stamina. In the 1910s, Eugen Sandow, widely considered to be the first modern bodybuilder in the West, advocated the use of dietary control to enhance muscle growth. Later, bodybuilder Earle Liederman advocated the use of "beef juice" or "beef extract" (basically, consomme) as a way to enhance muscle recovery. In 1950s with recreational and competitive bodybuilding becoming increasingly popular Irvin P. Johnson began to popularize and market egg-based protein powders marketed specifically at bodybuilders and physical athletes. The 1970s and 1980s marked an explosion in the growth of the bodybuilding supplement industry fueled by an unprecedented increase in mainstream recreational bodybuilding and the widespread use of modern marketing techniques.

In the USA, in October 1994, the Dietary Supplement Health and Education Act (DSHEA) was signed into law. Under DSHEA, a supplement manufacturer alone is responsible for determining that the dietary supplements it manufactures or distributes are safe. Dietary supplements did not henceforth need approval from the U.S. Food and Drug Administration (FDA) before they were marketed. Except in the case of a new dietary ingredient, a firm did not have to provide FDA with the evidence to substantiate safety or effectiveness. It is widely believed that the 1994 DSHEA further consolidated the position of the supplement industry and lead to unprecedented growth and sales figures.

Health problems

The US FDA reports 50,000 health problems a year due to dietary supplements. These often involve bodybuilding supplements.

For example, the "natural" best-seller Craze, 2012's "New Supplement of the Year" by bodybuilding.com, sold in Walmart, Amazon etc., was found to contain undisclosed amphetamine-like compounds. Also other products by Matt Cahill have contained dangerous substances causing blindness or liver damages, and experts say that Cahill is emblematic for the whole industry.

Liver damage

The incidence of liver damage from dietary supplements has tripled in a decade. Most of the supplements involved were bodybuilding supplements. Some of the patients require liver transplants and some die. One third of the supplements involved contained unlisted steroids. Dr. Victor Navarro, the chairman of the hepatology division at Einstein Healthcare Network in Philadelphia, said that "while liver injuries linked to supplements were alarming, he believed that a majority of supplements were generally safe. Most of the liver injuries tracked by a network of medical officials are caused by prescription drugs used to treat things like cancer, diabetes and heart disease"

Supplement categories

Modern bodybuilding supplements are often marketed as promoting various desirable processes related to improving nutrition, enhancing body composition or improving lifting performance. Supplements are often categorized accordingly. While many of these categories are based on scientifically based physiological or biochemical processes, their use in bodybuilding parlance is often heavily colored by bodybuilding lore and industry marketing and as such may deviate considerably from traditional scientific usages of these terms.

These supplements are set into place for the benefit of the consumer, but are only beneficial if used correctly. These include things like protein, creatine, and other workout substances used to maximize results. If supplements aren't used correctly, for example to much or to little, the body won't see results as advertised. Also supplements are only as effective in relation to the amount of effort/workout put in.

Protein shake

Bodybuilders often supplement their diets with a powdered form of protein. The powder is mixed with water, milk or juice. Protein powder is generally consumed immediately before and after exercising, or in place of a meal. Some types of protein are to be taken directly before and after a workout (whey protein), while others are to be taken before going to bed (casein protein). The theory behind this supplementation is that bodybuilders, by virtue of their unique training methods and end-goals, require higher-than-average quantities of protein to support maximal muscle growth.

"The Recommended Dietary Allowance (RDA) for both men and women is 0.80 g of good quality protein/kg body weight/d and is based on careful analyses of available nitrogen balance studies.". "In view of the lack of compelling evidence to the contrary, no additional dietary protein is suggested for healthy adults undertaking resistance or endurance exercise."

No consensus has been reached in determining whether or not an individual in exercise training can benefit from protein and amino acid supplements. Protein supplements come in various forms: ready to drink shakes, bars, bites, oats, gels and powders. Protein powders are available in a variety of flavors.

• Whey protein contains high levels of all the essential amino acids and branched-chain amino acids. It also has the highest content of the amino acid cysteine, which aids in the biosynthesis of glutathione. For bodybuilders whey protein provides amino acids used to aid in muscle recovery. Whey protein is derived from the process of making cheese from milk. There are three types of whey protein: whey concentrate, whey isolate, and whey hydrolysate. Whey concentrate is 29-89% protein by weight whereas whey isolate is 90%+ protein by weight. Whey hydrolysate is enzymatically predigested and therefore has the highest rate of digestion of all protein types.
• Casein protein (or milk protein) has glutamine, and casomorphin.
• Soy protein from soybeans contain isoflavones, a type of phytoestrogen.
• Egg-white protein is a lactose- and dairy-free protein.
• Hemp seed contains complete and highly-digestible protein and hemp oil is high in essential fatty acids.
• Rice protein, when made from the whole grain, is a complete protein source that is highly digestible and allergen free. Since rice protein is low in the amino acid lysine, it is often combined with pea protein powder to achieve a superior amino acid profile.
• Pea protein is a hypoallergenic protein with a lighter texture than most other protein powders. Pea protein has an amino acid profile similar to that of soy, but pea protein does not elicit concerns about unknown effects of phytoestrogens. Pea protein is also less allergenic than soy.

Although it is generally believed that athletes and bodybuilders need an increased intake of protein, the exact amount is highly individualized and dependent on the type and duration of the exercise as well as the physiological make up of the individual. Age, gender, and body size may vary this protein intake. Some health experts have criticized protein shakes as being unnecessary for most people that consume them, since most users already get enough protein in the normal varied diet with enough calories. However, there is some evidence to support the idea that protein shakes are superior to whole foods with regards to enhancing muscle hypertrophy in the one hour window following intensive exercise. Moreover, for athletes who do not have the time to prepare whole food meals on the run or immediately after exercise, a protein shake may be preferred for practical as well as performance reasons.

A dietitian has suggested that low-calorie dieters, vegetarians, haphazard eaters and those who train very heavily may benefit from protein supplements. However, at least in the case of people following vegetarian diets, the Institute of Medicine of the National Academies states: "Available evidence does not support recommending a separate protein requirement for vegetarians who consume complementary mixtures of plant proteins.".

Taking an overdose of protein can lead to a loss of appetite, which may be useful for some dieters. Nutritionists claim that osteoporosis occurs from excessive protein intake because protein can put pressure on the kidneys and lead to bone loss due to calcium leaching. However, recent research has cast doubts on these claims, and suggests that higher calcium excretion may be due to increased calcium absorption in the intestines due to protein intake. Indeed, it is well known that dietary protein is itself important for bone growth, and some studies have found increased bone formation in response to exchanging dietary carbohydrates for protein. Nutritionists also argue against increased protein consumption because weight gain may occur because, as the body cannot store protein, excess protein will either be burned as energy or stored as fat (if you are already getting the calories you need). However, dietary protein is converted to fat far less efficiently than either carbohydrates or lipids, so consuming a calorie excess in protein will result in far less fat gain than would a calorie excess of other macronutrients.

Research by Tarnopolsky et al. (1988) showed that for bodybuilding individuals, 0.96g of protein per kg of body weight per day is recommended, whereas endurance athletes require 1.34g per kg per day. Their findings indicated that protein requirements are actually much lower than might be expected and that protein supplements therefore may not be as effective as is popularly believed. It should be noted that both of these levels are significantly higher than the levels recommended for the general population (0.8 g protein / kg body weight). The study concluded that "Bodybuilders during habitual training require a daily protein intake only slightly greater than that for sedentary individuals in the maintenance of lean body mass and that endurance athletes require daily protein intakes greater than either bodybuilders or sedentary individuals to meet the needs of protein catabolism during exercise.".

Another study suggest that the protein requirements for anaerobic and aerobic exercise are opposite those presented by Tarnopolsky. Endurance athletes in aerobic activity may have increased daily protein intake at 1.2-1.4 g per kg body weight per day--the same as the aforementioned study--where strength training athletes performing anaerobic activity may have increased daily protein intake needs at 1.4-1.8 g per kg body weight so as to enhance muscle protein synthesis or to make up for the loss of amino acid oxidation during exercise.

Branched-chain amino acids

Amino acids are the building blocks of protein; the body breaks consumed protein into amino acids in the stomach and intestines. Amino Acids are classified as essential, conditionally essential and non-essential. There are three branched-chain amino acids (BCAAs): leucine, isoleucine, and valine. All three branched-chain amino acids are essential amino acids. Each has numerous benefits on various biological processes in the body. Unlike other amino acids, BCAAs are metabolised in the muscle and have an anabolic/anti-catabolic effect on it. BCAAs account for 33% of muscle protein.

Glutamine

Glutamine is the most abundant amino acid found in human muscle and is commonly found in supplements or as a micronized, instantly soluble powder because supplement manufacturers claim the body's natural glutamine stores are depleted during anaerobic exercise. Some studies have shown there to be no significant effect of glutamine on bench press strength, knee-extension torque or lean muscle mass when compared to controls taking a placebo, though another study found that glutamine is beneficial in raising T-helper/suppressor cell ratio in long-distance runners.

Essential fatty acids

The essential fatty acids (alpha-linolenic acid and linoleic acid) may be especially important to supplement while bodybuilding; these cannot readily be made in the body, but are required for various functions within the body to take place.

Fatty fish, such as fresh salmon and trout are rich in essential fatty acids and fish oils can also be taken in supplement form.

Flaxseed oil, often sold as a supplement on its own, is an ideal source of alpha-Linolenic acid, which can also be found in walnuts and pumpkin seeds.

Meal replacement products

Meal replacement products (MRPs) are either pre-packaged powdered drink mixes or edible bars designed to replace prepared meals. MRPs are generally high in protein, low in fat, have a low to moderate amount of carbohydrates, and contain a wide array of vitamins and minerals.

The majority of MRPs use whey protein, casein (often listed as calcium caseinate or micellar casein), soy protein, and/or egg albumin as protein sources. Carbohydrates are typically derived from maltodextrin, oat fiber, brown rice, and/or wheat flour. Some MRPs also contain flax oil powder as a source of essential fatty acids.

MRPs can also contain other ingredients, such as creatine monohydrate, glutamine peptides, L-glutamine, calcium alpha-ketoglutarate, additional amino acids, lactoferrin, conjugated linoleic acid, and medium-chain triglycerides.

A sub-class of MRPs are called 'weight gainers' and have a high ratio of carbohydrates:protein. Where a MRP would have a 0.25-2:1 ratio of Carbohydrates:Protein a weight gainer would have in the order of between 3-5:1 ratios.

Prohormones

Prohormones are precursors to hormones and are most typically sold to bodybuilders as a precursor to the natural hormone testosterone. This conversion requires naturally occurring enzymes in the body. Side effects are not uncommon, as prohormones can also convert further into DHT and estrogen. To deal with this, many supplements also have aromatase inhibitors and DHT blockers such as chrysin and 4-androstene-3,6,17-trione. To date most prohormone products have not been thoroughly studied, and the health effects of prolonged use are unknown. Although initially available over the counter, their purchase was made illegal without a prescription in the US in 2004, and they hold similar status in many other countries. They remain legal however in the United Kingdom and the wider European Union. Their use is proscribed by most sporting bodies.

Creatine

Creatine is an organic acid naturally occurring in the body that supplies energy to muscle cells for short bursts of energy (as required in lifting weights) via creatine phosphate replenishment of ATP. A number of scientific studies have shown that creatine can improve strength, energy, muscle mass, and recovery times. In addition, recent studies have also shown that creatine improves brain function. and reduces mental fatigue. Unlike steroids or other performance-enhancing drugs, creatine can be found naturally in many common foods such as herring, tuna, salmon, and beef.

Creatine increases what is known as cell volumization by drawing water into muscle cells, making them larger. This intracellular retention should not be confused with the common myth that creatine causes bloating (or intercellular water retention).

Creatine is sold in a variety of forms, including creatine monohydrate and creatine ethyl ester, amongst others. Though all types of creatine are sold for the same purposes, there are subtle differences between them, such as price and necessary dosage.

In The New Encyclopedia of Modern Bodybuilding, 2nd ed., author Arnold Schwarzenegger states:

Creatine monohydrate is regarded as a necessity by most bodybuilders. Creatine monohydrate is the most cost-effective dietary supplement in terms of muscle size and strength gains. ... There is no preferred creatine supplement, but it is believed that creatine works best when it is consumed with simple carbohydrates. This can be accomplished by mixing powdered creatine with grape juice, lemonade, or many high glycemic index drinks.

Some studies have suggested that consumption of creatine with protein and carbohydrates can have a greater effect than creatine combined with either protein or carbohydrates alone.

Thermogenic products

A thermogenic is a broad term for any supplement that the manufacturer claims will cause thermogenesis, resulting in increased body temperature, increased metabolic rate, and consequently an increased rate in the burning of body fat and weight loss. Until 2004 almost every product found in this supplement category comprised the "ECA stack": ephedrine, caffeine and aspirin. However, on February 6, 2004 the Food and Drug Administration (FDA) banned the sale of ephedra and its alkaloid, ephedrine, for use in weight loss formulas. Several manufacturers replaced the ephedra component of the "ECA" stack with bitter orange or citrus aurantium (containing synephrine) instead of the ephedrine.

See also

• Fish oil
• Glycocarn
• Instant breakfast
• Protein
• Protein bar
• ConsumerLab.com
• Examine.com
• Natural Standard

References

External links

• Dietary Supplement Health and Education Act of 1994

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