美國yoyo生活家-分享推薦文，歡迎來信生活交流~ez123us@gmail.com

yoyo在美國購買   ～Best Vite B-12舌下錠 120粒（Best Vite必賜力-台灣翻譯）----
沒有添加其他多餘的糖粉，含著就溶化了！

吃起來略甜---yoyo個人覺得像（櫻桃＋杏仁）的味道！

成份(1粒）
VitaminB-12-Methylcobalamin--5,000mcg--83,333%
Folic Acid-（葉酸）----    -----------400mcg---100%
服用方式----  一天一粒

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google網上搜尋B-12 有關資料補充如下--純屬yoyo個人食用選擇B-12參考用

一般所稱Vit B12 係Cyanocobalamin (CN-B12)(合成維他命B12)
在體內轉變成Hydroxocobalamin (OH-B12)
與蛋白結合而貯留於肝臟才能發揮生理作用，為正常生長和發育，細胞生殖，造血，以及核蛋白和髓鞘(Myelin)合成所必需的。

Methylcobalamin (甲基維生素B12)是維他命B12輔酶型式（不用再轉換）好吸收，可維持腦與神經，健康的結構和功能。 

美國yoyo生活交流請來信～ez123us@gmail.com

看看googil網上~B12的其他資料搜尋
-----VitaminB-12-Methylcobalamin和神經系統再生的關係

METHYLCOBALAMIN

甲烷基鈷胺素維他命B12

Methylcobalamin 是維他命B12輔酶型式，可維持腦與神經，健康的結構和功能。有幾個研究發現，人類有些神經上的症狀是特殊的Methylcobalamin 不足，甚至於當血液中B12，及血液檢查adenosylcobalamin 活性，是完全正常。大部分因為身體可以在肝臟和粒腺體儲存adenosylcobalamin ，而Methylcobalamin 是存放於液體裡面，像腦脊髓的液體中、血液中，所以從小便中流失的比儲存來得容易。
健康的人只需要一丁點Methylcobalamin 就可避免真正的不足，有大量的證據証明：大劑量補充Methylcobalamin ，而不是一般的B12，是可以保護腦部及神經對抗毒素，可以幫助醫療受損的神經元，甚至於提供強有力的營養保護神經退化的疾病。
保護大腦與神經
Methylcobalamin 已經顯示可以保護神經細胞對抗各種廣泛不有善的環境，包括缺乏重要細胞能源、B1不足、缺氧、和暴露在毒素中像甲基汞、大腸桿菌(毒素)、 硝基普酸鹽、和刺激神經毒性的神經介質穀氨酸鹽。然而直接測試Cyanocobalamin B12 ，一般綜合維他命，則沒有像Mehtylcobalamin保護神經和神經再生的這些好處。
癱瘓病毒
幾組科學家調查應用Methylcobalamin 在貝爾氏癱瘓患者，他們一致地發現Methylcobalamin可以加速復原正常神經功能。在幾組分開的病人實驗上：一組給服用Prednisone (類固醇藥治療貝爾氏癱瘓)，一組給服用Methylcobalamin ，一組給服用以上這兩種產品。結果發現單獨服用Methylcobalamin及服用兩種產品者，他們完全復原的時間都比單獨服用Prednisone 這組縮短很多。

Multiple Sclerosis多發性硬化症 (MS)
一個試驗性的實驗，有六個退化的MS 病人每天服用60mg Methylcobalamin ，半年後醫生做一個比較，兩年前還未服用該產品神經功能和服用六個月後的改變做一比較。結果顯示所有神經反應的數字、和改善的徵兆是未服用前的4倍半。
Lou Gehrig's Disease : Amyotrophic Lateral Sclerosis (ALS)
肌萎縮性脊髓側索硬化症：在隨機、雙盲、控制的試驗中24名病患注射高劑量Methylcobalamin (25mg 或500mcg 每天)。一個月後。服用高劑量的病患，已經經歷到他的神經有能力去啟動肌肉的反應。有兩人的步伐明顯改善。
Alzheimer’s Disease 阿滋海默症
兩組試驗發現給患者或相關的癡呆症患者服用Methylcobalamin 誘導病患與他人及周遭世界有較好的互動，同時改善情緒和解除神經上的一些症狀。家人和醫生對病人的評估都進步了。這次試驗發現智力的功能是不協調的：有些方面是改進但是某些並沒有。這可能跟Methylcobalamin 的用量有關。
A good guess: Parkinson's Disease 帕金森氏病值得一試
有很好的理由相信，因為帕金森氏病的原因或惡化，是刺激神經毒素作用，它又是過度刺激神經介質穀氨酸鹽的結果。西藥就是降低穀氨酸鹽的水平或拒絕它的受體，依此改善病患很多症狀，當藥品刺激受體時病情又惡化了。
所以說假如Methylcobalamin 保護神經元免受穀氨酸鹽之毒，它就有可能保護帕金森氏病患者？不幸地到現在還沒有診所做此試驗。但相信Methylcobalamin做為營養補充品，它的安全性及在其他神經退化症，清楚的好處是有目共賭。這重要的輔黴將給予潛在的希望來預防和治療使人衰弱疾病。
Caramelized Nerves 使神經成焦糖化
一連串診所試驗報告Methylcobalamin 改善糖尿病神經變性病的神經功能，如探知微弱的震動、減少刺痛感、麻木、和末梢的疼痛、減少腿部沉重感、恢復神經元有效地傳遞信息調節心跳。試驗中觀察病人整體神經變性病的症狀及徵兆，結果都得到顯著地改善。
Eyes Under pressure 眼壓問題
正常眼壓青光眼分成兩組，一組１４人服用Methylcobalamin ，另一組２２人沒服用，結果顯示沒服用這組５９％的病人情況惡化，有服用這組８６％的病人沒有失去眼睛的功能。
The Squeezing Spine擠壓脊椎
腰椎脊骨的狹窄(症)是脊椎下部神經擠壓因關節炎、脊椎退化、受傷、有時很不幸是基因的問題所引起的。受壓迫的神經導致下背部或屁股的疼痛，當換個姿勢疼痛就解除。有一實驗，１５０人有擠壓脊椎病患給予現代的治療（物理療法、標準西藥、教育管理疾病等），另一方面就是有的給很輕劑量的Methylcobalamin有的沒給。無論任何理由，選出做實驗的這組劑量非常少（０．５ｍｇ），與大多數成功使用Methylcobalamin競爭治安神情疾病相比。少劑量，疼痛沒有什麼改進，或者醫生對外表、感覺、神經功能的評價也一樣。然而不管用量不足，那些服用Methylcobalamin的患者發現他們自己可以走更遠的距離而沒有疼痛。

Let There Be Light… And Dark讓白晝黑夜有序
科學雜誌記載很多診所的實驗証明；Methylcobalamin 讓人們重回全天有節律生活，因此改善睡眠品質增進心理的健康。主要理由是Methylcobalamin 使部分大腦調節體內生理時鐘對光線感覺更敏銳。換句話說，讓身體釋放睡眠荷爾蒙melatonin 回歸正確的每日循環線上。另一荷爾蒙可體松全天高低調節和體溫的改變也因Methylcobalamin 回歸正常。
The Question of Dose 劑量的疑問
總的來說，大部分的實驗Methylcobalamin 使用在糖尿病患者神經變性病患者，非糖尿病患者神經變性病患者與尿毒症、週邊顏面麻痺(包括貝爾氏癱瘓)、正常眼壓青光眼、和癡呆症(包括紅肢病與阿滋海默症)， 所使用的劑量從1.5mg 到5mg而已。另一方面的試驗包括肌萎縮性脊髓側索硬化症、多發性硬化症就用較高的劑量前者每日25mg，後者每天60mg。因此在和有營養導向的醫師配合使用Methylcobalamin 時當依症狀之不同給予適當的用量或者較高一些可能較明顯的效果是可預期的。

Vitamin B12

Sources

The only dietary sources of vitamin B12 for human are from animal products, which have derived their cobalamins from micro-organisms. All naturally occurring vitamin B12 is produced by micro-organisms. 

The best sources of the cobalamins are meat and meat products, poultry, fish, shellfish (especially clams and oysters), and eggs (especially the yolk); the cobalamins in these products are predominantly adenosyl- and hydroxocobalamin.Milk and milk products such as cheese and yogurt contain less of the vitamin, mainly as methyl-and hydroxocobalamins. Cyancobalamin may be found in a few foods as well as tobacco; it is also the form, along with hydroxocobalamin, that is commercially available in vitamin preparation. Within the body, cyanocobalamin is converted to aquo- or hydroxocobalamin. 

Bioavailability of vitamin B12 may be impaired by vitamin C. Vitamin C in doses of 500mg or more, taken with meals or up to 1 hour after a meal, may diminish vitamin B12 availability from food or destroy the vitamin. Furthermore, incubation of 200mg of ascorbate with 25ug of vitamin B12, 400ug of folate, and 15mg of iron for 30 minutes in gastric juice (PH 5) resulted in a significant destruction of vitamin B12.

Digestion, Absorption, Transport, and Storage

Ingeste cobalamins must first be released from the polyprptides to which they are linked in foods. This release usually occcurs through the action of the gastric proteolytic enzyme pepsin in the stomach.

Once released from foods, vitamin B12 absorption involves contact with two proteins, intrinsic factor (IF) and R proteins. IF is a glycoprotein synthesized by the gastric parietal cells. Although it is made and released in the stomach, IF functions in the small intestine. R proteins, known collectively as cobalophilins or haptocorrins (HCs), are found in most body fluids, including saliva and gastric juice. R proteins have a high affinity for cobalamins. Free cobalamin released from food combines with R protein; the complex moves from the stomach into the small intestine. Within the duodenum, the R protein is hydrolyzed by pancreatic proteases, and free cobalamin is released. A pancreatic insufficiency could interfere with the release of cobalamin from the R protein and reduce the amount of the vitamin available for absorption. R proteins may also serve to protect vitamin B12 from bacterial use.

In the proximal small intestine, IF, which escapes the catabolic action of the proteases, binds the cobalamin, any of the forms, once released from the R proteins. The cobalamin-IF complex travels to the ileum, where receptor sites for vitamin B12 are present. Absorption of the vitamin occurs throughout the entire ileum, especially the distal third. 

The cobalamin absorption process is complex and poorly understood. it is known that calcium is needed for absorption to occur, and presently the belief is that calcium has some sort of specific action on the receptor site. Whether cellular uptake of IF occurs with the vitamin is unclear. 

Absorption of vitamin B12 is slow; after attachment of the IF-cobalamin complex to the receptor, there is a delay of 3 to 4 hours before the cobalamin appears in circulation. Peak levels of the vatimin in the blood may not be reach for 8 to 12 hours after ingestion. 

When pharmacological doses of vitamin B12 are ingested, passive diffusion can account for much of the absorption throughout the intestinal tract. However, passive diffusion can account for only about 1% and up to 3% of the total absorption fo the vitamin when it is being obtained from ordinary dietary sources. Absorption rate of the vitamin decreases with increased intake. At low levels of intake(0.1mg), absorption averages 80%, whereas at higher intakes, the absorption rate drops to 3%. 

Enterohepatic circulation is very important in vitamin B12 nutriture, accounting in part for the long biological half-life of cobalamin. When enterohepatic circulation is effective, much of the cobalamin in the bile and in other intestinal secrections can be reabsorbed. Malabsorption syndromes not only cause a decrease in absorption of ingested cobalamin but also interfere with enterohepatic circulation, thereby increasing the amount of vitamin B12 required to meet body needs.  

Vitamin B12, unlike other water-soluble vitamins, can be stored and retained in the body for long periods of time, even years. The vitamin is stored mainly in the liver, however, small amounts are also found in the muscle, bone, kidneys, heart, brain, and spleen. Adenosylcobalamin is the primary storage form of the vitamin in the liver, and possibley in other organs; however, hydroxocobalamin and methylcobalamin are also stored to lesser extent. Haptocorrin represents the circulating storage form of vitamin B12 that is in equilibrium with body stores of the vitamin. Hepatocytes have recepors for the uptake  of both haptocorrin and for TCII.

Functions and Mechanisms of Action

Three enzymatic reactions requiring vitamin B12 have been recognized in humans; one of these reactions requires methylcobalamin, while the other two must have adenosylcobalamin. Adenosyl-and-methylcobalamin are formed by a complex reaction sequence resulting in the production of a carbon-cobalt bond between the cobalt nucleus of the vitamin and either the methyl or 5'-deoxyadenosyl ligand.  

The reaction requiring methylcobalamin as a coenzyme is the conversion of omocysteine into methionine. This reaction occurs in the cytoplasm of the cell. To form the methylcobalamin needed in methionine synthesis, cobalamin, bound to the methionine synthetase (homocysteine methyl transferase) apoenzyme, picks up te methyl group from N methyl THF (Tetrahydrofolate) and transfers it to homocysteine, thereby producing methionine and free THF.THF can then be converted into any of its coenzyme forms. This reaction explains in large part the synergism between folate and vitamin B12.

Metabolism and Excretion

Very little evidence exists to support any extensive degradation of cobalamin. Whole-body turnover of vitamin B12 is approximately 0.1%/day and loss of the vitamin is due primarily to fecal excretion, not catabolism. Most of cobalamin excretion occurs via the bile. Little urinary excretion of vitamin B12 occurs.

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