Vitamin B12 – Info For WLS Gastric Bypass Post-ops

Vitamin B12

Vitamin B12 supplement is crucial for gastric bypass post-ops because this vitamin is normally absorbed in the stomach and the 1st part of the small intestine. Gastric bypass surgery removes a majority of the body’s B12 absorption system. In addition stomach acid is a major factor in converting B12 into a form that the body can utilize. The small remaining portion of the stomach left after gastric bypass produces much less acid. When you combine this with acid reducing medications that gastric bypass post-ops must take for the rest of their lives it results in significantly less B12 absorption after surgery. To maintain appropriate levels of B12, gastric bypass post-ops MUST supplement B12 for the rest of their lives.

Latter in this article we will describe signs and symptoms of B12 deficiency. What is critical for gastric bypass post-ops is to understand that damage resulting from B12 deficiency is often irreversible even after vitamin B12 levels in the body have been restored.

B12 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 body, especially affecting DNA synthesis and regulation, but also fatty acid synthesis and energy production.
Vitamin B12 is the name for a class of chemically-related compounds, all of which have vitamin activity. It is structurally the largest and one of the most complicated vitamins. It contains the biochemically metal ion element cobalt. Biosynthesis of the basic structure of the vitamin can only be accomplished by bacteria, but conversion between different forms of the vitamin is accomplished in the human body.

The most common synthetic form (man-made) of the vitamin, cyanocobalamin, does not occur in nature, but is used in many pharmaceuticals, supplements and as food additive, due to its stability and lower cost. In the body it is converted to the physiological forms, methylcobalamin and adenosylcobalamin, leaving behind a miniscule amount of cyanide, which is a by-product of production of the cyanocobalamin version of B12. More recently, hydroxocobalamin, methylcobalamin and, adenosylcobalamin can also be found in more expensive pharmacological products and food supplements. Although recent research questions any significant difference between the different types of B12, it would seem prudent to utilize the natural version over the more common man-made version if possible.

Symptoms and damage from 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. However, these symptoms by themselves are too nonspecific to diagnose deficiency of the vitamin.

Vitamin B12 deficiency can also cause symptoms of mania and psychosis.

Vitamin B12 deficiency has the following signs and symptoms:

They include a spongiform state of neural tissue along with edema of fibres and deficiency of tissue. The myelin decays, along with axial fibre. In later phases, fibric sclerosis of nervous tissues occurs. Those changes apply to dorsal parts of the spinal cord, and to pyramidal tracts in lateral cords. The resulting changes due to the lack of B12 causes a combined degeneration of spinal cord.

In the brain itself, changes are less severe. They occur as small sources of nervous fibres decay and accumulation of astrocytes, usually subcortically located, causing haemorrhages within the glial cells. Pathological changes can be noticed as well in the posterior roots of the cord and, to lesser extent, in peripheral nerves.

Clinical symptoms:

The main syndrome of vitamin B12 deficiency is Biermer’s disease (pernicious anemia). It is characterized by a triad of symptoms:
1. Anemia with bone marrow promegaloblastosis (megaloblastic anemia)
2. Gastrointestinal symptoms
3. Neurological symptoms

Each of those symptoms can occur either alone or along with others. The neurological complex, defined as myelosis funicularis, consists of the following symptoms:

1. Impaired perception of deep touch, pressure and vibration, abolishment of sense of touch, very annoying and persistent paresthesias.
2. Ataxia of dorsal cord type
3. Decrease or abolishment of deep muscle-tendon reflexes;
4. Pathological reflexes – Babinski, Rossolimo and others, also severe paresis.

During the course of disease, mental disorders can occur which include: irritability, focus/concentration problems, depressive state with suicidal tendencies, paraphrenia complex. These symptoms may not reverse after correction of hematological abnormalities, and the chance of complete reversal decreases with the length of time the neurological symptoms have been present.

Interactions with Drugs

* 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 grams/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 3.9mg/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 in order to decrease cholesterol, can decrease gastrointestinal (GI) absorption of vitamin B12. It is unlikely that 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. These changes can lead to hyperhomocysteinemia, adding to the risk of cardiovascular disease in people with diabetes.[citation needed] There are also rare reports of megaloblastic anemia in people who have taken metformin for 5 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.[58]
* Phenytoin (Dilantin), phenobarbital, primidone (Mysoline): These anticonvulsants have been associated with reduced vitamin B12 absorption, and reduced serum and cerebrospinal fluid levels 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, data suggests vitamin B12 supplements are not helpful for people taking zidovudine.

Interactions with Herbs and Dietary Supplements

* 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.

Food Sources

Vitamin B12 is present in animal products such as meat, poultry, fish (including shellfish), and to a lesser extent milk, but it is not generally present in plant products or yeast. Fresh pasteurized milk contains 0.9 mcg per cup.
Some foods with substantial amounts of vitamin B12 are listed in the table below along with their vitamin B12 content in micrograms (mcg).

Food Serving Vitamin B12 (mcg)
Clams (steamed) 3 ounces 84.0
Mussels (steamed) 3 ounces 20.4
Crab (steamed) 3 ounces 8.8
Salmon (baked) 3 ounces* 2.4
Rockfish (baked) 3 ounces 1.0
Beef (cooked) 3 ounces 2.1
Chicken (roasted) 3 ounces 0.3
Turkey (roasted) 3 ounces 0.3
Egg (poached) 1 large 0.6
Milk (skim) 8 ounces 0.9
Brie (cheese) 1 ounce 0.5
*A three-ounce serving of meat or fish is about the size of a deck of cards.

Dosage Recommendation:

- 1500 mcg Sublingual per week (dissolved under the tongue).
- 500 mcg intranasal taken 4 days per week (Nascobal) by prescription only
- Weekly injections – through your GP

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