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Vitamin B-12

 

B12 or cobalamin is a water-soluble vitamin. It helps maintain healthy nerve cells and red blood cells as well as assisting in making DNA. The Roux-en-Y gastric bypass (RYGB) transects or partitions off the lower stomach. The first one to four feet of intestine is also bypassed in a proximal/medial RYGB depending on the surgeon. In a distal RYGB, typically the last four feet or less of intestine (ileum) is left to absorb nutrients. The biliopancreatic diversion/duodenal switch (BPD/DS) leaves more of the stomach and the pyloric sphincter muscle in the stomach intact, but also only leaves four feet or less of small intestine left to absorb nutrients. This is somewhat simplified as the alimentary limb (where the food goes down) also absorbs some nutrients as well as the common channel.

The process of B12 absorption is as follows. Hydrochloric acid and pepsin released in the stomach are needed to separate B12 from protein. After the B12 is separated from protein, it attaches to R-binder proteins found in saliva and gastric juice. Next, pancreatic enzymes in the upper small intestine release the B12 from the R-binder proteins. The B12 then binds to intrinsic factor and is carried away to the distal ileum where it is absorbed. When part of the stomach is removed or partitioned off, cells are loss that secrete stomach acid and intrinsic factor.

Bypassing the upper part of the intestine can also interfere with the mechanism of B12 absorption as well as H2 blockers taken for treating stomal ulcers after RYGB and rapid transit time of nutrients. Other issues that can decrease absorption of B12 are inflammation of the stomach or intestine and excess bacteria in the stomach and small intestine.

Lack of intrinsic factor can lead to pernicious anemia which can result in permanent nerve damage if not treated. Pernicious anemia is a chronic condition that must be treated for life, usually with an intramuscular injection that goes directly into the bloodstream. B12 can also be absorbed via the mucous membranes of the nose or under the tongue to the bloodstream so these are also other viable ways of treating anemia in some individuals.

Clinical signs of B12 deficiency may include fatigue, weakness, nausea, constipation, gas, loss of appetite, and weight loss. Other physical signs are numbness and tingling of the hands and feet, difficulty in maintaining balance, depression, confusion, poor memory, and soreness of the mouth or tongue. Some of these symptoms can also result from a variety of other medical conditions so it is important to see your surgeon and discuss these issues should they arise. The Schilling test may be used to determine problems of intrinsic factor availability. Most surgeons are monitoring B12. If yours is not, you may want to urge him/her to do so.

The DRI for B12 is 2.4 mcg (micrograms) for men and women. In a study by Rhode, Tamim, Gilfix et al., it was found that it took a minimum of 350 mcg of oral crystalline B12 daily to sustain normal levels of B12 in 95% of RYGB patients. B12 is an unusual vitamin in that you actually store a year’s supply or more. Many patients don’t tolerate or eat foods high in B12 after bariatric surgery so their stores slowly dwindle along with the lack of absorption caused by the surgeries. It may not be possible to get enough B12 from food after surgery again because of the interference in the absorption process and lack of gastric juice and intrinsic factor. Deficiency may not show up for to two years or more after surgery depending on the person’s nutrition status before surgery. Vitamin C in doses of 500 mg or more, taken with meals or up to one hour after a meal, may diminish B12 availability from food or destroy the vitamin.

The normal range for serum B12 is 250 to 900 pg/ml, the range will vary depending on which lab your blood work is sent to. Anything under 160 is considered critical. B12 has no known toxicity level but there is no reason to have levels way over 900 either. B12 levels should be checked pre and post-operatively to make sure patients stay within their usual range if it was acceptable pre-surgery.

Some food sources of B12 are as follows: 3 ounces of beef liver, 60 mcg, ¾ cup of 100% fortified breakfast cereal, 6 mcg, 3 ounces of cooked rainbow trout, 5.3 mcg, 3 ounces of cooked beef, 2.1 mcg, 3 ounces of canned water packed tuna, .9 mcg, 1 cup of milk, .9 mcg, 3 ounces of cooked pork, .6 mcg, 1 egg, .5 mcg, 1 ounce of American cheese, .4 mcg, and 3 ounces of cooked chicken, .3 mcg.

In general, vitamin/mineral supplements should dissolve easily and be consumed with food so absorption and toleration will be greater. Smaller doses taken more often are more effective than one large dose as only 10 to 30% of any food or supplement consumed is absorbed at one time.

Loose powder, liquid, soft-gel caps or quick dissolving tablets usually allow for greatest absorption. Chelated minerals are best absorbed. When minerals are chelated, they are bound to other substances to aid in absorption. The highest absorption substances are malate, ethanolamine phosphate, ascorbate, citrate, fumarate, peptonate, succinate, lysinate, glycerate, picolinate, and acetate. Moderately high absorption substances are amino acid chelates, aspartate, chloride, sulfate, gluconate, and phosphate. Lowest absorbing are carbonate and oxide. Synthetic is fine as the cost of natural vitamins is usually too expensive. One exception is Vitamin E. Use the d form, not the dl. Synthetic fat-soluble vitamins are difficult for the liver to break down and utilize. Supplements should be used under medical supervision. A typical schedule for labs is every three months the first year, twice the second year, then on an annual basis after the first two years post-operatively to monitor nutrition status. It is important that patients take their supplements as directed and follow-up with their surgical team to optimize their health and surgical outcome.



Vitamin B-12 is essential to growth, cell reproduction, hematopoiesis (the process of formation and development of the various types of blood cells and other formed elements), and nucleoprotein and myelin synthesis. The plasma level of the B-12 compound reaches its peak within 1 hour after an intramuscular injection. The liver is the main organ for vitamin B-12 storage.

Within 48 hours after injection of vitamin B-12, 50 to 98% of the injected dose may appear in the urine. The major portion is excreted within the first eight hours.


Gastrointestinal absorption of vitamin B-12 depends upon the presence of sufficient intrinsic factor and calcium ions. The average diet supplies about 5 to 15 mcg/day of vitamin B-12 in a protein-bound form that is available for absorption after "normal digestion." Vitamin B-12 is not present in foods of plant origin, but is abundant in foods of animal origin.

Vitamin B-12 is bound to intrinsic factor during transit through the stomach, separation occurs in the terminal ileum (last part of the small intestines) in the presence of calcium.

Vitamin B-12 deficiencies due to malabsorption may be associated with the following conditions:

Addisonian (pernicious) anemia.
Gastrointestinal pathology, dysfunction or surgery, including gluten enteropahty or sprue, small intestine bacterial overgrowth, total or partial gastrectomy
Fish tapeworm infestation
Malignancy of pancreas or bowel
Folic acid deficiency

Warning – Vitamin B-12 deficiency that is allowed to progress for longer than 3 months may produce permanent degenerative lesions on the spinal cord.

Maximum dosage should not exceed 10 mcg daily. So, if you have the standard 1mg/mL vitamin B-12 this would be 1cc intramuscular injection per week.

Important Note:
Never Self Administer Intramuscular Vitamin B-12 Without Your Doctor’s Approval !!!

Serious complications can result from improper usage of this Vitamin. Anaphylactic shock and death have been reported with administration of Vitamin B-12.

This information was gathered from Steris Laboratories in Phoenix Arizona.

Causes of hypoferremia (iron deficiency)
Random transient variation in normal subject
Deficient iron stores (relatively late occurrence in the development of iron deficiency)
Chronic inflammatory or neoplastic disorders (see "anemia of chronic disease")

Miscellaneous:
1) Iron levels can decrease quickly even in relatively mild/acute injuries and trivial infections (e.g., colds in humans)
2) Corticosteroid excess: causes decreased iron (as much as half)

Iron circulates in the blood bound to transferrin. Transferrin is responsible for shuttling iron between sites of absorption, storage and utilization for the biosynthesis of iron-containing macromolecules. Receptors have been identified on the surface of reticulocytes (young red blood cells), hepatocytes (a type of liver cell), lymphocytes (white blood cells) and fibroblasts (a type of cell in connective tissue).

The best way to confirm iron deficiency is to demonstrate lack of iron stores in bone marrow.





 

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