B12 question do I need to take injections?

MOjs13

New member
insted of injecting 1000mg of B12 EOD i am gunna switch to the 1000mg a day tabs but i was just wondering if i should use the time relseased ones or not.
 
the body doesn't absorb b12 when it's supplimented oraly....thats why it is injected...Im the expert go to my site www.buyb12.com and read the articles...you will be wasting your time taking it oraly
 
I think theres a post somewhere proving that b12 has no difference b/w taken orally or injected.....
 
gymphreak ....you mean to tell us that all the medical studys are wrong ...maybe you should inform the Medical community. ......


when b12 is supplimented oraly the body see's it in the stomac and doesn't absorb it in the intestinal lining
 
Last edited:
the Lion said:
gymphreak ....you mean to tell us that all the medical studys are wrong ...maybe you should inform the Medical community. ......


when b12 is supplimented oraly the body see's it in the stomac and doesn't absorb it in the intestinal lining


Sorry but gymphreak is right about this, I'll see if I can find the study.
Maybe you should start selling tabs as well.......lol
 
Oral versus intramuscular cobalamin treatment in megaloblastic anemia: a single-center, prospective, randomized, open-label study.

Bolaman Z, Kadikoylu G, Yukselen V, Yavasoglu I, Barutca S, Senturk T.

Department of Internal Medicine, Division of Hematology, Adnan Menderes University Medical School, Aydin, Turkey. zahitb@yahoo.com

BACKGROUND: Cobalamin (vitamin B12) deficiency, the most common cause of megaloblastic anemia, is treated with intramuscular (IM) cobalamin. It has been suggested by some investigators that oral (p.o.) cobalamin treatment may be as effective in the treatment of this condition, with the advantages of ease of administration and lower cost. OBJECTIVE: This study assessed the effects and cost of p.o. versus i.m. cobalamin treatment in patients with megaloblastic anemia due to cobalamin deficiency. METHODS: This was a 90-day, prospective, randomized, open-label study conducted at the Division of Hematology, Department of Internal Medicine, Adnan Menderes University Research and Practice Hospital (Aydin, Turkey). Patients aged > or =16 years with megaloblastic anemia due to cobalamin deficiency were randomized to receive 1000-microg cobalamin p.o. once daily for 10 days (p.o. group) or 1000-microg cobalamin i.m. once daily for 10 days (i.m. group). After 10 days, both treatments were administered once a week for 4 weeks, and after that, once a month for life. Patients were assessed for the presence of reticulocytosis between treatment days 5 and 10 until it was detected. Therapeutic effectiveness was assessed by measuring hematologic parameters on days 0, 10, 30, and 90 and serum vitamin B12 concentration on days 0 and 90. The Mini-Mental State Examination was used before and after the B12 therapy for cognitive function assessment and 125-Hz diapozone was used for vibration threshold testing. Neurologic sensory assessment, including soft-touch and pinprick examinations, was used to identify neuropathy at baseline and study end. Tolerability was assessed using laboratory tests and patient interview. Cost was assessed using the cost of the study drug and of the injection. RESULTS: Sixty patients completed the study 26 in the p.o. group (16 men, 10 women; mean [SD] age, 60 [15] years) and 34 in the i.m. group (17 men, 17 women; mean [SD] age, 64 [10] years). Reticulocytosis was observed in all patients. In the p.o. group, at days 30 and 90, all hematologic parameters changed significantly versus day 0 (mean hemoglobin levels increased [both P<0.001]; mean corpuscular volume decreased [both P<0.001]; mean white blood cell count increased [day 30, P<0.01; day 90, P<0.001]; and mean platelet count increased [both P<0.001]). The mean serum vitamin B12 concentration increased significantly from day 0 to 90 (P<0.001). These hematologic parameters and the recovery patterns were similar between the 2 groups. Neurologic findings included sensitive peripheral neuropathy in 9 patients (15.0%), alteration of cognitive function (loss of memory, impaired concentration) in 7 patients (11.7%), and loss of sense of vibration in 5 patients (8.3%). Neurologic improvement was detected in 7 of 9 patients (77.8%) in the p.o. group and 9 of 12 patients (75.0%) in the i.m. group at day 30. CONCLUSIONS: In this study of patients with megaloblastic anemia due to cobalamin deficiency, p.o. cobalamin treatment was as effective as i.m. cobalamin treatment. P.o. treatment also was better tolerated and less expensive compared with IM treatment. However, because of the small sample size and the short term of this study, further long-term studies are needed to determine the efficacy of p.o. cobalamin treatment.
 
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