Vit B12 study for Type II Diabetes

Largest study to-date proves that Vitamin B12 is needed for patients with Type II Diabetes.  Metformin, the most commonly prescribed drug for DMII, and has a common side effect to not allowing Vitamin B12 to absorb into the body. Check out the study below, pass the info to family and friends.

Author: Steve Austin, N.D.

Reference: de Jager J, Kooy A, Lehert P, et al. Long term treatment with metformin in patients with type 2 diabetes and risk of vitamin B-12 deficiency: randomized placebo controlled trial. BMJ 2010;340:c2181.

Design: Randomized double blind intervention trial

Participants: 390 patients with type 2 diabetes (T2DM)

Study Medication and Dosage: 850 mg of metformin or placebo administered t.i.d. for 4.3 years

Primary Outcome Measures: Changes in serum B12, homocysteine, and folic acid

Key Findings: Metformin use decreased serum B12 levels by 90 pmol/L, a 19% reduction (P=0.001). By the end of the trial, the number of subjects with B12 deficiency (defined as serum levels <150 pmol/L) increased from 3 to 19 in those given metformin compared with an increase from 4 to 5 in the placebo group. For every 13.8 subjects given metformin, one was driven into a state of B12 deficiency. For every 8.9 subjects given metformin one developed low B12 status (defined as a serum level between 150 and 220 pmol/L) during the 4.3 year intervention.

Overall, metformin use led to a non-significant 5% increase in homocysteine (Hcy). In those in whom a B12 deficiency was induced, Hcy increased by 67% compared with those who maintained normal B12 status (P=0.005). Metformin use also led to a 5% decline in folate concentrations, but this change became statistically non-significant after adjustment for weight and smoking status.

Practice Implications: Metformin is the most frequently prescribed first-line treatment for patients with T2DM. Metformin was previously found to reduce absorption of vitamin B12. Vitamin B12 deficiency is common in T2DM patients, though previous to the publication of the new report, the likely cause of these deficiencies remained somewhat unclear. Before this new report only short-term data were available regarding the effect of metformin on B12 status. This is the first long-term trial.

As a result of these new findings, healthcare practitioners who work with natural medicine are likely to consider a variety of new therapeutic options. Many may routinely prescribe vitamin B12 to all diabetics taking metformin. Administration of 1mg/day of p.o. B12 is unlikely to cause side effects but would probably protect against deficiency without requiring i.m. or deep sub-cutaneous administration of B12.

More conventional practitioners may choose to simply check the B12 status of all patients taking metformin, supplementing only those showing laboratory evidence of deficiency. Indeed, the authors of the new report suggest that their "data provide a strong case for routine assessment of vitamin B-12 levels during long term treatment with metformin."

Regardless of one's medical perspective, however, practitioners should immediately investigate B12 status in all patients taking metformin who develop diabetic neuropathy, given that some of these patients might simply be suffering from a B12 deficiency (which also produces neuropathy), while others may have their neuropathic symptoms exacerbated by a B12 deficiency. I say this despite the fact that the new trial unfortunately did not explore the issue of how metformin-induced B12 deficiency affects diabetic neuropathy.

All patients in the current trial were also given varying doses of insulin despite the fact that they had type 2 disease. While it remains possible that the findings reported here may not apply to the much larger group of metformin-taking T2DM patients who are not taking insulin, there is no immediate reason to suspect that T2DM patients taking metformin but not taking insulin would respond any differently than the subjects in the current trial.

Alex Goldberg