Dr. Richard Deth of Northeastern University sent a letter to the editor at Toxicological and Environmental Chemisty
pointing out flaws in a published study criticizing the injectable form of MB12.
A press release
about the study begins with: " A new study, “An Autism Cohort Study of Cobalt Levels Following Vitamin B12 Injections”, published in the most recent issue of the peer-reviewed Toxicological & Environmental Chemistry1, confirms a significant association between the frequency of methylcobalamin (vitamin B12) injections and blood/urinary cobalt levels in subjects diagnosed with an autism spectrum disorder as well as a significant association between cobalt exposure and damage to human neurons.
Here is Dr. Deth's letter:Dear Dr. Frank
Having read the paper “An Autism Cohort Study of Cobalt Levels Following Vitamin B12 Injections”, I feel it necessary to write a follow-up “Letter to the Editor”. I hope such letters are published by the Journal. The text follows:
To the editor:
While I have a great deal of respect for the overall work of David and Mark Geier, their recent article “An Autism Cohort Study of Cobalt Levels Following Vitamin B12 Injections” misuses findings to create an unjustified level of fear about the use of methylcobalamin (methylB12) to treat autism. Since this treatment is widely recognized as being effective in a significant number of autistic individuals, it is critical to not allow a scientifically flawed paper to undermine its use. The authors found a mean plasma level of cobalt of 0.82 ug/liter for subjects receiving methylB12 injections, which corresponds to a concentration of 14 nM, and they found that neuroblastoma cells exhibit a toxic response to cobalt(II)nitrate hexahydrate with an LC50 of 559 uM. As a first significant problem, their comparison of cobalt in vitamin B12 with the free heavy metal form of cobalt is an inappropriate and misleading comparison. It would be as if supplements containing vitamin B12 actually contained the heavy metal cobalt, which is obviously not the case. The authors have an obligation to characterize the chemical form of cobalt, which is highly likely to be overwhelmingly in the form of vitamin B12, not in the form of free cobalt. Secondly, the difference between the plasma concentration and the toxic concentration is 40,000-fold, but the authors fail to make this comparison. If indeed the plasma form of cobalt is in the form of vitamin B12, the difference in free cobalt concentrations is actually much higher than 40,000-fold. These discrepancies make this article scientifically invalid and as such it should be withdrawn. Studies directed toward identifying optimal dosing regimens for methylB12, with minimal toxicity, are indeed important. Unfortunately, this is not such a study.
Richard C. Deth, PhD
Professor of Pharmacology
360 Huntington Avenue
Boston, MA 02115