Who Responds to the Drug GcMAF?

After researching, W.L. Karns and I have come to the conclusion that autism expert Dr. Amy Yasko is incorrect in saying that the G allele in the bsm/taq SNP (single nucleotide polymorphism) of the Vitamin D Receptor gene is the mutation.  Several Pubmed studies indicate that the more common G allele is the ancestral allele and the wild type—not the mutation.   

Thus, in our estimation, patients with the G allele in the bsm/taq SNP as well as the wild type C allele in the fok SNP of the Vitamin D Receptor are the ones that Belgium ME/CFS physician Kenny de Meirleir believes are most responsive to the drug GcMAF. Patients with a double A  allele in the bsm/taq and a double T allele in the fok would be least responsive, and those who are heterogeneous would fall in the middle.  The Gene Chart has been changed to reflect this. 

It makes a certain amount of sense that the SNPs most likely to respond to a drug that affects the Vitamin D Receptor are the wild types in that receptor, not the mutations.

de Meirleir and Yamamoto disagree
CFS Central contacted de Meirleir by email to confirm, but he didn’t respond to this particular question.   

However, Dr. Nobuto Yamamoto, the world’s foremost expert on GcMAF, says in his experience it makes absolutely no difference whether patients have mutations in these two SNPS.  “The efficacy of GcMAF depends on the capability of the patient’s macrophages [to be] activated,” he explained in an email. “Macrophage activation [has] nothing to do with VDR polymorphism.”  In fact, he wrote, an inability to respond to GcMAF would be fatal.

GcMAF works by turning on white blood cells called macrophages, which gobble up pathogens and activate other immune cells. In the large number of patients who've been treated with GcMAF, Yamamoto has never observed an inability to respond to the medication. 

“Since the molecular structure of [the drug] GcMAF is identical to that of the human MAF [Macrophage Activating Factor], it seems unlikely that subjects harboring the genotype ff/BB cannot be activated by MAF,” he explained.  “These conclusions were made by the response of human peripheral blood mononuclear cells (PBMCs), instead of monocytes alone, to GcMAF…. Unfortunately, people tend to use the same idea of the VDR polymorphism dependency for the efficacy of GcMAF (activation).”

When asked to comment on Yamamoto’s position, Kenny de Meirleir—who has reported that 80 percent of ME/CFS patients have significantly improved on GcMAF in concert with the antiviral Nexavir (Kutapressin)—wrote to CFS Central, “I will be able to give you an answer on this in a few months when statistics can be made on our experience. But at first glance it seems that I have to [disagree] with Dr Yamamoto.”

So the jury’s still out on whether certain SNPs in the Vitamin D Receptor gene influence the efficacy of the drug GcMAF in treating ME/CFS—or for that matter, any other diseases.