Originally Posted by zanpar321
New information regarding the methylation cycle and MTHFR gene mutations seem to strongly suggest that PD can be treated by fixing this. Maybe throwing L-Dopa at the symptoms may no longer be the best we can do!
See also a study below showing a link between MTHFR and Parkinson's'
Folks with a MTHFR 677 or 1298 gene mutation don't absorb B12 and their methylation cycle needs fixing. Has anyone had any success doing this?
I'm sorry Zanpar, but I respectfully believe your statements are way overboard. There is absolutely NO new research that "strongly suggest that PD can be treated" by controlling the methylation cycle.
With regard to your first linked study, that's very old information, not new. That study was conducted, on mice, in 2001. Just because some whole foods supporter with a web site comments about it today doesn't make it any more recent than 13 years. The second study linked was just a meta analysis of older research on the MTHFR C677 polymorphism and the increase in risk of getting PD. Again, this relationship between the MTHFR polymorphism and susceptibility to PD has been know for years. However, the relationship in no way means that (1) this is an actual cause of PD; or (2) that changing levels of folate and/or ultimately homocysteine, will either stop or slow the progression of neural cell death. In fact, to quote directly from the study you have referenced:
Recent findings suggest that homocysteine levels are increased in PD patients (Allain et al. 1995; Kuhn et al. 1998; Yasui et al. 2000), but it is not known whether this alteration precedes disease onset. In addition, the clinical data are mainly from studies of patients treated with levodopa, a drug that may itself affect homocysteine levels (Miller et al. 1997; Muller et al. 2001). It therefore remains unclear whether folate deficiency and/or elevated homocysteine levels play a critical role in the pathogenesis of PD.
What I personally find most interesting about this research is that it has shown that the adverse effects of homocysteine on dopaminergic cells is ameliorated by administration of the antioxidant uric acid. This may be the reason why there has been some recent studies that have shown possible progression slowing with the use of Inosine (which raises blood levels of uric acid). In that regard, the NIH is going to begin, later this year, a large multi-centered clinical study researching inosine on it's potential as a progression slowing drug. I'm not sure if they have posted the study yet, but I am sure that they haven't yet begun to recruit patients. This may be a better way to test your hypothesis re: MTHFR rather than taking B-12 shots, and certainly better than just increasing dietary folate.