Can Parkinson's be treated by fixing the methylation cycle?
 

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!

http://www.whfoods.com/genpage.php?tname=news&dbid=42

See also a study below showing a link between MTHFR and Parkinson's'

http://www.ncbi.nlm.nih.gov/pubmed/24064257

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?

Normal
 

My homocysteine levels have always been normal but here I am in the PD forum!

Hi Gerry,

Interesting. My homocysteine level is normal too, but I have one of the CBS mutations so apparently the CBS is upregulated, so I dump glutathione (dopamine) through the CBS gate too fast. One thing that was fascinating about the Hinz testing was that I had tons of dopamine in my urine so why is it not in the brain where it's needed? Maybe my always open CBS gate explains that. So I've lowered my intake of sulfur to close the CBS gate. Maybe that will help.

Homocysteine and Vitamin B12 Levels Related to MRI White Matter Abnormalities in Park
 

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.

Thanks,

Gary

Hi Gary,

From what I can discover from researching the methylation cycle, it seems apparent that this cycle clearly involves the creation of glutithione and dopamine, which are certainly factors in PD, so if broken would affect PD symptoms to some extent. I'm not saying it's the fix all solution. Throwing excess L-dopa at the symptoms may not be the best solution. The research may not have caught up to this yet, but I'm suggesting that there is something to be learned from the methylation cycle which pertains to PD treatment.

I agree that there is interest in the methylation cycle and its relationship with PD, and, ultimately you may be correct that it will lead to new treatments. However, that is much different than stating that new research strongly suggests that PD can be treated by fixing this. The research on the relationship between PD risk and problems with methylation is decades old. What would interest me, and probably many other members, would be if you can provide current research which gives evidence that controlling the cycle can be interventional (slow progression) or provide symptomatic relief. I certainly hope this can be found and, again, it's one of the reasons I'm interested in the inosine research. I was just unaware of any methylation research that supports your statements and would like to read it if available.

Dr Yasko and Dr Ben Lynch have apparently had good success treating autism, chronic fatigue patients etc. based on the methylation cycle mutations. I'm thinking PD patients also will benefit. Just not sure when big Pharma and NIH studies will get around to studying this in earnest (if ever), or if I have the years to wait. Just sayin . . . If I find any more recent studies I'll post. Best regards!

It's a big problem when totally unrelated data and reserach are sued to support a hypothesis.

The internet is great for something but it can also confuse,especially a little big of knowledge isn't the same thing as having the right amount of understanding ofa topic to really understand it in all its complexity.

I think you cand ask the question, but to expect the answer to come in a quick web link simply isn't going happen.

I would love this to be the missing liking to the PDpuzzle, I really would, but we are so different and science is only just starting to understand the reasons why a condition can have multiple causes. I think PD will eventually be on of those, and perhaps this will be one of our answers.

I caught a answers to a similar question, from this forum, being cited elsewhere to support a hypothesis. It was never meant to do that, so I am writing this for anyone who may see these being used in the say way. It's not evidence, its not even hypothesis, it is supposition, by people like me, who are hungry to find answers that other sources are not giving.

Please don't cite posts as evidence, and yes I am looking at someone posting on this thread.

I agree that PD will eventually be very treatable via multiple means as there do seem to be multiple causes (head injuries, toxins, stress etc.). All of us here are looking for answers, some which may be right in front of us (or not), while others will perhaps be discovered based on hypothesis that are presented here and elsewhere.