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?

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.

http://www.karger.com/Article/Pdf/345414

you had tons of dopamine in your urine? before or after you took mucana?
if before, where in the world did that dopamine come from? your're saying glutathione is a precursor to dopamine? btw, dopamine can't pass thru the BBB.

i take sinemet, carbidopa/l-dopa, and i get very nauseated if i take more than 200mg in 1 dose, i took A 25/250 TABLET once and was sick to my stomach which i assume was from the l-dopa getting converted into dopa in the blood stream.

I had alot of dopamine in my urine before I took the mucuna and about a third more after taking it. I don't understand why my body would produce excess dopamine and then dump it. I Guess it was being converted in the body/blood to dopamine but not in the brain. I understand dopamine doesn't pass thru the BBB, but L-dopa does. I never got nauseous at all. L-dopa andTyrosine are precursors to dopamine. Glutatione apparently allows dopamine to be more effective and is a master antioxidant, so if it's in short supply more damage can be done to mitrochondria and brain dopamine neurons.

The video below from Dr Rostenburg discusses the role of glutathione, dopamine and the methylation cycle:

http://www.youtube.com/watch?v=_eq28PCvfsg

I have only anecdotal evidence on this question and in time I'm sure the hardcore research will catch up. Yes, I think that correcting methylation is a worthy pursuit in efforts to heal from pd. But you need to have a sophisticated knowledge of biochemistry to fine tune methylation pathways. The folks who have that knowledge plus the clinical expertise are docs who work under the rubric of functional medicine, integrative medicine or Bioindividualised medicine.

Rather than throwing b12 or SAMe or glutathione at the problem in a random fashion they first run functional tests to see how u are performing as a methylator, not just looking at serum levels. Then they know what precursors to introduce, when and where and how to avoid triggering feedback inhibition. They also investigate underlying causes. Leaky gut seems to be extremely common. Triggers for that are common allergens like gluten, dairy or soy.

Folks are very focused on gluten as an issue but I suggest that you consider parasites and fungal overgrowth equally as they are just as implicated in dysbiosis. My functional med doc says that 80 percent of stool samples she submits are coming back positive for parasites (including my own and an acquaintance with pd). The problem is there if you look for it. This creates two problems. Toxins getting thru and malnutrition. I have shown up some major nutritional deficiencies which are now being corrected. I am also being treated for fungal overgrowth in gut as well as parasite. There's a long road ahead. Parasites are not easy to eliminate.

One such doc I spoke to said that when you treat such underlying conditions in pwps, their symptoms either abate or vanish completely. Worth a try. Pd aside, we'd all benefit from cleaning up our gut.

sorry, i can't take a video from a chiropractor seriously. you can believe what you want.
tyrosine is converted to dopamine in the brain and i believe also the adrenal glands, the eyes - i think forms melanin? and this is tightly regulated, how do you explain how eating ounces of tyrosine in an egg or piece of meat doesn't cause you to die by massive production of dopamine and every other enzyme in your system and on the flip side, why don't you exhibit pd symptoms if you fast for a week or don't eat protein? in addition, selegiline, a non-reversible mao-b inhibitor, was shown years ago not to slow pd progression, same with vitamin C and vitamin E.

people taking dopamine agonists have been shown to progress at the same rate as those taking l-dopa. NO DOPAMINE.

i guess my point is post whatever you want but i object to your constant claim that dopamine is harmful. before sinemet, what kind of life do you think pd'ers could look forward to? please think about the affect of what you post here on the less informed.

one double blinded trial with IV glutathione did not improve pd symptoms.
http://www.ncbi.nlm.nih.gov/pubmed/19230029
there's 1 study on nasal glutathione tested on pd'ers but no results published yet

Very informative link. Synthetic L-Dopa has definitely been shown to be damaging.

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