[lurkingforacure]

No, I don't think they are related....but maybe we can learn from the history of scurvy...

What if PD is caused (in whole or part) by some vitamin or mineral deficiency, either because our food no longer provides it (poor soil, massive farming practices, GMO seeds that change the bioavailability of whatever nutrients the poor plant can uptake from the crap soil they are being grown in) or because PWP cannot use it (genetic problem, like MHTFR mutation, or perhaps even a digestive disorder). With such a situation, one could understand how the condition would progressively worsen, and new symptoms would continue to emerge as the body continued suffering the relentless unavailability of a critical element.

I was wondering if given this, what parallels are there in the medical histories of such deficiencies and how they manifested over time? Scurvy being the easiest for me, I went with that one.

I was a bit shocked to learn the history of scurvy, the cure for which is now universally recognized as simply being vitamin C. It is actually considered by most laypeople to be a simple nutritional deficiency that is easily corrected. But look at what total and horrific devastation scurvy caused before we figured it out:

Here is a description of the course of the "disease" of scurvy, it actually killed people, lots of them: more British navymen than were suffered in all enemy action at the time....

"Robert Falcon Scott’s 1903 and 1911 expeditions were both struck with the disease. His description: “The symptoms of scurvy do not necessarily occur in a regular order, but generally the first sign is an inflamed, swollen condition of the gums. The whitish pink tinge next the teeth is replaced by an angry red; as the disease gains ground the gums become more spongy and turn to a purplish colour, the teeth become loose and the gums sore. Spots appear on the legs, and pain is felt in old wounds and bruises; later, from a slight oedema, the legs, and then the arms, swell to a great size and become blackened behind the joints. After this the patient is soon incapacitated, and the last horrible stages of the disease set in, from which death is a merciful release"

from: http://www.atlasobscura.com/articles/scurvy

As early as the 1200s, scurvy was being described and referenced, and in the 1550's BC, Hippocrates and the Egyptians identified it. Hundreds of years of more ghastly suffering followed, until in 1747 the first "clinical trial" for scurvy was undertaken, which showed the successful use of oranges. Unfortunately, the cheap powers that be began substituting limes (hence the term "limey") which not only did not pack the same vitamin C punch that oranges did, but they were stored in copper which further diminished the nutritional value of the fruit. People began doubting the whole vitamin C/cure theory until Hungarian biochemist Szent-Gyorgyi found the cause and cure in....1927. What was once a horrible, progressive, and fatal disease became suddenly not only curable, but preventable.

Without vitamin C, scurvy will get worse and worse, and new symptoms appear as the body continues to be deprived of what it needs until it simply gives out. Is there a lesson here for us? Maybe PD is the lack of some nutrient our body must have but is not getting, or not getting enough of? It could be B12, folic acid, oxygen, who knows, but it seems so obvious that the body can handle most things if it has the tools it needs to do so.

Which brings me to my real point: and thank you Laura, for your recent comments on MHTFR.

I have read that mutations in the MHTFR pathway are common: depending on the report you read, it can range form 40-70%. I find this huge, just as huge as vitamin D3, or B12. Now, maybe that mutation affects your health, maybe it does not, and never will, or maybe it hasn't affected it yet, but will at some point. I look at PD and how it is different but at the same time similar for PWP, but it does universally relentlessly get worse.

Are PWP routinely tested for mutuations in the methylation pathway? None of the many docs we have seen has ever offered us this, much less mentioned it....despite the large overlap in symptoms.

Who here has been tested, and with what result? Itwould be interesting if a large percentage of PWP tested positive for this, particularly since it appears to be something one can do something about. Please share your experience if you don't mind.

[Tupelo3]

Originally Posted by lurkingforacure

Are PWP routinely tested for mutuations in the methylation pathway? None of the many docs we have seen has ever offered us this, much less mentioned it....despite the large overlap in symptoms.

Who here has been tested, and with what result? Itwould be interesting if a large percentage of PWP tested positive for this, particularly since it appears to be something one can do something about. Please share your experience if you don't mind.

Lurking, thanks for a very interesting post. Just to expand on the detail, there are more than 400 MTHFR genes, which are located on the small leg of Chromosome 1. I believe the ones that we would be interested in are defects at points C677T and A1298C. The associated SNPs for the genes and risk letters are:

C677T Rs1801133 (risk letter A)
A1298C Rs1801131 (risk letter G)

My understanding is that you are at risk for various diseases if you are either heterozygous (1 copy of mutation) or homozygous (2 copies of the mutations).

As to your question regarding who has been tested, anyone who did 23andMe genetic testing can get their results. I haven't looked at their reports to see if it is readily available, but it is definitely available in the raw data if you download it.

In my case, I was heterozygous on both genes, meaning I have copy of the mutation for each of them.

[lurkingforacure]

Originally Posted by Tupelo3

Lurking, thanks for a very interesting post. Just to expand on the detail, there are more than 400 MTHFR genes, which are located on the small leg of Chromosome 1. I believe the ones that we would be interested in are defects at points C677T and A1298C. The associated SNPs for the genes and risk letters are:

C677T Rs1801133 (risk letter A)
A1298C Rs1801131 (risk letter G)

My understanding is that you are at risk for various diseases if you are either heterozygous (1 copy of mutation) or homozygous (2 copies of the mutations).

As to your question regarding who has been tested, anyone who did 23andMe genetic testing can get their results. I haven't looked at their reports to see if it is readily available, but it is definitely available in the raw data if you download it.

In my case, I was heterozygous on both genes, meaning I have copy of the mutation for each of them.

Thank you for sharing! 698 and 1277 are the mutations that seem to most commonly cause serious issues, at least so far as I have been able to research.

The next Q is: what, if anything, are you doing about the mutations? Have you seen Dr. Lynch's website and protocol for these two mutations? There are others as well, but I like his the best from what I have seen so far...