vitamin C, libido, and parkinson's

I took 12 grams vitamin C for much of about 10 years from age 27 to 37. Myself and the only two others I knew of who took more than 10 grams a day for more than a week or two noticed a large decrease in libido. I took so much because it greatly relieved stress. I stopped because I got married. Fast-forward 10 more years and at age 47 I seem to have Parkinson's. Then I remembered Dr Pauling's videos from about 1981 and on seem to show him displaying two symptoms of Parkinsons: weak voice, trembling hands, and head nodding just a tad more than you would expect. After some researching, I see that more than 2 grams a day causes copper to shift from the protein-bound state to free copper, and that the protein-bound state is needed to protect the part of the brain that is damaged in Parkinson's. The protein-bound state is needed to protect the brain from iron toxicity. If not, then the iron damages dopamine producing cells, which is directly related to libido. As a side note, my own research into how much vitamin C animals produce (and primates and guinea pigs need) would convert to 0.5 to 2 grams a day for a human. The biggest error in saying 10 grams a day is that it is based on body weight, but body weight is not the correct measure in converting nutrition and toxicity, but caloric intake is, which is lower for larger animals. Keep in mind, I've read all of Pauling, Hoffer, Cathcart, Cameron, and Stone's work on VitC and you can't find anyone these days who is as big a proponent as I was.

1500 mg/day decreases protein-bound copper "Serum ceruloplasmin activity was significantly reduced (p less than 0.01) at every data point throughout the ascorbic acid supplementation period."
http://www.ncbi.nlm.nih.gov/pubmed/6837490
1000 mg/day decreased:
http://nsft.sbmu.ac.ir/browse.php?a_code=A-10-1-8&slc_lang=en&sid=1
Effect not seen in guinea pigs and men
http://www.ncbi.nlm.nih.gov/pubmed/7891201
Also reduced in guinea pigs:
http://www.ncbi.nlm.nih.gov/pubmed/7429759
Also in rats:
http://www.ncbi.nlm.nih.gov/pubmed/3337044
Ceruloplasmin was not reduced at 605 mg/day in men, but its activity was
http://www.ncbi.nlm.nih.gov/pubmed/3694287
Magnesium was lowered in guinea pigs, but not ceruloplasmin
http://www.ncbi.nlm.nih.gov/pubmed/4077401
vitamin c in blood correlates with lower ceruloplasmin in humans
http://www.ncbi.nlm.nih.gov/pubmed/22841398
Small effect seen in monkeys on marginal copper diet
http://www.ncbi.nlm.nih.gov/pubmed/7304479

Low ceruloplasmin including from mutations is strongly implicated in PD and AD:
http://www.ncbi.nlm.nih.gov/pubmed/23144563
Low ceruloplasmin correlate with younger-onset PD
http://www.ncbi.nlm.nih.gov/pubmed/19159062
Mutations for low ceruloplasmin allow iron oxidation
http://www.ncbi.nlm.nih.gov/pubmed/16150804

Linus pauling institute:

Vitamin C

Although vitamin C supplements have produced copper deficiency in guinea pigs (17), the effect of vitamin C supplements on copper nutritional status in humans is less clear. Two small studies in healthy, young adult men indicate that the oxidase activity of ceruloplasmin may be impaired by relatively high doses of supplemental vitamin C. In one study, vitamin C supplementation of 1,500 mg/day for two months resulted in a significant decline in ceruloplasmin oxidase activity (18). In the other study, supplements of 605 mg/day of vitamin C for three weeks resulted in decreased ceruloplasmin oxidase activity, although copper absorption did not decline (19). Neither of these studies found vitamin C supplementation to adversely affect copper nutritional status.