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On Tue 10 Feb, Stephan Schwartz wrote: > Dear Brian: > I have a few questions: > 1. What is a 'big shot' of levodopa? It is purely levodopa, > without carbidopa? In what concentration? > 2. Do you have a citation to a clinical study where > researchers experimented with inducing levodopa into > non-PD subjects? > 3. In light of the fact that researchers have determined that > levodopa, without carbidopa, doesn't cross into the blood > stream without significant degradation in the liver (even before > it gets to the blood-brain barrier) is it possible that a > mechanism exists in the periphery to metabolize "excess" > levodopa, without the brain adjusting the dopamine > production in the neurons? > > Stephan 53/7 > > > Hello Stephan, My not-very-scientific answer to you is that it is so because my neuro says it is so. To me, it has been an established fact for several years, and I can't recall the details. I will see if I can get any references, but I have such confidence in my man that I accept his occasional uncorroborated statements as essentially true. I was not suggesting that raw levodopa was used : the reference was actually to Sinemet; it's just that I tend to talk in terms of the active ingredient. actually, I think I could make a good case, working from what I might call 'first principles':- As I expect you know, a newly-diagnosed PWP can accept doses like the Sinemet 250/25 tablet without any adverse reaction. (As a 19yr PWP, it sets me sweating just to think of doses that high.) If you think about it, if a Sinemet 250/25 is acceptable at the time of diagnosis (i.e. when 20% of Dopaminergic cells remain) then even higher doses should be acceptable earlier in a PWP's life. In other words, I do not regard the onset of symptoms as marking a significant change in the chemistry if the brain: it's just that the visible symptoms make themselves obvious at about the '20% of cells remaining' benchmark. -- Brian Collins <[log in to unmask]>