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]>