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Numerous postings include something like the folowing: <<The docs have me
on Wellbutrin for the "lability" and eldepryl for now. I'm at the point
where I could use some PD relief so we a trying the standard arsenal of
meds - before starting on Sinemet. ... Rick Barrett ([log in to unmask])>>>

I continue to be puzzled by the reticence to use the chemical that the body
normally uses!  levo-DOPA is the normal metabolic chemical that is
metabolized by the body as the pre-cursor for metabolizing dopamine.  It is
the natural chemical that is perhaps least likely to be toxic.

The philosophy of using least amount required is not emphasized by many
doctors.  This seems imprudent to me. The known peaking rapidly - then
decaying rapidly - concentration of levodopa in the bloodstream -
characteristic of carbidopa/levodopa medication means that the regular
medication should be taken every two to three hours - because the half-life
is about two hours.  If half of a 25/100 carbi/levo-dopa tablet is
sufficient to reduce the symptoms to tolerable level, then that dosage is
sufficient for that patient at that time.

Actually, the CR version is more convenient - and less affected by
digestive variations which affect amount of levodopa getting into the
bloodstream - because halves of the 25/100 Sinemet CR medicate for the
usual 4 to 5 hours between meals (without peaks).  If the beginning
medication is three half-25/100 Sinemet CR tablets per day at awakening,
lunch, and evening meal, the dosage is level in blood concentration for the
hours awake.  (this near constant supply of supplemental levodopa can be
approximated by taking six halves <or twelve quarters> of
carbidopa/levodopa medication at equal time intervals through the day - to
save money.)

The possibility exists that carbidopa by itself might raise the
concentration of natural levodopa that exists in the patient newly
diagnosed with mild symptoms.

The conjecture that l-deprenyl keeps the metabolism of dopamine from
occurring - thereby increasing the level of dopamine in the brain - is
cited as the reason that Eldepryl reduces symptoms.  This prompts me to ask
whether this selegiline hydrochloride functions in like manner throughout
the body where dopamine is part of the normal bio-chemicals.

Does anyone know of any data relevant to the two conjectures of
carbidopa-alone or l-deprenyl-alone?  Do measurements of levodopa in
bloodstream exist for normal persons? Same given carbidopa-alone,
Eldepryl-alone, placebo(?)?

Is carbidopa detrimental above some dosage? Eldepryl is potentially toxic
if SSRI effect inhibits type A instead of only type B if I recall the logic
for limiting to 10 mg. per day. Is carbidopa at high dosage entering the
brain and retarding conversion of levodopa to dopamine?  Have we sacrificed
a few small creatures to determine this? I would like to know. Does the
blood absorption level of levodopa have the effect of limiting how much
levodopa can be absorbed from the intestine? (In other words, does the
patient taking very large amounts get more into the bloodstream?) Also,
does the amount of carbidopa taken with it change this maximum levodopa
concentration in blood? This might tell those taking 50/200 Sinemet CR
medication every two hours that they are not absorbing much of it.  We are
told 69% of the levodopa concentration provided by the regular Sinemet is
typical of the CR tablet.  Does this percentage remain constant no matter
how many are taken? Not likely - IMNSHO. (id est, not likely in my not so
humble opinion.)

ron      1936, dz PD 1984  Ridgecrest, California
Ronald F. Vetter <[log in to unmask]>
http://www.ridgecrest.ca.us/~rfvetter/