They tested two quantities of mucuna against the 200 mg/50 mg levodopa/cardidopa pills. 15 grams of mucuna seed powder contained 500 mg natural levodopa; 30 grams of mucuna seed powder contained 1000 mg natural levodopa. They used these large amounts because the natural powder did not have the advantage of being swallowed along with cardidopa (which inhibits metabolism of levodopa allowing 3 to 5 times as much to get to the brain). So they were just levelling the playing field.
The 8 subjects had advanced PD and would normally take the 200/50 ld/cd pill every 4 hours to go from an "off" to an "on" state. When they took the pill (first thing in the morning), the time to "on" was 54.6 minutes; with 15 g mucuna, time to "on" was 27.8 minutes, with 30 g mucuna, time to "on" was 23.0 minutes.
Length of "on" time was 232 minutes for 200/50 pill, 170 minutes for 15 g mucuna, 278 minutes for 30 g mucuna.
15 g mucuna seed powder didn't last as long as the pill but it was twice as fast in producing an "on" state. It's not clear whether this speed is because of a temporary advantage of 500 mg levodopa in the powder versus 200 mg in the pill; or because levodopa from powder gets into the blood faster than levodopa in a pill; or because there are other things in the natural powder which lend a helping hand.
KenA
At 03:42 PM 02/11/2005, you wrote:
Thanks, Ken that is interesting. Theres obviously even more to this
than meets the eye. Feel free to pounce on my ropy chemistry or
anything else, the debate is a good outcome and I am intrigued. It
would be interesting to know whether the efficacy of the powder was
because it contained more than the 100mg L-dopa in a standard pill
or whether there was some more chemistry involved that resulted in
more reaching the brain or indeed whether some other pathway was
involved.
There was an interesting television documentary here which looked at
a young onset parkie who used the drug ecstacy (don't pounce, I
can't spell either!) for the occasional relief from his PD.Of course
I am not suggesting we all rush out and get some 'E' (there is some
evidence it may make PD worse in the long term) but what was
interesting was there was a pathway other than dopamine involved. A
scan showed that when he took the 'E' the dopamine levels in his
brain were almost negligibly affected (much much less than taking
sinemet) yet his symptoms were greatly improved.it was suggested
serantonin was involved (aargh is Peter going to pounce again?) When
the subject he took both 'E' and Sinemet together he was able to
perform gymnastics, quite amazing to see.
I guess it gives me hope that we are still finding out stuff about
this disease - one day we will know enough to fix it.
Cheers,
Barry
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Ken Allan
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