is not quantifiable as to how much l-dopa you are taking and it has no peripheral decarboxylase inhibitor. We have gone over this many times in the past, but it is never too often to stress the importance of certain subjects, because new people are coming here with the same questions, all the time.
Back when L-dopa was discovered, it worked well for a short time, then side effects such as dyskinesia came on rapidly. This was because the dose became too high to continue working as it did at the onset of treatment. Without Carbidopa (or Benserazide in the UK), too much of the dopa molecule is converted to dopamine outside the brain. Dopamine itself does not get into the brain to do it's work; it is the L-Dopa that gets into the brain and is transformed into dopamine by the same enzyme that converts L-Dopa into dopamine outside the brain. This enzyme removes the carboxyl group on the dopa molecule , converting it to dopamine. This dopamine outside the brain is worse than useless, it does not have the same effect as dopamine in the correct amount in the right brain compartments. Instead, it acts directly on muscle tissue, causing exacerbated movement disorder effects, ie., dyskinesias. It seems questionable why dyskinesias develop with time, even though you are taking a preparation of L-Dopa, that contains carbidopa (sinemet);but that happens with time, probably due to the efficiency of conversion from L-dopa to dopamine in the brain. The ever increasing doses needed for the same effect, without increasing the peripheral decarboxylase inhibitor, is probably responsible for dyskinesias that show up after a few months to years on a regular dose of dopa. Correct with me if i'm wrong.cs