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On Wed 11 Feb, Stephan Schwartz wrote: > > Now, your question: Why doesn't the amount of > carbidopa remain constant despite the rise in the amount of > levodopa in each pill? > > There is a highly specialized area of the brain at the > junction with the spinal cord called the vomiting center > (medical term?). There, nerve cells detect toxins in blood > circulation and provoke vomiting to prevent further absorption > of the poison by expelling the matter from the stomach. > The vomit center is sensitized to levodopa, in varying > degrees for patients, according to their individuality. In some > patients the vomit center can become desensitized to > levodopa over a period of time. Therefore, in some patients > the action of carbidopa as an inhibitor is not uniform. > Researchers estimate that the optimum daily level of > carbidopa in the bloodstream is approximately 75mg . . . > below that, some patients still experience nausea. However, > because of the differences among patients, that estimated > level could be less or more in practice. > Hence, the amount of carbidopa in the regular release pill > 10/100, even taken at several intervals throughout the day, > may not be sufficient over a 24 hour period for that patient to > avoid the formation of some levodopa in the bloodstream that > triggers the vomit center. The pills are purposely scored to > allow the patient to adjust the levels of carbidopa and > levodopa by adding some carbidopa during the day [breaking > a 25/100 to take half - 12.5/50] thereby getting just enough > extra carbidopa [12.5mg] to inhibit nausea, but not too much > additional levodopa [50mg] that could trigger dyskinesias. > Stephan 53/7 > > > Hello Stefan, your explanation of the effect of Carbidopa is ingenious, and may well be a part of the story. However I think there is another more straight-forward explanation: The level of levodopa in the bloodstream is very low, and is virtually unaffected by the amount of Sinemet taken by the PWP. This is because a) The Carbidopa does a good job of protecting the levodopa from attack on its way from the lower intestine to the brain, and b) As soon as any unprotected levodopa does get into the bloodstream, it is attacked and broken down. There is of course a lot of Dopamine in the bloodstream, but it exists in the body (made by the adrenal gland) for a totally different reason than the neuro-transmitter role in the brain. Dopamine cannot cross the blood-brain barrier, and so this dual role can exist. Similarly, the blood-brain barrier will not allow Carbidopa through, but does a very efficient job of stripping away the Carbidopa, thus allowing the levodopa to get through unscathed. The Carbidopa promptly sets off looking for any more large neutral amino acids to protect. This is the last thing the body wants - the reactive LNAAs are a vital part of the operation of our body- and if it is inhibited by large quantities of Carbidopa (protecting the LNAA whether it likes it or not). If the level of Carbidopa becomes too high, this unwanted protective role of the Carbidopa can cause loss of energy, and general torpor, and has been described as 'Carbidopa poisoning'. It is not a major or critical problem; the system needs about 75 mg to protect the levodopa in the Sinemet tablet, but the only people who I have encountered with symptoms of Carbidopa poisoning have been taking over 400 to 500 mg of Carbidopa. Regards, -- Brian Collins <[log in to unmask]>