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> > The level of levodopa in the bloodstream is very low, and is > > virtually unaffected by the amount of Sinemet taken by the PWP. > > The data do not show this. The concentration of levodopa rises quite rapidly > to a peak following taking a tablet. The regular tablet is in the blood plasma > in it's entirety (99%) at the peak. The decay in concentration is due to > metabolic effects including the usage of some of the levodopa by the brain. > > > 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. > > I believe this is mis-information. > > 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. > > Conversion of levodopa to dopamine IS the chemical signal that is the > proximate cause of nausea. Carbidopa retards the conversion of levodopa to > dopamine. This keeps the amount of levodopa from being reduced to zero much > more rapidly than if there is no retardation. (tolcapone and entacapone retard > another metabolic enzyme - that being the one that is labeled COMT - to make > the levodopa concentration remain high longer in the bloodstream.) > > This information is basic and needs to be clearly understood. We need to have > an accurate, valid, description of the processes and mass transport as well as > the chemistry. > -- > Ron Vetter 1936, '84 PD dz paradise is feeling good, not a place to go > [log in to unmask] > http://www.ridgecrest.ca.us/~rfvetter > > > > For Ron Vetter You are quite right Ron; What I had written is nonsense, and I am glad that you raised it. What I was intending to say was that the level of levodopa in the blood of a normal person, or a PWP before they take a Sinemet tablet , is very low. During the period that the Sinemet is present in the body, the level of levodopa in the bloodstream of course rises, but provided the 75 mg or more of Carbidopa is taken each day, the normal reaction which would otherwise convert the levodopa to dopamine in the body instead of in the brain is inhibited. The reason that I found Stefan's explanation of the effect of the levodopa on the vomit centre a little hard to swallow (!) is that he has had to assume differrent sensitivities for different people, and some people becoming desensitised over a period of time - and I'm not sure how you explain what happens to a person who accidentally takes a large dose of Sinemet, say first thing in the morning before the Carbidopa has time to build up. I am not saying that this mechanism does not exist, but I can't help thinking that if it was the only one, a much larger proportion of us would be going round throwing up whenever we got our dosage wrong. I think we can all agree on the history of Sinemet/Madopar : First- they invented the levodopa tablet, and it was actually used in that form for some time (I don't know the exact time, but I think it is about 1 to 2 years. Patients suffered from precisely the symptoms of nausea discussed above, to say nothing about colouring the urine black, and worst of all, without the protection of the carbidopa only a small percentage of the levodopa survived the journey to the brain. The levodopa was combined with carbidopa (in what strikes me as a brilliant bit of chemistry), resulting in the tablets which we take today. -- Brian Collins <[log in to unmask]>