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Sinemet vs gastroparesis and protein

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Pls help clarify my confusion...


If gastroparesis delays absorption and onset of action that causes a need for more sinemet, but sinemet has a 90 min lifespan and can be useless by the time it reaches the brain, how can it overlap with the next dosage causing overmedication? Also, one of your past replies has sinemet being effective for 3 hrs. How does that differ from the 90 min lifespan?


The pharmacist forum mentioned protein and medicine metabolism in the liver. Does that mean they go from small int to liver mostly whole, then come out as a.a. or activated medicine repectively, before traveling to the brain? Where does the competition for the 'carriers' occur?


Thank you. Your posts are thoughtful and thorough, and I've enjoyed reading them.

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Mae, these are very good questions, and I wish I had equally good answers. PD is so individualized and effects vary so greatly from one person to the next that many times we can only guess. However, here are some comments.


- Gastroparesis can prevent the absorption of levodopa into the bloodstream; however, the breakdown products of the "expired" levodopa can be problematic themselves. Instead of being transferred to the brain and converted to dopamine, it remains in the bloodstream as levodopa. Further, it appears that some levodopa does reach the bloodstream, but not the "critical mass" needed to be effective. Repeating a dose after the stomach is emptied, when some levodopa may still be present can cause an overlap and thus a larger-than-normal mass reaches the brain, causing overmedication.


Also, not everyone is taking regular Sinemet -- some use Sinemet CR which has a longer "lifespan." So, while it may delay the action of the Sinemet CR causing the person to take extra medication, the CR eventually may kick in causing overmedication effects.


Regarding the effective time -- regular Sinemet is generally effective for around 90 minutes, while Sinemet CR can last 3 or more hours.


The competition for levodopa carriers is not universal, especially in early stages of PD. Some people are more protein-sensitive from the very start, and others become more protein-sensitive in later stages. Competition for carriers occurs in the small intestine, where both amino acids from protein and particles of levodopa are absorbed across the intestinal wall into the bloodstream. A hamburger, for example, will contain far more competing amino acids than the tiny levodopa pill, so the protein competes very effectively in obtaining intestinal carriers.


I hope this addresses your concerns; let me know if you have further questions.

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