Quote:
Originally Posted by johnt
This post raises two related questions:
Why do many PwP go unmedicated with levodopa/carbidopa at night?
Is the apparent failure of levodopa/carbidopa to address the non-motor symptoms of PD due to an insufficient dose being used?
If this is the case, two approaches to consider are: increasing the daily dose of levodopa/carbidopa, especially by using the overnight slot; trying to target the dose, so that one amount goes to the brain, and a different amount goes to the ENS.
Any comments?
John
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John, once again you've raised a very interesting question. I can't say that I know much about PD and constipation, as luckily this is one symptom I haven't had to deal with. However, if we're just making some educated assumptions, or guessing, these would be my thoughts:
1. There hasn't been much, if any, research that has shown the L/C has had any beneficial impact on constipation, as a symptom. In fact, it's the opposite, as many studies on L/C have shown it to cause constipation as a side effect (as do many of the other drugs we take).
2. You are absolutely correct in your statements about the ENS, which functions as a second brain, autonomous to the CNS. The large majority of all of our neurotransmitters that the body uses (as much as 95%) are produced and used here.
3. The dopamine produced in the ENS doesn't pass through the BBB. This is the reason we take Levodopa (a dopamine precursor) along with Carbidopa (or Entacapone also) to get it through the BBB so it can be turned into dopamine.
4. If the above assumptions are generally accurate, then it is unlikely that consuming extra L/C will have much, if any, impact on constipation as it is mostly bypassing synthesis in the gut. Once it's synthesized in the brain, it can't pass through the BBB back to the gut.
I do wonder what the effect on the gut would be if levodopa was taken without carbidopa. Would that have any impact on constipation?
Just some thoughts which I honestly can't say are accurate.
Gary