[QUOTE=Conductor71;829786]Soccertese,

I was wondering this as well. According to research, the responsible component of grapefruit is the phytochemical bergamottin. This is perhaps why Ron had such an extra long duration. It boosts the amount of levodopa in our bloodstreams and then it enhances the COMT inhibition leaving more dopamine up there working for us?

Maybe if we are not on entacapone we do not get the extended on time? Just a guess.

Oh, and our genes play a role. I don't know how many have done this but 23 andMe tests for our genetic dispositions with the COMT gene. The Val/Met SNP also informs how well we respond to COMT inhibitors. 23andme will tell you what alleles you have by looking up SNP rs43680 in browse raw data then see abstract for your response to COMT inhibitors at the pubmed link:


The COMT Val158Met polymorphism affects the response to entacapone in Parkinson's disease: a randomized crossover clinical trial.

Laura[/QUOTE

what i find interesting is that if your detoxifying enzyme activity is inhibited by grapefruit juice and basically l-dopa is absorbed in just a small area of your small intestine via active transport, then i assume you have to have a higher concentration of l-dopa in your tissues and blood, and maybe that translates to a higher concentration in the brain but doesn't seem so, just a longer affect. so as an aside, it seems that the concentration of l-dopa in your brain must reach an equilibrium fairly quickly? i.e., the active transport into the brain gets saturated quickly and somehow shuts down until the concentration in the brain decreases? of course normally it's tyrosine that your brain uses to mfg dopamine but life's too short to research that pathway. amazingly complicated system, wonder how the kidneys look a l-dopa, how much l-dopa ends up in the urine?
and how much better are comt inhibitors vs selegiline and rasagiline, which gives the bigger bang for the buck?

have too much time on my hands.