Does anyone know if there is research on this topic? Does taking C/L actually discourage the brain from producing its own dopamine because it's being fed dopamine from an external source?
I just wondered if this question had ever been explored because the human body is lazy. For example, if you put testosterone into your body (via. TRT replacement therapy), your body stops producing its own testosterone and you literally cannot stop taking testosterone. Similarly, if you start putting corticosteroids into the body, the adrenal glands stop working for a year after you stop taking the steroid because the adrenal glands have not needed to work and simply shut down in the interim. Likewise, if you suddenly stop taking an SSRI antidepressant, you will be missing all of that extra serotonin and will crash.
Does a similar correlation exist when the body is given levodopa? Does the brain become "lazy" at producing its own dopamine? If you are aware of any scientific research on this topic, please do post it. Thank you.
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"Does taking C/L actually discourage the brain from producing its own dopamine because it's being fed dopamine from an external source?" YES, but if you have PD you can only have a huge net benefit by taking C/L and not vice versa. That's because if the brain cells producing dopamine are irreversibly dying, you can never benefit from starving your brain cells of C/L. But the big question is, are the brain cells death irreversible? No, I think not, but that's another story all together
A very good question. I can't find a paper that gives a good explanation of what is going on. The best I can do is to describe my symptoms in the time around when I take a dose of C/L, and descibe a simple experiment to measure what is going on
I sometimes notice that on taking my first dose of the day, say, 12 hours after my previous dose of C/L, that my symptoms get worse for perhaps 10 to 40 minutes after taking my pill, before the symptoms start to improve.
The way I measure this is using the side-to-side tap test. This involves using a computer keyboard on which I type alternately q followed by p for 30 seconds for each hand. An app to do this can be found at:
To get a baseline, I start testing at 20 minutes before taking the pill and then do the test every 10 minutes. Although I have done no proper statistical analysis of the results, they often show a decline relative to the baseline. Given the pharmacokinetic values for a half-life of about 90 minutes for C/L you would expect very little further decline after 12 hours, which is approximately 8 half-lifes.
hi johntPM, i just read your response and am interested in learning more. i have to say, i dont underatand how that helps answer the question? could you expand on your answer? i just read a post on a nootropic site, "boost your biology" which said thart macuna pruriens definately downregulates dopamine production and shouldnt be used by normal people seeking to boost brain dopamine levels. any thoughts on that?
I think johntPM is just trying to answer the same question by using his tool to measure and analyse his tremor level when taking cl. Perhaps that could indicate whether cl discourages dopamine production or not
Discogs asks "Does Levodopa cause your brain to produce less of "its own" dopamine?" Any such changes may be short term or long term. My reply attemps to throw some light on the short term effects. It assumes that the more levodopa or dopamine in the body the less the symptoms of PD. If we observe an increase in symptoms (here, a lower tap test score) that suggests that the total amount of levodopa from exogenous sources (here, the pill) and from endogenous sources (here, the body's continued but diminished production) has for a short time decreased. One way to balance the books is to suggest that endogenous production decreases for a short while. Eventually (here, after about 30 minutes) the brain is swamped by the levodopa from the pill causing levels to rise, and, with this, the symptoms decreasing before going into reverse. Please note that this is just a suggestion, not a proven fact.
Called negative feedback loop which maintains homeostasis in the body whereby a swamping exogenous source is likely to suppress endogenous production. I always thought this with a basic principle in physiology but not sure how it actually works out with PD but makes you wonder how much this occurs with use of levodopa
Some light on this question comes from the paper "BIOCHEMICAL AND FUNCTIONAL DIFFERENCE BETWEEN DOPAMINE FORMED FROM ENDOGENOUS TYROSINE AND EXOGENOUS L-DOPA IN NIGROSTRIATAL DOPAMINERGIC NEURONS" ELDAD MELAMED
"However, we wish to propose an alternative possibility, i.e. that the dopamine derived from exogenous L-dopa is handled in an entirely different manner than the tyrosine-generated dopamine. Normally, tyrosine is supplied to the brain mostly from dietary sources. Nigrostriatal nerve-terminals take up tyrosine from the extracellular space to be utilized, among others, for dopamine biosynthesis. There is no or only a negligible amount of L-dopa in the striatal extracellular space. However, following systemic administration of L-dopa, the striatum is artificially loaded with high concentrations of this precursor. Exogenous L-dopa may now become the major available substrate since it competes with tyrosine on entry from circulation into the"
!!! There ends that part of the paper that is available for free. The rest is behind a paywall. Kudos to anyone who can complete the sentence.
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