“Several amino acid decarboxylases have been identified in bacteria. Tyrosine decarboxylase (TDC) genes (tdc) have especially been encoded in the genome of several bacterial species in the genera Lactobacillus and Enterococcus17,18. Though TDC is named for its capacity to decarboxylate L-tyrosine into tyramine, it might also have the ability to decarboxylate levodopa to produce dopamine due to the high similarity of the chemical structures of these substrates. This implies that TDC activity of the gut microbiota might interfere with levodopa/decarboxylase inhibitor availability, thus the treatment of PD patients.”
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LAJ12345
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This paper is speculative, saying that because these bacterial enzymes affect tyrosine they might also affect levodopa because the two are similar. So no worries about tyrosine consumption.
With that said there is a very important reason to have plenty of tyrosine in your diet. Because levodopa so similar it can accidentally get substituted for tyrosine when your body builds proteins, which makes defective proteins. An abundance of tyrosine minimizes this.
I thought it might be also suggesting the bacteria were a problem? So reducing the bacteria would be better rather than reducing the tyrosine that is needed?
For myself, I see that in the first few years after symptoms are beginning to be seen that levodopa works well for most people labelled with a PD diagnosis. (Indeed, if we limit ourselves to a subset of PwP who respond well to levodopa, then levodopa works for all patients with PD. I know this is a circular argument!)
What then would be the effect, on prescribing and researching, of putting all the research efforts into just focusing on improving the efficacy of levodopa and its helpers (e.g. carbidopa)? Can the honeymoon period be extended? Can a larger, but more intelligent dosing regimen improve dyskinesia and dementia rates?
This is not for DIYing, but has any clinical trial tested PwP on very high doses of levodopa (with carbidopa), perhaps 2000 mg per day.
Increasing the dose is one way to look at this. Decreasing the waste, caused by levodopa metabolism outside of the brain, is another. The paper goes some way to persuading us that the gut is a good place for looking for such mechanisms.
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Is the levodopa in sinement any different then the levodopa in mucuna?
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