3 min
The Secret Life of Levodopa: 3 min youtube... - Cure Parkinson's
The Secret Life of Levodopa
Thanks for sharing
A study that confirms this:
pubmed.ncbi.nlm.nih.gov/220...
"Levodopa (L-DOPA), a close structural analogue of the protein amino acid L-tyrosine, can substitute for L-tyrosine in protein synthesis and be mistakenly incorporated into newly synthesised proteins in vitro. We show that L-DOPA-containing proteins are present in the brain in L-DOPA-treated Parkinson's disease patients and accumulate in specific brain regions."
Therefore it is important to have abundant tyrosine – a lot more than the amount of levodopa that we are taking in order to minimize this problem. There is usually plenty of tyrosine in the diet. So it is not usually necessary to supplement it unless a person is taking a lot of levodopa and not much protein:
en.wikipedia.org/wiki/Tyrosine
" Dietary requirements and sources[edit]
The Dietary Reference Intake (recommended dietary allowance, RDA) for phenylalanine and tyrosine is 42 mg per kilogram of body weight.[6] For a 70 kg person, this is 2.31 g (phenylalanine + tyrosine).
Tyrosine, which can also be synthesized in the body from phenylalanine, is found in many high-protein food products such as chicken, turkey, fish, milk, yogurt, cottage cheese, cheese, peanuts, almonds, pumpkin seeds, sesame seeds, soy products and lima beans, but also in avocados and bananas.[7] For example, the white of an egg has about 250 mg per egg,[8] while lean beef/lamb/pork/salmon/chicken/turkey contains about 1 g per 3 ounces (85 g) portion.[8]"
How does this fit in with:
1. alpha-synuclein and its role in the pathogenesis of PD.
2. The results that show levodopa does not hasten the progression of PD?
John
Good questions. Levodopa usage has been shown to not hasten the arrival of levodopa -induced dyskinesia.
Per the study I cited, fulltext:
researchgate.net/publicatio...
whether or not levodopa usage aggravates Parkinson's is unclear. The cell culture results give some reason for concern. However, levodopa may cause different problems. Here is a study associating increased levels of peripheral neuropathy with levodopa usage in Parkinson's patients:
pubmed.ncbi.nlm.nih.gov/205...
Association is not causation so the study does not stand as proof of causation.
With all that said, I think it is wise to see to it we have plenty of tyrosine on board as compared to levodopa usage.
We've talked a long time ago about dietary supplementation of L tyrosine and it's a good thing, and entirely consistent with the study you mentioned. Remembering that L tyrosine is the precursor basis for synthesis of all the catecholamines, one could think about it as a very very good thing, not just a good thing. Can't hurt and you can never have enough tyrosine, whether you're talking about PD or mental health issues in general, it's a pretty critical amino acid and dietary sources certainly seem well-founded as supplement, whether you're eating them as beef or nuts or whatever. Want absolute proof? I'm sorry I can't actually give it to you and more's the pity.
I can only speak for myself but i dislike videos.
Why? Is the video accurate is what matters to me.
It's ineficient. Its just me*. Which means it may be others.
To the broader topic: i think people are already generally aware that ldopa is not nutrituous, but accept it as part of the bargain. Coupled with numerous studies that show that levodopa at the very least doesnt appear to accelerate disease progression or bring about an earlier death, i think its open for people to reasonably conclude that the toxicity is more than offset by QOL improvements and the compounding health benefits derived from improved mobility.
There is a chance that what i just wrote is irrelevant horseshit tho, since i didnt watch the vid.
*i do a lot of my HU browsing whilst doing other things and this makes videos impractical
Do not know for sure. Possibly a title like "Levodopa Can Result In Defective Proteins" would attract more attention.
Marc,
When we are younger and melatonin levels in the Substantia Nigra pars compacta and brain are normal, the melatonin very likely prevents the aSyn aggregation and toxicity, but with the age related decline of melatonin production plus the additional melatonin decline seen in people with PD, the reduced melatonin level is no longer able to prevent aSyn aggregation and toxicity. That is one theory.
frontiersin.org/articles/10....
A relevant quote from the study :
>>> ' Melatonin blocked α-synuclein fibril formation and destabilized preformed fibrils by inhibiting protofibril formation and secondary structure transitions and by reducing α-synuclein cytotoxicity (169, 190). ' <<<
We are already aware of a multitude of other health benefits that melatonin offers in PD, but the two above apply to some degree to the video you posted.
Art
Thanks for sharing the video!