Hi folks,
Really interested in opinions here - especially from the more experienced and time-served 'warriors'. Diagnosed 2 years ago after about 18 months of tests to establish why I had been experiencing arm stiffness, loss of some finger dexterity and foot/toe curling - all on my right hand side. A SPECT/DAT scan result came back reporting a 'gross presynaptic dopaminergic deficit' - and Idiopathic PD was diagnosed. I was just shy of 49 (coming up for 51 now), and luckily still very active.
I was put onto Sinimet 25/100mg (C/L) three times a day. Did I notice a difference when I started these? I'm not sure - if there was a difference it wasn't much, though to be fair my symptoms were quite subtle /minimal.
2 years on, and I've gradually built a regime to optimise my health and give myself the best shot of keeping PD's impact to a minimum. When it's something this important, I reckon throwing the kitchen sink at it is the only way. Any nuggets of wisdom I've picked up from researching books, podcasts, forums like this (thanks people!👏), I've looked to implement, especially if there appears to be little in the way of risks/downsides.
My regime includes yoga, boxing, running, cycling, meditation, breath work, cold showers, diet (no dairy, less sugar, more fresh veg, especially peppers & berries), High Dose Vitamin B1, supplements (B Complex, Magnesium Glycinate, Vit D), playing my guitar and singing.
I count my blessings that all these things are available to me, and mostly I have to say, I feel great - mentally better than I've felt in years (more energy, less brain fog, less anxiety). 6 monthly Neuro nurse appointments have been showing improvements in reactions and touch tests.
Which brings me to my point.....given the often-stated link between long term Levodopa use and dyskinesia, and the lack of impact these meds may have had for me, I have been giving some serious thought to reducing C/L dose, then if no impact, considering eliminating. I do not experience on/off periods and if I mistakenly miss my 3rd tablet one day I notice no difference.
So I guess my questions are..
1. Is there a definite link between Levodopa use and dyskenesia?
2. Is this only at higher doses or after a longer period of use, or both?
3. Should I (carefully & with Doc's support) reduce C/L intake and monitor?
4. Or should I go for 'if it's not broke, don't fix it' strategy?
Maybe the meds are doing more than I give them credit for. I just feel it's worth exploring. Any feedback most welcome.
Best wishes,
Andy
How i beat Parkinson's
What to do when things go wrong with PD medications?
Medication not working 
HDT & TTFD–In my case, HBP was a return of symptoms and not a side-effect of TTFD.
Parkinson’s disease managing reversible neurodegeneration- retracted!
The link between levodopa usage and acceleration of the arrival of dyskinesia has been refuted. See this study: academic.oup.com/brain/arti...
However there is a long-term adverse effect of levodopa as set forth by this study: researchgate.net/publicatio...
This problem is at its worst with high levels of levodopa intake and low intake of protein. Less of an issue with low levodopa and normal diet. In any case, levodopa is strictly for symptom relief. If it makes no difference then it should not be taken. Do not quit all at once cold turkey but taper your dosage gradually.
Parkinson's is a wake-up call to adopt healthy habits and you have done well. Good work and carry on. 🙂
Thank you PB🙏🏼. Very enlightening post!
I think that’s a good rule for any medication - if you don’t need it, don’t take it. There’s pretty much always some kind of side effect.
Will set up a gradual taper and keep a close eye on things.
L-dopa was/is an incredible enhancement to the lives of so many, so I’m not knocking it, but need to be sure it’s working for me.
Thanks again. Your contributions are always interesting.
I agree with most of this. The 2nd study cited is not typical for you PB. An in-vitro study with a fairly weak conclusion.
"These data suggest that the accumulation of l-DOPA-containing proteins in vulnerable cells might negatively impact on cell function." (my emphsasis). And all of this based on test-tubes. And 12 years old. In the absence of anything in-vitro subsequently, I wouldn't rush to draw definitive conclusions.
As a levodopa user I would love to be able to disregard this study but not about to do so. They were guarded in their conclusions but they clearly found levodopa incorporated in proteins in the brains of levodopa treated patients where there should have been tyrosine. This cannot be good.
pb,
Should any concern be given to the differences in diet between Ghanaians, which is mostly starch and Italians which is the Mediterranean diet and therefore differences in their microbiota cause differences in absorption of levodopa should be taken into account in the sub-Saharan African study?
Since patients are individually titrated to their appropriate plasma levels of levodopa I'm inclined to think that such variations get calibrated out