Why should not we increase L-Dopa bioavai... - Cure Parkinson's

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Why should not we increase L-Dopa bioavailability in the Brain

Kia17 profile image
21 Replies

After watching this video you will find out why you shouldn’t manipulate the L Dopa bioavailability in the brain.

youtu.be/_eq28PCvfsg

You are trying to balance something but you will end up messing with the same thing, in this case the Dopamine.

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Kia17 profile image
Kia17
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21 Replies
Gioc profile image
Gioc

Very interesting , but what is solution ? Maybe I didn't understand it fully.

Kia17 profile image
Kia17 in reply to Gioc

With Fixing methylation.

reedboat2 profile image
reedboat2

I've seen other videos by Dr Rostenberg and generally like his approach. To simplify his message: PWP's need to de-tox not only from the substances that caused the inflammatory condition in our brains in the first place, but also from the L-Dopa we are taking to alleviate our symptoms. That's why supplements, diet, exercise, and stress-reducing lifestyle choices, (which are actually important for everyone), are absolutely crucial for us PWP's. One's health becomes a full time job. I'm not complaining about it. It's just how it is.

wriga profile image
wriga

I can't disagree with Dr Rostenburg. All these Metabolic pathways are known, but what is less known is which ones are dominant. With levodopa treatment, I agree that any overdose of levodopa or dopamine un the brain is bad for two reasons, 1) overdose stresses the synapses and causes dyskinesia, 2) we have to get rid of the waste products, the quinones that are oxidative reactants. That's why we need a stable supply of levodopa rather than a peak/trough supply which wastes much of the dopamine.

He's also right about antioxidants and anti-inflammatory agents in diet to mop up the waste products and protect the neurons. Not sure about St John's Wort though, it's a CYP3A4 inducer, so could also block levodopa getting into the blood.

Gioc profile image
Gioc in reply to wriga

Let's also consider two other things: peripheral levodopa and levodopa that goes beyond the BBB are two distinct cases. Thiamina is a powerful antioxidant for neuro cells.

ncbi.nlm.nih.gov/pmc/articl...

akgirlsrock profile image
akgirlsrock in reply to wriga

I think he uses st. Johns wort as a Mao B inhibitor

Kia17 profile image
Kia17

My dear friend Gio ,If you check my posts you will see information about methylation.

Gioc profile image
Gioc in reply to Kia17

Yep yep yep. I will do it. 🙏😊

Gioc profile image
Gioc in reply to Kia17

I am lazy these days, I was hoping for a summary in sequence with things to study and do. A small manual "read and do". I would find it interesting, an eBook that I would also be willing to pay. 👍

Kia17 profile image
Kia17 in reply to Gioc

Doing a simple Genetic testing with 23andme or AncestoryDNA is the first step to get your genome , then finding out which pathway of your methylation is blocked or not efficiently works then you can find a way to fix it.

Gioc profile image
Gioc in reply to Kia17

I will do.😊

I hate all this practical knowledge dispersed in the posts, you examine a small manual eBook on this topic not necessarily related to PD. You could write it in three days. 🙏

wriga profile image
wriga

Yes sure, but he's not aware of my research on levodopa and CYP3A4. Inducing CYP3A4 with St John's Wort is not a good idea.

LAJ12345 profile image
LAJ12345

Doesn’t carbidopa allow more l- dopa into the brain? By stopping it being converted in the blood? So is a smaller amount of l-dopa without carbidopa better than a larger amount with it?

Kia17 profile image
Kia17 in reply to LAJ12345

LAJ12345

It’s about the events after entering synthetic LDOPA or natural Dopamine in the brain.

LAJ12345 profile image
LAJ12345 in reply to Kia17

But by having carbidopa with the l dopa more gets into the brain meaning more dopamine in the brain. Without the carbidopa most converts in the blood and doesn’t get into the brain. So if we don’t want too much in the brain isn’t carbidopa making it worse?

I’m never sure if all of these enzymes work equally in the brain and outside of it or are they specific to different body parts?

LAJ12345 profile image
LAJ12345 in reply to Kia17

Is he saying we shouldn’t take any dopa supplements and work with what we have naturally?

Kia17 profile image
Kia17 in reply to LAJ12345

No, he doesn’t say that. He is discussing the imbalance of Dopamine in the brain and its consequences mostly due to SNPs in COMT , MAO and MTHFR.

Hikoi profile image
Hikoi in reply to LAJ12345

LAJ I dont follow your reasoning here. We want levadopa in the brain not in the periphery. so we want smaller amount with carbodopa rather than large amount without. Or have I misundersatood what you are writing?

LAJ12345 profile image
LAJ12345 in reply to Hikoi

Well the whole premise of this post is that we don’t want more l dopa availability in the brain isn’t it?

So I am saying if that is correct (and I don’t know if it is) does that mean any extra l dopa we make available to the brain by adding carbidopa to it (which stops it being converted in the blood) is not doing us any good? Of course not having the carbidopa means it isn’t available to the brain as the dopamine ends up in the blood so it doesn’t provide any benefit to symptoms. It is confusing. It sounds like it’s bad to allow more into the brain as it causes damage, but unless you do you’ll have the symptoms. And if it isn’t good to allow bioavailability in the brain is it good taking it at all? Maybe I have just misunderstood the whole thing!

I just read all the comments again. It seems like it is just better to make sure the bare minimum is taken with carbidopa and spread evenly over the day? That way there is no excess in the brain but none wasted by converting in the blood?

LAJ12345 profile image
LAJ12345

And if you have a fast mao a and mao b enzyme and fast COMT(lower dopamine) activity?Does that mean no dopamine sticks around long?

Kia17 profile image
Kia17

Having fast COMT or MAO means that you destroy the neurotransmitters faster.

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