This is PDWarrior ... i'm at a different computer
------------------------------
That's pretty DRAMATIC title to this post isn't?
And it may very well be ... TRUE.
Watch this video and you tell me...
------------------------------------------
only $5 million dollars will CURE ALL of US! - Cure Parkinson's
only $5 million dollars will CURE ALL of US!
Written by
NewGuywithPD
To view profiles and participate in discussions please or .
84 Replies
•
Not likely.
healthunlocked.com/cure-par...
so you changed your mind?
MBAnderson
7 days ago
Very interesting. He may be on to something. Good find Roo.
He was interviewed on "No Silver Bullet" last year.
I wanted to hear a fuller explanation of how his theory that we suffering from too much dopamine works, i.e., how inhibiting dopamine production stops the progression. (Maybe he explains that in the No Silver Bullet interview. I'll go back and listen to it again.)
Did you understand that?
I don't feel I endorsed his theory, but if you prefer, yes, I think he is wrong. He never does explain the mechanism - which I pointed out.
I confess, I do try to stay open minded, because conventional thinking has gotten us nothing so far.
Where does the dopamine that causes the progression come from?
If most of the dopamine producing neurons are dead or have shut down?
And that's a basic problem isn't it?
But I think what he is getting at is that there is a sort of a Goldilocks situation with dopamine, and if for some reason there is too much dopamine, with perhaps one kind of too much being if there is more dopamine than the vesicles can transport, then dopamine is stuck in the cell and while more dopamine is being made it amounts to too much dopamine accumulating in the cell, which poisons the cell and then that toxic effect kills off the dopamine producing capabilities of the cell and so now the cell produces not near enough because it's dead. Kind of like oversteer versus understeer in a car when you slide on the highway when it's too icy, you can overcorrect as well as under correct and both can happen to smash up your car. Well this happens with cocaine and amphetamine too and other stimulants... And by the way, dopamine is chemically a sister to epinephrine and norepinephrine, which used to be called adrenaline and noradrenaline, stimulants, all three being called the catecholamines, which is what is basically produced from tyrosine, which is dopamine's precursor. Tyrosine is processed by an enzyme, and that processing produces the three catecholamines, dopamine, adrenaline, and noradrenaline. AMPT inhibits the production of dopamine by defeating the enzyme that breaks down tyrosine in the sequence that converts tyrosine into the catecholamines, one of which is dopamine...thus reducing the production of dopamine. With this guy is suggesting is that too much dopamine can eat away at the dopamine producing cell if it isn't relieved by transporting the dopamine out of the cell through those vesicles. So when there's either too much dopamine or not enough vesicle power, dopamine is going to somehow accumulate without slowing down its production and eventually will damage the cell. That's his idea. And he gets the idea of AMPT because ampa settles down the stimulant effect of cocaine.
Like when you have perishable food so you put it in the refrigerator, but even in the refrigerator when it is very cold, eventually that food is transformed into toxins and byproducts by bacteria, it "goes bad." Then if you eat it you get sick. That's what he is suggesting could be going on with intracellular dopamine that doesn't get transported out of the cell by the vesicles, maybe the vesicles are impaired or there are too few vesicles or there is too much dopamine being produced. Either way, staying in the cell, the dopamine accumulates and there is something about the dopamine that eventually too much of it, or being in the cell too long, degrade something or damages something in the cell... makes the cell go bad, maybe like bacteria consumes all the nutrients in food while it's in the refrigerator, and after so long you don't have good food anymore, you have basically toxins, bacteria, dead bacteria, and bacteria poop, and maybe even some degradation of the cell wall or other cell functions.
I know, clear as mud. But it makes sense in terms of the chemistry and the idea is clear enough to be able to design experiments around it and test it pretty readily.
Absolutely facinatingthe guy is a legend what would we all give for 10 or15 years normality
but for someone 5 years plus diagnosis, with no dopamine supplementation (the era before sinemet pre 1971) where does this dopamine come from?
WTP: "where does this dopamine come from?"
Consider the (familial PD) case of duplication of the SNCA gene, which results in too much alpha-syn being produced. By strength of numbers, alpha-syn thus outcompetes dopamine for vesicular transport. Only some of the dopamine produced will thus make it into the vesicles, the rest will build up in the cytoplasm. Hence the (postmortem) observation that (these) PwP have more dopamine in the cytoplasm than (the average) non PwP.
Taking levodopa will result in more dopamine in the cytoplasm and thus more in the vesicles (i.e. by strength of numbers, dopamine now outcompetes alpha-syn for vesicular transport). The result is an improvement in symptoms but also an increase in toxicity.
EDIT: Just my 2 cents worth. Happy to be corrected.
Yes butBefore levadopa was available in 1971 people still had PD and it still progressed and so something else was responsible (and still is)
Ignore my 2nd paragraph. Just consider my 1st paragraph.
Yes, before 1971 it progressed, but their life span was shorter. Now the lifespan has lengthened with L-dopa. UP TO A POINT. Then all goes bad........So many try not to start medication, many try to use as low a dose as long as possible, and many when and if they feel better and symptoms are better cut the medication down. I have viewed his videos before and think he might have a point. I don't see a cure, but perhaps some alternative or different attitude toward how strong the prescription of L Dopa would need to be? Personally, in my brief exposure to PD (4 years - wife of PwP) I find more physicians not very well informed. Plus, I don't believe they read their medical journals either. Just my thoughts, very new to PD, always reading, always learning.
Great refrigerator analogy! Thanks!
Thank you so much MarionP for allowing everyone to understand what this means. You did a great job!!!
Now, can you go a little further and tell us what one can use in the meantime (til approval of his med)? Example, in my case, a little levodopa (25 mg) and I get terrible dystonia, no levodopa at all and I can’t move… I am sure you can come up with an alternative one could use instead of AMPT in the meanwhile.
Thanks, I wish I did know something, I thought like you did that "Gee then the next step would be... but what? I don't have the faintest clue." I just know what he said so I was able to put it in plain language. But I have no idea what kind of mechanisms or treatment or alterations, maybe he's got some inside track or maybe there were some other readers who are knowledgeable or readers who know doctors or like that to make suggestions. In which case I would like to know what to do in my own case as well. That's what he wants the money for, that's what it takes to start down the path, the formal clinical or experimental science path that is. But maybe in your case at least the obvious most glaring obvious and simple minded idea might be introduce L-dopa or its equivalent in a much slower or more gradual way, like drops or dribbles at a time instead of injections at a time or big dose of time. So somebody on our list here will learn more, because to tell you the truth I don't know jacks*** about L-dopa.
Anyway to continue on the principal of using lithium orotate as a substitute for prescribed lithium, that's what a lot of us who use the lithium orotate supplement do... You see lithium has been pretty standard treatment for bipolar depression, but it has to be prescribed, and the roots, doses, and probably mechanisms involved for some sensitive people it's like trying to drink from a fire hose instead of a garden hose. that's the principle behind the lithium orotate... Some of us either have a form of depression that response to lithium but lithium that you get for the doctor is too intense, too large, too bio-available, too fast, too extreme and we get terrible side effects like metallic taste to everything, which we can't tolerate for example. Well the orotate
supplement, is a much lower dose, and a much less bioavailable form, and may even have a mechanism that doesn't do what prescription lithium carbonate or prescription lithium does. Nobody really knows the mechanism of either lithium carbonate or lithium orotate. So it's a sort of clinical guessing by golly approach... LO is like I said probably much less bioavailable to cross the blood-brain barrier, and hello to some extent is taken up in adipose or fat tissue, which means even though it's a lower dose, that lower dose is still less available and may come out of that fat tissue and into your system slower and smaller, like a trickle, then the delivery of lithium carbonate that goes from your blood directly into your brain and is more intense available heavy blast dose. And that much smaller amount might contribute a little bit to somebody in the way of slight mood elevation but maybe helps put a floor on the person's mood disease even though it may not give a large boost it maybe a useful amount of help and does not trigger the high sensitivity of side effects or overwhelming effect. Ever hear of lithium water? I don't know where to get it and I have no idea if it's affordable and I have no idea if it's real or not, but same idea, to sensitive individuals it's maybe good for something.
But even in the lithium orotate for depression cases, it is an individual differences and individual response sort of situation and you have to purchase like that so you try some and see. But that means you're still having to walk through a whole lot of variables, like doses, time frames, between doses varying how long and how many days you try it, watching out for side effects and trying do more than one change at a time of that going into your body. Constantini with tell people his experience was with the one it might take months at high doses before you see some effect, and in the meantime you'd have to tolerate the B1 in terms of the side effects like agitation or skin problems or itching or flushing etc. So whatever you're trying maybe the same sort of long winding road.
Okay so that's the idea, now how does that apply to us with our parkinson's and parkinsonism? Well there are some dopa chemicals that kind of act in that way that lithium orotate might. People on our string might have better experience to talk about with those, two that I can think of are that fava bean extract mucuna, or maybe just cooking fava beans and having some of them (with a nice Chianti don't forget). And the sort of unrefined dopamine that is an oral supplement, mucuna pruriens, and last, I'm not sure but I think maybe L-Tyrosine maybe that some little bit of it gets through the blood-brain barrier.
Okay, well I guess it's three, not two. But as I used to say, there are three kinds of people in the world: those who can count and those who can't.
That would be on the input side, and the other end of the equation would be on the x breaking down Alto or dopamine inside your cells" side, what you have no idea what to try or what to try to do in order to either break down the bad excess dopamine or break it into components and flush them out of the cells, get the trash moving, maybe it has something to do with the dopamine or maybe it's some mechanism that is impaired that you can't flush properly the garbage out of yourselves, the eldopa or dopamine or bad dopamine precursors or bad dopamine byproducts out of your cells, that's the output and I have no idea and that will be with the sciences about. Or maybe it's something not in linear vision, like maybe something more to do with the Alzheimer's or other neurodegeneration generally diseases.
And maybe remember this is all talking about the input output mechanism of the l-dope picture, what if your problem is different entirely and maybe other people's experiences will help with you that aren't like this particular line of thinking. I have no clue whether maybe your particular symptoms are within the experience of somebody who's already solved that problem.
Maybe somebody here has some experience along that way of thinking or guessing or hypothesizing or having tried some things, I don't know. And a totally another direction might be try to make you less sensitive to the ldopa, maybe the answer is to start introducing B1 Anyway maybe somebody here has experience with L-tyrosine I used to have a bottle around somewhere but I just never got around to trying it.
Thank you so much for taking the time to answer. And thanks for the humor: ''there are three kinds of people in the world: those who can count and those who can't'' it is hilarious!
I also hope that those knowledgeable people on this forum (maybe Winnie the poo, or Hikoi, or anyone else, really...) that do know a lot about levodopa will manifest themselves with the beginning of a solution.
Meanwhile, I found this: but of course, i have no access to AMPT...
Low dose alpha-methyl-para-tyrosine (AMPT) in the treatment of dystonia and dyskinesia
Abstract
AMPT (alpha-methyl-para-tyrosine) is an inhibitor of tyrosine hydroxylase, the rate-limiting enzyme in dopamine biosynthesis. In clinical settings, AMPT is approved to treat pheochromocytoma. Dystonias and dyskinesias seem to have their origin in inconsistent regulation of dopamine function in dopamine pathways.
pubmed.ncbi.nlm.nih.gov/173....
As for exploring AMPT use to downregulate tyrosine hydroxylase activity to hinder catecholamine production, I'd think a better method would be to clear the built-up toxicity that prevents dopamine reuptake or norepinephrine conversion. When it comes to dopamine degradation, COMT and MAO enzyme inhibitors have been explored to improve dopamine in the synaptic cleft, so this seems contradictory to the proposed "too much dopamine" idea, as are the drugs that target DAT to prevent dopamine reuptake. So what's left is to try enhancing norepinephrine conversion to clear excess/toxic dopamine, but if you hinder the tyrosine hydroxylase enzyme through the use of AMPT, you may also affect subsequent norepinephrine conversion in the process while modulating all catecholamine. This doesn't seem to add up...in some ways, I can parallel the idea with the long-term toxic insulin effect in diabetes, but if your cells are running short on insulin due to cell toxicity that results in insulin resistance, preventing insulin production (that cells need to function) may cause more harm than addressing the core issue.
One potential idea worth investigating involves helping the conversion of dopamine to norepinephrine. This could be particularly relevant for addressing factors that might have initially contributed to sluggish enzyme activities, including tyrosine hydroxylase and the Dopamine-beta-hydroxylase enzyme responsible for converting dopamine to norepinephrine. Notably, these enzymes rely on copper as a cofactor. Lack of bioavailable copper (glyphosate chelates copper, iron toxicity hinders copper availability) and long-term disruptions in copper homeostasis can impact the activity of many copper-dependent enzymes and may have implications for neurotransmitter synthesis and needed conversions to clear built-up toxicity. As I've been mentioning repeatedly lately, I'd try improving measurable copper enzymes such as ceruloplasmin to improve overall copper bioavailability.
IMHO in summary, given the proposed idea, focusing on enhancing the conversion of dopamine to norepinephrine and addressing potential copper deficiencies might offer a more coherent strategy than inhibiting tyrosine hydroxylase with AMPT.
I had understood that i need to reduce norepinephrine not enhance it:
"enhancing the conversion of dopamine to norepinephrine and addressing potential copper deficiencies might offer a more coherent strategy than inhibiting tyrosine hydroxylase with AMPT
Yes, for PD treatment, the conventional prevailing idea is to improve the cell dopamine availability, which means you need to reduce norepinephrine conversion. This idea stands when you're already SHORT on dopamine, but not as Dr. Bernstein proposes for cell dopamine toxicity.
In the end, if either dopamine producing or dopamine clearing enzymes are not functional due to lack of crucial co-factors such as copper, B vitamins, or else, you're going to have an imbalance of either toxicity or deficiency from long-term disruptions in the enzyme homeostasis. .
I agree Rescuema,
From your post:
“In the end, if either dopamine producing or dopamine clearing enzymes are not functional due to lack of crucial co-factors such as copper, B vitamins, or else, you're going to have an imbalance of either toxicity or deficiency from long-term disruptions in the enzyme homeostasis. .”
In practice, supplementation with minerals containing zinc, copper, magnesium, vitamins C, B, and intramuscular thiamine injection as per the original HDT by Dr. C. This has kept my levodopa-induced dyskinesia at an acceptable level for ten years, despite the doses of levodopa considered medium/hight.
My opinion is that thiamine and levodopa are synergistic but accelerate diuresis and therefore the consumption of the mentioned minerals, which need to be supplemented in large amounts, including copper. Otherwise, in the absence of these minerals and vitamins, the body will undergo those toxic processes described above based on substances like manganese.
These are my personal experiences of PwP and opinions, and should not be taken as medical advice.
greeting from Italy
Alpi italiane
Yes, Gio. In order to get closer to a cure, we need to identify/address nutrient deficiencies or applicable toxicity affecting crucial co-factor availability, which unfortunately will differ per idiopathic PD patients. No silver-bullet repurposed drug hindering the natural NT mechanics will be the answer.
In reality I have simplified and abbreviated a lot but there is a lot of nutritional science done both on the general population and on animals, not mice.
I understand. While it's tough to pinpoint individual issues, supplementing certain beneficial and often deficient nutrients, such as thiamine and magnesium, might be a strategic approach when the potential benefits outweigh the risks to be worth trying blind. It gets trickier when we discuss certain minerals such as copper (high suspect), iron, and even manganese that are needed in precise trace amounts with needed co-factors, and if not end up being toxic if the bioavailability or the impaired enzyme functions, which also affects the detox of excess metals, are not addressed.
Here's a recent one that's easy to read, maybe:
cambridge.org/core/journals...
And for lovers of the “heavily scientific” genre another older one on the thiamine and copper manganese magnesium interactions , not humans ( made in japan):
jstage.jst.go.jp/article/ch...
They're good articles highlighting the importance and interactions of trace minerals and the deficiencies that contribute to impaired metabolic pathways dependent on these minerals. Lack of certain minerals can cause toxic displacement or stop the metabolic cogwheel from turning while accumulating other unused co-factors, including pyridoxine (needing methylation to turn into active P5P) or other toxicities affecting enzymatic functions. Unfortunately, popular supplements and multivitamin formulas can affect the delicate balance of nutrients that often oppose/block bioavailability. Copper, for example, easily gets blocked by excess iron, molybdenum, zinc, melatonin, ascorbic acid, niacin, curcumin, antioxidants, etc., etc. Separating the Cu intake with the needed co-factors while being cognizant of the opposing nutrients (including avoiding glyphosate) still required in certain ratios can make all the difference.
Just finished watching the posted video. At time stamp around 10:57, the Dr. touches on norepinephrine conversion, basically a double-edged sword for heart conditions he was more familiar with - "basically we were trying to do beta stimulation." The video mentions synaptic vesicles failing to gather the cytoplasmic dopamine, so again improving related enzyme activities, in this case, VMAT2 to improve the vesicular uptake/transport or the overall bio-mechanics neurotransmitter enzymes functions at the root cause seems more appropriate IMO.
Does this seem workable?
healthunlocked.com/cure-par...
Dr. Laurie Mischley made several videos talking about how citicoline increases the dopamine level in PD patients, which necessitated lowering of levodopa dosage to lower dyskinesia so this won't help in the context of "too much dopamine" theory while taking PD meds due to its dopaminergic agonist effect. However, in the absence of excess pharma l-dopa, citicoline does reduce toxic dopamine metabolites and help stabilize the dopamine and norepinephrine ratio along with other catecholamines, so I believe it acts as a methyl donor to help enzyme functions and may help with norepinephrine conversion and striatal dopamine release/turnover at less resource-starved/compromised state.
What I understood in layman terms was that Citicoline rebuilt the neuronal cell wall making them more efficient in releasing dopamine which means no more intracellular crowding of dopamine and no more neuronal death as a result
Let's discuss your recent post for what I mean.
healthunlocked.com/cure-par...
"This activation of tyrosine hydroxylase would lead to an inhibition of dopamine reuptake at the synapse, an action that has been shown in ex vivo studies"
In a resource starved state, ramping up the enzyme activity actually may result in inhibition of dopamine reuptake, meaning less clearing of toxic dopamine. This explains the dyskinesia experienced by many PD patients, which also stands against Dr. Bernstein's idea under discussion. However, I do think Citicoline is a beneficial supplement that helps stabilize NT functions as long as your enzyme functions are not compromised and competing for limited resource.
See my response.
Is copper even something one can use as a supplement? Because I really do not want to sacrifice my daily multi, it's worked so well for me in so many other ways I would hate to have to drop it. Is there a minimal copper supplement available? Or were you commenting about that one as the important illustrative example, but meaning there are multiple rabbit holes of other minerals etc that greatly complement (or complicate I guess) this delicate balance of many?
Hi Marion,
You can either eat copper-rich foods or supplement with copper bisglycinate. In order to precisely balance with zinc, I use the supplement although I may vary by day depending on my diet. You can find copper cheap pretty much anywhere. I'm currently using copper at 1:7 ratio with zinc in order to bring up my sodium to potassium ratio. Look at your multi label to see how much copper and zinc it contains, and then supplement copper in the morning away from the multi. For example, if your multi contains 1mg Cu and 10mg Zn, I'd start supplementing 2mg copper in the morning along with cod liver oil (for natural A and D), and then supplement extra 11 mg Zn with the multi in the pm for the target ratio. As your enzyme level recovers (serum ceruloplasmin), you want to titrate up copper depending on deficiency.
I'm no medico, nor am I bio-chem trained, but assuming (or in this case, endeavoring to find out IF) excess dopamine causes the PD progression may be as I think you wrote, that the artificially-added dopamine not being UTILIZED could be the problem causing a toxic accumulation which then kills off the dopamine-producing cells. Could it be death or injury of dopamine receptors?
Well, cells yes.
Receptors are a different target but possibly also could be modified, receptors are proteins on cells that when the proper chemical key is inserted a link in the protein opens ("depolarizes") a gap or gate in and out of a cell, like a door or "gate" or valve, through which the substance of interest passes or something else that is part of a reaction chain such as an electrolyte ion stream, or some other catalyst that starts a reaction, passes, and over time if there is a feedback mechanism then excess of that substance stimulates more of those gateway proteins to be produced and lack of that substance curtails the number of receptors on the cell surface... Changing number of receptors as referred to as regulation, as an upregulation and downregulation and regulation changes occur and accumulate over time if the amount of substance changed is persistent over time, because in essence the system has "deduced or determined" that the environment has changed with respect to that substance, and then the physical presence or number of the receptors changes in accordance, that's durable and possibly very resistant to subsequent changes. That's the basis of addiction for example, or when the drug that was once helpful seems to lose its effect and higher doses required to achieve the same effect. Sometimes if the cell is in a developmental stage then the location of the receptor can also move, causing a new illness when the substance goes to the proper location and the receptor isn't there to receive it... For example if a pregnant mother uses cannabis the baby's cannabinoid receptors may move, relocate to some other, wrong location on the child's cells and then become fixed there.
The drugs?
Which drugs? Pre 1971 there were no drugs. But PD kept progressing in people with very low dopamine (pwp} and not progressing in people with lots of dopamine (the rest of the population}
Sorry, didn’t read your comment properly. I guess the body makes it naturally still then. But it isn’t utilised properly.
No. The body doesn't make it naturally in PWP. In the first place we're talking about the brain not the rest of the body. Dopamine can't cross the BBB. 2nd pwp make much much much less dopamine than people who don't have PD, and yet the disease progressed in pwpSo maybe something other than toxic surplus dopamine is responsible
Maybe our esteemed cardiologist who has done NIL primary research but read a lot of articles has made a naieve error
Maybe that's why nobody wants to waste 5 million on him
I think it does initially make it but makes less and less as time and the condition progresses. It’s not like you are born with it not being made.
"pwp make much much much less dopamine than people who don't have PD"
Isn't that an assumption? i.e. they haven't measured it.
No
"This analysis reports that the dopamine levels inside these cells (called the cytosol) – the part of the brain cells where dopamine produces its toxicity – were higher than normal in the caudate and putamen of the brain in patients with advanced Parkinson’s disease. Prior to this publication by Sackner-Bernstein, the amount of dopamine inside these vital brain cells had never been reported."
linkedin.com/pulse/could-al...
And they were pre-1971?
Catch no ball. What does "they" refer to?
The pwp brains full of dopamine.
I'll have to get back to you. Some of JSB's references are from the 1960s.
what about this. (BBR= berberine,L-phenylalanine (Phe)). Presumably other compounds in various foods do similar?
nature.com/articles/s41392-...
“Discussion
BBR is an alkaloid that is poorly absorbed in the intestine,31,32,33,47 but it has been well documented by independent groups that oral administration of BBR showed therapeutic effects on energy metabolism and brain function in patients, as well as in animals,48 leaving us with a very interesting question in pharmacological research. We have recently discovered that BBR could stimulate synthetic pathways in gut microbiota to produce short-chain fatty acids, such as acetate, propionate, and butyrate, which steadily enter the blood and lower blood lipids and sugar.49 In continuing the searching for BBR-induced bioactive metabolites from gut microbiota, we discovered that the concentrations of Tyr, dopa, and dopamine significantly increased in the intestinal bacteria after exposure to BBR, while Phe decreased. The activity of TH and DDC in gut flora might play an important role in the mode of action of BBR…”
Hi, could you repost link about YOP and dr Mischley analysis for supplements. Thank you.
This is actually very very intriguing. I like the hypothesis it isvery much worth testing, definitely. Treatment with AMPT. Would have to be extremely careful when used with people who have co-occurring depression, that's going to take more careful exploration. I like it!
Excuse my ignorance is he saying too much or any levadopa can make you worse
He's saying too much dopamine . The stuff your own neurons make.
Sounds just like the mechanics of diabetes 😂
His theory as I understood it was this: the problem is not that we don't have or make dopamine, it's that we have plenty but it's not transported properly out of the neuron to be used. (If you think about it, DaT scans measure dopamine transport, not dopamine, BTW)
Anyway, dopamine IS toxic--or the breakdown products of dopamine are--I don't think anyone quibbles about that. So his point was, Here we are, flooding cells already stuffed with too much dopamine (that is useless since it can't get transported out where it needs to be to be useful) with more dopamine. And ultimately that kills the neuron.
He wants to stop adding dopamine to an already overstuffed cell and work on transporters instead.
I think
I read all your comments. ALL of you MISSED the point of my post.
Maybe he's right.
Maybe he's wrong.
All he needs is a LOUSY 5 million bucks to prove/ disprove his theory.
And he has to go around BEGGING for help.
(p.s. Thanks DEMOCRATS for allowing MILLIONS of ILLEGALS to INVADE and you're spending 100s of BILLIONS of dollars on these vermin while WE ... REAL AMERICANS ... are suffering from Parkinson when this highly credible doctor and brain researcher just needs a measly 5 ... million ... dollar.)
(p.p.s. Yeah I know I'm about to get bombarded by HATE. Piss off.)
People are not vermin. Please refrain from demeaning others. “Real Americans “? You mean native Americans, right? Those are the “real” ones. The rest of us are invaders and colonizers
The Moon Eyed people preceded, those who are referred to as native American. Unless you are disputing Cherokee history.
Mercifully the Atlantic and Pacific are both pretty substantial
Such a pathetic excuse for a human being! Let's ignore him and his hate!
The rest of us are invaders and colonizers
Dramatic! I just thought you were mostly dull people who happened to be born in the USA.
Que lastima que pienses así de los Ilegales, cuando esas personas se fueron a tu pais a trabajar en lo que tu y las personas que piensan como tu no lo hacen, que aguantan todos los desplantes de tipos como tu, que sin esos ilegales no tendrían mano de obra para sacar a tu país adelante, Sin embargo tu gobierno es el que no quiere destinar la cantidad de dinero para lograr encontrar cura a esta enfermedad, no le eches la culpa a los Ilegales.
Translated
What a pity that you think that way about Illegals, when those people went to your country to work in what you and the people who think like you do not do, who put up with all the rudeness of guys like you, who without those illegals would not have manpower to move your country forward. However, your government is the one that does not want to allocate the amount of money to find a cure for this disease, do not blame the Illegals.
Meanwhile--I TRIED his theory: took trytophan (which increases serotonin which in some completely complicated way depletes dopamine...supposedly) and felt miserable.
And I guess that made sense during the treatment, but I didn't miraculously feel better a few months later when I stopped the experiment, either.
Maybe I needed to do it for a year? Maybe it was nuts? I am a human guinea pig and take a million different things, plus eat a keto diet, so who knows?
Hi amykp,
I also wanted to try tryptophan, but then I realized that even if the theory is correct it would be inapplicable because as with levodopa you would still have to continually balance the drugs. He himself says that the problem is the dosage.
I use B3 niacin which addresses the deficiencies on this tryptophan line and others.
My basic idea is that the brain system is very complex structurally and a myriad of chemical processes take place in it, all balanced by membranes and various corpuscles that deal with acids , alkaloids , electric fields ,electronic flows of information and commands of some kind.
It is impossible to touch it without creating imbalances with consequences on function.
I think the only way is to remove what damages it, toxic substances like toxic alfasyn and superoxides, resolve the deficiencies and hope that it then has within itself (and it does) a self-repair mechanism.
Practically an anti-aging strategy.
For me is antioxidant, exercise, vitamins, good food and no stress whatever that means.
Greetings from Italy
Albero 🌲
Well, I wasn't taking levodopa at all, so that simplified it...sort of. I agree, from the way I felt, SOMETHING was out of balance! The brain is very complex. It would be nice if there was a simple answer, eh?
Italy looks very nice, nicer than muggy Florida at this time of year! As it happens, we are taking my mom to Rome in a week, but only for a few days. Then we embark on a cruise around the Mediterranean.
Very good!😊
There is a motto that unites all the peoples of the Mediterranean, "if you give them stones they build houses" and this is how you feel traveling around the Mediterranean:
at home.
With all the spiritual values that derive from this.
It's in the DNA 😁.
Happy cruising to all of you.🤗
Colosseo, lot of stones.🪨
I do know my husband has felt worse in the past when they increase the dose of L/C .
I do know he has a very fast running dopamine beta hydroxylase from his gene test which means that dopamine is very quickly burned through . So I have been trying to find a dopamine beta hydroxylase inhibitor that is natural so the dopamine lingers in there a bit longer before breaking down to the toxic biproduct.
Chatgpt says flavonoids. There are many of these in bright coloured foods.
He also has the same reaction to seratonin drugs.
Neurologist refuses to even engage on this one. Looks at me blankly.
** edit
I have just found this which I haven’t seen before
medchemexpress.com/Targets/...
Dopamine β-hydroxylase
Dopamine beta-hydroxylase; Dopamine beta-monooxygenase; Dopamine β-monooxygenase
Dopamine β-hydroxylase
Related Products
PDF 0.13 MB
Dopamine β-hydroxylase (Dopamine beta-hydroxylase, Dopamine beta-monooxygenase) is an enzyme that in humans is encoded by the DBH gene. Dopamine β-monooxygenase catalyzes the chemical reaction with 3 substrates of 3,4-dihydroxyphenethylamine, ascorbate, and O2, whereas its 3 products are noradrenaline, dehydroascorbate, and H2O. Dopamine β-hydroxylase belongs to the family of oxidoreductases, specifically those acting on paired donors, with O2 as oxidant and incorporation or reduction of oxygen. Dopamine β-hydroxylase participates in tyrosine metabolism. Dopamine β-hydroxylase has 3 cofactors: copper, PQQ, and Fumarate. Dopamine β-hydroxylase is in the catecholamine biosynthetic pathway. Dopamine β-hydroxylase has been shown to be associated with decision making and addictive behaviors such as alcohol and smoking, attention deficit hyperactivity disorder, and also with neurological diseases such as Schizophrenia and Alzheimer's.
Dopamine β-hydroxylase Related Products (12):
Cat. No. Product Name Effect Purity
HY-N0453
Hypericin Inhibitor ≥98.0%
Hypericin is a naturally occurring substance found in Hyperlcurn perforatum L. Hypericin is an inhibitor of PKC (protein kinase C), MAO (monoaminoxidase), dopamine-beta-hydroxylase, reverse transcriptase, telomerase and CYP (cytochrome P450). Hypericin shows antitumor, antiviral, antidepressive activities, and can induce apoptosis.
HY-128483
Fusaric acid Inhibitor 99.83%
Fusaric acid is a potent dopamine β-hydroxylase inhibitor.
HY-W115718
Cuprizone
Cuprizone is a copper chelating agent that forms a deep blue copper ketone complex with copper (II). The copper ketone reaction can be used in colorimetric tests for the presence of trace copper. Cuprizone can be used to induce some schizophrenia-like behavior in mice. Cuprizone acts on copper enzymes, including SOD1, cytochrome oxidase, and DβH, thereby causing oxidative stress and increasing DA levels in certain brain regions such as the medial prefrontal cortex (PFC).
HY-N7204
4-Hydroxyderricin Inhibitor 99.97%
4-Hydroxyderricin, the major active ingredients of Angelica keiskei Koidzumi, is a potent selective MAO-B (Monoamine oxidase inhibitors) inhibitor with an IC50 of 3.43 μM. 4-Hydroxyderricin also mildly inhibits DBH (dopamine β-hydroxylase) activity. 4-Hydroxyderricin has antidepressant activity.
HY-13289A
Nepicastat hydrochloride Inhibitor 99.48%
Nepicastat hydrochloride (SYN-117 hydrochloride) is a selective, potent, and orally active inhibitor of dopamine-beta-hydroxylase. Nepicastat hydrochloride produces concentration-dependent inhibition of bovine (IC50=8.5 nM) and human (IC50=9 nM) dopamine-beta-hydroxylase. Nepicastat hydrochloride can cross the blood-brain barrier (BBB).
HY-116158
Oosponol Inhibitor
Oosponol is a dopamine beta-hydroxylase inhibitor exhibiting hypotensive effects.Oospongol has strong antifungal activity against many antagonistic fungi.
HY-106004
Zamicastat Inhibitor ≥98.0%
Zamicastat (BIA 5-1058) is a dopamine β-hydroxylase (DBH) inhibitor and can cross the blood-brain barrier (BBB) to cause central as well as peripheral effects. Zamicastat is also a concentration-dependent dual P-gp and BCRP inhibitor with IC50 values of 73.8 μM and 17.0 μM, respectively. Zamicastat reduces high blood pressure.
HY-14838A
Etamicastat hydrochloride Inhibitor 98.14%
Etamicastat hydrochloride (BIA 5-453 hydrochloride) is a potent and reversible dopamine-β-hydroxylase (DBH) inhibitor with an IC50 value of 107 nM. Etamicastat can be used in the research of cardiovascular diseases.
HY-148001
EWP 815 Inhibitor 98.25%
EWP 815 is a disulfiram analogue, is a potent inhibitor of Ins(1,4)P2 phosphatase and Ins(1,4,5)P3 5-phosphatase. EWP 815 also inhibits enzyme dopamine β-hydroxylase activity.
HY-14838
Etamicastat Inhibitor
Etamicastat (BIA 5-453) is a potent and reversible dopamine-β-hydroxylase (DBH) inhibitor with an IC50 value of 107 nM. Etamicastat can be used in the research of cardiovascular diseases.
HY-13289
Nepicastat Inhibitor
Nepicastat (SYN117) is a selective, potent, and orally active inhibitor of dopamine-beta-hydroxylase. Nepicastat (SYN117) produces concentration-dependent inhibition of bovine (IC50=8.5 nM) and human (IC50=9 nM) dopamine-beta-hydroxylase. Nepicastat (SYN117) can cross the blood-brain barrier (BBB).
HY-100796
Guanoclor Inhibitor
Guanoclor is an antihypertensive compound. Guanoclor is an adrenergic neurone-blocking agent, which also interferes with noradrenaline synthesis by inhibition of the enzyme dopamine beta-hydroxylase.
That's really interesting, and I think I might be experiencing this myself. I was diagnosed with PD five years ago, at 55. Started taking Levadopa and experienced the honeymoon phase for about 12 months. After that, my disease progression seemed to accelerate, so I was taking even more Levadopa. Eventually, I was taking 2000mg a day.However, my PD diagnosis was questioned about 12 months ago when I experienced a particularly stressful situation and took powerful pain killers to deal with the physical fallout. For a couple of weeks I had better movement control, virtually no off times, and less symptoms overall. My neurologist examined me and began to question his diagnosis. We started to slowly reduce the Levadopa to test the theory. I'm currently taking 500mg a day, and while the first couple of days after each reduction can be difficult, my body seems to adjust fairly quickly. I have less symptoms now on 500mg than when I was taking 2000mg, so in theory, my body is doing what the doctor suggests in the video. I have another visit with my neurologist in a month, by which time I will only be taking 400mg, so it will be interesting to assess then.
Hello,I just read your post and I think I have a similar problem minus the honeymoon phase which I never experienced.
I started taking 500 mg per day Levodopa and a small dose of Pramipexole. In a year Pramipexole was replaced by Rotigotine transdermal patches (the maximum dose I received was 10 mg per 24 h). During this time I had to increase the dose of Levodopa to cope with the negative symptoms caused by the patch, thus reaching 1000 mg Levodopa per day. My condition worsened so I started reducing the Madopar and felt better (and almost complete eliminated the patches).
However, I'm experiencing severe withdrawal episodes (arrhythmia, whole-body shaking that is so bad that I can't get up, and a total paralysis when I can't make any voluntary movement) when I try to reduce the Madopar.
I was wondering if you have any withdrawal symptoms and how you managed them.
Any advice would be highly appreciated.
Well mjf foundation certainly has that kind of money sitting around, or at least the equivalent of what the funding stream would have to be in order to ramp into it. So one wonders whether they would be interested, although perhaps not this particular guy or doing it his way... Unless he is also looking to patent something and make it his legacy... There are certainly enough billionaires around in the world now, including mega billionaires, families with that kind of money and more, foundations with that kind of money and more... Venture capital firms. $5M is petty cash to them, a rounding error... Maybe some of them even have friends or family or members with PD.
Maybe it is a question of delivering a dopamine β-hydroxylase (the enzyme that breaks down dopamine) to the right location. And also not to the wrong location. There is also a question of whether what is desired is less dopamine, or instead quicker degradation of dopamine, or instead changing the byproduct that is toxic into a less toxic substance, or instead perhaps finding way to transport and evacuate the excess dopamine out of the cell by replacing or redeveloping the vesicles in the cell that are tasked with moving the dopamine out of the cell and into the synapse. And maybe these are each separate questions for separate individuals' problems or needs.
We already know for example that too much dopamine, "too much" being a very relative term (because the individual case may not be too much dopamine, it just may be dopamine in the wrong place, or too much toxic degradation byproduct, failure to transport it away from where it is produced or stored which can't tolerate it for too long, and instead transported to where it needs to be so it is properly effective and consumed (or broken down where it should be broken down and toxic byproducts in turn metabolically eliminated)...
Anyway where I started going with my example is: an example is that we know too much dopamine results in psychotic like behavior, and too little dopamine results in severe depressive and catatonic-like behavior since dopamine is involved in several things, perhaps many things, it is a widely distributed chemical messenger playing a number of roles around the body. You get the point that there are a lot of assumptions and variables that might need to be involved in order to establish facts and work their way through the hypotheses.
No just doing something clinically in the meantime is more simple, provided people are willing to take the risks. Just try a bunch of things and see what works and doesn't work, ad nauseum.
That was an amazing video. I whole heartedly agree that dopamine at high dose is toxic. I treat my parkinson symptoms with a homemade fava bean pod tincture only when they arise. (and only take the most minimal amount possible to aleviate symptoms. Food is medicine to me. I watch my friends with PD going downhill taking drugs when I have had no side effects from fava beans. It would be nice to be able to get in touch with this doctor and share my journey with him. Nice to hear someone else talk about how the dopamine supplements are not the answer. Thank you for posting this. Sandra (Aunt Bean)
Hope you don’t mind a few questions. I have seen your posts over the years but feel I know very little about you. How were you diagnosed Fava -1 and by whom? Have you ever had your diagnosis questioned and do you take any conventional medicines.?
I was diagnosed by general family MD. My PD is hereditary. My father, his father, my grandfather's brother , my brother, several cousins all had PD. Many of my symptoms were at a very young age. All of them were alleviated from using natural ldopa from both fava beans and mucuna puriens. No, I have never taken pharmaceuticals for PD. So far I am able to subdue symptoms . God is so good.
If he is sugesting inhibiting tyrosine hydroxylase then the result would be tyrosine hydroxylase deficiency, wouldn't it? But if that is the case then what about this? medlineplus.gov/genetics/co...
"Meanwhile--I TRIED his theory: took trytophan (which increases serotonin which in some completely complicated way depletes dopamine...supposedly) and felt miserable..."
How does taking tryptophan reduce serotonin? My understanding is dopamine is produced and stored in vesicles and released into the cytosol as needed. The basic argument is whether dopamine excess/deficiency causes PD? Necropsy studies show elevated dopamine in the brain?
Not what you're looking for?
You may also like...
If you had 10 million dollars to spend on your Parkinson's treatment...
If you had $ 10 million to spend on your Parkinson's treatment, what specifically would you spend it
Is a cure for Parkinson’s disease hiding inside us?
025-1
Previous post on LL-37 .
https://healthunlocked.com/cure-parkinsons/posts/146412914/ll-37-a
Photomodulation - which device would you choose?
would you pick based on the wavelength and price? Have you tried any of these devices? Do you think...
Supplements to Stop Before Holmium Laser Enucleation of the Prostate (HoLEP) Surgery
one explain that to me, why stop B complex?
Thank you!
ELON MUSK gets FDA approval for 'BRAIN CHIP' to treat PD and other neuro conditions!
Parkinson’s, dementia and Alzheimer’s.\\"...
Related Posts
Is the \"tetrahydrofurfury disulfide in (TTFD)\" a B1 with a \"DMSO\" attached?
I make trying to suppress EBV a leg of my supplement strategy.
How significant is the strain in bacillus subtilis PXN21?- Patients with Parkinson’s disease (PD) report a strong craving for sweets
Had To Come Off All Meds and Supplements 5 Days
