Supplements For Parkinson Disease

Kasper

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Hi all,

My uncle is diagnosed with Parkinson, which is very bad news of course. It is good to finally understand what is going on, but the traditional outlook for Parkinson is not that good.

I think that he is not someone that will change his diet too radically (I can try of course), so that is why I post this in supplements. Are there any supplements that he could try out that may help Parkinson?

I heard Vitamin B1 may be beneficial. I also saw this in the Wikipedia of trehalose:

Trehalose induces autophagy via an mTOR independent pathway. It may have use for treatments of Huntington's disease, Parkinson disease or tauopathies, as it may correct defects in autophagy seen in these diseases and improve removal of these aggregated proteins.[18]

Not sure what this really means, I was just investigating trehalose today and I saw this.

Now he was really devastated to hear this, and according to the doctor, there is not much that can really cure Parkinson. I don't want to give him false hope, but what do you guys think, especially asking @haidut here, is there any hope with supplements and maybe making slight adjustments in his diet (like avoiding PUFA at least). He eats a typical dutch diet, with bread/animal food/vegetables/potatoes/milk and probably bad oils for cooking.
 
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tara

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As well as looking up threads here for various tactics, maybe check out lisuride? Antiserotonin drug often prescribed against Parkninsons.

Give his household a big tub of coconut oil ad encourage them to use it in place of any seed oils they have?
 

Matt1951

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Nicotine gum or patch?
The only things I know of that help Parkinson are coffee and tobacco. Nicotine is probably the right way to start, then consider one or two cigars a day. Reference the studies cited in the book "The Health Benefits of Tobacco" by Dr William Campbell Douglas MD.
 
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This Ayurvedic herb is used for Parkinson's in India with excellent results and no long-term side effects, it's a nootropic with a high percentage of L-Dopa... I think the dose for Parkinson's patients is higher than recommended in the link below, something close to 5 grams depending on the patient.

Mucuna Pruriens Side Effects | Powder City
 

Giraffe

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RP: It's known that aspirin prevents most of these degenerative conditions. People who have chronically used some aspirin are much less likely to have Parkinson's or Alzheimer's. And caffeine is another generally protective thing against inflammation, fibrosis and degeneration. And avoidance of the polyunsaturated fats I think is the basic and most important thing — and avoid the anti-thyroid foods. The worst anti-thyroid foods are these polyunsaturated fats.

Politics & Science: Autoimmune Diseases and Movement Disorders (2012) | Ray Peat Forum
 

haidut

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Hi all,

My uncle is diagnosed with Parkinson, which is very bad news of course. It is good to finally understand what is going on, but the traditional outlook for Parkinson is not that good.

I think that he is not someone that will change his diet too radically (I can try of course), so that is why I post this in supplements. Are there any supplements that he could try out that may help Parkinson?

I heard Vitamin B1 may be beneficial. I also saw this in the Wikipedia of trehalose:



Not sure what this really means, I was just investigating trehalose today and I saw this.

Now he was really devastated to hear this, and according to the doctor, there is not much that can really cure Parkinson. I don't want to give him false hope, but what do you guys think, especially asking @haidut here, is there any hope with supplements and maybe making slight adjustments in his diet (like avoiding PUFA at least). He eats a typical dutch diet, with bread/animal food/vegetables/potatoes/milk and probably bad oils for cooking.
Thiamine (b1) Reverses Parkinson Disease In Humans - Before/after Videos | Ray Peat Forum

Watch this short before and after movies. The improvements are tremendous and speak for themselves. I would try it with B1.
You can also write an email to Dr Costantini.


And here is the actual study:
Thiamine (B1) reverses Parkinson disease in humans | Ray Peat Forum
 

Peata

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"Increased intracellular calcium, in association with excess nitric oxide and excitatory amino acids, is involved in several neurodegenerative diseases, including ALS, Alzheimers disease, Parkinsons disease, Huntingtons chorea, and epilepsy. Magnesium, nicotine, progesterone, and many other substances are known to protect against excitotoxic calcium overload, but there is no coherent effort in the health professions to make rational use of the available knowledge." - Ray Peat

Calcium and Disease: Hypertension, organ calcification, & shock, vs. respiratory energy
 

DrAbs

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Hi, sorry about your grandfather. Polyamines such as spermidine hold promise as potential treatments for Parkinsons. Polyamines are found in high concentrations in peas and corn. Sarcosine aka n-methylglycine I've heard may be effective though has a quick half and would require frequent dosings. Vit k2 as well could be effective. Look into d-serine while your at it. I've read somewhere something like 30% of all ingested serine is converted to d-serine. Best of luck sir
 
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haidut

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"Increased intracellular calcium, in association with excess nitric oxide and excitatory amino acids, is involved in several neurodegenerative diseases, including ALS, Alzheimers disease, Parkinsons disease, Huntingtons chorea, and epilepsy. Magnesium, nicotine, progesterone, and many other substances are known to protect against excitotoxic calcium overload, but there is no coherent effort in the health professions to make rational use of the available knowledge." - Ray Peat

Calcium and Disease: Hypertension, organ calcification, & shock, vs. respiratory energy

This is actually really timely quote as I just read this study, which showed that NMDA antagonists like magnesium will lower NO and calcium overload and should be therapeutic for conditions like PD, AD, and even ALS.
Inflammatory mediators leading to protein misfolding and uncompetitive/fast off-rate drug therapy for neurodegenerative disorders. - PubMed - NCBI
"...Inflammatory mediators, including free radicals such as nitric oxide (NO) and reactive oxygen species (ROS), can contribute to neurodegenerative diseases in part by triggering protein misfolding. In this chapter, we will discuss a newly discovered pathway for this phenomenon and possible novel treatments. Excitotoxicity, defined as overstimulation of glutamate receptors, has been implicated in a final common pathway contributing to neuronal injury and death in a wide range of acute and chronic neurological disorders, ranging from Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), multiple sclerosis, and Alzheimer's disease (AD) to stroke and trauma. Excitotoxic cell death is due, at least in part, to excessive activation of N-methyl-d-aspartate (NMDA)-type glutamate receptors, leading to excessive Ca(2+) influx through the receptor's associated ion channel and subsequent free radical production, including NO and ROS. These free radicals can trigger a variety of injurious pathways, but newly discovered evidence suggests that some proteins are S-nitrosylated (transfer of NO to a critical thiol group), and this reaction can mimic the effect of rare genetic mutations. This posttranslational modification can contribute to protein misfolding, triggering neurodegenerative diseases. One such molecule affected is protein disulfide isomerase (PDI), an enzyme responsible for normal protein folding in the endoplasmic reticulum (ER). We found that when PDI is S-nitrosylation (forming SNO-PDI), the function of the enzyme is compromised, leading to misfolded proteins and contributing to neuronal cell injury and loss. Moreover, SNO-PDI occurs at pathological levels in several human diseases, including AD and PD. This discovery thus links protein misfolding to excitotoxicity and free radical formation in a number of neurodegenerative disorders. Another molecule whose S-nitrosylation can lead to abnormal protein accumulation is the E3 ubiquitin ligase, parkin, which contributes to the pathogenesis of PD. One way to ameliorate excessive NO production and hence abnormal S-nitrosylations would be to inhibit NMDA receptors. In fact, blockade of excessive NMDA receptor activity can in large measure protect neurons from this type of injury and death. However, inhibition of the NMDA receptor by high-affinity antagonists also blocks the receptor's normal function in synaptic transmission and leads to unacceptable side effects. For this reason, many NMDA receptor antagonists have disappointingly failed in advanced clinical trials. Our group was the first to demonstrate that gentle blockade of NMDA receptors by memantine, via a mechanism of uncompetitive open-channel block with a rapid "off-rate," can prevent this type of damage in a clinically efficacious manner without substantial side effects. For these Uncompetitive/Fast Off-rate therapeutics, we use the term "UFO drugs" because like Unidentified Flying Objects, they leave very quickly as soon as their job is finished. As a result, memantine blocks excessive NMDA receptor activity without disrupting normal activity. Memantine does this by preferentially entering the receptor-associated ion channel when it is excessively open, and, most importantly, when its off-rate from the channel is relatively fast so that it does not accumulate to interfere with normal synaptic transmission. Hence, memantine is clinically well tolerated, has been used in Europe for PD for many years, and recently passed multiple phase III trials for dementia, leading to its approval by the FDA and European Union for moderate-to-severe AD. Clinical studies of memantine for additional neurological disorders, including other dementias, neuropathic pain, and glaucoma, are underway. We have also developed a series of second-generation drugs that display greater neuroprotective properties than memantine. These second-generation drugs take advantage of the fact that the NMDA receptor has other modulatory sites, including critical thiol groups that are S-nitrosylated. In this case, in contrast to PDI or parkin, S-nitrosylation proves to be neuroprotective by decreasing excessive NMDA receptor activity. Targeted S-nitrosylation of the NMDA receptor can be achieved by coupling NO to memantine, yielding second-generation "UFO drugs" known as NitroMemantines."

So, once again, either Peat wrote that study or he is prescient (as usual) about stuff that is just being discovered.
 

DrAbs

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If I remember correctly Sarcosine is a reverse agonist at the nmda receptor glycine site. Polyamines are nmda receptor modulators and d-serine is the true ligand for the glycine site. Steroids like dhea and progesterone are also nmda modulators as are their sulfated counterparts.
 

haidut

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If I remember correctly Sarcosine is a reverse agonist at the nmda receptor glycine site. Polyamines are nmda receptor modulators and d-serine is the true ligand for the glycine site. Steroids like dhea and progesterone are also nmda modulators as are their sulfated counterparts.

The study says that it has to be a very specific type of NMDA antagonist = i.e. an "uncompetitive antagonist" to be precise. Magnesium and a few pharma drugs seems to fit this bill, but I am not sure about serine and the others even though any decrease of NO synthesis would be beneficial in theory.
NMDA receptor antagonist - Wikipedia, the free encyclopedia
 

DrAbs

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The study says that it has to be a very specific type of NMDA antagonist = i.e. an "uncompetitive antagonist" to be precise. Magnesium and a few pharma drugs seems to fit this bill, but I am not sure about serine and the others even though any decrease of NO synthesis would be beneficial in theory.
NMDA receptor antagonist - Wikipedia, the free encyclopedia

Some Nmda receptors are coupled to nitric oxide synthase in my eyes meaning that they are meant to release nitric oxide. Activation of this subtype of nmda coactivates NOS. http://www.nature.com/mp/journal/v4/n1/pdf/4000437a.pdf?origin=publication_detail
I suspect there is a natural means by which NO is dealt with before it can cause damage and in parkinsonian and other types of neurological disorders this function would be missing.(theory) I'd have to do more research. Some of the substances I mentioned previously would likely limit nitric oxide production by limiting nmda activity.
 

haidut

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Some Nmda receptors are coupled to nitric oxide synthase in my eyes meaning that they are meant to release nitric oxide. Activation of this subtype of nmda coactivates NOS. http://www.nature.com/mp/journal/v4/n1/pdf/4000437a.pdf?origin=publication_detail
I suspect there is a natural means by which NO is dealt with before it can cause damage and in parkinsonian and other types of neurological disorders this function would be missing.(theory) I'd have to do more research. Some of the substances I mentioned previously would likely limit nitric oxide production by limiting nmda activity.

One of the these natural NO deactivation mechanisms is cytochrome C oxidase (CCOX). CCOX levels are greatly diminished in pretty much all chronic conditions, and CCOX levels depend primarily on availability of T3. This links suboptimal thyroid status to pretty much all such degenerative conditions. Also, in a state of low thyroid function there would not be enough CO2 produced and as such NO levels will rise adaptively. NO and CO2 are antagonistic like pituitary and thyroid - i.e. the higher the activity levels of one the lower the activity/level of the other.
 

DaveFoster

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As a result, memantine blocks excessive NMDA receptor activity without disrupting normal activity. Memantine does this by preferentially entering the receptor-associated ion channel when it is excessively open, and, most importantly, when its off-rate from the channel is relatively fast so that it does not accumulate to interfere with normal synaptic transmission. Hence, memantine is clinically well tolerated, has been used in Europe for PD for many years, and recently passed multiple phase III trials for dementia, leading to its approval by the FDA and European Union for moderate-to-severe AD. Clinical studies of memantine for additional neurological disorders, including other dementias, neuropathic pain, and glaucoma, are underway. We have also developed a series of second-generation drugs that display greater neuroprotective properties than memantine. These second-generation drugs take advantage of the fact that the NMDA receptor has other modulatory sites, including critical thiol groups that are S-nitrosylated. In this case, in contrast to PDI or parkin, S-nitrosylation proves to be neuroprotective by decreasing excessive NMDA receptor activity. Targeted S-nitrosylation of the NMDA receptor can be achieved by coupling NO to memantine, yielding second-generation "UFO drugs" known as NitroMemantines."
By "coupling" I'd assume that this suppresses the activity of NO. I keep hearing great things about memantine; it's a shame it's so expensive.

Preventing neurodegeneration seems like the primary concern, but do you know of any ways to raise intelligence haidut? Peat talks about LSD's ability to accelerate learning, but I can't find very much on improving mathematical/logical intelligence.
 

DrAbs

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By "coupling" I'd assume that this suppresses the activity of NO. I keep hearing great things about memantine; it's a shame it's so expensive.

Preventing neurodegeneration seems like the primary concern, but do you know of any ways to raise intelligence haidut? Peat talks about LSD's ability to accelerate learning, but I can't find very much on improving mathematical/logical intelligence.
Coupling of nos and nmda means that activation of nmda increases nitric oxide. A cofactor of Nos is bh4 without which nos will release superoxide instead of NO, bh4 formation is in part regulated by the thyroid. Bh4 also is a cofactor in the formation of tyrosine which is necessary for producing t4 and t3.

Nmda activation increases learning and memory. D-aspartate increases dendrite formation. Polyamines which have a site on the nmda receptor helps prevent age related memory deficits.
 
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Kasper

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Thanks for all the posts and advices :D

Excitotoxicity, defined as overstimulation of glutamate receptors, has been implicated in a final common pathway contributing to neuronal injury and death in a wide range of acute and chronic neurological disorders, ranging from Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), multiple sclerosis, and Alzheimer's disease (AD) to stroke and trauma.

Isn't theanine preventing overstimulation of glutamate receptors as well? Could that be beneficial then in parkinson disease?

I will see my uncle next weekend, I think I will advise him to start with b-mix (energin) and extra b1, fat solubles (estroban), taurine, theanine, extra gelatin and maybe aspirin. Getting all vegetable and seed oils out of his house and replace it with coconut oil. I think that would be a good start to begin with.
 

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