Parkinson's disease: any Peat recommendations?

I am asking for a friend of a friend. I was told the person was trying acupuncture for relief but was seeing no benefit. My Peat-influenced thought was to stop something that wasn't yielding a benefit. I did a search this morning and didn't find a lot of Parkinson's and Peat. What do you think his recommendations would be? Thank you.

Lilac said:

I am asking for a friend of a friend. I was told the person was trying acupuncture for relief but was seeing no benefit. My Peat-influenced thought was to stop something that wasn't yielding a benefit. I did a search this morning and didn't find a lot of Parkinson's and Peat. What do you think his recommendations would be? Thank you.

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I would think that implementing the general dietary guidelines could only help. I also read in the email depository that Peat mentioned nicotine can be protective in people with a Parkinson's diagnosis. If this person is interested in trying nicotine the patch seems like the safest way to go. I will try to find the specific email I'm referring to.

I plugged " Parkinsons" in raypeat.com search engine and there are
29 articles mentioning Parkinsons. I clicked the first article and got this quote

Ray Peat said:

A disease or its treatment can obscure the presence of hypothyroidism. Parkinson's disease is a clear example of this. (Garcia-Moreno and Chacon, 2002: “... in the same way hypothyroidism can simulate Parkinson's disease, the latter can also conceal hypothyroidism.”) http://raypeat.com/articles/articles/hy ... dism.shtml

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It looks like it's sign of hypothyroidism.

Another quote on Parkinsons

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.http://raypeat.com/articles/articles/calcium.shtml

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Here is the quote from the email depository: Ray said

In old people, a little nicotine can have a balancing effect, improving alertness, and probably protecting nerves, for example in the negative association with Parkinson's disease.

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I'm not sure if that would help your friend but it's something to consider. I'm on a mobile device so I couldn't link but you can find the quote by searching the email depository for Parkinson's disease.

That email may just mean nicotine decreased the chances of developing Parkinson's disease not that it's helpful once someone has the condition. A Peat Inspired approach always helps though.

Thank you for the replies. I never noticed the search engine on Peat's site before. Duh.

Post by member Haidut might be of use to you as well: viewtopic.php?f=10&t=4260 and viewtopic.php?f=10&t=3467

You want to consider large amounts of coconut oil [ https://healthunlocked.com/parkinsonsmo ... ed-my-life ] gelatin and Noopept [ http://www.ncbi.nlm.nih.gov/m/pubmed/21986202/ ].

Lilac said:

...asking for a friend of a friend....

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Among other factors, Dr. Peat has mentioned iron deposition in Parkinson's disease.

Based on recent experience with close friends and family, in addition to basic and other Peat specific recommendations, I suggest exploring three supports mentioned by Dr. Peat in other contexts:
Pregnenolone
Thiamine
Theanine

Each of the three facors in anecdotal experience has reduced Parkinson's type symptoms, even apart from more full metabolic support as outlined by Dr. Peat. Various orthomolecular advocates mention the dopamine precursor tyrosine.
--
http://raypeat.com/articles/articles/iron-dangers.shtml
"Excess iron's role in infectious diseases is now well established, and many recent studies show that it is involved in degenerative brain diseases, such as Parkinson's, ALS (Lou Gehrig's disease), Huntington's chorea, and Alzheimer's disease. Iron is now believed to have a role in skin aging, atherosclerosis, and cataracts of the lenses of the eyes, largely through its formation of the 'age pigment.' "
---
http://www.ncbi.nlm.nih.gov/pubmed/21671084
J Mol Neurosci. 2012 Jan;46(1):177-83. doi: 10.1007/s12031-011-9570-y. Epub 2011 Jun 14.
Modifications of neuroactive steroid levels in an experimental model of nigrostriatal degeneration: potential relevance to the pathophysiology of Parkinson's disease.
Melcangi RC1, Caruso D, Levandis G, Abbiati F, Armentero MT, Blandini F.

"Among the neuroactive steroid levels assessed (i.e., pregnenolone, progesterone, dihydroprogesterone, tetrahydroprogesterone, isopregnanolone, testosterone, dihydrotestosterone, 3α-diol, dehydroepiandrosterone, 17α-estradiol, and 17β-estradiol), we observed a significant decrease of pregnenolone in the striatum. A similar effect was also observed on the levels of dihydroprogesterone present in this cerebral area and also in the cerebral cortex. Interestingly, an increase of isopregnanolone also occurred in the striatum and in the cerebral cortex."

http://www.ncbi.nlm.nih.gov/pubmed/18772319
J Pharmacol Exp Ther. 2008 Dec;327(3):840-5. doi: 10.1124/jpet.108.143958. Nanomolar concentrations of pregnenolone sulfate enhance striatal dopamine overflow in vivo.
Sadri-Vakili G1, Janis GC, Pierce RC, Gibbs TT, Farb DH.

"Pregnenolone sulfate (PS) is a neuroactive steroid that can modulate the activity of ionotropic glutamate and GABA(A) receptors either positively or negatively,....The results demonstrate that exogenous PS, at nanomolar concentrations, is able to increase DA overflow in the striatum through an NMDA receptor-mediated pathway."

J Neurol Sci. 2012 May 15;316(1-2):1-8. doi: 10.1016/j.jns.2012.02.008. Thiamine and Parkinson's disease. Lu'o'ng Kv1, Nguyên LT.

Parkinson's disease (PD) is the second most common form of neurodegeneration in the elderly population. PD is clinically characterized by tremors, rigidity, slowness of movement and postural imbalance. A significant association has been demonstrated between PD and low levels of thiamine in the serum, which suggests that elevated thiamine levels might provide protection against PD. Genetic studies have helped identify a number of factors that link thiamine to PD pathology, including the DJ-1 gene, excitatory amino acid transporters (EAATs), the α-ketoglutarate dehydrogenase complex (KGDHC), coenzyme Q10 (CoQ10 or ubiquinone), lipoamide dehydrogenase (LAD), chromosome 7, transcription factor p53, the renin-angiotensin system (RAS), heme oxygenase-1 (HO-1), and poly(ADP-ribose) polymerase-1 gene (PARP-1). Thiamine has also been implicated in PD through its effects on L-type voltage-sensitive calcium channels (L-VSCC), matrix metalloproteinases (MMPs), prostaglandins (PGs), cyclooxygenase-2 (COX-2), reactive oxygen species (ROS), and nitric oxide synthase (NOS). Recent studies highlight a possible relationship between thiamine and PD. Genetic studies provide opportunities to determine which proteins may link thiamine to PD pathology. Thiamine can also act through a number of non-genomic mechanisms that include protein expression, oxidative stress, inflammation, and cellular metabolism. Further studies are needed to determine the benefits of using thiamine as a treatment for PD.
PMID: 22385680

Innov Clin Neurosci. 2013 Apr;10(4):26-32.
Thiamine deficiency and delirium.
Osiezagha K1, Ali S, Freeman C, Barker NC, Jabeen S, Maitra S, Olagbemiro Y, Richie W, Bailey RK.
Abstract
Thiamine is an essential vitamin that plays an important role in cellular production of energy from ingested food and enhances normal neuronal actives. Deficiency of this vitamin leads to a very serious clinical condition known as delirium. Studies performed in the United States and other parts of the world have established the link between thiamine deficiency and delirium. This literature review examines the physiology, pathophysiology, predisposing factors, clinical manifestations (e.g., Wernicke's encephalopathy, Wernicke-Korsakoff syndrome, structural and functional brain injuries) and diagnosis of thiamine deficiency and delirium. Current treatment practices are also discussed that may improve patient outcome, which ultimately may result in a reduction in healthcare costs.

Amino Acids. 2009 Jan;36(1):21-7. doi: 10.1007/s00726-007-0020-7. Epub 2008 Jan 15.
Theanine, gamma-glutamylethylamide, a unique amino acid in tea leaves, modulates neurotransmitter concentrations in the brain striatum interstitium in conscious rats. Yamada T1, Terashima T, Kawano S, Furuno R, Okubo T, Juneja LR, Yokogoshi H.

http://www.ncbi.nlm.nih.gov/pubmed/18452993
Neurotoxicology. 2008 Jul;29(4):656-62. doi: 10.1016/j.neuro.2008.03.004. Epub 2008 Mar 20.
Protective effect of the green tea component, L-theanine on environmental toxins-induced neuronal cell death.
Cho HS1, Kim S, Lee SY, Park JA, Kim SJ, Chun HS.

"Several environmental neurotoxins and oxidative stress inducers are known to damage the nervous system and are considered major factors associated with the selective vulnerability of nigral dopaminergic neurons in Parkinson's disease (PD).....These results suggest that L-theanine directly provide neuroprotection against PD-related neurotoxicants and may be clinically useful for preventing PD symptoms."

As aguilaroja pointed about iron's role in Parkinsons, it would be a good idea to
measure total iron storage from Serum Ferritin and Transferrin saturation index.
RP mentioned that saturation index below 25 is protective against cancer.
Only serum iron level does not reflect total iron storage. Stored iron turns problematic in
hypothyroid people. A good thyroid function keeps stored iron's in safe mode.
Phlebotomy is used in lowering iron level .I do not know if there are side effect
from traditional iron lowering meds. Here is a thread on Iron Chelation
viewtopic.php?f=56&t=2384


Two more studies on high dose Thiamine treating PD. Thiamine reacts with iron.
One abstract did not give the size of the dose and another one used 100-200 mg. It would be very easy to convince someone to take a simple vitamin like B1 to treat PD
If possible measuring serum thiamine level can be helpful. Your friend can consult
with physician if it is safe to use high dose thiamine. Here is a quote from Linus Pauling
Institute page "Toxicity :The Food and Nutrition Board did not set a tolerable upper intake level (UL) for thiamin because there are no well-established toxic effects from consumption of excess thiamin in food or through long-term, oral supplementation (up to 200 mg/day). A small number of life-threatening anaphylactic reactions have been observed with large intravenous doses of thiamin (29)." http://lpi.oregonstate.edu/infocenter/vitamins/thiamin/

1. Only Abstract
High-dose thiamine as initial treatment for Parkinson's disease.
Costantini A1, Pala MI, Compagnoni L, Colangeli M.
Author information
Abstract

Parkinson's disease (PD) is a systemic disease with motor and non-motor deficits. We recruited three patients with newly diagnosed PD. They were not under anti-Parkinson's therapy. Plasmatic thiamine was within healthy reference range. We performed the Unified Parkinson's Disease Rating Scale (UPDRS) and started a parenteral therapy with high doses of thiamine. The therapy led to a considerable improvement in the motor part of the UPDRS ranging from 31.3% to 77.3%. From this clinical observation, it is reasonable to infer that a focal, severe thiamine deficiency due to a dysfunction of thiamine metabolism could cause a selective neuronal damage in the centres that are typically hit in this disease. Injection of high doses of thiamine was effective in reversing the symptoms, suggesting that the abnormalities in thiamine-dependent processes could be overcome by diffusion-mediated transport at supranormal thiamine concentrations.

http://www.ncbi.nlm.nih.gov/pubmed/23986125

2 Full-text Case Study

The Beneficial Role of Thiamine in Parkinson’s Disease:
Preliminary Report

Abstract
Parkinson’s disease (PD) is the second most common form of neuro-degeneration in the elderly population. PD is clinically characterized by tremors, rigidity, slowness of movement and postural imbalance. A significant association has been demonstrated between
PD and low levels of serum thiamine. Five PD patients presented
with stone face, right-hand tremors, Parkinsonian gait and bradykinesia with occasional freezing. Two patients presented with sialorrhea and the plasma transkelosase activity was low in one patient.All of the patients received 100 - 200 mg daily doses of parenteral thiamine. Within days of thiamine treatment, the patients had smiles on their faces, walked normally with longer steps, increased their arm swings, and experienced no tremors or sialorrhea. Three patients did not require carbidopa and levodopa without effects on their movements. Thiamine may benefit to PD. Further investigation of thiamine in PD patients is needed

http://www.neurores.org/index.php/neuro ... le/155/155

Mittir said:

...High-dose thiamine as initial treatment for Parkinson's disease.
Costantini A1, Pala MI, Compagnoni L, Colangeli M.
Author information
Abstract
... Injection of high doses of thiamine was effective in reversing the symptoms, suggesting that the abnormalities in thiamine-dependent processes could be overcome by diffusion-mediated transport at supranormal thiamine concentrations.

http://www.ncbi.nlm.nih.gov/pubmed/23986125....

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Thanks. Constantini has studied thiamine in several medical situations, with gratifying results. Oral Thiamine was used in many of these patients. If it were a pharmaceutical, imagine how relentless its marketing would be. I am not saying that enthusiasts here should all take thiamine, or use large doses. I am suggesting these findings further expands an open view of metabolism in disease.

http://www.ncbi.nlm.nih.gov/pubmed/24351023
J Altern Complement Med. 2014 Mar;20(3):208-11. doi: 10.1089/acm.2012.0612. Epub 2013 Sep 25.
Thiamine and Hashimoto's thyroiditis: a report of three cases.
Costantini A1, Pala MI.
"RESULTS: Treatment with thiamine led to partial or complete regression of the fatigue within a few hours or days.
CONCLUSION:
As the administration of thiamine led to a partial or complete regression of the fatigue and related disorders, it is reasonable to infer that the administration of large quantities of thiamine restores thiamine-dependent processes."

http://www.ncbi.nlm.nih.gov/pubmed/23379830
J Altern Complement Med. 2013 Aug;19(8):704-8. doi: 10.1089/acm.2011.0840. Epub 2013 Feb 4.
Thiamine and fatigue in inflammatory bowel diseases: an open-label pilot study.
Costantini A1, Pala MI.
"RESULTS: Ten patients out of twelve showed complete regression of fatigue, while the remaining two patients showed nearly complete regression of fatigue compared to the chronic fatigue syndrome scale scores before therapy.
CONCLUSIONS: The absence of blood thiamine deficiency and the efficacy of high-dose thiamine in our patients suggest that fatigue is the manifestation of a thiamine deficiency, likely due to a dysfunction of the active transport of thiamine inside the cells, or due to structural enzymatic abnormalities. The administration of large quantities of thiamine increases the concentration in the blood to levels in which the passive transport restores the normal glucose metabolism in all cells and leads to a complete regression of fatigue."

You know what, I haven't had one IBS attack since I've been giving blood. Meat was always a huge trigger. Mild anemia was always present regardless of ferritin levels. I don't know how long doctors will take to understand this.

Such_Saturation said:

post 54862 You know what, I haven't had one IBS attack since I've been giving blood. Meat was always a huge trigger. Mild anemia was always present regardless of ferritin levels. I don't know how long doctors will take to understand this.

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Are you still eating some liver?

First step would be to lower iron in the brain from continuing oxidation.

Parsifal said:

post 108937

Such_Saturation said:

post 54862 You know what, I haven't had one IBS attack since I've been giving blood. Meat was always a huge trigger. Mild anemia was always present regardless of ferritin levels. I don't know how long doctors will take to understand this.

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Are you still eating some liver?

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Yea I eat almost a pound a week now, because without small daily doses like Estroban you just need so much more for pimples. If you want to take methylene blue that only leaves space for about one meal a week.