So I was bouncing around and found this article: Palmitoylethanolamide/Luteolin as Adjuvant Therapy to Improve an Unusual Case of Camptocormia in a Patient with Parkinson’s Disease: A Case Report 2021 ncbi.nlm.nih.gov/labs/pmc/a... This is a single case report about a fairly unusual condition related to PD and did not hold my attention.
But then I stumbled upon: Randomized clinical trial "olfactory dysfunction after COVID-19: olfactory rehabilitation therapy vs. intervention treatment with Palmitoylethanolamide and Luteolin" 2021 pubmed.ncbi.nlm.nih.gov/341... and this showed the combination of Palmitoylethanolamide and Luteolin improved the sense of smell in people who had COVID, and it worked better the longer their sense of smell had been diminished.
So... It treats Camptocormia in a patient with PD AND rehabilitates the olfactory system. Let's search on "Palmitoylethanolamide" + "Parkinson's":
Ultra-micronized Palmitoylethanolamide: An Efficacious Adjuvant Therapy for Parkinson's Disease pubmed.ncbi.nlm.nih.gov/283...
" Background: Parkinson's disease (PD) is the subject of intense efforts to develop strategies that slow down or stop disease progression and disability. Substantial evidence points to a prominent role for neuroinflammation in the underlying dopaminergic cell death. Ultramicronized palmitoylethanolamide (um-PEA) is well-known for its ability to promote the resolution of neuroinflammation and exert neuroprotection. This study was designed to assess the efficacy of um-PEA as adjuvant therapy in patients with advanced PD.
Method: Thirty PD patients receiving levodopa were included in the study. The revised- Movement Disorder Society/Unified Parkinson's Disease Rating Scale (MDS-UPDRS) questionnaire was used to assess motor and non-motor symptoms. Clinical assessments were carried out before and after addition of um-PEA (600 mg). MDS-UPDRS questionnaire total score for parts I, II, III, and IV was analyzed using the Generalized Linear Mixed Model, followed by the Wilcoxon signed-rank test to evaluate the difference of each item's mean score between baseline and end of um-PEA treatment.
Results: Addition of um-PEA to PD patients receiving levodopa therapy elicited a significant and progressive reduction in the total MDS-UPDRS score (parts I, II, III and IV). For each item, the mean score difference between baseline and end of um-PEA treatment showed a significant reduction in most nonmotor and motor symptoms. The number of patients with symptoms at basal was reduced after one year of um-PEA treatment. None of the participants reported side effects attributable to the addition of um-PEA.
Conclusion: um-PEA slowed down disease progression and disability in PD patients, suggesting that um-PEA may be an efficacious adjuvant therapy for PD. "
Seems like kind of a big deal.
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Bolt_Upright
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"In this study, 30 Parkinson’s patients averaging 73 years of age received 1,200 mg a day of Normast for three months, along with Levadopa (L-DOPA) and other Parkinson’s medications in some cases, and then given 600 mg daily for up to a year.
Researchers used the Motor Disease Society Unified Parkinson’s Disease Rating Scale (MDS-UPDRS) to evaluate motor and non-motor symptoms of Parkinson’s in their patients. The MDS-UPDRS questionnaire covers four sections: nonmotor aspects of daily living experience, motor aspects of daily living experience, motor examination and motor complications.
After 12 months, non-motor symptoms scores, using the Non-Motor Aspects of Experiences of Daily Living scale, had fallen from 9.7 to 4.5 in patients receiving Normast and Levadopa (L-DOPA). The average score on the Motor Aspects of Experiences of Daily Living scale dropped from 12.7 to 7.6 over the one-year period, while the average total motor complication score dropped from 8.8 to 4.2. Normast caused no side effects."
So... that is 1,200 X 90 = 108,000 mg + 600 X 365 = 219,000 mg, = 327,000 mg = 327 grams!
If you Google Ultra-micronized Palmitoylethanolamide you will find you can get 250 grams for only $140.
I have a High School degree and am prone to making mistakes. Please do your own research.
It's like you were looking over my shoulder 😂 bought PEA too. What I just learned is there is an inverse relationship between acetylcholine and catecholamines.
Acetylcholine excess depresses the catacholamines, epinephrine, norepinephrine and dopamine. (Catecholamines act both as neurotransmitters and hormones vital to the maintenance of homeostasis through the autonomic nervous system.)
When I tested my catecholamines, dopamine was below the limit of detection. My DaTscan didn't show substantia nigra degeneration. The problem, for me anyway, is upstream in the hypothalamus. This is the origin of autonomic dysfunction. How do we heal the hypothalamus?! Heal the gut? Supplements at the top of my list are Chromium and Biotin.
I'm retesting neurotransmitters first and if it's determined that I have acetylcholine excess (likely) then I want to increase acetylcholinesterase and correct the deficiency (likely) of the enzyme that breaks down acetylcholine. I am considering Betaine Hcl supplementation.
I strongly believe that degeneration of the SN is an effect of higher order brain injury of the hypothalamus leading to parkinsonism. Haven't seen these studies.
A little off track, wasn't there a discussion on shoulder pain and PD? It's one of the areas Mayo Clinic identified for pain in fibromyalgia 🤔
"Just to be clear: Everything after "I bought PEA too" was unrelated to PEA?"
Sorry if I was unclear. It's related. Palmitoylethanolamide (PEA) boosts catecholamines similar to Ritalin and Adderall without being addictive. But, if the cause of the low catecholamines is excess acetylcholine then it should be addressed first.
Citicholine is used for Parkinson’s. I can’t find if you can take citicholine and anticholergenic drugs like procyclidine , a PD drug together . Do they counteract each other ? And how does that relate to acetylcholine?
I think you should talk to your doctor about how citicholine might interact with procyclidine. Seems logical to me that citicholine would counteract the effect of an anticholinergic.
Anticholinergics block the neurotransmitter acetylcholine.
Acetylcholine is so important and is said to be Neuroprotective. Yet anticholinergics are said to have some neuro protection. What am I missing here? I’m assuming it’s a matter of finding the delicate balance? I feel like I’m throwing darts in the dark sometimes.
It depends on the diagnosis. "The etiology and pathogenesis of these NDDs are complex and unique for each disease." Acetylcholine excess is treated with anticholinergics, but over time they increase dementia risk. A 2019 study found a link between dementia and several classes of anticholinergics used to treat depression, schizophrenia, bipolar disorder, seizures, Parkinson's disease, and overactive bladder. health.harvard.edu/mind-and...
I tested my catecholamines a few years ago, they were very low - esp dopamine. I had no idea what caused this. I just learned that excess acetylcholine depresses catecholamines. I want to know my status before supplementing.
If you feel better on citicholine, then that's probably your answer. I just want more information before deciding.
This is the test I'm doing now. I'm especially interested in my acetylcholine, glutamate, GABA, kyneurenic acid and oxytocin levels. nutritionallyyourstestkits....
There is a recommendation. Dosage: PEA is proposed for use at a daily dose range of 400 mg/day to 800 mg/day. Typical use is expected to be a starting dose of up to 400 mg BID for 3 - 4 days and a maintenance dose of 300 mg BID for up to 1 year.
Let's just look at the abstract and selected heading titles in this document: Palmitoylethanolamide: A Natural Compound for Health Management 2021 mdpi.com/1422-0067/22/10/53...
Abstract
All nations which have undergone a nutrition transition have experienced increased frequency and falling latency of chronic degenerative diseases, which are largely driven by chronic inflammatory stress. Dietary supplementation is a valid strategy to reduce the risk and severity of such disorders. Palmitoylethanolamide (PEA) is an endocannabinoid-like lipid mediator with extensively documented anti-inflammatory, analgesic, antimicrobial, immunomodulatory and neuroprotective effects. It is well tolerated and devoid of side effects in animals and humans. PEA’s actions on multiple molecular targets while modulating multiple inflammatory mediators provide therapeutic benefits in many applications, including immunity, brain health, allergy, pain modulation, joint health, sleep and recovery. PEA’s poor oral bioavailability, a major obstacle in early research, has been overcome by advanced delivery systems now licensed as food supplements. This review summarizes the functionality of PEA, supporting its use as an important dietary supplement for lifestyle management.
2. PEA and Immunity
2.1. PEA’s Antiviral Activities
2.2. PEA’s Antibacterial Activities
2.3. PEA’s Modulation of Gut-Derived Immunity
2.4. Future Directions of PEA’s Role as An Immunomodulator
3. PEA and Inflammatory Reactions
4. PEA and Brain Health
4.1. PEA’s Neuroprotective Effects
4.2. PEA’s Effects on Mood, Cognition and Behavior
4.3. PEA’s Modulation of the Gut–Brain Axis
5. PEA and Pain
5.1. PEA’s Effects on Primary Headache
5.2. PEA’s Effects on Menstrual Pain
6. PEA and Joint Health
7. PEA and Exercise Recovery
8. PEA and Sleep
9. Overcoming Challenges in PEA’s Bioavailability (make sure you get ultra-micronized)
Conflicts of Interest
M.H., N.B. and S.S. are employed by Gencor Pacific, who own the patented PEA formulations, Levagen® and Levagen®+. R.V. has personal relations to one of the members of Gencor Pacific. There is no other conflict of interest involved.
Palmitoylethanolamide: A Nutritional Approach to Keep Neuroinflammation within Physiological Boundaries—A Systematic Review 2020 mdpi.com/1422-0067/21/24/95...
" 3.1. Parkinson’s Disease
Under physiological conditions, non-neuronal cells like microglia and astrocytes support the well-being and well-function of the brain through diverse functions, including neurotrophic factor secretion. On the contrary, in the course of Parkinson’s disease (PD) a shift from neuroprotective to neuroinflammatory phenotype occurs and the non-neuronal cells sustain disease onset and progression [157,158,159]. The efficacy of PEA in controlling neuroinflammation-associated neurodegeneration has been demonstrated in an animal model of PD induced by 1-methyl-4-phenyl-1 2 3 6-tetrahydropyridine (MPTP). Chronic treatment with PEA (10 mg/kg for 7 days) protected against MPTP-induced loss of tyrosine hydroxylase neurons, reduced MPTP-induced microglial activation and the number of glial fibrillary acidic protein (GFAP)-positive astrocytes [84]. Moreover, PEA exerted a positive effect on the cognitive and motor deficits, which was shown to be mediated at least in part by PPAR-α receptor [84]. A formulation containing PEA co-ultra-micronized with luteolin (co-ultraPEA-Lut) has been investigated in the same animal model of PD. The administration of co-ultraPEA-Lut (for 7 days at 1 mg/kg dose) re-established the normal expression of the enzyme tyrosine hydroxylase, and most importantly, reduced the increased expression of GFAP (a marker of astrocyte activation), inducible nitric oxide synthase (iNOS), and pro-inflammatory cytokines in the brain [85]. In a further study performed on MPTP-induced PD in aged mice, chronic pre-treatment with PEA-m (10 mg/kg for 60 days) was found to counteract the behavioral deficits, the reduced expression of tyrosine hydroxylase and dopamine transporter, as well as the up-regulation of α-synuclein and β3-tubulin in the substantia nigra [80]. Importantly, PEA-m also reduced the expression of pro-inflammatory cytokines and showed a pro-neurogenic effect in the hippocampus [80]. A different animal model of PD was also used to investigate the protective effect of PEA against PD-associated neuroinflammation. In particular, the disease was induced by 6-hydroxydopamine (6-OHDA) and PEA was administered at 3, 10, or 30 mg/kg for 28 days [86]. Results showed that PEA was able to (i) improve 6-OHDA-induced behavioral impairments, (ii) increase tyrosine hydroxylase expression, (iii) exert an anti-apoptotic effect and, most importantly, (iv) reduce oxidative stress and neuroinflammation (i.e., reduced iNOS and cyclooxygenase-2 (COX-2) expression) [86]. The observed effects were PPAR-α receptor-mediated [86]. These pre-clinical studies suggest that PEA-m and PEA-um (alone or in association with Luteolin) are effective in improving PD motor function through mechanisms aimed at controlling neuroinflammation and protecting neurons. Accordingly, the clinical utility of FSMP containing PEA-m has been evaluated in a study conducted on 30 patients affected by PD [87]. Add-on oral administration of PEA-um (3 months at 600 mg/bid followed by 600 mg/die for 12 months) to PD patients receiving levodopa therapy produced a significant and progressive reduction in the total Movement Disorder Society/Unified Parkinson’s Disease Rating Scale (MDS-UPDRS) score (parts I, II, III, and IV) [87]. In other words, oral supplementation with PEA-um slowed down the disease progression and disability scores, and proved to be a valuable add-on option in PD patients [87]."
Palmitoylethanolamide as adjunctive therapy in major depressive disorder: A double-blind, randomized and placebo-controlled trial 2018 sciencedirect.com/science/a...
• We assessed the safety and efficacy of PEA on depressive symptoms of patients MDD.
• Over 6 weeks, patients who received PEA showed significant and rapid-onset improvement in Ham-D scores.
• Treatment with PEA seems to be well tolerated with no serious adverse event.
Palmitoylethanolamide Modulates GPR55 Receptor Signaling in the Ventral Hippocampus to Regulate Mesolimbic Dopamine Activity, Social Interaction, and Memory Processing 2017 liebertpub.com/doi/10.1089/...
Targeting CB 1 and GPR55 Endocannabinoid Receptors as a Potential Neuroprotective Approach for Parkinson's Disease 2019pubmed.ncbi.nlm.nih.gov/306...
Palmitoylethanolamide (P.E.A.) and the Microbiome (please watch the entire video, I just set it to start at the Microbiome portion): youtu.be/dGhh8oAJONE?t=2681
Bolt, It does seem amazing. Thank you for finding this!! I’ve learned to temper my enthusiasm but so far I’m not finding any negatives other than that it is peculiar that it is so obscure
Yes. In that long video I posted they said the studies were published in Italian and they went under the radar. It seems crazy, I know. They actually said "slows progression" in the report. I am still looking for the best product.
Bolt thank you thank you thank you for your determination and tenacity. And
It appears you
Found a good one!!!
I found one tonight that I’m going to try. I almost never order something I have just found but the one I just posted about had me at “reduced insomnia and anxiety”
That PD study was not double blind. I don't have time to sort through these now, but I collected a lot of papers on this yesterday if you are interested:
Ultra-micronized Palmitoylethanolamide: An Efficacious Adjuvant Therapy for Parkinson's Disease pubmed.ncbi.nlm.nih.gov/283...
Palmitoylethanolamide/Luteolin as Adjuvant Therapy to Improve an Unusual Case of Camptocormia in a Patient with Parkinson’s Disease: A Case Report ncbi.nlm.nih.gov/pmc/articl...
Randomized clinical trial “olfactory dysfunction after COVID-19: olfactory rehabilitation therapy vs. intervention treatment with Palmitoylethanolamide and Luteolin”: preliminary results europeanreview.org/article/...
Palmitoylethanolamide: A Nutritional Approach to Keep Neuroinflammation within Physiological Boundaries—A Systematic Review mdpi.com/1422-0067/21/24/95...
Palmitoylethanolamide as adjunctive therapy in major depressive disorder: A double-blind, randomized and placebo-controlled trial sciencedirect.com/science/a...
Palmitoylethanolamide Modulates GPR55 Receptor Signaling in the Ventral Hippocampus to Regulate Mesolimbic Dopamine Activity, Social Interaction, and Memory Processing liebertpub.com/doi/10.1089/...
Targeting CB 1 and GPR55 Endocannabinoid Receptors as a Potential Neuroprotective Approach for Parkinson's Disease pubmed.ncbi.nlm.nih.gov/306...
The anti-inflammatory effect of bacterial short chain fatty acids is partially mediated by endocannabinoids tandfonline.com/doi/full/10...
Ultramicronized palmitoylethanolamide reduces inflammation an a Th1-mediated model of colitis journals.sagepub.com/doi/10...
Effect of Palmitoylethanolamide (PEA) and Oleoylethanolamide (OEA) Compared to a Placebo on the Gut Microbiome in an Adult Population – A double blind, randomised controlled trial. anzctr.org.au/Trial/Registr...
Pharmacological and nutritional control of dysbiosis related to CNS disorders: gut-brain axis fedoa.unina.it/12578/
Palmitoylethanolamide and Cannabidiol Prevent Inflammation-induced Hyperpermeability of the Human Gut In Vitro and In Vivo-A Randomized, Placebo-controlled, Double-blind Controlled Trial pubmed.ncbi.nlm.nih.gov/310...
Palmitoylethanolamide, a naturally occurring lipid, is an orally effective intestinal anti-inflammatory agent ncbi.nlm.nih.gov/pmc/articl...
An Update of Palmitoylethanolamide and Luteolin Effects in Preclinical and Clinical Studies of Neuroinflammatory Events mdpi-res.com/d_attachment/a...
Anybody been taking um-PEA with or without luteolin? If so have you noticed anything? I just started taking it a week ago (um-PEA w/luteolin). I'm taking 630/mg/day. Nothing noticeable yet, but it is very early. I'm not so sure i'd notice anything anyways, just hoping to slow the progression.
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A Simple Request for Kindness
Any suggestions for managing this kind of dyskinesia?
