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Diabetic Neuropathy
Published in Charles Theisler, Adjuvant Medical Care, 2023
Palmitoylethanolamide (PEA): A number of patients not responding well to conventional therapy were started on PEA 600 mg sublingually twice daily for quick absorption and to avoid first-pass effects. After 10 days, they were switched to tablets of 600 mg PEA twice daily, and if pain was sufficiently reduced, the dose was thereafter reduced to 300 mg twice daily. In case studies of patients suffering with metastatic prostate cancer pain, failed low-back surgery, diabetic neuropathy, polyneuropathy, and a female with partial vulvectomy from vulvar intraepithelial neoplasia II, all responded to the previous regimen. Most results were seen between weeks one and three of treatment, but some cases improved only after five weeks of treatment.13
Endocannabinoids & Phytocannabinoids in Pain Management *
Published in Betty Wedman-St Louis, Cannabis as Medicine, 2019
A promising new strategy for resolving pain is to use palmitoylethanolamide (PEA) in combination with CBD. When in pain, the body produces PEA, which acts as a natural painkiller.46 PEA is also found in foods such as egg yolks, peanuts, and soybeans. It is not found in cannabis and is not classified as an endocannabinoid. However, it acts on the endocannabinoid system by helping the body use anandamide more effectively.46
Pea
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
The topic of peroxisome proliferator-activated receptor (PPAR) ligands typically involves a discussion of the lipid-lowering effects of fibrates and the blood sugar-lowering effects of thiazolidinediones. However, more recent research has investigated the role of the endogenous PPAR-α ligand, palmitoylethanolamide (PEA) on inflammation, pain, neurodegenerative diseases, stroke, spinal cord injury, and neuropsychiatric disorders.1 Palmitoylethanolamide is a naturally occurring fatty acid belonging to the N-acylethanolamine (NAE) class of signaling molecules and can be isolated from egg yolks, peanut meal, and lecithin. It is rapidly metabolized in the human body via fatty acid amide hydrolase (FAAH) and N-acylethanolamine-hydrolyzing acid amidase (NAAA) to inactive metabolites palmitic acid and ethanolamide.2,3 Initial pharmacokinetic research by Lambert et al.2 assumed a ligand-binding relationship between PEA and the endogenous cannabinoid 2 (CB2) receptor. However, these initial claims proved to be incorrect and were explained as the entourage effect, where PEA competes with the endocannabinoid anandamide (AEA) for FAAH, resulting in higher concentrations of AEA.4 Although it does have a structural relationship to AEA and other endocannabinoids, PEA was found to have pharmacologic activity at PPAR-α, PPAR-γ, PPAR-δ, G protein-coupled receptor (GPR) 55, GPR119, transient receptor potential channel type (TRP) V1, ATP-sensitive potassium channels, and calcium-activated potassium channels. Additionally, PEA appears to inhibit ceramidases, and potassium channels Kv4.3 and Kv1.5, as well as interacting with NF-κB, cyclooxygenase (COX), TNFα, interleukin (IL)-4, IL-6, IL-8, nitric oxide (NO), and substance P mast cell activation. This variety of interactions has afforded PEA the title of being “promiscuous.”4,5
Nutritional intervention in chronic pain: an innovative way of targeting central nervous system sensitization?
Published in Expert Opinion on Therapeutic Targets, 2020
Jo Nijs, Sevilay Tumkaya Yilmaz, Ömer Elma, Joe Tatta, Patrick Mullie, Luc Vanderweeën, Peter Clarys, Tom Deliens, Iris Coppieters, Nathalie Weltens, Lukas Van Oudenhove, Eva Huysmans, Anneleen Malfliet
Another potential therapeutic way of targeting neuroinflammation in chronic pain relates to the mast-cell glial axis in neuroinflammation. Activated mast cells may contribute to glial activation through its release of an array of mediators after degranulation, including pro-inflammatory cytokines (IL-1β, TNF-α) and nerve growth factor [80]. Mast cells and microglia interact in a bidirectional fashion, including through Toll-like receptor isoforms-2 and −4, mast-cell tryptase, and proteinase-activated receptor 2 on microglia [80]. The naturally occurring fatty acid N-palmitoylethanolamine (or palmitoylethanolamide) is an endogenous molecule abundant in the mammalian brain with established anti-inflammatory and analgesic properties, potentially through inhibiting mast-cell activation [80]. This way, they hold potential as innovative therapeutic target for chronic postsurgical and nonsurgical pain.
Herpes simplex virus type 1 and Alzheimer’s disease: link and potential impact on treatment
Published in Expert Review of Anti-infective Therapy, 2019
Roberta Mancuso, Mariaconcetta Sicurella, Simone Agostini, Peggy Marconi, Mario Clerici
Other natural products with an antiviral action and the ability of inducing protection from neurodegeneration are Resveratrol (RSV) and Quercetin, which are known activators of Sirt1 (NAD+-dependent deacetylase sirtuin 1) and AMPK (5ʹAMP-activated protein kinase) [154–157]. Several studies have demonstrated that, during neuronal infection, HSV-1 modulates the AMPK/Sirt1 axis. Particularly, AMPK is down-regulated during early infection; on the other hand, the levels of Sirt1 increase, suggesting that the AMPK/Sirt1 axis is differentially modulated by the virus during infection [158]. RSV and Quercetin activate the AMPK/Sirt1 axis and induce neuroprotective and antiviral effects in HSV-1-infected neuronal cultures [159]. Other studies have demonstrated the capacity of RSV and Quercetin to delay axonal degeneration after injury [158], to block accumulation of Aβ peptide in vitro [159], to reduce BACE-1, which mediates the APP cleavage [158], and to provide protection from brain ischemia in both adult and neonatal rodents [160,161]. Palmitoylethanolamide (PEA), an endogenous lipid mediator is also endowed with anti-inflammatory and neuroprotective effects [162]. A murine model showed that PEA counteracted the activation and inflammation seen in AD-like mouse astrocytes and promoted neuronal viability [163]. Table 3 summarizes the drugs discussed in this paragraph.
Recent developments in interferon-based therapies for multiple sclerosis
Published in Expert Opinion on Biological Therapy, 2018
Laura Dumitrescu, Cris S. Constantinescu, Radu Tanasescu
All classical IFN-β formulations show good long-term safety profiles but have frequent tolerability and adherence issues, mainly related to injection-site reactions, and dose-related flu-like syndrome [66]. The former there are seen in up to 90% of the patients receiving subcutaneous formulations, and in about a third of those using the intramuscular route [90]. Reactions are usually mild and do not require IFN-β cessation. The flu-like syndrome includes fever, chills, fatigue, myalgia, and headache, beginning 4–6 h after IFN-β administration, and persisting for up to 24 h [41]. During the first months of treatment, these symptoms may affect up to ~75% of the patients, but subsequently their incidence decreases [91]. Some patients also experience dose-related transient worsening of MS symptoms, typically resolving 3 months after treatment initiation [41]. Strategies to mitigate these side effects include gradual titration to full-dose schedules, optimal scheduling of IFN-β administration, and the use of acetaminophen or non-steroidal anti-inflammatory drugs [90]. A recent placebo-controlled trial showed that adding oral ultramicronized palmitoylethanolamide (600 mg/day), an endogenous bioactive lipid, to subcutaneous IFN-β-1a, may reduce injection-related pain and increase the perceived cognitive performance and health status of RRMS patients [92]. A small randomized, placebo-controlled, cross-over trial that found no benefit in reducing flu-like symptoms from adding cetirizine (a second-generation histamine 1 antagonist) to the standard IFN-β-1b treatment [91].