Vitalitus is the only reputable supplier of PEA in the US – palmitoylethanolamide


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Strong Warning

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 Purchase PEA only from *Vitalitus* in the U.S.

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I have previously warned readers, but I continue to be bombarded with fake comments about the toxic contaminated Chinese powder with a fake address in Florida that sells on the web at a “bargain” so that people think they will save money. 

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Do not buy from any other source than Vitalitus in the U.S. Or purchase PeaPure in the Netherlands. 

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Take the capsules with something fatty to help them absorb (glass of whole milk, peanut butter, etc) and continue for 2 to 3 months to determine if they work. The PEA Cream called Soothamide will give relief in a few minutes when it works for pain. 

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The material on this site is for informational purposes only.

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It is not legal for me to provide medical advice without an examination.

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It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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Comments are welcome.

This site is not for email, not for medical questions, and not for appointments.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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Please IGNORE THE ADS BELOW. They are not from me.

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PEA in US (palmitoylethanolamide), PeaPure in Netherlands – DO NOT BUY OTHER SOURCES


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PEA in US is palmitoylethanolamide from Vitalitus

PeaPure in  Netherlands

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DO NOT BUY OTHER SOURCES

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PEA is thankfully available in the US since Spring 2016 from ONE company: Vitalitus. It is a trusted source. Buy PEA only from Vitalitus in the US, others are fraudulent sources.

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I strongly recommend that you AVOID any product with a “PEA-type” name trying to sell elsewhere in the US or on the web.

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One such fraudulent source is a foreign entity pretending to be in the US, and they are now listing a US address on Brickell Avenue, Miami, FL 33131 United States. But that is a virtual office address which is still listed for rent at $60/month.

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It looks like they’ve morphed the website and their product label. Very professional looking but AVOID THEM LIKE POISON. They keep trying to post comments on my website. They may even be buying advertising on my free site – anyone can advertise but I do not endorse products with this one exception, PEA, because it is unique.

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I have also seen “PEA-type” powder available on the web. Do not buy powders claiming they are pure palmitoylethanolamide. They are not trustworthy sources.

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Make sure your PEA comes only from a trustworthy source. In the US, that is Vitalitus. PEA works on the innate immune system, mast cells, and much more. There are more than 400 scientific publications on palmitoylethanolamide since it was rediscovered by a Nobel Prize Winner in 1993. Vitalitus’ PEA capsules are 100% palmitoylethanolamide. Pain relief is one of its immune functions. Your body makes it, plants make it, it has no toxicity, but follow directions or capsules will not fully absorb.

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The material on this site is for informational purposes only.
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It is not legal for me to provide medical advice without an examination.

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It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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This site is not for email and not for appointments.

If you wish an appointment, please telephone the office to schedule.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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Please IGNORE THE ADS BELOW. They are not from me.

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The material on this site is for informational purposes only.
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It is not legal for me to provide medical advice without an examination.

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It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

~~
This site is not for email and not for appointments.

If you wish an appointment, please telephone the office to schedule.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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Please ignore the ads below. They are not from me.

 

PEA (palmitoylethanolamide) made in America – like PeaPure


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Vitalitus

now sells PEA

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Palmitoylethanolamide is now sold in the US as PEA by Vitalitus. It should be very comparable with the product PeaPure from the Netherlands. Since a Nobel Prize winner rediscovered it in 1993, over 400 scientific papers have been published on it. It is a food supplement, your brain makes it, plants make it. It is nontoxic, a glial modulator that works on the innate immune system, inflammation and mast cells, among many functions.

 

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Remember, you need to take PEA capsules with something a little fatty, like milk, or peanut butter, or buttered toast. Otherwise, it will not absorb. Because it is lipophilic, i.e. likes fat, it does not dissolve in water. Only oil.

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Dosage – use the search functions on left column for PEA or palmitoylethanolamide or PeaPure. You will find where I previously imported the instructions from the Netherlands website.

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PeaPure has helped intractable nerve pain. We published in 2014 the case of a woman in remission after 8 years of vulvodynia, treated with PeaPure.

 

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I have been very pleased with PeaPure (palmitoylethanolamide) for neuropathic pain. It is available in a capsule as a food supplement called PEA, without prescription.

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[Edited 12-13-16 for repetitious comments. Link added.]

 

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The material on this site is for informational purposes only.

It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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Update on PeaPure – Palmitoylethanolamide


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Please refer to this post for context. Here is the addition:

 

UPDATE SEPTEMBER 2014

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It is with a heavy heart that I report this news:

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Palmitoylethanolamide is

now available only from the Netherlands,

sold as PeaPure, a food supplement.

www.peapure.com – click on UK flag for English.

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It can no longer be imported in the USA in larger quantities.

My local pharmacy is trying hard to find alternatives,

but it may take years, if they are successful at all.

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.I have published this year, 2014, on the treatment of

vulvodynia and proctodynia with PeaPure and a topical cream.

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There are no studies to show us how often it may relieve nerve pain,

but it is astonishing when it works.

No toxicity, no side effects.

Your brain makes it, plants make it.

There is a growing literature on it and I have posted on some of its mechanisms,

in particular, its Anti-inflammatory, Analgesic, Neuroprotective Mechanisms.

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The material on this site is for informational purposes only, and is not a substitute for

medical advice, diagnosis or treatment provided by a qualified health care provider.

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Please understand that it is not legal for me to give medical advice without a consultation.

If you wish an appointment, please telephone my office or contact your local psychiatrist.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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Palmitoylethanolamide “PEA” – Review of Anti-inflammatory, Analgesic, Neuroprotective Mechanisms


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A review of palmitoylethanolamide, or PEA, has been published this June by Mireille Alhouayek and Guilio G. Muccioli from the Bioanalysis and Pharmacology of Bioactive Lipids Research Group, Louvain Drug Research Institute, Bruxelles, Belgium.

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The authors review the impact of PEA on inflammatory and neurodegenerative diseases, and show that inhibiting the breakdown of PEA (the hydrolysis) may increase levels of PEA. This could lead to treatment of inflammatory and neurodegenerative diseases.

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To address the loss of PEA that occurs in various diseases we must either

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1.  replace the decreased levels of endogenous PEA that is made by the brain by taking a capsule such as PeaPure,  a food supplement that contains 100% palmitoylethanolamide, to reconstitute the needed levels

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2.  inhibit the breakdown (hydrolysis) of PEA.

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.I directly quote palmitoylethanolamide4pain that has outlined key quotes from that scientific review:

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They start outlining the focus of the paper:

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Our focus here is on PEA, which is a known anti-inflammatory compound with analgesic, neuroprotective and antiallergic properties.

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Important for understanding the therapeutic relevance of PEA is the next remark:

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Evidence suggests that PEA metabolism is disturbed during inflammation, and that a decrease in PEA levels contributes to the inflammatory response.

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This explains why it is so useful to administer exogenous PEA as a supplement during states of chronic inflammation. Decreased PEA levels induce more inflammation and a vicious circle has started. Administering PEA (for instance as PeaPure capsules of 400 mg, a foodsupplement) can stop this circle and help the organism to restore the PEA levels and decrease inflammation.

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PEA’s mechanism of action

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The next quote is related to PEA’s main mechanism of action:

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Although it is now clear that PEA is a ligand for PPAR-a, some of its effects occur through as yet unidentified receptors.

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Although there are many ways PEA acts in the cell, the PPAR-a receptor indeed seems the most important one; through that receptor PEA can downregulate overactive inflammatory responses.

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PEA levels also decreased following sciatic nerve constriction injury or ligation of the sciatic nerve in spinal cord and brain areas involved in nociception

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PEA levels are not only decreased during chronic inflammation, also during chronic pain states, such as in sciatic pain.

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The fact that an anti-inflammatory treatment restores PEA levels reinforces the role of PEA as an anti-inflammatory mediator.

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PEA levels can be restored also by treatment with classical anti-inflammatory compounds such as NSAIDs, this however triggers many side effects and that can be avoided by treating with PEA itself!

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PEA as a protective molecule

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In the brain, PEA levels seem to be increased following injurious stimuli, and this has been proposed as a homeostatic mechanism aimed at counteracting inflammation and blunting the inflammatory response.

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PEA has self-reparative properties and indeed can be defined as the molecule of self-reparation and self-protection.

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This ‘pro-homeostatic’ increase, although probably slowing disease progression, seems insufficient to exert anti-inflammatory effects in itself, and should be further amplified…

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One of the classical ways to amplify PEA is to administer it as food supplement: start dose is 1200 mg/daily and in cases of insufficient response we suggest to double the dose.

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Although the first identification of PEA as an anti-inflammatory compound occurred more than 50 years ago, general interest in its anti-inflammatory and analgesic properties was not sparked again until the mid-1990s.

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It was due to the work of the Nobel laureate professor Rita Levi-Montalcini that the scientific community understood the importance of PEA in the 90s. However, as patents on this natural compound were not possible, no great interest emerged, as pharmaceutical companies were uninterested. It was due to the work of small companies, such as Epitech Srl and JP Russell Science that PEA was brought to the attention of the general public.

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Mechanism of action in addition to the PPAR receptor

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The authors nicely summarized the effects of PEA:

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PEA inhibits phosphorylation of kinases involved in activation of pro-inflammatory pathways, such as mitogen-activated protein kinase (MAPK), c- Jun N-terminal kinase (JNK) and extracellular signal-regulated kinases (ERK), and the nuclear translocation of the transcription factors nuclear factor (NF)-kB and activator protein 1 (AP-1) and prevents degradation of the inhibitory IkB-a, which when associated to NF-kB prevents its nuclear translocation.

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Besides reducing inflammatory cells activation and recruitment, PEA modulates the expression of enzymes involved in pro-inflammatory processes, such as COX-2 and inducible nitric oxide synthase (iNOS) and reduces nitric oxide and pro-inflammatory cytokines production in vitro and in vivo.

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Relevance for Alzheimer, Parkinson’s and MS

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The neuroprotective effects of PEA are in part the result of its effects on downregulating the inflammatory cascade. Indeed, many neurodegenerative diseases are associated with a strong inflammatory component, such as Alzheimer’s disease (AD), Parkinson’s disease (PD) or MS

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The follow stating:

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This neuroinflammation is no longer simply considered as a consequence of neurodegeneration, but might be a primary factor in some cases; therefore, anti-inflammatory treatments might represent interesting therapeutic strategies in these diseases

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After discussing modern pharmaceutical ways to block the hydrolysis of PEA with pharmaceutical new compounds, they end their overview with an important statement:

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The potential of using PEA as a beneficial endogenous bioactive lipid in the setting of inflammation is well established

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My thanks to palmitoylethanolamide4pain for the outline of key points in this review of PEA.

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The material on this site is for informational purposes only.

It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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PEA Palmitoylethanolamide – “Glia & Mast Cells as Target, An Anti-Inflammatory & Neuroprotective Lipid Mediator”


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Another oustanding article on palmitoylethanolamide “PEA.” I have seen profound results with it relieving intractable neuropathic pain in a woman with CRPS for years, and I suspect it may help Major Depressive Disorder but that remains to be tested.

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I need to add that opioids create pain. One mechanism by which that occurs is that opioids create pro-inflammatory cytokines, which creates more pain. Patients may see no response to essential pain relieving medications untill they taper off all opioids and allow the system to stabilize. Otherwise, they will have pain forever and it may increase.

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Glia and mast cells as targets for palmitoylethanolamide,

an anti-inflammatory and neuroprotective lipid mediator

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Authors  Skaper SD, Facci L, Giusti P.

Mol Neurobiol. 2013 Oct;48(2):340-52.  Epub 2013 Jun 28.

Abstract

Glia are key players in a number of nervous system disorders. Besides releasing glial and neuronal signaling molecules directed to cellular homeostasis, glia respond also to pro-inflammatory signals released from immune-related cells, with the mast cell being of particular interest. A proposed mast cell-glia communication may open new perspectives for designing therapies to target neuroinflammation by differentially modulating activation of non-neuronal cells normally controlling neuronal sensitization-both peripherally and centrally. Mast cells and glia possess endogenous homeostatic mechanisms/molecules that can be upregulated as a result of tissue damage or stimulation of inflammatory responses. Such molecules include the N-acylethanolamines, whose principal family members are the endocannabinoid N-arachidonoylethanolamine (anandamide), and its congeners N-stearoylethanolamine, N-oleoylethanolamine, and N-palmitoylethanolamine (PEA). A key role of PEA may be to maintain cellular homeostasis when faced with external stressors provoking, for example, inflammation: PEA is produced and hydrolyzed by microglia, it downmodulates mast cell activation, it increases in glutamate-treated neocortical neurons ex vivo and in injured cortex, and PEA levels increase in the spinal cord of mice with chronic relapsing experimental allergic encephalomyelitis. Applied exogenously, PEA has proven efficacious in mast cell-mediated experimental models of acute and neurogenic inflammation. This fatty acid amide possesses also neuroprotective effects, for example, in a model of spinal cord trauma, in a delayed post-glutamate paradigm of excitotoxic death, and against amyloid β-peptide-induced learning and memory impairment in mice. These actions may be mediated by PEA acting through “receptor pleiotropism,” i.e., both direct and indirect interactions of PEA with different receptor targets, e.g., cannabinoid CB2 and peroxisome proliferator-activated receptor-alpha.

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The material on this site is for informational purposes only.

It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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Vulvodynia & proctodynia treated with topical baclofen 5 % & palmitoylethanolamide


 

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Vulvodynia and proctodynia (rectal pain) treated with topical baclofen 5 % and palmitoylethanolamide

Abstract

Background

The prevalence of idiopathic vulvodynia and proctodynia is high. Pain management with anti-depressants and anti-epileptics may induce undesirable side effects. Therefore, topical baclofen cream and palmitoylethanolamide might be new therapeutic options.

Case

A 33-year-old woman with intractable chronic vulvar and anal pain had to abstain from sexual intercourse and could neither cycle nor sit for more than 5 min. The patient did not respond to standard treatments. We prescribed a combination of topical baclofen 5 % and palmitoylethanolamide 400 mg, three times daily. After 3 months her symptoms decreased more than 50 % and sexual intercourse was possible again without pain.

Conclusion

Topical baclofen and palmitoylethanolamide can be a viable treatment option in chronic vulvodynia and proctodynia.

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I have been very pleased with palmitoylethanolamide for neuropathic pain. It is made in the brain and by plants and I have never seen toxicity. PJ’s Prescription Shoppe imports it from the Netherlands for my patients, and it is available in a capsule as a food supplement called PeaPure, without prescription. I have posted on it and its mechanisms a few times elsewhere on this website.

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The material on this site is for informational purposes only.

It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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PEA (palmitoylethanolamide) inhibits TLR4


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New insight into the mechanism of action of palmitoylethanolamide was presented in 2013 at EFIC, a Congress for European Pain Specialists:

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“… Dr Svik Assaw and colleagues from the School of Life Sciences, Medical School, University of Nottingham, United Kingdom presented new exciting data on the mechanism of action of the fatty acid amide N-Palmitoyethanoalamide (PEA) and presented the effects of PEA after activation of toll-like receptors (TLRs) by the inflammatory substance carrageenan.”

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1. PEA inhibits chemotaxis of monocytes, but not neutrophils (clearly a sign that PEA downregulates chronic inflammation but not acute inflammation)

2. PEA decrease in the carrageenan induced induction of the pro-inflammatory genes IL-1b, CCL4 and NOS2 in the inflamed skin.

3. PEA also blocks CCL4 induced monocyte migration in a chemotaxis assay.

4. PEA clearly modulates the TLR4 mediated inflammatory responses and dose-related inhibits inflammatory evoked TNFa and IL-1b gene expression.”

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The material on this site is for informational purposes only.

It is not a substitute for medical advice,

diagnosis or treatment provided by a qualified health care provider.

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Please understand that it is not legal for me

to give medical advice without a consultation.

If you wish an appointment, please telephone my office.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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Palmitoylethanolamide (PEA) – Boosting Its Anti-inflammatory Immune Response


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Discovery could lead to new immune-response drugs for allergies, illnesses and injuries

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Improved spinal cord injury & inflammation in mice

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Medical news November 17, 2009, announced that “UC Irvine pharmacology researchers have discovered a way to boost levels of a natural body fat that helps decrease inflammation, pointing to possible new treatments for allergies, illnesses and injuries related to the immune system.”

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“For decades, it has been known that this fat, called palmitoylethanolamide (PEA), is a potent anti-inflammatory substance that reduces both allergic symptoms and occurrences of rheumatic fever, but researchers understood little about how PEA works.”

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I”n a study appearing online in the Proceedings of the National Academy of Sciences, Daniele Piomelli, the Louise Turner Arnold Chair in Neurosciences at UCI, and colleagues found that levels of PEA are tightly regulated by immune system cells. In turn, PEA helps control the activity of these cells, which are called into action to fight infection, disease and injury in the body.”

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They found a protein, an enzyme that breaks down molecules that control cell inflammation and deactivates PEA. They then created a novel compound that prevents the breakdown.

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“When given to rodents, the compound increased the levels of PEA in their immune cells and reduced the amount of inflammation elicited by an inflammatory substance. Furthermore, when administered to the spinal cords of mice after spinal cord injury, the compound decreased inflammation associated with the trauma and improved the recovery of motor function.”

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UCI is collaborating with the Italian Institute of Technology in Genoa to develop a range of immune-response drugs. 

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Source: University of California – Irvine

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Refer an earlier post on PEA here.

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Palmitoylethanolamide is sold as PeaPure, a food supplement, available from the Netherlands and imported by a local pharmacy here. I have submitted a paper for publication on the treatment of vulvodynia and proctodynia with PeaPure and a topical cream. That source will be posted once it is accepted.

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I have been seeing some exciting responses to treatment of intractable pain with PeaPure. I invite others who use it to add comments below so that we may all learn from your experience.

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The material on this site is for informational purposes only.

It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

~~~~~

Please understand that it is not legal for me

to give medical advice without a consultation.

If you wish an appointment, please telephone my office.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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PeaPure – Palmitoylethanolamide for Nerve Pain or Migraine


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PeaPure is a glial modulator. It is available in Italy and the Netherlands as a food supplement and has been studied in multicenter clinical trials in Europe for several years. It is well tolerated with no side effects and is very helpful for neuropathic pain, headache, and osteoarthritis. It is anti-inflammatory and neuroprotective.

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Because it inhibits astrocyte activation and the over-expression of pro-inflammatory molecules and signals, it is being investigated in Alzheimer’s Disease.

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The mechanism of action of PEA was discovered in 1993 by Nobel laureate Rita Levi-Montalcini in her work on nerve growth factors. She found it is involved in metabolism of mast cells and published a series of papers on its self-healing effect of the body in response to inflammation and pain. Two recent publications from Jan M Keppel Hesselink, MD, PhD, and his colleagues at the Institute for Neuropathic Pain, Amsterdam, The Netherlands, describe case reports, one of which is the case of a woman with CRPS.

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The purpose of this post is to clarify dosing of PeaPure and how to take it for a sudden flare of pain. My apologies for failing to recall the source of these instructions which I believe was from the manufacturer and from here and here. The latter includes an excellent review of its mechanism.

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Description of PeaPure® 400 mg capsules
PeaPure® is a food supplement based on a natural and fatty-acid like compound.
The substance palmitoylethanolamide (PEA) is a physiologically active molecule that the body produces naturally.
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What the user should know prior to ingestion:
•    There are no known significant side effects.
•    PeaPure® can be taken simultaneously with other medicine. In case of doubt, it is recommended to first consult your doctor or a pharmacist.
•    Use during pregnancy is NOT recommended.
•    PeaPure® does not contain sugar, yeast, allergens, sorbitol, magnesium stearate, povidone or other ingredients.

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Dosage and administration – please refer to the manufacturer.

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UPDATE SEPTEMBER 2014

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It is with a heavy heart that I report this news:

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Palmitoylethanolamide is

now available only from the Netherlands,

sold as PeaPure, a food supplement.

  It is no longer able to be imported by a pharmacy, but we are hoping

that may change if we can interest a supplement manufacturer to make it available for the US.

Patent rights, attorneys are far beyond the resources of my local pharmacy.

 

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I have published this year, 2014, on the treatment of

vulvodynia and proctodynia with PeaPure and a topical cream.

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There are no studies to show us how often it may relieve nerve pain, but it is astonishing when it works. No toxicity, no side effects. Your brain makes it, plants make it. There is a growing literature on it and I have posted on some of its mechanisms. And in particular, its Anti-inflammatory, Analgesic, Neuroprotective Mechanisms.

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The material on this site is for informational purposes only, and is not a substitute for

medical advice, diagnosis or treatment provided by a qualified health care provider.

.

~

Please understand that it is not legal for me to give medical advice without a consultation.

If you wish an appointment, please telephone my office or contact your local psychiatrist.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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PEA Capsules & PEA Cream from Vitalitus – Soothamide


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Palmitoylethanolamide (Pea in the US, PeaPure in Netherlands) is a glial modulator, analgesic, anti-inflammatory, neuroprotective and anticonvulsant  with mechanisms involving the innate immune system and mast cells. It binds to a receptor in the cell nucleus. The major focus of hundreds of publications on it has been inflammation, neuropathic pain states and mast cell related disorders from University of Oxford,  Journal of Arthritis Research and Therapy, Journal of Pain Research, University of Bologna School of Dentistry (a study for TMJD pain), etc.

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It is a food supplement. It is a naturally occurring lipid amide, i.e. the body makes it, plants make it. It is available as a capsule and a cream without prescription. It may take days to weeks to work, but I’ve seen the cream work in two minutes – shock!  The relief is amazing for someone who has failed everything for intractable pain.

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Soothamide Cream is 2% palmitoylethanolamide from Vitalitus in the US.

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It’s been fascinating to see the cream work for so many pain syndromes including severe CRPS/RSD nerve pain! arthritis, muscle and severe ligamentous strain – often in less than two minutes! Not everyone, not every pain benefits but it is well worth trying and very affordable for large amount.

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One senior whose osteoarthritis in finger joints has been painful, very stiff, and prevents him from only very slightly being able to bend four fingers on his right hand. It’s been years since he’s been able to touch tips of the fingers to his palm because of stiffness and pain. They just would not go.

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After applying Soothamide cream, in less than 20 minutes he was able to fully, easily and painlessly bend all four fingers to the palm without any trace of stifness – quite astonishing. And the next day, three of the four fingers still had complete 100% relief 20 hours later, but it did not last for the index finger, even applying it later to that finger over those 20 hours. Twenty hours relief is amazing for three fingers after years of severe stiffness and pain. Relief may have been hours longer, but he took off for the day and data like this is difficult to pay attention to, and then to make a memory note of how long.

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Another with knee pain and significant joint effusion (fluid that creates pressure inside the joint), had relief for 3 hours after one application in the office.

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I have seen the cream relieve low back pain completely in less than two minutes. This was the father of a patient who had tried it in the office and it failed to help that patient, but she had a little left on her hand and schmeared it across her dad’s back. All pain gone in less than two minutes!  I am assuming this was muscle strain, not deep mechanical structures in the spine.

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Another patient with RSD pain on the foot had no benefit, but she then applied the Soothamide to a very severe pain from torn ligament in the arm that was more painful than her RSD. It was gone in less than two minutes, to her shock and delight.

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The cream has only recently been available in the US, and I have seen it help so many patients including those with CRPS/ RSD nerve pain. Most relief from creams is short lived, but if you see 4 hours of relief, or 20 plus hours as the patient above, it is very special.

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The cream has been such fun! Having seen even the severe nerve pain of CRPS/RSD improve or be astonishingly gone -!- in less than two minutes -!- it helps doctors forget the pain of being unable to offer anything more. Here we have capsules and cream that do not require prescription. And even in the most extreme pain syndromes is worthy of a try.

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PEA capsules – open and place powder under tongue for instant relief of breakthrough pain.

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That was a blessing in the middle of last night for one of my patients with RSD who was having a severe flare of pain. In August, she had started PEA capsules 3 twice daily – always take with something fatty (milk, peanut butter, etc) to aid absorption. In 3 weeks it had reduced her lower limb pain from severe to mild-moderate while in bed. Now months later, after reducing another medication briefly due to side effects, pain flared severely. What to do?

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I instructed her to open the PEA capsule and place the powder under tongue to absorb there. She had relief. I don’t have data to relate more as yet but hope to post as I learn from her and hopefully other patients who write in their comments. How much is safe? I will try to find more information. We know the body makes it, plants make it and at doses of 6 capsules daily it causes no side effects.

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The material on this site is for informational purposes only.
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It is not legal for me to provide medical advice without an examination.

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It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

~~
This site is not for email and not for appointments.

If you wish an appointment, please telephone the office to schedule.

~~~~~

For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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Please IGNORE THE ADS BELOW. They are not from me.

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Medication Summary for Intractable Pain, CRPS/RSD


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  Medication Summary for

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Intractable Pain, CRPS/RSD

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I spoke only briefly this morning at the RSDSA conference but there is so much to add. Most importantly, thanks to RSDSA for helping so many people with CRPS. They fund pain research, they are starting a free children’s camp, and now offer physicians one hour free CME teaching about CRPS.

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Holistic view, 36 points – that’s how I view caring for brain and nerves, very similar to the details used by UCLA Alzheimers Research Unit. In June 2015, I posted on their work on memory loss, dementia. We know chronic pain means inflammation in the brain, excess of proinflammatory cytokines. CT scans show memory loss and brain atrophy in those with chronic low back pain.  Can this inflammation lead to Alzheimers? Even if it doesn’t, why not maximize what we know we can do to help brain. As I view it, simply be meticulously detailed in giving the central nervous system (CNS) the best chance to relieve or prevent pain or disease.

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Below is a brief list.

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To find detail and sometimes depth, check the alphabetical lists on either side column until you see the category or tag when I first posted on that. Or simply plow through 7.5 years of detail with references. You do the work to check the side columns as I have no time to embed links below, taken from throughout this site.

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For now just a list of medication players that may be strikingly important in trying to bring intractable pain into remission even after 20 years. Yes, even chronic for decades.

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The list applies to intractable pain of all causes. I omitted listing standard interdisciplinary approaches commonly used by every pain specialist around the world. My patients have failed all those.

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Some patients with CRPS combine my medications with ketamine infusions.

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For those who remain on opioids, ultra low dose naltrexone (10 to 60 mcg three times daily) can significantly reduce pain, reduce opioid induced hyperalgesia, reduce windup, and thus reduce the dose of opioid needed to give improved relief.

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Opioids cause pain and trigger pro-inflammatory cytokines that create more pain.

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I strongly recommend slowly, gently tapering off opioid, and remaining off for 3 weeks before the following is trialed:

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 1. Vitamin D is anti-inflammatory. Important. Helps pain, depression. If bone loss is an issue, you will not absorb calcium from food if D is low. Mayo Clinic’s publication in 2012 showed more morphine is needed for pain if D is low. Huge literature of its benefit for depression. First topic I posted on – it is that important.

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2. Vitamin B6 can cause burning pain from scalp to toe, a toxic neuropathy. It can be toxic to brain. It is loaded in tons of soft drinks, “energy” drinks, supplements.

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3. MTHFR mutation may be present. Body cannot process  the B12 and folic acid you are eating or taking in supplement. A simple blood test, costly. Treatment is as simple as buying methyl folate and methyl B12 – no prescription needed. Folic acid in particular is profoundly important for one of the major energy cycles in the body. Can cause multiple conditions, some fatal, all from one single cause.

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4. Minocycline 100 mg/day is the dose I use but higher doses could be given. It is used daily for decades for acne. I may prevent spread of CRPS if given before surgery, dental work, even minor procedures. I start 24 hrs before, and continue for days after full recovery from surgery.

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5. Testosterone  in either male or female is depleted by opioids, it may be depleted by stress. Low T is a risk for depression, weakness and osteoporosis.

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6. Naltrexone low dose (LDN) – profoundly important. A glial modulator. Lifelong use.

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7. Dextromethorphan – reduces hyperexcitable glutamate

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8. Oxytocin

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9. Memantine – double the Alzheimers dose for CRPS. Like ketamine, it blocks the NMDA receptor.

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10. Lamotrigine

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11. Palmitoylethanolamide (PEA, PeaPure) a glial modulator, also acts on mast cells. A food supplement. No Rx. Your body makes it. Plants make it. Capsules & cream

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12. Ketamine via nasal spray, under tongue combined with IV or not, works on glutamate-NMDA receptor. Not an essential drug. Where ketamine has stopped working, patients have become pain free after years of CRPS.

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13. Creams combinations, so many

most of my CRPS pts very much like   Mg++/guai  10% each.

You may or may not trial various combinations lido/keto/keta, etc. Numerous. DMSO 50%.

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14. Medical Marijuana (CBD, THC, terpenes) Marijuana saves lives. Entire issue of Science, November 4, 2016, devoted to pain.

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NAC and alpha lipoic acid are noted by research from the Netherlands.

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Appendicitis

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If it has not burst, treat it like the infection that it is. Surgery may never be needed. I posted details of publications early 2016 with a case report. That young man was being rolled into the OR, instead was discharged 100% better without surgery 2 days later.
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Medications target 3 main systems

as discussed at the conference

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The opioid receptor – opioids create pain. They trigger glia to produce pro-inflammatory cytokines. Opioid induced hyperalgesia may occur. Cannot be used with low dose naltrexone.

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The glutamate NMDA receptor – ketamine, memantine

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Glia, the innate immune system – glial modulators

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Before they see me, my patients have failed all prior therapies even ketamine coma. I view it like football. You have one guy running down the field with one ball. Do you want to win the game? You’ve dealt with this for years. Let’s not prolong it. Hit it with my main choice of meds all at once. Jump on it. What if you get 10% relief – will you even notice 10% after many years of severe pain? But if you get 10% from each of 5 meds, then you are talking 50% relief as a start. Address those 3 main pain systems – even without ketamine – and I have posted a case report after 20 years and 3 suicide attempts before seeing me, she has been pain free for about 4 years as I recall. A surgeon nicked her sciatic nerve when she was 27. Two years ago, pain free, running on her treadmill, she twisted her ankle. She has permanent foot drop from the sciatic nerve injury, but even spraining her ankle did not flare her CRPS. Twenty years of CRPS, pain free for about 4 years. And ultimately, years ago, she was tapered off all the drugs with one exception: LDN lifelong.

 

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Most importantly, I did not have time to relay a very special message from my patient in Brooklyn:

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.Surround yourself with friends and family who love you.

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.Never give up hope.

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She had her first 2 or 3 pain free days this week, as she slowly increases doses of medication. She’s not yet at maximal effect and even then there can be increases. Sending love and courage.

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MOVEMENT

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Watch this on the RSDSA video, afternoon speakers, the parents of young ones who had RSD discussed today all the toys and games they had to devise to slowly force yourself to move through the pain, every single day, several times a day, all day, begin to move the body as much as you can. Set goals and slowly, at a pace you set, do the work. Make progress. Go forward. Keep moving. Do whatever you can to keep moving.

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RSD support groups are essential and I am glad to see the RSDSA list of so many throughout the country.

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There is so much more. Indeed, at least 36 points discussed on June 2015.

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The material on this site is for informational purposes only.
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It is not legal for me to provide medical advice without an examination.

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It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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This site is not for email and not for appointments.

If you wish an appointment, please telephone the office to schedule.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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Please ignore the ads below. They are not from me.

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Vulvodynia Topical Treatment – Monotherapy Obsolete


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New topical treatment of vulvodynia based on the pathogenetic role of cross talk between nociceptors, immunocompetent cells, and epithelial cells

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Authors Keppel Hesselink JM, Kopsky DJ, Sajben N
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Journal of Pain Research 2016, 9:757-762

 

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Abstract: Topical treatments of localized neuropathic pain syndromes in general are mostly neglected, mainly due to the fact that most pain physicians expect that a topical formulation needs to result in a transdermal delivery of the active compounds. On the basis of the practical experience, this study brings forth a new, somewhat neglected element of the vulvodynia pathogenesis: the cross talk between the nerve endings of nociceptors, the adjacent immunocompetent cells, and vaginal epithelial cells. Insight into this cross talk during a pathogenic condition supports the treatment of vulvodynia with topical (compounded) creams. Vulvodynia was successfully treated with an analgesic cream consisting of baclofen 5% together with the autacoid palmitoylethanolamide 1% [Pea, PeaPure], an endogenous anti-inflammatory compound. In this review, data is presented to substantiate the rationale behind developing and prescribing topical products for localized pain states such as vulvodynia. Most chronic inflammatory disorders are based on a network pathogenesis, and monotherapeutic inroads into the treatment of such disorders are obsolete.

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[Vitalitus, the American manufacturer of PEA, expects to have their first batch of cream for sale in 2 weeks. It’s a 2% PEA cream.]

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The material on this site is for informational purposes only, and is not a substitute for medical advice,

diagnosis or treatment provided by a qualified health care provider.

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Please understand that it is not legal for me to give medical advice without a consultation.

If you wish an appointment, please telephone my office.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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The advertising below is not recommended by me.

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PEA Vitalitus Micronized/ultramicronized superior


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From the Journal of Neuroinflammation comes this 2014 discussion of PEA related to the recent post on Vitalitus PEA product. PEA is micronized.

 

Micronized/ultramicronized palmitoylethanolamide displays superior oral efficacy compared to nonmicronized palmitoylethanolamide in a rat model of inflammatory pain

 

… PEA’s ability to modulate inflammation and pain in animal studies led to the proposal of this endogenous fatty acid amide as a component of a complex homeostatic system controlling the basal threshold of both inflammation and pain. The fact that PEA is produced during inflammatory conditions supports this role. Further, data showing selective inhibition of PEA degradation to be anti-inflammatory points more directly to PEA’s involvement in the control of pain and inflammation. As an endogenous compound, PEA has no adverse effects at pharmacological doses while possessing a double therapeutic effect (that is, anti-inflammatory and antinociceptive) (see [8,9] for recent reviews).

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This study allows me to be confident that the product sold in USA is as helpful as PeaPure sold in Netherlands.

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PEA is a glial modulator. It clearly modulates the TLR4 mediated inflammatory responses and dose-related inhibits inflammatory evoked TNFa and IL-1b gene expression. This and other mechanisms are summarized by Jan Keppel Hesselink in 2013.

 

 

 

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The material on this site is for informational purposes only, and is not a substitute for medical advice,

diagnosis or treatment provided by a qualified health care provider.

~

Please understand that it is not legal for me to give medical advice without a consultation.

If you wish an appointment, please telephone my office.

~

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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The advertising below is not recommended by me.

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