Amyotrophic Lateral Sclerosis or Lou Gehrig’s disease is a chronic inflammation of nervous tissue, leading to severe neurological deficits, such as weaknes in muscles, up to the respiratory and swallowing miuscles and ends in death within some years.
Now it seems that compounds belonging to the class of signaling lipids, such as Cannabinoids and endogenous lipids such as palmitoylethanolamide, can inhibit the neuro-inflammation, quite relevant for patients suffering from ALS.
Palmitoylethanolamide is available in the Netherlands as a food supplement, up to November 2012 as een PEA-houdend product and from November 2012 onwards as a new supplement, under the brandname PeaPure.
There are some differences between een PEA-houdend product and PeaPure, but both supplements contain the body own anti-inflammatory compound palmitoylethanolamide.
In PeaPure you find in one package 30 capsules of 400 mg pure palmitoylethanolamide, without any other pharmaceutical substance, nor sweeteners added.
In een PEA-houdend product you find in one package either 20 sachets containing 600 mg palmitoylethanolamide and other substances to sweeten and to stabilize: 300 mg sorbitol (a sweetener), polysorbate80 and sucrose palmitate. In a package with 20 tablets 600 mg you find 600 mg palmitoylethanolamide, and added magnesium stearate, croscaramelose, povidone and other pharmaceutical excipients.
The capsules of PeaPure are specially designed to be used either for obtaining filely powdered palmitoylethanolamide, to administer under the tongue (the capsule has been developed so that opening is easy and one can sprinkel the powder or directly in the mouth, or on a spoon and then under the tongue). The company developed PeaPure without any sweetener, because patients gave the input that the sweetener induced sometimes diarree. Or the sweetener, most of the time, induced so much slime/saliva in the mouth, that it was difficult not to swallow.
Russell Science Ltd therefore developed this content of the capsule, only with pure palmitoylethanolamide, with a neutral taste by not adding sorbitol nor any other pharmaceutical compound, to not attrack saliva and so to avoid the side effect of diarree and hypersalivation. This can be quite of use in ALS patients, who sometimes have difficulty swallowing saliva. The palmitoylethanolamide in PeaPure melts in the mouth without inducing extra saliva.
How to take PEA in the ALS?
The best is to start with either een PEA-houdend product in 2 times 600 mg sachets or with 3 capsules of PeaPure 400 mg and sprinkel the powder in the mouth. After the second day double the dose, and use 3 times 2 capsules. After 10 days, if it is convenient, one can swallow a capsule three times a day and use also the pwder from 3 capsules three times a day under the tongue.
If started with een PEA-houdend product powder, add een PEA-houdend product 600 mg tablets after a week, to increase the dose, or even double the dose.
The discoverer of PEA as a treatment for ALS patients and first results
Discoverer of the principle of palmitoylethanolamide in ALS is Dr. Simonetta Clemente, the Rehabilitation Specialist who directs the Center for Rehabilitation of Macon ASL of Nuoro, assisted by a team of other female professionals.
Since November of 2011 two patients with ALS (sporadic form in one case and another in the hereditary form), diagnosed with certainty at prestigious universities, have been subjected to administration of PEA.
“My goal – explains Dr. Clemente – was to improve the effects of rehabilitation, that in ALS patients is rendered completely ineffective due to the degeneration of motor neurons and progressive muscle atrophy.”
“The study – continues Clement – has shown that the PEA determines an immediate motor effect, blocking the progression of the disease, while the patient has a subjective perception of improvement and can do things which before were closed. This effect allows you to implement a rehabilitation plan that quickly determines the functional recovery, accompanied by the reappearance of the muscles.”
” Of course, two cases are few. I hope that it is possible to begin a multicenter research protocol with patients at different stages of severity, experiencing the active ingredient together with a targeted rehabilitation in order to drive the re-innervation, as in the two cases described“.
Recently, in November 2012 a paper appeared in a high ranked peer reviewed medical journal describing the results of the first patient treated with PEA.
The patient she treated was a 64-year-old male experienced the first symptoms around 2 months after returning from a long hiking tour. 
These appeared as pain in the right hand, followed by muscle waisting in the hand, with pain and limited use of all fingers accompanied by difficulty in fine movements like writing.
Symptoms progressed and in addition diffuse cramps in the lower limbs appeared, as well as swallow problems and mild respiratory problems.
A diagnosis of primary and secondary motor neuron disease (ALS) was made and the patient admitted to the Macomer Rehabilitation Center in July 2011. Respiratory symptoms worsened progressively.
Treatment with PEA in the ALS patient: results
Based on the anti-inflammatory action, the patient received PEA mg sublingual, twice daily.
The patient noticed a clear improvement in respiration and taking after about 15 min as well as diminished fascicular contractions after 1 week, and continued progress was observed in the following days.
At first only the accessory muscles in breathing were used but then the improvement progressed to the entire respiratory musculature, with movement on the order of 2 cm in the upper pulmonary fields, and continued expansion to the lower fields almost exceeding 2 cm.
Dose was increased to 3 powders under the tongie and 2 tablets of 600 mg. The positive effects could be measured in the blood, with clear signs of better lung functions.
Als the neurophysiological measures of nerve and muscle function were clearly and measurable better.
Conclusion of the author:
“Conceivably, the beneficial effects of PEA observed for this case of sporadic ALS could be due to its anti- inflammatory and/or immunomodulatory characteristic.
Clearly, a controlled clinical trial will be critical to confirm our preliminary findings. It also remains to be seen if long-term treatment of ALS patients affects lifespan.
It is important to point out that there have never been any reports of adverse events related to PEA administration in man.”
Recently it was communicated in an scientific article on ALS and the molecular target of PEA (PPAR) that:
Recent evidence highlights the peroxisome proliferator-activated receptors (PPARs) as critical neuroprotective factors in several neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS).
This might be one of the explanations why PEA (as PPAR-agonist) makes sense in ALS, and PEA might help in a neuroprotective way. In addition to this there is a great number of papers on PEA as a neuroprotectant, all available in PubMed.