Amyotrophic lateral sclerosis and the use of the natural anti-inflammatory compound Palmitoylethanolamide

Dutch people know the advertisement with the shocking content: “In the meantime I have passed away”. The campaign uses expressive faces of people with ALS that have already passed away.

Amyotrophic lateral sclerosis (first described in 1869 by the prominent neurologist Charcot) is a dreadful and rapidly progressive disease causing you to lose muscle function and strength and affects all muscles in the body. This includes the respiratory muscles. There still is no effective treatment for the condition. People generally pass away within a few years.

That’s why the results of an Italian revalidation-clinic on Sardinia are so impressive. Two ALS patients were treated there with the natural anti-inflammatory and pain relieving bodily substance palmitoylethanolamide (PEA), available as the supplement Normast. The positive effects were measurable almost immediately.

Elsewhere in the world ALS patients have started to use PEA. Especially patients with bulbar ASL seem to notice a relatively quick and positive effect.  Our body naturally produces palmitoylethanolamide as a reparation molecule with ALS.

Of course everything is still in its infancy. Patients will often try anything, without guidance of a doctor. The dose should be between 10-30mg per kg of body weight, which is relatively unknown and we suspect many people are using too small a dose to properly decrease the inflammation.


ALS and neuroinflammation

It has become more and more clear over the last years that ALS is an active inflammation of the nervous system, a so-called neuroinflammatory process. [1] [2] These new discoveries have caused substances that can modulate neuroinflammation to suddenly appear as a possible therapy. In 2010, this was described as follows:

“The multiple aspects of the immune response in ALS are beginning to be appreciated, and their potential as pharmacologic targets in neurologic disease is being explored.” [3]

Mast cells play an important role in many cases of inflammation, and activated mast cells have also been found in case of ALS.

“Our data suggest that inflammation in ALS spinal cord and cortex is based on innate immune responses by macrophages and mast cells and adaptive immune responses by T cells.” [4] The overactive mast cell is a factor that can cause problems and palmitoylethanolamide has the ability to calm exactly that cell. The fact that mast cells play an important role in ALS has been mentioned before. [5] Furthermore there is a type of connective tissue, called the glia cells, which can cause damage with ALS due to over activity. [6]


Palmitoylethanolamide for Amyotrophic lateral sclerosis

The clinical observations before and after treatment with palmitoylethanolamide (PEA) were clear. The muscle strength that has severely decreased in the hands, mouth and respiratory system, increased measurably within several weeks, without any negative side effects.

The authors concluded:

Lo studio dimostra che il PEA determina un immediato effetto motorio anche in condizioni di grave ipoamiotrofi a muscolare.

Tale effetto consente di attuare un progetto riabilitativo che, in tempi brevi, determina recupero funzionale accompagnato dalla ricomparsa dei muscoli. 

L’efficacia del trattamento è sicuramente dovuta al fatto che lo stress neuromuscolare causa un processo infiammatorio mediato da cellule non neuronali (mastociti e microglia). L’azione del PEA è quella di modulare l’azione di queste cellule.

Or, palmitoylethanolamide has a quite direct and positive effect on the muscle strength and functionality with Amyotrophic lateral sclerosis. The effects could be caused by the positive effects of palmitoylethanolamide on the non-neural cells, the glia tissue and mast cells.

The last statement has indeed been proven, and there are strong indications that ALS is a chronic inflammation of the nervous system in which mast cells play a certain role. [7] [3] A substance like palmitoylethanolamide can decrease the inflammation stress in the central nervous system. [9] [10] [11]The anti-inflammatory effect of palmitoylethanolamide has been demonstrated by many preclinical and clinical studies, as was recently summarized by the chairman of our foundation.

Every ALS patient can try this supplement, because palmitoylethanolamide has no important side effects.

These observations are not the only ones. On the internet we can see stories of ALS patients who use palmitoylethanolamide and experience benefits, here are some examples:

Case 1: Less fasciculation, better eating and drinking after amyotrophic lateral sclerosis treatment with palmitoylethanolamide

My husband started taking Normast on May 21st and he has had some interesting results. Two days after starting it, he noticed a decrease in Fasciculation. A couple of nights later, he noticed that during the night he was able to move his hand a bit more and his fingers were moving on their own. He said that it was hard for him to explain, but it wasn’t the usual twitching.

Three days ago, I noticed that he was drinking liquids with no choking. That hasn’t happened in quite a while. He is not doing any exercising except walking, as his legs are not affected yet.

I know that the literature on Normast states that it could take up to 50 days to see any pain relief from taking it, so perhaps given a little more time, it might start show positive results for other PALS.

FYI – my husband was diagnosed May 1st, but he has had symptoms for about a year previous. It was probably bulbar onset because we noticed slurred speech first, but we attributed it to some heavy-duty narcotics that he was taking for back pain.

Case 2: Palmitoylethanolamide: easier breathing and less salivating

Ten days of normast (tablets 600 mg x 2) Early May ALS had taken over: my breathing got worse, I needed my Bi-Pap almost 24h/24, I had no more appetite, my voice got weak, my speech was no longer understandable, excess saliva…

Normast not only put a hold but I’ve been experiencing some improvements: Breathing: slightly better, I can breathe again 20’ without my Bi-Pap , I eat a little more.

My voice is stronger, my speech is better. Excess saliva: I’ve got a small window in the morning, and another one of around 2 hours in the afternoon during which my saliva is back to normal Arms: a little stronger I now hope that it’s only the beginning. We’ll see. I add some Indian ginseng believing the combination of the two will be more powerful.

Gone with ALS!

The ALS foundation clearly summarizes it one more time:

ALS (amyotrophic lateral sclerosis) is a very serious muscle/nerve-condition, which causes the nerve cells in the spine and brain to slowly die off. One after the other muscle group stops functioning.

When diagnosed, a person has an average of three more years to live. Little is still known about the cause.

That’s why the ALS foundation is raising funds for research. We are also active in raising awareness about the disease and improving the quality of care for the 500 people that are affected by ALS every year. We have a long way to go before we can cure or slow down ALS. ALS needs to go! Help us to fight ALS.


Palmitoylethanolamide for ALS: dose recommendations

Palmitoylethanolamide could open a new chapter in the treatment of ALS. In our opinion, a test treatment could be considered for every ALS patient, as there are no side effects.

It is best to dose high: first week 3 times 400 mg capsules (select only capsules which have been clinically tested for safety and efficacy for some years, capsules with the PEA-opt mark. Second week double dose. Try for 2 month. If no result stop. Sometimes the effect becomes quite clear after stopping abruptly.



[1] Fujita K, Izumi Y, Kaji R. | [Inflammatory mechanisms in amyotrophic lateral sclerosis]. |Brain Nerve. | 2012 Mar;64(3):273-8.

[2] Li G, Esiri MM, Ansorge O, DeLuca GC. | Concurrent multiple sclerosis and amyotrophic lateral sclerosis: where inflammation and neurodegeneration meet? | J Neuroinflammation. |2012 Jan 24;9:20. doi: 10.1186/1742-2094-9-20.

[3] Calvo A, Moglia C, Balma M, Chiò A. | Involvement of immune response in the pathogenesis of amyotrophic lateral sclerosis: a therapeutic opportunity? | CNS Neurol Disord Drug Targets. | 2010 Jul;9(3):325-30.

[4] Graves MC, Fiala M, Dinglasan LA, Liu NQ, Sayre J, Chiappelli F, van Kooten C, Vinters HV.Inflammation in amyotrophic lateral sclerosis spinal cord and brain is mediated by activated macrophages, mast cells and T cells. | Amyotroph Lateral Scler Other Motor Neuron Disord. |2004 Dec;5(4):213-9.

[5] Purcell WM, Westgate C, Atterwill CK. | Rat brain mast cells: an in vitro paradigm for assessing the toxic effects of neurotropic therapeutics. | Neurotoxicology. | 1996 Fall-Winter;17(3-4):845-50.

[6] Lewis CA, Manning J, Rossi F, Krieger C. | The Neuroinflammatory Response in ALS: The Roles of Microglia and T Cells. | Neurol Res Int. | 2012;2012:803701. doi: 10.1155/2012/803701. Epub 2012 May 15.

[7] Fiala M, Chattopadhay M, La Cava A, Tse E, Liu G, Lourenco E, Eskin A, Liu PT, Magpantay L, Tse S, Mahanian M, Weitzman R, Tong J, Nguyen C, Cho T, Koo P, Sayre J, Martinez-Maza O, Rosenthal MJ, Wiedau-Pazos M. | IL-17A is increased in the serum and in spinal cord CD8 and mast cells of ALS patients. | J Neuroinflammation. | 2010 Nov 9;7:76. doi: 10.1186/1742-2094-7-76.

[8] Calvo A, Moglia C, Balma M, Chiò A. | Involvement of immune response in the pathogenesis of amyotrophic lateral sclerosis: a therapeutic opportunity? | CNS Neurol Disord Drug Targets. | 2010 Jul;9(3):325-30.

[9] Pacher P, Mackie K. | Interplay of cannabinoid 2 (CB2) receptors with nitric oxide synthases, oxidative and nitrative stress, and cell death during remote neurodegeneration. | J Mol Med (Berl). | 2012 Apr;90(4):347-51. doi: 10.1007/s00109-012-0884-1.

[10] Moreno-Martet M, Mestre L, Loría F, Guaza C, Fernández-Ruiz J, de Lago E. |Identification of receptors and enzymes for endocannabinoids in NSC-34 cells: relevance for in vitro studies with cannabinoids in motor neuron diseases. | Neurosci Lett. | 2012 Feb 6;508(2):67-72. doi: 10.1016/j.neulet.2011.12.020. Epub 2011 Dec 22.

[11] Rossi S, Bernardi G, Centonze D. | The endocannabinoid system in the inflammatory and neurodegenerative processes of multiple sclerosis and of amyotrophic lateral sclerosis. | Exp Neurol. | 2010 Jul;224(1):92-102. doi: 10.1016/j.expneurol.2010.03.030. Epub 2010 Mar 29


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