Lou Gehrig’s disease (ALS) treated with palmitoylethanolamide
Palmitoylethanolamide (PEA) is an anti-inflammatory body own molecule and might be able to fight off part of the neuro-inflammation in ALS.
Simonetta Clemente (MD) from the Macomer Rehabilitation Center, Nuoro Health Care Center, Italy published an important mile stone paper in 2012, title: 'Amyotrophic Lateral Sclerosis Treatment with Ultramicronized Palmitoylethanolamide: A Case Report'.
In this paper she descibes the positive effect of the natural and body-own compound palmitoylethanolamide (PEA) in ALS, amyotrophic lateral sclerosis, a devasting neurological disorder also known as Lou Gehrig's disease in the USA.
In her article she points out that PEA has potent anti-inflammatory activity in many acute and inflammatory and chronic pain models, that PEA reduces spinal cord trauma in mice, and has neuroprotective properties.
She refers to the recent findings from professor's Cruccu's group, that PEA has seen to improve myelinated-fibre function in patients with chemotherapy-induced painful neuropathy and to other recent publications were PEA was seen to reduce pain severity in patients with pain associated to different pathological conditions who were undergoing standard therapies with unsatisfactory results or in those patients who discontinued standard therapy because of important side effects.
Given the lack of an effective therapy for ALS, as she correctly stated, she explored and reported the effects of PEA in a case of ALS.
The ALS patient
The patient she treated was a 64-year-old male experienced the first symptoms around 2 months
after returning from a long hiking tour. 
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
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.
important to point out that there have never been any reports
of adverse events related to PEA administration in man.
More science on endocannabinoids and amyotrophic lateral sclerosis
In a recent overview in the
International Journal of Basic & Clinical Pharmacology (September-October 2012 | Vol 1 | Issue 2 Page 48) , title: Cannabinoids and their medicinal potential Deepika Tikoo and colleagues presented some more preclinical data to support the use of PEA in ALS:
In SOD1G93A mice, a model of ALS, cannabinoids was seen to delay onset of symptoms and prolong survival by non CB1 receptor mechanism.
15 Genetic ablation of FAAH, the enzyme responsible for metabolizing endocannabinoids, prevented the onset of disease signs in these mice. CB1 receptor induced mechanism did not seem to play a role in this.
A safety study of THC done on ALS patients showed beneficial effects in spasticity, insomnia and appetite.
Very few clinical studies evaluating the benefits of cannabinoids are available in ALS patients and there seems to be hope for them as preclinical studies have shown the neuroprotective effect of cannabinoids.
Availability and use & dose of PEA in ALS
PEA is available under two brandnames: Normast and PeaPure. Normast has separate powder for under the tongue (including quite a bit sorbitol (384 mg);this is the cause for some ALS patients to suffer from diarree. We quote a patient:
This is 3rd day of taking 2 PEA satchels a day. Have had diarrhea each day, not a common thing.
PeaPure is also available as powder for under the tongue via capsules of 400 mg which are easy to open. PeaPure does not contain any sorbitol and thus does not cause diarree.
Normast sachets are sweet and thus induce quite a bit of saliva, making sublingual resorption a bit difficult. PeaPure has no taste, and it does not induce salivation. Especially in ALS were sublingual resportion might be important, this could be an advantage.
Dose recomendation for PeaPure: At least 1600 mg daily powder under the tongue, or in the mounth, without swalling it. Start taking 2 capsules onder the tongue on day 1, 3 on day 2 and 4 on day 4, to taper in.
We never saw troublesome side effects, even if starting directly high, but we like startng slow, to give the body time to adapt. Stay on 4 capusules for a week before deciding to go higher. You can add 2 more capsules, just by aditional swollowing, but always keep at least 3-4 capsules per day to ingest via the buccal mucosa, the mouth.
It is probably not necessary to go higher, so stay somewehere between 1200 mg and 2400 daily (6 capsules).
 Clemente S. | Amyotrophic lateral sclerosis treatment with ultramicronized palmitoylethanolamide: a case report. | CNS Neurol Disord Drug Targets. | 2012 Nov 1;11(7):933-6.