Ulcerative Colitis patients: new hope!

Ulcerative Colitis patients: new hope!

Ulcerative Colitis is an unpleasant, chronic inflammation of the colon. Treatment is difficult, as many of the drugs that are used have nasty side effects. However, there’s exciting news, as two recent studies have emphasized the value of the anti-inflammatory supplement palmitoylethanolamide (PEA).

An experiment in a 2013 study by scientist of the university of Rome (Italy) and Harvard University (USA) showed that the natural substance palmitoylethanolamide (the supplement PEA) can calm the inflamed cells in the colon on the patients.

A 2014 article showed that palmitoylethanolamide can normalize the accelerated passage of food through the intestines. Both are important advantages for Crohn’s and ulcerative colitis.

Ulcerative Colitis: an unpleasant bowel disease! Firstly researchers pose that the glial cells of the intestinal wall play an active roll in inflammation and chronic pain in the colon. This hyperactivity of the glial cells can be reduced with PEA (short for palmitoylethanolamide):

  1. Enteric glial cells actively participate in regulating intestinal pathophysiology.
  2. Enteric glial cells overexpress S100B and are activated during ulcerative colitis.
  3. PEA is able to counteract astroglial activation in a model of Alzheimer disease.

Then, researchers explain what they found in this new study: ulcerative colitis patients and relevant animal models have a series of hyperactive inflammatory cells. PEA can reduce this hyperactivity and inflammation. PEA calms the cells by turning off a certain gene in the cell nucleus which functions as a sort of inflammation switch (the PPAR receptor). [1]

  1. The expression of TLR4/S100B proteins, together with p38/p-ERK/pJNK-pathway signalling molecules and NF-κB expression, are upregulated in EGCs deriving from DSS-treated mice and UC patients.
  2. PEA is able to counteract enteroglial activation, to inhibit macrophages and neutrophils infiltration in colonic mucosa and to downregulate the expression and release of all the proinflammatory markers typical of UC, in mice and humans.
  3. PEA anti-inflammatory effects are mediated mainly by the selective targeting of PPARα site in gut mucosa.

Finally, the researchers state that these results can be of great importance to patients as this offers a new treatment possibility for patients suffering from ulcerative colitis:

This study, by in vitro, ex vivo and in vivo analysis, adds further data on the role of EGCs in intestinal pathophysiology. Additionally, since PEA can counteract inflammatory signals in mice and humans, it might represent a novel and potential pharmacological tool to modulate inflammation during ulcerative colitis. [2]

Ulcerative colitis: less bloody diarrhea and normal bowel movements

Animal tests served as a good reflection on what happens with patients suffering from ulcerative colitis, as the animals also had bloody diarrhea. After giving them PEA, less blood was found in the stool and bowel movement normalized.

On top of that, it turned out that the tissue was already producing PEA during the colitis as a way of natural healing, only that this concentration was too low to create a self-healing effect. PEA had to be supplemented to achieve this. This data is in line with earlier discovered research that pointed in the same direction concerning ulcerative colitis. [3] Other models also showed that PEA has a protective effect in the bowel. [4] This is one of many studies that prove the anti inflammatory effect of PEA, and considered a breakthrough because the healing effect on ulcerative colitis has now been proven effective on human tissue.


PEA: an inviting natural treatment

In 2013, an editorial about the value of PEA for Inflammatory Bowel Disease was published in the prominent journal ‘GUT’. The title of piece the speaks volumes:

Here’s a sample of some of the writing:

Anti-inflammatory effects of PEA depend upon its ability to activate peroxisome proliferator-activated receptors (PPARs), members of the nuclear hormone receptor superfamily of ligand-activated transcription factors.9 The multiple approaches employed in the paper by Esposito et al and the large number of inflammatory markers/mediators measured make a convincing case for PEA-induced anti- inflammatory effects, mediated via PPAR-α. The results demonstrate convincingly that PEA reduces immune cell infiltration and activity in the colon of dextran sodium sulfate (DSS)-treated mice and human UC biopsies.


The data suggest that PEA may represent a viable therapeutic option for the effective treatment of Ulcerative Colitis…


Recommendations for patients

Because PEA has been studied since 1957 and is completely safe in high doses, and because there is a lot of clinical literature supporting the anti-inflammatory and pain relieving effects of PEA, a green light for PEA with ulcerative colitis. As PEA is only available as a supplement and the pharmaceutical industry has no financial gain from the product, we fear that further large clinical research will fail to appear and this information is all that’s available. How should it be dosed?

It is worth it to try PEA for ulcerative colitis. Start with a dose of 1200 mg a day, spread out in 2 or 3 doses over the day, for example 2 times 400mg with breakfast and 1 after dinner. After several weeks, increase the dose to the double amount (a total of 2400mg a dag). If the bowel movements improved after 2-3 months the doses can be lowered to 1200mg a day again. Pea is available as PEA on the internet, just Google the brand name.

PEA can be taken in combination with any other medicine or supplement, as no negative interactions are known.

In another model for bowel disease (post-inflammatory irritable bowel syndrome) PEA also showed to have a clear positive effect on bowel function. [5] PEA can prevent diarrhea and accelerated passage of food. The authors noted: “PEA counteracted the accelerated transit”



[1] Zhang ZF1, Yang N, Zhao G, Zhu L, Wang LX. | Association between the Pro12Ala polymorphism of peroxisome proliferator-activated receptor gamma 2 and inflammatory bowel disease: a meta-analysis. | PLoS One. | 2012;7(1):e30551. doi: 10.1371/journal.pone.0030551. Epub 2012 Jan 19.

[2] Esposito G, Capoccia E, Turco F, Palumbo I, Lu J, Steardo A, Cuomo R, Sarnelli G, Steardo L. | Palmitoylethanolamide improves colon inflammation through an enteric glia/toll like receptor 4-dependent PPAR-? activation. | Gut. | 2013 Sep 30. doi: 10.1136/gutjnl-2013-305005. [Epub ahead of print]

[3] Romano B, Borrelli F, Fasolino I, Capasso R, Piscitelli F, Cascio M, Pertwee R, Coppola D, Vassallo L, Orlando P, Di Marzo V, Izzo A. | The cannabinoid TRPA1 agonist cannabichromene inhibits nitric oxide production in macrophages and ameliorates murine colitis. | Br J Pharmacol. | 2013 May;169(1):213-29. doi: 10.1111/bph.12120.

[4] Di Paola R, Impellizzeri D, Torre A, Mazzon E, Cappellani A, Faggio C, Esposito E, Trischitta F, Cuzzocrea S. | Effects of palmitoylethanolamide on intestinal injury and inflammation caused by ischemia-reperfusion in mice. | J Leukoc Biol. | 2012 Jun;91(6):911-20. doi: 10.1189/jlb.0911485. Epub 2012 Apr 2.

[5] Capasso R1, Orlando P, Pagano E, Aveta T, Buono L, Borrelli F, Di Marzo V, Izzo AA. |Ultramicronized palmitoylethanolamide normalizes intestinal motility in a murine model of post-inflammatory accelerated transit: involvement of CB1 receptors and TRPV1. | Br J Pharmacol. | 2014 May 12. doi: 10.1111/bph.12759. [Epub ahead of print]