Unique properties of PeaPure

• The most pure PEA product
• A natural substance identical to the body's own
• Optimized formula without stearic acid, magnesium stearate and other ingredients.
• Patent on formulation pending

Information from Wikipedia

• PEA seems to be produced in human as well as in animals as a biological response and a repair mechanism in chronic inflammation and chronic pain.
• Several papers have demonstrated that alterations in the endogenous levels of PEA occur in chronic inflammation. Chronic inflammation is thought to underlie glaucoma.
• PEA has been shown to have anti-inflammatory, anti-nociceptive (anti-pain), neuroprotective, and anticonvulsant properties.
• PEA inhibits the release of both preformed and newly synthesized mast cell mediators, such as histamine and TNF-alpha.
• PEA can also reduce reperfusion injury.

For references, see:
Palmitoylethanolamide - Wikipedia, the free encyclopedia

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Research

A new treatment paradigm for Glaucoma?

Ophthalmology Times Europe

Jan 1, 2013
By: Dr Caterina Gagliano
Volume 9, Issue 1

Following on from earlier studies demonstrating that systemic administration of palmitoylethanolamide (PEA), a fatty acid ethanolamide, reduces intraocular pressure (eye pressure or "IOP") in patients with glaucoma and ocular hypertension,^1–3 Dr Caterina Gagliano has conducted a further study into the effects of systemic PEA on glaucoma. The results of the study — Clinical trial for the evaluation of neuroprotective effects of palmitoylethanolamide: Visual Field and Pattern-ERG — were communicated through an oral presentation at the EVER congress, held in Nice, France.

While previous studies have focused solely on the eye pressure-lowering effect of PEA, this study increased the dose of PEA administered and measured change in visual field, to assess the impact of PEA on the trabecular meshwork (TM) and its potential neuroprotective activity in glaucoma patients.

Discussing the rationale for the trial and its potential applications in glaucoma, Dr Gagliano explained, "Activation of the glial cells and the consequent neuroinflammatory response is increasingly recognized as a prominent neuropathological feature of glaucoma damage and should therefore be addressed."

About the trial

The prospective, randomised, crossover, double-blind clinical trial evaluated the effects of PEA on intraocular pressure, visual field (VF) and pattern-ERG (PERG) in primary open angle glaucoma (POAG) and ocular hypertension (OH) patients.

Prior to enrolment in the study, the 36 patients included were all receiving topical treatment with timolol 0.5% and had undergone a minimum of five VF tests using the Humphrey Visual Field Analyzer (Threshold 30-2) over a 2-year period. Upon enrolment, study subjects were randomly assigned to either Group A (PEA 300 mg orally twice daily) or Group B (placebo), and were examined at baseline and after 6, 12, 18 and 24 months of treatment. The assessment parameters were change of progression rate of VF using mean deviation (MD) and pattern standard deviation (PSD). Comparison of means was performed with the paired t-test.

"To monitor progressive change of retinal ganglion cell function, we used the pattern electroretinograms twice annually over at least 2 years," noted Dr Gagliano. "The evaluation of the pattern ERG used the amplitude of P50 and N95, and each of the parameters were respected."

Results in traditional parameters

PEA-treated patients experienced a statistically significant reduction in intraocular pressure compared with the eye pressure lowering achieved by subjects receiving placebo (16.94 ± 3.96 vs 13.8 ± 3.24 mmHg; P < 0.001). There was also a statistically significant difference in the MD between the two groups (Group A: –2.9 dB ± 2.93; Group B, –8.55 dB ± 6.51; P = 0.001). The change in PSD reached statistical significance after 24 months of treatment (Group A, 2.64 dB ± 1.47; Group B, 6.59 dB ± 6.51; P = 0.002). PERG amplitude increased significantly (P < 0.01) in Group B patients compared with in Group A patients: at 6, 12, 18 and 24 months, a significant decrease of P50 and N95 amplitude in PEA-treated patients was observed.

"Significant intraocular pressure reduction was observed in Group A," summarized Dr Gagliano. "At 24 months, the mean intraocular pressure decreased 16% from baseline. Additionally, Circadian rhythm variance reduced from baseline by 10%, and a statistically significant difference in the MD was found between the two groups after 12, 18 and 24 months."

Moreover, throughout the 2-year treatment period, PEA medication remained safe and well tolerated, with no drug-related adverse events.

"These findings show substantial clinical benefits of PEA treatment in POAG patients: reduction of intraocular pressure as well as significant improvement in VF and PERG," Dr Gagliano noted. "Based on this evidence we also assessed the relevance of this neuroprotective effect of PEA to treatment in glaucoma patients."

Neuroprotection

Dr Gagliano reported that the reason her team had chosen to research the neuroprotective effect of PEA had been to examine the hypothesis that the effect of PEA — which has been demonstrated to reduce the activation of microglial cells, reducing chronic inflammation — could also work in the same way to preserve or repair cells in glaucoma.

"We believe that targeting the signalling pathways in glial cells responsible for neuroinflammation represents a promising new therapeutic approach in glaucoma," she asserted, adding, moreover, that PEA may also be able to protect against neurotoxicity, and should continue to function even once an insult has been initiated. "Treatment with PEA has an impact on the degree of apoptosis, with up-regulation of pro-apoptotic BAX and down-regulation of anti-apoptotic BCL-2 among the changes," Dr Gagliano noted, to explain this hypothesis.

"All these actions — the intraocular pressure-lowering effect as well as neuroprotection — are mediated by receptor mechanism peroxisome proliferator activated receptor alfa (PPR-alfa) and G-protein coupled receptor 55 (GPR55)."

The future of glaucoma management?

Dr Gagliano concluded her presentation by asserting that, if other clinical trials and laboratory evidence support the results of this study, the treatment paradigm in glaucoma has the potential to shift beyond the current efforts to reduce intraocular pressure and will in addition begin to focus on our ability to preserve visual function for glaucoma patients.

"Although there's still much work to be done in this area, we shouldn't forget what a long way we've already come," she asserted.

References

1. C. Gagliano et al., Invest. Ophthalmol. Vis. Sci., 2011;52(9):6096–6100.

2. A. Kumar et al., Invest. Ophthalmol. Vis. Sci., 2012;53(8):4416–4425.

3. E. Strobbe et al., Invest. Ophthalmol. Vis. Sci., Published on-line before print 10 January 2013, doi: 10.1167/iovs.12-10899