Palmitoylethanolamide (PEA) as a Treatment of Normal Tension Glaucoma

People with Normal Tension Glaucoma (NTG) may have “normal” or high normal IOP yet still develop nerve damage. Although the cause of Normal Tension Glaucoma is unknown, a number of risk factors have been discovered including:

  • Systemic hypotension (low blood pressure)[1]
  • Cardiovascular (heart) disease[2]
  • Vasospasm[3]
    • Conditions including migraine and Raynaud’s disease
  • Defective vascular autoregulation[4]
  • Autoimmune disease[5]
  • Hemorheologic (blood “thickening”) abnormalities[6]
  • Cerebral microvascular ischemia[7]

As with the more common forms of glaucoma, Normal Tension Glaucoma is treated by lowering the intraocular pressure (IOP). As you might surmise, however, this can be a challenge when the IOP is already in the “normal” range. Eye drops, laser therapies, and many of the lower-risk surgical treatments simply don’t work as well at lowering the IOP when it is already within the physiologic range. As such, many patients with Normal Tension Glaucoma end up requiring trabeculectomy surgery in order to slow vision loss.

The supplement Ginkgo biloba has been studied as a potential treatment of Normal Tension Glaucoma. Unfortunately, due to its blood thinning properties, it may not be safe for those already taking prescription blood thinners to also take Ginkgo biloba. Fortunately, it appears that Ginkgo biloba may not be the only natural supplement with a potential role in the treatment of Normal Tension Glaucoma.

What it is Palmitoylethanolamide (PEA)?

Palmitoylethanolamide (PEA) is a naturally occurring substance that mimics chemicals known as endocannabinoids[8]. Our bodies naturally produce PEA.[9] Certain foods such as peanut oil, egg yolk, and soybean lecithin also contain PEA.[10] If the term “endocannabinoid” sounds familiar it is because “cannabis” is the term used to describe plants that produce delta-9-tetrahydrocannabinol (the main active ingredient in marijuana). There is evidence that cannabinoids can be used to treat glaucoma.[11] What about PEA?

Evidence that PEA can be used to Treat Normal Tension Glaucoma (NTG)

PEA has been shown to increase the flow of aqueous fluid out of the eye.[12] Additionally, PEA is naturally found in the ciliary body (the eye tissue that produces aqueous fluid). In patients with glaucoma there is a reduced amount of PEA in the ciliary body[13]. If patients with glaucoma have a decreased amount of PEA in their eyes could increasing the amount of PEA treat glaucoma?

The answer appears to be “yes”. An Italian study evaluated the effect of taking 300mg of PEA twice daily over a six month period. Patients with Normal Tension Glaucoma were randomized into treatment or no treatment (it would have been a more convincing study had there been a placebo control). Those patients who received PEA experienced both lower IOP (average 14.4mmHg -> 11.1mmHg) and visual field improvement.[14]

Potential Side Effects and Risks of PEA

No serious ocular or systemic side effects have been noted at a dose of 300mg taken twice daily.

Potential Drug Interaction

No known drug interactions.[15]

Recommended Dosage

In the above mentioned study patients were instructed to take 300mg of PEA by mouth twice daily (after breakfast and dinner).

Where to Buy

PEA is not cheap. The purest commercially available form (PeaPureTM) is $30-50 for a package of 30 (thirty) 400mg capsules. I am aware of only one US reseller who currently stocks PeaPureTM: FitEyes.

The formulation used in the Normal Tension Glaucoma study referenced earlier was Visimast® 300mg (taken twice daily). Although commonly available in Italy, Visimast® is not commercially available in the USA. Of the Italian pharmacies that are willing to ship Visimast® to the USA, the quoted delivery fees alone can be upwards of $100. So, unless someone is purchasing a year’s supply, this would not be a very economical option.

Regardless of the form of PEA taken, the expected monthly cost of this treatment would be in the range of $45-100 USD.

Summary

Because the IOP is in the normal range, those with Normal Tension Glaucoma are often diagnosed late in the disease after significant vision loss has occurred. Even when diagnosed early, Normal Tension Glaucoma tends to be one of the more challenging forms of glaucoma to control with standard lower-risk therapies. The only other supplement with decent evidence of benefit in those with Normal Tension Glaucoma, Ginkgo biloba, cannot be safely taken in those who are also on prescription blood thinners. PEA, on the other hand, has no known serious side effects or drug interactions. Thus, I currently recommend that my patients with Normal Tension Glaucoma who can afford to do so take 300mg of PEA twice daily.

References
  1. Graham SL, Drance SM, Wijsman K, et al. Ambulatory blood pressure monitoring in glaucoma: the nocturnal dip. Ophthalmology 1995;102:61–9.

    Leighton DA, Phillips CI. Systemic blood pressure in open-angle glaucoma, low tension glaucoma, and the normal eye. Br J Ophthalmol 1972;56:447–53.

    Chumbley LC, Brubaker RF. Low-tension glaucoma. Am J Ophthalmol 1976;81:761–7.

    Goldberg I, Hollows FC, Kass MA, Becker B. Systemic factors in patients with low-tension glaucoma. Br J Ophthalmol 1981;65:56–62.

    Hayreh SS, Podhajsky P, Zimmermann MB. Role of nocturnal arterial hypotension in optic nerve head ischemic disorders.Ophthalmologica 1999;213:76–96.

  2. Goldberg I, Hollows FC, Kass MA, Becker B. Systemic factors in patients with low-tension glaucoma. Br J Ophthal-mol 1981;65:56–62.

    Johnson DG, Drance SM. Some studies on the circulation in patients with advanced open angle glaucoma. Can J Ophthalmol 1968;3:149–53.

    Drance SM. Some factors in the production of low tension glaucoma. Br J Ophthalmol 1972;56:229–42.

    Drance SM, Sweeney VP, Morgan RW, Feldman F. Studies of factors involved in the production of low tension glaucoma. Arch Ophthalmol 1973;89:457–65.

  3. Klein BEK, Klein R, Meuer SM, Goetz LA. Migraine headache and its association with open-angle glaucoma: the Beaver Dam Eye Study. Invest Ophthalmol Vis Sci 1993;34:3024–7.

    Wang JJ, Mitchell P, Smith W. Is there an association between migraine headache and open-angle glaucoma? Findings from the Blue Mountains Eye Study. Ophthalmology 1997;104:1714–9.

    Phelps CD, Corbett JJ. Migraine and low-tension glaucoma. A case-control study. Invest Ophthalmol Vis Sci 1985;26:1105–8.

    Gasser P, Flammer J. In?uence of vasospasm on visual function. Doc Ophthalmol 1987;66:3–18.

    Guthauser U, Flammer J, Mahler F. The relationship between digital and ocular vasospasm. Graefes Arch Clin Exp Ophthalmol 1988;226:224–6.

    Drance SM, Douglas GR, Wijsman K, et al. Response of blood ?ow to warm and cold in normal and low-tension glaucoma patients. Am J Ophthalmol 1988;105:35–9.

    Lewis RA, Vijayan N, Watson C, et al. Visual ?eld loss in migraine. Ophthalmology 1989;96:321–6.

    Gasser P, Flammer J, Guthauser U, Mahler F. Do vasospasms provoke ocular diseases? Angiology 1990;41:213–20.

  4. Pillunat LE, Stodtmeister R, Wilmanns I, Christ T. Autoregulation of ocular blood ?ow during changes in intraocular pressure: preliminary results. Graefes Arch Clin Exp Ophthalmol 1985;223:219–23.
  5. Wax MB, Tezel G, Saito I, et al. Anti-Ro/SS-A positivity and heat shock protein antibodies in patients with normal-pressure glaucoma. Am J Ophthalmol 1998;125:145–57.

    Wax MB, Barrett DA, Pestronk A. Increased incidence of paraproteinemia and autoantibodies in patients with normal-tension glaucoma. Am J Ophthalmol 1994;117:561–8.

  6. Drance SM, Sweeney VP, Morgan RW, Feldman F. Studies of factors involved in the production of low tension glaucoma. Arch Ophthalmol 1973;89:457–65.

    Mary A, Serre I, Brun JF, et al. Erythrocyte deformability measurements in patients with glaucoma. J Glau

  7. Stroman GA, Stewart WC, Golnik KC, et al. Magnetic resonance imaging in patients with low-tension glaucoma. Arch Ophthalmol 1995;113:168–72.
  8. Lambert DM, Di Marzo V. The palmitoylethanolamide and oleamide enigmas: are these two fatty acid amides cannabimimetic? Curr Med Chem. 1999;6:757–773.
  9. Bachur NR, Masek K, Melmon KL, Udenfriend S. Fatty acid amides of ethanolamine in mammalian tissues. J Biol Chem.1965;240:1019–1024.
  10. Kuehl FA, Jacob TA, Ganley OH, Ormond RE, Meisinger MAP. The identi?cation of N-(2-hydroxyethyl)-palmitamide as a naturally occurring anti-in?ammatory agent. J Am Chem Soc. 1957;79:5577–5578.
  11. Buchwald A, Browne CE, Wu WM, Ji F, Bodor N. Soft cannabinoid analogues as potential anti-glaucoma agents. Pharmazie. 2000;55:196–201.
  12. Kumar A, Qiao Z, Kumar P, Song ZH. Effects of palmitoylethanolamide on aqueous humor outflow. Invest Ophthalmol Vis Sci. 2012 Jul 3;53(8):4416-25.
  13. Chen J, Matias I, Dinh T, et al. Finding of endocannabinoids in human eye tissues: implications for glaucoma. Biochem Biophys Res Commun. 2005;330:1062–1067.
  14. Costagliola C, Romano MR, dell’Omo R, Russo A, Mastropasqua R, Semeraro F. Effect of palmitoylethanolamide on visual field damage progression in normal tension glaucoma patients: results of an open-label six-month follow-up. J Med Food. 2014 Sep;17(9):949-54.
  15. Keppel Hesselink JM. New targets in pain, non-neuronal cells, and the role of palmitoylethanolamide. Open Pain J. 2012;5:12–23.

Don’t delay getting checked for glaucoma.

Make an appointment with an eye doctor in your area now.  If you live in the greater Los Angeles area and would like Dr. Richardson to evaluate your eyes for glaucoma call 626-289-7856 now. No referral required. Same day or next day appointments are available, Tuesday through Saturday.

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