Omega-3 Fatty Acids, Inflammation Resolution, and Glaucoma Progression

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Omega-3 Fatty Acids in Glaucoma: Inflammation and Eye HealthGlaucoma is a progressive optic neuropathy often driven by elevated intraocular pressure (IOP) and chronic neuroinflammation. By contrast, omega-3 polyunsaturated fatty acids (PUFAs) – notably eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) – give rise to specialized pro-resolving mediators (SPMs). SPMs (including resolvins, protectins, and maresins) actively turn off inflammation and promote tissue healing. Emerging research suggests SPMs from EPA/DHA might improve the trabecular meshwork outflow of aqueous humor, dampen retinal inflammation, and support blood vessel health in glaucoma () (). This article reviews how these mechanisms could influence eye pressure and retinal neurons, surveys the clinical trials on omega-3 supplements in glaucoma (focusing on IOP, visual function, and ocular blood flow), and connects eye outcomes with broader longevity and cardiovascular findings. Finally, we discuss supplement safety, fish vs. algal omega-3 sources, and quality control concerns.Mechanisms: SPMs, Inflammation Resolution, and the EyeTrabecular Outflow and IOP Regulation The trabecular meshwork (TM) is the eye’s drainage system for aqueous humor. In glaucoma, TM cells are often damaged by oxidative stress and inflammation () (). SPMs derived from omega-3s can counteract chronic inflammation: they shift immune cells from a pro-inflammatory to a healing mode, reduce cytokines (e.g. TNF-α, IL-6) via nuclear factor-κB (NF-κB) inhibition, and reverse tissue damage () (). In the TM, this could mean less endothelial dysfunction and more normal outflow resistance. For example, preclinical studies (though not yet in glaucoma patients) show lipoxins and resolvins protect microvascular endothelium and promote vasodilation by increasing nitric oxide () (). If similar actions occur in the TM or Schlemm’s canal, aqueous drainage might improve, tending to lower IOP. Indeed, dietary omega-3 was shown in mice to enhance trabecular outflow facility and lower age-related IOP, supporting this mechanism (). Retinal Neuroinflammation Glaucoma involves “sterile” inflammation in the retina and optic nerve head. Activated glial cells (astrocytes/microglia) secrete inflammatory mediators that kill retinal ganglion cells (RGCs) () (). SPMs are potent anti-inflammatories: DHA and EPA metabolites (D-series and E-series resolvins, protectins, etc.) promote resolution of neuroinflammation () (). In ocular tissues, pro-resolving lipids have been shown to preserve photoreceptors and RGCs in injury models. For example, lipoxin A₄ (an AA-derived SPM) injected into mouse eyes reduced retinal cell death and restored photoreceptor function in degenerative models (). Similarly, resolvin D1 blunts retinal cytokine responses and protects against retinal injury () (). While direct glaucoma trials are pending, these results suggest EPA/DHA intake could limit the low-grade retinal inflammation seen in glaucoma, complementing IOP lowering.Vascular Function and Ocular Perfusion Glaucoma is also associated with vascular dysregulation and reduced ocular blood flow (). SPMs and omega-3s are well-known to support blood vessels. In cardiovascular studies, SPM receptor activation in endothelium reduces leukocyte adhesion and oxidative stress, restores nitric oxide, and improves vasodilation (). For example, resolvin E1 and others improve endothelial function and reduce vascular inflammation, thereby preventing atherosclerosis in animal mode