Ginkgo biloba for Ocular Perfusion and Visual Field Preservation: Promise and Precautions

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Ginkgo Biloba and Ocular Perfusion in GlaucomaGinkgo biloba extract (GBE) is a botanical supplement long studied for its circulatory and neuroprotective effects. In glaucoma – especially normal-tension glaucoma (NTG) where intraocular pressure is not elevated – vascular dysregulation and poor optic nerve perfusion are thought to contribute to retinal ganglion cell loss. GBE’s flavonoids and terpenoids (e.g. ginkgolides) may improve microcirculation, inhibit platelet-activating factor (PAF) and support neuronal health () (). This article reviews GBE’s mechanisms of action, evidence for visual field and blood flow effects in glaucoma, relevant data from cognitive and cerebrovascular aging studies, and addresses safety (bleeding risk, drug interactions). We also outline optimal trial designs to test GBE in glaucoma patients.Mechanisms of ActionMicrocirculation and Vasodilation Ginkgo’s polyphenolic flavonoids and terpenoids enhance small-vessel circulation. In vitro and clinical studies show that GBE improves blood rheology: it increases erythrocyte deformability, lowers fibrinogen, and reduces blood viscosity and elastic resistance () (). GBE also promotes endothelium-dependent vasodilation. For example, GBE increases nitric oxide (NO) and prostacyclin release, and can lower systemic vascular resistance () (). In healthy elderly adults, intravenous GBE raised coronary artery blood flow and brachial artery flow‐mediated dilation (). Improved vasodilation and blood fluidity in small vessels could enhance ocular perfusion pressure and retinal capillary flow, which are often reduced in NTG () ().Platelet-Activating Factor (PAF) Antagonism Ginkgolides (B, A, C, J) in GBE are potent PAF receptor antagonists. In vitro, ginkgolides block PAF-induced platelet aggregation (a step in microthrombosis) () (). This anti-thrombotic action can theoretically reduce microvascular ischemia in the optic nerve. However, clinically relevant effects are unclear: one lab study found 50% inhibition of human platelet PAF aggregation by ginkgolide B required ~2.5 μg/mL (much higher than blood levels achieved with standard doses) (). Because PAF per se is a weak platelet activator, it remains uncertain if GBE meaningfully prolongs bleeding time or causes hemorrhage () (). In short, ginkgo’s PAF antagonism may improve microcirculation, but does not appear to dramatically disrupt normal hemostasis at usual doses ().Neuroprotection and Antioxidant Effects GBE contains flavonoid glycosides (quercetin, kaempferol etc.) with strong antioxidant activity. These can scavenge free radicals, stabilize mitochondria and inhibit oxidative apoptosis () (). Experimental studies show EGb761 (standard extract) protects mitochondrial membrane potential under stress and boosts ATP generation () (). GBE also reduces low-grade inflammation: it suppresses inducible nitric oxide synthase and pro-inflammatory cytokines in neural tissues () (). Such neuroprotective actions could plausibly slow retinal ganglion cell (RGC) death in glaucoma. Indeed, animal models suggest GBE counters glutamate excitotoxicity and oxidative injury to neurons (). Clinical Evidence in GlaucomaVisual Field Outcomes Several small studies have tested GBE in NTG patients to see if visual fields stabilize. A prospective double-blind crossover trial of 27 NTG patients (40 mg GBE three times daily for 4 weeks) found significant short-term improvements in visual field indices: mean