Secondary Neuroprotection in Glaucoma from Change in Lifestyle

Abstract

Glaucoma therapy usually includes lowering IOP, but a healthy lifestyle may also be recommended. We discuss how this can be defined and the underlying secondary neuroprotective mechanisms. One neuroprotective measure is to avoid common neurotoxic pollution like cigarette smoking, ethanol, methanol or lead. Nutrition should be rich in variety and prevent vitamin B12 and folate deficiency. Supernutrition may lead to the metabolic syndrome and increase IOP, arterial hypertension and serum steroid levels. The metabolic syndrome can also lead to decreased renal function, which can cause accumulation of neurotoxic substances in the blood. Enhanced physical activities is useful, as this burns calories and reduces caloric intake. In contrast to supernutrition, during starvation ketone bodies like acetone, acetoacetate and β-hydroxybutyrate are synthesised. These are thought to have neuroprotective effects, due to the additional power supply to the mitochondria. Ketosis can also occur after increased intake of fatty acids - which is generally not recommended, due to the cardiovascular risks involved. In addition to burning calories, endurance sports can reduce fear and depression, and neurotrophins with neuroprotective effects are released. Genetically determined or acquired mitochondrial dysfunction can both play a role in glaucomatous optic nerve impairment. Therefore, knowledge of secondary neuroprotective mechanisms can help in giving patient professional advice to minimise risks and to restore homeostasis in optic nerve metabolism.