Rüfer Florian
Glaukomdepartment, nordBLICK Augenklinik Bellevue, Kiel.
Klin Monbl Augenheilkd. 2020 Feb;237(2):158-162. doi: 10.1055/a-1078-1333. Epub 2020 Feb 10.
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 B 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.
青光眼治疗通常包括降低眼压,但也可能建议采取健康的生活方式。我们讨论如何定义这一点以及潜在的继发性神经保护机制。一种神经保护措施是避免常见的神经毒性污染,如吸烟、乙醇、甲醇或铅。营养应丰富多样,预防维生素B和叶酸缺乏。过度营养可能导致代谢综合征,并增加眼压、动脉高血压和血清类固醇水平。代谢综合征还可能导致肾功能下降,从而导致神经毒性物质在血液中积累。加强体育活动是有益的,因为这能燃烧卡路里并减少热量摄入。与过度营养相反,在饥饿期间会合成丙酮、乙酰乙酸和β-羟基丁酸等酮体。由于为线粒体提供了额外的能量供应,这些物质被认为具有神经保护作用。增加脂肪酸摄入量后也可能发生酮症——由于涉及心血管风险,一般不建议这样做。除了燃烧卡路里,耐力运动还可以减轻恐惧和抑郁,并释放具有神经保护作用的神经营养因子。遗传决定的或后天获得的线粒体功能障碍都可能在青光眼性视神经损伤中起作用。因此,了解继发性神经保护机制有助于为患者提供专业建议,以将风险降至最低并恢复视神经代谢的稳态。