Sir,Nutritional and toxic optic neuropathy (TON) is a condition where bilateral progressive and symmetrical loss of vision occurs.[1] We present a chronic case of alcohol and tobacco abuse-related TON in a 65-year-old lady who recovered almost fully by change in her lifestyle. The symptoms had been noticed about a year ago and were gradually progressive in nature. The patient was a chronic alcoholic (about 6 L of wine per day) and also a heavy smoker (40 cigarettes per day) for past 7 years.The clinical examination revealed visual acuities of 6/72 in the right, counting fingers in the left eye. The pupils were sluggish, without any afferent papillary defect. The color vision was impaired to 6/17 plates. The fundus examination revealed pale optic discs and the visual fields showed constriction of right visual field (left field was not recordable due to poor vision) Optical coherence tomography (OCT) on optic nerve head showed bilateral temporal thinning of the nerve fibre layer and macular OCT showed loss of papillomacular bundle.A clinical diagnosis of toxic neuropathy was made. Serum vitamin B 12 was low 156 ng/L (normal range: 180-650) and folate level was normal. Imaging of the visual pathway was normal. Electrophysiological test results were highly suggestive of optic neuropathy.The patient was commenced on vitamin B12 oral supplements and advised a change in her lifestyle. In 12 months, her vision improved to 6/38 in the right and 6/60 in the left eye by reducing the alcohol to 1 L per day and smoking to 10/day and with improvement of the diet. By 24 months, her vision was 6/9 in the right and 6/12 in the left and her field tests and color vision in both eyes improved significantly. Serum B12 became normal. Electrophysiological tests showed a marked improvement in N95 component of pattern electroretinography which suggests improvement in the ganglion cell function. Repeat visually evoked potential (VEP) showed only mild optic nerve dysfunction.Alcohol and tobacco abuse-related optic neuropathy is characterized by papillomacular bundle damage, central or centrocecal scotoma, and reduced color vision.[2] A detailed history and ocular examination including color vision and field test and investigations for serum B12 and red cell folate levels are essential in the diagnosis. Neuroimaging is usually normal but is indicated to rule out causes of compressive neuropathy.[3] VEP and OCT are helpful in the diagnosis.[45] The management is by reducing/stopping smoking and the intake of alcohol, along with vitamin B12 and folate supplementation and improvement in the diet. This case shows that by early intervention and dietary improvement, the optic nerve functions could be recovered almost fully in TON.