Is Occasional Alcohol Drinking and Smoking Related to the Development of Age-Related Cataract?

We have read with interest the article by Jiang et al.,¹ in which the authors analyzed the association between alcohol drinking, cigarette smoking, and other general and ocular diseases with the risk of age-related cataract. To assess potential causal effects, a two-sample Mendelian randomization analysis was conducted based on data from the Genetic Epidemiology Research on Adult Health and Aging (United States, all non-Hispanic Whites) and the UK Biobank (all European-descent individuals) cohorts was conducted. 

The study found no association between alcohol consumption and cataract risk (P > 0.05).¹ The existing evidence evaluating the relation between alcohol intake and the risk of developing cataract has been inconsistent. In a recent study on Chinese individuals, Im et al.² found that regular drinkers had a nonsignificantly greater risk of developing cataract compared to occasional drinkers (hazard risk [HR], 1.08; 95% confidence interval [CI], 1.03–1.12); however, cataract has been significantly more common among current drinkers (280 g/week; HR, 1.21; 95% CI, 1.09–1.33). The results were stratified by age at risk and study area and were adjusted for education and smoking. Chua et al.³ found a decreased likelihood of needing cataract surgery among individuals who engage in low to moderate alcohol consumption in a multiethnic UK cohort. This association was particularly noticeable in relation to the consumption of wine. Kanthan et al.⁴ noted a U-shaped relationship between alcohol intake and the long-term likelihood of requiring cataract surgery among the older participants in Wisconsin. Moderate alcohol consumption was associated with a 50% reduced incidence of cataract surgery compared to both abstaining from alcohol and consuming it heavily. A meta-analysis by Gong et al.⁵ also found that moderate consumption may be protective for cataracts, although heavy consumption was associated with risk of age-related cataract. The results shown by the study of Im et al. seem to resonate with these findings; drinkers of a mild amount of alcohol (<140 g/week) tended to have lower HR than the controls (0.96; 95% CI, 0.89–1.03) and similar results are seen for patients with any eye and adnexa pathologies, with a HR of 0.94 (95% CI, 0.88–1.00), which seems to be borderline protective. 

Potentially, oxidative stress plays a role in the development of cataracts. Heavy alcohol consumption has the potential to trigger the production of microsomal enzyme cytochrome CYP2E1 in the liver. When metabolizing ethanol, this enzyme generates free radicals that can contribute to the aggregation of lens proteins, which do not metabolize, ultimately leading to cataract formation in elderly individuals. This factor could explain the differences between drinking habits and the risk of developing cataract with a potentially more harmful effect of drinking spirits versus wine. Other potential mechanisms include alteration of calcium levels within the lens and increased permeability of lens fiber cell membrane caused by alcohol exposure. There also might be different genetic susceptibility between European and Asian populations due to different variants of alcohol and aldehyde dehydrogenase variants.⁶ 

The study found no significant association between cigarette smoking and cataract (P > 0.05).¹ The current literature analyzing the influence of smoking on cataract development is more consistent. The meta-analysis by Ye et al.,⁷ which included 13 cohort and 8 case-control studies, concluded that smoking is linked to a higher risk of age-related cataract, particularly nuclear cataract. Moreover, current smokers were at a higher risk of cataract than past smokers. Cataract formation is believed to involve significant oxidative damage. Smoking introduces additional oxidative stress by triggering free radical activity, promoting oxidation, and lipid peroxidation. Furthermore, tobacco byproducts contain heavy metals like cadmium, lead, and copper, which accumulate in the lens and cause direct toxicity. 

Acknowlegements

Disclosure: P. Kanclerz, fees from Alcon, Carl Zeiss Meditec, nonfinancial support from Visim and Optopol Technology; I. Hecht, None; R. Tuuminen, scientific adviser (advisory board, honoraria) to Alcon Laboratories, Inc., Allergan, Inc., Bayer AG, F. Hoffmann–La Roche, Ltd., and Novartis AG, and has received clinical trial support (study medicines) from Bayer AG and Laboratoires Théa