In Germany, beer gardens have been allowed to gradually reopen1. But what does this have to do with ophthalmology? Today's blog looks into this.
Only recently, a scientific study was published that looked at the effect of alcohol on the eye's accommodation capacity. This was investigated using different doses of alcohol in a total of 20 emmetropic test persons. The results of this Spanish study were printed in the renowned scientific journal "Graefe's Archive" in April 2021.2 More about this in today's article.
A distinction is made between acute ethanol effects and neuroimmunological changes in chronic alcohol abuse. After the first sip of an alcoholic drink, the toxin enters the brain after only 6 minutes to influence various neurotransmitters. GABA (gamma-aminobutyric acid) production is stimulated and at the same time glutamate is inhibited. GABA itself has an inhibitory effect on neuronal brain activity. Glutamate, on the other hand, stimulates neuronal activity under physiological circumstances - i.e. without the ethanol influence.
Overall, it can be said that there is an attenuation of brain activity. Besides this effect, ethanol has many others up its sleeve. It promotes the release of adrenalin, cortisol, serotonin and dopamine.3-9 Chronic and excessive alcohol abuse leads to neuroimmunological remodelling processes of the brain after only 5 years. The degree of excessive alcohol abuse correlates positively with the loss of grey brain matter in the frontal lobe.10 However, not only the grey brain matter decreases in volume. The white brain matter is also affected. Magnetic resonance imaging measurements showed a reduction of choline-containing areas in the frontal cortex region.11-13 According to neuropathological studies, the number of neurons in the superior frontal cortex is reduced by 22% in persons with alcohol abuse. Chronic alcohol abuse can lead to significant impairment of cognition, non-verbal memory, sense of balance and visuospatial processing.14-16
The human lens is elastic in the early years of life and would assume a spherical shape without the help of the ring-shaped ciliary muscle. It is attached to the ciliary muscle by the zonula fibres. The spherical shape of the lens has a high refractive power. This makes it possible for the eye to move closer. This happens when the ciliary muscle tenses, causing the zonula fibres to relax and the lens to return to its natural spherical shape due to its inherent elasticity. Distance vision is possible in the flattened elliptical shape. The accommodation period is around 0.5 to 1.5 seconds.
Accommodation, convergence and pupil constriction are summarised as the accommodative triad. The maximum increase in refractive power of the lens is also called the accommodative width. The refractive power of a lens is mathematically calculated with the formula "D=1/f" (D=refractive power; f=focal length). The refractive power for the focal length f=20cm can be calculated as follows: D=1/0.2m = 5m-1 = +5 dpt (dioptre). If the accommodation width is less than 3 dioptres, presbyopia is present.17-19
In the present study, accommodation dynamics were measured with and without the influence of alcohol using an autorefractometer (Grand Seiko WAM-5500). All subjects were sober at baseline. Changes in accommodation ability were measured in the fasting state and after ingestion of 300 ml of red wine and 450 ml of red wine. The accommodation tests were carried out for 2.5 D and 5 D. After analysing their data, the research group was able to make the following observation: Alcohol consumption correlated positively with an impairment of the accommodation dynamics of the eyes. There was a significant reduction in the speed of accommodation after the consumption of 450 ml of red wine.
The impairment of the accommodation dynamics correlated positively with the breath alcohol content. The accommodation velocity peaks at 2.5 dpt and 5 dpt were negatively affected by higher alcohol consumption. Accommodative microfluctuations could be observed with higher alcohol consumption.2
So, now we have it in black and white. If you want to read a book in the sun in the near future, you should be careful when choosing your drink.
References:
1. https://www.br.de/nachrichten/bayern/aussengastronomie-in-passau-darf-ab-montag-oeffnen,SWvEG8v (In Geman only).
2. Casares-López M. et al. (2021). Changes in accommodation dynamics after alcohol consumption, for two different doses.Graefes Arch Clin Exp Ophthalmol 259, 919–928 (2021).
3. Claus D. et al. (1970). Einfluss von Aethanol auf die Neurotransmitter Glutamat und GABA [Effect of ethanol on the neurotransmitters glutamate and GABA]. Arch Psychiatr Nervenkr (1970). 1982;232(2):183-9. (In German).
4. Cuzon Carlson V. C. et al. (2018). GABA and Glutamate Synaptic Coadaptations to Chronic Ethanol in the Striatum. Handb Exp Pharmacol. 2018; 248:79-112.
5. Hodge C. W. et al. (2006). Understanding how the brain perceives alcohol: neurobiological basis of ethanol discrimination. Alcohol Clin Exp Res. 2006 Feb;30(2):203-13.
6. Mon A. et al. (2012). Glutamate, GABA, and other cortical metabolite concentrations during early abstinence from alcohol and their associations with neurocognitive changes. Drug Alcohol Depend. 2012 Sep 1;125(1-2):27-36.
7. Zimmermann U. et al. (2004). Effect of ethanol on hypothalamic-pituitary-adrenal system response to psychosocial stress in sons of alcohol-dependent fathers. Neuropsychopharmacology. 2004 Jun;29(6):1156-65.
8. Blaine S. K. et al. (2017). Alcohol, stress, and glucocorticoids: From risk to dependence and relapse in alcohol use disorders. Neuropharmacology. 2017;122: 136-147.
9. Rachdaoui N. et al. (2013). Effects of alcohol on the endocrine system. Endocrinol Metab Clin North Am. 2013;42(3):593-615.
10. Pfefferbaum A. et al. (1995). Longitudinal changes in magnetic resonance imaging brain volumes in abstinent and relapsed alcoholics. Alcohol, Clinical and Experimental Research. 1995; 19:1177–1191.
11. Ende G. et al. (2006). Alcohol consumption significantly influences the MR signal of frontal choline-containing compounds. NeuroImage. 2006; 32:740–746.
12. Harper C. et al (1987). Are we drinking our neurones away? British Medical Journal (Clinical Research Ed) 1987; 294:534–536.
13. Gansler D. A. et al. (2000). Hypoperfusion of inferior frontal brain regions in abstinent alcoholics: A pilot SPECT study. Journal of Studies on Alcohol. 2000; 61:32–37.
14. Oscar-Berman M. et al. (2007). Alcohol: Effects on neurobehavioral functions and the brain. Neuropsychology Review. 2007; 17:239–257.
15. Parsons O. A. (1993). Impaired neuropsychological cognitive functioning in sober alcoholics. In: Hunt WA, Nixon SJ, editors. Alcohol-induced brain damage. Rockville: NIAAA/NIH; 1993.
16. Crews F. T. et al. (2014). Neuroimmune basis of alcoholic brain damage. Int Rev Neurobiol. 2014; 118:315-357.
17. Coleman, D. J. (1986). On the hydraulic suspension theory of accommodation. Trans Am Ophthalmol Soc 84, 846-868.
18. [35] Coleman, D. J., Fish, S. K. (2001). Presbyopia, accommodation and the mature catenary. Ophthalmology 108, 1544.
19. Helmholtz, H. von (1855). Über die Accommodation des Auges. Graefes Arch Ophthalmol 1, Abt II: 1-74 (In German only).