Given the above physiology of dark adaptation it is clear why initial dark adaptation is reported to occur over 20 minutes. Over this time the accumulated vitamin A is converted to Retinene and then to Rhodopsin. The physiology also explains the lack of loss of dark adaptation reported by some amateurs following short exposures even to bright light. In these cases the Rhodopsin although bleached by the light exposure is quickly regenerated from Retinene which did not go on to be converted to the stable vitamin A. Clearly from the physiology and physics any mechanism which hinders the function of nerves, muscles and the protein synthesis will have a detrimental effect on achieving and maintaining dark adaptation As is evident from the discussion above both protein synthesis and neural responses are important in vision and dark adaptation. Neural response is important in initiating and maintaining a dilated pupil and for conducting the retinal image to the visual cortex.
Protein synthesis is important in amplifying the visual signal presented to the retina.
Below is a review of the effects of alcohol and smoking on some of the parameters which influence dark adaptation as well as on the process of dark adaptation as a whole. The study found that the maximum pupillary diameter of non users was 6.2mm while those using alcohol regularly the maximum diameter was 5.7mm. The effects are illustrated in figure 1. The above study did not look at the acute effects of alcohol but rather the effects of chronic alcohol use. Alcohol reduces both the speed and extent to which the pupil dilates.