Anyone who drinks regularly aged whiskey can feel a certain difference compared to the young one, with the same alcohol content. This, perceived in the brain, is caused by the kinetics of ethanol (ethyl alcohol) which, in the two products, appears to be discrepant.
The maturation of the distillates induces a change in the relationship between ethanol congeners, consequently improving the olfactory and gustatory qualities of the product.
" What does congenere mean? "These are NOT isomeric molecules but belong to the same genus.
On the other hand, this process has been found to significantly modify the pharmacokinetics and neuropharmacological effects of ethanol.
In a study entitled: "Maturation of whiskey changes ethanol elimination kinetics and neural effects by increasing nonvolatile congeners", the effects of maturation alcohol on ethanol metabolism and the consequent state of drunkenness were observed.
Mice were fed at a dose of 3g / kg of 5-year (5-y) or 20-year (20-y) "single malt" whiskey, having a concentration of 20% ethanol. Between the two groups were compared: the density of ethyl alcohol in the blood, its metabolites and the duration of the "loss of the righting reflex" (LORR). Furthermore, the effects of the non-volatile whiskey congeners on the biomedical reactivity of ethanol were studied, by administering a volatile fraction (obtained by evaporating 16-y whiskey) to a 20% ethanol solution. The activity of hepatic alcohol dehydrogenase (ADH - enzyme that allows the "disposal" of alcohol) was also measured with whiskey and non-volatile ethanol congeners.
The elimination rate of ethanol (mmol / kg / h) was lower in the 20-y whiskey group than in the 5-y group; concentrations of acetaldehyde and acetate in the blood were lower in the first group than in the second. Non-volatile congeners added to the ethanol solution depressed the rate of ethanol elimination. In vitro studies have shown that the activity of hepatic ADH measured on whiskey as a substrate is reduced as a function of the whiskey age, and that the activity of ADH measured on ethanol as a substrate is strongly inhibited by non-volatile congeners . The duration of the LORR is greater in the group that takes the 20-y whiskey compared to the 5-y group. When administered together with ethanol, non-volatile congeners also prolong the duration of the corresponding LORR.
Whiskey maturation delays the metabolism of ethanol, lowers the levels of acetaldehyde and acetate in the blood and increases the inhibition of hepatic ADH due to non-volatile alcohol congeners. Furthermore, it prolongs the intoxication by enhancing the neurodepressive effects of ethanol, due to an increase in the quantity of non-volatile congeners.
These biomedical effects of whiskey maturation can reduce adverse reactions and cytotoxicity caused by acetaldehyde, and may also limit alcohol abuse and the associated excessive excessive neurodepression.
