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Research shows that older people may turn to alcohol as a result of changes in their circumstances1. This could be because they retired and don’t have as much to occupy their time, because they’re less mobile and can’t get out to socialise as much, or because they’re mourning the loss of a loved one. About a quarter of all adults report drinking more than the recommended weekly limit of alcohol. Hard seltzer is the popular summer beverage that’s taken the US and now Britain by storm. We burst the bubble on many of the health myths surrounding this fizzy alcoholic drink. This is a very common problem in older people, especially women – 1 in 2 women and 1 in 5 men over 50 will break a bone because of osteoporosis.
Another subfield analysis conducted cross-sectionally in AUD subjects abstinent from alcohol for 3–60 months found significant volume deficits in AUD relative to controls in the subiculum, presubiculum, and fimbria in addition to the whole hippocampus (Lee et al., 2016). Evidence for AUD-related hippocampal involvement has clear implications for the emergence of dementia-like symptoms of explicit memory impairment in older men and women with AUD. Early MRI studies embraced volumetric quantification and semi-automated segmentation of different tissue classes, CSF spaces (ventricles and sulci), and brain structures. The study, published in Alcoholism Clinical and Experimental Research, utilized five different epigenetic clocks, a measure of an individual’s biological age, and examined the effects of varying levels of alcohol consumption on biological age.
Early studies used crude imaging and analysis methods based on inferior image quality, poor registration across scanning sessions, and linear (rather than volumetric) measurements made on Polaroid photographs of CT slices. Ample cross-sectional data indicate that regional volume deficits are consistently forthcoming in controlled, quantitative study, and correlational evidence is accruing to support accelerated aging of the brain in AUD subjects. Establishing excessive alcohol consumption as a causative factor of observation-identified volume deficits, however, requires longitudinal examination. Ideally, investigations would be prospective, that is, conducting MRI before initiating drinking and then following drinkers henceforth. Given the potential role of ALC in the aging process, it is important to gain a better understanding of this relationship on a molecular, epigenetic level.
Although the relationship between ALC and aging has not been extensively studied using Horvath’s epigenetic clock, Quach et al.15 found a small negative correlation of age acceleration with moderate alcohol consumption in blood in an analysis of behavioral and lifestyle factors15. Similarly, an analysis using blood samples and a blood-specific epigenetic clock developed by Hannum revealed accelerated biological aging in light and heavy drinkers, and a deceleration in moderate drinkers16. Although these studies provide interesting preliminary findings, more specific studies focusing on alcohol consumption as the primary exposure are required to better understand the role of both moderate and heavy alcohol consumption in aging on the molecular does alcohol accelerate aging level. Consequently, tolerance development to alcohol must result primarily from an overall decrease in the organism’s response to a given amount of alcohol after repeated alcohol consumption (i.e., functional tolerance). As indicated in the study by Spencer and McEwen (1997), this functional tolerance appears to develop more slowly in aged rats than in younger ones, providing some important clues to the aging process in general and to adaptation mechanisms to alcohol in particular. Researchers have examined several factors that may contribute to functional tolerance development, including direct changes in the cells’ response to alcohol, as well as changes in various systems that may help the body compensate for alcohol’s effects.
Observations of disproportionately higher diffusivity with older age marked groups with AUD (e.g., Pfefferbaum et al., 2006a). An early study using TBSS to explore regional effects of AUD on white matter systems found low FA and high diffusivity in frontal, limbic, and commissural circuitry that correlated with low scores on a visuospatial memory test (Yeh, Simpson, Durazzo, Gazdzinski, & Meyerhoff, 2009). Other TBSS analyses have revealed widespread FA deficits also related to older age of AUD individuals (but see Pandey et al., 2018) but not to sex or years of heavy drinking (Kisner et al., 2021). By contrast, another study reported that in women but not men with AUD, lower scores on a latent white matter factor calculated from FA values in five pre-selected tracts correlated with a higher proportion of days drinking over the previous 60 or 90 days (Monnig et al., 2015). DTI has also revealed FA deficits in women with AUD who did not exhibit volume deficits in the underlying white matter macrostructure (Pfefferbaum & Sullivan, 2002).
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