Like all adults, older adults should avoid or limit alcohol consumption. In fact, aging can lead to social and physical changes that make older adults more susceptible to alcohol misuse and abuse and more vulnerable to the consequences of alcohol. Alcohol dependence or heavy drinking affects every organ in the body, including the brain.
A comprehensive study from the National Institute on Alcohol Abuse and Alcoholism shows that alcohol consumption among older adults, especially women, is on the rise. The researchers also found evidence that certain brain regions show signs of premature aging in alcohol-dependent men and women. In addition, heavy drinking for extended periods of time in older adults may contribute to poor heart health, as shown in this 2016 study. These studies suggest that stopping or limiting the use of alcohol could improve heart health and prevent the accelerated aging seen with heavy alcohol use.
Individuals Who Drink Heavily And Smoke May Show Early Aging Of The Brain
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Other research shows that the younger children and adolescents are when they start to drink, the more likely they will be to engage in behaviors that harm themselves and others. For example, frequent binge drinkers (nearly 1 million high school students nationwide) are more likely to engage in risky behaviors, including using other drugs such as marijuana and cocaine, having sex with six or more partners, and earning grades that are mostly Ds and Fs in school (10).
Research shows that COAs may have subtle brain differences which could be markers for developing later alcohol problems (28). For example, using high-tech brain-imaging techniques, scientists have found that COAs have a distinctive feature in one brainwave pattern (called a P300 response) that could be a marker for later alcoholism risk (29,30). Researchers also are investigating other brainwave differences in COAs that may be present long before they begin to drink, including brainwave activity recorded during sleep (31) as well as changes in brain structure (32) and function (33).
Whatever it is that leads adolescents to begin drinking, once they start they face a number of potential health risks. Although the severe health problems associated with harmful alcohol use are not as common in adolescents as they are in adults, studies show that young people who drink heavily may put themselves at risk for a range of potential health problems.
Difficulty walking, blurred vision, slurred speech, slowed reaction times, impaired memory: Clearly, alcohol affects the brain. Some of these impairments are detectable after only one or two drinks and quickly resolve when drinking stops. On the other hand, a person who drinks heavily over a long period of time may have brain deficits that persist well after he or she achieves sobriety. Exactly how alcohol affects the brain and the likelihood of reversing the impact of heavy drinking on the brain remain hot topics in alcohol research today.
Chronic health conditions tend to develop as part of aging, and older adults are often prescribed more medicines than other age groups, leading to a higher rate of exposure to potentially addictive medications. One study of 3,000 adults aged 57-85 showed common mixing of prescription medicines, nonprescription drugs, and dietary supplements. More than 80% of participants used at least one prescription medication daily, with nearly half using more than five medications or supplements,5 putting at least 1 in 25 people in this age group at risk for a major drug-drug interaction.5
Teen drinkers are more likely to get fat or have health problems, too. One study by the University of Washington found that people who regularly had five or more drinks in a row starting at age 13 were much more likely to be overweight or have high blood pressure by age 24 than their nondrinking peers. People who continue drinking heavily well into adulthood risk damaging their organs, such as the liver, heart, and brain.
Heavy alcohol consumption has been associated with brain atrophy, neuronal loss, and poorer white matter fiber integrity. However, there is conflicting evidence on whether light-to-moderate alcohol consumption shows similar negative associations with brain structure. To address this, we examine the associations between alcohol intake and brain structure using multimodal imaging data from 36,678 generally healthy middle-aged and older adults from the UK Biobank, controlling for numerous potential confounds. Consistent with prior literature, we find negative associations between alcohol intake and brain macrostructure and microstructure. Specifically, alcohol intake is negatively associated with global brain volume measures, regional gray matter volumes, and white matter microstructure. Here, we show that the negative associations between alcohol intake and brain macrostructure and microstructure are already apparent in individuals consuming an average of only one to two daily alcohol units, and become stronger as alcohol intake increases.
Alcohol-consumption related white matter (WM) microstructural alterations are a hallmark change associated with AUD18,19,20. Neuroimaging studies have consistently shown WM degeneration of the corpus callosum in AUD3,21,22. However, the effects of AUD on WM microstructure, as evidenced by decreased fractional anisotropy (FA) and increased mean diffusivity (MD), are not limited to the corpus callosum but are also seen in the internal and external capsules, fornix, frontal forceps, superior cingulate, and longitudinal fasciculi3,21,23. Further, research indicates that anterior and superior WM systems are more likely to show changes associated with AUD than posterior and inferior systems24. However, because conventional diffusion tensor imaging (DTI) measures (FA and MD) are based on a simplistic brain tissue microstructure model, they fail to account for the complexities of neurite geometry25. For example, the lower FA observed in individuals with AUD may reflect lower neurite density and/or greater orientation dispersion of neurites, which conventional DTI measures do not differentiate26,27.
Despite an extensive literature on the associations of alcohol consumption with brain structure and microstructure in individuals with AUD, there is limited research exploring these associations in individuals who consume alcohol but do not have AUD. In some studies of middle-aged and older adults, moderate alcohol consumption was associated with lower total cerebral volume28, gray matter atrophy29,30, and lower density of gray matter in frontal and parietal brain regions30. However, other studies have failed to show an association31, and one study showed a positive association of light-to-moderate alcohol consumption and GMV in older men32. One interpretation of these findings is that an inverse U-shaped, dose-dependent association exists between alcohol consumption and brain structure32. However, this interpretation was not supported by a longitudinal cohort study, which showed no difference in structural brain measures between individuals who did not consume alcohol and those who consumed between 1 and
Notably, the negative associations we observe with global IDPs are detectable in individuals who consume between 1 and 2 alcohol units daily. Thus, in the UK, consuming just one alcoholic drink daily (or two units of alcohol) could be associated with changes in GMV and WMV in the brain.
The negative associations between alcohol intake and total GMV and WMV are consistent with prior studies of early middle-aged46 and older adults28,47. Based on Figs. 2 and 3, which show that males consumed more alcohol units per day and had larger global GMV and WMV, we further examine the influence of sex in detail. We find negative associations between alcohol intake and the global IDPs for both sexes and weak evidence for interactive effects between alcohol intake and sex on the brain. These findings are similar to a recent study of early middle-aged adult moderate drinkers that showed smaller brain volumes associated with moderate alcohol consumption in men and women46. The weak sex-by-alcohol interactions also comport with the findings of an earlier longitudinal study in individuals with AUD38; however, other cross-sectional studies have reported greater volume changes in women than men48,49.
Although nearly 90% of all regional GMVs show significant negative associations with alcohol intake, the most extensively affected regions included the frontal, parietal, and insular cortices, with changes also in temporal and cingulate regions. Associations are also marked in the brain stem, putamen, and amygdala. The share of variance explained by alcohol intake for these regions is smaller in size than for global GMV, suggesting that the latter results from an aggregation of many small effects that are widespread, rather than a localized effect that is limited to specific regions. Alcohol intake is further associated with poorer WM microstructure (lower FA and higher ISOVF and MD) in specific classes of WM tract regions. The commissural fibers (genu and body of the corpus callosum, bilateral tapetum), projection fibers (bilateral anterior corona radiata), associative bundles (fornix, fornix cres+stria terminalis, left inferior longitudinal fasciculus), and the bilateral anterior thalamic radiations show the most consistent associations with alcohol intake, with the fornix showing the strongest associations. The fornix is the primary outgoing pathway from the hippocampus50, and WM microstructural alterations in the fornix are consistently associated with heavy alcohol consumption and memory impairments3,51.
Our study has several limitations. First, we rely on a sample of middle-aged individuals of European ancestry living in the UK. We hope that future work will test the generalizability of our findings to individuals from other populations and in other age groups. It is reasonable to expect that the relationship we observe would differ in younger individuals who have not experienced the chronic effects of alcohol on the brain. An additional limitation stems from the self-reported alcohol intake measures in the UK Biobank, which cover only the year prior to participation. Such estimates may not adequately reflect drinking prior to the past year and are susceptible to reporting and recall bias38,39. 2ff7e9595c
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