Alcohol Intake and Risk of Dementia

Jose A. Luchsinger, MD; Ming-Xin Tang, PhD; Maliha Siddiqui, MPH; Steven Shea, MD; Richard Mayeux, MD

Disclosures

J Am Geriatr Soc. 2004;52(4) 

In This Article

Results

The 980 individuals contributed 4,023 years of observation (mean observation time= 4.1±1.5 years). The mean age of the sample was 73.3±5.8, and 67% were women. One hundred forty-four individuals reported beer intake (15%), 138 reported liquor intake (14%), 162 reported wine intake (17%), and 690 reported no intake of alcoholic beverages (70%). The incidence of AD was 4.9 cases per 100 person-years (199 cases), and the incidence of DAS was 1.5 per 100 person years (61 cases).

Table 1 shows the comparison of clinical characteristics among different levels of intake for beer, liquor, and wine. Individuals with light to moderate intake of beer were less likely to be female (70.9% vs 46.0%; P<.001) and have heart disease (31.0% vs 18.7%; P = .003) than subjects who did not report drinking beer. Individuals with heavy intake were less likely to be female (70.9% vs 33.3%; P = .044) than nondrinkers. Individuals who reported light to moderate intake were less likely to be female (70.5% vs 50.3%; P<.001), had more years of education (9 vs 12 years; P<.001), and were less likely to have heart disease (30.6% vs 21.5%; P = .008) than individuals who reported no intake of liquor. Those who reported light to moderate intake of wine were less likely to be female (71.3 vs 42.0; P<.001), had more years of education (9 vs 12; P<.001), and were less likely to have heart disease (30.6 vs 19.6; P = .019) than those who reported no wine intake. Similar differences were observed for total alcohol intake.

Analyses using multivariate proportional hazards models examining the association between each alcoholic beverage type individually and the outcomes of interest revealed that only light to moderate intake of wine was significantly associated with a lower risk of incident dementia (hazard ratio (HR)= 0.64, 95% confidence interval (CI)= 0.43-0.96; P = .031) compared with individuals who reported no wine intake. In similar analyses examining AD as an outcome ( Table 2 ), a similar result was found in a model adjusting for age and sex (HR= 0.59, 95% CI= 0.38-0.91; P = .018), but this association became nonsignificant after including education and APOE-ε4 in the model (HR= 0.69, 95% CI= 0.45-1.09; P = .118). Analyses examining dementia associated with stroke as an outcome ( Table 3 ) showed that, in the full model, the HR for light to moderate wine intake was similarto that in the previous analyses but not statisticallysignificant (HR= 0.47, 95% CI= 0.18,1.20; P = .116). The analyses relating beer and liquor intake didnot reveal a significant association with any of the outcomes.

Analyses were conducted relating total alcohol intake in grams to dementia. Daily intake of alcohol in grams was categorized to resemble the classification by servings used for the analyses by beverage type assuming that each serving was approximately 12 g of alcohol: 0 g (no intake), 0.1-36 g (light to moderate intake), and more than 36 g (heavy intake). None of the HRs and CIs was suggestive of a significant association between any level of alcohol intake and dementia or its subtypes. The adjusted HRs of AD and DAS related to intake of 0.1-36 g of alcohol were 0.97 (95% CI= 0.69-1.35; P = .85) and 0.93 (95% CI= 0.50-1.72; P = .82), respectively.

Analyses were conducted using proportional hazards models including dummy variables for beer, liquor, and wine in the same model; this is akin to adjusting the association of each beverage type with the outcome by intake of other beverage types and their associated traits. It was found that only light to moderate intake of wine was associated with a significant lower risk of dementia (HR= 0.52, 95% CI= 0.34-0.80; P = .003); light to moderate intake of wine was also associated with a lower risk of AD (HR= 0.55, 95% CI= 0.34-0.89; P = .015) ( Table 4 ). The HR relating light to moderate intake of wine and DAS ( Table 4 ) also suggested a lower risk of dementia and was close to statistical significance (HR= 0.42, 95% CI= 0.15-1.15; P = .091).

Stratified analyses by APOE-ε4 allele revealed that, in 667 individuals without the allele, light to moderate intake of wine was associated with a lower risk of dementia (HR= 0.44, 95% CI= 0.25-0.77; P = .004), and AD (HR= 0.45, 95% CI= 0.24-0.85; P = .013) compared with nondrinkers, whereas this association disappeared for individuals heterozygous or homozygous for the APOE-ε4 allele (HR for dementia= 1.10, 95% CI= 0.59-2.04; P = .093; HR for AD= 1.32, 95% CI= 0.67-2.60; P = .427). The interaction terms for alcohol category and the APOE-ε4 allele in the models with dementia and AD as outcomes were both statistically significant (P = .056 and P = .032, respectively). No effect modification by sex, diabetes mellitus, hypertension, heart disease, or smoking was found.

All analyses were repeated with and without the 210 individuals with diet data who were lost to follow-up, using age at onset of dementia or age at censoring as the time-to-event variable; the results were virtually unchanged from those reported above.

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