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American Journal of Epidemiology Advance Access originally published online on June 29, 2005
American Journal of Epidemiology 2005 162(3):295-296; doi:10.1093/aje/kwi191
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American Journal of Epidemiology Copyright © 2005 by the Johns Hopkins Bloomberg School of Public Health All rights reserved

LETTERS TO THE EDITOR

THREE AUTHORS REPLY

Mark A. Espeland1, Kamal H. Masaki2 and Stephen R. Rapp1,3

1 Department of Public Health Sciences, Wake Forest University School of Medicine, Winston-Salem, NC 27157
2 Department of Geriatric Medicine, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI 96817
3 Department of Psychiatry, Wake Forest University School of Medicine, Winston-Salem, NC 27157

We thank Drs. Rozzini and Trabucchi for their comments (1Go) on our paper (2Go). Rozzini et al. (3Go) originally reported their findings in a letter questioning a recent paper by Luchsinger et al. (4Go), in which moderate wine intake was found to be associated with a reduced risk of Alzheimer's disease among individuals with the apolipoprotein E {varepsilon}4 allele. We agree with the points made by the authors of this earlier paper in response to that original letter (5Go). These points include the fact that findings from observational studies such as ours cannot fully distinguish whether alcohol intake is a marker of individuals at less risk of cognitive decline or whether it is part of a causal pathway related to reduced risk, a pathway that could include biologic and behavioral mechanisms. In addition, as we state in our report, randomized clinical trials are necessary to provide definitive evidence of any cause-effect associations.

Several additional points should be made. The study by Rozzini et al. (3Go) involved examining the relation between a baseline questionnaire (which the authors describe as "ad hoc") to assess usual alcohol intake and a single questionnaire-based reassessment of cognitive status 12 years later (of survivors and those otherwise not lost to follow-up). The cognitive measure used was a brief screener from which Rozzini et al. (3Go) extrapolated incident dementia cases. It is quite possible that measurement error and differential follow-up may have attenuated the observed relation. The argument for the possibility of differential follow-up is strengthened by the finding of a positive association between overall mortality and moderate alcohol intake. It is also possible that the differences between our findings from the Women's Health Initiative Memory Study (WHIMS) (2Go) and the cohort from Brescia, Italy (1Go), may reflect chance variability, since the point estimates we report are within the bounds of the 95 percent confidence interval for relative risks reported by Rozzini et al. (i.e., 0.5, 1.6). The diversity of the WHIMS cohort, drawn using a variety of recruitment strategies at sites throughout the United States, makes it less likely that moderate alcohol intake serves as an omnibus marker for a particular social group. We found that statistical adjustment for a range of demographic and clinical characteristics was unable to account for associations between cognitive status and alcohol intake.

Furthermore, Zhang et al. (6Go) recently reported that the relation between alcohol intake and reduced verbal memory impairment is strongest in the subset of individuals with the greatest levels of educational attainment. Since these individuals likely include the greater part of the subpopulation that Rozzini et al. describe as "more able to exert mastery over their own lives" (1Go, p. 295), one would expect that if alcohol intake is merely a marker for this population, the arguments of these authors would appear to predict the opposite of this finding.

Our results (2Go) are similar to those of several other large population-based longitudinal studies. However, in the absence of data from randomized clinical trials, we are not recommending that individuals consume alcohol to prevent dementia and cognitive decline.


    ACKNOWLEDGMENTS
 
Conflict of interest: none declared.


    References
 TOP
 References
 

  1. Rozzini R, Trabucchi M. Re: "Association between reported alcohol intake and cognition: results from the Women's Health Initiative Memory Study." (Letter). Am J Epidemiol 2005;162:294–5.[Free Full Text]
  2. Espeland MA, Gu L, Masaki KH, et al. Association between reported alcohol intake and cognition: results from the Women's Health Initiative Memory Study. Am J Epidemiol 2005;161:228–38.[Abstract/Free Full Text]
  3. Rozzini R, Sabatini T, Trabucchi M. Alcohol consumption and the risk of dementia: biological and psychological mechanisms. (Letter). J Am Geriatr Soc 2005;53:175–6.[CrossRef][ISI][Medline]
  4. Luchsinger JA, Tang MX, Siddiqui M, et al. Alcohol intake and risk of dementia. J Am Geriatr Soc 2004;52:540–6.[CrossRef][ISI][Medline]
  5. Luchsinger JA, Mayeux R. Response to letter by Rozzini et al. (Letter). J Am Geriatr Soc 2005;53:176–7.[CrossRef]
  6. Zhang Y, Heeren T, Ellison CR. Education modifies the effect of alcohol on memory impairment: The Third National Health and Nutrition Examination Survey. Neuroepidemiology 2005;24:63–9.[CrossRef][ISI][Medline]

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This Article
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