Copyright © 2004 by the Johns Hopkins Bloomberg School of Public Health
LETTERS TO THE EDITOR |
FOUR AUTHORS REPLY
1 Neuroepidemiology Section, Laboratory of Epidemiology, Demography, and Biometry, National Institute on Aging, Bethesda, MD 20892
2 Pacific Health Research Institute, Honolulu, HI 96813
We appreciate the letter by Hoffmann and Bergmann (1) about our paper (2) in the Journal. In this letter, we would like to address some of their concerns.
First, we agree that use of a single 24-hour recall may not be optimal for assessing long-term individual dietary intake. In nutritional epidemiology, the 24-hour recall is seldom used because it requires standardized and skilled interviewers, detailed information about food preparation methods, recipe ingredients, and so forth (3). Although the 24-hour recall may be limited by the fact that a single day of intake is not likely to be representative of a person’s usual intake, it is adequate for estimating group means. Our study sample included dietary information from a large sample of subjects (n = 2,459); multiple measures of intake are obviously not feasible. The stability of midlife dietary intake in this population has been investigated in a published study (4) on the reproducibility of dietary frequency data over a 6-year period (between examination 1 and examination 3).
Second, we adjusted our relative risks for stroke and cardiovascular disease, which in this cohort are risk factors for Alzheimer’s disease and vascular dementia (5). On the other hand, intakes of antioxidants were not associated with the risk of stroke and cardiovascular disease in our study sample, which minimizes the extent to which they may be statistically in the causal pathway between the exposure and the outcome. Furthermore, dietary assessment of antioxidants was carried out before stroke and cardiovascular disease occurred so the men would not have changed their diet because of the disease.
Third, epidemiologic studies of diet and disease should be directed at the effect of nutrient intakes independent of total caloric intake, particularly when caloric intake is associated with disease. It is reasonably well accepted that statistical adjustment of nutrient intakes for caloric intake and use of the nutrient residuals as the independent variable will minimize the correlation between nutrient intake and caloric intake (6). Use of calorie-adjusted values in multivariate models can reduce the problem of high collinearity frequently observed between nutritional factors. We also included energy intake in the regression models. As noted, however, doing so may not entirely eliminate confounding due to energy intake.
In summary, the Honolulu-Asia Aging Study provided us the unique opportunity to examine the associations between dietary antioxidants and the risk of dementia. Previous results from prospective studies have been difficult to interpret because assessment of dietary intake was closer in time to onset of disease. Eating patterns might be influenced by the presence of preclinical disease. Our analysis overcame this problem by examining the diet during midlife, not late in life. Dietary assessment was carried out in a large sample of subjects followed extensively for over 30 years. Our results showed no association between antioxidant intakes and dementia. No associations were observed between antioxidant intakes by the means of dietary supplements during late life and dementia (7). In our cohort, dietary intake of antioxidants does not seem to contribute to prevention of dementia late in life.
REFERENCES
- Hoffmann K, Bergmann MM. Re: "Midlife dietary intake of antioxidants and risk of late-life incident dementia: the Honolulu-Asia Aging Study." (Letter). Am J Epidemiol 2004;160:717–18.
[Free Full Text] - Laurin D, Masaki KH, Foley DJ, et al. Midlife dietary intake of antioxidants and risk of late-life incident dementia: the Honolulu-Asia Aging Study. Am J Epidemiol 2004;159:959–67.
[Abstract/Free Full Text] - Buzzard M. 24-hour dietary recall and food record methods. In: Willett W, ed. Nutritional epidemiology. 2nd ed. New York, NY: Oxford University Press, 1998:50–73.
- Hankin JH, Nomura A, Rhoads GG. Dietary patterns among men of Japanese ancestry in Hawaii. Cancer Res 1975;35:3259–64.
[Abstract/Free Full Text] - Kalmijn S, Foley D, White L, et al. Metabolic cardiovascular syndrome and risk of dementia in Japanese-American elderly men. The Honolulu-Asia Aging Study. Arterioscler Thromb Vasc Biol 2000;20:2255–60.
[Abstract/Free Full Text] - Willett W, Stampfer MJ. Total energy intake: implications for epidemiologic analyses. Am J Epidemiol 1986;124:17–27.
[Free Full Text] - Laurin D, Foley DJ, Masaki KH, et al. Vitamin E and C supplements and risk of dementia. JAMA 2002;288:2266–8.
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