German Institute of Human Nutrition, Potsdam-Rehbrücke, Germany
We read with interest the recent Journal paper on intake of antioxidants and risk of dementia. In that paper, Laurin et al. (1) reported that midlife intake of antioxidants does not modify the risk of late-life dementia or its most prevalent subtypes.
However, we have several concerns about the assessment of dietary intake and the statistical analysis of the data. First, assessing dietary intake by using a single 24-hour recall is unusual in nutritional epidemiology because the recall covers a very short time period that cannot reflect individual long-term intake. Although the authors addressed this problem in the Discussion section and excluded subjects who stated that the 24-hour recall was atypical, the bias due to the short time period of exposure assessment remains serious. The exclusion criterion referred to under- or overeating in general and not to micronutrient intake, so that participants who were not excluded (93.6 percent) may have had an atypical intake of antioxidants on the sampling day. A number of researchers have demonstrated a day-to-day variability in vitamin intake and have shown that this intraindividual variation tends to be even higher than the variation between individuals (2). Thus, misclassification will take place when subjects are assigned to quartiles of dietary intake according to a single 24-hour recall compared with long-term or repeated short-term intake measurements. Consequently, estimates of relative risks by quartiles of vitamin intake will be biased (3).
To illustrate this issue, we estimated the intra- and interindividual variance components for beta-carotene, vitamin C, and vitamin E by using data from the 19951996 European Prospective Investigation into Cancer and NutritionPotsdam validation study. In this study, twelve 24-hour dietary recall interviews were conducted, three interviews per season (4). About 80 percent of the total variance for each antioxidant could be attributed to day-to-day variation in individual intake. To ensure that our estimates were compatible with those of Laurin et al. (1), we categorized the exposure by quartiles of log-transformed energy-adjusted antioxidant intakes. If we did so for intake regarding the first sampling day and for mean intake of the twelve recalls, a misclassification rate of 59.762.7 percent would occur if the first 24-hour dietary recall was used instead of all twelve recalls (table 1).
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Third, levels of antioxidants in the diet are highly correlated. Thus, the combined effect of antioxidants on dementia may be quite different from the effects of single antioxidants. The regression models applied by Laurin et al. (1), with only one antioxidant as predictor adjusting for some covariates, are neither appropriate to model the combined effect nor to get unbiased estimates of single effects. To adjust each antioxidant for the other ones, all antioxidants should be included in the same regression model.
In conclusion, careful attention should be given to the very short time period covered by the dietary assessment method and the insufficient adjustment of antioxidant intake before a conclusive statement can be made about midlife dietary intake of antioxidants not being associated with late-life dementia.
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