Recall and selection bias in reporting alcohol consumption among breast cancer cases

Harvard Medical School, Boston, MA.
Cancer Causes and Control (Impact Factor: 2.74). 10/1993; 4(5):441-8. DOI: 10.1007/BF00050863
Source: PubMed


Recall and selection bias are well-recognized potential problems in case-control studies of alcohol and cancer, but few analyses have attempted to assess the direction and the magnitude of these potential biases. We thus examined alcohol consumption in relation to risk of breast cancer using dietary questionnaires administered both before and after the diagnosis of breast cancer in the Nurses' Health Study (United States). Among cohort members who completed a dietary questionnaire in 1986 and who were free of cancer, 616 were diagnosed with breast cancer during follow-up to December 1989. These cases and 1,277 controls (a random sample of cohort members who did not develop cancer up to 1990) then were sent another questionnaire inquiring about their diet in 1985. Four hundred and ninety-four cases (80.2 percent) and 999 controls (78.2 percent) responded to the second questionnaire. The analysis based on the prospective (1986) questionnaire demonstrated an elevated risk of breast cancer among women who drank 30 or more g of alcohol daily (about two drinks) relative to nondrinkers (odds ratio [OR] = 1.55, 95 percent confidence interval [CI] = 1.01-2.39). The analysis based on the retrospective questionnaire also indicated a similar but slightly attenuated elevation of risk of breast cancer among women who drank at least 30 g daily (OR = 1.42, CI = 0.85-2.40). In these data, bias due to selection and recall had only minor effects on reported intake of alcohol consumption.

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    • "The CLDH used in the study has been shown to have high test-retest reliability for estimates of lifetime alcohol consumption (Russell et al., 1997). While recall bias may be a concern for case control study, there is evidence that there is not much bias in recall of alcohol in case control studies of breast cancer (Friedenreich et al., 1991; Giovannucci et al., 1993). Further, it is unlikely that biased recall of alcohol intake would be related to gene promoter methylation, and thus would not differentially affect the case-case comparisons. "
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    ABSTRACT: The mechanism for the observed association of alcohol consumption breast cancer risk is not known; understanding that mechanism could improve understanding of breast carcinogenesis and optimize prevention strategies. Alcohol may impact breast malignancies or tumor progression by altering DNA methylation. We examined promoter methylation of three genes, the E-cadherin, p16, and retinoic acid-binding receptor-β2 (RAR-β2) genes in archived breast tumor tissues from participants in a population-based case-control study. Real time methylation-specific PCR was performed on 803 paraffin-embedded samples, and lifetime alcohol consumption was queried. Unordered polytomous and unconditional logistic regression were used to derive adjusted odds ratios (ORs) and 95% confidence intervals (CIs). RAR-β2 methylation was not associated with drinking. Among premenopausal women, alcohol consumption was also not associated with promoter methylation for E-cadherin and p16 genes. In case-case comparisons of postmenopausal breast cancer, compared with lifetime never drinkers, promoter methylation likelihood was increased for higher alcohol intake for E-cadherin (OR=2.39; 95% CI, 1.15-4.96), in particular for those with estrogen receptor-negative tumors (OR=4.13; 95% CI, 1.16-14.72), and decreased for p16 (OR=0.52; 95% CI, 0.29-0.92). There were indications that the association with p16 was stronger for drinking at younger ages. Methylation was also associated with drinking intensity independent of total consumption for both genes. We found alcohol consumption was associated with DNA methylation in postmenopausal breast tumors, suggesting that the association of alcohol and breast cancer may be related, at least in part, to altered methylation, and may differ by drinking pattern.
    Alcohol (Fayetteville, N.Y.) 12/2010; 45(7):689-99. DOI:10.1016/j.alcohol.2010.11.006 · 2.01 Impact Factor
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    • "Self-report of alcohol intake tends to underestimate actual intake (Pernanen, 1974; Polich, 1981; Alanko, 1984; Simpura, 1987), thereby over-emphasizing the apparent relative health risk estimates. Nevertheless, a comparison of retrospective vs prospective alcohol and cigarette consumption data has shown that information bias is unlikely to exert much impact on effect size estimates based on retrospective information (Giovannucci et al., 1993). Our results demonstrate that the biochemical markers of alcohol abuse, CDT, GGT and their combination, may prove useful as indicators of health risks in a general population. "
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    ABSTRACT: Although most data support an overall relation of alcohol consumption with risk of breast cancer, the timing of alcohol consumption as it relates to risk of breast cancer is still debatable. The authors examined this issue in a case-control study conducted among non-Hispanic white and Hispanic women in Los Angeles. Cases aged 55-64 years at diagnosis in 1987-1989 were enrolled through the Cancer Surveillance Program of Los Angeles County (a Surveillance, Epidemiology, and End Results Program registry). Community controls were individually matched to cases by age (+/- 3 years), ethnicity, and neighborhood. In-person interviews were completed with 1510 matched pairs, of which 1431 met the inclusion criteria for the present analysis. In a multivariate conditional logistic regression model that simultaneously included terms for alcohol consumption at age 25 years, age 40 years, and in the recent past, clear differences among the age-specific associations were not observed, and the results suggested associations were not observed, and the results suggested that intake at each time independently contributed to risk. The odds ratios associated with estimated average lifetime intake were: for <6 g/day, 1.01; for 6-11 g/day, 1.21; for 12-18 g/day, 0.94; for 19-32 g/day, 1.63; for 33-45 g/day, 2.45 and for > or = 46 g/day, 0.94 compared with abstainers (P for trend = 0.01). Use of estrogen replacement therapy did not modify the risk associated with alcohol consumption, in contrast with the findings in two previous studies. This large study supports a relation between risk of breast cancer and alcohol consumption and suggests that lifetime intake may be the best indicator of alcohol-associated risk.
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