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PubMed1996

[Prediction of the epidemiological efficiency rate of preventive antiviral drugs from laboratory findings].

Based on the dose-response dependence represented as a generating distribution function of infecting doses of a pathogen, a value for the epidemiological efficiency rate of preventive agents was derived. For an arbitrary distribution of infecting doses, EEC mean values is shown to always no greater than 1: ED50v/ED50w where ED50v and ED50w are 50% of the infective doses of the pathogen assessed for those treated with the agent and intact persons, respectively. This relation is also valid when differences in pathogenic resistance are determined not only due to the use of drugs, but for any other variables (age-, sex-specific and other factors). This was verified by experiments.

Animals↗
PubMed2001

Selection and validation of biomarkers for chemoprevention: the contribution of epidemiology.

This chapter considers the epidemiological contribution of DNA adducts as an example of markers for use in chemoprevention studies, and highlights the potential biases inherent in the conduct of epidemiological studies with molecular markers. Although adducts have been interpreted mainly as biomarkers of exposure, 'bulky' DNA adducts such as those measured by 32P-postlabelling or ELISA in white blood cells are more correctly interpretable as markers of cumulative unrepaired DNA damage. The latter concept can prove useful in cancer epidemiology, since it is consistent with existing knowledge on the importance of duration of exposure in the etiology of chemically-induced cancers. Increasing evidence suggests that in addition to prolonged exposure to genotoxic chemicals, inter-individual variability in carcinogen metabolism and DNA repair is predictive of cancer risk. Also from this point of view, measurements of 'bulky' DNA adducts can be useful as biomarkers for studies in populations, since they express the amount of carcinogen linked to DNA after repair, taking into account individual repair capacity. Finally, we suggest a theory of causality based on the work of Wesley Salmon and the concept of 'propagating mark', which is particularly attractive for molecular epidemiologists.

Biomarkers, Tumor↗
PubMed1996

Optimizing power in allocating resources to exposure assessment in an epidemiologic study.

We consider an epidemiologic study with a fixed budget, in which resources may be put into increasing sample size or into improving accuracy of exposure assessments. To maximize study power (efficiency), improving accuracy is preferable if and only if the proportional increase in the square of the validity coefficient is more than the proportional increase in total study costs per subject that is required to achieve it. (The validity coefficient is the correlation between the true exposure and the approximate assessment in the study base.) This is most likely to be so if the cost of exposure measurement remains a small proportion of the overall costs per subject. The design with maximum power will not generally have minimum bias in measure of effect, so that alternative optimality criteria are required if this bias is important.

Bias↗
PubMed2004

The interview mode effect on the Center for Epidemiological Studies Depression (CES-D) scale: an item response theory analysis.

BACKGROUND: Evidence of a mode effect has raised concerns about the comparability and validity of self- versus interviewer-administered versions of the Center for Epidemiological Studies Depression (CES-D) scale. Response anonymity has been proposed to explain this effect. However, the factors that contribute to this mode effect are not well understood. We used item response theory (IRT) to examine the nature of the CES-D mode effect. METHODS: A sample of depressed primary care patients from the Partners-in-Care Study were randomized to receive either a phone interview (N=139) or a mail survey (N=139) of the CES-D. We used likelihood ratio tests to identify differentially functioning items in the 2 groups. Category response curves are used to describe these effects. RESULTS: Twelve items manifested differential functioning. Category response curves consistently indicate that phone respondents had a lower probability of endorsing the third of 4 response categories than mail respondents, suggesting a possible cognitive effect. CONCLUSION: Although response anonymity could be important in mode effects observed in surveys of sensitive topics, cognitive factors appear more important to the mode effect in the CES-D.

Adult↗
PubMed1989

Diet history: questionnaire and interview techniques used in some retrospective studies of cancer.

A detailed diet history method that has been used by the Epidemiology Unit of the National Cancer Institute of Canada, Toronto, in retrospective case-control studies is discussed. The questionnaire format and the method of administration by trained interviewers, together with instructions used to train the interviewers, are described. The questionnaire items elicited the usual frequency of foods consumed in the Canadian diet for one or two specified periods of time, including current and/or past diet history. Various probes required to elicit proper information on frequency, serving size, and additions to food are discussed. Portions were quantified by using geometric food models made of papier-mâché, wood, and plastic. The frequency and volumetric measurements obtained from the diet history questionnaire were converted to gram weights using the density of each food consumed; the nutrient intakes were then computed.

Canada↗
PubMed2004

Assessing interaction in case-control studies: type I errors when using both additive and multiplicative scales.

Epidemiologic researchers often explore effect modification in case-control studies on more than one statistical scale, an approach that one expects would increase the rate of false-positive findings of interaction. For example, researchers have measured effect modification by using both a multiplicative interaction coefficient (M) in a logistic regression model and a measure of interaction on the additive scale such as the interaction coefficient from an additive relative risk regression model (A). We performed computer simulations to investigate the degree to which type I error may be inflated when statistical interactions are evaluated by using both M and A. The overall type I error rate was often greater than 5% when both tests were performed together. These results provide empiric evidence of the limited validity of a common approach to assessing etiologic effect modification. When the scale has not been specified before analysis, interaction hypothesis tests of effect modification should be interpreted particularly cautiously. Researchers are not justified in choosing the interaction test with the lowest P value.

Case-Control Studies↗
PubMedDate not supplied

Is weight loss a modifier of the cholesterol-heart disease relationship in older persons? Data from the NHANES I Epidemiologic Follow-up Study.

The relationship between cholesterol and 14-year incidence of coronary heart disease was compared for men and women of two age groups, 25 to 64 years and 65 to 74 years. While cholesterol levels of 6.2 mmol/L or higher were associated with a risk of coronary heart disease in the younger group, this was not true for either men or women aged 65 to 74. Further analyses for older persons showed that weight loss modified the cholesterol-heart disease relationship. Those with stable weight showed a positive relationship between cholesterol and coronary heart disease, similar to the younger age group (relative risk [RR] = 1.8 [95% confidence interval: 1.1, 2.9] for men; RR = 1.6 [.7, 3.4] for women). Among those with a weight loss of 10% or more, the relationship of cholesterol to heart disease was inverse (RR = .8 [.5, 1.2] for men; RR = .6 [.3, 1.0] for women). These data suggest that the relationship of cholesterol to coronary disease in healthier older persons may be similar to that in younger persons, and that health status should be considered in analyses of cholesterol risk in old age.

Adult↗
PubMed2006

Estimation of direct causal effects.

Many common problems in epidemiologic and clinical research involve estimating the effect of an exposure on an outcome while blocking the exposure's effect on an intermediate variable. Effects of this kind are termed direct effects. Estimation of direct effects is typically the goal of research aimed at understanding mechanistic pathways by which an exposure acts to cause or prevent disease, as well as in many other settings. Although multivariable regression is commonly used to estimate direct effects, this approach requires assumptions beyond those required for the estimation of total causal effects. In addition, when the exposure and intermediate variables interact to cause disease, multivariable regression estimates a particular type of direct effect-the effect of an exposure on an outcome when the intermediate is fixed at a specified level. Using the counterfactual framework, we distinguish this definition of a direct effect (controlled direct effect) from an alternative definition, in which the effect of the exposure on the intermediate is blocked, but the intermediate is otherwise allowed to vary as it would in the absence of exposure (natural direct effect). We illustrate the difference between controlled and natural direct effects using several examples. We present an estimation approach for natural direct effects that can be implemented using standard statistical software, and we review the assumptions underlying our approach (which are less restrictive than those proposed by previous authors).

Clinical Trials as Topic↗
PubMed2004

Stroke prevention, blood cholesterol, and statins.

The risk of stroke increases with age, and hence the disease particularly affects the elderly, who are also at high risk for coronary heart disease. Epidemiological and observational studies have not shown a clear association between cholesterol concentrations and all causes of stroke. Large, long-term statin trials in patients with established or high risk for coronary heart disease have shown that statins decrease stroke incidence. These statin trials in a combined total of 70,020 patients indicate relative and absolute risk reductions for stroke of 21% and 0.9%, respectively. By comparison, the number of strokes prevented per 1000 patients treated for 5 years in patients with coronary heart disease is nine for statins versus 17.3 for antiplatelet drugs and 17 for antihypertensive drugs. Although the Heart Protection Study showed that statins lower the risk of major coronary events in patients with a previous stroke, statins may not lower stroke recurrence in these patients. In this review, we discuss the potential reasons for the effects of statins on stroke and the mechanisms of action. Treatment strategies on the basis of global cardiovascular risk may be most effective. Additional studies in patients representative of the typical stroke population are needed.

Anticholesteremic Agents↗
PubMed2003

Correcting for nonrandom ascertainment in generalized linear mixed models (GLMMs), fitted using Gibbs sampling.

Gibbs sampling-based generalized linear mixed models (GLMMs) provide a convenient and flexible way to extend variance components models for multivariate normally distributed continuous traits to other classes of phenotype. This includes binary traits and right-censored failure times such as age-at-onset data. The approach has applications in many areas of genetic epidemiology. However, the required GLMMs are sensitive to nonrandom ascertainment. In the absence of an appropriate correction for ascertainment, they can exhibit marked positive bias in the estimated grand mean and serious shrinkage in the estimated magnitude of variance components. To compound practical difficulties, it is currently difficult to implement a conventional adjustment for ascertainment because of the need to undertake repeated integration across the distribution of random effects. This is prohibitively slow when it must be repeated at every iteration of the Markov chain Monte Carlo (MCMC) procedure. This paper motivates a correction for ascertainment that is based on sampling random effects rather than integrating across them and can therefore be implemented in a general-purpose Gibbs sampling environment such as WinBUGS. The approach has the characteristic that it returns ascertainment-adjusted parameter estimates that pertain to the true distribution of determinants in the ascertained sample rather than in the general population. The implications of this characteristic are investigated and discussed. This paper extends the utility of Gibbs sampling-based GLMMs to a variety of settings in which family data are ascertained nonrandomly.

Age of Onset↗
PubMed1996

Age-period-cohort analysis of suicide mortality rates in Spain, 1959-1991.

BACKGROUND: Although there is evidence that suicide rates may be increasing in Spain, formal epidemiological studies have been limited to specific cities or counties. The objective of this study was to investigate nationwide trends in suicide mortality from 1959 to 1991 in Spain, with emphasis on age, period, and cohort effects. METHODS: Age- and sex-specific suicide mortality rates from 1959 until 1991 were obtained from official vital statistics tables from the Instituto Nacional de Estadística, the official registry of vital statistics in Spain. Poisson regression and graphical methods were used to model and estimate age, period and cohort effects. RESULTS: Suicide mortality rates increased with age, with a proportional increment for each decade of life of 45% (95% confidence interval: 45-46%). In both males and females, age-adjusted suicide mortality rates decreased from 1959 until the late 1970s and early 1980s. In 1982, trends started to increase, returning to the levels of 1959 in less than 6 years. Cohort effects were small for cohorts born prior to 1940. For cohorts born after 1950, suicide rates increased markedly. CONCLUSIONS: The increase in suicide mortality in younger cohorts and the high rates of suicide in the elderly demand further investigation to establish causal mechanisms and preventive strategies.

Adolescent↗
PubMed1999

The Latino mortality paradox: a test of the "salmon bias" and healthy migrant hypotheses.

OBJECTIVES: Relative to non-Latino Whites, Latinos have a worse socioeconomic profile but a lower mortality rate, a finding that presents an epidemiologic paradox. This study tested the salmon bias hypothesis that Latinos engage in return migration to their country of origin and are thereby rendered "statistically immortal" and the alternative hypothesis that selection of healthier migrants to the United States accounts for the paradox. METHODS: National Longitudinal Mortality Study data were used to examine mortality rates of the following groups for whom the salmon hypothesis is not feasible: Cubans, who face barriers against return migration; Puerto Ricans, whose deaths in Puerto Rico are recorded in US national statistics; and US-born individuals, who are not subject to either salmon or healthy migrant effects. RESULTS: The sample included 301,718 non-Latino Whites and 17,375 Latino Whites 25 years or older. Cubans and Puerto Ricans had lower mortality than non-Latino Whites. Moreover, US-born Latinos had lower mortality than US-born non-Latino Whites. CONCLUSIONS: Neither the salmon nor the healthy migrant hypothesis explains the pattern of findings. Other factors must be operating to produce the lower mortality.

Adult↗
PubMed1997

Interviewer effects in a cohort study. Results from the Massachusetts Women's Health Study.

Although interviewer error is widely recognized as an important source of variation in epidemiologic investigations, scant published information exists documenting the impact of interviewer variation on study findings. Using data from the Massachusetts Women's Health Study, a population-based cohort study of 2,569 middle-aged women (1982-1987), the authors evaluated interviewer variation in responses to different types of questions, and assessed the impact of interviewer variation on inferences derived from study data. Respondent sociodemographic and lifestyle characteristics were similar for the four study interviewers at the first follow-up. No interviewer variation was detected for questions concerning recall of specific events, but responses to questions regarding recall of subjective or personal information or those which required further probing did differ significantly by interviewer. Adjustment for interviewer effects had no impact on the conclusions obtained from one analysis of predictors of depression, despite significant interviewer variation in the outcome and predictor variables, but it did change conclusions from an analysis of the impact of support networks on psychological symptoms, wherein the interviewer variable was strongly related to the outcome after data were controlled for predictor variables. Given these findings, examination of data for interviewer effects is advisable despite incorporation of quality control measures in a study's design.

Depression↗
PubMedDate not supplied

Differences in histology between first and second primary lung cancer.

Data from the Surveillance, Epidemiology, and End Results (SEER) Program were used to compare the histological distribution of second lung cancer following an initial cancer of the lung, head and neck, and breast to primary lung carcinoma occurring as a first cancer. Following initial head and neck cancer or initial squamous cell carcinoma of the lung, the proportion of second primary lung cancer which was of squamous cell histology rose dramatically, while the proportion of pulmonary adenocarcinomas rose following initial adenocarcinoma of the lung. The histological distribution of lung cancer following an initial breast cancer in women was similar to the distribution of de novo lung cancer in women. These results persisted as the time interval between diagnosis of the two primaries was increased from 12 to 48 months. We conclude that the histology of a second primary lung cancer following an initial cancer of the lung or head and neck tends to repeat the histology of the initial cancer (field effect), and this observation is not likely to be due to misdiagnosis of a recurrence of the initial cancer.

Adenocarcinoma↗
PubMed2001

Sample size determination for studies of gene-environment interaction.

BACKGROUND: The search for interaction effects is common in epidemiological studies, but the power of such studies is a major concern. This is a practical issue as many future studies will wish to investigate potential gene-gene and gene-environment interactions and therefore need to be planned on the basis of appropriate sample size calculations. METHODS: The underlying model considered in this paper is a simple linear regression and relating a continuous outcome to a continuously distributed exposure variable. RESULTS: The slope of the regression line is taken to be dependent on genotype, and the ratio of the slopes for each genotype is considered as the interaction parameter. Sample size is affected by the allele frequency and whether the genetic model is dominant or recessive. It is also critically dependent upon the size of the association between exposure and outcome, and the strength of the interaction term. The link between these determinants is graphically displayed to allow sample size and power to be estimated. An example of the analysis of the association between physical activity and glucose intolerance demonstrates how information from previous studies can be used to determine the sample size required to examine gene-environment interactions. CONCLUSIONS: The formulae allowing the computation of the sample size required to study the interaction between a continuous environmental exposure and a genetic factor on a continuous outcome variable should have a practical utility in assisting the design of studies of appropriate power.

Effect Modifier, Epidemiologic↗
PubMed2000

Serum carotenoids and markers of inflammation in nonsmokers.

One explanation for discrepant results between epidemiologic studies and randomized trials of beta-carotene and cardiovascular disease may be a failure to consider inflammation as a confounder. To evaluate the potential for such confounding, the authors relate the serum concentrations of five carotenoids (alpha-carotene, beta-carotene, beta-cryptoxanthin, lycopene, and lutein/zeaxanthin) to levels of three inflammatory markers (C-reactive protein, fibrinogen, and white blood cell count) measured during the Third National Health and Nutrition Survey, 1988-1994. The analysis included 4,557 nonsmoking participants aged 25-55 years. Adjusted concentrations of all five carotenoids were significantly lower in those with C-reactive protein levels above 0.88 mg/dl (p = 0.001). There was a trend toward lower adjusted beta-cryptoxanthin concentrations with increasing level of fibrinogen (p value test for trend = 0.01), but other carotenoids were not related. Many of the carotenoid concentrations were lower among participants with high white blood cell counts. After log transformation, only adjusted mean beta-carotene levels were significantly lower in those with white blood cell counts above 7.85 x 10(9)/liter (p < 0.01). These cross-sectional data do not clarify the biologic relation between carotenoids and C-reactive protein but, to the extent that the carotenoids are associated with C-reactive protein levels, a carotenoid-heart disease association may be, in part, an inflammation-heart disease association.

Acute-Phase Proteins↗
PubMedDate not supplied

A randomized trial of vitamin E supplementation and cognitive function in women.

BACKGROUND: Oxidative stress may play a key role in the development of cognitive impairment. Long-term supplementation with vitamin E, a strong antioxidant, may provide cognitive benefits. METHODS: The Women's Health Study is a randomized, double-blind, placebo-controlled trial of vitamin E supplementation (600 IU [alpha-tocopherol acetate], on alternate days) begun between 1992 and 1995 among 39 876 healthy US women. From 1998, 6377 women 65 years or older participated in a cognitive substudy. Three cognitive assessments of general cognition, verbal memory, and category fluency were administered by telephone at 2-year intervals. The primary outcome was a global composite score averaging performance on all tests. Repeated measures analyses were conducted to examine mean performance and mean differences in cognitive change, and logistic regression was used to estimate relative risks of substantial decline. RESULTS: There were no differences in global score between the vitamin E and placebo groups at the first assessment (5.6 years after randomization: mean difference, -0.01; 95% confidence interval [CI], -0.04 to 0.03) or at the last assessment (9.6 years of treatment: mean difference, 0.00; 95% CI, -0.04 to 0.04). Mean cognitive change over time was also similar in the vitamin E group compared with the placebo group for the global score (mean difference in change, 0.02; 95% CI, -0.01 to 0.05; P = .16). The relative risk of substantial decline in the global score in the vitamin E group compared with the placebo group was 0.92 (95% CI, 0.77 to 1.10). CONCLUSION: Long-term use of vitamin E supplements did not provide cognitive benefits among generally healthy older women.

Aged↗
PubMed1998

Olfaction in neurodegenerative disease: a meta-analysis of olfactory functioning in Alzheimer's and Parkinson's diseases.

BACKGROUND: Olfactory deficits in Alzheimer's disease (AD) and idiopathic Parkinson's disease (PD) have been well established. OBJECTIVE: To clarify and review the literature by evaluating the evidence for olfactory deficits in 3 olfactory domains, including odor identification, recognition, and detection threshold. DATA SOURCES: A literature search of English-language studies of olfaction in AD, PD, and healthy controls was conducted via online databases (PsycInfo and MEDLINE) and reference lists from review articles. STUDY SELECTION: To meet selection criteria for meta-analysis, each study required a control group and complete and usable data. This review yielded 26 publications of olfactory identification, recognition, and/or detection threshold. Because of the inclusion of more than 1 relevant study of olfaction in several of these publications (eg, both identification and threshold assessed), 43 studies were ultimately appropriate for meta-analysis. DATA EXTRACTION: Effect sizes were calculated for each study by expressing differences between patient and control group means in SD units (Cohen's d). DATA SYNTHESIS: Extremely large effect sizes were shown across all tasks in both AD and PD groups. Both between-group analyses using the Mann-Whitney U test and within-group analyses using Friedman 2-way analysis of variance did not reveal any significant differences (all P > .30). CONCLUSIONS: As expected, severe deficits were found for both patients with AD and PD in each of the 3 olfactory domains relative to controls. However, no discriminating olfactory deficits were seen between patient groups or among the 3 measured olfactory domains, suggesting a similar disturbance in olfactory function between patients with AD and PD.

Adult↗