Dataset Information

Cigarette experimentation and the population attributable fraction for associated genetic and non-genetic risk factors.

ABSTRACT:

Background

We, and others, have shown that experimenting with cigarettes is a function of both non-genetic and genetic factors. In this analysis we ask: how much of the total risk of experimenting with cigarettes, among those who had not experimented with cigarettes when they enrolled in a prospective cohort, is attributable to genetic factors and to non-genetic factors?

Methods

Participants (N?=?1,118 Mexican origin youth), recruited from a large population-based cohort study in Houston, Texas, provided prospective data on cigarette experimentation over three years. Non-genetic data were elicited twice - baseline and follow-up. Participants were genotyped for 672 functional and tagging variants in the dopamine, serotonin and opioid pathways.

Results

In the overall model, the adjusted combined non-genetic PAF was 71.2% and the adjusted combined genetic PAF was 58.5%. Among committed never smokers the adjusted combined non-genetic PAF was 67.0% and the adjusted combined genetic PAF was 53.5%. However, among cognitively susceptible youth, the adjusted combined non-genetic PAF was 52.0% and the adjusted combined genetic PAF was 68.4%.

Conclusions

Our results suggest there may be differences in genotypes between youth who think they will try cigarettes in the future compared to their peers who think they will not and underscore the possibility that the relative influence of genetic vs. non-genetic factors on the uptake of smoking may vary between these two groups of youth.

Impact

A clearer understanding of the relative role of genetic vs. non-genetic factors in the uptake of smoking may have implications for the design of prevention programs.

SUBMITTER: Wilkinson AV

PROVIDER: S-EPMC3547034 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Cigarette experimentation and the population attributable fraction for associated genetic and non-genetic risk factors.

Wilkinson Anna V AV Swartz Michael D MD Yu Xiaoying X Spitz Margaret R MR Shete Sanjay S

PloS one 20130116 1

<h4>Background</h4>We, and others, have shown that experimenting with cigarettes is a function of both non-genetic and genetic factors. In this analysis we ask: how much of the total risk of experimenting with cigarettes, among those who had not experimented with cigarettes when they enrolled in a prospective cohort, is attributable to genetic factors and to non-genetic factors?<h4>Methods</h4>Participants (N = 1,118 Mexican origin youth), recruited from a large population-based cohort study in ...[more]

PMID: 23342024

Similar Datasets

Project description:BackgroundSevere maternal morbidity is an important proxy for maternal mortality. Population attributable fraction is the proportion of a disease that is attributable to a given risk factor and can be used to estimate the reduction in the disease that would be anticipated if a risk factor was reduced or eliminated.ObjectiveWe sought to determine the population-attributable fraction (PAF) of potentially modifiable risk factors for severe maternal morbidity.Study designWe used a retrospective cohort of 86,260 delivery hospitalizations from Magee-Womens Hospital, Pittsburgh, PA for this analysis (2003-2012). Severe maternal morbidity was defined as any of the following: Centers for Disease Control and Prevention International Classification of Diseases 9th Revision diagnosis and procedure codes for the identification of maternal morbidity; prolonged postpartum length of stay (defined as >3 standard deviations beyond the mean length of stay: >3 days for vaginal deliveries and >5 days for Cesarean deliveries); or maternal intensive care unit admission. We used multivariable logistic regression with generalized estimating equations to estimate the association of prepregnancy overweight or obesity, maternal age ≥35 years, preexisting hypertension, preexisting diabetes, excessive gestational weight gain, smoking, education, and marital status with severe maternal morbidity. We then calculated the PAF for each risk factor. We also examined the impact of modest reductions and elimination of risk factors on the PAF of severe maternal morbidity.ResultsThe overall rate of severe maternal morbidity was 2.0%. Overweight and obesity, maternal age ≥35 years, preexisting hypertension, excessive gestational weight gain, and lack of a college degree had PAF ranging from 4.5% to 13%. If all risk factors were eliminated, 36% of cases could have been prevented. Modest reductions in the prevalence of excessive BMI and advanced maternal age had minimal impact on preventing severe maternal morbidity. Smoking during pregnancy and marital status were not associated with severe maternal morbidity.ConclusionsOur data suggest maternal morbidity can be reduced by modifying common, individual-level risk factors. Nevertheless, the majority of cases were not attributable to the patient level risk factors we examined. These data support the need for large studies of patient-, provider-, system- and population-level factors to identify high-impact interventions to reduce maternal morbidity.

Project description:ImportanceIdentifying modifiable risk factors that are associated with dementia burden across racial and ethnic groups in the population can yield insights into the potential effectiveness of interventions in preventing dementia and reducing disparities.ObjectiveTo calculate the population attributable fraction (PAF) of dementia associated with 12 established modifiable risk factors for all US adults, as well as separately by race and ethnicity.Design, setting, and participantsThis cross-sectional study used survey data from nationally representative samples of US adults. PAFs were calculated using relative risks and prevalence estimates for 12 risk factors. Relative risks were taken from meta-analyses, as reported in a 2020 systematic review. Prevalence estimates for risk factors were derived from nationally representative cross-sectional survey data collected between 2011 and 2018. Combined PAFs were adjusted for risk factor communality using weights derived from the Atherosclerosis Risk in Communities (ARIC) study (1987-2018). Analyses were conducted May through October 2021.ExposuresLow education, hearing loss, traumatic brain injury, hypertension, excessive alcohol consumption, obesity, smoking, depression, social isolation, physical inactivity, diabetes, and air pollution.Main outcomes and measuresPAF for each dementia risk factor, a combined PAF, and the decrease in the number of prevalent dementia cases in 2020 that would be expected given a 15% proportional decrease in each exposure.ResultsAmong all US adults, an estimated 41.0% (95% CI, 22.7%-55.9%) of dementia cases were attributable to 12 risk factors. A 15% proportional decrease in each risk factor would reduce dementia prevalence in the population by an estimated 7.3% (95% CI, 3.7%-10.9%). The estimated PAF was greater for Black and Hispanic than it was for White and Asian individuals. The greatest attributable fraction of dementia cases was observed for hypertension (PAF, 20.2%; 95% CI, 6.3%-34.4%), obesity (PAF, 20.9%; 95% CI, 13.0%-28.8%), and physical inactivity (PAF, 20.1%; 95% CI, 9.1%-29.6%). These factors were also highest within each racial and ethnic group, although the proportions varied.Conclusions and relevanceA large fraction of dementia cases in the US were associated with potentially modifiable risk factors, especially for Black and Hispanic individuals. Targeting and reducing these risk factors may curb the projected rise in dementia cases over the next several decades.

Project description:BackgroundChlamydia trachomatis infection is highly prevalent among young women in the United States. Prevention of long-term sequelae of infection, including tubal factor infertility, is a primary goal of chlamydia screening and treatment activities. However, the population-attributable fraction of tubal factor infertility associated with chlamydia is unclear, and optimal measures for assessing tubal factor infertility and prior chlamydia in epidemiological studies have not been established. Black women have increased rates of chlamydia and tubal factor infertility compared with White women but have been underrepresented in prior studies of the association of chlamydia and tubal factor infertility.ObjectivesThe objectives of the study were to estimate the population-attributable fraction of tubal factor infertility associated with Chlamydia trachomatis infection by race (Black, non-Black) and assess how different definitions of Chlamydia trachomatis seropositivity and tubal factor infertility affect population-attributable fraction estimates.Study designWe conducted a case-control study, enrolling infertile women attending infertility practices in Birmingham, AL, and Pittsburgh, PA, during October 2012 through June 2015. Tubal factor infertility case status was primarily defined by unilateral or bilateral fallopian tube occlusion (cases) or bilateral fallopian tube patency (controls) on hysterosalpingogram. Alternate tubal factor infertility definitions incorporated history suggestive of tubal damage or were based on laparoscopic evidence of tubal damage. We aimed to enroll all eligible women, with an expected ratio of 1 and 3 controls per case for Black and non-Black women, respectively. We assessed Chlamydia trachomatis seropositivity with a commercial assay and a more sensitive research assay; our primary measure of seropositivity was defined as positivity on either assay. We estimated Chlamydia trachomatis seropositivity and calculated Chlamydia trachomatis-tubal factor infertility odds ratios and population-attributable fraction, stratified by race.ResultsWe enrolled 107 Black women (47 cases, 60 controls) and 620 non-Black women (140 cases, 480 controls). Chlamydia trachomatis seropositivity by either assay was 81% (95% confidence interval, 73-89%) among Black and 31% (95% confidence interval, 28-35%) among non-Black participants (P < .001). Using the primary Chlamydia trachomatis seropositivity and tubal factor infertility definitions, no significant association was detected between chlamydia and tubal factor infertility among Blacks (odds ratio, 1.22, 95% confidence interval, 0.45-3.28) or non-Blacks (odds ratio, 1.41, 95% confidence interval, 0.95-2.09), and the estimated population-attributable fraction was 15% (95% confidence interval, -97% to 68%) among Blacks and 11% (95% confidence interval, -3% to 23%) among non-Blacks. Use of alternate serological measures and tubal factor infertility definitions had an impact on the magnitude of the chlamydia-tubal factor infertility association and resulted in a significant association among non-Blacks.ConclusionLow population-attributable fraction estimates suggest factors in addition to chlamydia contribute to tubal factor infertility in the study population. However, high background Chlamydia trachomatis seropositivity among controls, most striking among Black participants, could have obscured an association with tubal factor infertility and resulted in a population-attributable fraction that underestimates the true etiological role of chlamydia. Choice of chlamydia and tubal factor infertility definitions also has an impact on the odds ratio and population-attributable fraction estimates.

Dataset Information

Cigarette experimentation and the population attributable fraction for associated genetic and non-genetic risk factors.

Background

Methods

Results

Conclusions

Impact

Publications

Cigarette experimentation and the population attributable fraction for associated genetic and non-genetic risk factors.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets