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"I don't believe it." Acceptance and skepticism of genetic health information among African-American and White smokers.

ABSTRACT: Effective translation of genomics research into practice depends on public acceptance of genomics-related health information.To explore how smokers come to accept or reject information about the relationship between genetics and nicotine addiction.Thirteen focus groups (N = 84) were stratified by education (seven < Bachelor's degree, six ? Bachelor's degree) and race (eight black, five white). Participants viewed a 1-min video describing the discovery of a genetic variant associated with increased risk of nicotine addiction and lung cancer. Next, they provided their opinions about the information. Two coders analyzed the data using grounded theory.Pre-video knowledge about why people smoke cigarettes and what genetic risk means informed beliefs about the relationship between genes and addiction. These beliefs were not always consistent with biomedical explanations, but formed the context through which participants processed the video's information. This, in turn, led to information acceptance or skepticism. Participants explained their reactions in terms of the scientific merits of the research and used their existing knowledge and beliefs to explain their acceptance of or skepticism about the information.Laypeople hold complex understandings of genetics and addiction. However, when lay and biomedical explanations diverge, genetics-related health information may be rejected.

SUBMITTER: Waters EA

PROVIDER: S-EPMC5535773 | biostudies-other | 2017 Jul

REPOSITORIES: biostudies-other

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"I don't believe it." Acceptance and skepticism of genetic health information among African-American and White smokers.

Waters Erika A EA Ball Linda L Gehlert Sarah S

Social science & medicine (1982) 20170503

<h4>Rationale</h4>Effective translation of genomics research into practice depends on public acceptance of genomics-related health information.<h4>Objective</h4>To explore how smokers come to accept or reject information about the relationship between genetics and nicotine addiction.<h4>Methods</h4>Thirteen focus groups (N = 84) were stratified by education (seven < Bachelor's degree, six ≥ Bachelor's degree) and race (eight black, five white). Participants viewed a 1-min video describing the di ...[more]

PMID: 28527373

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Project description:BackgroundIdentifying sources of variation in the nicotine and nitrosamine metabolic inactivation pathways is important to understanding the relationship between smoking and cancer risk. Numerous UGT1A and UGT2B enzymes are implicated in nicotine and nitrosamine metabolism in vitro; however, little is known about their roles in vivo.MethodsWithin UGT1A1, UGT1A4, UGT1A9, UGT2B7, UGT2B10, and UGT2B17, 47 variants were genotyped, including UGT2B10*2 and UGT2B17*2. The association between variation in these UGTs and glucuronidation activity within European and African American current smokers (n = 128), quantified as urinary ratios of the glucuronide over unconjugated compound for nicotine, cotinine, trans-3'-hydroxycotinine, and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), was investigated in regression models assuming a dominant effect of variant alleles.ResultsCorrecting for multiple testing, three UGT2B10 variants were associated with cotinine glucuronidation, rs2331559 and rs11726322 in European Americans and rs835309 in African Americans (P ≤ 0.0002). Additional variants predominantly in UGT2B10 were nominally associated with nicotine (P = 0.008-0.04) and cotinine (P = <0.001-0.02) glucuronidation in both ethnicities in addition to UGT2B10*2 in European Americans (P = 0.01, P < 0.001). UGT2B17*2 (P = 0.03) in European Americans and UGT2B7 variants (P = 0.02-0.04) in African Americans were nominally associated with 3HC glucuronidation. UGT1A (P = 0.007-0.01), UGT2B10 (P = 0.02), and UGT2B7 (P = 0.02-0.03) variants in African Americans were nominally associated with NNAL glucuronidation.ConclusionsFindings from this initial in vivo study support a role for multiple UGTs in the glucuronidation of tobacco-related compounds in vivo, in particular UGT2B10 and cotinine glucuronidation.ImpactFindings also provide insight into ethnic differences in glucuronidation activity, which could be contributing to ethnic disparities in the risk for smoking-related cancers. Cancer Epidemiol Biomarkers Prev; 24(1); 94-104. ©2014 AACR.

Project description:ImportanceUnexplained sudden cardiac death (SCD) describes SCD with no cause identified. Genetic testing helps to diagnose inherited cardiac diseases in unexplained SCD; however, the associations between pathogenic or likely pathogenic (P/LP) variants of inherited cardiomyopathies (CMs) and arrhythmia syndromes and the risk of unexplained SCD in both White and African American adults living the United States has never been systematically examined.ObjectiveTo investigate cases of unexplained SCD to determine the frequency of P/LP genetic variants of inherited CMs and arrhythmia syndromes.Design, setting, and participantsThis genetic association study included 683 African American and White adults who died of unexplained SCD and were included in an autopsy registry. Overall, 413 individuals had DNA of acceptable quality for genetic sequencing. Data were collected from January 1995 to December 2015. A total of 30 CM genes and 38 arrhythmia genes were sequenced, and variants in these genes, curated as P/LP, were examined to study their frequency. Data analysis was performed from June 2018 to March 2021.Main outcomes and measuresThe frequency of P/LP variants for CM or arrhythmia in individuals with unexplained SCD.ResultsThe median (interquartile range) age at death of the 413 included individuals was 41 (29-48) years, 259 (62.7%) were men, and 208 (50.4%) were African American adults. A total of 76 patients (18.4%) with unexplained SCD carried variants considered P/LP for CM and arrhythmia genes. In total, 52 patients (12.6%) had 49 P/LP variants for CM, 22 (5.3%) carried 23 P/LP variants for arrhythmia, and 2 (0.5%) had P/LP variants for both CM and arrhythmia. Overall, 41 P/LP variants for hypertrophic CM were found in 45 patients (10.9%), 9 P/LP variants for dilated CM were found in 11 patients (2.7%), and 10 P/LP variants for long QT syndrome were found in 11 patients (2.7%). No significant difference was found in clinical and heart characteristics between individuals with or without P/LP variants. African American and White patients were equally likely to harbor P/LP variants.Conclusions and relevanceIn this large genetic association study of community cases of unexplained SCD, nearly 20% of patients carried P/LP variants, suggesting that genetics may contribute to a significant number of cases of unexplained SCD. Our findings regarding both the association of unexplained SCD with CM genes and race-specific genetic variants suggest new avenues of study for this poorly understood entity.

Dataset Information

"I don't believe it." Acceptance and skepticism of genetic health information among African-American and White smokers.

Publications

"I don't believe it." Acceptance and skepticism of genetic health information among African-American and White smokers.

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