91 research outputs found

    A framework for conceptualizing how narratives from health-care consumers might improve or impede the use of information about provider quality

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    Consumers choosing a health-care provider have access to diverse information including narratives by patients about their prior experiences. However, little research has examined how narratives might improve or impede the use of information about the quality of providers’ performance. This paper describes a conceptual framework for examining mechanisms by which narrative information might influence consumer judgments and decisions about providers. We conducted a conceptual review of risk communication and behavioral decision research. We synthesized the literature to form the foundation of a conceptual framework for assessing how narrative information about provider quality impacts consumer decisions about providers. We identified four key characteristics of narratives (convey emotion; explain logic; provide relational information; and capture naturalistic experience) that may address four consumer needs (avoid surprise and regret; recognize dominant options; motivate to act or not act; and make multi-attribute tradeoff decisions). We also identified three main functions of narratives (provide a simple, powerful cue; imbue quality information with meaning; and stimulate cognition and behavior) in four decision contexts (short-term treatments; external disruptions; chronic illness; problematic experiences). A rigorous research program can be derived from the conceptual framework to generate evidence-based recommendations about whether and how patient narratives might encourage: (1) more reasoned decisions; (2) consistency with a patient’s own values/preferences; and (3) engagement with provider quality information. Research results can be used then to develop robust guidance for health communicators reporting diverse and often incommensurate performance metrics

    Consumer Response to Drug Risk Information:The Role of Positive Affect

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    Risk disclosure is an essential element of the marketing of prescription drugs and other medical products. This study examines how consumers respond to verbal information about the frequency and severity of medical-product risks and how media-induced affect can moderate such responses. The study finds that consumers tend to overestimate the actual likelihood of adverse events described with words such as “common” or “rare” (compared with the probabilities such terms are typically intended to convey) and that consumers tend to give little weight to such probability language when forming product use intentions. However, consumers in positive media-induced moods seem to engage in more nuanced evaluation of product risk information, weighing both frequency and severity information and using such information to make inferences about other product attributes (e.g., product efficacy). These findings suggest that medical marketers and regulators need to devise more effective means of communicating risk probability to consumers and that positive mood induction (e.g., by placing advertisements in upbeat media environments) can enhance consumers' ability to process product risk information

    Shared heritability and functional enrichment across six solid cancers

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    Correction: Nature Communications 10 (2019): art. 4386 DOI: 10.1038/s41467-019-12095-8Quantifying the genetic correlation between cancers can provide important insights into the mechanisms driving cancer etiology. Using genome-wide association study summary statistics across six cancer types based on a total of 296,215 cases and 301,319 controls of European ancestry, here we estimate the pair-wise genetic correlations between breast, colorectal, head/neck, lung, ovary and prostate cancer, and between cancers and 38 other diseases. We observed statistically significant genetic correlations between lung and head/neck cancer (r(g) = 0.57, p = 4.6 x 10(-8)), breast and ovarian cancer (r(g) = 0.24, p = 7 x 10(-5)), breast and lung cancer (r(g) = 0.18, p = 1.5 x 10(-6)) and breast and colorectal cancer (r(g) = 0.15, p = 1.1 x 10(-4)). We also found that multiple cancers are genetically correlated with non-cancer traits including smoking, psychiatric diseases and metabolic characteristics. Functional enrichment analysis revealed a significant excess contribution of conserved and regulatory regions to cancer heritability. Our comprehensive analysis of cross-cancer heritability suggests that solid tumors arising across tissues share in part a common germline genetic basis.Peer reviewe

    Genomic analyses identify hundreds of variants associated with age at menarche and support a role for puberty timing in cancer risk

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    The timing of puberty is a highly polygenic childhood trait that is epidemiologically associated with various adult diseases. Using 1000 Genomes Project-imputed genotype data in up to similar to 370,000 women, we identify 389 independent signals (P <5 x 10(-8)) for age at menarche, a milestone in female pubertal development. In Icelandic data, these signals explain similar to 7.4% of the population variance in age at menarche, corresponding to similar to 25% of the estimated heritability. We implicate similar to 250 genes via coding variation or associated expression, demonstrating significant enrichment in neural tissues. Rare variants near the imprinted genes MKRN3 and DLK1 were identified, exhibiting large effects when paternally inherited. Mendelian randomization analyses suggest causal inverse associations, independent of body mass index (BMI), between puberty timing and risks for breast and endometrial cancers in women and prostate cancer in men. In aggregate, our findings highlight the complexity of the genetic regulation of puberty timing and support causal links with cancer susceptibility

    Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

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    Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe
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