Lauren Navrady
University of Edinburgh
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Featured researches published by Lauren Navrady.
Cognition | 2012
Oriel FeldmanHall; Dean Mobbs; D. W. Evans; Lucy V. Hiscox; Lauren Navrady; Tim Dalgleish
Highlights ► We show people are unable to appropriately judge outcomes of moral behaviour. ► Moral beliefs have weaker impact when there is a presence of significant self-gain. ► People make highly self-serving choices in real moral situations. ► Real moral choices contradict responses to simple hypothetical moral probes. ► Enhancing context can cause hypothetical decisions to mirror real moral decisions.
Clinical psychological science | 2013
Tim Dalgleish; Lauren Navrady; Elinor Bird; Emma Hill; Barnaby D. Dunn; Ann-Marie Golden
Depression impairs the ability to retrieve positive, self-affirming autobiographical memories. To counteract this difficulty, we trained individuals with depression, either in episode or remission, to construct an accessible mental repository for a preselected set of positive, self-affirming memories using an ancient mnemonic technique—the method-of-loci (MoL). Participants in a comparison condition underwent a similar training protocol where they chunked the memories into meaningful sets and rehearsed them (rehearsal). Both protocols enhanced memory recollection to near ceiling levels after 1 week of training. However, on a surprise follow-up recall test a further week later, recollection was maintained only in the MoL condition, relative to a significant decrease in memories recalled in the rehearsal group. There were no significant performance differences between those currently in episode and those in remission. The results support use of the MoL as a tool to facilitate access to self-affirming memories in those with depression.
European Psychiatry | 2017
Lauren Navrady; Stuart J. Ritchie; Stella W. Y. Chan; D Kerr; Mark J. Adams; Emma Hawkins; David J. Porteous; Ian J. Deary; Catharine R. Gale; G. D. Batty; Andrew M. McIntosh
Background Neuroticism is a risk factor for selected mental and physical illnesses and is inversely associated with intelligence. Intelligence appears to interact with neuroticism and mitigate its detrimental effects on physical health and mortality. However, the inter-relationships of neuroticism and intelligence for major depressive disorder (MDD) and psychological distress has not been well examined. Methods Associations and interactions between neuroticism and general intelligence (g) on MDD, self-reported depression, and psychological distress were examined in two population-based cohorts: Generation Scotland: Scottish Family Health Study (GS:SFHS, n = 19,200) and UK Biobank (n = 90,529). The Eysenck Personality Scale Short Form-Revised measured neuroticism and g was extracted from multiple cognitive ability tests in each cohort. Family structure was adjusted for in GS:SFHS. Results Neuroticism was strongly associated with increased risk for depression and higher psychological distress in both samples. Although intelligence conferred no consistent independent effects on depression, it did increase the risk for depression across samples once neuroticism was adjusted for. Results suggest that higher intelligence may ameliorate the association between neuroticism and self-reported depression although no significant interaction was found for clinical MDD. Intelligence was inversely associated with psychological distress across cohorts. A small interaction was found across samples such that lower psychological distress associates with higher intelligence and lower neuroticism, although effect sizes were small. Conclusions From two large cohort studies, our findings suggest intelligence acts a protective factor in mitigating the effects of neuroticism on psychological distress. Intelligence does not confer protection against diagnosis of depression in those high in neuroticism.
International Journal of Epidemiology | 2018
Lauren Navrady; Maria Wolters; Donald J. MacIntyre; Toni-Kim Clarke; Archibald Campbell; Alison D. Murray; Kathryn L. Evans; Jonathan R. Seckl; Chris S. Haley; Keith Milburn; Joanna M. Wardlaw; David J. Porteous; Ian J. Deary; Andrew M. McIntosh
Funding: STRADL is supported by the Wellcome Trust through a Strategic Award (reference 104036/Z/14/Z). The Chief Scientist Office of the Scottish Government Health Department (CZD/16/6) and the Scottish Funding Council (HR03006) provided core support for Generation Scotland. A.M.M. is supported by the Dr Mortimer and Theresa Sackler Foundation. D.J.M. is supported by an NRS Fellowship, funded by the CSO. J.S., J.M.W., K.L.E., D.J.P., I.J.D. and A.M.M. are members of the Centre for Cognitive Ageing and Cognitive Epidemiology which also supports I.J.D.; funding from the Medical Research Council and Biotechnology and Biological Sciences Research Council is gratefully acknowledged (MR/K026992/1). Acknowledgments: We would like to express gratitude to all individuals who have taken part in both GS:SFHS and STRADL, and the entire project team including academic researchers, administrative staff, research managers and statisticians. Conflict of interest: The authors declare that they have no conflicting interests.
Social Psychological and Personality Science | 2016
Oriel FeldmanHall; Tim Dalgleish; D. W. Evans; Lauren Navrady; Ellen Tedeschi; Dean Mobbs
Moral perceptions of harm and fairness are instrumental in guiding how an individual navigates moral challenges. Classic research documents that the gender of a target can affect how people deploy these perceptions of harm and fairness. Across multiple studies, we explore the effect of an individual’s moral orientations (their considerations of harm and justice) and a target’s gender on altruistic behavior. Results reveal that a target’s gender can bias one’s readiness to engage in harmful actions and that a decider’s considerations of harm—but not fairness concerns—modulate costly altruism. Together, these data illustrate that moral choices are conditional on the social nature of the moral dyad: Even under the same moral constraints, a target’s gender and a decider’s gender can shift an individual’s choice to be more or less altruistic, suggesting that gender bias and harm considerations play a significant role in moral cognition.
Psychological Medicine | 2017
Lauren Navrady; Mark J. Adams; Sarah Chan; Stuart J. Ritchie; Andrew M. McIntosh
Background Polygenic risk scores (PRS) for depression correlate with depression status and chronicity, and provide causal anchors to identify depressive mechanisms. Neuroticism is phenotypically and genetically positively associated with depression, whereas psychological resilience demonstrates negative phenotypic associations. Whether increased neuroticism and reduced resilience are downstream mediators of genetic risk for depression, and whether they contribute independently to risk remains unknown. Methods Moderating and mediating relationships between depression PRS, neuroticism, resilience and both clinical and self-reported depression were examined in a large, population-based cohort, Generation Scotland: Scottish Family Health Study (N = 4166), using linear regression and structural equation modelling. Neuroticism and resilience were measured by the Eysenck Personality Scale Short Form Revised and the Brief Resilience Scale, respectively. Results PRS for depression was associated with increased likelihood of self-reported and clinical depression. No interaction was found between PRS and neuroticism, or between PRS and resilience. Neuroticism was associated with increased likelihood of self-reported and clinical depression, whereas resilience was associated with reduced risk. Structural equation modelling suggested the association between PRS and self-reported and clinical depression was mediated by neuroticism (43–57%), while resilience mediated the association in the opposite direction (37–40%). For both self-reported and clinical diagnoses, the genetic risk for depression was independently mediated by neuroticism and resilience. Conclusions Findings suggest polygenic risk for depression increases vulnerability for self-reported and clinical depression through independent effects on increased neuroticism and reduced psychological resilience. In addition, two partially independent mechanisms – neuroticism and resilience – may form part of the pathway of vulnerability to depression.
Journal of Clinical Epidemiology | 2017
Jonathan D. Hafferty; Archie Campbell; Lauren Navrady; Mark J. Adams; Donald J. MacIntyre; Stephen M. Lawrie; David J. Porteous; Andrew M. McIntosh
Objectives Researchers need to be confident about the reliability of epidemiologic studies that quantify medication use through self-report. Some evidence suggests that psychiatric medications are systemically under-reported. Modern record linkage enables validation of self-report with national prescribing data as gold standard. Here, we investigated the validity of medication self-report for multiple medication types. Study Design and Setting Participants in the Generation Scotland population-based cohort (N = 10,244) recruited 2009–2011 self-reported regular usage of several commonly prescribed medication classes. This was matched against Scottish NHS prescriptions data using 3- and 6-month fixed time windows. Potential predictors of discordant self-report, including general intelligence and psychological distress, were studied via multivariable logistic regression. Results Antidepressants self-report showed very good agreement (κ = 0.85, [95% confidence interval (CI) 0.84–0.87]), comparable to antihypertensives (κ = 0.90 [CI 0.89–0.91]). Self-report of mood stabilizers showed moderate-poor agreement (κ = 0.42 [CI 0.33–0.50]). Relevant past medical history was the strongest predictor of self-report sensitivity, whereas general intelligence was not predictive. Conclusion In this large population-based study, we found self-report validity varied among medication classes, with no simple relationship between psychiatric medication and under-reporting. History of indicated illness predicted more accurate self-report, for both psychiatric and nonpsychiatric medications. Although other patient-level factors influenced self-report for some medications, none predicted greater accuracy across all medications studied.
Emotion | 2017
Susanne Schweizer; Lauren Navrady; Lauren Breakwell; Rachel M. Howard; Ann-Marie Golden; Aliza Werner-Seidler; Tim Dalgleish
We currently know little about how performance on assessments of working memory capacity (WMC) that are designed to mirror the concurrent task demands of daily life are impacted by the presence of affective information, nor how those effects may be modulated by depression—a syndrome where sufferers report global difficulties with executive processing. Across 3 experiments, we investigated WMC for sets of neutral words in the context of processing either neutral or affective (depressogenic) sentences, which had to be judged on semantic accuracy (Experiments 1 and 2) or self-reference (Experiment 3). Overall, WMC was significantly better in the context of depressogenic compared with neutral sentences. However, there was no support for this effect being modulated by symptoms of depression (Experiment 1) or the presence of recurrent major depressive disorder (MDD; Experiments 2 and 3). Implications of these findings for cognitive theories of the role of WM in depression are discussed in the context of a growing body of research showing no support for a differential impact of depressogenic compared with neutral information on WM accuracy.
bioRxiv | 2018
Aleix Arnau-Soler; Mark J. Adams; Toni-Kim Clarke; Donald J. MacIntyre; Keith Milburn; Lauren Navrady; Generation Scotland; Caroline Hayward; Andrew M. McIntosh; Pippa A. Thomson
Depression has well-established influences from genetic and environmental risk factors. This has led to the diathesis-stress theory, which assumes a multiplicative gene-by-environment interaction (GxE) effect on risk. Recently, Colodro-Conde et al. empirically tested this theory, using the polygenic risk score for major depressive disorder (PRS, genes) and stressful life events (SLE, environment) effects on depressive symptoms, identifying significant GxE effects with an additive contribution to liability. We have tested the diathesis-stress theory on an independent sample of 4 919 individuals. We identified nominally significant positive GxE effects in the full cohort (R2 = 0.08%, p = 0.049) and in women (R2 = 0.19%, p = 0.017), but not in men (R2 = 0.15%, p = 0.07). GxE effects were nominally significant, but only in women, when SLE were split into those in which the respondent plays an active or passive role (R2 = 0.15%, p = 0.038; R2 = 0.16%, p = 0.033, respectively). High PRS increased the risk of depression in participants reporting high numbers of SLE (p = 2.86 × 10−4). However, in those participants who reported no recent SLE, a higher PRS appeared to increase the risk of depressive symptoms in men (β = 0.082, p = 0.016) but had a protective effect in women (β = −0.061, p = 0.037). This difference was nominally significant (p = 0.017). Our study reinforces the evidence of additional risk in the aetiology of depression due to GxE effects. However, larger sample sizes are required to robustly validate these findings.
Wellcome Open Research | 2018
Lauren Navrady; Yanni Zeng; Toni-Kim Clarke; Mark J. Adams; David M. Howard; Ian J. Deary; Andrew M. McIntosh
Background: Twin studies indicate that genetic and environmental factors contribute to both psychological resilience and coping style, but estimates of their relative molecular and shared environmental contributions are limited. The degree of overlap in the genetic architectures of these traits is also unclear. Methods: Using data from a large population- and family-based cohort Generation Scotland (N = 8,734), we estimated the genetic and shared environmental variance components for resilience, task-, emotion-, and avoidance-oriented coping style in a linear mixed model (LMM). Bivariate LMM analyses were used to estimate the genetic correlations between these traits. Resilience and coping style were measured using the Brief Resilience Scale and Coping Inventory for Stressful Situations, respectively. Results: The greatest proportion of the phenotypic variance in resilience remained unexplained, although significant contributions from common genetic variants and family-shared environment were found. Both task- and avoidance-oriented coping had significant contributions from common genetic variants, sibling- and couple-shared environments, variance in emotion-oriented coping was attributable to common genetic variants, family- and couple-shared environments. The estimated correlation between resilience and emotion-oriented coping was high for both common-variant-associated genetic effects (r G = -0.79, se = 0.19), and for the additional genetic effects from the pedigree (r K = -0.94, se = 0.30). Genetic correlations between resilience and task- and avoidance-oriented coping did not meet statistical significance. Conclusions: Both genetics and shared environmental effects were major contributing factors to coping style, whilst the variance in resilience remains largely unexplained. Strong genetic overlap between resilience and emotion-oriented coping suggests a relationship whereby genetic factors that increase negative emotionality also lead to decreased resilience. We suggest that genome-wide family-based studies of resilience and coping may help to elucidate tractable methodologies to identify genetic architectures and modifiable environmental risk factors to protect against psychiatric illness, although further work with larger sample sizes is needed.