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Drawing on early work on ethical leadership, we argue that when leaders engage in leader moral hypocrisy (i.e., ethical promotion without ethical demonstration), followers can experience psychological reactance—a negative response to a perceived restriction of freedom—which can have negative downstream consequences. In a survey of employee–manager dyads (study 1), we demonstrate that leader moral hypocrisy is positively associated with follower psychological reactance, which increases follower deviance. In two subsequent laboratory experiments, we find similar patterns of results (study 2) and explore potential alternative mechanisms (study 3). We demonstrate in a final experiment with working adults that the relationship between leader moral hypocrisy and psychological reactance is partly explained by increased perceptions of a leader’s use of power (study 4). We discuss the implications of our findings and advocate for further understanding of the risks associated with psychological reactance in response to leaders and other workplace situations.
Major depressive disorder (MDD) is moderately heritable, however genome-wide association studies (GWAS) for MDD, as well as for related continuous outcomes, have not shown consistent results. Attempts to elucidate the genetic basis of MDD may be hindered by heterogeneity in diagnosis. The Center for Epidemiological Studies Depression (CES-D) scale provides a widely used tool for measuring depressive symptoms clustered in four different domains which can be combined together into a total score but also can be analysed as separate symptom domains.
We performed a meta-analysis of GWAS of the CES-D symptom clusters. We recruited 12 cohorts with the 20- or 10-item CES-D scale (32 528 persons).
One single nucleotide polymorphism (SNP), rs713224, located near the brain-expressed melatonin receptor (MTNR1A) gene, was associated with the somatic complaints domain of depression symptoms, with borderline genome-wide significance (pdiscovery = 3.82 × 10−8). The SNP was analysed in an additional five cohorts comprising the replication sample (6813 persons). However, the association was not consistent among the replication sample (pdiscovery+replication = 1.10 × 10−6) with evidence of heterogeneity.
Despite the effort to harmonize the phenotypes across cohorts and participants, our study is still underpowered to detect consistent association for depression, even by means of symptom classification. On the contrary, the SNP-based heritability and co-heritability estimation results suggest that a very minor part of the variation could be captured by GWAS, explaining the reason of sparse findings.
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