Cyber-Risikomanagement in der Finanzdienstleistungsbranche, Spillover-Effekte und Cyber-Versicherungsprodukte für Privatkunden

This thesis consists of four essays on open research questions with respect to cyber risks. The first and second research essays address cyber risk management and spillover effects from cyberattacks in the US financial services industry, while the third has a regional focus on Europe. The last essay discusses the cyber insurance products for private clients provided in six different countries. First, we empirically analyze the consciousness, determinants, and value-relevance of cyber risk management in the US banking and insurance industry, as well as the spillover effects, which to the best of our knowledge have not been examined so far. By means of a text mining approach applied to annual reports and regression analyses, we find an increasing cyber risk consciousness and point out, inter alia, that cyber risk management contributes to value creation. We also observe significant competitive effects to large- and mid-cap firms and contagion effects to the entire sample when using event study methodology. Second, as the implications of cyberattacks on announcing firms could spill over to a third party, we empirically examine spillover effects to the stocks of US (cyber) insurers in the US financial services industry which have not been investigated in closer detail. By applying an event study, we find evidence for significant contagion effects to the US (cyber) insurance industry, reflecting the deterioration of the reputation of non-announcing firms. For “mega cyberattacks”, we observe competitive effects to US cyber insurers. Studying possible influencing factors confirms that spillover effects are information-based. Third, we also empirically study the cyber risk consciousness, firm characteristics, and value of cyber risk management for European banks and insurers, as well as possible spillover effects from cyberattacks and IT risk events, which has not been done so far, as the current literature neglects the focus on Europe. When applying similar research methodologies which are in line with the two previous US studies, we correspondingly observe an increasing cyber risk consciousness and relevant determinants, as well as a positive relationship between cyber risk management and firm value, in addition to significant spillover effects. Fourth, a comparison of the cyber insurance products for private clients offered in Austria, Canada, Germany, Switzerland, the United Kingdom and the US is provided. Thereby, coverage components regarding first and third party risk, legal advice and the additional services of stand-alone cyber insurance and add-ons are identified and compared by conducting a qualitative analysis to reveal new insights regarding product features. We find that first party risk and additional services play a crucial role in stand-alone cyber insurance and add-ons, while the overall comparison of coverage components (across different regions) is challenging.Diese Arbeit besteht aus vier Aufsätzen zu offenen Forschungsfragen in Bezug auf Cyber-Risiken. Der erste und zweite Forschungsaufsatz befassen sich mit dem Cyber-Risikomanagement und Spillover-Effekten von Cyber-Angriffen in der US-amerikanischen Finanzdienstleistungsbranche, während der dritte den regionalen Fokus auf Europa hat. Der letzte Aufsatz behandelt die Cyber-Versicherungsprodukte für Privatkunden, die in sechs verschiedenen Ländern angeboten werden. Zuerst analysieren wir empirisch das Bewusstsein, die Determinanten und die Wertrelevanz des Cyber-Risikomanagements in der US-amerikanischen Banken- und Versicherungsbranche sowie Spillover-Effekte, die nach unserem Kenntnisstand bisher nicht untersucht wurden. Anhand eines auf Geschäftsberichte und Regressionsanalysen angewandten Text-Mining-Ansatzes stellen wir ein zunehmendes Cyber-Risikobewusstsein fest und weisen unter anderem darauf hin, dass Cyber-Risikomanagement zur Wertschöpfung beiträgt. Wir beobachten auch signifikante Wettbewerbseffekte auf Large- und Mid-Cap-Unternehmen und Ansteckungseffekte auf die gesamte Stichprobe, wenn wir die Event-Studienmethodik verwenden. Da zweitens die Auswirkungen von Cyber-Angriffen ankündigender Unternehmen auf Dritte übertragen werden könnten, untersuchen wir empirisch Spillover-Effekte auf Aktien von US-amerikanischen (Cyber-)Versicherern in der US-amerikanischen Finanzdienstleistungsbranche, die noch nicht näher untersucht wurden. Durch die Anwendung einer Ereignisstudie finden wir Hinweise auf erhebliche Ansteckungseffekte auf die US-amerikanische (Cyber-)Versicherungsbranche, die die Verschlechterung der Reputation von nicht ankündigenden Unternehmen widerspiegeln. Bei „Mega-Cyber-Attacken“ beobachten wir Wettbewerbseffekte auf US-amerikanische Cyber-Versicherer. Die Untersuchung möglicher Einflussfaktoren bestätigt, dass Spillover-Effekte informationsbasiert sind. Drittens untersuchen wir auch empirisch das Cyber-Risikobewusstsein, die Unternehmenseigenschaften und den Wert des Cyber-Risikomanagements für europäische Banken und Versicherungen sowie mögliche Spillover-Effekte von Cyber-Angriffen und IT-Risikoereignissen, was bisher noch nicht erfolgt ist, da die Literatur den Fokus auf Europa vernachlässigt. Bei der Anwendung ähnlicher Forschungsmethoden, die mit den beiden vorangegangenen US-Studien übereinstimmen, beobachten wir neben signifikanten Spillover-Effekten ein zunehmendes Cyber-Risikobewusstsein und relevante Determinanten sowie einen positiven Zusammenhang zwischen Cyber-Risikomanagement und Unternehmenswert. Viertens erfolgt ein Vergleich der in Österreich, Kanada, Deutschland, der Schweiz, Großbritannien und den USA angebotenen Cyber-Versicherungsprodukten für Privatkunden. Dabei werden Deckungskomponenten zu Eigen- und Drittrisiko, Rechtsberatung und den Zusatzleistungen von Stand-Alone Cyber-Versicherungen und Add-Ons identifiziert und durch eine qualitative Analyse verglichen, um neue Erkenntnisse zu den Produkteigenschaften zu gewinnen. Wir stellen fest, dass das Eigenrisiko und zusätzliche Services eine entscheidende Rolle bei Stand-Alone Cyber-Versicherungen und Add-Ons spielen, während der Gesamtvergleich der Deckungskomponenten (über verschiedene Regionen) eine Herausforderung darstellt

Cyber risk management in the US banking and insurance industry: A textual and empirical analysis of determinants and value

Abstract In this paper, we first construct a cyber risk consciousness score using a text mining algorithm, applied to annual reports of large‐ and mid‐cap US banks and insurers from 2011 to 2018. We next categorize the firms' cyber risk management based on keywords to study determinants and value‐relevance. Our results show an increasing cyber risk consciousness, regardless of the industry. In addition, for the entire sample we find that firms belonging to the banking industry, with a higher cyber risk consciousness score and a higher general risk awareness are more likely to implement cyber risk management, which also holds for both industries separately. We find the opposite in the case of profitable firms for the entire sample and the insurer subsample. Finally, we observe a significant positive relationship between cyber risk management and firm value measured by Tobin's Q for the entire sample and the subsamples of banks and insurers

No Reliable Association between Runs of Homozygosity and Schizophrenia in a Well-Powered Replication Study

It is well known that inbreeding increases the risk of recessive monogenic diseases, but it is less certain whether it contributes to the etiology of complex diseases such as schizophrenia. One way to estimate the effects of inbreeding is to examine the association between disease diagnosis and genome-wide autozygosity estimated using runs of homozygosity (ROH) in genome-wide single nucleotide polymorphism arrays. Using data for schizophrenia from the Psychiatric Genomics Consortium (n = 21,868), Keller et al. (2012) estimated that the odds of developing schizophrenia increased by approximately 17% for every additional percent of the genome that is autozygous (β = 16.1, CI(β) = [6.93, 25.7], Z = 3.44, p = 0.0006). Here we describe replication results from 22 independent schizophrenia case-control datasets from the Psychiatric Genomics Consortium (n = 39,830). Using the same ROH calling thresholds and procedures as Keller et al. (2012), we were unable to replicate the significant association between ROH burden and schizophrenia in the independent PGC phase II data, although the effect was in the predicted direction, and the combined (original + replication) dataset yielded an attenuated but significant relationship between Froh and schizophrenia (β = 4.86,CI(β) = [0.90,8.83],Z = 2.40,p = 0.02). Since Keller et al. (2012), several studies reported inconsistent association of ROH burden with complex traits, particularly in case-control data. These conflicting results might suggest that the effects of autozygosity are confounded by various factors, such as socioeconomic status, education, urbanicity, and religiosity, which may be associated with both real inbreeding and the outcome measures of interest

Gene expression imputation across multiple brain regions provides insights into schizophrenia risk

Transcriptomic imputation approaches combine eQTL reference panels with large-scale genotype data in order to test associations between disease and gene expression. These genic associations could elucidate signals in complex genome-wide association study (GWAS) loci and may disentangle the role of different tissues in disease development. We used the largest eQTL reference panel for the dorso-lateral prefrontal cortex (DLPFC) to create a set of gene expression predictors and demonstrate their utility. We applied DLPFC and 12 GTEx-brain predictors to 40,299 schizophrenia cases and 65,264 matched controls for a large transcriptomic imputation study of schizophrenia. We identified 413 genic associations across 13 brain regions. Stepwise conditioning identified 67 non-MHC genes, of which 14 did not fall within previous GWAS loci. We identified 36 significantly enriched pathways, including hexosaminidase-A deficiency, and multiple porphyric disorder pathways. We investigated developmental expression patterns among the 67 non-MHC genes and identified specific groups of pre- and postnatal expression

Age at first birth in women is genetically associated with increased risk of schizophrenia

Prof. Paunio on PGC:n jäsenPrevious studies have shown an increased risk for mental health problems in children born to both younger and older parents compared to children of average-aged parents. We previously used a novel design to reveal a latent mechanism of genetic association between schizophrenia and age at first birth in women (AFB). Here, we use independent data from the UK Biobank (N = 38,892) to replicate the finding of an association between predicted genetic risk of schizophrenia and AFB in women, and to estimate the genetic correlation between schizophrenia and AFB in women stratified into younger and older groups. We find evidence for an association between predicted genetic risk of schizophrenia and AFB in women (P-value = 1.12E-05), and we show genetic heterogeneity between younger and older AFB groups (P-value = 3.45E-03). The genetic correlation between schizophrenia and AFB in the younger AFB group is -0.16 (SE = 0.04) while that between schizophrenia and AFB in the older AFB group is 0.14 (SE = 0.08). Our results suggest that early, and perhaps also late, age at first birth in women is associated with increased genetic risk for schizophrenia in the UK Biobank sample. These findings contribute new insights into factors contributing to the complex bio-social risk architecture underpinning the association between parental age and offspring mental health.Peer reviewe

Genetic correlation between amyotrophic lateral sclerosis and schizophrenia

A. Palotie on työryhmän Schizophrenia Working Grp Psychiat jäsen.We have previously shown higher-than-expected rates of schizophrenia in relatives of patients with amyotrophic lateral sclerosis (ALS), suggesting an aetiological relationship between the diseases. Here, we investigate the genetic relationship between ALS and schizophrenia using genome-wide association study data from over 100,000 unique individuals. Using linkage disequilibrium score regression, we estimate the genetic correlation between ALS and schizophrenia to be 14.3% (7.05-21.6; P = 1 x 10(-4)) with schizophrenia polygenic risk scores explaining up to 0.12% of the variance in ALS (P = 8.4 x 10(-7)). A modest increase in comorbidity of ALS and schizophrenia is expected given these findings (odds ratio 1.08-1.26) but this would require very large studies to observe epidemiologically. We identify five potential novel ALS-associated loci using conditional false discovery rate analysis. It is likely that shared neurobiological mechanisms between these two disorders will engender novel hypotheses in future preclinical and clinical studies.Peer reviewe

Estimation of Genetic Correlation via Linkage Disequilibrium Score Regression and Genomic Restricted Maximum Likelihood

J. Lönnqvist on työryhmän Psychiat Genomics Consortium jäsen.Genetic correlation is a key population parameter that describes the shared genetic architecture of complex traits and diseases. It can be estimated by current state-of-art methods, i.e., linkage disequilibrium score regression (LDSC) and genomic restricted maximum likelihood (GREML). The massively reduced computing burden of LDSC compared to GREML makes it an attractive tool, although the accuracy (i.e., magnitude of standard errors) of LDSC estimates has not been thoroughly studied. In simulation, we show that the accuracy of GREML is generally higher than that of LDSC. When there is genetic heterogeneity between the actual sample and reference data from which LD scores are estimated, the accuracy of LDSC decreases further. In real data analyses estimating the genetic correlation between schizophrenia (SCZ) and body mass index, we show that GREML estimates based on similar to 150,000 individuals give a higher accuracy than LDSC estimates based on similar to 400,000 individuals (from combinedmeta-data). A GREML genomic partitioning analysis reveals that the genetic correlation between SCZ and height is significantly negative for regulatory regions, which whole genome or LDSC approach has less power to detect. We conclude that LDSC estimates should be carefully interpreted as there can be uncertainty about homogeneity among combined meta-datasets. We suggest that any interesting findings from massive LDSC analysis for a large number of complex traits should be followed up, where possible, with more detailed analyses with GREML methods, even if sample sizes are lesser.Peer reviewe

Interaction Testing and Polygenic Risk Scoring to Estimate the Association of Common Genetic Variants with Treatment Resistance in Schizophrenia

Importance: About 20% to 30% of people with schizophrenia have psychotic symptoms that do not respond adequately to first-line antipsychotic treatment. This clinical presentation, chronic and highly disabling, is known as treatment-resistant schizophrenia (TRS). The causes of treatment resistance and their relationships with causes underlying schizophrenia are largely unknown. Adequately powered genetic studies of TRS are scarce because of the difficulty in collecting data from well-characterized TRS cohorts. Objective: To examine the genetic architecture of TRS through the reassessment of genetic data from schizophrenia studies and its validation in carefully ascertained clinical samples. Design, Setting, and Participants: Two case-control genome-wide association studies (GWASs) of schizophrenia were performed in which the case samples were defined as individuals with TRS (n = 10501) and individuals with non-TRS (n = 20325). The differences in effect sizes for allelic associations were then determined between both studies, the reasoning being such differences reflect treatment resistance instead of schizophrenia. Genotype data were retrieved from the CLOZUK and Psychiatric Genomics Consortium (PGC) schizophrenia studies. The output was validated using polygenic risk score (PRS) profiling of 2 independent schizophrenia cohorts with TRS and non-TRS: a prevalence sample with 817 individuals (Cardiff Cognition in Schizophrenia [CardiffCOGS]) and an incidence sample with 563 individuals (Genetics Workstream of the Schizophrenia Treatment Resistance and Therapeutic Advances [STRATA-G]). Main Outcomes and Measures: GWAS of treatment resistance in schizophrenia. The results of the GWAS were compared with complex polygenic traits through a genetic correlation approach and were used for PRS analysis on the independent validation cohorts using the same TRS definition. Results: The study included a total of 85490 participants (48635 [56.9%] male) in its GWAS stage and 1380 participants (859 [62.2%] male) in its PRS validation stage. Treatment resistance in schizophrenia emerged as a polygenic trait with detectable heritability (1% to 4%), and several traits related to intelligence and cognition were found to be genetically correlated with it (genetic correlation, 0.41-0.69). PRS analysis in the CardiffCOGS prevalence sample showed a positive association between TRS and a history of taking clozapine (r2 = 2.03%; P =.001), which was replicated in the STRATA-G incidence sample (r2 = 1.09%; P =.04). Conclusions and Relevance: In this GWAS, common genetic variants were differentially associated with TRS, and these associations may have been obscured through the amalgamation of large GWAS samples in previous studies of broadly defined schizophrenia. Findings of this study suggest the validity of meta-analytic approaches for studies on patient outcomes, including treatment resistance

Germinant Synergy Facilitates Clostridium difficile Spore Germination under Physiological Conditions

Clostridium difficile is an anaerobic spore-forming human pathogen that is the leading cause of nosocomial infectious diarrhea worldwide. Germination of infectious spores is the first step in the development of a C. difficile infection (CDI) after ingestion and passage through the stomach. This study investigates the specific conditions that facilitate C. difficile spore germination, including the following: location within the gastrointestinal (GI) tract, pH, temperature, and germinant concentration. The germinants that have been identified in culture include combinations of bile salts and amino acids or bile salts and calcium, but in vitro, these function at concentrations that far exceed normal physiological ranges normally found in the mammalian GI tract. In this work, we describe and quantify a previously unreported synergy observed when bile salts, calcium, and amino acids are added together. These germinant cocktails improve germination efficiency by decreasing the required concentrations of germinants to physiologically relevant levels. Combinations of multiple germinant types are also able to overcome the effects of inhibitory bile salts. In addition, we propose that the acidic conditions within the GI tract regulate C. difficile spore germination and could provide a biological explanation for why patients taking proton pump inhibitors are associated with increased risk of developing a CDI.Clostridium difficile is a Gram-positive obligate anaerobe that forms spores in order to survive for long periods in the unfavorable environment outside a host. C. difficile is the leading cause of nosocomial infectious diarrhea worldwide. C. difficile infection (CDI) arises after a patient treated with broad-spectrum antibiotics ingests infectious spores. The first step in C. difficile pathogenesis is the metabolic reactivation of dormant spores within the gastrointestinal (GI) tract through a process known as germination. In this work, we aim to elucidate the specific conditions and the location within the GI tract that facilitate this process. Our data suggest that C. difficile germination occurs through a two-step biochemical process that is regulated by pH and bile salts, amino acids, and calcium present within the GI tract. Maximal germination occurs at a pH ranging from 6.5 to 8.5 in the terminal small intestine prior to bile salt and calcium reabsorption by the host. Germination can be initiated by lower concentrations of germinants when spores are incubated with a combination of bile salts, calcium, and amino acids, and this synergy is dependent on the availability of calcium. The synergy described here allows germination to proceed in the presence of inhibitory bile salts and at physiological concentrations of germinants, effectively decreasing the concentrations of nutrients required to initiate an essential step of pathogenesis

Intestinal calcium and bile salts facilitate germination of <i>Clostridium difficile</i> spores

<div><p><i>Clostridium difficile</i> (<i>C</i>. <i>difficile</i>) is an anaerobic gram-positive pathogen that is the leading cause of nosocomial bacterial infection globally. <i>C</i>. <i>difficile</i> infection (CDI) typically occurs after ingestion of infectious spores by a patient that has been treated with broad-spectrum antibiotics. While CDI is a toxin-mediated disease, transmission and pathogenesis are dependent on the ability to produce viable spores. These spores must become metabolically active (germinate) in order to cause disease. <i>C</i>. <i>difficile</i> spore germination occurs when spores encounter bile salts and other co-germinants within the small intestine, however, the germination signaling cascade is unclear. Here we describe a signaling role for Ca²⁺ during <i>C</i>. <i>difficile</i> spore germination and provide direct evidence that intestinal Ca²⁺ coordinates with bile salts to stimulate germination. Endogenous Ca²⁺ (released from within the spore) and a putative AAA+ ATPase, encoded by <i>Cd630_32980</i>, are both essential for taurocholate-glycine induced germination in the absence of exogenous Ca²⁺. However, environmental Ca²⁺ replaces glycine as a co-germinant and circumvents the need for endogenous Ca²⁺ fluxes. <i>Cd630_32980</i> is dispensable for colonization in a murine model of <i>C</i>. <i>difficile</i> infection and <i>ex vivo</i> germination in mouse ileal contents. Calcium-depletion of the ileal contents prevented mutant spore germination and reduced WT spore germination by 90%, indicating that Ca²⁺ present within the gastrointestinal tract plays a critical role in <i>C</i>. <i>difficile</i> germination, colonization, and pathogenesis. These data provide a biological mechanism that may explain why individuals with inefficient intestinal calcium absorption (<i>e</i>.<i>g</i>., vitamin D deficiency, proton pump inhibitor use) are more prone to CDI and suggest that modulating free intestinal calcium is a potential strategy to curb the incidence of CDI.</p></div