Browsing by Subject "Causality"

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  • O'Hare, Kirstie J. M.; Korhonen, Tellervo; Latvala, Antti; Kaprio, Jaakko; Linscott, Richard J. (2020)
    Subclinical psychosis, including schizotypal indicators and psychotic experiences, predicts future suicidal ideation. This relationship may reflect unmeasured confounding from environmental factors, genetic factors, or both. We used a genetically-informative twin design to understand if the association between subclinical psychosis and suicidal ideation is independent of shared genetic and environmental factors. We analysed cross-sectional associations of age-22 self-reported subclinical psychosis (positive, negative, and disorganised features) with suicidal ideation in twins participating in the FinnTwin12 study (maximum n = 1213). Then, we analysed the reverse association of age-14 suicidal ideation with age-22 subclinical psychosis. Associations were studied first among individuals and then within monozygotic (MZ) and dizygotic (DZ) pairs. Individual-level analyses showed that all subclinical psychosis factors were associated with suicidal ideation. In within-pair analyses, estimates of associations were lower for MZ pairs than DZ pairs, except for the negative schizotypy-suicidal ideation association where estimates were consistent across individual-level and within-pair analyses. Findings provide evidence that the association between negative features and suicide ideation is not explained by familial factors and may be causal, though the possibility of confounding by individual-specific environmental factors and reverse causation cannot be ruled out. The relationships of positive and disorganised subclinical psychosis features with suicidal ideation cannot be explained by confounding due to environmental factors shared between siblings, but their associations may be due to shared genetic factors. (C) 2020 Elsevier B.V. All rights reserved.
  • Pigorini, Andrea; Sarasso, Simone; Proserpio, Paola; Szymanski, Caroline; Arnulfo, Gabriele; Casarotto, Silvia; Fecchio, Matteo; Rosanova, Mario; Mariotti, Maurizio; Lo Russo, Giorgio; Palva, J. Matias; Nobili, Lino; Massimini, Marcello (2015)
    During non-rapid eye movement (NREM) sleep (stage N3), when consciousness fades, cortico-cortical interactions are impaired while neurons are still active and reactive. Why is this? We compared cortico-cortical evoked-potentials recorded during wakefulness and NREM by means of time-frequency analysis and phase-locking measures in 8 epileptic patients undergoing intra-cerebral stimulations/recordings for clinical evaluation. We observed that, while during wakefulness electrical stimulation triggers a chain of deterministic phase-locked activations in its cortical targets, during NREM the same input induces a slow wave associated with an OFF-period (suppression of power > 20 Hz), possibly reflecting a neuronal down-state. Crucially, after the OFF-period, cortical activity resumes to wakefulness-like levels, but the deterministic effects of the initial input are lost, as indicated by a sharp drop of phase-locked activity. These findings suggest that the intrinsic tendency of cortical neurons to fall into a down-state after a transient activation (i.e. bistability) prevents the emergence of stable patterns of causal interactions among cortical areas during NREM. Besides sleep, the same basic neurophysiological dynamics may play a role in pathological conditions in which thalamo-cortical information integration and consciousness are impaired in spite of preserved neuronal activity. (C) 2015 The Authors. Published by Elsevier Inc.
  • Ference, Brian A.; Ginsberg, Henry N.; Graham, Ian; Ray, Kausik K.; Packard, Chris J.; Bruckert, Eric; Hegele, Robert A.; Krauss, Ronald M.; Raal, Frederick J.; Schunkert, Heribert; Watts, Gerald F.; Boren, Jan; Fazio, Sergio; Horton, Jay D.; Masana, Luis; Nicholls, Stephen J.; Nordestgaard, Borge G.; van de Sluis, Bart; Taskinen, Marja-Riitta; Tokgözoglu, Lale; Landmesser, Ulf; Laufs, Ulrich; Wiklund, Olov; Stock, Jane K.; Chapman, M. John; Catapano, Alberico L. (2017)
    Aims To appraise the clinical and genetic evidence that low-density lipoproteins (LDLs) cause atherosclerotic cardiovascular disease (ASCVD). Methods and results We assessed whether the association between LDL and ASCVD fulfils the criteria for causality by evaluating the totality of evidence from genetic studies, prospective epidemiologic cohort studies, Mendelian randomization studies, and randomized trials of LDL-lowering therapies. In clinical studies, plasma LDL burden is usually estimated by determination of plasma LDL cholesterol level (LDL-C). Rare genetic mutations that cause reduced LDL receptor function lead to markedly higher LDL-C and a dose-dependent increase in the risk of ASCVD, whereas rare variants leading to lower LDL-C are associated with a correspondingly lower risk of ASCVD. Separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies, and randomized trials including more than 2 million participants with over 20 million person-years of follow-up and over 150 000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C. Both the naturally randomized genetic studies and the randomized intervention trials consistently demonstrate that any mechanism of lowering plasma LDL particle concentration should reduce the risk of ASCVD events proportional to the absolute reduction in LDL-C and the cumulative duration of exposure to lower LDL-C, provided that the achieved reduction in LDL-C is concordant with the reduction in LDL particle number and that there are no competing deleterious off-target effects. Conclusion Consistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD.
  • Valtonen, Jussi; Ahn, Woo-kyoung; Cimpian, Andrei (2021)
    People commonly think of the mind and the brain as distinct entities that interact, a view known as dualism. At the same time, the public widely acknowledges that science attributes all mental phenomena to the workings of a material brain, a view at odds with dualism. How do people reconcile these conflicting perspectives? We propose that people distort claims about the brain from the wider culture to fit their dualist belief that minds and brains are distinct, interacting entities: Exposure to cultural discourse about the brain as the physical basis for the mind prompts people to posit that mind–brain interactions are asymmetric, such that the brain is able to affect the mind more than vice versa. We term this hybrid intuitive theory neurodualism. Five studies involving both thought experiments and naturalistic scenarios provided evidence of neurodualism among laypeople and, to some extent, even practicing psychotherapists. For example, lay participants reported that “a change in a person's brain” is accompanied by “a change in the person's mind” more often than vice versa. Similarly, when asked to imagine that “future scientists were able to alter exactly 25% of a person's brain,” participants reported larger corresponding changes in the person's mind than in the opposite direction. Participants also showed a similarly asymmetric pattern favoring the brain over the mind in naturalistic scenarios. By uncovering people's intuitive theories of the mind–brain relation, the results provide insights into societal phenomena such as the allure of neuroscience and common misperceptions of mental health treatments.
  • Nurmi, Miska Juhani (Helsingin yliopisto, 2021)
    Objectives The purpose of this thesis is to consider what the cognitive models of online causal learning are and what they have to offer for the interactive AI approach. In this thesis, an interactive AI system is considered one that focuses on understanding and collaborating with a human user and which can therefore benefit from cognitive models. The general overview of the models is given by replicating some of the computational results of Bramley et al. (2017) which explored cognitive models for online causal learning. The earlier paper contained four models on how people might learn their causal beliefs, and five models on how people might choose where they place their tests, also known as interventions. Thesis also discusses the implications that the replicated models have for interactive AI, both by considering how these models could be better extended into the interactive AI framework, but also by considering a simple AI based system that could make use of such models. Replication The replication was done by reimplementing the original models of Bramley et al. in R and by reproducing the corresponding figures. Out of the four models used for causal belief updating, two were successfully replicated so that the results corresponded to the original paper. It is not certain why the two other models could not be replicated, and the task is left open for future work. Out of the five intervention choice models, four were implemented and three successfully replicated. One of the models was very close to the original results, but this thesis could not conclude whether it fully reproduces the original results. Implications The simple AI model proposed in this performed poorly but was able to show that in theory, an interactive AI system that incorporates such a model might be feasible in the future with further development. Some recommendations to better extend the replicated models into the interactive AI framework were made. Main recommendations were that a better model on how people might choose where they focus their local attention is needed. Furthermore, it should be ensured that the models approximate human behaviour in larger graphs as well.