Unveiling the interplay between evidence, values and cognitive biases. The case of the failure of the AstraZeneca COVID-19 vaccine

This paper depicts a Covid science case, that of the AstraZeneca Vaxzevria vaccine, with specific focus on what happened in Italy. Given that we believe acknowledging the role of non-evidential factors in medicine is an important insight into the recent philosophy of science, we illustrate how in the case of Vaxzevria, the interplay between facts, values (both epistemic and non-epistemic) and cognitive biases may have possibly led to different institutional decisions based on the same evidence. The structure of the paper is as follows. First, we provide a glossary of the relevant terms involved, that is to say, epistemic values, non-epistemic values and cognitive biases. Second, we sketch a timeline of Vaxzevria's approvals and suspensions by relevant institutional healthcare authorities with special focus on Italy and the Italian Medicines Agency. Then we show the interplay between the evidence base, epistemic as well as non-epistemic values and cognitive biases using a narrative review of political decisions along with newspaper and social media content pertaining to Vaxzevria. We briefly compare Italy with other European countries to show that different political decisions were made on the basis of the same evidence

The Notion of Gender in Psychiatry: A Focus on DSM-5

In this paper I review how the notion of gender is understood in psychiatry, specifically in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). First, I examine the contraposition between sex and gender, and argue that it is still retained by DSM-5, even though with some caveats. Second, I claim that, even if genderqueer people are not pathologized and gender pluralism is the background assumption, some diagnostic criteria still conceal a residue of gender dualism and essentialism. Third, I consider gender dysphoria, which is characterized by an incongruence between one’s experienced or expressed gender and one’s assigned gender; since this condition pertains to distress and disability, not to the incongruence per se, it does not pathologize transgender people. Still, I contend that it should be removed from DSM-5 for theoretical reasons

Wherein is the concept of disease normative? From weak normativity to value-conscious naturalism

In this paper we focus on some new normativist positions and compare them with traditional ones. In so doing, we claim that if normative judgments are involved in determining whether a condition is a disease only in the sense identified by new normativisms, then disease is normative only in a weak sense, which must be distinguished from the strong sense advocated by traditional normativisms. Specifically, we argue that weak and strong normativity are different to the point that one \u2018normativist\u2019 label ceases to be appropriate for the whole range of positions. If values and norms are not explicit components of the concept of disease, but only intervene in other explanatory roles, then the concept of disease is no more value-laden than many other scientific concepts, or even any other scientific concept. We call the newly identified position \u201cvalue-conscious naturalism\u201d about disease, and point to some of its theoretical and practical advantages

Non-Epistemic Factors in Epidemiological Models. The Case of Mortality Data

The COVID-19 pandemic has made it especially visible that mortality data are a key component of epidemiological models, being a single indicator that provides information about various health aspects, such as disease prevalence and effectiveness of interventions, and thus enabling predictions on many fronts. In this paper we illustrate the interrelation between facts and values in death statistics, by analyzing the rules for death certification issued by the World Health Organization. We show how the notion of the underlying cause of death can change in view of public health goals. This brings us to a general point about how non-epistemic factors, such as values and goals, are reflected in the choice of different measures in epidemiological models. We finally argue that this analysis is not only relevant from a theoretical point of view but also has important practical consequences

The DSM-5 introduction of the Social (Pragmatic) Communication Disorder as a new mental disorder: a philosophical review

The latest edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) included the Social (Pragmatic) Communication Disorder (SPCD) as a new mental disorder characterized by deficits in pragmatic abilities. Although the introduction of SPCD in the psychiatry nosography depended on a variety of reasons—including bridging a nosological gap in the macro-category of Communication Disorders—in the last few years researchers have identified major issues in such revision. For instance, the symptomatology of SPCD is notably close to that of (some forms of) Autism Spectrum Disorder (ASD). This opens up the possibility that individuals with very similar symptoms can be diagnosed differently (with either ASD or SPCD) and receive different clinical treatments and social support. The aim of this paper is to review recent debates on SPCD, particularly as regards its independence from ASD. In the first part, we outline the major aspects of the DSM-5 nosological revision involving ASD and SPCD. In the second part, we focus on the validity and reliability of SPCD. First, we analyze literature on three potential validators of SPCD, i.e., etiology, response to treatment, and measurability. Then, we turn to reliability issues connected with the introduction of the grandfather clause and the use of the concepts of spectrum and threshold in the definition of ASD. In the conclusion, we evaluate whether SPCD could play any role in contemporary psychiatry other than that of an independent mental disorder and discuss the role that non-epistemic factors could play in the delineation of the future psychiatry nosography

Cortical thinning over two years after first-episode psychosis depends on age of onset

First-episode psychosis (FEP) patients show structural brain abnormalities at the first episode. Whether the cortical changes that follow a FEP are progressive and whether age at onset modulates these changes remains unclear. This is a multicenter MRI study in a deeply phenotyped sample of 74 FEP patients with a wide age range at onset (15–35 years) and 64 neurotypical healthy controls (HC). All participants underwent two MRI scans with a 2-year follow-up interval. We computed the longitudinal percentage of change (PC) for cortical thickness (CT), surface area (CSA) and volume (CV) for frontal, temporal, parietal and occipital lobes. We used general linear models to assess group differences in PC as a function of age at FEP. We conducted post-hoc analyses for metrics where PC differed as a function of age at onset. We found a significant age-by-diagnosis interaction effect for PC of temporal lobe CT (d = 0.54; p = 002). In a post-hoc-analysis, adolescent-onset (≤19 y) FEP showed more severe longitudinal cortical thinning in the temporal lobe than adolescent HC. We did not find this difference in adult-onset FEP compared to adult HC. Our study suggests that, in individuals with psychosis, CT changes that follow the FEP are dependent on the age at first episode, with those with an earlier onset showing more pronounced cortical thinning in the temporal lobe

Cognitive functioning throughout adulthood and illness stages in individuals with psychotic disorders and their unaffected siblings

Important questions remain about the profile of cognitive impairment in psychotic disorders across adulthood and illness stages. The age-associated profile of familial impairments also remains unclear, as well as the effect of factors, such as symptoms, functioning, and medication. Using cross-sectional data from the EU-GEI and GROUP studies, comprising 8455 participants aged 18 to 65, we examined cognitive functioning across adulthood in patients with psychotic disorders (n = 2883), and their unaffected siblings (n = 2271), compared to controls (n = 3301). An abbreviated WAIS-III measured verbal knowledge, working memory, visuospatial processing, processing speed, and IQ. Patients showed medium to large deficits across all functions (ES range = -0.45 to -0.73, p <0.001), while siblings showed small deficits on IQ, verbal knowledge, and working memory (ES = -0.14 to -0.33, p <0.001). Magnitude of impairment was not associated with participant age, such that the size of impairment in older and younger patients did not significantly differ. However, first-episode patients performed worse than prodromal patients (ES range = -0.88 to -0.60, p <0.001). Adjusting for cannabis use, symptom severity, and global functioning attenuated impairments in siblings, while deficits in patients remained statistically significant, albeit reduced by half (ES range = -0.13 to -0.38, p <0.01). Antipsychotic medication also accounted for around half of the impairment in patients (ES range = -0.21 to -0.43, p <0.01). Deficits in verbal knowledge, and working memory may specifically index familial, i.e., shared genetic and/or shared environmental, liability for psychotic disorders. Nevertheless, potentially modifiable illness-related factors account for a significant portion of the cognitive impairment in psychotic disorders

Cognitive functioning throughout adulthood and illness stages in individuals with psychotic disorders and their unaffected siblings.

Important questions remain about the profile of cognitive impairment in psychotic disorders across adulthood and illness stages. The age-associated profile of familial impairments also remains unclear, as well as the effect of factors, such as symptoms, functioning, and medication. Using cross-sectional data from the EU-GEI and GROUP studies, comprising 8455 participants aged 18 to 65, we examined cognitive functioning across adulthood in patients with psychotic disorders (n = 2883), and their unaffected siblings (n = 2271), compared to controls (n = 3301). An abbreviated WAIS-III measured verbal knowledge, working memory, visuospatial processing, processing speed, and IQ. Patients showed medium to large deficits across all functions (ES range = -0.45 to -0.73, p < 0.001), while siblings showed small deficits on IQ, verbal knowledge, and working memory (ES = -0.14 to -0.33, p < 0.001). Magnitude of impairment was not associated with participant age, such that the size of impairment in older and younger patients did not significantly differ. However, first-episode patients performed worse than prodromal patients (ES range = -0.88 to -0.60, p < 0.001). Adjusting for cannabis use, symptom severity, and global functioning attenuated impairments in siblings, while deficits in patients remained statistically significant, albeit reduced by half (ES range = -0.13 to -0.38, p < 0.01). Antipsychotic medication also accounted for around half of the impairment in patients (ES range = -0.21 to -0.43, p < 0.01). Deficits in verbal knowledge, and working memory may specifically index familial, i.e., shared genetic and/or shared environmental, liability for psychotic disorders. Nevertheless, potentially modifiable illness-related factors account for a significant portion of the cognitive impairment in psychotic disorders.The European Community’s Seventh Framework Programme under grant agreement No. HEALTH-F2-2010-241909 (EU-GEI)

The continuity of effect of schizophrenia polygenic risk score and patterns of cannabis use on transdiagnostic symptom dimensions at first-episode psychosis: findings from the EU-GEI study

Abstract: Diagnostic categories do not completely reflect the heterogeneous expression of psychosis. Using data from the EU-GEI study, we evaluated the impact of schizophrenia polygenic risk score (SZ-PRS) and patterns of cannabis use on the transdiagnostic expression of psychosis. We analysed first-episode psychosis patients (FEP) and controls, generating transdiagnostic dimensions of psychotic symptoms and experiences using item response bi-factor modelling. Linear regression was used to test the associations between these dimensions and SZ-PRS, as well as the combined effect of SZ-PRS and cannabis use on the dimensions of positive psychotic symptoms and experiences. We found associations between SZ-PRS and (1) both negative (B = 0.18; 95%CI 0.03–0.33) and positive (B = 0.19; 95%CI 0.03–0.35) symptom dimensions in 617 FEP patients, regardless of their categorical diagnosis; and (2) all the psychotic experience dimensions in 979 controls. We did not observe associations between SZ-PRS and the general and affective dimensions in FEP. Daily and current cannabis use were associated with the positive dimensions in FEP (B = 0.31; 95%CI 0.11–0.52) and in controls (B = 0.26; 95%CI 0.06–0.46), over and above SZ-PRS. We provide evidence that genetic liability to schizophrenia and cannabis use map onto transdiagnostic symptom dimensions, supporting the validity and utility of the dimensional representation of psychosis. In our sample, genetic liability to schizophrenia correlated with more severe psychosis presentation, and cannabis use conferred risk to positive symptomatology beyond the genetic risk. Our findings support the hypothesis that psychotic experiences in the general population have similar genetic substrates as clinical disorders