INCET conference 'Bioethics Meets Philosophy of Science'
The conference organized by the Interdisciplinary Centre for Ethics at the Jagiellonian University explored practical, theoretical, and regulatory issues in biomedical research through the joint perspective of bioethics and philosophy of science. The conference took place from the 20th till the 21st of May 2022 at Larisch Palace, Bracka 12, Kraków.
Short descriptionThe conference explored practical, theoretical, and regulatory issues in biomedical research through the joint perspective of bioethics and philosophy of science.
The solution to many biomedical questions often lies at the intersection of theory and practice. On the one hand, philosophy of science can inform bioethical and legal debates by advancing our theoretical understanding of biomedical issues, helping decide between alternative ethical positions, or even undermining a moral conjecture on an empirical basis. On the other hand, philosophy of science can benefit from a bioethical perspective, as many scientific debates and disagreements do not just depend on empirical results or theoretical aspects, but also require the analysis of moral, social, and political factors and values.
Typical questions involving this sort of interdisciplinary effort are, for instance: To what extent do ethical principles limit technological advancements and research, e.g., in case of human embryos or embryonic models? How do inclusion and exclusion criteria in clinical trials need to balance the trade-off between statistical inferences and ethical considerations? How can philosophical analysis of the genetic and epigenetic basis of human diseases reframe questions regarding reproductive decision and prevention? May work in philosophy of comparative psychology change the way scientists characterize, operationalize, and interpret cognitive similarities and differences among species? Can the acceptance or refutation of categories and concepts depend on ethical factors? Are there ethical reasons to revise concepts that are widely used in biomedical sciences, such as race, gender, sex, disease, normality, and dysfunction?
Friday, May 20
9.00-9.30 Registration and Welcome
9.30-10.20 Maxence Gaillard (Catholic University of Louvain): "Ontological foundations of the ethical discourse on organoid research"
10.20-11.10 Davide Battisti (University of Milan): "Attitudes, intentions, and procreative responsibility in assisted reproduction"
11.10-11.40 Coffee Break
11.40-12.30 Cristina Amoretti (University of Genoa) & Elisabetta Lalumera (University of Bologna): "Evidence-based, value-laden, or cognitively biased? The case of the failure of Astrazeneca Covid-19 vaccine”
12.30-14.00 Lunch Break
14.00-15.30 Keynote Talk: Rachel Ankeny (University of Adelaide): “Causation and explanation in overdiagnosis: Epistemic and ethical implications”
15.30-16.00 Coffee Break
16.00-16.50 Valentina Petrolini (University of the Basque Country) & Davide Serpico (Jagiellonian University): "Categories versus dimensions in psychiatry: A hybrid and value-sensitive alternative"
16.50-17.40 Jon Rueda (University of Granada): "The science of human genetic enhancement: From myth to close reality?"
Saturday, May 21
9.30-10.20 Jordan Parsons (University of Bristol): "Nothing About Us Without Us? The challenges of involving people with cognitive impairments in biomedical research"
10.20-11.10 Charlotte Zemmel (University of Cambridge): "Holistic inductive risk management in clinical trials"
11.10-11.40 Coffee Break
11.40-12.30 Joanna Malinowska (Adam Mickiewicz University): "Concept of racialisation in biomedical research: a step toward the ethical and credible use of racial classifications"
12.30-14.00 Lunch Break
14.00-15.30 Keynote Talk: Sven Hansson (Royal Institute of Technology, Stockholm): “Causality and morality”
15.30-16.00 Coffee Break
16.00-16.50 Vilius Dranseika (Jagiellonian University): "How to count conjoined twins?"
List of accepted abstracts
Astrazeneca Covid-19 vaccine (AZD1222), also known as Vaxzevria, received a conditional marketing authorization by the European Medicines Association (EMA) on 29 January 2021, and it was soon later assessed by WHO’s Strategic Advisory Group of Experts on Immunization (SAGE), who recommended its use for all age groups 18 and above (EMA 2021, WHO 2021). However, a series of events occurred in the subsequent months, including reports of adverse effects (blood clots), miscommunication, and controversies between Astrazeneca and institutions, which resulted in suspensions, partial re-authorizations, and definitive bans of the vaccine in different countries. This variety and heterogeneity of institutional decisions in face of the same evidence has been called a public relation disaster, that determined a loss of trust in Vaxzevria and in all Covid-19 vaccines, too (Wise 2021). As public trust has been identified as a key element in vaccination uptake, its disruption is to be considered harmful to the whole population (Larson & Broniatowski 2021). This paper describes Vaxzevria failure as a case where institutional and individual decisions were partly evidence-based, but also value-laden, and cognitively biased. We believe that acknowledging the role of non-evidential factors in medicine – not only epistemic values, but also non-epistemic ones, such as, practical motivations, ethical and political issues, as well as cognitive biases – is an important insight in recent philosophy of science.
The structure of the paper is the following. First, we provide a timeline of Vaxzevria’s approvals and suspensions by institutional healthcare authorities, focusing on UK Medicines and Healthcare products Regulatory Agency (MHRA), EMA, SAGE, and Canadian National Advisory Committee on Immunization (NACI). Then we show the interplay between the evidence base, epistemic values, non-epistemic values, and cognitive biases, through a narrative review of political decisions as well as newspaper and social media contents about Vaxzevria and its adverse effects from Italy, Germany, Canada, and UK. In particular, we identify the role of moral, political, and economic values, as well as the following non-evidential factors in assessing and complementing scientific evidence: the priming effect (most recent experience of a stimulus affects perception and judgment), the framing effect (how a content is delivered influences its uptake), the social conformity bias (we tend to think and behave as the others do), and the moralization of a pharmaceutical product (things or brands acquire moral properties on inappropriate grounds). Finally, we consider some very recent assessments of Vaxzevria failure in the literature, which partially converge with ours, and tentatively offer a list of key concepts for a guideline for scenarios of (emergency) health communication.
Specifically, we argue that within non-evidential factors, values should be distinguished from biases, in that the former, but not the latter, can be critically and rationally discussed in a public debate. To restore and promote public trust in Vaxzevria, vaccines, and, more generally, in medicine, we believe that the interplay between the evidence base and values, both epistemic and non-epistemic, should be made explicit and publicly assessed, while cognitive biases should be detected and possibly removed from the process of decision making, both at the individual and institutional level.
- Albanese, A.; Fallucchi, F.; Verheyden, B. (2021) Can a supranational medicines agency restore trust after vaccine suspensions? The case of Vaxzevria, GLO Discussion Paper, 878, Global Labor Organization (GLO), Essen.
- European Medicines Agency (2021) Vaxzevria (previously COVID-19 Vaccine AstraZeneca)
- Larson, H. J., & Broniatowski, D. A. (2021). Volatility of vaccine confidence. Science 371(6536), 1289-1289.
- Wise, J. (2021). Covid-19: How AstraZeneca lost the vaccine PR war. BMJ: British Medical Journal (Online), 373.
- World Health Organization (WHO) (2021) The Oxford/AstraZeneca COVID-19 vaccine: what you need to know, retrieved 25 September 2021.
Overdiagnosis typically refers to the making of a diagnosis that does not benefit an individual patient because the diagnosed condition is in fact not a harmful disease in that individual. Overdiagnosis has been identified as a problem in a range of types of medical domains including cancer screening, common chronic diseases such as diabetes, and a range of mental illnesses. Overdiagnosis has been increasingly recognised in the bioethics literature as an important phenomenon which can expose individuals to significant risk and even harm. Practices associated with overdiagnosis are particularly prevalent in clinical and population genetics related fields, including via screening programs, personal genomic assessments, and risk reduction via genetic testing (e.g., for common and chronic diseases, as well as some forms of cancers) with some preventive healthcare practices being argued to be not ethically justifiable. This paper explores these issues from the point of view of philosophy of science and medicine where discussions on this issue have been limited (one important exception is Biddle 2016 which focuses on overdiagnosis as a revealing example for understanding inductive risk). I focus on the diverse and conflicting underlying models of causation and explanation at use by medical and public health professionals particularly when they engage in what arguably can be considered to be overdiagnosis, in order to cast additional light on problems associated with overdiagnosis in preventive genetic medicine, and to contribute to the debates in bioethics which focus on the complexities in this domain to attempt to refine practices in transparent and ethical ways.
Procreative responsibility in assisted reproduction is generally discussed considering the consequences of reproductive actions or omissions; less attention is paid to the moral role of intentions and attitudes. In this paper, I address this issue considering procreative decisions firstly involving Preimplantation Genetic Diagnosis (PGD), and secondly involving future (and still hypothetical) techniques such as reproductive Genome Editing (rGE) and Ectogenesis. My thesis is twofold: intentions and attitudes can play a role in informing reproductive decisions involving PGD; this also leads us to have moral reasons to evaluate reproduction via rGE and Ectogenesis as morally preferable to natural reproduction.
As far as PGD is concerned, I first discuss three normative accounts dealing with procreative intentions and attitudes: i) virtue ethics, ii) the principle of deliberate impossibility, and iii) the collective interests’ argument. Stemming from different ethical justifications, these views claim that reproducers should already have some parental attitudes during the procreative process. I argue that (i) and (ii) cannot justify this conclusion, since they do not convincingly explain why a procreator should have parental attitudes towards an individual whose identity depends on them. I consider (iii) as better suited to justify the aforementioned conclusion, but still problematic: socializing procreative attitudes and intentions could lead to legitimizing moralistic attitudes towards private reproductive choices.
I then propose a “parent-child relationship” strategy, drawing a moral distinction between the intention to create and that of having a child. When we decide to have a child – and thus to create a new relationship – through in vitro fertilization plus PGD, our procreative intention involves two morally different desires: first, that of creating a child with some genetic characteristics; second, that the embryo that will be transferred in utero actually develops into a child with those characteristics. The former is not subject to moral blame, since there is no specific individual towards whom attitudes are directed; on the contrary, the latter could be blameworthy because it refers to a specific future person, even though her/his identity is unknown at the moment of decision. Hence, some procreative choices involving PGD are morally problematic – although they do not directly harm anyone – due to moral defects concerning the second desire. Indeed, having a second desire in contrast to parental care and protection (e.g., hoping that the embryo will develop into a child with disability) could undermine the parent-child relationship.
I therefore apply this strategy to rGE and Ectogenesis, arguing that parents-to-be who will decide to use these technologies may have a second desire to allow future children, whatever their identity, to develop under ideal conditions to avoid suffering conditions. Accordingly, employing such techniques with this second desire may enhance the parent-child relationship, showing greater propensity by parents to take care of their child's interests and protect them (e.g., Ectogenesis would allow embryos or fetuses to be treated more safely than in utero, if necessary). Hence, I conclude that we may have moral reasons to prefer reproduction through these technologies rather than through natural reproduction, leading to an extension of procreative responsibility.
- Battisti, D. (2021). Affecting future individuals: Why and when germline genome editing entails a greater moral obligation towards progeny. Bioethics, 35(5), 487-495.
- Chambers, K. L. (2019). Wronging Future Children. Ergo: An Open Access Journal of Philosophy, 6.
- Kahane, G. (2009). Non-identity, self-defeat, and attitudes to future children. Philosophical studies, 145(2), 193-214.
- Lotz, M. (2011). Rethinking procreation: Why it matters why we have children. Journal of applied philosophy, 28(2), 105-121.
- McDougall, R. (2007). Parental virtue: A new way of thinking about the morality of reproductive actions. Bioethics, 21(4), 181-190.
- Noggle, R. (2019). Impossible obligations and the non-identity problem. Philosophical Studies, 176(9), 2371-2390.
- Overall, C. (2012). Why have children?: The ethical debate. Mit press.
- Wasserman, D. (2005). The nonidentity problem, disability, and the role morality of prospective parents. Ethics, 116(1), 132-152.
- Wilkinson, S. (2010). Choosing tomorrow's children: the ethics of selective reproduction. Oxford University Press.
The debate on psychosortalism and antipsychosortalism in psychology and philosophy (Blok et al. 2007; Carey & Xu 1999; Leonard & Rips 2015) focuses on two questions: (a) Is the way people track objects through time furnished by the identity conditions provided by a given sortal category? (b) Is the way people count objects furnished by the individuation conditions provided by a given sortal category? While most of the empirical research so far was focused on (a), I provide new empirical data bearing on (b). In a set of studies, I use drawings of two-headed conjoined twins (parapagus dicephalus, either human or animal) and ask participants to count individuals under different sortal categories. In addition to providing support to psychosortalism, the studies explore several other issues spanning from the conceptualization of conjoined twinning to biological individuality.
Organoids – small stem-cell-derived 3D physiological systems – are conveying many uncertainties: epistemic uncertainty, as research is progressing at a fast pace and the scientific nomenclature is itself unstable; ontological uncertainty, as there is no consensus on what they are (e.g., small organs? living entities? models of development? artifacts?); and, as a consequence, ethical and regulatory uncertainties. The failure to identify correctly these entities can indeed result in behaviors that might be inappropriate from a moral point of view. In this talk, we analyze from a philosophy of science perspective the bioethical discourse surrounding organoid research as the production of new entities populating our laboratories.
Organoids (including especially, embryo models and brain organoids) are most of the time described as “new entities,” with emerging properties that would make them distinct from blobs of cells that are “just” cell cultures (Rivron et al. 2018; Lavazza and Pizzetti 2020; Koplin, Carter, and Savulescu 2021). But how to assess such a claim? Are organoids really novel entities? Or are they a compound of older entities? The latest stage of a continuum in the large family of biotechnological objects made from stem cells? This would be a question of ontology, i.e., what kind of entities organoids exactly are. This is a complex and debated issue, as can be seen through the ongoing discussions on organoid nomenclature (Marsee et al. 2021) and historiographic quarrels (Simian and Bissell 2017).
If certain organoids are considered as radically new entities grown in laboratories, then a natural inference is that questions should be raised about their moral status, according to their complexity. And if these are “new entities,” there is a temptation to revise the ethical framework guiding research, on the assumption that we would lack explicit directives for dealing with these supposedly new entities. Here, we unpack the connection between the discourse on biotechnological novelty and ethical assessment. We suggest that this entanglement of ontological and ethical novelty could be formalized in terms of four different stances, representing one’s position on the novelty of the entities of interest, and the need for a renewal of already-existing ethical conventions.
We present and discuss the implications of each of these stances, relating them to different positions in the field such as those expressed in the recent revision of the ISSCR guidelines (ISSCR 2021). Unfolding the four options is useful as it goes beyond the opposition of progressive vs. conservative attitudes (for or against new technologies). The focus is not on being in favor of or against the development of organoids, but rather on how we assess the novelty (or lack thereof) of these entities to appropriately adapt our ethical framework. This is typically a case at the junction of bioethical issues and issues in philosophy of science. We conclude with a reflection on how we can inform the bioethical discussion – and also, in our case, guidelines and regulations – with ontological considerations based on philosophy of science.
- ISSCR. 2021. “International Society for Stem Cell Research Guidelines for Stem Cell Research and Clinical Translation.”
- Koplin, Julian J., Olivia Carter, and Julian Savulescu. 2021. “Moral Status of Brain Organoids.” In Rethinking Moral Status, edited by Steve Clarke, Hazem Zohny, and Julian Savulescu, 250–68. Oxford: Oxford University Press.
- Lavazza, Andrea, and Federico Gustavo Pizzetti. 2020. “Human Cerebral Organoids as a New Legal and Ethical Challenge.” Journal of Law and the Biosciences 7 (1): lsaa005. https://doi.org/10.1093/jlb/lsaa005.
- Marsee, Ary, Floris J. M. Roos, Monique M. A. Verstegen, HPB Organoid Consortium, Helmuth Gehart, Eelco de Koning, Frédéric Lemaigre, et al. 2021. “Building Consensus on Definition and Nomenclature of Hepatic, Pancreatic, and Biliary Organoids.” Cell Stem Cell 28 (5): 816–32. https://doi.org/10.1016/j.stem.2021.04.005.
- Rivron, Nicolas, Martin Pera, Janet Rossant, Alfonso Martinez Arias, Magdalena Zernicka-Goetz, Jianping Fu, Susanne van den Brink, et al. 2018. “Debate Ethics of Embryo Models from Stem Cells.” Nature 564 (7735): 183–85. https://doi.org/10.1038/d41586-018-07663-9.
- Simian, Marina, and Mina J. Bissell. 2017. “Organoids: A Historical Perspective of Thinking in Three Dimensions.” The Journal of Cell Biology 216 (1): 31–40. https://doi.org/10.1083/jcb.201610056.
The term “causality” has two major meanings. It can refer to world causality, the ways in which events at different locations in time and space are connected with each other. It can also refer to causality models, the ways in which we think about world causality. In ethics, in everyday life, and in most of science, our thinking about world causality is dominated by the cause–effect model (CE causality). It describes developments in the world in terms of chains of cause-effect relationships. Usually, it serves us well, but it is only a model and, unfortunately, it is insufficient for many purposes. Many complex developments in the world are better described in terms of a large number of mutual interactions than in terms of causal chains. The dominance of the CE model in ethics makes it difficult to deal with situations in which the combination of many actions, each with small and uncertain effects, creates undesirable developments. Such situations arise in many issues of health and safety, and also in climate and environmental policies. In this contribution I will try to clarify the two meanings of causality and give indications of what bioethics can learn from these insights. Traditional moral virtues such as setting good examples and doing one’s part in joint endeavours may in many contexts provide better moral guidance than principles focusing on the causal effects of individual actions. I will also discuss the impact that our moral appraisals have on our assignments of (agent) causality. Contrary to traditional assumptions, causality assignments are not always prior to and independent of moral judgments. The relationship between causality and morality is much less orderly and clear-cut than what we usually believe it to be.
While in the field of bioethics, race is usually interpreted to be a socio-cultural construct that has no biological basis (Mithani 2021; Yearby 2021), there are arguments in the field of philosophy of science that it may be a good proxy for some real biological features (Sesardic 2010; Spencer 2014) or the contrary – that it is a misleading category because human races (both in a biological and social sense) do not exist (Hochman 2017, 2019). Also, in biomedical research itself, race appears in various meanings, hindering effective scientific communication (Popejoy et al. 2020; Singh & Steeves 2020; Byeon et al. 2021). However, I agree with the position that revising the concept of race is unlikely to improve this situation satisfyingly, if only due to the fact that it perpetuates existing racial stereotypes and it fails to reflect the complexity of the phenomena to which it relates (Hochman 2017, 2019, 2021). Instead, I will aim at developing a concept of racialisation on the example of the use of racial categories in biomedical research.
I understood racialisation as a continuous processes running on several different levels (and their complex interactions) due to which individuals come to be understood by others (as well as recognise themselves) as a representatives of a major biological entities and human lineages, formed due to reproductive isolation, in which membership is transmitted through biological descent (cf., Hochman 2017, 2019, 2021). In this perspective, race is just a social construct contributing to the racialisation, but it doesn’t refer to any existing entities (biological nor social groups). Thus, the concept of racialisation can be used e.g., to analyse the impact of systemic racism on health without reifying the category of race.
My talk will be as follows: First, I will briefly reconstruct some ethical and empirical arguments against using the category of race (in both socio-cultural and biological meaning) in research. Then, I will present model of multileveled processes affecting and co-shaping racialisation of an individual. These levels are: (1) phylogenetic, (2) epigenetic, (3) phenotypic, (4) neuronal, (5) environmental, (6) socio-cultural. I will discuss them in regard to the biomedical research. I will also argue that processualism and processual terminology is important for the conceptualisation of racialisation. This is for at least two reasons. First, it reflects its anti-essentialist, dynamic and constructivist character. Second, the concepts and terminology that emphasizes the processualism of racialisation may be less prone to psychological essentialisation unlike more generic and static concepts and terms (cf., Hollander et al. 2009; Sutherland & Cimpian 2019). I will finish by discussing the potential benefits of using the above concept in biomedical research and bioethics.
- Byeon, Y. J. J., Islamaj, R., Yeganova, L., Wilbur, W. J., Lu, Z., Brody, L. C., & Bonham, V. L. (2021). Evolving use of ancestry, ethnicity, and race in genetics research—A survey spanning seven decades. The American Journal of Human Genetics, 108(12), 2215-2223.
- Hochman, A. (2021). FURTHER DEFENSE OF THE RACIALIZATION CONCEPT: A Reply to Uyan. Du Bois Review: Social Science Research on Race, 18(1), 31-48.
- Hochman, A. (2019). Racialization: A defense of the concept. Ethnic and Racial Studies, 42(8), 1245-1262.
- Hochman, A. (2017). Replacing race: Interactive constructionism about racialized groups. Ergo: An open Access Journal of Philosophy, 4.
- Hollander, M. A., Gelman, S. A., & Raman, L. (2009). Generic language and judgements about category membership: Can generics highlight properties as central?. Language and Cognitive Processes, 24(4), 481-505.
- Mithani, Z., Cooper, J., & Boyd, J. W. (2021). Race, power, and COVID-19: A call for advocacy within bioethics. The American Journal of Bioethics, 21(2), 11-18.
- Popejoy, A. B., Crooks, K. R., Fullerton, S. M., Hindorff, L. A., Hooker, G. W., Koenig, B. A., ... & Diversity Working Group. (2020). Clinical genetics lacks standard definitions and protocols for the collection and use of diversity measures. The American Journal of Human Genetics, 107(1), 72-82.
- Sesardic, N. (2010). Race: a social destruction of a biological concept. Biology & Philosophy, 25(2), 143-162.
- Singh, S., and Steeves, V. (2020). The Contested Meanings of Race and Ethnicity in Medical Research: A Case Study of the DynaMed Point of Care Tool. Social Science and Medicine, 113112.
- Spencer, Q. (2014). A radical solution to the race problem. Philosophy of Science, 81(5), 1025-1038.
- Sutherland, S. L., & Cimpian, A. (2019). Developmental evidence for a link between the inherence bias in explanation and psychological essentialism. Journal of Experimental Child Psychology, 177, 265-281.
- Yearby, R. (2021). Race based medicine, colorblind disease: How racism in medicine harms us all. The American Journal of Bioethics, 21(2), 19-27.
The slogan ‘nothing about us without us’ gained prominence in disability activism in the 1990s. Given how policy often disproportionately impacts those with disabilities, it ensures those affected play a role in a policy’s development – arguably due to the historic inability of policymakers to position themselves behind a Rawlsian veil of ignorance (Rawls 1999) on such matters. In the healthcare context, this idea is advocated in biomedical research. However, the focus remains largely on physical disability. In this paper, I shift the focus to cognitive disability.
Actioning ‘nothing about us without us’ is especially challenging where individuals suffer cognitive impairments. Historic language around mental capacity has created a lasting perception of cognitive impairment not as one of many aspects of a person, but of the person as an embodiment of such impairment. Those affected by cognitive impairments are often immediately deemed unable to make decisions or even participate in the decision-making process. In healthcare, the paternalistic approach that has significantly faded in recent decades remains prominent – and explicitly so – when patients have cognitive impairments. This creates barriers to involving these individuals in research related to their own healthcare.
In this paper, I reflect on my experience of conducting empirical research with individuals who have both cognitive impairments and renal failure. I explore the value of ‘nothing about us without us’ in this context and the barriers to practicing it. In particular, I consider the gatekeeping role healthcare professionals occupy and how paternalistic inclinations can result in concerning approaches – even if from a place of good will.
Drawing on these experiences, and the concept of ‘nothing about us without us’, I suggest a need to reevaluate perspectives on the ethics of involving those with cognitive impairments in biomedical research. To do so, I look to phenomenological work concerning ‘skillful coping’ (Dreyfus 2005) and ‘absorbed coping’ (Kong 2017). I argue it is necessary for all parties in biomedical research to recognise the capabilities of those with cognitive impairments, and that systemic failings on this front are rooted in a narrow focus that disregards atypical communication. It is important such individuals are not excluded from research by virtue of their cognitive impairment, and that appropriate systems enable their consent (or, possibly, assent).
Even where such individuals may be less able to communicate, I argue their involvement in research can be in their best interests. However, importantly, they require additional evaluative steps to prevent undue burden and potential exploitation. This is due to a risk of the pursuit of ‘nothing about us without us’ going full circle such that those with cognitive impairments are vulnerable to being automatically involved in research to the point that it disadvantages them further. As such, it must be confirmed that their involvement is not disproportionately harmful and that it has the potential to directly improve the care of the particular patient group. In the example context, it is insufficient that research may benefit patients with renal failure – it must instead have the potential to benefit those with both renal failure and cognitive impairment.
- Dreyfus HL. 2005. Overcoming the myth of the mental: how philosophers can profit from the phenomenology of everyday expertise. Proceedings and Addresses of the American Philosophical Association 79(2):47-65.
- Kong C. 2017. Mental Capacity in Relationship: Decision-Making, Dialogue, and Autonomy. Cambridge: Cambridge University Press.
- Rawls J. 1999. A Theory of Justice. Cambridge, MA: Belknap.
Recent trends in psychiatry and biomedicine involve a transition from categorical to dimensional frameworks, according to which the boundary between health and pathology should be seen as a difference in degree, rather than as a difference in kind. The current trend towards dimensionality is sometimes based on the empirical observation that symptoms of mental disorders vary along a spectrum from normality to abnormality (APA 2013). However, this trend is also often motivated by non-epistemic considerations involving social, economic, and clinical factors (Amoretti et al. 2021; Solomon 2017; Cooper 2005).
In this talk we first argue that non-epistemic values alone are not decisive to guide the choice between categorical and dimensional approaches. Then, we turn to epistemic considerations to show that current theories of psychopathology risk oversimplifying the distinction between health and pathology. A novel theoretical framework is thus required to address the issues raised by both approaches. Our argument unfolds as follows.
In the first part of the talk, we show that equally plausible ethical perspectives generate contrasting judgments among scholars, practitioners, and patients. For instance, there are compelling ethical reasons to avoid essentialist attitudes towards psychiatric labels as they risk perpetuating stigma and discrimination (Zachar 2015; Jablensky 2012; see also Wijsen et al. 2021). Nevertheless, in many cases, proponents of neurodiversity movements and ideals perceive their own diagnosis as an essential aspect of their identity and forcefully reject the claim that “we are all a little bit X”, where X stands for any psychiatry condition (Botha et al. 2020; Spencer & Carel 2021). It is thus unclear which model would be more desirable on ethical grounds.
In the second part, we outline a hybrid model that sets out to combine a range of desiderata from both categorical and dimensional approaches. Drawing on contemporary epigenetics and developmental biology, we offer a characterization of mental disorders as dynamic, stable, and emerging complex states. According to this view, although symptoms appear to be varying quantitatively, pathologies are constellations of multi-level variables that differ qualitatively from one another.
In the third part, we show that our model fares better than the alternatives both on nonepistemic and epistemic grounds. Indeed, our proposal succeeds in escaping the conflicting ethical intuitions fleshed out in the first part, and exhibits remarkable epistemic advantages over categorical as well as dimensional frameworks. Contra categorical approaches, our model avoids essentialist labels and does justice to the idea that symptom severity varies quantitatively along some relevant dimensions. At the same time, it also avoids two potential downsides of dimensional frameworks: a) the reduction of individual variability to single (or a few) quantitative dimensions; b) the oversimplification of the health-pathology distinction based on the continuity observed at the behavioral level.
- American Psychiatric Association, APA. (2013). Diagnostic and statistical manual of mental disorders, fifth edition: DSM-5. American Psychiatric Publishing.
- Amoretti, M. C., Lalumera, E., & Serpico, D. (2021). The DSM-5 introduction of the Social (Pragmatic) Communication Disorder as a new mental disorder: a philosophical review. History and Philosophy of the Life Sciences, 43(4).
- Botha, M., Dibb, B., & Frost, D. M. (2020). “Autism is me”: an investigation of how autistic individuals make sense of autism and stigma. Disability & Society, 1-27.
- Cooper, R. (2005). Classifying madness. Springer.
- Jablensky, A. (2012). The nosological entity in psychiatry: a historical illusion or a moving target. Philosophical issues in psychiatry II Nosology. Oxford University Press, Oxford, 77-94.
- Solomon, M. (2017). “A messy business”: Balancing considerations in revising the psychiatric nosology. In K. S. Kendler & J. Parnas (Eds.), Philosophical issues in psychiatry IV: Psychiatric nosology (pp. 70–74). Oxford University Press.
- Spencer, L., & Carel, H. (2021). ‘Isn’t Everyone a Little OCD?’ The Epistemic Harms of Wrongful Depathologization. Philosophy of Medicine, 2(1).
- Wijsen, L. D., Borsboom, D., & Alexandrova, A. (2021). Values in Psychometrics. Perspectives on Psychological Science.
- Zachar, P. (2015). Psychiatric disorders: Natural kinds made by the world or practical kinds made by us? World Psychiatry, 14(3), 288–290.
Human enhancement is the debate that has grown the most in the bioethics literature within the last decade (Bystranowski et al., under review). The issue of genetic enhancement has particularly been one of the most discussed. However, this topic suffers from an important paradox. While articles that have addressed the normative problems of the debate have abounded, this discussion has received scant attention from a perspective closer to the philosophy of science. This is puzzling since both proponents and detractors base their ethical views, either hopes or concerns, on underlying scientific premises about the near possibility of human genetic enhancement.
One of the most notable exceptions has been the article “The myth of genetic enhancement” by Philip M. Rosoff (2012), which I believe has not unfortunately been sufficiently discussed in the subsequent literature. Rosoff developed an interesting science-based skepticism according to which human “genetic enhancement is conceptually and scientifically unlike” (p. 173). In other words, he argued that the deepseated expectations about genetic enhancement are based on false factual premises and misleading scientific assumptions. A decade after its publication, I consider it appropriate to revisit his objections to the possibility of human genetic enhancement and to problematize them in the light of the theoretical and scientific advances of the last ten years.
Therefore, my argument will proceed as follows. I will start by clarifying the very meaning of ‘human genetic enhancement’, presenting some of the most important definitions and assessing their advantages and weaknesses. Then, I will discuss Rosoff’s science-based critique of the possibility of genetic enhancement in humans. I will focus on two distinct objections—although they may sometimes overlap. The first one is what we shall call the Reductionism Objection. Regarding this topic, I will discuss issues related to the reification of genes, genetic determinism, behavioral genetics and polygenic scores. The second argument shall be called the Complexity Objection. It encompasses different problems around the pleiotropic effects of genes, new discoveries about epigenetics and phenotypic expression. I will show contra Rosoff that, although both objections show relevant difficulties, they are not sufficient to dismiss the possibility of human genetic enhancement in the light of the latest scientific and biotechnological advances. After that, in the last section, I will approach the challenges of embedding cutting-edge science in public bioethical controversies. My proposal is what I shall call the Mutual Stewardship Ideal, according to which I advocate a mutually attentive relationship between (the philosophy of) science and bioethical discourse. Applied to the genetic enhancement debate, this ideal demands a bidirectional engagement between scientists and bioethicists to establish the most reasonable expectations in the short, medium, and long term. To conclude, human genetic enhancement is an empirically sensitive topic, where scientific assumptions clearly influence the normative debate, so we need the public engaging in the bioethics discussion to be informed by the highest standards of scientific evidence. After all, if genetic enhancement is closer to being a realistic possibility than an unfounded myth, we, as a society, have a lot to discuss.
- Alexander, D. (2020). Are We Slaves to our Genes?. Cambridge: CUP.
- Barbara, T., & Staffan, B. (2010). Genetics of personalities: no simple answers for complex traits. Molecular Ecology, 19(4), 624–626. http://dx.doi.org/10.1111/j.1365-294X.2009.04519.x
- Bystranowski, P., Dranseika, V. and Zuradzki, T. (under review). Half a Century of Bioethics and Philosophy of Medicine. A Topic-Modeling Study.
- Griffiths, P., & Stotz, K. (2013). Genetics and Philosophy: An Introduction. In Cambridge Introductions to Philosophy and Biology (pp. 1-8). Cambridge, UK: CUP.
- Kampourakis, K. (2021). Understanding Genes. Cambridge: CUP.
- Munday, S., & Savulescu, J. (2021). Three models for the regulation of polygenic scores in reproduction. Journal of Medical Ethics, 47(12), E91. https://doi.org/10.1136/medethics-2020-106588
- Paige Harden, Kathryn (2021). The Genetic Lottery: Why DNA Matters for Social Equality. Princeton University Press.
- Plomin R. (2018). Blueprint: How DNA makes us who we are. Cambridge, Massachusetts: The MIT Press.
- Rosoff, P. M. (2010). In search of the mommy gene: Truth and consequences in behavioral genetics. Science Technology and Human Values, 35(2), 200–243. https://doi.org/10.1177/0162243909340260
- Rosoff, P. M. (2012). The myth of genetic enhancement. Theoretical Medicine and Bioethics, 33(3), 163–178. https://doi.org/10.1007/s11017-012-9220-6
- Sober, E. (2000). The Meaning of Genetic Causation. In A. Buchanan, D. W. Brock, N. Daniels, & D. Wikler (2000). From Chance to Choice: Genetics and Justice (pp. 347-370). Cambridge: CUP.
- Tabery, J. (Winter 2021 Edition). Genetics. In Edward N. Zalta (ed.). The Stanford Encyclopedia of Philosophy. Retrieved from https://plato.stanford.edu/archives/win2021/entries/genetics/ (last access 25th January 2021).
- Turkheimer, E. (2015). Genetic prediction. Hastings Center Report, 45(S1), S32-S38.
Clinical trials are designed to assess the effectiveness of novel medical interventions. In order to help minimise the risk to the trial subjects, and to ensure that an effective intervention is licensed as quickly as possible, researchers must design maximally informative trials that last the shortest feasible amount of time. Consequently, researchers must devise ways to develop reliable inferences using the minimum amount of trial data necessary. However, researchers will always incur some risk of making a false inference from the trial data (Stegenga 2017; Bluhm 2017). The argument from inductive risk (AIR) has shed light on how the ethical constraints within clinical trials should impact our assessments and management of inferential uncertainty. The AIR stipulates that scientists should use ethical concerns surrounding clinical trials to set standards for what constitutes sufficient evidence to conclude experimental interventions are (in)effective (Rudner 1953; Douglas 2009; 2000; Steel 2010). As a risk-management strategy, the AIR instructs researchers to choose experimental methods in a way that makes the inductive risk within the trial procedure conform to an acceptable level. However, how to operationalise this guideline as a strategy for in-trial risk management is currently unexplored. To address this, I outline the ideal conditions under which methodological choices that conform to this guideline can be made:
- Ideal Holistic risk management: The risk of making a false inference about the nature of an experimental intervention being trialled is ideally managed when each methodological choice in the trial procedure is informed by methodological choices made elsewhere in the research procedure.
- Ideal Holistic agential perspective: In order to achieve holistic risk management, some researchers must occupy a perspective in which they can see all methodological choices made at all points in the inquiry. These researchers can therefore judge the inductive risk generated/mitigated as a result of each choice and make subsequent methodological choices accordingly.
These ideal conditions follow from two properties of trial methods and inferences. Firstly, no methodological outcome has a straightforward relationship to the eventual inference made about the intervention: for example, meeting statistical significance is sometimes insufficient and sometimes unnecessary for justifying an inference on drug effectiveness (Ellenberg, Fleming, and DeMets 2019; Zannad et al. 2012). Without the context of the complete trial procedure and all methodological choices made wherein, the inductive risk associated with an individual method choice remains elusive (Biddle and Kukla 2017). Secondly, the risk associated with each method depends on previous choices made. For example, the chance that any statistical test outputs significant results depends on what clinical endpoint was chosen to measure the intervention’s effectiveness.
Outlining these conditions makes clearer why social approaches to risk management are better than individual approaches (Contessa 2021; Wilholt 2016; 2009). As I show through examples of Data Monitoring Committees, certain social-organisational structures bring trial experimenters closer to the ideal holistic agential perspective by making then well-situated to view the research procedure holistically. The upshot of my thesis is that making modifications to the social-organisational structure of clinical trials brings in-trial inductive risk management closer to the ideal.
- Biddle, Justin B., and Rebecca Kukla. 2017. ‘The Geography of Epistemic Risk’. Exploring Inductive Risk: Case Studies of Values in Science, 215–37.
- Bluhm, Robyn. 2017. ‘Inductive Risk and the Role of Values in Clinical Trials’. Exploring Inductive Risk: Case Studies of Values in Science, 193–212.
- Contessa, Gabriele. 2021. ‘On the Mitigation of Inductive Risk’.
- Douglas, Heather. 2000. ‘Inductive Risk and Values in Science’. Philosophy of Science 67 (4): 559–79.
- ———. 2009. Science, Policy, and the Value-Free Ideal. University of Pittsburgh Pre.
- Ellenberg, Susan S., Thomas R. Fleming, and David L. DeMets. 2019. Data Monitoring Committees in Clinical Trials: A Practical Perspective. John Wiley & Sons.
- Rudner, Richard. 1953. ‘The Scientist qua Scientist Makes Value Judgments’. Philosophy of Science 20 (1): 1–6.
- Steel, Daniel. 2010. ‘Epistemic Values and the Argument from Inductive Risk*’. Philosophy of Science 77 (1): 14–34. https://doi.org/10.1086/650206.
- Stegenga, Jacob. 2017. ‘Drug Regulation and the Inductive Risk Calculus’. Exploring Inductive Risk: Case Studies of Values in Science, 17–36.
- Wilholt, Torsten. 2009. ‘Bias and Values in Scientific Research’. Studies in History and Philosophy of Science Part A 40 (1): 92–101.
- ———. 2016. ‘Collaborative Research, Scientific Communities, and the Social Diffusion of Trustworthiness’. The Epistemic Life of Groups: Essays in the Epistemology of Collectives, 2182–33.
- Zannad, Faiez, Wendy Gattis Stough, John J. V. McMurray, Willem J. Remme, Bertram Pitt, Jeffrey S. Borer, Nancy L. Geller, and Stuart J. Pocock. 2012. ‘When to Stop a Clinical Trial Early for Benefit: Lessons Learned and Future Approaches’. Circulation: Heart Failure, March. https://doi.org/10.1161/CIRCHEARTFAILURE.111.965707.