Jonathan Y. Tsou examines and defends positions on central issues in philosophy of psychiatry. The positions defended assume a naturalistic and realist perspective and are framed against skeptical perspectives on biological psychiatry. Issues addressed include the reality of mental disorders; mechanistic and disease explanations of abnormal behavior; definitions of mental disorder; natural and artificial kinds in psychiatry; biological essentialism and the projectability of psychiatric categories; looping effects and the stability of mental disorders; psychiatric classification; and the validity of the DSM's (...) diagnostic categories. The main argument defended by Tsou is that genuine mental disorders are biological kinds with harmful effects. This argument opposes the dogma that mental disorders are necessarily diseases that result from biological dysfunction. Tsou contends that the broader ideal of biological kinds offers a more promising and empirically ascertainable naturalistic standard for assessing the reality of mental disorders and the validity of psychiatric categories. (shrink)

Since the turn of the twenty-first century, biomedical psychiatry around the globe has embraced the so-called precision medicine paradigm, a model for medical research that uses innovative techniques for data collection and analysis to reevaluate traditional theories of disease. The goal of precision medicine is to improve diagnostics by restratifying the patient population on the basis of a deeper understanding of disease processes. This paper argues that precision is ill-fitting for psychiatry for two reasons. First, in psychiatry, unlike in fields (...) like oncology, precision medicine has been understood as an attempt to improve medicine by casting out, rather than merely revising, traditional taxonomic tools. Second, in psychiatry the term “biomarker” is often used in reference to signs or symptoms that allow patients to be classified and then matched with treatments; however, in oncology “biomarker” usually refers to a disease mechanism that is useful not only for diagnostics, but also for discovering causal pathways that drug therapies can target. Given these differences between how the precision medicine paradigm operates in psychiatry and in other medical fields like oncology, while precision psychiatry may offer successful rhetoric, it is not a promising paradigm. (shrink)

We argue that Madole & Harden's distinction between shallow versus deep genetic causes can bring some clarity to causal claims arising from genome-wide association studies (GWASs). However, the authors argue that GWAS only finds shallow genetic causes, making GWAS commensurate with the environmental studies they hope to supplant. We also assess whether their distinction applies best to explanations or causes.

In 1976, the Genetics Society of America published a document entitled “Resolution of Genetics, Race, and Intelligence.” This document laid out the Society’s position in the IQ controversy, particularly that on scientific and ethical questions involving the genetics of intellectual differences between human populations. Since the GSA was the largest scientific society of geneticists in the world, many expected the document to be of central importance in settling the controversy. Unfortunately, the Resolution had surprisingly little influence on the discussion. In (...) 1979, William Provine analyzed the possible factors that decreased the impact of the Resolution, among them scientists’ limited understanding of the relationship between science and ethics. Through the analysis of unpublished versions of the Resolution and exchanges between GSA members, I will suggest that the limited impact of the statement likely depended on a shift in the aims of the GSA due to the controversies that surrounded the preparation of the document. Indeed, the demands of the membership made it progressively more impartial in both scientific and political terms, decreasing its potential significance for a wider audience. Notably, the troubled history of the Resolution raises the question of what can make effective or ineffective the communication between scientists and the public—a question with resonance in past and present discussions on topics of social importance. (shrink)

Research in pharmacogenomics and precision medicine has recently introduced the concept of Polygenic Scores (PGSs), namely, indexes that aggregate the effects that many genetic variants are predicted to have on individual disease risk. The popularity of PGSs is increasing rapidly, but surprisingly little attention has been paid to the idealisations they make about phenotypic development. Indeed, PGSs rely on quantitative genetics models and methods, which involve considerable theoretical assumptions that have been questioned on various grounds. This comes with epistemological and (...) ethical concerns about the use of PGSs in clinical decision-making. In this paper, I investigate to what extent idealisations in genetics models can impact the data gathering and clinical interpretation of genomics findings, particularly the calculation and predictive accuracy of PGSs. Although idealisations are considered ineliminable components of scientific models, they may be legitimate or not depending on the epistemic aims of a model. I thus analyse how various idealisations have been introduced in classical models and progressively readapted throughout the history of genetic theorising. Notably, this process involved important changes in the epistemic purpose of such idealisations, which raises the question of whether they are legitimate in the context of contemporary genomics. (shrink)

In the last two decades few topics in philosophy of science have received as much attention as mechanistic explanation. A significant motivation for these accounts is that scientists frequently use the term “mechanism” in their explanations of biological phenomena. While scientists appeal to a variety of causal concepts in their explanations, many philosophers argue or assume that all of these concepts are well understood with the single notion of mechanism. This reveals a significant problem with mainstream mechanistic accounts– although philosophers (...) use the term “mechanism” interchangeably with other causal concepts, this is not something that scientists always do. This paper analyses two causal concepts in biology–the notions of “mechanism” and “pathway”–and how they figure in biological explanation. I argue that these concepts have unique features, that they are associated with distinct strategies of causal investigation, and that they figure in importantly different types of explanation. (shrink)

According to the homeostatic property cluster family of accounts, one of the main conditions for groups of properties to count as natural is that these properties be frequently co-instantiated. I argue that this condition is, in fact, not necessary for natural-kindness. Furthermore, even when it is present, the focus on co-occurrence distorts the role natural kinds play in science. Co-occurrence corresponds to what information theorists call redundancy: observing the presence of some of the properties in a frequently co-occurrent cluster makes (...) observations of other members of the cluster comparatively uninformative. Yet, scientific practice often, and increasingly often, singles out as natural groups of properties that are not redundant, but synergic: instantiations of properties in synergic clusters are not necessarily informative about instantiations of other properties in the cluster; rather, it is their joint instantiation that plays the explanatory role for which the natural kind is recruited. (shrink)

Because biologization of psychiatric constructs does not involve derivation of laws, or reduce the number of entities involved, the traditional term of ‘reduction’ should be replaced. This paper describes biologization in terms of redefinition, which involves changing the definition of terms sharing the same extension. Redefinition obtains through triangulation and calibration, that is, respectively, detection of an object from two different spots, and tweaking parameters of detection in order to optimize the picture. The unity of the different views of the (...) same object does not occur through derivation from one of them, as reduction suggests, nor does it obtain through mechanistic unity or the goal of explaining one mechanism, as the phrase ‘mosaic unity’ suggests. Instead, it depends on finding a specific angle of observation, from which linguistic consistency matches sound localization in the brain, so that all observations make sense together, just as an anamorphic picture makes clear sense only when observed from the right spot. (shrink)

Journal of Social Philosophy, EarlyView.

In biology and philosophy of biology, discussing the notion of interaction leads to an examination of interactionism, which is, broadly speaking, the view that rejects gene-centrism and gene determinism and instead emphasizes the fact that traits of organisms are always the result of genes and environments. It has long been asserted that the nature-nurture problem requires an interactionist solution of sorts, the so-called interactionist consensus. This consensus, however, has been deemed insufficient and challenged by several authors triggering an extension of (...) the debate among contestants and defenders. Unfortunately, part of the problem is that the views on causation that would ground claims about interactionism are not always made explicit in this debate, which renders those views somewhat complicated to assess. Moreover, it seems to be assumed that causal complexity excludes the possibility of characterizing, distinguishing, or comparing among causal contributions. By turning to a detailed survey of the origin of the debate and to some developments in the philosophy of causation, we will contend that this view is unwarranted, and that much of the debate around interactionism is based on the drawing of this conclusion. We also examine implications of this analysis for the project to develop a framework based on the notion of inter-identities. (shrink)

Causation has multiple distinct meanings in genetics. One reason for this is meaning slippage between two concepts of the gene: Mendelian and molecular. Another reason is that a variety of genetic methods address different kinds of causal relationships. Some genetic studies address causes of traits in individuals, which can only be assessed when single genes follow predictable inheritance patterns that reliably cause a trait. A second sense concerns the causes of trait differences within a population. Whereas some single genes can (...) be said to cause population-level differences, most often these claims concern the effects of many genes. Polygenic traits can be understood using heritability estimates, which estimate the relative influences of genetic and environmental differences to trait differences within a population. Attempts to understand the molecular mechanisms underlying polygenic traits have been developed, although causal inference based on these results remains controversial. Genetic variation has also recently been leveraged as a randomizing factor to identify environmental causes of trait differences. This technique—Mendelian randomization—offers some solutions to traditional epidemiological challenges, although it is limited to the study of environments with known genetic influences. (shrink)

My doctoral project is a study of epistemological and ethical issues in Evidence-Based Medicine, a movement in medicine which emphasizes the use of randomized controlled trials. Much of the research on EBM suggests that, for a large part of the movement's history, EBM considered expertise, mechanisms, and values to be forces contrary to its goals and has sought to remove them, both from medical research and from the clinical encounter. I argue, however, that expertise, mechanisms and values have important epistemological (...) and ethical roles to play and can be incorporated into the current EBM movement. (shrink)