Supposing someone earnestly seeks God but to no avail. Does this mean God does not exist? Or might it be instead that the seeker seeks God without awareness of the peculiar method that must be employed in order for the seeking to be productive?

This chapter considers the concept of proximal and distal causes in various health science fields and common reference to the “proximal–distal model” of disease causation. In many cases, this model is used to capture the interaction of social and biological factors, with social factors as distal causes and biological factors as proximal causes. The authors examine Krieger’s (2008) criticism of this framework and suggestion that proximal–distal language confuses causal thinking, reasoning, and distinctions in health science domains. While Krieger (2008) has recommended the elimination of language of proximal and distal causes, Ross and Kendler argue for another alternative, specifically that while the proximal–distal model captures some etiological scenarios, it should not be applied to all cases. They examine three ways in which social and biological causes lead to health outcomes and argue for the value (and possibility) of clear notions of proximal and distal causes.

The subject of Peter Zachar’s chapter is classification, with a focus on psychiatry (of course). He suggests that classificatory choices should be “understood from the perspective of scientific conventionalism.” I agree that there is an important conventional element in current systems for the classification of mental disorders. Rather than seeing this as necessarily a limitation that needs to be overcome, my view is that many scientific theories, including very successful ones, contain conventional elements. (I take Zachar to agree.) In what follows I try to distinguish or disentangle different ways in which a scientific theory can contain conventional elements and to assess the implications of the presence of conventions in psychiatry.

In their chapter, Eric Turkheimer and Jonathan Kaplan assert that Galton’s quincunx “unifies discrete and continuous, binary and normally distributed, random and deterministic, predetermined and epigenetic.” What starts as an anodyne recitation of antinomies, quickly raises questions about how they intend to use the quincunx model as they move from statistical couplets to the contrast of “predetermined and epigenetic.” In so doing, Turkheimer and Kaplan seem to reduce epigenetics, a diverse and complex set of biological processes, into a synecdoche standing in for all nongenetic factors (stochastic and environmental) in development (the pins of the quincunx). Epigenetics refers to a complex (and variably reversible) group of biological processes that regulate gene expression. Epigenetic mechanisms are involved in gametogenesis, the earliest stages of embryonic development, and throughout life. In early development, chromatin (complexes of DNA with histones and other proteins) packages DNA and forms the basis for epigenetic regulation mediated by chemical modifications of the chromatin. Early on, epigenetics establishes cell fate and cell identities; later in development and through postnatal life, epigenetic mechanisms transduce diverse physiological signals that may originate in the body or in the environment to reversibly regulate gene expression. Epigenetic regulation of gene expression represents one of many biological mechanisms (including such important processes as learning and memory) that utilize and build on genomic information to support an organism’s development, homeostasis, adaptation, and change. In so doing these processes, along with chance, increase the heterogeneity (“individuality”) of organisms and significantly degrade the possibility of making precise long-term predictions from DNA sequences. From genetics alone we cannot predict with certainty whether a person will suffer from a mental illness, finish graduate school, or get divorced. Even the effects of Mendelian alleles, such as the precise age at which a carrier will develop Huntington’s disease (Genetic Modifiers of Huntington’s Disease Consortium, 2015), are not deterministically predictable in the context of modifier genes, chance, and additional layers of regulation.

The International Convention on the Elimination of All Forms of Racial Discrimination is the oldest UN human rights treaty, and for over forty years, the Committee overseeing its implementation, CERD, has had the power to decide individual communications. Despite this long history, a settled evidentiary framework has not materialised yet. The Committee rarely discussed evidence, and when it did, the results could differ markedly: In Dawas and Shava v. Denmark (2012), a case on mob violence, the Committee did not directly engage with the evidence, which led to a resurfacing of evidentiary questions during the follow-up phase, when they could no longer be addressed. Far preferable is the approach adopted in Zapescu v. Moldova (2021), dealing with discriminatory employment practices, where the Committee discussed the standard of proof for procedural violations and the necessary evidence. More elaborations of this kind are needed for a clear evidentiary pathway to emerge.

In his chapter Steven Hyman describes several paths forward for a more mechanistic understanding of psychiatric disorder, articulating the promise of such an approach as well as illustrating how it encompasses a variety of projects.

The author of the following chapter, Denny Borsboom, has played a leading role in the rise of the network model in psychopathology. This model has developed into a viable alternative to the older conventional common-factor model. These two models provide quite different explanations for why psychiatric disorders tend to cluster together in disorders. Let us illustrate this using two commonly co-occurring symptoms in individuals with major depression: insomnia and tiredness. The common-factor model assumes that the two symptoms co-occur because they are both caused by a latent construct: the psychobiological state of depression. By contrast, the network model implies a more common (and perhaps naïve) presentation, assuming a direct causal link between the two symptoms, especially in the direction of “I sleep poorly on night x” followed by “during day x + 1 I am tired.”

This introductory chapter illustrates why evidence in the individual communications procedure of the United Nations human rights treaty bodies (UNTB) is an issue requiring reflection and clarification. The chapter firstly contextualises this central topic of this book by broadly introducing the UNTBs’ mandates, composition and ways of working, as well as some general features of their individual communications procedures. Indications are given of how this legal, institutional and procedural setting interacts with the handling of evidence by the UNTBs, as well as some of the key questions it raises. The chapter further outlines some of the particular research challenges encountered in tackling the questions at the heart of this book, and how they have been addressed. It then goes on to introduce the four-part structure of the book and its ten chapters, including the final chapter, containing recommendations. Finally, this introduction discusses cross-cutting themes which emerge from the contributions.

Campbell’s contribution investigates the possible function of scientific laws in psychopathology, specifically the idea that the standard notion of scientific law could function in the way it has traditionally done in scientific explanation. An important way of thinking about this, as outlined by Campbell, is to introduce scientific laws as general axioms that act as premises in a deductive argument through a covering law. Properties of an individual case then feature as the explanandum. Variants on this approach generally emulate Aristotle’s well-known modus ponens argument scheme that deduces the mortality of Socrates from the premises that all men are mortal and that Socrates is a man. Although many different theories of explanation have been produced over the past century, I think it is fair to say that most working scientists have something like this model in mind when they think about explanations of individual cases.

This chapter starts from the well-known episode in which Pope supposedly spiked a glass of wine with an emetic in order to ‘poison’ Curll. This prompted one of Pope’s most hilarious works in prose, the short pamphlet entitled A Full and True Account of a Horrid and Barbarous Revenge by Poison, On the Body of Mr. Edmund Curll, Bookseller (1716). This was a parody of Curll’s numerous biographies of recently deceased celebrities with their will attached. The chapter looks at examples in earlier literature using the motif of lacing a drink as an act of revenge. A number of satiric writers are cited, beginning with Horace and Lucian. However, the most direct precedent involves Crispinus (‘curly’, from the Latin), the central character in Ben Jonson’s comedy Poetaster (1602). Succeeding passages consider the use Pope makes of these texts, pointing out that the need to vomit is regularly inflicted on bad writers. Pope departed from the tradition in having the draught delivered to a bookseller, suggestive of a change in the nature of print culture.