There may be nothing of such obvious importance to human knowledge that is more elusive than the concept of causation. It sits as the crossroads of many disciplines, including philosophy, statistics, epidemiology, psychology, and clinical medicine. Causal theories in psychiatry trace back to the very beginning of the discipline and have often been speculative – and incorrect. These include the humoral theories of the Galenists from Roman times, ideas about vibrating nerves and intestinal vapors in the 18th century, degeneration theory the 19th century, Oedipal conflicts in the middle of the 20th century, and the dopamine theory of schizophrenia and other rudimentary “chemical imbalance” perspectives of the late 20th century.
Ironically, nearly every one of these perspectives was formulated using a causal framework that remains relevant today. This is the notion that people differ in their degree of vulnerability to illness, some are more and others less likely to become ill, but life events both random and systematic – and how those events are interpreted – play an important role in the generation and maintenance of illness (and health). In other words, although causal theory after causal theory from the past has been abandoned, one of the oldest theories – a broad framework including predisposing and precipitating factors – is still considered accurate.
In this book we examine causation as it applies to the origins of psychiatric disorders and related distress and dysfunction utilizing a multidisciplinary framework, from the perspectives of psychiatry, philosophy, and psychological science. Although members of all three disciplines discuss many of the same problems, they do not always share the same framework for studying those problems. This can lead them to focus on different features of the shared causal issues.
There is of course variation within each discipline – also evident in these chapters – making it misleading to lump all members of a discipline together. Nevertheless, different training, histories, and types of expertise establish disciplinary identities that can influence perspectives, including perspectives on causation. The issue is not the identity of disciplines themselves, but what a discipline is more likely to emphasize in contrast to other related disciplines. Our articulation of these perspectives, we contend, highlights some relevant differences that can be gleaned in this volume as members of the different disciplines interact with perspectives from the other disciplines.
For psychiatrists, causal theorizing had one great success, now rarely discussed: the discovery that general paresis of the insane was a late-stage manifestation of syphilis. This discovery, combined with the introduction of a range of treatments and eventually antibiotics, resulted in the disappearance of one of the most prevalent institutionalized mental disorders of the 19th century. For psychiatry the core elements of causation include etiology (what initiated an illness) and the pathological process that constitutes the disorder in question. For many psychiatrists it is nearly canonical that establishing the etiopathological validity for psychiatric disorders would increase the discipline’s medical respectability and, most importantly, lead to better therapeutic success. Even for thinkers who do not favor reductive accounts, and in proportion to how strongly they identify with medicine, etiopathological validity is not something they want to abandon.
For philosophers (especially philosophers of science), as briefly described by Lauren Ross in Chapter 21, the issue of causation is entwined with the nature of scientific explanation. In the 18th century, following the work of David Hume, scientifically minded philosophers viewed the very idea of causation to be speculative metaphysics – and not an appropriate candidate for being a defining feature of scientific explanation. Alternative candidates not directly based on causation included laws of nature, relationships of probability, and unifying theoretical frameworks (like the Newtonian model in physics).
However, aside from Darwin’s theory of evolution, laws of nature and grand unifying theories are not prevalent in the life sciences, so causal approaches to explanation have become more important for philosophers who study those sciences. These approaches include causal pathway accounts, mechanistic accounts, interventionist accounts, and cascade accounts. Many of these approaches emphasize how causal claims are understood and validated in the sciences. Such accounts, however, do not just trail the sciences but dig deeper. For example, a psychiatrist may talk loosely about endophenotypes or biomarkers as “mechanistic,” but a philosopher would point out that endophenotypes may be a part of a mechanism but are not mechanisms. Philosophers will have detailed accounts of what mechanisms in science are and will also distinguish them from other kinds of causal accounts.
To characterize psychological scientists, we will contrast them with what we said about psychiatry and philosophy of science. With respect to psychiatry, neuroscience and genetics are an increasingly important part of training in psychology, but developmental psychology, personality and social psychology, and cognitive psychology are still core subjects. In trying to put this all together, the resulting notion of complex psychological states makes it less likely for psychologists to prioritize etiopathological validity. Psychometric construct validity would typically be front and center in psychological science.
With respect to questions about the nature of scientific explanation and causation, psychologists are unlikely to dig down as deeply as do the philosophers of science. Especially in clinical psychological science, the questions that would be of direct interest in philosophy either take a back seat to or are viewed by psychological scientists as entangled with issues relating to measurement, quantification, and scientific methodology.
This book is the sixth volume in a series documenting philosophical issues in psychiatry conferences that have been held in Copenhagen, Denmark. The first conference was in 2006. The meeting for the current volume occurred May 15–17, 2023. Although these books have been described as being based on the Copenhagen conferences, over time we have come to see that description as inaccurate. A better description is that we selected a book topic and invited specific people to contribute chapters. The initial drafts of these chapters were presented at the meeting in Copenhagen.
The conference was co-sponsored by the University of Copenhagen Center for Subjectivity Research. The funding for the conference, including travel and accommodations for all presenters, was generously provided by the Lundbeck Foundation. The conference itself was free and open to the public.
Although presenters were invited based on the quality and relevance of their prior work, everyone was free to select their own topic related to the issue of causation. Once the specific topics coalesced, we organized them into four different sections: The Causes Themselves; Causes, Genes, and Neuroscience; Causality and Nosology; and Causality and Phenomenology. A key feature of the conference phase of the book is that every main presentation is followed by a commentary by another presenter, a brief response to the commentary, and then a general discussion with questions taken from anyone in the audience. The interaction between presenter and commentator is designed to continue after the conference as final versions of the chapters are written.
Each presentation–commentary section in the book is preceded by a brief introduction by one of the editors. These introductions were shared with the section authors, who provided suggestions for improvement. The purpose of the brief introductions is to increase the accessibility of the chapters to those from multiple disciplines.
We have no better summary of this meeting than the final comments Kenneth Kendler gave at the formal close of the conference phase of the book:
This now brings the first phase of our joint venture to a close. Our three days together has well demonstrated the richness of the issues involved in causality for the multilevel field of psychiatry.
We explored the benefits and potential limitations of counterfactual methods, especially the interventionist approach of Woodward. We debated about the nature of mechanisms, from sketches at a high psychosocial level to worked-out biological pathways and large-effect molecular variants. We pondered the boundaries between mechanisms and the more generic concept of causal pathways and examined the possible contribution of network approaches. We examined the notion that our measurements index disorders versus constituting them, looking that what implication a constituting relation might have for causal models.
We looked at how meaning and explanation aided understanding. We explored how phenomenological approaches should be integrated into our causal approach, how to clarify the sometime confusing division into so-called proximal and distal causes, and had a peek into how we might learn about the key feature of agency from deep-brain-stimulation studies. We debated whether optimism about the reductionist molecular approach is warranted. We examined in some detail how brain-based imaging, molecular genetics, and molecular neuroscience approaches to the etiology of psychiatry disorders could clarify causal pathways.
For us, the best return on our organization effort would be for new collaborations to spring up among the participants (or expansions of prior work). Most of all, the speakers engaged with energy the topics they selected. We had some good-spirited discussions that, for me, were the epitome of our academic mission – the pursuit of truth in the company of friends. It doesn’t get much better.