Elena Popa, “Mechanisms, Activities, and Biopsychosocial Causation”
Channel: CEFISES at UCLouvain
Date: 2023-08-08

Talk given at the Mechanisms and Ontic Causation in the Life Sciences conference, the second workshop of the MeCauLife group.

Abstract: This paper aims to develop a metaphysical background for mechanistic causation within the biopsychosocial model of health and disease. Bolton & Gillett's (2019) defence of this model refers to criticism regarding its being vague and underdeveloped with regards to ontology, and also discusses causation. Some of the implications of Bolton and Gillett's views on causality, particularly metaphyiscal questions about normativity have been criticized, with the suggested use of interventionist approaches (Maung 2021). In response, Bolton (2021) has emphasized the importance of a deeper metaphysical background for theorizing biological, psychological, and social components, stressing the role of mechanisms. Yet, Bolton and Gillett do not elaborate the ontic aspects of mechanistic causation, namely relevant entities and activities within the biopsychosocial model and how different mechanisms interact. I aim to further develop the account of mechanistic causation withing the biopsychosocial model by using this debate alongside contributions regarding causality in psychiatry spelling out diseases as mechanistic property clusters (Kendler et al. 2011) as starting points.

Mechanistic property clusters are defined as ‘complex, mutually reinforcing networks of causal mechanisms' (Kendler et al. 2011: 1143). Components of mechanistic property clusters include an underlying state, causes, and clinical manifestations. For instance, inflammation resulting from stress can be an underlying state, with excessive social demands and low psychological resources as causes, while clinical manifestations can include high blood pressure. One important feature of mechanistic property clusters is that they can account for self-reinforcing patterns that obtain in mental disorders, as well as other illnesses with psychosocial components. Further spelling out what causal mechanisms amount to in this context alongside how different mechanisms interact with one another requires more in-depth metaphysical analysis. The challenge for the biopsychosocial model (which interventionist approaches may avoid) is to explain how entities and activities belonging to different spheres come together. I will sketch this out by looking at a top-down and bottom-up model of neuro-endocrime-immune pathways in irritable bowel syndrome (IBS) (Stasi et al. 2012) and considering broader mechanistic property clusters so as to also include social and psychological phenomena.

While different accounts of causal mechanisms have been brought forward (see review by Craver and Tabery 2015), my analysis will rely on the activity account (Machamer 2004; Bogen 2005), applying it to causality in biomedical contexts. On this view, causal mechanisms consist of productive activities in a sense introduced by Anscombe. Features of activities depend on the scientific domain where they operate. Using the example of IBS, several mechanisms are involved, in connection to exteroceptive stress (top-down) and interoceptive stress (bottom-up) (see figure 1). The model for the Hypothalamic–pituitary–adrenal axis (HPA) includes a mechanism connecting the experience of chronic stress to changes in the amygdala and hippocampus function which affect the pituitary and adrenal gland resulting in low grade inflammation of the enteric nervous system. The bottom-up mechanism operates from inflammation of the enteric nervous system through afferent fibers and to changes in amygdala and hippocampus function. The entities here are the relevant components of the nervous and enteric system, while activities include neural processes, immune response, and hormonal changes. On a mechanistic property cluster view, these mechanisms interact without circularity, explaining how chronic stress leads to worsening IBS through a top-down mechanism, while the resulting changes in the enteric system affect brain function through a bottom-up mechanism.

As it can be seen from the above, the activities in this model are neuronal, biological, or chemical. A broader model, taking into account stress and its uncontrollability feature may also consider activities involving psychological and social states, such as dynamics between demands and responses. These could all be brought together under a more complex mechanistic property cluster, but it should be noted that different mechanisms may be underlain by different types of activities (e.g., psychological and neuronal). Thus, a puzzle to explore for the biopsychosocial model and mechanistic causation is whether activities neatly overlap with corresponding mechanisms, or whether activities of social or psychological nature can be traced in mechanisms such as the top-down and bottom-up model of IBS beyond their neural manifestations.