This is a report on the 2014 Oxford Loebel Lectures by Rebecca Roache, Lecturer in Philosophy at Royal Holloway, University of London.
The biopsychosocial model in psychiatry tells us that psychiatric disorders arise from a combination of biological, psychological, and social factors. But how do causes at these three ‘levels’ interact, and how do we put this insight to use in treating mental illness? Professor Kenneth Kendler addressed these questions in Oxford’s inaugural Loebel Lectures.
In his first lecture (which you can watch here or listen to here), Kendler shared fascinating empirical data to demonstrate the aetiological complexity of psychiatric disorders. He showed that whilst one’s genes can make it more likely that one will suffer certain disorders, the causal pathway does not run directly from genes to the development of a disorder. Rather, causal pathways often—to use Kendler’s expression—‘loop out’ into the environment. For example, having a genetic predisposition to depression makes you more likely to be depressed, but this is because you will be more sensitive than other people to stressful life events that can cause depression. Another example: alcohol dependency does not simply arise from one’s genes, but via one’s genetically-induced tendency to seek out social groups where drinking is encouraged.
In Kendler’s second lecture (view it here or listen here), he observed that before the middle of the 19th century, mental disorders were not thought to have single, clear aetiologies. This changed in the late 19th century, when scientific advances meant that various somatic diseases were explained in terms of elegant, simple causal mechanisms, paving the way for a reductionist quest to discover single causal aetiologies for psychiatric disorders. However, with the exception of the discovery that general paresis is caused by syphilis, attempts to discover such simple aetiologies have been unsuccessful.
What does this lack of success tell us? Kendler thinks that finding simple aetiologies for psychiatric disorders is an unrealistic goal, since there is generally no privileged level of explanation for these disorders in terms of which such aetiologies could be characterised. It is not the case, for example, that the best causal story for any given psychiatric disorder is one couched purely in terms of neuropathology, or molecular genetics, or environmental stressors, or some other narrowly-focused set of explanatory factors. On the contrary, invariably, we need to consider all these explanatory factors and more in order to explain psychiatric disorders: a phenomenon that Kendler terms ‘dappling’.