Lecture 2 Audio [MP3] | YouTube link [MP4]
Grove Auditorium, Magdalen College, Longwall Street, Oxford
4 November 2015, 6-8pm
i. A half-century of stasis in psychiatric therapeutics reflects the enormous scientific hurdles posed by psychiatric disorders.
ii. However, it also reveals the need for new ways of thinking and a more honest response to evidence.
iii. Psychiatry has yet to grasp the complexity that lies at the heart of human cognition and behavior as well as psychopathology.
a. There are few, if any, main effects in the genesis of psychopathology
i. Hundreds, perhaps thousands of genes, contribute small incremental to the pathogenesis of mental illness
ii. Current ‘candidate’ gene by environment approaches are still reductive heuristics, not explanations of psychopathology.
b. Overly reductive pharmacologic and endocrine models persist in academic research despite contrary evidence, as do failed animal models rejected by industry.
c. Linear, causal psychological narratives may be comforting, even helpful, but are not veridical
i. Motivation and decision-making are opaque to introspection (as Freud knew, but lacked the tools to investigate).
ii. Cognitive and computational neuroscience are beginning to draw a better picture
d. The DSM classification, based on drawing a large number of fictive categories, has proved damaging to science
iv. Epochal technological advances (genomics, computation, stem cell biology, genome engineering, microscopy, and brain-machine interfaces) are fundamentally changing the science relevant to psychiatry; new ideas are following from technologically enabled observations.
v. The complexity is humbling, but the emerging picture of psychopathology will be one of biological mechanisms, whether of molecular targets within protein complexes (cellular machines) affected by drugs, or synapses and circuits affected by cognitive therapies, adaptive therapies, or neuromodulation.