In this episode of Chewing It Over, Jack is joined again by Asaf Weisman for a deliberately challenging discussion about some of the prevailing ideas within modern pain science.
Asaf argues that pain medicine has spent decades on a series of intellectual “side quests”, particularly following the development of the biopsychosocial model and modern definitions of pain in the 1970s. His criticism isn't that psychological, social or neurological factors are irrelevant, but that theoretical possibilities have sometimes been promoted with greater certainty than the evidence warrants.
A central theme is nociception and the role of the brain. Asaf challenges descriptions of pain as simply an output of the brain or a neurological expression of perceived threat. Instead, he argues that pain requires underlying somatic signalling, while the brain participates in processing and modulating that experience rather than independently generating it.
The discussion explores the language clinicians use around pain, the distinction between modulation and causation, and whether attempts to explain persistent pain have sometimes made the subject unnecessarily complex.
Importantly, the conversation also identifies areas of agreement. Asaf accepts that psychological and social factors can substantially alter an individual's pain experience, even when underlying nociceptive signalling remains unchanged. Stress, context and other factors can influence pain through modulation.
For clinicians, this creates a more practical discussion about management. Rather than becoming trapped in theoretical explanations, Asaf argues for identifying and addressing modifiable risk factors associated with persistent pain, while using exercise, modalities and other interventions where they help patients pursue meaningful activity.
It's a provocative conversation that challenges clinicians not simply to replace one pain model with another, but to scrutinise the assumptions underneath both.
Be precise about causation versus modulation. A psychosocial factor influencing the intensity of someone's pain doesn't necessarily establish that it independently caused the pain. That distinction is central to Asaf's argument.
Don't turn theoretical models into established biological facts. Models can help generate hypotheses and guide research without every component of the model having been empirically demonstrated.
The brain isn't being dismissed. Asaf's position is more nuanced than “pain is peripheral”. He explicitly accepts that the brain processes and modulates pain and that stress and psychosocial circumstances can change the resulting experience.
Language matters clinically. Terms such as “pain output”, “threat”, “nociception” and “biopsychosocial” carry assumptions. Using them casually can make a proposed mechanism sound more established than it actually is.
Don't let the theoretical debate distract from modifiable factors. Whatever model a clinician favours, the practical priority remains identifying things that can meaningfully be changed — including activity, physical health and relevant psychosocial stressors — and helping the patient address them.
5 clinical/professional takeaways