As a rheumatologist Dr. Jones specializes in autoimmune diseases where the body’s immune system starts to attack your own body.   He describes how his understanding of pain associated with the inflammation produced by the immune system in the healing process changed from a biomedical model to a biopsychosocial model.   Previously it was based on the biomedical model that a painful stimulus from an injured location sends a pain signal to the brain, which produces the pain experience.  He has previously done research on osteoarthritis bone samples looking for a protein signature in the sample that might correlate with arthritic pain.

Five years ago he encountered the ‘Pain Triangle based’ explanation of an incident where a worker was in extreme pain with a spike through his boot, but the spike passed between his toes so he had no injury.   The biopsychosocial explanation of the unexpected incident prompted him to rethink how he cared for patients, and he now understands inflammation symptoms are for protection, but inflammation is harmful when overexpressed.

In an injured area, immune cells (cytokines) leak from capillaries, and nerves release them, to cause the inflammation.  He shows research results demonstrating that individuals exposed to psychogenic stress had more inflammation than unstressed individuals when capsaicin was applied to their skin.  Cytokines in synovium fluid cause joint swelling in rheumatoid arthritis.   He briefly discusses anti-CCP antibodies, neuroimmune factors, interleukin-6, and TNF associated with rheumatoid arthritis.

He reports the 16-fold increase of inflammatory arthritis in teenagers with more than 4 adverse childhood events, which suggests a relationship between the disease and the brain being in a higher state of threat.   PTSD is also related to a higher incidence of rheumatoid arthritis.

He shows the hands of a man with rheumatoid arthritis, (which almost always occurs symmetrically in both hands or feet), and then shows his normal left hand two year later as the result of a stroke.  Half of his brain was not functional after the stroke, which produced the unusual non-symmetrical arthritis.

Patients with very active rheumatoid arthritis, that did not respond to multiple medications, experienced a decrease of about one third in the disease activity after a six-minute daily treatment for 42 days with a vagal nerve stimulator.   That result from a nonmedication intervention was an amazing demonstration of the relationship between the disease and the nervous system.

He poses a variation to the model of inflammation; it remains a protective response to threat to tissue, but neural activity may also simulate and direct inflammatory response.  So together with medication to control inflammation, he anticipates that decreasing the sense of threat can help change the neural stimulation and enable decreased medication.

A heightened sense of threat can lead to increased pain and increased inflammation.   So treatment of rheumatoid arthritis is focused on both the immune cells and the state to the brain.