The introduction is also posted on Spotify as a podcast by “Gerry at The Health Equation”

You can search Spotify for “Gerry at The Health Equation”

Or use the link below

https://podcasters.spotify.com/pod/show/gerrygaj

Below is the specific link

“Please follow this show on Spotify. It really helps!”

Gerry Gajadharsingh writes:

“For many years, the management of chronic rheumatic disease has focused primarily on suppressing inflammation. While this remains essential, an increasing body of research demonstrates that controlling inflammation alone does not necessarily resolve a patient’s symptoms. Many individuals continue to experience significant pain, fatigue and disability despite excellent control of inflammatory markers.

This important article from Medscape, reporting presentations from the 2026 European Alliance of Associations for Rheumatology (EULAR) Congress, highlights a fundamental shift in clinical thinking. The evidence suggests that persistent pain often reflects the complex interaction of multiple physiological regulatory systems rather than ongoing inflammatory disease alone. Sleep disturbance, altered pain processing within the nervous system, psychological stress, fear of movement (kinesiophobia), physical deconditioning and metabolic changes may all contribute to symptom persistence long after inflammatory activity has been controlled.

From the perspective of the Integrated Regulatory Systems Framework (IRSF), these findings are entirely consistent with a systems-based approach to clinical reasoning. Rather than viewing pain as a direct measure of tissue inflammation, the clinician is encouraged to consider how neural regulation, immune and inflammatory regulation, metabolic function, endocrine physiology, respiratory regulation and musculoskeletal adaptation interact to influence the patient’s overall physiological resilience. Dysfunction within one regulatory system can amplify dysfunction in another, creating self-perpetuating cycles that conventional disease-centred models may fail to recognise.

The message is an important one. Successful management of chronic pain requires clinicians to move beyond asking, “Where is the inflammation?” and instead ask, “Which regulatory systems are no longer working together effectively?” It is often the answer to this second question that provides the greatest opportunity for meaningful and sustained clinical improvement.

Looking Ahead

Many of the concepts discussed in this article are explored in my forthcoming book, Clinical Reasoning for Complex Patients: An Integrated Regulatory Systems Framework (IRSF). The book sets out a practical model for understanding patients whose symptoms cannot be fully explained through a single-system or disease-based perspective.

Drawing on nearly four decades of clinical practice, the book examines how interactions between the neural, respiratory, circulatory, endocrine, metabolic, immune and musculoskeletal regulatory systems influence health, disease and recovery. Through real clinical case studies, it demonstrates how the IRSF can help clinicians move beyond symptom management towards identifying the underlying physiological drivers of complex presentations.”

The manuscript has now been completed and is entering the publication process. I look forward to sharing further details, including the publisher and release date, in due course.

Clinical Disclaimer

This article is intended for educational and informational purposes only. It does not constitute medical advice and should not replace individual consultation with a qualified healthcare professional.

 

Sleep, Fear, and Hidden Drivers of Chronic Rheumatic Pain

Manuela Callari

Medscape

LONDON — Suppress inflammation and the pain will go away. While that approach has been the dominant rule of thumb in rheumatology for decades, clinicians and researchers alike have in recent years pivoted to a more nuanced view of the factors that influence chronic pain. Data presented at the European Alliance of associations for rheumatology (EULAR) 2026 annual meeting further underscore how the traditional playbook leaves a massive and largely unresolved burden of chronic pain that persists long after inflammation is controlled.

“About a third of our patients still report unacceptable pain 15 years after diagnosis, despite receiving anti-inflammatory treatment,” said Zoe Rutter-Locher, MD, PhD, a rheumatologist and clinical researcher at Guy’s Hospital and King’s College London, both in London, England, speaking at the meeting.

“The greatest misconception of all, though, is when kinesiophobia, which is an irrational and debilitating fear of physical movement, rooted in the belief that motion will cause pain or reinjury, is widely misused or misconstrued as being the same as pain-related fear,” Nadia Malliou, MSc, a cognitive psychologist at the Aristotle University of Thessaloniki in Thessaloniki, Greece, and general secretary of the Axial Spondyloarthritis International Federation, told Medscape Medical News. Malliou, who presented data on the behavioral realities of axial spondyloarthritis (axSpA), said that the solution to this unresolved pain burden lies in early phenotyping and addressing the highly individualized, noninflammatory drivers of chronic symptoms.

Pain Sensitivity Persists Long After Remission 

Clinicians often fall into the trap of assuming that a patient’s pain is merely a proxy for active inflammation. In reality, the signal is highly processed in the nervous system and modulated by overlapping biological, psychological, and social factors. To bring order to this chaos, Rutter-Locher pointed to the International Association for the Study of Pain definitions that distinguish classic nociceptive pain from nociplastic pain — altered nociception that drives hypersensitivity despite no clear evidence of tissue or nerve damage.

“Fibromyalgia is that prototypical central sensitivity syndrome,” Rutter-Locher explained, citing data showing its prevalence  in patients with rheumatoid arthritis (RA) sits at 21%, nearly 10-fold higher than that in the general population. In addition, a systematic review  she led tracking over 13,000 patients found that up to 42% reported distinct pain sensitization, which was significantly associated with worse reported disease activity, profound disability, lower quality of life, and low mood.

This central sensitization is not just a late-stage byproduct of chronic wear and tear. “Contrary to my hypothesis that most people would have just inflammatory pain, I actually found that about 20%-30% of people have these features of centrally mediated pain already at diagnosis,” Rutter-Locher said. Over a two year follow-up,  baseline features of centrally mediated pain and psychological distress strongly predicted long-term persistent pain, whereas baseline inflammatory markers did not.

Sleep as a Pain Mediator 

If nociplastic processes drive residual pain, what drives nociplastic sensitivity? According to Yvonne Lee, MD, a professor of medicine and rheumatologist at the Northwestern University Feinberg School of Medicine in Chicago, a major, modifiable culprit is sleep.

Lee described sleep as the “Swiss Army knife of health.” In rheumatology, the relationship between sleep and disease is increasingly recognized as a bidirectional, vicious cycle. Recent data from the English longitudinal study of aging showed that poor sleep quality and short sleep duration are independently associated with an increased risk of developing RA, with each 1-hour reduction in sleep duration carrying a 7% higher disease risk.

For patients who already have an established diagnosis, sleep disturbances are pervasive.  In RA, insomnia affects 63%-73% of patients, whereas obstructive sleep apnea can affect up to 64% of patients, depending on measurement parameters.

While it is intuitive that joint pain disrupts a night’s sleep, Lee said the opposite is also true: Sleep deprivation directly induces pain hypersensitivity.Data from the Canadian Early Arthritis Cohort tracked over 1000 patients with newly diagnosed RA to see what baseline variables predicted remaining in a state of unacceptable pain 12 months later. While baseline pain intensity was a predictor, sleep problems were also significantly and independently predictive of persistent pain in a clear dose-response relationship.

Using objective wrist actigraphy, her team found that wake after sleep onset and low sleep efficiency directly correlate with a higher temporal summation of pain (pain facilitation). “Sleep problems are not just a consequence of pain; they can lead to increased pain sensitivity and greater and more widespread pain,” Lee said.

Lee said that optimizing targeted biological or synthetic therapy to control baseline nocturnal joint inflammation, systematically tapering down sleep-disrupting glucocorticoids such as prednisone to under 7.5 mg daily, and treating concurrent depression might break this cycle. For directly managing insomnia, she strongly advocated for cognitive-behavioral therapy for insomnia, which utilizes behavioral strategies such as sleep restriction and stimulus control via digital apps if local specialists are unavailable.

Kinesiophobia: The ‘Mother of All Evil’

Nowhere is the complex intersection of pain, psychology, and behavior more evident than in axSpA. Deniz Bayraktar, a physiotherapist and researcher at the University of Iceland in Reykjavik, Iceland, introduced a major behavioral barrier to management: kinesiophobia, or the fear of movement.

“From a physiotherapist’s perspective, the mother of all evil is actually kinesiophobia,” Bayraktar said. When patients experience pain upon moving, they instinctively stop. This physical inactivity triggers a cascade: a positive energy balance, accumulation of visceral fat, and infiltration of macrophages into adipose tissue, which then secrete proinflammatory cytokines that compound the systemic inflammation already driving the arthritis.

To overcome this phobia, Bayraktar said that simply telling a fearful patient to exercise is rarely effective. Instead, clinicians must use complementary strategies to lower the barrier to movement. “[In] my experience as a physiotherapist, I always try to distract the patients from that fear,” Bayraktar said, suggesting gamification, virtual reality, or shifting to an inherently safer environment such as a heated pool for aquatic therapy. Also, combining movement with pain science education greatly improves the efficacy of interventions.

Malliou said that clinicians frequently misinterpret these deep-seated fears. “Clinicians approach kinesiophobia merely as reluctance or nonadherence to their suggestions. They could even propose escalation of exercise or suggest to patients that they need to ‘push through pain.’ What they might be missing when suggesting that is that persistent pain might not be inflammatory but neuropathic or nociplastic,” she warned.

“Avoidance is not equal to nonadherence,” she said.

The Sweet Spot

Alexandros Mitropoulos, PhD, a clinical exercise physiologist and research fellow at Sheffield Hallam University in Sheffield, England, said that a vast array of modalities, from aerobic protocols and high-intensity interval training to Pilates and yoga, all demonstrate robust, clinically meaningful reductions in axSpA disease activity, fatigue, and pain.

However, the panel agreed that trying to enforce highly rigid, intensive exercise or lifestyle overhauls often backfires, causing overwhelmed patients to drop out entirely. Rather than treating these modalities as optional extras, they must be seamlessly integrated with targeted therapeutics to tackle the remaining pain burden.

“The best exercise program is the one that we can maintain for the long term,” Mitropoulos said. Small, consistent behavioral steps matter far more than clinical perfection, he said. In the clinic, this translates to shifting the conversation away from a demanding directive to “move more” and instead guiding patients to “move in a way that feels safe and best fits you.”

The experts cited in this article had no relevant disclosures.

Manuela Callari is a freelance science journalist specializing in human and planetary health. Her work has been published in The Medical Republic, Rare Disease Advisor, The Guardian, MIT Technology Review, and others.