Obesity and Chronic Pain. Non-Obvious Facts
Obesity and Chronic Pain. Three Mechanisms of Connection
Dr. Nehama Milson Ben-Gershon
The connection between excess weight and chronic pain is usually explained simply. More weight means more load on the joints, hence pain. And there is undoubtedly some truth to this. The mechanical component accounts, by various estimates, for fifteen to twenty-five percent of the total contribution to the pain syndrome. The rest is distributed between two other mechanisms, and it is these that explain why pain in obesity often localizes where there is no mechanical load, and why it does not resolve with moderate weight loss.
biomechanics
systemic inflammation
neuroinflammation
Mechanism One
Biomechanics, Obvious and Not So Obvious
The obvious part. Each additional kilogram of body weight increases the axial load on the knee joint during walking by about three to four times, and when climbing stairs by six to seven times. This has been confirmed by biomechanical studies using force platforms since the 1990s. Messier et al., in studies by the Wake Forest group, showed that losing one kilogram reduces the load on the knee with each step by approximately four kilograms.
The less obvious part, and much more important. Excess weight changes not only the load but also the movement pattern. Gait changes, the pelvic tilt angle, lumbar curvature, and the position of the head relative to the shoulder girdle all shift. Compensatory musculature is activated, which is not designed for this work. Chronically overloaded myofascial zones, trigger points, and local spasms arise. Pain forms not in the joint itself but in the soft tissues around it, often where weight should not matter. In the neck, jaw muscles, wrists.
Mechanism Two
Adipose Tissue as an Endocrine Organ
Until the late 1990s, adipose tissue was considered a passive triglyceride storage. The discovery of leptin in 1994 and subsequent work identifying other adipokines overturned this view. Today, adipose tissue, especially visceral fat, is classified as a full-fledged endocrine and immune organ.
Visceral adipocytes and infiltrating macrophages in obesity secrete proinflammatory cytokines. Key players:
TNF-α
interleukin-1β
leptin ↑
resistin
adiponectin ↓
The result is chronic low-grade systemic inflammation, referred to in the literature as metaflammation or low-grade chronic inflammation. C-reactive protein in patients with visceral obesity is chronically elevated, often two to four times above normal, without an apparent focus of infection.
Mechanism Three
Neuroinflammation and Central Sensitization
Proinflammatory cytokines from the systemic circulation penetrate the blood-brain barrier, especially when the barrier itself becomes more permeable due to chronic inflammation, which is also proven. Once in the central nervous system, they activate microglia, the resident immune cells of the brain and spinal cord.
Activated microglia shift from a resting state to a proinflammatory M1 phenotype, begin producing cytokines, glutamate, and reactive oxygen species themselves. This state is called neuroinflammation.
Neuroinflammation leads to functional remodeling of pain pathways. In the dorsal horns of the spinal cord, neurons become hyperexcitable. The activation threshold decreases, the response to a standard stimulus intensifies, receptive fields expand. This phenomenon, central sensitization, was well described by Clifford Woolf and his school since the 1980s and is now considered a key mechanism in the transition from acute to chronic pain.
In a patient with obesity and neuroinflammation, central sensitization develops without acute injury, gradually, against the background of years of smoldering systemic inflammation. Clinically, this presents as diffuse pain of unclear localization, hyperalgesia, allodynia, poor sleep, fatigue, cognitive impairments. A picture very similar to fibromyalgia, and not coincidentally.
A Closed System of Excess Weight and Pain
These three mechanisms mutually reinforce each other. Pain limits physical activity. Reduced activity worsens visceral fat accumulation. Visceral fat increases systemic inflammation. Systemic inflammation sustains neuroinflammation. Neuroinflammation reduces sleep quality. Sleep deprivation, in turn, increases proinflammatory cytokine levels and lowers the pain threshold. Chronic pain and poor sleep together disrupt appetite regulation through the leptin-ghrelin system, enhancing overeating.
Feedback Loop
pain → decreased activity → increased visceral fat → systemic inflammation → neuroinflammation → poor sleep → increased cytokines → lowered pain threshold → appetite dysregulation → overeating → back to start
This is not a vicious circle with a single entry point; it is a network of connections, and breaking it at one point is often insufficient. Therefore, the standard recommendation “lose weight, and it will pass” usually does not work or works slowly and poorly. Weight loss without addressing the inflammatory and neuroinflammatory components provides a partial and unstable effect.
Clinical Practice Implications
Chronic pain in a patient with obesity should not be considered simply a consequence of mechanical load. It is a multicomponent condition requiring intervention at least at three levels.
Treating this as one diagnosis, not as two adjacent ones, is the only approach that provides a sustainable result for both problems, excess weight and chronic pain.
