Title : Managing neuroinflammation in fibromyalgia

Effective management of fibromyalgia requires a personalised approach to identify and modulate the systemic and neuroinflammatory drivers that contribute to symptom persistence. Current evidence indicates that chronic systemic inflammation and neuroinflammation are important contributors to fibromyalgia pathophysiology, however, their origins and clinical expression vary between individuals.

Potential risk factors may include biological contributors such as genetic polymorphisms, nutrient deficiency and gut dysbiosis; psychological contributors such as childhood trauma, adult sexual violence and comorbid depression; environmental contributors such as mycotoxins, heavy metals, biotoxins, viral illness and tick-borne disease; and lifestyle contributors such as poor diet and physical inactivity.

Key mechanisms implicated in fibromyalgia include oxidative stress, impaired mitochondrial and autonomic function, inappropriate activation of microglia and mast cells as well as peripheral and central sensitisation.

Studies have reported altered pro-inflammatory and anti-inflammatory mediators in the blood and cerebrospinal fluid of individuals with fibromyalgia, supporting an association between chronic systemic inflammation, neuroinflammation and pain initiation.

Oxidative stress can impair mitochondrial function, which may further promote microglial activation and altered glutamatergic neurotransmission, contributing to neuroinflammation, peripheral muscle pain and central pain sensitisation.

Multiple studies have reported coexisting nutrient deficiencies in patients with fibromyalgia, including ubiquinol, magnesium and vitamin D3, which may affect mitochondrial respiratory enzyme activity, microglial homeostasis and neurotransmitter production.

Mast cells are increasingly recognised as important mediators in neuroendocrine and chronic pain disorders, including fibromyalgia, because they provide a functional bridge between the immune and nervous systems. Pro-inflammatory mediators released from mast cells and sustained inappropriate mast cell activation may contribute to mast cell activation syndrome, blood–brain barrier dysregulation, microglial activation and ongoing neuroinflammation.

This presentation will outline a practical, personalised framework for addressing individual risk factors, reducing oxidative stress, supporting mitochondrial function, and modulating mast cell and microglial activation, with discussion of both oral and topical nutraceutical and pharmaceutical management options.

To be updated shortly..