For decades, fibromyalgia has stood as one of medicine’s most perplexing enigmas. Millions of people have endured persistent pain, disabling fatigue, and, all too often, the misunderstanding of those unable to grasp a condition as real as it is difficult to explain. Today, that landscape is beginning to shift.
The lecture delivered by Professor Jesús A. Fernández Tresguerres at the Real Academia Nacional de Medicina de España (Ordinary Scientific Session, July 14th, 2026) offers an integrative biological explanation that deepens our understanding of the origins of fibromyalgia and opens a promising line of therapeutic research focused on restoring mitochondrial function and cellular energy metabolism.
This perspective brings encouraging news for those living with the disease and for their families. Research is no longer directed solely at alleviating symptoms; it now ventures into the cellular mechanisms that may lie at the very root of the disorder.
The origin of the problem: Fibromyalgia is no longer an inscrutable mystery. The findings presented by Professor Fernández Tresguerres place one of the fundamental processes of the disease within the mitochondria—the small organelles responsible for producing the energy required by all our cells.
When mitochondria lose efficiency, ATP production—the cell’s primary energy source—declines. This energy deficit triggers a cascade of events that ultimately affects the nervous system and promotes the appearance of the disease’s characteristic symptoms.
Among them:
- Intense, persistent fatigue that scarcely improves with rest.
- Generalized musculoskeletal pain, stemming from heightened sensitivity of neural pathways.
- Cognitive fog, with difficulties in concentration, memory, and sustained attention.
A key piece of the puzzle: Reduced cellular energy favors the activation of the NLRP3 inflammasome, a molecular complex involved in the body’s inflammatory response.
When it remains chronically activated, it sustains a state of low grade inflammation that contributes to the sensitization of the central nervous system and helps explain the persistence of pain and fatigue.
The strength of this perspective lies in integrating processes that previously appeared unrelated. Mitochondrial dysfunction, inflammation, and altered energy metabolism become components of a single biological mechanism.
Restoring cellular function: Building on this knowledge, Professor Fernández Tresguerres proposes an innovative therapeutic approach based on the complementary action of three compounds:
- Metformin, at low doses, to activate the AMPK pathway and modulate inflammasome activity.
- Coenzyme Q10, to enhance mitochondrial function and reduce oxidative stress.
- Melatonin, to support circadian rhythm synchronization and protect mitochondria through its potent antioxidant effects.
Guiding scheme
| Compound | Suggested daily dose | Main objective |
|---|---|---|
| Metformin | 500 mg | Activation of the AMPK pathway and modulation of neuroinflammation |
| Coenzyme Q10 | 300–400 mg | Restoration of mitochondrial function and improvement of ATP production |
| Melatonin | Individualized dose | Regulation of circadian rhythm and mitochondrial protection |
This approach always requires individualized medical assessment and follow up, as fibromyalgia varies greatly among patients.
One of the most original aspects of this proposal is the use of metformin at doses below those typically prescribed for type 2 diabetes. Its purpose is not to reduce blood glucose, but to activate AMPK—one of the principal regulators of cellular energy metabolism. Its activation supports natural mechanisms of cellular repair and recycling, improves mitochondrial function, and attenuates inflammatory responses.
Coenzyme Q10 complements this action by optimizing the mitochondrial respiratory chain and promoting more efficient ATP production. According to the data presented, initial benefits usually appear after about six weeks of continuous treatment, while maximum response requires several months.
Knowledge restores hope: The history of medicine demonstrates that every major advance commences when a mystery finds its explanation. Fibromyalgia still raises many questions, but today we understand far better the mechanisms that may give rise to it, and we have new strategies to attempt to correct them. Professor Fernández Tresguerres’s lecture represents an important step in that direction. It is not yet the definitive solution to fibromyalgia, but it offers a solid pathophysiological model and a coherent therapeutic strategy that merit confirmation through increasingly extensive clinical trials.
For patients and their families, this shift in perspective is profoundly valuable. Understanding that pain has an identifiable biological basis helps dispel misunderstanding and restores confidence in scientific research.
The strongest hope is never born of promises, but of knowledge. And each discovery brings us a little closer to the moment when living with fibromyalgia will no longer inevitably mean living with suffering. When science illuminates the origin of pain, it also illuminates the path toward hope.
An important clarification: Every person with fibromyalgia presents unique characteristics. For this reason, any treatment must be prescribed and supervised by a physician. This article aims to disseminate the scientific advances presented at the Royal National Academy of Medicine of Spain and to contribute to a better understanding of the disease.
Today’s research is tomorrow’s therapy