For years we have been combing the scientific literature in search of data that could point us toward a better diagnostic assessment of fibromyalgia and potential therapies for it. A disease that, after years of research, still remains essentially unknown. We do not know its causes, we struggle to diagnose it (the diagnosis is almost always made after ruling out other inflammatory or rheumatic diseases) and we do not have therapies capable of solving the underlying problem. So much so that, even today, fibromyalgia is not recognized as an autonomous nosological entity, with major implications for the patients who suffer from it.
In this context, identifying one or more biological mechanisms underlying the disease could allow us to make giant strides. The excellent Roberta Gualtierotti of the Policlinico di Milano, together with other colleagues including the pharmacologist Massimiliano Ruscica, has completed a study on fibromyalgia patients in which the function of the mitochondria was analyzed with a very sophisticated technique.
What mitochondria are
Mitochondria are our power plants. When they stop working, the entire cellular system goes into crisis. And that is not all: a non-functioning mitochondrion becomes a burden for the cell because it triggers inflammatory processes that end up affecting the whole tissue. The data from the study, still considered preliminary although very convincing, say that the mitochondria of fibromyalgia patients do not work as they should. The idea was in the air, but the data were lacking.
The implications of the study
If the data are confirmed, not only will we have a very useful laboratory test for diagnosing the disease, but we will also have new potential therapies in hand. Renewing mitochondria may not be so difficult. Some molecules of natural origin, above all urolithin, can help us. But so can NADNAD (Nicotinamide adenindinucleotide ) is a co-enzyme essential to the metabolism of the cell, intervening in the activity of more than 200 enzyme proteins that govern the energy process of the cell itself. With age, one becomes deficient in this co-enzyme by altering cell catabolism. boosters and other molecules that work on the energy generation cycle. We also have techniques from the world of “biohacking” that seem to work quite well, although they require further experimental evidence. Not forgetting that very similar mechanisms underlie long COVID syndrome. Perhaps this study will also provide useful information for these patients.


