In fibromyalgia, fatigue is a key symptom. Fatigue is thought to be caused by a combination of genetic predisposition and environmental factors. By looking at single nucleotide polymorphisms in 34 fibromyalgia candidate genes, gene interactions, and gene-physical activity interactions, we were able to investigate the importance of genetic vulnerability for fatigue in southern Spanish women with fibromyalgia. To research gene polymorphisms, we extracted DNA from the saliva of 276 fibromyalgia patients. Physical activity and sedentary behavior were tracked using accelerometers.
The Multidimensional Fatigue Inventory was used to measure fatigue.
We discovered that the genotype of the rs4453709 polymorphism (sodium channel protein type 9 subunit alpha, SCN9A, gene) was linked to reduced motivation (AT carriers showed the most reduced motivation) and reduced behavior using Bonferroni’s and False Discovery Rate values (AA carriers showed the lowest reduced activity).
Physically active people with the heterozygous genotype of the rs1801133 (methylene tetrahydrofolate reductase, MTHFR, gene) or rs4597545 (SCN9A gene) polymorphisms had lower fatigue scores than inactive people.
Highly sedentary carriers of the rs7607967 polymorphism (AA/GG genotype; SCN9A gene) had lower levels of activity (a dimension of fatigue) than those with lower levels of sedentary conduct.
Overall, the results of this research indicate that genetics and the gene-physical activity relationship play a minor role in fibromyalgia fatigue.
