Juan M Guerrero-González
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Juan M Guerrero-González has a total of 14 co-authors. Here are the top co-authors by number of shared publications:
Alberto Soriano-Maldonado
Department of Education, Faculty of Education Sciences, and SPORT Research Group (CTS-1024) , CERNEP Research Center, University of Almería, Almería, Spain
1 shared publication- Blanca Gavilán-Carrera
Sport and Health University Research Institute (IMUDS), University of Granada, Granada, Spain
1 shared publication Daniel Camiletti-Moirón
Department of Physical Education, Faculty of Education Sciences, University of Cádiz , Cádiz
1 shared publicationDiego Salazar-Tortosa
Department of Ecology and Evolutionary Biology, University of Arizona , Tucson, AZ, USA
1 shared publication- Fernando Estévez-López
Department of Education, Faculty of Education Sciences, CIBIS Research Centre (Centro de Investigación para el Bienestar y la Inclusión Social), and SPORT Research Group (CTS-1024), University of Almería, Almería, Spain
1 shared publication Inmaculada C Álvarez-Gallardo
Department of Physical Education, Faculty of Education Sciences, University of Cádiz , Cádiz
1 shared publication
Latest Publications
- Open Access
- 7 December 2021
- Published by Oxford University Press (OUP) in Rheumatology
- Vol. 61 (8) , 3180-3191
Interplay between genetics and lifestyle on pain susceptibility in women with fibromyalgia: the al-Ándalus project
It is widely acknowledged that the experience of pain is promoted by both genetic susceptibility and environmental factors such as engaging in physical activity (PA), and that pain-related cognitions are also important. Thus, the purpose of the present study was to test the association of 64 polymorphisms (34 candidate genes) and the gene–gene, gene–PA and gene–sedentary behaviour interactions with pain and pain-related cognitions in women with FM. Saliva samples from 274 women with FM [mean (s.d.) age 51.7 (7.7) years] were collected for extracting DNA. We measured PA and sedentary behaviour by accelerometers for a week, pain with algometry and questionnaires, and pain-related cognitions with questionnaires. To assess the robustness of the results, a meta-analysis was also performed. The rs6311 and rs6313 polymorphisms (5-hydroxytryptamine receptor 2A, HTR2A) were individually related to algometer scores. The interaction of rs4818 (catechol-O-methyltransferase, COMT) and rs1799971 (opioid receptor μ gene, OPRM1) was related to pain catastrophizing. Five gene–behaviour interactions were significant: the interactions of sedentary behaviour with rs1383914 (adrenoceptor alpha 1A, ADRA1A), rs6860 (charged multivesicular body protein 1A, CHMP1A), rs4680 (COMT), rs165599 (COMT) and rs12994338 (SCN9A) on bodily pain subscale of the Short Form 36. Furthermore, the meta-analysis showed an association between rs4680 (COMT) and severity of FM symptoms (codominant model, P-value 0.032). The HTR2A gene (individually), COMT and OPRM1 gene–gene interaction, and the interactions of sedentary behaviour with ADRA1A, CHMP1A, COMT and SCN9A genes were associated with pain-related outcomes. Collectively, findings from the present study indicate a modest contribution of genetics and gene–sedentary behaviour interaction to pain and pain catastrophizing in women with FM. Future research should examine whether reducing sedentary behaviour is particularly beneficial for reducing pain in women with genetic susceptibility to pain.
- 7 December 2021
- Published by Oxford University Press (OUP) in Rheumatology
- Vol. 61 (8) , 3180-3191
Open AccessInterplay between genetics and lifestyle on pain susceptibility in women with fibromyalgia: the al-Ándalus project
It is widely acknowledged that the experience of pain is promoted by both genetic susceptibility and environmental factors such as engaging in physical activity (PA), and that pain-related cognitions are also important. Thus, the purpose of the present study was to test the association of 64 polymorphisms (34 candidate genes) and the gene–gene, gene–PA and gene–sedentary behaviour interactions with pain and pain-related cognitions in women with FM. Saliva samples from 274 women with FM [mean (s.d.) age 51.7 (7.7) years] were collected for extracting DNA. We measured PA and sedentary behaviour by accelerometers for a week, pain with algometry and questionnaires, and pain-related cognitions with questionnaires. To assess the robustness of the results, a meta-analysis was also performed. The rs6311 and rs6313 polymorphisms (5-hydroxytryptamine receptor 2A, HTR2A) were individually related to algometer scores. The interaction of rs4818 (catechol-O-methyltransferase, COMT) and rs1799971 (opioid receptor μ gene, OPRM1) was related to pain catastrophizing. Five gene–behaviour interactions were significant: the interactions of sedentary behaviour with rs1383914 (adrenoceptor alpha 1A, ADRA1A), rs6860 (charged multivesicular body protein 1A, CHMP1A), rs4680 (COMT), rs165599 (COMT) and rs12994338 (SCN9A) on bodily pain subscale of the Short Form 36. Furthermore, the meta-analysis showed an association between rs4680 (COMT) and severity of FM symptoms (codominant model, P-value 0.032). The HTR2A gene (individually), COMT and OPRM1 gene–gene interaction, and the interactions of sedentary behaviour with ADRA1A, CHMP1A, COMT and SCN9A genes were associated with pain-related outcomes. Collectively, findings from the present study indicate a modest contribution of genetics and gene–sedentary behaviour interaction to pain and pain catastrophizing in women with FM. Future research should examine whether reducing sedentary behaviour is particularly beneficial for reducing pain in women with genetic susceptibility to pain.