Margot J Overman1, Neil Pendleton2, Terence W O'Neill3, Gyorgy Bartfai4, Felipe F Casanueva5, Gianni Forti6, Giulia Rastrelli7, Aleksander Giwercman8, Thang S Han9, Ilpo T Huhtaniemi10, Krzysztof Kula11, Michael E J Lean12, Margus Punab13, David M Lee14, Elon S Correa15, Tomas Ahern15, Michaël R Laurent16, Sabine M P Verschueren17, Leen Antonio18, Evelien Gielen19, Martin K Rutter20, Dirk Vanderschueren21, Frederick C W Wu15, Jos Tournoy19. 1. Gerontology and Geriatrics, Department of Clinical and Experimental Medicine, KU Leuven, Leuven, Belgium. Electronic address: margot.overman@ndcn.ox.ac.uk. 2. Clinical & Cognitive Neurosciences, Institute of Brain, Behaviour and Mental Healthy, The University of Manchester, UK. 3. Arthritis Research UK Centre for Epidemiology, Institute of Inflammation and Repair, the University of Manchester, Manchester, UK; NIHR Manchester Musculoskeletal Biomedical Research Unit, Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK. 4. Department of Obstetrics, Gynaecology and Andrology, Albert Szent-György Medical University, Szeged, Hungary. 5. Department of Medicine, Instituto Salud Carlos III, Complejo Hospitalario Universitario de Santiago (CHUS), A Coruña, Spain. 6. Endocrinology Unit, University of Florence, Florence, Italy. 7. Sexual Medicine and Andrology Unit, Department of Experimental, Clinical, and Biomedical Sciences, University of Florence, Florence, Italy. 8. Reproductive Medicine Centre, Skåne University Hospital, University of Lund, Lund, Sweden. 9. Department of Endocrinology, Ashford and St Peter's NHS Foundation Trust, Chertsey, UK. 10. Department of Surgery and Cancer, Imperial College London, Hammersmith Campus, London, UK. 11. Department of Andrology and Reproductive Endocrinology, Medical University of Łódź, Łódź, Poland. 12. Department of Human Nutrition, University of Glasgow, Glasgow, UK. 13. Andrology Unit, United Laboratories of Tartu University Clinics, Tartu, Estonia. 14. School of Social Sciences, Cathie Marsh Institute for Social Research, The University of Manchester, Manchester, UK. 15. Andrology Research Unit, The University of Manchester, Manchester, UK. 16. Gerontology and Geriatrics, Department of Clinical and Experimental Medicine, KU Leuven, Leuven, Belgium; Laboratory of Molecular Endocrinology, KU Leuven, Heverlee, Belgium. 17. Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium. 18. Department of Andrology and Endocrinology, KU Leuven, Leuven, Belgium; Department of Clinical and Experimental Medicine, KU Leuven, Leuven, Belgium. 19. Gerontology and Geriatrics, Department of Clinical and Experimental Medicine, KU Leuven, Leuven, Belgium; Geriatric Medicine, University Hospitals Leuven, Leuven, Belgium. 20. The Endocrinology and Diabetes, Research Group, Faculty of Medical and Human Sciences, Institute of Human Development, University of Manchester, Manchester, UK; Manchester Diabetes Centre, Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK. 21. Department of Andrology and Endocrinology, KU Leuven, Leuven, Belgium.
Abstract
OBJECTIVE: Previous research has indicated that components of the metabolic syndrome (MetS), such as hyperglycemia and hypertension, are negatively associated with cognition. However, evidence that MetS itself is related to cognitive performance has been inconsistent. This longitudinal study investigates whether MetS or its components affect cognitive decline in aging men and whether any interaction with inflammation exists. METHODS: Over a mean of 4.4 years (SD ± 0.3), men aged 40-79 years from the multicenter European Male Ageing Study were recruited. Cognitive functioning was assessed using the Rey-Osterrieth Complex Figure (ROCF), the Camden Topographical Recognition Memory (CTRM) task, and the Digit Symbol Substitution Test (DSST). High-sensitivity C-reactive protein (hs-CRP) levels were measured using a chemiluminescent immunometric assay. RESULTS: Overall, 1,913 participants contributed data to the ROCF analyses and 1,965 subjects contributed to the CTRM and DSST analyses. In multiple regression models the presence of baseline MetS was not associated with cognitive decline over time (p > 0.05). However, logistic ordinal regressions indicated that high glucose levels were related to a greater risk of decline on the ROCF Copy (β = -0.42, p < 0.05) and the DSST (β = -0.39, p < 0.001). There was neither a main effect of hs-CRP levels nor an interaction effect of hs-CRP and MetS at baseline on cognitive decline. CONCLUSION: No evidence was found for a relationship between MetS or inflammation and cognitive decline in this sample of aging men. However, glycemia was negatively associated with visuoconstructional abilities and processing speed.
OBJECTIVE: Previous research has indicated that components of the metabolic syndrome (MetS), such as hyperglycemia and hypertension, are negatively associated with cognition. However, evidence that MetS itself is related to cognitive performance has been inconsistent. This longitudinal study investigates whether MetS or its components affect cognitive decline in aging men and whether any interaction with inflammation exists. METHODS: Over a mean of 4.4 years (SD ± 0.3), men aged 40-79 years from the multicenter European Male Ageing Study were recruited. Cognitive functioning was assessed using the Rey-Osterrieth Complex Figure (ROCF), the Camden Topographical Recognition Memory (CTRM) task, and the Digit Symbol Substitution Test (DSST). High-sensitivity C-reactive protein (hs-CRP) levels were measured using a chemiluminescent immunometric assay. RESULTS: Overall, 1,913 participants contributed data to the ROCF analyses and 1,965 subjects contributed to the CTRM and DSST analyses. In multiple regression models the presence of baseline MetS was not associated with cognitive decline over time (p > 0.05). However, logistic ordinal regressions indicated that high glucose levels were related to a greater risk of decline on the ROCF Copy (β = -0.42, p < 0.05) and the DSST (β = -0.39, p < 0.001). There was neither a main effect of hs-CRP levels nor an interaction effect of hs-CRP and MetS at baseline on cognitive decline. CONCLUSION: No evidence was found for a relationship between MetS or inflammation and cognitive decline in this sample of aging men. However, glycemia was negatively associated with visuoconstructional abilities and processing speed.
Authors: Richard D Semba; Marta Gonzalez-Freire; Ruin Moaddel; Kai Sun; Elisa Fabbri; Pingbo Zhang; Olga D Carlson; Mohammed Khadeer; Chee W Chia; Norman Salem; Luigi Ferrucci Journal: J Clin Endocrinol Metab Date: 2018-09-01 Impact factor: 5.958
Authors: Jigar Gosalia; Polly S Montgomery; Shangming Zhang; William A Pomilla; Ming Wang; Menglu Liang; Anna Csiszar; Zoltan Ungvari; Andriy Yabluchanskiy; David N Proctor; Andrew W Gardner Journal: Geroscience Date: 2022-08-18 Impact factor: 7.581
Authors: Aditi Gupta; Jonathan D Mahnken; David K Johnson; Tashra S Thomas; Dipti Subramaniam; Tyler Polshak; Imran Gani; G John Chen; Jeffrey M Burns; Mark J Sarnak Journal: BMC Nephrol Date: 2017-05-12 Impact factor: 2.388