Associations Between Sex Steroids and the Development of Metabolic Syndrome: A Longitudinal Study in European Men
Context:Low testosterone (T) has been associated with incident metabolic syndrome (MetS), but it remains unclear if this association is independent of sex hormone binding globulin (SHBG). Estradiol (E2) may also be associated with MetS, but few studies have investigated this.Objective:To study the a...
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| Published in | The journal of clinical endocrinology and metabolism Vol. 100; no. 4; pp. 1396 - 1404 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Oxford University Press
01.04.2015
Copyright by The Endocrine Society |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0021-972X 1945-7197 1945-7197 |
| DOI | 10.1210/jc.2014-4184 |
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| Abstract | Context:Low testosterone (T) has been associated with incident metabolic syndrome (MetS), but it remains unclear if this association is independent of sex hormone binding globulin (SHBG). Estradiol (E2) may also be associated with MetS, but few studies have investigated this.Objective:To study the association between baseline sex steroids and the development of incident MetS and to investigate the influence of SHBG, body mass index (BMI) and insulin resistance on this risk.Methods:Three thousand three hundred sixty nine community-dwelling men aged 40–79 years were recruited for participation in EMAS. MetS was defined by the updated NCEP ATP III criteria. Testosterone and E2 levels were measured by liquid and gas chromatography/mass spectrometry, respectively. Logistic regression was used to assess the association between sex steroids and incident MetS.Results:One thousand six hundred fifty one men without MetS at baseline were identified. During follow-up, 289 men developed incident MetS, while 1362 men did not develop MetS. Men with lower baseline total T levels were at higher risk for developing MetS [odds ratio (OR) = 1.72, P < .001), even after adjustment for SHBG (OR = 1.43, P = .001), BMI (OR = 1.44, P < .001) or homeostasis model assessment of insulin resistance (HOMA-IR) (OR = 1.64, P < .001). E2 was not associated with development of MetS (OR = 1.04; P = .56). However, a lower E2/T ratio was associated with a lower risk of incident MetS (OR = 0.38; P < .001), even after adjustment for SHBG (OR = 0.48; P < .001), BMI (OR = 0.60; P = .001) or HOMA-IR (OR = 0.41; P < .001).Conclusions:In men, lower T levels, but not E2, are linked with an increased risk of developing MetS, independent of SHBG, BMI or insulin resistance. A lower E2/T ratio may be protective against developing MetS. |
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| AbstractList | Low testosterone (T) has been associated with incident metabolic syndrome (MetS), but it remains unclear if this association is independent of sex hormone binding globulin (SHBG). Estradiol (E2) may also be associated with MetS, but few studies have investigated this.CONTEXTLow testosterone (T) has been associated with incident metabolic syndrome (MetS), but it remains unclear if this association is independent of sex hormone binding globulin (SHBG). Estradiol (E2) may also be associated with MetS, but few studies have investigated this.To study the association between baseline sex steroids and the development of incident MetS and to investigate the influence of SHBG, body mass index (BMI) and insulin resistance on this risk.OBJECTIVETo study the association between baseline sex steroids and the development of incident MetS and to investigate the influence of SHBG, body mass index (BMI) and insulin resistance on this risk.Three thousand three hundred sixty nine community-dwelling men aged 40-79 years were recruited for participation in EMAS. MetS was defined by the updated NCEP ATP III criteria. Testosterone and E2 levels were measured by liquid and gas chromatography/mass spectrometry, respectively. Logistic regression was used to assess the association between sex steroids and incident MetS.METHODSThree thousand three hundred sixty nine community-dwelling men aged 40-79 years were recruited for participation in EMAS. MetS was defined by the updated NCEP ATP III criteria. Testosterone and E2 levels were measured by liquid and gas chromatography/mass spectrometry, respectively. Logistic regression was used to assess the association between sex steroids and incident MetS.One thousand six hundred fifty one men without MetS at baseline were identified. During follow-up, 289 men developed incident MetS, while 1362 men did not develop MetS. Men with lower baseline total T levels were at higher risk for developing MetS [odds ratio (OR) = 1.72, P < .001), even after adjustment for SHBG (OR = 1.43, P = .001), BMI (OR = 1.44, P < .001) or homeostasis model assessment of insulin resistance (HOMA-IR) (OR = 1.64, P < .001). E2 was not associated with development of MetS (OR = 1.04; P = .56). However, a lower E2/T ratio was associated with a lower risk of incident MetS (OR = 0.38; P < .001), even after adjustment for SHBG (OR = 0.48; P < .001), BMI (OR = 0.60; P = .001) or HOMA-IR (OR = 0.41; P < .001).RESULTSOne thousand six hundred fifty one men without MetS at baseline were identified. During follow-up, 289 men developed incident MetS, while 1362 men did not develop MetS. Men with lower baseline total T levels were at higher risk for developing MetS [odds ratio (OR) = 1.72, P < .001), even after adjustment for SHBG (OR = 1.43, P = .001), BMI (OR = 1.44, P < .001) or homeostasis model assessment of insulin resistance (HOMA-IR) (OR = 1.64, P < .001). E2 was not associated with development of MetS (OR = 1.04; P = .56). However, a lower E2/T ratio was associated with a lower risk of incident MetS (OR = 0.38; P < .001), even after adjustment for SHBG (OR = 0.48; P < .001), BMI (OR = 0.60; P = .001) or HOMA-IR (OR = 0.41; P < .001).In men, lower T levels, but not E2, are linked with an increased risk of developing MetS, independent of SHBG, BMI or insulin resistance. A lower E2/T ratio may be protective against developing MetS.CONCLUSIONSIn men, lower T levels, but not E2, are linked with an increased risk of developing MetS, independent of SHBG, BMI or insulin resistance. A lower E2/T ratio may be protective against developing MetS. CONTEXT:Low testosterone (T) has been associated with incident metabolic syndrome (MetS), but it remains unclear if this association is independent of sex hormone binding globulin (SHBG). Estradiol (E2) may also be associated with MetS, but few studies have investigated this. OBJECTIVE:To study the association between baseline sex steroids and the development of incident MetS and to investigate the influence of SHBG, body mass index (BMI) and insulin resistance on this risk. METHODS:Three thousand three hundred sixty nine community-dwelling men aged 40–79 years were recruited for participation in EMAS. MetS was defined by the updated NCEP ATP III criteria. Testosterone and E2 levels were measured by liquid and gas chromatography/mass spectrometry, respectively. Logistic regression was used to assess the association between sex steroids and incident MetS. RESULTS:One thousand six hundred fifty one men without MetS at baseline were identified. During follow-up, 289 men developed incident MetS, while 1362 men did not develop MetS. Men with lower baseline total T levels were at higher risk for developing MetS [odds ratio (OR) = 1.72, P < .001), even after adjustment for SHBG (OR = 1.43, P = .001), BMI (OR = 1.44, P < .001) or homeostasis model assessment of insulin resistance (HOMA-IR) (OR = 1.64, P < .001). E2 was not associated with development of MetS (OR = 1.04; P = .56). However, a lower E2/T ratio was associated with a lower risk of incident MetS (OR = 0.38; P < .001), even after adjustment for SHBG (OR = 0.48; P < .001), BMI (OR = 0.60; P = .001) or HOMA-IR (OR = 0.41; P < .001). CONCLUSIONS:In men, lower T levels, but not E2, are linked with an increased risk of developing MetS, independent of SHBG, BMI or insulin resistance. A lower E2/T ratio may be protective against developing MetS. Context:Low testosterone (T) has been associated with incident metabolic syndrome (MetS), but it remains unclear if this association is independent of sex hormone binding globulin (SHBG). Estradiol (E2) may also be associated with MetS, but few studies have investigated this.Objective:To study the association between baseline sex steroids and the development of incident MetS and to investigate the influence of SHBG, body mass index (BMI) and insulin resistance on this risk.Methods:Three thousand three hundred sixty nine community-dwelling men aged 40–79 years were recruited for participation in EMAS. MetS was defined by the updated NCEP ATP III criteria. Testosterone and E2 levels were measured by liquid and gas chromatography/mass spectrometry, respectively. Logistic regression was used to assess the association between sex steroids and incident MetS.Results:One thousand six hundred fifty one men without MetS at baseline were identified. During follow-up, 289 men developed incident MetS, while 1362 men did not develop MetS. Men with lower baseline total T levels were at higher risk for developing MetS [odds ratio (OR) = 1.72, P < .001), even after adjustment for SHBG (OR = 1.43, P = .001), BMI (OR = 1.44, P < .001) or homeostasis model assessment of insulin resistance (HOMA-IR) (OR = 1.64, P < .001). E2 was not associated with development of MetS (OR = 1.04; P = .56). However, a lower E2/T ratio was associated with a lower risk of incident MetS (OR = 0.38; P < .001), even after adjustment for SHBG (OR = 0.48; P < .001), BMI (OR = 0.60; P = .001) or HOMA-IR (OR = 0.41; P < .001).Conclusions:In men, lower T levels, but not E2, are linked with an increased risk of developing MetS, independent of SHBG, BMI or insulin resistance. A lower E2/T ratio may be protective against developing MetS. Context: Low testosterone (T) has been associated with incident metabolic syndrome (MetS), but it remains unclear if this association is independent of sex hormone binding globulin (SHBG). Estradiol (E2) may also be associated with MetS, but few studies have investigated this. Objective: To study the association between baseline sex steroids and the development of incident MetS and to investigate the influence of SHBG, body mass index (BMI) and insulin resistance on this risk. Methods: Three thousand three hundred sixty nine community-dwelling men aged 40-79 years were recruited for participation in EMAS. MetS was defined by the updated NCEP ATP III criteria. Testosterone and E2 levels were measured by liquid and gas chromatography/mass spectrometry, respectively. Logistic regression was used to assess the association between sex steroids and incident MetS. Results: One thousand six hundred fifty one men without MetS at baseline were identified. During follow-up, 289 men developed incident MetS, while 1362 men did not develop MetS. Men with lower baseline total T levels were at higher risk for developing MetS [odds ratio (OR) = 1.72, P < .001), even after adjustment for SHBG (OR = 1.43, P < .001), BMI (OR = 1.44, P < .001) or homeostasis model assessment of insulin resistance (HOMA-IR) (OR = 1.64, P < .001). E2 was not associated with development of MetS (OR = 1.04; P = .56). However, a lower E2/T ratio was associated with a lower risk of incident MetS (OR = 0.38; P < .001), even after adjustment for SHBG (OR = 0.48; P < .001), BMI (OR = 0.60; P = .001) or HOMA-IR (OR = 0.41; P < .001). Conclusions: Inmen, lower Tlevels, but not E2, are linked with an increased risk of developing MetS, independent of SHBG, BMI or insulin resistance. A lower E2/T ratio may be protective against developing MetS. Low testosterone (T) has been associated with incident metabolic syndrome (MetS), but it remains unclear if this association is independent of sex hormone binding globulin (SHBG). Estradiol (E2) may also be associated with MetS, but few studies have investigated this. To study the association between baseline sex steroids and the development of incident MetS and to investigate the influence of SHBG, body mass index (BMI) and insulin resistance on this risk. Three thousand three hundred sixty nine community-dwelling men aged 40-79 years were recruited for participation in EMAS. MetS was defined by the updated NCEP ATP III criteria. Testosterone and E2 levels were measured by liquid and gas chromatography/mass spectrometry, respectively. Logistic regression was used to assess the association between sex steroids and incident MetS. One thousand six hundred fifty one men without MetS at baseline were identified. During follow-up, 289 men developed incident MetS, while 1362 men did not develop MetS. Men with lower baseline total T levels were at higher risk for developing MetS [odds ratio (OR) = 1.72, P < .001), even after adjustment for SHBG (OR = 1.43, P = .001), BMI (OR = 1.44, P < .001) or homeostasis model assessment of insulin resistance (HOMA-IR) (OR = 1.64, P < .001). E2 was not associated with development of MetS (OR = 1.04; P = .56). However, a lower E2/T ratio was associated with a lower risk of incident MetS (OR = 0.38; P < .001), even after adjustment for SHBG (OR = 0.48; P < .001), BMI (OR = 0.60; P = .001) or HOMA-IR (OR = 0.41; P < .001). In men, lower T levels, but not E2, are linked with an increased risk of developing MetS, independent of SHBG, BMI or insulin resistance. A lower E2/T ratio may be protective against developing MetS. |
| Author | Kula, Krzysztof Keevil, Brian G. O'Neill, Terence W. Finn, Joseph D. Lean, Michael E. J. Carter, Emma L. Claessens, Frank Antonio, Leen Rutter, Martin K. Huhtaniemi, Ilpo T. Casanueva, Felipe F. Laurent, Michaël R. Giwercman, Aleksander Pye, Stephen R. Vanderschueren, Dirk Han, Thang S. Wu, Frederick C. W. Pendleton, Neil Decallonne, Brigitte Rastrelli, Giulia Forti, Gianni Bartfai, Gyorgy Punab, Margus |
| AuthorAffiliation | Department of Clinical and Experimental Medicine (L.A., B.D., D.V.), KU Leuven, Laboratory of Clinical and Experimental Endocrinology, B-3000 Leuven, Belgium; Department of Cellular and Molecular Medicine (L.A., M.R.L., F.C.), KU Leuven, Laboratory of Molecular Endocrinology, B-3000 Leuven, Belgium; Department of Endocrinology (L.A., B.D., D.V.), University Hospitals Leuven, B-3000 Leuven, Belgium; Andrology Research Unit (F.C.W.W., E.L.C., J.D.F., M.K.R.), Endocrinology and Diabetes Research Group, Institute of Human Development, Faculty of Medical and Human Sciences, The University of Manchester, Manchester M13 9WL, United Kingdom; Manchester Royal Infirmary (F.C.W.W.), Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester M13 9WL, United Kingdom; Arthritis Research UK Centre of Epidemiology (T.W.O., S.R.P.), The University of Manchester, Manchester Academic Health Science Centre, Manchester M13 9WL, United Kingdom; NIHR M |
| AuthorAffiliation_xml | – name: Department of Clinical and Experimental Medicine (L.A., B.D., D.V.), KU Leuven, Laboratory of Clinical and Experimental Endocrinology, B-3000 Leuven, Belgium; Department of Cellular and Molecular Medicine (L.A., M.R.L., F.C.), KU Leuven, Laboratory of Molecular Endocrinology, B-3000 Leuven, Belgium; Department of Endocrinology (L.A., B.D., D.V.), University Hospitals Leuven, B-3000 Leuven, Belgium; Andrology Research Unit (F.C.W.W., E.L.C., J.D.F., M.K.R.), Endocrinology and Diabetes Research Group, Institute of Human Development, Faculty of Medical and Human Sciences, The University of Manchester, Manchester M13 9WL, United Kingdom; Manchester Royal Infirmary (F.C.W.W.), Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester M13 9WL, United Kingdom; Arthritis Research UK Centre of Epidemiology (T.W.O., S.R.P.), The University of Manchester, Manchester Academic Health Science Centre, Manchester M13 9WL, United Kingdom; NIHR Manchester Musculoskeletal Biomedical Research Unit (T.W.O.), Central Manchester NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester M13 9WL, United Kingdom; The Endocrinology and Diabetes Research Group (M.K.R.), Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, Manchester Academic Health Science Centre, Manchester M13 9WL United Kingdom; Manchester Diabetes Centre (M.K.R.), Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester M13 9WL, United Kingdom; Department of Clinical and Experimental Medicine (M.R.L.), KU Leuven, Laboratory of Gerontology and Geriatrics, B-3000 Leuven, Belgium; Department of Surgery and Cancer (I.T.H.), Imperial College London, Hammersmith Campus, London W12 ONN, United Kingdom; Department of Endocrinology (T.S.H.), Ashford and St. Peterʼs NHS Foundation Trust Hospital, Chertsey, Surrey, KT16 0PZ, United Kingdom; Department of Human Nutrition (M.E.J.L.), University of Glasgow, Glasgow G12 8TA, United Kingdom; Department of Clinical Biochemistry (B.G.K.), University Hospital of South Manchester, Manchester M23 9TL, United Kingdom; School of Community Based Medicine (N.P.), The University of Manchester, Salford Royal NHS Trust, Salford M6 8HD, United Kingdom; Endocrinology Unit, Department of Experimental Clinical And Biochemical Sciences (G.R., G.F.), University of Florence, 50121 Florence, Italy; Department of Sexual Medicine and Andrology Unit (G.R.), Department of Experimental, Clinical and Biochemical Sciences, University Of Florence, 50121 Florence Italy; Department of Obstetrics (G.B.), Gynaecology and Andrology, Albert Szent-György Medical University, H-6721 Szeged, Hungary; Department of Medicine (F.F.C.), Santiago de Compostela University, Complejo Hospitalario Universitario de Santiago; CIBER de Fisiopatología Obesidad y Nutricion (CB06/03), Instituto Salud Carlos III; 15705 Santiago de Compostela, Spain; Department of Andrology and Reproductive Endocrinology (K.K.), Medical University of Łódź, 90-149 Łódź, Poland; Andrology Unit (M.P.), United Laboratories of Tartu University Clinics, 51054 Tartu, Estonia; and Reproductive Medicine Centre (A.G.), Skåne University Hospital, University of Lund, SE-22184 Lund Sweden |
| Author_xml | – sequence: 1 givenname: Leen surname: Antonio fullname: Antonio, Leen email: leen.antonio@med.kuleuven.be organization: 1Department of Clinical and Experimental Medicine (L.A., B.D., D.V.), KU Leuven, Laboratory of Clinical and Experimental Endocrinology, B-3000 Leuven, Belgium – sequence: 2 givenname: Frederick C. W. surname: Wu fullname: Wu, Frederick C. W. organization: 4 Andrology Research Unit (F.C.W.W., E.L.C., J.D.F., M.K.R.), Endocrinology and Diabetes Research Group, Institute of Human Development, Faculty of Medical and Human Sciences, The University of Manchester, Manchester M13 9WL, United Kingdom – sequence: 3 givenname: Terence W. surname: O'Neill fullname: O'Neill, Terence W. organization: 6 Arthritis Research UK Centre of Epidemiology (T.W.O., S.R.P.), The University of Manchester, Manchester Academic Health Science Centre, Manchester M13 9WL, United Kingdom – sequence: 4 givenname: Stephen R. surname: Pye fullname: Pye, Stephen R. organization: 6 Arthritis Research UK Centre of Epidemiology (T.W.O., S.R.P.), The University of Manchester, Manchester Academic Health Science Centre, Manchester M13 9WL, United Kingdom – sequence: 5 givenname: Emma L. surname: Carter fullname: Carter, Emma L. organization: 4 Andrology Research Unit (F.C.W.W., E.L.C., J.D.F., M.K.R.), Endocrinology and Diabetes Research Group, Institute of Human Development, Faculty of Medical and Human Sciences, The University of Manchester, Manchester M13 9WL, United Kingdom – sequence: 6 givenname: Joseph D. surname: Finn fullname: Finn, Joseph D. organization: 4 Andrology Research Unit (F.C.W.W., E.L.C., J.D.F., M.K.R.), Endocrinology and Diabetes Research Group, Institute of Human Development, Faculty of Medical and Human Sciences, The University of Manchester, Manchester M13 9WL, United Kingdom – sequence: 7 givenname: Martin K. surname: Rutter fullname: Rutter, Martin K. organization: 4 Andrology Research Unit (F.C.W.W., E.L.C., J.D.F., M.K.R.), Endocrinology and Diabetes Research Group, Institute of Human Development, Faculty of Medical and Human Sciences, The University of Manchester, Manchester M13 9WL, United Kingdom – sequence: 8 givenname: Michaël R. surname: Laurent fullname: Laurent, Michaël R. organization: 2 Department of Cellular and Molecular Medicine (L.A., M.R.L., F.C.), KU Leuven, Laboratory of Molecular Endocrinology, B-3000 Leuven, Belgium – sequence: 9 givenname: Ilpo T. surname: Huhtaniemi fullname: Huhtaniemi, Ilpo T. organization: 11 Department of Surgery and Cancer (I.T.H.), Imperial College London, Hammersmith Campus, London W12 ONN, United Kingdom – sequence: 10 givenname: Thang S. surname: Han fullname: Han, Thang S. organization: 12Department of Endocrinology (T.S.H.), Ashford and St. Peter's NHS Foundation Trust Hospital, Chertsey, Surrey, KT16 0PZ, United Kingdom – sequence: 11 givenname: Michael E. J. surname: Lean fullname: Lean, Michael E. J. organization: 13 Department of Human Nutrition (M.E.J.L.), University of Glasgow, Glasgow G12 8TA, United Kingdom – sequence: 12 givenname: Brian G. surname: Keevil fullname: Keevil, Brian G. organization: 14Department of Clinical Biochemistry (B.G.K.), University Hospital of South Manchester, Manchester M23 9TL, United Kingdom – sequence: 13 givenname: Neil surname: Pendleton fullname: Pendleton, Neil organization: 15 School of Community Based Medicine (N.P.), The University of Manchester, Salford Royal NHS Trust, Salford M6 8HD, United Kingdom – sequence: 14 givenname: Giulia surname: Rastrelli fullname: Rastrelli, Giulia organization: 16 Endocrinology Unit, Department of Experimental Clinical And Biochemical Sciences (G.R., G.F.), University of Florence, 50121 Florence, Italy – sequence: 15 givenname: Gianni surname: Forti fullname: Forti, Gianni organization: 16 Endocrinology Unit, Department of Experimental Clinical And Biochemical Sciences (G.R., G.F.), University of Florence, 50121 Florence, Italy – sequence: 16 givenname: Gyorgy surname: Bartfai fullname: Bartfai, Gyorgy organization: 18Department of Obstetrics (G.B.), Gynaecology and Andrology, Albert Szent-György Medical University, H-6721 Szeged, Hungary – sequence: 17 givenname: Felipe F. surname: Casanueva fullname: Casanueva, Felipe F. organization: 19 Department of Medicine (F.F.C.), Santiago de Compostela University, Complejo Hospitalario Universitario de Santiago – sequence: 18 givenname: Krzysztof surname: Kula fullname: Kula, Krzysztof organization: 20 CIBER de Fisiopatología Obesidad y Nutricion (CB06/03), Instituto Salud Carlos III; 15705 Santiago de Compostela, Spain; Department of Andrology and Reproductive Endocrinology (K.K.), Medical University of Łódź, 90-149 Łódź, Poland – sequence: 19 givenname: Margus surname: Punab fullname: Punab, Margus organization: 21 Andrology Unit (M.P.), United Laboratories of Tartu University Clinics, 51054 Tartu, Estonia – sequence: 20 givenname: Aleksander surname: Giwercman fullname: Giwercman, Aleksander organization: 22Reproductive Medicine Centre (A.G.), Skåne University Hospital, University of Lund, SE-22184 Lund Sweden – sequence: 21 givenname: Frank surname: Claessens fullname: Claessens, Frank organization: 2 Department of Cellular and Molecular Medicine (L.A., M.R.L., F.C.), KU Leuven, Laboratory of Molecular Endocrinology, B-3000 Leuven, Belgium – sequence: 22 givenname: Brigitte surname: Decallonne fullname: Decallonne, Brigitte organization: 1Department of Clinical and Experimental Medicine (L.A., B.D., D.V.), KU Leuven, Laboratory of Clinical and Experimental Endocrinology, B-3000 Leuven, Belgium – sequence: 23 givenname: Dirk surname: Vanderschueren fullname: Vanderschueren, Dirk organization: 1Department of Clinical and Experimental Medicine (L.A., B.D., D.V.), KU Leuven, Laboratory of Clinical and Experimental Endocrinology, B-3000 Leuven, Belgium |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25636052$$D View this record in MEDLINE/PubMed |
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| Snippet | Context:Low testosterone (T) has been associated with incident metabolic syndrome (MetS), but it remains unclear if this association is independent of sex... CONTEXT:Low testosterone (T) has been associated with incident metabolic syndrome (MetS), but it remains unclear if this association is independent of sex... Low testosterone (T) has been associated with incident metabolic syndrome (MetS), but it remains unclear if this association is independent of sex hormone... Context: Low testosterone (T) has been associated with incident metabolic syndrome (MetS), but it remains unclear if this association is independent of sex... |
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| SubjectTerms | 17β-Estradiol Adult Aged Aging - metabolism Body Composition Body Mass Index Clinical Medicine Endocrinology and Diabetes Endokrinologi och diabetes Europe - epidemiology Gas chromatography Globulins Gonadal Steroid Hormones - blood Homeostasis Humans Incidence Insulin Resistance Klinisk medicin Longitudinal Studies Male Mass spectroscopy Medical and Health Sciences Medicin och hälsovetenskap Metabolic syndrome Metabolic Syndrome - blood Metabolic Syndrome - epidemiology Middle Aged Sex hormones Steroid hormones Steroids Testosterone |
| Title | Associations Between Sex Steroids and the Development of Metabolic Syndrome: A Longitudinal Study in European Men |
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