Evidence for Accelerated Biological Aging in Young Adults with Prader–Willi Syndrome
Abstract Objective Adults with Prader–Willi syndrome (PWS) are at increased risk of developing age-associated diseases early in life and, like in premature aging syndromes, aging might be accelerated. We investigated leukocyte telomere length (LTL), a marker of biological age, in young adults with P...
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| Published in | The journal of clinical endocrinology and metabolism Vol. 105; no. 6; pp. 2053 - 2059 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
US
Oxford University Press
01.06.2020
Copyright Oxford University Press |
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| Online Access | Get full text |
| ISSN | 0021-972X 1945-7197 1945-7197 |
| DOI | 10.1210/clinem/dgz180 |
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| Abstract | Abstract
Objective
Adults with Prader–Willi syndrome (PWS) are at increased risk of developing age-associated diseases early in life and, like in premature aging syndromes, aging might be accelerated. We investigated leukocyte telomere length (LTL), a marker of biological age, in young adults with PWS and compared LTL to healthy young adults of similar age. As all young adults with PWS were treated with growth hormone (GH), we also compared LTL in PWS subjects to GH-treated young adults born short for gestational age (SGA).
Design
Cross-sectional study in age-matched young adults; 47 with PWS, 135 healthy, and 75 born SGA.
Measurements
LTL measured by quantitative polymerase chain reaction, expressed as telomere/single copy gene ratio.
Results
Median (interquartile range) LTL was 2.6 (2.4–2.8) at a median (interquartile range) age of 19.2 (17.7–21.3) years in PWS, 3.1 (2.9–3.5) in healthy young adults and 3.1 (2.8–3.4) in the SGA group. Median LTL in PWS was significantly lower compared to both control groups (P < .01). In PWS, a lower LTL tended to be associated with a lower total IQ (r = 0.35, P = .08). There was no association between LTL and duration of GH treatment, cumulative GH dose, or several risk factors for type 2 diabetes mellitus or cardiovascular disease.
Conclusions
Young adults with PWS have significantly shorter median LTL compared to age-matched healthy young adults and GH-treated young adults born SGA. The shorter telomeres might play a role in the premature aging in PWS, independent of GH. Longitudinal research is needed to determine the influence of LTL on aging in PWS. |
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| AbstractList | Adults with Prader-Willi syndrome (PWS) are at increased risk of developing age-associated diseases early in life and, like in premature aging syndromes, aging might be accelerated. We investigated leukocyte telomere length (LTL), a marker of biological age, in young adults with PWS and compared LTL to healthy young adults of similar age. As all young adults with PWS were treated with growth hormone (GH), we also compared LTL in PWS subjects to GH-treated young adults born short for gestational age (SGA).OBJECTIVEAdults with Prader-Willi syndrome (PWS) are at increased risk of developing age-associated diseases early in life and, like in premature aging syndromes, aging might be accelerated. We investigated leukocyte telomere length (LTL), a marker of biological age, in young adults with PWS and compared LTL to healthy young adults of similar age. As all young adults with PWS were treated with growth hormone (GH), we also compared LTL in PWS subjects to GH-treated young adults born short for gestational age (SGA).Cross-sectional study in age-matched young adults; 47 with PWS, 135 healthy, and 75 born SGA.DESIGNCross-sectional study in age-matched young adults; 47 with PWS, 135 healthy, and 75 born SGA.LTL measured by quantitative polymerase chain reaction, expressed as telomere/single copy gene ratio.MEASUREMENTSLTL measured by quantitative polymerase chain reaction, expressed as telomere/single copy gene ratio.Median (interquartile range) LTL was 2.6 (2.4-2.8) at a median (interquartile range) age of 19.2 (17.7-21.3) years in PWS, 3.1 (2.9-3.5) in healthy young adults and 3.1 (2.8-3.4) in the SGA group. Median LTL in PWS was significantly lower compared to both control groups (P < .01). In PWS, a lower LTL tended to be associated with a lower total IQ (r = 0.35, P = .08). There was no association between LTL and duration of GH treatment, cumulative GH dose, or several risk factors for type 2 diabetes mellitus or cardiovascular disease.RESULTSMedian (interquartile range) LTL was 2.6 (2.4-2.8) at a median (interquartile range) age of 19.2 (17.7-21.3) years in PWS, 3.1 (2.9-3.5) in healthy young adults and 3.1 (2.8-3.4) in the SGA group. Median LTL in PWS was significantly lower compared to both control groups (P < .01). In PWS, a lower LTL tended to be associated with a lower total IQ (r = 0.35, P = .08). There was no association between LTL and duration of GH treatment, cumulative GH dose, or several risk factors for type 2 diabetes mellitus or cardiovascular disease.Young adults with PWS have significantly shorter median LTL compared to age-matched healthy young adults and GH-treated young adults born SGA. The shorter telomeres might play a role in the premature aging in PWS, independent of GH. Longitudinal research is needed to determine the influence of LTL on aging in PWS.CONCLUSIONSYoung adults with PWS have significantly shorter median LTL compared to age-matched healthy young adults and GH-treated young adults born SGA. The shorter telomeres might play a role in the premature aging in PWS, independent of GH. Longitudinal research is needed to determine the influence of LTL on aging in PWS. Abstract Objective Adults with Prader–Willi syndrome (PWS) are at increased risk of developing age-associated diseases early in life and, like in premature aging syndromes, aging might be accelerated. We investigated leukocyte telomere length (LTL), a marker of biological age, in young adults with PWS and compared LTL to healthy young adults of similar age. As all young adults with PWS were treated with growth hormone (GH), we also compared LTL in PWS subjects to GH-treated young adults born short for gestational age (SGA). Design Cross-sectional study in age-matched young adults; 47 with PWS, 135 healthy, and 75 born SGA. Measurements LTL measured by quantitative polymerase chain reaction, expressed as telomere/single copy gene ratio. Results Median (interquartile range) LTL was 2.6 (2.4–2.8) at a median (interquartile range) age of 19.2 (17.7–21.3) years in PWS, 3.1 (2.9–3.5) in healthy young adults and 3.1 (2.8–3.4) in the SGA group. Median LTL in PWS was significantly lower compared to both control groups (P < .01). In PWS, a lower LTL tended to be associated with a lower total IQ (r = 0.35, P = .08). There was no association between LTL and duration of GH treatment, cumulative GH dose, or several risk factors for type 2 diabetes mellitus or cardiovascular disease. Conclusions Young adults with PWS have significantly shorter median LTL compared to age-matched healthy young adults and GH-treated young adults born SGA. The shorter telomeres might play a role in the premature aging in PWS, independent of GH. Longitudinal research is needed to determine the influence of LTL on aging in PWS. Objective Adults with Prader–Willi syndrome (PWS) are at increased risk of developing age-associated diseases early in life and, like in premature aging syndromes, aging might be accelerated. We investigated leukocyte telomere length (LTL), a marker of biological age, in young adults with PWS and compared LTL to healthy young adults of similar age. As all young adults with PWS were treated with growth hormone (GH), we also compared LTL in PWS subjects to GH-treated young adults born short for gestational age (SGA). Design Cross-sectional study in age-matched young adults; 47 with PWS, 135 healthy, and 75 born SGA. Measurements LTL measured by quantitative polymerase chain reaction, expressed as telomere/single copy gene ratio. Results Median (interquartile range) LTL was 2.6 (2.4–2.8) at a median (interquartile range) age of 19.2 (17.7–21.3) years in PWS, 3.1 (2.9–3.5) in healthy young adults and 3.1 (2.8–3.4) in the SGA group. Median LTL in PWS was significantly lower compared to both control groups (P < .01). In PWS, a lower LTL tended to be associated with a lower total IQ (r = 0.35, P = .08). There was no association between LTL and duration of GH treatment, cumulative GH dose, or several risk factors for type 2 diabetes mellitus or cardiovascular disease. Conclusions Young adults with PWS have significantly shorter median LTL compared to age-matched healthy young adults and GH-treated young adults born SGA. The shorter telomeres might play a role in the premature aging in PWS, independent of GH. Longitudinal research is needed to determine the influence of LTL on aging in PWS. Adults with Prader-Willi syndrome (PWS) are at increased risk of developing age-associated diseases early in life and, like in premature aging syndromes, aging might be accelerated. We investigated leukocyte telomere length (LTL), a marker of biological age, in young adults with PWS and compared LTL to healthy young adults of similar age. As all young adults with PWS were treated with growth hormone (GH), we also compared LTL in PWS subjects to GH-treated young adults born short for gestational age (SGA). Cross-sectional study in age-matched young adults; 47 with PWS, 135 healthy, and 75 born SGA. LTL measured by quantitative polymerase chain reaction, expressed as telomere/single copy gene ratio. Median (interquartile range) LTL was 2.6 (2.4-2.8) at a median (interquartile range) age of 19.2 (17.7-21.3) years in PWS, 3.1 (2.9-3.5) in healthy young adults and 3.1 (2.8-3.4) in the SGA group. Median LTL in PWS was significantly lower compared to both control groups (P < .01). In PWS, a lower LTL tended to be associated with a lower total IQ (r = 0.35, P = .08). There was no association between LTL and duration of GH treatment, cumulative GH dose, or several risk factors for type 2 diabetes mellitus or cardiovascular disease. Young adults with PWS have significantly shorter median LTL compared to age-matched healthy young adults and GH-treated young adults born SGA. The shorter telomeres might play a role in the premature aging in PWS, independent of GH. Longitudinal research is needed to determine the influence of LTL on aging in PWS. Objective: Adults with Prader-Willi syndrome (PWS) are at increased risk of developing age-associated diseases early in life and, like in premature aging syndromes, aging might be accelerated. We investigated leukocyte telomere length (LTL), a marker of biological age, in young adults with PWS and compared LTL to healthy young adults of similar age. As all young adults with PWS were treated with growth hormone (GH), we also compared LTL in PWS subjects to GH-treated young adults born short for gestational age (SGA). Design: Cross-sectional study in age-matched young adults; 47 with PWS, 135 healthy, and 75 born SGA. Measurements: LTL measured by quantitative polymerase chain reaction, expressed as telomere/single copy gene ratio. Results: Median (interquartile range) LTL was 2.6 (2.4-2.8) at a median (interquartile range) age of 19.2 (17.7-21.3) years in PWS, 3.1 (2.9-3.5) in healthy young adults and 3.1 (2.8-3.4) in the SGA group. Median LTL in PWS was significantly lower compared to both control groups (P < .01). In PWS, a lower LTL tended to be associated with a lower total IQ (r = 0.35, P = .08). There was no association between LTL and duration of GH treatment, cumulative GH dose, or several risk factors for type 2 diabetes mellitus or cardiovascular disease. Conclusions: Young adults with PWS have significantly shorter median LTL compared to age-matched healthy young adults and GH-treated young adults born SGA. The shorter telomeres might play a role in the premature aging in PWS, independent of GH. Longitudinal research is needed to determine the influence of LTL on aging in PWS. (J Clin Endocrinol Metab 105: 2053-2059, 2020) Key Words: Prader-Willi syndrome, telomere length, growth hormone |
| Audience | Academic |
| Author | van der Velden, Janiëlle A E M Hokken-Koelega, Anita C S Damen, Layla Denniff, Matthew Donze, Stephany H Codd, Veryan Samani, Nilesh J Goedegebuure, Wesley J |
| AuthorAffiliation | Dutch Growth Research Foundation, Rotterdam, The Netherlands Department of Pediatrics, Subdivision of Endocrinology, Erasmus University Medical Center-Sophia Children’s Hospital, Rotterdam, The Netherlands Department of Cardiovascular Sciences and Leicester NIHR Biomedical Research Centre, University of Leicester, Glenfield General Hospital, Leicester, United Kingdom Department of Pediatrics, Subdivision of Endocrinology, Radboud University Medical Centre-Amalia Children’s Hospital, Nijmegen, The Netherlands |
| AuthorAffiliation_xml | – name: Dutch Growth Research Foundation, Rotterdam, The Netherlands Department of Pediatrics, Subdivision of Endocrinology, Erasmus University Medical Center-Sophia Children’s Hospital, Rotterdam, The Netherlands Department of Cardiovascular Sciences and Leicester NIHR Biomedical Research Centre, University of Leicester, Glenfield General Hospital, Leicester, United Kingdom Department of Pediatrics, Subdivision of Endocrinology, Radboud University Medical Centre-Amalia Children’s Hospital, Nijmegen, The Netherlands – name: 2 Department of Pediatrics, Subdivision of Endocrinology, Erasmus University Medical Center-Sophia Children’s Hospital , Rotterdam, The Netherlands – name: 4 Department of Pediatrics, Subdivision of Endocrinology, Radboud University Medical Centre-Amalia Children’s Hospital , Nijmegen, The Netherlands – name: 1 Dutch Growth Research Foundation , Rotterdam, The Netherlands – name: 3 Department of Cardiovascular Sciences, University of Leicester, NIHR Leicester Cardiovascular Biomedical Research Unit, Glenfield Hospital , Leicester, United Kingdom |
| Author_xml | – sequence: 1 givenname: Stephany H orcidid: 0000-0002-9249-4284 surname: Donze fullname: Donze, Stephany H email: S.Donze@kindengroei.nl organization: Dutch Growth Research Foundation, Rotterdam, The Netherlands – sequence: 2 givenname: Veryan surname: Codd fullname: Codd, Veryan organization: Department of Cardiovascular Sciences, University of Leicester, NIHR Leicester Cardiovascular Biomedical Research Unit, Glenfield Hospital, Leicester, United Kingdom – sequence: 3 givenname: Layla surname: Damen fullname: Damen, Layla organization: Dutch Growth Research Foundation, Rotterdam, The Netherlands – sequence: 4 givenname: Wesley J surname: Goedegebuure fullname: Goedegebuure, Wesley J organization: Department of Pediatrics, Subdivision of Endocrinology, Erasmus University Medical Center-Sophia Children’s Hospital, Rotterdam, The Netherlands – sequence: 5 givenname: Matthew surname: Denniff fullname: Denniff, Matthew organization: Department of Cardiovascular Sciences, University of Leicester, NIHR Leicester Cardiovascular Biomedical Research Unit, Glenfield Hospital, Leicester, United Kingdom – sequence: 6 givenname: Nilesh J surname: Samani fullname: Samani, Nilesh J organization: Department of Cardiovascular Sciences, University of Leicester, NIHR Leicester Cardiovascular Biomedical Research Unit, Glenfield Hospital, Leicester, United Kingdom – sequence: 7 givenname: Janiëlle A E M surname: van der Velden fullname: van der Velden, Janiëlle A E M organization: Department of Pediatrics, Subdivision of Endocrinology, Radboud University Medical Centre-Amalia Children’s Hospital, Nijmegen, The Netherlands – sequence: 8 givenname: Anita C S surname: Hokken-Koelega fullname: Hokken-Koelega, Anita C S organization: Dutch Growth Research Foundation, Rotterdam, The Netherlands |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31689713$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1210_clinem_dgad312 crossref_primary_10_1155_2020_8041616 crossref_primary_10_1093_ejendo_lvad084 crossref_primary_10_3390_ijms22073727 crossref_primary_10_3390_jcm14051470 |
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| Keywords | telomere length Prader–Willi syndrome growth hormone |
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Adults with Prader–Willi syndrome (PWS) are at increased risk of developing age-associated diseases early in life and, like in premature... Adults with Prader-Willi syndrome (PWS) are at increased risk of developing age-associated diseases early in life and, like in premature aging syndromes, aging... Objective: Adults with Prader-Willi syndrome (PWS) are at increased risk of developing age-associated diseases early in life and, like in premature aging... Objective Adults with Prader–Willi syndrome (PWS) are at increased risk of developing age-associated diseases early in life and, like in premature aging... |
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| SubjectTerms | Adolescent Adult Age Aging Aging, Premature - epidemiology Aging, Premature - genetics Cardiovascular diseases Care and treatment Case-Control Studies Clinical s Cross-Sectional Studies Diabetes mellitus (non-insulin dependent) Female Follow-Up Studies Genetic aspects Gestational age Growth hormones Health aspects Humans Incidence Male Netherlands - epidemiology Polymerase chain reaction Prader-Willi syndrome Prader-Willi Syndrome - physiopathology Prognosis Risk factors Structure Telomere - genetics Telomeres Young Adult Young adults |
| Title | Evidence for Accelerated Biological Aging in Young Adults with Prader–Willi Syndrome |
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