Mette W Christensen1,2, David L Keefe3, Fang Wang3, Christine S Hansen4, Isaac J Chamani3, Carolyn Sommer3, Mette Nyegaard5, Palle D Rohde6, Anders L Nielsen5, Jonas Bybjerg-Grauholm4, Ulrik S Kesmodel7,8, Ulla B Knudsen9,10, Kirstine Kirkegaard11, Hans Jakob Ingerslev10,7. 1. Fertility Clinic, Department of Obstetrics and Gynecology, Horsens Regional Hospital, Horsens, Denmark. mwch@clin.au.dk. 2. Department of Clinical Medicine, Aarhus University, Aarhus, Denmark. mwch@clin.au.dk. 3. Department of Obstetrics and Gynecology, New York University Langone Medical Center, New York, NY, USA. 4. Center for Neonatal Screening, Department of Congenital Disorders, Statens Serum Institut, Copenhagen, Denmark. 5. Department of Biomedicine, Aarhus University, Aarhus, Denmark. 6. Department of Chemistry and Bioscience, Aalborg University, Aalborg, Denmark. 7. Fertility Unit, Aalborg University Hospital, Aalborg, Denmark. 8. Department of Clinical Medicine, Aalborg University, Aalborg, Denmark. 9. Fertility Clinic, Department of Obstetrics and Gynecology, Horsens Regional Hospital, Horsens, Denmark. 10. Department of Clinical Medicine, Aarhus University, Aarhus, Denmark. 11. Department of Obstetrics and Gynecology, Aarhus University Hospital, Aarhus, Denmark.
Abstract
PURPOSE: To evaluate whether young women with idiopathic early ovarian aging, as defined by producing fewer oocytes than expected for a given age over multiple in vitro fertilization (IVF) cycles, have changes in telomere length and epigenetic age indicating accelerated biological aging (i.e., increased risk of morbidity and mortality). METHODS: A prospective cohort study was conducted at two Danish public fertility clinics. A total of 55 young women (≤ 37 years) with at least two IVF cycles with ≤ 5 harvested oocytes despite sufficient stimulation with follicle-stimulating hormone (FSH) were included in the early ovarian aging group. As controls, 52 young women (≤ 37 years) with normal ovarian function, defined by at least eight harvested oocytes, were included. Relative telomere length (rTL) and epigenetic age acceleration (AgeAccel) were measured in white blood cells as markers of premenopausal accelerated biological aging. RESULTS: rTL was comparable with a mean of 0.46 (± SD 0.12) in the early ovarian aging group and 0.47 (0.14) in the normal ovarian aging group. The AgeAccel of the early ovarian aging group was, insignificantly, 0.5 years older, but this difference disappeared when adjusting for chronological age. Sub-analysis using Anti-Müllerian hormone (AMH) as selection criterion for the two groups did not change the results. CONCLUSION: We did not find any indications of accelerated aging in whole blood from young women with idiopathic early ovarian aging. Further investigations in a similar cohort of premenopausal women or other tissues are needed to fully elucidate the potential relationship between premenopausal accelerated biological aging and early ovarian aging.
PURPOSE: To evaluate whether young women with idiopathic early ovarian aging, as defined by producing fewer oocytes than expected for a given age over multiple in vitro fertilization (IVF) cycles, have changes in telomere length and epigenetic age indicating accelerated biological aging (i.e., increased risk of morbidity and mortality). METHODS: A prospective cohort study was conducted at two Danish public fertility clinics. A total of 55 young women (≤ 37 years) with at least two IVF cycles with ≤ 5 harvested oocytes despite sufficient stimulation with follicle-stimulating hormone (FSH) were included in the early ovarian aging group. As controls, 52 young women (≤ 37 years) with normal ovarian function, defined by at least eight harvested oocytes, were included. Relative telomere length (rTL) and epigenetic age acceleration (AgeAccel) were measured in white blood cells as markers of premenopausal accelerated biological aging. RESULTS: rTL was comparable with a mean of 0.46 (± SD 0.12) in the early ovarian aging group and 0.47 (0.14) in the normal ovarian aging group. The AgeAccel of the early ovarian aging group was, insignificantly, 0.5 years older, but this difference disappeared when adjusting for chronological age. Sub-analysis using Anti-Müllerian hormone (AMH) as selection criterion for the two groups did not change the results. CONCLUSION: We did not find any indications of accelerated aging in whole blood from young women with idiopathic early ovarian aging. Further investigations in a similar cohort of premenopausal women or other tissues are needed to fully elucidate the potential relationship between premenopausal accelerated biological aging and early ovarian aging.
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