Antimüllerian hormone and leukocyte aging markers in the Coronary Artery Risk Development in Young Adults study

Catherine Kim; Eli Puterman; Lifang Hou; James C. Slaughter; James G. Terry; Melissa F. Wellons

doi:10.1016/j.fertnstert.2022.03.021

Antimüllerian hormone and leukocyte aging markers in the Coronary Artery Risk Development in Young Adults study

Catherine Kim^*, Eli Puterman, Lifang Hou, James C. Slaughter, James G. Terry, Melissa F. Wellons

^*Corresponding author for this work

Preventive Medicine

Research output: Contribution to journal › Article › peer-review

3 Scopus citations

Abstract

Objective: To examine whether premenopausal reproductive age, as indicated by serum antimüllerian hormone (AMH), is associated with leukocyte aging biomarkers. Design: Prospective cohort analysis. Setting: The Coronary Artery Risk Development in Young Adults study, a population-based study of Black and White adults from four US communities (Birmingham, AL; Chicago, IL; Minneapolis, MN; Oakland, CA). Patient(s): Premenopausal women with serum AMH measures at examination year 15 as well as leukocyte aging markers. Intervention(s): None. Main Outcome Measure(s): Telomere length, mitochondrial deoxyribonucleic acid (mtDNA) copy number, and intrinsic and extrinsic epigenetic age acceleration (EAA) at examination years 15, 20, and 25 as well as change between examination years. Result(s): Women were 40.2 (standard deviation, 3.7) years of age at examination year 15 when the AMH and initial measures of telomere length and mtDNA copy number (n = 386) were obtained and EAA occurred. After adjustment for chronological age, race, and smoking history, AMH quartile at examination year 15 was not associated with telomere length at examination years 15 and 25 or telomere length change between these years, mtDNA copy number at examination years 15 and 25 or change between these years, or intrinsic EAA at examination years 15 and 20 or change between these years. Women in the second AMH quartile had faster extrinsic EAA than women in the lowest AMH quartile (β-coefficient, 1.84; 95% confidence interval, 0.20–3.49). Conclusion(s): In a population-based cohort, AMH did not have associations with leukocyte telomere length, mtDNA copy number, or intrinsic EAA.

Original language	English (US)
Pages (from-to)	125-133
Number of pages	9
Journal	Fertility and Sterility
Volume	118
Issue number	1
DOIs	https://doi.org/10.1016/j.fertnstert.2022.03.021
State	Published - Jul 2022

Funding

The Coronary Artery Risk Development in Young Adults (CARDIA) Study is conducted and supported by the National Heart, Lung, and Blood Institute (NHLBI) in collaboration with the University of Alabama at Birmingham (HHSN268201800005I and HHSN268201800007I), Northwestern University (HHSN268201800003I), University of Minnesota (HHSN268201800006I), and Kaiser Foundation Research Institute (HHSN268201800004I). The CARDIA Study is also partially supported by the Intramural Research Program of the National Institute on Aging (NIA) and an intra-agency agreement between the NIA and NHLBI (AG0005). The laboratory work and analytic component were funded by the American Heart Association (17SFRN33700278 and 14SFRN20790000). The telomere ancillary study was funded by the MacArthur Foundation SES and Health Network. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIA, NHLBI, or MacArthur Foundation. This manuscript has been reviewed by the CARDIA Study for scientific content. The CARDIA Women's Study (R01-HL-065611) was supported by the NHLBI. Anti-Müllerian hormone measurement was supported by a National Heart, Lung, and Blood Institute Career Development Award (K23-HL-87114).

Keywords

antimüllerian hormone (AMH)
epigenetic
mitochondrial DNA copy number
telomere

ASJC Scopus subject areas

Reproductive Medicine
Obstetrics and Gynecology

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10.1016/j.fertnstert.2022.03.021

Cite this

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title = "Antim{\"u}llerian hormone and leukocyte aging markers in the Coronary Artery Risk Development in Young Adults study",

abstract = "Objective: To examine whether premenopausal reproductive age, as indicated by serum antim{\"u}llerian hormone (AMH), is associated with leukocyte aging biomarkers. Design: Prospective cohort analysis. Setting: The Coronary Artery Risk Development in Young Adults study, a population-based study of Black and White adults from four US communities (Birmingham, AL; Chicago, IL; Minneapolis, MN; Oakland, CA). Patient(s): Premenopausal women with serum AMH measures at examination year 15 as well as leukocyte aging markers. Intervention(s): None. Main Outcome Measure(s): Telomere length, mitochondrial deoxyribonucleic acid (mtDNA) copy number, and intrinsic and extrinsic epigenetic age acceleration (EAA) at examination years 15, 20, and 25 as well as change between examination years. Result(s): Women were 40.2 (standard deviation, 3.7) years of age at examination year 15 when the AMH and initial measures of telomere length and mtDNA copy number (n = 386) were obtained and EAA occurred. After adjustment for chronological age, race, and smoking history, AMH quartile at examination year 15 was not associated with telomere length at examination years 15 and 25 or telomere length change between these years, mtDNA copy number at examination years 15 and 25 or change between these years, or intrinsic EAA at examination years 15 and 20 or change between these years. Women in the second AMH quartile had faster extrinsic EAA than women in the lowest AMH quartile (β-coefficient, 1.84; 95% confidence interval, 0.20–3.49). Conclusion(s): In a population-based cohort, AMH did not have associations with leukocyte telomere length, mtDNA copy number, or intrinsic EAA.",

keywords = "antim{\"u}llerian hormone (AMH), epigenetic, mitochondrial DNA copy number, telomere",

author = "Catherine Kim and Eli Puterman and Lifang Hou and Slaughter, {James C.} and Terry, {James G.} and Wellons, {Melissa F.}",

note = "Publisher Copyright: {\textcopyright} 2022 American Society for Reproductive Medicine",

year = "2022",

month = jul,

doi = "10.1016/j.fertnstert.2022.03.021",

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T1 - Antimüllerian hormone and leukocyte aging markers in the Coronary Artery Risk Development in Young Adults study

AU - Kim, Catherine

AU - Puterman, Eli

AU - Hou, Lifang

AU - Slaughter, James C.

AU - Terry, James G.

AU - Wellons, Melissa F.

PY - 2022/7

Y1 - 2022/7

N2 - Objective: To examine whether premenopausal reproductive age, as indicated by serum antimüllerian hormone (AMH), is associated with leukocyte aging biomarkers. Design: Prospective cohort analysis. Setting: The Coronary Artery Risk Development in Young Adults study, a population-based study of Black and White adults from four US communities (Birmingham, AL; Chicago, IL; Minneapolis, MN; Oakland, CA). Patient(s): Premenopausal women with serum AMH measures at examination year 15 as well as leukocyte aging markers. Intervention(s): None. Main Outcome Measure(s): Telomere length, mitochondrial deoxyribonucleic acid (mtDNA) copy number, and intrinsic and extrinsic epigenetic age acceleration (EAA) at examination years 15, 20, and 25 as well as change between examination years. Result(s): Women were 40.2 (standard deviation, 3.7) years of age at examination year 15 when the AMH and initial measures of telomere length and mtDNA copy number (n = 386) were obtained and EAA occurred. After adjustment for chronological age, race, and smoking history, AMH quartile at examination year 15 was not associated with telomere length at examination years 15 and 25 or telomere length change between these years, mtDNA copy number at examination years 15 and 25 or change between these years, or intrinsic EAA at examination years 15 and 20 or change between these years. Women in the second AMH quartile had faster extrinsic EAA than women in the lowest AMH quartile (β-coefficient, 1.84; 95% confidence interval, 0.20–3.49). Conclusion(s): In a population-based cohort, AMH did not have associations with leukocyte telomere length, mtDNA copy number, or intrinsic EAA.

AB - Objective: To examine whether premenopausal reproductive age, as indicated by serum antimüllerian hormone (AMH), is associated with leukocyte aging biomarkers. Design: Prospective cohort analysis. Setting: The Coronary Artery Risk Development in Young Adults study, a population-based study of Black and White adults from four US communities (Birmingham, AL; Chicago, IL; Minneapolis, MN; Oakland, CA). Patient(s): Premenopausal women with serum AMH measures at examination year 15 as well as leukocyte aging markers. Intervention(s): None. Main Outcome Measure(s): Telomere length, mitochondrial deoxyribonucleic acid (mtDNA) copy number, and intrinsic and extrinsic epigenetic age acceleration (EAA) at examination years 15, 20, and 25 as well as change between examination years. Result(s): Women were 40.2 (standard deviation, 3.7) years of age at examination year 15 when the AMH and initial measures of telomere length and mtDNA copy number (n = 386) were obtained and EAA occurred. After adjustment for chronological age, race, and smoking history, AMH quartile at examination year 15 was not associated with telomere length at examination years 15 and 25 or telomere length change between these years, mtDNA copy number at examination years 15 and 25 or change between these years, or intrinsic EAA at examination years 15 and 20 or change between these years. Women in the second AMH quartile had faster extrinsic EAA than women in the lowest AMH quartile (β-coefficient, 1.84; 95% confidence interval, 0.20–3.49). Conclusion(s): In a population-based cohort, AMH did not have associations with leukocyte telomere length, mtDNA copy number, or intrinsic EAA.

KW - antimüllerian hormone (AMH)

KW - epigenetic

KW - mitochondrial DNA copy number

KW - telomere

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Antimüllerian hormone and leukocyte aging markers in the Coronary Artery Risk Development in Young Adults study

Abstract

Funding

Keywords

ASJC Scopus subject areas

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