Vasomotor symptoms and lipids/lipoprotein subclass metrics in midlife women: Does level of endogenous estradiol matter? The SWAN HDL Ancillary Study.
Estrogen
Lipoproteins
Menopause
Nuclear magnetic resonance spectroscopy
Vasomotor symptoms
Journal
Journal of clinical lipidology
ISSN: 1933-2874
Titre abrégé: J Clin Lipidol
Pays: United States
ID NLM: 101300157
Informations de publication
Date de publication:
Historique:
received:
16
03
2020
revised:
30
06
2020
accepted:
02
07
2020
pubmed:
5
8
2020
medline:
18
9
2021
entrez:
5
8
2020
Statut:
ppublish
Résumé
A greater frequency of vasomotor symptoms (VMSs) has been associated with higher low-density lipoprotein cholesterol (LDL-C), but the association with high-density lipoprotein cholesterol (HDL-C) remains unclear. Endogenous estradiol (E2) levels are associated with both VMS and lipid levels and thus may confound such associations. To assess the relationship of VMS frequency with HDL-C, LDL-C, and lipoprotein concentrations (HDL and LDL particles [HDL-P; LDL-P]) and lipoprotein sizes in midlife women and to evaluate whether these associations are explained by E2. Participants were from the Study of Women's Health Across the Nation (SWAN) HDL ancillary study who had both nuclear magnetic resonance (NMR) spectroscopy lipoprotein subclass metrics and self-reported frequency of VMS measured 2-5 times over the menopause transition. VMS frequency was categorized into none, 1-5 days (infrequent), or ≥6 days (frequent) within the past 2 weeks. We evaluated 522 women [at baseline: mean age 50.3 (SD: 2.8) years; infrequent VMS: 29.8%, frequent VMS: 16.5%]. Adjusting for potential confounders except E2, frequent VMS was associated with smaller HDL size [β(SE): -0.06 (0.03); P = .04] and higher concentrations of LDL-C [β(SE): 3.58 (1.77); P = .04] and intermediate LDL-P [β(SE): 0.09 (0.05); P = .04] than no VMS. These associations were largely explained by E2, all P's > .05. Frequent VMSs were associated with smaller HDL size and higher concentrations of LDL-C and intermediate LDL-P. These associations were explained by endogenous E2. Whether treating frequent VMS with exogenous E2 could simultaneously improve lipids/lipoproteins profile should be assessed in future studies.
Sections du résumé
BACKGROUND
A greater frequency of vasomotor symptoms (VMSs) has been associated with higher low-density lipoprotein cholesterol (LDL-C), but the association with high-density lipoprotein cholesterol (HDL-C) remains unclear. Endogenous estradiol (E2) levels are associated with both VMS and lipid levels and thus may confound such associations.
OBJECTIVES
To assess the relationship of VMS frequency with HDL-C, LDL-C, and lipoprotein concentrations (HDL and LDL particles [HDL-P; LDL-P]) and lipoprotein sizes in midlife women and to evaluate whether these associations are explained by E2.
METHODS
Participants were from the Study of Women's Health Across the Nation (SWAN) HDL ancillary study who had both nuclear magnetic resonance (NMR) spectroscopy lipoprotein subclass metrics and self-reported frequency of VMS measured 2-5 times over the menopause transition. VMS frequency was categorized into none, 1-5 days (infrequent), or ≥6 days (frequent) within the past 2 weeks.
RESULTS
We evaluated 522 women [at baseline: mean age 50.3 (SD: 2.8) years; infrequent VMS: 29.8%, frequent VMS: 16.5%]. Adjusting for potential confounders except E2, frequent VMS was associated with smaller HDL size [β(SE): -0.06 (0.03); P = .04] and higher concentrations of LDL-C [β(SE): 3.58 (1.77); P = .04] and intermediate LDL-P [β(SE): 0.09 (0.05); P = .04] than no VMS. These associations were largely explained by E2, all P's > .05.
CONCLUSIONS
Frequent VMSs were associated with smaller HDL size and higher concentrations of LDL-C and intermediate LDL-P. These associations were explained by endogenous E2. Whether treating frequent VMS with exogenous E2 could simultaneously improve lipids/lipoproteins profile should be assessed in future studies.
Identifiants
pubmed: 32747311
pii: S1933-2874(20)30212-9
doi: 10.1016/j.jacl.2020.07.002
pmc: PMC7642056
mid: NIHMS1610375
pii:
doi:
Substances chimiques
Estrogens
0
Lipoproteins, HDL
0
Lipoproteins, LDL
0
Estradiol
4TI98Z838E
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
685-694.e2Subventions
Organisme : NIA NIH HHS
ID : U01 AG012554
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG058690
Pays : United States
Organisme : NIA NIH HHS
ID : U01 AG012505
Pays : United States
Organisme : NIA NIH HHS
ID : U01 AG012535
Pays : United States
Organisme : NIA NIH HHS
ID : U01 AG012553
Pays : United States
Organisme : NINR NIH HHS
ID : U01 NR004061
Pays : United States
Organisme : NIA NIH HHS
ID : U01 AG012539
Pays : United States
Organisme : NIA NIH HHS
ID : U01 AG012546
Pays : United States
Organisme : NIA NIH HHS
ID : U19 AG063720
Pays : United States
Organisme : NIA NIH HHS
ID : U01 AG012495
Pays : United States
Organisme : NIA NIH HHS
ID : U01 AG012531
Pays : United States
Organisme : NIA NIH HHS
ID : U01 AG017719
Pays : United States
Informations de copyright
Copyright © 2020 National Lipid Association. Published by Elsevier Inc. All rights reserved.
Références
J Clin Lipidol. 2016 Jul-Aug;10(4):962-969
pubmed: 27578129
J Am Geriatr Soc. 2013 Jun;61(6):1011-8
pubmed: 23692449
Am J Public Health. 2006 Jul;96(7):1226-35
pubmed: 16735636
J Clin Endocrinol Metab. 2011 Mar;96(3):746-54
pubmed: 21159842
Menopause. 2011 Jun;18(6):603-10
pubmed: 21358352
Menopause. 2015 Nov;22(11):1239-45
pubmed: 25899005
Curr Opin Lipidol. 2017 Aug;28(4):328-336
pubmed: 28459707
BBA Clin. 2015 Jun;3:243-250
pubmed: 25825692
Fertil Steril. 2013 Sep;100(3):793-800
pubmed: 23755948
J Clin Lipidol. 2009 Oct;3(5):345-50
pubmed: 21291833
JAMA. 2002 Jul 3;288(1):49-57
pubmed: 12090862
Am J Obstet Gynecol. 1996 Mar;174(3):897-902
pubmed: 8633665
Maturitas. 2010 Jul;66(3):285-90
pubmed: 20400247
Am J Cardiol. 2002 Oct 17;90(8A):71i-76i
pubmed: 12419483
Maturitas. 2004 Apr 15;47(4):299-303
pubmed: 15063483
JAMA. 2002 Jul 17;288(3):321-33
pubmed: 12117397
Ann Hepatol. 2017 Oct 28;16(Suppl. 1: s3-105.):s27-s42
pubmed: 29080338
Fertil Steril. 2005 Mar;83(3):558-66
pubmed: 15749481
Maturitas. 2015 Apr;80(4):399-405
pubmed: 25631350
Am J Epidemiol. 2000 Mar 15;151(6):584-93
pubmed: 10733040
Women Health. 2017 Sep;57(8):891-904
pubmed: 27617395
Clin Endocrinol (Oxf). 2011 Jan;74(1):97-103
pubmed: 21050255
Menopause. 2008 May-Jun;15(3):429-34
pubmed: 18204407
Fertil Steril. 2001 May;75(5):898-915
pubmed: 11334901
J Lipid Res. 1978 Jan;19(1):65-76
pubmed: 202660
Atherosclerosis. 2004 Dec;177(2):329-36
pubmed: 15530907
Obstet Gynecol. 2012 Apr;119(4):753-61
pubmed: 22433339
Menopause. 2011 Apr;18(4):352-8
pubmed: 21242820
Clin Chem. 1972 Jun;18(6):499-502
pubmed: 4337382
Med Sci Sports Exerc. 2000 Jul;32(7):1327-38
pubmed: 10912901
J Am Coll Cardiol. 2012 Aug 7;60(6):508-16
pubmed: 22796256
Menopause. 2011 Apr;18(4):376-84
pubmed: 21107300
Clin Infect Dis. 2015 Sep 1;61(5):840-9
pubmed: 25979307
Menopause. 2011 Oct;18(10):1044-51
pubmed: 21926929
J Obstet Gynecol Neonatal Nurs. 2014 Mar-Apr;43(2):226-35; quiz E18-9
pubmed: 24502325
J R Soc Med. 1979 Nov;72(11):835-41
pubmed: 399622
Obes Res. 1998 May;6(3):246-54
pubmed: 9618130
Maturitas. 2015 May;81(1):62-8
pubmed: 25804951
J Clin Lipidol. 2011 Mar-Apr;5(2):105-13
pubmed: 21392724
Metabolism. 2008 Aug;57(8):1101-7
pubmed: 18640388
Br J Math Stat Psychol. 2015 May;68(2):246-67
pubmed: 25098455
J Lipid Res. 2014 Jul;55(7):1498-504
pubmed: 24852168
Circulation. 2009 Feb 24;119(7):931-9
pubmed: 19204302
JAMA. 1995 Jan 18;273(3):199-208
pubmed: 7807658
Oxid Med Cell Longev. 2017;2017:1273042
pubmed: 28572872
Menopause. 2006 Mar-Apr;13(2):265-79
pubmed: 16645540
Arterioscler Thromb Vasc Biol. 2018 Sep;38(9):2236-2244
pubmed: 30026268
Circulation. 2008 Sep 16;118(12):1234-40
pubmed: 18765392
Menopause. 2010 Jan-Feb;17(1):145-51
pubmed: 19602991
Clin Lab Med. 2006 Dec;26(4):847-70
pubmed: 17110242
J Am Coll Cardiol. 2013 Jan 29;61(4):440-446
pubmed: 23265337