title: Are changes in cardiovascular disease risk factors in midlife women due to chronological aging or to the menopausal transition?
abstract: OBJECTIVE
  This prospective study examined whether changes in traditional and novel coronary heart disease (CHD) risk factors are greater within a year of the final menstrual period (FMP), relative to changes that occur before or after that interval, in a multiethnic cohort.
  
  
  BACKGROUND
  Understanding the influence of menopause on CHD risk remains elusive and has been evaluated primarily in Caucasian samples.
  
  
  METHODS
  SWAN (Study of Women's Health Across the Nation) is a prospective study of the menopausal transition in 3,302 minority (African American, Hispanic, Japanese, or Chinese) and Caucasian women. After 10 annual examinations, 1,054 women had achieved an FMP not due to surgery and without hormone therapy use before FMP. Measured CHD risk factors included lipids and lipoproteins, glucose, insulin, blood pressure, fibrinogen, and C-reactive protein. We assessed which of 2 models provided a better fit with the observed risk factor changes over time in relation to the FMP: a linear model, consistent with chronological aging, or a piecewise linear model, consistent with ovarian aging.
  
  
  RESULTS
  Only total cholesterol, low-density lipoprotein cholesterol, and apolipoprotein B demonstrated substantial increases within the 1-year interval before and after the FMP, consistent with menopause-induced changes. This pattern was similar across ethnic groups. The other risk factors were consistent with a linear model, indicative of chronological aging.
  
  
  CONCLUSIONS
  Women experience a unique increase in lipids at the time of the FMP. Monitoring lipids in perimenopausal women should enhance primary prevention of CHD.
authors.affiliation: Department of Psychiatry and Psychology, University of Pittsburgh, Pittsburgh, PA 15213, USA. matthewska@upmc.edu
authors.forename: Karen A
authors.initials: KA
authors.lastname: Matthews
authors.forename: Sybil L
authors.initials: SL
authors.lastname: Crawford
authors.forename: Claudia U
authors.initials: CU
authors.lastname: Chae
authors.forename: Susan A
authors.initials: SA
authors.lastname: Everson-Rose
authors.forename: Mary Fran
authors.initials: MF
authors.lastname: Sowers
authors.forename: Barbara
authors.initials: B
authors.lastname: Sternfeld
authors.forename: Kim
authors.initials: K
authors.lastname: Sutton-Tyrrell
mesh_terms: D000375:Aging / Q000502:physiology*; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure; D002097:C-Reactive Protein / Q000032:analysis; D002318:Cardiovascular Diseases / Q000097:blood* / Q000503:physiopathology*; D002784:Cholesterol / Q000097:blood; D005167:Factor VII / Q000032:analysis; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D006801:Humans; D007328:Insulin / Q000097:blood; D016014:Linear Models; D008074:Lipoproteins / Q000097:blood; D008137:Longitudinal Studies; D008875:Middle Aged; D047648:Perimenopause / Q000502:physiology*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011446:Prospective Studies; D044469:Racial Groups; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood; D014481:United States
chemical_list: D001786:Blood Glucose; D007328:Insulin; D008074:Lipoproteins; D017395:Plasminogen Activator Inhibitor 1; D014280:Triglycerides; D005167:Factor VII; D005340:Fibrinogen; D002097:C-Reactive Protein; D002784:Cholesterol