Vasomotor symptoms (VMS) may be associated with an increased risk of cardiovascular disease. One candidate mechanism may involve alterations in physiological responses to stress. The current study therefore examined the relationship between self-reported VMS bother and cardiovascular, hemodynamic, neuroendocrine, and inflammatory responses to an acute psychosocial stress protocol.
One hundred eighty-six women in the menopausal transition or early postmenopausal stage (age 45-60 y) provided the data for this article. Subjective hot flash and night sweat bother were assessed using the Greene Climacteric Scale. Women also underwent a stressor battery involving a speech and a mental arithmetic task while cardiovascular, hemodynamic, neuroendocrine, and inflammatory responses were assessed. Repeated measures regression analyses were used to examine the relationship between self-reported VMS and physiologic responses to the stressor.
In multivariate analyses adjusting for potential confounders, self-reported hot flash bother was associated with lower overall cardiac index and stroke volume index and higher overall vascular resistance index and levels of the inflammatory cytokine interleukin-6. Hot flash bother also tended to be associated with higher overall cortisol levels and higher baseline levels of plasma norepinephrine. Night sweat bother, on the other hand, was associated with higher overall cortisol levels and tended to be associated with higher interleukin-6.
Self-reported VMS bother is associated with an unfavorable hemodynamic and neuroendocrine profile characterized by increased hypothalamic-pituitary-adrenal axis and central sympathetic activation, inflammation, and vasoconstriction. Further research investigating this profile in relation to VMS, and the potential health implications of this association, is warranted.
1Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, NC
2Departments of Psychiatry, Epidemiology and Psychology, University of Pittsburgh, PA
3Section on Behavioral Endocrinology, Department of Health and Human Services, National Institute of Mental Health, Bethesda, MD.
Address correspondence to: Susan S. Girdler, PhD, Department of Psychiatry, University of North Carolina at Chapel Hill School of Medicine, CB# 7160, 101 Manning Drive, Chapel Hill, NC 27599-3366. E-mail: Susan_Girdler@med.unc.edu
Received 24 October, 2015
Revised 6 April, 2016
Accepted 6 April, 2016
Funding/support: This research was supported by NIH grant RO1-MH087619.
Financial disclosure/conflicts of interest: J.L.G. is the recipient of a postdoctoral fellowship of the Fonds de la Recherche du Québec—Santé (FRQS). D.R.R. serves on the editorial board of Servier Laboratories, is a consultant for Sage Therapeutics Inc, and has received grant funding from the Foundation of Hope. Both D.R.R. and S.S.G. have received grant funding from NIH.