TY - JOUR
T1 - Insomnia symptoms and biomarkers of monocyte activation, systemic inflammation, and coagulation in HIV
T2 - Veterans Aging Cohort Study
AU - Polanka, Brittanny M.
AU - Kundu, Suman
AU - So-Armah, Kaku A.
AU - Freiberg, Matthew S.
AU - Gupta, Samir K.
AU - Zapolski, Tamika C.B.
AU - Hirsh, Adam T.
AU - Bedimo, Roger J.
AU - Budoff, Matthew J.
AU - Butt, Adeel A.
AU - Chang, Chung Chou H.
AU - Gottlieb, Stephen S.
AU - Marconi, Vincent C.
AU - Womack, Julie A.
AU - Stewart, Jesse C.
N1 - Publisher Copyright:
Copyright: This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.
PY - 2021/2
Y1 - 2021/2
N2 - Background Insomnia may be a risk factor for cardiovascular disease in HIV (HIV-CVD); however, mechanisms have yet to be elucidated. Methods We examined cross-sectional associations of insomnia symptoms with biological mechanisms of HIV-CVD (immune activation, systemic inflammation, and coagulation) among 1,542 people with HIV from the Veterans Aging Cohort Study (VACS) Biomarker Cohort. Past-month insomnia symptoms were assessed by the item, "Difficulty falling or staying asleep?,"with the following response options: "I do not have this symptom"or "I have this symptom and. . .""it doesn't bother me,""it bothers me a little,""it bothers me,""it bothers me a lot."Circulating levels of the monocyte activation marker soluble CD14 (sCD14), inflammatory marker interleukin-6 (IL-6), and coagulation marker D-dimer were determined from blood specimens. Demographic- and fully-adjusted (CVD risk factors, potential confounders, HIV-related factors) regression models were constructed, with log-transformed biomarker variables as the outcomes. We present the exponentiated regression coefficient (exp[b]) and its 95% confidence interval (CI). Results We observed no significant associations between insomnia symptoms and sCD14 or IL-6. For D-dimer, veterans in the "Bothers a Lot"group had, on average, 17% higher D-dimer than veterans in the "No Difficulty Falling or Staying Asleep"group in the demographicadjusted model (exp[b] = 1.17, 95%CI = 1.01-1.37, p = .04). This association was nonsignificant in the fully-adjusted model (exp[b] = 1.09, 95%CI = 0.94-1.26, p = .27). Conclusion We observed little evidence of relationships between insomnia symptoms and markers of biological mechanisms of HIV-CVD. Other mechanisms may be responsible for the insomnia- CVD relationship in HIV; however, future studies with comprehensive assessments of insomnia symptoms are warranted.
AB - Background Insomnia may be a risk factor for cardiovascular disease in HIV (HIV-CVD); however, mechanisms have yet to be elucidated. Methods We examined cross-sectional associations of insomnia symptoms with biological mechanisms of HIV-CVD (immune activation, systemic inflammation, and coagulation) among 1,542 people with HIV from the Veterans Aging Cohort Study (VACS) Biomarker Cohort. Past-month insomnia symptoms were assessed by the item, "Difficulty falling or staying asleep?,"with the following response options: "I do not have this symptom"or "I have this symptom and. . .""it doesn't bother me,""it bothers me a little,""it bothers me,""it bothers me a lot."Circulating levels of the monocyte activation marker soluble CD14 (sCD14), inflammatory marker interleukin-6 (IL-6), and coagulation marker D-dimer were determined from blood specimens. Demographic- and fully-adjusted (CVD risk factors, potential confounders, HIV-related factors) regression models were constructed, with log-transformed biomarker variables as the outcomes. We present the exponentiated regression coefficient (exp[b]) and its 95% confidence interval (CI). Results We observed no significant associations between insomnia symptoms and sCD14 or IL-6. For D-dimer, veterans in the "Bothers a Lot"group had, on average, 17% higher D-dimer than veterans in the "No Difficulty Falling or Staying Asleep"group in the demographicadjusted model (exp[b] = 1.17, 95%CI = 1.01-1.37, p = .04). This association was nonsignificant in the fully-adjusted model (exp[b] = 1.09, 95%CI = 0.94-1.26, p = .27). Conclusion We observed little evidence of relationships between insomnia symptoms and markers of biological mechanisms of HIV-CVD. Other mechanisms may be responsible for the insomnia- CVD relationship in HIV; however, future studies with comprehensive assessments of insomnia symptoms are warranted.
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U2 - 10.1371/journal.pone.0246073
DO - 10.1371/journal.pone.0246073
M3 - Article
C2 - 33561176
AN - SCOPUS:85101259960
SN - 1932-6203
VL - 16
JO - PloS one
JF - PloS one
IS - 2 February
M1 - e0246073
ER -