4.5 Article

Sleep quantity and quality and cardiometabolic risk factors in Indigenous Australians

期刊

JOURNAL OF SLEEP RESEARCH
卷 30, 期 2, 页码 -

出版社

WILEY
DOI: 10.1111/jsr.13067

关键词

Aboriginal and Torres Strait Islander people; cardiometabolic risk; cardiovascular disease; Indigenous Australian; metabolic syndrome; sleep

资金

  1. Australian Catholic University
  2. NHMRC Centre for Research Excellence to Reduce Inequality in Heart Disease
  3. Victorian Government's Operational Infrastructure Support Program
  4. Gender Equity Award, Baker Heart and Diabetes Institute
  5. NHMRC Practitioner Fellowship
  6. National Heart Foundation of Australia [100802]
  7. Aboriginal community-controlled health services and councils
  8. Tangentyere Town Camp Council
  9. Central Australian Aboriginal Congress in the Northern Territory
  10. Yarrabah and Palm Island Councils in North Queensland
  11. Wurli-wurlinjang Health Service

向作者/读者索取更多资源

The study found that a large proportion of indigenous Australians experience short sleep durations and poor sleep quality, with over one-third of participants obtaining less than 7 hours of sleep per night. Short sleep duration and poor sleep quality are associated with increased cardiometabolic risk in this population.
Poor sleep is associated with increased risk of cardiovascular disease (CVD). Indigenous Australians have 1.3 times higher risk of CVD compared to non-indigenous Australians. However, there are limited data describing sleep problems and cardiometabolic risk in this population. This study aimed to investigate sleep quantity and quality in indigenous Australians and assess its association with cardiometabolic risk. Two hundred and forty-five indigenous Australians aged > 18 years were recruited via convenience sampling from communities in the Northern Territory and Queensland. Sleep quantity and quality was assessed subjectively with questionnaires including the Epworth Sleepiness Scale. In a sub-population (n = 46), objective sleep assessment was performed over three nights of actigraphy. Cardiometabolic risk measures included glycated haemoglobin, lipids, anthropometric measurements and sitting blood pressure. Sleep duration measured subjectively and objectively averaged 7.5 +/- 2.0 hr/night; however, over one-third of participants (self-report 35%; actigraphy 39%) obtained < 7 hr/night. Overall, more than a third of participants experienced poor-quality sleep, with 27% reporting severe daytime sleepiness (ESS score > 10) and a high number of objectively measured awakenings/night (6 +/- 4). Short sleep duration (<6 hr/night) measured both subjectively and objectively was an independent predictor of diastolic (beta = 5.37,p = .038) and systolic blood pressure (beta = 14.30,p = .048). More objectively measured night-time awakenings were associated with increased glycated haemoglobin levels (beta = 0.07,p = .020) and greater sleep fragmentation was associated with lower high-density lipoprotein levels (beta = -0.01,p = .025). A large proportion of indigenous Australians experienced short sleep durations and had significant sleep disruption. Poor sleep quantity and quality may contribute to heightened cardiometabolic risk in this population.

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