Associations of Adverse Childhood Experiences, Sleep Disruption, and Vascular Dysfunction in Young Adults: The Iowa ACEs and Sleep Cohort and Manipulating Sleep in Young Adults With ACEs Studies
Overview
- Phase
- Not Applicable
- Intervention
- Not specified
- Conditions
- Adverse Childhood Experiences
- Sponsor
- Nathaniel Jenkins
- Enrollment
- 70
- Locations
- 1
- Primary Endpoint
- Vascular Endothelial Function
- Status
- Recruiting
- Last Updated
- 4 months ago
Overview
Brief Summary
The overall purpose of this study is to understand the role of disrupted sleep in the association of exposure to early life adversity (adverse childhood experiences (ACEs)) with vascular endothelial (dys)function.
In Aim 1 (The Iowa ACEs and Sleep Cohort Study), the investigators will utilize a cross-sectional cohort design with a state-of-the-art translational approach. Participants will be recruited to objectively characterize the degree to which lower sleep quality and quantity contribute to ACEs-related endothelial dysfunction, inflammation, and oxidative stress in young adults using:
- rigorous at home sleep monitoring using 7-nights of wrist actigraphy and 2 nights of home-based polysomnography to objectively measure sleep quality (sleep efficiency, wakefulness after sleep onset and sleep depth), and total sleep duration,
- in vivo assessment of endothelial function via flow-mediated dilation testing, and
- in vitro determination of endothelial cell inflammation and oxidative stress from biopsied endothelial cells. This study to achieve this Aim.
In Aim 2, approximately 70 eligible participants from Aim 1 (The Iowa ACEs and Sleep Cohort Study) will then be randomized to either a 6-week behavioral sleep intervention (cognitive behavioral therapy for insomnia) or a wait-list control to determine the mechanistic contribution of sleep disruption to vascular dysfunction in young adults with moderate-to-high exposure to adverse childhood experiences (ACEs). Following the intervention, participants will again complete:
- rigorous at home sleep monitoring using 7-nights of wrist actigraphy and 2 nights of home-based polysomnography to objectively measure sleep quality (sleep efficiency, wakefulness after sleep onset and sleep depth), and total sleep duration,
- in vivo assessment of endothelial function via flow-mediated dilation testing, and
- in vitro determination of endothelial cell inflammation and oxidative stress from biopsied endothelial cells.
Investigators
Nathaniel Jenkins
Assistant Professor, Principal Investigator
University of Iowa
Eligibility Criteria
Inclusion Criteria
- •18-29 years of age
- •SBP \<129 and DBP \<90 mmHg
- •Body Mass Index \> 18.5 kg/m2 and \<35 kg/m2
- •Willing to complete in-home sleep studies
Exclusion Criteria
- •Currently undergoing treatment for a sleep disorder or diagnosed with restless leg syndrome, hypersomnia, parasomnia or narcolepsy, or obstructive sleep apnea
- •Currently performing overnight shift work
- •Lifetime history of any psychiatric disorder with psychotic features or bipolar disorder, currently undergoing treatment for substance-induced mood disorder
- •Endorsed suicidal ideation as indicated by a Moderate or High risk determination on the Columbia Suicide Risk Protocol
- •Diagnosed neurological disorder or illness affecting the central nervous system
- •Diagnosed acute or chronic autoimmune disease or chronic inflammatory condition
- •Current or previous cancer diagnosis
- •History of moderate or severe traumatic brain injury
- •Current or previous history of CBT-I treatment or sleep restriction or cognitive restructuring therapy for sleep
- •History of cardiometabolic disease (e.g., ischemic heart disease, coronary artery disease, stroke, chronic kidney disease, diabetes mellitus), pulmonary disease, or renal disease
Outcomes
Primary Outcomes
Vascular Endothelial Function
Time Frame: Week 0 (Pre-Intervention) and Week 7 (Post-Intervention)
The brachial artery flow-mediated dilation (FMD) technique, a non-invasive bioassay of endothelium-dependent vasodilatory function, will be used as the primary determinant of in-vivo vascular endothelial function.
Secondary Outcomes
- Endothelial nitrotyrosine expression.(Week 0 (Pre-Intervention) and Week 7 (Post-Intervention))
- Circulating IL1-RA(Week 0 (Pre-Intervention) and Week 7 (Post-Intervention))
- Anti-oxidant (Superoxide Dismutase) Activity in Peripheral Blood Mononuclear Cells(Week 0 (Pre-Intervention) and Week 7 (Post-Intervention))
- Anti-oxidant (Glutathione Reductase) Activity in Peripheral Blood Mononuclear Cells(Week 0 (Pre-Intervention) and Week 7 (Post-Intervention))
- Endothelial NFκB p65 expression.(Week 0 (Pre-Intervention) and Week 7 (Post-Intervention))
- Endothelial TNF-α expression.(Week 0 (Pre-Intervention) and Week 7 (Post-Intervention))
- Endothelial MCP-1 expression.(Week 0 (Pre-Intervention) and Week 7 (Post-Intervention))
- Circulating CRP(Week 0 (Pre-Intervention) and Week 7 (Post-Intervention))
- Circulating oxidized low density lipoprotein(Week 0 (Pre-Intervention) and Week 7 (Post-Intervention))
- Circulating 8-iso prostaglandin F2α(Week 0 (Pre-Intervention) and Week 7 (Post-Intervention))
- Endothelial NADPH-oxidase p47phox expression.(Week 0 (Pre-Intervention) and Week 7 (Post-Intervention))
- Anti-oxidant (Catalase) Activity in Peripheral Blood Mononuclear Cells(Week 0 (Pre-Intervention) and Week 7 (Post-Intervention))
- Perceived Stress(Week 0 (Pre-Intervention) and Week 7 (Post-Intervention))
- Distress(Week 0 (Pre-Intervention) and Week 7 (Post-Intervention))
- Circulating TNF-α(Week 0 (Pre-Intervention) and Week 7 (Post-Intervention))
- Circulating MCP-1(Week 0 (Pre-Intervention) and Week 7 (Post-Intervention))