Principal Investigator: Assistant Professor Philip Gehrman
University of Pennsylvania
Perelman School of Medicine
3535 Market Street, Suite 670
Philadelphia PA 19104
United StatesTags: 16434, cognitive function, epidemiology, featured, public health, sleep
Professor Mary Morrell and Professor Michael Grandner
Collaborating Institutions and Addresses:
University of Arizona
Department of Psychiatry
Sleep and Health Research Program
1501 N Campbell Avenue
Tucson AZ 85274-5002
Imperial College London
Royal Brompton Hospital
London SW3 6NP
1a: There is a body of literature showing that in the laboratory, sleep deprivation leads to cardiometabolic dysregulation. This literature is mirrored at the epidemiologic level, showing increased incidence and prevalence of obesity, diabetes, and cardiovascular disease. Similarly, there is a body of literature showing that in the laboratory, sleep deprivation leads to cognitive dysfunction. However, there are very few studies at the epidemiologic level that have attempted to show whether these findings translate into real-world effects. The UK Biobank has the screening measures for working memory, basic verbal functioning, and basic abstract reasoning. We wish to investigate (1) the associations between sleep duration and cognitive function [is short or long sleep associated with impaired cognitive function?], (2) a potential mediating role of daytime sleepiness [is this effect due to increased sleepiness/fatigue?], (3) a potential moderating role of these relationships on self-reported health outcomes [do cognitive impairments track with health impairments?], and (4) whether there are common genetic variants that are associated with sleep duration.
1b: This study will leverage the sleep, cognitive, and genomic data obtained via the UK Biobank to address an issue of public health relevance that has not been previously examined.
1c: This study will be a secondary analysis of existing data. The first portion of the analyses will focus on self-reported sleep duration (independent variable), sleep duration assessed with actigraphy (independent variable), cognitive function (dependent variables), covariates (demographics, socioeconomics, and health factors), and potential moderating factors (sleepiness/fatigue). The second portion of the analyses will use the genotyping data to conduct a GWA analysis of sleep duration assessed with both self-report and actigraphy. The analyses will examine whether habitual sleep duration will is associated with cognitive function variables, whether these relationships persist in the presence of covariates, the potential role of cardiometabolic and other comorbidities, whether the effects of sleep duration are mediated by sleepiness/fatigue, and whether genetic variants are associated with sleep duration.
1d: All cohort members with sleep duration, cognitive data and genotyping. Actigraphy analyses will focus on the subsent (~100,000) who participated in this portion of the study.