Associations of sleep duration and quality with serum and hepatic lipids: The Netherlands Epidemiology of Obesity Study

Abstract

Short and long sleep duration and poor sleep quality may affect serum and hepatic lipid content, but available evidence is inconsistent. Therefore, we aimed to investigate the associations of sleep duration and quality with serum and hepatic lipid content in a large population‐based cohort of middle‐aged individuals. The present cross‐sectional study was embedded in the Netherlands Epidemiology of Obesity (NEO) study and consisted of 4260 participants (mean age, 55 years; proportion men, 46%) not using lipid‐lowering agents. Self‐reported sleep duration and quality were assessed using the Pittsburgh Sleep Quality Index questionnaire (PSQI). Outcomes of this study were fasting lipid profile (total cholesterol, low‐density lipoprotein [LDL]‐cholesterol, high‐density lipoprotein [HDL]‐cholesterol and triglycerides), postprandial triglyceride (response) levels, and hepatic triglyceride content (HTGC) as measured with magnetic resonance spectroscopy. We performed multivariable linear regression analyses, adjusted for confounders and additionally for measures that link to adiposity (e.g. body mass index [BMI] and sleep apnea). We observed that relative to the group with median sleep duration (≈7.0 hr of sleep), the group with shortest sleep (≈5.0 hr of sleep) had 1.5‐fold higher HTGC (95% confidence interval [CI]: 1.0‐2.2). The group with PSQI score ≥ 10 had a 1.1‐fold (95% CI: 1.0‐1.2) higher serum triglyceride level compared with the group with PSQI ≤ 5. However, these associations disappeared after adjustment for BMI and sleep apnea. Therefore, we concluded that previously observed associations of shorter sleep duration and poorer sleep quality with an adverse lipid profile, may be explained by BMI and sleep apnea, rather than by a direct effect of sleep on the lipid profile.

Sex-specific association of sleep duration with subclinical indicators of metabolic diseases among asymptomatic adults

“…Existed evidence have revealed the associations of sleep duration with simple lipid and glucose metabolism indicators, such as WC [32], HDL-C [33], and TG [34,35]. However, the conclusions were, to a large extent, controversial.…”

“…In the current study, 7-9 h was the reference, and only sleep duration <7 h was associated with higher LAP. Existed evidence have revealed the associations of sleep duration with simple lipid and glucose metabolism indicators, such as WC [ 32 ], HDL-C [ 33 ], and TG [ 34 , 35 ]. However, the conclusions were, to a large extent, controversial.…”

Investigating the relationships between unfavourable habitual sleep and metabolomic traits: evidence from multi-cohort multivariable regression and Mendelian randomization analyses

“…There is some evidence of poor sleep quality, shorter sleep duration, and having an evening chronotype being associated with higher triglyceride, total cholesterol and low-density lipoprotein cholesterol (LDL-C) levels, and lower high-density lipoprotein cholesterol (HDL-C) concentrations [ 10 – 12 ]. However, the extent to which these associations are explained by confounding factors, such as body mass index [ 11 ], is unclear. Beyond conventional multivariable-adjusted regression analyses, we have previously demonstrated that sleep duration modifies the associations of genetic variation with triglycerides, LDL-C and HDL-C in a large sleep-gene interaction analysis, suggesting that possible different biological mechanisms underlie the associations of short and long sleep duration with these lipid traits [ 13 ].…”

Multi-ancestry analysis of gene-sleep interactions in 126,926 individuals identifies multiple novel blood lipid loci that contribute to our understanding of sleep-associated adverse blood lipid profile

“…Sleep is increasingly recognized as a fundamental behavior that influences a wide range of physiological processes 14 . A large volume of epidemiological research implicates disturbed sleep in the pathogenesis of atherosclerosis 15 , and specifically, both a long and short sleep duration are associated with an adverse blood lipid profile [16][17][18][19][20][21][22][23][24][25][26] . However, it is unknown whether sleep duration modifies genetic risk factors for adverse blood lipid profiles.…”

“…Given that there are differences among ancestry groups in sleep behaviours and lipid levels, analysis of data from cohorts of varying ancestries may further the discovery of robust interactions between genetic loci and sleep traits. We focused on short total sleep time (STST; defined as the lower 20% of age-and sex-adjusted sleep duration residuals) and long total sleep time (LTST; defined as the upper 20% of age-and sex-adjusted sleep duration residuals) as exposures compared to the remaining individuals in the study population, given that each extreme sleep trait has been associated with multiple metabolic and health outcomes[15][16][17][18][19][20][21][22][23][24][25][26][30][31][32][33][34] . Within the present study, we report multi-ancestry sleep-by-SNP interaction analyses for blood lipid levels that successfully identified several novel loci for blood lipid traits.…”