Abstract:ObjectiveMost studies of rheumatoid arthritis (RA) and sleep have focused on established RA. We here investigate sleep quality and sleep duration in patients with newly diagnosed RA and during 1–12 years after diagnosis.MethodsData were collected on sleep 1–12 years after diagnosis from patients diagnosed 1998–2018 in the Swedish study Epidemiological Investigation of RA. Six sleep domains (sleep problems, non-restorative sleep, insomnia, insufficient sleep, sleep quality perceived as poor and sleep considered… Show more
“…The Swedish “RA Epidemiological Survey” from 1998 to 2018 collected sleep data from 1 to 12 years after diagnosis and did not find any major sleep problems. The existing sleep problems were mainly related to pain and functional decline ( 47 ). This may explain to a certain extent that short sleep time may be the cause of RA, and there is a one-way causal relationship between short sleep time and RA.…”
Currently, the causal association between sleep disorders and rheumatoid arthritis (RA) has been poorly understood. In this two-sample Mendelian randomization (TSMR) study, we tried to explore whether sleep disorders are causally associated with RA. Seven sleep-related traits were chosen from the published Genome-Wide Association Study (GWAS): short sleep duration, frequent insomnia, any insomnia, sleep duration, getting up, morningness (early-to-bed/up habit), and snoring, 27, 53, 57, 57, 70, 274, and 42 individual single-nucleotide polymorphisms (SNPs) (P < 5 × 10−8) were obtained as instrumental variables (IVs) for these sleep-related traits. Outcome variables were obtained from a public GWAS study that included 14,361 cases and 43,923 European Ancestry controls. The causal relationship between sleep disturbances and RA risk were evaluated by a two-sample Mendelian randomization (MR) analysis using inverse variance weighted (IVW), MR-Egger regression, weighted median, and weight mode methods. MR-Egger Regression and Mendelian randomization pleiotropy residual sum and outlier (MR-PRESSO) were used to test for horizontal pleomorphism and outliers. There was no evidence of a link between RA and frequent insomnia (IVW, odds ratio (OR): 0.99; 95% interval (CI): 0.84–1.16; P = 0.858), any insomnia (IVW, OR: 1.09; 95% CI: 0.85–1.42; P = 0.489), sleep duration (IVW, OR: 0.65, 95% CI: 0.38–1.10, P = 0.269), getting up (IVW, OR: 0.56, 95% CI: 0.13–2.46, P = 0.442), morningness (IVW, OR: 2.59; 95% CI: 0.73–9.16; P = 0.142), or snoring (IVW, OR: 0.95; 95% CI: 0.68–1.33; P = 0.757). Short sleep duration (6h) had a causal effect on RA, as supported by IVW and weighted median (OR: 1.47, 95% CI: 1.12–1.94, P = 0.006; OR: 1.43, 95%CI:1.01–2.05, P = 0.047). Sensitivity analysis showed that the results were stable. Our findings imply that short sleep duration is causally linked to an increased risk of RA. Therefore, sleep length should be considered in disease models, and physicians should advise people to avoid short sleep duration practices to lower the risk of RA.
“…The Swedish “RA Epidemiological Survey” from 1998 to 2018 collected sleep data from 1 to 12 years after diagnosis and did not find any major sleep problems. The existing sleep problems were mainly related to pain and functional decline ( 47 ). This may explain to a certain extent that short sleep time may be the cause of RA, and there is a one-way causal relationship between short sleep time and RA.…”
Currently, the causal association between sleep disorders and rheumatoid arthritis (RA) has been poorly understood. In this two-sample Mendelian randomization (TSMR) study, we tried to explore whether sleep disorders are causally associated with RA. Seven sleep-related traits were chosen from the published Genome-Wide Association Study (GWAS): short sleep duration, frequent insomnia, any insomnia, sleep duration, getting up, morningness (early-to-bed/up habit), and snoring, 27, 53, 57, 57, 70, 274, and 42 individual single-nucleotide polymorphisms (SNPs) (P < 5 × 10−8) were obtained as instrumental variables (IVs) for these sleep-related traits. Outcome variables were obtained from a public GWAS study that included 14,361 cases and 43,923 European Ancestry controls. The causal relationship between sleep disturbances and RA risk were evaluated by a two-sample Mendelian randomization (MR) analysis using inverse variance weighted (IVW), MR-Egger regression, weighted median, and weight mode methods. MR-Egger Regression and Mendelian randomization pleiotropy residual sum and outlier (MR-PRESSO) were used to test for horizontal pleomorphism and outliers. There was no evidence of a link between RA and frequent insomnia (IVW, odds ratio (OR): 0.99; 95% interval (CI): 0.84–1.16; P = 0.858), any insomnia (IVW, OR: 1.09; 95% CI: 0.85–1.42; P = 0.489), sleep duration (IVW, OR: 0.65, 95% CI: 0.38–1.10, P = 0.269), getting up (IVW, OR: 0.56, 95% CI: 0.13–2.46, P = 0.442), morningness (IVW, OR: 2.59; 95% CI: 0.73–9.16; P = 0.142), or snoring (IVW, OR: 0.95; 95% CI: 0.68–1.33; P = 0.757). Short sleep duration (6h) had a causal effect on RA, as supported by IVW and weighted median (OR: 1.47, 95% CI: 1.12–1.94, P = 0.006; OR: 1.43, 95%CI:1.01–2.05, P = 0.047). Sensitivity analysis showed that the results were stable. Our findings imply that short sleep duration is causally linked to an increased risk of RA. Therefore, sleep length should be considered in disease models, and physicians should advise people to avoid short sleep duration practices to lower the risk of RA.
“…Several recent studies have reported SS times for individuals with RA (11,21), and one study found that SS duration (≤6 hours) was causally linked to an increased risk of RA (22). However, other studies have noted sleep times similar to those in the general population (23). Poor sleep is commonly reported in rheumatoid arthritis (RA) and has potentially significant health implications, yet little research has examined the prevalence of specific sleep disorders in RA.Rate of each sleep disorder studied (obstructive sleep apnea, restless leg syndrome, short sleep) were higher in this cohort of individuals with RA than in the general population.RA disease activity and pain were significantly associated with each disorder.Additional research is needed to tease out the causal pathway for associations noted between sleep disorders and RA disease activity and pain, as well as to identify the long‐term consequences of sleep disorders in RA.…”
Section: Introductionmentioning
confidence: 52%
“…Several recent studies have reported SS times for individuals with RA (11,21), and one study found that SS duration (≤6 hours) was causally linked to an increased risk of RA (22). However, other studies have noted sleep times similar to those in the general population (23).…”
Objective
Self‐reported sleep problems are common in rheumatoid arthritis (RA), with potential negative health implications, yet relatively little research has focused on sleep in RA. We examined the prevalence of obstructive sleep apnea (OSA) risk, restless legs syndrome (RLS) symptoms, and short sleep (SS) in a large RA cohort (n = 4,200) and factors associated with each.
Methods
Data are from FORWARD, The National Databank for Rheumatic Diseases. Validated screening measures assessed OSA risk and RLS symptoms. SS was based on self‐reported average sleep time (<6 hours). The Medical Outcomes Study Sleep Problems Index I measured self‐reported sleep quality. Multivariable logistic regression models identified independent predictors of sleep disorders and sleep quality and the independent association of OSA risk, RLS symptoms, and SS with self‐reported poor sleep quality.
Results
Twenty‐one percent (n = 899) had OSA diagnosis or risk, 30% (n = 1,272) had RLS symptoms or diagnosis, and 43% (n = 1,737) reported SS, and RA disease activity was associated with each sleep disorder. Abatacept use was associated with lower odds of RLS and SS. Use of conventional disease‐modifying antirheumatic drugs or abatacept was less frequent in the SS group. No medications were associated with OSA in multivariable analyses. Both RLS and SS was associated with worse perceived sleep quality.
Discussion
Almost two‐thirds met criteria for at least one sleep disorder. RA disease activity and pain were significantly associated with each sleep condition. Additional research is needed to identify the causal pathway between sleep disorders and RA disease activity and pain and the long‐term consequences of sleep disorders in RA.
“…First, the total and direct effects of sleep disturbance on subsequent pain were small, and the beta coefficients for the indirect effects were low. Prior studies reporting associations between sleep disturbance and pain intensity have either been cross-sectional analyses or analyses examining next-day pain (4,36,37). It is possible that the magnitude of association would be higher if the duration between sleep assessment and pain intensity assessment were shorter.…”
Objective
Many patients with rheumatoid arthritis (RA) experience sleep disturbances, commonly attributed to joint pain. Sleep disturbances could also influence pain. One mechanism may be through dysregulated pain processing, manifested by enhanced pain sensitivity. The present study was undertaken to examine the role of pain sensitization, measured by quantitative sensory testing (QST), as a mediator in the pathway of sleep disturbance leading to subsequent pain.
Methods
We used longitudinal data from 221 patients with active RA who were followed for 12 weeks after initiating a disease‐modifying antirheumatic drug. Baseline QST included pressure pain thresholds at articular (wrists, knees) and nonarticular (trapezius, thumbnails) sites, temporal summation (TS) at the wrist and forearm, and conditioned pain modulation (CPM). Baseline sleep disturbance and subsequent pain intensity were assessed using the Patient‐Reported Outcomes Measurement Information System (PROMIS). We evaluated correlations between sleep disturbance, QSTs, and subsequent pain intensity. Mediation analyses separately assessed each QST as a mediator, adjusting for baseline confounding factors.
Results
Sleep disturbance was correlated with all QST measures except wrist TS and CPM. Sleep disturbance significantly predicted subsequent pain (coefficient for a meaningful increase of 5 units in sleep disturbance = 0.32 (95% confidence interval 0.11, 0.50) in multiple regression. QST mediated 10–19% of this effect.
Conclusion
Pain sensitization may be one mechanism through which sleep disturbance contributes to pain. The small magnitude of association indicates that unmeasured pathways may contribute to this relationship. Intervention studies are needed to establish causality and determine whether improving sleep can improve pain in patients with RA.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
