A Machine Learning Model for Predicting Sleep and Wakefulness Based on Accelerometry, Skin Temperature and Contextual Information.

Purpose: Body-worn accelerometers are commonly used to estimate sleep duration in population-based studies. However, since accelerometry-based sleep/wake-scoring relies on detecting body movements, the prediction of sleep duration remains a challenge. The aim was to develop and evaluate the performance of a machine learning (ML) model to predict accelerometry-based sleep duration and to explore if this prediction can be improved by adding skin temperature data, circadian rhythm based on the estimated midpoint of sleep, and cyclic time features to the model. Patients and Methods: Twenty-nine adults (17 females), mean (SD) age 40.2 (15.0) years (range 17-70) participated in the study. Overnight polysomnography (PSG) was recorded in a sleep laboratory or at home along with body movement by two accelerometers with an embedded skin temperature sensor (AX3, Axivity, UK) positioned at the low back and thigh. The PSG scoring of sleep/wake was used as ground truth for training the ML model. Results: Based on pure accelerometer data input to the ML model, the specificity and sensitivity for predicting sleep/wake was 0.52 (SD 0.24) and 0.95 (SD 0.03), respectively. Adding skin temperature data and contextual information to the ML model improved the specificity to 0.72 (SD 0.20), while sensitivity remained unchanged at 0.95 (SD 0.05). Correspondingly, sleep overestimation was reduced from 54 min (228 min, limits of agreement range [LoAR]) to 19 min (154 min LoAR). Conclusion: An ML model can predict sleep/wake periods with excellent sensitivity and moderate specificity based on a dual-accelerometer set-up when adding skin temperature data and contextual information to the model.

Incidence of sick leave and disability pension in adults with musculoskeletal pain and co-occurring long-term conditions: data from the Norwegian HUNT study and national registries.

BACKGROUND: Musculoskeletal pain is one of the leading causes of work productivity loss. Long-term conditions (LTCs) commonly occur alongside musculoskeletal pain. However, the incidence of sick leave and disability pension according to LTC status in people with musculoskeletal pain has not been previously described. METHODS: Working-age participants (20-65 years) with persistent musculoskeletal pain who participated in the HUNT3 Study (1995-97) were included. Twenty-five LTCs were classified into 8 LTC groups according to the International Classification of Diseases version 11. Data on sickness and disability benefits were obtained from the National Insurance Database and linked to the HUNT3 data using participants' personal identification number. Age-adjusted incidence rates (IRs) (per 10,000 person-years) and hazard ratios (HRs) of sick leave during 5-year follow-up and disability pension during ~ 25-year follow-up were estimated with 95% confidence intervals (CIs) and presented according to LTC status. RESULTS: Overall, 11,080 participants with musculoskeletal pain were included. Of those, 32% reported one LTC and 45% reported ≥ 2 LTCs. During the follow up period, 1,312 participants (12%) received disability pension due to musculoskeletal conditions. The IR of sick leave and disability pension due to musculoskeletal conditions increased with number of LTCs. Specifically, the IR of sick leave was 720 (95% CI 672 to 768) in participants without any LTCs and 968 (95% CI 927 to 1,009) if they had ≥ 2 LTCs. The IRs of disability pension were 87 (95% CI 75 to 98) and 167 (95% CI 154 to 179) among those with no LTCs and ≥ 2 LTCs, respectively. The incidence of sick leave and disability pension due to musculoskeletal conditions was largely similar across LTCs, although the incidence of disability pension was somewhat higher among people with sleep disorders (IR: 223, 95% CI 194 to 252). CONCLUSIONS: Among people with persistent musculoskeletal pain, the incidence of prematurely leaving the work force due to musculoskeletal conditions was twice as high for those with multiple LTCs compared to those without any LTCs. This was largely irrespective of the type of LTC, indicating that the number of LTCs are an important feature when evaluating work participation among people with musculoskeletal pain.

Inpatient multimodal rehabilitation and the role of pain intensity and mental distress on return-to-work: causal mediation analyses of a randomized controlled trial.

OBJECTIVE: Studies suggest that symptom reduction is not necessary for improved return-to-work after occupational rehabilitation programmes. This secondary analysis of a randomized controlled trial examined whether pain intensity and mental distress mediate the effect of an inpatient programme on sustainable return-to-work. METHODS: The randomized controlled trial compared inpatient multimodal occupational rehabilitation (n = 82) with outpatient acceptance and commitment therapy (n = 79) in patients sick-listed due to musculoskeletal and mental health complaints. Pain and mental distress were measured at the end of each programme, and patients were followed up on sick-leave for 12 months. Cox regression with an inverse odds weighted approach was used to assess causal mediation. RESULTS: The total effect on return-to-work was in favour of the inpatient programme compared with the control (hazard ratio (HR) 1.96; 95% confidence interval (95% CI) 1.15-3.35). There was no evidence of mediation by pain intensity (indirect effect HR, 0.98; 95% CI, 0.61-1.57, direct effect HR, 2.00; 95% CI, 1.02-3.90), but mental distress had a weak suppression effect (indirect effect HR, 0.89; 95% CI, 0.59-1.36, direct effect HR, 2.19; 95% CI, 1.13-4.26). CONCLUSION: These data suggest that symptom reduction is not necessary for sustainable return-to-work after an inpatient multimodal occupational rehabilitation intervention.

The joint association of insomnia disorder and lifestyle on the risk of activity-limiting spinal pain: the HUNT Study.

OBJECTIVES: To investigate whether the combination of multiple healthy lifestyle factors modify the well-established association between insomnia disorder and risk of activity-limiting spinal pain. METHODS: We conducted a prospective study of 10,228 individuals who participated in two surveys over ∼11 years and were free of chronic pain in the neck, upper back, and lower back at baseline. Adjusted risk ratios (RRs) were calculated for the risk of activity-limiting chronic spinal pain (i.e., pain that impairs daily activities at work or leisure time) at follow-up associated with the joint association of insomnia disorder and the combination of five lifestyle factors (body mass index, leisure time physical activity, alcohol consumption, diet, and smoking) at baseline. RESULTS: Our data indicate an additive interaction between insomnia disorder and lifestyle on risk of activity-limiting spinal pain, i.e., compared with participants without insomnia disorder and the best lifestyle score, participants with insomnia disorder and the worst lifestyle score had a RR of activity-limiting spinal pain of 3.57 (95 % CI: 2.65-4.80); participants with insomnia disorder and the best lifestyle score had a RR of 1.56 (95 % CI: 0.97-2.50); and those without insomnia disorder and the worst lifestyle score had a RR of 1.32 (95 % CI: 1.12-1.55). CONCLUSIONS: Poor lifestyle behaviour amplifies the adverse effect of insomnia disorder on the risk of activity-limiting chronic spinal pain.

Can the bias of self-reported sitting time be corrected? A statistical model validation study based on data from 23 993 adults in the Norwegian HUNT study.

BACKGROUND: Despite apparent shortcomings such as measurement error and low precision, self-reported sedentary time is still widely used in surveillance and research. The aim of this study was threefold; (i) to examine the agreement between self-reported and device-measured sitting time in a general adult population; (ii), to examine to what extent demographics, lifestyle factors, long-term health conditions, physical work demands, and educational level is associated with measurement bias; and (iii), to explore whether correcting for factors associated with bias improves the prediction of device-measured sitting time based on self-reported sitting time. METHODS: A statistical validation model study based on data from 23 993 adults in the Trøndelag Health Study (HUNT4), Norway. Participants reported usual sitting time on weekdays using a single-item questionnaire and wore two AX3 tri-axial accelerometers on the thigh and low back for an average of 3.8 (standard deviation [SD] 0.7, range 1-5) weekdays to determine their sitting time. Statistical validation was performed by iteratively adding all possible combinations of factors associated with bias between self-reported and device-measured sitting time in a multivariate linear regression. We randomly selected 2/3 of the data (n = 15 995) for model development and used the remaining 1/3 (n = 7 998) to evaluate the model. RESULTS: Mean (SD) self-reported and device-measured sitting time were 6.8 (2.9) h/day and 8.6 (2.2) h/day, respectively, corresponding to a mean difference of 1.8 (3.1) h/day. Limits of agreement ranged from - 8.0 h/day to 4.4 h/day. The discrepancy between the measurements was characterized by a proportional bias with participants device-measured to sit less overestimating their sitting time and participants device-measured to sit more underestimating their sitting time. The crude explained variance of device-measured sitting time based on self-reported sitting time was 10%. This improved to 24% when adding age, body mass index and physical work demands to the model. Adding sex, lifestyle factors, educational level, and long-term health conditions to the model did not improve the explained variance. CONCLUSIONS: Self-reported sitting time had low validity and including a range of factors associated with bias in self-reported sitting time only marginally improved the prediction of device-measured sitting time.

Investigating the causal interplay between sleep traits and risk of acute myocardial infarction: a Mendelian randomization study.

BACKGROUND: Few studies have investigated the joint effects of sleep traits on the risk of acute myocardial infarction (AMI). No previous study has used factorial Mendelian randomization (MR) which may reduce confounding, reverse causation, and measurement error. Thus, it is prudent to study joint effects using robust methods to propose sleep-targeted interventions which lower the risk of AMI. METHODS: The causal interplay between combinations of two sleep traits (including insomnia symptoms, sleep duration, or chronotype) on the risk of AMI was investigated using factorial MR. Genetic risk scores for each sleep trait were dichotomized at their median in UK Biobank (UKBB) and the second survey of the Trøndelag Health Study (HUNT2). A combination of two sleep traits constituting 4 groups were analyzed to estimate the risk of AMI in each group using a 2×2 factorial MR design. RESULTS: In UKBB, participants with high genetic risk for both insomnia symptoms and short sleep had the highest risk of AMI (hazard ratio (HR) 1.10; 95% confidence interval (CI) 1.03, 1.18), although there was no evidence of interaction (relative excess risk due to interaction (RERI) 0.03; 95% CI -0.07, 0.12). These estimates were less precise in HUNT2 (HR 1.02; 95% CI 0.93, 1.13), possibly due to weak instruments and/or small sample size. Participants with high genetic risk for both a morning chronotype and insomnia symptoms (HR 1.09; 95% CI 1.03, 1.17) and a morning chronotype and short sleep (HR 1.11; 95% CI 1.04, 1.19) had the highest risk of AMI in UKBB, although there was no evidence of interaction (RERI 0.03; 95% CI -0.06, 0.12; and RERI 0.05; 95% CI -0.05, 0.14, respectively). Chronotype was not available in HUNT2. CONCLUSIONS: This study reveals no interaction effects between sleep traits on the risk of AMI, but all combinations of sleep traits increased the risk of AMI except those with long sleep. This indicates that the main effects of sleep traits on AMI are likely to be independent of each other.

App-Delivered Cognitive-Behavioral Therapy for Insomnia Among Patients with Comorbid Musculoskeletal Complaints and Insomnia Referred to 4-Week Inpatient Multimodal Rehabilitation: Protocol for a Randomized Clinical Trial.

Background: Insomnia is prevalent among patients receiving treatment for long-term musculoskeletal complaints in inpatient rehabilitation settings. Cognitive-behavioral therapy for insomnia (CBT-I) is effective for improving sleep quality in patients with pain, but a lack of therapists often limits the capacity to use this therapy in rehabilitation programs. The aim of this randomized clinical trial (RCT) is to evaluate the effectiveness of app-delivered CBT-I adjunct to inpatient multimodal rehabilitation for individuals with comorbid musculoskeletal complaints and insomnia, compared with rehabilitation (usual care) only. Methods: This RCT has two parallel arms: 1) inpatient multimodal rehabilitation and 2) app-delivered CBT-I adjunct to inpatient multimodal rehabilitation. Patients referred to Unicare Helsefort (Norway) with long-term chronic musculoskeletal complaints are invited to the study. Eligible and consenting participants will be randomized to the intervention and usual care at a ratio of 2:1. Assessments will be carried out at baseline (prior to randomization), 6 weeks (at the end of rehabilitation), 3 months (primary outcome), as well as 6 and 12 months after the rehabilitation. The primary outcome is insomnia severity measured at 3 months. Secondary outcomes include pain intensity, health-related quality of life, fatigue, physical function, work ability, expectations about sick leave length, sick leave, and prescribed medication. Exploratory analyses are planned to identify moderators and mediators of the effect of the app-delivered intervention. Discussion: This RCT will provide novel knowledge about the effectiveness of app-delivered CBT-I as an adjunct to usual care among patients participating in inpatient multimodal pain rehabilitation. Regardless of the results from this trial, the results will improve our understanding of the utility of dCBT-I in the field of rehabilitation and the importance of adding sleep therapy to this patient group. Trial Registration: This trial was prospectively registered in ClinicalTrials.gov October 10, 2022 (ClinicalTrials.gov identifier: NCT05572697).

Group-delivered cognitive behavioural therapy versus waiting list in the treatment of insomnia in primary care: study protocol for a pragmatic, multicentre randomized controlled trial.

BACKGROUND: Insomnia is common in the general population and is a risk factor for ill-health, which highlights the importance of treating insomnia effectively and cost-efficiently. Cognitive-behavioural therapy for insomnia (CBT-I) is recommended as first-line treatment due to its long-term effectiveness and few side-effects, but its availability is limited. The aim of this pragmatic, multicentre randomized controlled trial is to investigate the effectiveness of group-delivered CBT-I in primary care compared to a waiting-list control group. METHODS: A pragmatic multicentre randomized controlled trial will be conducted with about 300 participants recruited across 26 Healthy Life Centres in Norway. Participants will complete online screening and provide consent before enrolment. Those who meet the eligibility criteria will be randomized to a group-delivered CBT-I or to a waiting list according to a 2:1 ratio. The intervention consists of four two-hour sessions. Assessments will be performed at baseline, 4 weeks, 3- and 6 months post-intervention, respectively. The primary outcome is self-reported insomnia severity at 3 months post-intervention. Secondary outcomes include health-related quality of life, fatigue, mental distress, dysfunctional beliefs and attitudes about sleep, sleep reactivity, 7-day sleep diaries, and data obtained from national health registries (sick leave, use of relevant prescribed medications, healthcare utilization). Exploratory analyses will identify factors influencing treatment effectiveness, and we will conduct a mixed-method process evaluation to identify facilitators and barriers of participants' treatment adherence. The study protocol was approved by the Regional Committee for Medical and Health Research ethics in Mid-Norway (ID 465241). DISCUSSION: This large-scale pragmatic trial will investigate the effectiveness of group-delivered cognitive behavioural therapy versus waiting list in the treatment of insomnia, generating findings that are generalizable to day-to-day treatment of insomnia in interdisciplinary primary care services. The trial will identify those who would benefit from the group-delivered therapy, and will investigate the rates of sick leave, medication use, and healthcare utilization among adults who undergo the group-delivered therapy. TRIAL REGISTRATION: The trial was retrospectively registered in the ISRCTN registry (ISRCTN16185698).

Self-reported insomnia symptoms, sleep duration, chronotype and the risk of acute myocardial infarction (AMI): a prospective study in the UK Biobank and the HUNT Study.

Insomnia and short/long sleep duration increase the risk of AMI, but their interaction with each other or with chronotype is not well known. We investigated the prospective joint associations of any two of these sleep traits on risk of AMI. We included 302 456 and 31 091 participants without past AMI episodes from UK Biobank (UKBB; 2006-10) and the Trøndelag Health Study (HUNT2; 1995-97), respectively. A total of 6 833 and 2 540 incident AMIs were identified during an average 11.7 and 21.0 years follow-up, in UKBB and HUNT2, respectively. Compared to those who reported normal sleep duration (7-8 h) without insomnia symptoms, the Cox proportional hazard ratios (HRs) for incident AMI in UKBB among participants who reported normal, short and long sleep duration with insomnia symptoms were 1.07 (95% CI 0.99, 1.15), 1.16 (95% CI 1.07, 1.25) and 1.40 (95% CI 1.21, 1.63), respectively. The corresponding HRs in HUNT2 were 1.09 (95% CI 0.95, 1.25), 1.17 (95% CI 0.87, 1.58) and 1.02 (95% CI 0.85, 1.23). The HRs for incident AMI in UKBB among evening chronotypes were 1.19 (95% CI 1.10, 1.29) for those who had insomnia symptoms, 1.18 (95% CI 1.08, 1.29) for those with short sleep duration, and 1.21 (95% CI 1.07, 1.37) for those with long sleep duration, compared to morning chronotypes without another sleep symptom. The relative excess risk for incident AMI in UKBB due to interaction between insomnia symptoms and long sleep duration was 0.25 (95% CI 0.01, 0.48). Insomnia symptoms with long sleep duration may contribute more than just an additive effect of these sleep traits on the risk of AMI.

A bidirectional study of the association between insomnia, high-sensitivity C-reactive protein, and comorbid low back pain and lower limb pain.

OBJECTIVES: To examine the possible bidirectional association between insomnia and comorbid chronic low back pain (LBP) and lower limb pain and to explore whether high-sensitivity C-reactive protein (hsCRP) amplifies these associations. METHODS: We calculated adjusted risk ratios (RR) with 95% confidence intervals (CI) for the development of insomnia and mild-to-severe chronic LBP and lower limb pain at 11 years follow-up in participants aged ≥32 years and with hsCRP ≤10 mg/L at baseline in 2007-2008: 3,714 without chronic LBP or lower limb pain (sample 1) and 7,892 without insomnia (sample 2). RESULTS: Compared to participants without chronic pain, participants with comorbid chronic LBP and lower limb pain had a RR of insomnia of 1.37 (95% CI 1.12-1.66). Compared with participants without insomnia, participants with insomnia did not have an increased risk of comorbid chronic LBP and lower limb pain (RR: 1.06, 95% CI 0.76-1.46); however, participants with insomnia had a RR of chronic LBP of 1.20 (95% CI 1.02-1.42). There was no strong amplifying effect of elevated hsCRP (3.00-10.0 mg/L) on these associations. CONCLUSIONS: These findings suggest that elevated hsCRP does not amplify the associations between insomnia and mild-to-severe chronic LBP and lower limb pain. Further research using data on the temporal relation between insomnia, chronic pain, and inflammatory responses are required to fully understand the causal pathways.

The joint effect of sleep duration and insomnia symptoms on the risk of recurrent spinal pain: The HUNT study.

Although sleep quantity and quality appear to be interrelated, most previous studies have considered sleep duration and insomnia symptoms as distinct entities. We therefore examined whether there is a joint effect of sleep duration and long-term changes in insomnia symptoms on the risk of recurrent chronic spinal pain. We performed a prospective study of 8,788 participants who participated in three surveys over ∼22 years and reported chronic spinal pain at the first, second, or both surveys. Adjusted risk ratios (RRs) were calculated for the risk of recurrent spinal pain at the last survey associated with self-reported sleep duration at the first survey and changes in insomnia symptoms between the two first surveys. Compared to participants with normal sleep duration (7-9 h) and no insomnia symptoms at the two first surveys, participants with insomnia symptoms over the same period had RRs of spinal pain of 1.33 (95% CI 1.26-1.41) in the last survey if they reported normal sleep duration and 1.50 (95% CI 1.34-1.67) if they reported short sleep (≤6 h). The corresponding RRs for spinal pain for participants who improved their sleep symptoms were 1.09 (95% CI 1.00-1.19) for those with normal sleep and 1.13 (95% CI 0.88-1.45) for those with short sleep. In conclusion, people who reported insomnia symptoms over ∼10 years in combination with short sleep had a particularly increased risk of recurrent spinal pain. Improvement in insomnia symptoms was associated with a favorable prognosis.

The interplay between multisite pain and insomnia on the risk of anxiety and depression: the HUNT study.

BACKGROUND: Chronic musculoskeletal pain and insomnia frequently co-occur and are known independent risk factors for anxiety and depression. However, the interplay between these two conditions on the risk of anxiety and depression has not been explored. METHODS: A population-based prospective study of 18,301 adults in the Norwegian HUNT Study without anxiety or depression at baseline (2006-2008). We calculated adjusted risk ratios (RRs) with 95% confidence intervals (CIs) for anxiety and/or depression at follow-up (2017-2019), associated with i) number of chronic pain sites, and ii) chronic pain and insomnia symptoms jointly. RESULTS: At follow-up, 2155 (11.8%) participants reported anxiety and/or depression. The number of pain sites was positively associated with risk of anxiety and/or depression (Ptrend, < 0.001). Compared to people without chronic pain and insomnia symptoms, people with ≥5 pain sites and no insomnia symptoms had a RR of 1.52 (95% CI: 1.28 to 1.81) for anxiety and/or depression, those with no chronic pain but with insomnia had a RR of 1.78 (95% CI: 1.33 to 2.38), whereas the RR among people with both ≥5 pain sites and insomnia was 2.42 (95% CI: 1.85 to 3.16). We observed no synergistic effect above additivity for the combination of ≥5 pain sites and insomnia on risk of anxiety and/or depression. CONCLUSIONS: This study shows that people with multisite chronic pain who also suffer from insomnia are at a particularly high risk for anxiety and/or depression, suggesting that insomnia symptoms are important contributors to the association between multisite pain and common mental health problems.

Insomnia is Associated with the Effect of Inpatient Multimodal Occupational Rehabilitation on Work Participation in Workers with Musculoskeletal or Mental Health Disorders: Secondary Analyses of a Randomized Clinical Trial.

STUDY OBJECTIVES: Insomnia is common among people with musculoskeletal and/or mental health disorders. This study aimed to assess whether insomnia is associated with the favorable effect from inpatient multimodal occupational rehabilitation on future work participation among individuals with these conditions. METHODS: Insomnia was measured at baseline through a randomized clinical trial that compared the effect of inpatient multimodal occupational rehabilitation with a less-comprehensive program of outpatient acceptance and commitment therapy on future work participation. The inpatient multimodal program lasted 3.5 weeks at the rehabilitation center, comprising psychoeducational sessions (including sleep education), fixed schedules, acceptance and commitment therapy, physical exercise and work-related problem-solving, whereas the outpatient program comprised mainly six weekly acceptance and commitment therapy sessions. Both programs were group-based. The study tracked cumulative sick leave during the 12 months of follow-up using national registry data. RESULTS: Among the 163 adults included in this subgroup analysis, 56% (n=91) reported insomnia. Overall, we found statistical evidence of interaction between the occupational program and insomnia concerning cumulative sick leave (p=0.03). Compared with people without insomnia in the comprehensive inpatient multimodal program, people with insomnia had 12 (95% CI: -48 to 24) fewer days with sick leave if they participated in the inpatient program and 46 (95% CI: 8 to 83) more days if they participated in the outpatient program. CONCLUSION: These findings suggest that insomnia should be addressed specifically before individuals on sick leave are considered for participation in occupational rehabilitation and that individuals with insomnia may benefit in particular from inpatient rehabilitation.

Subtypes of insomnia and the risk of chronic spinal pain: the HUNT study.

OBJECTIVE: To examine the association between subtypes of insomnia and the risk of chronic spinal pain. METHODS: The study comprised 16,401 participants without chronic spinal pain at baseline who were followed for ∼11 years. People were categorized into 'no insomnia symptoms', 'subthreshold insomnia', and 'insomnia'. Insomnia was defined according to the diagnostic classification system requiring both daytime and nighttime symptoms, and further categorized into subtypes based on nighttime symptoms (ie, sleep onset latency [SOL-insomnia], wake after sleep onset [WASO-insomnia], early morning awakening [EMA-insomnia], or combinations of these). Subthreshold insomnia comprised those with only daytime impairment or one or more nighttime symptoms. Chronic spinal pain was defined as pain in either 'neck', 'low back', or 'upper back', or a combination of these. RESULTS: In multivariable regression analysis using people without insomnia as reference, people with subthreshold insomnia or insomnia had relative risks (RRs) of chronic spinal pain of 1.29 (95% confidence interval [CI] 1.21-1.38) and 1.50 (95% CI 1.34-1.68), respectively. The RRs for people with one nighttime symptom were 1.30 (95% CI 0.83-2.05) for WASO-insomnia, 1.32 (95% CI 1.06-1.65) for EMA-insomnia, and 1.70 (95% CI 1.32-2.18) for SOL-insomnia, respectively. Combinations of nighttime insomnia symptoms gave RRs from 1.45 (95% CI 1.08-1.94) for WASO + EMA-insomnia to 1.72 (95% CI 1.36-2.19) for all nighttime symptoms (SOL + WASO + EMA-insomnia). CONCLUSIONS: These findings suggest that the risk of chronic spinal pain is highest among persons with insomnia subtypes characterized by sleep onset latency or among those having insomnia symptoms in all parts of the sleep period.

The effect of long-term poor sleep quality on risk of back-related disability and the modifying role of physical activity.

Sleep problems and regular leisure time physical activity (LTPA) are interrelated and have contrasting effects on risk of back pain. However, no studies have investigated the influence of long-term poor sleep quality on risk of back-related disability, or if LTPA modifies this association. The study comprised data on 8601 people who participated in three consecutive surveys over ~ 22 years, and who reported no chronic back pain at the two first surveys. Adjusted risk ratios (RRs) for back-related disability were calculated at the last survey, associated with the joint effect of changes in sleep quality between the two first surveys and meeting physical activity guidelines at the second survey. Compared to people with long-term good sleep, people with long-term poor sleep had nearly twice the risk of back-related disability (RR 1.92, 95% CI 1.48-2.49). There was no statistical interaction between sleep and LTPA but people who reported long-term poor sleep and meeting the physical activity guidelines had 35% lower risk of back-related disability compared to people with same level of sleep problems, but who not met the guidelines. These findings suggest that long-term poor sleep quality contributes to a substantially increased risk of chronic and disabling back pain irrespective of LTPA.

Long-term changes in self-reported sleep quality and risk of chronic musculoskeletal pain: The HUNT Study.

We examined the association between long-term (~10 years) changes in self-reported sleep quality and risk of any chronic musculoskeletal pain and chronic widespread pain. The study comprised data on 6,033 people who participated in three consecutive surveys in the Norwegian HUNT Study (1995-1997, 2006-2008 and 2017-2019) and who were without chronic musculoskeletal pain at the first two surveys. We used a modified Poisson regression model to calculate adjusted risk ratios for chronic pain at follow-up (2017-2019) associated with categories of poor and good sleep quality reported in 1995-1997 and 2006-2008. Compared with people who reported good sleep at both surveys (crude absolute risk: 32.4%), the risk ratios of any chronic pain were 1.20 (95% confidence interval: 1.02-1.41) for those who changed from poor to good sleep; 1.25 (95% confidence interval: 1.12-1.39) for those who changed from good to poor sleep; and 1.41 (95% confidence interval: 1.21-1.63) for those who reported long-term poor sleep. The corresponding risk ratios for chronic widespread pain were 1.35 (95% confidence interval: 0.82-2.23), 1.55 (95% confidence interval: 1.14-2.12) and 2.09 (95% confidence interval: 1.38-3.17), respectively. In conclusion, these findings indicate that people with long-term poor sleep quality have a markedly higher risk of chronic musculoskeletal pain and chronic widespread pain, compared with people who remain good sleep quality.

Genetic variants related to physical activity or sedentary behaviour: a systematic review.

BACKGROUND: Research shows that part of the variation in physical activity and sedentary behaviour may be explained by genetic factors. Identifying genetic variants associated with physical activity and sedentary behaviour can improve causal inference in physical activity research. The aim of this systematic review was to provide an updated overview of the evidence of genetic variants associated with physical activity or sedentary behaviour. METHODS: We performed systematic literature searches in PubMed and Embase for studies published from 1990 to April 2020 using keywords relating to "physical activity", "exercise", "sedentariness" and "genetics". Physical activity phenotypes were either based on self-report (e.g., questionnaires, diaries) or objective measures (e.g., accelerometry, pedometer). We considered original studies aiming to i) identify new genetic variants associated with physical activity or sedentary behaviour (i.e., genome wide association studies [GWAS]), or ii) assess the association between known genetic variants and physical activity or sedentary behaviour (i.e., candidate gene studies). Study selection, data extraction, and critical appraisal were carried out by independent researchers, and risk of bias and methodological quality was assessed for all included studies. RESULTS: Fifty-four out of 5420 identified records met the inclusion criteria. Six of the included studies were GWAS, whereas 48 used a candidate gene approach. Only one GWAS and three candidate gene studies were considered high-quality. The six GWAS discovered up to 10 single nucleotide polymorphisms (SNPs) associated with physical activity or sedentariness that reached genome-wide significance. In total, the candidate gene studies reported 30 different genes that were associated (p < 0.05) with physical activity or sedentary behaviour. SNPs in or close to nine candidate genes were associated with physical activity or sedentary behaviour in more than one study. CONCLUSION: GWAS have reported up to 10 loci associated with physical activity or sedentary behaviour. Candidate gene studies have pointed to some interesting genetic variants, but few have been replicated. Our review highlights the need for high-quality GWAS in large population-based samples, and with objectively assessed phenotypes, in order to establish robust genetic instruments for physical activity and sedentary behaviour. Furthermore, consistent replications in GWAS are needed to improve credibility of genetic variants. TRIAL REGISTRATION: Prospero CRD42019119456 .

It is never too late to start: adherence to physical activity recommendations for 11-22 years and risk of all-cause and cardiovascular disease mortality. The HUNT Study.

OBJECTIVES: To examine associations between long-term (11-22 years) adherence to physical activity recommendations and mortality from all causes and from cardiovascular disease. DESIGN: Prospective population-based study with repeated assessments of self-reported physical activity (1984-86, 1995-97 and 2006-08) and follow-up until the end of 2013. SETTING: County of Nord-Trøndelag, Norway. PARTICIPANTS: Men and women aged ≥20 years; 32 811 who participated in 1984-86 and 1995-97; 22 058 in 1984-86 and 2006-08; 31 948 in 1995-97 and 2006-09 and 19 349 in all three examinations (1984-1986, 1995-95 and 2006-08). MAIN OUTCOME MEASURES: All-cause mortality and cardiovascular disease mortality from the national Cause of Death Registry. RESULTS: Compared with the reference category comprising individuals who adhered to the physical activity recommendations (≥150 min of moderate intensity or ≥60 min of vigorous intensity physical activity per week) over time, individuals who remained inactive (reporting no or very little physical activity) from 1984-86 to 1995-97 had HRs (95% CI) of 1.56 (1.40 to 1.73) for all-cause mortality and 1.94 (1.62 to 2.32) for cardiovascular disease mortality. Individuals who were inactive in 1984-86 and then adhered to recommendations in 2006-08 had HRs of 1.07 (0.85 to 1.35) for all-cause mortality and 1.31 (0.87 to 1.98) for cardiovascular disease mortality. In a subsample of individuals who participated at all three time points, those who were inactive or physically active below the recommended level across three decades (1984-86, 1995-97 and 2006-2008) had an HR of 1.57 (1.22 to 2.03) for all-cause mortality and 1.72 (1.08 to 2.73) for cardiovascular disease mortality. CONCLUSION: Individuals who remained, or became, physically inactive had substantially greater risk of all-cause and cardiovascular disease mortality compared with those who met the physical activity recommendations throughout the lifespan.