Search

Summary: Both short (< 6 hr) and long (> 8 hr) sleep are associated with increased mortality. We here investigated whether the association between sleep duration and all‐cause, cardiovascular disease and cancer mortality differs between men and women. A cohort of 34,311 participants (mean age and standard deviation = 50.5 ± 15.5 years, 65% women), with detailed assessment of sleep at baseline and up to 20.5 years of follow‐up (18 years for cause‐specific mortality), was analysed using Cox proportional hazards model to estimate HRs with 95% confidence intervals. After adjustment for covariates, all‐cause, cardiovascular disease and cancer mortalities were increased for both < 5 hr and ≥ 9 hr sleep durations (with 6 hr as reference). For all‐cause mortality, women who slept < 5 hr had a hazard ratio = 1.54 (95% confidence interval = 1.32–1.80), while the corresponding hazard ratio was 1.05 (95% confidence interval = 0.88–1.27) for men, the interaction being significant (p < 0.05). For cardiovascular disease mortality, exclusion of the first 2 years of exposure, as well as competing risk analysis eliminated the originally significant interaction. Cancer mortality did not show any significant interaction. Survival analysis of the difference between the reference duration (6 hr) and the short duration (< 5 hr) during follow‐up showed a gradually steeper reduction of survival time for women than for men for all‐cause mortality. We also observed that the lowest cancer mortality appeared for the 5‐hr sleep duration. In conclusion, the pattern of association between short sleep duration and all‐cause mortality differed between women and men, and the difference between men and women increased with follow‐up time. [ABSTRACT FROM AUTHOR]

Background: Clinical guidelines recommend monitoring of creatinine and lithium throughout treatment with lithium. We here assessed the extent to which this occurs in healthcare in Sweden. Methods: This is an observational study of all adults with bipolar disorder starting lithium therapy in Stockholm, Sweden, during 2007–2018. The main outcome was monitoring of blood lithium and creatinine at therapy initiation and/or once annually. The secondary outcome was monitoring of calcium and thyroid‐stimulating hormone (TSH). Patients were followed up until therapy cessation, death, out‐migration, or to the end of 2018. Results: We identified 4428 adults with bipolar disorder who started lithium therapy and were followed up for up to 11 years. Their median age was 39 years, and 63% were women. The median duration on lithium therapy was 4.3 (IQR: 1.9–7.45) years, and the majority who discontinued therapy started another mood stabilizer soon after. Overall, 21% started lithium therapy without assessing the serum/plasma concentration of creatinine. The proportion of people who did not have both lithium and creatinine measured increased from 21% in the first year to 33% in the eleventh year. The proportion with annual testing for TSH or calcium was slightly lower. As few as 16% of patients had both lithium and creatinine tested once annually during their complete time on lithium. Conclusions: In a Swedish community sample, lithium and creatinine monitoring was inconsistent with guideline recommendations that call for measurement of annual biomarker levels. [ABSTRACT FROM AUTHOR]

Summary: Previous work has shown that both long and short sleep duration is associated with increased mortality, with lowest risk around 7 hr. This has had widespread impact on views on the optimal sleep duration. However, age, being employed/retired, and blue‐/white‐collar status, may influence the time available for sleep and thus, confound the association. We investigated the role of these factors on the association between sleep duration and mortality. We used employed and retired participants (N = 25,430) from the Swedish National March Cohort and Cox proportional hazards regression to model the shape of the association. We found a significant U‐shaped association in a multivariable model with a hazard ratio (HR) of 1.24 (95% confidence interval [CI] 1.10, 1.39) for <5‐hr sleep duration, and a HR of 1.30 (95% CI 1.12, 1.51) for ≥9‐hr sleep duration, with the lowest HR for 7 hr, but with a span of low HRs from 5 to 8 hr. Unadjusted values showed a pronounced U‐shape. Adjusting for age accounted for most of the attenuation in the multivariable model. Stratification into five age groups showed a significant U‐shape only in those aged >60.3 years at baseline. The shape of the association did not differ between blue‐/white‐collar workers, nor between employed and retired groups. We conclude that the U‐shaped association between sleep duration and mortality is present only in older individuals. [ABSTRACT FROM AUTHOR]

Systemic inflammation is thought to mediate the link between sleep and cardiovascular outcomes, but previous studies on sleep habits and inflammation markers have found inconsistent results. This study investigated the relationship between sleep characteristics and C‐reactive protein (CRP), interleukin‐6 (IL‐6) and tumor necrosis factor α (TNFα). A representative sample of 319 Swedish women was randomly selected from the general population for in‐home polysomnography, sleep questionnaire and blood samples. As variables were highly correlated, principal component analysis was used to reduce the number of original variables. Linear regression with log‐transformation of the outcomes (lnCRP, lnIL‐6 and lnTNFα) and quantile regression were fitted to estimate cross‐sectional relationships. Multivariable linear regression models suggested a significant association of insomnia symptoms (self‐reported) with higher lnCRP levels (β = 0.11; 95% confidence interval [CI] = 0.02; 0.21), but not with lnIL‐6 and lnTNFα. From quantile regression analysis we found that a high non‐restorative index (subjective) and insomnia symptoms (self‐reported) were associated with higher values of CRP, especially in the highest quantiles of the CRP distribution (90th percentile: β = 0.71; 95% CI = 0.17; 1.24. β = 1.23; 95% CI = 0.44; 2.02, respectively). Additionally, higher amounts of rapid eye movement (REM) sleep were associated with lower CRP values (90th percentile: β = −0.80; 95% CI = −0.14; −1.46). In conclusion, sleep disturbances (self‐reported), specifically difficulties maintaining sleep and early morning awakenings, but not sleep duration (neither subjective nor objective), were associated with higher CRP levels. No association was found with IL‐6 or TNFα. Elevated REM sleep was associated with lower CRP levels. The results suggest that inflammation might be an intermediate mechanism linking sleep and health in women. [ABSTRACT FROM AUTHOR]

Marginal structural Cox models have been used to estimate the causal effect of a time-varying treatment on a survival outcome in the presence of time-dependent confounders. These methods rely on the positivity assumption, which states that the propensity scores are bounded away from zero and one. Practical violations of this assumption are common in longitudinal studies, resulting in extreme weights that may yield erroneous inferences. Truncation, which consists of replacing outlying weights with less extreme ones, is the most common approach to control for extreme weights to date. While truncation reduces the variability in the weights and the consequent sampling variability of the estimator, it can also introduce bias. Instead of truncated weights, we propose using optimal probability weights, defined as those that have a specified variance and the smallest Euclidean distance from the original, untruncated weights. The set of optimal weights is obtained by solving a constrained quadratic optimization problem. The proposed weights are evaluated in a simulation study and applied to the assessment of the effect of treatment on time to death among people in Sweden who live with human immunodeficiency virus and inject drugs. [ABSTRACT FROM AUTHOR]

Background: Concerns for hyperkalaemia limit the use of mineralocorticoid receptor antagonists (MRAs). The frequency of MRA-associated hyperkalaemia in real-world settings and the extent of subsequent MRA discontinuation are poorly quantified.Methods and Results: Observational study including all Stockholm citizens initiating MRA therapy during 2007-2010. Hyperkalaemias were identified from all potassium (K+ ) measurements in healthcare. MRA treatment lengths and dosages were obtained from complete collection of pharmacy dispensations. We assessed the 1-year incidence and clinical hyperkalaemia predictors, and quantified drug prescription changes after an episode of hyperkalaemia. Overall, 13 726 new users of MRA were included, with median age of 73 years, 53% women and median plasma K+ of 3.9 mmol/L. Within a year, 18.5% experienced at least one detected hyperkalaemia (K+  > 5.0 mmol/L), the majority within the first 3 monthsnthsnthsnthsnths of therapy. As a comparison, hyperkalaemia was detected in 6.4% of propensity-matched new beta-blocker users. Chronic kidney disease (CKD), older age, male sex, heart failure, peripheral vascular disease, diabetes and concomitant use of angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, beta-blockers and diuretics were associated with increased hyperkalaemia risk. After hyperkalaemia, 47% discontinued MRA and only 10% reduced the prescribed dose. Discontinuation rates were higher after moderate/severe (K+  > 5.5 mmol/L) and early in therapy (<3 months from initiation) hyperkalaemias. CKD participants carried the highest risk of MRA discontinuation in adjusted analyses. When MRA was discontinued, most patients (76%) were not reintroduced to therapy during the subsequent year.Conclusion: Among real-world adults initiating MRA therapy, hyperkalaemia was very common and frequently followed by therapy interruption, especially among participants with CKD. [ABSTRACT FROM AUTHOR]

While smoking is a well-established risk factor for pancreatic cancer, the effect of smokeless tobacco is less well understood. We used pooled individual data from the Swedish Collaboration on Health Effects of Snus Use to assess the association between Swedish snus use and the risk of pancreatic cancer. A total of 424,152 male participants from nine cohort studies were followed up for risk of pancreatic cancer through linkage to health registers. We used shared frailty models with random effects at the study level, to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) adjusted for confounding factors. During 9,276,054 person-years of observation, 1,447 men developed pancreatic cancer. Compared to never-snus use, current snus use was not associated with risk of pancreatic cancer (HR 0.96, 95% CI 0.83-1.11) after adjustment for smoking. Swedish snus use does not appear to be implicated in the development of pancreatic cancer in men. Tobacco smoke constituents other than nicotine or its metabolites may account for the relationship between smoking and pancreatic cancer. [ABSTRACT FROM AUTHOR]

To investigate the association between hysterectomy and thyroid cancer subtypes based on histopathology. They did a nationwide, population-based, cohort study from 1973 to 2009 in Sweden. All women above 18 years of age during the period between January 1, 1973 and December 31, 2009 from the Register of Population ( n = 5.704,202) were identified as the study population. Individual case ascertainment of primary thyroid cancer subtypes were restricted to 1993-2009 based on histological pathologic-anatomical-diagnosis from the Cancer Register. Thyroid cancer subtypes were categorized based on histological morphology as: papillary, follicular and others (including anaplastic and medullary thyroid carcinoma). Information on benign hysterectomy derived from the Swedish Inpatient Register. Women with a hysterectomy (exposed) were compared with women not having had a hysterectomy (unexposed) using Cox's proportional hazard ratios (HRs). The adjusted HR for papillary thyroid cancer was significantly increased in exposed as compared with unexposed women (HR 1.70, 95% CI 1.04-2.79). There was no significant association between hysterectomy and follicular carcinoma or other thyroid cancers. There was a clear shift in the occurrence of thyroid cancer toward a lower attained age at the time of diagnosis among the exposed but no significant difference in overall survival when comparing exposed and unexposed (HR 1.02, 95% CI 0.48-2.16) Hysterectomy was associated with an increased risk for subsequent papillary thyroid cancer and diagnosis at a younger age compared with women not having had a hysterectomy but there were no differences in survival. [ABSTRACT FROM AUTHOR]

Objectives To explore the association between genes that may be related to human mortality, taking into account the possible contribution of morbidity, and investigate whether lifestyle behaviors may attenuate genetic risk. Design Twenty-five-year population-based cohort study. Setting Kungsholmen cohort, Stockholm, Sweden. Participants Individuals aged 75 and older (N = 1,229). Measurements The associations between single-nucleotide variations in 14 genes (previously associated with mortality or to diseases linked to mortality), relevant lifestyle risk behaviors (smoking; mental, physical, or social inactivity; moderate or poor social network), and mortality were estimated using Cox regression. Results People with allelic variation in four genes related to cardiovascular diseases and metabolism were more likely to die: apolipoprotein ( APO)C1 GG and AG carriers, APOE ɛ4 carriers, insulin-degrading enzyme ( IDE) TC carriers, and phosphatidylinositol 3-kinase ( PI3 KCB) GG carriers. Individuals with multiple adverse alleles had 62% higher mortality rate than those with none. In contrast, people with no risk behaviors (low-risk profile) had 65% lower mortality rate than people with all examined risk behaviors (high-risk profile). Combining the genetic and environmental factors, it was found that, independent of genetic profile, individuals with a low-risk profile had up to 64% lower mortality rate than those with a moderate high- or high-risk profile and at least one genetic risk factor. Conclusion This study supports and expands evidence that genetic variations in APOE, IDE, and PI3 KCB are associated with lower mortality rate, although lifestyle behaviors can modulate their effects. [ABSTRACT FROM AUTHOR]

A favorable role of fruit and vegetables on colorectal cancer risk has been related to the antioxidant properties of their components. We used data from an Italian case-control study including 1,953 patients with incident, histologically confirmed colorectal cancer (1,225 colon and 728 rectal cancers). Controls were 4,154 patients admitted to hospital for acute, non-neoplastic conditions. A reproducible and valid food frequency questionnaire was used to assess subjects' usual diet. Total antioxidant capacity (TAC) was measured using Italian food composition tables in terms of ferric reducing-antioxidant power (FRAP), Trolox equivalent antioxidant capacity (TEAC) and total radical-trapping antioxidant parameter (TRAP). We estimated the odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) through multiple logistic regression models, including terms for potential confounding factors, and energy intake. TAC was inversely related with colorectal cancer risk: the OR for the highest versus the lowest quintile was 0.68 (95% CI, 0.57-0.82) for FRAP, 0.69 (95% CI, 0.57-0.83) for TEAC and 0.69 (95% CI, 0.57-0.83) for TRAP. Corresponding values, excluding TAC deriving from coffee, were 0.75 (95% CI, 0.61-0.93) for FRAP, 0.76 (95% CI, 0.61-0.93) for TEAC and 0.71 (95% CI, 0.57-0.89) for TRAP. The inverse association was apparently-though not significantly-stronger for rectal than for colon cancer. This is the first case-control study indicating consistent inverse relations between dietary TAC and colorectal cancer risk. [ABSTRACT FROM AUTHOR]

Copyright of Tropical Medicine & International Health is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

A fundamental challenge in meta-analyses of published epidemiological dose-response data is the estimate of the function describing how the risk of disease varies across different levels of a given exposure. Issues in trend estimate include within studies variability, between studies heterogeneity, and nonlinear trend components. We present a method, based on a two-step process, that addresses simultaneously these issues. First, two-term fractional polynomial models are fitted within each study included in the meta-analysis, taking into account the correlation between the reported estimates for different exposure levels. Second, the pooled dose-response relationship is estimated considering the between studies heterogeneity, using a bivariate random-effects model. This method is illustrated by a meta-analysis aimed to estimate the shape of the dose-response curve between alcohol consumption and esophageal squamous cell carcinoma (SCC). Overall, 14 case-control studies and one cohort study, including 3000 cases of esophageal SCC, were included. The meta-analysis provided evidence that ethanol intake was related to esophageal SCC risk in a nonlinear fashion. High levels of alcohol consumption resulted in a substantial risk of esophageal SCC as compared to nondrinkers. However, a statistically significant excess risk for moderate and intermediate doses of alcohol was also observed, with no evidence of a threshold effect. Copyright © 2010 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Although anemia is widely considered an early sign of malignant disease, little is known about the pattern of hemoglobin decline before diagnosis. As an approach to understanding the duration of the preclinical phase of different types of malignant diseases, we investigated prediagnostic hemoglobin concentration changes in a large cohort of blood donors. Using a nested case-control design, we analyzed a population-based cohort comprising 1.1 million Scandinavian blood donors with complete follow-up through record linkage to population and cancer registers. A total of 16,375 cancer cases were identified, for whom we selected 161,995 controls. We used conditional logistic regression to estimate the risk of cancer in relation to hemoglobin concentration during the 5 years preceding the cancer diagnosis. Hemoglobin concentration decline began already 3 years before diagnosis of stomach cancer, multiple myeloma, and lymphatic leukemia; 2 years before diagnosis of small intestinal and colon cancer as well as of Hodgkin lymphoma. A decline was evident during the last year for non-Hodgkin lymphoma and myeloid/monocytic leukemia, whereas no change was found for cancer of the esophagus, breast or prostate. In conclusion, in this study, we have demonstrated that the pattern of declining hemoglobin concentration before cancer diagnosis varies considerably between malignancies without being a suitable screening tool for any of them. For some malignancies, however, the long duration of hemoglobin decline before clinical diagnosis suggests a substantial lead-time with systemic effects, during which earlier diagnosis should be achievable by emerging diagnostic tools. [ABSTRACT FROM AUTHOR]

Objective To assess the relative risk for amyotrophic lateral sclerosis (ALS) in families of ALS patients. Methods We conducted a cohort study based on the Swedish Multi-Generation Register in 1961 to 2005. Among 6,671 probands (first ALS case in the family), 1,909 full siblings, 13,947 children, and 5,405 spouses were identified (exposed group). Other persons in the Multi-Generation Register, who were siblings, children, or spouses to persons without ALS, served as the reference group. Relative risks for ALS among the exposed group, compared with the reference group, were calculated from Poisson regression models. Concurrence of ALS within twins was assessed in 86,441 twin pairs registered in the Swedish Twin Register. Results Nine cases of ALS were noted among the siblings and 37 cases among the children of the probands, giving a 17-fold risk among the siblings (95% confidence interval, 8.1-30.4) and a 9-fold risk among the children (95% confidence interval, 6.2-12.0), compared with the reference group. Siblings and children had a greater excess risk if the proband was diagnosed at a younger age, and the excess risks decreased with increasing age at diagnosis of the proband ( p < 0.001). Spouses had no significantly increased risk ( p = 0.27). Two cases were identified among the cotwins of ALS probands, giving a relative risk of 32 (95% confidence interval, 5.2-102.6). Interpretation The siblings and children of ALS patients have an about 10-fold risk for ALS compared with the reference group. The excess risks vary with both age and kinship, indicating a major genetic role in familial ALS. Ann Neurol 2009;66:94-99 [ABSTRACT FROM AUTHOR]

Aims To study the association between measured or perceived overweight in adolescence and subsequent uptake of cigarette smoking and of the Swedish smokeless tobacco ‘snus’ (oral moist snuff). Design Population-based prospective cohort study with 7 years' follow-up. Setting Self-administered questionnaires and school nurses' visits. Participants A total of 2922 children of both sexes and mean age 11.6 years at recruitment, resident in the Stockholm region, Sweden. Measurements Tobacco use was self-reported at baseline and on six subsequent surveys. Subjects' height and weight were measured by school nurses during the first 4 years, self-reported thereafter. Overweight perception was self-reported at the age of 15 years. Findings Overweight and perception of overweight were not associated with subsequent uptake of either smoking or snus among males. Among females, overweight at baseline was associated with uptake of smoking [adjusted hazard ratio (HR) 1.34, 95% confidence interval (CI) 1.09–1.63], but not of snus. A similar pattern was found with overweight status during follow-up. Among girls with low-educated parents, overweight at baseline predicted the uptake of both snus and smoking. Among 15-year-old females who never used tobacco perceived overweight was associated with subsequent uptake of smoking (adjusted HR 1.71, 95% CI 1.20–2.46), but not of snus. Conclusions In Sweden, adolescent girls with actual or perceived overweight are at increased risk to start smoking, while indications that this increased risk applies to smokeless tobacco (snus) are limited to girls of low socio-economic status. [ABSTRACT FROM AUTHOR]

Ovarian cancer is the leading cause of death from gynecologic malignancies among women worldwide. Little is known about reproductive factors or lifestyle determinants and ovarian cancer prognosis. The objective of this study was to examine whether ovarian cancer survival is influenced by reproductive history, anthropometric characteristics, prediagnostic life-style factors and family history of breast or ovarian cancer. The study population consisted of 635 epithelial ovarian cancer (EOC) cases derived from a nationwide population-based case-control study conducted in Sweden between 1993 and 1995. Exposure data on prediagnostic factors of interest were collected through questionnaires at the beginning of the parent study. Clinical data were abstracted from medical records. Cases were followed-up by means of record linkage to nationwide registers until December 31, 2002. Cox proportional hazard regression model was used to estimate the prognostic effect of each factor in terms of hazard ratios (HR) and 95% confidence intervals (CI), following adjustment for age at diagnosis, FIGO tumor stage and WHO grade of tumor differentiation. Tumor characteristics significantly influenced the risk of death from EOC. After adjustment for these, no clear associations were detected between reproductive history (parity, age at first or last birth, oral contraceptive use, age at menarche or menopause), anthropometric characteristics (body size and shape in different periods of life), lifestyle factors before diagnosis (alcohol consumption, smoking and physical activity over lifetime), nor family history of breast cancer or ovarian cancer and EOC survival. Our findings indicate that these prediagnostic factors do not influence the EOC survival. Nevertheless, among women with early stage disease (FIGO stage I and II), there was some indication that overweight in young adulthood or recent years increased the risk of death, while physical activity in young adult life appeared to reduce the risk of death due to EOC. © 2008 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Use of hormone replacement therapy (HRT) has been hypothesized to affect survival of epithelial ovarian cancer (EOC). We studied 5-year survival in patients with invasive EOC and borderline ovarian tumors (BOT) according to HRT use before and after diagnosis in a prospective nation-wide cohort study of 799 women diagnosed with EOC ( n = 649) and BOT ( n = 150) aged 50-74 years in 1993-1995 in Sweden. Cox regression was used to obtain multivariate age-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs). Multivariate models included indicator variables for age, tumor stage, grade and histological subtype. After 5 years of follow-up, 45% of the patients with EOC and 93% of the patients with BOT were alive. For women with BOT there were no associations between HRT-use pre- or postdiagnosis and survival. There was no overall difference in 5-year EOC survival according to use HRT before diagnosis (multivariate HR = 0.83, 95% CI = 0.65-1.08), except for serous EOC (HR = 0.69, 95% CI = 0.48-0.98). Analyses of different HRT preparations, duration and recency of use did not reveal any variations in pattern of survival. We observed a better survival for EOC-patients who used HRT after diagnosis (multivariate HR = 0.57, 95% CI = 0.42-0.78). We conclude that HRT-use prior to diagnosis of EOC does not affect 5-year survival, except for a possible survival advantage in serous EOC. Women using HRT after diagnosis had a better survival than women with no use, but we cannot rule out that this latter finding may reflect a subtle selection process. © 2006 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Background Methods Results Conclusion Although glomerular diseases are the third most frequent cause of end‐stage kidney disease worldwide, little is known about their long‐term outcomes.In patients with chronic kidney disease (CKD) stage 3–5 enrolled in the Swedish Renal Registry, we compared risks of hospitalization, kidney replacement therapy (KRT), major cardiovascular events (MACE), and death of the four most frequent primary glomerular diseases (IgA nephropathy [IgAN], focal segmental glomerulosclerosis [FSGS], minimal change disease [MCD], and membranous nephropathy [MN]), and patients with CKD due to the most common non‐communicable diseases (control‐CKD).We identified 2396 patients with glomerular disease (97% biopsy‐proven, 69% men, 57 years, eGFR 29 mL/min/1.73 m2, uACR 88 mg/mmol, 1524 with IgAN, 398 FSGS, 94 MCD, and 380 MN) and 37,697 controls (64% men, 74 years, eGFR 25 mL/min/1.73 m2, uACR 23 mg/mmol), mainly with diabetic nephropathy and nephroangiosclerosis. The median follow‐up was 6.3 (3.3; 9.9) years. Compared with control‐CKD, patients with primary glomerular diseases generally had a lower risk of hospitalization, MACE (adjusted hazard ratios [HRs] ranging from 0.44 to 0.88 depending on the etiology) and death (HRs ranging 0.45–0.76). Patients with IgAN and FSGS had a faster eGFR decline and a higher rate of KRT (HRs 1.26 [95%CI: 1.15–1.37] and 1.34 [1.15–1.57], respectively). Conversely, patients with MN and MCD had a lower KRT rate and slower eGFR decline.Despite having a lower relative risk of hospitalization, cardiovascular events and mortality, patients with IgAN and FSGS are at higher risk of CKD progression than the most common etiologies of CKD, emphasizing the need for more stringent treatment strategies in these patients. [ABSTRACT FROM AUTHOR]

Summary: Previous studies have found a U‐shaped relationship between mortality and (weekday) sleep duration. We here address the association of both weekday and weekend sleep duration with overall mortality. A cohort of 43,880 subjects was followed for 13 years through record‐linkages. Cox proportional hazards regression models with attained age as time‐scale were fitted to estimate multivariable‐adjusted hazard ratios and 95% confidence intervals for mortality; stratified analyses on age (<65 years, ≥65 years) were conducted. Among individuals <65 years old, short sleep (≤5 hr) during weekends at baseline was associated with a 52% higher mortality rate (hazard ratios 1.52; 95% confidence intervals 1.15–2.02) compared with the reference group (7 hr), while no association was observed for long (≥9 hr) weekend sleep. When, instead, different combinations of weekday and weekend sleep durations were analysed, we observed a detrimental association with consistently sleeping ≤5 hr (hazard ratios 1.65; 95% confidence intervals 1.22–2.23) or ≥8 hr (hazard ratios 1.25; 95% confidence intervals 1.05–1.50), compared with consistently sleeping 6–7 hr per day (reference). The mortality rate among participants with short sleep during weekdays, but long sleep during weekends, did not differ from the rate of the reference group. Among individuals ≥65 years old, no association between weekend sleep or weekday/weekend sleep durations and mortality was observed. In conclusion, short, but not long, weekend sleep was associated with an increased mortality in subjects <65 years. In the same age group, short sleep (or long sleep) on both weekdays and weekend showed increased mortality. Possibly, long weekend sleep may compensate for short weekday sleep. [ABSTRACT FROM AUTHOR]