Background Ideal cardiovascular health (CVH) can be assessed by 7 metrics: smoking, body mass index, physical activity, diet, hypertension, dyslipidemia and diabetes, proposed by the American Heart Association. We examined the association of ideal CVH metrics with risk of all-cause, CVD and non-CVD death in a large cohort. Methods A total of 29,557 participants in the Swedish National March Cohort were included in this study. We ascertained 3,799 deaths during a median follow-up of 19 years. Cox regression models were used to estimate hazard ratios with 95% confidence intervals (95% CIs) of the association between CVH metrics with risk of death. Laplace regression was used to estimate 25th, 50th and 75th percentiles of age at death. Results Compared with those having 6-7 ideal CVH metrics, participants with 0-2 ideal metrics had 107% (95% CI = 46-192%) excess risk of all-cause, 224% (95% CI = 72-509%) excess risk of CVD and 108% (31-231%) excess risk of non-CVD death. The median age at death among those with 6-7 vs. 0-2 ideal metrics was extended by 4.2 years for all-causes, 5.8 years for CVD and 2.9 years for non-CVD, respectively. The observed associations were stronger among females than males. Conclusions The strong inverse association between number of ideal CVH metrics and risk of death supports the application of the proposed seven metrics for individual risk assessment and general health promotion.

Importance  Bereavement following parental death experienced in adulthood may be associated with suicide over many years, but this risk has received scant attention.

Objective  To investigate whether the risk of suicide increases among adult children around the anniversary of a parent’s death.

Design, Setting, and Participants  This case-crossover study used Swedish register-based longitudinal data from 1990 to 2016, based on the entire national population. Participants included all adults aged 18 to 65 years who experienced parental death and subsequently died by suicide. Conditional logistic regression was used to quantify the association between the anniversary (or preanniversary and postanniversary periods) and suicide, controlling for time-invariant confounding. All analyses were stratified by sex of the offspring. The analyses were also stratified by the sex of the deceased parent, time since parental death, age, and marital status. Data analyses were performed in June 2022.

Exposures  Anniversary of a parent’s death (or preanniversary and postanniversary periods).

Main Outcomes and Measures  Suicide.

Results  Of 7694 individuals who died by suicide (76% intentional self-harm), 2255 (29%) were women, and the median (IQR) age at suicide was 55 (47-62) years. There was evidence of an anniversary reaction among women, with a 67% increase in the odds of suicide when exposed to the period from the anniversary to 2 days after the anniversary, compared with when not being exposed (odds ratio [OR], 1.67; 95% CI, 1.07-2.62). The risk was particularly pronounced among maternally bereaved women (OR, 2.29; 95% CI, 1.20-4.40) and women who were never married (OR, 2.08; 95% CI, 0.99-4.37), although the latter was not statistically significant. An increased risk of suicide from the day before up to the anniversary was observed among women bereaved between the ages of 18 and 34 years (OR, 3.46; 95% CI, 1.14-10.56) and between the ages of 50 and 65 years (OR, 2.53; 95% CI, 1.04-6.15). Men had an attenuated suicide risk for the period from the day before up to the anniversary (OR, 0.57; 95% CI, 0.36-0.92).

Objective: Consumption of antioxidant-rich foods has been associated with a reduced risk for stroke. However, antioxidant supplementation is not recommended owing to controversial findings reported in clinical trials. The aim of this study was to better understand the effect of dietary antioxidants by investigating the effect of dietary non-enzymatic antioxidant capacity (NEAC), reflecting the antioxidant potential of the whole diet, on the risk for stroke. Methods: In the Women's Lifestyle and Health Cohort, 45 882 women 30 to 49 y of age and free from cardiovascular diseases were followed through record linkages from 1991 to 2012. Dietary NEAC was assessed by a validated food frequency questionnaire collected at baseline and categorized into quintiles. Multivariable Cox proportional hazard regression models were fitted to estimate hazard ratios with 95% confidence intervals for overall stroke and ischemic and hemorrhagic stroke separately. Results: During a mean follow-up time of 20.2 y, we detected 871 incidence cases of stroke (516 ischemic, 296 hemorrhagic, and 59 unspecified strokes). After adjusting for potential confounders, we did not find any association between dietary NEAC and stroke, either overall, or ischemic or hemorrhagic stroke (P-trend > 0.05). Conclusion: Higher dietary NEAC was not associated with any type of stroke in young and middle-aged Swedish women.

Foods rich in antioxidants have been associated with a reduced risk of myocardial infarction. However, findings from randomized clinical trials on the role of antioxidant supplementation remain controversial. It has been suggested that antioxidants interact with each other to promote cardiovascular health. We therefore investigated the association between dietary Non Enzymatic Antioxidant Capacity (NEAC), measuring the total antioxidant potential of the whole diet, and the risk of myocardial infarction. We followed 45,882 women aged 30-49 years and free from cardiovascular diseases through record linkages from 1991 until 2012. Dietary NEAC was assessed by a validated food frequency questionnaire collected at baseline. Total dietary NEAC was categorized into quintiles and multivariable Cox proportional hazard regression models were fitted to estimate hazard ratios (HR) with 95% confidence intervals (CI). During a mean follow-up time of 20.3 years we detected 657 incident cases of myocardial infarction. After adjusting for potential confounders, we found a significant 28% lower risk of myocardial infarction among women in the fourth (HR: 0.72; 95% CI 0.55-0.95) and a 40% lower risk among women in the fifth quintile (HR: 0.60, 95% CI 0.45-0.81) of dietary NEAC compared to women in the first quintile, with a significant trend (p-value < 0.001). Higher dietary NEAC is associated with a lower risk of myocardial infarction in young to middle-aged women. These findings support the hypothesis that dietary antioxidants protect from myocardial infarction and that this effect might be exerted through interactions between antioxidants.

Background: Following progressive aging of the population worldwide, the prevalence of Parkinson disease is expected to increase in the next decades. Primary prevention of the disease is hampered by limited knowledge of preventable causes. Recent evidence regarding diet and Parkinson disease is inconsistent and suggests that dietary habits such as fat intake may have a role in the etiology.

Objective: To investigate the association between intake of total and specific types of fat with the incidence of Parkinson disease.

Methods: Participants from the Swedish National March Cohort were prospectively followed-up from 1997 to 2016. Dietary intake was assessed at baseline using a validated food frequency questionnaire. Food items intake was used to estimate fat intake, i.e. the exposure variable, using the Swedish Food Composition Database. Total, saturated, monounsaturated and polyunsaturated fat intake were categorized into quartiles. Parkinson disease incidence was ascertained through linkages to Swedish population-based registers. Cox proportional hazards regression models were used to estimate hazard ratios (HR) with 95% confidence intervals (CI) of the association between fat intake from total or specific types of fats and the incidence of Parkinson disease. The lowest intake category was used as reference. Isocaloric substitution models were also fitted to investigate substitution effects by replacing energy from fat intake with other macronutrients or specific types of fat.

Results: 41,597 participants were followed up for an average of 17.6 years. Among them, 465 developed Parkinson disease. After adjusting for potential confounders, the highest quartile of saturated fat intake was associated with a 41% increased risk of Parkinson disease compared to the lowest quartile (HR Q4 vs. Q1: 1.41; 95% CI: 1.04–1.90; p for trend: 0.03). Total, monounsaturated or polyunsaturated fat intake were not significantly associated with Parkinson disease. The isocaloric substitution models did not show any effect.

Conclusions: We found that a higher consumption of large amounts of saturated fat might be associated with an increased risk of Parkinson disease. A diet low in saturated fat might be beneficial for disease prevention.

Background

Previous studies have shown that the experience of parental death during childhood is associated with increased mortality risk. However, few studies have examined potential pathways that may explain these findings. The aim of this study is to examine whether familial and behavioural factors during adolescence and socioeconomic disadvantages in early adulthood mediate the association between loss of a parent at age 0 to 12 and all-cause mortality by the age of 63.

Methods and findings

A cohort study was conducted using data from the Stockholm Birth Cohort Multigenerational Study for 12,615 children born in 1953, with information covering 1953 to 2016. Familial and behavioural factors at age 13 to 19 included psychiatric and alcohol problems in the surviving parent, receipt of social assistance, and delinquent behaviour in the offspring. Socioeconomic disadvantage in early adulthood included educational attainment, occupational social class, and income at age 27 to 37. We used Cox proportional hazard regression models, combined with a multimediator analysis, to separate direct and indirect effects of parental death on all-cause mortality.

Among the 12,582 offspring in the study (men 51%; women 49%), about 3% experienced the death of a parent in childhood. During follow-up from the age of 38 to 63, there were 935 deaths among offspring. Parental death was associated with an elevated risk of mortality after adjusting for demographic and household socioeconomic characteristics at birth (hazard ratio [HR]: 1.52 [95% confidence interval: 1.10 to 2.08, p-value = 0.010]). Delinquent behaviour in adolescence and income during early adulthood were the most influential mediators, and the indirect associations through these variables were HR 1.03 (1.00 to 1.06, 0.029) and HR 1.04 (1.01 to 1.07, 0.029), respectively. After accounting for these indirect paths, the direct path was attenuated to HR 1.35 (0.98 to 1.85, 0.066). The limitations of the study include that the associations may be partly due to genetic, social, and behavioural residual confounding, that statistical power was low in some of the subgroup analyses, and that there might be other relevant paths that were not investigated in the present study.

Conclusions

Our findings from this cohort study suggest that childhood parental death is associated with increased mortality and that the association was mediated through a chain of disadvantages over the life course including delinquency in adolescence and lower income during early adulthood. Professionals working with bereaved children should take the higher mortality risk in bereaved offspring into account and consider its lifelong consequences. When planning and providing support to bereaved children, it may be particularly important to be aware of their increased susceptibility to delinquency and socioeconomic vulnerability that eventually lead to higher mortality.

Background Parental death and its anniversaries, including anticipation of these dates, might cause distress andincrease the risk of substance use disorder and suicide-related behaviour in bereaved adolescents and young adults.We examined whether the risk of substance use disorder and suicide-related behaviour increases around the date ofparental death and subsequent anniversaries.

Methods Using Swedish national registers, we conducted a cohort study of individuals aged 12–24 years. We includedindividuals aged 12–24 years between Jan 1, 2001, and Dec 31, 2014, whose parents were alive at entry (n=1 858 327)and followed up with them until the end of age 24 years. We excluded individuals with a half-sibling, a history ofemigration, a previous record of the outcome events, a parental death before study entry, two parental deaths on thesame day during the follow-up, or missing data for relevant variables. Follow-up ended on the day of an outcomeevent or on Dec 31, 2014; at age 25 years, emigration, or death; or a year before the second parental death. We studiedsubstance use disorder and suicide-related behaviour outcomes separately and included non-fatal and fatal events inboth outcomes. We used Cox regression to estimate hazard ratios (HRs), controlling for baseline psychiatric,demographic, and socioeconomic characteristics. Parental death was modelled as a time-varying exposure over72 monthly periods, starting from 1 year before the parental death to the fifth year and later after the death.Unmeasured confounding was also addressed in within-individual comparisons using a case-crossover design.

Findings During follow-up (median 7·5 [IQR 4·3–10·6] years), there were 42 854 substance use disorder events, witha crude rate of 3·1 per 1000 person-years. For suicide-related behaviour, there were 19 827 events, with a crude rate of1·4 per 1000 person-years. Most of the events studied were non-fatal. In the month of parental death, the HR forsubstance use disorder risk was 1·89 (95% CI 1·07–3·33) among male participants, and, for suicide-related behaviour,was 3·76 (1·79–7·89) among male participants and 2·90 (1·61–5·24) among female participants. In male participants,there was an increased risk around the first anniversary (substance use disorder: HR 2·64 [95% CI 1·56–4·46] duringthe anniversary month; 2·21 [1·25–3 ·89] for the subsequent month; and for suicide-related behaviour: 3·18[1·32–7·66] for the subsequent month). Among female participants, an increased risk of substance use disorderrecurred around every year consistently in the month before the anniversary of the death and there was an increasedrisk for suicide-related behaviour in the months of the first and second anniversaries.

Interpretation Although effect sizes were large in this cohort study, the number of individuals who had the outcomeswas small. Nevertheless, adolescents and young adults, especially women and girls, who had the death of a parentshowed increased risk of substance use disorder and suicide-related behaviour around the first few death anniversaries.Adolescents and young adults, especially women and girls, who had the death of a parent could benefit from preventivemeasures to reduce distress around the first few years of death anniversaries

Potential health risks for informal caregivers have been hypothesised to be partly related to adverse changes in health-related behaviour, but evidence is limited. We examined whether smoking, drinking, eating, physical activity or leisure pursuits change in relation to co-resident or out-of-home caregiving (for someone outside the household), and if associations differ by sex, educational attainment, and welfare state typology. We conducted a longitudinal study using six waves of the Survey of Health, Ageing and Retirement in Europe, collecting data repeatedly from 2004 to 2017 for adults aged 50 years and older living in 17 European countries (57,962 individuals). To control for measured and unmeasured within-individual time-invariant confounders, we used fixed effects logistic models to analyse the repeated measures of caregiving, behaviour and covariates and estimated odds ratios (OR) with 95% confidence intervals (95%CI). Among male participants, unhealthy eating increased while smoking decreased [ORs 1.26 (95%CI 1.01–1.58) and 0.53 (0.36–0.78), respectively] in survey waves in which they provided co-resident care, compared with the waves that they did not. Among female participants, there was little change in behaviour between waves with and without co-resident caregiving. When providing out-of-home care, lacks of physical activity and leisure pursuits declined. But in the same time, drinking increased both men and women, and especially among individuals with lower educational attainment and residing in non-Nordic countries. To conclude, overall, increased drinking when providing out-of-home care was most consistent, especially among individuals with lower educational attainment and residing in non-Nordic countries. Otherwise, the associations varied by the type of care, behaviour and population subgroups. These findings indicated that not all caregivers are susceptible to behavioural changes, and that not all behaviour may be involved similarly in linking caregiving to health risks. This opens possibilities to target specific behaviour and groups to prevent adverse changes in health behaviour in caregivers.

Background: Cycling is increasingly encouraged in many countries as an inexpensive and healthy choice of transportation. Operating any vehicle on the road requires high visual acuity, but few studies to our knowledge have examined the association between vision and cycling injuries.

Methods: We examined whether poorer visual acuity is associated with increased risk of fatal and nonfatal cycling injuries. We used prospectively recorded register data for 691,402 men born between 1970 and 1992 in Sweden. We followed these men from an average age of 18 years, when visual acuity was assessed during the conscription assessment, to age 45 at the latest. We identified fatal and nonfatal cycling and car injuries using Patient and Cause of Death registers. Cox regression models were used to estimate hazard ratios and 95% confidence intervals.

Results: Based on visual acuity for the eye with the best vision, moderately impaired acuity 0.9 to 0.6 when wearing refractive correction was associated with increased risk for cycling injuries (hazard ratio = 1.44 [95% confidence interval = 1.16, 1.79]) compared with unimpaired vision (uncorrected visual acuity 1.0) and after adjustment for a wide range of potential confounders. This association remained consistent across various sensitivity analyses. Visual acuity was not associated with car injury risk.

Conclusions: In this cohort study, poorer vision was specifically associated with a higher rate of cycling injuries.

Background The link between workplace bullying and poor mental health is well-known. However, little is known about the prospective and potentially reciprocal association between workplace bullying and mental health-related sickness absence. This 2-year prospective study examined bidirectional associations between exposure to workplace bullying and sickness absence due to common mental disorders (SA-CMD) while controlling for confounding factors from both work and private life.

Methods The study was based on propensity score-matched samples (N = 3216 and N = 552) from the Swedish Longitudinal Occupational Survey of Health, using surveys from years 2012, 2014 and 2016. Self-reported exposure to workplace bullying was linked to registry-based information regarding medically certified SA-CMD (≥ 14 consecutive days). The associations were examined by means of Cox proportional hazards regression and via conditional logistic regression analysis. Hazard ratios and odds ratios with 95% confidence intervals were estimated.

Results Exposure to workplace bullying was associated with an increased risk of incident SA-CMD (HR: 1.3, 95% CI: 1.0–1.8), after accounting for the influence of job demands, decision authority, previous SA-CMD, as well as other sociodemographic covariates. However, we found no statistically significant association between SA-CMD and subsequent workplace bullying (OR 1.2, 95% CI 0.7–1.9).

Conclusions The results support an association between self-reported workplace bullying and SA-CMD, independent of other sociodemographic factors and workplace stressors. Preventing workplace bullying could alleviate a share of the individual and societal burden caused by SA globally.

Background. Research shows that early childbearing is associated negatively with educational attainment and socioeconomic status (SES). Children born to young versus older mothers often do less well in school, and many have early first births. Some studies suggest that mothers' early childbearing operates through SES to influence the daughters' early childbearing, and some argue that the association is strong net of SES. The current study tests these direct and indirect associations. Methods. We estimate the pathways through which mothers' early childbearing influences daughters' early childbearing in several steps. First, we examine bivariate associations between mothers' early childbearing and SES, followed by bivariate associations between mothers' SES outcomes and their daughters' early childbearing. We then estimate the average marginal effects (AMEs) of mothers' early children on daughters', and a KHB decomposition to examine direct and indirect associations. Results. Findings suggest both direct and indirect associations. Nested models show that, net of a range of SES characteristics, mothers' early childbearing increases the probability of daughters' by approximately 8%; and KHB results suggest 37% mediation, with daughters' school performance (12%) and household educational attainment (10%) contributing the highest shares. Conclusion. Mothers' early childbearing and subsequent SES collectively influence the long-term wellbeing of children. Thus, early childbearing has consequences both within and across generations.

BACKGROUND Phosphodiesterase-5 inhibitor (PDE5i) treatment for erectile dysfunction is associated with lower mortality compared with no treatment for erectile dysfunction after myocardial infarction (MI). There are conflicting results regarding the impact of PDE5i treatment on mortality in conjunction with nitrate medication. OBJECTIVES The purpose of this study was to investigate the association between PDE5i treatment and cardiovascular outcomes in men with stable coronary artery disease treated with nitrate medication. METHODS Using the Swedish Patient Register and the Prescribed Drug Register we included men with previous MI or revascularization in 2006-2013 who had 2 dispensed nitrate prescriptions within 6 months. Exposure was defined as at least 2 filled prescriptions of any PDE5i. We performed multivariable Cox proportional hazard regression to estimate HRs with 95% CIs for all -cause, cardiovascular, and noncardiovascular mortality, MI, heart failure, cardiac revascularization, and major cardiovascular events (MACE). RESULTS In total, 55,777 men were treated with nitrates and 5,710 men with nitrates and a PDE5i. The combined use of PDE5i treatment with nitrates was associated with higher mortality (HR: 1.39; 95% CI: 1.28-1.51), cardiovascular mortality (HR: 1.34; 95% CI: 1.11-1.62), noncardiovascular mortality (HR: 1.40; 95% CI: 1.27-1.54), MI (HR: 1.72; 95% CI: 1.55-1.90), heart failure (HR: 1.67; 95% CI: 1.48-1.90), cardiac revascularization (HR: 1.95; 95% CI: 1.78-2.13), and MACE (HR: 1.70; 95% CI: 1.58-1.83). CONCLUSIONS The use of a PDE5i in combination with nitrate medication in men with stable coronary artery disease may pose an increased hazard for cardiovascular morbidity and mortality. Careful patient -centered consideration before prescribing PDE5is to patients with cardiovascular disease using nitrate medication is warranted. (J Am Coll Cardiol 2024;83:417-426) (c) 2024 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation. This is an open access article under the CC BY -NC -ND license (http://creativecommons.org/licenses/by-nc-nd/ 4.0/).

Importance  To better support children with the experience of parental death, it is crucial to understand whether parental death increases the risk of adverse school outcomes.

Objectives  To examine whether parental death is associated with poorer school outcomes independent of factors unique to the family, and whether children of certain ages are particularly vulnerable to parental death.

Design, Setting, and Participants  This population-based sibling cohort study used Swedish national register-based longitudinal data with linkage between family members. Register data were collected from January 1, 1990, to December 31, 2016. Data analyses were performed on July 14, 2021. The participants were all children born between 1991 and 2000 who lived in Sweden before turning age 17 years (N = 908 064).

Exposure  Parental death before finishing compulsory school.

Main Outcomes and Measures  Mean school grades (year-specific z scores) and ineligibility for upper secondary education on finishing compulsory school at age 15 to 16 years. Population-based cohort analyses were conducted to examine the association between parental death and school outcomes using conventional linear and Poisson regression models, after adjustment for demographic and parental socioeconomic and health indicators measured before childbirth. Second, using fixed-effect linear and Poisson regression models, children who experienced parental death before finishing compulsory school were compared with their siblings who experienced the death after. Third, the study explored the age-specific associations between parental death and school outcomes.

Results  In the conventional population-based analyses, bereaved children (N = 22 634; 11 553 boys [51.0%]; 11 081 girls [49.0%]; mean [SD] age, 21.0 [2.8] years) had lower mean school grade z scores (adjusted β coefficient, −0.19; 95% CI, −0.21 to −0.18; P < .001) and a higher risk of ineligibility for upper secondary education than the nonbereaved children (adjusted risk ratio, 1.36; 95% CI, 1.32-1.41; P < .001). Within-sibling comparisons using fixed-effects models showed that experiencing parental death before finishing compulsory school was associated with lower mean school grade z scores (−0.06; 95% CI, −0.10 to −0.01; P = .02) but not with ineligibility for upper secondary education (adjusted risk ratio, 1.07; 95% CI, 0.93-1.23; P = .34). Independent of birth order, losing a parent at a younger age was associated with lower grades within a family.

Conclusions and Relevance  In this cohort study, childhood parental death was associated with lower school grades after adjustment for familial confounders shared between siblings. Children who lost a parent may benefit from additional educational support that could reduce the risk of adverse socioeconomic trajectories later in life.

Background Population-based longitudinal studies on bereaved children and youth’s mental health care use are scarce and few have assessed the role of surviving parents’ mental health status.

Methods Using register data of individuals born in Sweden in 1992–1999, we performed a matched cohort study(n = 117,518) on the association between parental death and subsequent initiation of antidepressant treatment among individuals bereaved at ages 7–24 years. We used flexible parametric survival models to estimate the hazard ratios (HRs) over time after bereavement, adjusting for individual and parental factors. We further examined if the association varied by age at loss, sex, parental sociodemographic factors, cause of death, and the surviving parents’psychiatric care.

Findings The bereaved were more likely to initiate antidepressants treatment than the nonbereaved matched individuals during follow-up (incidence rate per 1000 person years 27.5 [26.5–28.5] vs. 18.2 [17.9–18.6]). The HRs peaked in the first year after bereavement and remained higher than the nonbereaved individuals until the end of the follow-up. The average HR over the 12 years of follow-up was 1.48 (95% confidence interval [1.39–1.58]) for father’s death and 1.33 [1.22–1.46] for mother’s death. The HRs were particularly high when the surviving parents received psychiatric care before bereavement (2.11 [1.89–2.56] for father’s death; 2.14 [1.79–2.56] for mother’s death) or treated for anxiety or depression after bereavement (1.80 [1.67–1.94]; 1.82 [1.59–2.07]).

Interpretation The risk of initiating antidepressant treatment was the highest in the first year after parental death and remained elevated over the next decade. The risk was particularly high among individuals with surviving parentsaffected by psychiatric morbidity.

Objective Causes of Parkinson disease are largely unknown, but recent evidence suggests associations with physical activity and anthropometric measures.

Methods We prospectively analyzed a cohort of 41,638 Swedish men and women by detailed assessment of lifestyle factors at baseline in 1997. Complete follow-up until 2010 was achieved through linkage to population-based registers. We used multivariable Cox proportional hazards models to estimate hazard ratios with 95% confidence intervals (CIs).

Results We identified 286 incident cases of Parkinson disease during follow-up. Multivariable adjusted hazard ratios were 1.06 (95% CI 0.76-1.47) for sitting time >= 6 vs <6 hours per day; and 1.13 (95% CI 0.60-2.12) for body mass index >= 30 vs < 25 kg/m(2). Results did not differ by sex.

Conclusions No association between prolonged sitting time per day or obesity and risk of Parkinson disease was found.

Prior work has shown that both short and long sleep predict mortality. However, sleep duration decreases with age and this may affect the relationship of sleep duration with mortality. The purpose of the present study was to assess whether the association between sleep duration and mortality varies with age. Prospective cohort study. 43,863 individuals (64% women), recruited in September 1997 during the Swedish National March and followed through record-linkages for 13 years. Sleep duration was self-reported and measured using the Karolinska Sleep Questionnaire, and grouped into 4 categories: ae5, 6, 7 (reference) and 8 h. Up to 2010 3548 deaths occurred. Multivariable Cox proportional hazards regression models with attained age as time scale were fitted to estimate mortality rate ratios. Among individuals < 65 years, short (ae5 h) and long (8 h) sleep duration showed a significant relationship with mortality (HR 1.37, 95% CI 1.09-1.71, and HR 1.27, 95% CI 1.08-1.48). Among individuals 65 years or older, no relationships between sleep duration and mortality were observed. The effect of short and long sleep duration on mortality was highest among young individuals and decreased with increasing age. The results suggest that age plays an important role in the relationship between sleep duration and mortality.

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.