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Scandinavian electronic health-care registers provide a unique setting to investigate potential unidentified side effects of drugs. We analysed the association between prescription drugs dispensed in Norway and Sweden and the short-term risk of developing pulmonary embolism. A total of 12,104 pulmonary embolism cases were identified from patient- and cause-of-death registries in Norway (2004-2014) and 36,088 in Sweden (2005-2014). A case-crossover design was used to compare individual drugs dispensed 1-30 days before the date of pulmonary embolism diagnosis with dispensation in a 61-90 day time-window, while controlling for the receipt of other drugs. A BOLASSO approach was used to select drugs that were associated with short-term risk of pulmonary embolism. Thirty-eight drugs were associated with pulmonary embolism in the combined analysis of the Norwegian and Swedish data. Drugs associated with increased risk of pulmonary embolism included certain proton-pump inhibitors, antibiotics, antithrombotics, vasodilators, furosemide, anti-varicose medications, corticosteroids, immunostimulants (pegfilgrastim), opioids, analgesics, anxiolytics, antidepressants, antiprotozoals, and drugs for cough and colds. Mineral supplements, hydrochlorothiazide and potassium-sparing agents, beta-blockers, angiotensin 2 receptor blockers, statins, and methotrexate were associated with lower risk. Most associations persisted, and several additional drugs were associated, with pulmonary embolism when using a longer time window of 90 days instead of 30 days. These results provide exploratory, pharmacopeia-wide evidence of medications that may increase or decrease the risk of pulmonary embolism. Some of these findings were expected based on the drugs' indications, while others are novel and require further study as potentially modifiable precipitants of pulmonary embolism., (© 2024. The Author(s).)

Background: With the global population growing older, there is a need for more knowledge of how to improve and/or maintain functional capacities to promote healthy ageing. In this study we aimed to assess the effect of several known health-promoting behaviors in old age with intrinsic capacity ten years later., Methods: This was a prospective cohort study looking at participants that were ≥ 65 years at the time of the third wave of the Trøndelag Health Study (HUNT3, 2006-2008) who also took part in the 70 + sub-study of the fourth wave (HUNT4 70+, 2017-2019). Self-reported behavior data from short questionnaires, including diet and physical activity, were collected in HUNT3, and data on the five domains of intrinsic capacity defined by the World Health Organization were collected in HUNT4 70+. A composite index was created for both healthy life and intrinsic capacity, awarding points for how well participants adhered to guidelines for healthy living and their level of functional impairment, respectively. Ordinal logistic regression was used to assess the relationship between health-promoting behaviors and intrinsic capacity., Results: Of 12,361 participants in HUNT3 ≥ 65 years, 4699 (56.5% women) also participated in HUNT4 70+. On the health-promoting behaviors, lowest adherence to healthy living guidelines were seen for fruit and vegetables intake (47.2%), milk intake (46.7%) and physical activity (31.1%). On intrinsic capacity domains, highest impairment was seen in the domains of locomotion (29.7%), hearing (11.1%) and vitality (8.3%). A higher adherence to guidelines for healthy living was associated with higher intrinsic capacity 10 years later. A one-point increase in the healthy life index was associated with a 1.15 (95% confidence interval 1.10-1.21) times increased odds of being in a higher intrinsic capacity category., Conclusion: Health-promoting behaviors in old age are associated with better intrinsic capacity ten years later. In clinical settings assessment of health-promoting behaviors could potentially be done using short questionnaires., (© 2024. The Author(s).)

In March 2020, the World Health Organization declared the global COVID-19 pandemic outbreak and the Norwegian government declared lockdown to stop the virus from spreading. In Norway, universities were immediately closed, and all teaching and learning were done digitally for the rest of the spring semester 2020. Our aim was to explore nursing students experience with studying and learning, as well as the psychological consequences it may incur during a period of social isolation during the Covid-19 pandemic lockdown. The study is a qualitative study based on a focus group with 6 nursing students. The analysis was conducted following Kvale's approach to qualitative analysis. Three main categories were identified: (1) psychosocial learning environment, (2) personal and social challenges, and (3) communication. We found that the restrictions due to social isolation and pandemic restrictions such as closing of the university campus, has impacted students` study situation significantly, both psychosocially and academically. If social isolation should be necessary in the future, universities need to use methods such as group discussions, quizzes, and short breaks in the lectures to prevent unnecessary problems among the students. Personal challenges due to the social isolation, such as anxiety or other mental health issues are more difficult to avoid or prevent, but the universities must be better prepared to give students more personal communication, have unformal meetings and providing more information to the students in times of crisis., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Background: Loneliness has become a significant public health problem and should be addressed with more research over a broader period. This study investigates the variations in the prevalence of loneliness among a nationally representative study population of Norwegian adolescents over the last three decades and whether age, gender, self-rated health, and mental distress are associated with these changes., Methods: Adolescents aged 13-19 years completed the structured and validated questionnaires from the three waves of the Young-HUNT Study: 1995-1997, 2006-2008, and 2017-2019. Loneliness was measured with one item asking, 'Are you lonely?'. Hopkins Symptom Checklist-5 was used to measure mental distress (cut-off ≥ 2). Self-rated health was assessed by a single question 'How is your health at the moment?' Measures were provided by self-report. Descriptive analyses were stratified by age, gender, self-rated health, and mental distress. Linear-by-Linear association test across survey years was performed to test time trends of loneliness. Logistic regression was used to analyze the cross-sectional associations of self-rated health and mental distress with loneliness, adjusting for sociodemographic factors in all three waves of Young-HUNT., Results: Loneliness prevalence doubled from 5.9% in 1995/97 to 10.2% in 2017/19 in the total population sample. The highest loneliness prevalence and an increase from 8.9% in 1995/97 to 16.7% in 2017/19 was observed in girls of 16-19 years. Among mentally distressed adolescents, loneliness increased from 22.3% in 1995/97 to 32.8% in 2006/08 and lowered to 27% in 2017/19. Increasing loneliness prevalence was seen in those with poor self-rated health, i.e., 14.6% in 1995-97 and 26.6% in 2017-19. Mental distress and poor self-rated health were associated with higher odds of loneliness in each wave (p < 0.001)., Conclusion: The results highlight the increasing burden of loneliness in the Norwegian adolescent population, especially girls. Those with mental distress and poor self-rated health have a higher risk of experiencing loneliness. Thus, health-promoting upbringing environments for children and adolescents that support mutual affinity, social support, integration, and belongingness in adolescents' daily arenas are essential., (© 2023. The Author(s).)

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., (© 2023. BioMed Central Ltd., part of Springer Nature.)

Background: Higher BMI in middle age is associated with ischemic stroke, but little is known about BMI over adulthood, and the risk for ischemic stroke as most studies relied on a single measurement of BMI., Methods: BMI was measured four times over a period of 42 years. We calculated average BMI values and group-based trajectory models and related these to the prospective risk of ischemic stroke after the last examination in Cox models with a follow-up time of 12 years., Results: A total of 14,139 participants, with a mean age of 65.2 years and 55.4% women, had information on BMI from all four examinations, and we observed 856 ischemic strokes. People with overweight and obesity over adulthood had a higher risk for ischemic stroke with a multivariable-adjusted hazard ratio of 1.29 (95% CI 1.11-1.48) and 1.27 (95% CI 0.96-1.67), respectively, when compared to normal weight participants. Excess weight tended to have stronger effects earlier than later in life. A trajectory of developing obesity throughout life was associated with higher risk than other trajectories., Conclusions: High average BMI, especially at an early age, is a risk factor for ischemic stroke. Early weight control and long-term weight reduction for those with high BMI may decrease the later occurrence of ischemic stroke.

We examined the short-term risk of stroke associated with drugs prescribed in Norway or Sweden in a comprehensive, hypothesis-free manner using comprehensive nation-wide data. We identified 27,680 and 92,561 cases with a first ischemic stroke via the patient- and the cause-of-death registers in Norway (2004-2014) and Sweden (2005-2014), respectively, and linked these data to prescription databases. A case-crossover design was used that compares the drugs dispensed within 1 to 14 days before the date of ischemic stroke occurrence with those dispensed 29 to 42 days before the index event. A Bolasso approach, a version of the Lasso regression algorithm, was used to select drugs that acutely either increase or decrease the apparent risk of ischemic stroke. Application of the Bolasso regression algorithm selected 19 drugs which were associated with increased risk for ischemic stroke and 11 drugs with decreased risk in both countries. Morphine in combination with antispasmodics was associated with a particularly high risk of stroke (odds ratio 7.09, 95% confidence intervals 4.81-10.47). Several potentially intriguing associations, both within and across pharmacological classes, merit further investigation in focused, follow-up studies., (© 2021. The Author(s).)

Background and Purpose: Obesity is one of the most prevalent modifiable risk factors of ischemic stroke. However, it is still unclear whether obesity itself or the metabolic abnormalities due to obesity increase the risk of ischemic stroke. We therefore investigated the association between metabolic health, weight, and risk of ischemic stroke in a large prospective cohort study., Methods: In the Norwegian HUNT study (Trøndelag Health Study), we included 35 105 participants with complete information on metabolic risk factors and relevant covariates. Metabolically unhealthy state was defined as sex specific increased waist circumference in addition to 2 or more of the following criteria: hypertension, increased blood pressure, decreased high-density lipoprotein, triglycerides or glucose, or self-reported diagnosis of diabetes. We then applied Cox proportional hazard models to estimate the risk for ischemic stroke among overweight and obese metabolically healthy and unhealthy participants compared with metabolically healthy, normal weight participants., Results: A total of 1161 ischemic stroke cases occurred after an average observation time of 11.9 years. In general, metabolically unhealthy participants were at increased risk of ischemic stroke (for obese participants: hazard ratio, 1.30 [95% CI, 1.09–1.56] compared with metabolically healthy participants with a normal body mass index). Hypertension appeared to be the most important metabolic risk factor. Metabolically healthy participants with overweight or obesity were at similar risk of ischemic stroke compared with normal weight participants (hazard ratio, 1.02 [95% CI, 0.81–1.28] for participants with obesity). Obesity and overweight even over an extended period of time seems to be benign about ischemic stroke, as long as it was not associated with metabolic abnormalities., Conclusions: Obesity was not an independent ischemic stroke risk factor in this cohort, and the risk depended more on the metabolic consequences of obesity.

Aims: Although obesity has been associated with risk of atrial fibrillation (AF), the associations of long-term obesity, recent obesity, and weight change with AF risk throughout adulthood are uncertain., Methods and Results: An ambispective cohort study was conducted which included 15 214 individuals. The cohort was created from 2006 to 2008 (the baseline) and was followed for incident AF until 2015. Weight and height were directly measured at baseline. Data on previous weight and height were retrieved retrospectively from measurements conducted 10, 20, and 40 years prior to baseline. Average body mass index (BMI) over time and weight change was calculated. During follow-up, 1149 participants developed AF. The multivariable-adjusted hazard ratios were 1.2 (95% confidence interval 1.0-1.4) for average BMI 25.0-29.9 kg/m2 and 1.6 (1.2-2.0) for average BMI ≥30 kg/m2 when compared with normal weight. The association of average BMI with AF risk was only slightly attenuated after adjustment for most recent BMI. In contrast, current BMI was not strongly associated with the risk of AF after adjustment for average BMI earlier in life. Compared with stable BMI, both loss and gain in BMI were associated with increased AF risk. After adjustment for most recent BMI, the association of BMI gain with AF risk was largely unchanged, while the association of BMI loss with AF risk was weakened., Conclusion: Long-term obesity and BMI change are associated with AF risk. Obesity earlier in life and weight gain over time exert cumulative effects on AF development even after accounting for most recent BMI., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2019. For permissions, please email: journals.permissions@oup.com.)

Excessive daytime sleepiness (EDS) affects 10-20% of the population and is associated with substantial functional deficits. Here, we identify 42 loci for self-reported daytime sleepiness in GWAS of 452,071 individuals from the UK Biobank, with enrichment for genes expressed in brain tissues and in neuronal transmission pathways. We confirm the aggregate effect of a genetic risk score of 42 SNPs on daytime sleepiness in independent Scandinavian cohorts and on other sleep disorders (restless legs syndrome, insomnia) and sleep traits (duration, chronotype, accelerometer-derived sleep efficiency and daytime naps or inactivity). However, individual daytime sleepiness signals vary in their associations with objective short vs long sleep, and with markers of sleep continuity. The 42 sleepiness variants primarily cluster into two predominant composite biological subtypes - sleep propensity and sleep fragmentation. Shared genetic links are also seen with obesity, coronary heart disease, psychiatric diseases, cognitive traits and reproductive ageing.

Wholesale, unbiased assessment of Scandinavian electronic health-care databases offer a unique opportunity to reveal potentially important undiscovered drug side effects. We examined the short-term risk of acute myocardial infarction (AMI) associated with drugs prescribed in Norway or Sweden. We identified 24,584 and 97,068 AMI patients via the patient- and the cause-of-death registers and linked to prescription databases in Norway (2004-2014) and Sweden (2005-2014), respectively. A case-crossover design was used to compare the drugs dispensed 1-7 days before the date of AMI diagnosis with 15-21 days' time -window for all the drug individually while controlling the receipt of other drugs. A BOLASSO approach was used to select drugs that acutely either increase or decrease the apparent risk of AMI. We found 48 drugs to be associated with AMI in both countries. Some antithrombotics, antibiotics, opioid analgesics, adrenergics, proton-pump inhibitors, nitroglycerin, diazepam, metoclopramide, acetylcysteine were associated with higher risk for AMI; whereas angiotensin-II-antagonists, calcium-channel blockers, angiotensin-converting-enzyme inhibitors, serotonin-specific reuptake inhibitors, allopurinol, mometasone, metformin, simvastatin, levothyroxine were inversely associated. The results were generally robust in different sensitivity analyses. This study confirms previous findings for certain drugs. Based on the known effects or indications, some other associations could be anticipated. However, inverse associations of hydroxocobalamin, levothyroxine and mometasone were unexpected and needs further investigation. This pharmacopeia-wide association study demonstrates the feasibility of a systematic, unbiased approach to pharmacological triggers of AMI and other diseases with acute, identifiable onsets.

Objective: Atrial fibrillation (AF) is the most common arrhythmia and has been described as a global epidemic. Although AF is associated with both obesity and its metabolic consequences, little is known about the association between metabolically healthy obesity and AF., Methods: In a population-based study, 47,870 adults were followed for incident AF from 2006 to 2008 until 2015. Participants were classified according to BMI and metabolic status (using waist circumference, triglycerides, high-density lipoprotein cholesterol, blood pressure, and glucose) at baseline., Results: During a median follow-up of 8.1 years, 1,758 participants developed AF. Compared with metabolically healthy individuals with BMI < 25 kg/m 2 , the multivariable-adjusted hazard ratios for metabolically healthy and unhealthy obesity were 1.6 (95% CI: 1.2 to 2.1) and 1.6 (95% CI: 1.3 to 1.9), respectively. AF risk increased according to the severity of obesity., Conclusions: Metabolically healthy and unhealthy obesity increased AF risk to a similar extent. Severity of obesity was positively associated with AF risk regardless of metabolic status., (© 2019 The Obesity Society.)

Objectives: A significant proportion of cardiovascular disease (CVD) cannot be explained by well-known risk factors such as high cholesterol, hypertension and diabetes. One potential novel risk factor for CVD is asthma. We aimed to investigate the association between asthma and mortality due to CVD., Design: Prospective cohort study., Setting: A large health check-up programme from 1994 to 2011 in Taipei, Taiwan., Participants: 446 346 Taiwanese adults. Each participant answered questions regarding asthma history (yes/no) and current daily use of asthma medications (yes/no). Active asthma was defined as those using current daily medications for asthma., Outcomes: The participants were followed for mortality from CVD, coronary heart disease (CHD) and stroke obtained through linkage to the cause-of-death register until 31 December 2011., Results: We found an increased risk of dying from CVD in individuals with active asthma (adjusted HR (aHR) 1.32, 95% CI 1.08 to 1.62). The risk of death from CHD or stroke was increased in a similar manner (aHR 1.16, 95% CI 0.78 to 1.73 and aHR 1.23, 95% CI 0.86 to 1.74, respectively) although the HR estimates were less precise than that of CVD. For deaths from CVD, CHD and stroke, we found stronger associations with active asthma than non-active asthma, and for CVD and stroke stronger associations in men than women., Conclusion: Our study suggests that asthma, particularly active asthma, may be associated with adverse cardiovascular consequences., Competing Interests: Competing interests: None declared., (© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Objectives: To investigate the association between alcohol consumption and left ventricular (LV) function in a population with low average alcohol intake., Design, Setting and Participants: A total of 1296 healthy participants, free from cardiovascular diseases, were randomly selected from the third wave of the Norwegian HUNT study (2006-2008) and underwent echocardiography. After validation of the inclusion criteria, 30 participants were excluded due to arrhythmias or myocardial or valvular pathology. Alcohol consumption, sociodemographic and major cardiovascular risk factors were assessed by questionnaires and clinical examination in the HUNT3. General linear models were used to analyse the cross-sectional associations between alcohol intake and LV indices., Primary and Secondary Outcome Measures: LV functional and structural indices were measured with tissue Doppler and speckle tracking echocardiography., Results: We observed no associations between alcohol consumption and multivariable-adjusted LV functional indices. Excluding abstainers who reported regular alcohol consumption 10 years prior to the baseline did not change the results. Alcohol consumption was positively associated with LV mass indices (p<0.01 for linear trend of the means); there was no such association among participants with non-risky drinking characteristics (p=0.67 for linear trend of the means)., Conclusions: We found no clear evidence that light-moderate alcohol consumption is associated with measures of LV function, although our results indicate that consumption, especially when marked by binge drinking, is progressively associated with greater LV mass., Competing Interests: Competing interests: None declared., (© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Objective: To examine the length of time between receiving funding and publishing the protocol and main paper for randomised controlled trials., Design: An observational study using survival analysis., Setting: Publicly funded health and medical research in Australia., Participants: Randomised controlled trials funded by the National Health and Medical Research Council of Australia between 2008 and 2010., Main Outcome Measures: Time from funding to the protocol paper and main results paper. Multiple variable survival models examining whether study characteristics predicted publication times., Results: We found 77 studies with a total funding of $A59 million. The median time to publication of the protocol paper was 6.4 years after funding (95% CI 4.1 to 8.1). The proportion with a published protocol paper 8 years after funding was 0.61 (95% CI 0.48 to 0.74). The median time to publication of the main results paper was 7.1 years after funding (95% CI 6.3 to 7.6). The proportion with a published main results paper 8 years after funding was 0.72 (95% CI 0.56 to 0.87). The HRs for how study characteristics might influence timing were generally close to one with narrow CIs, the notable exception was that a longer study length lengthened the time to the main paper (HR=0.62 per extra study year, 95% CI 0.43 to 0.89)., Conclusions: Despite the widespread registration of clinical trials, there remain serious concerns of trial results not being published or being published with a long delay. We have found that these same concerns apply to protocol papers, which should be publishable soon after funding. Funding agencies could set a target of publishing the protocol paper within 18 months of funding., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.)

Insomnia is highly prevalent among asthmatics; however, few studies have investigated insomnia symptoms and asthma development. We aimed to investigate the association between insomnia and the risk of incident asthma in a population-based cohort.Among 17 927 participants free from asthma at baseline we calculated odds ratios and 95% confidence intervals for the risk of incident asthma among those with insomnia compared to those without. Participants reported sleep initiation problems, sleep maintenance problems and nonrestorative sleep. Chronic insomnia was defined as those reporting one or more insomnia symptom at baseline and 10 years earlier. Incident asthma was defined by questions on asthma at baseline and follow-up (average 11 years).The prevalence of sleep initiation problems, sleep maintenance problems and nonrestorative sleep were 1%, 1% and 5%, respectively. The multi-adjusted odds ratios were 1.18 (95% CI 0.97-1.44), 1.30 (95% CI 1.03-1.64) and 1.70 (95% CI 1.37-2.11) for people with one, two and three insomnia symptoms, respectively, compared with people without symptoms (p<0.01 for trend). The risk of developing asthma in those with chronic insomnia was three times higher (adjusted OR 3.16, 95% CI 1.37-6.40) than those without.Insomnia symptoms were associated with increased risk of incident asthma in this study., (Copyright ©ERS 2017.)

Objective: Symptoms of anxiety and depression often co-exist with cardiovascular disease (CVD), yet little is known about the association with left ventricular (LV) subclinical dysfunction. We aimed to study the cross-sectional associations of previous, current and repeated depression or anxiety symptoms, with sensitive indices of LV systolic and diastolic function, based on tissue Doppler (TD) and speckle tracking (ST) imaging methods., Methods: A random selection of 1296 individuals free from known CVD, hypertension and diabetes were examined with echocardiography at baseline of the third Nord-Trøndelag Health Study, (HUNT3, 2006-2008). The primary outcomes were LV diastolic function (e') and LV systolic function (longitudinal global strain). The primary exposures were self-report on the Hospital Anxiety and Depression Scale (HADS). Associations between outcomes and baseline exposures were available for 1034 (80%), and with previous and repeated exposures for 700 participants who also participated in HUNT2 (1995-1997)., Results: Previous and repeated depression symptoms, but not current depression, were linearly associated with a reduction in e'. The average sum of two repeated HADS-D scores 10 years apart had the strongest effect on e' (-8.3%; 95% CI -13.9% to -2.7%) per 5 units. We observed a sex difference between depression symptoms and longitudinal global strain (p for interaction 0.019), where women had a marginal negative effect. Anxiety symptoms, neither previous, current nor repeated were associated with subclinical LV dysfunction., Conclusions: In a healthy sample, confirmed free of CVD, past and repeated depression symptoms were associated with subclinical LV dysfunction. Thus, depression symptoms might represent a modifiable risk factor for future CVD.

Objective: We examined the associations of symptoms of sleep-disordered breathing (SDB), which was defined as loud snoring, stopping breathing for a while during sleep, and daytime sleepiness, and insomnia with glucose metabolism and incident type 2 diabetes in older adults., Research Design and Methods: Between 1989 and 1993, the Cardiovascular Health Study recruited 5,888 participants ≥65 years of age from four U.S. communities. Participants reported SDB and insomnia symptoms yearly through 1989-1994. In 1989-1990, participants underwent an oral glucose tolerance test, from which insulin secretion and insulin sensitivity were estimated. Fasting glucose levels were measured in 1989-1990 and again in 1992-1993, 1994-1995, 1996-1997, and 1998-1999, and medication use was ascertained yearly. We determined the cross-sectional associations of sleep symptoms with fasting glucose levels, 2-h glucose levels, insulin sensitivity, and insulin secretion using generalized estimated equations and linear regression models. We determined the associations of updated and averaged sleep symptoms with incident diabetes in Cox proportional hazards models. We adjusted for sociodemographics, lifestyle factors, and medical history., Results: Observed apnea, snoring, and daytime sleepiness were associated with higher fasting glucose levels, higher 2-h glucose levels, lower insulin sensitivity, and higher insulin secretion. The risk of the development of type 2 diabetes was positively associated with observed apnea (hazard ratio [HR] 1.84 [95% CI 1.19-2.86]), snoring (HR 1.27 [95% CI 0.95-1.71]), and daytime sleepiness (HR 1.54 [95% CI 1.13-2.12]). In contrast, we did not find consistent associations between insomnia symptoms and glucose metabolism or incident type 2 diabetes., Conclusions: Easily collected symptoms of SDB are strongly associated with insulin resistance and the incidence of type 2 diabetes in older adults. Monitoring glucose metabolism in such patients may prove useful in identifying candidates for lifestyle or pharmacological therapy. Further studies are needed to determine whether insomnia symptoms affect the risk of diabetes in younger adults., (© 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.)

Aims: Insomnia is highly prevalent among heart failure patients, but only a few small studies have investigated insomnia symptoms and risk of heart failure. We aimed to assess the prospective association between self-reported insomnia symptoms and the risk of incident heart failure in a large Norwegian cohort., Methods and Results: Baseline data on insomnia symptoms, including difficulty initiating sleep, difficulty maintaining sleep and having non-restorative sleep, socio-demographic variables, and health status, including established cardiovascular risk factors, were collected from 54 279 men and women 20-89 years of age who participated in the Nord-Trøndelag Health study (HUNT) between 1995 and 1997 and were free from known heart failure at baseline. The cohort was followed for incident heart failure from baseline through 2008. We used Cox proportional hazard models to assess the association of baseline insomnia symptoms with the risk of heart failure. A total of 1412 cases of heart failure occurred during a mean follow-up of 11.3 years (SD = 2.9 years), either identified at hospitals or by the National Cause of Death Registry. There was a dose-dependent association between the number of insomnia symptoms and risk of heart failure. The multi-adjusted hazard ratios were 0.96 (0.57-1.61), 1.35 (0.72-2.50), and 4.53 (1.99-10.31) for people with one, two, and three insomnia symptoms, compared with people with none of the symptoms (P for trend 0.021)., Conclusions: Insomnia is associated with an increased risk of incident heart failure. If our results are confirmed by others and causation is proved, evaluation of insomnia symptoms might have consequences for cardiovascular prevention., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2013. For permissions please email: journals.permissions@oup.com.)

Almost 10% of all births are preterm, and 2.2% are stillbirths. Recent research has suggested that environmental factors may be a contributory cause of these adverse birth outcomes. The authors examined the relation between ambient temperature and preterm birth and stillbirth in Brisbane, Australia, between 2005 and 2009 (n = 101,870). They used a Cox proportional hazards model with livebirth and stillbirth as competing risks. They also examined whether there were periods in pregnancy where exposure to high temperatures had a greater effect. Higher ambient temperatures in the last 4 weeks of the pregnancy increased the risk of stillbirth. The hazard ratio for stillbirth was 0.3 at 12°C relative to the reference temperature of 21°C. The temperature effect was greatest at less than 36 weeks of gestation. There was an association between higher temperature and shorter gestation, as the hazard ratio for livebirth was 0.96 at 15°C and 1.02 at 25°C. This effect was greatest at later gestational ages. These results provide strong evidence of an association between increased temperature and increased risk of stillbirth and shorter gestation.

Background: Insomnia is associated with increased risk of coronary heart disease (CHD), but the underlying mechanisms are not understood. To our knowledge, no previous studies have examined insomnia in relation to endothelial function, an indicator of preclinical atherosclerosis. Our aim was to assess the association of insomnia with endothelial function in a large population based study of healthy individuals., Methods: A total of 4 739 participants free from known cardiovascular or pulmonary diseases, cancer, and sarcoidosis, and who were not using antihypertensive medication were included in the study. They reported how often they had experienced difficulties falling asleep at night, repeated awakenings during the night, early awakenings without being able to go back to sleep, and daytime sleepiness. Endothelial function was measured by flow mediated dilation (FMD) derived from the brachial artery., Results: We found no consistent association between the insomnia symptoms and endothelial function in multiadjusted models, but individual insomnia symptoms may be related to endothelial function. Among women who reported early awakenings, endothelial function may be lower than in women without this symptom (p = 0.03)., Conclusions: This study provided no evidence that endothelial function, an early indicator of atherosclerosis, is an important linking factor between insomnia and CHD. Further studies are needed to explore the complex interrelation between sleep and cardiovascular pathology.

Background: Many previous studies have found seasonal patterns in birth outcomes, but with little agreement about which season poses the highest risk. Some of the heterogeneity between studies may be explained by a previously unknown bias. The bias occurs in retrospective cohorts which include all births occurring within a fixed start and end date, which means shorter pregnancies are missed at the start of the study, and longer pregnancies are missed at the end. Our objective was to show the potential size of this bias and how to avoid it., Methods: To demonstrate the bias we simulated a retrospective birth cohort with no seasonal pattern in gestation and used a range of cohort end dates. As a real example, we used a cohort of 114,063 singleton births in Brisbane between 1 July 2005 and 30 June 2009 and examined the bias when estimating changes in gestation length associated with season (using month of conception) and a seasonal exposure (temperature). We used survival analyses with temperature as a time-dependent variable., Results: We found strong artificial seasonal patterns in gestation length by month of conception, which depended on the end date of the study. The bias was avoided when the day and month of the start date was just before the day and month of the end date (regardless of year), so that the longer gestations at the start of the study were balanced by the shorter gestations at the end. After removing the fixed cohort bias there was a noticeable change in the effect of temperature on gestation length. The adjusted hazard ratios were flatter at the extremes of temperature but steeper between 15 and 25°C., Conclusions: Studies using retrospective birth cohorts should account for the fixed cohort bias by removing selected births to get unbiased estimates of seasonal health effects.

Seasonal patterns of birth outcomes, such as low birth weight, preterm birth and stillbirth, have been found around the world. As a result, there has been an increasing interest in evaluating short-term exposure to ambient temperature as a determinant of adverse birth outcomes. This paper reviews the epidemiological evidence on seasonality of birth outcomes and the impact of prenatal exposure to ambient temperature on birth outcomes. We identified 20 studies that investigated seasonality of birth outcomes, and reported statistically significant seasonal patterns. Most of the studies found peaks of preterm birth, stillbirth and low birth weight in winter, summer or both, which indicates the extremes of temperature may be an important determinant of poor birth outcomes. We identified 13 studies that investigated the influence of exposure to ambient temperature on birth weight and preterm birth (none examined stillbirth). The evidence for an adverse effect of high temperatures was stronger for birth weight than for preterm birth. More research is needed to clarify whether high temperatures have a causal effect on fetal health., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Background: There is overwhelming scientific evidence that human activities have changed and will continue to change the climate of the Earth. Eco-environmental health, which refers to the interdependencies between ecological systems and population health and well-being, is likely to be significantly influenced by climate change. The aim of this study was to examine perceptions from government stakeholders and other relevant specialists about the threat of climate change, their capacity to deal with it, and how to develop and implement a framework for assessing vulnerability of eco-environmental health to climate change., Methods: Two focus groups were conducted in Brisbane, Australia with representatives from relevant government agencies, non-governmental organisations, and the industry sector (n = 15) involved in the discussions. The participants were specialists on climate change and public health from governmental agencies, industry, and non-governmental organisations in South-East Queensland., Results: The specialists perceived climate change to be a threat to eco-environmental health and had substantial knowledge about possible implications and impacts. A range of different methods for assessing vulnerability were suggested by the participants and the complexity of assessment when dealing with multiple hazards was acknowledged. Identified factors influencing vulnerability were perceived to be of a social, physical and/or economic nature. They included population growth, the ageing population with associated declines in general health and changes in the vulnerability of particular geographical areas due to for example, increased coastal development, and financial stress. Education, inter-sectoral collaboration, emergency management (e.g. development of early warning systems), and social networks were all emphasised as a basis for adapting to climate change. To develop a framework, different approaches were discussed for assessing eco-environmental health vulnerability, including literature reviews to examine the components of vulnerability such as natural hazard risk and exposure and to investigate already existing frameworks for assessing vulnerability., Conclusion: The study has addressed some important questions in regard to government stakeholders and other specialists' views on the threat of climate change and its potential impacts on eco-environmental health. These findings may have implications in climate change and public health decision-making.