Objective:

Few studies have investigated the persistence over time of experiences of harm from a known person's drinking. The aim of this study was to describe 1-year persistence and investigate its predictors at baseline. Potential predictors included the harmed person's sociodemographic factors, their own drinking habits, their relationship to the person causing harm, and the type of negative experience.

Method:

The sample included respondents who reported experiencing harm from a known person's drinking in a general population survey in 2013 and participated in a follow-up survey in 2014 (n = 1,203). One-year persistence of experienced harm was defined as reporting any harm in both surveys. We investigated potential baseline predictors of persistence by estimating relative risks and 95% confidence intervals through modified binary Poisson regression analyses with robust error variance.

Results:

One-year persistence of experiencing any type of harm from a known person's drinking was seen in 52.5% of those reporting harm at baseline and was higher among women (56.7%) than men (43.3%). Reporting harm from a partner, parent, or other household member significantly predicted 1-year persistence, as did severity of overall perceived harm at baseline.

Conclusions:

In Sweden, 1-year persistence of experienced harm from a known person's drinking is common in most individuals. The risk of experiencing such harm is higher among women, when harm occurs within close relationships, and when it is experienced as severe at baseline. Support to individuals in these situations is crucial.

Background: School pressure is a significant stressor in the lives of adolescents, recognised to be associated with psychosomatic complaints. Therefore, the exploration of potential buffering factors is a relevant task. This study aimed to examine the association between school pressure and psychosomatic complaints and the potentially moderating role of physical activity in a Swedish national sample of adolescents. Methods: Data were derived from the 2017/2018 Swedish Health Behaviour in School-aged Children (HBSC) survey, involving 3,745 participants aged 11–15 years. School pressure and physical activity were measured using single items. Psychosomatic complaints were assessed through an additive index based on the frequency of eight complaints. Covariates included gender, grade, and family affluence. Results: Linear regression analyses demonstrated a positive graded association between school pressure and psychosomatic complaints, while an inversely graded association was observed between physical activity and psychosomatic complaints. Physical activity did, however, not moderate the link between school pressure and psychosomatic complaints. Conclusion: Even though physical activity did not serve as a buffer, the direct effects of school pressure and physical activity on psychosomatic complaints suggest that supporting young people in managing school demands and promoting their engagement in physical activities could be effective measures in alleviating psychosomatic complaints.

Background: Socioeconomic inequalities in labour market participation are well established. However, we do not fully know what causes these inequalities. The present study aims to examine to what extent factors in childhood and late adolescence can explain educational differences in early labour market exit among older workers.

Methods: All men born in 1951–1953 who underwent conscription examination for the Swedish military in 1969–1973 (n = 145 551) were followed from 50 to 64 years of age regarding early labour market exit (disability pension, long-term sickness absence, long-term unemployment and early old-age retirement with and without income). Early life factors, such as cognitive ability, stress resilience, and parental socioeconomic position, were included. Cox proportional-hazards regressions were used to estimate the association between the level of education and each early labour market exit pathway, including adjustment for early life factors.

Results: The lowest educated men had a higher risk of exit through disability pension (HR: 2.72), long-term sickness absence (HR: 2.29), long-term unemployment (HR: 1.45), and early old-age retirement with (HR: 1.29) and without income (HR: 1.55) compared to the highest educated men. Factors from early life explained a large part of the educational differences in disability pension, long-term sickness absence and long-term unemployment but not for early old-age retirement. Important explanatory factors were cognitive ability and stress resilience, whilst cardiorespiratory fitness had negligible impact.

Conclusions: The association between education and early exit due to disability pension, long-term sickness absence and long-term unemployment was to a large part explained by factors from early life. However, this was not seen for early old-age retirement. These results indicate the importance of taking a life-course perspective when examining labour market participation in later working life.

BackgroundThe distribution of sickness absence tends to be socially patterned less is however known about the underlying mechanisms and pathways of the social gradient found in sickness absence. The present study aims to investigate (i) if the risk function between average volume of alcohol consumption and sickness absence is modified by socio-economic position (SEP), and (ii) whether such an effect modification can be attributed to differences in drinking patterns and other risk factors including other lifestyle behaviours, health status, and working conditions.MethodsThe study was based on data from the Stockholm public health cohort 2006, with an analytical sample of 13 855 respondents aged 18-64 years. Self-reported information on occupational class (a measure of SEP), alcohol consumption, other lifestyle behaviour, health and working conditions was collected from the survey. The outcome of long-term (> 14 days) sickness absence between 2006 and 2008 was obtained from national registers. Negative binomial regression was used to estimate the Incidence Rate Ratios (IRR) with 95% confidence intervals (CI).ResultsIn the initial analyses, heavy drinking manual workers had a 5-fold increased risk of long-term sickness absence compared to non-manual employees who were moderate drinkers, and approximately 60% of the excess risk among heavy drinking manual workers was attributable to an interaction between alcohol use and SEP. Adjusting for working conditions was associated with the largest attenuation of the risk estimate, compared to other lifestyle behaviors and health. In the fully adjusted model, the IRR was further attenuated for the manual workers and the joint effect of SEP and heavy drinking remained in the final model with an attributable proportion of 49%.ConclusionsIndividuals in Sweden with lower levels of SEP appear to be more vulnerable to alcohol consumption in relation to sickness absence, where differences in working conditions explained a large part but not all of the differential vulnerability.

A large number of observational studies have found a J-shaped relationship between alcohol intake and ischemic heart disease (IHD) risk. However, some studies suggest that the alleged cardio-protective effect may be an artifact in the way that the elevated risk for abstainers is due to self-selection on risk factors for IHD. The aim of this paper is to estimate the association between alcohol and IHD-mortality on the basis of aggregate time-series data, where the problem with selection effects is not present. In addition, we will analyze SES-specific mortality to investigate whether there is any socio-economic gradient in the relationship at issue. SES was measured by educational level. We used IHD-mortality in three educational groups as outcome. Per capita alcohol consumption was proxied by Systembolaget’s alcohol sales (litres of alcohol 100% per capita 15+). Swedish quarterly data on mortality and alcohol consumption spanned the period 1991Q1–2020Q4. We applied SARIMA time-series analysis. Survey data were used to construct an indicator of heavy SES-specific episodic drinking. The estimated association between per capita consumption and IHD-mortality was positive and statistically significant in the two groups with primary and secondary education, but not in the group with postsecondary education. The association was significantly stronger the lower the educational group. Although the associations were generally stronger for males than for females, these differences were not statistically significant (P > 0.05). Our findings suggest that the detrimental impact of per capita consumption on IHD-mortality was stronger the lower the educational group.

Introduction: The social gradient in consumption behaviours has been suggestedto partly explain health inequalities. The majority of previous studies have onlyincluded baseline measurements and not considered potential changes in behav-iours over time. The study aimed to investigate the contribution of alcohol con-sumption and smoking to the social gradient in mortality and to assess whetherthe use of repeated measurements results in larger attenuations of the main asso-ciation compared to using single baseline assessments.

Methods: Longitudinal survey data from the population-based Stockholm PublicHealth Cohort from 2006 to 2014 was linked to register data on mortality until2018 for 13,688 individuals and analysed through Cox regression.

Results: Low socioeconomic position (SEP) was associated with increased mortal-ity compared with high SEP; hazard ratios 1.56 (95% CI 1.30–1.88) for occupa-tional status and 1.77 (95% CI 1.49–2.11) for education, after adjustment fordemographic characteristics. Using repeated measurements, alcohol consumptionand smoking explained 44% of the association between occupational status andall-cause mortality. Comparing repeated and baseline measures, the percentageattenuation due to alcohol consumption increased from 11% to 18%, whereas itremained similar for smoking (25–23%).

Discussion and Conclusions: Smoking and alcohol consumption explained alarge part of the association between SEP and mortality. Comparing results fromtime-fixed and time-varying models, there was an increase in overall percentageattenuation that was mainly due to the increased proportion explained by alcoholconsumption. Repeated measurements provide a better estimation of the contri-bution of alcohol consumption, but not smoking, for the association between SEPand mortality.

Introduction: There is limited knowledge about how individual experiences of harm from others’ drinking are influenced by heavy episodic drinking (HED) at the country level. The present study aimed to assess (1) the association between the country-level prevalence of HED and the risk of experiencing harm from others’ drinking-related aggression and (2) if HED at the country level modifies the association between consumption of alcohol per capita (APC) and such harm. Methods: Outcome data from 32,576 participants from 19 European countries stem from the RARHA SEAS study. Self-reported harm from others’ drinking included having been verbally abused, harmed physically, or having serious arguments. Data on country-level drinking patterns were derived from the World Health Organization. Associations between country-level prevalence of monthly HED and experiences of aggression (at least 1 of 3 studied harms) were derived through multilevel models – adjusted for country-level age structure and by including the respondent’s own HED patterns as a mediator. Results: A 1% increase in the prevalence of monthly HED was associated with 5% higher odds (odds ratio [OR] 1.05) of experiencing others’ alcohol-related aggression among men, and 6% (OR 1.06) among women. The results suggest that the association between APC and harm was stronger in countries with high prevalences of HED, but the modifying effect could not be confirmed. Discussion/Conclusion: Harm from others’ drinking-related aggression depends not only on individual factors but is also influenced by the drinking patterns of the population. However, the country-level prevalence of HED only explains a small part of the variance of this type of harm.