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Context It is widely recognised that the COVID-19 pandemic has negatively impacted individuals’ mental health. However, little emphasis has been put on the possible influence of socio-economic factors in the relationship. In the context of the COVID-19 pandemic, our objectives were (i) to assess the relationship between education level and mental health in French adults, and (ii) to study the influence of the economic, social, health and the COVID-19-related factors in men and women respectively. Method Data are from 32,581 individuals representative of the French population who responded to the weekly survey “Baromètre COVID-19” between April 7 th and May 31 st 2020. Education level was self-reported (university degree, high school qualification, vocational certificate/qualification, no diploma). Anxiety-depressive state was derived from four items related to the frequency of occurrence of depressive and anxiety symptoms, and summarized in an overall validated anxiety-depressive score. Multivariate linear regression analyses were carried out with nested adjustments of variables related to economic, social, health and COVID-19 contexts to assess the relationship between education and anxiety-depressive state. Results In total, 45% of individuals reported symptoms of anxiety-depressive state (53% in women versus 36% in men). Among men, those with a vocational certificate/qualification and those with no diploma had a greater risk of having a higher anxiety-depressive state compared to those with a university degree (β Vocational certificate/qualification  = 0.16 [0.04; 0.27]; β No diploma  = 0.75 [0.43; 1.07]) while among women, the risk of anxiety-depressive state increased as education level decreased (β Baccalaureate  = 0.37 [0.25; 0.49]; β Vocational certificate/qualification  = 0.41 [0.28; 0.54]; β No diploma  = 0.8 [0.49; 1.12]). For both men and women, economic, health, and COVID-19 factors partly attenuate these associations while social factors marginally modified the relationship. After accounting for confounders and intermediate variables, the absence of a diploma remained associated with anxiety-depressive state among men, while the whole educational gradient of anxiety-depressive state persisted among women. Conclusion In France, at the end of the first wave of COVID-19, individuals with a lower level of education had a higher risk of anxiety-depressive state. This association was more pronounced for women, highlighting a process of social inequality in health possibly related to gender. This should be considered in future prevention and public health interventions.

This study examines hypertension control beyond the cascade of care framework, which assesses awareness, treatment, and control sequentially. The analysis included 52 434 hypertensive adults (blood pressure (BP) ≥140/90 mm Hg and/or treatment in the past 6 months), aged 25–69, from the French population‐based CONSTANCES cohort from 2012 to 2021. The authors assessed the typical “awareness, treatment, and control” scenario and characterized other possible control patterns. The authors found that 13% achieved control. This percentage rose to 19% when considering individuals who were not aware but treated and controlled. This alternative control scenario was associated with female sex, younger age, higher education, Northern‐African origin, and reporting prior cardiovascular diseases (CVD). Sub‐Saharan African origin, diabetes and overweight/obesity were associated with the typical control scenario. This study highlights that applying a typical sequential cascade of care approach may lead to the exclusion of some specific groups of participants who do not fit into the defined categories.

Adverse childhood experiences (ACEs) have emerged as a major research theme. They make reference to an array of potentially harmful exposures occurring from birth to eighteen years of age and may be involved in the construction of health inequalities over the lifecourse. As with many simplified concepts, ACEs present limitations. They include diverse types of exposures, are often considered cumulatively, can be identified using prospective and retrospective approaches, and their multidimensional nature may lead to greater measurement error. From a public health perspective, ACEs are useful for describing the need to act upon complex social environments to prevent health inequalities at a population level. As the ACEs concept becomes popular in the context of policy interventions, concerns have emerged. As a probabilistic and population-level tool, it is not adapted to diagnose individual-level vulnerabilities, an approach which could ultimately exacerbate inequalities. Here, we present a critique of the ACEs framework, discussing its strengths and limits.

Disadvantaged socioeconomic position (SEP) is widely associated with disease and mortality, and there is no reason to think this will not be the case for the newly emerged coronavirus disease 2019 (COVID-19) that has reached a pandemic level. Individuals with a more disadvantaged SEP are more likely to be affected by most of the known risk factors of COVID-19. SEP has been previously established as a potential determinant of infectious diseases in general. We hypothesise that SEP plays an important role in the COVID-19 pandemic either directly or indirectly via occupation, living conditions, health-related behaviours, presence of comorbidities and immune functioning. However, the influence of socioeconomic factors on COVID-19 transmission, severity and outcomes is not yet known and is subject to scrutiny and investigation. Here we briefly review the extent to which SEP has been considered as one of the potential risk factors of COVID-19. From 29 eligible studies that reported the characteristics of patients with COVID-19 and their potential risk factors, only one study reported the occupational position of patients with mild or severe disease. This brief overview of the literature highlights that important socioeconomic characteristics are being overlooked when data are collected. As COVID-19 spreads worldwide, it is crucial to collect and report data on socioeconomic determinants as well as race/ethnicity to identify high-risk populations. A systematic recording of socioeconomic characteristics of patients with COVID-19 will be beneficial to identify most vulnerable groups, to identify how SEP relates to COVID-19 and to develop equitable public health prevention measures, guidelines and interventions.

In 2011, WHO member states signed up to the 25 × 25 initiative, a plan to cut mortality due to non-communicable diseases by 25% by 2025. However, socioeconomic factors influencing non-communicable diseases have not been included in the plan. In this study, we aimed to compare the contribution of socioeconomic status to mortality and years-of-life-lost with that of the 25 × 25 conventional risk factors. We did a multicohort study and meta-analysis with individual-level data from 48 independent prospective cohort studies with information about socioeconomic status, indexed by occupational position, 25 × 25 risk factors (high alcohol intake, physical inactivity, current smoking, hypertension, diabetes, and obesity), and mortality, for a total population of 1 751 479 (54% women) from seven high-income WHO member countries. We estimated the association of socioeconomic status and the 25 × 25 risk factors with all-cause mortality and cause-specific mortality by calculating minimally adjusted and mutually adjusted hazard ratios [HR] and 95% CIs. We also estimated the population attributable fraction and the years of life lost due to suboptimal risk factors. During 26·6 million person-years at risk (mean follow-up 13·3 years [SD 6·4 years]), 310 277 participants died. HR for the 25 × 25 risk factors and mortality varied between 1·04 (95% CI 0·98–1·11) for obesity in men and 2 ·17 (2·06–2·29) for current smoking in men. Participants with low socioeconomic status had greater mortality compared with those with high socioeconomic status (HR 1·42, 95% CI 1·38–1·45 for men; 1·34, 1·28–1·39 for women); this association remained significant in mutually adjusted models that included the 25 × 25 factors (HR 1·26, 1·21–1·32, men and women combined). The population attributable fraction was highest for smoking, followed by physical inactivity then socioeconomic status. Low socioeconomic status was associated with a 2·1-year reduction in life expectancy between ages 40 and 85 years, the corresponding years-of-life-lost were 0·5 years for high alcohol intake, 0·7 years for obesity, 3·9 years for diabetes, 1·6 years for hypertension, 2·4 years for physical inactivity, and 4·8 years for current smoking. Socioeconomic circumstances, in addition to the 25 × 25 factors, should be targeted by local and global health strategies and health risk surveillance to reduce mortality. European Commission, Swiss State Secretariat for Education, Swiss National Science Foundation, the Medical Research Council, NordForsk, Portuguese Foundation for Science and Technology.

The infection fatality rate of COVID-19 is several-fold higher than that of seasonal influenza,2 and infection can lead to persisting illness, including in young, previously healthy people (ie, long COVID).3 It is unclear how long protective immunity lasts,4 and, like other seasonal coronaviruses, SARS-CoV-2 is capable of re-infecting people who have already had the disease, but the frequency of re-infection is unknown.5 Transmission of the virus can be mitigated through physical distancing, use of face coverings, hand and respiratory hygiene, and by avoiding crowds and poorly ventilated spaces. PK reports personal fees from Kymab, outside the submitted work; PK also has a patent ‘Monoclonal antibodies to treat and prevent infection by SARS-CoV-2 (Kymab)’ pending and is a scientific advisor to the Serology Working Group (Public Heath England), Testing Advisory Group (Department of Health and Social Care) and the Vaccines Task force (Department for Business, Energy and Industrial Strategy). CS reports grants from BMS, Ono-Pharmaceuticals, and Archer Dx (collaboration in minimal residual disease sequencing technologies), outside the submitted work; personal fees from Bristol Myers Squibb, Roche-Ventana, Ono Pharmaceutical, GlaxoSmithKline, Novartis, Celgene, Illumina, MSD, Sarah Canon Research Institute, Genentech, Bicycle Therapeutics, and Medicixi, outside the submitted work; personal fees and stock options from GRAIL and Achilles Therapeutics, outside the submitted work; and stock options from Epic Biosciences and Apogen Biotechnologies, outside the submitted work.

BackgroundMental health conditions are increasing worldwide and can have substantial consequences on all aspects of life. Exposure to adverse childhood experiences (ACEs) at a young age increases the risk of mental health problems later in life. ACEs are characterized as stressful psychosocial conditions, outside of the child’s control, which can occur during sensitive periods of development and impact health throughout the life-course. In addition, obesity across the life-course is related to exposure to ACEs and associated with an increased risk in mental illness. A long-term association between ACEs and mental health requires further investigation of intermediate variables and their effect such as, obesity. Hence, the aim of this study is to examine the association between prospectively measured ACEs and an outcome of mental health in adulthood and to examine the role of obesity as an intermediate variable.MethodsThe study used data from the 1958 National Child Development Study, an observational prospective birth cohort study conducted in Great Britain (N = 18, 558). ACEs were measured prospectively (7, 11 and 16 years) using reports of (1) Child in care; (2) Physical neglect; (3) Contact with probation; (4) Parental separation; (5) Family mental illness and (6) Alcohol abuse. Exposures were counted and combined into a categorical ACEs variable (No ACEs, one ACEs and ≥ 2 ACEs). Depression and anxiety related symptoms were assessed at age 44/45 using an abbreviated version of the Clinical Interview Schedule-Revised. Obesity at 16y was determined as the upper BMI sex-specific quartile. Sequential nested logistic regression modelling was performed adjusting for early life covariates: individual’s characteristics, mother characteristics, parental socioeconomic background. In view of imputing data, analyses were conducted on complete cases.ResultsIn our study sample of 5 509 participants, we found a robust graded association between ACEs and CIS-R after accounting for covariates. The odds of having depression-anxiety symptoms at 44/45 was 2 times larger in participants who experienced two or more ACEs versus those with no ACEs, after adjusting for confounders (OR [95%CI]: 2.31[1.72–3.09], p<0.001). Further adjustment for obesity at 16y had no effect on the observed association (OR [95%CI]: 2.30[1.71–3.08], p<0.001).ConclusionThis study consolidates findings on the long-term cumulative effects of ACEs with late life psychopathology, independent of covariates and obesity status at 16y. In future analyses, testing the potential effects of intermediate variables during different time periods will be considered. Interventions that target early life stressors are recommended for primary prevention of adult psychopathology.

Events causing stress responses during sensitive periods of rapid neurological development in childhood may be early determinants of all-cause premature mortality. Using a British birth cohort study of individuals born in 1958, the relationship between adverse childhood experiences (ACE) and mortality ≤50 year was examined for men (n = 7,816) and women (n = 7,405) separately. ACE were measured using prospectively collected reports from parents and the school: no adversities (70 %); one adversity (22 %), two or more adversities (8 %). A Cox regression model was carried out controlling for early life variables and for characteristics at 23 years. In men the risk of death was 57 % higher among those who had experienced 2+ ACE compared to those with none (HR 1.57, 95 % CI 1.13, 2.18, p = 0.007). In women, a graded relationship was observed between ACE and mortality, the risk increasing as ACE accumulated. Women with one ACE had a 66 % increased risk of death (HR 1.66, 95 % CI 1.19, 2.33, p = 0.003) and those with ≥2 ACE had an 80 % increased risk (HR 1.80, 95 % CI 1.10, 2.95, p = 0.020) versus those with no ACE. Given the small impact of adult life style factors on the association between ACE and premature mortality, biological embedding during sensitive periods in early development is a plausible explanatory mechanism.

Background Epidemiologists need tools to measure effects of gender , a complex concept originating in the social sciences which is not easily operationalized in the discipline. Our aim is to clarify useful concepts, measures, paths, effects, and analytical strategies to explore mechanisms of health difference between men and women. Methods We reviewed concepts to clarify their definitions and limitations for their translation into usable measures in Epidemiology. Then we conducted methodological research using a causal framework to propose methodologically appropriate strategies for measuring sex and gender effects in health. Results (1) Concepts and measures. We define gender as a set of norms prescribed to individuals according to their attributed-at-birth sex. G ender pressure creates a systemic gap, at population level, in behaviors, activities, experiences, etc., between men and women. A pragmatic individual measure of gender would correspond to the level at which an individual complies with a set of elements constituting femininity or masculinity in a given population, place and time. (2) Main analytical strategy. Defining and measuring gender are not sufficient to distinguish the effects of sex and gender on a health outcome. We should also think in terms of mechanisms, i.e., how the variables are linked together, to define appropriate analytical strategies. A causal framework can help us to conceptualize “sex” as a “parent” of a gender or gendered variable. This implies that we cannot interpret sex effects as sexed mechanisms, and that we can explore gendered mechanisms of sex-differences by mediation analyses. (3) Alternative strategy. Gender could also be directly examined as a mechanism, rather than through a variable representing its realization in the individual, by approaching it as an interaction between sex and social environment. Conclusions Both analytical strategies have limitations relative to the impossibility of reducing a complex concept to a single or a few measures, and of capturing the entire effect of the phenomenon of gender. However, these strategies could lead to more accurate analyses of the mechanisms underlying health differences between men and women. Highlights A pragmatic individual measure of individual gender would correspond to the level at which an individual complies with a set of elements constituting femininity or masculinity in a given population, place and time Comparing outcomes by sex and gender is not sufficient, and even misleading, to understand the mechanisms underlying biological and health differences between men and women Causal analysis framework is a powerful tool for refining hypotheses and identifying the effects that can and should be estimated to meet the objectives Gender could also be measured at the populational-level as an interaction between sex and environment, which would be more compatible with the sociological concept of gender

Chronic inflammation has been proposed as having a prominent role in the construction of social inequalities in health. Disentangling the effects of early life and adulthood social disadvantage on inflammation is key in elucidating biological mechanisms underlying socioeconomic disparities. Here we explore the relationship between socioeconomic position (SEP) across the life course and inflammation (as measured by CRP levels) in up to 23,008 participants from six European cohort studies from three countries conducted between 1958 and 2013. We find a consistent inverse association between SEP and CRP across cohorts, where participants with a less advantaged SEP have higher levels of inflammation. Educational attainment is most strongly related to inflammation, after adjusting for health behaviours, body mass index and later-in-life SEP. These findings suggest socioeconomic disadvantage in young adulthood is independently associated with later life inflammation calling for further studies of the pathways operating through educational processes. Here, the authors explore the relationship between socioeconomic position (SEP) across the life course and inflammation in a multi-cohort study and show that educational attainment is most strongly related to inflammation, suggesting that socioeconomic disadvantage in young adulthood is independently associated with later life inflammation.