Usefulness of a single-item measure of depression to predict mortality: the GAZEL prospective cohort study.: single-item of depression and mortality

International audienceBACKGROUND: It remains unknown whether short measures of depression perform as well as long measures in predicting adverse outcomes such as mortality. The present study aims to examine the predictive value of a single-item measure of depression for mortality. METHODS: A total of 14,185 participants of the GAZEL cohort completed the 20-item Center-for-Epidemiologic-Studies-Depression (CES-D) scale in 1996. One of these items (I felt depressed) was used as a single-item measure of depression. All-cause mortality data were available until 30 September 2009, a mean follow-up period of 12.7 years with a total of 650 deaths. RESULTS: In Cox regression model adjusted for baseline socio-demographic characteristics, a one-unit increase in the single-item score (range 0-3) was associated with a 25% higher risk of all-cause mortality (95% CI: 13-37%, P<0.001). Further adjustment for health-related behaviours and physical chronic diseases reduced this risk by 36% and 8%, respectively. After adjustment for all these variables, every one-unit increase in the single-item score predicted a 15% increased risk of death (95% CI: 5-27%, P<0.01). There is also an evidence of a dose-reponse relationship between reponse scores on the single-item measure of depression and mortality. CONCLUSION: This study shows that a single-item measure of depression is associated with an increased risk of death. Given its simplicity and ease of administration, a very simple single-item measure of depression might be useful for identifying middle-aged adults at risk for elevated depressive symptoms in large epidemiological studies and clinical settings

Socio-economic trajectories and cardiovascular disease mortality in older people: the English Longitudinal Study of Ageing

Background: Socio-economic status from early life has been linked to cardiovascular disease risk, but the impact of life-course socio-economic trajectories, as well as the mechanisms underlying social inequalities in cardiovascular disease risk, is uncertain. Objectives: We assessed the role of behavioural, psychosocial and physiological (including inflammatory) factors in the association between life-course socio-economic status and cardiovascular disease mortality in older adults. Methods: Participants were 7846 individuals (44% women) from the English Longitudinal Study of Ageing, a representative study of individuals aged ≥ 50 years, established in 2002–03. Comprising four indicators of socio-economic status (father’s social class, own education, occupational position and wealth), we computed an index of socio-economic trajectory and a lifetime cumulative socio-economic score. Behavioural (smoking, physical activity, alcohol consumption, body mass index) and psychosocial (social relations, loneliness) factors, physiological (blood pressure, total cholesterol, triglycerides) and inflammatory markers (C-reactive protein, fibrinogen), measured repeatedly over time, were potential explanatory variables. Cardiovascular disease mortality was ascertained by linkage of study members to a national mortality register. Mediation was calculated using the traditional ‘change-in-estimate method’ and alternative approaches such as counterfactual mediation modelling could not be applied in this context. Results: During the 8.4-year follow-up, 1301 study members died (438 from cardiovascular disease). A stable low-social-class trajectory was associated with around double the risk of cardiovascular disease mortality (hazard ratio; 95% confidence interval: 1.94, 1.37; 2.75) compared with a stable high social class across the life course. Individuals in the lowest relative to the highest life-course cumulative socio-economic status group were also more than twice as likely to die of cardiovascular disease (2.57, 1.81; 3.65). Behavioural factors and inflammatory markers contributed most to explaining this gradient, whereas the role of psychosocial and other physiological risk factors was modest. Conclusions: In a population-based cohort of older individuals living in England, we provide evidence that disadvantage across the life course is linked to cardiovascular mortality. That behavioural factors and inflammatory markers partially explain this gradient may provide insights into the potential for intervention

Life-course socioeconomic status and DNA methylation of genes regulating inflammation

Background: In humans, low socioeconomic status (SES) across the life course is associated with greater diurnal cortisol production, increased inflammatory activity and higher circulating antibodies for several pathogens, all suggesting a dampened immune response. Recent evidence suggests that DNA methylation of pro-inflammatory genes may be implicated in the biological embedding of the social environment. Methods: The present study examines the association between life-course SES and DNA methylation of candidate genes, selected on the basis of their involvement in SES-related inflammation, in the context of a genome-wide methylation study. Participants were 857 healthy individuals sampled from the EPIC Italy prospective cohort study. Results: Indicators of SES were associated with DNA methylation of genes involved in inflammation. NFATC1, in particular, was consistently found to be less methylated in individuals with low vs high SES, in a dose-dependent manner. IL1A, GPR132 and genes belonging to the MAPK family were also less methylated among individuals with low SES. In addition, associations were found between SES and CXCL2 and PTGS2, but these genes were consistently more methylated among low SES individuals. Conclusions: Our findings support the hypothesis that the social environment leaves an epigenetic signature in cells. Although the functional significance of SES-related DNA methylation is still unclear, we hypothesize that it may link SES to chronic disease ris

Life course socioeconomic conditions and frailty at older ages

Objectives: This paper aimed to assess associations of childhood socioeconomic conditions (CSC) with the risk of frailty in old age and whether adulthood socioeconomic conditions (ASC) influence this association. Methods: Data from 21 185 individuals aged 50 years and older included in the longitudinal Survey of Health, Ageing, and Retirement in Europe were used. Frailty was operationalized as a sum of presenting weakness, shrinking, exhaustion, slowness, or low activity. Confounder-adjusted multilevel logistic regression models were used to analyze associations of CSC and ASC with frailty. Results: While disadvantaged CSC was associated with higher odds of (pre-)frailty in women and men (OR=1.73, 95%CI 1.34, 2.24; OR=1.84, 95%CI 1.27, 2.66, respectively), this association was mediated by ASC. Personal factors and demographics, such as birth cohort, chronic conditions and difficulties with activities of daily living, increased the odds of being (pre-)frail. Discussion: Findings suggest that CSC are associated with frailty at old age. However, when taking into account ASC, this association no longer persists. The results show the importance of improving socioeconomic conditions over the whole life course in order to reduce health inequalities in old age

Socio-demographic and behavioural determinants of weight gain in the Swiss population

© 2015 Guerra et al.; licensee BioMed Central. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0),which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.Background: In Switzerland, socio-demographic and behavioural factors are associated with obesity, but no study ever assessed their impact on weight gain using prospective data. Methods: Data from 4,469 participants (53.0% women), aged 35 to 75 years at baseline and followed for 5.5 years. Weight gain was considered as a rate (kg/year) or as gaining ≥5 kg during the study period. Results: Rate of weight gain was lower among participants who were older (mean ± standard deviation: 0.46 ± 0.92, 0.33 ± 0.88, 0.21 ± 0.86 and 0.06 ± 0.74 kg/year in participants aged [35-45], [45-55], [55–65] and [65+] years, respectively, P<0.001); physically active (0.27 ± 0.82 vs. 0.35 ± 0.95 kg/year for sedentary, P < 0.005) or living in couple (0.29 ± 0.84 vs. 0.35 ± 0.96 kg/year for living single, P < 0.05), and higher among current smokers (0.41 ± 0.97, 0.26 ± 0.84 and 0.29±0.85 kg/year for current, former and never smokers, respectively, p<0.001). These findings were further confirmed by multivariable analysis. Multivariable logistic regression showed that receiving social help, being a current smoker or obese increased the likelihood of gaining ≥5 Kg: Odds ratio (OR) and 95% confidence interval (CI) 1.43 (1.16-1.77); 1.63 (1.35-1.95) and 1.95 (1.57-2.43), respectively, while living in couple or being physically active decreased the risk: 0.73 (0.62-0.86) and 0.72 (0.62-0.83), respectively. No association was found between weight gain and gender, being born in Switzerland or education. Conclusions: In Switzerland, financial difficulties (indicated by receiving social help) and current smoking were associated with increases in body weight over a 5 years follow-up. Living in couple, being older or physically active were protective against weight gain.The CoLaus study was supported by grants from the Swiss National Science Foundation [grant no: 33CSCO-122661 and FN 33CSC0-139468]; GlaxoSmithKline and the Faculty of Biology and Medicine of Lausanne, Switzerland. FG was supported by a Scientific Mobility Grant from the Lisbon Faculty of Medicine/Calouste Gulbenkian Foundation. SS is supported by an Ambizione Grant. (n° PZ00P3_147998) from the Swiss National Science Foundation (SNSF)

The radically unequal distribution of Covid-19 vaccinations: a predictable yet avoidable symptom of the fundamental causes of inequality

The Covid-19 pandemic—and its social and economic fallout—has thrust social and health-related inequalities into the spotlight. The pandemic, and our response to it, has induced new inequalities both within and between nations. However, now that highly efficacious vaccines are available, one might reasonably presume that we have in our hands the tools to address pandemic-associated inequalities. Nevertheless, two prominent social science theories, fundamental cause theory and diffusion of innovation theory suggest otherwise. Together, these theories predict that better resourced individuals and countries will jockey to harness the greatest vaccine benefit for themselves, leaving large populations of disadvantaged people unprotected. While many other life-saving prevention measures have been distributed unequally in ways these theories would predict, the COVID-19 vaccines represent a different kind of case. As the disease is so highly infectious and because mutations lead to new variants so rapidly, any inequality-generating process that leaves disadvantaged individuals and countries behind acts to put everyone—rich and poor—at risk. It is time that we ensure the equitable distribution of this life-saving benefit. As the fundamental cause and diffusion of innovation theories help illuminate processes that regularly produce inequities, we turn to them to reason about the rollout of the COVID-19 vaccines. Specifically, employ them to suggest countermoves that may be necessary to avoid an irrational and inequitable vaccine rollout that ends up unfavorably affecting all people.publishedVersio

Socioeconomic status, non-communicable disease risk factors, and walking speed in older adults: Multi-cohort population based study

Objective To assess the association of low socioeconomic status and risk factors for non-communicable diseases (diabetes, high alcohol intake, high blood pressure, obesity, physical inactivity, smoking) with loss of physical functioning at older ages. Design Multi-cohort population based study. Setting 37 cohort studies from 24 cou

Biological marks of early-life socioeconomic experience is detected in the adult inflammatory transcriptome.

Consistent evidence is accumulating to link lower socioeconomic position (SEP) and poorer health, and the inflammatory system stands out as a potential pathway through which socioeconomic environment is biologically embedded. Using bloodderived genome-wide transcriptional profiles from 268 Italian participants of the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, we evaluated the association between early life, young and later adulthood SEP and the expression of 845 genes involved in human inflammatory responses. These were examined individually and jointly using several inflammatory scores. Our results consistently show that participants whose father had a manual (as compared to nonmanual) occupation exhibit, later in life, a higher inflammatory score, hence indicating an overall increased level of expression for the selected inflammatory-related genes. Adopting a life course approach, these associations remained statistically significant upon adjustment for later-in-life socioeconomic experiences. Sensitivity analyses indicated that our findings were not affected by the way the inflammatory score was calculated, and were replicated in an independent study. Our study provides additional evidence that childhood SEP is associated with a sustainable upregulation of the inflammatory transcriptome, independently of subsequent socioeconomic experiences. Our results support the hypothesis that early social inequalities impacts adult physiology