Economic crises are complex events that affect behavioral patterns (including alcohol consumption) via opposing mechanisms. With this realist systematic review, we aimed to investigate evidence from studies of previous or ongoing crises on which mechanisms (How?) play a role among which individuals (Whom?). Such evidence would help understand and predict the potential impact of economic crises on alcohol consumption. Medical, psychological, social, and economic databases were used to search for peer-reviewed qualitative or quantitative empirical evidence (published January 1, 1990-May 1, 2014) linking economic crises or stressors with alcohol consumption and alcohol-related health problems. We included 35 papers, based on defined selection criteria. From these papers, we extracted evidence on mechanism(s), determinant, outcome, country-level context, and individual context. We found 16 studies that reported evidence completely covering two behavioral mechanisms by which economic crises can influence alcohol consumption and alcohol-related health problems. The first mechanism suggests that psychological distress triggered by unemployment and income reductions can increase drinking problems. The second mechanism suggests that due to tighter budget constraints, less money is spent on alcoholic beverages. Across many countries, the psychological distress mechanism was observed mainly in men. The tighter budget constraints mechanism seems to play a role in all population subgroups across all countries. For the other three mechanisms (i.e., deterioration in the social situation, fear of losing one's job, and increased non-working time), empirical evidence was scarce or absent, or had small to moderate coverage. This was also the case for important influential contextual factors described in our initial theoretical framework. This realist systematic review suggests that among men (but not among women), the net impact of economic crises will be an increase in harmful drinking. Such a different net impact between men and women could potentially contribute to growing gender-related health inequalities during a crisis.

Despite similar body composition, the offspring of nonagenarian siblings showed a lower prevalence of metabolic syndrome and better glucose tolerance than their partners, centralizing the role of favorable glucose metabolism in familial longevity.

In many fields, including the field of nephrology, missing data are unfortunately an unavoidable problem in clinical/epidemiological research. The most common methods for dealing with missing data are complete case analysis-excluding patients with missing data--mean substitution--replacing missing values of a variable with the average of known values for that variable-and last observation carried forward. However, these methods have severe drawbacks potentially resulting in biased estimates and/or standard errors. In recent years, a new method has arisen for dealing with missing data called multiple imputation. This method predicts missing values based on other data present in the same patient. This procedure is repeated several times, resulting in multiple imputed data sets. Thereafter, estimates and standard errors are calculated in each imputation set and pooled into one overall estimate and standard error. The main advantage of this method is that missing data uncertainty is taken into account. Another advantage is that the method of multiple imputation gives unbiased results when data are missing at random, which is the most common type of missing data in clinical practice, whereas conventional methods do not. However, the method of multiple imputation has scarcely been used in medical literature. We, therefore, encourage authors to do so in the future when possible.

The current evidence is in line with the hypothesis that drug use increases in times of recession because unemployment increases psychological distress which increases drug use. During times of recession, psychological support for those who lost their job and are vulnerable to drug use (relapse) is likely to be important.

BackgroundConcerns are present on the limited value of renal function alone in defining the optimal moment to start dialysis. Disease-related symptoms and health-related quality of life (HRQOL) may have additional clinical value in defining this moment, but little is known about how these parameters change during pre-dialysis care. The aims of our study were to describe the course of symptoms and HRQOL during pre-dialysis care and to investigate their association with poor health outcomes.MethodsIn the prospective PREPARE-2 cohort, incident patients starting specialized pre-dialysis care were included when referred to one of the 25 participating Dutch outpatient clinics (2004–2011). In the present analysis, 436 patients with data available on symptoms and HRQOL were included. Clinical data, symptoms (revised illness perception questionnaire), and HRQOL (short form-36 questionnaire; physical and mental summary score) were collected every 6-month interval. A time-dependent Cox proportional hazard model was used to associate symptoms and HRQOL with the combined poor health outcome (i.e. starting dialysis, receiving a kidney transplant, and death).ResultsAll symptoms increased, especially fatigue and loss of strength, and both the physical and mental summary score decreased over time, with the most pronounced change during the last 6–12 months of follow-up. Furthermore, each additional symptom (adjusted HR 1.04 (95% CI, 1.00–1.09)) and each 3-point lower physical and mental summary score (adjusted HR 1.04 (1.02–1.06) and 1.04 (1.02–1.06) respectively) were associated with a higher risk of reaching the combined poor health outcome within the subsequent 6 months.ConclusionsThe number of symptoms increased and both the physical and mental HRQOL score decreased during pre-dialysis care and these changes were associated with starting dialysis, receiving a kidney transplant, and death. These results may indicate that symptoms and HRQOL are good markers for the medical condition and disease stage of pre-dialysis patients.

IntroductionSNPs rs2981582 and rs2981578, located in a linkage disequilibrium block (LD block) within intron 2 of the fibroblast growth factor receptor 2 gene (FGFR2), are associated with a mildly increased breast cancer risk. Allele-specific regulation of FGFR2 mRNA expression has been reported previously, but the molecular basis for the association of these variants with breast cancer has remained elusive to date.MethodsmRNA levels of FGFR2 and three fibroblast growth factor genes (FGFs) were measured in primary fibroblast and epithelial cell cultures from 98 breast cancer patients and correlated to their rs2981578 genotype. The phosphorylation levels of downstream FGFR2 targets, FGF receptor substrate 2α (FRS2α) and extracellular signal-regulated kinases 1 and 2 (ERK1/2), were quantified in skin fibroblasts exposed to FGF2. Immunohistochemical markers for angiogenesis and lymphocytic infiltrate were semiquantitatively assessed in 25 breast tumors.ResultsThe risk allele of rs2981578 was associated with increased FGFR2 mRNA levels in skin fibroblasts, but not in skin epithelial cell cultures. FGFR2 mRNA levels in skin fibroblasts and breast fibroblasts correlated strongly in the patients from whom both cultures were available. Tumor-derived fibroblasts expressed, on average, eight times more FGFR2 mRNA than the corresponding fibroblasts from normal breast tissue. Fibroblasts with higher FGFR2 mRNA expression showed more FRS2α and ERK1/2 phosphorylation after exposure to FGF2. In fibroblasts, higher FGFR2 expression correlated with higher FGF10 expression. In 25 breast tumors, no associations between breast tumor characteristics and fibroblast FGFR2 mRNA levels were found.ConclusionsThe influence of rs2981578 genotypes on FGFR2 mRNA expression levels is cell type-dependent. Expression differences correlated well with signaling levels of the FGFR2 pathway. Our results suggest that the increased breast cancer risk associated with SNP rs2981578 is due to increased FGFR2 signaling activity in stromal fibroblasts, possibly also involving paracrine FGF10 signaling.

The association of Hb levels with HRQOL differs by age and use of ESA/iron medication on predialysis care. Therefore, medical care should aim for shared decision-making regarding the appropriate Hb target leading to more individualized care.

SummaryBackground and objectives Studies performed in the United States showed that blacks progress from CKD to ESRD faster than do whites. Possible explanations are differences in health care system factors. This study investigated whether progression is also faster in a universal health care system, where all patients receive comparable care.Design, setting, participants, & measurements Data from the PREdialysis PAtient REcord study, a multicenter follow-up study of patients with CKD who started predialysis care in The Netherlands (1999)(2000)(2001)(2002)(2003)(2004)(2005)(2006)(2007)(2008)(2009)(2010)(2011), were analyzed. Time-dependent Cox proportional hazards models were used to estimate the hazard ratio (HR) for starting renal replacement therapy (RRT), and linear mixed models were used to compare renal function decline (RFD) between blacks and whites. To explore possible mechanisms, analyses were adjusted for patient characteristics.Results At initiation of predialysis care, blacks (n=49) were younger and had more diabetes mellitus, higher proteinuria levels, and a higher estimated GFR than whites (n=946). Median follow-up time in months was similar (blacks: 13.9 [boundaries of interquartile range (IQR), 5.3 to 19.5]; whites: 13.1 [IQR, 5.1 to 24.0]). For blacks compared with whites, the crude HR for starting RRT within the first 15 months was 0.86 (95% confidence interval [CI], 0.55 to 1.34) and from 15 months onward, 1.93 (95% CI, 1.02 to 3.68), which increased after adjustment. RFD was faster by 0.18 (95% CI, 0.05 to 0.32) ml/min per 1.73 m 2 per month in blacks compared with whites.Conclusion Blacks receiving predialysis care in a universal health care system have faster disease progression than whites, suggesting that health care system factors have a less influential role than had been thought in explaining black-white differences.