Search Results

High Na intake has been associated with different health problems. However, serious controversies exist over studies investigating associations of Na intake with mortality from all-causes and CVD. The present systematic review and meta-analysis was done to investigate, for the first time, the dose–response association of dietary Na intake with all-cause and CVD mortality among prospective studies.

Relevant papers published up to August 2017 were searched in MEDLINE, EMBASE and Google Scholar databases. Prospective cohort studies on the association of dietary Na intake with all-cause or/and CVD mortality were included. Linear and non-linear dose–response associations between Na intake and CVD and all-cause mortality were examined.

Overall, twenty publications met inclusion criteria. A significant non-linear association (P<0·001) was found between Na intake and CVD mortality risk among studies assessing urinary Na excretion, with a relatively steep slope at Na intakes above 2400mg/d. However, the association was not significant in studies using dietary Na intake (P=0·61). Additionally, the non-linear association of Na intake with all-cause mortality was also non-significant. No linear association (effect size; 95 % CI; I2) was seen between 100mg/d increment in Na intake and CVD mortality (1·01; 0·97, 1·05; 98·4 %) or all-cause mortality (1·01; 1·00, 1·02; 89·2 %). Following subgroup analyses, the association between Na intake and CVD mortality was observed only among studies conducted in the USA (0·99; 0·99, 1·00; 20·0 %).

The study showed a direct association between urinary Na excretion and CVD mortality which was more considerable at intakes above 2400mg/d. In contrast, no significant association was found between Na intake and all-cause mortality. Further long-term prospective studies on different populations are required to confirm these findings.

Individuals with bipolar disorder (BD) have a higher prevalence of obesity and metabolic syndrome (MetS) compared with the general population. Obesity and MetS are associated with cognitive deficits and brain imaging abnormalities in the general population. Obesity and components of MetS might potentially associate with neuroimaging and neurocognitive findings in BD.

A literature search of studies investigating the association between obesity (and other components of MetS) and neurocognitive and neuroimaging findings in BD was conducted. In addition to a systematic review, a random-effects meta-analysis was conducted when sufficient data were available.

Twenty-three studies were included in the current systematic review. Overweight/obese patients were significantly associated with impaired neurocognition compared normal weight individuals with BD (d = 0.37). The most robust association between obesity and cognitive deficits in BD was observed in the cognitive subdomain of executive functions (d = 0.61). There was also evidence for a significant relationship between cognitive impairment in BD and other components of MetS including hypertension, dyslipidemia, and diabetes. Overweight/obese individuals with BD had more pronounced brain imaging abnormalities than normal weight individuals with BD.

Obesity and related cardiovascular risk factors significantly are associated with more severe cognitive and brain imaging abnormalities in BD. Medical co-morbidities can potentially contribute to functional decline observed in some patients throughout the course of BD.

The purpose of the present meta-analysis was to evaluate the association between the inflammatory potential of diet, determined by the dietary inflammatory index (DII®) score, and depression.

Systematic review and meta-analysis.

A comprehensive literature search was conducted in PubMed, Web of Science and EMBASE databases up to August 2018. All observational studies that examined the association of the DII score with depression/depressive symptoms were included.

Four prospective cohorts and two cross-sectional studies enrolling a total of 49 584 subjects.

Overall, individuals in the highest DII v. the lowest DII category had a 23 % higher risk of depression (risk ratio (RR)=1·23; 95 % CI 1·12, 1·35). When stratified by study design, the pooled RR was 1·25 (95 % CI 1·12, 1·40) for the prospective cohort studies and 1·16 (95 % CI 0·96, 1·41) for the cross-sectional studies. Gender-specific analysis showed that this association was observed in women (RR=1·25; 95 % CI 1·09, 1·42) but was not statistically significant in men (RR=1·15; 95 % CI 0·83, 1·59).

The meta-analysis suggests that pro-inflammatory diet estimated by a higher DII score is independently associated with an increased risk of depression, particularly in women. However, more well-designed studies are needed to evaluate whether an anti-inflammatory diet can reduce the risk of depression.

Personality disorder is a severe health issue. However, the epidemiology of personality disorders is insufficiently described and surveys report very heterogeneous rates.

We aimed to conduct a meta-analysis on the prevalence of personality disorders in adult populations and examine potential moderators that affect heterogeneity.

We searched PsycINFO, PSYNDEX and Medline for studies that used standardised diagnostics (DSM-IV/-5, ICD-10) to report prevalence rates of personality disorders in community populations in Western countries. Prevalence rates were extracted and aggregated by random-effects models. Meta-regression and sensitivity analyses were performed and publication bias was assessed.

The final sample comprised ten studies, with a total of 113 998 individuals. Prevalence rates were fairly high for any personality disorder (12.16%; 95% CI, 8.01–17.02%) and similarly high for DSM Clusters A, B and C, between 5.53 (95% CI, 3.20–8.43%) and 7.23% (95% CI, 2.37–14.42%). Prevalence was highest for obsessive–compulsive personality disorder (4.32%; 95% CI, 2.16–7.16%) and lowest for dependent personality disorder (0.78%; 95% CI, 0.37–1.32%). A low prevalence was significantly associated with expert-rated assessment (versus self-rated) and reporting of descriptive statistics for antisocial personality disorder.

Epidemiological studies on personality disorders in community samples are rare, whereas prevalence rates are fairly high and vary substantially depending on samples and methods. Future studies investigating the epidemiology of personality disorders based on the DSM-5 and ICD-11 and models of personality functioning and traits are needed, and efficient treatment should be a priority for healthcare systems to reduce disease burden.

None.

Suicide attempt (SA), which is one of the strongest predictors of completed suicide, is common in major depressive disorder (MDD) but its prevalence across epidemiological studies has been mixed. The aim of this comprehensive meta-analysis was to examine the pooled prevalence of SA in individuals with MDD.

A systematic literature search was conducted in PubMed, Embase, PsycINFO, Web of Science and Cochrane Library from their commencement date until 27 December 2017. Original studies containing data on prevalence of SA in individuals with MDD were analyzed.

In all, 65 studies with a total of 27 340 individuals with MDD were included. Using the random effects model, the pooled lifetime prevalence of SA was 31% [95% confidence interval (CI) 27–34%], 1-year prevalence was 8% (95% CI 3–14%) and 1-month prevalence was 24% (95% CI 15–34%). Subgroup analyses revealed that the lifetime prevalence of SA was significantly associated with the patient setting, study region and income level, while the 1-month prevalence of SA was associated with only the patient setting.

This meta-analysis confirmed that SA was common in individuals with MDD across the world. Careful screening and appropriate interventions should be implemented for SA in the MDD population.

A reliable biomarker signature for bipolar disorder sensitive to illness phase would be of considerable clinical benefit. Among circulating blood-derived markers there has been a significant amount of research into inflammatory markers, neurotrophins and oxidative stress markers.

To synthesise and interpret existing evidence of inflammatory markers, neurotrophins and oxidative stress markers in bipolar disorder focusing on the mood phase of illness.

Following PRISMA (Preferred Reporting Items for Systematic reviews and Meta-analyses) guidelines, a systematic review was conducted for studies investigating peripheral biomarkers in bipolar disorder compared with healthy controls. We searched Medline, Embase, PsycINFO, SciELO and Web of Science, and separated studies by bipolar mood phase (mania, depression and euthymia). Extracted data on each biomarker in separate mood phases were synthesised using random-effects model meta-analyses.

In total, 53 studies were included, comprising 2467 cases and 2360 controls. Fourteen biomarkers were identified from meta-analyses of three or more studies. No biomarker differentiated mood phase in bipolar disorder individually. Biomarker meta-analyses suggest a combination of high-sensitivity C-reactive protein/interleukin-6, brain derived neurotrophic factor/tumour necrosis factor (TNF)-α and soluble TNF-α receptor 1 can differentiate specific mood phase in bipolar disorder. Several other biomarkers of interest were identified.

Combining biomarker results could differentiate individuals with bipolar disorder from healthy controls and indicate a specific mood-phase signature. Future research should seek to test these combinations of biomarkers in longitudinal studies.

None.

To determine the impact of specialized treatments, relative to comparator treatments, upon the weight and psychological symptoms of anorexia nervosa (AN) at end-of-treatment (EOT) and follow-up.

Randomized controlled trials (RCTs) between January 1980 and December 2017 that reported the effects of at least two treatments on AN were screened. Weight and psychological symptoms were analyzed separately for each study. PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines were followed, and studies were assessed using the GRADE (Grading of Recommendations, Assessment, Development and Evaluation) criteria and Cochrane risk of bias tool.

We identified 35 eligible RCTs, comprising data from 2524 patients. Meta-analyses revealed a significant treatment effect on weight outcomes at EOT [g = 0.16, 95% CI (0.05–0.28), p = 0.006], but not at follow-up [g = 0.11, 95% CI (−0.04 to 0.27), p = 0.15]. There was no significant treatment effect on psychological outcomes at either EOT [g = −0.03, 95% CI (−0.14 to 0.08), p = 0.63], or follow-up [g = −0.001, 95% CI (−0.11 to 0.11), p = 0.98]. There was no strong evidence of publication bias or significant moderator effects for illness duration, mean age, year of publication, comparator group category, or risk of bias (all p values > 0.05).

Current specialized treatments are more adept than comparator interventions at imparting change in weight-based AN symptoms at EOT, but not at follow-up. Specialized treatments confer no advantage over comparator interventions in terms of psychological symptoms. Future precision treatment efforts require a specific focus on the psychological symptoms of AN.

To determine the association between the sleep duration and the risk of all-cause mortality in adults.

A search strategy was conducted in the MEDLINE, CENTRAL, EMBASE and LILACS databases. Searches were also conducted in other databases and unpublished literature. Cohort studies were included without language, time or setting restrictions. The risk of bias was evaluated with a modified Cochrane Collaboration's tool. An analysis of random effects was conducted. The primary outcome was all-cause mortality. The measure of the effect was the risk difference (RD) with a 95% confidence interval (CI). The planned comparisons were 7–9 h of sleep v. <7 h and the same reference v. >9 h.

Thirty-nine studies were included in our qualitative analysis, regarding the quantitative analysis, 19 studies were included in <7 v. 7–9 h analysis, and 18 studies in the >9 v. 7–9 h. A low risk of bias was shown for most of the study items. The overall RD for all-cause mortality was 0.09 (95% CI 0.07–0.11) favouring the >9 h group compared with our reference. In contrast, no differences were found between the <7 h and the reference sleep duration groups (RD 0.00, 95% CI 0.00–0.01).

We found a probable association of long sleep duration and higher mortality; however, it could reflect an underlying systemic or neurological disease that cause sleep fragmentation, deterioration in quality and micro-awakenings.

Interpersonal violence is a leading cause of morbidity and mortality. The strength and population effect of modifiable risk factors for interpersonal violence, and the quality of the research evidence is not known.

We aimed to examine the strength and population effect of modifiable risk factors for interpersonal violence, and the quality and reproducibility of the research evidence.

We conducted an umbrella review of systematic reviews and meta-analyses of risk factors for interpersonal violence. A systematic search was conducted to identify systematic reviews and meta-analyses in general population samples. Effect sizes were extracted, converted into odds ratios and synthesised, and population attributable risk fractions (PAF) were calculated. Quality analyses were performed, including of small study effects, adjustment for confounders and heterogeneity. Secondary analyses for aggression, intimate partner violence and homicide were conducted, and systematic reviews (without meta-analyses) were summarised.

We identified 22 meta-analyses reporting on risk factors for interpersonal violence. Neuropsychiatric disorders were among the strongest in relative and absolute terms. The neuropsychiatric risk factor that had the largest effect at a population level were substance use disorders, with a PAF of 14.8% (95% CI 9.0–21.6%), and the most important historical factor was witnessing or being a victim of violence in childhood (PAF = 12.2%, 95% CI 6.5–17.4%). There was evidence of small study effects and large heterogeneity.

National strategies for the prevention of interpersonal violence may need to review policies concerning the identification and treatment of modifiable risk factors.

J.R.G. is an NIHR Senior Investigator. The views expressed within this article are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health and Social Care.

The aim of this study was to reanalyse the data from Cuijpers et al.'s (2018) meta-analysis, to examine Eysenck's claim that psychotherapy is not effective. Cuijpers et al., after correcting for bias, concluded that the effect of psychotherapy for depression was small (standardised mean difference, SMD, between 0.20 and 0.30), providing evidence that psychotherapy is not as effective as generally accepted.

The data for this study were the effect sizes included in Cuijpers et al. (2018). We removed outliers from the data set of effects, corrected for publication bias and segregated psychotherapy from other interventions. In our study, we considered wait-list (WL) controls as the most appropriate estimate of the natural history of depression without intervention.

The SMD for all interventions and for psychotherapy compared to WL controls was approximately 0.70, a value consistent with past estimates of the effectiveness of psychotherapy. Psychotherapy was also more effective than care-as-usual (SMD = 0.31) and other control groups (SMD = 0.43).

The re-analysis reveals that psychotherapy for adult patients diagnosed with depression is effective.

Increasing evidence has suggested an association between food insecurity and the risk of anaemia. Therefore, a systematic review and meta-analysis were performed to examine the associations between food insecurity and anaemia risk.

Pertinent studies were identified by searching PubMed and EMBASE databases up to August 2017. Data were available from nineteen studies; seventeen studies were cross-sectional and two studies were longitudinal. Risk ratios of 95993 individual participants from twelve different countries in these studies were pooled for the meta-analysis.

The results showed that there was an overall positive relationship between food insecurity and anaemia risk (OR=1·27; 95 % CI 1·13, 1·40). Similar results were observed for Fe-deficiency anaemia (OR=1·45; 95 % CI 1·04, 1·86). These results revealed that food insecurity at two levels, including mild food insecurity (OR=1·15; 95 % CI 1·00, 1·31) and moderate food insecurity (OR=1·36; 95 % CI 1·23, 1·48), increased the risk of anaemia. In addition, it was found that age had an impact on the associations between food insecurity and anaemia risk (OR=1·22; 95 % CI 1·09, 1·36). Age subgroup analysis indicated that food insecurity significantly increased the risk of anaemia among infants/toddlers (OR=1·17; 95 % CI 1·05, 1·29) and adult women (OR=1·35; 95 % CI 1·16, 1·54).

It seems that infants, toddlers and adult women in food-insecure households are at a higher risk of anaemia. To prevent anaemia in food-insecure households, these age groups may require more nutritional support.