Meta-Analysis on the Association of Neuropeptide Y rs16139 Variant With the Risk of Alcoholism

Introduction: The neuropeptide-Y (NPY) is involved in the development of alcoholism through NPY receptors. A T>C mutation causes substitution of leucine to proline at codon 7 (L7P; rs16139) in the signal peptide of neuropeptide Y is known to cause a 42% increase in plasma NPY levels. Studies that analyzed the association between NPY rs16139 and alcoholism risk did not demonstrate conclusive evidence for this relationship. The present study aims to evaluate the association between NPY gene rs16139 variant and alcohol dependence.Method: An electronic search of databases including PubMed and Google Scholar was performed to retrieve studies investigating the association between NPY rs16139 and alcoholism. The pooled odds ratio (OR) with 95% confidence interval (CI) was calculated in allelic and dominant genetic models. Sensitivity analyses and publication bias were assessed in our meta-analysis. The meta-analysis was conducted using the MetaGenyo web tool.Result: Significant heterogeneity was observed across studies (p < 0.001). Our results have shown that there is no significant association between NPY rs16139 variant and the risk of alcoholism in allelic (OR = 0.98, 95% CI 0.70–1.38, p = 0.921) and dominant models (OR = 0.98, 95% CI 0.69–1.40, p = 0.919). Begg's funnel plot and Egger's test have not shown publication bias (p = 0.332).Conclusion: To the best of our knowledge, this is the first meta-analysis that evaluates the relationship between the NPY rs16139 polymorphism and the risk of alcoholism. Our large-scale meta-analysis suggests that NPY rs16139 polymorphism is not associated with alcoholism. However, further studies are needed to increase our understanding of the relationship between NPY variants in alcoholism.

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The impact of time to adjuvant chemotherapy (AC) on survival in colorectal cancer (CRC): A systematic review and meta-analysis.

Journal of Clinical Oncology ◽

10.1200/jco.2011.29.4_suppl.364 ◽

2011 ◽

Vol 29 (4_suppl) ◽

pp. 364-364 ◽

Cited By ~ 4

Author(s):

J. J. Biagi ◽

M. Raphael ◽

W. D. King ◽

W. Kong ◽

W. J. Mackillop ◽

...

Keyword(s):

Systematic Review ◽

Prognostic Factors ◽

Adjuvant Chemotherapy ◽

Publication Bias ◽

Meta Analysis ◽

Disease Free Survival ◽

Significant Heterogeneity ◽

Risk Of Death ◽

The Impact ◽

The Relationship

364 Background: The optimal timing from CRC surgery to initiation of AC is unknown. We report a systematic review and meta-analysis to determine the relationship between time to adjuvant chemotherapy (TTAC) and survival. Methods: A systematic review of literature was done to identify studies that described the relationship between TTAC and survival. Studies were only included if the distribution of relevant prognostic factors was adequately described, and either comparative groups were balanced or results adjusted for the prognostic factors. Hazard ratio (HR) and TTAC for overall survival (OS) and disease free survival (DFS) from each study were converted to a regression coefficient (β) and standard error (SE) corresponding to a continuous representation per 4 weeks of TTAC. The adjusted β from individual studies were combined using a fixed-effect model. Inverse-variance (1/SE2) was used to weight individual studies. The possible effect of publication bias was investigated using the trim and fill approach. Results: We identified 9 eligible studies involving 14,357 patients (4 published articles, 5 abstracts). Two studies were randomized trials and 7 were cohort studies. Six studies reported TTAC as a binary variable and 3 reported TTAC as ≥3 categories. An estimate of HR for OS was derived from all 9 studies and estimate for DFS was derived from 5 studies. Meta-analysis demonstrated that a 4-week increase in TTAC was associated with a significant decrease in both OS (HR = 1.12, 95% CI 1.09-1.15), and DFS (HR = 1.15, 95% CI 1.11-1.20). The analysis showed no significant heterogeneity among studies. These TTAC associations remained significant after analysis for potential publication bias, and when the analysis was repeated excluding the two studies of largest weight. Conclusions: This study demonstrates a 12% increase in the risk of death for each 4 week of delay in the start of AC for CRC. These findings indicate the need for clinicians and health systems managers to take the steps necessary to keep TTAC as short as reasonably achievable. In addition, our results suggest there may be some benefit to AC after a 3-month TTAC delay. No significant financial relationships to disclose.

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BDNF Val66Met and clinical response to antipsychotic drugs: A systematic review and meta-analysis

European Psychiatry ◽

10.1016/j.eurpsy.2015.12.001 ◽

2016 ◽

Vol 33 (1) ◽

pp. 45-53 ◽

Cited By ~ 10

Author(s):

S. Cargnin ◽

A. Massarotti ◽

S. Terrazzino

Keyword(s):

Clinical Response ◽

Publication Bias ◽

Antipsychotic Drugs ◽

Meta Analysis ◽

Individual Variability ◽

Sensitivity Analyses ◽

Significant Heterogeneity ◽

Relevant Effect ◽

Quantitative Synthesis ◽

The Impact

AbstractBackgroundThe polymorphic brain-derived neurotrophic factor (BDNF) gene has been postulated to be involved in inter-individual variability response to antipsychotic drugs.PurposeTo perform a qualitative and quantitative synthesis of studies evaluating the influence of BDNF genetic variation on clinical response to antipsychotics.MethodsThe review protocol was published in the PROSPERO database (Reg. no CRD42015024614). A comprehensive search was performed through PubMed, Web of Knowledge and Cochrane databases up to July 2015. The methodological quality of identified studies was assessed using the MINORS criteria. Publication bias was estimated and potential sources of heterogeneity were investigated via meta-regression, subgroup and sensitivity analyses.ResultsNine studies including a total of 2461 antipsychotic-treated patients fulfilled inclusion criteria for meta-analysis of BDNF Val66Met. Using the random-effects model, the pooled results showed no significant association with antipsychotic response for the dominant (Met carriers vs Val/Val, OR: 0.93, 95% CI: 0.72–1.19, P = 0.55), codominant (Met/Met vs Val/Val, OR: 0.82, 95% CI: 0.59–1.15, P = 0.25), recessive (Met/Met vs Val carriers, OR: 0.81, 95% CI 0.60–1.10, P = 0.18) or the allelic contrast (Met vs Val, OR: 0.92, 95% CI 0.76–1.10, P = 0.34). Visual inspection of funnel plots and further evaluation with Egger's test did not suggest evidence of publication bias. Despite lack of significant heterogeneity in most comparisons, no evidence of association also emerged in the subgroup and sensitivity analyses conducted.ConclusionThe present meta-analysis excludes a clinically relevant effect of BDNF Val66Met on antipsychotic drug response per se. Nevertheless, further investigation is still needed to clarify in well-designed, large sample-based studies, the impact of BDNF haplotypes containing the Val66Met polymorphism.

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Correcting for Bias in Psychology: A Comparison of Meta-Analytic Methods

Advances in Methods and Practices in Psychological Science ◽

10.1177/2515245919847196 ◽

2019 ◽

Vol 2 (2) ◽

pp. 115-144 ◽

Cited By ~ 63

Author(s):

Evan C. Carter ◽

Felix D. Schönbrodt ◽

Will M. Gervais ◽

Joseph Hilgard

Keyword(s):

Publication Bias ◽

Large Scale ◽

Meta Analysis ◽

Sensitivity Analyses ◽

Simulation Studies ◽

Research Practices ◽

Simulation Code ◽

Questionable Research Practices ◽

Analytic Methods ◽

Primary Literature

Publication bias and questionable research practices in primary research can lead to badly overestimated effects in meta-analysis. Methodologists have proposed a variety of statistical approaches to correct for such overestimation. However, it is not clear which methods work best for data typically seen in psychology. Here, we present a comprehensive simulation study in which we examined how some of the most promising meta-analytic methods perform on data that might realistically be produced by research in psychology. We simulated several levels of questionable research practices, publication bias, and heterogeneity, and used study sample sizes empirically derived from the literature. Our results clearly indicated that no single meta-analytic method consistently outperformed all the others. Therefore, we recommend that meta-analysts in psychology focus on sensitivity analyses—that is, report on a variety of methods, consider the conditions under which these methods fail (as indicated by simulation studies such as ours), and then report how conclusions might change depending on which conditions are most plausible. Moreover, given the dependence of meta-analytic methods on untestable assumptions, we strongly recommend that researchers in psychology continue their efforts to improve the primary literature and conduct large-scale, preregistered replications. We provide detailed results and simulation code at https://osf.io/rf3ys and interactive figures at http://www.shinyapps.org/apps/metaExplorer/ .

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The Relationship between Natriuretic Peptide Precursor a Gene T2238C Polymorphism and Hypertension: A Meta-Analysis

International Journal of Hypertension ◽

10.4061/2011/653698 ◽

2011 ◽

Vol 2011 ◽

pp. 1-8 ◽

Cited By ~ 6

Author(s):

Wenquan Niu

Keyword(s):

Publication Bias ◽

Study Design ◽

Meta Analysis ◽

Analysis Data ◽

Population Based ◽

Significant Heterogeneity ◽

Study Heterogeneity ◽

Peptide Precursor ◽

Meta Regression Analysis ◽

The Relationship

Single studies attempting to associate ANP gene T2238C (rs5065) polymorphism with hypertension have so far reported inconclusive results. We therefore aimed to evaluate this association via a meta-analysis. Data on 7 studies with a total of 4068 subjects were available and analyzed using the random-effects model with assessment of heterogeneity and publication bias. Overall comparison of 2238C with 2238T yielded a 23% reduced, albeit nonsignificant, risk for hypertension (95% CI: 0.38–1.59;P=.485), while accompanying significant heterogeneity (I2=88.3%) and publication bias (P=.051). Subgroup analysis by study design demonstrated opposite associations between population-based (OR=0.33; 95% CI: 0.13–0.80;P=.015) and hospital-based studies (OR=1.15; 95% CI: 0.79–1.68;P=.454). Further meta-regression analysis exclusively indicated the significant influence of study design (P=.042) on heterogeneity. Taken together, these findings support the notion that carriers of 2238C allele were at moderate decreased risk of developing hypertension, whereas study design was identified as a potentially significant source of between-study heterogeneity.

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Correcting for bias in psychology: A comparison of meta-analytic methods

10.31234/osf.io/9h3nu ◽

2017 ◽

Cited By ~ 7

Author(s):

Evan C Carter ◽

Felix D. Schönbrodt ◽

Will M Gervais ◽

Joseph Hilgard

Keyword(s):

Publication Bias ◽

Large Scale ◽

Meta Analysis ◽

Sensitivity Analyses ◽

Simulation Studies ◽

Research Practices ◽

Simulation Code ◽

Questionable Research Practices ◽

Analytic Methods ◽

Primary Literature

Publication bias and questionable research practices in primary research can lead to badly overestimated effects in meta-analysis. Methodologists have proposed a variety of statistical approaches to correct for such overestimation. However, much of this work has not been tailored specifically to psychology, so it is not clear which methods work best for data typically seen in our field. Here, we present a comprehensive simulation study to examine how some of the most promising meta-analytic methods perform on data that might realistically be produced by research in psychology. We created such scenarios by simulating several levels of questionable research practices, publication bias, heterogeneity, and using study sample sizes empirically derived from the literature. Our results clearly indicated that no single meta-analytic method consistently outperformed all others. Therefore, we recommend that meta-analysts in psychology focus on sensitivity analyses—that is, report on a variety of methods, consider the conditions under which these methods fail (as indicated by simulation studies such as ours), and then report how conclusions might change based on which conditions are most plausible. Moreover, given the dependence of meta-analytic methods on untestable assumptions, we strongly recommend that researchers in psychology continue their efforts on improving the primary literature and conducting large-scale, pre-registered replications. We provide detailed results and simulation code at https://osf.io/rf3ys and interactive figures at http://www.shinyapps.org/apps/metaExplorer/.

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Pre-eclampsia and the risk of autism-spectrum disorder in offspring: meta-analysis

The British Journal of Psychiatry ◽

10.1192/bjp.2017.27 ◽

2018 ◽

Vol 212 (3) ◽

pp. 142-147 ◽

Cited By ~ 30

Author(s):

Berihun Assefa Dachew ◽

Abdullah Mamun ◽

Joemer Calderon Maravilla ◽

Rosa Alati

Keyword(s):

Autism Spectrum Disorder ◽

Publication Bias ◽

Meta Analysis ◽

Autism Spectrum ◽

Spectrum Disorder ◽

Sensitivity Analyses ◽

Significant Heterogeneity ◽

Early Screening ◽

Intrauterine Exposure ◽

Relative Risks

BackgroundEvidence about the effect of intrauterine exposure to pre-eclampsia on offspring autism-spectrum disorder (ASD) is not well established.AimsTo examine the association between pre-eclampsia and ASD.MethodPubMed, Embase and PsycINFO databases were searched. Pooled relative risks (RR) with 95% confidence intervals were calculated. Subgroup and sensitivity analyses were performed. Heterogeneity was assessed using Cochran'sQ- and theI2−test. The presence of publication bias was evaluated by Egger's test and visual inspection of the symmetry in funnel plots.ResultsTen studies meet the inclusion criteria. The risk of ASD was 32% higher in offspring who had intrauterine exposure to pre-eclampsia compared with those not exposed (RR = 1.32, 95% CI 1.20–1.45). Sensitivity analysis revealed consistent pooled estimates ranging from RR = 1.30 (95% CI 1.17–1.44) to RR = 1.37 (95% CI 1.26–1.48). We found no significant heterogeneity and evidence of publication bias.ConclusionPre-eclampsia increased the risk of ASD in offspring. The finding suggests a need for early screening for ASD in offspring of women with pre-eclampsia.Declaration of interestNone.

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Relationship between total plasma homocysteine and the risk of aneurysms – a meta-analysis

VASA ◽

10.1024/0301-1526/a000891 ◽

2020 ◽

pp. 1-6

Author(s):

Hanji Zhang ◽

Dexin Yin ◽

Yue Zhao ◽

Yezhou Li ◽

Dejiang Yao ◽

...

Keyword(s):

Large Scale ◽

Meta Analysis ◽

Single Species ◽

Total Plasma ◽

Control Groups ◽

Randomized Controlled ◽

Randomized Controlled Studies ◽

The Difference ◽

The Relationship ◽

Healthy Participants

Summary: Our meta-analysis focused on the relationship between homocysteine (Hcy) level and the incidence of aneurysms and looked at the relationship between smoking, hypertension and aneurysms. A systematic literature search of Pubmed, Web of Science, and Embase databases (up to March 31, 2020) resulted in the identification of 19 studies, including 2,629 aneurysm patients and 6,497 healthy participants. Combined analysis of the included studies showed that number of smoking, hypertension and hyperhomocysteinemia (HHcy) in aneurysm patients was higher than that in the control groups, and the total plasma Hcy level in aneurysm patients was also higher. These findings suggest that smoking, hypertension and HHcy may be risk factors for the development and progression of aneurysms. Although the heterogeneity of meta-analysis was significant, it was found that the heterogeneity might come from the difference between race and disease species through subgroup analysis. Large-scale randomized controlled studies of single species and single disease species are needed in the future to supplement the accuracy of the results.

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Identification of and Correction for Publication Bias: Comment

10.31222/osf.io/dh87m ◽

2019 ◽

Author(s):

Amanda Kvarven ◽

Eirik Strømland ◽

Magnus Johannesson

Keyword(s):

Publication Bias ◽

False Positive ◽

Large Scale ◽

Meta Analysis ◽

False Positive Rate ◽

Effect Sizes ◽

Replication Studies ◽

Moderate Reduction ◽

Positive Rate ◽

Meta Analyses

Andrews & Kasy (2019) propose an approach for adjusting effect sizes in meta-analysis for publication bias. We use the Andrews-Kasy estimator to adjust the result of 15 meta-analyses and compare the adjusted results to 15 large-scale multiple labs replication studies estimating the same effects. The pre-registered replications provide precisely estimated effect sizes, which do not suffer from publication bias. The Andrews-Kasy approach leads to a moderate reduction of the inflated effect sizes in the meta-analyses. However, the approach still overestimates effect sizes by a factor of about two or more and has an estimated false positive rate of between 57% and 100%.

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Emotional intelligence, Personality Variables and Career Adaptability: A Systematic Review and Meta-analysis

Vision The Journal of Business Perspective ◽

10.1177/0972262921989877 ◽

2021 ◽

pp. 097226292198987

Author(s):

Sakshi Vashisht ◽

Poonam Kaushal ◽

Ravi Vashisht

Keyword(s):

Systematic Review ◽

Emotional Intelligence ◽

Publication Bias ◽

Meta Analysis ◽

Career Adaptability ◽

Personality Variables ◽

Regression Test ◽

Size Measure ◽

Fail Safe ◽

The Relationship

This study conducted a systematic review and meta-analysis to examine the relationship between emotional intelligence, personality variables (Big V personality traits, self-esteem, self-efficacy, optimism and proactive personality) and career adaptability of students. Data were coded on CMA software version 3.0. Product–moment correlation coefficient (r) was considered as the effect size measure for this study. Publication bias was assessed using Egger’s regression test along with Orwin’s fail-safe N, but no significant publication bias was detected. From the results of 54 studies, it was found that all variables of the study had meta-analytic correlation with career adaptability of students. For heterogeneity, subgroup analysis was conducted, and significant differences were found.

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Risk of dementia in gout and hyperuricaemia: a meta-analysis of cohort studies

BMJ Open ◽

10.1136/bmjopen-2020-041680 ◽

2021 ◽

Vol 11 (6) ◽

pp. e041680

Author(s):

Shu-Yue Pan ◽

Rui-Juan Cheng ◽

Zi-Jing Xia ◽

Qiu-Ping Zhang ◽

Yi Liu

Keyword(s):

Cohort Studies ◽

Quality Assessment ◽

Publication Bias ◽

Data Extraction ◽

Meta Analysis ◽

Sensitivity Analyses ◽

Cochrane Library ◽

Crystal Formation ◽

Medical Subject Headings ◽

Eligibility Criteria

ObjectivesGout, characterised by hyperuricaemia with monosodium urate crystal formation and inflammation, is the most common inflammatory arthritis in adults. Recent studies have found that elevated uric acid levels are related to the occurrence of dementia. We conducted a study to investigate the association between dementia and gout or hyperuricaemia.DesignSystematic review and meta-analysis of cohort studies.Data sourcesStudies were screened from inception to 28 June 2019 by searching Medline, Embase and the Cochrane Library databases.Eligibility criteriaCohort studies comparing the risk of dementia in patients with gout and hyperuricaemia versus non-gout and non-hyperuricaemia controls were enrolled.Data extraction and analysisTwo reviewers separately selected studies and extracted data using the Medical Subject Headings without restriction on languages or countries. The adjusted HRs were pooled using the DerSimonian and Laird random effects model. Sensitivity analyses were conducted to evaluate the stability of the results. Publication bias was evaluated using Egger’s and Begg’s tests. Quality assessment was performed according to the Newcastle-Ottawa Scale.ResultsFour cohort studies that met the inclusion criteria were included in our meta-analysis. We found that gout and hyperuricaemia did not increase the risk of dementia, with a pooled HR of 0.94 (95% CI 0.69 to 1.28), but might decrease the risk of Alzheimer’s disease (AD), with a pooled HR of 0.78 (95% CI 0.64 to 0.95). There was little evidence of publication bias. Quality assessment of the included studies was high (range: 6–8 points).ConclusionsOur study shows that gout and hyperuricaemia do not increase the risk of dementia. However, gout and hyperuricaemia might have a protective effect against AD. Due to the limited number of research articles, more investigations are needed to demonstrate the potential relationship between dementia and gout or hyperuricaemia.

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