Relationship between Hypothyroidism and Non-Alcoholic Fatty Liver Disease: A Systematic Review and Meta-analysis
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Previous studies propose that hypothyroidism might play a crucial role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD), but findings from published studies on the relationship between hypothyroidism and NAFLD are still controversial. Our study aimed to make a comprehensive evaluation of the relationship between hypothyroidism and NAFLD through a meta-analysis.PubMed, China Dissertation Database, and EMBASE databases were searched to find observational studies assessing the relationship between hypothyroidism and NAFLD. The pooled odds ratios (ORs) with 95% confidence intervals (95% CIs) were calculated to evaluate the strength of the relationship between hypothyroidism and NAFLD through meta-analysis.Thirteen articles were ultimately included in our meta-analysis. Meta-analysis of the 13 studies found a high correlation between hypothyroidism and NAFLD (OR = 1.52, 95% CI 1.24-1.87, P < 0.001). Meta-analysis of 9 studies providing adjusted ORs found that hypothyroidism was independently correlated with NAFLD (OR = 1.72, 95% CI 1.32-2.23, P < 0.001). Subgroup analysis found that both overt hypothyroidism and subclinical hypothyroidism were significantly correlated with NAFLD, and the pooled ORs were 1.70 (95% CI 1.23-2.36, P = 0.002) and 1.40 (95% CI 1.10-1.77, P = 0.006), respectively. Besides, meta-analysis of studies providing adjusted ORs also found that both overt hypothyroidism and subclinical hypothyroidism were independently correlated with NAFLD, and the pooled ORs were 1.81 (95% CI 1.30-2.52, P < 0.001) and 1.63 (95% CI 1.19-2.24, P = 0.002), respectively.The meta-analysis provides strong epidemiological evidence for the relationship between hypothyroidism and NAFLD. Both individuals with subclinical and overt hypothyroidism are at higher risk for NAFLD than euthyroid subjects.Keywords:
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Publication bias is a substantial problem for the credibility of research in general and of meta-analyses in particular, as it yields overestimated effects and may suggest the existence of non-existing effects. Although there is consensus that publication bias exists, how strongly it affects different scientific literatures is currently less well-known. We examined evidence of publication bias in a large-scale data set of primary studies that were included in 83 meta-analyses published in Psychological Bulletin (representing meta-analyses from psychology) and 499 systematic reviews from the Cochrane Database of Systematic Reviews (CDSR; representing meta-analyses from medicine). Publication bias was assessed on all homogeneous subsets (3.8% of all subsets of meta-analyses published in Psychological Bulletin) of primary studies included in meta-analyses, because publication bias methods do not have good statistical properties if the true effect size is heterogeneous. The Monte-Carlo simulation study revealed that the creation of homogeneous subsets resulted in challenging conditions for publication bias methods since the number of effect sizes in a subset was rather small (median number of effect sizes equaled 6). No evidence of bias was obtained using the publication bias tests. Overestimation was minimal but statistically significant, providing evidence of publication bias that appeared to be similar in both fields. These and other findings, in combination with the small percentages of statistically significant primary effect sizes (28.9% and 18.9% for subsets published in Psychological Bulletin and CDSR), led to the conclusion that evidence for publication bias in the studied homogeneous subsets is weak, but suggestive of mild publication bias in both psychology and medicine.
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Effective obesity interventions in adolescent populations have been identified as an immediate priority action to stem the increasing prevalence of adult obesity. The purpose of this meta-analysis was to make a quantitative analysis of the impact of school-based interventions on body mass index during adolescence. Studies were retrieved from PubMed, Scopus, Science Direct and Web of Science databases. Results were pooled using a random-effects model with 95% confidence interval considered statistically significant. Of the 18 798 possible relevant articles identified, 12 articles were included in this meta-analysis. The global result showed a low magnitude effect, though it was statistically significant (N = 14 428), global e.s. = -0.055, P = 0.004 (95% CI = -0.092, -0.017). Heterogeneity was low among the studies (I2 = 9.017%). The funnel plot showed no evidence of publication bias. The rank-correlation test of Begg (P = 0.45641) and Egger's regression (P = 0.19459) confirmed the absence of bias. This meta-analysis reported a significant effect favoring the interventions; however, future research are needed since the reported the evidence was of low magnitude, with the studies following a substantial range of approaches and mostly had a modest methodological quality.
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Publication bias is a substantial problem for the credibility of research in general and of meta-analyses in particular, as it yields overestimated effects and may suggest the existence of non-existing effects. Although there is consensus that publication bias exists, how strongly it affects different scientific literatures is currently less well-known. We examined evidence of publication bias in a large-scale data set of primary studies that were included in 83 meta-analyses published in Psychological Bulletin (representing meta-analyses from psychology) and 499 systematic reviews from the Cochrane Database of Systematic Reviews (CDSR; representing meta-analyses from medicine). Publication bias was assessed on all homogeneous subsets (3.8% of all subsets of meta-analyses published in Psychological Bulletin) of primary studies included in meta-analyses, because publication bias methods do not have good statistical properties if the true effect size is heterogeneous. Publication bias tests did not reveal evidence for bias in the homogeneous subsets. Overestimation was minimal but statistically significant, providing evidence of publication bias that appeared to be similar in both fields. However, a Monte-Carlo simulation study revealed that the creation of homogeneous subsets resulted in challenging conditions for publication bias methods since the number of effect sizes in a subset was rather small (median number of effect sizes equaled 6). Our findings are in line with, in its most extreme case, publication bias ranging from no bias until only 5% statistically nonsignificant effect sizes being published. These and other findings, in combination with the small percentages of statistically significant primary effect sizes (28.9% and 18.9% for subsets published in Psychological Bulletin and CDSR), led to the conclusion that evidence for publication bias in the studied homogeneous subsets is weak, but suggestive of mild publication bias in both psychology and medicine.
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Abstract Visfatin levels have been reported to be abnormal in many types of cancers. However, epidemiological studies yielded inconsistent results. Therefore, a meta‐analysis was performed to assess the association between circulating visfatin levels and cancer risk. A systematic search was conducted for relevant studies in health‐related electronic databases up to March 2018. Data related to standard mean difference (SMD) and overall odds ratio (ORS) were collected and analyzed. Summary SMD and pooled OR with 95% CIs were calculated using a random‐effect model. Funnel plot and Egger's linear regression test were conducted to examine the risk of publication bias. A total of 27 studies with 2,693 cases and 3,040 healthy controls were included in meta‐analysis for pooling SMD analysis. The results of the meta‐analysis showed a significant higher visfatin levels in patients with various cancers than in controls, with a pooled SMD of 0.88, 95% CI = 0.56–1.20, p = 0.000. In subgroup, metaregression, Galbraith plot, and sensitivity analysis showed no substantial difference among all the analyzed factors. Data from 14 studies were also used for pooling ORs analysis. Metaresults revealed that high visfatin levels were associated with cancer risk (OR = 1.24, 95% CI: 1.14–1.34, p = 0.000). No evidence of publication bias was observed for pooling ORs and SMD analysis. This meta‐analysis indicated a significant association between high circulating visfatin levels and increased risk of various cancers. Visfatin may represent a potential biomarker for early detection of cancers who may benefit from preventive treatment.Note.
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Selective publication and reporting in individual papers compromise the scientific record, but are meta-analyses as compromised as their constituent studies? We systematically sampled 63 meta-analyses (each comprising at least 40 studies) in PLOS One, top medical journals, top psychology journals, and Metalab, an online, open-data database of developmental psychology meta-analyses. We empirically estimated publication bias in each. Across all meta-analyses, “statistically significant” results in the expected direction were only 1.17 times more likely to be published than “nonsignificant” results or those in the unexpected direction (95%CI: [0.94, 1.47]), with a confidence interval substantially overlapping the null. Comparable estimates were 0.83 for meta-analyses in PLOS One, 1.02 for top medical journals, 1.54 for top psychology journals, and 4.70 for Metalab. The severity of publication bias did differ across individual meta-analyses; in a small minority (10%; 95% CI: [2%, 21%]), publication bias appeared to favor "significant" results in the expected direction by more than 3-fold. We estimated that for 89% of meta-analyses, the amount of publication bias that would be required to attenuate the point estimate to the null exceeded the amount of publication estimated to be actually present in the vast majority of meta-analyses from the relevant scientific discipline (exceeding the 95th percentile of publication bias). Study-level measures (“statistical significance” with a point estimate in the expected direction and point estimate size) did not indicate more publication bias in higher-tier versus lower-tier journals, nor in the earliest studies published on a topic versus later studies. Overall, the mere act of performing a meta-analysis with a large number of studies (at least 40) and that includes non-headline results may largely mitigate publication bias in meta-analyses, suggesting optimism about the validity of meta-analytic results.
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BackgroundObservational studies suggest that the risk and clinical prognosis of coronavirus disease 2019 (COVID-19) are related to low vitamin D status; however, the data are inconsistent.ObjectivesWe conducted a systematic review and meta-analysis to assess the association between low vitamin D status and COVID-19.MethodsA systematic search was conducted with PubMed, Embase, and the Cochrane Library from database inception to September 25, 2020. The standardized mean difference (SMD) or odds ratio (OR) and corresponding 95% confidence interval (CI) was applied to estimate pooled results. Random - or fixed-effect models based on heterogeneity were used for the meta-analysis. Funnel plots and Egger regression tests were used to assess publication bias.ResultsA total of ten articles with 361,934 participants were selected for meta-analysis. Overall, the pooled OR in the fixed-effect model showed that vitamin D deficiency or insufficiency was associated with an increased risk of COVID-19 (OR = 1.43, 95% CI 1.00–2.05). In addition, COVID-19-positive individuals had lower vitamin D levels than COVID-19-negative individuals (SMD = -0.37, 95% CI = -0.52 to -0.21). Significant heterogeneity existed in both endpoints. Funnel plots and Egger regression tests revealed significant publication bias.ConclusionsThis systematic review and meta-analysis indicated that low vitamin D status might be associated with an increased risk of COVID-19 infection. Further studies are needed to evaluate the impact of vitamin D supplementation on the clinical severity and prognosis in patients with COVID-19.Systematic Review RegistrationPROSPERO registration no: CRD42020216740.
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Background The evidence for association between Epstein-Barr virus (EBV) infection and risk of oral squamous cell carcinoma (OSCC) is inconsistent in the literature. Therefore, this meta-analysis was conducted to clarify this association. Methods A literature search was conducted in electronic databases for English- and Chinese-language publications until March 31, 2017 to include eligible case-control studies. The pooled odds ratio (OR) and 95% confidence interval (95% CI) were estimated to determine the association between EBV infection and OSCC risk using a fixed- or random-effects model based on heterogeneity. Publication bias was assessed using funnel plot analysis. Results A total of 13 case-control studies with 686 OSCC patients and 433 controls were included based on predetermined inclusion and exclusion criteria. The pooled OR with 95% CI between EBV infection and OSCC risk was 5.03 (1.80–14.01) with significant heterogeneity observed (I2 = 87%). The subgroup analysis indicates that the year of publication, study location, economic level, sample size, tissue type, detection method and marker, control type, and language might explain potential sources of heterogeneity. Publication bias was not observed, and sensitivity analysis showed stable results. Conclusions The results of the current meta-analysis suggest that EBV infection is statistically associated with increased risk of OSCC. However, additional high-quality studies with larger sample sizes are needed to further confirm the relationship between EBV and OSCC.
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