Dietary Inflammatory Index and Pancreatic Cancer Risk—A Systematic Review and Dose-response Meta-analysis

2021 ◽  
pp. 1-24
Author(s):  
Zhangyou Guo ◽  
Yuan Hong ◽  
Yao Cheng

Abstract Objective: The meta-analysis was conducted to test the link between pancreatic cancer (PC) risk and dietary inflammatory index (DII®) score. Design: Systematic review and meta-analysis. Setting: We searched PubMed, Embase, Web of Science, and the Cochrane Library up to November 22, 2020, to identify the relevant studies. Studies that reported the risk estimates and the corresponding 95% confidence intervals (CIs) for the DII category and PC risk were included. The effect sizes were pooled using the random-effects model. Dose–response analysis was conducted where possible. Participants: Two prospective cohort studies of 634 705 participants (3 152 incident cases), and four case-control studies of 2 737 cases and 4 861 controls. Results: Overall, the pooled risk ratio (RR) indicated that individuals in the highest category compared with the lowest category had an increased PC risk (RR=1.45; 95% CI 1.11, 1.90; P=0.006). Meanwhile, significant heterogeneity was also revealed. The dose-response meta-analysis indicated that a 1-unit increase in the DII score was associated with the PC risk (RR=1.08; 95% CI 1.002, 1.166; P=0.045; I 2 =94.1%, P<0.001). Nonlinear result showed an increased risk of moving from fewer to more inflammatory borders with increasing DII score (Pnonlinearity = 0.003; I 2 =76.5%, P<0.001). Subgroup analyses found that significant positive association between PC risk and DII score appeared to be in case-control studies (RR=1.70; 95% CI 1.16, 2.50; P=0.007) and studies with ≤31 DII components (RR=1.76; 95% CI 1.14, 2.72; P=0.011). Conclusion: These findings suggested dietary habits with high inflammatory features (high DII score) might increase PC risk.

2017 ◽  
Vol 20 (17) ◽  
pp. 3183-3192 ◽  
Author(s):  
Yanhong Huang ◽  
Hongru Chen ◽  
Liang Zhou ◽  
Gaoming Li ◽  
Dali Yi ◽  
...  

AbstractObjectiveTo examine and quantify the potential dose–response relationship between green tea intake and the risk of gastric cancer.DesignWe searched PubMed, EMBASE, Web of Science, CBM, CNKI and VIP up to December 2015 without language restrictions.SettingA systematic review and dose–response meta-analysis of observational studies.SubjectsFive cohort studies and eight case–control studies.ResultsCompared with the lowest level of green tea intake, the pooled relative risk (95 % CI) of gastric cancer was 1·05 (0·90, 1·21, I2=20·3 %) for the cohort studies and the pooled OR (95 % CI) was 0·84 (0·74, 0·95, I2=48·3 %) for the case–control studies. The pooled relative risk of gastric cancer was 0·79 (0·63, 0·97, I2=63·8 %) for intake of 6 cups green tea/d, 0·59 (0·42, 0·82, I2=1·0 %) for 25 years of green tea intake and 7·60 (1·67, 34·60, I2=86·5 %) for drinking very hot green tea.ConclusionsDrinking green tea has a certain preventive effect on reducing the risk of gastric cancer, particularly for long-term and high-dose consumption. Drinking too high-temperature green tea may increase the risk of gastric cancer, but it is still unclear whether high-temperature green tea is a risk factor for gastric cancer. Further studies should be performed to obtain more detailed results, including other gastric cancer risk factors such as smoking and alcohol consumption and the dose of the effective components in green tea, to provide more reliable evidence-based medical references for the relationship between green tea and gastric cancer.


2013 ◽  
Vol 23 (3) ◽  
pp. 437-441 ◽  
Author(s):  
Maria Inês Rosa ◽  
Geraldo Doneda Silva ◽  
Priscyla Waleska Targino de Azedo Simões ◽  
Meriene Viquetti Souza ◽  
Ana Paula Ronzani Panatto ◽  
...  

ObjectiveWe performed a systematic review and a meta-analysis to estimate the prevalence of human papillomavirus (HPV) in ovarian cancer.MethodsA comprehensive search of the Cochrane Library, MEDLINE, CANCERLIT, LILACS, Grey literature and EMBASE was performed for articles published from January 1990 to March 2012. The following MeSH (Medical Subject Headings) terms were searched: “ovarian tumor” or “ovarian cancers” and “HPV” or “human papillomavirus.” Included were case-control and cross-sectional studies, prospective or retrospective, that evaluated clinical ovarian cancer and provided a clear description of the use of in situ hybridization, Southern blot hybridization, and polymerase chain reaction. The statistical analysis was performed using REVMAN 5.0.ResultsIn total, 24 primary studies were included in this meta-analysis. Studies from 11 countries on 3 continents contained data on HPV and ovarian cancer, including 889 subjects. Overall, the HPV prevalence in patients with ovarian cancer was 17.5 (95% confidence interval [CI], 15.0%–20.0%). Human papillomavirus prevalence ranged from 4.0% (95% CI, 1.7%–6.3%) in Europe to 31.4% (95% CI, 26.9%–35.9%) in Asia. An aggregate of 4 case-control studies from Asia showed an odds ratio of 2.48 (95% CI, 0.64–9.57).ConclusionsWe found a high prevalence of HPV-positive DNA in ovarian cancer cases, but the role of HPV in ovarian cancer remains inconclusive. Further studies are needed to control case to answer this question.


2021 ◽  
pp. 1-31
Author(s):  
Raymond Pranata ◽  
Andrea Feraldho ◽  
Michael Anthonius Lim ◽  
Joshua Henrina ◽  
Rachel Vania ◽  
...  

Abstract In this systematic review and dose-response meta-analysis, we aim to assess whether coffee and tea consumption is related to the risk of glioma. We performed a systematic literature search using PubMed, Embase, Scopus, and the EuropePMC up until 1st October 2020. Exposures in this study were coffee and tea consumption. The main outcome of this study was the incidence of glioma. This study compares the association between the exposure of coffee and tea with the incidence of glioma, the results are reported in Relative Risks (RRs). There are 12 unique studies comprising of 1,960,731 participants with 2,987 glioma cases. Higher coffee consumption was associated with a statistically non-significant trend towards lower risk of glioma (RR 0.77 [0.55, 1.03], p=0.11; I2: 75.27%). Meta-regression showed that the association between coffee and glioma was reduced by smoking (p=0.029). Higher tea consumption was associated with the lower risk of glioma (RR 0.84 [0.71, 0.98], p=0.030; I2: 16.42%). Sensitivity analysis by removal of case-control studies showed that higher coffee consumption (RR 0.85 [0.72, 1.00], p=0.046; I2: 0%) and higher tea consumption (RR 0.81 [0.70, 0.93], p=0.004; I2: 0%, Pnon-linearity=0.140) were associated with lower risk of glioma. Dose-response meta-analysis showed that every 1 cup of coffee per day decreases the risk of glioma by 3% (RR 0.97 [0.94, 0.99], p=0.016, Pnon-linearity=0.054) and every 1 cup of tea per day decreases the risk of glioma by 3% (RR 0.97 [0.94, 1.00], p=0.048). This meta-analysis showed apparent association between coffee and tea intake and risk of glioma.


2014 ◽  
Vol 1 (2) ◽  
pp. 31-37 ◽  
Author(s):  
Khalid Bouti ◽  
Rajae Borki ◽  
Hicham Fenane ◽  
Laila Harrak

Background: Cannabis is the illicit psychoactive substance the most consumed in the world. Little is known about the association between the use of cannabis and the risk of lung cancer. Objective:The objective of this meta-analysis is to determine whether use of cannabis is a risk factor for lung cancer. Methods: We conducted a systematic review and meta-analyses of all languages articles using relevant computerised databases. MEDLINE (online PubMed), Web of knowledge, Embase, EBSCO CINAHL, ScienceDirect, Scopus, Cochrane Library, and Directory of Open Access Journals were searched to September 2014 for cohorts and case-control studies that assessed the risk of lung cancer associated with cannabis smoking. The literature search was performed with a combination of medical subject headings terms, "cannabis" and "lung neoplasms". Data extraction: Two investigators independently analysed and extracted results from eligible studies. Our study's registration number on PROSPERO is CRD42014008872. Results: The search strategy identified 2476 citations. 13 studies were eligible for inclusion: 2 pooled analysis of 9 case-control studies, one case-control study and 3 cohorts. The cumulative analysis for all the studies under a fixed-effects model showed that cannabis smoking determined an increased risk of developing lung cancer in the future (relative risk 1.22, 95% confidence interval 0.999–1.5; p=0.051), with no evidence of heterogeneity across the studies (I2: 34%; p¼0.01). Conclusions: The use of cannabis with or without tobacco smoking is associated with an increased risk for lung cancer


2021 ◽  
Vol 8 ◽  
Author(s):  
Peng Miao ◽  
Lin Guan

Background: Many case–control studies have investigated the association between dietary cholesterol and gastric cancer, yielding inconsistent findings. We carried out a systematic review and meta-analysis of observational studies to assess the relationship between dietary cholesterol intake and gastric cancer among adults.Methods: PubMed, Scopus, and Google Scholar were systematically searched to identify articles that evaluated the association of dietary cholesterol with gastric cancer up to May 2021. Pooled odds ratio (ORs) and 95% confidence intervals (CIs) were computed using random-effects models. Dose–response analysis was used to explore the shape and strength of the association.Results: Fourteen case–control studies with 6,490 gastric cancer patients and 17,793 controls met our inclusion criteria. In the meta-analysis of the highest vs. the lowest dietary cholesterol categories, a significantly higher (~35%) risk of gastric cancer was observed in association with high cholesterol consumption (pooled OR: 1.35, 95% CI: 1.29–1.62, I2 = 68%; 95%CI: 45–81%). Subgroup analysis also showed this positive relationship in population-based case–control studies, those conducted on non-US countries, those with a higher number of cases and high-quality studies, those that collected dietary data via interviews, studies not adjusted for Helicobacter pylori infection, and studies where the body mass index was controlled. Besides, a non-linear dose–response association was also identified (P = 0.03).Conclusion: This study demonstrated that dietary cholesterol intake could significantly augment the risk of gastric cancer in case–control studies. Prospective cohort studies with large sample sizes and long durations of follow-up are required to verify our results.


Author(s):  
Mahdi Vajdi ◽  
Mahdieh Abbasalizad Farhangi ◽  
Mahsa Mahmoudi-Nezhad

Abstract. Background: The available data on the relationship between dietary inflammatory index (DII®) and serum lipids are controversial. This systematic review and meta-analysis aimed to investigate the relationship between DII® and serum lipids, including total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglyceride (TG) in general populations. Methods: PubMed, Web of Science, SCOPUS, and Cochrane electronic databases were systematically searched from inception to December 2019. Case-control, cohort or cross-sectional studies that evaluated the relationship between DII® and serum lipids were included. The random-effects model was applied to evaluate the pooled weighted mean difference (WMD) and 95% confidence intervals (CI). Results: In total, twenty-four cross-sectional and one case-control studies with a total sample size of 129,759 were included in the meta-analysis. The pooled results showed that the highest category of DII® was associated with 5.16 mg/dl increase in TC (Pooled WMD: 5.16; 95% CI: 0.58–9.73, p = 0.02) and 3.99 mg/dl increase in LDL-C (Pooled WMD: 3.99; 95% CI: 1.16–6.81, p = 0.006). However, no significant association between DII® scores, HDL-C and TG was found. In subgroup analysis, the geographical region, gender, and dietary assessment methods were potent sources of heterogeneity. Conclusion: This study showed that a higher level of DII® was associated with higher levels of TC and LDL-C in apparently healthy populations. Since the included studies had observational designs, therefore, no conclusion of causality was possible. More studies with interventional designs are required to elucidate the causality of the observed association between DII® and the risk of abnormal lipid profile.


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