Dietary fat intake and endometrial cancer risk: A dose response meta-analysis.
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ABSTRACT:
SUBMITTER: Zhao J
PROVIDER: S-EPMC5058849 | biostudies-other | 2016 Jul
REPOSITORIES: biostudies-other
Publications
Dietary fat intake and endometrial cancer risk: A dose response meta-analysis.
Zhao Jing J Lyu Chen C Gao Jian J Du Li L Shan Boer B Zhang Hong H Wang Hua-Ying HY Gao Ying Y
Medicine 20160701 27
Since body fatness is a convincing risk factor for endometrial cancer, dietary fat intake was speculated to be associated with endometrial cancer risk. However, epidemiological studies are inconclusive. We aimed to conduct a meta-analysis to assess the associations between dietary fat intake and endometrial cancer risk. We searched the PubMed, Embase, and Web of science databases updated to September 2015. In total, 7 cohort and 14 case-control studies were included. Pooled analysis of case-cont ...[more]
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Project description:Epidemiological studies have provided controversial evidence of the association between dietary fat intake and endometrial cancer (EC) risk. To address this inconsistency, we conducted this dose-response meta-analysis by total dietary fat intake, based on epidemiological studies published up to the end of June 2015 identified from PubMed, EMBASE and Web of Science. Two authors (RH and Q-JW) independently performed the eligibility evaluation and data extraction. All differences were resolved by discussion with the third investigator (LJ). Random-effects models were used to estimate summary relative risks (RRs) and 95% confidence intervals (CIs). Overall, the search yielded 16 studies (6 cohort and 10 case-control studies) that involved a total of 7556 EC cases and 563,781 non-cases. The summary RR for EC for each 30 g/day increment intake was 0.98 (95%CI = 0.95-1.001; I(2) = 0%; n = 11) for total dietary fat. Non-significant results were observed in plant-based fat (summary RR = 1.05, 95%CI = 0.94-1.18; I(2) = 0%; n = 5) and animal-based fat (summary RR = 1.17, 95%CI = 0.92-1.36; I(2) = 85.0%; n = 6). Additionally, the null associations were observed in almost all the subgroup and sensitivity analyses. In conclusion, findings of the present meta-analysis suggested a lack of association between total dietary fat intake and EC risk. Further studies, especially prospective designed studies are warranted to confirm our findings.
| S-EPMC4645223 | biostudies-other
Project description:BackgroundSeveral epidemiological studies have investigated the association between dietary fat intake and cardiovascular disease. However, dietary recommendations based on systematic review and meta-analysis might be more credible.Methods and resultsPubmed, Embase and Cochrane library were searched up to July 1st 2018 for cohort studies reporting associations of dietary fat intake and risk of CVDs. By comparing the highest vs. the lowest categories of fat or fatty acids intake, we found that higher dietary trans fatty acids (TFA) intake was associated with increased risk of CVDs [RR:1.14(1.08-1.21)]. However, no association was observed between total fat, monounsaturated fatty acids (MUFA), saturated fatty acids (SFA), and polyunsaturated fatty acids (PUFA), and risk of CVDs. Subgroup analysis found a cardio-protective effect of PUFA in the studies that has been followed up more than 10 years [0.95(0.91-0.99), I2 = 62.4%]. Dose-response analysis suggested that the risk of CVDs increased 16% [1.16 (1.07-1.25), Plinearity = 0.033] for an increment of 2% energy/day of TFA intake.ConclusionsThis current meta-analysis of cohort studies suggested that total fat, SFA, MUFA, and PUFA intake were not associated with the risk of cardiovascular disease. However, we found that higher TFA intake is associated with greater risk of CVDs in a dose-response fashion. Furthermore, the subgroup analysis found a cardio-protective effect of PUFA in studies followed up for more than 10 years.
| S-EPMC6451787 | biostudies-literature
Project description:Background and objectivesConsumption of dietary fat has been reported to be associated with gastric cancer risk, but the results of epidemiologic studies remain inconsistent. We conducted a meta-analysis to summarize the evidence regarding the association between dietary fat intake and gastric cancer risk.MethodsA comprehensive search of PubMed and EMBASE was performed to identify observational studies providing quantitative estimates between dietary fat and gastric cancer risk. Random effects model was used to calculate the summary relative risk(SRR) in the highest versus lowest analysis. Categorical dose-response analysis was conducted to quantify the association between dietary fat intake and gastric cancer risk. Heterogeneity among studies was evaluated using I2 and tau2(between study variance)statistics. Subgroup analysis and publication bias analysis were also performed.ResultsTwenty-two articles were included in the meta-analysis. The SRR for gastric cancer was 1.18 for individuals with highest intake versus lowest intake of total fat (95% confidence interval [CI]: 0.999-1.39; n = 28; P< 0.001; tau2 = 0.12; I2 = 69.5%, 95% CI: 55%-79%) and 1.08 with a daily increase in total fat intake (20 g/d) (95%CI: 1.02-1.14; n = 6; P = 0.09; tau2 = 0.002; I2 = 46.8%, 95% CI: 0%-79%). Positive association between saturated fat intake (SRR = 1.31; 95%CI: 1.09-1.58;n = 18;P<0.001; tau2 = 0.08; I2 = 60.6%, 95% CI: 34%-76%), inverse association between polyunsaturated fat intake (SRR = 0.77; 95%CI: 0.65-0.92; n = 16; P = 0.003; tau2 = 0.06; I2 = 56.2%, 95% CI: 23%-75%) and vegetable fat intake (SRR = 0.55; 95%CI: 0.41-0.74; n = 4;P = 0.12; tau2 = 0.04; I2 = 48.6%, 95% CI: 0%-83%), and no association between monounsaturated fat intake (SRR = 1.00; 95%CI: 0.79-1.25; n = 14; P< 0.001; tau2 = 0.10; I2 = 63.0%, 95% CI: 34%-79%) and animal fat intake (SRR = 1.10; 95%CI: 0.90-1.33; n = 6; P = 0.13;tau2 = 0.02; I2 = 42.0%, 95% CI: 0%-70%) and gastric cancer risk were observed.ConclusionsOur results suggest that intake of total fat is potentially positively associated with gastric cancer risk, and specific subtypes of fats account for different effects. However, these findings should be confirmed by further well-designed cohort studies with detailed dietary assessments and strict control of confounders.
| S-EPMC4581710 | biostudies-literature
Project description:Evidence between age at menarche and endometrial cancer risk have been controversial. Therefore, we conducted a meta-analysis of prospective studies to analyze the aforementioned association. Relevant studies were identified by searching PubMed and EMBASE databases until the end of June 2015. A random-effects model was used to estimate summary relative risks (RRs) and 95% confidence intervals (CIs) for associations between menarcheal age and endometrial cancer risk. Our meta-analysis included eight prospective studies involving 4553 subjects with endometrial cancer. The summarized RRs of endometrial cancer for menarcheal age were 0.68 (95%CI = 0.58-0.81, I(2) = 41.9%, P = 0.099, n = 8) when comparing women with oldest category of menarcheal age with women with youngest category of menarcheal age. Notably, there was an 4% reduction in risk for per 2 years delay in menarcheal age (summarized RR = 0.96; 95%CI = 0.94-0.98, I(2) = 45.7%, P = 0.101, n = 6). Additionally, significant inverse associations were consistent within all stratified analyses. There was no evidence of publication bias or significant heterogeneity between subgroups detected by meta-regression analyses. Our findings support the hypothesis that late menarcheal age is inversely associated with endometrial cancer risk. Further larger prospective or pooled studies are warranted to fully adjust for potential confounders and distinguish whether the associations differ by histological subtypes of endometrial cancer.
| S-EPMC4566123 | biostudies-other
Project description:Dietary sodium intake has received considerable attention as a potential risk factor of cardiovascular disease. However, evidence on the dose-response association between dietary sodium intake and cardiovascular disease risk is unclear. Embase and PubMed were searched from their inception to 17 August 2020 and studies that examined the association between sodium intake and cardiovascular disease in adolescents were not included in this review. We conducted a meta-analysis to estimate the effect of high sodium intake using a random effects model. The Newcastle-Ottawa Scale assessment was performed. A random-effects dose-response model was used to estimate the linear and nonlinear dose-response relationships. Subgroup analyses and meta-regression were conducted to explain the observed heterogeneity. We identified 36 reports, which included a total of 616,905 participants, and 20 of these reports were also used for a dose-response meta-analysis. Compared with individuals with low sodium intake, individuals with high sodium intake had a higher adjusted risk of cardiovascular disease (Rate ratio: 1.19, 95% confidence intervals = 1.08-1.30). Our findings suggest that there is a significant linear relationship between dietary sodium intake and cardiovascular disease risk. The risk of cardiovascular disease increased up to 6% for every 1 g increase in dietary sodium intake. A low-sodium diet should be encouraged and education regarding reduced sodium intake should be provided.
| S-EPMC7601012 | biostudies-literature
Project description:Several B vitamins are essential in the one-carbon metabolism pathway, which is central to DNA methylation, synthesis, and repair. Moreover, an imbalance in this pathway has been linked to certain types of cancers. Here, we performed a meta-analysis in order to investigate the relationship between the intake of four dietary one-carbon metabolism-related B vitamins (B2, B6, folate, and B12) and the risk of esophageal cancer (EC). We searched PubMed, Web of Science, and Embase for relevant studies published through 1 March 2018. The odds ratio (OR) with 95% confidence interval (CI) for the highest versus the lowest level of each dietary B vitamin was then calculated. From 21 articles reporting 26 studies including 6404 EC cases and 504,550 controls, we found an inverse correlation between the consumption of vitamin B6 and folate and the risk of EC; this association was specific to the US, Europe, and Australia, but was not found in Asia. A dose-response analysis revealed that each 100 μg/day increase in folate intake reduced the risk of EC by 12%. Moreover, each 1 mg/day increase in vitamin B6 intake decreased the risk of EC by 16%. Surprisingly, we found that each 1 μg/day increase in vitamin B12 intake increased the risk of esophageal adenocarcinoma by 2%, particularly in the US and Europe, suggesting both geographic and histological differences. Together, our results suggest that an increased intake of one-carbon metabolism-related B vitamins may protect against EC, with the exception of vitamin B12, which should be consumed in moderation.
| S-EPMC6073467 | biostudies-literature
Project description:Since the late 1960s, the average global supply of fat has increased by 20 g per capita per day. While fat intake has been considered a potential risk factor for prostate cancer (Pca), the hypothesis from previous epidemiologic studies remained equivocal.Relevant cohort studies were identified through a literature search in PubMed, ScienceDirect and Wiley Online Library up to March 1, 2015. A systematic review and dose-response meta-analysis were used to assess the relationship between fat intake and the risk for Pca.We identified 14 cohort studies, which included 37,349 cases and a total of 751,030 participants. We found no evidence of a non-linear association between fat intake and the risk for Pca. Overall, the summarized relative risks for every 28.35 g increment a day was 0.99 (95%CI: 0.98, 1.01; P=0.94; n=13) for total fat intake, 1.00 (95%CI: 1.00, 1.00; P=0.72; n=9) for saturated fat, 0.99 (95%CI: 0.95, 1.03; P=0.55; n=7) for polyunsaturated fat, and 1.00 (95%CI: 0.95, 1.04; P=0.85; n=8) for monounsaturated fat. Additionally, there was no link to the risk for advanced stage Pca regarding total fat intake (RR=1.02, 95%CI: 0.96, 1.08; P=0.63; n=5), saturated fat (RR=0.96, 95%CI: 0.84, 1.11; P=0.61; n=6), polyunsaturated fat (RR=0.96, 95%CI: 0.79, 1.17; P=0.68; n=6), or monounsaturated fat (RR=0.96, 95%CI: 0.86, 1.07; P=0.42; n=6). Subgroup and sensitively analyses showed consistent results.Little evidence from published cohort studies supports the statement that total fat, saturated fat or unsaturated fat intake increases the risk for Pca or advanced stage Pca.
| S-EPMC4505895 | biostudies-literature
Project description:ObjectiveTo assess whether dietary fat intake influences Parkinson's disease risk.Data sourcesWe systematically surveyed the Embase and PubMed databases, reviewing manuscripts published prior to October 2018. The following terms were used: ("Paralysis agitans" OR "Parkinson disease" OR "Parkinson" OR "Parkinson's" OR "Parkinson's disease") AND ("fat" OR "dietary fat" OR "dietary fat intake").Data selectionIncluded studies were those with both dietary fat intake and Parkinson's disease risk as exposure factors. The Newcastle-Ottawa Scale was adapted to investigate the quality of included studies. Stata V12.0 software was used for statistical analysis.Outcome measuresThe primary outcomes included the relationship between high total energy intake, high total fat intake, and Parkinson's disease risk. The secondary outcomes included the relationship between different kinds of fatty acids and Parkinson's disease risk.ResultsNine articles met the inclusion criteria and were incorporated into this meta-analysis. Four studies scored 7 and the other five studies scored 9 on the Newcastle-Ottawa Scale, meaning that all studies were of high quality. Meta-analysis results showed that high total energy intake was associated with an increased risk of Parkinson's disease (P = 0.000, odds ratio (OR) = 1.49, 95% confidence interval (CI): 1.26-1.75); in contrast, high total fat intake was not associated with Parkinson's disease risk (P = 0.123, OR = 1.07, 95% CI: 0.91-1.25). Subgroup analysis revealed that polyunsaturated fatty acid intake (P = 0.010, OR = 1.03, 95% CI: 0.88-1.20) reduced the risk of Parkinson's disease, while arachidonic acid (P = 0.026, OR = 1.15, 95% CI: 0.97-1.37) and cholesterol (P = 0.002, OR = 1.09, 95% CI: 0.92-1.29) both increased the risk of Parkinson's disease. Subgroup analysis also demonstrated that, although the results were not significant, consumption of n-3 polyunsaturated fatty acids (P = 0.071, OR = 0.88, 95% CI: 0.73-1.05), ?-linolenic acid (P = 0.06, OR = 0.86, 95% CI: 0.72-1.02), and the n-3 to n-6 ratio (P = 0.458, OR = 0.89, 95% CI: 0.75-1.06) were all linked with a trend toward reduced Parkinson's disease risk. Monounsaturated fatty acid (P = 0.450, OR = 1.06, 95% CI: 0.91-1.23), n-6 polyunsaturated fatty acids (P = 0.100, OR = 1.15, 95% CI: 0.96-1.36) and linoleic acid (P = 0.053, OR = 1.11, 95% CI: 0.94-1.32) intakes were associated with a non-significant trend toward higher PD risk. Saturated fatty acid (P = 0.619, OR = 1.01, 95% CI: 0.87-1.18) intake was not associated with Parkinson's disease.ConclusionDietary fat intake affects Parkinson's disease risk, although this depends on the fatty acid subtype. Higher intake of polyunsaturated fatty acids may reduce the risk of Parkinson's disease, while higher cholesterol and arachidonic acid intakes may elevate Parkinson's disease risk. However, further studies and evidence are needed to validate any link between dietary fat intake and Parkinson's disease.
| S-EPMC6788237 | biostudies-literature
Project description:The association of dietary fat intake with ovarian cancer risk has been inconsistent across populations. We examined dietary fat intake, overall and by type and ovarian cancer risk in two prospective cohort studies. We assessed long-term dietary fat intake among Nurses' Health Study (NHS) and NHSII participants using food frequency questionnaires administered every 2-4 years beginning in 1984 and 1991, respectively. We examined cumulative energy-adjusted intake of total fat, specific types of fat (animal, vegetable, saturated, monounsaturated, polyunsaturated and trans fat) and cholesterol. We identified 700 ovarian cancer cases in NHS and 196 in NHSII with dietary information. Cox proportional hazards regression was used to estimate associations between intake and ovarian cancer risk. Dietary fat intake changed over time in both cohorts and was lower in NHS than NHSII. Higher cumulative average intakes of animal fat and cholesterol were significantly positively associated with risk of ovarian cancer in NHS (relative risk [RR] comparing extreme quartiles = 1.57, 95% CI: 1.20, 2.06 and 1.35, 95% CI: 1.08, 1.69, respectively), but not in NHSII. Other dietary fat sources were not clearly associated with risk in either population. We did not observe clear associations between dietary fat and ovarian cancer risk in two large prospective cohort studies.
| S-EPMC7201382 | biostudies-literature
Project description:Aim: A dose-response meta-analysis was conducted in order to summarize the evidence from prospective cohort studies regarding the association between coffee intake and breast cancer risk. Methods: A systematic search was performed in electronic databases up to March 2017 to identify relevant studies; risk estimates were retrieved from the studies and linear and non-linear dose-response analysis modelled by restricted cubic splines was conducted. A stratified and subgroup analysis by menopausal and estrogen/progesterone receptor (ER/PR) status, smoking status and body mass index (BMI) were performed in order to detect potential confounders. Results: A total of 21 prospective studies were selected either for dose-response, the highest versus lowest category of consumption or subgroup analysis. The dose-response analysis of 13 prospective studies showed no significant association between coffee consumption and breast cancer risk in the non-linear model. However, an inverse relationship has been found when the analysis was restricted to post-menopausal women. Consumption of four cups of coffee per day was associated with a 10% reduction in postmenopausal cancer risk (relative risk, RR 0.90; 95% confidence interval, CI 0.82 to 0.99). Subgroup analyses showed consistent results for all potential confounding factors examined. Conclusions: Findings from this meta-analysis may support the hypothesis that coffee consumption is associated with decreased risk of postmenopausal breast cancer.
| S-EPMC5852688 | biostudies-other