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Dietary Fat Intake and Risk of Gastric Cancer: A Meta-Analysis of Observational Studies.

Han J, Jiang Y, Liu X, Meng Q, Xi Q, Zhuang Q, Han Y, Gao Y, Ding Q, Wu G - PLoS ONE (2015)

Bottom Line: Random effects model was used to calculate the summary relative risk(SRR) in the highest versus lowest analysis.Twenty-two articles were included in the meta-analysis.Our results suggest that intake of total fat is potentially positively associated with gastric cancer risk, and specific subtypes of fats account for different effects.

View Article: PubMed Central - PubMed

Affiliation: The Clinical Nutrition Center of Shanghai, Department of General Surgery, Zhongshan Hospital of Fudan University, Shanghai, China.

ABSTRACT

Background and objectives: Consumption 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.

Methods: A 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.

Results: Twenty-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.

Conclusions: Our 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.

No MeSH data available.


Related in: MedlinePlus

Dose-response relationship for total fat intake level and the RR of gastric cancer risk (P-nonlinearity = 0.50).
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pone.0138580.g004: Dose-response relationship for total fat intake level and the RR of gastric cancer risk (P-nonlinearity = 0.50).

Mentions: Unfortunately, only one cohort article (2studies) and 3case-control articles (4studies) providing the distribution of cases and controls (person-year)were eligible for the dose-response analysis. The results showed that the SRR per 20 g/d total fat increase intake was 1.08 (95%CI: 1.02–1.14), with moderate heterogeneity (P = 0.09; tau2 = 0.002;I2 = 46.8%, 95% CI: 0%-79%).However, the increased risk of total fat increase intake per 20 g/d was only found in 4 case-control studies(SRR = 1.12;95% CI: 1.03–1.22;P = 0.07; I2 = 57.5%)but not in 2 cohort studies (SRR = 1.03;95% CI: 0.97–1.09;P = 0.67; I2 = 0.0%).There was no evident non-linear association between total fat intake and gastric cancer risk(P-nonlinearity = 0.50; Fig 4).


Dietary Fat Intake and Risk of Gastric Cancer: A Meta-Analysis of Observational Studies.

Han J, Jiang Y, Liu X, Meng Q, Xi Q, Zhuang Q, Han Y, Gao Y, Ding Q, Wu G - PLoS ONE (2015)

Dose-response relationship for total fat intake level and the RR of gastric cancer risk (P-nonlinearity = 0.50).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4581710&req=5

pone.0138580.g004: Dose-response relationship for total fat intake level and the RR of gastric cancer risk (P-nonlinearity = 0.50).
Mentions: Unfortunately, only one cohort article (2studies) and 3case-control articles (4studies) providing the distribution of cases and controls (person-year)were eligible for the dose-response analysis. The results showed that the SRR per 20 g/d total fat increase intake was 1.08 (95%CI: 1.02–1.14), with moderate heterogeneity (P = 0.09; tau2 = 0.002;I2 = 46.8%, 95% CI: 0%-79%).However, the increased risk of total fat increase intake per 20 g/d was only found in 4 case-control studies(SRR = 1.12;95% CI: 1.03–1.22;P = 0.07; I2 = 57.5%)but not in 2 cohort studies (SRR = 1.03;95% CI: 0.97–1.09;P = 0.67; I2 = 0.0%).There was no evident non-linear association between total fat intake and gastric cancer risk(P-nonlinearity = 0.50; Fig 4).

Bottom Line: Random effects model was used to calculate the summary relative risk(SRR) in the highest versus lowest analysis.Twenty-two articles were included in the meta-analysis.Our results suggest that intake of total fat is potentially positively associated with gastric cancer risk, and specific subtypes of fats account for different effects.

View Article: PubMed Central - PubMed

Affiliation: The Clinical Nutrition Center of Shanghai, Department of General Surgery, Zhongshan Hospital of Fudan University, Shanghai, China.

ABSTRACT

Background and objectives: Consumption 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.

Methods: A 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.

Results: Twenty-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.

Conclusions: Our 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.

No MeSH data available.


Related in: MedlinePlus