Nutrition and health

Objectives:
Even though many studies have examined the possible effect of low-fat diet on breast cancer survival, the relationship remains unclear. Therefore, this review article has been conducted.

Does low-fat diet reduce risk of recurrence of breast cancer?

Study design:
This review article included 2 randomized controlled trials (RCTs) and 1 large multi-center prospective cohort study with 9,966 breast cancer patients.

Results and conclusions:
The investigators found post-diagnostic low-fat diet significantly reduced risk of recurrence of breast cancer by 23% [HR = 0.77, 95% CI = 0.63 to 0.94, p = 0.009] and all cause mortality of breast cancer by 17% [HR = 0.83, 95% CI = 0.69 to 1.00, p = 0.05].

The investigators concluded post-diagnostic low-fat diet reduces risk of recurrence of breast cancer. However, more trials of the relationship between low-fat diet and all-cause mortality of breast cancer are still needed.

Original title:
Effect of low-fat diet on breast cancer survival: a meta-analysis by Xing MY, Xu SZ and Shen P.

Link:
https://pubmed.ncbi.nlm.nih.gov/24606431/

Additional information of El Mondo:
Find more information/studies on fat consumption and breast cancer right here.

A low-fat diet is a diet with maximum 30 En% fat and maximum 7 En% saturated fat.  
30 En% fat means that the amounts of fat contribute 30% to the total calories (kcal) of the diet.
If the diet contains 2000 kcal, 66.7 grams of fat contribute 30% to this 2000 kcal.
1 gram of fat gives 9 kcal. Thus, 66.7 grams of fat provide 600 kcal and 600 kcal is 30% of 2000 kcal.

The most easy way to follow a diet a diet with maximum 30 En% fat and maximum 7 En% saturated fat is to choose only meals/products with maximum 30 En% fat and maximum 7 En% saturated fat. Check here which products contain maximum 30 En% fat and maximum 7 En% saturated fat.

However, the most practical way to follow a diet with maximum 30 En% fat and maximum 7 En% saturated fat is, all meals/products that you eat on a daily basis should contain on average maximum 30 En% fat and maximum 7 En% saturated fat.

To do this, use the 7-points nutritional profile app to see whether your daily diet contains maximum 30 En% fat and maximum 7 En% saturated fat.

Objectives:
Epidemiological studies regarding the association between dietary fiber intake and ovarian cancer risk are still inconsistent. Therefore, this review article has been conducted.

Does dietary fiber intake reduce ovarian cancer risk?

Study design:
This review article included 10 case-control studies and 3 cohort studies, with a total of 5,777 ovarian cancer cases and 142,189 participants.

All the included studies provided RRs that were adjusted for energy intake and most provided RRs that were adjusted for age, oral contraceptive use, menopausal status and parity.
All the original studies measured dietary intakes using a food-frequency questionnaire. NOS scores ranged from 6 to 8 and 7 studies were considered high quality.

Funnel plot shapes demonstrated a symmetrical distribution and no evidence of publication bias was detected by the Egger’s regression test [p = 0.73].

Results and conclusions:
The investigators found for the highest vs. the lowest category of dietary fiber intake a significantly reduced risk of 22% [pooled multivariable RR = 0.78, 95% CI = 0.70 to 0.88, I2 = 4.20%, p = 0.40] for ovarian cancer.

The investigators found a significantly reduced risk of 12% [summarized RR = 0.88, 95% CI = 0.82 to 0.93, I2 = 7.3%, p = 0.38] for ovarian cancer per 10 g/day increase of dietary fiber intake.

The investigators found there was no evidence for a nonlinear association between dietary fiber intake and ovarian cancer risk [p for nonlinearity = 0.83].

The investigators found in subgroup analysis a significantly reduced risk of 23% [pooled RR = 0.77, 95% CI = 0.66 to 0.90] for ovarian cancer in case-control studies. However, the reduced risk was not significant in cohort studies [pooled RR = 0.84, 95% CI = 0.65 to 1.10].

The investigators found sensitivity analysis showed that none of the studies influenced the combined results substantially, with a range from 0.77 [95% CI = 0.68 to 0.87] to 0.81 [95% CI = 0.71 to 0.91].

The investigators concluded that 10g dietary fiber intake per day may reduce the risk of ovarian cancer with 12%. May reduce because the reduced risk was not significant in cohort studies.

Original title:
Dietary fiber intake and reduced risk of ovarian cancer: a meta-analysis by Zheng B, Shen H, […], Qin Y.

Link:
https://nutritionj.biomedcentral.com/articles/10.1186/s12937-018-0407-1

Additional information of El Mondo:
Find more information/studies on meta-analysis/cohort studies, fiber intake and cancer right here.

Objectives:
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. Therefore, this review article has been conducted.

Is there a relationship between dietary vitamin intake and risk of esophageal cancer (EC)?

Study design:
This review article included 24 patient-control studies and 2 cohort studies with a total of 510,954 participants and 6,404 esophageal cancer cases, which included 1,919 esophageal adenocarcinoma (EAC) patients, 2,010 esophageal squamous cell carcinoma (ESCC) patients and 2,475 esophageal cancer (EC) patients.

The quality scores of all studies ranged from 6 to 8, with a median score of 7.

There was no significant publication bias in the final analysis with respect to vitamin B2 [p = 0.244], vitamin B6 [p = 0.068], folate [p = 0.054] or vitamin B12 [p = 0.093].

A sensitivity analysis revealed that no individual study affected the pooled effect size.

Results and conclusions:
The investigators found for the highest level versus the lowest level of dietary folate intake, a significantly reduced risk of 38% [pooled OR = 0.62, 95% CI = 0.56-0.68, I2 = 40.2%] for esophageal cancer.
Subgroup analysis revealed that this inverse correlation (reduced risk) was present in the US [OR = 0.58, 95% CI = 0.51-0.67], Europe [OR = 0.51, 95% CI = 0.40-0.65] and Australia [OR = 0.74, 95% CI = 0.58-0.95], but not in Asia [OR = 0.77, 95% CI = 0.59-1.01].

The investigators found in dose-response analysis that each 100 μg/day increase in dietary folate intake significantly reduced the risk of esophageal cancer by 12% [OR = 0.88, 95% CI = 0.86-0.91].
Significant means that there is an association with a 95% confidence.

The investigators found for the highest level versus the lowest level of dietary vitamin B6 intake, a significantly reduced risk of 41% [pooled OR = 0.59, 95% CI = 0.52-0.66, I2 = 46.8%] for esophageal cancer.
This inverse relationship remained significant in subgroup analyses for esophageal adenocarcinoma [OR = 0.58, 95% CI = 0.49-0.68] and esophageal squamous cell carcinoma [OR = 0.47, 95% CI = 0.33-0.67].

The investigators found in dose-response analysis, a significantly reduced risk of 18% [OR = 0.82, 95% CI = 0.76-0.88] for esophageal cancer for 2.0 mg/day of dietary vitamin B6 intake.

The investigators found in dose-response analysis, a significantly reduced risk of 33% [OR = 0.67, 95% CI = 0.59-0.75] for esophageal cancer for 2.5 mg/day of dietary vitamin B6 intake.

The investigators found in dose-response analysis, a significantly reduced risk of 45% [OR = 0.55, 95% CI = 0.44-0.67] for esophageal cancer for 3.0 mg/day of dietary vitamin B6 intake.

The investigators found in dose-response analysis that each 1 mg/day increase in dietary B6 increase significantly reduced the risk of esophageal cancer by 16% [OR = 0.84, 95% CI = 0.80-0.89].

The investigators found for the highest level versus the lowest level of dietary vitamin B12 intake, a significantly increased risk of 30% [pooled OR = 1.30, 95% CI = 1.05-1.62, I2 = 73.5%] for esophageal cancer.
A subgroup analysis based on geographic location revealed similar results in the US [OR = 1.26, 95% CI = 1.03-1.53] and Europe [OR = 2.54, 95% CI = 1.16-5.53], but not in Australia [OR = 0.93, 95% CI = 0.73-1.19].
A subgroup analysis based on histological type revealed that this correlation was present among patients with esophageal adenocarcinoma [OR = 1.47, 95% CI = 1.02-2.11], but not among patients with esophageal squamous cell carcinoma [OR = 1.00, 95% CI = 0.63-1.61].

The investigators found in dose-response analysis that each 1 μg/day increase in dietary B12 intake significantly increased the risk of esophageal cancer by 2% [OR = 1.02, 95% CI = 1.00-1.03].

The investigators concluded that both dietary vitamin B6 intake (at least 1 mg/day) and dietary folate intake (at least 100 μg/day) are inversely correlated with esophageal cancer risk, whereas dietary vitamin B12 intake (at least 1 μg/day) increases esophageal cancer risk.

Original title:
Intake of Dietary One-Carbon Metabolism-Related B Vitamins and the Risk of Esophageal Cancer: A Dose-Response Meta-Analysis by Qiang Y, Li Q, […], Wang F.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6073467/

Additional information of El Mondo:
Find more information/studies on folate, vitamin B6 and B12 and cancer right here.

Objectives:
Many studies were conducted to explore the relationship between dietary protein intake and risk of prostate cancer, obtaining inconsistent results. Therefore, this review article has been conducted.

Does dietary protein intake increase risk of prostate cancer?

Study design:
This review article included a total of 8 cohort studies, 5 case-control studies and 1 RCT, comprising 13,483 prostate cancer cases among 286,245 participants.

Begg’s funnel plots and Egger’s test [p = 0.296] indicated that no publication bias was found in overall analysis.

Results and conclusions:
The investigators found in the overall analysis there was no association with prostate cancer risk when comparing the highest protein intake with the lowest protein intake [summary RR = 0.993, 95% CI = 0.930-1.061, I2 = 0.0%, p = 0.656].
The sensitivity analysis showed that there is no single study that had potential effects on the overall result while removing a study at a time.

The investigators found in the stratified analysis by protein type, the association was non-significant on prostate cancer risk in both animal protein intake [RR = 1.001, 95% CI = 0.917-1.092] and vegetable protein intake [RR = 0.986, 95% CI = 0.904-1.076].
Non-significant because RR of 1 was found in the 95% CI of 0.917 to 1.092. RR of 1 means no risk/association.

The investigators found there was also no significant association in cohort studies [RR = 1.080, 95% CI = 0.964-1.209] and in case-control studies [RR = 0.960, 95% CI = 0.874-1.055].

The investigators found there was no association with prostate cancer localized-stage disease risk when comparing the highest protein intake with the lowest protein intake [summary RR = 1.263, 95% CI = 0.953-1.674].

The investigators found there was no association with prostate cancer advanced-stage disease risk when comparing the highest protein intake with the lowest protein intake [summary RR = 0.973, 95% CI = 0.745-1.272].

The investigators concluded that there is no effect on prostate cancer with high-protein intake. Since some limitations exited in this review article, future studies are wanted to confirm the result.

Original title:
Association between dietary protein intake and prostate cancer risk: evidence from a meta-analysis by Ye M, Yan T and Jing D.

Link:
https://wjso.biomedcentral.com/articles/10.1186/s12957-018-1452-0

Additional information of El Mondo:
Find more information/studies on protein and cancer right here.

Objectives:
There has been accumulating evidence that several micronutrients may play a protective role in the risk of solid cancers. However, their role in hematological malignancies remains to be elucidated. Therefore, this review article has been conducted.

Is there a relationship between vitamin intake and risk of non-Hodgkin lymphoma?

Study design:
This review article included a total of 12 cohort studies.

Results and conclusions:
The investigators found null associations regarding
-supplemented vitamin A [pooled RR = 0.92, 95% CI = 0.80-1.07];
-supplemented vitamin C [pooled RR = 1.00, 95% CI = 0.90-1.12];
-total vitamin D [pooled RR = 1.05, 95% CI = 0.91-1.20];
-supplemented vitamin E [pooled RR = 0.98, 95% CI = 0.88-1.10] and;
-dietary lycopene intake [pooled RR = 1.00, 95% CI = 0.86-1.16] and risk of non-Hodgkin lymphoma.

The investigators found no summary estimates were provided for other hematological malignancies due to the limited number of studies.

The investigators concluded there is no association between vitamin A, C, D, E and lycopene and risk of non-Hodgkin lymphoma.

Original title:
Micronutrient Intake and Risk of Hematological Malignancies in Adults: A Systematic Review and Meta-analysis of Cohort Studies by Psaltopoulou T, Ntanasis-Stathopoulos I, […], Sergentanis TN.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/30288994

Additional information of El Mondo:
Find more information/studies on vitamin A, C, D, E and lycopene right here.

Objectives:
There were inconsistent results with respect to the correlation between consumption of wine and the development of colorectal cancer (CRC). Therefore, this review article has been conducted.

Does consumption of wine increase colorectal cancer risk?

Study design:
This review article included a total of 8 case-control studies and 9 cohort studies, involving 12,110 colorectal cancer cases.

Results and conclusions:
The investigators found that wine drinking was not associated with any greater risk for colorectal cancer [SRR = 0.99, 95% CI = 0.89-1.10, p-heterogeneity 0.001] compared with nondrinkers.

The investigators found subgroup analyses (to get more information) indicated that null associations were observed in men and women for colon and rectal cancer.

The investigators found subgroup analyses showed neither light to moderate [2 drinks/day: SRR = 0.93, 95% CI = 0.80-1.08, I2 = 69.2%] nor heavy [≥2 drinks/day: SRR = 1.00, 95% CI = 0.86-1.16, I2 = 39.9%] consumption of wine was associated statistically with colorectal cancer risk.

The investigators concluded that wine consumption is not associated with the risk of colorectal cancer. Furthermore, null associations are found in men and women for colon and rectal cancer.

Original title:
Wine consumption and colorectal cancer risk: a meta-analysis of observational studies by Xu W, Fan H, [...], Ge Z.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/30247171

Additional information of El Mondo:
Find more information/studies on review article/significant/heterogeneity, colorectal cancer and wine consumption right here.

Objectives:
Does dietary carrot intake reduce breast cancer risk?

Study design:
This review article included a total of 10 articles involving 13,747 cases (women with breast cancer).

A significant heterogeneity was observed among studies.

Results and conclusions:
The investigators found for the highest compared with the lowest dietary carrot intake a significantly reduced risk of 21% for breast cancer [OR = 0.79, 95% CI = 0.68 to 0.90]. Omission of any single study (=sensitivity analysis) had little effect on the combined risk estimate.

The investigators found in the subgroup analyses separated by study design, the inverse associations were more pronounced in the case-control studies than in the cohort studies, while the associations did not significantly differ by geographical region, study quality, exposure assessment.

The investigators concluded that high intake of dietary carrot reduces breast cancer risk.

Original title:
Association between dietary carrot intake and breast cancer: A meta-analysis by Chen H, Shao F, […], Miao Q.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/30212943

Additional information of El Mondo:
Find more information/studies on review article/significant/heterogeneity, breast cancer and carrot consumption right here.

Objectives:
Do dietary flavonoid intake reduce colorectal cancer risk?

Study design:
This review article included 5 prospective cohort and 7 case-control studies with a tolal of 17,481 cases (persons with colorectal cancer) and 740,859 controls (persons without colorectal cancer).

All studies were adjusted for a wide range of potential confounders of colorectal cancer, such as age, gender, BMI, physical activity, family history of colorectal cancer, education, energy intake, alcohol, fiber intake, red and processed meat intake, tobacco, aspirin and non-steroidal anti-inflammatory drug.

There was no publication bias.

Results and conclusions:
The investigators found that there was no significant association between colorectal cancer risk and total flavonoid intake, with a pooled OR from the combination of the included studies of 0.73 [95% CI = 0.48-1.10] for the highest category of intake vs. the lowest category. Similarly, no association between the intake of flavanones or flavan-3-ols and the risk of colorectal cancer was observed.

The investigators found in subgroup analysis of both cohort and case-control studies that when compared with the lowest, the highest intake of dietary flavonols significanty reduced risk of colorectal cancer with 30% [OR = 0.70, 95% CI = 0.54-0.90]. Nevertheless, substantial heterogeneities existed across the studies.
However, this reduced risk was not significant in cohort studies [pooled RR = 1.00, 95% CI = 0.92-1.08].

The investigators found in subgroup analysis of both cohort and case-control studies that when compared with the lowest, the highest intake of dietary flavones significanty reduced risk of colorectal cancer with 21% [OR = 0.79, 95% CI = 0.83-0.99]. Nevertheless, substantial heterogeneities existed across the studies.
However, this reduced risk was not significant in cohort studies [pooled RR = 1.02, 95% CI = 0.94-1.11].

The investigators found in subgroup analysis of both cohort and case-control studies that when compared with the lowest, the highest intake of dietary anthocyanidins significanty reduced risk of colorectal cancer with 22% [OR = 0.78, 95% CI = 0.64-0.95]. Nevertheless, substantial heterogeneities existed across the studies. 
However, this reduced risk was not significant in cohort studies [pooled RR = 1.00, 95% CI = 0.91-1.10].

The investigators found dose-response meta-analysis indicated that an increment of dietary flavones intake of 1 mg per day significantly reduced risk of colorectal cancer with 9% [pooled OR = 0.91, 95% CI = 0.84-0.99].

The investigators found dose-response meta-analysis indicated that an increment of dietary flavonols intake of 10 mg per day significantly reduced risk of colorectal cancer with 14% [pooled OR = 0.86, 95% CI = 0.76-0.97].

The investigators found that high intake of flavonols significantly decreased risk of colon cancer with 20% [OR = 0.80, 95% CI = 0.68-0.94].
Significantly means that there is an association with a 95% confidence.

The investigators found that high intake of flavones significantly decreased risk of rectal cancer with 18% [OR = 0.82, 95% CI = 0.70-0.97].
Significantly because OR of 1 was not found in the 95% CI of 0.70 to 0.97. OR of 1 means no risk/association.

The investigators concluded that high intake of dietary flavonols, flavones and anthocyanidins may decrease the risk of colorectal cancer. May decrease because substantial heterogeneities existed across the studies and the reduced risk was not significant in cohort studies.

Original title:
Dietary Flavonoids and the Risk of Colorectal Cancer: An Updated Meta-Analysis of Epidemiological Studies by Chang H, Lin Lei L, […], Guohua Zhao G.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6073812/

Additional information of El Mondo:
Find more information/studies on review article/significant/publication bias, colorectal cancer and flavonoids right here.

The results of a review article are only reliable when they are also found in cohort studies. Thus, the significantly reduced risk must be found in both patient-control studies (more sensitive to errors) and cohort studies (less susceptible to errors).

Objectives:
Controversial results have been reported concerning the influence of calcium intake on prostate cancer risk. Therefore, this review article has been conducted.

Does calcium intake increase prostate cancer risk?

Study design:
This review article included 11 cohort studies and 1 case control study.

The average age of majority was between 50-70 years and also about 83%of articles had been performed in the USA.

Begg’s test showed the effect of publication bias was significant for relationship between calcium intake and total prostate cancer [p = 0.02] and the relationship between total calcium and localized prostate cancer [p = 0.03].

Results and conclusions:
The investigators found that total calcium intake significantly increased the total prostate cancer risk with 15% [overall RR = 1.15, 95% CI = 1.04-1.27, I2 = 59.7%, p = 0.006].
Sensitivity analysis by removing one study at the same time indicated that the overall RR was robust.

The investigators found in studies with follow-up more than 10 years a significantly increased risk of 22% [RR = 1.22, 95% CI = 1.07-1.38] for total prostate for total calcium intake.

The investigators found in 9 studies a significantly increased risk of 9% [RR = 1.09, 95% CI = 1.01-1.18] for total prostate cancer for 750 mg calcium intake per day.

The investigators found in 8 cohort studies, no association between total calcium intake and localized prostate cancer [RR = 1.05, 95% CI = 0.96-1.14].

The investigators found in 7 cohort studies, no association between total calcium intake and advance prostate cancer [RR = 1.15, 95% CI = 0.89-1.50].

The investigators concluded that calcium intake of 750 mg per day could be considered as a risk factor for total prostate cancer. Could be because there was publication bias.

Original title:
Total Calcium (Dietary and Supplementary) Intake and Prostate Cancer: a Systematic Review and Meta-Analysis by Rahmati S, Azami M, […], Sayehmiri K.

Link:
http://journal.waocp.org/?sid=Entrez:PubMed&id=pmid:29936714&key=2018.19.6.1449

Additional information of El Mondo:
Find more information/studies on cancer and calcium right here.

Objectives:
Prostate cancer (PCa) is one of the leading cause cancer among men worldwide. Many epidemiologic studies have reported an association between carbohydrate intake and prostate cancer. However, the evidence from epidemiologic studies is inconsistent. Therefore, this review article has been conducted.

Does carbodydrate intake increase prostate cancer risk?

Study design:
This review article included 21 studies published from 1980 to 2018, including 98,739 participants and 11,573 cases (persons with prostate cancer).

Multivariate-adjusted odds ratios (ORs) were pooled using random-effect models.

Results and conclusions:
The investigators found no association between higher carbohydrate intake and prostate cancer risk [OR =1.11, 95% CI = 0.98-1.26, I2 = 62.7%].
No association because OR of 1 was found in the 95% CI of 0.98 to 1.26. RR of 1 means no risk/association.

The investigators found no association between higher carbohydrate intake and advanced prostate cancer risk [OR = 0.95, 95% CI = 0.78-1.16, I2 = 14.1%].

The investigators found no association between higher carbohydrate intake and non-advanced prostate cancer risk [OR = 1.01, 95% CI = 0.79-1.29, I2 = 64.4%].

The investigators found there was not a significant dose-response association observed for carbohydrate intake with prostate cancer risk and advanced prostate cancer risk.

The investigators concluded that there is no association between carbohydrate intake and prostate cancer risk. Nor is association detected about carbohydrate intake with advanced or non-advanced prostate cancer risk. More studies are needed for a further dose-response meta-analysis.

Original title:
Carbohydrate intake and the risk of prostate cancer by Fan LL, Su HX, […], Nan CJ.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/29778541

Additional information of El Mondo:
Find more information/studies on cancer and carbohydrate right here.

Objectives:
Several epidemiological studies have assessed the ability of vitamin B2 to prevent colorectal cancer (CRC), but the results are controversial. Therefore, this review article has been conducted.

Does vitamin B2 intake reduce colorectal cancer risk?

Study design:
This review article included a total of 14 studies reporting vitamin B2 intake and 2 studies reporting blood vitamin B2 concentration, comprising 14,934 cases (persons with colorectal cancer) and 1,593 cases (persons with colorectal cancer), respectively.

Results and conclusions:
The investigators found in pooled analysis a significantly reduced risk of 13% [RR = 0.87, 95% CI = 0.81-0.93] for colorectal cancer for vitamin B2 intake.
Significant means that there is an association with a 95% confidence.

The investigators found in subgroup analysis a significantly reduced risk of 14% [RR = 0.86, 95% CI = 0.78-0.94] for colorectal cancer for vitamin B2 intake from diet and supplements.

The investigators found in subgroup analysis a significantly reduced risk of 11% [RR = 0.89, 95% CI = 0.82-0.98] for colorectal cancer for dietary vitamin B2 intake.

The investigators found the dose-response model indicated a non-linear trend and colorectal cancer risk was reduced by 10% when vitamin B2 intake increased to 5 mg/day.

The investigators found that high blood concentrations of vitamin B2 significantly reduced the colorectal cancer risk with 26% [RR = 0.74, 95% CI = 0.59-0.92].

The investigators concluded that both higher vitamin B2 intake (5 mg per dag) and higher blood vitamin B2 concentration reduce colorectal cancer risk. These results suggest the importance of vitamin B2 intake in the prevention of colorectal cancer.

Original title:
Vitamin B2 intake reduces the risk for colorectal cancer: a dose-response analysis by Ben S, Du M, [...], Wang M.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/29744609

Additional information of El Mondo:
Find more information/studies on vitamin B2 and colorectal cancer right here.

Objectives:
Is there an association between wine consumption and prostate cancer risk?

Study design:
This review article included 6 cohort and 8 case-control studies with a total of 455,413 subjects regarding moderate wine consumption and risk of prostate cancer.

There was no evidence of publication bias.

Results and conclusions:
The investigators found in pooled analysis of cohort studies (438,302 subjects from which 19,238 developed prostate cancer during observation/follow-up) no association between moderate wine consumption and prostate cancer risk [pooled RR = 1.06, 95% CI = 0.96-1.15, p = 0.22, I2 = 0%]. 

The investigators found in multivariable analysis that moderate red wine consumption was associated with a significantly decreased risk of 12% for prostate cancer [pooled RR = 0.88, 95% CI = 0.78-0.999, p = 0.047, I2 = 0%]. 

The investigators found in multivariable analysis that moderate white wine consumption increased significantly the risk of prostate cancer with 26% [pooled RR = 1.26, 95% CI = 1.10-1.43, p = 0.001, I2 = 34.4%].

The investigators concluded that moderate consumption of white wine increases the risk of prostate cancer, whereas moderate consumption of red wine has a protective role. This hypothesis-generating data should serve as a rationale for uncovering the molecular underpinnings of this differential effect in order to potentially devise prevention strategies in the at-risk population.

Original title:
The impact of moderate wine consumption on the risk of developing prostate cancer by Vartolomei MD, Kimura S, […], Shariat SF.
 
Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5909789/

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Objectives:
Esophageal cancer (EC) is the eighth most common cancer and the sixth most frequent cause of cancer death in the whole world. Many studies have investigated the association between citrus fruit intake and the risk of esophageal cancer, but the results are inconsistent and not analyzed by category. Therefore, this review article has been conducted.

Does citrus fruit intake reduce esophageal cancer risk?

Study design:
This review article included 20 case-control studies and 5 cohort studies.
The studies were published between 1983 and 2015 with a total of 2,456 esophageal squamous cell carcinoma (ESCC) (range 47-395), 1,284 esophageal adenocarcinoma (EAC) (range 67-282) and 1,990 esophageal cancer (EC) (range 53-1,246).

The Newcastle-Ottawa Quality Assessment Scale (NOS) scores of 25 clinical trials range from 5 to 9, with an average of approximately 7. The median score was 6.75 for case-control studies and 8 for cohort studies.

There was no evidence of publication bias. 

Results and conclusions:
The investigators found in 10 case-control studies and 3 cohort studies a significantly reduced risk of 41% [pooled RR = 0.59, 95% CI = 0.47-0.76, I2 = 60.7%, p  = 0 .002] for esophageal squamous cell carcinoma in the citrus fruit consumption group.
Significant because RR of 1 was not found in the 95% CI of 0.47 to 0.76. RR of 1 means no risk/association.

The investigators found in 5 case-control studies and 3 cohort studies a non-significantly reduced risk of 14% [pooled RR = 0.86, 95% CI = 0.74-1.01, I2 = 0.0%, p = 0.598] for esophageal adenocarcinoma in the citrus fruit consumption group.
Non-significantly because RR of 1 was found in the 95% CI of 0.74 to 1.01. RR of 1 means no risk/association.

The investigators found in 20 case-control studies and 5 cohort studies a significantly reduced risk of 35% [pooled RR = 0.65, 95% CI = 0.56-0.75, I2 = 51.1%, p = 0.001] for esophageal cancer in the citrus fruit consumption group.

The investigators found in subgroup analysis significant inverse associations between citrus fruit intake and the risk of esophageal squamous cell carcinoma in cohort studies [OR  =  0.66, 95% CI = 0.49-0.88] and hospital-based cohort studies [OR  =  0.82, 95% CI = 0.33-0.75], but not in population-based cohort studies [OR  =  0.82, 95% CI = 0.62-1.09].

The investigators found in subgroup analysis significant inverse associations between citrus fruit intake and the risk of esophageal squamous cell carcinoma in >7 scores studies [OR =  0.56, 95% CI = 0.43-0.72].

The investigators concluded that citrus fruit intake reduces risk of esophageal cancer, particularly esophageal squamous cell carcinoma. However, further studies are warranted to find which constituents in citrus fruit prevent esophageal cancer and its mechanism.

Original title:
Intakes of citrus fruit and risk of esophageal cancer: A meta-analysis by Zhao W, Liu L and Xu S.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5895383/

Additional information of El Mondo:
Find more information/studies on fruit consumption and cancer right here.

Objectives:
The relationship between vitamin intake and pancreatic cancer (PC) risk is disputed. Therefore, this review article has been conducted.

Is there a relationship between dietary vitamin intake and pancreatic cancer risk?

Study design:
This review article included 25 observational studies with a total of 1,214,995 individuals, of which 8,000 pancreatic cancer cases.

In the identified studies, 10 were population-based case-control studies, 4 were hospital-based case-control studies, 2 were RCTs, 9 were cohort studies, 11 were prospective studies and 14 were retrospective studies.
The number of participants ranged from 305 to 537,218 and pancreatic cancer cases ranged from 79 to 2,383.
Quality scores of included case-control and cohort studies ranged from 7 to 9 with an average score of about 8.

Results and conclusions:
The investigators found in prospective cohort studies a significantly reduced risk of 10% [multivariable-adjusted RR = 0.90, 95% CI = 0.83-0.98, I2 = 11%] for pancreatic cancer when comparing the highest dietary vitamin intake with the lowest, particularly for 10 μg/d dietary intake of vitamin D [multivariable-adjusted RR = 0.75, 95% BI = 0.60-0.93, I2  =  59%].

The investigators concluded that a high dietary vitamin intake decreases the risk of pancreatic cancer, particularly for 10 μg/d dietary intake of vitamin D.

Original title:
Vitamin intake and pancreatic cancer risk reduction: A meta-analysis of observational studies by Liu Y, Wang X, [...], Liu S.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5895396/

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A review article (a collection of scientific studies on a specific topic) of cohort studies or case-control studies will answer the following question:
"Should I change my diet?".

Objectives:
Breast cancer is the most common cancer in women worldwide. The association between body mass index (BMI) and breast cancer risk has been paid more attention in the past few years, but the findings are still controversial. Therefore, this review article has been conducted.

Is there a relationship between BMI and breast cancer risk among women?

Study design:
This review article included 12 prospective cohort studies comprising 22,728,674 women.

All studies were published from 2004 to 2014, with the mean duration of follow-up varying from 4.29 to 10.8 years.
The sample size of included studies ranged from 15,054 to 1,222,630 women.
The Newcastle-Ottawa scale was applied to assess the quality of the included studies and the results showed all studies were of high quality, with a Newcastle-Ottawa scale score of ≥7.
There was no evidence of publication bias with Egger’s test [p = 0.74] and the funnel plot showed no sign of asymmetry by visual inspection.

Results and conclusions:
The investigators found overall results showed a weak positive association between a 5-unit increase in BMI and breast cancer risk, indicating that a 5 kg/m2 increase in BMI corresponded to a 2% increase in breast cancer risk [SRR = 1.02, 95% CI = 1.01-1.04, p 0.001, I2 = 74.2%, p = 0.00]. The results were statistically robust in sensitivity analyses.

The investigators found in subgroup analysis that higher BMI significantly reduced breast cancer risk with 2% among premenopausal women [SRR = 0.98, 95% CI = 0.96-0.99, p 0.001].

The investigators found there was evidence of a linear association between BMI and breast cancer risk in both premenopausal and postmenopausal women [p nonlinearity = 0.892 and p nonlinearity = 0.630, respectively].

The investigators concluded that every 5 kg/m² increase in BMI corresponds to a 2% increase in breast cancer risk in women. However, higher BMI is a protective factor of breast cancer risk for premenopausal women. Further studies are necessary to verify these findings and elucidate the pathogenic mechanisms.

Original title:
Association between body mass index and breast cancer risk: evidence based on a dose-response meta-analysis by Liu K, Zhang W, [...], Dai Z.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5783020/

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Objectives:
Multiple epidemiologic studies have evaluated the relationship between dietary cholesterol and lung cancer risk, but the association is controversial and inconclusive. Therefore, this review article has been conducted.

Does consumption of dietary cholesterol increase risk of lung cancer?

Study design:
This review article included 10 case-control studies (6,894 lung cancer cases and 29,736 controls/persons with no lung cancer) and 6 cohort studies (1,769 lung cancer cases among 241,920 participants).

The Newcastle-Ottawa Scale scores for the included studies ranged from 6 to 9 and all studies were deemed to be of high quality (≥6).

There was no evidence of publication bias observed. Case-control studies: Egger’s test, p = 0.737, Begg’s test, p = 0.213 and cohort studies: Egger’s test, p = 0.459, Begg’s test, p = 1.000.

Results and conclusions:
The investigators found in case-control studies that a high dietary cholesterol intake significantly increased lung cancer risk with 70% [OR = 1.70, 95% CI = 1.43-2.03, I2 = 42.3%, p = 0.067]. No significant change in the result was found in the sensitivity analysis.

The investigators found in cohort studies no association between a high dietary cholesterol intake and lung cancer risk [RR = 1.08, 95% CI = 0.94-1.25, I2 = 0.0%, p = 0.833]. No significant change in the result was found in the sensitivity analysis.

The investigators found in 6 case-control studies that a high dietary total fat intake significantly increased lung cancer risk with 64% [OR = 1.64, 95% BI = 1.16-2.33, I2 = 68.7%, p = 0.004]. No significant change in the result was found in the sensitivity analysis.

The investigators concluded that a high dietary cholesterol intake might increase lung cancer risk. Might increase because the increased risk was not significant in cohort studies. Therefore, carefully designed and well-conducted cohort studies are needed to identify the association between dietary cholesterol and lung cancer risk.

Original title:
Dietary Cholesterol Intake and Risk of Lung Cancer: A Meta-Analysis by Lin X, Liu L, […], Lian X.

Link:
http://www.mdpi.com/2072-6643/10/2/185/htm

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A high dietary cholesterol intake is an intake of more than 200-300 mg cholesterol per day.

The result of a review article is only reliable when the result is also significant in cohort studies (thus not only significant in case-control studies).
 

Objectives:
Does the consumption of various types of tomato products reduce prostate cancer risk and is there a potential dose-response relationship?

Study design:
This review article included 30 studies, which summarized data from 24,222 cases (subjects with prostate cancer) among 260,461 participants.

Results and conclusions:
The investigators found that higher total tomato consumption was associated with a reduced risk of 19% for prostate cancer [RR = 0.81, 95% CI = 0.71 to 0.92, p = 0.001].

The investigators found in subgroup analysis that higher tomato foods consumption was associated with a reduced risk of 16% for prostate cancer [RR = 0.84, 95% CI = 0.72 to 0.98, p = 0.030].

The investigators found in subgroup analysis that higher cooked tomatoes and sauces consumption was associated with a reduced risk of 16% for prostate cancer [RR = 0.84, 95% CI = 0.73 to 0.98, p = 0.029]. 

The investigators found in subgroup analysis, however, no association between higher raw tomatoes consumption and prostate cancer risk [RR = 0.96, 95% CI = 0.84 to 1.09, p = 0.487].

The investigators found there was a significant dose-response association for total tomato consumption [p = 0.040], cooked tomatoes and sauces [p  0.001] and raw tomatoes [p = 0.037], but there was not a significant association with tomato foods [p-linear = 0.511, p-nonlinear = 0.289].

The investigators concluded that increased tomato consumption, particularly cooked tomatoes and sauces reduces prostate cancer risk. Furthermore, there are dose-response relationships for total tomato consumption and for cooked tomatoes and sauces. Further studies are required to determine the underlying mechanisms of these associations.

Original title:
Processed and raw tomato consumption and risk of prostate cancer: a systematic review and dose-response meta-analysis by Rowles JL, Ranard KM, […], Erdman JW Jr.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/29317772

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Objectives:
Evidence shows cruciferous vegetables exhibit chemoprotective properties, commonly attributed to their rich source of isothiocyanates. However, epidemiological data examining the association between cruciferous vegetable intake and colorectal neoplasms have been inconclusive. Therefore, this review article (meta-analysis) has been conducted.

Does cruciferous vegetable intake decrease colon cancer risk?

Study design:
This review article included 33 articles.
Subgroup analysis for individual cruciferae types (n = 8 studies) and GST polymorphism (n = 8 studies) were performed. Pooled adjusted odds ratios (ORs) comparing highest and lowest categories of dietary pattern scores were calculated.

Results and conclusions:
The investigators found when comparing highest with lowest categorie, cruciferous vegetable intake significantly reduced risk of colon cancer with 16% [OR = 0.84, 95% CI = 0.72-0.98, p value heterogeneity 0.001].

The investigators found when comparing highest with lowest categorie, broccoli intake significantly reduced risk of colorectal neoplasms with 20% [OR = 0.80, 95% CI = 0.65-0.99, p value heterogeneity = 0.02].

The investigators found stratification by GST genotype showed that the GSTT1 null genotype confered a reduction in colorectal neoplasms risk of 22% [OR = 0.78, 95% CI = 0.64-0.95, p value heterogeneity = 0.32].

The investigators concluded this meta-analysis provides support to the hypothesis that cruciferous vegetable intake protects against cancer of the colon. This meta-analysis also demonstrates the significance of gene-diet interactions and the importance of assessing individual cruciferous vegetables.

Original title:
Cruciferous vegetables and risk of colorectal neoplasms: a systematic review and meta-analysis by Tse G and Eslick GD.

Link:
http://www.ncbi.nlm.nih.gov/pubmed/24341734

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Objectives:
Does physical activity reduce gastric cancer risk?

Study design:
This review article included 7 cohort studies (with mean reported follow-up ranging from 6 to 18.8 years) and 9 case control studies reporting 11,111 cases of gastric cancer among 1,606,760 patients.

There was no evidence of publication bias, both quantitatively [Begg and Mazumdar rank correlation test, p = 0.62] and qualitatively, on visual inspection of the funnel plot.

Results and conclusions:
The investigators found the risk of gastric cancer was 21% [OR = 0.79, 95% CI = 0.71-0.87, I2 = 55%]  lower among the most physically active people as compared with the least physically active people, after adjustment for important confounders, including age, obesity, and other risk factors for gastric cancer (smoking, alcohol, dietary patterns and socioeconomic status).
This protective effect was seen for gastric cancers in the cardia [OR = 0.80, 95% CI = 0.63-1.00, 4 studies] and distal stomach [OR = 0.63, 95% CI = 0.52-0.76, 5 studies].

The investigators found increasing physical activity was associated with a reduced risk of gastric cancer in both men [OR = 0.86, 95% CI = 0.75-0.99, 10 studies] and women [OR = 0.72, 95% CI = 0.55-0.94, 3 studies].

The investigators found in 12 studies that increased recreational physical activity showed an 18% reduction in gastric cancer risk [OR = 0.82, 95% CI = 0.72-0.94].

The investigators found the effect size was significantly smaller in high-quality studies [OR = 0.86, 95% CI = 0.75-0.99, 6 studies] as compared with low-quality studies [OR = 0.74, 95% CI = 0.69-0.81, 10 studies]. The results were consistent across sex, study quality, study design and geographic location.

The investigators concluded physical activity - especially recreational physical activity - is associated with reduced risk of gastric cancer. Lifestyle interventions focusing on increasing physical activity may decrease the global burden of gastric cancer, in addition to a myriad of other health benefits with being physically active, which include cardiovascular, metabolic and psychologic wellbeing.

Original title:
Physical Activity Is Associated with Reduced Risk of Gastric Cancer: A Systematic Review and Meta-analysis by Singh S, Varayil JE, […], Iyer PG.

Link:
http://cancerprevention.aacrjournals.org/content/7/1/12.abstract

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Objectives:
The association of red meat consumption with the risk of stomach cancer has been reported by many studies, with inconclusive results. Therefore, this review article has been conducted.

Does a high red meat consumption increase stomach cancer risk?

Study design:
This review article included a total of 18 studies (cohort and case-control studies) involving 1,228,327 subjects.

Results and conclusions:
The investigators found for the highest versus lowest categories of red meat intake a significant increased risk of 37% for gastric cancer [pooled RR = 1.37, 95% CI = 1.18-1.59, I2 = 67.6%, p 0.001].

The investigators found in population-based case-control studies, a significant increased risk of 58% for gastric cancer [pooled RR = 1.58, 95% CI = 1.22-2.06, I2 = 73.0%, p 0.001].

The investigators found in hospital-based case-control studies, a significant increased risk of 63% for gastric cancer [pooled RR = 1.63, 95% CI = 1.38-1.92, I2 = 19.1%, p = 0.284].

The investigators found, however, no association among cohort studies [RR = 1.00, 95% CI = 0.83-1.20, I2 = 33.9%, p = 0.158].

The investigators found the significant association was also presented in the subgroup analysis by geographic area (Asia, Europe), publication year (≥2000), sample size (1,000, ≥1,000) and quality score (7 stars, ≥7 stars).

The investigators found in dose-response analysis that every 100 g/day increment in red meat intake significant increased gastric cancer risk with 17% [RR = 1.17, 95% CI = 1.05-1.32].

The investigators found in linear regression model that the risk of gastric cancer increased with increasing level of red meat consumption.

The investigators concluded that a increased intake of red meat might be a risk factor for stomach cancer. Might be because the risk was not significant among cohort studies. Therefore, further larger prospective cohort studies are warranted to verify this association.

Original title:
Red meat consumption and stomach cancer risk: a meta-analysis by Song P, Lu M, […], Zhao Q.

Link:
https://link.springer.com/article/10.1007/s00432-014-1637-z

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Objectives:
The association between meat consumption and the risk of hepatocellular carcinoma (HCC) is still inconclusive. Therefore, this review article has been conducted.

Does meat consumption increase risk of hepatocellular carcinoma?

Study design:
This review article included 7 cohort studies and 10 case-control studies.

Results and conclusions:
The investigators found for the highest vs. lowest consumption levels a non-significant increased risk for hepatocellular carcinoma of 10% [RR = 1.10, 95% CI = 0.85-1.42] for red meat, a non-significant increased risk of 1% [RR = 1.01, 95% CI = 0.79-1.28] for processed meat and a non-significant decreased risk of 3% [RR = 0.97, 95% CI = 0.85-1.11] for total meat. Non-significant means, there is no association with a 95% confidence.

The investigators found for the highest vs. lowest consumption levels a significant decreased risk for hepatocellular carcinoma of 31% [RR = 0.69, 95% CI = 0.58-0.81] for white meat and a significant decreased risk of 22% [RR = 0.78, 95% CI = 0.67-0.90] for fish. The results remained quite stable after stratification by the confounding factors.
Significant means, there is an association with a 95% confidence.

The investigators concluded a high level of white meat or fish consumption reduces the risk of hepatocellular carcinoma, while intake of red meat, processed meat or total meat is not associated with hepatocellular carcinoma risk. These results suggest that dietary intervention may be a promising approach for prevention of hepatocellular carcinoma, which still need to be confirmed by further well-designed prospective studies and experimental research.

Original title:
Systematic review with meta-analysis: meat consumption and the risk of hepatocellular carcinoma by Luo J, Yang Y, [...], Zhu Y.

Link:
http://www.ncbi.nlm.nih.gov/pubmed/24588342

Additional information of El Mondo:
Find more studies/information on fish consumption, meat consumption and cancer right here.

A review article of cohort studies or case-control studies will answer the following question:
"Should I change my diet?".

Objectives:
Is there an association between meat intake and risk of esophageal cancer?

Study design:
This review article included 7 cohort studies and 28 case-control studies.

Results and conclusions:
The investigators found for the highest versus lowest total meat consumption categories a non-significant increased risk of 19% [95% CI = 0.98-1.46] for esophageal cancer.

The investigators found for the highest versus lowest red meat consumption categories a significant increased risk of 55% [95% CI = 1.22-1.96] for esophageal cancer.

The investigators found for the highest versus lowest processed meat consumption categories a significant increased risk of 33% [95% CI = 1.04-1.69] for esophageal cancer.

The investigators found for the highest versus lowest white meat consumption categories a significant decreased risk of 28% [95% CI = 0.60-0.86] for esophageal cancer.

The investigators found for the highest versus lowest poultry consumption categories a significant decreased risk of 17% [95% CI = 0.72-0.96] for esophageal cancer.

The investigators found for the highest versus lowest fish consumption categories a non-significant decreased risk of 5% [95% CI = 0.76-1.19] for esophageal cancer.

The investigators found when stratified by histological subtype, positive associations among esophageal squamous cell carcinoma and red meat, white meat and poultry and esophageal adenocarcinoma with total meat and processed meat.

The investigators concluded red meat and processed meat consumption increase risk of esophageal cancer, while white meat and poultry decrease risk of esophageal cancer. Fish consumption is not associated with incidence of esophageal cancer.

Original title:
Meat consumption is associated with esophageal cancer risk in a meat- and cancer-histological-type dependent manner by Zhu HC, Yang X, […], Sun XC.

Link:
http://www.ncbi.nlm.nih.gov/pubmed/24395380

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Objectives:
Previous observational studies regarding the existence of an association between folate intake and the risk of breast cancer have been inconsistent. Therefore, this review article has been conducted.

Does a higher dietary folate intake reduce breast cancer risk?

Study design:
This review article included 14 prospective cohort studies that reported data on 677,858 individuals.
The participant follow-up period ranged 4.7-17.4 years and the number of individuals per study ranged 11,699-88,818.
There was no publication bias.

Results and conclusions:
The investigators found no association between dietary folate intake and breast cancer risk for highest versus lowest category  [RR =  0.97, 95% CI = 0.90-1.05, p  = 0.451, I2 =  57.5%, p = 0.004].

The investigators found dose-response meta-analysis findings showed no association between the risk of breast cancer and a 100 µg/day increase in dietary folate intake [RR = 0.99, 95% CI = 0.98-1.01, p = 0.361, I2 = 66.2%, p 0.001].

The investigators found evidence of a nonlinear relationship between dietary folate intake and the risk of breast cancer.

A daily dietary folate intake of 200-320 µg was associated with a reduced risk of breast cancer. However, daily folate intake levels >400 µg was associated with a increased risk of breast cancer.

The investigators found overall folate intake level was associated with a reduced breast cancer risk of 36% if the patients had a daily alcohol intake >10 g [RR for highest versus lowest category = 0.64, 95% CI = 0.43-0.97].

The investigators concluded there are no effects of increased dietary folate intake on the incidence of breast cancer. But, a daily dietary folate intake of 200-320 µg was associated with a reduced risk of breast cancer. However, daily folate intake levels >400 µg was associated with a increased risk of breast cancer. Future studies should focus on specific populations in order to analyze primary breast cancer prevention.

Original title:
Folate Intake and the Risk of Breast Cancer: A Dose-Response Meta-Analysis of Prospective Studies by Zhang YF, Shi WW, […], Zhou YH.

Link:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4059748/

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