Nutritional advice

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

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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

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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

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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/

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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

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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

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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

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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/

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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:
Lung cancer is the most common cause of cancer death. Fruits and vegetables containing carotenoids and other antioxidants have been hypothesized to decrease lung cancer risk. Therefore, this meta-analysis (systematic review) has been conducted.

Do fruits and vegetables reduce lung cancer risk?

Study design:
This review article included prospective cohort studies up to December 2014.

Results and conclusions:
The investigators found in 18 studies, when comparing the highest fruits and vegetables with the lowest intakes, a significantly reduced risk of 14% for lung cancer [summary RR = 0.86 [95% CI = 0.78-0.94].

The investigators found in 25 studies, when comparing the highest vegetables with the lowest intakes, a significantly reduced risk of 8% for lung cancer [summary RR = 0.92 [95% CI = 0.87-0.97].

The investigators found in 29 studies, when comparing the highest fruits with the lowest intakes, a significantly reduced risk of 18% for lung cancer [summary RR = 0.82, 95% CI = 0.76-0.89].

The investigators found the association with fruit and vegetable intake was marginally significant in current smokers and inverse but not significant in former or never smokers.

The investigators found in 4 studies for each 100 g/day increase of fruits and vegetables, a significantly reduced risk of 4% for lung cancer [RR = 0.96, 95% CI = 0.94-0.98, I2 = 64%, n (cases) = 9,609].

The investigators found in 20 studies for each 100 g/day increase of vegetables, a significantly reduced risk of 6% for lung cancer [RR = 0.94, 95% CI = 0.89-0.98, I2 = 48%, n (cases) = 12,563].

The investigators found in 23 studies for each 100 g/day increase of fruits, a significantly reduced risk of 8% for lung cancer [RR = 0.92, 95% CI = 0.89-0.95, I2 = 57%, n (cases) = 14,506].

The investigators found the results were consistent among the different types of fruits and vegetables. However, the strength of the association differed across locations.

The investigators found evidence of a non-linear relationship [p 0.01] between fruit and vegetable intake and lung cancer risk showing that no further benefit is obtained when increasing consumption above ∼400g per day.

The investigators concluded fruits and/or vegetables intakes reduce risk of lung cancer with no further benefit when increasing consumption of fruits and vegetables above ∼400g per day.

Original title:
Fruits, vegetables and lung cancer risk: a systematic review and meta-analysis by Vieira AR, Abar L, […], Norat T.

Link:
http://www.ncbi.nlm.nih.gov/pubmed/26371287

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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:
What is the relationship between dietary intake of 12 major food groups, including whole grains, refined grains, vegetables, fruit, nuts, legumes, eggs, dairy, fish, red meat, processed meat and sugar-sweetened beverages and colorectal cancer (CRC) risk?

Study design:
This review article included cohort studies.

Results and conclusions:
The investigators found in the linear dose-response meta-analysis, that every 30 g/d whole grains significantly reduced risk of colorectal cancer with 5% [RR = 0.95, 95% CI = 0.93 to 0.97, n = 9 cohort studies].

The investigators found in the linear dose-response meta-analysis, that every 100 g/d vegetables significantly reduced risk of colorectal cancer with 3% [RR = 0.97, 95% CI = 0.96 to 0.98, n = 15 cohort studies].

The investigators found in the linear dose-response meta-analysis, that every 100 g/d fruit significantly reduced risk of colorectal cancer with 3% [RR = 0.97, 95% CI = 0.95 to 0.99, n = 16 cohort studies]. 

The investigators found in the linear dose-response meta-analysis, that every 200 g/d dairy products significantly reduced risk of colorectal cancer with 7% [RR = 0.93, 95% CI = 0.91 to 0.94, n = 15 cohort studies]. 

The investigators found in the linear dose-response meta-analysis, that every 100 g/d red meat significantly increased risk of colorectal cancer with 12% [RR = 1.12, 95% CI = 1.06 to 1.19, n = 21 cohort studies].

The investigators found in the linear dose-response meta-analysis, that every 50 g/d processed meat significantly increased risk of colorectal cancer with 17% [RR = 1.17, 95% CI = 1.10 to 1.23, n = 16 cohort studies].

The investigators found some evidence for a nonlinear relationship between dietary intake of vegetables, fruit and dairy products and risk of colorectal cancer.

The investigators concluded that daily dietary intake of 30g whole grains, 100g vegetables,100g fruit and 200g dairy products reduce risk of colorectal cancer, while daily dietary intake of 100g red meat and 50g processed meat increase risk of colorectal cancer.

Original title:
Food groups and risk of colorectal cancer by Schwingshackl L, Schwedhelm C, [...], Schlesinger S.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/29210053

Additional information of El Mondo:
Find more information/studies on different food groups and colorectal cancer right here.

Objectives:
Carnitine deficiency has been implicated as a potential pathway for cancer-related fatigue that could be treated with carnitine supplementation. Therefore, this review article (meta-analysis) has been conducted.

Does carnitine supplementation reduce cancer-related fatigue?

Study design:
This review article included 3 RCTs involving a total of 659 participants.

There were not enough studies to conduct sensitivity analyses to isolate potential sources of heterogeneity and test the robustness of findings.

Results and conclusions:
The investigators found in 3 RCTs involving a total of 659 participants that carnitine supplementation did not significantly reduce cancer-related fatigue [SMD = 0.06 points, 95% CI = -0.09 to 0.21, p = 0.45, I2 = 0%].
Clinical heterogeneity was evident from these studies in regards to the dose (2-4 g of carnitine per day), patient demographics (40-100% females included) and carnitine status.

The investigators concluded there is no evidence to support the use of carnitine supplementation (2-4 g of carnitine per day) for cancer-related fatigue.

Original title:
Efficacy and Effectiveness of Carnitine Supplementation for Cancer-Related Fatigue: A Systematic Literature Review and Meta-Analysis by Marx W, Teleni L, [...], Isenring E.

Link:
http://www.mdpi.com/2072-6643/9/11/1224/htm

Additional information of El Mondo:
Find more information/studies on carnitine, randomized controlled trials/cohort studies/subgroup analysis and cancer right here.

Objectives:
Previous studies regarding the relationship between carrot intake and risk of urothelial cancer have reported conflicting results. Therefore, this review article (meta-analysis) has been conducted.

Does a high consumption of carrot reduce urothelial cancer risk?

Study design:
This review article included a total of 6 epidemiological studies (4 case-control and 2 cohort studies) with 1,523 urothelial cancer cases.

There was no significant publication bias by Begg's test (p = 0.348) or Egger's test (p = 0.130).

Results and conclusions:
The investigators found overall analysis indicated a significantly reduced risk of 37% for urothelial cancer for high intake of carrot [OR = 0.63, 95% CI = 0.44-0.90, I2 = 79.6%, p 0.001].

The investigators found in the subgroup analysis by study design, a significantly reduced risk of 55% for urothelial cancer in case-control studies [OR = 0.45, 95% CI = 0.25-0.81]. However, this reduced risk was not significant in cohort studies [OR = 0.91, 95% CI = 0.67-1.24].
Not significant because OR of 1 was found in the 95% CI of 0.67 to 1.24. OR of 1 means no risk/association.

The investigators found, when separately analyzed by carrot type, a significantly reduced risk of 31% for cooked carrot [OR = 0.69, 95% CI 0.51-0.94], but the reduced risk was not significant for raw carrot [OR = 0.84, 95% CI = 0.37-1.93].

The investigators found in the stratified analysis by geographical region, a non-significantly reduced risk of 38% [OR = 0.62, 95% CI = 0.37-1.06], a non-significantly reduced risk of 30% [OR = 0.70, 95% CI = 0.29-1.67] and a non-significantly reduced risk of 47% [OR = 0.53, 95% CI = 0.22-1.26] for Europe, Asia and USA, respectively.

The investigators also found a non-significantly reduced risk of 44% [OR = 0.56, 95% CI = 0.27-1.17] and a non-significantly reduced risk of 27% [OR = 0.73, 95% CI = 0.12-4.60] for male and female, respectively.

The investigators concluded that a high intake of carrot might be associated with a low incidence of urothelial cancer. Might be associated because the reduced risk was not significant in cohort studies. Considering the limited included studies and huge heterogeneity, further large well-designed prospective cohort studies are warranted to confirm these findings.

Original title:
Carrot intake and incidence of urothelial cancer: a systematic review and meta-analysis by Luo X, Lu H, [...], Wang S.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5652827/

Additional information of El Mondo:
Find more information/studies on carrot consumption, randomized controlled trials/cohort studies/subgroup analysis and cancer right here.

Objectives:
Surgical resection remains the primary treatment for gastrointestinal (GI) malignancy including early-stage cancer. Omega-3 polyunsaturated fatty acids (n-3 PUFAs) have been reported to have beneficial clinical and immune-modulating effects in the prognosis of gastrointestinal cancer patients undergoing surgery. Therefore, this review article (meta-analysis) has been conducted.

What is the impact of n-3 PUFA supplementation on postoperative inflammation status and immune function of gastrointestinal cancer patients?

Study design:
This review article included a total of 9 RCTs with 623 participants.

The homogeneous test detected no statistical heterogeneity between studies.

There was no evidence of publication bias following assessment by funnel plot, Egger’s test [p > 0.05] and Begg’s test [p > 0.05].

Results and conclusions:
The investigators found the n-3 PUFAs regime significantly resulted in lower levels of C-reactive protein [p 0.05], interleukin-6 [p 0.01] and higher levels of albumin, CD3+ T cells, CD4+ T cells and CD4+/CD8+ ratio [p 0.05] compared with the isocaloric nutrition regime.

The investigators found, however, no significant difference in the level of tumor necrosis factor-α between the n-3 PUFAs regime and the isocaloric nutrition regime [p = 0.17].

The investigators found that the level of CD8 + T cells significantly decreased compared with the isocaloric nutrition regime [p 0.0001].

The investigators concluded that n-3 PUFAs are effective in improving the nutritional status and immune function of gastrointestinal cancer patients undergoing surgery as they effectively enhance immunity and attenuate the inflammatory response. Although further larger trials are needed, these fatty acids should be widely used in the clinic.

Original title:
Effects of omega-3 fatty acids on patients undergoing surgery for gastrointestinal malignancy: a systematic review and meta-analysis by Yu J, Liu L, [...], Yang F.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5391568/

Additional information of El Mondo:
Find more information/studies on n-3 PUFA consumption and cancer right here.
 

Objectives:
The aim of this review article (meta-analysis) is to compare empirically derived dietary patterns in relation to cancer risk.

Study design:
This review article included observational studies, which evaluated the association with cancer risk between a posteriori derived dietary patterns.

Results and conclusions:
The investigators found a significantly 64% increased risk of cancer for the adoption of high-meat compared to plant-based dietary patterns [RR = 1.64, 95% CI = 1.02-2.63].

The investigators found a significantly 12% lower risk of cancer for individuals adopting a plant-based dietary pattern over a mixed one [RR = 0.88, 95% BI = 0.82-0.95].

The investigators concluded that plant-based dietary patterns decrease cancer risk; meanwhile meat-based dietary patterns increase cancer risk.

Original title:
Differences in the association between empirically derived dietary patterns and cancer: a meta-analysis by Bella F, Godos J, […], Sciacca S.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/27894200

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

Objectives:
Increasing evidence suggests that high consumption of meat is linked to lung cancer but the previous meta-analyses did not properly address the role of tobacco smoking as a potential confounder. Therefore, this review article (meta-analysis) has been conducted.

Does high consumption of meat increase lung cancer risk among never and non-smokers?

Study design:
This review article included 14 independent observational studies and a total of 5,368 subjects with lung cancer.
There was no indication of publication bias.

Results and conclusions:
The investigators found in 11 studies, a statistically significant 24% increased risk of lung cancer for high consumption of red meat [Summary Relative Risk = 1.24, 95% CI = 1.01-1.51, I2 = 31%].

The investigators found no significant associations between high consumption of other types of meat, fish or for heterocyclic amines and lung cancer risk.

The investigators found no significant risk estimates for the increase of one serving per week of any type of meat or fish.

The investigators concluded a high intake of red meat increases the risk of lung cancer among never and non-smokers.

Original title:
Carcinogenicity of High Consumption of Meat and Lung Cancer Risk Among Non-Smokers: A Comprehensive Meta-Analysis by Gnagnarella P, Caini S, […], Gandini S.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/29016198

Additional information of El Mondo:
Find more information/studies on meat consumption, randomized controlled trials/cohort studies/subgroup analysis and cancer right here.

According to international recommendations, adults should aim to have a maximum of 70g red meat per day or 500g per week (cooked weight).
 

Objectives:
Several studies have investigated the relationship between serum selenium concentration and cervical cancer, but the results were inconsistent. Therefore, this review article (meta-analysis) has been conducted.

Do high serum selenium levels reduce risk of cervical cancer among women?

Study design:
This review article included 12 studies investigating the association by univariate analysis and 5 studies by multivariate analysis.

Results and conclusions:
The investigators found in univariate analysis, that serum selenium levels in women with cervical cancer were significantly lower than in women without cervical cancer [SMD = -4.86, 95% CI = -6.03 to -3.69]. Subgroup analysis showed consistent results.

The investigators found in multivariate analysis, that serum selenium levels in women with cervical cancer were significantly lower than in women without cervical cancer [OR = 0.55, 95% CI = 0.42-0.73].

The investigators found after treatment, the serum selenium levels increased significantly [SMD = 2.59, 95% CI = 0.50-4.69].

The investigators concluded high serum selenium levels reduce risk of cervical cancer among women.

Original title:
Serum Selenium Levels and Cervical Cancer: Systematic Review and Meta-Analysis by He D, Wang Z, […], Chen D.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/28255860

Additional information of El Mondo:
Find more information/studies on selenium, randomized controlled trials/cohort studies/subgroup analysis and cancer right here.

Univariate analysis is the simplest form of analyzing data. "Uni" means "one", thus in other words your data has only one variable.

High serum selenium levels can be obtained by consuming selenium-rich food items and/or taking selenium supplements.
 

Objectives:
Several epidemiological studies have suggested that vitamin E could reduce the risk of uterine cervical neoplasm. However, controversial data were presented by different reports. Therefore, this review article (meta-analysis) has been conducted.

Do both high vitamin E intake and circulating vitamin E levels reduce risk of uterine cervical neoplasm?

Study design:
This review article included 15 case-control studies, involving 3,741 cases (those with uterine cervical neoplasm) and 6,328 controls (those without uterine cervical neoplasm).

There was no obvious publication bias.

Results and conclusions:
The investigators found in pooled analysis that the highest intake of vitamin E significantly reduced risk of cervical neoplasia with 42% [OR = 0.58, 95% CI = 0.47-0.72, I2 = 83%]. In addition, both vitamin E intake and blood levels of vitamin E were negatively correlated with cervical neoplasia risk.

The investigators found in subgroup analysis that the highest intake of dietary vitamin E significantly reduced risk of cervical neoplasia with 32% [OR = 0.68, 95% CI = 0.49-0.94, I2 = 70%].

The investigators found in subgroup analysis that the highest vitamin E blood levels significantly reduced risk of cervical neoplasia with 48% [OR = 0.52, 95% CI = 0.40-0.69, I2 = 86%].

The investigators found in subgroup analysis that vitamin E significantly reduced risk of cervical neoplasia with 40% [OR = 0.60, 95% CI = 0.45-0.78, I2 = 84%] in studies conducted in America and Europe.

The investigators found in subgroup analysis that the highest intake of vitamin E significantly reduced risk of cervical neoplasia with 46% [OR = 0.54, 95% CI = 0.39-0.76, I2 = 75%] in studies conducted in Asia.

The investigators found subgroup analysis stratified by different types of cervical neoplasm indicated that the highest intake (or serum level) of vitamin E significantly decreased risk of cervical cancer with 47% [OR = 0.53, 95% CI = 0.390.73, I2 = 77%] and cervical intraepithelial neoplasia (CIN) with 46% [OR = 0.54, 95% CI = 0.43-0.70, I2 = 79%]. Meanwhile, sensitivity analysis to assess the influence of each single study on the pooled ORs by omitting a research in each turn, showed combined ORs were not substantially different, indicating that the results of this meta-analysis were stable and reliable.

The investigators concluded that both vitamin E intake and circulating vitamin E levels could reduce cervical neoplasia risk, including cervical cancer and cervical intraepithelial neoplasia. In other words, sufficient supplementation of vitamin E might reduce the risk of cervical neoplasia. However, more randomized controlled trials and cohort studies with high quality are required to further validate this inverse relationship.

Original title:
Effect of vitamin E supplementation on uterine cervical neoplasm: A meta-analysis of case-control studies by Hu X, Li S, [...], Zhu X.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5567498/

Additional information of El Mondo:
Find more information/studies on vitamin E, randomized controlled trials/cohort studies/subgroup analysis and cancer right here.

Higher intake of vitamin E is an intake which covers the recommended daily allowance of vitamin E of at least 1 day.

Objectives:
Dietary fat may play a role in lung carcinogenesis. Findings from epidemiologic studies, however, remain inconsistent. Therefore, this review article (meta-analysis) has been conducted.

Is there an association between dietary fat intake and the risk of lung cancer?

Study design:
This review article included 10 prospective cohort studies with a total of 1,445,850 participants, of which 18,822 incident cases (subjects with lung cancer).

The mean follow-up was 9.4 years. 

Results and conclusions:
The investigators found high intakes of total fat were associated with a 7% significant increased risk of lung cancer [for highest v lowest quintile: HR = 1.07, 95% CI = 1.00 to 1.15].

The investigators found high intakes of saturated fat were associated with a 14% significant increased risk of lung cancer [for highest v lowest quintile: HR = 1.14, 95% CI = 1.07 to 1.22].

The investigators found high intakes of saturated fat were associated with a 23% significant increased risk of lung cancer among current smokers [for highest v lowest quintile: HR = 1.23, 95% CI = 1.13 to 1.35, p for trend 0.001].

The investigators found high intakes of saturated fat were associated with a 61% significant increased risk of squamous cell lung cancer [for highest v lowest quintile: HR = 1.61, 95% CI = 1.38 to 1.88].

The investigators found high intakes of saturated fat were associated with a 40% significant increased risk of small cell carcinoma lung cancer [for highest v lowest quintile: HR = 1.40, 95% CI = 1.17 to 1.67].

The investigators found a high intake of polyunsaturated fat was associated with a 8% significant decreased risk of lung cancer [for highest v lowest quintile: HR = 0.92, 95% CI = 0.87 to 0.98, p for trend = 0.02].

The investigators found a 5% energy substitution of saturated fat with polyunsaturated fat was associated with a 16% and 17% lower risk of small cell and squamous cell carcinoma, respectively.

The investigators found no associations for monounsaturated fat.

The investigators concluded that high intakes of polyunsaturated fat decrease risk of lung cancer, while high intakes of saturated fat increase risk of lung cancer, particularly among smokers and for squamous cell and small cell carcinoma.

Original title:
Dietary Fat Intake and Lung Cancer Risk: A Pooled Analysis by Yang JJ, Yu D1, […], Shu XO.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/28742456

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

A daily diet with high intakes of saturated fat is a diet that is largely made up of meals/products with more than 10 En% saturated fat, with a small part of meals/products with less than 10 En% saturated fat. Practically, this means that all meals/products that you eat on a daily basis should contain on average more than 10 En% saturated fat.
Check here which products contain more than 10% En% saturated fat.

A daily diet with low intakes of saturated fat is a diet that is largely made up of meals/products with less than 7 En% saturated fat, with a small part of meals/products with more than 7 En% saturated fat. Practically, this means that all meals/products that you eat on a daily basis should contain on average less than 7 En% saturated fat.
Check here which products contain less than 7% En% saturated fat.

Objectives:
Recently, several randomized controlled trials (RCTs) reported the association between the use of vitamin or antioxidant supplements and the risk of bladder cancer. However, those findings remain inconsistent and some studies even reported that vitamin and antioxidant supplements increased the risk of bladder cancer. Therefore, this review article (meta-analysis) has been conducted.

Is there an association between the use of vitamin or antioxidant supplements and the risk of bladder cancer?

Study design:
This review article included 14 RCTs with a total of 147,383 participants, which involved 89,972 in the supplement group and 57,411 in the control group.

The supplementation and follow-up periods ranged between 1 and 13 years.

The types of vitamin and antioxidant supplements were as follows: vitamin A, vitamin B6, vitamin C, vitamin D, vitamin E, beta-carotene, folic acid and selenium.
The dosage regimens in individual trials were as follows: vitamin A (200 mg or 25,000, 36,000 or 40,000 IU daily), vitamin B6 (25 or 100 mg daily), vitamin C (2,000 mg daily), vitamin D (1,600 IU daily), vitamin E (50 mg or 400 IU daily), beta-carotene (20 or 30 mg daily; 50 mg alternate day; 75 mg daily for 3-month cycles), folic acid (1.6 mg daily) and selenium (200 μg daily).

Publication bias was not observed [Begg's funnel plot, symmetrical and Egger's test, p for bias = 0.378].

Results and conclusions:
The investigators found in fixed-effect meta-analysis of all 14 trials that vitamin or antioxidant supplementation was not associated with the risk of bladder cancer [RR = 1.04, 95% CI = 0.92-1.17, I2 = 39.7%].

The investigators found regarding types of supplements, any type of vitamin and antioxidant supplements had no beneficial effect on the risk of bladder cancer:
-vitamin A [RR = 0.86, 95% CI = 0.65-1.13, I2 = 61.7%, n = 5];
-vitamin B6 [RR = 0.77, 95% CI = 0.49-1.20, I2 = 78.8%, n = 3];
-vitamin C [RR = 0.74, 95% CI = 0.36-1.54, I2 = 88.8%, n = 2];
-vitamin D [RR = 1.05, 95% CI = 0.85-1.29, n = 1];
-vitamin E [RR = 0.91, 95% CI = 0.69-1.19, I2 = 60.9%, n = 6];
-beta-carotene [RR = 1.19, 95% CI = 0.96-1.46, I2 = 0.0%, n = 6];
-folate [RR = 1.05, 95% CI = 0.85-1.29, n = 1] and
-selenium [RR = 1.09, 95% CI = 0.81-1.46, I2 = 0.0%, n = 2].

The investigators found overall, there was no significant effect of vitamin and antioxidant supplements in the subgroup meta-analyses by various factors such as dose of supplements, type of cancer prevention, methodological quality, duration of treatment, provider of supplements, type of control and number of participants.
However, the risk of bladder cancer was marginally increased in trials with the use of beta-carotene alone [RR = 1.44, 95% CI = 1.00-2.09, I2 = 0.0%, n = 3].

The investigators concluded that vitamin and antioxidant supplements have no overall preventive effect against bladder cancer. Instead, subgroup meta-analyses showed that beta-carotene supplementation marginally increased the risk of bladder cancer. Even though further large, high-quality trials are required to confirm these associations, the effects (either beneficial or harmful) of vitamin or antioxidant supplements on bladder cancer should not be overemphasized.

Original title:
Effects of Vitamin and Antioxidant Supplements in Prevention of Bladder Cancer: a Meta-Analysis of Randomized Controlled Trials by Park SJ, Myung SK, […], Lee YJ.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5334161/

Additional information of El Mondo:
Find more information/studies on vitamins, selenium, beta-carotene, antioxidants and cancer right here.

Objectives:
Protective effects of calcium supplementation against colorectal adenomas have been documented in systematic reviews; however, the results have not been conclusive. Therefore, this review article (meta-analysis) has been conducted.

Does calcium supplementation reduce colorectal adenomas?

Study design:
This review article included 5 RCTs involving 2,234 patients with a history of adenomas.
Based on visual inspection of the funnel plots as well as on quantitative measurement that used the Egger regression test, there was weak evidence of publication bias.
No major serious adverse events were associated with the use of calcium, but there was an increase in the incidence of hypercalcemia [p  = 0 .0095].
Random errors were evaluated with trial sequential analyses (TSAs). However, TSA indicated a lack of firm evidence for a beneficial effect of calcium supplementation.

Results and conclusions:
The investigators found quantitative pooling of results from all 5 RCTs indicated that the use of supplemental calcium lasting 3 to 5 years showed a statistically significant 17% reduction in risk of any recurrent colorectal adenomas [RR = 0.83, 95% CI = 0.75-0.93, I2  =  8.5%, p  =  0.36].

The investigators found in the sensitivity analysis of 3 trials with low bias risk a statistically significant 12% reduction in the recurrence of any colorectal adenomas [RR = 0.88, 95% CI = 0.79-0.99, I2  =  0%, p  =  0.54] in patients who were administered supplemental calcium versus placebo.

The investigators found no association between supplemental calcium and recurrence of advanced colorectal adenomas in trials with low risk of bias [RR = 1.02, 95% CI = 0.67-1.55, I2 =  17.5%].

The investigators found in the subgroup analysis of 3 trials with elemental calcium dose ≤ 1200 mg/day, a statistically significant 16% reduction in the recurrent of any colorectal adenomas [RR = 0.84, 95% CI = 0.73-0.97, I2  =  38.5%, p  = 0 .19].

However, a greater reduction of 26% [RR = 0.74, 95% CI = 0.56-0.97, I2  =  0%, p  = 0 .70] was observed in the subgroup analysis of 2 trials with elemental calcium dose ≥ 1600 mg/day.
Subgroup analyses demonstrated no statistically significant association with the reduction of advanced colorectal adenomas in any doses.

The investigators concluded the available good quality RCTs suggests a possible beneficial effect of calcium supplementation – preferably at least 1600 mg/day elemental calcium – on the recurrence of colorectal adenomas. However, TSA indicated that the accumulated evidence is still inconclusive. Therefore, large well-designed randomized trials with low risk of bias are needed.

Original title:
Effects of calcium on the incidence of recurrent colorectal adenomas: A systematic review with meta-analysis and trial sequential analysis of randomized controlled trials by Veettil SK, Ching SM, […], Chaiyakunapruk N.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5556213/

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

Colorectal adenomas can lead to colorectal cancer.