Nutrition and health

Objectives:
Chemotherapy-induced peripheral neuropathy (CIPN) is a common symptom, but prophylactic measures cannot still be carried out effectively. In addition, the efficacy of vitamin E in preventing peripheral neurotoxicity caused by chemotherapy is inconclusive. Therefore, this review article has been conducted.

Does vitamin E supplementation decrease risk of chemotherapy-induced peripheral neuropathy?

Study design:
This review article included 8 RCTs with a total of 488 patients.
The number of participants in each arm ranged from 13 to 96.
The experimental intervention was vitamin E supplementation as an adjuvant to cisplatin, paclitaxel and other chemotherapies.
There was no publication bias.

Results and conclusions:
The investigators found patients who received vitamin E supplementation of 600 mg/day had a significantly lower incidence of chemotherapy-induced peripheral neuropathy of 69% [risk ratio = 0.31, 95% CI = 0.14 to 0.65, p = 0.002, I2 = 0%] than the placebo group (group without vitamin E).

The investigators found patients in the cisplatin chemotherapy group who received vitamin E supplementation had a significantly lower incidence of chemotherapy-induced peripheral neuropathy of 72% [risk ratio = 0.28, 95% CI = 0.14 to 0.54, p = 0.0001, I2 = 0%]  than the placebo group.

The investigators found, moreover, vitamin E supplementation significantly decreased patients’ sural amplitude after 3 rounds of chemotherapy [MD = -2.66, 95% CI = -5.09 to -0.24, p = 0.03, I2 = 0%] in contrast with that of placebo supplementation, while no significant difference was observed when patients were treated with vitamin E after 6 rounds of chemotherapy [MD = -1.28, 95% CI = -3.11 to 0.54, p = 0.17, I2 = 40%].

The investigators found, in addition, the vitamin E-supplemented group had better improvement in the neurotoxicity score and lower incidence of reflexes and distal paraesthesias than the control group.

The investigators concluded that vitamin E supplementation of 600 mg/day decreases risk of chemotherapy-induced peripheral neuropathy, particularly in the cisplatin chemotherapy group. More high-quality trials with standardized reporting of clinical outcomes about peripheral neuropathy are needed to explore the exact role of vitamin E in the prevention of chemotherapy-induced peripheral neuropathy.

Original title:
Protective Effects of Vitamin E on Chemotherapy-Induced Peripheral Neuropathy: A Meta-Analysis of Randomized Controlled Trials by Miao H, Li R [...], Wen Z.

Link:
https://www.karger.com/Article/FullText/515620

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

Objectives:
The efficacy of dendritic cell vaccine for newly diagnosed glioblastoma remains controversial. Therefore, this review article has been conducted.

Does dendritic cell vaccine provide benefits for the newly diagnosed glioblastoma?

Study design:
This review article included 3 randomized controlled trials (RCTs).

Results and conclusions:
The investigators found overall, compared with control group for newly diagnosed glioblastoma, dendritic cell vaccine showed no substantial effect on:
-median overall survival [SMD = 0.11, 95% CI = -0.18 to 0.41, p = 0.45];
-median progression-free survival [SMD = 0.12, 95% CI = -0.24 to 0.48, p = 0.50];
-progression-free survival rate [risk ratio = 1.29, 95% CI = 0.82 to 2.04, p = 0.27];
-overall survival rate [risk ratio = 1.29, 95% CI = 0.61 to 2.72, p = 0.50] or;
-nervous system disorders [risk ratio = 0.80, 95% CI= 0.59 to 1.08, p = 0.14].

The investigators concluded dendritic cell vaccine provides no obvious benefits for the newly diagnosed glioblastoma.

Original title:
The Efficacy of Dendritic Cell Vaccine for Newly Diagnosed Glioblastoma: A Meta-analysis of Randomized Controlled Studies by Tan L, Peng J, […], Wu Q.

Link:
https://pubmed.ncbi.nlm.nih.gov/34767325/

Additional information of El Mondo:
Find more information/studies on RCTs/cohort/significantly/review article and cancer right here.

Dendritic cells (DCs) are professional antigen-presenting cells that link innate and adaptive immunity and are critical for the induction of protective immune responses against pathogens.

Glioblastoma is an aggressive type of cancer that can occur in the brain or spinal cord.

Objectives:
Does breastfeeding reduce risk of ovarian cancer in women with BRCA1 mutation or BRCA2 mutation?

Study design:
This review article included 1 cohort study and 4 case-control studies with a total of 14,601 women with a BRCA1 or BRCA2 mutation.

There was no publication bias.

Results and conclusions:
The investigators found ever having performed breastfeeding significantly reduced risk of ovarian cancer with 23.3% [pooled OR = 0.767, 95% CI = 0.688 to 0.856, I2 = 0%] in women with BRCA1 mutation.

The investigators found ever having performed breastfeeding non-significantly reduced risk of ovarian cancer with 18.3% [pooled OR = 0.817, 95% CI = 0.650 to1.028, I2 = 0%] in women with BRCA2 mutation.

The investigators found breastfeeding for >1 year significantly reduced risk of ovarian cancer with 21.3% [pooled OR = 0.787, 95% CI = 0.682 to 0.907, I2 = 0%] in women with BRCA1 mutation.

The investigators found breastfeeding for >1 year significantly reduced risk of ovarian cancer with 43.3% [pooled OR = 0.567, 95% CI = 0.400 to 0.802, I2 = 0%] in women with BRCA2 mutation.

The investigators concluded that ever having performed breastfeeding reduces risk of ovarian cancer in women with BRCA1 mutation and breastfeeding for >1 year reduces risk of ovarian cancer in women with BRCA2 mutation.

Original title:
The preventive effect of breastfeeding against ovarian cancer in BRCA1 and BRCA2 mutation carriers: A systematic review and meta-analysis by Eoh KJ, Park EY, […], Lim MC.

Link:
https://pubmed.ncbi.nlm.nih.gov/34304906/

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

Objectives:
Previous studies have provided limited evidence for the effect of carrot intake on bladder cancer incidence. Therefore, this review article has been conducted.

Is there a relationship between dietary carrot intake and bladder cancer incidence?

Study design:
This review article included 3 cohort studies.

Results and conclusions:
The investigators found in a meta-analyse of 3 cohort studies no significant association between dietary carrot intake and bladder cancer risk [summary HR = 1.02, 95% CI = 0.95 to 1.10, I2 = 0.0%, p = 0.859].

The investigators concluded that there is no association between dietary consumption of carrot and the risk of bladder cancer.

Original title:
Association of Dietary Carrot Intake With Bladder Cancer Risk in a Prospective Cohort of 99,650 Individuals With 12.5 Years of Follow-Up by Xu X, Zhu Y, […], Xia D.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8349976/

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

Objectives:
Omega-3 polyunsaturated fatty acid (PUFA) supplementation has been proposed as a potential therapy for cancer-related malnutrition, which affects up to 70% of patients with cancer. Therefore, this review article has been conducted.

Do patients with cancer benefit from oral omega-3 PUFA supplements?

Study design:
This review article included 31 RCTs.
Trials supplementing ≥600 mg/d omega-3 PUFA (oral capsules, pure fish oil or oral nutritional supplements) compared with a control intervention for ≥3 weeks.

The Cochrane risk of bias tool graded most trials as “unclear” or “high” risk of bias.

Results and conclusions:
The investigators found meta-analyses showed no significant difference between omega-3 PUFA supplements and control intervention on muscle mass, quality of life and body weight.

The investigators found oral omega-3 PUFA supplements significantly reduced the likelihood of developing chemotherapy-induced peripheral neuropathy with 80% [OR = 0.20, 95% CI = 0.10 to 0.40, p 0.001, I2 = 0%].  

The investigators concluded that oral omega-3 PUFA supplementation may reduce the incidence of chemotherapy-induced peripheral neuropathy in patients with cancer. May reduce because most trials were graded as “unclear” or “high” risk of bias.

Original title:
The effect of oral omega-3 polyunsaturated fatty acid supplementation on muscle maintenance and quality of life in patients with cancer: A systematic review and meta-analysis by Lam CN, Watt AE, [...], van der Meij BS.

Link:
https://pubmed.ncbi.nlm.nih.gov/34130028/

Additional information of El Mondo:
Find more information/studies on omega- 3 fatty acids and cancer right here.

Chemotherapy-induced peripheral neuropathy (CIPN) is one of the most frequent side effects caused by antineoplastic agents. Antineoplastic drugs are medications used to treat cancer. Antineoplastic drugs are also called anticancer, chemotherapy, chemo, cytotoxic or hazardous drugs.

Objectives:
There appears to be a sex-specific association between obesity and colorectal neoplasia in patients with Lynch Syndrome (LS). Therefore, this review article has been conducted.

Does obesity (BMI>30) increase colorectal cancer in patients with Lynch Syndrome?

Study design:
This review article included 3 prospective cohort studies with 2,463 subjects (persons), of which 735 subjects with colorectal cancer.

All studies with a prospective study design (cohort studies) expressed the association between obesity and colorectal cancer in terms of adjusted HR (95% CI).

There was no publication bias.

Results and conclusions:
The investigators found a twofold risk of colorectal cancer in obese men with Lynch Syndrome compared to nonobese men with Lynch Syndrome [SRR = 2.09, 95% CI = 1.23 to 3.55, I2 = 33%].  
No significantly increased risk due to obesity was found for women [SRR = 1.41, 95% CI = 0.46 to 4.27, I2 = 68%].  

The investigators found a significantly 49% increased colorectal cancer risk for obesity (BMI>30) for subjects with an MLH1 mutation [SRR = 1.49, 95% CI = 1.11 to 1.99, I2 = 0%].

The investigators concluded that obesity (BMI>30) increases colorectal cancer in men with Lynch Syndrome, particularly with an MLH1 mutation.

Original title:
A Meta-Analysis of Obesity and Risk of Colorectal Cancer in Patients with Lynch Syndrome: The Impact of Sex and Genetics by Lazzeroni M, Bellerba F, […], Gandini S.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8160758

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

Lynch syndrome, also known as hereditary non-polyposis colorectal cancer (HNPCC), is an autosomal dominantly inherited disease. People with Lynch syndrome have about a 40% to 80% chance of getting colorectal cancer by age 70. They’re also at risk for cancer of the uterus, ovaries or stomach. And they tend to get cancer at younger ages than other people, often in their 30s and 40s.

An error or mutation, in one copy of the MLH1 gene is one of the causes of Lynch syndrome. Men and women with a mutation in MLH1 have a 52-82% lifetime risk (up to age 70) to develop colon or rectal cancer.
 

Objectives:
Does calcium reduce the risk of incidence and recurrence of colorectal adenomas and advanced adenomas?

Study design:
This review article included 37 relevant clinical trials and observational studies involving over 10,964 cases.

Results and conclusions:
The investigators found that calcium consumption significantly reduced the risk of colorectal adenomas incidence by 8% [RR = 0.92, 95% CI = 0.89 to 0.96].

The investigators found that calcium intake as a food significantly reduced the risk of colorectal adenomas incidence by 21% [RR = 0.79, 95% CI = 0.72 to 0.86].

The investigators found that calcium intake as dairy product significantly reduced the risk of colorectal adenomas incidence by 12% [RR = 0.88, 95% CI = 0.78 to 0.98].

The investigators found, however, calcium supplements did not show a significant effect on colorectal adenomas incidence [RR = 0.97, 95% CI = 0.89 to 1.05].

The investigators found that total calcium intake significantly reduced the risk of advanced colorectal adenomas incidence by 21% [RR = 0.79, 95% CI = 0.73 to 0.85].

The investigators found that total calcium intake significantly reduced the risk of recurrence of adenomas by 12% [RR = 0.88, 95% CI = 0.84 to 0.93].

The investigators concluded that natural sources of calcium such as dairy products and foods have more effective role than supplementary calcium in terms of reducing the risk of incidence and recurrence of colorectal adenomas and advanced adenomas.

Original title:
Calcium and dairy products in the chemoprevention of colorectal adenomas: a systematic review and meta-analysis by Emami MH, Salehi M, […], Maghool F.

Link:
https://pubmed.ncbi.nlm.nih.gov/33951958/

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

The colorectal adenoma is a benign glandular tumor of the colon and the rectum. It is a precursor lesion of the colorectal adenocarcinoma (colon cancer).

Objectives:
Apart from ruminant fat, trans fatty acids are produced during the partial hydrogenation of vegetable oils, (eg, in the production of ultraprocessed foods). Harmful cardiovascular effects of trans fatty acids are already proven, but the link with cancer risk has not yet been summarized. Therefore, this review article has been conducted.

Does high consumption of dietary trans fat increase risk of cancer?

Study design:
This review article included 17 cohort and case-control studies on breast cancer, 11 cohort and case-control studies on prostate cancer and 9 cohort and case-control studies on colorectal cancer.

Results and conclusions:
The investigators found that high consumption of dietary total trans fat significantly increased prostate cancer with 49% [OR = 1.49, 95% CI = 1.13 to 1.95].
Significantly means that there is an association with a 95% confidence.

The investigators found that high consumption of dietary total trans fat significantly increased colorectal cancer with 26% [OR = 1.26, 95% CI = 1.08 to 1.46].
Significant because OR of 1 was not found in the 95% CI of 1.08 to 1.46. OR of 1 means no risk/association.

The investigators found no association between high consumption of dietary total trans fat and the risk of breast cancer [OR = 1.12, 95% CI = 0.99 to 1.26].
No association ant because OR of 1 was found in the 95% CI of 0.99 to 1.26. OR of 1 means no risk/association.

The investigators found results were dependent on the fatty acid subtype, with even cancer-protective associations for some partially hydrogenated vegetable oils.

The investigators found enhancing moderators in the positive transfat-cancer relation were gender (direction was cancer-site specific), European ancestry, menopause, older age and overweight.

The investigators concluded that high consumption of dietary total trans fat increases prostate cancer and colorectal cancer. Future studies need methodological improvements (eg, using long-term follow-up cancer data and intake biomarkers). Owing to the lack of studies testing trans-fatty acid subtypes in standardized ways, it is not clear which subtypes (eg, ruminant sources) are more carcinogenic.

Original title:
Dietary trans-fatty acid intake in relation to cancer risk: a systematic review and meta-analysis by Michels N, Specht IO and Huybrechts I.

Link:
https://pubmed.ncbi.nlm.nih.gov/34104953/

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

A diet high in trans fat is a diet with more than 1 En% trans fat.

Trans fat can be found in doughnuts, cakes, pie crusts, biscuits, frozen pizza, cookies, crackers and stick margarines and other spreads.

Objectives:
Despite the widespread increase in the incidence of early-onset colorectal cancer (EoCRC), the reasons for this increase remain unclear. Therefore, this review article has been conducted.

What are the risk factors of early-onset colorectal cancer?

Study design:
This review article included 20 studies.

With the exception of alcohol consumption, there was considerable heterogeneity among studies [I2 > 60%].

Results and conclusions:
The investigators found colorectal cancer history in a first-degree relative was significantly associated with a 4.21-fold enhanced risk of early-onset colorectal cancer [RR = 4.21, 95% CI = 2.61 to 6.79].

The investigators found hyperlipidemia significantly increased risk of early-onset colorectal cancer with 62% [RR = 1.62, 95% CI = 1.22 to 2.13].

The investigators found obesity (BMI>30) significantly increased risk of of early-onset colorectal cancer with 54% [RR = 1.54, 95% CI = 1.01 to 2.35].

The investigators found compared to non-drinkers, high alcohol consumption significantly increased risk of of early-onset colorectal cancer with 71% [RR = 1.71, 95% CI = 1.62 to 1.80].

The investigators concluded that colorectal cancer history in a first-degree relative, hyperlipidemia (a high level of lipids (fats, cholesterol and triglycerides) circulating in the blood), obesity and high alcohol consumption are risk factors of early-onset colorectal cancer. High-quality studies conducted on generalizable populations and that comprehensively examine risk factors for early-onset colorectal cancer are required to inform primary and secondary prevention strategies.

Original title:
Risk Factors for Early-Onset Colorectal Cancer: A Systematic Review and Meta-analysis by O'Sullivan DE, Sutherland RL, […], Brenner DR.

Link:
https://pubmed.ncbi.nlm.nih.gov/33524598/

Additional information of El Mondo:
Find more information/studies on obesity, alcohol consumption and colorectal cancer right here.

Early-onset colorectal cancer is colorectal cancer diagnosed in a patient younger than age 50.

 

Objectives:
Does guarana supplementation reduce cancer-related fatigue?

Study design:
This review article included 7 RCTs with a total of 427 cancer patients.
Some studies presented a low risk of bias for all the categories.
Meta-analysis was conducted for 3 studies about breast cancer, which presented sufficient data.

The instruments used to analyze fatigue were the Brief Fatigue Inventory (BFI), the Chalder Fatigue Scale, the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-FATIGUE) and the Piper Scale.

Results and conclusions:
The investigators found guarana supplementation did not reduce cancer-related fatigue compared with placebo groups [mean = -0.02, 95% CI = -1.54 to 1.50, p = 0.98] and the quality of evidence according to GRADE was very low.

The investigators concluded that guarana supplementation did not reduce cancer-related fatigue. However, further studies with better methodological quality are needed.

Original title:
The use of guarana (Paullinia cupana) as a dietary supplement for fatigue in cancer patients: a systematic review with a meta-analysis by de Araujo DP, Pereira PTVM, […], Garcia JBS.

Link:
https://pubmed.ncbi.nlm.nih.gov/34146166/

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

 

Objectives:
Systemic inflammation and oxidative stress (OS) are associated with breast cancer. Coenzyme Q10 (CoQ10) as an adjuvant treatment with conventional anti-cancer chemotherapy has been demonstrated to help in the inflammatory process and oxidative stress. Therefore, this review article has been conducted.

Does coenzyme Q10 supplementation reduce levels of inflammatory markers, oxidative stress parameters and matrix metalloproteinases/tissue inhibitor of metalloproteinases (MMPs/TIMPs) in patients with breast cancer?

Study design:
This review article included 9 RCTs.

Results and conclusions:
The investigators found that coenzyme Q10 supplementation (100 mg/day for 45-90 days) significantly decreased the levels of
-vascular endothelial growth factor (VEGF) [SMD = -1.88, 95% CI = -2. 62 to -1.13, I2 = 93.1%, p 0.001];
-IL-8 [SMD = -2.24, 95% CI = -2.68 to -1.8, I2 = 79.6%, p = 0.001];
-matrix metalloproteinase-2 (MMP-2) [SMD = -1.49, 95% CI = -1.85 to -1.14, I2 = 76.3%, p = 0.005] and
-matrix metalloproteinase-9 (MMP-9) [SMD = -1.58, 95% CI = -1.97 to -1.19, I2 = 79.6%, p = 0.002].

The investigators concluded that 100 mg/day coenzyme Q10 supplementation for 45-90 days reduces some of the important markers of inflammation and matrix metalloproteinases in patients with breast cancer. However, further studies with controlled trials for other types of cancer are needed to better understand and confirm the effect of coenzyme Q10 on tumor therapy.

Original title:
Effects of coenzyme Q10 supplementation on inflammation, angiogenesis, and oxidative stress in breast cancer patients: a systematic review and meta-analysis of randomized controlled trials by Alimohammadi M, Rahimi A, […], Rafiei A.

Link:
https://pubmed.ncbi.nlm.nih.gov/34008150/

Additional information of El Mondo:
Find more information/studies on coenzyme Q10 and breast cancer right here.

Vascular endothelial growth factor (VEGF) plays a central role in promoting angiogenesis and is over-expressed in breast cancer.

IL-8 is a marker of ER-negative and/or HER2-positive breast cancer.

Matrix metalloproteinases (MMPs) are a group of zinc-containing, calcium dependent endopeptidases which play a substantial role in breast carcinogenesis through several mechanisms. These mechanisms include remodeling of extracellular matrix (ECM), cell proliferation and angiogenesis which promote metastasis and result in tumor progression.

Objectives:
Branched-chain amino acids (BCAAs; leucine, isoleucine and valine) are essential amino acids involved in immune responses and may have roles in protein malnutrition and sarcopenia (a type of muscle loss (muscle atrophy) that occurs with aging and/​or immobility). Furthermore, certain liver diseases have been associated with a decreased Fischer's ratio (BCAAs to aromatic amino acids; phenylalanine, tyrosine and tryptophan). However, a comprehensive synthesis of the evidence from human controlled studies on the supplemental use of BCAAs during the oncology peri-operative period has not been published. Therefore, this review article (meta-analysis) has been conducted.

Does branched-chain amino acids (BCAAs) supplementation during the oncological surgical period reduce post-operative morbidity from infections and ascites?

Study design:
This review article included 13 RCTs and 6 cohort studies with 2,019 participants.
Mean (or median) ages of the RCTs populations were from 53 to 67 years old and all of the RCTs had a predominantly male population.
9 RCTs (69%) evaluated oral intake of BCAAs and 4 (31%) administered (parenteral) BCAAs intravenously in hospital.
Duration of treatment use in the RCTs ranged from intra-operatively (single intravenous administration) up to a maximum duration of 13 months (oral administration).

Among 13 RCTs, 77% involved liver cancer. Methodological study quality scored substantial risk-of-bias across most RCTs.

Overall, 6 cohort studies were of low methodological quality.

Results and conclusions:
The investigators found meta-analysis of RCTs showed a 38% significantly decreased risk of post-operative infections in BCAAs group compared to controls [RR = 0.62, 95% CI = 0.44 to 0.87, p= 0.006, I2 = 0%, number of RCTs, k = 6, total sample size, n = 389].

The investigators found BCAAs supplementation was also beneficial for ascites [RR = 0.55, 95% CI = 0.35 to 0.86, p = 0.008, I2 = 0%, k = 4, n = 296], body weight [MD = 3.24 kg, 95% CI = 0.44 to 6.04, p = 0.02, I2 = 24%, k = 3, n = 196] and hospitalization length [MD = -2.07 days, 95% CI = -3.97 to -0.17, p = 0.03, I2 = 59%, k = 5, n = 362].

The investigators found no differences between BCAAs and controls for mortality, recurrence, other post-operative complications (liver failure, edema, pleural effusion), blood loss, quality of life, ammonia level and prothrombin time.

The investigators found no serious adverse events were related to BCAAs; however, serious adverse events were reported due to intravenous catheters. No safety concerns from observational studies were identified.

The investigators concluded that branched-chain amino acids (BCAAs) supplementation during the oncological surgical period may reduce important post-operative morbidity from infections and ascites compared to controls. May reduce because the included studies were of low methodological quality. Therefore, blinded, placebo-controlled confirmatory trials of higher methodological quality are warranted, especially using oral, short-term BCAAs-enriched supplements within the context of recent ERAS programs.

Original title:
Are Supplemental Branched-Chain Amino Acids Beneficial During the Oncological Peri-Operative Period: A Systematic Review and Meta-Analysis by Cogo E, Elsayed  M, […], Papadogianis P.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7930658/

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

Ascites is the buildup of fluid in the space around the organs in the abdomen. When ascites is caused by cancer, it is called malignant ascites.
 

Objectives:
Due to the rapid increase of primary liver cancer incidence and the poor prognosis, it is imperative to identify new modifiable factors such as diet and nutrition for the prevention of liver cancer. Diet high in saturated fatty acids (SFA) has been hypothesized to be associated with increased risk of cancers. However, the associations between dietary fatty acids and liver cancer are not consistent. Therefore, this review article has been conducted.

Does a diet high in saturated fatty acids or cholesterol increase risk of liver cancer?

Study design:
This review article included 14 prospective cohort studies with 15,890 liver cancer cases.

Results and conclusions:
The investigators found for the highest dietary saturated fat versus lowest intake, a significantly increased risk of 34% [RR = 1.34, 95% CI = 1.06 to 1.69, I2 = 16.9%, n = 5] for liver cancer.

The investigators found for every increase with 1 En% saturated fat, a significantly increased risk of 4% [RR = 1.04, 95% CI = 1.01 to 1.07, I2 = 16.8%, n = 5] for liver cancer.

The investigators found per 0.1-unit increase in ratio of monounsaturated fatty acids (MUFA): saturated fat (SFA), a significantly decreased risk of 9% [RR = 0.91, 95% CI = 0.86 to 0.95] for liver cancer.

The investigators found per 0.1-unit increase in ratio of unsaturated fatty acids (UFA):saturated fat (SFA), a significantly decreased risk of 6% [RR = 0.94, 95% CI = 0.90 to 0.97] for liver cancer.

The investigators found for every increase with 100 mg dietary cholesterol intake per day, a significantly increased risk of 16% [RR = 1.16, 95% CI = 1.01 to 1.07, I2 = 0%, n = 2] for liver cancer.

The investigators found for the highest serum total cholesterol levels versus lowest levels, a significantly decreased risk of 58% [RR = 0.42, 95% CI = 0.33 to 0.54, I2 = 90.7%, n = 7] for liver cancer.

The investigators found for the highest serum total cholesterol levels versus lowest levels, a significantly decreased risk of 61% [RR = 0.39, 95% CI = 0.27 to 0.57] for liver cancer among men. 

The investigators found for the highest serum total cholesterol levels versus lowest levels, a significantly decreased risk of 69% [RR = 0.31, 95% CI = 0.26 to 0.38] for liver cancer among women. 

The investigators found for every increase with 1 mmol/L in serum cholesterol level, a significantly decreased risk of 28% [RR = 0.72, 95% CI = 0.69 to 0.75, I2 = 75.3%, n = 7] for liver cancer.

The investigators found for every increase with 1 mmol/L in serum HDL cholesterol level, a significantly decreased risk of 58% [RR = 0.42, 95% CI = 0.27 to 0.64, I2 = 0%, n = 2] for liver cancer.

The investigators found these findings were generally robust and stable in sensitivity analyses.

The investigators concluded there is an increased risk for dietary saturated fat with liver cancer using both category and dose-response analyses. Higher ratios of monounsaturated fatty acids (MUFA):saturated fat (SFA) and unsaturated fatty acids (UFA):saturated fat (SFA) are associated with a lower risk of developing liver cancer. Higher serum total and HDL cholesterol are associated with a lower risk of liver cancer with high between-studies variability.

Original title:
Dietary Fats, Serum Cholesterol and Liver Cancer Risk: A Systematic Review and Meta-Analysis of Prospective Studies by Zhao L, Deng C, [...], Zhang X.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8037522/

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

A diet high in saturated fat (unhealthy fat) is a diet with more than 10 En% saturated fat.

The easiest way to follow a diet with more than 10 En% saturated fat is to choose only products/meals that also contain more than 10 En% saturated fat. Check here which products contain more than 10 En% saturated fat.

More than 10% saturated fat means that the total amounts of saturated fat make up more than 10% of the total kcal of the diet. So a 2000 kcal diet with more than 10 En% saturated fat contains more than 22 grams of saturated fat. 22 grams of saturated fat provides 22x9 kcal = 198 kcal. 198 kcal is 10% of 2000 kcal.

However, products with more than 10 En% saturated fat are unhealthy products.

Objectives:
Does mushroom dietary intake reduce risk of cancer at any site?

Study design:
This review article included 11 case-control studies and 6 cohort studies.

Results and conclusions:
The investigators found higher mushroom consumption significantly reduced total cancer with 34% [pooled RR for the highest compared with the lowest consumption groups = 0.66, 95% CI = 0.55 to 0.78, n = 17].

The investigators found higher mushroom consumption significantly reduced breast cancer with 35% [pooled RR for the highest compared with the lowest consumption groups = 0.65, 95% CI = 0.52 to 0.81, n = 10].

The investigators found higher mushroom consumption significantly reduced nonbreast cancer with 20% [pooled RR for the highest compared with the lowest consumption groups = 0.80, 95% CI = 0.66 to 0.97, n = 13].

The investigators found there was evidence of a significant nonlinear dose-response association between mushroom consumption and the risk of total cancer [p-nonlinearity = 0.001, n = 7].

The investigators concluded higher mushroom consumption reduces risk of cancer, particularly breast cancer.

Original title:
Higher Mushroom Consumption Is Associated with Lower Risk of Cancer: A Systematic Review and Meta-Analysis of Observational Studies by Ba DM, Ssentongo P, […], Richie JP.

Link:
https://pubmed.ncbi.nlm.nih.gov/33724299/

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

Objectives:
Controversial results of the association between green tea consumption and risk for esophageal cancer (EC) were reported by previous meta-analysis. Therefore, this review article (meta-analysis) has been conducted.

Does green tea consumption reduce esophageal cancer risk?

Study design:
This review article included 14 studies with a total of 5,057 esophageal cancer cases among 493,332 participants.

Results and conclusions:
The investigators found in the dose-response analysis, no association for a 1 cup/d increase in green tea and esophageal cancer risk [the summary OR = 1.00, 95% CI = 0.95 to 1.04, I2 = 77%].

The investigators found no nonlinearity association was observed between tea consumption and risk for esophageal cancer [p = 0.71 for nonlinearity].

The investigators found in the subgroup analysis of sex, a significantly reduced risk of 21% for esophageal cancer among women for a 1 cup/d increase in green tea [summary OR = 0.79, 95% CI = 0.68 to 0.91, I2 = 0%].
However, this reduced risk was not found for men [summary OR for a 1 cup/d increase in green tea = 1.03, 95% CI = 0.95 to 1.11, I2 = 67%].
Significant because OR of 1 was not found in the 95% CI of 0.68 to 0.91. OR of 1 means no risk/association.

The investigators concluded that a 1 cup/d increase in green tea consumption reduces esophageal cancer among women. Notably, these findings might be influenced by limited studies and potential bias, such as dose of green tea assessment and select bias of case-control studies. Further larger number, prospective and well-designed larger-scale studies are needed to provide more precise evidence, especially in women and more regions (United States and Europe).

Original title:
Green tea consumption and risk for esophageal cancer: A systematic review and dose-response meta-analysis by Zhao H, Mei K, […], Lixia Xie L.

Link:
https://pubmed.ncbi.nlm.nih.gov/33744644/

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

Objectives:
The etiology of cancer type may vary significantly due to anatomy, embryology and physiology of the cancer site. Although the association between potato consumption and colorectal cancer (CRC) was summarized in a 2018 meta-analysis of 5 cohort studies, however, no meta-analysis has evaluated potato consumption in relation to multiple cancer sites in adults. Therefore, this review article has been conducted.

Do potato intakes increase multiple cancer sites risk?

Study design:
This review article included 20 prospective cohort studies (with a total of 785,348 participants, of which 19,882 incident cases (persons with cancer)) and 36 case-control studies ( with a total of 21,822 cases (persons with cancer) and 66,502 controls (persons without cancer)).

Certainty of the evidence was low for total cancer, colorectal cancer, colon, rectal, renal, pancreatic, breast, prostate and lung cancer and very low for gastric and bladder cancer.

Results and conclusions:
The investigators found among cohort studies, no association between high versus low intake of total potato (white and yellow) consumption and overall cancers [RR = 1.04, 95% CI = 0.96 to 1.11, tau2 = 0.005, n = 18].

The investigators found no relation between total potato consumption (high compared with low intake) and risk of colorectal, pancreatic, colon, gastric, breast, prostate, kidney, lung or bladder cancer in cohort or case-control studies.

The investigators found no association between high versus low consumption of potato preparations (boiled/fried/mashed/roasted/baked) and risk of gastrointestinal-, sex-hormone-, or urinary-related cancers in cohort or case-control studies.

The investigators concluded that potato intakes or potato preparations are not associated with multiple cancer sites when comparing high and low intake categories. This finding is consistent with the findings from the 2018 meta-analysis regarding potato intake and risk of colorectal cancer.

Original title:
Potato Consumption and Risk of Site-Specific Cancers in Adults: A Systematic Review and Dose-Response Meta-Analysis of Observational Studies by Mofrad MD, Mozaffari H, […], Azadbakht L.

Link:
https://pubmed.ncbi.nlm.nih.gov/33861304/

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Objectives:
Does citrus dietary intake reduce the risk of lung cancer?

Study design:
This review article included 21 observational studies.

Results and conclusions:
The investigators found pooled analyses showed that those with the highest citrus fruit dietary intake compared to the lowest intake had a 9% reduction in lung cancer risk [OR = 0.91, 95% CI = 0.84 to 0.98].

The investigators found a nonlinear association between citrus dietary intake and lung cancer risk in the dose-response analysis [p = 0.0054] and that the risk reached the minimum [OR = 0.91] around 60 g/d.
However, no obvious dose-response association was observed with intakes above 80 g/d.

The investigators concluded that citrus fruit dietary intake is negatively associated with the risk of lung cancer. Besides, there is a nonlinear dose-response relationship between citrus fruit dietary intake and lung cancer risk within a certain range (60-80g per day).

Original title:
Citrus fruit intake and lung cancer risk: A meta-analysis of observational studies by Wang J, Gao J, [...], Qian BY.

Link:
https://pubmed.ncbi.nlm.nih.gov/33529754/

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Citrus fruits include oranges, lemons, limes and grapefruits.

Objectives:
Does a low selenium level in human tissues increase the risk of breast cancer?

Study design:
This review article included 18 case-control studies with 3,374 women diagnosed with breast cancer (case group) and 3,582 healthy controls (women without breast cancer).

Results and conclusions:
The investigators found selenium level of the case group (group with women diagnosed with breast cancer) was significantly lower than the control group (group with women without breast cancer) [-0.53 μg/L, 95% CI = -0.72 to -0.34, p 0.001].

The investigators found in subgroup analysis that serum selenium level of the case group was significantly lower than the control group [-1.14 μg/L, 95% CI = -1.70 to -0.58, p 0.001].

The investigators found in subgroup analysis that plasma selenium level of the case group was significantly lower than the control group [-0.21 μg/L, 95% CI = -0.37 to -0.04, p 0.014].

The investigators found in subgroup analysis that selenium level of toenail of the case group was significantly lower than the control group [-0.21 μg/L, 95% CI = -0.38 to -0.03, p 0.021].

The investigators concluded that a low selenium level in human tissues increases the risk of breast cancer, which may improve the understanding of the effects of selenium on human health.

Original title:
Relationship Between Selenium in Human Tissues and Breast Cancer: a Meta-analysis Based on Case-Control Studies by Zhu X, Pan D, […], Sun G.

Link:
https://pubmed.ncbi.nlm.nih.gov/33420696/

Additional information of El Mondo:
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Objectives:
Although several epidemiological studies have investigated associations between poultry and fish consumption and pancreatic cancer (PC) risk, these findings have been inconsistent. Therefore, this review article has been conducted.

Do high dietary poultry or fish intakes increase risk of pancreatic cancer?

Study design:
This review article included 25 studies (cohort studies and case-control studies).

Results and conclusions:
The investigators found for the highest vs. lowest poultry intake category a significantly increased risk of 14% for pancreatic cancer [pooled RR = 1.14, 95% CI = 1.02 to 1.26] in cohort studies.
Significant because RR of 1 was not found in the 95% CI of 1.02 to 1.26. RR of 1 means no risk/association.

The investigators found there was no association between fish intake and pancreatic cancer risk [RR = 1.00, 95% CI = 0.93 to 1.07].
No association because RR of 1 was found in the 95% CI of 0.93 to 1.07. RR of 1 means no risk/association.

The investigators concluded that large amount of poultry intake increases pancreatic cancer risk, while fish intake is unlikely to be linked to pancreatic cancer risk. These findings require further investigation, particularly between poultry and pancreatic cancer.

Original title:
Poultry and Fish Intake and Pancreatic Cancer Risk: A Systematic Review and Meta-Analysis by Gao Y, Ma Y, […], Wang X.

Link:
https://pubmed.ncbi.nlm.nih.gov/33432844/

Additional information of El Mondo:
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Objectives:
Does dietary acrylamide intake increase risk of breast, endometrial and ovarian cancer?

Study design:
This review article included 14 prospective cohort studies.

Results and conclusions:
The investigators found no significant association between dietary acrylamide intake and the risk of breast [RR = 0.95, 95% CI = 0.90 to 1.01], endometrial [RR = 1.03, 95% CI = 0.89 to 1.19] and ovarian cancers [RR = 1.02, 95% CI = 0.84 to 1.24].
In addition, no significant association between dietary acrylamide intake and the risk of breast, endometrial and ovarian cancers in different subgroup analyses by smoking status, menopausal status, BMI status and different types of breast cancer.

The investigators concluded there is no significant association between dietary acrylamide intake and the risk of breast, endometrial and ovarian cancers.

Original title:
Dietary acrylamide intake and risk of women's cancers: a systematic review and meta-analysis of prospective cohort studies by Benisi-Kohansal S, Salari-Moghaddam A, […], Esmaillzadeh A.

Link:
https://pubmed.ncbi.nlm.nih.gov/33413725/

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

Acrylamide is a chemical that naturally forms in starchy food products during high-temperature cooking processes, such as frying, roasting and baking. Acrylamide in food forms from sugars and an amino acid that are naturally present in food.
 

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:
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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:
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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

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