Nutrition and health

Objectives:
Do diets rich in protein causually reduce body weight of adults with overweight or obesity? 

Study design:
This review article included 37 RCTs.
The diets were included during a mean of 32 weeks interventions, ranging from 8 to 104 weeks.

There was no publication bias.

Results and conclusions:
The investigators found protein intake (ranging from 18-59 energy percentage [En%]) significantly reduced body weight by 1.6 kg [95% CI = 1.2 to 2.0 kg, I2 = 56%] compared to controls (digestible carbohydrate, fiber, fat or no supplementation (no placebo used)).
This result was also found in sensitivity analysis.

The investigators found the effect size of dietary protein in body weight management was dependent on specific phenotypes, where individuals with prediabetes had more benefit compared to individuals with normoglycemia.
Furthermore, individuals without the obesity risk allele (AA genotype) had more benefit compared to individuals with the obesity risk alleles (AG and GG genotypes).

The investigators concluded that diets rich in protein (18-59 energy percentage [En%]) during 32 weeks causally have a moderate beneficial effect on body weight management of adults with overweight or obesity.

Original title:
Are Dietary Proteins the Key to Successful Body Weight Management? A Systematic Review and Meta-Analysis of Studies Assessing Body Weight Outcomes after Interventions with Increased Dietary Protein by Hansen TT, Astrup A and Sjödin A.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8468854/

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

A diet rich in protein with 18-59 energy percentage [E%] or a diet with 18-59 En% protein means that the amounts of protein contribute 18 to 59% to the total calories (kcal) of the diet.
If the diet contains 2000 kcal, 90 grams of protein contribute 18% to this 2000 kcal.
1 gram of protein gives 4 kcal. Thus 90 grams of protein provide 360 kcal (90x4 kcal) and 360 kcal is 18% of 2000 kcal.

The most easy way to follow a diet rich in protein with 18-59 energy percentage is to choose only meals/products with 18-59 En% protein. Check here which products contain 18-59 En% protein.

However, the most practical way to follow a diet with 18-59 En% protein is, all meals/products that you eat on a daily basis should contain on average 18-59 En% protein.

To do this, use the 7-points nutritional profile app to see whether your daily diet contains 18-59 En% protein.

A high-protein diet is a diet with at least 20 En% protein.

 

Objectives:
The association between vitamin C and metabolic syndrome (MetS) has been evaluated in several epidemiological studies with conflicting results. Therefore, this review article has been conducted.

Do dietary vitamin C intake and circulating vitamin C level reduce risk of metabolic syndrome? 

Study design:
This review article included 26 cross-sectional studies and 2 cohort studies with a total number of 110,771 participants. 23 studies were related to the dietary vitamin C level.
The sample size ranged from 143 to 27,656 persons.
The dietary vitamin C level was assessed by food-frequency questionnaire (FFQ) in 4 studies, a 24-h or 3-day recall in 18 studies and a 4-day record in 1 study.

No evidence of publication bias existed according to Begg's rank correlation test [p = 0.495].

Results and conclusions:
The investigators found when compared to the lowest dietary vitamin C intake, that the highest dietary vitamin C intake significantly reduced risk of metabolic syndrome with 7% [overall multivariable-adjusted RR = 0.93, 95% CI = 0.88 to 0.97, p = 0.003, I2 = 54.5%, p = 0.003]. The above findings were confirmed in cross-sectional studies [RR = 0.92, 95% CI = 0.87 to 0.97, p = 0.001] and 24-h or 3-day recall [RR = 0.89, 95% CI = 0.86 to 0.93, p 0.001] studies.

The investigators found when compared to the lowest circulating vitamin C level, that the highest circulating vitamin C level significantly reduced risk of metabolic syndrome with 40% [overall multivariable-adjusted RR = 0.60, 95% CI = 0.49 to 0.74, p 0.001, I2 = 22.7%, p = 0.249].

The investigators concluded that both the dietary and the circulating vitamin C level reduce risk of metabolic syndrome. However, due to the limitation of the available evidence, more well-designed prospective studies are still needed.

Original title:
Vitamin C and Metabolic Syndrome: A Meta-Analysis of Observational Studies by Guo H, Ding J, [...], Zhang Y.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8531097/

Additional information of El Mondo:
Find more information/studies on vitamin C consumption and overweight right here.

In practice, a lot of dietary vitamin C intake amounts to 200 to 300 grams of vegetables and 2-5 pieces of fruit per day. Vitamin C is found in fruit and vegetables.

A high circulating vitamin C level can be obtained through vitamin C-rich food and/or taking vitamin C supplements.

 

Objectives:
The associations between dietary carbohydrate and diverse health outcomes remain controversial and confusing. Therefore, this review article (meta-analyse) has been conducted.

What is the association between dietary carbohydrate intake and diverse health outcomes?

Study design:
This review article included 43 meta-analyses of observational research studies with 23 health outcomes, including cancer (n = 26), mortality (n = 4), metabolic diseases (n = 4), digestive system outcomes (n = 3) and other outcomes [coronary heart disease (n = 2), stroke (n = 1), Parkinson's disease (n = 1) and bone fracture (n = 2)].

This umbrella review summarized 281 individual studies with 13,164,365 participants.

33.3% studies were considered to be of high quality and 66.7% of moderate quality.

Results and conclusions:
The investigators found highly suggestive evidence showed that dietary carbohydrate intake significantly increased risk of metabolic syndrome with 25% [adjusted summary odds ratio = 1.25, 95% CI = 1.15 to 1.37].

The investigators found suggestive evidence showed that dietary carbohydrate intake significantly decreased risk of esophageal adenocarcinoma with 43% [adjusted summary hazard ratio = 0.57, 95% CI = 0.42 to 0.78].

The investigators found suggestive evidence showed that dietary carbohydrate intake significantly increased risk of all-cause mortality with 19% [adjusted summary hazard ratio 1.19, 95% CI = 1.09 to 1.30].

The investigators concluded despite the fact that numerous systematic reviews and meta-analyses have explored the relationship between carbohydrate intake and diverse health outcomes, there is no convincing evidence of a clear role of carbohydrate intake. However, highly suggestive evidence shows carbohydrate intake is associated with higher risk of metabolic syndrome. Suggestive evidence shows carbohydrate intake is associated with higher risk of all-cause mortality and lower risk of esophageal adenocarcinoma.

Original title:
Dietary Carbohydrate and Diverse Health Outcomes: Umbrella Review of 30 Systematic Reviews and Meta-Analyses of 281 Observational Studies by Liu YS, Wu QJ […], Zhao YH.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8116488/

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

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:
What is the association between red meat and poultry consumption and the risk of metabolic syndrome?

Study design:
This review article included 9 prospective cohort studies, which involved a total of 21,869 participants.
Among them, 8 studies were identified for red meat consumption.

No publication bias was observed according to the Begg's rank-correlation test and the Egger's test.  

Results and conclusions:
The investigators found that red meat consumption was significantly associated with a higher risk of 35% for metabolic syndrome [multi-variable adjusted RR = 1.35, 95% CI = 1.13 to 1.62, p = 0.001, I2 = 54.4%, p = 0.032].  
The same results were obtained in subgroup analysis for >5 years follow-up [RR = 1.36, 95% CI = 1.09 to 1.7, p = 0.006], non-National Cholesterol Education Program-Adult Treatment Panel (NCEP-ATP III) [RR = 1.34, 95% CI = 1.12 to 1.62, p = 0.002], Non-Asia [RR = 1.51, 95% CI = 1.29 to 1.77, p 0.001], adjustment of BMI [RR = 1.4, 95% CI = 1.23 to 1.6, p 0.001] and physical activity studies [RR = 1.48, 95% CI = 1.29 to 1.71, p 0.001].

The investigators found that unprocessed red meat consumption was significantly associated with a higher risk of 32% for metabolic syndrome [multi-variable adjusted RR = 1.32, 95% CI = 1.14 to 1.54, p = 0.0003, I2 = 0%, p = 0.397].  

The investigators found that processed red meat consumption was significantly associated with a higher risk of 48% for metabolic syndrome [multi-variable adjusted RR = 1.48, 95% CI = 1.11 to 1.97, p = 0.007, I2 = 64.7%, p = 0.097].  

The investigators found that poultry consumption was significantly associated with a lower risk of 15% for metabolic syndrome [multi-variable adjusted RR = 0.85, 95% CI = 0.75 to 0.97, p = 0.02, I2 = 0%, p = 0.707].  

The investigators concluded that red meat (processed and unprocessed) consumption is associated with a higher risk of metabolic syndrome, whereas, poultry consumption is associated with a lower risk of metabolic syndrome. More well-designed randomized controlled trials are still needed to address the issues further.

Original title:
Association of Red Meat and Poultry Consumption With the Risk of Metabolic Syndrome: A Meta-Analysis of Prospective Cohort Studies by Guo H, Ding J, [...], Zhang Y.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8295459/

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

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:
Nuts are recommended for cardiovascular health, yet concerns remain that nuts may contribute to weight gain due to their high energy density. Therefore, this review article has been conducted.

Does nut consumption contribute to an increased adiposity risk?

Study design:
This review article included 6 prospective cohort studies with 569,910 participants and 86 RCTs with 114 comparisons and 5,873 participants.

Results and conclusions:
The investigators found nuts consumption was significantly associated with a lower risk of 7% for incidence of overweight/obesity [RR = 0.93, 95% CI = 0.88 to 0.98, p 0.001, moderate certainty of evidence] in prospective cohort studies.

The investigators found RCTs showed no adverse effect of nuts on body weight [MD = 0.09 kg, 95% CI = -0.09 to 0.27 kg, p 0.001, high certainty of evidence].

The investigators found meta-regression showed that higher nut intake was significantly associated with reductions in body weight and body fat.

The investigators concluded that current evidence demonstrates the concern that nut consumption contributes to increased adiposity appears unwarranted.

Original title:
Are fatty nuts a weighty concern? A systematic review and meta-analysis and dose-response meta-regression of prospective cohorts and randomized controlled trials by Nishi SK, Viguiliouk E, [...], Sievenpiper JL.

Link:
https://pubmed.ncbi.nlm.nih.gov/34494363/

Additional information of El Mondo:
Find more information/studies on nut consumption and obesity/overweight 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:
Diets with high glycemic index (GI) or high glycemic load (GL) have been linked to important risk factors associated with the development of metabolic syndrome (MetS), such as dyslipidemia, higher blood glucose and insulin concentrations. However, the role of GI and GL in relation to metabolic syndrome is still understudied and controversial. Therefore, this review article has been conducted.

Does high dietary GI or GL increase risk of metabolic syndrome?

Study design:
This review article included 1 cohort study and 11 cross-sectional studies with a total sample size of 36,295 subjects.

Results and conclusions:
The investigators found, the pooled effect sizes from the 9 studies indicated high versus low dietary GI was significantly associated with increased risk of 5% for metabolic syndrome [OR = 1.05, 95% CI = 1.01 to 1.09, I2 = 58.1%, p = 0.004].
This finding was supported by all subgroup analyses except where studies used 24-h recalls for dietary assessment.

The investigators found, additionally, a linear dose-response investigation revealed that each 5-point increment in GI was associated with 2% increase in the risk of metabolic syndrome [OR = 1.02, 95% CI = 1.01 to 1.02].
Howver, non-linear pattern was insignificant [p-nonlinearity = 0.63].

The investigators found, moreover, pooled effect sizes from 10 studies suggested that no association was found between the GL and metabolic syndrome with results remaining consistent in all subgroup analyses.

The investigators concluded that high dietary GI increases risk of metabolic syndrome. Nutrition policy and clinical practices should encourage a diet with low GI. Future studies should include both GI and GL and different criteria of metabolic syndrome to provide a better comparison.

Original title:
Glycemic index, but not glycemic load, is associated with an increased risk of metabolic syndrome: Meta-analysis of observational studies by Askari M, Dehghani A, […], Alizadeh S.

Link:
https://pubmed.ncbi.nlm.nih.gov/33928722/

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

A diet with low GI is a diet with GI of 55 or lower.

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:
Excess body weight, including overweight and obesity, is one of the major factors influencing human health and plays an important role in the global burden of disease. Carotenoids serve as precursors of vitamin A-related retinoids and are considered to have potential effects on many diseases. However, the influence of carotenoids on people with excess body weight is unclear. Therefore, this review article has been conducted.

Does carotenoid supplementation reduce risk of overweight and obesity in overweight or obese subjects?

Study design:
This review article included 7 randomized controlled trials (RCTs) and 8 observational studies with 28,944 subjects and data on multiple carotenoid subgroups, including lycopene, astaxanthin, cryptoxanthin, α-carotene, and β-carotene.

In all included RCTs, the intervention duration was 20 days at the shortest and 16 weeks at the longest and the range of intervention doses was 1.2-60 mg/d.

Results and conclusions:
The investigators found that the insufficiency of serum carotenoids significantly increased risk of overweight and obesity with 73% [OR = 1.73, 95% CI = 1.57 to 1.91, p 0.001].

The investigators found, moreover, carotenoid supplementation was significantly associated with body weight reductions [SMD = -2.34 kg, 95% CI = -3.80 to -0.87 kg, p 0.001], body mass index decrease [SMD = -0.95 kg/cm², 95% CI = -1.88 to -0.01 kg/cm², p 0.001] and waist circumference losses [SMD = -1.84 cm, 95% CI = -3.14 to -0.54 cm, p 0.001].

The investigators concluded that 1.2-60 mg/d carotenoid supplementation reduces risk of overweight and obesity in overweight or obese subjects. Furthermore, an insufficiency of serum carotenoids is a risk factor for overweight and obesity. Additional data from large clinical trials are needed.

Original title:
The association between carotenoids and subjects with overweight or obesity: a systematic review and meta-analysis by Yao N, Yan S, […], Cui W.

Link:
https://pubmed.ncbi.nlm.nih.gov/33977977/

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

Am I overweight?
 

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:
The evidence on the association between obesity and atrial fibrillation (AF) recurrence was equivocal. Therefore, this review article (meta-analysis) has been conducted.

Does obesity increase risk of atrial fibrillation recurrence in patients undergoing catheter ablation?

Study design:
This review article included 20 studies with 52,771 patients.

Results and conclusions:
The investigators found that obesity was significantly associated with higher atrial fibrillation recurrence [OR = 1.30, 95% C = 1.16 to 1.47, p 0.001, I2 = 72.7%] and similar rate of adverse events [OR = 1.21, 95% CI = 0.87 to 1.67, p = 0.264, I2 = 23.9%] in patients undergoing catheter ablation.

The investigators found meta-regression showed that the association varied by age [coefficient = -0.03, p = 0.024].

The investigators found meta-analysis of highest versus lowest BMI showed that the highest group had higher atrial fibrillation recurrence [OR = 1.37, 95% CI = 1.18 to 1.58, p 0.001, I2 = 64.9%] and adverse events [OR = 2.02, 95% CI = 1.08 to 3.76, p = 0.028, I2 = 49.5%] in patients undergoing catheter ablation.

The investigators found the dose-response relationship for BMI and atrial fibrillation recurrence was nonlinear [p nonlinearity 0.001], the curve became steeper at 30-35 kg/m².

The investigators found for adverse events, an increase of 1% for every 1 kg/m² increase in BMI [OR = 1.01, 95% CI = 1.00 to 1.02, p = 0.001], the relationship was nonlinear [p nonlinearity = 0.001].

The investigators concluded that obesity is associated with higher atrial fibrillation recurrence in patients undergoing catheter ablation. High BMI is associated with a higher risk for adverse events.

Original title:
BMI and atrial fibrillation recurrence post catheter ablation: A dose-response meta-analysis by Pranata R, Henrina J, […], Munawar M.

Link:
https://pubmed.ncbi.nlm.nih.gov/33544873/

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

Catheter ablation is a procedure that uses radiofrequency energy (similar to microwave heat) to destroy a small area of heart tissue that is causing rapid and irregular heartbeats. Destroying this tissue helps restore your heart’s regular rhythm. Catheter ablation is also called radiofrequency ablation.

Am I overweight?
 

Objectives:
A few randomized controlled trials (RCTs) have assessed the effect of brown rice consumption on metabolic parameters (such as, weight, height, waist circumference, fasting glucose, LDL, HDL, total cholesterol, triglycerides and blood pressure) compared to white rice, with inconsistent findings. Therefore, this review article has been conducted.

Is the effect of brown rice on adiposity indices (such as, weight, height and waist circumference), lipid profile (such as, LDL, HDL, total cholesterol and triglycerides) and glycemic markers (such as, fasting blood glucose) higher compared to white rice in adult subjects?

Study design:
This review article included 13 RCTs.
In accordance with Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach, the certainly of the included evidence was low and very low.

Results and conclusions:
The investigators found brown rice significantly reduced:
weight by -1.63 kg [95% CI = -2.15 to -1.11, I2 = 97%, n = 6];
body mass index (BMI) by -0.58 kg/m² [95% CI = -0.78 to -0.37, I2 = 96%, n = 6] and;
waist circumference by -2.56 cm [95% CI = -4.86 to -0.26, I2 = 88%, n = 5] compared with white rice.

The investigators found, moreover, brown rice had no significant effect on lipid profile and glycemic markers.

The investigators found pre-germinated brown rice significantly declined:
weight by -1.75 kg [95% CI = -2.70 to -0.81, I2 = 99%, n = 4];
total cholesterol by -24.22 mg/dL [95% CI = -33.03 to -15.41, I2 = 78%, n = 5];
triglyceride (TG) by -43.28 mg/dL [95% CI = -74.05 to -12.50, I2 = 90%, n = 5];
low-density lipoprotein (LDL or bad cholesterol) by -20.05 mg/dL [95% CI = -29.57 to -10.52, I2 = 71%, n = 5] and;
fasting blood glucose (FBG) by -15.83 mg/dL [95% CI = -25.20 to -6.46, I2 = 91%, n = 5] compared to white rice.

The investigators concluded brown rice has anti-obesity effects in comparison with white rice. However, it has no beneficial effects on lipid profile and glycemic markers. Furthermore, pre-germinated brown rice has better functional effects on promoting lipid profile and fasting blood glucose compared to brown rice.

Original title:
The effect of brown rice compared to white rice on adiposity indices, lipid profile, and glycemic markers: a systematic review and meta-analysis of randomized controlled trials by Golzarand M, Toolabi K, […], Mirmiran P.

Link:
https://pubmed.ncbi.nlm.nih.gov/33905269

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

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:
Several mechanisms have been proposed for the effect of vitamin E on weight loss. Yet various interventional studies with wide ranges of doses and durations have reported contradictory results. Therefore, this review article has been conducted.

Does vitamin E supplementation reduce overweight?

Study design:
This review article included 24 RCTs.

Results and conclusions:
The investigators found there was no significant effect of vitamin E supplements on weight [WMD = 0.15, 95% CI = -1.35 to 1.65, p = 0.847], body mass index (BMI) [WMD = 0.04, 95% CI = -0.29 to 0.37, p = 0.815] and waist circumference (WC) [WMD = -0.19 kg, 95% CI = -2.06 to 1.68, p = 0.842], respectively.

The investigators found, however, subgroup analysis revealed that vitamin E supplementation in studies conducted on participants with normal BMI (18.5-24.9) had increasing impact on BMI [p = 0.047].  

The investigators concluded there is no significant effect of vitamin E supplementation on weight, BMI and waist circumference (WC). However, vitamin E supplementation increases BMI in participants with normal BMI (18.5-24.9).

Original title:
Can vitamin E supplementation affect obesity indices? A systematic review and meta-analysis of twenty-four randomized controlled trials by Emami MR, Jamshidi S, […], Aryaeian N.

Link:
https://pubmed.ncbi.nlm.nih.gov/33632535/

Additional information of El Mondo:
Find more information/studies on vitamin E and obesity/overweight 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.