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Sedentary behavior and cancer-an umbrella review and meta-analysis.
Hermelink, R, Leitzmann, MF, Markozannes, G, Tsilidis, K, Pukrop, T, Berger, F, Baurecht, H, Jochem, C
European journal of epidemiology. 2022;37(5):447-460
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Globally, cancer is one of the leading causes of death. In modern day-to-day life, sedentary behaviour is prevalent, with adults spending an average of 8.2 hours without any physical activity. It is believed that sedentary behaviour plays a significant role in the increase in all-cause mortality, obesity, chronic diseases, and cancer risk. The purpose of this review and meta-analysis was to examine previous studies that reported associations between sedentary behaviour and cancer incidence and all-cancer mortality. A total of 14 meta-analyses were included in the study, and the strength of the evidence for each association was rated. A significant association was found between sedentary behaviour and cancer incidence across various cancer sites, including ovarian, endometrial, colon, breast, rectal, and prostate cancers. All-cancer mortality also showed positively significant associations with sedentary behaviour. There is a need for further research to evaluate the mechanisms associated with sedentary behaviour and the development of cancer at various sites. However, the results of this study can be used by healthcare professionals to better understand the importance of recommending physical activity and other therapeutic strategies.
Abstract
Several systematic reviews and meta-analyses have summarized the association between sedentary behavior (SB) and cancer. However, the level of evidence and the potential for risk of bias remains unclear. This umbrella review summarized the current data on SB in relation to cancer incidence and mortality, with a particular emphasis on assessing the risk of bias. We searched PubMed, Web of Science and Cochrane Database for systematic reviews and meta-analyses on the association between SB and cancer incidence and mortality. We also searched for recent observational studies not yet included in existing meta-analyses. We re-calculated summary risk estimates for cancer incidence and mortality using random effects models. We included 14 meta-analyses covering 17 different cancer sites from 77 original studies. We found that high SB levels increase the risk for developing ovarian, endometrial, colon, breast, prostate, and rectal cancers, with relative risks of 1.29 (95% confidence interval (CI) = 1.08-1.56), 1.29 (95% CI = 1.16-1.45), 1.25 (95% CI = 1.16-1.33), 1.08 (95% CI = 1.04-1.11), 1.08 (95% CI = 1.00-1.17), and 1.07 (95% CI = 1.01-1.12), respectively. Also, we found an increased risk of cancer mortality of 1.18 (95% CI = 1.09-1.26). Most associations between SB and specific cancer sites were supported by a "suggestive" level of evidence. High levels of SB are associated with increased risk of several types of cancer and increased cancer mortality risk.
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Coffee Consumption and Cancer Risk: An Assessment of the Health Implications Based on Recent Knowledge.
Pauwels, EKJ, Volterrani, D
Medical principles and practice : international journal of the Kuwait University, Health Science Centre. 2021;30(5):401-411
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Coffee is one of the most consumed beverages worldwide. Coffee is a good source of polyphenolic antioxidant and anti-inflammatory compounds such as caffeine, cafestol, kahweol, and chlorogenic acids. This review included one hundred and five cohort studies and meta-analyses to evaluate the relationship between coffee consumption and cancer of the breast, liver, oesophagus, stomach, pancreas, colorectum, kidney, bladder, prostate, and ovaries. The results of this review found an inverse association between coffee consumption and reduced risk of hepatocellular cancer. A slight risk reduction is observed against breast cancer in postmenopausal women. This review found no considerable association between coffee consumption and decreased cancer risk in other organs. Further robust studies are required to investigate the benefits of coffee consumption on cancer risk reduction due to the high heterogeneity of included studies. However, healthcare professionals can use the results of this study to understand the benefits of coffee consumption.
Abstract
A significant number of studies suggest that coffee consumption reduces cancer risk. This beneficial effect is usually ascribed to the presence of polyphenolic antioxidants and anti-inflammatory agents, including caffeine, cafestol, kahweol, and chlorogenic acids. To summarize recent literature on this subject, we performed a bibliographic search in PubMed and Embase over the period January 2005 to December 2020 to identify cohort studies and meta-analysis (with data collection ensuring quality of selected reports) that could provide quantitative data on the relationship between coffee consumption and common cancers. The totality of eligible scientific articles supports the evidence that coffee intake is inversely associated with risk of hepatocellular cancer and, to a slight extent, risk of breast cancer among postmenopausal women. As to the association with other organs, including the esophagus, pancreas, colorectum, kidneys, bladder, ovaries, and prostate, the results are less clear as reports reveal conflicting results or statistically nonsignificant data. Therefore, this overview does not provide broad-based conclusions. Important uncertainties include general study design, inhomogeneous patient sampling, different statistical analysis (deliberate), misreporting of socioeconomic status, education, coffee-brewing methods, consumption of caffeinated or decaffeinated coffee, smoking habits, and alcohol intake. Clearly, more epidemiologic research needs to be conducted before solid science-based recommendations can be made with regard to coffee consumption.
3.
Coenzyme Q10 for heart failure.
Al Saadi, T, Assaf, Y, Farwati, M, Turkmani, K, Al-Mouakeh, A, Shebli, B, Khoja, M, Essali, A, Madmani, ME
The Cochrane database of systematic reviews. 2021;(2):CD008684
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As per the definition given by the NHS, heart failure happens when the heart fails to pump blood around the body due to stiffness or weakness of the heart muscle. Coenzyme Q10 reduces oxidative stress and toxic effects in the body by acting as a fat-soluble antioxidant nutrient. Due to these beneficial effects, CoQ10 may effectively reduce damage to cardiac cells and disruption to cellular signalling. CoQ10 is also a cell membrane stabiliser, and previous studies have shown a correlation between the severity of heart failure and CoQ10 deficiency. In addition, dietary absorption of CoQ10 is relatively slow and ineffective; therefore, supplementation is effective and safe with no side effects. This review included eleven randomised controlled studies to compare the beneficial effects of Coenzyme Q10 for the treatment of people with heart disease. This review showed that Coenzyme Q10 might reduce all-cause mortality and hospitalisation due to heart failure. In addition, CoQ10 may stabilise myocardial calcium‐dependent ion channels and encourage adenosine‐5'‐triphosphate (ATP) synthesis. However, the effectiveness of CoQ10 in lowering the risk of myocardial infarction or stroke, left ventricular ejection fraction and exercise capacity is inconclusive. Healthcare professionals can use this study's results to understand the potential beneficial effects of CoQ10 supplementation on maintaining heart health. However, due to the high heterogeneity in the current research, further robust long-term studies are required to evaluate the therapeutic value of Coenzyme Q10 in managing heart disease.
Abstract
BACKGROUND Coenzyme Q10, or ubiquinone, is a non-prescription nutritional supplement. It is a fat-soluble molecule that acts as an electron carrier in mitochondria, and as a coenzyme for mitochondrial enzymes. Coenzyme Q10 deficiency may be associated with a multitude of diseases, including heart failure. The severity of heart failure correlates with the severity of coenzyme Q10 deficiency. Emerging data suggest that the harmful effects of reactive oxygen species are increased in people with heart failure, and coenzyme Q10 may help to reduce these toxic effects because of its antioxidant activity. Coenzyme Q10 may also have a role in stabilising myocardial calcium-dependent ion channels, and in preventing the consumption of metabolites essential for adenosine-5'-triphosphate (ATP) synthesis. Coenzyme Q10, although not a primary recommended treatment, could be beneficial to people with heart failure. Several randomised controlled trials have compared coenzyme Q10 to other therapeutic modalities, but no systematic review of existing randomised trials was conducted prior to the original version of this Cochrane Review, in 2014. OBJECTIVES To review the safety and efficacy of coenzyme Q10 in heart failure. SEARCH METHODS We searched CENTRAL, MEDLINE, Embase, Web of Science, CINAHL Plus, and AMED on 16 October 2020; ClinicalTrials.gov on 16 July 2020, and the ISRCTN Registry on 11 November 2019. We applied no language restrictions. SELECTION CRITERIA We included randomised controlled trials of either parallel or cross-over design that assessed the beneficial and harmful effects of coenzyme Q10 in people with heart failure. When we identified cross-over studies, we considered data only from the first phase. DATA COLLECTION AND ANALYSIS We used standard Cochrane methods, assessed study risk of bias using the Cochrane 'Risk of bias' tool, and GRADE methods to assess the quality of the evidence. For dichotomous data, we calculated the risk ratio (RR); for continuous data, the mean difference (MD), both with 95% confidence intervals (CI). Where appropriate data were available, we conducted meta-analysis. When meta-analysis was not possible, we wrote a narrative synthesis. We provided a PRISMA flow chart to show the flow of study selection. MAIN RESULTS We included eleven studies, with 1573 participants, comparing coenzyme Q10 to placebo or conventional therapy (control). In the majority of the studies, sample size was relatively small. There were important differences among studies in daily coenzyme Q10 dose, follow-up period, and the measures of treatment effect. All studies had unclear, or high risk of bias, or both, in one or more bias domains. We were only able to conduct meta-analysis for some of the outcomes. None of the included trials considered quality of life, measured on a validated scale, exercise variables (exercise haemodynamics), or cost-effectiveness. Coenzyme Q10 probably reduces the risk of all-cause mortality more than control (RR 0.58, 95% CI 0.35 to 0.95; 1 study, 420 participants; number needed to treat for an additional beneficial outcome (NNTB) 13.3; moderate-quality evidence). There was low-quality evidence of inconclusive results between the coenzyme Q10 and control groups for the risk of myocardial infarction (RR 1.62, 95% CI 0.27 to 9.59; 1 study, 420 participants), and stroke (RR 0.18, 95% CI 0.02 to 1.48; 1 study, 420 participants). Coenzyme Q10 probably reduces hospitalisation related to heart failure (RR 0.62, 95% CI 0.49 to 0.78; 2 studies, 1061 participants; NNTB 9.7; moderate-quality evidence). Very low-quality evidence suggests that coenzyme Q10 may improve the left ventricular ejection fraction (MD 1.77, 95% CI 0.09 to 3.44; 7 studies, 650 participants), but the results are inconclusive for exercise capacity (MD 48.23, 95% CI -24.75 to 121.20; 3 studies, 91 participants); and the risk of developing adverse events (RR 0.70, 95% CI 0.45 to 1.10; 2 studies, 568 participants). We downgraded the quality of the evidence mainly due to high risk of bias and imprecision. AUTHORS' CONCLUSIONS The included studies provide moderate-quality evidence that coenzyme Q10 probably reduces all-cause mortality and hospitalisation for heart failure. There is low-quality evidence of inconclusive results as to whether coenzyme Q10 has an effect on the risk of myocardial infarction, or stroke. Because of very low-quality evidence, it is very uncertain whether coenzyme Q10 has an effect on either left ventricular ejection fraction or exercise capacity. There is low-quality evidence that coenzyme Q10 may increase the risk of adverse effects, or have little to no difference. There is currently no convincing evidence to support or refute the use of coenzyme Q10 for heart failure. Future trials are needed to confirm our findings.
4.
Ultra-Processed Foods and Health Outcomes: A Narrative Review.
Elizabeth, L, Machado, P, Zinöcker, M, Baker, P, Lawrence, M
Nutrients. 2020;12(7)
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Ultra-processed food (UPF) is prevalent in diets world-wide. This review aims to look at the results of studies that have investigated associations between levels of UPF consumption and health outcomes on healthy participants. 43 studies were reviewed; studies covered all age groups (including children and adolescents) in a number of different countries. Studies looked at overweight, obesity and cardio-metabolic risks as outcomes as well as cancer, cardiovascular disease, type 2 diabetes, mortality, gastrointestinal disorders, depression, frailty and asthma. In 37 studies, there was at least one statistically significant association between UPF exposure and at least one adverse health outcome. No study reported an association between UPF exposure and beneficial health outcomes. This review has shown that a high intake of UPFs is associated with a range of adverse health outcomes, disorders and conditions. This has the potential to significantly influence the global burden of disease. As well as this; evidence suggests a higher risk of all-cause mortality with high consumption of UPFs. No study reported an association between UPF and beneficial health outcomes. The review has also shown beneficial outcomes were associated with diets higher in unprocessed and minimally processed foods.
Abstract
The nutrition literature and authoritative reports increasingly recognise the concept of ultra-processed foods (UPF), as a descriptor of unhealthy diets. UPFs are now prevalent in diets worldwide. This review aims to identify and appraise the studies on healthy participants that investigated associations between levels of UPF consumption and health outcomes. This involved a systematic search for extant literature; integration and interpretation of findings from diverse study types, populations, health outcomes and dietary assessments; and quality appraisal. Of 43 studies reviewed, 37 found dietary UPF exposure associated with at least one adverse health outcome. Among adults, these included overweight, obesity and cardio-metabolic risks; cancer, type-2 diabetes and cardiovascular diseases; irritable bowel syndrome, depression and frailty conditions; and all-cause mortality. Among children and adolescents, these included cardio-metabolic risks and asthma. No study reported an association between UPF and beneficial health outcomes. Most findings were derived from observational studies and evidence of plausible biological mechanisms to increase confidence in the veracity of these observed associations is steadily evolving. There is now a considerable body of evidence supporting the use of UPFs as a scientific concept to assess the 'healthiness' of foods within the context of dietary patterns and to help inform the development of dietary guidelines and nutrition policy actions.