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Polyphenols as potential metabolism mechanisms regulators in liver protection and liver cancer prevention.
Li, S, Yin, S, Ding, H, Shao, Y, Zhou, S, Pu, W, Han, L, Wang, T, Yu, H
Cell proliferation. 2023;56(1):e13346
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Multiple risk factors could lead to the development of liver cancer, one of the most common malignant tumours in the world. These risk factors include hepatitis infection, non-alcoholic fatty liver disease and excessive alcohol consumption. Polyphenols are bioactive compounds with antioxidant, anti-inflammatory, anti-mutagenic, anti-viral, hypoglycaemic, anti-hypertensive, antibacterial and anti-proliferative properties. Polyphenols may be effective in reducing the risk of developing liver cancer by altering the metabolism. This review evaluated the effectiveness of polyphenols in protecting the liver and inhibiting hepatocarcinoma development. In addition, the review evaluated several mechanisms by which polyphenols affect glucose and lipid metabolism and mitochondrial metabolism and reduce the effects of oxidative stress, inflammation and toxic metabolites. Further robust studies are required to assess the beneficial effects of polyphenols as a therapeutic agent, as the current knowledge is limited. However, healthcare professionals can use the results of this study to understand the protective effects of polyphenols against liver disease.
Abstract
BACKGROUND Liver cancer is one of the common malignancies. The dysregulation of metabolism is a driver of accelerated tumourigenesis. Metabolic changes are well documented to maintain tumour growth, proliferation and survival. Recently, a variety of polyphenols have been shown to have a crucial role both in liver disease prevention and metabolism regulation. METHODS We conducted a literature search and combined recent data with systematic analysis to comprehensively describe the molecular mechanisms that link polyphenols to metabolic regulation and their contribution in liver protection and liver cancer prevention. RESULTS Targeting metabolic dysregulation in organisms prevents and resists the development of liver cancer, which has important implications for identifying new therapeutic strategies for the management and treatment of cancer. Polyphenols are a class of complex compounds composed of multiple phenolic hydroxyl groups and are the main active ingredients of many natural plants. They mediate a broad spectrum of biological and pharmacological functions containing complex lipid metabolism, glucose metabolism, iron metabolism, intestinal flora imbalance, as well as the direct interaction of their metabolites with key cell-signalling proteins. A large number of studies have found that polyphenols affect the metabolism of organisms by interfering with a variety of intracellular signals, thereby protecting the liver and reducing the risk of liver cancer. CONCLUSION This review systematically illustrates that various polyphenols, including resveratrol, chlorogenic acid, caffeic acid, dihydromyricetin, quercetin, catechins, curcumin, etc., improve metabolic disorders through direct or indirect pathways to protect the liver and fight liver cancer.
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Plasma anthocyanins and their metabolites reduce in vitro migration of pancreatic cancer cells, PANC-1, in a FAK- and NF-kB dependent manner: Results from the ATTACH-study a randomized, controlled, crossover trial in healthy subjects.
Mostafa, H, Behrendt, I, Meroño, T, González-Domínguez, R, Fasshauer, M, Rudloff, S, Andres-Lacueva, C, Kuntz, S
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. 2023;158:114076
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Pancreatic cancer is commonly associated with poor prognosis and low overall five-year survival rate (5–7%) due to the early metastatic potential of pancreatic cancer cells. Strategies to improve the health outcomes in pancreatic cancer are challenging. The aims of this study where to investigate: - whether plasma metabolites, isolated after a 28-day intervention, would reduce migration of two pancreatic cancer cell lines (PANC-1 and AsPC-1); - whether expression of adhesion molecules on cancer and endothelial cells were influenced by plasma anthocyanins (ACN) metabolites; - which molecular mechanisms were involved; and - which metabolites in plasma and urine were altered during a long-term ACN intake and how they associate with the inhibitory effects on migration. This study is a randomised, double-blind, placebo-controlled, cross-over, 28-days intervention - ATTACH study (Anthocyanins Target Tumor cell Adhesion—Cancer vs. Endothelial Cell (HUVEC)). Thirty-five (female n = 27 and male n = 8) young, healthy volunteers participated in the intervention. Results show that ACN and metabolites isolated from plasma after a long-term ACN-rich juice intervention reduced the migration and expression of cell adhesion molecules in PANC-1 cancer cells in vitro through activation of two pathways [focal adhesion kinase- and nuclear factor kappa light chain enhancer of activated B cells (NF-kB)-pathways] as well as the reduction of reactive oxygen species. Authors conclude that their findings can lead to the investigation of interactions of ACNs with classical cancer prevention strategies.
Abstract
Pancreatic cancer is primarily considered to be a metastatic disease with a low 5-year survival rate. We aimed to detect if plasma-isolated anthocyanins and their metabolites (PAMs) modulate pancreatic cancer cells migration and to describe molecular targets of PAMs in this process. Plasma metabolites were isolated by solid-phase extraction before and after a 28-days intervention trial involving 35 healthy subjects comparing effects of a daily anthocyanin-rich juice intake vs. placebo. Plasma extracts were used for migration and mechanistic in vitro studies as well as for metabolomic analysis. Pancreatic PANC-1 and AsPC-1 were used for migration studies in a Boyden chamber co-cultured with endothelial cells. Expression of adhesion molecules on cancer and endothelial cells were determined by flow cytometry and NF-kB (nuclear factor-kappa B) p65 and focal adhesion kinase activation were measured by immunoassays. UHPLC-MS/MS metabolomics was done in plasma and urine samples. Plasma extracts isolated after the intake of the anthocyanin-rich juice significantly reduced PANC-1 migration, but not AsPC-1 migration. In PANC-1, and to a lower extent in endothelial cells, plasma extracts after juice intake decreased the expression of ß1- and ß4-integrins and intercellular adhesion molecule-1. Pooled plasma from volunteers with the highest inhibition of PANC-1 migration (n = 10) induced a reduction of NF-kB-p65 and FAK-phosphorylation in cancer and in endothelial cells. Concerning metabolites, 14 were significantly altered by juice intervention and PANC-1 migration was inversely associated with the increase of o-coumaric acid and peonidin-3-galactoside. PAMs were associated with lower PANC-1 cell migration opening new strategies for metastatic pancreatic cancer treatment.
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Resistance Exercise Training Increases Muscle Mass and Strength in Prostate Cancer Patients on Androgen Deprivation Therapy.
Houben, LHP, Overkamp, M, VAN Kraaij, P, Trommelen, J, VAN Roermund, JGH, DE Vries, P, DE Laet, K, VAN DER Meer, S, Mikkelsen, UR, Verdijk, LB, et al
Medicine and science in sports and exercise. 2023;55(4):614-624
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Androgen deprivation therapy (ADT) forms the cornerstone in the treatment of localised high-risk, locally advanced, and metastatic prostate cancer (PCa). The hypothesis of this study was that protein supplementation augments the benefits of prolonged resistance exercise training to attenuate the decline in muscle mass, reduce fat mass accrual, and increase strength and physical performance in PCa patients on ADT. This study is a multicentre partly randomised controlled trial, comparing two intervention groups with a separately recruited control group. One hundred and twenty-six patients were included, and ninety-six patients finished the study. Results show that 20 week of resistance exercise training was feasible, safe, and well tolerated, and effectively counteracted the negative effect of ADT treatment on body composition, muscle mass, leg strength, and aerobic capacity in men with advanced PCa. Protein supplementation did not further augment the benefits of resistance exercise training. Authors conclude that protein supplementation is not required to further augment gains in muscle mass and strength after resistance exercise training in PCa patients who habitually consume ample protein.
Abstract
PURPOSE This study aimed to assess the effects of 20 wk resistance exercise training with or without protein supplementation on body composition, muscle mass, muscle strength, physical performance, and aerobic capacity in prostate cancer patients receiving androgen deprivation therapy (ADT). METHODS Sixty prostate cancer patients receiving ADT were randomly assigned to perform 20 wk of resistance exercise training with supplementation of 31 g whey protein (EX + PRO, n = 30) or placebo (EX + PLA, n = 30), consumed immediately after exercise and every night before sleep. A separate control group (CON, n = 36) only received usual care. At baseline and after 20 wk, body composition (dual-energy x-ray absorptiometry), muscle mass (computed tomography scan), muscle strength (1-repetition maximum strength tests), physical performance (Timed Up and Go Test, 30-Second Chair Stand Test, and Stair Climb Test), aerobic capacity (cardiopulmonary exercise test), and habitual dietary intake (food diary) were assessed. Data were analyzed using a two-factor repeated-measures ANOVA. RESULTS Over time, muscle mass and strength increased in EX + PRO and EX + PLA and decreased in CON. Total fat mass and fat percentage increased in EX + PRO and CON, but not in EX + PLA. Physical performance did not significantly change over time in either group. Aerobic capacity was maintained in EX + PLA, but it decreased in EX + PRO and CON. Habitual protein intake (without supplements) averaged >1.0 g·kg body weight -1 ·d -1 , with no differences over time or between groups. CONCLUSIONS In prostate cancer patients, resistance exercise training counteracts the adverse effects of ADT on body composition, muscle mass, muscle strength, and aerobic capacity, with no additional benefits of protein supplementation.
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Influence of methyl donor nutrients as epigenetic regulators in colorectal cancer: A systematic review of observational studies.
Chávez-Hidalgo, LP, Martín-Fernández-de-Labastida, S, M de Pancorbo, M, Arroyo-Izaga, M
World journal of gastroenterology. 2023;29(7):1219-1234
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Colorectal cancer (CRC) is the third most frequent type of cancer and yet has the second highest mortality rate in cancer patients worldwide. Hence there is an urgency to understand more about dietary and lifestyle factors that can help to prevent this type of cancer. It is known that folate has a preventive function in CRC, possibly due to its role in DNA methylation. Methylation is the addition of methyl groups to DNA, which influences gene expression and regulation. This systematic review investigated how folate and other dietary methyl groups and methyl influencers such as B vitamins and alcohol influence the development of CRC, whilst also considering various genetic variants in methyl-metabolising enzymes (polymorphisms). The analysis included a total of 19 case-control and cohort studies and highlighted that potential interactions between methyl donor nutrients, genetic variants, and alcohol influence CRC risk. For most, high levels of folate intake were considered a protective factor, while high alcohol consumption proved to be a risk factor. Yet these interactions appear to be complex, with gender, genetic variations and folate status appearing to contribute to variable and, in some cases, contradictory outcomes. The authors suggested in their findings that Vitamin B6, Vitamin B3 (Niacin), and alcohol may affect CRC by influencing its risk by acting on both the genetic code itself and the epigenetic factors that control gene activity. Further research is needed to better understand the complexity of these mechanisms, and to help clarify the influence of methyl group donors as epigenetic regulators of gene activity in CRC development.
Abstract
BACKGROUND Dietary methyl donors might influence DNA methylation during carcinogenesis of colorectal cancer (CRC). However, whether the influence of methyl donor intake is modified by polymorphisms in such epigenetic regulators is still unclear. AIM: To improve the current understanding of the molecular basis of CRC. METHODS A literature search in the Medline database, Reference Citation Analysis (https:// www.referencecitationanalysis.com/), and manual reference screening were performed to identify observational studies published from inception to May 2022. RESULTS A total of fourteen case-control studies and five cohort studies were identified. These studies included information on dietary methyl donors, dietary components that potentially modulate the bioavailability of methyl groups, genetic variants of methyl metabolizing enzymes, and/or markers of CpG island methylator phenotype and/or microsatellite instability, and their possible interactions on CRC risk. CONCLUSION Several studies have suggested interactions between methylenetetrahydrofolate reductase polymorphisms, methyl donor nutrients (such as folate) and alcohol on CRC risk. Moreover, vitamin B6, niacin, and alcohol may affect CRC risk through not only genetic but also epigenetic regulation. Identification of specific mechanisms in these interactions associated with CRC may assist in developing targeted prevention strategies for individuals at the highest risk of developing CRC.
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Consumption of industrial processed foods and risk of premenopausal breast cancer among Latin American women: the PRECAMA study.
Romieu, I, Khandpur, N, Katsikari, A, Biessy, C, Torres-Mejía, G, Ángeles-Llerenas, A, Alvarado-Cabrero, I, Sánchez, GI, Maldonado, ME, Porras, C, et al
BMJ nutrition, prevention & health. 2022;5(1):1-9
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Ultra-processed food intake has been linked to an increased risk of breast cancer in Western populations. This is the first study on ultra-processed food and breast cancer in young women from Latin America. In Latin America around 27% of breast cancers occur between 20 and 45 years and this is increasing. This population is currently undergoing rapid lifestyle and nutritional changes switching from a varied traditional diet (including corn tortillas, corn flour cakes, beans and other legumes, soup, homemade stew, vegetable, whole fruit) towards a more homogenous diet rich in industrial ultra-processed foods. In this case control study, the association of ultra-processed food intake to breast cancer risk was evaluated. 525 cases were included (women aged 20–45 years) and 525 matched population-based controls from Chile, Colombia, Costa Rica and Mexico. The degree of processing of foods was classified according to the NOVA classification. The results show an adverse effect of ultra-processed food intake on the risk of breast cancer in young Latin American women. Further studies are needed to confirm the results. Given the already proven chronic adverse health effects of ultra-processed foods, a decrease in these types of foods should be encouraged.
Abstract
Ultra-processed food intake has been linked to an increased risk of breast cancer in Western populations. No data are available in the Latin American population although the consumption of ultra-processed foods is increasing rapidly in this region. We evaluated the association of ultra-processed food intake to breast cancer risk in a case-control study including 525 cases (women aged 20-45 years) and 525 matched population-based controls from Chile, Colombia, Costa Rica and Mexico. The degree of processing of foods was classified according to the NOVA classification. Overall, the major contributors to ultra-processed food intake were ready-to-eat/heat foods (18.2%), cakes and desserts (16.7%), carbonated and industrial fruit juice beverages (16.7%), breakfast cereals (12.9%), sausages and reconstituted meat products (12.1%), industrial bread (6.1%), dairy products and derivatives (7.6%) and package savoury snacks (6.1%). Ultra-processed food intake was positively associated with the risk of breast cancer in adjusted models (OR T3-T1=1.93; 95% CI=1.11 to 3.35). Specifically, a higher risk was observed with oestrogen receptor positive breast cancer (ORT3-T1=2.44, (95% CI=1.01 to 5.90, P-trend=0.049), while no significant association was observed with oestrogen receptor negative breast cancer (ORT3-T1=1.87, 95% CI=0.43 to 8.13, P-trend=0.36). Our findings suggest that the consumption of ultra-processed foods might increase the risk of breast cancer in young women in Latin America. Further studies should confirm these findings and disentangle specific mechanisms relating ultra-processed food intake and carcinogenic processes in the breast.
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Effect of Tart Cherry on Aromatase Inhibitor-Induced Arthralgia (AIA) in Nonmetastatic Hormone-Positive Breast Cancer Patients: A Randomized Double-Blind Placebo-Controlled Trial.
Shenouda, M, Copley, R, Pacioles, T, Lebowicz, Y, Jamil, M, Akpanudo, S, Tirona, MT
Clinical breast cancer. 2022;22(1):e30-e36
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Aromatase inhibitors (AIs) are used as a treatment in breast cancer; however, a side effect of their use is often the development of aromatase inhibitor induced arthralgia (AIA), which manifests as pain in the joints, muscle weakness and reduced grip strength. Subsequently, many individuals stop taking AIs, resulting in poorer disease prognosis. Tart cherries (TC) have been shown in studies to help relieve joint pain and pain associated with exercise and so this RCT aimed to determine the effect of TC consumption on 60 breast cancer patients with AIA. The results showed that after 6-weeks individuals given TC had less pain, with some individuals reporting no pain at all. It was concluded that TC is a reliable and safe option for the management of AIA in breast cancer patients. This study could be used by healthcare professionals to recommend TC as an adjunct to aromatase inhibitor therapy in individuals with breast cancer who are experiencing pain.
Abstract
BACKGROUND Aromatase Inhibitor induced Arthralgia (AIA) can cause noncompliance leading to decreased breast-cancer survival. Effective interventions for AIA are limited. Tart cherry (TC) showed beneficial effect on musculoskeletal pain. 48 patients (Pts) randomized to TC versus placebo over 6 weeks, TC (23pts) had 34.7% mean pain decrease versus 1.4% in Placebo (25pts). TC can improve AIA in nonmetastatic breast-cancer patients. METHODS Randomized, placebo-controlled, double-blind trial. Eligible patients with NMHPBC on AI for at least 4 weeks were randomized to TC concentrate [50 tart cherries] vs. placebo (P) [syrup] in 1:1 model. Patients instructed to consume 1 Oz of concentrate in 8 Oz water daily for 6 weeks, and document their pain intensity at baseline, weekly and at study completion in a diary using Visual Analog Scale (VAS), with 0 mm indicating no pain, and 100 mm indicating highest pain. RESULTS Sixty patients were enrolled. Two patients did not complete the study due to diarrhea, and 10 patients were noncompliant. Forty-eight patients were included in the final analysis. TC group (23 pts) had 34.7% mean decrease in pain compared to 1.4% in P group (25 pts). This difference was statistically significant (Mann-Whitney U Test, P = .034). CONCLUSIONS Tart cherry can significantly improve AIA in nonmetastatic breast cancer patient.
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Mycotoxin-Linked Mutations and Cancer Risk: A Global Health Issue.
Ekwomadu, T, Mwanza, M, Musekiwa, A
International journal of environmental research and public health. 2022;19(13)
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Mycotoxins are toxic substances produced by fungi, which can be found in common foods like maize, wheat, nuts, and foods containing them. Mycotoxins such as aflatoxins, ochratoxin, fumonisins, zearalenone, and some Penicillium toxins can alter genetic material. According to previous studies, they can damage genetic material and affect cell growth. Usage of chemicals such as fertilizers and fungicides is a common practice in the agricultural industry to protect plants from fungus and to feed them. However, fungicides can accelerate mycotoxin production. 16 studies were included in this Systematic Review and 11 in Meta-Analysis. This research looked at the harmful effects of mycotoxins such as aflatoxins, fumonisins, ochratoxin, T2, zearalenone, and some Penicillium toxins in causing cancers. The researchers evaluated the link between aflatoxin exposure and liver cancer, fumonisin B1 exposure and liver cancer, zearalenone exposure and breast cancer, zearalenone exposure and cervical cancer, citrinine and patulin exposure and colorectal cancer, and NEO, HT-2, and T-2 exposure and Oesophageal cancer. This research did not show significant associations between various mycotoxins and cancer risk. As currently, most studies are primarily focused on aflatoxin; more robust studies are needed to assess the cancer risk associated with different mycotoxin exposure. Using the results of this study, healthcare professionals can gain a better understanding of how mycotoxins affect our bodies.
Abstract
Humans continue to be constantly exposed to mycotoxins, mainly through oral exposure (dietary), inhalation, or dermal contact. Recently, it has been of increasing interest to investigate mycotoxin-linked carcinogenicity. This systematic review was conducted to synthesize evidence of the association between mycotoxin-linked mutations and the risk of cancer, to provide an overview of the data linking exposure to different mycotoxins with human cancer risk, and to provide an update on current research on the risk of cancer associated with human exposure to mycotoxins. PRISMA guidelines were used when conducting the systematic review. PubMed, MEDLINE, and CINAHL electronic databases were comprehensively searched to extract the relevant studies published from inception to May 2022. A total of sixteen relevant studies (4907 participants) were identified and included in this review. Of these, twelve studies were from Asia, while four of the studies were conducted in Africa. The overall meta-analysis result found no significant association, although some of the studies confirmed an association between mycotoxin-linked mutations and primary liver cancer risk. Mainly, the experimental studies have shown associations between mycotoxin-linked mutations and cancer risk, and there is a need for researchers to confirm these links in epidemiological studies in order to guide public health policies and interventions.
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Association of Retinol and Carotenoids Content in Diet and Serum With Risk for Colorectal Cancer: A Meta-Analysis.
Han, X, Zhao, R, Zhang, G, Jiao, Y, Wang, Y, Wang, D, Cai, H
Frontiers in nutrition. 2022;9:918777
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The incident rate of malignant tumours has been increasing, and so has colo-rectal cancer (CRC), which is now the third most frequent cancer and the second most common cause of cancer death. CRC development is influenced by environmental and genetic factors. Diet, diabetes, obesity, lack of physical activity, age, family history and history of benign adenomatous polyps and inflammatory bowel disease are all known risk factors. Modulating diet is one way to modify cancer risk. Vitamin A (retinol) and carotenoids, which are precursors to Vitamin A, are indispensable in the human body and widely occur in a range of vegetables, fruits and animal-derived foods. In some studies high dietary intake of retinol and carotenoids had been linked to a decreased risk of CRC, however, this was not consistent in all findings. To get a better understanding of this matter, the authors of this meta-analysis analysed 22 clinical studies from the last 20 years. The authors found an inverse association with carotenoids in blood serum, so higher blood serum of carotenoids seemed to decrease CRC risk. In regards to dietary intake, total carotenoid intake did not increase CRC risk and in fact the carotenoids carotenes, lycopene, and β-cryptoxanthin reduced risk, which was particularly noticeable in men. In women, high dietary intake of retinol also showed to reduce CRC risk, but it appeared to increase the risk in men. This raised the idea of gender-specific differences. Of clinical relevance are that carotenoids can be an important dietary contributors in reducing CRC risk. However the protective role of retinol appears to be gender-specific and only seems to benefit women, with the opposite effect in men.
Expert Review
Conflicts of interest:
None
Take Home Message:
The results of this study were mixed:
- Total dietary intake of carotenoids was not associated with CRC risk.
- Case control studies found that high serum carotenoids may increase CRC risk.
- There were differences in findings between males and females.
- Larger, well-controlled studies over long time frames are needed to further explore the relationship between dietary intake and serum concentrations of carotenoids and retinol with CRC. These studies should include results by sex, race and dose response.
Evidence Category:
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X
A: Meta-analyses, position-stands, randomized-controlled trials (RCTs)
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B: Systematic reviews including RCTs of limited number
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C: Non-randomized trials, observational studies, narrative reviews
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D: Case-reports, evidence-based clinical findings
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E: Opinion piece, other
Summary Review:
Colorectal cancer (CRC) is the third most common cancer worldwide, and second in terms of mortality. Diet and environmental factors may have a strong influence and causative effect. Research has linked dietary consumption and serum levels of carotenoids and retinol with CRC. However, results have been mixed.
The aim of this meta analysis was to identify a potential association between CRC and carotenoid and retinol intake. A total of 22 cohort and case control studies published between 2000-2019 from across Europe, North America and Asia were included. The number of CRC cases totalled 19,293 from a sample of more than 450,000 people.
Eligible studies reported data in either relative risk (RR) or odds ratios (OR) with 95% confidence intervals (95% CI). In the meta analysis, data were combined and expressed as OR with 95% CI.
Cases and control groups were based on high or low carotenoid intake as defined by the included studies and based on dietary intake or serum concentration. Sub-group analysis was undertaken by study type, sex and tumour type. A sensitivity analysis tested the robustness of the results.
Due to the heterogeneity between studies, adjustments were made for potential covariates and confounding factors including age, gender, a family history of CRC, smoking, alcohol consumption and levels of physical activity.
The quality of the studies was assessed against predefined inclusion and exclusion criteria and scored using the Newcastle-Ottawa Scale (NOS).
The nutrients studied included; beta-carotene, alpha-carotene, lycopene, lutein/zeaxanthin, beta-cryptoxanthin and retinol. These were assessed through dietary intake or serum concentrations.
Key Findings
- High dietary intake of beta-carotene was not associated with an increased risk of CRC in females (OR = 0.97; 95%CI 0.79-1.19), however, it may lower CRC risk in males (OR = 0.74; 95% CI 0.55-0.99).
- High dietary intake of retinol was not associated with CRC risk (OR = 0.99; 95% CI 0.89-1.10). However, the findings suggested that it may reduce CRC risk in females but increase CRC risk in males.
- There was a tendency towards a slightly decreased risk of CRC with high dietary intakes of alpha-carotene), lycopene, and beta-cryptoxanthin. The results were more pronounced in males.
- No association was found between high consumption of high lutein/zeaxanthin, retinol or total carotenoids and the risk of CRC
- Case control studies found a negative association between serum carotenoids and CRC risk. This relationship was not found in cohort studies and therefore remains uncertain.
Conclusions
This was a well-conducted meta-analysis that was not subject to any conflicts of interest. Larger, well controlled prospective studies adjusting for sex and with long-term follow-up are needed to confirm the relationship between dietary intake and serum levels of carotenoids and CRC.
Notes: The authors had no conflicts of interest to disclose.
Clinical practice applications:
- Healthcare practitioners working with people with a family history of CRC or those who may be at increased risk may like to consider increasing carotenoid intake modestly.
- A modest increase in dietary intake of beta-carotene for males may be beneficial.
- A modest increase in dietary retinol may be beneficial for females.
Considerations for future research:
- Further research is needed to explore the differences between sexes for dietary intake of carotenoids and retinol and CRC risk
- Further studies are needed to investigate the relationship between serum carotenoids and CRC
- Analysis of results by race and continent may be beneficial
- Further research is needed to define dose response
- Due to heterogeneity between studies, large, well controlled studies over long time frames are needed
Abstract
Background: Colorectal cancer (CRC) risk is linked to serum and dietary retinol and carotenoids, according to clinical and epidemiological research. However, the findings are not consistent. As a result, we did this meta-analysis to determine the link between them. Methods: From 2000 through 2022, the PubMed, Web of Science, and Embase databases, as well as pertinent article references, were searched and filtered based on inclusion and exclusion criteria and literature quality ratings. High and low intake were used as controls, and OR (odds ratio) or RR (relative risk) and 95% confidence interval were extracted. The extracted data were plotted and analyzed using Stata12.0 software. Results: A total of 22 relevant studies were included, including 18 studies related to diet and 4 studies related to serum. For high and low intake or concentration controls, the pooled OR was as follows: β-carotene (OR = 0.89, 95% CI: 0.78-1.03), α-carotene (OR = 0.87, 95% CI: 0.72-1.03), lycopene (OR = 0.93, 95% CI: 0.81-1.07), lutein/zeaxanthin (OR = 0.96, 95% CI: 0.87-1.07), β-cryptoxanthin (OR = 0.70, 95% CI: 0.48-1.01), total carotenoids (OR = 0.97, 95% CI: 0.81-1.15), retinol (OR = 0.99, 95% CI: 0.89-1.10), serum carotenoids (OR = 0.73, 95% CI: 0.58-0.93), serum retinol (OR = 0.62, 95% CI: 0.26-1.49). Subgroup analysis was performed according to tumor type, study type and sex. Conclusion: Total carotenoid intake and Lutein/Zeaxanthin intake were not associated with CRC risk. High β-carotene, α-carotene, lycopene, and β-cryptoxanthin all tended to reduce CRC risk. Serum carotenoid concentrations were significantly inversely associated with CRC risk.
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The Dose-Response Associations of Sugar-Sweetened Beverage Intake with the Risk of Stroke, Depression, Cancer, and Cause-Specific Mortality: A Systematic Review and Meta-Analysis of Prospective Studies.
Wang, Y, Zhao, R, Wang, B, Zhao, C, Zhu, B, Tian, X
Nutrients. 2022;14(4)
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The consumption of sugar-sweetened beverages is high in today's society, which may lead to weight gain, inflammation, and a number of obesity-associated diseases. The objective of this systematic review and meta-analysis was to investigate the associations and causal links between the consumption of sugar-sweetened beverages and cancer, stroke, depression, and cause-specific mortality. Consumption of sugar-sweetened beverages significantly increased the risk of cancer, strokes, depression, and cause-specific mortality when compared with the consumption of low or no-sugar-sweetened beverages. As little as a 250ml increment of sugar-sweetened beverages was associated with an increase in risk. Consumption of sugar-sweetened beverages increases the risk of ischemic stroke by 10%, CVD-caused mortality by 13%, and cancer-caused mortality by 6.0% compared to those who consume less or no sugar-sweetened beverages. These findings can be used by healthcare professionals to understand the clinical significance of intervention strategies that reduce the consumption of sugar-sweetened beverages. It is imperative to conduct additional robust studies as there is an insufficient amount of evidence at present to establish a causal connection between the consumption of sugary beverages and the risk of depression, stroke, cancer, and cause-specific mortality.
Abstract
The associations between sugar-sweetened beverage (SSB) consumption and the risk of stroke, depression, cancer, and cause-specific mortality have not been determined, and the quantitative aspects of this link remain unclear. This meta-analysis therefore conducted a systematic review and dose-response analysis to determine their causal links. The database searches were conducted in PubMed, Cochrane library, Embase, Web of Science up to 10 November 2021. The intervention effects were evaluated by relative risk (RR) with 95% confidences (CI). Thirty-two articles met the inclusion criteria. Higher levels of SSB consumption significantly increased the risk of stroke (RR 1.12, 95% CI 1.03-1.23), depression (1.25, 1.11-1.41), cancer (1.10, 1.03-1.17), and all-cause mortality (1.08, 1.05-1.11) compared with none or lower SSB intake. The associations were dose-dependent, with per 250 mL increment of SSB intake daily increasing the risk of stroke, depression, cancer, and all-cause mortality by RR 1.09 (1.03-1.15), 1.08 (1.06-1.10), 1.17 (1.04-1.32), and 1.07 (1.03-1.11), respectively. The link was curved for depression and cancer risk (pnon-linear < 0.05). Subgroup analysis suggested that higher SSB intake increased ischemic stroke by 10%, CVD-caused mortality by 13%, and cancer-caused mortality by 6.0% than none or lower SSB consumption. It is suggested that SSB accounts for a leading risk factor of stroke, depression, cancer, and mortality, and that the risk rises in parallel with the increment of SSB intake (and is affected by participant characteristics).
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10.
Lipid Intake and Breast Cancer Risk: Is There a Link? A New Focus and Meta-Analysis.
Lodi, M, Kiehl, A, Qu, FL, Gabriele, V, Tomasetto, C, Mathelin, C
European journal of breast health. 2022;18(2):108-126
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Incidence of breast cancer is the leading cause of cancer-related mortality, accounting for 15.5% of all cancer-related deaths. However, there is a lack of complete understanding of the effects of different types of dietary lipids on breast cancer development, such as saturated fatty acids (SFA), monounsaturated fatty acids (MUFA), dietary cholesterol, polyunsaturated fatty acids (PUFA), and unsaturated trans fatty acids (TFA). An evaluation of the effect of lipid consumption on breast cancer and the impact it has on menopausal status was conducted in this meta-analysis, which included forty-four studies. Increased saturated fatty acid intake was associated with an increased risk of breast cancer in postmenopausal women. However, breast cancer risk was not associated with increased consumption of total fat, SFA, MUFA, PUFA, and cholesterol in premenopausal women. The effects of estrogen and the release of proinflammatory cytokines by adipocytes should be evaluated, as well as other pathways that contribute to the development of breast cancer. There is a need for further robust studies to evaluate the effects of different types of lipid consumption on breast cancer. Although the association between SFA and breast cancer is weak, healthcare professionals can use this study's findings to better understand the detrimental effect of SFA, despite the fact that there is a great deal of heterogeneity in the current analysis.
Expert Review
Conflicts of interest:
None
Take Home Message:
- The authors found no association between total fat, saturated fatty-acids, mono and poly-unsaturated fatty acids and cholesterol intake and breast cancer incidence in the general population and in pre-menopausal women.
Evidence Category:
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X
A: Meta-analyses, position-stands, randomized-controlled trials (RCTs)
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B: Systematic reviews including RCTs of limited number
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C: Non-randomized trials, observational studies, narrative reviews
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D: Case-reports, evidence-based clinical findings
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E: Opinion piece, other
Summary Review:
- Among lifestyle-related breast cancer risk factors, the role of diet in breast cancer remains uncertain.
- The authors highlight a weak association between high SFA consumption and breast cancer risk in post-menopausal women.
- The authors found no association between total fat, saturated fatty-acids, mono and poly-unsaturated fatty acids and cholesterol intake and breast cancer incidence in the general population and in pre-menopausal women.
Objectives
- To determine if there is an association between total lipid intake, saturated fatty acid (SFA), Poly- and Mono-Unsaturated Fatty Acid (PUFA and MUFA) and cholesterol intake and breast cancer risk.
Results
- Forty-four articles were included in the meta-analysis, consisting of 28 case-control studies and 16 cohort studies.
- In total, this meta-analysis involved 1,185,896 women, of whom 54,553 had breast cancer.
- There was no association between total fat, SFA, MUFA, PUFA and cholesterol intake and breast cancer in the general population and in pre-menopausal women.
- In postmenopausal women, high SFA consumption was associated with increased breast cancer risk in case-control studies [relative risk (RR): 1.12; confidence interval (CI) 95%: 1.03–1.21; p = 0.006 but not in cohort studies (RR: 1.01; CI 95%: 0.85–1.19; p = 0.93).
Limitations
- Studies included in the meta-analysis were carried out on populations from five continents with significant cultural and dietary diversity, and well as different types of oils used in the diet
Conclusion
- At this stage, the authors state it is not possible to establish nutritional recommendations regarding the consumption of lipids to decrease breast cancer risk.
Clinical practice applications:
- The results of this meta-analysis does not demonstrate a statistically significant link between high consumption of total lipids, PUFA, MUFA and cholesterol and the occurrence of breast cancer.
- However, the results suggest that there is an association between SFA intake and breast cancer risk in postmenopausal women, although this was only found in case-controlled studies and not cohort studies.
- While obesity is a known breast cancer risk factor after menopause, the link between the effect of diet and the effect of obesity on the breast may be through different mechanisms.
- The authors investigated if high lipid consumption acts on breast tissue by the same mechanisms as obesity, and found the association between SFA intake and breast cancer risk in postmenopausal women must be through other biological explanations.
- The authors found that while high SFA consumption may increase breast cancer risk among post-menopausal women, biological mechanisms linking SFA and breast cancerogenesis are still unknown.
- The meta-analysis found high blood cholesterol levels appear to increase the risk of breast cancer. However, the authors could not confirm that high dietary cholesterol intake is a risk factor for breast cancer. The authors postulated this may be in part due to the low proportion of cholesterol (about 30%) in the diet, while the rest comes from the degradation of lipids and carbohydrates by the liver.
Considerations for future research:
- As lipids can have different actions in the same family, studies should rather focus on specific lipid consumption
Abstract
Objective: To determine if there is an association between total lipid intake, saturated fatty acid (SFA), Poly- and Mono-Unsaturated Fatty Acid (PUFA and MUFA) and cholesterol intake and breast cancer risk. Materials and Methods: We conducted a systematic review of the literature and a meta-analysis following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. We included all cohort and case-control studies published up to December 2020 with subgroup analysis according to menopausal status. Results: We included 44 articles for analysis. There was no association between total fat, SFA, MUFA, PUFA and cholesterol intake and breast cancer in the general population and in pre-menopausal women. In postmenopausal women, high SFA consumption was associated with increased breast cancer risk in case-control studies [relative risk (RR): 1.12; confidence interval (CI) 95%: 1.03-1.21; p = 0.006 but not in cohort studies (RR: 1.01; CI 95%: 0.85-1.19; p = 0.93). Conclusion: There was a weak association between high SFA consumption and breast cancer risk in post-menopausal women, however there was high heterogeneity for this analysis. As lipids can have different actions in the same family, studies should rather focus on specific lipid consumption.