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Ultra-processed Foods and Drinks - NED Infobite
BANT's scientific NED InfoBites are designed to provide key elements of the latest research using plain language. They provide quick overviews on particular health issues and nutrition topics for a speedy introduction to the science. Visually attractive and easily shareable with clients and social media followers.
2024
Abstract
Ultra-processed foods and drinks (UPF) are mostly or entirely lacking in whole foods and fibre and are often high is salt, fat, sugars and chemical additives. Regular consumption of these foods and drinks has been associated with obesity and metabolic dysregulation. This NED Infobite includes articles on childhood health impacts of UPF consumption and associations between UPFs and Type 2 diabetes, hypertension and low-grade inflammation.
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Unhealthy Food and Beverage Consumption in Children and Risk of Overweight and Obesity: A Systematic Review and Meta-analysis.
Rousham, EK, Goudet, S, Markey, O, Griffiths, P, Boxer, B, Carroll, C, Petherick, ES, Pradeilles, R
Advances in nutrition (Bethesda, Md.). 2022
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Plain language summary
Infants and children are consuming increasing amounts of foods with added sugars, high in salt, and high in saturated or trans fats. Commercially prepared foods are more likely to be high in energy, low in nutrients (energy dense, nutrient-poor), and ultra-processed. The aim of this study was to examine, in children aged ≤10.9 y, the risks of greater consumption of unhealthy foods and beverages compared with no or low consumption on overweight and obesity. This study is a systematic review and meta-analysis which included the summarized characterises of 71 articles from 60 included studies. Results indicate that in children aged ≤10.9 years, consumption of sugar-sweetened beverages and unhealthy foods may increase body mass index, percentage body fat, or the odds of overweight/obesity (low to very-low certainty). Furthermore, there was little or no difference to body mass index, percentage body fat, or overweight/obesity outcomes (low certainty) after consumption of artificially sweetened beverages and 100% fruit juices. Authors conclude that policy recommendations are needed to address the growing burden of overweight and obesity that children are experiencing worldwide.
Abstract
This WHO-commissioned review contributed to the update of complementary feeding recommendations, synthesizing evidence on effects of unhealthy food and beverage consumption in children on overweight and obesity. We searched PubMed (Medline), Cochrane CENTRAL and Embase for articles, irrespective of language or geography. Inclusion criteria were: 1) randomized controlled trials (RCTs); non-RCTs; cohort studies and pre/post studies with control; 2) participants ≤ 10.9 y at exposure; 3) studies reporting greater consumption of unhealthy foods/beverages vs. no or low consumption; 4) studies assessing anthropometric and/or body composition; and 5) publication date ≥ 1971. Unhealthy foods and beverages were defined using nutrient- and food-based approaches. Risk of bias was assessed using the ROBINS-I and RoB2 tools for non-randomized and randomized studies, respectively. Narrative synthesis was complemented by meta-analyses where appropriate. Certainty of evidence was assessed using GRADE. Of 26,542 identified citations, 60 studies from 71 articles were included. Most studies were observational (59/60), and no included studies were from low-income countries. The evidence base was low quality, as assessed by ROBINS-I and RoB2 tools. Evidence synthesis was limited by the different interventions and comparators across studies. Evidence indicated that consumption of sugar-sweetened beverages (SSB) and unhealthy foods in childhood may increase body mass index (BMI)/BMI z-score, % body fat or odds of overweight/obesity (low certainty of evidence). Artificially-sweetened beverages and 100% fruit juice consumption may make little/no difference to BMI, % body fat or overweight/obesity outcomes (low certainty of evidence). Meta-analyses of a subset of studies indicated a positive association between SSB intake and % body fat, but no association with change in BMI and BMI z-score. High-quality epidemiological studies that are designed to assess the effects of unhealthy food consumption during childhood on risk of overweight/obesity are needed to contribute to a more robust evidence base upon which to design policy recommendations. This protocol was registered at https://www.crd.york.ac.uk/PROSPERO as CRD42020218109.
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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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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.
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Association between dietary inflammatory index and oral cancer risk: A systematic review and dose-response meta-analysis.
Luo, Z, Zhu, X, Hu, Y, Yan, S, Chen, L
Frontiers in oncology. 2022;12:920452
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Oral cancer is the most prevalent subtype of head and neck cancers. Inflammation and oxidative stress triggered by certain dietary components may be a potential mechanism for oral cancer. The aim of this study was to comprehensively assess the dose–response relationship between dietary inflammatory index (DII) and oral cancer risk. This study is a systematic review and meta-analysis of five studies. The studies were all case–control studies with a total of 1,278 cases and 5,137 controls. Results show that a more pro-inflammatory diet, represented by the higher DII score, was associated with an elevated risk of oral cancer. Authors conclude that reducing pro-inflammatory food components and promoting anti-inflammatory food components would be beneficial in the prevention and control of oral cancer.
Abstract
Background: Dietary inflammatory index (DII) has been suggested to be associated with oral cancer risk. However, a quantitative comprehensive assessment of the dose-response relationship has not been reported. We performed a meta-analysis to clarify the risk of oral cancer with DII. Methods: We searched PubMed, Embase, Cochrane Library, and Web of Science databases for relevant articles published up to 1 March 2022. Fixed- or random-effects models were utilized to estimate the pooled odds ratio (OR) of oral cancer with DII, as appropriate. Restricted cubic splines were used to model the dose-response relationship. Results: We included five case-control studies involving 1,278 cases and 5,137 controls in the meta-analysis. Risk of oral cancer was increased by 135% with the highest versus lowest DII level [OR: 2.35, 95% confidence interval (CI): 1.88-2.94], and 79% with higher versus lower DII level (OR: 1.79, 95% CI: 1.49-2.15). We found no evidence of a nonlinear dose-response association of DII with oral cancer (pnon-linearity = 0.752), and the risk was increased by 17% (OR: 1.17, 95% CI: 1.05-1.30) with 1 unit increment in DII score. Conclusion: This meta-analysis suggested that a higher DII score was associated with increased risk of oral cancer. Therefore, reducing pro-inflammatory components and promoting anti-inflammatory components of diet may be effective in the prevention of oral cancer.
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Nutrients, Genetic Factors, and Their Interaction in Non-Alcoholic Fatty Liver Disease and Cardiovascular Disease.
Lombardi, R, Iuculano, F, Pallini, G, Fargion, S, Fracanzani, AL
International journal of molecular sciences. 2020;21(22)
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Non-alcoholic fatty liver disease (NAFLD) and heart disease are influenced by diet and genetics. NAFLD cannot be managed with drugs and so lifestyle modification is the main recommendation, which is also advised in heart disease. The aim of this large review of 176 papers was to discuss the role of nutrients and genetics in NAFLD and heart disease. Amongst the main nutrients, excess fructose (a simple sugar) and high saturated and trans-fats were all shown to contribute to the development of both diseases. The influence of protein on NAFLD is controversial. Animal studies suggest that protein can be of benefit, but studies on humans have failed to support this. This is similar for heart disease where large scale trials in humans are not definitive. The role of fibre in NAFLD and heart disease appears to be beneficial. Several micronutrients were also reviewed including vitamins D, K, curcumin, plant chemicals and caffeine. The complex interplay involving genetics was also discussed and although fairly new science, evidence is mounting in support of genetic considerations when making dietary recommendations. It was concluded that diet and genetics influence the development of NAFLD, and heart disease and dietary recommendations need to reflect this. This study could be used by health care professionals to understand the interaction between diet and genetics and the importance of making personalised nutrition recommendations to individuals with NAFLD or heart disease.
Abstract
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in Western countries and expose patients to increased risk of hepatic and cardiovascular (CV) morbidity and mortality. Both environmental factors and genetic predisposition contribute to the risk. An inappropriate diet, rich in refined carbohydrates, especially fructose, and saturated fats, and poor in fibers, polyunsaturated fats, and vitamins is one of the main key factors, as well as the polymorphism of patatin-like phospholipase domain containing 3 (PNPLA3 gene) for NAFLD and the apolipoproteins and the peroxisome proliferator-activated receptor (PPAR) family for the cardiovascular damage. Beyond genetic influence, also epigenetics modifications are responsible for various clinical manifestations of both hepatic and CV disease. Interestingly, data are accumulating on the interplay between diet and genetic and epigenetic modifications, modulating pathogenetic pathways in NAFLD and CV disease. We report the main evidence from literature on the influence of both macro and micronutrients in NAFLD and CV damage and the role of genetics either alone or combined with diet in increasing the risk of developing both diseases. Understanding the interaction between metabolic alterations, genetics and diet are essential to treat the diseases and tailoring nutritional therapy to control NAFLD and CV risk.