Nutritional composition of ultra-processed plant-based foods in the out-of-home environment: a multi-country survey with plant-based burgers.

Ultra-processed plant-based foods, such as plant-based burgers, have gained in popularity. Particularly in the out-of-home (OOH) environment, evidence regarding their nutritional profile and environmental sustainability is still evolving. Plant-based burgers available at selected OOH sites were randomly sampled in Amsterdam, Copenhagen, Lisbon and London. Plant-based burgers (patty, bread and condiment) (n 41) were lab analysed for their energy, macronutrients, amino acids and minerals content per 100 g and serving and were compared with reference values. For the plant-based burgers, the median values per 100 g were 234 kcal, 20·8 g carbohydrates, 3·5 g dietary fibre and 12·0 g fat, including 0·08 g TFS and 2·2 g SFA. Protein content was 8·9 g/100 g, with low protein quality according to amino acid composition. Median Na content was 389 mg/100 g, equivalent to 1 g salt. Compared with references, the median serving provided 31% of energy intake based on a 2000 kcal per day and contributed to carbohydrates (17-28%), dietary fibre (42%), protein (40%), total fat (48%), SFA (26%) and Na (54%). One serving provided 15-23% of the reference values for Ca, K and Mg, while higher contributions were found for Zn, Mn, P and Fe (30-67%). The ultra-processed plant-based burgers provide protein, dietary fibre and essential minerals and contain relatively high levels of energy, Na and total fats. The amino acid composition indicated low protein quality. The multifaceted nutritional profile of plant-based burgers highlights the need for manufacturers to implement improvements to better support healthy dietary habits, including reducing energy, Na and total fats.

Tuberculosis and malnutrition: The European perspective.

Tuberculosis (TB) is a leading infectious cause of death worldwide, despite ongoing efforts to limit its incidence and mortality. Although the European Region has made gains in TB incidence and mortality, it now contends with increasing numbers of multidrug- and rifampicin-resistant tuberculosis (MDR/RR-TB). Malnutrition is a major contributor to the burden of TB and may also be directly caused or enhanced by the onset of TB. The presence of malnutrition may worsen TB and MDR/RR-TB related treatment outcomes and contribute to growing TB drug-resistance. Preventing and treating all forms of malnutrition is an important tool to limit the spread of TB worldwide and improve TB outcomes and treatment efficacy. We carried out a scoping review of the existing evidence that addresses malnutrition in the context of TB. Our review found malnutrition increased the risk of developing TB in high-burden settings and increased the likelihood of developing unfavorable treatment outcomes, including treatment failure, loss to follow-up, and death. The potential impact of nutritional care and improved nutritional status on patient prognosis was more difficult to evaluate due to heterogeneity of patient populations, treatment protocols, and treatment durations and goals. High-quality trials that consider malnutrition as a major risk factor and relevant treatment target when designing effective strategies to limit TB spread and mortality are needed to inform evidence-based practice. In TB patients, we suggest that widespread and regular nutritional screening, assessment, and counselling, has the potential to increase effectiveness of TB management strategies and improve patient quality of life, overall outcomes, and survival.

Relative validity of a brief dietary survey to assess food intake and adherence to national dietary guidelines among Sri Lankan adults.

BACKGROUND: Suboptimal diet is the leading cause of global morbidity and mortality. Addressing this problem requires context-specific solutions informed by context-specific data collected by context-specific tools. This study aimed to assess the relative validity of a newly developed brief dietary survey to estimate food intake and adherence to the Food Based Dietary Guidelines for Sri Lankans. METHODS: Between December 2018 and February 2019, we interviewed 94 Sri Lankan adults living in Colombo (Western Province), Kalutara (Western Province), and Trincomalee (Eastern Province). We assessed the relative validity of the Sri Lankan Brief Dietary Survey (SLBDS) with Wilcoxon rank-sum tests, Spearman's Rho correlation coefficients, Bland-Altman plots, and Cohen's kappa tests using a 24-h Dietary Recall (24DR) as reference. RESULTS: Ninety-four adults (40.7 years ±12.6; 66% female) completed both surveys during the same interview. With the exception of 'Fish, pulses, meat and eggs' food group median intake, which was underestimated by the SLBDS compared to the 24DR, there was no strong evidence of difference between median intakes reported by the two methods. Correlation coefficients were highest for 'Milk and dairy products' (0.84) at the food group level and for 'dosa', 'hoppers', 'milk rice', and 'dried fish' (1.00) among individual food and beverages. Visual exploration of Bland-Altman plots showed acceptable agreement between the SLBDS and 24DR, with the SLBDS tending to overestimate consumption as the number of servings of 'Rice, bread, other cereals and yams' and 'Vegetables' consumed increased and slightly underestimate consumption as the number of servings of 'Fish, pulses, meat and eggs', 'Milk and dairy products', and 'Nuts' increased. Kappa values ranged from from 0.59 (95% CI: 0.32-0.86) for 'Vegetables' to 0.81 (95% CI: 0.66-0.96) for 'Fruit' indicating a moderate to strong level of agreement. CONCLUSIONS: Having been developed for and relatively validated with the study population in question, our study shows that the SLBDS can be used as a fit for purpose research tool. Additional research is needed to assess SLBDS test-retest reliability and to validate further the reporting of salt, oil, and coconut intake.

Practices related to sharps disposal among diabetic patients in Sri Lanka.

BACKGROUND: Patients with diabetes on insulin therapy use sharps (e.g., needles) on a regular basis and a considerable proportion of them, within their home environments. These sharps and other bloodstained materials, if not disposed of appropriately has the potential to be a public health hazard. OBJECTIVE: Our objective was to explore the practices related to sharps disposal among patients with diabetes from North Colombo Teaching Hospital (CNTH), Ragama, Sri Lanka. METHODS: We conducted a cross-sectional study on 158 patients with diabetes from the CNTH. Patients had to use sharps for the daily management of their disease for inclusion into the study group. Data were collected on sharps disposal practices using an interviewer-administered questionnaire. Clinic records were also used as a secondary data source. RESULTS: Most patients, 153/158 (96.8%) used syringes to inject insulin. Forty-three patients (27%) involved others (e.g., family) when disposing of sharps. Used sharps were commonly disposed to the household garbage bin by 66 participants (41.7%). Other methods used for sharps disposal were: sharps container, toilet pit, household garbage dump and indiscriminate measures. Importantly most patients, 147 (93%) had received no information on how to dispose of sharps after usage. CONCLUSION: Patients commonly used unsafe practices in home-based sharps disposal. These included disposing of in the household garbage bin, burning sharps in the household garbage dump and disposing of into the common garbage dump of the community. Being male and being > 60 years of age was associated with a higher dependence on family members for sharps disposal. Patient education and public resources for sharps handling can help improve this situation.

What national and subnational interventions and policies based on Mediterranean and Nordic diets are recommended or implemented in the WHO European Region, and is there evidence of effectiveness in reducing noncommunicable diseases?

This review focuses on national and subnational Mediterranean diet (MD) and Nordic diet (ND) interventions and policies in the WHO European Region. In the context of increasing noncommunicable disease (NCD) burden and unhealthy diets, there is a need to continue identifying optimal, evidence-informed diets and interventions for the prevention and control of NCDs. The MD and ND have been identified as region-specific healthy diets. To support decision-makers in shaping context-specific diet and nutrition policies, this review provides a summary of the NCD burden and activities in the Region; outlines the NCD-related health benefits of the MD and ND; describes interventions and policies in 15 countries; reviews four identified studies into the effectiveness of MD and ND policies on NCD outcomes; and discusses policy implications and options. In the context of MD and ND interventions for NCDs, there remains a Region-wide need to increase translation of evidence into action, monitor and evaluate the impact of existing policies on NCD outcomes and share activities through public platforms to support information sharing.

Contribution of healthy and unhealthy primary school meals to greenhouse gas emissions in England: linking nutritional data and greenhouse gas emission data of diets.

BACKGROUND/OBJECTIVES: School meals represent the largest sector in Government food procurement in the United Kingdom. This paper aims to quantify, simultaneously, the nutritional quality and carbon footprint of meals provided by primary schools in England. SUBJECTS/METHODS: The School Food Trust conducted the 'Primary School Food Survey 2009' in a nationally representative sample of 139 primary schools in England. The survey included 6690 students who consumed school lunches and 3488 students who brought packed lunches. We estimated the total greenhouse gas emissions (GHGEs) per Kg of the food items contributing to those lunches based on the results of a systematic review of life-cycle analyses. RESULTS: In both school lunches and packed lunches, the 'meat, fish and alternatives' group contributed the largest share of GHGEs. The mean GHGE value per school lunch was estimated to be 0.72 (95% uncertainty interval 0.52-1.34) KgCO2e and per packed lunch was 0.70 (0.58-0.94) KgCO2e. The total GHGE due to primary school meals in England per year is 578.1 million KgCO2e (455-892 million). CONCLUSIONS: If all children achieved a healthy meal defined by having a low level of salt, free sugars and saturated fat, the total GHGEs from primary school meals would be 441.2 million KgCO2e (384-1192), saving 136.9 million KgCO2e compared with the current total emissions from primary school meals. This paper demonstrates that changes in the primary school food sector can have an impact on UK GHGEs.

Modelling the health impact of environmentally sustainable dietary scenarios in the UK.

BACKGROUND/OBJECTIVES: Food is responsible for around one-fifth of all greenhouse gas (GHG) emissions from products consumed in the UK, the largest contributor of which is meat and dairy. The Committee on Climate Change have modelled the impact on GHG emissions of three dietary scenarios for food consumption in the UK. This paper models the impact of the three scenarios on mortality from cardiovascular disease and cancer. SUBJECTS/METHODS: A previously published model (DIETRON) was used. The three scenarios were parameterised by fruit and vegetables, fibre, total fat, saturated fat, monounsaturated fatty acids, polyunsaturated fatty acids, cholesterol and salt using the 2008 Family Food Survey. A Monte Carlo simulation generated 95% credible intervals. RESULTS: Scenario 1 (50% reduction in meat and dairy replaced by fruit, vegetables and cereals: 19% reduction in GHG emissions) resulted in 36,910 (30,192 to 43,592) deaths delayed or averted per year. Scenario 2 (75% reduction in cow and sheep meat replaced by pigs and poultry: 9% reduction in GHG emissions) resulted in 1999 (1739 to 2389) deaths delayed or averted. Scenario 3 (50% reduction in pigs and poultry replaced with fruit, vegetables and cereals: 3% reduction in GHG emissions) resulted in 9297 (7288 to 11,301) deaths delayed or averted. CONCLUSION: Modelled results suggest that public health and climate change dietary goals are in broad alignment with the largest results in both domains occurring when consumption of all meat and dairy products are reduced. Further work in real-life settings is needed to confirm these results.

The use of refused tea as litter material for broiler chickens.

A completely randomized design experiment was conducted to determine the suitability of refused tea (RT) as a litter material for broiler chickens. Physiochemical properties of RT were compared with paddy husk (PH). Subsequently, broilers were raised on RT- or PH-based litter to compare the performances and litter qualities. Twenty-day-old broiler chicks (n = 150) were randomly allocated into 6 deep litter pens so that each treatment had 3 replicates. Chicks received 0.8 ft(2) of floor spacing until d 28 and 1.3 ft(2) thereafter. Each cage had a feeder and a drinker. Litter materials and litter samples taken on 28, 35, and 39 d were analyzed for bulk density, moisture, ash, and N. Chick mortality was low (1.3%) and similar on 2 types of litters. Live weights on d 28, 35, 39, and weight gains, feed intakes, dressing percentages, and feed conversion ratios were not affected by the type of litter material. The bulk density, moisture level, and pH of the RT were comparable with PH. Even though the water-holding capacity of PH (213%) was significantly higher (P < 0.01) than RT (70%), the latter material had significantly higher (P < 0.01) water-releasing capacity compared with the former (17.9 vs. 13.6%). Throughout the experiment the RT litter had around 10% units higher moisture level than PH litter. By d 39, the moisture content of the RT litter was (48%) significantly higher (P = 0.05) than PH litter (37%). The N contents of RT litter were higher (P < 0.05) than those of PH on d 28, 35, and 39, being 8.1, 7.8, and 7% and 3.4, 3.6, and 3%, respectively. It was concluded that RT could be successfully used as an alternative litter material for broilers. A higher N content in RT-based spent broiler litter would make it be a better organic fertilizer and ruminant feed compared with PH-based litter.

Is intestinal metaplasia a necessary precursor lesion for adenocarcinomas of the distal esophagus, gastroesophageal junction and gastric cardia?

Adenocarcinoma of the distal esophagus and gastroesophageal junction are believed to arise in Barrett's esophagus with intestinal metaplasia. Whether adenocarcinoma can arise in columnar lined esophagus without intestinal metaplasia is in doubt. Whether adenocarcinoma of the gastric cardia arises in intestinal metaplasia of the gastric cardia is also in doubt. We aim to evaluate the relationship of size and stage of adenocarcinoma of the distal esophagus, gastroesophageal junction and gastric cardia to intestinal metaplasia and other types of columnar epithelium. Seventy-four patients who had esophagogastrectomy for adenocarcinomas in this region were examined histologically to assess the frequency of residual intestinal metaplasia in the surrounding epithelium. Tumors without residual intestinal metaplasia were evaluated for the presence of other columnar epithelia and correlated with tumor size and stage. Cardiac mucosa was present around all tumors. Residual intestinal metaplasia was present in 48 (65%) tumors, including 33/38 (87%) distal esophageal, 10/25 (45%) junctional and 5/11 (45%) gastric cardia tumors. The prevalence of intestinal metaplasia was 100% in all tumors that were less than 1 cm in maximum diameter and all intramucosal tumors. The prevalence of residual intestinal metaplasia decreased with increasing tumor size and stage. These data strongly support the contention that adenocarcinomas of this region, including those in the gastric cardia, arise in intestinal metaplastic epithelium. The absence of residual intestinal metaplasia in larger tumors is the result of tumor overgrowing the intestinal metaplasia from which it arose.

Ki67 expression in different epithelial types in columnar lined oesophagus indicates varying levels of expanded and aberrant proliferative patterns.

AIMS: To evaluate proliferative patterns in metaplastic columnar epithelia of the oesophagus, classified as oxynto-cardiac (n = 43), cardiac (n = 45) intestinal without dysplasia (n = 41), dysplastic intestinal epithelium (n = 25), and adenocarcinoma (n = 15) by Ki67 immunohistochemistry. METHODS AND RESULTS: Abnormal patterns of Ki67 immunoreactivity were classified into (i) expanded proliferation, characterized by increased levels of Ki67 expression in the deep and mid third of the foveolar pit; and (ii) aberrant proliferation, characterized by positive staining in the surface epithelium and superficial third of the foveolar pit. A significant step-wise increase in the frequency of expanded proliferation was seen in oxynto-cardiac, cardiac, intestinal and dysplastic intestinal epithelium indicative of increasing levels of damage. Aberrant proliferation was absent in oxynto-cardiac mucosa, present at a low and similar level in cardiac, intestinal and low-grade dysplastic epithelia and at a significantly increased frequency in high-grade dysplasia. CONCLUSIONS: These findings suggest that oxynto-cardiac mucosa occurs in a low damage environment and intestinal metaplasia in a high damage environment along the length of the columnar lined oesophageal segment. Aberrant proliferative patterns with Ki67 staining are not useful in differentiating reactive epithelia from low-grade dysplasia, but may prove useful in the diagnosis of high-grade dysplasia.

Etiology of intestinal metaplasia at the gastroesophageal junction.

BACKGROUND: Intestinal metaplasia occurs in the esophagus as a consequence of gastroesophageal reflux disease and in the stomach secondary to H. pylori infection. The etiology of intestinal metaplasia limited to the gastroesophageal junction or cardia (CIM) is disputed. We hypothesized that CIM has dual etiologies: gastroesophageal reflux in some, H. pylori infection in others, and that cytokeratin immunostaining can help to differentiate between these two etiologies. METHODS: We defined CIM as the presence of intestinal metaplasia within cardiac mucosa on biopsy from an endoscopically normal-appearing gastroesophageal junction. Thirty patients with CIM who had multiple biopsy specimens taken from the esophagus, gastroesophageal junction, and stomach were identified. Tissue blocks from biopsy specimens taken at the gastroesophageal junction were sectioned and immunostained for cytokeratins 7 and 20. The cytokeratin 7/20 staining of the CIM in each patient was determined to be either a Barrett's or non-Barrett's pattern. H. pylori infection was assessed by Giemsa staining of antral biopsy specimens. RESULTS: H. pylori infection was present in 16 patients. A Barrett's cytokeratin 7/20 staining pattern in the CIM was present in only 46% of the H. pylori-positive patients, as compared to 86% in the 14 patients with CIM and no H. pylori (p = 0.025). Objective evidence of reflux disease was present in 71% of patients with CIM and no H. pylori, as compared to 31% of patients with H. pylori. CONCLUSIONS: The two different patterns of cytokeratin 7/20 staining found in patients with CIM support the concept of dual etiologies for CIM. A Barrett's staining pattern was associated with objective evidence of gastroesophageal reflux and the absence of H. pylori, suggesting that cytokeratin 7/20 immunostaining is useful to determine the likely etiology of CIM.

Adenomatous polyposis coli gene promoter hypermethylation in non-small cell lung cancer is associated with survival.

Methylation of 5' CpG islands in promoter and upstream coding regions has been identified as a mechanism for transcriptional inactivation of tumor suppressor genes. The purpose of this study was to determine whether hypermethylation of the adenomatous polyposis coli (APC) gene promoter occurs in primary non-small cell lung cancer (NSCLC), and whether hypermethylated APC has any relationship with survival. APC promoter 1A methylation was determined in normal and corresponding tumor tissue from 91 NSCLC patients and in a control group of 10 patients without cancer, using a quantitative fluorogenic real-time PCR (Taqman) system. APC promoter methylation was detectable in 86 (95%) of 91 tumor samples, but also in 80 (88%) of 91 normal samples of NSCLC patients, and in only two (20%) of 10 normal lung tissues of the control group. The median level of APC promoter methylation was 4.75 in tumor compared to 1.57 in normal lung tissue (P<0.001). Patients with low methylation status showed significantly longer survival than did patients with high methylation status (P=0.041). In a multivariate analysis of prognostic factors, APC methylation was a significant independent prognostic factor (P=0.044), as were pT (P=0.050) and pN (P<0.001) classifications. This investigation shows that APC gene promoter methylation occurs in the majority of primary NSCLCs. High APC promoter methylation is significantly associated with inferior survival, showing promise as a biomarker of biologically aggressive disease in NSCLC.

Epigenetic patterns in the progression of esophageal adenocarcinoma.

Esophageal adenocarcinoma (EAC) arises after normal squamous mucosa undergoes metaplasia to specialized columnar epithelium (intestinal metaplasia or Barrett's esophagus), which can then ultimately progress to dysplasia and subsequent malignancy. Epigenetic studies of this model have thus far been limited to the DNA methylation analysis of a few genes. In this study, we analyzed a panel of 20 genes using a quantitative, high-throughput methylation assay, METHYLIGHT: We used this broader approach to gain insight into concordant methylation behavior between genes and to generate epigenomic fingerprints for the different histological stages of EAC. Our study included a total of 104 tissue specimens from 51 patients with different stages of Barrett's esophagus and/or associated adenocarcinoma. We screened 84 of these samples with the full panel of 20 genes and found distinct classes of methylation patterns in the different types of tissue. The most informative genes were those with an intermediate frequency of significant hypermethylation [ranging from 15% (CDKN2A) to 60% (MGMT) of the samples]. This group could be further subdivided into three classes, according to the absence (CDKN2A, ESR1, and MYOD1) or presence (CALCA, MGMT, and TIMP3) of methylation in normal esophageal mucosa and stomach, or the infrequent methylation of normal esophageal mucosa accompanied by methylation in all normal stomach samples (APC). The other genes were less informative, because the frequency of hypermethylation was below 5% (ARF, CDH1, CDKN2B, GSTP1, MLH1, PTGS2, and THBS1), completely absent (CTNNB1, RB1, TGFBR2, and TYMS1), or ubiquitous (HIC1 and MTHFR), regardless of tissue type. Each class undergoes unique epigenetic changes at different steps of disease progression of EAC, suggesting a step-wise loss of multiple protective barriers against CpG island hypermethylation. The aberrant hypermethylation occurs at many different loci in the same tissues, suggestive of an overall deregulation of methylation control in EAC tumorigenesis. However, we did not find evidence for a distinct group of tumors with a CpG island methylator phenotype. Finally, we found that normal and metaplastic tissues from patients with evidence of associated dysplasia or cancer had a significantly higher incidence of hypermethylation than similar tissues from patients with no further progression of their disease. The fact that the samples from these two groups of patients were histologically indistinguishable, yet molecularly distinct, suggests that the occurrence of such hypermethylation may provide a clinical tool to identify patients with premalignant Barrett's who are at risk for further progression.

Fields of aberrant CpG island hypermethylation in Barrett's esophagus and associated adenocarcinoma.

Esophageal adenocarcinoma (EAC) is thought to develop through a multistage process in which Barrett's metaplasia progresses through low- and high-grade dysplasia to invasive cancer. Transcriptional silencing of tumor suppressor genes by promoter CpG island hypermethylation has been observed in many types of human cancer. Analysis of CpG island hypermethylation in EAC has thus far been limited to the CDKN2A (p16) gene. In this study, we extend the methylation analysis of EAC to include three other genes, APC, CDH1 (E-cadherin), and ESR1 (ER, estrogen receptor alpha), in addition to CDKN2A. Molecular analysis can provide insight into the complex relationships between tissues with different histologies in Barrett's esophagus and associated adenocarcinoma. Therefore, we have mapped the spatial distribution of methylation patterns in six esophagectomy cases in detail. Hypermethylation of the four CpG islands was analyzed by the MethyLight technique in 107 biopsies derived from these six patients for a total of 428 methylation analyses. Our results show that normal esophageal squamous epithelium is unmethylated at all four CpG islands. CDH1 is unmethylated in most other tissue types as well. Hypermethylation of ESR1 is seen at high frequency in inflammatory reflux esophagitis and at all subsequent stages, whereas APC and CDKN2A hypermethylation is found in Barrett's metaplasia, dysplasia, and EAC. When it occurs, hypermethylation of APC, CDKN2A, and ESR1 is usually found in a large contiguous field, suggesting either a concerted methylation change associated with metaplasia or a clonal expansion of cells with abnormal hypermethylation.