Search

Background: Food plays a dual role in promoting human health and environmental sustainability. Yet, current food systems jeopardize both. Food waste poses a major global challenge due to its significant economic, social, and environmental impacts. Healthcare facilities generate the largest amounts of food waste compared to other forms of catering provision. Food waste correlates with environmental unsustainability and diminished patient satisfaction, compounding the prevalent challenge of hospital malnutrition and contributing to suboptimal patient outcomes. Materials and methods: In a three-year interventional study (2020-2022) at a psychiatric tertiary care center, we assessed and mitigated food waste using evidence-based measures. We conducted systematic food wastage audits over three years (2020-2022) in May and June, each lasting four weeks. Costs were analyzed comprehensively, covering food, staff, infrastructure, and disposal. Environmental impact was assessed using Umweltbelastungspunkte (UBP) and CO2e/kg emissions, alongside water usage (H2O - l/kg). Results: Economic losses due to food wastage were substantial, primarily from untouched plates and partially consumed dinners, prompting meal planning adjustments. Despite a >3% increase in meals served, both food waste mass and costs decreased by nearly 6%. Environmental impact indicators showed a reduction >20%. Vegetables, salad, and fruits constituted a significant portion of waste. Overproduction minimally contributed to waste, validating portion control efficacy. Conclusion: Our study highlights significant economic and environmental losses due to hospital food waste, emphasizing the importance of resource efficiency. The strategies outlined offer promising avenues for enhanced efficiency. The decrease in food waste observed over the three-year period underscores the potential for improvement. [ABSTRACT FROM AUTHOR]

Summary: Background: Primary sclerosing cholangitis (PSC) is a progressive bile duct disease associated with inflammatory bowel disease (PSC‐IBD). Aim: To investigate whether patients with PSC‐IBD benefit from a gluten‐free and amylase trypsin inhibitor (ATI)‐free diet (GFD). Methods: We performed a prospective clinical pilot study administering an eight‐week GFD. The primary outcomes were colonic inflammation assessed by proctosigmoidoscopy, and liver stiffness (surrogate for fibrosis, inflammation and cholestasis) measured by transient elastography before and after GFD. Amongst the secondary (exploratory) outcomes were colonic mucosal and serum cytokine/chemokine changes, the intestinal microbiome and transcriptome dynamics, and shifts in serum markers of hepatic fibrogenesis. Results: Fifteen patients with PSC‐IBD completed the study. The study did not meet its primary outcome: the endoscopic score and liver stiffness remained unchanged. However, the expression of pro‐inflammatory mucosal cytokines and chemokines such as IL6, IL8, CCL2, and TNFα was significantly down‐regulated. Two critical markers of liver fibrosis and matrix remodelling, thrombospondin‐2 and ‐4, decreased significantly. The microbiota composition changed slightly, including a decrease in the pathogen Romboutsia ilealis. The intestinal transcriptome indicated a gut barrier improvement. Pruritus, fatigue, overall well‐being, faecal calprotectin levels, and serum alkaline phosphatase did not change significantly. Conclusions: This study did not demonstrate a clinical improvement with short‐term GFD in patients with PSC‐IBD. However, a gluten/ATI‐free diet may improve biomarkers of intestinal inflammation and barrier function in these patients with associated changes in the enteric microbiota. Further investigation of the therapeutic potential of the GFD in PSC‐IBD is warranted. [ABSTRACT FROM AUTHOR]

Purpose: Currently, information on the psychometric properties of the Medical outcomes study-social support survey (MOS-SSS) for patients with chronic disease in primary health care, suggests problems in the dimensionality, specifically predominant unidimensionality in a multidimensional measure. The aim of this study was to determine the internal structure (dimensionality, measurement invariance and reliability) and association with other variables. Methods: A total of 470 patients with chronic disease from a Family Medicine Unit at the Instituto Mexicano del Seguro Social, IMSS, with a mean age of 51.51 years were included. Participants responded to the Questionnaire of Sociodemographic Variables (Q-SV), SF-36 Health-Related Quality of Life Scale--version 1.1, and MOS-SSS.Results: Non-parametric (Mokken scaling analysis) and parametric (confirmatory factor analysis) analyses indicated unidimensionality, and three-factor model was not representative. A new 8-item version (MOS-S) was developed, where measurement invariance, equivalence with the long version, reliability, and relationship with the SF-36 were satisfactory. Conclusion: The MOS-SSS scale is unidimensional, and the shortened version yields valid and reliable scores for measuring social support in patients with chronic disease at the primary health care. [ABSTRACT FROM AUTHOR]

Summary: Background: The pathogenesis of autoimmune hepatitis (AIH) is poorly understood and little is known about enteric microbiota in AIH. Aim: To investigate disease‐specific microbiome alterations in AIH. Methods: The V1‐V2 variable regions of the 16S rRNA gene were sequenced in faecal samples from 347 patients with AIH and controls (AIH n = 72, healthy controls (HC) n = 95, primary biliary cholangitis (PBC) n = 99 and ulcerative colitis (UC) n = 81). Results: Biodiversity (Shannon entropy) was decreased in AIH patients compared to HC (P = 0.016), which was partially reversed by azathioprine (P = 0.011). Regarding between‐sample diversity, AIH patients separated from HC, PBC and UC individuals (all P = 0.001). Compared to HC, decreased relative abundance of anaerobic genera such as Faecalibacterium and an increase of Veillonella and the facultative anaerobic genera Streptococcus and Lactobacillus were detected. Importantly, a disease‐specific decline of relative abundance of Bifidobacterium was observed in AIH patients. Lack of Bifidobacterium was associated with failure to achieve remission of AIH (P < 0.001). Of potential therapeutic implication, Bifidobacterium abundance correlated with average protein intake (P < 0.001). Random forests classification between AIH and PBC on the microbiome signature yielded an area under receiver operating characteristic curve (AUC) of 0.787 in the training cohort, and an AUC of 0.849 in an external validation cohort. Conclusion: Disease‐specific faecal microbial alterations were identified in patients with AIH. Intestinal dysbiosis in AIH was characterised by a decline of Bifidobacterium, which was associated with increased disease activity. These results point to the contribution of intestinal microbiota to AIH pathogenesis and to novel therapeutic targets. [ABSTRACT FROM AUTHOR]