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On 11 March 2020, coronavirus disease 2019 (COVID-19) was declared a pandemic by the World Health Organization (WHO) and, up to 1837 a.m. on 9 December 2021, it has produced 268,440,530 cases and 5,299,511 deaths. selleckchem This disease, in some patients, included pneumonia and shortness of breath, being transmitted through droplets and aerosols. To date, there is no scientific literature to justify transmission directly from foods. In this review, we applied the precautionary principle for the home and the food industry using the known "Five Keys to Safer Food" manual developed by the World Health Organization (WHO) and extended punctually in its core information from five keys, in the light of new COVID-19 evidence, to guarantee a possible food safety tool.Eating disorders are potentially life-threatening mental health disorders that require management by a multidisciplinary team including medical, psychological and dietetic specialties. This review systematically evaluated the available literature to determine the effect of including a dietitian in outpatient eating disorder (ED) treatment, and to contribute to the understanding of a dietitian's role in ED treatment. Six databases and Google Scholar were searched for articles that compared treatment outcomes for individuals receiving specialist dietetic treatment with outcomes for those receiving any comparative treatment. Studies needed to be controlled trials where outcomes were measured by a validated instrument (PROSPERO CRD42021224126). The searches returned 16,327 articles, of which 11 articles reporting on 10 studies were included. Two studies found that dietetic intervention significantly improved ED psychopathology, and three found that it did not. Three studies reported that dietetic input improved other psychopathological markers, and three reported that it did not. One consistent finding was that dietetic input improved body mass index/weight and nutritional intake, although only two and three studies reported on each outcome, respectively. A variety of instruments were used to measure each outcome type, making direct comparisons between studies difficult. Furthermore, there was no consistent definition of the dietetic components included, with many containing psychological components. Most studies included were also published over 20 years ago and are now out of date. Further research is needed to develop consistent dietetic guidelines and outcome measures; this would help to clearly define the role of each member of the multidisciplinary team, and particularly the role of dietitians, in ED treatment.Avocado is a nutrient-rich food that has been shown to benefit the health and diet quality of adults. link2 In this paper, we examined if habitual intake of avocado among adolescents is associated with their diet quality, food and nutrient intake, and measures of obesity and body composition. Participants aged 12-18 years old (n = 534) from selected public and Adventist middle-high schools reported their dietary intake in a web-based food frequency questionnaire (FFQ); anthropometrics were measured during school visits. Diet quality (DQI-I) and avocado intake were calculated from the FFQ; BMI z-scores (BMIz), waist-to-height ratio (WHtR), and fat mass (FM), fat-free mass (FFM), and %body fat (%BF) were determined from the anthropometric data. Compared to non-consumers, avocado consumers had significantly higher covariate-adjusted mean scores on total DQI-I (68.3 vs. 64.6) and energy-adjusted mean scores on variety (18.8 vs. 18.0) and adequacy (36.4 vs. 33.4). Avocado consumption was significantly associated with DQI-I components adequacy (β [SE] = 0.11 [0.03]) and moderation (β [SE] = 0.06 [0.03]) but not with BMIz, WHtR, FM, FFM, and %BF. Mean intakes of fruits, vegetables, and plant protein foods, total and vegetable proteins, dietary fiber, retinol, vitamin C, calcium, magnesium, iron, and potassium were significantly higher for avocado consumers; saturated and trans fats intakes were significantly higher for non-consumers. In our adolescent population, avocado consumption was associated with higher diet quality and intake of plant-based foods and shortfall nutrients, but not with measures of obesity and body composition. Studies are needed to determine the optimal amount of avocado that would confer health benefits during adolescence.Obesity and cardiometabolic risk have been associated with vitamin D levels even in children. link3 The objective of the present study was to evaluate the association between insulin resistance (IR), cardiometabolic risk factors, and vitamin D in children from prepubertal to pubertal stages. A total of 76 children from the PUBMEP study, aged 4-12 years at baseline, were included. Children were evaluated in prepubertal and pubertal stages. Anthropometric measurements and selected cardiometabolic risk biomarkers, such as plasma glucose, blood lipids, insulin, adiponectin, leptin, and blood pressure, and serum 25-hydroxyvitamin D (25(OH)D) were determined. Children were categorized by obesity degree and IR status combined before and after puberty. Paired t-test and multivariate linear regression analyses were conducted. During puberty, the increase in triacylglycerols, insulin, and HOMA-IR and the decrease in QUICKI were significantly associated with the reduction in 25(OH)D (B = -0.274, p = 0.032; B = -0.219, p = 0.019; B = -0.250, p = 0.013; B = 1.574, p = 0.013, respectively) after adjustment by BMI-z, sex, and pubertal stage. Otherwise, prepubertal non-IR children with overweight/obesity that became IR during puberty showed a significant decrease in 25(OH)D and HDL-c, and an increase in waist circumference and triacylglycerol concentrations (p less then 0.05 for all) over time. These results suggest that changes in IR seem to be associated with an effect on 25(OH)D levels during puberty, especially in children with overweight.It is suggested that clock genes link the circadian rhythm to glucose and lipid metabolism. In this study, we explored the role of the clock gene Bmal1 in the hypothalamic paraventricular nucleus (PVN) in glucose metabolism. The Sim1-Cre-mediated deletion of Bmal1 markedly reduced insulin secretion, resulting in impaired glucose tolerance. The pancreatic islets' responses to glucose, sulfonylureas (SUs) and arginine vasopressin (AVP) were well maintained. To specify the PVN neuron subpopulation targeted by Bmal1, the expression of neuropeptides was examined. In these knockout (KO) mice, the mRNA expression of Avp in the PVN was selectively decreased, and the plasma AVP concentration was also decreased. However, fasting suppressed Avp expression in both KO and Cre mice. These results demonstrate that PVN BMAL1 maintains Avp expression in the PVN and release to the circulation, possibly providing islet β-cells with more AVP. This action helps enhance insulin release and, consequently, glucose tolerance. In contrast, the circadian variation of Avp expression is regulated by feeding, but not by PVN BMAL1.Synbiotics have emerged as a therapeutic strategy for modulating the gut microbiome and targeting novel cardiovascular risk factors, including uremic toxins indoxyl sulfate (IS) and p-cresyl sulfate (PCS). This study aims to evaluate the feasibility of a trial of long-term synbiotic supplementation in adults with stage 3-4 chronic kidney disease (CKD). Adult participants with CKD and estimated glomerular filtration rate (eGFR) of 15-60 mL/min/1.73 m2) were recruited between April 2017 and August 2018 to a feasibility, double-blind, placebo-controlled, randomized trial of synbiotic therapy or matched identical placebo for 12 months. The primary outcomes were recruitment and retention rates as well as acceptability of the intervention. Secondary outcomes were treatment adherence and dietary intake. Exploratory outcomes were evaluation of the cardiovascular structure and function, serum IS and PCS, stool microbiota profile, kidney function, blood pressure, and lipid profile. Of 166 potentially eligible patients, 68 (41%) were recruited into the trial (synbiotic n = 35, placebo n = 33). Synbiotic and placebo groups had acceptable and comparable 12-month retention rates (80% versus 85%, respectively, p = 0.60). Synbiotic supplementation altered the stool microbiome with an enrichment of Bifidobacterium and Blautia spp., resulting in a 3.14 mL/min/1.73 m2 (95% confidence interval (CI), -6.23 to -0.06 mL/min/1.73 m2, p less then 0.01) reduction in eGFR and a 20.8 µmol/L (95% CI, 2.97 to 38.5 µmol/L, p less then 0.01) increase in serum creatinine concentration. No between-group differences were observed in any of the other secondary or exploratory outcomes. Long-term synbiotic supplementation was feasible and acceptable to patients with CKD, and it modified the gastrointestinal microbiome. However, the reduction in kidney function with synbiotics warrants further investigation.Chronic high-fat diet (HFD) is associated with the onset and progression of hepatic steatosis, and oxidative stress is highly involved in this process. The potential role of sesamol (SEM) against oxidative stress and inflammation at the transcriptional level in a mice model of hepatic steatosis is not known. In this study, we aimed to investigate the scavenging effects of SEM towards reactive oxygen generated by lipid accumulation in the liver of obese mice and to explore the mechanisms of protection. Markers of oxidative stress, vital enzymes involved in stimulating oxidative stress or inflammation, and nuclear transcription of Nrf2 were examined. Our results showed that SEM significantly inhibited the activity of the HFD-induced hepatic enzymes CYP2E1 and NOX2, associated with oxidative stress generation. Additionally, SEM reversed HFD-induced activation of NF-κB, a redox-sensitive transcription factor, and attenuated the expression of hepatic TNF-α, a proinflammatory molecule. Moreover, SEM enhanced HFD-induced hepatic Nrf2 nuclear transcription and increased the levels of its downstream target genes Ho1 and Nqo1, which indicated antiinflammation and antioxidant properties. Our study suggests that chronic HFD led to hepatic steatosis, while SEM exhibited protective effects on the liver by counteracting the oxidative stress and inflammation induced by HFD. The underlying mechanism might involve multiple pathways at the transcriptional level; the antioxidant defense mechanism was in partly mediated by the upregulation of Nrf2.We aim to describe temporal eating patterns in a population of adults with overweight or obesity. In this cross-sectional analysis, data were combined from two separate pilot studies during which participants entered the timing of all eating occasions (>0 kcals) for 10-14 days. Data were aggregated to determine total eating occasions, local time of the first and last eating occasions, eating window, eating midpoint, and within-person variability of eating patterns. Eating patterns were compared between sexes, as well as between weekday and weekends. Participants (n = 85) had a median age of 56 ± 19 years, were mostly female (>70%), white (56.5%), and had a BMI of 31.8 ± 8.0 kg/m2. The median eating window was 14 h 04 min [12 h 57 min-15 h 21 min], which was significantly shorter on the weekend compared to weekdays (p 14 h/d). Future trials should examine the contribution of a prolonged eating window on adiposity independent of energy intake.