Avoidant restrictive food intake disorder: recent advances in neurobiology and treatment.

Avoidant restrictive food intake disorder (ARFID) is an eating disorder characterized by persistent insufficient nutritional and/or energy intake. ARFID, before referred to as "selective eating disorder", was introduced recently in the DSM-5 as a replacement for and expansion of the previous diagnosis. Individuals with ARFID may limit food variety and intake due to avoidance based on the sensory characteristics of the food or related to any adverse consequences of eating without the intention of losing weight and concerns of body image. The limited understanding of avoidant and restrictive eating poses challenges to effective treatment and management, impacting directly on the growth and development of children and adolescents. The ARFID neurobiological concept has not yet been clearly defined to clinical practice for nutritionists, thereby hindering screening and impeding the development of treatment recommendations. This narrative review provide useful practical information to consult the pathophysiology, the neurobiology, the clinical features, the assessment and the treatment for healthcare professionals seeking to enhance their clinical knowledge and management of this disorder.

Avoidant restrictive food intake disorder (ARFID) is an eating disorder characterized by persistent insufficient nutritional and/or energy intake. Individuals with ARFID exhibit limited food intake and variety, often due to a lack in eating, without the primary goal of weight loss. The limited understanding of avoidant and restrictive eating poses challenges in terms of effective treatment and management, which directly impacts the growth and development of children and adolescents, as well as their nutrition and psychosocial well-being. ARFID is a relatively recent diagnostic classification, representing a burgeoning field of study. The identification of diagnostic criteria and the pursuit of new knowledge in this area have only recently begun. Consequently, assessment tools and treatment strategies are still in the process of development and validation. This narrative review explored the neurobiological perspective of ARFID using the three-dimensional model, examined its etiology and risk factors, evaluated clinical screening and evaluation tools, discussed common clinical complications, and presented different types of nutritional, behavioural, and pharmacological interventions used in ARFID treatment.

Long-term Effect of Lifestyle Interventions on the Cardiovascular and All-Cause Mortality of Subjects With Prediabetes and Type 2 Diabetes: A Systematic Review and Meta-analysis.

BACKGROUND: Lifestyle interventions improve the metabolic control of individuals with hyperglycemia. PURPOSE: We aimed to determine the effect of lifestyle interventions on cardiovascular and all-cause mortality in this population. DATA SOURCES: Searches were made through MEDLINE, Cochrane CENTRAL, Embase, and Web of Science (no date/language restriction, until 15 May 2022). STUDY SELECTION: We included randomized clinical trials (RCTs) of subjects with prediabetes and type 2 diabetes, comparing intensive lifestyle interventions with usual care, with a minimum of 2 years of active intervention. DATA EXTRACTION: Data from the 11 RCTs selected were extracted in duplicate. A frequentist and arm-based meta-analysis was performed with random-effects models to estimate relative risk (RR) for mortality, and heterogeneity was assessed through I2 metrics. A generalized linear mixed model (GLMM) was used to confirm the findings. DATA SYNTHESIS: Lifestyle interventions were not superior to usual care in reducing cardiovascular (RR 0.99; 95% CI 0.79-1.23) or all-cause (RR 0.93; 95% CI 0.85-1.03) mortality. Subgroup, sensitivity, and meta-regression analyses showed no influence of type of intervention, mean follow-up, age, glycemic status, geographical location, risk of bias, or weight change. All of these results were confirmed with the GLMM. Most studies had a low risk of bias according to the RoB 2.0 tool and the certainty of evidence was moderate for both outcomes. LIMITATIONS: Most studies had a low risk of bias according to the RoB 2.0 tool, and the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach resulted in moderate certainty of evidence for both outcomes. Differences in lifestyle programs and in usual care between the studies should be considered in the interpretation of our results. CONCLUSIONS: Intensive lifestyle interventions implemented so far did not show superiority to usual care in reducing cardiovascular or all-cause mortality for subjects with prediabetes and type 2 diabetes.

Effects of obesity on kidney transplantation outcomes: a systematic review and meta-analysis.

BACKGROUND: The effects of obesity on outcomes reported after kidney transplantation have been controversial. The purpose of this systematic review and meta-analysis was to elucidate this issue. METHODS: MEDLINE, EMBASE, Cochrane Library, and gray literature were searched up to August 6, 2013. Studies that compared obese and nonobese patients who underwent kidney transplantation and evaluated one of these outcomes-delayed graft function (DGF), acute rejection, graft or patient survival at 1 or 5 years after transplantation, or death by cardiovascular disease (CVD)-were included. Two independent reviewers extracted the data and assessed the quality of the studies. RESULTS: From 1,973 articles retrieved, 21 studies (9,296 patients) were included. Obesity was associated with DGF (relative risk, 1.41; 95% confidence interval, 1.26-1.57; I=8%; Pheterogeneity=0.36), but not with acute rejection. Graft loss and death were associated with obesity only in the analysis of studies that evaluated patients who received a kidney graft before year 2000. No association of obesity with graft loss and death was found in the analysis of studies that evaluated patients who received a kidney graft after year 2000. Death by CVD was associated with obesity (relative risk, 2.07; 95% confidence interval, 1.17-3.64; I=0%; Pheterogeneity=0.59); however, most studies included in this analysis evaluated patients who received a kidney graft after year 2000. CONCLUSION: In conclusion, obese patients have increased risk for DGF. In the past years, obesity was a risk factor for graft loss, death by CVD, and all-cause mortality. However, for the obese transplanted patient today, the graft and patient survival is the same as that of the nonobese patient.

Association between 276G/T adiponectin gene polymorphism and new-onset diabetes after kidney transplantation.

BACKGROUND: New-onset diabetes after transplantation (NODAT) is a well-recognized complication of kidney transplantation and is associated with poor outcomes. Both adiponectin and chemokine ligand 5 (CCL5) proteins are related to glucose metabolism and genetic variations in their genes can lead to development of NODAT. The aim of this study was to investigate the association of adiponectin and CCL5 genes polymorphisms with NODAT in a population of Caucasian kidney transplant recipients. METHODS: Two hundred seventy Caucasian kidney transplant recipients (83 with NODAT and 187 without NODAT) were included in a nested case-control study. Patients with pretransplantation diabetes mellitus and multiorgan transplantation were excluded. NODAT diagnosis was determined by American Diabetes Association criteria. Subjects were genotyped for 276G/T adiponectin gene polymorphism (rs1501299) and rs2280789 and rs3817655 CCL5 gene polymorphisms by real-time polymerase chain reaction. RESULTS: The TT genotype of 276G/T adiponectin gene polymorphism was significantly more frequent in NODAT than non-NODAT patients compared with GG/GT genotypes (recessive model; P=0.031). TT genotype was identified as an independent risk factor for NODAT in Caucasian kidney transplant recipients after adjusting for age at transplantation, pretransplantation body mass index, and use of tacrolimus (TT vs. GG/GT, hazard ratio=1.88, 95% confidence interval=1.03-3.45, P=0.041). There were no differences in genotype distribution and allele frequency of rs2280789 and rs3817655 CCL5 gene polymorphisms between NODAT and non-NODAT groups. CONCLUSIONS: The 276G/T adiponectin gene polymorphism is associated with NODAT in Caucasian kidney transplant recipients.