Associations of disordered eating with the intestinal microbiota and short-chain fatty acids among young adults with type 1 diabetes

Background and aimsDisordered eating (DE) in type 1 diabetes (T1D) includes insulin restriction for weight loss with serious complications. Gut microbiota-derived short chain fatty acids (SCFA) may benefit host metabolism but are reduced in T1D. We evaluated the hypothesis that DE and insulin restriction were associated with reduced SCFA-producing gut microbes, SCFA, and intestinal microbial diversity in adults with T1D.Methods and resultsWe collected stool samples at four timepoints in a hypothesis-generating gut microbiome pilot study ancillary to a weight management pilot in young adults with T1D. 16S ribosomal RNA gene sequencing measured the normalized abundance of SCFA-producing intestinal microbes. Gas-chromatography mass-spectrometry measured SCFA (total, acetate, butyrate, and propionate). The Diabetes Eating Problem Survey—Revised (DEPS-R) assessed DE and insulin restriction. Covariate-adjusted and Bonferroni-corrected generalized estimating equations modeled the associations. COVID-19 interrupted data collection, so models were repeated restricted to pre-COVID-19 data.Data were available for 45 participants at 109 visits, which included 42 participants at 65 visits pre-COVID-19. Participants reported restricting insulin “At least sometimes” at 53.3% of visits. Pre-COVID-19, each 5-point DEPS-R increase was associated with a ?0.34 (95% CI -0.56, ?0.13, p = 0.07) lower normalized abundance of genus Anaerostipes; and the normalized abundance of Lachnospira genus was ?0.94 (95% CI -1.5, ?0.42), p = 0.02 lower when insulin restriction was reported “At least sometimes” compared to “Rarely or Never”.ConclusionDE and insulin restriction were associated with a reduced abundance of SCFA-producing gut microbes pre-COVID-19. Additional studies are needed to confirm these associations to inform microbiota-based therapies in T1D.     

French practical guidelines for the diagnosis and management of relapsing polychondritis

Relapsing polychondritis is a rare systemic disease. It usually begins in middle-aged individuals. This diagnosis is mainly suggested in the presence of chondritis, i.e. inflammatory flares on the cartilage, in particular of the ears, nose or respiratory tract, and more rarely in the presence of other manifestations. The formal diagnosis of relapsing polychondritis cannot be established with certainty before the onset of chondritis, which can sometimes occur several years after the first signs. No laboratory test is specific of relapsing polychondritis, the diagnosis is usually based on clinical evidence and the elimination of differential diagnoses. Relapsing polychondritis is a long-lasting and often unpredictable disease, evolving in the form of relapses interspersed with periods of remission that can be very prolonged. Its management is not codified and depends on the nature of the patient's symptoms and association or not with myelodysplasia/vacuoles, E1 enzyme, X linked, autoinflammatory, somatic (VEXAS). Some minor forms can be treated with non-steroidal anti-inflammatory drugs, or a short course of corticosteroids with possibly a background treatment of colchicine. However, the treatment strategy is often based on the lowest possible dosage of corticosteroids combined with background treatment with conventional immunosuppressants (e.g. methotrexate, azathioprine, mycophenolate mofetil, rarely cyclophosphamide) or targeted therapies. Specific strategies are required if relapsing polychondritis is associated with myelodysplasia/VEXAS. Forms limited to the cartilage of the nose or ears have a good prognosis. Involvement of the cartilage of the respiratory tract, cardiovascular involvement, and association with myelodysplasia/VEXAS (more frequent in men over 50 years of age) are detrimental to the prognosis of the disease.     

Trait self-acceptance mediates parental childhood abuse predicting depression and anxiety symptoms in adulthood

BackgroundBiopsychosocial models posit that experiencing parental childhood abuse increases vulnerability to psychopathology in adulthood. There are a lack of studies investigating mediators of the parental childhood abuse–adulthood psychopathology relation. The current study investigated if trait self-acceptance mediated the parental childhood abuse–adulthood major depressive disorder (MDD), generalized anxiety disorder (GAD), and panic disorder (PD) severity relations.MethodsParticipants (n = 3294) partook in the 18-year Midlife Development in the United States (MIDUS) study at three time-points. We conducted structural equation modeling analyses to test how maternal and paternal childhood abuse at Time 1 would independently positively predict MDD, GAD, and PD severity at Time 3, and if self-acceptance at Time 2 mediated those relations while controlling for adulthood MDD, GAD, and PD severity at Time 1.ResultsSelf-acceptance notably mediated the parental childhood abuse-adulthood MDD, GAD, and PD relations. Overall, higher paternal and maternal childhood abuse was associated with lower self-acceptance. Reduced self-acceptance predicted heightened adulthood MDD, GAD, and PD.ConclusionFindings highlight the importance of understanding the parental childhood abuse–adulthood psychopathology relation and the possible mechanisms of its long-term impact.