Investigating the Role of Self-Disgust in Nonsuicidal Self-Injury

Self-directed disgust, a component of self-criticism, may present an important, yet unexplored emotion in the context of nonsuicidal self-injury (NSSI). The aim of this study was to examine the role of self-disgust in NSSI, specifically as a potential mediator in the relations between depression and NSSI as well as sexual abuse and NSSI, and to also better understand characteristics that might differentiate recent and past self-injurers. A total of 549 college students completed measures assessing NSSI, self-disgust, depression, anxiety sensitivity, and physical and sexual abuse. Results indicated self-disgust fully mediated the relation between depressive symptoms and NSSI status and partially mediated the relation between sexual abuse and NSSI status. Additionally, compared to past self-injurers (4.6%; n = 25), recent self-injurers (6.4%; n = 35) endorsed significantly higher self-disgust and depressive symptoms. Self-disgust may be an important component in NSSI and should be addressed in treatment.     

Influence of Periodontal Status and Periodontopathogens on Levels of Oral Human β‐Defensin‐2 in Saliva

Background: Expression patterns of human β‐defensin‐2 (HBD‐2) mRNA or HBD‐2 protein concentration and periodontal diseases have been a focus of scientific research. This study compares the salivary levels of HBD‐2 protein concentration of healthy patients and patients with gingivitis and chronic periodontitis (CP) and correlates these levels with the presence of periodontopathogens. Methods: A total of 89 patients were enrolled in this study: 31 periodontally healthy, 27 with gingivitis, and 31 with CP. Plaque and gingival indices, probing depth, and clinical attachment level were measured. The presence of Campylobacter rectus, Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, and Prevotella intermedia was evaluated qualitatively by conventional polymerase chain reaction. HBD‐2 quantification in saliva was performed using an immune enzymatic assay. Frequency of periodontopathogens and HBD‐2 protein concentration was assessed. Association between HBD‐2 protein concentration (≥100 pg/mL) and the simultaneous presence of one to two, three to four, or five to six periodontopathogens was tested. Results: Although periodontally healthy individuals and patients with gingivitis showed similar HBD‐2 levels, the CP group displayed an increased level of HBD‐2. P. gingivalis, P. intermedia, T. forsythia, and T. denticola were more prevalent in CP; however, their mere presence was not related to the increased levels of HBD‐2 (Pearson correlation and multinomial logistic regression model). Conclusions: Salivary HBD‐2 protein concentration was higher in patients with CP compared with healthy individuals or patients with gingivitis. These different protein concentrations were not related to the frequency of periodontopathogens. Clinical inflammatory profile had a higher impact on salivary HBD‐2 levels than bacteria.     

Effects of 8 weeks of continuous positive airway pressure on abdominal adiposity in obstructive sleep apnoea

The aim of the present study was to investigate the effect of continuous positive airway pressure (CPAP) treatment on regional adipose tissue distribution in patients with moderate or severe obstructive sleep apnoea. Patients received both therapeutic and sham CPAP in a random order for 2 months each with an intervening 1-month washout. Abdominal subcutaneous, visceral and liver fat were quantified using magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS). Liver enzymes and plasma glucose were also determined. Measurements were obtained at baseline and at the end of both treatment arms. 38 eligible patients were randomly assigned to a treatment order, with 27 patients having complete MRI/MRS data. No significant difference was observed in subcutaneous (-28.6 cm(3); p=0.49) or visceral (-16.8 cm(3); p=0.59) adipose tissue, intrahepatic lipid (-0.2%; p=0.21), or fasting glucose measurements (-0.1 mmol·L(-1); p=0.46) between treatment modalities. Alkaline phosphatase decreased (-3.1 U·L(-1); p=0.02) while on therapeutic CPAP compared with sham CPAP but other liver enzymes, including aspartate aminotransferase (0.3 U·L(-1); p=0.82), alanine aminotransferase (1.34 U·L(-1); p=0.59) and γ-glutamyltransferase (-2.3 U·L(-1); p=0.33), remained unchanged. In this first randomised, sham-controlled trial, there was no change in adipose tissue distribution after 8 weeks of therapeutic CPAP compared with 8 weeks of sham CPAP. Longer duration of CPAP use may be necessary to demonstrate a difference.     

Altered thermogenesis and impaired bone remodeling in Misty mice

Fat mass may be modulated by the number of brown‐like adipocytes in white adipose tissue (WAT) in humans and rodents. Bone remodeling is dependent on systemic energy metabolism and, with age, bone remodeling becomes uncoupled and brown adipose tissue (BAT) function declines. To test the interaction between BAT and bone, we employed Misty (m/m) mice, which were reported be deficient in BAT. We found that Misty mice have accelerated age‐related trabecular bone loss and impaired brown fat function (including reduced temperature, lower expression of Pgc1a, and less sympathetic innervation compared to wild‐type (+/ +)). Despite reduced BAT function, Misty mice had normal core body temperature, suggesting heat is produced from other sources. Indeed, upon acute cold exposure (4°C for 6 hours), inguinal WAT from Misty mice compensated for BAT dysfunction by increasing expression of Acadl, Pgc1a, Dio2, and other thermogenic genes. Interestingly, acute cold exposure also decreased Runx2 and increased Rankl expression in Misty bone, but only Runx2 was decreased in wild‐type. Browning of WAT is under the control of the sympathetic nervous system (SNS) and, if present at room temperature, could impact bone metabolism. To test whether SNS activity could be responsible for accelerated trabecular bone loss, we treated wild‐type and Misty mice with the β‐blocker, propranolol. As predicted, propranolol slowed trabecular bone volume/total volume (BV/TV) loss in the distal femur of Misty mice without affecting wild‐type. Finally, the Misty mutation (a truncation of DOCK7) also has a significant cell‐autonomous role. We found DOCK7 expression in whole bone and osteoblasts. Primary osteoblast differentiation from Misty calvaria was impaired, demonstrating a novel role for DOCK7 in bone remodeling. Despite the multifaceted effects of the Misty mutation, we have shown that impaired brown fat function leads to altered SNS activity and bone loss, and for the first time that cold exposure negatively affects bone remodeling.