Attachment-Based Family Therapy to Improve Family Functioning in Adolescent Binge-Spectrum Eating Disorders: An Initial Evaluation Via Case Series Design.

Binge-spectrum eating disorders (EDs; bulimia nervosa, binge eating disorder) often develop during adolescence and are associated with serious psychological and physical consequences. Current treatments for adolescents are highly behavioral in nature and while efficacious, many patients do not reach remission indicating that current treatments fail to target a key maintenance factor for EDs. One potential maintenance factor is poor family functioning (FF). In particular, high family conflict (e.g., arguing, critical comments) and low family cohesion (e.g., warmth, support) are known to maintain ED behaviors. Poor FF can (1) cause or exacerbate an adolescent's use of ED behaviors to cope with life stress and/or (2) inhibit parents from being a resource to adolescents during ED treatment. Attachment-Based Family Therapy (ABFT) is specifically designed to improve FF, and thus may be a promising adjunct to behavioral ED intervention strategies. ABFT, however, has not been tested in adolescents with binge-spectrum EDs. Thus, the current study is the first to evaluate a 16-week adapted ABFT treatment for adolescents with EDs (N = 8, Mage = 16.00, 71.43% female, 71.43% White) fusing together behavioral treatment for EDs with ABFT for highest possible impact. Eight families were treated in an open pilot trial to examine treatment feasibility, acceptability, and preliminary efficacy on FF and eating pathology. Overall, findings were promising. ABFT + B treatment was feasible and acceptable and showed preliminary evidence that it could improve FF and ED behaviors. Future research will test this intervention in a larger sample and further examine the role of FF in maintaining ED symptoms.

Micronutrient-fortified rice improves haemoglobin, anaemia prevalence and cognitive performance among schoolchildren in Gujarat, India: a case-control study.

Anaemia is a public health problem in India. A case-control, quasi-experimental study was conducted to evaluate the effect of a multiple micronutrient fortified rice intervention among school children (6-12 years) through the midday meal programme in Gujarat, India, over 8 months. The fortified rice provided approximately 10% Recommended Dietary Allowance of iron; 25-33% of vitamin A, thiamine, niacin and vitamin B6; and 100% of folic acid and vitamin B12. Outcomes of interest included haemoglobin concentration, anaemia prevalence, and cognitive performance. Cognitive performance was evaluated using J-PAL-validated Pratham reading and mathematics testing tools. 973 children completed the study (cases n = 484; controls n = 489). The intervention significantly increased mean haemoglobin by 0.4 g/dL (p = 0.001), reduced anaemia prevalence by 10% (p < 0.00001), and improved average cognitive scores by 11.3 points (p < 0.001). Rice fortification can help address anaemia in settings where rice is a staple food.

Consequences of TCDD treatment on intra-hepatic lymphocytes during liver regeneration.

Increasing evidence demonstrates a physiological role for the aryl hydrocarbon receptor (AhR) in regulating hepatocyte cell cycle progression. Previous studies have used a murine model of liver regeneration to show that exposure to the potent exogenous AhR ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), suppresses hepatocyte proliferation in vivo. Based on recent reports that natural killer (NK) cells negatively regulate liver regeneration, coupled with the well-established immunomodulatory effects of TCDD, it was hypothesized that alterations in lymphocyte activation contribute to the suppression of liver regeneration in TCDD-treated mice. To test this, mice were treated with TCDD (20 µg/kg) 1 day prior to 70% partial hepatectomy (PH), in which two-thirds of the liver was surgically resected. Lymphocytes were collected from the remnant liver and analyzed by flow cytometry. Whereas exposure to TCDD did not alter the number of NK cells or CD3(+) T-cells recovered from the regenerating liver, it reduced the percentage and number of intra-hepatic NKT cells 42 h after PH. With regard to lymphocyte activation, TCDD treatment transiently increased CD69 expression on NK and NKT cells 12 h after PH, but had no effect on intracellular levels of IFNγ in NK, NKT, or CD3(+) T-cells. To determine the relevance of NK cells to the suppression of liver regeneration by TCDD, mice were treated with anti-Asialo GM-1 (ASGM-1) antibody to deplete NK cells prior to TCDD treatment and PH, and hepatocyte proliferation was measured using bromodeoxyuridine incorporation. Exposure to TCDD was found to inhibit hepatocyte proliferation in the regenerating liver of NK cell-depleted mice and control mice to the same extent. Hence, it is unlikely that enhanced numbers or increased activation of NK cells contribute to the suppression of liver regeneration in TCDD-treated mice.