In depression, bacterial translocation may drive inflammatory responses, oxidative and nitrosative stress (O&NS) and autoimmune responses directed against O&NS- damaged neoepitopes

Objective: Depression is accompanied by activation of immuno-inflammatory and oxidative and nitrosative stress (IO&NS) pathways, and increased IgM/IgA responses to lipopolysaccharide (LPS) of gram-negative commensal bacteria. The latter suggests that bacterial translocation has caused IgM/IgA responses directed against LPS. Bacterial translocation may drive IO&NS responses.

Method: To examine the associations between IgM/IgA responses to LPS and IO&NS measurements, including plasma/serum interleukin-1 (IL-1), tumor necrosis factor (TNF)α, neopterin, lysozyme, oxidized LDL (oxLDL) antibodies, peroxides, and IgM (auto)immune responses against malondialdehyde (MDA), azelaic acid, phophatidyl inositol (Pi), NO-tryptophan and NO-tyrosine in depressed patients and controls.

Results: We found significant positive associations between IgM/IgA responses to LPS and oxLDL antibodies, IgM responses against MDA, azelaic acid, Pi, NO-tryptophan, and NO-tyrosine. The IgA responses to LPS were correlated with lysozyme. There were no significant positive correlations between the IgM/IgA responses to LPS and IL-1 and neopterin.

Conclusion: The findings show that in depression there is an association between increased bacterial translocation and lysozyme production, an antibacterial compound, O&NS processes, and autoimmune responses directed against O&NS generated neoantigenic determinants. It is suggested that bacterial translocation may drive IO&NS pathways in depression and thus play a role in its pathophysiology.

Nutrient and core and non-core food intake of Australian schoolchildren differs on school days compared to non-school days.

Overall the diets of Australian schoolchildren are suboptimal, but differences in nutrient and food intake on school versus non-school days have not been assessed. The aim of this study was to examine differences in nutrient and core and non-core food intake on school days versus non-school days in Australian schoolchildren aged 6-16 years. Cross-sectional analysis of the 2007 Australian Children's Nutrition and Physical Activity Survey. Dietary intake was assessed via one 24-h dietary recall. A school day was defined as Monday-Friday, a non-school day included Saturday, Sunday and public/school holidays. Independent t-tests and χ(2) tests were used to assess differences in continuous and categorical variables, respectively. Multiple linear and logistic regression was used to adjust for confounders. Forty-eight per cent of recalls were completed on a non-school day. On non-school days primary schoolchildren aged 6-11 years (n = 1334) and secondary schoolchildren aged 12-16 years (n = 1362) had significantly higher absolute intakes of sugars, total fat and saturated fat (all P < 0.05). In addition the energy density of foods consumed was greater (P < 0.001), but there was no difference in the energy density of fluids. The sodium density of the diet did not differ across day types. On non-school days, total core food intake was ~30% higher and children were more likely to consume sugar-sweetened beverages, fried potatoes and take-away pizzas and burgers (all P < 0.05). Important differences in the intake of sugar, total fat, and saturated fat and noncore foods exist on non-school days compared to school days in Australian schoolchildren. To improve the diets of schoolchildren there is scope for strategies that target non-school day eating practices.

Metabolic remodelling in obesity and type 2 diabetes: pathological or protective mechanisms in response to nutrient excess?

Altered metabolism in tissues such as the liver, skeletal muscle and adipose tissue is observed in metabolic diseases characterized by nutrient excess and energy imbalance, such as obesity and type 2 diabetes. These alterations in metabolism can include resistance to the hormone insulin, lipid accumulation, mitochondrial dysfunction and transcriptional remodelling of major metabolic pathways. The underlying assumption has been that these same alterations in metabolism are fundamental to the pathogenesis of metabolic diseases. An alternative view is that these alterations in metabolism occur to protect cell and tissue viability in the face of constant positive energy balance. This speculative review presents evidence that many of the metabolic adaptations that occur in metabolic diseases characterized by nutrient excess can be viewed as protective in nature, rather than pathogenic per se for disease progression. Finally, we also briefly discuss the usefulness and potential pitfalls of therapeutic approaches that attempt to correct these same metabolic defects when energy balance is not altered, and the potential links between metabolic survival responses and other chronic diseases such as cancer.