Mediators of longitudinal associations between television viewing and eating behaviours in adolescents

Background: Television viewing has been associated with poor eating behaviours in adolescents. Changing unhealthy eating behaviours is most likely to be achieved by identifying and targeting factors shown to mediate the association between these behaviours. However, little is known about the mediators of the associations between television viewing and eating behaviours. The aim of this study was to examine mediators of the longitudinal associations between television viewing (TV) and eating behaviours among Australian adolescents.
Method: Eating behaviours were assessed using a web-based survey completed by a community-based sample of 1729 adolescents from years 7 and 9 of secondary schools in Victoria, Australia, at baseline (2004-2005) and two years later. TV viewing and the potential mediators (snacking while watching TV and perceived value of TV viewing) were assessed via the web-based survey at baseline.
Results: Adolescents who watched more than two hours of TV/day had higher intakes of energy-dense snacks and beverages, and lower intakes of fruit two years later. Furthermore, the associations between TV viewing and consumption of energy-dense snacks, energy-dense drinks and fruit were mediated by snacking while watching TV. Perceived value of TV viewing mediated the association between TV viewing and consumption of energy-dense snacks, beverages and fruit.
Conclusion: Snacking while watching TV and perceived value of TV viewing mediated the longitudinal association between TV viewing and eating behaviours among adolescents. The efficacy of methods to reduce TV viewing, change snacking habits while watching TV, and address the values that adolescents place on TV viewing should be examined in an effort to promote healthy eating among adolescents.

Correlates of socio-economic inequalities in women’s television viewing : a study of intrapersonal, social and environmental mediators

Introduction

Socio-economically disadvantaged women are at a greater risk of spending excess time engaged in television viewing, a behavior linked to several adverse health outcomes. However, the factors which explain socio-economic differences in television viewing are unknown. This study aimed to investigate the contribution of intrapersonal, social and environmental factors to mediating socio-economic (educational) inequalities in women's television viewing.
Methods

Cross-sectional data were provided by 1,554 women (aged 18-65) who participated in the 'Socio-economic Status and Activity in Women study' of 2004. Based on an ecological framework, women self-reported their socio-economic position (highest education level), television viewing, as well as a number of potential intrapersonal (enjoyment of television viewing, preference for leisure-time sedentary behavior, depression, stress, weight status), social (social participation, interpersonal trust, social cohesion, social support for physical activity from friends and from family) and physical activity environmental factors (safety, aesthetics, distance to places of interest, and distance to physical activity facilities).
Results

Multiple mediating analyses showed that two intrapersonal factors (enjoyment of television viewing and weight status) and two social factors (social cohesion and social support from friends for physical activity) partly explained the educational inequalities in women's television viewing. No physical activity environmental factors mediated educational variations in television viewing.
Conclusions

Acknowledging the cross-sectional nature of this study, these findings suggest that health promotion interventions aimed at reducing educational inequalities in television viewing should focus on intrapersonal and social strategies, particularly providing enjoyable alternatives to television viewing, weight-loss/management information, increasing social cohesion in the neighborhood and promoting friend support for activity.

Early inflammatory and myogenic responses to resistance exercise in the elderly

Introduction and Methods: This study compared changes in myokine and myogenic genes following resistance exercise (3 sets of 12 repetitions of maximal unilateral knee extension) in 20 elderly men (67.8 ± 1.0 years) and 15 elderly women (67.2 ± 1.5 years). Results: Monocyte chemotactic protein (MCP)-1, macrophage inhibitory protein (MIP)-1β, interleukin (IL)-6 and MyoD mRNA increased significantly (P < 0.05), whereas myogenin and myostatin mRNA decreased significantly after exercise in both groups. Macrophage-1 (Mac-1) and MCP-3 mRNA did not change significantly after exercise in either group. MIP-1β, Mac-1 and myostatin mRNA were significantly higher before and after exercise in men compared with women. In contrast, MCP-3 and myogenin mRNA were significantly higher before and after exercise in the women compared with the men. Conclusions: In elderly individuals, gender influences the mRNA expression of certain myokines and growth factors, both at rest and after resistance exercise. These differences may influence muscle regeneration following muscle injury.

New drug targets in depression : inflammatory, cell-mediated immune, oxidative and nitrosative stress, mitochondrial, antioxidant, and neuroprogressive pathways. And new drug candidates—Nrf2 activators and GSK-3 inhibitors

This paper reviews new drug targets in the treatment of depression and new drug candidates to treat depression. Depression is characterized by aberrations in six intertwined pathways: (1) inflammatory pathways as indicated by increased levels of proinflammatory cytokines, e.g. interleukin-1 (IL-1), IL-6, and tumour necrosis factor α. (2) Activation of cell-mediated immune pathways as indicated by an increased production of interferon γ and neopterin. (3) Increased reactive oxygen and nitrogen species and damage by oxidative and nitrosative stress (O&NS), including lipid peroxidation, damage to DNA, proteins and mitochondria. (4) Lowered levels of key antioxidants, such as coenzyme Q10, zinc, vitamin E, glutathione, and glutathione peroxidase. (5) Damage to mitochondria and mitochondrial DNA and reduced activity of respiratory chain enzymes and adenosine triphosphate production. (6) Neuroprogression, which is the progressive process of neurodegeneration, apoptosis, and reduced neurogenesis and neuronal plasticity, phenomena that are probably caused by inflammation and O&NS. Antidepressants tend to normalize the above six pathways. Targeting these pathways has the potential to yield antidepressant effects, e.g. using cytokine antagonists, minocycline, Cox-2 inhibitors, statins, acetylsalicylic acid, ketamine, ω3 poly-unsaturated fatty acids, antioxidants, and neurotrophic factors. These six pathways offer new, pathophysiologically guided drug targets suggesting that novel therapies could be developed that target these six pathways simultaneously. Both nuclear factor (erythroid-derived 2)-like 2 (Nrf2) activators and glycogen synthase kinase-3 (GSK-3) inhibitors target the six above-mentioned pathways. GSK-3 inhibitors have antidepressant effects in animal models of depression. Nrf2 activators and GSK-3 inhibitors have the potential to be advanced to phase-2 clinical trials to examine whether they augment the efficacy of antidepressants or are useful as monotherapy.

Depression and sickness behavior are Janus-faced responses to shared inflammatory pathways

It is of considerable translational importance whether depression is a form or a consequence of sickness behavior. Sickness behavior is a behavioral complex induced by infections and immune trauma and mediated by pro-inflammatory cytokines. It is an adaptive response that enhances recovery by conserving energy to combat acute inflammation. There are considerable phenomenological similarities between sickness behavior and depression, for example, behavioral inhibition, anorexia and weight loss, and melancholic (anhedonia), physio-somatic (fatigue, hyperalgesia, malaise), anxiety and neurocognitive symptoms. In clinical depression, however, a transition occurs to sensitization of immuno-inflammatory pathways, progressive damage by oxidative and nitrosative stress to lipids, proteins, and DNA, and autoimmune responses directed against self-epitopes. The latter mechanisms are the substrate of a neuroprogressive process, whereby multiple depressive episodes cause neural tissue damage and consequent functional and cognitive sequelae. Thus, shared immuno-inflammatory pathways underpin the physiology of sickness behavior and the pathophysiology of clinical depression explaining their partially overlapping phenomenology. Inflammation may provoke a Janus-faced response with a good, acute side, generating protective inflammation through sickness behavior and a bad, chronic side, for example, clinical depression, a lifelong disorder with positive feedback loops between (neuro)inflammation and (neuro)degenerative processes following less well defined triggers.

Depression's multiple comorbidities explained by (neuro)inflammatory and oxidative & nitrosative stress pathways

There is now evidence that depression, as characterized by melancholic symptoms, anxiety, and fatigue and somatic (F&S) symptoms, is the clinical expression of peripheral cell-mediated activation, inflammation and induction of oxidative and nitrosative stress (IO&NS) pathways and of central microglial activation, decreased neurogenesis and increased apoptosis. This review gives an explanation for the multiple “co-morbidities” between depression and a large variety of a) brain disorders related to neurodegeneration, e.g. Alzheimer’s, Parkinson’s and Huntington’s disease, multiple sclerosis and stroke; b) medical disorders, such as cardiovascular disorder, chronic fatigue syndrome, chronic obstructive pulmonary disease, rheumatoid arthritis, psoriasis, systemic lupus erythematosus, inflammatory bowel disease, irritable bowel syndrome, leaky gut, diabetes type 1 and 2, obesity and the metabolic syndrome, and HIV infection; and c) conditions, such as hemodialysis, interferon-α-based immunotherapy, the postnatal period and psychosocial stressors. The common denominator of all those disorders/conditions is the presence of microglial activation and/or activation of peripheral IO&NS pathways. There is evidence that shared peripheral and / or central IO&NS pathways underpin the pathophysiology of depression and the previously mentioned disorders and that activation of these IO&NS pathways contributes to shared risk. The IO&NS pathways function as a smoke sensor that detect threats in the peripheral and central parts of the body and signal these threats as melancholic, anxiety, and fatigue and somatic (F&S) symptoms. The presence of concomitant depression is strongly associated with a lower quality of life and increased morbidity and mortality in medical disorders. This may be explained since depression contributes to increased (neuro)inflammatory burden and may therefore drive the inflammatory and degenerative progression. It is concluded that the activation of peripheral and / or central IO&NS pathways may explain the co-occurrence of depression with the above disorders. This shows that depression belongs to the spectrum of inflammatory and degenerative disorders.