Health-related quality of life in food hypersensitive schoolchildren and their families: parents' perceptions

BACKGROUND: About 20% of schoolchildren and adolescents in Sweden suffer from perceived food hypersensitivity (e.g. allergy or intolerance). Our knowledge of how child food hypersensitivity affects parents HRQL and what aspects of the hypersensitivity condition relate to HRQL deterioration in the family is limited. Thus the aim of this study was to investigate the parent-reported HRQL in families with a schoolchild considered to be food hypersensitive. The allergy-associated parameters we operated with were number of offending food items, adverse food reactions, additional hypersensitivity, allergic diseases and additional family members with food hypersensitivity. These parameters, along with age and gender were assessed in relation to child, parent and family HRQL. METHODS: In May 2004, a postal questionnaire was distributed to parents of 220 schoolchildren with parent-reported food hypersensitivity (response rate 74%). Two questionnaires were used: CHQ-PF28 and a study-specific questionnaire including questions on allergy-associated parameters. In order to find factors that predict impact on HRQL, stepwise multiple linear regression analyses were carried out. RESULTS: An important predictor of low HRQL was allergic disease (i.e. asthma, eczema, rhino conjunctivitis) in addition to food hypersensitivity. The higher the number of allergic diseases, the lower the physical HRQL for the child, the lower the parental HRQL and the more disruption in family activities. Male gender predicted lower physical HRQL than female gender. If the child had sibling(s) with food hypersensitivity this predicted lower psychosocial HRQL for the child and lower parental HRQL. Food-induced gastro-intestinal symptoms predicted lower parental HRQL while food-induced breathing difficulties predicted higher psychosocial HRQL for the child and enhanced HRQL with regards to the family's ability to get along. CONCLUSION: The variance in the child's physical HRQL was to a considerable extent explained by the presence of allergic disease. However, food hypersensitivity by itself was associated with deterioration of child's psychosocial HRQL, regardless of additional allergic disease. The results suggest that it is rather the risk of food reactions and measures to avoid them that are associated with lower HRQL than the clinical reactivity induced by food intake. Therefore, food hypersensitivity must be considered to have a strong psychosocial impact

A Common Carcinogen Benzo[a]pyrene Causes Neuronal Death in Mouse via Microglial Activation

BACKGROUND: Benzo[a]pyrene (B[a]P) belongs to a class of polycyclic aromatic hydrocarbons that serve as micropollutants in the environment. B[a]P has been reported as a probable carcinogen in humans. Exposure to B[a]P can take place by ingestion of contaminated (especially grilled, roasted or smoked) food or water, or inhalation of polluted air. There are reports available that also suggests neurotoxicity as a result of B[a]P exposure, but the exact mechanism of action is unknown. METHODOLOGY/PRINCIPAL FINDINGS: Using neuroblastoma cell line and primary cortical neuron culture, we demonstrated that B[a]P has no direct neurotoxic effect. We utilized both in vivo and in vitro systems to demonstrate that B[a]P causes microglial activation. Using microglial cell line and primary microglial culture, we showed for the first time that B[a]P administration results in elevation of reactive oxygen species within the microglia thereby causing depression of antioxidant protein levels; enhanced expression of inducible nitric oxide synthase, that results in increased production of NO from the cells. Synthesis and secretion of proinflammatory cytokines were also elevated within the microglia, possibly via the p38MAP kinase pathway. All these factors contributed to bystander death of neurons, in vitro. When administered to animals, B[a]P was found to cause microglial activation and astrogliosis in the brain with subsequent increase in proinflammatory cytokine levels. CONCLUSIONS/SIGNIFICANCE: Contrary to earlier published reports we found that B[a]P has no direct neurotoxic activity. However, it kills neurons in a bystander mechanism by activating the immune cells of the brain viz the microglia. For the first time, we have provided conclusive evidence regarding the mechanism by which the micropollutant B[a]P may actually cause damage to the central nervous system. In today's perspective, where rising pollution levels globally are a matter of grave concern, our study throws light on other health hazards that such pollutants may exert

An intervention study of individual, apoE genotype-based dietary and physical-activity advice: impact on health behavior

Issue release date: March 2015201

Supplementary Material for: An Intervention Study of Individual, apoE Genotype-Based Dietary and Physical-Activity Advice: Impact on Health Behavior

<b><i>Aim:</i></b> To assess the behavioral effects of receiving personal genetic information, using apoE genotypes as a tool for promoting lifestyle changes. apoE was chosen because it has a significant impact on lipid metabolism and cholesterol absorption, both factors in cardiovascular disease. <b><i>Methods:</i></b> This study was a 1-year intervention study of healthy adults aged 20-67 years (n = 107). Their behavioral changes were measured by diet (e.g., fat quality, as well as consumption of vegetables, berries, fruits, and fatty and sugary foods), alcohol consumption, and exercise. Health and taste attitudes were assessed with the Health and Taste Attitude Scales (HTAS). The measurements were performed 4 times: at baseline (T0), as well as 10 weeks (T1), 6 months (T2), and 12 months after baseline (T3). These behavioral effects were assessed for three groups: a high-risk (Ɛ4+; n = 16), a low-risk (Ɛ4-; n = 35), and a control group (n = 56). <b><i>Results:</i></b> Personal genetic information affected health behavior. Dietary fat quality improved more in the Ɛ4+ group than in the Ɛ4- and control groups after personal, genotype-based health advice. This change differed significantly between the Ɛ4+ and the control group (p < 0.05), but only for a short time. <b><i>Conclusion:</i></b> Personal genetic information, based on apoE, may affect dietary fat quality. More research is required to determine how to utilize genotype-based health information and how to efficiently achieve long-term changes in the prevention of lifestyle-related diseases

APOE Genotype Disclosure and Lifestyle Advice in a Randomized Intervention Study with Finnish Participants

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