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Celiac disease (CD) is an immune-mediated enteropathy triggered in genetically susceptible individuals by gluten-containing cereals. A central role in the pathogenesis of CD is played by the HLA-restricted gliadin-specific intestinal T cell response generated in a pro-inflammatory environment. The mechanisms that generate this pro-inflammatory environment in CD is now starting to be addressed. In vitro study on CD cells and organoids, shows that constant low-grade inflammation is present also in the absence of gluten. In vivo studies on a population at risk, show before the onset of the disease and before the introduction of gluten in the diet, cellular and metabolic alterations in the absence of a T cell-mediated response. Gluten exacerbates these constitutive alterations in vitro and in vivo. Inflammation, may have a main role in CD, adding this disease tout court to the big family of chronic inflammatory diseases. Nutrients can have pro-inflammatory or anti-inflammatory effects, also mediated by intestinal microbiota. The intestine function as a crossroad for the control of inflammation both locally and at distance. The aim of this review is to discuss the recent literature on the main role of inflammation in the natural history of CD, supported by cellular fragility with increased sensitivity to gluten and other pro-inflammatory agents. [ABSTRACT FROM AUTHOR]

Celiac disease (CD) is an immune-mediated enteropathy triggered in genetically susceptible individuals by gluten-containing cereals. A central role in the pathogenesis of CD is played by the HLA-restricted gliadin-specific intestinal T cell response generated in a pro-inflammatory environment. The mechanisms that generate this pro-inflammatory environment in CD is now starting to be addressed. In vitro study on CD cells and organoids, shows that constant low-grade inflammation is present also in the absence of gluten. In vivo studies on a population at risk, show before the onset of the disease and before the introduction of gluten in the diet, cellular and metabolic alterations in the absence of a T cell-mediated response. Gluten exacerbates these constitutive alterations in vitro and in vivo. Inflammation, may have a main role in CD, adding this disease tout court to the big family of chronic inflammatory diseases. Nutrients can have pro-inflammatory or anti-inflammatory effects, also mediated by intestinal microbiota. The intestine function as a crossroad for the control of inflammation both locally and at distance. The aim of this review is to discuss the recent literature on the main role of inflammation in the natural history of CD, supported by cellular fragility with increased sensitivity to gluten and other pro-inflammatory agents.

Social disadvantage and diet composition independently impact myriad dimensions of health. They are closely entwined, as social disadvantage often yields poor diet quality, and may interact to fuel differential health outcomes. This paper reviews effects of psychosocial stress and diet composition on health in nonhuman primates and their implications for aging and human health. We examined the effects of social subordination stress and Mediterranean versus Western diet on multiple systems. We report that psychosocial stress and Western diet have independent and additive adverse effects on hypothalamic-pituitary-adrenal and autonomic nervous system reactivity to psychological stressors, brain structure, and ovarian function. Compared to the Mediterranean diet, the Western diet resulted in accelerated aging, nonalcoholic fatty liver disease, insulin resistance, gut microbial changes associated with increased disease risk, neuroinflammation, neuroanatomical perturbations, anxiety, and social isolation. This comprehensive, multisystem investigation lays the foundation for future investigations of the mechanistic underpinnings of psychosocial stress and diet effects on health, and advances the promise of the Mediterranean diet as a therapeutic intervention on psychosocial stress. • Social disadvantage is accompanied by poor diet quality, both of which impact health. • Social stress and Western diet have additive adverse effects on multiple systems. • Mediterranean diet protects against many of the deleterious effects of social stress. • Mediterranean diet may be an efficacious intervention on psychosocial stress. [ABSTRACT FROM AUTHOR]

Background/Objectives:To observe fruit and vegetable consumption as it relates to body mass index (BMI) and other variables, by analyzing the health surveys of two countries—the United States and France—with traditionally distinct diets, and identifying factors that may explain the differences.Subjects/Methods:Two nationally representative surveys that assess food intake via 24-h diet recalls. Respondents include 2126 women and 1911 men from the US National Health and Nutrition Examination Survey, and 1572 women and 1141 men from the French Nutrition Barometer Survey. Standard linear regression models and t-tests of both simple and predictive marginal means were run employing the software package SUDAAN.Results:Americans appear to consume fruits and vegetables less often than their French counterparts (1.04 vs 1.33 times per day fruits; 1.98 vs 2.29 times per day vegetables). American men consume fruits and vegetables least often (0.98 times per day fruits; 1.88 times per day vegetables) than do American women or French men (1.10 vs 1.25 times per day fruits; 2.07 vs 2.18 times per day vegetables). French women consume fruits and vegetables most often (1.41 times per day fruits; 2.41 times per day vegetables). The French have lower mean BMI than Americans (23.34 vs 28.22 women; 25.20 vs 28.02 men). Regression analyses showed that age, BMI and educational attainment are strongly associated with frequency of consumption.Conclusions:These results support our hypothesis that the French tend to eat fruits and vegetables more often than Americans. This study proves to be an important first step in determining some of the influential factors that may affect various populations' consumption of fruits and vegetables.European Journal of Clinical Nutrition (2009) 63, 11–17; doi:10.1038/ejcn.2008.2; published online 13 February 2008 [ABSTRACT FROM AUTHOR]