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      A Positive Association between T. gondii Seropositivity and Obesity

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          Abstract

          Obesity is a global public health problem that is linked with morbidity, mortality, and functional limitations and has limited options for sustained interventions. Novel targets for prevention and intervention require further research into the pathogenesis of obesity. Consistently, elevated markers of inflammation have been reported in association with obesity, but their causes and consequences are not well understood. An emerging field of research has investigated the association of infections and environmental pathogens with obesity, potential causes of low grade inflammation that may mediate obesity risk. In this study, we estimate the possible association between Toxoplasma gondii ( T. gondii) infection and obesity in a sample of 999 psychiatrically healthy adults. Individuals with psychiatric conditions, including personality disorders, were excluded because of the association between positive serology to T. gondii and various forms of serious mental illness that have a strong association with obesity. In our sample, individuals with positive T. gondii serology had twice the odds of being obese compared to seronegative individuals ( p = 0.01). Further, individuals who were obese had significant higher T. gondii IgG titers compared to individuals who were non-obese. Latent T. gondii infection is very common worldwide, so potential public health interventions related to this parasite can have a high impact on associated health concerns.

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          Most cited references34

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          Inflammation: the link between insulin resistance, obesity and diabetes.

          Recent data have revealed that the plasma concentration of inflammatory mediators, such as tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), is increased in the insulin resistant states of obesity and type 2 diabetes, raising questions about the mechanisms underlying inflammation in these two conditions. It is also intriguing that an increase in inflammatory mediators or indices predicts the future development of obesity and diabetes. Two mechanisms might be involved in the pathogenesis of inflammation. Firstly, glucose and macronutrient intake causes oxidative stress and inflammatory changes. Chronic overnutrition (obesity) might thus be a proinflammatory state with oxidative stress. Secondly, the increased concentrations of TNF-alpha and IL-6, associated with obesity and type 2 diabetes, might interfere with insulin action by suppressing insulin signal transduction. This might interfere with the anti-inflammatory effect of insulin, which in turn might promote inflammation.
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            Food-borne diseases — The challenges of 20 years ago still persist while new ones continue to emerge

            The burden of diseases caused by food-borne pathogens remains largely unknown. Importantly data indicating trends in food-borne infectious intestinal disease is limited to a few industrialised countries, and even fewer pathogens. It has been predicted that the importance of diarrhoeal disease, mainly due to contaminated food and water, as a cause of death will decline worldwide. Evidence for such a downward trend is limited. This prediction presumes that improvements in the production and retail of microbiologically safe food will be sustained in the developed world and, moreover, will be rolled out to those countries of the developing world increasingly producing food for a global market. In this review evidence is presented to indicate that the microbiological safety of food remains a dynamic situation heavily influenced by multiple factors along the food chain from farm to fork. Sustaining food safety standards will depend on constant vigilance maintained by monitoring and surveillance but, with the rising importance of other food-related issues, such as food security, obesity and climate change, competition for resources in the future to enable this may be fierce. In addition the pathogen populations relevant to food safety are not static. Food is an excellent vehicle by which many pathogens (bacteria, viruses/prions and parasites) can reach an appropriate colonisation site in a new host. Although food production practices change, the well-recognised food-borne pathogens, such as Salmonella spp. and Escherichia coli, seem able to evolve to exploit novel opportunities, for example fresh produce, and even generate new public health challenges, for example antimicrobial resistance. In addition, previously unknown food-borne pathogens, many of which are zoonotic, are constantly emerging. Current understanding of the trends in food-borne diseases for bacterial, viral and parasitic pathogens has been reviewed. The bacterial pathogens are exemplified by those well-recognized by policy makers; i.e. Salmonella, Campylobacter, E. coli and Listeria monocytogenes. Antimicrobial resistance in several bacterial food-borne pathogens (Salmonella, Campylobacter, Shigella and Vibrio spp., methicillin resistant Staphylcoccus aureas, E. coli and Enterococci) has been discussed as a separate topic because of its relative importance to policy issues. Awareness and surveillance of viral food-borne pathogens is generally poor but emphasis is placed on Norovirus, Hepatitis A, rotaviruses and newly emerging viruses such as SARS. Many food-borne parasitic pathogens are known (for example Ascaris, Cryptosporidia and Trichinella) but few of these are effectively monitored in foods, livestock and wildlife and their epidemiology through the food-chain is poorly understood. The lessons learned and future challenges in each topic are debated. It is clear that one overall challenge is the generation and maintenance of constructive dialogue and collaboration between public health, veterinary and food safety experts, bringing together multidisciplinary skills and multi-pathogen expertise. Such collaboration is essential to monitor changing trends in the well-recognised diseases and detect emerging pathogens. It will also be necessary understand the multiple interactions these pathogens have with their environments during transmission along the food chain in order to develop effective prevention and control strategies.
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              The Neurotropic Parasite Toxoplasma Gondii Increases Dopamine Metabolism

              The highly prevalent parasite Toxoplasma gondii manipulates its host's behavior. In infected rodents, the behavioral changes increase the likelihood that the parasite will be transmitted back to its definitive cat host, an essential step in completion of the parasite's life cycle. The mechanism(s) responsible for behavioral changes in the host is unknown but two lines of published evidence suggest that the parasite alters neurotransmitter signal transduction: the disruption of the parasite-induced behavioral changes with medications used to treat psychiatric disease (specifically dopamine antagonists) and identification of a tyrosine hydroxylase encoded in the parasite genome. In this study, infection of mammalian dopaminergic cells with T. gondii enhanced the levels of K+-induced release of dopamine several-fold, with a direct correlation between the number of infected cells and the quantity of dopamine released. Immunostaining brain sections of infected mice with dopamine antibody showed intense staining of encysted parasites. Based on these analyses, T. gondii orchestrates a significant increase in dopamine metabolism in neural cells. Tyrosine hydroxylase, the rate-limiting enzyme for dopamine synthesis, was also found in intracellular tissue cysts in brain tissue with antibodies specific for the parasite-encoded tyrosine hydroxylase. These observations provide a mechanism for parasite-induced behavioral changes. The observed effects on dopamine metabolism could also be relevant in interpreting reports of psychobehavioral changes in toxoplasmosis-infected humans.
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                Author and article information

                Contributors
                Journal
                Front Public Health
                Front Public Health
                Front. Public Health
                Frontiers in Public Health
                Frontiers Media S.A.
                2296-2565
                22 October 2013
                25 December 2013
                2013
                : 1
                : 73
                Affiliations
                [1] 1Child and Adolescent Mental Health Innovations Center, Department of Psychiatry, University of Maryland, School of Medicine , Baltimore, MD, USA
                [2] 2Division of Child and Adolescent Psychiatry, Department of Psychiatry, University of Maryland, School of Medicine , Baltimore, MD, USA
                [3] 3St. Elizabeths Hospital, Psychiatry ResidencyTraining Program , Washington, DC, USA
                [4] 4Division of Endocrinology, Diabetes, and Nutrition, Department of Medicine, University of Maryland, School of Medicine , Baltimore, MD, USA
                [5] 5Department of Epidemiology and Public Health, University of Maryland, School of Medicine , Baltimore, MD, USA
                [6] 6Department of Psychiatry, Martin-Luther-Universität Halle-Wittenberg , Halle, Germany
                [7] 7Department of Psychiatry and Behavioral Sciences, The University of Texas Health Science Center at Houston , TX, USA
                [8] 8Colleges of Nursing and Medicine, University of South Florida , Tampa, FL, USA
                [9] 9Research Unit on Lifestyle and Inflammation-associated Risk Biomarkers, Clinical Institute for Medical and Chemical Laboratory Diagnosis, Medical University of Graz , Graz, Austria
                [10] 10Department of Pediatrics, Paracelsus Medical School , Salzburg, Austria
                [11] 11Section on Statistical Genetics, Department of Biostatistics, Nutrition Obesity Research Center, University of Alabama at Birmingham , Birmingham, AL, USA
                [12] 12Mood and Anxiety Disorder Program, Department of Psychiatry, University of Maryland, School of Medicine , Baltimore, MD, USA
                Author notes

                Edited by: Joav Merrick, Ministry of Social Affairs, Israel

                Reviewed by: Cihad Dundar, Ondokuz Mayis University, Turkey; Mohammed Morad, Clalit Health Services, Israel

                *Correspondence: Teodor T. Postolache, Mood and Anxiety Program, Department of Psychiatry, University of Maryland, School of Medicine, 685 West Baltimore Street, MSTF Building Room 930, Baltimore, MD 21201, USA e-mail: teopostolache@ 123456gmail.com

                Dan Rujescu and Teodor T. Postolache share senior authorship of this paper and contributed equally in this role.

                This article was submitted to Child Health and Human Development, a section of the journal Frontiers in Public Health.

                Article
                10.3389/fpubh.2013.00073
                3872312
                24400300
                6ac05681-62d6-4a41-b865-3550e3e52d89
                Copyright © 2013 Reeves, Mazaheri, Snitker, Langenberg, Giegling, Hartmann, Konte, Friedl, Okusaga, Groer, Mangge, Weghuber, Allison, Rujescu and Postolache.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 04 October 2013
                : 09 December 2013
                Page count
                Figures: 0, Tables: 2, Equations: 0, References: 46, Pages: 6, Words: 4995
                Categories
                Public Health
                Original Research

                obesity,parasitic infection,inflammation,body weight,toxoplasma gondii

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