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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"><channel rdf:about="http://onlinelibrary.wiley.com/rss/journal/10.1111/(ISSN)1753-4887" xmlns="http://purl.org/rss/1.0/"><title>Nutrition Reviews</title><description> Wiley Online Library : Nutrition Reviews</description><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2F%28ISSN%291753-4887</link><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc</dc:publisher><dc:language xmlns:dc="http://purl.org/dc/elements/1.1/">en</dc:language><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/">© International Life Sciences Institute</dc:rights><prism:issn xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">0029-6643</prism:issn><prism:eIssn xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">1753-4887</prism:eIssn><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-01T00:00:00-05:00</dc:date><prism:coverDisplayDate xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">May 2013</prism:coverDisplayDate><prism:volume xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">71</prism:volume><prism:number xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">5</prism:number><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">257</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">318</prism:endingPage><image rdf:resource="http://onlinelibrary.wiley.com/store/10.1111/nure.2013.71.issue-5/asset/cover.gif?v=1&amp;s=6ebe389d55d68795475dacdfb89f2f8b5b3d3caf"/><items><rdf:Seq><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12030"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12027"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12038"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12034"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12033"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12025"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12032"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12026"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12037"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12036"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12024"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12028"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12023"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12012"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12020"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12031"/></rdf:Seq></items></channel><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12030" xmlns="http://purl.org/rss/1.0/"><title>The epigenome as a potential mediator of cancer and disease prevention in prenatal development</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12030</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The epigenome as a potential mediator of cancer and disease prevention in prenatal development</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Pushpinder Kaur, Lyndsey E Shorey, Emily Ho, Roderick H Dashwood, David E Williams</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-15T09:32:51.189163-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/nure.12030</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/nure.12030</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12030</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Special Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Epigenetic events establish a particular gene expression signature for each cell type during differentiation and fertilization. Disruption of these epigenetic programs in response to environmental stimuli during prenatal exposure dysregulates the fetal epigenome, potentially impacting susceptibility to disease later in life (the fetal basis of adult disease). Maternal dietary modifications during gestation and lactation play a pivotal role in the period of fetal (re)programming. Recently, many studies have demonstrated the impact of maternal nutrition on the fetal epigenome. This review discusses the complex interplay among various environmental factors and epigenetic mechanisms that have been found to affect offspring in human and animal models. Further, it summarizes the impact of various dietary phytochemicals capable of modulating the epigenome with regard to diverse human cancers and childhood cancer, specifically those with potential environmental etiology through maternal consumption during pregnancy and lactation. Other dietary agents that are still untested as to their effectiveness in transplacental studies are also discussed. The recent developments discussed herein enhance current understanding of how chemopreventive agents act and their potential to impact the prenatal epigenome; they may also aid efforts to identify dietary interventions that can be beneficial in treating and preventing disease.</p></div>
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Epigenetic events establish a particular gene expression signature for each cell type during differentiation and fertilization. Disruption of these epigenetic programs in response to environmental stimuli during prenatal exposure dysregulates the fetal epigenome, potentially impacting susceptibility to disease later in life (the fetal basis of adult disease). Maternal dietary modifications during gestation and lactation play a pivotal role in the period of fetal (re)programming. Recently, many studies have demonstrated the impact of maternal nutrition on the fetal epigenome. This review discusses the complex interplay among various environmental factors and epigenetic mechanisms that have been found to affect offspring in human and animal models. Further, it summarizes the impact of various dietary phytochemicals capable of modulating the epigenome with regard to diverse human cancers and childhood cancer, specifically those with potential environmental etiology through maternal consumption during pregnancy and lactation. Other dietary agents that are still untested as to their effectiveness in transplacental studies are also discussed. The recent developments discussed herein enhance current understanding of how chemopreventive agents act and their potential to impact the prenatal epigenome; they may also aid efforts to identify dietary interventions that can be beneficial in treating and preventing disease.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12027" xmlns="http://purl.org/rss/1.0/"><title>Ethanol metabolism and its effects on the intestinal epithelial barrier</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12027</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Ethanol metabolism and its effects on the intestinal epithelial barrier</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Elhaseen E Elamin, Ad A Masclee, Jan Dekker, Daisy M Jonkers</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-06T09:45:57.649261-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/nure.12027</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/nure.12027</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12027</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Special Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Ethanol is widely consumed and is associated with an increasing global health burden. Several reviews have addressed the effects of ethanol and its oxidative metabolite, acetaldehyde, on the gastrointestinal (GI) tract, focusing on carcinogenic effects or alcoholic liver disease. However, both the oxidative and the nonoxidative metabolites of ethanol can affect the epithelial barrier of the small and large intestines, thereby contributing to GI and liver diseases. This review outlines the possible mechanisms of ethanol metabolism as well as the effects of ethanol and its metabolites on the intestinal barrier. Limited studies in humans and supporting in vitro data have indicated that ethanol as well as mainly acetaldehyde can increase small intestinal permeability. Limited evidence also points to increased colon permeability following exposure to ethanol or acetaldehyde. In vitro studies have provided several mechanisms for disruption of the epithelial barrier, including activation of different cell-signaling pathways, oxidative stress, and remodeling of the cytoskeleton. Modulation via intestinal microbiota, however, should also be considered. In conclusion, ethanol and its metabolites may act additively or even synergistically in vivo. Therefore, in vivo studies investigating the effects of ethanol and its byproducts on permeability of the small and large intestines are warranted.</p></div>
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Ethanol is widely consumed and is associated with an increasing global health burden. Several reviews have addressed the effects of ethanol and its oxidative metabolite, acetaldehyde, on the gastrointestinal (GI) tract, focusing on carcinogenic effects or alcoholic liver disease. However, both the oxidative and the nonoxidative metabolites of ethanol can affect the epithelial barrier of the small and large intestines, thereby contributing to GI and liver diseases. This review outlines the possible mechanisms of ethanol metabolism as well as the effects of ethanol and its metabolites on the intestinal barrier. Limited studies in humans and supporting in vitro data have indicated that ethanol as well as mainly acetaldehyde can increase small intestinal permeability. Limited evidence also points to increased colon permeability following exposure to ethanol or acetaldehyde. In vitro studies have provided several mechanisms for disruption of the epithelial barrier, including activation of different cell-signaling pathways, oxidative stress, and remodeling of the cytoskeleton. Modulation via intestinal microbiota, however, should also be considered. In conclusion, ethanol and its metabolites may act additively or even synergistically in vivo. Therefore, in vivo studies investigating the effects of ethanol and its byproducts on permeability of the small and large intestines are warranted.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12038" xmlns="http://purl.org/rss/1.0/"><title>Diet beverages and the risk of obesity, diabetes, and cardiovascular disease: a review of the evidence</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12038</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Diet beverages and the risk of obesity, diabetes, and cardiovascular disease: a review of the evidence</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Mark A Pereira</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-02T10:36:34.34792-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/nure.12038</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/nure.12038</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12038</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Special Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>“Diet beverage” is a common term used to describe beverages that are sweetened with non-nutritive or artificial sweeteners (ASBs). Marketing strategies often imply that consuming these beverages holds promise for weight control or weight loss. The objective of the present review is to provide a synthesis of the literature on the effects of ASBs on body weight, cardiovascular disease, and type 2 diabetes. Consumption of diet beverages is much lower than that of sugar-sweetened beverages (SSBs), and people trying to lose weight report the highest levels of ASB consumption. To date, prospective observational studies have revealed mixed results, and it appears that reverse causality is a particular problem, since individuals who are at higher risk for weight gain may choose to consume ASBs in an attempt to control their weight or reduce disease risk. As for experimental studies, the evidence currently suggests that obesity risk may be lower when ASBs replace SSBs in the diet. Still, additional evidence from experimental studies is needed to more definitively determine the benefits and risks of frequent ASB consumption.</p></div>
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“Diet beverage” is a common term used to describe beverages that are sweetened with non-nutritive or artificial sweeteners (ASBs). Marketing strategies often imply that consuming these beverages holds promise for weight control or weight loss. The objective of the present review is to provide a synthesis of the literature on the effects of ASBs on body weight, cardiovascular disease, and type 2 diabetes. Consumption of diet beverages is much lower than that of sugar-sweetened beverages (SSBs), and people trying to lose weight report the highest levels of ASB consumption. To date, prospective observational studies have revealed mixed results, and it appears that reverse causality is a particular problem, since individuals who are at higher risk for weight gain may choose to consume ASBs in an attempt to control their weight or reduce disease risk. As for experimental studies, the evidence currently suggests that obesity risk may be lower when ASBs replace SSBs in the diet. Still, additional evidence from experimental studies is needed to more definitively determine the benefits and risks of frequent ASB consumption.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12034" xmlns="http://purl.org/rss/1.0/"><title>Association between weight gain during pregnancy and postpartum weight retention and obesity: a bias-adjusted meta-analysis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12034</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Association between weight gain during pregnancy and postpartum weight retention and obesity: a bias-adjusted meta-analysis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Munim Mannan, Suhail AR Doi, Abdullah A Mamun</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-02T10:36:29.75265-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/nure.12034</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/nure.12034</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12034</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Special Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Gestational weight gain (GWG) is associated with postpartum weight retention (PPWR) in women. The strength of the association between GWG and long-term PPWR and body mass index (BMI), however, is still unclear. Publications from different databases were systematically extracted and the articles relevant to this study were reviewed to quantify the effect estimate of GWG on PPWR and BMI using a bias-adjusted method. The Institute of Medicine categories of “inadequate,” “adequate,” and “excess” were used to define GWG. The time span for PPWR was divided into three periods (<em>&lt;</em>1 year, 1 year to 9 years, and <em>≥</em>15 years) to determine outcome at different times postpartum. Twelve studies met the eligibility criteria and were included in the analyses. Women with an inadequate GWG had a significantly lower mean PPWR of −2.14 kg (95%CI, −2.61 to −1.66) than women with an adequate GWG, who had a mean PPWR of 3.15 kg (95%CI, 2.47 to 3.82) up to 21 years postpartum. Over the postpartum time span, a U-shaped relationship was observed between the weighted mean difference calculated for women with excess GWG and the weighted mean difference calculated for women with adequate GWG, and this relationship was time independent between these two groups. Postpartum BMI showed a similar relationship and magnitude of change, but the exact loss or gain was difficult to assess due to fewer studies (<em>n</em> <em>=</em> 5) with considerable heterogeneity of BMI measurements. The findings of this study suggest that GWG outside of the Institute of Medicine recommendations can lead to both short-term and long-term postpartum weight imbalance.</p></div>
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Gestational weight gain (GWG) is associated with postpartum weight retention (PPWR) in women. The strength of the association between GWG and long-term PPWR and body mass index (BMI), however, is still unclear. Publications from different databases were systematically extracted and the articles relevant to this study were reviewed to quantify the effect estimate of GWG on PPWR and BMI using a bias-adjusted method. The Institute of Medicine categories of “inadequate,” “adequate,” and “excess” were used to define GWG. The time span for PPWR was divided into three periods (&lt;1 year, 1 year to 9 years, and ≥15 years) to determine outcome at different times postpartum. Twelve studies met the eligibility criteria and were included in the analyses. Women with an inadequate GWG had a significantly lower mean PPWR of −2.14 kg (95%CI, −2.61 to −1.66) than women with an adequate GWG, who had a mean PPWR of 3.15 kg (95%CI, 2.47 to 3.82) up to 21 years postpartum. Over the postpartum time span, a U-shaped relationship was observed between the weighted mean difference calculated for women with excess GWG and the weighted mean difference calculated for women with adequate GWG, and this relationship was time independent between these two groups. Postpartum BMI showed a similar relationship and magnitude of change, but the exact loss or gain was difficult to assess due to fewer studies (n = 5) with considerable heterogeneity of BMI measurements. The findings of this study suggest that GWG outside of the Institute of Medicine recommendations can lead to both short-term and long-term postpartum weight imbalance.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12033" xmlns="http://purl.org/rss/1.0/"><title>Evidence of health benefits of canola oil</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12033</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Evidence of health benefits of canola oil</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Lin Lin, Hanja Allemekinders, Angela Dansby, Lisa Campbell, Shaunda Durance-Tod, Alvin Berger, Peter JH Jones</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-02T10:36:19.907556-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/nure.12033</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/nure.12033</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12033</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Special Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Canola oil-based diets have been shown to reduce plasma cholesterol levels in comparison with diets containing higher levels of saturated fatty acids. Consumption of canola oil also influences biological functions that affect various other biomarkers of disease risk. Previous reviews have focused on the health effects of individual components of canola oil. Here, the objective is to address the health effects of intact canola oil, as this has immediate practical implications for consumers, nutritionists, and others deciding which oil to consume or recommend. A literature search was conducted to examine the effects of canola oil consumption on coronary heart disease, insulin sensitivity, lipid peroxidation, inflammation, energy metabolism, and cancer cell growth. Data reveal substantial reductions in total cholesterol and low-density lipoprotein cholesterol, as well as other positive actions, including increased tocopherol levels and improved insulin sensitivity, compared with consumption of other dietary fat sources. In summary, growing scientific evidence supports the use of canola oil, beyond its beneficial actions on circulating lipid levels, as a health-promoting component of the diet.</p></div>
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Canola oil-based diets have been shown to reduce plasma cholesterol levels in comparison with diets containing higher levels of saturated fatty acids. Consumption of canola oil also influences biological functions that affect various other biomarkers of disease risk. Previous reviews have focused on the health effects of individual components of canola oil. Here, the objective is to address the health effects of intact canola oil, as this has immediate practical implications for consumers, nutritionists, and others deciding which oil to consume or recommend. A literature search was conducted to examine the effects of canola oil consumption on coronary heart disease, insulin sensitivity, lipid peroxidation, inflammation, energy metabolism, and cancer cell growth. Data reveal substantial reductions in total cholesterol and low-density lipoprotein cholesterol, as well as other positive actions, including increased tocopherol levels and improved insulin sensitivity, compared with consumption of other dietary fat sources. In summary, growing scientific evidence supports the use of canola oil, beyond its beneficial actions on circulating lipid levels, as a health-promoting component of the diet.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12025" xmlns="http://purl.org/rss/1.0/"><title>Use of dual X-ray absorptiometry to measure body mass during short- to medium-term trials of nutrition and exercise interventions</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12025</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Use of dual X-ray absorptiometry to measure body mass during short- to medium-term trials of nutrition and exercise interventions</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Christopher PF Marinangeli, Amira N Kassis</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-02T10:36:13.326903-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/nure.12025</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/nure.12025</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12025</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Lead Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Dual X-ray absorptiometry (DXA) has a range of clinical applications, from assessing associations between adipose or lean body mass and the risk of disease to measuring the effects of dietary interventions on adipose deposition and oxidation and/or muscle accumulation. Many lifestyle-related studies, however, are short- to medium-term interventions, and inter- or intradevice variation between DXA scanners can facilitate type I and type II errors during data analysis. Studies demonstrate that variation in body composition measurements exist not only between DXA instruments using fan-beam and pencil-beam technologies but also between DXA instruments produced by different manufacturers. Moreover, studies show inter- and intrainstrument variation between identical DXA instruments. Such inter- and intrascan variability between instruments can be compounded by the particular patient population being investigated. The objective of this review is to discuss inter- and intradevice variation of DXA instruments and to outline quality control procedures that should be implemented prior to initiating short-term single or multicenter clinical trials that use DXA to investigate the effects of an intervention on loss or accretion of lean or fat mass.</p></div>
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Dual X-ray absorptiometry (DXA) has a range of clinical applications, from assessing associations between adipose or lean body mass and the risk of disease to measuring the effects of dietary interventions on adipose deposition and oxidation and/or muscle accumulation. Many lifestyle-related studies, however, are short- to medium-term interventions, and inter- or intradevice variation between DXA scanners can facilitate type I and type II errors during data analysis. Studies demonstrate that variation in body composition measurements exist not only between DXA instruments using fan-beam and pencil-beam technologies but also between DXA instruments produced by different manufacturers. Moreover, studies show inter- and intrainstrument variation between identical DXA instruments. Such inter- and intrascan variability between instruments can be compounded by the particular patient population being investigated. The objective of this review is to discuss inter- and intradevice variation of DXA instruments and to outline quality control procedures that should be implemented prior to initiating short-term single or multicenter clinical trials that use DXA to investigate the effects of an intervention on loss or accretion of lean or fat mass.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12032" xmlns="http://purl.org/rss/1.0/"><title>Dietary fiber and the risk of precancerous lesions and cancer of the esophagus: a systematic review and meta-analysis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12032</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Dietary fiber and the risk of precancerous lesions and cancer of the esophagus: a systematic review and meta-analysis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Helen G Coleman, Liam J Murray, Blanaid Hicks, Shivaram K Bhat, Ai Kubo, Douglas A Corley, Chris R Cardwell, Marie M Cantwell</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-24T12:32:24.595528-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/nure.12032</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/nure.12032</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12032</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Special Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Dietary fiber has several anticarcinogenic effects and is thought to be protective against esophageal cancer. The aim of this systematic review was to quantify the association between dietary fiber and the risk of esophageal cancer by investigating histological subtypes of esophageal cancer and the stage at which fiber may influence the carcinogenic pathway. Systematic search strategies were used to identify relevant studies, and adjusted odds ratios (ORs) were combined using random-effects meta-analyses to assess the risk of cancer when comparing extreme categories of fiber intake. Ten relevant case-control studies were identified within the timeframe searched. Pooled estimates from eight studies of esophageal adenocarcinoma revealed a significant inverse association with the highest fiber intakes (OR 0.66; 95% confidence interval (CI) 0.44–0.98). Two studies also identified protective effects of dietary fiber against Barrett's esophagus. Similar, though nonsignificant, associations were observed when results from five studies of fiber intake and risk of squamous cell carcinoma were combined (OR 0.61; 95%CI 0.31–1.20). Dietary fiber is associated with protective effects against esophageal carcinogenesis, most notably esophageal adenocarcinoma. Potential methods of action include modification of gastroesophageal reflux and/or weight control.</p></div>
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Dietary fiber has several anticarcinogenic effects and is thought to be protective against esophageal cancer. The aim of this systematic review was to quantify the association between dietary fiber and the risk of esophageal cancer by investigating histological subtypes of esophageal cancer and the stage at which fiber may influence the carcinogenic pathway. Systematic search strategies were used to identify relevant studies, and adjusted odds ratios (ORs) were combined using random-effects meta-analyses to assess the risk of cancer when comparing extreme categories of fiber intake. Ten relevant case-control studies were identified within the timeframe searched. Pooled estimates from eight studies of esophageal adenocarcinoma revealed a significant inverse association with the highest fiber intakes (OR 0.66; 95% confidence interval (CI) 0.44–0.98). Two studies also identified protective effects of dietary fiber against Barrett's esophagus. Similar, though nonsignificant, associations were observed when results from five studies of fiber intake and risk of squamous cell carcinoma were combined (OR 0.61; 95%CI 0.31–1.20). Dietary fiber is associated with protective effects against esophageal carcinogenesis, most notably esophageal adenocarcinoma. Potential methods of action include modification of gastroesophageal reflux and/or weight control.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12026" xmlns="http://purl.org/rss/1.0/"><title>Bioavailability of vitamin E in humans: an update</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12026</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Bioavailability of vitamin E in humans: an update</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Patrick Borel, Damien Preveraud, Charles Desmarchelier</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-24T12:32:16.720332-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/nure.12026</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/nure.12026</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12026</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Lead Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Vitamin E is essential for human health and may play a role in the prevention of some degenerative diseases. Its bioavailability, however, is wide ranging and is affected by numerous factors. Recent findings showing that the intestinal absorption of vitamin E involves proteins have raised new relevant questions about factors that can affect bioavailability. It is, therefore, opportune to present a current overview of this topic. This review begins by exploring what is known, as well as what is unknown, about the metabolization of vitamin E in the human upper gastrointestinal tract and then presents a methodical evaluation of factors assumed to affect vitamin E bioavailability. Three main conclusions can be drawn. First, the proteins ABCA1, NPC1L1, and SR-BI are implicated in the absorption of vitamin E. Second, the efficiency of vitamin E absorption is widely variable, though not accurately known (i.e., between 10% and 79%), and is affected by several dietary factors (e.g., food matrix, fat, and fat-soluble micronutrients). Finally, numerous unanswered questions remain about the metabolization of vitamin E in the intestinal lumen and about the factors affecting the efficiency of vitamin E absorption.</p></div>
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Vitamin E is essential for human health and may play a role in the prevention of some degenerative diseases. Its bioavailability, however, is wide ranging and is affected by numerous factors. Recent findings showing that the intestinal absorption of vitamin E involves proteins have raised new relevant questions about factors that can affect bioavailability. It is, therefore, opportune to present a current overview of this topic. This review begins by exploring what is known, as well as what is unknown, about the metabolization of vitamin E in the human upper gastrointestinal tract and then presents a methodical evaluation of factors assumed to affect vitamin E bioavailability. Three main conclusions can be drawn. First, the proteins ABCA1, NPC1L1, and SR-BI are implicated in the absorption of vitamin E. Second, the efficiency of vitamin E absorption is widely variable, though not accurately known (i.e., between 10% and 79%), and is affected by several dietary factors (e.g., food matrix, fat, and fat-soluble micronutrients). Finally, numerous unanswered questions remain about the metabolization of vitamin E in the intestinal lumen and about the factors affecting the efficiency of vitamin E absorption.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12037" xmlns="http://purl.org/rss/1.0/"><title>Effect of iron intervention on growth during gestation, infancy, childhood, and adolescence: a systematic review with meta-analysis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12037</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Effect of iron intervention on growth during gestation, infancy, childhood, and adolescence: a systematic review with meta-analysis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Vesna Vucic, Cristiana Berti, Christiane Vollhardt, Katalin Fekete, Irene Cetin, Berthold Koletzko, Mirjana Gurinovic, Pieter Veer</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-12T10:35:24.297322-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/nure.12037</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/nure.12037</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12037</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Special Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>To evaluate the effect of iron intervention on physical growth in fetuses, infants, children, and adolescents up to 18 years of age, a systematic review with meta-analysis of randomized controlled trials (RCTs) was conducted. Structured electronic searches were conducted to February 2010 using MEDLINE, Embase, and the Cochrane Library databases. RCTs that included iron-fortified foods, iron-fortified formula, or iron supplements and in which height, weight, mid-arm circumference (MAC), head circumference, birth weight, or length of gestation was evaluated were analyzed for inclusion. In total, 21 RCTs in infants, children, and adolescents and 7 studies in pregnant women met the inclusion criteria. The overall pooled result (random-effects model) showed no significant effects of iron intervention on any of the parameters measured. To accommodate wide heterogeneity, studies were stratified according to dose of iron, duration of intervention, age, and baseline iron status. However, only doses of 40–66 mg of supplemental iron and intervention in children <em>≥</em>6 years of age showed a slight but significant association with weight and MAC.</p></div>
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To evaluate the effect of iron intervention on physical growth in fetuses, infants, children, and adolescents up to 18 years of age, a systematic review with meta-analysis of randomized controlled trials (RCTs) was conducted. Structured electronic searches were conducted to February 2010 using MEDLINE, Embase, and the Cochrane Library databases. RCTs that included iron-fortified foods, iron-fortified formula, or iron supplements and in which height, weight, mid-arm circumference (MAC), head circumference, birth weight, or length of gestation was evaluated were analyzed for inclusion. In total, 21 RCTs in infants, children, and adolescents and 7 studies in pregnant women met the inclusion criteria. The overall pooled result (random-effects model) showed no significant effects of iron intervention on any of the parameters measured. To accommodate wide heterogeneity, studies were stratified according to dose of iron, duration of intervention, age, and baseline iron status. However, only doses of 40–66 mg of supplemental iron and intervention in children ≥6 years of age showed a slight but significant association with weight and MAC.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12036" xmlns="http://purl.org/rss/1.0/"><title>Dietary sodium, potassium, and alcohol: key players in the pathophysiology, prevention, and treatment of human hypertension</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12036</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Dietary sodium, potassium, and alcohol: key players in the pathophysiology, prevention, and treatment of human hypertension</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Chrysi Koliaki, Nicholas Katsilambros</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-11T11:02:25.792157-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/nure.12036</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/nure.12036</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12036</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Nutrition in Clinical Care</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Western industrialized societies are currently experiencing an epidemic expansion of hypertension (HTN), which extends alarmingly even to children and adolescents. HTN constitutes an independent risk factor for cardiorenal disease and represents an extremely common comorbidity of diabetes and obesity. Numerous randomized clinical trials and meta-analyses have provided robust scientific evidence that reduced dietary salt intake, increased dietary potassium intake, moderation of alcohol consumption, optimal weight maintenance, and the adoption of “heart-friendly” dietary patterns such as the Dietary Approaches to Stop Hypertension or the Mediterranean diet can effectively lower blood pressure. Interestingly, the susceptibility of blood pressure to nutritional interventions is greatly variable among individuals, depending on age, race, genetic background, and comorbidities. The purpose of this review is to provide a comprehensive overview of currently available scientific evidence in the constantly evolving field of diet and HTN, placing particular emphasis on the key role of dietary sodium, dietary potassium, and alcohol intake in the pathophysiology, prevention, and treatment of human hypertension.</p></div>
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Western industrialized societies are currently experiencing an epidemic expansion of hypertension (HTN), which extends alarmingly even to children and adolescents. HTN constitutes an independent risk factor for cardiorenal disease and represents an extremely common comorbidity of diabetes and obesity. Numerous randomized clinical trials and meta-analyses have provided robust scientific evidence that reduced dietary salt intake, increased dietary potassium intake, moderation of alcohol consumption, optimal weight maintenance, and the adoption of “heart-friendly” dietary patterns such as the Dietary Approaches to Stop Hypertension or the Mediterranean diet can effectively lower blood pressure. Interestingly, the susceptibility of blood pressure to nutritional interventions is greatly variable among individuals, depending on age, race, genetic background, and comorbidities. The purpose of this review is to provide a comprehensive overview of currently available scientific evidence in the constantly evolving field of diet and HTN, placing particular emphasis on the key role of dietary sodium, dietary potassium, and alcohol intake in the pathophysiology, prevention, and treatment of human hypertension.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12024" xmlns="http://purl.org/rss/1.0/"><title>Use of natural AhR ligands as potential therapeutic modalities against inflammatory disorders</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12024</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Use of natural AhR ligands as potential therapeutic modalities against inflammatory disorders</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Philip B Busbee, Michael Rouse, Mitzi Nagarkatti, Prakash S Nagarkatti</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-01T09:38:08.04329-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/nure.12024</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/nure.12024</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12024</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Special Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>The aim of this review is to discuss research involving ligands for the aryl hydrocarbon receptor (AhR) and their role in immunomodulation. While activation of the AhR is well known for its ability to regulate the biochemical and toxic effects of environmental chemicals, more recently an exciting discovery has been made indicating that AhR ligation can also regulate T-cell differentiation, specifically through activation of Foxp3<sup>+</sup> regulatory T cells (Tregs) and downregulation of the proinflammatory Th17 cells. Such findings have opened new avenues of research on the possibility of targeting the AhR to treat inflammatory and autoimmune diseases. Specifically, this review will discuss the current research involving natural and dietary AhR ligands. In addition, evidence indicating the potential use of these ligands in regulating inflammation in various diseases will be highlighted. The importance of the AhR in immunological processes can be illustrated by expression of this receptor on a majority of immune cell types. In addition, AhR signaling pathways have been reported to influence a number of genes responsible for mediating inflammation and other immune responses. As interest in the AhR and its ligands increases, it seems prudent to consolidate current research on the contributions of these ligands to immune regulation during the course of inflammatory diseases.</p></div>
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The aim of this review is to discuss research involving ligands for the aryl hydrocarbon receptor (AhR) and their role in immunomodulation. While activation of the AhR is well known for its ability to regulate the biochemical and toxic effects of environmental chemicals, more recently an exciting discovery has been made indicating that AhR ligation can also regulate T-cell differentiation, specifically through activation of Foxp3+ regulatory T cells (Tregs) and downregulation of the proinflammatory Th17 cells. Such findings have opened new avenues of research on the possibility of targeting the AhR to treat inflammatory and autoimmune diseases. Specifically, this review will discuss the current research involving natural and dietary AhR ligands. In addition, evidence indicating the potential use of these ligands in regulating inflammation in various diseases will be highlighted. The importance of the AhR in immunological processes can be illustrated by expression of this receptor on a majority of immune cell types. In addition, AhR signaling pathways have been reported to influence a number of genes responsible for mediating inflammation and other immune responses. As interest in the AhR and its ligands increases, it seems prudent to consolidate current research on the contributions of these ligands to immune regulation during the course of inflammatory diseases.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12028" xmlns="http://purl.org/rss/1.0/"><title>Meat, fish, and esophageal cancer risk: a systematic review and dose-response meta-analysis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12028</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Meat, fish, and esophageal cancer risk: a systematic review and dose-response meta-analysis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Maryam Salehi, Maziar Moradi-Lakeh, Mohhamad Hossein Salehi, Marziyeh Nojomi, Fariba Kolahdooz</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-11T11:02:15.985622-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/nure.12028</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/nure.12028</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12028</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Lead Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">257</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">267</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Risk factors for esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC) are well defined, while the role of diet in these conditions remains controversial. To help elucidate the role of particular dietary components, major bibliographic databases were searched for published studies (1990–2011) on associations between esophageal cancer risk (EC) and consumption of various types of meat and fish. Random-effects models and dose-response meta-analyses were used to pool study results. Subgroup analyses were conducted by histological subtype, study design, and nationality. Four cohorts and 31 case-control studies were identified. The overall pooled relative risk (RR) of EC and the confidence intervals (CIs) for the groups with the highest versus the lowest levels of intake were as follows: 0.99 (95% CI: 0.85–1.15) for total meat; 1.40 (95%CI: 1.09–1.81) for red meat; 1.41 (95%CI: 1.13–1.76) for processed meat; 0.87 (95%CI: 0.60–1.24) for poultry; and 0.80 (95%CI: 0.64–1.00) for fish. People with the highest levels of red meat intake had a significantly increased risk of ESCC. Processed meat intake was associated with increased risk of EAC. These results suggest that low levels of red and processed meat consumption and higher levels of fish intake might reduce EC risk.</p></div>
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Risk factors for esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC) are well defined, while the role of diet in these conditions remains controversial. To help elucidate the role of particular dietary components, major bibliographic databases were searched for published studies (1990–2011) on associations between esophageal cancer risk (EC) and consumption of various types of meat and fish. Random-effects models and dose-response meta-analyses were used to pool study results. Subgroup analyses were conducted by histological subtype, study design, and nationality. Four cohorts and 31 case-control studies were identified. The overall pooled relative risk (RR) of EC and the confidence intervals (CIs) for the groups with the highest versus the lowest levels of intake were as follows: 0.99 (95% CI: 0.85–1.15) for total meat; 1.40 (95%CI: 1.09–1.81) for red meat; 1.41 (95%CI: 1.13–1.76) for processed meat; 0.87 (95%CI: 0.60–1.24) for poultry; and 0.80 (95%CI: 0.64–1.00) for fish. People with the highest levels of red meat intake had a significantly increased risk of ESCC. Processed meat intake was associated with increased risk of EAC. These results suggest that low levels of red and processed meat consumption and higher levels of fish intake might reduce EC risk.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12023" xmlns="http://purl.org/rss/1.0/"><title>Mechanisms of behavioral, atopic, and other reactions to artificial food colors in children</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12023</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Mechanisms of behavioral, atopic, and other reactions to artificial food colors in children</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Laura J Stevens, Thomas Kuczek, John R Burgess, Mateusz A Stochelski, L Eugene Arnold, Leo Galland</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-13T10:34:11.231703-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/nure.12023</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/nure.12023</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12023</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Special Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">268</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">281</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>This review examines the research on mechanisms by which artificial food colors (AFCs) and common foods may cause behavioral changes in children with and without attention-deficit/hyperactivity disorder (ADHD). Children with ADHD show excess inattention, impulsivity, and hyperactivity. Studies have shown that a subgroup of children (with or without ADHD) react adversely to challenges with AFCs. Many early studies found few children who reacted to challenges with 20–40 mg of AFCs. However, studies using at least 50 mg of AFCs showed a greater percentage of children who reacted to the challenge. Three types of potential mechanisms are explored: toxicological, antinutritional, and hypersensitivity. Suggestions for future studies in animals and/or children include dose studies as well as studies to determine the effects of AFCs on the immune system, the intestinal mucosa, and nutrient absorption. Given the potential negative behavioral effects of AFCs, it is important to determine why some children may be more sensitive to AFCs than others and to identify the tolerable upper limits of exposure for children in general and for children at high risk.</p></div>
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This review examines the research on mechanisms by which artificial food colors (AFCs) and common foods may cause behavioral changes in children with and without attention-deficit/hyperactivity disorder (ADHD). Children with ADHD show excess inattention, impulsivity, and hyperactivity. Studies have shown that a subgroup of children (with or without ADHD) react adversely to challenges with AFCs. Many early studies found few children who reacted to challenges with 20–40 mg of AFCs. However, studies using at least 50 mg of AFCs showed a greater percentage of children who reacted to the challenge. Three types of potential mechanisms are explored: toxicological, antinutritional, and hypersensitivity. Suggestions for future studies in animals and/or children include dose studies as well as studies to determine the effects of AFCs on the immune system, the intestinal mucosa, and nutrient absorption. Given the potential negative behavioral effects of AFCs, it is important to determine why some children may be more sensitive to AFCs than others and to identify the tolerable upper limits of exposure for children in general and for children at high risk.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12012" xmlns="http://purl.org/rss/1.0/"><title>Effect of garlic on serum lipids: an updated meta-analysis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12012</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Effect of garlic on serum lipids: an updated meta-analysis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Karin Ried, Catherine Toben, Peter Fakler</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-07T11:43:22.626731-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/nure.12012</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/nure.12012</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12012</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Special Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">282</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">299</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Hypercholesterolemia is associated with an increased risk of heart disease. The effect of garlic on blood lipids has been studied in numerous trials and summarized in meta-analyses, with conflicting results. This meta-analysis, the most comprehensive to date, includes 39 primary trials of the effect of garlic preparations on total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides. The findings suggest garlic to be effective in reducing total serum cholesterol by 17 ± 6 mg/dL and low-density lipoprotein cholesterol by 9 ± 6 mg/dL in individuals with elevated total cholesterol levels (&gt;200 mg/dL), provided garlic is used for longer than 2 months. An 8% reduction in total serum cholesterol is of clinical relevance and is associated with a 38% reduction in risk of coronary events at 50 years of age. High-density lipoprotein cholesterol levels improved only slightly, and triglycerides were not influenced significantly. Garlic preparations were highly tolerable in all trials and were associated with minimal side effects. They might be considered as an alternative option with a higher safety profile than conventional cholesterol-lowering medications in patients with slightly elevated cholesterol.</p></div>
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Hypercholesterolemia is associated with an increased risk of heart disease. The effect of garlic on blood lipids has been studied in numerous trials and summarized in meta-analyses, with conflicting results. This meta-analysis, the most comprehensive to date, includes 39 primary trials of the effect of garlic preparations on total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides. The findings suggest garlic to be effective in reducing total serum cholesterol by 17 ± 6 mg/dL and low-density lipoprotein cholesterol by 9 ± 6 mg/dL in individuals with elevated total cholesterol levels (&gt;200 mg/dL), provided garlic is used for longer than 2 months. An 8% reduction in total serum cholesterol is of clinical relevance and is associated with a 38% reduction in risk of coronary events at 50 years of age. High-density lipoprotein cholesterol levels improved only slightly, and triglycerides were not influenced significantly. Garlic preparations were highly tolerable in all trials and were associated with minimal side effects. They might be considered as an alternative option with a higher safety profile than conventional cholesterol-lowering medications in patients with slightly elevated cholesterol.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12020" xmlns="http://purl.org/rss/1.0/"><title>Developmental changes and fructose absorption in children: effect on malabsorption testing and dietary management</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12020</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Developmental changes and fructose absorption in children: effect on malabsorption testing and dietary management</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hilary F Jones, Ross N Butler, David J Moore, Doug A Brooks</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-16T12:41:16.012075-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/nure.12020</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/nure.12020</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12020</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Special Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">300</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">309</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Fructose malabsorption came to prominence in the pediatric arena as so-called “apple juice diarrhea,” with excess consumption of fructose being linked to gastrointestinal symptoms such as diarrhea and abdominal pain. Over the past two decades the amount of fructose in children's diets has been increasing in the United States. A test for fructose malabsorption has yet to be fully validated, due mainly to the lack of an established etiology. In animal models, however, the fructose transporter GLUT5 is developmentally regulated, and this could be consistent with the greater susceptibility of children, especially toddlers, to fructose malabsorption. Additionally, the available evidence indicates the fructose breath hydrogen test has no apparent diagnostic utility in infants younger than 1 year; it may, therefore, be advisable to test for malabsorption by dietary exclusion in these patients. The present review aims to expound on the biological basis for fructose malabsorption in children and evaluate the current evidence for diagnostic procedures in order to identify clinical testing strategies that can be recommended and areas where further investigation is required.</p></div>
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Fructose malabsorption came to prominence in the pediatric arena as so-called “apple juice diarrhea,” with excess consumption of fructose being linked to gastrointestinal symptoms such as diarrhea and abdominal pain. Over the past two decades the amount of fructose in children's diets has been increasing in the United States. A test for fructose malabsorption has yet to be fully validated, due mainly to the lack of an established etiology. In animal models, however, the fructose transporter GLUT5 is developmentally regulated, and this could be consistent with the greater susceptibility of children, especially toddlers, to fructose malabsorption. Additionally, the available evidence indicates the fructose breath hydrogen test has no apparent diagnostic utility in infants younger than 1 year; it may, therefore, be advisable to test for malabsorption by dietary exclusion in these patients. The present review aims to expound on the biological basis for fructose malabsorption in children and evaluate the current evidence for diagnostic procedures in order to identify clinical testing strategies that can be recommended and areas where further investigation is required.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12031" xmlns="http://purl.org/rss/1.0/"><title>Nutritional challenges and health implications of takeaway and fast food</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12031</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Nutritional challenges and health implications of takeaway and fast food</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Agnieszka Jaworowska, Toni Blackham, Ian G Davies, Leonard Stevenson</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-11T11:02:21.079259-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/nure.12031</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/nure.12031</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fnure.12031</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Nutrition Science ↔ Policy</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">310</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">318</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Consumption of takeaway and fast food continues to increase in Western societies and is particularly widespread among adolescents. Since food is known to play an important role in both the development and prevention of many diseases, there is no doubt that the observed changes in dietary patterns affect the quality of the diet as well as public health. The present review examines the nutritional characteristics of takeaway and fast food items, including their energy density, total fat, and saturated and trans fatty acid content. It also reports on the association between the consumption of such foods and health outcomes. While the available evidence suggests the nutrient profiles of takeaway and fast foods may contribute to a variety of negative health outcomes, findings on the specific effects of their consumption on health are currently limited and, in recent years, changes have been taking place that are designed to improve them. Therefore, more studies should be directed at gaining a firmer understanding of the nutrition and health consequences of eating takeaway and fast foods and determining the best strategy to reduce any negative impact their consumption may have on public health.</p></div>
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Consumption of takeaway and fast food continues to increase in Western societies and is particularly widespread among adolescents. Since food is known to play an important role in both the development and prevention of many diseases, there is no doubt that the observed changes in dietary patterns affect the quality of the diet as well as public health. The present review examines the nutritional characteristics of takeaway and fast food items, including their energy density, total fat, and saturated and trans fatty acid content. It also reports on the association between the consumption of such foods and health outcomes. While the available evidence suggests the nutrient profiles of takeaway and fast foods may contribute to a variety of negative health outcomes, findings on the specific effects of their consumption on health are currently limited and, in recent years, changes have been taking place that are designed to improve them. Therefore, more studies should be directed at gaining a firmer understanding of the nutrition and health consequences of eating takeaway and fast foods and determining the best strategy to reduce any negative impact their consumption may have on public health.
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