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<title><![CDATA[Contents]]></title>
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<dc:date>Tue, 10 Nov 2009 09:23:36 PST</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxp012</dc:identifier>
<dc:title><![CDATA[Contents]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>31</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
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<title><![CDATA[Subscription]]></title>
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<dc:date>Tue, 10 Nov 2009 09:23:36 PST</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxp013</dc:identifier>
<dc:title><![CDATA[Subscription]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>31</prism:volume>
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<prism:publicationDate>2009-11-01</prism:publicationDate>
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<title><![CDATA[Editorial Board]]></title>
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<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Tue, 10 Nov 2009 09:23:36 PST</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxp014</dc:identifier>
<dc:title><![CDATA[Editorial Board]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>31</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
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<prism:section>STANDING MATERIAL</prism:section>
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<title><![CDATA[Cover]]></title>
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<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Tue, 10 Nov 2009 09:23:36 PST</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxp015</dc:identifier>
<dc:title><![CDATA[Cover]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>31</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>NP</prism:startingPage>
<prism:section>COVER</prism:section>
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<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/31/1/1?rss=1">
<title><![CDATA[Epidemiologic Research on Health Disparities: Some Thoughts on History and Current Developments]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/31/1/1?rss=1</link>
<description><![CDATA[
<p>In this introduction to volume 31 of <I>Epidemiologic Reviews</I>, the author traces the history of health disparities research in epidemiology and situates the 10 review articles comprising this edition within this history. With the aid of a conceptual model describing the key determinants of health disparities, he offers several suggestions for improving future epidemiologic research on health disparities.</p>
]]></description>
<dc:creator><![CDATA[James, S. A.]]></dc:creator>
<dc:date>Tue, 10 Nov 2009 09:23:36 PST</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxp010</dc:identifier>
<dc:title><![CDATA[Epidemiologic Research on Health Disparities: Some Thoughts on History and Current Developments]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>31</prism:volume>
<prism:endingPage>6</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/31/1/7?rss=1">
<title><![CDATA[Built Environments and Obesity in Disadvantaged Populations]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/31/1/7?rss=1</link>
<description><![CDATA[
<p>In the United States, health disparities in obesity and obesity-related illnesses have been the subject of growing concern. To better understand how obesity-related health disparities might relate to obesogenic built environments, the authors conducted a systematic review of the published scientific literature, screening for studies with relevance to disadvantaged individuals or areas, identified by low socioeconomic status, black race, or Hispanic ethnicity. A search for related terms in publication databases and topically related resources yielded 45 studies published between January 1995 and January 2009 with at least 100 participants or area residents that provided information on 1) the built environment correlates of obesity or related health behaviors within one or more disadvantaged groups or 2) the relative exposure these groups had to potentially obesogenic built environment characteristics. Upon consideration of the obesity and behavioral correlates of built environment characteristics, research provided the strongest support for food stores (supermarkets instead of smaller grocery/convenience stores), places to exercise, and safety as potentially influential for disadvantaged groups. There is also evidence that disadvantaged groups were living in worse environments with respect to food stores, places to exercise, aesthetic problems, and traffic or crime-related safety. One strategy to reduce obesity would involve changing the built environment to be more supportive of physical activity and a healthy diet. Based on the authors' review, increasing supermarket access, places to exercise, and neighborhood safety may also be promising strategies to reduce obesity-related health disparities.</p>
]]></description>
<dc:creator><![CDATA[Lovasi, G. S., Hutson, M. A., Guerra, M., Neckerman, K. M.]]></dc:creator>
<dc:date>Tue, 10 Nov 2009 09:23:36 PST</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxp005</dc:identifier>
<dc:title><![CDATA[Built Environments and Obesity in Disadvantaged Populations]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>31</prism:volume>
<prism:endingPage>20</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>7</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/31/1/21?rss=1">
<title><![CDATA[Associations Between Childhood Socioeconomic Position and Adulthood Obesity]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/31/1/21?rss=1</link>
<description><![CDATA[
<p>Childhood socioeconomic position (SEP) is inversely associated with cardiovascular disease and all-cause mortality. Obesity in adulthood may be a biologic mechanism. Objectives were to systematically review literature published between 1998 and 2008 that examined associations of childhood SEP with adulthood obesity. Five databases (Cochrane Library, MEDLINE, EMBASE, PsycINFO, Web of Science) were searched for studies from any country, in any language. Forty-eight publications based on 30 studies were identified. In age-adjusted analyses, inverse associations were found between childhood SEP and adulthood obesity in 70% (14 of 20) of studies in females and 27% (4 of 15) in males. In studies of females showing inverse associations between childhood SEP and adulthood obesity, typical effect sizes in age-adjusted analyses for the difference in body mass index between the highest and lowest SEP were 1.0&ndash;2.0 kg/m<sup>2</sup>; for males, effect sizes were typically 0.2&ndash;0.5 kg/m<sup>2</sup>. Analyses adjusted for age and adult SEP showed inverse associations in 47% (8 of 17) of studies in females and 14% (2 of 14) of studies in males. When other covariates were additionally adjusted for, inverse associations were found in 4 of 12 studies in females and 2 of 8 studies in males; effect sizes were typically reduced compared with analyses adjusted for age only. In summary, the findings suggest that childhood SEP is inversely related to adulthood obesity in females and not associated in males after adjustment for age. Adulthood SEP and other obesity risk factors may be the mechanisms responsible for the observed associations between childhood SEP and adulthood obesity.</p>
]]></description>
<dc:creator><![CDATA[Senese, L. C., Almeida, N. D., Fath, A. K., Smith, B. T., Loucks, E. B.]]></dc:creator>
<dc:date>Tue, 10 Nov 2009 09:23:37 PST</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxp006</dc:identifier>
<dc:title><![CDATA[Associations Between Childhood Socioeconomic Position and Adulthood Obesity]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>31</prism:volume>
<prism:endingPage>51</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>21</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/31/1/52?rss=1">
<title><![CDATA[Do Lifestyle or Social Factors Explain Ethnic/Racial Inequalities in Breast Cancer Survival?]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/31/1/52?rss=1</link>
<description><![CDATA[
<p>Despite numerous studies documenting ethnic inequalities in breast cancer survival between minority and majority ethnic groups worldwide, reasons for these inequalities remain unclear. The authors performed a systematic review of published literature to identify studies that investigated the explanatory power of smoking, alcohol consumption, body mass index (BMI), and socioeconomic position (SEP) on ethnic inequalities in breast cancer survival. Sixteen studies were included in the review. From 5 studies, the authors found that differences in breast cancer survival between ethnic groups may be in part explained by BMI, but there was little evidence to implicate smoking or alcohol consumption as explanatory factors of this inequality. From 12 studies, the authors found that SEP explains part of the ethnic inequality in all-cause survival but that it was not evident for breast-cancer-specific survival. SEP explains more of the disparities among African-American versus white women in the United States compared with other ethnic comparisons. Furthermore, given social patterning of BMI and other lifestyle habits, it is possible that results for SEP and BMI are measuring the same effect. In this review, the authors make suggestions regarding the role of epidemiology in facilitating further research to better inform the development of effective policies to address ethnic differences in survival.</p>
]]></description>
<dc:creator><![CDATA[McKenzie, F., Jeffreys, M.]]></dc:creator>
<dc:date>Tue, 10 Nov 2009 09:23:37 PST</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxp007</dc:identifier>
<dc:title><![CDATA[Do Lifestyle or Social Factors Explain Ethnic/Racial Inequalities in Breast Cancer Survival?]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>31</prism:volume>
<prism:endingPage>66</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>52</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/31/1/67?rss=1">
<title><![CDATA[Environmental Contributions to Disparities in Pregnancy Outcomes]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/31/1/67?rss=1</link>
<description><![CDATA[
<p>One of the most persistent disparities in American health status is the pronounced difference in birth outcomes between non-Hispanic black and non-Hispanic white women. Poor pregnancy outcomes have a substantial impact on mortality, morbidity, and health care costs. Increasing evidence indicates that environmental exposures are associated with poor birth outcomes. This paper reviews the latest research on how environmental exposures affect pregnancy outcomes and then discusses how these exposures may be embedded within a context of significant social and host factor stress. The analysis suggests that environmental, social, and host factors are cumulatively stressing non-Hispanic black women and that this cumulative stress may be a cause of the persistent disparities in pregnancy outcomes.</p>
]]></description>
<dc:creator><![CDATA[Miranda, M. L., Maxson, P., Edwards, S.]]></dc:creator>
<dc:date>Tue, 10 Nov 2009 09:23:37 PST</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxp011</dc:identifier>
<dc:title><![CDATA[Environmental Contributions to Disparities in Pregnancy Outcomes]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>31</prism:volume>
<prism:endingPage>83</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>67</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/31/1/84?rss=1">
<title><![CDATA[What Causes Racial Disparities in Very Preterm Birth? A Biosocial Perspective]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/31/1/84?rss=1</link>
<description><![CDATA[
<p>Very preterm birth (&lt;32 weeks&rsquo; gestation) occurs in approximately 2% of livebirths but is a leading cause of infant mortality and morbidity in the United States. African-American women have a 2-fold to 3-fold elevated risk compared with non-Hispanic white women for reasons that are incompletely understood. This paper reviews the evidence for the biologic and social patterning of very preterm birth, with attention to leading hypotheses regarding the etiology of the racial disparity. A systematic review of the literature in the MEDLINE, CINAHL, PsycInfo, and EMBASE indices was conducted. The literature to date suggests a complex, multifactorial causal framework for understanding racial disparities in very preterm birth, with maternal inflammatory, vascular, or neuroendocrine dysfunction as proximal pathways and maternal exposure to stress, racial differences in preconceptional health, and genetic, epigenetic, and gene-environment interactions as more distal mediators. Interpersonal and institutionalized racism are mechanisms that may drive racially patterned differences. Current literature is limited in that research on social determinants and biologic processes of prematurity has been generally disconnected. Improved etiologic understanding and the potential for effective intervention may come with better integration of these research approaches.</p>
]]></description>
<dc:creator><![CDATA[Kramer, M. R., Hogue, C. R.]]></dc:creator>
<dc:date>Tue, 10 Nov 2009 09:23:37 PST</dc:date>
<dc:identifier>info:doi/10.1093/ajerev/mxp003</dc:identifier>
<dc:title><![CDATA[What Causes Racial Disparities in Very Preterm Birth? A Biosocial Perspective]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>31</prism:volume>
<prism:endingPage>98</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>84</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/31/1/99?rss=1">
<title><![CDATA[Health Disparities in the Latino Population]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/31/1/99?rss=1</link>
<description><![CDATA[
<p>In this review, the authors provide an approach to the study of health disparities in the US Latino population and evaluate the evidence, using mortality rates for discrete medical conditions and the total US population as a standard for comparison. They examine the demographic structure of the Latino population and how nativity, age, income, and education are related to observed patterns of health and mortality. A key issue discussed is how to interpret the superior mortality indices of Latino immigrants and the subsequent declining health status of later generations. Explanations for differences in mortality include selection, reverse selection, death record inconsistencies, inequalities in health status, transnational migration, social marginality, and adaptation to environmental conditions in the United States. The utility of the public health social inequality framework and the status syndrome for explaining Latino disparities is discussed. The authors examine excess mortality from 8 causes: diabetes, stomach cancer, liver cancer, cervical cancer, human immunodeficiency virus/acquired immunodeficiency syndrome, liver disease, homicide, and work-related injuries. The impact of intergenerational changes in health behavior within the Latino population and the contributory role of suboptimal health care are interpreted in the context of implications for future research, public health programs, and policies.</p>
]]></description>
<dc:creator><![CDATA[Vega, W. A., Rodriguez, M. A., Gruskin, E.]]></dc:creator>
<dc:date>Tue, 10 Nov 2009 09:23:37 PST</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxp008</dc:identifier>
<dc:title><![CDATA[Health Disparities in the Latino Population]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>31</prism:volume>
<prism:endingPage>112</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>99</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/31/1/113?rss=1">
<title><![CDATA[Cardiometabolic Health Disparities in Native Hawaiians and Other Pacific Islanders]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/31/1/113?rss=1</link>
<description><![CDATA[
<p>Elimination of health disparities in the United States is a national health priority. Cardiovascular disease, diabetes, and obesity are key features of what is now referred to as the "cardiometabolic syndrome," which disproportionately affects racial/ethnic minority populations, including Native Hawaiians and other Pacific Islanders (NHOPI). Few studies have adequately characterized the cardiometabolic syndrome in high-risk populations such as NHOPI. The authors systematically assessed the existing literature on cardiometabolic disorders among NHOPI to understand the best approaches to eliminating cardiometabolic health disparities in this population. Articles were identified from database searches performed in PubMed and MEDLINE from January 1998 to December 2008; 43 studies were included in the review. There is growing confirmatory evidence that NHOPI are one of the highest-risk populations for cardiometabolic diseases in the United States. Most studies found increased prevalences of diabetes, obesity, and cardiovascular risk factors among NHOPI. The few experimental intervention studies found positive results. Methodological issues included small sample sizes, sample bias, inappropriate racial/ethnic aggregation of NHOPI with Asians, and a limited number of intervention studies. Significant gaps remain in the understanding of cardiometabolic health disparities among NHOPI in the United States. More experimental intervention studies are needed to examine promising approaches to reversing the rising tide of cardiometabolic health disparities in NHOPI.</p>
]]></description>
<dc:creator><![CDATA[Mau, M. K., Sinclair, K., Saito, E. P., Baumhofer, K. N., Kaholokula, J. K.]]></dc:creator>
<dc:date>Tue, 10 Nov 2009 09:23:37 PST</dc:date>
<dc:identifier>info:doi/10.1093/ajerev/mxp004</dc:identifier>
<dc:title><![CDATA[Cardiometabolic Health Disparities in Native Hawaiians and Other Pacific Islanders]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>31</prism:volume>
<prism:endingPage>129</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>113</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/31/1/130?rss=1">
<title><![CDATA[Racial Discrimination and Health Among Asian Americans: Evidence, Assessment, and Directions for Future Research]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/31/1/130?rss=1</link>
<description><![CDATA[
<p>Research shows that racial discrimination is related to illness among diverse racial and ethnic populations. Studies of racial discrimination and health among Asian Americans, however, remain underdeveloped. In this paper, the authors review evidence on racial discrimination and health among Asian Americans, identify gaps in the literature, and provide suggestions for future research. They identified 62 empirical articles assessing the relation between discrimination and health among Asian Americans. The majority of articles focused on mental health problems, followed by physical and behavioral problems. Most studies find that discrimination was associated with poorer health, although the most consistent findings were for mental health problems. This review suggests that future studies should continue to investigate the following: 1) the measurement of discrimination among Asian Americans, whose experiences may be qualitatively different from those of other racial minority groups; 2) the heterogeneity among Asian Americans, including those factors that are particularly salient in this population, such as ethnic ancestry and immigration history; and 3) the health implications of discrimination at multiple ecologic levels, ranging from the individual level to the structural level.</p>
]]></description>
<dc:creator><![CDATA[Gee, G. C., Ro, A., Shariff-Marco, S., Chae, D.]]></dc:creator>
<dc:date>Tue, 10 Nov 2009 09:23:37 PST</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxp009</dc:identifier>
<dc:title><![CDATA[Racial Discrimination and Health Among Asian Americans: Evidence, Assessment, and Directions for Future Research]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>31</prism:volume>
<prism:endingPage>151</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>130</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/31/1/152?rss=1">
<title><![CDATA[Epi + demos + cracy: Linking Political Systems and Priorities to the Magnitude of Health Inequities--Evidence, Gaps, and a Research Agenda]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/31/1/152?rss=1</link>
<description><![CDATA[
<p>A new focus within both social epidemiology and political sociology investigates how political systems and priorities shape health inequities. To advance&mdash;and better integrate&mdash;research on political determinants of health inequities, the authors conducted a systematic search of the ISI Web of Knowledge and PubMed databases and identified 45 studies, commencing in 1992, that explicitly and empirically tested, in relation to an a priori political hypothesis, for either 1) changes in the magnitude of health inequities or 2) significant cross-national differences in the magnitude of health inequities. Overall, 84% of the studies focused on the global North, and all clustered around 4 political factors: 1) the transition to a capitalist economy; 2) neoliberal restructuring; 3) welfare states; and 4) political incorporation of subordinated racial/ethnic, indigenous, and gender groups. The evidence suggested that the first 2 factors probably increase health inequities, the third is inconsistently related, and the fourth helps reduce them. In this review, the authors critically summarize these studies&rsquo; findings, consider methodological limitations, and propose a research agenda&mdash;with careful attention to spatiotemporal scale, level, time frame (e.g., life course, historical generation), choice of health outcomes, inclusion of polities, and specification of political mechanisms&mdash;to address the enormous gaps in knowledge that were identified.</p>
]]></description>
<dc:creator><![CDATA[Beckfield, J., Krieger, N.]]></dc:creator>
<dc:date>Tue, 10 Nov 2009 09:23:37 PST</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxp002</dc:identifier>
<dc:title><![CDATA[Epi + demos + cracy: Linking Political Systems and Priorities to the Magnitude of Health Inequities--Evidence, Gaps, and a Research Agenda]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>31</prism:volume>
<prism:endingPage>177</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>152</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/31/1/178?rss=1">
<title><![CDATA[Is Segregation Bad for Your Health?]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/31/1/178?rss=1</link>
<description><![CDATA[
<p>For decades, racial residential segregation has been observed to vary with health outcomes for African Americans, although only recently has interest increased in the public health literature. Utilizing a systematic review of the health and social science literature, the authors consider the segregation-health association through the lens of 4 questions of interest to epidemiologists: How is segregation best measured? Is the segregation-health association socially or biologically plausible? What evidence is there of segregation-health associations? Is segregation a modifiable risk factor? Thirty-nine identified studies test an association between segregation and health outcomes. The health effects of segregation are relatively consistent, but complex. Isolation segregation is associated with poor pregnancy outcomes and increased mortality for blacks, but several studies report health-protective effects of living in clustered black neighborhoods net of social and economic isolation. The majority of reviewed studies are cross-sectional and use coarse measures of segregation. Future work should extend recent developments in measuring and conceptualizing segregation in a multilevel framework, build upon the findings and challenges in the neighborhood-effects literature, and utilize longitudinal data sources to illuminate opportunities for public health action to reduce racial disparities in disease.</p>
]]></description>
<dc:creator><![CDATA[Kramer, M. R., Hogue, C. R.]]></dc:creator>
<dc:date>Tue, 10 Nov 2009 09:23:37 PST</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxp001</dc:identifier>
<dc:title><![CDATA[Is Segregation Bad for Your Health?]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>31</prism:volume>
<prism:endingPage>194</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>178</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/1?rss=1">
<title><![CDATA[The Burden of Mental Disorders]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/1?rss=1</link>
<description><![CDATA[
<p>In the last decade, there has been an increase in interest in the burden of chronic and disabling health conditions that are not necessarily fatal, such as the mental disorders. This review systematically summarizes data on the burden associated with 11 major mental disorders of adults. The measures of burden include estimates of prevalence, mortality associated with the disorders, disabilities and impairments related to the disorders, and costs. This review expands the range of mental disorders considered in a report on the global burden of disease, updates the literature, presents information on the range and depth of sources of information on burden, and adds estimates of costs. The purpose is to provide an accessible guide to the burden of mental disorders, especially for researchers and policy makers who may not be familiar with this subfield of epidemiology.</p>
]]></description>
<dc:creator><![CDATA[Eaton, W. W., Martins, S. S., Nestadt, G., Bienvenu, O. J., Clarke, D., Alexandre, P.]]></dc:creator>
<dc:date>Wed, 29 Oct 2008 01:14:58 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxn011</dc:identifier>
<dc:title><![CDATA[The Burden of Mental Disorders]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>30</prism:volume>
<prism:endingPage>14</prism:endingPage>
<prism:publicationDate>2008-11-01</prism:publicationDate>
<prism:startingPage>1</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/15?rss=1">
<title><![CDATA[Dementia of the Alzheimer Type]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/15?rss=1</link>
<description><![CDATA[
<p>Dementia of the Alzheimer type is a progressive, fatal neurodegenerative condition characterized by deterioration in cognition and memory, progressive impairment in the ability to carry out activities of daily living, and a number of neuropsychiatric symptoms. This narrative review summarizes the literature regarding descriptive epidemiology, clinical course, and characteristic neuropathological changes of dementia of the Alzheimer type. Although there are no definitive imaging or laboratory tests, except for brain biopsy, for diagnosis, brief screening instruments and neuropsychiatric test batteries used to assess the disease are discussed. Insufficient evidence exists for the use of biomarkers in clinical practice for diagnosis or disease management, but promising discoveries are summarized. Optimal treatment requires both nonpharmacological and pharmacological interventions, yet none have been shown to modify the disease's clinical course. This review describes the current available options and summarizes promising new avenues for treatment. Issues related to the care of persons with dementia of the Alzheimer type, including caregiver burden, long-term care, and the proliferation of dementia special care units, are discussed. Although advances have been made, more research is needed to address the gaps in our understanding of the disease.</p>
]]></description>
<dc:creator><![CDATA[Jalbert, J. J., Daiello, L. A., Lapane, K. L.]]></dc:creator>
<dc:date>Wed, 29 Oct 2008 01:14:58 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxn008</dc:identifier>
<dc:title><![CDATA[Dementia of the Alzheimer Type]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>30</prism:volume>
<prism:endingPage>34</prism:endingPage>
<prism:publicationDate>2008-11-01</prism:publicationDate>
<prism:startingPage>15</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/35?rss=1">
<title><![CDATA[Dementia Prevention: Methodological Explanations for Inconsistent Results]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/35?rss=1</link>
<description><![CDATA[
<p>The prevention of neurodegenerative dementias, such as Alzheimer disease, is a growing public health concern, because of a lack of effective curative treatment options and a rising global prevalence. Various potential risk or preventive factors have been suggested by epidemiologic research, including modifiable lifestyle factors, such as social contacts, leisure activities, physical exercise, and diet, as well as some preventive pharmacologic strategies, such as hormone replacement therapy, nonsteroidal antiinflammatory drugs, and <I>Ginkgo biloba</I>. Some factors have been targeted by interventions tested in randomized controlled trials, but many of the results are in conflict with observational evidence. The aim of this paper is to review the epidemiologic data linking potential protective factors to dementia or cognitive decline and to discuss the methodological limitations that could explain conflicting results. A thorough review of the literature suggests that, even if there are consistent findings from large observational studies regarding preventive or risk factors for dementia, few randomized controlled trials have been designed specifically to prove the protective effects of interventions based on such factors on dementia incidence. Because of the multifactorial origin of dementia, it appears that multidomain interventions could be a suitable candidate for preventive interventions, but designing such trials remains very challenging for researchers.</p>
]]></description>
<dc:creator><![CDATA[Coley, N., Andrieu, S., Gardette, V., Gillette-Guyonnet, S., Sanz, C., Vellas, B., Grand, A.]]></dc:creator>
<dc:date>Wed, 29 Oct 2008 01:14:58 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxn010</dc:identifier>
<dc:title><![CDATA[Dementia Prevention: Methodological Explanations for Inconsistent Results]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>30</prism:volume>
<prism:endingPage>66</prism:endingPage>
<prism:publicationDate>2008-11-01</prism:publicationDate>
<prism:startingPage>35</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/67?rss=1">
<title><![CDATA[Schizophrenia: A Concise Overview of Incidence, Prevalence, and Mortality]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/67?rss=1</link>
<description><![CDATA[
<p>Recent systematic reviews have encouraged the psychiatric research community to reevaluate the contours of schizophrenia epidemiology. This paper provides a concise overview of three related systematic reviews on the incidence, prevalence, and mortality associated with schizophrenia. The reviews shared key methodological features regarding search strategies, analysis of the distribution of the frequency estimates, and exploration of the influence of key variables (sex, migrant status, urbanicity, secular trend, economic status, and latitude). Contrary to previous interpretations, the incidence of schizophrenia shows prominent variation between sites. The median incidence of schizophrenia was 15.2/100,000 persons, and the central 80% of estimates varied over a fivefold range (7.7&ndash;43.0/100,000). The rate ratio for males:females was 1.4:1. Prevalence estimates also show prominent variation. The median lifetime morbid risk for schizophrenia was 7.2/1,000 persons. On the basis of the standardized mortality ratio, people with schizophrenia have a two- to threefold increased risk of dying (median standardized mortality ratio = 2.6 for all-cause mortality), and this differential gap in mortality has increased over recent decades. Compared with native-born individuals, migrants have an increased incidence and prevalence of schizophrenia. Exposures related to urbanicity, economic status, and latitude are also associated with various frequency measures. In conclusion, the epidemiology of schizophrenia is characterized by prominent variability and gradients that can help guide future research.</p>
]]></description>
<dc:creator><![CDATA[McGrath, J., Saha, S., Chant, D., Welham, J.]]></dc:creator>
<dc:date>Wed, 29 Oct 2008 01:14:58 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxn001</dc:identifier>
<dc:title><![CDATA[Schizophrenia: A Concise Overview of Incidence, Prevalence, and Mortality]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>30</prism:volume>
<prism:endingPage>76</prism:endingPage>
<prism:publicationDate>2008-11-01</prism:publicationDate>
<prism:startingPage>67</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/77?rss=1">
<title><![CDATA[Population-based Cohort Studies on Premorbid Cognitive Function in Schizophrenia]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/77?rss=1</link>
<description><![CDATA[
<p>Many previous studies have found associations between poor cognitive function and schizophrenia. However, the majority of these studies used retrospective data, leading to the possibility of selection and recall biases. Retrospective studies are also unable to distinguish whether cognitive deficits exist prior to the onset of schizophrenia, suggesting that they are important in etiology, or following onset, suggesting that they are secondary to the disorder or its treatment. The current review used a systematic search strategy to identify and summarize the results of all studies that have used population-based cohorts to examine associations between prospectively collected data on premorbid cognitive functioning in childhood or adolescence and subsequent risk for schizophrenia. Three broad categories of study have addressed these questions: birth cohort designs with cognitive testing during childhood, army conscript designs with cognitive performance measured at conscription, and studies using school grades. Birth cohort and conscript studies are consistent in reporting strong associations between poor performance on cognitive batteries and increased risk of schizophrenia. Studies on school performance have been less consistent, although the largest such study showed strong associations across all school subjects. In conclusion, children and adolescents with poor cognitive abilities in childhood are at increased risk of schizophrenia. This suggests that poor cognitive function is either directly causal or associated with causal factors that are involved in etiology.</p>
]]></description>
<dc:creator><![CDATA[MacCabe, J. H.]]></dc:creator>
<dc:date>Wed, 29 Oct 2008 01:14:58 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxn007</dc:identifier>
<dc:title><![CDATA[Population-based Cohort Studies on Premorbid Cognitive Function in Schizophrenia]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>30</prism:volume>
<prism:endingPage>83</prism:endingPage>
<prism:publicationDate>2008-11-01</prism:publicationDate>
<prism:startingPage>77</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/84?rss=1">
<title><![CDATA[Psychosis and Place]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/84?rss=1</link>
<description><![CDATA[
<p>One important line of epidemiologic inquiry implicating social context in the etiology of psychosis is the examination of spatial variation in the distribution of psychotic illness. The authors conducted a systematic review of evidence from urbanicity and neighborhood studies regarding spatial variation in the incidence of psychosis in developed countries since 1950. A total of 44 studies (20 of urbanicity and 24 of neighborhood) were culled from three databases with similar time frames: Medline (1950&ndash;2007), PsychInfo (1950&ndash;2007), and Sociological Abstracts (1952&ndash;2007). With a special emphasis on social factors potentially relevant to etiology, the authors elucidated contributions, limitations, and issues related to study design, measurement, and theory. Evidence from both arenas supports a possible etiologic role for social context. Studies of urbanicity indicate that early-life exposure may be important; dose-response relations, spatial patterning of schizophrenia, and interactions with other factors may exist. Neighborhood studies indicate heterogeneity in rates, hint at spatial patterning of schizophrenia, and offer intriguing evidence implying more proximal social (as opposed to physical) exposures. The authors encourage the exploration of social pathways engaging theory, methodological advances, and the life-course perspective. They also propose a conceptual shift from studies of spatial variation in outcomes to research addressing the etiologic effect of exposures shaped by place as a reservoir of risk or resilience.</p>
]]></description>
<dc:creator><![CDATA[March, D., Hatch, S. L., Morgan, C., Kirkbride, J. B., Bresnahan, M., Fearon, P., Susser, E.]]></dc:creator>
<dc:date>Wed, 29 Oct 2008 01:14:58 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxn006</dc:identifier>
<dc:title><![CDATA[Psychosis and Place]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>30</prism:volume>
<prism:endingPage>100</prism:endingPage>
<prism:publicationDate>2008-11-01</prism:publicationDate>
<prism:startingPage>84</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/101?rss=1">
<title><![CDATA[Blues from the Neighborhood? Neighborhood Characteristics and Depression]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/101?rss=1</link>
<description><![CDATA[
<p>Unipolar major depression ranks among the leading contributors to the global burden of disease. Although established risk factors for depression include a variety of individual-level characteristics, neighborhood etiologic factors have been relatively understudied, with several such attributes (neighborhood socioeconomic status, physical conditions, services/amenities, social capital, social disorder) possessing plausible linkages to depression. Using the PubMed database (1966&ndash;2008) and the Social Sciences Citation Index database (1956&ndash;2008), the author undertook a systematic review of the published literature on the associations between these characteristics and depression in adults. Across studies, the evidence generally supports harmful effects of social disorder and, to a lesser extent, suggests protective effects for neighborhood socioeconomic status. Few investigations have explored the relations for neighborhood physical conditions, services/amenities, and social capital, and less consistently point to salutary effects. The unsupportive findings may be attributed to the lack of representative studies within and across societies or to methodological gaps, including lack of control for other neighborhood/non-neighborhood exposures and lack of implementation of more rigorous methodological approaches. Establishing mediating pathways and effect-modifying factors will vitally advance understanding of neighborhood effects on depression. Overall, addressing these gaps will help to identify what specific neighborhood features matter for depression, how, and for whom, and will contribute to curtailing the burden of disease associated with this major disorder.</p>
]]></description>
<dc:creator><![CDATA[Kim, D.]]></dc:creator>
<dc:date>Wed, 29 Oct 2008 01:14:58 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxn009</dc:identifier>
<dc:title><![CDATA[Blues from the Neighborhood? Neighborhood Characteristics and Depression]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>30</prism:volume>
<prism:endingPage>117</prism:endingPage>
<prism:publicationDate>2008-11-01</prism:publicationDate>
<prism:startingPage>101</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/118?rss=1">
<title><![CDATA[The Relation between Work-related Psychosocial Factors and the Development of Depression]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/118?rss=1</link>
<description><![CDATA[
<p>This review is based on a literature search made in January 2007 on request by the Danish National Board of Industrial Injuries. The search in PubMed, EMBASE, and PsycINFO resulted in more than 1,000 publications. This was reduced to 14 after the titles, abstracts, and papers were evaluated by using the following criteria: 1) a longitudinal study, 2) exposure to work-related psychosocial factors, 3) the outcome a measure of depression, 4) relevant statistical estimates, and 5) nonduplicated publication. Of the 14 studies, seven used standardized diagnostic instruments as measures of depression, whereas the other seven studies used self-administered questionnaires. The authors found moderate evidence for a relation between the psychological demands of the job and the development of depression, with relative risks of approximately 2.0. However, indication of publication bias weakens the evidence. Social support at work was associated with a decrease in risk for future depression, as all four studies dealing with this exposure showed associations with relative risks of about 0.6. Even if this literature study has identified work-related psychosocial factors that in high-quality epidemiologic studies predict depression, studies are still needed that assess in more detail the duration and intensity of exposure necessary for developing depression.</p>
]]></description>
<dc:creator><![CDATA[Netterstrom, B., Conrad, N., Bech, P., Fink, P., Olsen, O., Rugulies, R., Stansfeld, S.]]></dc:creator>
<dc:date>Wed, 29 Oct 2008 01:14:58 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxn004</dc:identifier>
<dc:title><![CDATA[The Relation between Work-related Psychosocial Factors and the Development of Depression]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>30</prism:volume>
<prism:endingPage>132</prism:endingPage>
<prism:publicationDate>2008-11-01</prism:publicationDate>
<prism:startingPage>118</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/133?rss=1">
<title><![CDATA[Suicide and Suicidal Behavior]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/133?rss=1</link>
<description><![CDATA[
<p>Suicidal behavior is a leading cause of injury and death worldwide. Information about the epidemiology of such behavior is important for policy-making and prevention. The authors reviewed government data on suicide and suicidal behavior and conducted a systematic review of studies on the epidemiology of suicide published from 1997 to 2007. The authors' aims were to examine the prevalence of, trends in, and risk and protective factors for suicidal behavior in the United States and cross-nationally. The data revealed significant cross-national variability in the prevalence of suicidal behavior but consistency in age of onset, transition probabilities, and key risk factors. Suicide is more prevalent among men, whereas nonfatal suicidal behaviors are more prevalent among women and persons who are young, are unmarried, or have a psychiatric disorder. Despite an increase in the treatment of suicidal persons over the past decade, incidence rates of suicidal behavior have remained largely unchanged. Most epidemiologic research on suicidal behavior has focused on patterns and correlates of prevalence. The next generation of studies must examine synergistic effects among modifiable risk and protective factors. New studies must incorporate recent advances in survey methods and clinical assessment. Results should be used in ongoing efforts to decrease the significant loss of life caused by suicidal behavior.</p>
]]></description>
<dc:creator><![CDATA[Nock, M. K., Borges, G., Bromet, E. J., Cha, C. B., Kessler, R. C., Lee, S.]]></dc:creator>
<dc:date>Wed, 29 Oct 2008 01:14:58 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxn002</dc:identifier>
<dc:title><![CDATA[Suicide and Suicidal Behavior]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>30</prism:volume>
<prism:endingPage>154</prism:endingPage>
<prism:publicationDate>2008-11-01</prism:publicationDate>
<prism:startingPage>133</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/155?rss=1">
<title><![CDATA[Comorbid Forms of Psychopathology: Key Patterns and Future Research Directions]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/155?rss=1</link>
<description><![CDATA[
<p>The purpose of this review is to systematically appraise the peer-reviewed literature about clustered forms of psychopathology and to present a framework that can be useful for studying comorbid psychiatric disorders. The review focuses on four of the most prevalent types of mental health problems: anxiety, depression, conduct disorder, and substance abuse. The authors summarize existing empirical research on the distribution of concurrent and sequential comorbidity in children and adolescents and in adults, and they review existing knowledge about exogenous risk factors that influence comorbidity. The authors include articles that used a longitudinal study design and used psychiatric definitions of the disorders. A total of 58 articles met the inclusion criteria and were assessed. Current evidence demonstrates a reciprocal, sequential relation between most comorbid pairs, although the mechanisms that mediate such links remain to be explained. Methodological concerns include the inconsistency of measurement of the disorders across studies, small sample sizes, and restricted follow-up times. Given the significant mental health burden placed by comorbid disorders, and their high prevalence across populations, research on the key risk factors for clustering of psychopathology is needed.</p>
]]></description>
<dc:creator><![CDATA[Cerda, M., Sagdeo, A., Galea, S.]]></dc:creator>
<dc:date>Wed, 29 Oct 2008 01:14:58 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxn003</dc:identifier>
<dc:title><![CDATA[Comorbid Forms of Psychopathology: Key Patterns and Future Research Directions]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>30</prism:volume>
<prism:endingPage>177</prism:endingPage>
<prism:publicationDate>2008-11-01</prism:publicationDate>
<prism:startingPage>155</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/29/1/1?rss=1">
<title><![CDATA[The Global Epidemic of Obesity: An Overview]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/29/1/1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Caballero, B.]]></dc:creator>
<dc:date>Thu, 12 Jul 2007 07:39:19 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxm012</dc:identifier>
<dc:title><![CDATA[The Global Epidemic of Obesity: An Overview]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>29</prism:volume>
<prism:endingPage>5</prism:endingPage>
<prism:publicationDate>2007-01-01</prism:publicationDate>
<prism:startingPage>1</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/29/1/6?rss=1">
<title><![CDATA[The Obesity Epidemic in the United States Gender, Age, Socioeconomic, Racial/Ethnic, and Geographic Characteristics: A Systematic Review and Meta-Regression Analysis]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/29/1/6?rss=1</link>
<description><![CDATA[
<p>This review of the obesity epidemic provides a comprehensive description of the current situation, time trends, and disparities across gender, age, socioeconomic status, racial/ethnic groups, and geographic regions in the United States based on national data. The authors searched studies published between 1990 and 2006. Adult overweight and obesity were defined by using body mass index (weight (kg)/height (m)<sup>2</sup>) cutpoints of 25 and 30, respectively; childhood "at risk for overweight" and overweight were defined as the 85th and 95th percentiles of body mass index. Average annual increase in and future projections for prevalence were estimated by using linear regression models. Among adults, obesity prevalence increased from 13% to 32% between the 1960s and 2004. Currently, 66% of adults are overweight or obese; 16% of children and adolescents are overweight and 34% are at risk of overweight. Minority and low-socioeconomic-status groups are disproportionately affected at all ages. Annual increases in prevalence ranged from 0.3 to 0.9 percentage points across groups. By 2015, 75% of adults will be overweight or obese, and 41% will be obese. In conclusion, obesity has increased at an alarming rate in the United States over the past three decades. The associations of obesity with gender, age, ethnicity, and socioeconomic status are complex and dynamic. Related population-based programs and policies are needed.</p>
]]></description>
<dc:creator><![CDATA[Wang, Y., Beydoun, M. A.]]></dc:creator>
<dc:date>Thu, 12 Jul 2007 07:39:19 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxm007</dc:identifier>
<dc:title><![CDATA[The Obesity Epidemic in the United States Gender, Age, Socioeconomic, Racial/Ethnic, and Geographic Characteristics: A Systematic Review and Meta-Regression Analysis]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>29</prism:volume>
<prism:endingPage>28</prism:endingPage>
<prism:publicationDate>2007-01-01</prism:publicationDate>
<prism:startingPage>6</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/29/1/29?rss=1">
<title><![CDATA[Socioeconomic Status and Obesity]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/29/1/29?rss=1</link>
<description><![CDATA[
<p>The objective of this review was to update Sobal and Stunkard's exhaustive review of the literature on the relation between socioeconomic status (SES) and obesity (<I>Psychol Bull</I> 1989;105:260&ndash;75). Diverse research databases (including CINAHL, ERIC, MEDLINE, and Social Science Abstracts) were comprehensively searched during the years 1988&ndash;2004 inclusive, using "obesity," "socioeconomic status," and synonyms as search terms. A total of 333 published studies, representing 1,914 primarily cross-sectional associations, were included in the review. The overall pattern of results, for both men and women, was of an increasing proportion of positive associations and a decreasing proportion of negative associations as one moved from countries with high levels of socioeconomic development to countries with medium and low levels of development. Findings varied by SES indicator; for example, negative associations (lower SES associated with larger body size) for women in highly developed countries were most common with education and occupation, while positive associations for women in medium- and low-development countries were most common with income and material possessions. Patterns for women in higher- versus lower-development countries were generally less striking than those observed by Sobal and Stunkard; this finding is interpreted in light of trends related to globalization. Results underscore a view of obesity as a social phenomenon, for which appropriate action includes targeting both economic and sociocultural factors.</p>
]]></description>
<dc:creator><![CDATA[McLaren, L.]]></dc:creator>
<dc:date>Thu, 12 Jul 2007 07:39:19 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxm001</dc:identifier>
<dc:title><![CDATA[Socioeconomic Status and Obesity]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>29</prism:volume>
<prism:endingPage>48</prism:endingPage>
<prism:publicationDate>2007-01-01</prism:publicationDate>
<prism:startingPage>29</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/29/1/49?rss=1">
<title><![CDATA[Genetic Epidemiology of Obesity]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/29/1/49?rss=1</link>
<description><![CDATA[
<p>Obesity has become a global epidemic and contributes to the increasing burden of type 2 diabetes, cardiovascular disease, stroke, some types of cancer, and premature death worldwide. Obesity is highly heritable and arises from the interactions of multiple genes, environmental factors, and behavior. In this paper, the authors reviewed recent developments in genetic epidemiologic research, focusing particularly on several promising genomic regions and obesity-related genes. Gene-gene and gene-environment interactions of obesity were also discussed. Published studies were accessed through the MEDLINE database. The authors also searched the Obesity Gene Map Database (<inter-ref locator="http://obesitygene.pbrc.edu/" locator-type="url">http://obesitygene.pbrc.edu/</inter-ref>) and conducted a manual search using references cited in relevant papers. Heritabilities for obesity-related phenotypes varied from 6% to 85% among various populations. As of October 2005, 253 quantitative trait loci for obesity-related phenotypes have been localized in 61 genome-wide linkage scans, and genetic variants in 127 biologic candidate genes have been reported to be associated with obesity-related phenotypes from 426 positive findings. Gene-gene interactions were also observed in several genes, and some genes were found to influence the effect of dietary intake and physical activity on obesity-related phenotypes. Integration of genetic epidemiology with functional genomics and proteomics studies will be required to fully understand the role of genetic variants in the etiology and prevention of obesity.</p>
]]></description>
<dc:creator><![CDATA[Yang, W., Kelly, T., He, J.]]></dc:creator>
<dc:date>Thu, 12 Jul 2007 07:39:19 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxm004</dc:identifier>
<dc:title><![CDATA[Genetic Epidemiology of Obesity]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>29</prism:volume>
<prism:endingPage>61</prism:endingPage>
<prism:publicationDate>2007-01-01</prism:publicationDate>
<prism:startingPage>49</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/29/1/62?rss=1">
<title><![CDATA[Childhood Overweight, Obesity, and the Metabolic Syndrome in Developing Countries]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/29/1/62?rss=1</link>
<description><![CDATA[
<p>The incidence of chronic disease is escalating much more rapidly in developing countries than in industrialized countries. A potential emerging public health issue may be the increasing incidence of childhood obesity in developing countries and the resulting socioeconomic and public health burden faced by these countries in the near future. In a systematic review carried out through an electronic search of the literature from 1950&ndash;2007, the author compared data from surveys on the prevalence of overweight, obesity, and the metabolic syndrome among children living in developing countries. The highest prevalence of childhood overweight was found in Eastern Europe and the Middle East, whereas India and Sri Lanka had the lowest prevalence. The few studies conducted in developing countries showed a considerably high prevalence of the metabolic syndrome among youth. These findings provide alarming data for health professionals and policy-makers about the extent of these problems in developing countries, many of which are still grappling with malnutrition and micronutrient deficiencies. Time trends in childhood obesity and its metabolic consequences, defined by uniform criteria, should be monitored in developing countries in order to obtain useful insights for primordial and primary prevention of the upcoming chronic disease epidemic in such communities.</p>
]]></description>
<dc:creator><![CDATA[Kelishadi, R.]]></dc:creator>
<dc:date>Thu, 12 Jul 2007 07:39:20 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxm003</dc:identifier>
<dc:title><![CDATA[Childhood Overweight, Obesity, and the Metabolic Syndrome in Developing Countries]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>29</prism:volume>
<prism:endingPage>76</prism:endingPage>
<prism:publicationDate>2007-01-01</prism:publicationDate>
<prism:startingPage>62</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/29/1/77?rss=1">
<title><![CDATA[Abdominal Obesity and Fatty Liver]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/29/1/77?rss=1</link>
<description><![CDATA[
<p>It has been hypothesized that visceral fat releases free fatty acids and adipokines and thereby exposes the liver to fat accumulation. The authors aimed to evaluate current epidemiologic evidence for an association between abdominal fat and liver fat content. Clinical and epidemiologic studies with data on abdominal fat and liver fat content were reviewed. Studies using waist circumference to estimate abdominal fat mass suggested a direct association between abdominal fat and liver fat content. Studies using imaging methods suggested a direct association between intraabdominal fat and liver fat content, but not between subcutaneous abdominal fat and liver fat content. In conclusion, clinical and epidemiologic studies of abdominal fat and liver fat content suggest a direct association between abdominal fat and liver fat content which is probably accounted for by visceral fat. However, results from the included studies do not allow strong conclusions regarding the temporal sequence of events. Future longitudinal studies are recommended to obtain additional information on associations and mechanisms. Both abdominal fat depots and other body compartments of interest should be included to further investigate the association between specific fat depots and liver fat content. Biomarkers may provide insight into underlying mechanisms.</p>
]]></description>
<dc:creator><![CDATA[Jakobsen, M., Berentzen, T, Sorensen, T., Overvad, K]]></dc:creator>
<dc:date>Thu, 12 Jul 2007 07:39:20 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxm002</dc:identifier>
<dc:title><![CDATA[Abdominal Obesity and Fatty Liver]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>29</prism:volume>
<prism:endingPage>87</prism:endingPage>
<prism:publicationDate>2007-01-01</prism:publicationDate>
<prism:startingPage>77</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/29/1/88?rss=1">
<title><![CDATA[Obesity and Prostate Cancer: Making Sense out of Apparently Conflicting Data]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/29/1/88?rss=1</link>
<description><![CDATA[
<p>Both obesity and prostate cancer are epidemic in Western society. Although initial epidemiologic data appeared conflicting, recent studies, especially large prospective studies published in the past 6&ndash;12 months, have clarified the association between obesity and prostate cancer. The aim of this paper is to review the epidemiologic data linking obesity and prostate cancer, with an emphasis on new data published since 2005. A PubMed search was done on the keywords, "prostate cancer" and "obesity." Relevant articles and their references were reviewed for data on the association between obesity and prostate cancer. Recent data suggest that obesity is associated with reduced risk of nonaggressive disease but increased risk of aggressive disease. This may in part be explained by an inherent bias in our ability to detect prostate cancer in obese men (lower prostate-specific antigen values and larger sized prostates making biopsy less accurate for finding an existing cancer). Ultimately, this leads to increased risk of cancer recurrence after primary therapy and increased risk of prostate cancer mortality. The biologic causes of these associations are likely multifactorial, although the lower testosterone levels among obese men appear to be one of the most promising explanations. The association between obesity and prostate cancer is complex. Emerging data suggest a differential effect of obesity by disease aggressiveness: obesity may reduce the risk of nonaggressive disease while it may promote aggressive disease.</p>
]]></description>
<dc:creator><![CDATA[Freedland, S. J., Platz, E. A.]]></dc:creator>
<dc:date>Thu, 12 Jul 2007 07:39:20 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxm006</dc:identifier>
<dc:title><![CDATA[Obesity and Prostate Cancer: Making Sense out of Apparently Conflicting Data]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>29</prism:volume>
<prism:endingPage>97</prism:endingPage>
<prism:publicationDate>2007-01-01</prism:publicationDate>
<prism:startingPage>88</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/29/1/98?rss=1">
<title><![CDATA[Biomarkers of Obesity and Subsequent Cardiovascular Events]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/29/1/98?rss=1</link>
<description><![CDATA[
<p>Obesity is a major risk factor for cardiovascular diseases, but the mechanisms for increased cardiovascular risk in obesity are still unclear. Inflammation and increased oxidative stress are two potential mechanisms proposed to play a major role in the morbidity associated with obesity. Studies that investigate these mechanisms rely on biomarkers, but validated biomarkers for obesity-related cardiovascular outcomes are lacking. By finding optimal biomarkers, diagnostic criteria for cardiovascular diseases can be refined in the obese beyond "traditional" risk factors to identify early pathologic processes. The objective of this review is to identify potential early biomarkers resulting from obesity and associated with cardiovascular disease. Studies were initially identified through the search engine PubMed by using the keywords "obesity" and "biomarker." Subsequently, combinations of the keywords "obesity," "biomarker," "cardiovascular risk," "adipose tissue," "adipokine," "adipocytokine," and "oxidative stress" were used. The SOURCE database and Online Mendelian Inheritance in Man (OMIM) were used to obtain more information on the biomarkers. Results of the searches yielded a large number of potential biomarkers that occur in obesity and which either correlate with traditional cardiovascular risk factors or predict subsequent cardiovascular events. Several biomarkers are promising regarding their biologic properties, but they require further validation in humans.</p>
]]></description>
<dc:creator><![CDATA[Musaad, S., Haynes, E. N.]]></dc:creator>
<dc:date>Thu, 12 Jul 2007 07:39:20 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxm005</dc:identifier>
<dc:title><![CDATA[Biomarkers of Obesity and Subsequent Cardiovascular Events]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>29</prism:volume>
<prism:endingPage>114</prism:endingPage>
<prism:publicationDate>2007-01-01</prism:publicationDate>
<prism:startingPage>98</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/29/1/115?rss=1">
<title><![CDATA[Comparison of Body Mass Index, Waist Circumference, and Waist/Hip Ratio in Predicting Incident Diabetes: A Meta-Analysis]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/29/1/115?rss=1</link>
<description><![CDATA[
<p>Body mass index, waist circumference, and waist/hip ratio have been shown to be associated with type 2 diabetes. From the clinical perspective, central obesity (approximated by waist circumference or waist/hip ratio) is known to generate diabetogenic substances and should therefore be more informative than general obesity (body mass index). Because of their high correlation, from the statistical perspective, body mass index and waist circumference are unlikely to yield different answers. To compare associations of diabetes incidence with general and central obesity indicators, the authors conducted a meta-analysis based on published studies from 1966 to 2004 retrieved from a PubMed search. The analysis was performed with 32 studies out of 432 publications initially identified. Measures of association were transformed to log relative risks per standard deviation (pooled across all studies) increase in the obesity indicator and pooled using random effects models. The pooled relative risks for incident diabetes were 1.87 (95% confidence interval (CI): 1.67, 2.10), 1.87 (95% CI: 1.58, 2.20), and 1.88 (95% CI: 1.61, 2.19) per standard deviation of body mass index, waist circumference, and waist/hip ratio, respectively, demonstrating that these three obesity indicators have similar associations with incident diabetes. Although the clinical perspective focusing on central obesity is appealing, further research is needed to determine the usefulness of waist circumference or waist/hip ratio over body mass index.</p>
]]></description>
<dc:creator><![CDATA[Vazquez, G., Duval, S., Jacobs, D. R., Silventoinen, K.]]></dc:creator>
<dc:date>Thu, 12 Jul 2007 07:39:20 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxm008</dc:identifier>
<dc:title><![CDATA[Comparison of Body Mass Index, Waist Circumference, and Waist/Hip Ratio in Predicting Incident Diabetes: A Meta-Analysis]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>29</prism:volume>
<prism:endingPage>128</prism:endingPage>
<prism:publicationDate>2007-01-01</prism:publicationDate>
<prism:startingPage>115</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/29/1/129?rss=1">
<title><![CDATA[The Built Environment and Obesity]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/29/1/129?rss=1</link>
<description><![CDATA[
<p>Obesity results from a complex interaction between diet, physical activity, and the environment. The built environment encompasses a range of physical and social elements that make up the structure of a community and may influence obesity. This review summarizes existing empirical research relating the built environment to obesity. The Medline, PsychInfo, and Web of Science databases were searched using the keywords "obesity" or "overweight" and "neighborhood" or "built environment" or "environment." The search was restricted to English-language articles conducted in human populations between 1966 and 2007. To meet inclusion criteria, articles had to 1) have a direct measure of body weight and 2) have an objective measure of the built environment. A total of 1,506 abstracts were obtained, and 20 articles met the inclusion criteria. Most articles (84%) reported a statistically significant positive association between some aspect of the built environment and obesity. Several methodological issues were of concern, including the inconsistency of measurements of the built environment across studies, the cross-sectional design of most investigations, and the focus on aspects of either diet or physical activity but not both. Given the importance of the physical and social contexts of individual behavior and the limited success of individual-based interventions in long-term obesity prevention, more research on the impact of the built environment on obesity is needed.</p>
]]></description>
<dc:creator><![CDATA[Papas, M. A., Alberg, A. J., Ewing, R., Helzlsouer, K. J., Gary, T. L., Klassen, A. C.]]></dc:creator>
<dc:date>Thu, 12 Jul 2007 07:39:20 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxm009</dc:identifier>
<dc:title><![CDATA[The Built Environment and Obesity]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>29</prism:volume>
<prism:endingPage>143</prism:endingPage>
<prism:publicationDate>2007-01-01</prism:publicationDate>
<prism:startingPage>129</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/29/1/144?rss=1">
<title><![CDATA[Promoting Physical Activity Participation among Children and Adolescents]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/29/1/144?rss=1</link>
<description><![CDATA[
<p>With global increases in the prevalence of overweight and obesity among children and adolescents, there has never been a more urgent need for effective physical activity programs. The aim of this narrative review is to summarize the evidence of the effectiveness of interventions that report physical activity outcomes in children aged 4&ndash;12 years and adolescents aged 13&ndash;19 years. A systematic search of electronic databases identified 76 interventions. Most interventions were delivered via the school setting (57 interventions), nine through the family setting, six via primary care, and four in community- or Internet-based settings. Children's physical activity interventions that were most effective in the school setting included some focus on physical education, activity breaks, and family strategies. Interventions delivered in the family setting were not highly effective, but many were pilot studies. The use of motivationally tailored strategies and program delivery in the primary care setting showed promise among adolescents. Many studies had methodological and reporting flaws (e.g., no baseline data, poor study design, physical activity measures of unknown reliability and validity, and poor reporting of sample size, response rates, attrition/retention, compliance, year of intervention, and duration of intervention). Publications reporting the results of evaluations of intervention studies should follow the Consolidated Standards of Reporting Trials guidelines or, for nonrandomized studies, should follow the Transparent Reporting of Evaluations with Nonrandomized Designs guidelines. Further evidence of the effectiveness of interventions promoting young people's physical activity in family and community settings is needed.</p>
]]></description>
<dc:creator><![CDATA[Salmon, J., Booth, M. L., Phongsavan, P., Murphy, N., Timperio, A.]]></dc:creator>
<dc:date>Thu, 12 Jul 2007 07:39:20 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxm010</dc:identifier>
<dc:title><![CDATA[Promoting Physical Activity Participation among Children and Adolescents]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>29</prism:volume>
<prism:endingPage>159</prism:endingPage>
<prism:publicationDate>2007-01-01</prism:publicationDate>
<prism:startingPage>144</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/29/1/160?rss=1">
<title><![CDATA[The Real Contribution of Added Sugars and Fats to Obesity]]></title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/29/1/160?rss=1</link>
<description><![CDATA[
<p>Obesity rates in the United States are a function of socioeconomic status. Higher rates are found among groups with lower educational and income levels, among racial and ethnic minorities, and in high-poverty areas. Yet, the relation between obesity, nutrition, and diet continues to be viewed in biologic terms, with the search for likely causes focused on consumption of specific macronutrients, foods, or food groups. Epidemiologic evidence linking diet composition and body weight has mostly relied on ecologic comparisons, time trends, and analyses of cross-sectional studies. Plausible physiologic mechanisms have included the metabolic effects of dietary components, mostly sugars and fats, on regulation of food intake and deposition of body fat. However, the evidence could not have been convincing since the blame for rising obesity rates seems to shift regularly, every 10 years or so, from fats to sugars and then back again. This review demonstrates that much of past epidemiologic research is consistent with a single parsimonious explanation: obesity has been linked repeatedly to consumption of low-cost foods. Refined grains, added sugars, and added fats are inexpensive, good tasting, and convenient. The fact that energy-dense foods (megajoules/kilogram) cost less per megajoule than do nutrient-dense foods means that energy-dense diets are not only cheaper but may be preferentially selected by the lower-income consumer. In other words, the low cost of dietary energy (dollars/megajoule), rather than specific food, beverage, or macronutrient choices, may be the main predictor of population weight gain. Examining past studies of the contribution of added sugars and fats to obesity rates through the prism of food prices and diet costs is the purpose of this review.</p>
]]></description>
<dc:creator><![CDATA[Drewnowski, A.]]></dc:creator>
<dc:date>Thu, 12 Jul 2007 07:39:20 PDT</dc:date>
<dc:identifier>info:doi/10.1093/epirev/mxm011</dc:identifier>
<dc:title><![CDATA[The Real Contribution of Added Sugars and Fats to Obesity]]></dc:title>
<dc:publisher>Society for Epidemiologic Research</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>29</prism:volume>
<prism:endingPage>171</prism:endingPage>
<prism:publicationDate>2007-01-01</prism:publicationDate>
<prism:startingPage>160</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

</rdf:RDF>