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            type="text/xsl"?><rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"><channel rdf:about="http://onlinelibrary.wiley.com/rss/journal/10.1002/(ISSN)1520-6300" xmlns="http://purl.org/rss/1.0/"><title>American Journal of Human Biology</title><description> Wiley Online Library : American Journal of Human Biology</description><link>http://dx.doi.org/10.1002%2F%28ISSN%291520-6300</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/">Copyright © 2012 Wiley Periodicals Inc.</dc:rights><prism:issn xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">1042-0533</prism:issn><prism:eIssn xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">1520-6300</prism:eIssn><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><prism:coverDisplayDate xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">March/April 2012</prism:coverDisplayDate><prism:volume xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">24</prism:volume><prism:number xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">2</prism:number><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">101</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">256</prism:endingPage><image rdf:resource="http://onlinelibrary.wiley.com/store/10.1002/ajhb.v24.2/asset/cover.gif?v=1&amp;s=5aa3a7f0b3b007951e8b9087e0d8390c0a53731b"/><items><rdf:Seq><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22235"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22238"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22239"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22240"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22244"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22222"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22207"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22224"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22221"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22220"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22219"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22243"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22232"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22218"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22236"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22209"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22201"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22202"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22200"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22212"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22214"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22216"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22217"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22210"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22211"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22213"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22215"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22225"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22226"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22227"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22228"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22229"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22230"/><rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fajhb.22242"/></rdf:Seq></items></channel><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22235" xmlns="http://purl.org/rss/1.0/"><title>β-Globin polymorphisms in amerindian populations from the brazilian amazon</title><link>http://dx.doi.org/10.1002%2Fajhb.22235</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">β-Globin polymorphisms in amerindian populations from the brazilian amazon</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">João Farias Guerreiro</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Diogo Meyer</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Isabela Guerreiro Diniz</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ândrea Ribeiro Dos Santos</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Eduardo José Melo Dos Santos</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">John B. Clegg</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-10T07:32:41.283878-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22235</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/">10.1002/ajhb.22235</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22235</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original 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[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Objectives:</b> This investigation was performed to examine genetic variation at the β-globin locus in a sample of 30 healthy individuals from native populations in South America. The patterns of haplotypic variation were compared with those of previous studies including samples for various worldwide populations in an attempt to make inferences about the occupation of the Americas from a deeper temporal perspective than is typically available with haploid markers.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Methods:</b> A 2.67-kb segment containing the β-globin gene and its flanking regions was examined for genetic variation in a sample of 60 chromosomes from native populations in South America. The fragment was PCR-amplified and directly sequenced. To determine linkage relationships in compound heterozygotes, we used the amplification refractory mutation system. In addition, we assessed genetic variability and differentiation among populations, and we performed tests of selective neutrality. These analyses were performed for Brazilian Amerindian group and other worldwide populations previously studied.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Results:</b> Eleven polymorphic sites were found in the studied fragment, which distinguished eight different haplotypes, three recombinants haplotypes (present as single copies) and five previously described haplotypes, including some of those most highly differentiated. Genetic variation found in the pooled sample is substantial.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Conclusions:</b> Although only five known haplotypes are observed in Amazonia, some of these are highly divergent, resulting in patterns of molecular polymorphism equal to or higher than those from other world regions. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</p></div>]]></content:encoded><description>Objectives: This investigation was performed to examine genetic variation at the β-globin locus in a sample of 30 healthy individuals from native populations in South America. The patterns of haplotypic variation were compared with those of previous studies including samples for various worldwide populations in an attempt to make inferences about the occupation of the Americas from a deeper temporal perspective than is typically available with haploid markers.Methods: A 2.67-kb segment containing the β-globin gene and its flanking regions was examined for genetic variation in a sample of 60 chromosomes from native populations in South America. The fragment was PCR-amplified and directly sequenced. To determine linkage relationships in compound heterozygotes, we used the amplification refractory mutation system. In addition, we assessed genetic variability and differentiation among populations, and we performed tests of selective neutrality. These analyses were performed for Brazilian Amerindian group and other worldwide populations previously studied.Results: Eleven polymorphic sites were found in the studied fragment, which distinguished eight different haplotypes, three recombinants haplotypes (present as single copies) and five previously described haplotypes, including some of those most highly differentiated. Genetic variation found in the pooled sample is substantial.Conclusions: Although only five known haplotypes are observed in Amazonia, some of these are highly divergent, resulting in patterns of molecular polymorphism equal to or higher than those from other world regions. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22238" xmlns="http://purl.org/rss/1.0/"><title>Body image concerns and reduced breastfeeding duration in primiparous overweight and obese women</title><link>http://dx.doi.org/10.1002%2Fajhb.22238</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Body image concerns and reduced breastfeeding duration in primiparous overweight and obese women</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Laura E. Hauff</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ellen W. Demerath</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-05T06:50:01.937084-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22238</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/">10.1002/ajhb.22238</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22238</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original 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[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="section" id="abs1-1" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/"><b xmlns="http://www.w3.org/1999/xhtml">Objectives:</b></h3><div class="para"><p>To test differences in breastfeeding duration by prepregnant maternal weight status, and determine whether body image concerns mediate any differences.</p></div></div><div class="section" id="abs1-2" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/"><b xmlns="http://www.w3.org/1999/xhtml">Methods:</b></h3><div class="para"><p>A prospective longitudinal cohort of primiparous women was followed from pregnancy to, at minimum, 6 months postpartum. Questionnaire responses on body concerns were obtained during pregnancy and at 4 months postpartum. Kaplan-Meier curves compared breastfeeding duration in overweight/obese and normal weight groups. Cox proportional hazard regression was used to determine whether body image variables mediated the relationship between maternal weight and duration.</p></div></div><div class="section" id="abs1-3" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/"><b xmlns="http://www.w3.org/1999/xhtml">Results:</b></h3><div class="para"><p>Although intended duration was similar between groups, overweight/obese women had a shorter median duration of any breastfeeding (38.6 weeks) compared to normal weight women (48.9 weeks) (<em>P</em> &lt; 0.01) and they experienced higher risk of breastfeeding cessation over the entire first year postpartum [hazard risk (HR) = 1.43; confidence interval (CI) = 1.02–2.01; <em>P</em> &lt; 0.05]. Overweight/obese women reported lack of body comfort/confidence postpartum more frequently than normal BMI women (<em>P</em> &lt; 0.01). Lack of body comfort/confidence postpartum was negatively associated with duration after adjusting for maternal BMI (<em>P</em> = 0.01). Thus, the effect of BMI on duration was reduced by this variable (HR = 1.31; CI = 0.93, 1.86; <em>P</em> = 0.13), suggesting mediation.</p></div></div><div class="section" id="abs1-4" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/"><b xmlns="http://www.w3.org/1999/xhtml">Conclusions:</b></h3><div class="para"><p>Women with high prepregnant BMI have reduced lactation duration that is mediated by lack of comfort/confidence with one's body. Further research into the interplay between body image, weight status, and breastfeeding outcomes may point to behavioral targets amenable to intervention and modification that may in turn improve breastfeeding outcomes for overweight/obese women and their infants. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</p></div></div>]]></content:encoded><description>Objectives:To test differences in breastfeeding duration by prepregnant maternal weight status, and determine whether body image concerns mediate any differences.Methods:A prospective longitudinal cohort of primiparous women was followed from pregnancy to, at minimum, 6 months postpartum. Questionnaire responses on body concerns were obtained during pregnancy and at 4 months postpartum. Kaplan-Meier curves compared breastfeeding duration in overweight/obese and normal weight groups. Cox proportional hazard regression was used to determine whether body image variables mediated the relationship between maternal weight and duration.Results:Although intended duration was similar between groups, overweight/obese women had a shorter median duration of any breastfeeding (38.6 weeks) compared to normal weight women (48.9 weeks) (P &lt; 0.01) and they experienced higher risk of breastfeeding cessation over the entire first year postpartum [hazard risk (HR) = 1.43; confidence interval (CI) = 1.02–2.01; P &lt; 0.05]. Overweight/obese women reported lack of body comfort/confidence postpartum more frequently than normal BMI women (P &lt; 0.01). Lack of body comfort/confidence postpartum was negatively associated with duration after adjusting for maternal BMI (P = 0.01). Thus, the effect of BMI on duration was reduced by this variable (HR = 1.31; CI = 0.93, 1.86; P = 0.13), suggesting mediation.Conclusions:Women with high prepregnant BMI have reduced lactation duration that is mediated by lack of comfort/confidence with one's body. Further research into the interplay between body image, weight status, and breastfeeding outcomes may point to behavioral targets amenable to intervention and modification that may in turn improve breastfeeding outcomes for overweight/obese women and their infants. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22239" xmlns="http://purl.org/rss/1.0/"><title>Physical activity, cardio-respiratory fitness, and metabolic traits in rural mexican tarahumara</title><link>http://dx.doi.org/10.1002%2Fajhb.22239</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Physical activity, cardio-respiratory fitness, and metabolic traits in rural mexican tarahumara</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Dirk Lund Christensen</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Imelda Alcalá-Sánchez</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Irene Leal-Berumen</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Miguel Conchas-Ramirez</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Soren Brage</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-05T06:48:02.518171-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22239</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/">10.1002/ajhb.22239</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22239</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Short Report</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[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Objectives:</b> To study the association between physical activity energy expenditure (PAEE) and cardio-respiratory fitness (CRF) with key metabolic traits and anthropometric measures in the Tarahumara of Mexico.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Methods:</b> A cross-sectional study was carried out in five rural communities in Chihuahua, México including 64 adult Tarahumara, mean (SD) age 40.7 (12.9) years. Using a combined accelerometer and heart rate sensor, PAEE was measured over three consecutive days and nights and a sub-maximal step test was carried out in order to (1) calibrate heart rate at the individual level and (2) to estimate CRF. Random blood glucose level and resting blood pressure (BP) were measured with standard anthropometrics.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Results:</b> Mean (SD) PAEE was 71.2 (30.3) kJ kg<sup>−1</sup> day<sup>−1</sup> and CRF was 36.6 (6.5) mlO<sub>2</sub> min<sup>−1</sup> kg<sup>−1</sup>. Mean (SD) glucose was 127.9 (32.4) mg/dl, with 3.3% having diabetes. Mean (SD) systolic and diastolic BP was 122 (20.8) and 82 (14.8) mm Hg, respectively, with 28.1% having hypertension. Mean body mass index was 27.5 (4.2) kg m<sup>−2</sup>, with 71.9% being overweight. Following adjustment for age and sex, weak inverse associations were observed between PAEE and systolic BP (β = −0.20, <em>P</em> = 0.27) and diastolic BP (β = −0.16, <em>P</em> = 0.23); and between CRF and systolic BP (β = −0.51, <em>P</em> = 0.14) and diastolic BP (β = −0.53, <em>P</em> = 0.06). The inverse associations with glucose were also weak and not statistically significant for neither PAEE (β = −0.01, <em>P</em> = 0.63) nor CRF (β = −0.05, <em>P</em> = 0.27).</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Conclusions:</b> This study suggests high levels of overweight and hypertension in the Tarahumara, and points to fitness and physical activity as potential intervention targets although findings should be confirmed in larger samples. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</p></div>]]></content:encoded><description>Objectives: To study the association between physical activity energy expenditure (PAEE) and cardio-respiratory fitness (CRF) with key metabolic traits and anthropometric measures in the Tarahumara of Mexico.Methods: A cross-sectional study was carried out in five rural communities in Chihuahua, México including 64 adult Tarahumara, mean (SD) age 40.7 (12.9) years. Using a combined accelerometer and heart rate sensor, PAEE was measured over three consecutive days and nights and a sub-maximal step test was carried out in order to (1) calibrate heart rate at the individual level and (2) to estimate CRF. Random blood glucose level and resting blood pressure (BP) were measured with standard anthropometrics.Results: Mean (SD) PAEE was 71.2 (30.3) kJ kg−1 day−1 and CRF was 36.6 (6.5) mlO2 min−1 kg−1. Mean (SD) glucose was 127.9 (32.4) mg/dl, with 3.3% having diabetes. Mean (SD) systolic and diastolic BP was 122 (20.8) and 82 (14.8) mm Hg, respectively, with 28.1% having hypertension. Mean body mass index was 27.5 (4.2) kg m−2, with 71.9% being overweight. Following adjustment for age and sex, weak inverse associations were observed between PAEE and systolic BP (β = −0.20, P = 0.27) and diastolic BP (β = −0.16, P = 0.23); and between CRF and systolic BP (β = −0.51, P = 0.14) and diastolic BP (β = −0.53, P = 0.06). The inverse associations with glucose were also weak and not statistically significant for neither PAEE (β = −0.01, P = 0.63) nor CRF (β = −0.05, P = 0.27).Conclusions: This study suggests high levels of overweight and hypertension in the Tarahumara, and points to fitness and physical activity as potential intervention targets although findings should be confirmed in larger samples. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22240" xmlns="http://purl.org/rss/1.0/"><title>Extreme behavioral lateralization and the remodeling of the distal humerus</title><link>http://dx.doi.org/10.1002%2Fajhb.22240</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Extreme behavioral lateralization and the remodeling of the distal humerus</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Baris Ozener</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-05T06:45:35.027855-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22240</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/">10.1002/ajhb.22240</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22240</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original 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[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Objectives:</b> The effects of extreme behavioral lateralization (i.e., extreme handedness) on the epicondylar breadth are poorly understood. This study was conducted in order to determine the effects of high levels of right- and left-handedness on epicondyle of the humerus.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Methods:</b> Elbow width of 186 healthy male university students who completed their physical development (extreme left handed = 92, mean age = 18.67, SD = 0.61; extreme right handed = 94, mean age = 18.55, SD = 0.58) were measured with 0.01 mm sensitivity and Edinburgh Handedness Inventory was applied to determine the handedness of the individuals. Participants with scores of +100 were designated as extreme right-handers, and participants with scores of −100 were designed as extreme left-handers.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Results:</b> According to the findings, the degree of directional asymmetry was +1.22 (SD = 2.24) in the extreme right handed, whereas in extreme left handed −0.59 (SD = 1.74). The relative deviation percentage in the extreme right handed was 3.1% whereas 2.2% in the extreme left handed.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Conclusions:</b> It could be stated that extreme handedness has an influence on the asymmetry of epicondyle of the humerus; nevertheless, this effect is more significant in the extreme right handed. This is likely to result from the necessity for left-handed people to adapt themselves to the conditions of a dominantly “right-handed” world. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</p></div>]]></content:encoded><description>Objectives: The effects of extreme behavioral lateralization (i.e., extreme handedness) on the epicondylar breadth are poorly understood. This study was conducted in order to determine the effects of high levels of right- and left-handedness on epicondyle of the humerus.Methods: Elbow width of 186 healthy male university students who completed their physical development (extreme left handed = 92, mean age = 18.67, SD = 0.61; extreme right handed = 94, mean age = 18.55, SD = 0.58) were measured with 0.01 mm sensitivity and Edinburgh Handedness Inventory was applied to determine the handedness of the individuals. Participants with scores of +100 were designated as extreme right-handers, and participants with scores of −100 were designed as extreme left-handers.Results: According to the findings, the degree of directional asymmetry was +1.22 (SD = 2.24) in the extreme right handed, whereas in extreme left handed −0.59 (SD = 1.74). The relative deviation percentage in the extreme right handed was 3.1% whereas 2.2% in the extreme left handed.Conclusions: It could be stated that extreme handedness has an influence on the asymmetry of epicondyle of the humerus; nevertheless, this effect is more significant in the extreme right handed. This is likely to result from the necessity for left-handed people to adapt themselves to the conditions of a dominantly “right-handed” world. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22244" xmlns="http://purl.org/rss/1.0/"><title>Microbial exposures in infancy predict levels of the immunoregulatory cytokine interleukin-4 in filipino young adults</title><link>http://dx.doi.org/10.1002%2Fajhb.22244</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Microbial exposures in infancy predict levels of the immunoregulatory cytokine interleukin-4 in filipino young adults</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Paula Skye Tallman</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Christopher Kuzawa</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Linda Adair</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Judith B. Borja</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Thomas W. McDade</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-05T06:42:01.628073-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22244</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/">10.1002/ajhb.22244</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22244</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original 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[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="section" id="abs1-1" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Objectives:</h3><div class="para"><p>Infancy represents a window of development during which long-term immunological functioning can be influenced. In this study, we evaluate proxies of microbial exposures in infancy as predictors of interleukin-4 (IL-4) in young adulthood. IL-4 is an immunoregulatory cytokine that plays a role in the pathogenesis of atopic and allergic diseases.</p></div></div><div class="section" id="abs1-2" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Methods:</h3><div class="para"><p>Data were obtained from 1,403 participants in the Cebu Longitudinal Health and Nutrition Survey, an ongoing population-based study in the Philippines. Relationships between microbial and nutritional environments in infancy and plasma IL-4 concentrations in adulthood were evaluated using tobit regression models.</p></div></div><div class="section" id="abs1-3" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Results:</h3><div class="para"><p>Having older siblings and more episodes of respiratory illness in infancy significantly predicted lower concentrations of plasma IL-4 in adulthood. Unexpectedly, more episodes of diarrheal illness in infancy were associated with higher IL-4 in adulthood. Interactions between a composite household pathogen exposure score and the duration of exclusive breastfeeding approached significance. This interaction showed that the negative association between household pathogen exposure in infancy and adult IL-4 was only significant for individuals who had been exclusively breastfed for a short duration of time. Finally, currently living in an urban household was unexpectedly, negatively associated with adult IL-4. Associations were independent of early nutrition, socioeconomic status (SES), and urbanicity, as well as current measures of infection, body fat, SES, and smoking.</p></div></div><div class="section" id="abs1-4" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Conclusions:</h3><div class="para"><p>This study builds on a growing body of literature demonstrating that early ecological conditions have long-term effects on human biology by providing evidence that multiple proxies of microbial exposures in infancy are associated with adult IL-4. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</p></div></div>]]></content:encoded><description>Objectives:Infancy represents a window of development during which long-term immunological functioning can be influenced. In this study, we evaluate proxies of microbial exposures in infancy as predictors of interleukin-4 (IL-4) in young adulthood. IL-4 is an immunoregulatory cytokine that plays a role in the pathogenesis of atopic and allergic diseases.Methods:Data were obtained from 1,403 participants in the Cebu Longitudinal Health and Nutrition Survey, an ongoing population-based study in the Philippines. Relationships between microbial and nutritional environments in infancy and plasma IL-4 concentrations in adulthood were evaluated using tobit regression models.Results:Having older siblings and more episodes of respiratory illness in infancy significantly predicted lower concentrations of plasma IL-4 in adulthood. Unexpectedly, more episodes of diarrheal illness in infancy were associated with higher IL-4 in adulthood. Interactions between a composite household pathogen exposure score and the duration of exclusive breastfeeding approached significance. This interaction showed that the negative association between household pathogen exposure in infancy and adult IL-4 was only significant for individuals who had been exclusively breastfed for a short duration of time. Finally, currently living in an urban household was unexpectedly, negatively associated with adult IL-4. Associations were independent of early nutrition, socioeconomic status (SES), and urbanicity, as well as current measures of infection, body fat, SES, and smoking.Conclusions:This study builds on a growing body of literature demonstrating that early ecological conditions have long-term effects on human biology by providing evidence that multiple proxies of microbial exposures in infancy are associated with adult IL-4. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22222" xmlns="http://purl.org/rss/1.0/"><title>A possible link between the pubertal growth of girls and prostate cancer in their sons</title><link>http://dx.doi.org/10.1002%2Fajhb.22222</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">A possible link between the pubertal growth of girls and prostate cancer in their sons</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">David J.P. Barker</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Clive Osmond</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Kent L. Thornburg</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Eero Kajantie</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Johan G. Eriksson</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-01-27T06:58:52.477474-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22222</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/">10.1002/ajhb.22222</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22222</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original 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[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="section" id="abs1-1" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Objectives:</h3><div class="para"><p>Among women attending antenatal clinics during 1934–1944 a large intercristal diameter, the maximum distance between the pelvic iliac crests, was associated with a raised incidence of breast and ovarian cancer in the daughters in later life. At puberty, the intercristal diameter of girls enlarges rapidly under the influence of estrogen. We speculated that high maternal estrogen concentrations during pregnancy initiate hormonal cancers in their daughters. Here, we examine the association between the mothers' intercristal diameters and prostate cancer in their sons.</p></div></div><div class="section" id="abs1-2" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Methods:</h3><div class="para"><p>Using the national cancer registry we identified 221 cases of prostate cancer among 6,975 men born during 1934–1944 in Helsinki, Finland. Four thousand four hundred and one of these men had their mother's bony pelvic measurements recorded: there were 149 cases among them.</p></div></div><div class="section" id="abs1-3" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Results:</h3><div class="para"><p>Hazard ratios for prostate cancer rose as the mother's intercristal diameter increased; but this association was restricted to men who were born before 40 weeks of gestation. Among these men the hazard ratio was 1.27 (95% CI 1.09–1.48; <em>P</em> = 0.002). The hazard ratio was 2.2 (1.3–3.7; <em>P</em> &lt; 0.001) in men whose mothers weighed more than 80 kg in late pregnancy compared with those whose mothers weighed 60 kg or less.</p></div></div><div class="section" id="abs1-4" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Conclusions:</h3><div class="para"><p>These findings are consistent with a conceptual framework for the origins of hormonally dependent cancers that invokes exposure of embryonic tissue to maternal sex hormones followed by resetting of the fetal hypothalamic-gonadotropin axis in late gestation. We hypothesize that compensatory prepubertal growth among girls is associated with hormonal cancers in the next generation. Am. J. Hum. Biol. © 2012Wiley Periodicals, Inc.</p></div></div>]]></content:encoded><description>Objectives:Among women attending antenatal clinics during 1934–1944 a large intercristal diameter, the maximum distance between the pelvic iliac crests, was associated with a raised incidence of breast and ovarian cancer in the daughters in later life. At puberty, the intercristal diameter of girls enlarges rapidly under the influence of estrogen. We speculated that high maternal estrogen concentrations during pregnancy initiate hormonal cancers in their daughters. Here, we examine the association between the mothers' intercristal diameters and prostate cancer in their sons.Methods:Using the national cancer registry we identified 221 cases of prostate cancer among 6,975 men born during 1934–1944 in Helsinki, Finland. Four thousand four hundred and one of these men had their mother's bony pelvic measurements recorded: there were 149 cases among them.Results:Hazard ratios for prostate cancer rose as the mother's intercristal diameter increased; but this association was restricted to men who were born before 40 weeks of gestation. Among these men the hazard ratio was 1.27 (95% CI 1.09–1.48; P = 0.002). The hazard ratio was 2.2 (1.3–3.7; P &lt; 0.001) in men whose mothers weighed more than 80 kg in late pregnancy compared with those whose mothers weighed 60 kg or less.Conclusions:These findings are consistent with a conceptual framework for the origins of hormonally dependent cancers that invokes exposure of embryonic tissue to maternal sex hormones followed by resetting of the fetal hypothalamic-gonadotropin axis in late gestation. We hypothesize that compensatory prepubertal growth among girls is associated with hormonal cancers in the next generation. Am. J. Hum. Biol. © 2012Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22207" xmlns="http://purl.org/rss/1.0/"><title>How culture shapes the body: Cultural consonance and body mass in urban brazil</title><link>http://dx.doi.org/10.1002%2Fajhb.22207</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">How culture shapes the body: Cultural consonance and body mass in urban brazil</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">William W. Dressler</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Kathryn S. Oths</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Mauro C. Balieiro</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Rosane P. Ribeiro</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">José Ernesto Dos Santos</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-01-24T09:52:35.556715-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22207</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/">10.1002/ajhb.22207</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22207</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original 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[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="section" id="abs1-1" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Objectives:</h3><div class="para"><p>The aim of this article is to develop a model of how culture shapes the body, based on two studies conducted in urban Brazil.</p></div></div><div class="section" id="abs1-2" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Methods:</h3><div class="para"><p>Research was conducted in 1991 and 2001 in four socioeconomically distinct neighborhoods. First, cultural domain analyses were conducted with samples of key informants. The cultural domains investigated included lifestyle, social support, family life, national identity, and food. Cultural consensus analysis was used to confirm shared knowledge in each domain and to derive measures of cultural consonance. Cultural consonance assesses how closely an individual matches the cultural consensus model for each domain. Second, body composition, cultural consonance, and related variables were assessed in community surveys. Multiple regression analysis was used to examine the association of cultural consonance and body composition, controlling for standard covariates and competing explanatory variables.</p></div></div><div class="section" id="abs1-3" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Results:</h3><div class="para"><p>In 1991, in a survey of 260 individuals, cultural consonance had a curvilinear association with the body mass index that differed for men and women, controlling for sociodemographic and dietary variables. In 2001, in a survey of 267 individuals, cultural consonance had a linear association with abdominal circumference that differed for men and women, controlling for sociodemographic and dietary variables. In general, as cultural consonance increases, body mass index and abdominal circumference decline, more strongly for women than men.</p></div></div><div class="section" id="abs1-4" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Conclusions:</h3><div class="para"><p>As individuals, in their own beliefs and behaviors, more closely approximate shared cultural models in socially salient domains, body composition also more closely approximates the cultural prototype of the body. Am. J. Hum. Biol. © 2012Wiley Periodicals, Inc.</p></div></div>]]></content:encoded><description>Objectives:The aim of this article is to develop a model of how culture shapes the body, based on two studies conducted in urban Brazil.Methods:Research was conducted in 1991 and 2001 in four socioeconomically distinct neighborhoods. First, cultural domain analyses were conducted with samples of key informants. The cultural domains investigated included lifestyle, social support, family life, national identity, and food. Cultural consensus analysis was used to confirm shared knowledge in each domain and to derive measures of cultural consonance. Cultural consonance assesses how closely an individual matches the cultural consensus model for each domain. Second, body composition, cultural consonance, and related variables were assessed in community surveys. Multiple regression analysis was used to examine the association of cultural consonance and body composition, controlling for standard covariates and competing explanatory variables.Results:In 1991, in a survey of 260 individuals, cultural consonance had a curvilinear association with the body mass index that differed for men and women, controlling for sociodemographic and dietary variables. In 2001, in a survey of 267 individuals, cultural consonance had a linear association with abdominal circumference that differed for men and women, controlling for sociodemographic and dietary variables. In general, as cultural consonance increases, body mass index and abdominal circumference decline, more strongly for women than men.Conclusions:As individuals, in their own beliefs and behaviors, more closely approximate shared cultural models in socially salient domains, body composition also more closely approximates the cultural prototype of the body. Am. J. Hum. Biol. © 2012Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22224" xmlns="http://purl.org/rss/1.0/"><title>Newborn's condition at birth does not depend on maternal sexual strategy—evidence against the “hunting for good genes” hypothesis</title><link>http://dx.doi.org/10.1002%2Fajhb.22224</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Newborn's condition at birth does not depend on maternal sexual strategy—evidence against the “hunting for good genes” hypothesis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Boguslaw Pawlowski</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Agnieszka Zelazniewicz</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-01-24T09:52:07.622532-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22224</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/">10.1002/ajhb.22224</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22224</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Research 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[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="section" id="abs1-1" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Objectives:</h3><div class="para"><p>Neonatal weight and health depend on many epigenetic and environmental factors and also on a child's genes as inherited from the mother and the father. The “Hunting for Good Genes” (HfGG) hypothesis claims that women pursue short-term mating strategies in order to obtain good genes for their progeny. If this is true, one should expect that in comparison to children born in long-term relationships (LR), children born in short-term relationships (SR) should have a larger neonatal size and be healthier.</p></div></div><div class="section" id="abs1-2" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Methods:</h3><div class="para"><p>To test the HfGG hypothesis, and whether sexual strategy influences neonatal parameters, we used an on-line questionnaire aimed at mothers. Totally, 1,558 women took part in this study, and among them 130 conceived their first-born child in a short-term relationship (SR mothers) and 1,428 in a long-term relationship (LR mothers).</p></div></div><div class="section" id="abs1-3" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Results:</h3><div class="para"><p>There was no difference between those two groups of children in terms of birth weight and Apgar score. Although we found no difference in the occurrence of genetic diseases and birth defects between SR and LR boys, the girls born by LR mothers were healthier than those born by SR mothers. We also did not find any difference in the sex ratio of the children born to SR and LR mothers.</p></div></div><div class="section" id="abs1-4" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Conclusions:</h3><div class="para"><p>The results of our study do not support the “Hunting for Good Genes” hypothesis for the first born child. In the contemporary western society of the study, women do not seem to derive genetic benefits expressed as child condition at birth from short-term relationships. © 2012 Wiley Periodicals, Inc.</p></div></div>]]></content:encoded><description>Objectives:Neonatal weight and health depend on many epigenetic and environmental factors and also on a child's genes as inherited from the mother and the father. The “Hunting for Good Genes” (HfGG) hypothesis claims that women pursue short-term mating strategies in order to obtain good genes for their progeny. If this is true, one should expect that in comparison to children born in long-term relationships (LR), children born in short-term relationships (SR) should have a larger neonatal size and be healthier.Methods:To test the HfGG hypothesis, and whether sexual strategy influences neonatal parameters, we used an on-line questionnaire aimed at mothers. Totally, 1,558 women took part in this study, and among them 130 conceived their first-born child in a short-term relationship (SR mothers) and 1,428 in a long-term relationship (LR mothers).Results:There was no difference between those two groups of children in terms of birth weight and Apgar score. Although we found no difference in the occurrence of genetic diseases and birth defects between SR and LR boys, the girls born by LR mothers were healthier than those born by SR mothers. We also did not find any difference in the sex ratio of the children born to SR and LR mothers.Conclusions:The results of our study do not support the “Hunting for Good Genes” hypothesis for the first born child. In the contemporary western society of the study, women do not seem to derive genetic benefits expressed as child condition at birth from short-term relationships. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22221" xmlns="http://purl.org/rss/1.0/"><title>Body mass index versus dual energy x-ray absorptiometry-derived indexes: Predictors of cardiovascular and diabetic disease risk factors</title><link>http://dx.doi.org/10.1002%2Fajhb.22221</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Body mass index versus dual energy x-ray absorptiometry-derived indexes: Predictors of cardiovascular and diabetic disease risk factors</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Dan S. Sharp</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Michael E. Andrew</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Cecil M. Burchfiel</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">John M. Violanti</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jean Wactawski-Wende</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-01-24T09:51:59.558639-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22221</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/">10.1002/ajhb.22221</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22221</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Research 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[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="section" id="abs1-1" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/"><b xmlns="http://www.w3.org/1999/xhtml">Objectives:</b></h3><div class="para"><p>The body mass index (BMI), a ratio of weight/height<sup>2</sup>, dominates estimation of adiposity in population studies. BMI, however, does not distinguish among fat, muscle, or bone mass. Accordingly, its usage to assess and manage obesity in the population is limited. This study compares the use of BMI with direct measures of fat- and lean-mass to predict established cardiovascular and diabetes risk factors: blood pressure, lipids, and glucose.</p></div></div><div class="section" id="abs1-2" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Methods:</h3><div class="para"><p>The entire Buffalo Police Department was the object of recruitment to a baseline study of physiological and psychological stress. Four hundred nine officers constitute the sample for this analysis. Regression methods focusing on explained variance in blood pressure, high density lipoprotein (HDL) cholesterol, and blood glucose compare the use of BMI to that of fat- and lean-mass indexes derived from dual energy X-ray absorptiometry (DEXA).</p></div></div><div class="section" id="abs1-3" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Results:</h3><div class="para"><p>DEXA indexes explain 1.6%–3.3% (<em>P</em> &lt; 0.05, all risk factors) more variance than BMI. Fat mass drives the association for blood pressure, trunk lean mass for HDL cholesterol, and both for blood glucose. High degrees of multicollinearity complicate interpretation of predictive models jointly containing BMI and DEXA indexes.</p></div></div><div class="section" id="abs1-4" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Conclusions:</h3><div class="para"><p>In police officers, DEXA indexes are better predictors of cardiovascular disease and diabetes risk factors. However, populations with different distributions of fitness, diet, and health conditions may demonstrate differentfeatures. In contrast to BMI, DEXA-derived measurements suggest avenues to explore metabolic processes, which relate to an index's underlying association with risk and may suggest more effective intervention strategies. © 2012 Wiley Periodicals, Inc.</p></div></div>]]></content:encoded><description>Objectives:The body mass index (BMI), a ratio of weight/height2, dominates estimation of adiposity in population studies. BMI, however, does not distinguish among fat, muscle, or bone mass. Accordingly, its usage to assess and manage obesity in the population is limited. This study compares the use of BMI with direct measures of fat- and lean-mass to predict established cardiovascular and diabetes risk factors: blood pressure, lipids, and glucose.Methods:The entire Buffalo Police Department was the object of recruitment to a baseline study of physiological and psychological stress. Four hundred nine officers constitute the sample for this analysis. Regression methods focusing on explained variance in blood pressure, high density lipoprotein (HDL) cholesterol, and blood glucose compare the use of BMI to that of fat- and lean-mass indexes derived from dual energy X-ray absorptiometry (DEXA).Results:DEXA indexes explain 1.6%–3.3% (P &lt; 0.05, all risk factors) more variance than BMI. Fat mass drives the association for blood pressure, trunk lean mass for HDL cholesterol, and both for blood glucose. High degrees of multicollinearity complicate interpretation of predictive models jointly containing BMI and DEXA indexes.Conclusions:In police officers, DEXA indexes are better predictors of cardiovascular disease and diabetes risk factors. However, populations with different distributions of fitness, diet, and health conditions may demonstrate differentfeatures. In contrast to BMI, DEXA-derived measurements suggest avenues to explore metabolic processes, which relate to an index's underlying association with risk and may suggest more effective intervention strategies. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22220" xmlns="http://purl.org/rss/1.0/"><title>The dual origin of tati-speakers from dagestan as written in the genealogy of uniparental variants</title><link>http://dx.doi.org/10.1002%2Fajhb.22220</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The dual origin of tati-speakers from dagestan as written in the genealogy of uniparental variants</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Stefania Bertoncini</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Kazima Bulayeva</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Gianmarco Ferri</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Luca Pagani</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Laura Caciagli</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Luca Taglioli</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Igor Semyonov</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Oleg Bulayev</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Giorgio Paoli</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Sergio Tofanelli</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-01-24T09:51:48.883108-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22220</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/">10.1002/ajhb.22220</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22220</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Research 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[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="section" id="abs1-1" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Objectives:</h3><div class="para"><p>Tat language is classified in an Iranian subbranch of the Indo-European family. It is spoken in the Caucasus and in the West Caspian region by populations with heterogeneous cultural traditions and religion whose ancestry is unknown. The aim of this study is to get a first insight about the genetic history of this peculiar linguistic group.</p></div></div><div class="section" id="abs1-2" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Methods:</h3><div class="para"><p>We investigated the uniparental gene pools, defined by NRY and mtDNA high-resolution markers, in two Tati-speaking communities from Dagestan: Mountain Jews or Juhur, who speak the Judeo-Tat dialect, and the Tats, who speak the Muslim-Tat dialect. The samples have been collected in monoethnic rural villages and selected on the basis of genealogical relationships. A novel approach aimed at resolving cryptic cases in the recent history of human populations, which combines the properties of uniparental genetic markers with the potential of “forward-in-time” computer simulations, is presented.</p></div></div><div class="section" id="abs1-3" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Results:</h3><div class="para"><p>Judeo-Tats emerged as a group with tight matrilineal genetic legacy who separated early from other Jewish communities. Tats exhibited genetic signals of a much longer <em>in situ</em> evolution, which appear as substantially unlinked with other Indo-Iranian enclaves in the Caucasus.</p></div></div><div class="section" id="abs1-4" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Conclusions:</h3><div class="para"><p>The independent demographic histories of the two samples, with mutually reversed profiles at paternally and maternally transmitted genetic systems, suggest that geographic proximity and linguistic assimilation of Tati-speakers from Dagestan do not reflect a common ancestry. © 2012 Wiley Periodicals, Inc.</p></div></div>]]></content:encoded><description>Objectives:Tat language is classified in an Iranian subbranch of the Indo-European family. It is spoken in the Caucasus and in the West Caspian region by populations with heterogeneous cultural traditions and religion whose ancestry is unknown. The aim of this study is to get a first insight about the genetic history of this peculiar linguistic group.Methods:We investigated the uniparental gene pools, defined by NRY and mtDNA high-resolution markers, in two Tati-speaking communities from Dagestan: Mountain Jews or Juhur, who speak the Judeo-Tat dialect, and the Tats, who speak the Muslim-Tat dialect. The samples have been collected in monoethnic rural villages and selected on the basis of genealogical relationships. A novel approach aimed at resolving cryptic cases in the recent history of human populations, which combines the properties of uniparental genetic markers with the potential of “forward-in-time” computer simulations, is presented.Results:Judeo-Tats emerged as a group with tight matrilineal genetic legacy who separated early from other Jewish communities. Tats exhibited genetic signals of a much longer in situ evolution, which appear as substantially unlinked with other Indo-Iranian enclaves in the Caucasus.Conclusions:The independent demographic histories of the two samples, with mutually reversed profiles at paternally and maternally transmitted genetic systems, suggest that geographic proximity and linguistic assimilation of Tati-speakers from Dagestan do not reflect a common ancestry. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22219" xmlns="http://purl.org/rss/1.0/"><title>Does inadequate sleep play a role in vulnerability to obesity?</title><link>http://dx.doi.org/10.1002%2Fajhb.22219</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Does inadequate sleep play a role in vulnerability to obesity?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Kristen L. Knutson</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-01-24T09:51:39.165005-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22219</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/">10.1002/ajhb.22219</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22219</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review</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[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>The prevalence of obesity is increasing rapidly worldwide, which is cause for concern because obesity increases the risk of cardiovascular disease and diabetes, reduces life expectancy, and impairs quality of life. A better understanding of the risk factors for obesity is therefore a critical global health concern, and human biologists can play an important role in identifying these risk factors in various populations. The objective of this review is to present the evidence that inadequate sleep may be a novel risk factor associated with increased vulnerability to obesity and associated cardiometabolic disease. Experimental studies have found that short-term sleep restriction is associated with impaired glucose metabolism, dysregulation of appetite, and increased blood pressure. Observational studies have observed cross-sectional associations between short sleep duration (generally &lt;6 h per night) and increased body mass index or obesity, prevalent diabetes, and prevalent hypertension. Some studies also reported an association between self-reported long sleep duration (generally &gt;8 h per night) and cardiometabolic disease. A few prospective studies have found a significant increased risk of weight gain, incident diabetes, and incident hypertension associated with inadequate sleep. Given the potential link between inadequate sleep and obesity, a critical next step is to identify the social, cultural, and environmental determinants of sleep, which would help to identify vulnerable populations. Future human biology research should consider variation in sleep characteristics among different populations and determine whether the associations between sleep and obesity observed in Western populations persist elsewhere. © 2012 Wiley Periodicals, Inc.</p></div>]]></content:encoded><description>The prevalence of obesity is increasing rapidly worldwide, which is cause for concern because obesity increases the risk of cardiovascular disease and diabetes, reduces life expectancy, and impairs quality of life. A better understanding of the risk factors for obesity is therefore a critical global health concern, and human biologists can play an important role in identifying these risk factors in various populations. The objective of this review is to present the evidence that inadequate sleep may be a novel risk factor associated with increased vulnerability to obesity and associated cardiometabolic disease. Experimental studies have found that short-term sleep restriction is associated with impaired glucose metabolism, dysregulation of appetite, and increased blood pressure. Observational studies have observed cross-sectional associations between short sleep duration (generally &lt;6 h per night) and increased body mass index or obesity, prevalent diabetes, and prevalent hypertension. Some studies also reported an association between self-reported long sleep duration (generally &gt;8 h per night) and cardiometabolic disease. A few prospective studies have found a significant increased risk of weight gain, incident diabetes, and incident hypertension associated with inadequate sleep. Given the potential link between inadequate sleep and obesity, a critical next step is to identify the social, cultural, and environmental determinants of sleep, which would help to identify vulnerable populations. Future human biology research should consider variation in sleep characteristics among different populations and determine whether the associations between sleep and obesity observed in Western populations persist elsewhere. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22243" xmlns="http://purl.org/rss/1.0/"><title>The caloric restriction paradigm: Implications for healthy human aging</title><link>http://dx.doi.org/10.1002%2Fajhb.22243</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The caloric restriction paradigm: Implications for healthy human aging</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Rozalyn M. Anderson</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Richard Weindruch</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22243</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/">10.1002/ajhb.22243</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22243</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Feature Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">101</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">106</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>Underlying the importance of research on the biology of aging is the fact that many nations face the demographic reality of a rapidly aging populace and the looming healthcare challenges that it brings. This reality is a result of aging itself being the most significant risk factor for a range of the most prevalent diseases, including many cancers, cardiovascular disease, and diabetes. Accordingly, interventions are sorely needed that would be able to delay or prevent diseases and disorders associated with the aging process and thereby increase the period of time that aging individuals are in good health (the health-span). Caloric restriction (CR) has emerged as a model of major interest as it is widely agreed that CR is the most potent environmental intervention that delays the onset of aging and extends life span in diverse experimental organisms. A better understanding of the mechanisms by which CR delays aging will reveal new insights into the aging process and the underlying causes of disease vulnerability with age. These novel insights will allow the development of novel treatments and preventive measures for age-associated diseases and disorders. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</p></div>]]></content:encoded><description>Underlying the importance of research on the biology of aging is the fact that many nations face the demographic reality of a rapidly aging populace and the looming healthcare challenges that it brings. This reality is a result of aging itself being the most significant risk factor for a range of the most prevalent diseases, including many cancers, cardiovascular disease, and diabetes. Accordingly, interventions are sorely needed that would be able to delay or prevent diseases and disorders associated with the aging process and thereby increase the period of time that aging individuals are in good health (the health-span). Caloric restriction (CR) has emerged as a model of major interest as it is widely agreed that CR is the most potent environmental intervention that delays the onset of aging and extends life span in diverse experimental organisms. A better understanding of the mechanisms by which CR delays aging will reveal new insights into the aging process and the underlying causes of disease vulnerability with age. These novel insights will allow the development of novel treatments and preventive measures for age-associated diseases and disorders. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22232" xmlns="http://purl.org/rss/1.0/"><title>Human biology eats: Contemporary research and future directions</title><link>http://dx.doi.org/10.1002%2Fajhb.22232</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Human biology eats: Contemporary research and future directions</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Andrea S. Wiley</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">John S. Allen</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Alexandra Brewis</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22232</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/">10.1002/ajhb.22232</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22232</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Feature Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">107</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">109</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22218" xmlns="http://purl.org/rss/1.0/"><title>Paleolithic diets as a model for prevention and treatment of western disease</title><link>http://dx.doi.org/10.1002%2Fajhb.22218</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Paleolithic diets as a model for prevention and treatment of western disease</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Staffan Lindeberg</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22218</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/">10.1002/ajhb.22218</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22218</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Feature Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">110</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">115</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="section" id="abs1-1" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Objectives:</h3><div class="para"><p>To explore the possibility that a paleolithic-like diet can be used in the prevention of age-related degenerative Western disease.</p></div></div><div class="section" id="abs1-2" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Methods:</h3><div class="para"><p>Literature review of African Paleolithic foods in relation to recent evidence of healthy nutrition.</p></div></div><div class="section" id="abs1-3" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Results and Discussion:</h3><div class="para"><p>Available evidence lends weak support in favor and little against the notion that lean meat, fish, vegetables, tubers, and fruit can be effective in the prevention and treatment of common Western diseases. There are no obvious risks with avoiding dairy products, margarine, oils, refined sugar, and cereal grains, which provide 70% or more of the dietary intake in northern European populations. If stroke, coronary heart disease, type 2 diabetes, and cancer are preventable by dietary changes, an ancestral-like diet may provide an appropriate template. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</p></div></div>]]></content:encoded><description>Objectives:To explore the possibility that a paleolithic-like diet can be used in the prevention of age-related degenerative Western disease.Methods:Literature review of African Paleolithic foods in relation to recent evidence of healthy nutrition.Results and Discussion:Available evidence lends weak support in favor and little against the notion that lean meat, fish, vegetables, tubers, and fruit can be effective in the prevention and treatment of common Western diseases. There are no obvious risks with avoiding dairy products, margarine, oils, refined sugar, and cereal grains, which provide 70% or more of the dietary intake in northern European populations. If stroke, coronary heart disease, type 2 diabetes, and cancer are preventable by dietary changes, an ancestral-like diet may provide an appropriate template. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22236" xmlns="http://purl.org/rss/1.0/"><title>The human obesity epidemic, the mismatch paradigm, and our modern “captive” environment</title><link>http://dx.doi.org/10.1002%2Fajhb.22236</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The human obesity epidemic, the mismatch paradigm, and our modern “captive” environment</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Michael L. Power</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22236</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/">10.1002/ajhb.22236</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22236</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">116</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">122</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>In the distant past obesity in humans was rare and likely caused by metabolic dysregulation due to genetic or disease-related pathology. External factors precluded the ability of most people to overeat or under exert. Socio-cultural obesity came about due to the rareness of obesity and its difficulty to achieve. What is rare becomes valuable and what is difficult to achieve becomes a badge of prestige. The modern human obesity epidemic would appear to represent a third class of obesity: environmental obesity. Much like the captive environments which humans construct for the captive/companion animals in our care, the modern human environment has greatly decreased the challenges of life that would restrict food intake and enforce exertion. And like us, our captive/companion animal populations are also experiencing obesity epidemics. A further concern is that maternal obesity alters maternal signaling to offspring, <em>in utero</em> through the placenta and after birth through breast milk, in ways that perpetuate an enhanced vulnerability to obesity. Molecules such as leptin, produced by adipose tissue and placenta, have significant developmental effects on brain areas associated with feeding behavior. Leptin and other cytokines and growth factors are found in breast milk. These molecules have positive effects on gut maturation; their effects on metabolism and brain development are unclear. Placenta and brain also are hotspots for epigenetic regulation, and epigenetic changes may play significant roles in the later vulnerability to obesity and to the development of a diverse array of diseases, including heart disease, hypertension, and noninsulin-dependent diabetes. Am. J. Hum. Biol., 2012. © 2012 Wiley Periodicals, Inc.</p></div>]]></content:encoded><description>In the distant past obesity in humans was rare and likely caused by metabolic dysregulation due to genetic or disease-related pathology. External factors precluded the ability of most people to overeat or under exert. Socio-cultural obesity came about due to the rareness of obesity and its difficulty to achieve. What is rare becomes valuable and what is difficult to achieve becomes a badge of prestige. The modern human obesity epidemic would appear to represent a third class of obesity: environmental obesity. Much like the captive environments which humans construct for the captive/companion animals in our care, the modern human environment has greatly decreased the challenges of life that would restrict food intake and enforce exertion. And like us, our captive/companion animal populations are also experiencing obesity epidemics. A further concern is that maternal obesity alters maternal signaling to offspring, in utero through the placenta and after birth through breast milk, in ways that perpetuate an enhanced vulnerability to obesity. Molecules such as leptin, produced by adipose tissue and placenta, have significant developmental effects on brain areas associated with feeding behavior. Leptin and other cytokines and growth factors are found in breast milk. These molecules have positive effects on gut maturation; their effects on metabolism and brain development are unclear. Placenta and brain also are hotspots for epigenetic regulation, and epigenetic changes may play significant roles in the later vulnerability to obesity and to the development of a diverse array of diseases, including heart disease, hypertension, and noninsulin-dependent diabetes. Am. J. Hum. Biol., 2012. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22209" xmlns="http://purl.org/rss/1.0/"><title>“Theory of food” as a neurocognitive adaptation</title><link>http://dx.doi.org/10.1002%2Fajhb.22209</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">“Theory of food” as a neurocognitive adaptation</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">John S. Allen</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22209</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/">10.1002/ajhb.22209</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22209</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">123</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">129</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>Human adult cognition emerges over the course of development via the interaction of multiple critical neurocognitive networks. These networks evolved in response to various selection pressures, many of which were modified or intensified by the intellectual, technological, and sociocultural environments that arose in connection with the evolution of genus <em>Homo</em>. Networks related to language and theory of mind clearly play an important role in adult cognition. Given the critical importance of food to both basic survival and cultural interaction, a “theory of food” (analogous to theory of mind) may represent another complex network essential for normal cognition. I propose that theory of food evolved as an internal, cognitive representation of our diets in our minds. Like other complex cognitive abilities, it relies on complex and overlapping dedicated neural networks that develop in childhood under familial and cultural influences. Normative diets are analogous to first languages in that they are acquired without overt teaching; they are also difficult to change or modify once a critical period in development is passed. Theory of food suggests that cognitive activities related to food may be cognitive enhancers, which could have implications for maintaining healthy brain function in aging. Am. J. Hum. Biol., 2012. © 2012 Wiley Periodicals, Inc.</p></div>]]></content:encoded><description>Human adult cognition emerges over the course of development via the interaction of multiple critical neurocognitive networks. These networks evolved in response to various selection pressures, many of which were modified or intensified by the intellectual, technological, and sociocultural environments that arose in connection with the evolution of genus Homo. Networks related to language and theory of mind clearly play an important role in adult cognition. Given the critical importance of food to both basic survival and cultural interaction, a “theory of food” (analogous to theory of mind) may represent another complex network essential for normal cognition. I propose that theory of food evolved as an internal, cognitive representation of our diets in our minds. Like other complex cognitive abilities, it relies on complex and overlapping dedicated neural networks that develop in childhood under familial and cultural influences. Normative diets are analogous to first languages in that they are acquired without overt teaching; they are also difficult to change or modify once a critical period in development is passed. Theory of food suggests that cognitive activities related to food may be cognitive enhancers, which could have implications for maintaining healthy brain function in aging. Am. J. Hum. Biol., 2012. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22201" xmlns="http://purl.org/rss/1.0/"><title>Cow milk consumption, insulin-like growth factor-I, and human biology: A life history approach</title><link>http://dx.doi.org/10.1002%2Fajhb.22201</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Cow milk consumption, insulin-like growth factor-I, and human biology: A life history approach</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Andrea S. Wiley</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22201</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/">10.1002/ajhb.22201</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22201</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">130</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">138</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="section" id="abs1-1" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Objective:</h3><div class="para"><p>To assess the life history consequences of cow milk consumption at different stages in early life (prenatal to adolescence), especially with regard to linear growth and age at menarche and the role of insulin-like growth factor I (IGF-I) in mediating a relationship among milk, growth and development, and long-term biological outcomes.</p></div></div><div class="section" id="abs1-2" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Methods:</h3><div class="para"><p>United States National Health and Nutrition Examination Survey (NHANES) data from 1999 to 2004 and review of existing literature.</p></div></div><div class="section" id="abs1-3" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Results:</h3><div class="para"><p>The literature tends to support milk's role in enhancing growth early in life (prior to age 5 years), but there is less support for this relationship during middle childhood. Milk has been associated with early menarche and with acceleration of linear growth in adolescence. NHANES data show a positive relationship between milk intake and linear growth in early childhood and adolescence, but not middle childhood, a period of relatively slow growth. IGF-I is a candidate bioactive molecule linking milk consumption to more rapid growth and development, although the mechanism by which it may exert such effects is unknown.</p></div></div><div class="section" id="abs1-4" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Conclusions:</h3><div class="para"><p>Routine milk consumption is an evolutionarily novel dietary behavior that has the potential to alter human life history parameters, especially vis-à-vis linear growth, which in turn may have negative long-term biological consequences. Am. J. Hum. Biol. 2012. © 2011 Wiley Periodicals, Inc.</p></div></div>]]></content:encoded><description>Objective:To assess the life history consequences of cow milk consumption at different stages in early life (prenatal to adolescence), especially with regard to linear growth and age at menarche and the role of insulin-like growth factor I (IGF-I) in mediating a relationship among milk, growth and development, and long-term biological outcomes.Methods:United States National Health and Nutrition Examination Survey (NHANES) data from 1999 to 2004 and review of existing literature.Results:The literature tends to support milk's role in enhancing growth early in life (prior to age 5 years), but there is less support for this relationship during middle childhood. Milk has been associated with early menarche and with acceleration of linear growth in adolescence. NHANES data show a positive relationship between milk intake and linear growth in early childhood and adolescence, but not middle childhood, a period of relatively slow growth. IGF-I is a candidate bioactive molecule linking milk consumption to more rapid growth and development, although the mechanism by which it may exert such effects is unknown.Conclusions:Routine milk consumption is an evolutionarily novel dietary behavior that has the potential to alter human life history parameters, especially vis-à-vis linear growth, which in turn may have negative long-term biological consequences. Am. J. Hum. Biol. 2012. © 2011 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22202" xmlns="http://purl.org/rss/1.0/"><title>What's NOT to eat—food adulteration in the context of human biology</title><link>http://dx.doi.org/10.1002%2Fajhb.22202</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">What's NOT to eat—food adulteration in the context of human biology</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Lawrence M. Schell</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Mia V. Gallo</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Katsi Cook</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22202</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/">10.1002/ajhb.22202</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22202</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">139</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">148</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>Food has nutritional and non-nutritional components. The latter are not well-studied despite the fact that food adulteration has been common. Food adulteration may have reached its peak in cities of Western Europe and the US in the 18th and 19th centuries when foods were often purposely contaminated with additives to increase bulk, attractiveness, disguise spoilage, and increase profit. Effective regulation of food began in the late 19th and 20th centuries. Nevertheless, today food recalls for bacterial contamination are common, while pesticides and compounds from manufacturing are detected in many foods. Foods with strong reputations for healthiness, such as salmon, may have sizable contaminant contents. The contaminant content of many foods varies by origin and season. Nearly all commercially raised salmon has higher contaminant levels than wild caught salmon. Opting out of the commercial food distribution system is an option, but the value depends on the habitat in which the food is obtained. Traditionally, the Akwesasne Mohawk Nation has depended on local fish and wildlife for their diet. Now pollution of local waterways has led to the contamination of many local foods, and levels of the contaminant polychlorinated biphenyls in the Akwesasne Mohawk people reflect current or past dietary patterns. Many other communities in nonurban settings are exposed to contaminants through long-trail distribution of contaminants in food, air, and/or water. Human biologists considering nutrition, disease, growth, reproduction, aging, to name a few areas, may consider the non-nutritional components of food as many have the ability to alter physiological functioning. Am. J. Hum. Biol., 2012. © 2012 Wiley Periodicals, Inc.</p></div>]]></content:encoded><description>Food has nutritional and non-nutritional components. The latter are not well-studied despite the fact that food adulteration has been common. Food adulteration may have reached its peak in cities of Western Europe and the US in the 18th and 19th centuries when foods were often purposely contaminated with additives to increase bulk, attractiveness, disguise spoilage, and increase profit. Effective regulation of food began in the late 19th and 20th centuries. Nevertheless, today food recalls for bacterial contamination are common, while pesticides and compounds from manufacturing are detected in many foods. Foods with strong reputations for healthiness, such as salmon, may have sizable contaminant contents. The contaminant content of many foods varies by origin and season. Nearly all commercially raised salmon has higher contaminant levels than wild caught salmon. Opting out of the commercial food distribution system is an option, but the value depends on the habitat in which the food is obtained. Traditionally, the Akwesasne Mohawk Nation has depended on local fish and wildlife for their diet. Now pollution of local waterways has led to the contamination of many local foods, and levels of the contaminant polychlorinated biphenyls in the Akwesasne Mohawk people reflect current or past dietary patterns. Many other communities in nonurban settings are exposed to contaminants through long-trail distribution of contaminants in food, air, and/or water. Human biologists considering nutrition, disease, growth, reproduction, aging, to name a few areas, may consider the non-nutritional components of food as many have the ability to alter physiological functioning. Am. J. Hum. Biol., 2012. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22200" xmlns="http://purl.org/rss/1.0/"><title>Household food insecurity and caregiver distress: Equal threats to child nutritional status?</title><link>http://dx.doi.org/10.1002%2Fajhb.22200</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Household food insecurity and caregiver distress: Equal threats to child nutritional status?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Craig Hadley</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Fasil Tessema</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ayalew T. Muluneh</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22200</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/">10.1002/ajhb.22200</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22200</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">149</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">157</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="section" id="abs1-1" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Objectives:</h3><div class="para"><p>There is considerable interest in the link between household food insecurity and child wellbeing, and the extent to which caregiver wellbeing mediates the relationship between food insecurity and child wellbeing. The aim of this was to assess these relationships among a rural population in Ethiopia.</p></div></div><div class="section" id="abs1-2" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Methods:</h3><div class="para"><p>We used existing survey data from a maximum of 1,006 children under 5 years of age with matched data on household-level data on food insecurity, caregiver distress, and asset ownership, along with other sociodemographic information. All respondents lived in a predominately rural, primarily subsistence-based area in southwest Ethiopia. Multivariable regression models were used to test hypothesized associations.</p></div></div><div class="section" id="abs1-3" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Results:</h3><div class="para"><p>Household food insecurity, distress, and socioeconomic status predicted children's weight for age and undernutrition, defined as weight for age Z (WAZ) less than −2SD from the reference median. A small portion of the household food insecurity effect was mediated by caregiver distress but these were largely independent effects. Maternal distress was associated with greater odds of a child having any illness, and any illness was associated with lower WAZ and higher odds of being undernourished. The effect of maternal distress on undernutrition was mediated by diarrhea.</p></div></div><div class="section" id="abs1-4" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Conclusions:</h3><div class="para"><p>This study suggests that household food insecurity, maternal distress, and household SES are independent contributors to children's undernutrition. Our results are consistent with others but are not generally consistent with the hypothesis that maternal distress is a primary pathway through which food insecurity impacts on child nutritional wellbeing. Am. J. Hum. Biol. 2012. © 2011 Wiley Periodicals, Inc.</p></div></div>]]></content:encoded><description>Objectives:There is considerable interest in the link between household food insecurity and child wellbeing, and the extent to which caregiver wellbeing mediates the relationship between food insecurity and child wellbeing. The aim of this was to assess these relationships among a rural population in Ethiopia.Methods:We used existing survey data from a maximum of 1,006 children under 5 years of age with matched data on household-level data on food insecurity, caregiver distress, and asset ownership, along with other sociodemographic information. All respondents lived in a predominately rural, primarily subsistence-based area in southwest Ethiopia. Multivariable regression models were used to test hypothesized associations.Results:Household food insecurity, distress, and socioeconomic status predicted children's weight for age and undernutrition, defined as weight for age Z (WAZ) less than −2SD from the reference median. A small portion of the household food insecurity effect was mediated by caregiver distress but these were largely independent effects. Maternal distress was associated with greater odds of a child having any illness, and any illness was associated with lower WAZ and higher odds of being undernourished. The effect of maternal distress on undernutrition was mediated by diarrhea.Conclusions:This study suggests that household food insecurity, maternal distress, and household SES are independent contributors to children's undernutrition. Our results are consistent with others but are not generally consistent with the hypothesis that maternal distress is a primary pathway through which food insecurity impacts on child nutritional wellbeing. Am. J. Hum. Biol. 2012. © 2011 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22212" xmlns="http://purl.org/rss/1.0/"><title>The relationship between breast size and anthropometric characteristics</title><link>http://dx.doi.org/10.1002%2Fajhb.22212</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The relationship between breast size and anthropometric characteristics</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Nicola Brown</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jennifer White</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Alexandra Milligan</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Debbie Risius</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Bessie Ayres</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Wendy Hedger</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Joanna Scurr</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22212</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/">10.1002/ajhb.22212</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22212</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">158</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">164</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="section" id="abs1-1" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Objectives:</h3><div class="para"><p>Current clinical selection criteria for mammaplasty use weight-related parameters, and weight loss is recommended as a nonsurgical intervention to reduce breast size. However, research has not firmly established if breast size is related to body size and composition. This study aims to investigate anthropometric characteristics in smaller and larger breasted women and identify predictors of breast mass.</p></div></div><div class="section" id="abs1-2" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Methods:</h3><div class="para"><p>A bra fitter determined underband and cup size of 93 A to H cup size women (mean ± standard deviation, age 25.7 ± 5.6 years, height 1.67 ± 0.6 cm, and mass 65.6 ± 11.0 kg). Estimations of breast mass (g) were made, and participants were categorized as smaller (&lt;500 g) or larger (&gt;500 g) breasted. Restricted anthropometric profiles determined body mass, height, body mass index (BMI), waist-to-hip ratio, sum of eight skinfolds, subscapular to triceps skinfold ratio, somatotype, percent body fat, fat and fat-free mass, and suprasternal notch to nipple distance.</p></div></div><div class="section" id="abs1-3" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Results:</h3><div class="para"><p>All variables (excluding height, subscapular to triceps skinfold ratio, and age) were significantly greater in larger breasted women. Body mass-related parameters and suprasternal notch to nipple distance were positively related to breast mass, with BMI and suprasternal notch to nipple distance accounting for half of the variance in breast mass.</p></div></div><div class="section" id="abs1-4" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Conclusion:</h3><div class="para"><p>Smaller and larger breasted women demonstrate differences in anthropometry, with body mass and BMI demonstrating strong relationships to breast mass. Measures of BMI and suprasternal notch to nipple distance enable predictions of breast mass and suggest that weight-related parameters are not appropriate exclusion criteria for mammaplasty. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</p></div></div>]]></content:encoded><description>Objectives:Current clinical selection criteria for mammaplasty use weight-related parameters, and weight loss is recommended as a nonsurgical intervention to reduce breast size. However, research has not firmly established if breast size is related to body size and composition. This study aims to investigate anthropometric characteristics in smaller and larger breasted women and identify predictors of breast mass.Methods:A bra fitter determined underband and cup size of 93 A to H cup size women (mean ± standard deviation, age 25.7 ± 5.6 years, height 1.67 ± 0.6 cm, and mass 65.6 ± 11.0 kg). Estimations of breast mass (g) were made, and participants were categorized as smaller (&lt;500 g) or larger (&gt;500 g) breasted. Restricted anthropometric profiles determined body mass, height, body mass index (BMI), waist-to-hip ratio, sum of eight skinfolds, subscapular to triceps skinfold ratio, somatotype, percent body fat, fat and fat-free mass, and suprasternal notch to nipple distance.Results:All variables (excluding height, subscapular to triceps skinfold ratio, and age) were significantly greater in larger breasted women. Body mass-related parameters and suprasternal notch to nipple distance were positively related to breast mass, with BMI and suprasternal notch to nipple distance accounting for half of the variance in breast mass.Conclusion:Smaller and larger breasted women demonstrate differences in anthropometry, with body mass and BMI demonstrating strong relationships to breast mass. Measures of BMI and suprasternal notch to nipple distance enable predictions of breast mass and suggest that weight-related parameters are not appropriate exclusion criteria for mammaplasty. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22214" xmlns="http://purl.org/rss/1.0/"><title>Sex ratios in the arctic—do man-made chemicals matter?</title><link>http://dx.doi.org/10.1002%2Fajhb.22214</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Sex ratios in the arctic—do man-made chemicals matter?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Peter Bjerregaard</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Susan Chatwood</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Bryany Denning</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Lawrence Joseph</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">T. Kue Young</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22214</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/">10.1002/ajhb.22214</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22214</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">165</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">169</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="section" id="abs1-1" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Objectives:</h3><div class="para"><p>The objective was to analyze the variation of secondary sex ratios across the Arctic and to estimate the time trend. The rationale for this was claims in news media that, in the Arctic, sex ratios have become reduced due to exposure to anthropogenic contaminants in the environment.</p></div></div><div class="section" id="abs1-2" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Methods:</h3><div class="para"><p>Data was collected from 27 circumpolar jurisdictions from public websites of the eight Arctic countries. Sex ratios at birth were calculated for each jurisdiction and each available year. Linear regression models of the sex ratios across time were fit within each jurisdiction to estimate the change in sex ratio over time.</p></div></div><div class="section" id="abs1-3" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Results:</h3><div class="para"><p>All male:female sex ratios were close to 1.05 with time trends close to 0. In a Bayesian hierarchical model overall sex ratio was estimated at 1.054 (95% confidence interval 1.048, 1.058). The estimate for the 10-year slope across all jurisdictions was 0.0010 (95% confidence interval −0.0021, 0.0046). Separate analyses of indigenous populations in Alaska and Greenland gave similar results and similar sex ratios were found among Greenland Inuit in 1900 and today.</p></div></div><div class="section" id="abs1-4" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Conclusions:</h3><div class="para"><p>The absence of deviation of the secondary sex ratio in any of the Arctic jurisdictions indicates that the contaminants that are present are not disrupting endocrine systems to the extent that sex ratios are being affected. Am. J. Hum. Biol., 2012. © 2012 Wiley Periodicals, Inc.</p></div></div>]]></content:encoded><description>Objectives:The objective was to analyze the variation of secondary sex ratios across the Arctic and to estimate the time trend. The rationale for this was claims in news media that, in the Arctic, sex ratios have become reduced due to exposure to anthropogenic contaminants in the environment.Methods:Data was collected from 27 circumpolar jurisdictions from public websites of the eight Arctic countries. Sex ratios at birth were calculated for each jurisdiction and each available year. Linear regression models of the sex ratios across time were fit within each jurisdiction to estimate the change in sex ratio over time.Results:All male:female sex ratios were close to 1.05 with time trends close to 0. In a Bayesian hierarchical model overall sex ratio was estimated at 1.054 (95% confidence interval 1.048, 1.058). The estimate for the 10-year slope across all jurisdictions was 0.0010 (95% confidence interval −0.0021, 0.0046). Separate analyses of indigenous populations in Alaska and Greenland gave similar results and similar sex ratios were found among Greenland Inuit in 1900 and today.Conclusions:The absence of deviation of the secondary sex ratio in any of the Arctic jurisdictions indicates that the contaminants that are present are not disrupting endocrine systems to the extent that sex ratios are being affected. Am. J. Hum. Biol., 2012. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22216" xmlns="http://purl.org/rss/1.0/"><title>Divergent body mass index trajectories between aboriginal and non-aboriginal canadians 1994–2009—an exploration of age, period, and cohort effects</title><link>http://dx.doi.org/10.1002%2Fajhb.22216</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Divergent body mass index trajectories between aboriginal and non-aboriginal canadians 1994–2009—an exploration of age, period, and cohort effects</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Carmina NG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Paul N. Corey</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">T. Kue Young</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22216</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/">10.1002/ajhb.22216</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22216</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">170</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">176</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="section" id="abs1-1" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Objectives:</h3><div class="para"><p>Aboriginal Canadians have a high burden of obesity and obesity-related chronic conditions. Body mass index (BMI) trajectories from 1994 to 2009 were estimated for Aboriginal and non-Aboriginal Canadians using self-reported height and weight data from the National Population Health Survey to explore age, period, and cohort effects of BMI change.</p></div></div><div class="section" id="abs1-2" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Methods:</h3><div class="para"><p>Linear growth curve models were estimated for 311 Aboriginal and 10,967 non-Aboriginal respondents divided into five birth cohorts born in the 1940s, 50s, 60s, 70s, and 80s.</p></div></div><div class="section" id="abs1-3" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Results:</h3><div class="para"><p>Overall, Aboriginal Canadians experienced higher rates of BMI increase over the 14-year period. Rate of BMI increase was specifically higher for Aboriginal adults born in the 1960s and 1970s when compared with non-Aboriginal adults. At ages 25, 35, and 45, recent-born cohorts had consistently higher BMIs compared with earlier-born cohorts with magnitudes of differences typically larger in the Aboriginal population. Recent-born cohorts also exhibited steeper BMI trajectories.</p></div></div><div class="section" id="abs1-4" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Conclusions:</h3><div class="para"><p>Cohort effects may be responsible for the divergent BMI trajectories between Aboriginal and non-Aboriginal Canadians born in the 1960s and 1970s. Aboriginal Canadians, particularly of more recent-born cohorts, experienced faster increases in BMI from 1994 to 2009 than non-Aboriginal Canadians, suggesting that prevalence of obesity will continue to rise in this population without intervention. Am. J. Hum. Biol., 2012. © 2012 Wiley Periodicals, Inc.</p></div></div>]]></content:encoded><description>Objectives:Aboriginal Canadians have a high burden of obesity and obesity-related chronic conditions. Body mass index (BMI) trajectories from 1994 to 2009 were estimated for Aboriginal and non-Aboriginal Canadians using self-reported height and weight data from the National Population Health Survey to explore age, period, and cohort effects of BMI change.Methods:Linear growth curve models were estimated for 311 Aboriginal and 10,967 non-Aboriginal respondents divided into five birth cohorts born in the 1940s, 50s, 60s, 70s, and 80s.Results:Overall, Aboriginal Canadians experienced higher rates of BMI increase over the 14-year period. Rate of BMI increase was specifically higher for Aboriginal adults born in the 1960s and 1970s when compared with non-Aboriginal adults. At ages 25, 35, and 45, recent-born cohorts had consistently higher BMIs compared with earlier-born cohorts with magnitudes of differences typically larger in the Aboriginal population. Recent-born cohorts also exhibited steeper BMI trajectories.Conclusions:Cohort effects may be responsible for the divergent BMI trajectories between Aboriginal and non-Aboriginal Canadians born in the 1960s and 1970s. Aboriginal Canadians, particularly of more recent-born cohorts, experienced faster increases in BMI from 1994 to 2009 than non-Aboriginal Canadians, suggesting that prevalence of obesity will continue to rise in this population without intervention. Am. J. Hum. Biol., 2012. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22217" xmlns="http://purl.org/rss/1.0/"><title>Effect of ADA1 mother–fetus and wife–husband phenotypic differences on the ratio birth weight/placental weight in fertile women and on reproductive success in couples with RSA</title><link>http://dx.doi.org/10.1002%2Fajhb.22217</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Effect of ADA1 mother–fetus and wife–husband phenotypic differences on the ratio birth weight/placental weight in fertile women and on reproductive success in couples with RSA</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Fulvia Gloria-Bottini</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Maria Nicotra</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ada Amante</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Sara Ambrosi</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Eliana Cozzoli</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Patrizia Saccucci</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Egidio Bottini</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Andrea Magrini</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22217</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/">10.1002/ajhb.22217</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22217</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">177</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">182</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="section" id="abs1-1" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Objectives:</h3><div class="para"><p>To study the effect Adenosine Deaminase locus 1 (ADA<sub>1</sub>) mother–fetus and wife–husband phenotypic differences on the ratio Birth Weight/Placental Weight (BW/PW) in fertile women and on reproductive success in couples with repeated spontaneous abortion (RSA).</p></div></div><div class="section" id="abs1-2" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Methods:</h3><div class="para"><p>209 couples with primary RSA and a consecutive series of 379 healthy puerperae with their newborn infants from the White Caucasian population of central Italy were studied. In primary RSA women reproductive success was indicated by the presence of at least one live-born infant within 5 years of follow up. Two way contingency tables were analyzed by chi-square.</p></div></div><div class="section" id="abs1-3" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Results:</h3><div class="para"><p>The proportion of primary RSA couples with at least a live-born infant shows the highest value in couples mother ADA<sub>1</sub>1/father carrier of ADA<sub>1</sub>*2 allele (55.2%) and the lowest value in reciprocal couples mother carrier of ADA<sub>1</sub>*2 allele /father ADA<sub>1</sub>1 (18.7 %) (O.R. = 5.33; <em>P</em> = 0.023). The highest ratio BW/PW is observed in the class mother ADA<sub>1</sub>1/newborn carrier of ADA<sub>1</sub>*2 allele while the lowest ratio is observed in the reciprocal class mother carrier of ADA<sub>1</sub>*2 allele/ newborn ADA<sub>1</sub>1.</p></div></div><div class="section" id="abs1-4" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Conclusions:</h3><div class="para"><p>Differences between mother and fetus in ADA<sub>1</sub> phenotype may influence the ratio BW/PW in healthy women and reproductive success in RSA women. Am. J. Hum. Biol., 2012. © 2012 Wiley Periodicals, Inc.</p></div></div>]]></content:encoded><description>Objectives:To study the effect Adenosine Deaminase locus 1 (ADA1) mother–fetus and wife–husband phenotypic differences on the ratio Birth Weight/Placental Weight (BW/PW) in fertile women and on reproductive success in couples with repeated spontaneous abortion (RSA).Methods:209 couples with primary RSA and a consecutive series of 379 healthy puerperae with their newborn infants from the White Caucasian population of central Italy were studied. In primary RSA women reproductive success was indicated by the presence of at least one live-born infant within 5 years of follow up. Two way contingency tables were analyzed by chi-square.Results:The proportion of primary RSA couples with at least a live-born infant shows the highest value in couples mother ADA11/father carrier of ADA1*2 allele (55.2%) and the lowest value in reciprocal couples mother carrier of ADA1*2 allele /father ADA11 (18.7 %) (O.R. = 5.33; P = 0.023). The highest ratio BW/PW is observed in the class mother ADA11/newborn carrier of ADA1*2 allele while the lowest ratio is observed in the reciprocal class mother carrier of ADA1*2 allele/ newborn ADA11.Conclusions:Differences between mother and fetus in ADA1 phenotype may influence the ratio BW/PW in healthy women and reproductive success in RSA women. Am. J. Hum. Biol., 2012. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22210" xmlns="http://purl.org/rss/1.0/"><title>Pubertal muscle mass and diabetes markers in chinese adolescents</title><link>http://dx.doi.org/10.1002%2Fajhb.22210</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Pubertal muscle mass and diabetes markers in chinese adolescents</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Shi Lin Lin</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">So Lun Lee</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Lai Ling Hui</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Shiu Lun Au Yeung</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Michael A. Tse</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Gabriel M. Leung</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">C. Mary. Schooling</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22210</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/">10.1002/ajhb.22210</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22210</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Short Report</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">183</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">185</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Objectives:</b> Diabetes is common in China despite a relatively nonobese population. We hypothesized that testosterone driven muscle mass acquisition at puberty may be relevant. We examined the associations of testosterone with muscle mass and of muscle mass with fasting glucose in Chinese adolescents.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Methods:</b> In 40 adolescents (20 boys and 20 girls, age 12.9 ± 0.1 years) from Hong Kong's “Children of 1997” birth cohort, we used multivariable linear regression to assess adjusted associations of testosterone and fasting glucose (from a morning blood sample) with muscle and fat mass from a dual-energy X-ray absorptiometry scan.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Results:</b> Testosterone was positively associated with muscle mass (0.05 kg, 95% confidence interval (CI) 0.01 to 0.09, per pg/ml testosterone). Muscle mass was associated with lower glucose (−0.04 mmol/l, 95% CI −0.08 to −0.01 per kg muscle mass) adjusted for sex and fat mass.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Conclusions:</b> Environmentally driven muscle mass acquisition at puberty could influence diabetes. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</p></div>]]></content:encoded><description>Objectives: Diabetes is common in China despite a relatively nonobese population. We hypothesized that testosterone driven muscle mass acquisition at puberty may be relevant. We examined the associations of testosterone with muscle mass and of muscle mass with fasting glucose in Chinese adolescents.Methods: In 40 adolescents (20 boys and 20 girls, age 12.9 ± 0.1 years) from Hong Kong's “Children of 1997” birth cohort, we used multivariable linear regression to assess adjusted associations of testosterone and fasting glucose (from a morning blood sample) with muscle and fat mass from a dual-energy X-ray absorptiometry scan.Results: Testosterone was positively associated with muscle mass (0.05 kg, 95% confidence interval (CI) 0.01 to 0.09, per pg/ml testosterone). Muscle mass was associated with lower glucose (−0.04 mmol/l, 95% CI −0.08 to −0.01 per kg muscle mass) adjusted for sex and fat mass.Conclusions: Environmentally driven muscle mass acquisition at puberty could influence diabetes. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22211" xmlns="http://purl.org/rss/1.0/"><title>Adenylate kinase genetic polymorphism and spontaneous abortion</title><link>http://dx.doi.org/10.1002%2Fajhb.22211</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Adenylate kinase genetic polymorphism and spontaneous abortion</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Fulvia Gloria-Bottini</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Maria Nicotra</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ada Amante</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Adalgisa Pietropolli</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Anna Neri</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Egidio Bottini</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Andrea Magrini</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22211</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/">10.1002/ajhb.22211</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22211</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Short Report</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">186</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">188</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="section" id="abs1-1" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Objective:</h3><div class="para"><p>Recent studies on healthy puerperae suggest that Adenylate kinase locus 1 (Ak<sub>1</sub>) genetic polymorphism could be involved in intrauterine selection. In this article, we have searched for a possible relationship between Ak<sub>1</sub> polymorphism and spontaneous abortion.</p></div></div><div class="section" id="abs1-2" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Methods:</h3><div class="para"><p>178 women with primary repeated spontaneous abortion (RSA), 487 healthy consecutive puerperae, 251 puerperae with diabetes, and 361 consecutive healthy female newborns from the White Caucasian population of Central Italy delivered at the Maternal Department have been studied.</p></div><div class="para"><p>In these subjects, Ak<sub>1</sub> phenotype was determined to study the relationship between this enzyme and spontaneous abortion.</p></div></div><div class="section" id="abs1-3" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Results:</h3><div class="para"><p>The proportion of Ak<sub>1</sub>2-1 phenotype is higher in women with history of two or more spontaneous abortion than in puerperae with a negative history of spontaneous abortion and in female newborns infants (O.R. 1.930; 95%C.I. 1.113–3.280). Moreover, RSA women carrying the Ak<sub>1</sub>2-1 phenotype have a reduced probability of having live-born infants.</p></div></div><div class="section" id="abs1-4" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Conclusions:</h3><div class="para"><p>Our findings suggest a reduced reproductive efficiency of women carrying the Ak<sub>1</sub>2-1 phenotype: this observation could have practical importance in predicting the probability of reproductive success in couples with RSA and in the practice of in vitro fertilization. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</p></div></div>]]></content:encoded><description>Objective:Recent studies on healthy puerperae suggest that Adenylate kinase locus 1 (Ak1) genetic polymorphism could be involved in intrauterine selection. In this article, we have searched for a possible relationship between Ak1 polymorphism and spontaneous abortion.Methods:178 women with primary repeated spontaneous abortion (RSA), 487 healthy consecutive puerperae, 251 puerperae with diabetes, and 361 consecutive healthy female newborns from the White Caucasian population of Central Italy delivered at the Maternal Department have been studied.In these subjects, Ak1 phenotype was determined to study the relationship between this enzyme and spontaneous abortion.Results:The proportion of Ak12-1 phenotype is higher in women with history of two or more spontaneous abortion than in puerperae with a negative history of spontaneous abortion and in female newborns infants (O.R. 1.930; 95%C.I. 1.113–3.280). Moreover, RSA women carrying the Ak12-1 phenotype have a reduced probability of having live-born infants.Conclusions:Our findings suggest a reduced reproductive efficiency of women carrying the Ak12-1 phenotype: this observation could have practical importance in predicting the probability of reproductive success in couples with RSA and in the practice of in vitro fertilization. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22213" xmlns="http://purl.org/rss/1.0/"><title>Inaccuracy of self-reported low sodium diet</title><link>http://dx.doi.org/10.1002%2Fajhb.22213</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Inaccuracy of self-reported low sodium diet</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Linda M. Gerber</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Samuel J. Mann</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22213</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/">10.1002/ajhb.22213</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22213</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Short Report</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">189</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">191</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="section" id="abs1-1" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Objectives:</h3><div class="para"><p>This study evaluates how often the self-report of a low sodium (Na) intake is reflected by a low 24-h urinary sodium excretion and examines the influence of incomplete urinary collections on this comparison.</p></div></div><div class="section" id="abs1-2" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Methods:</h3><div class="para"><p>In a study in which 24-h urine collections were obtained for measurement of Na and creatinine excretion, 120 participants were asked whether their Na intake was low, medium, or high. A 24-h urine collection was considered complete if creatinine excretion was ≥20 mg/kg in men or ≥15 mg/kg in women, and incomplete if below those amounts. The kappa statistic was computed to assess the level of agreement between 24-h Na excretion, dichotomized at 100 meq and self-report responses.</p></div></div><div class="section" id="abs1-3" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Results:</h3><div class="para"><p>Agreement between self-reported and actual Na excretion was poor. The kappa statistic was 0.18 for the total sample, 0.04 for complete collectors, and 0.51 for incomplete collectors, respectively. Overall, 24-h Na excretion exceeded 100 meq among 75% of those reporting an average or high Na intake, but it also exceeded 100 meq among 57% of those reporting a low sodium intake. Further, among those reporting a low sodium intake, Na excretion exceeded 100 meq in 80% of those who submitted a complete collection, but in only 29% of those who submitted an incomplete collection.</p></div></div><div class="section" id="abs1-4" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Conclusions:</h3><div class="para"><p>These findings suggest that many individuals who report a low salt diet actually excrete ≥100 meq/day. Na intake is also frequently underestimated because many 24-h urine collections are incomplete. Am. J. Hum. Biol., 2012. © 2012 Wiley Periodicals, Inc.</p></div></div>]]></content:encoded><description>Objectives:This study evaluates how often the self-report of a low sodium (Na) intake is reflected by a low 24-h urinary sodium excretion and examines the influence of incomplete urinary collections on this comparison.Methods:In a study in which 24-h urine collections were obtained for measurement of Na and creatinine excretion, 120 participants were asked whether their Na intake was low, medium, or high. A 24-h urine collection was considered complete if creatinine excretion was ≥20 mg/kg in men or ≥15 mg/kg in women, and incomplete if below those amounts. The kappa statistic was computed to assess the level of agreement between 24-h Na excretion, dichotomized at 100 meq and self-report responses.Results:Agreement between self-reported and actual Na excretion was poor. The kappa statistic was 0.18 for the total sample, 0.04 for complete collectors, and 0.51 for incomplete collectors, respectively. Overall, 24-h Na excretion exceeded 100 meq among 75% of those reporting an average or high Na intake, but it also exceeded 100 meq among 57% of those reporting a low sodium intake. Further, among those reporting a low sodium intake, Na excretion exceeded 100 meq in 80% of those who submitted a complete collection, but in only 29% of those who submitted an incomplete collection.Conclusions:These findings suggest that many individuals who report a low salt diet actually excrete ≥100 meq/day. Na intake is also frequently underestimated because many 24-h urine collections are incomplete. Am. J. Hum. Biol., 2012. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22215" xmlns="http://purl.org/rss/1.0/"><title>Sampling strategies in a linguistic isolate: Results from mtDNA analysis</title><link>http://dx.doi.org/10.1002%2Fajhb.22215</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Sampling strategies in a linguistic isolate: Results from mtDNA analysis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Carla Maria Calò</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Laura Corrias</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Giuseppe Vona</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Valeria Bachis</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Renato Robledo</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22215</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/">10.1002/ajhb.22215</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22215</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Short Report</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">192</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">194</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="section" id="abs1-1" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Objectives:</h3><div class="para"><p>Sampling strategies are crucial issues in population genetics and anthropological studies. The sampling choice is related to the research question and the type of markers used. In this research, we compared two different sampling strategies in the Sardinian linguistic isolate of Carloforte (Italy).</p></div></div><div class="section" id="abs1-2" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Methods:</h3><div class="para"><p>A first sampling (<em>N</em> = 49) was carried out through grandparents criterion: individuals selected for the study were born and resident in Carloforte, and unrelated for at least three generations. A second sampling (<em>N</em> = 50) was based on founders surnames (FS): selected participants were proved to be descendants of the village founders, and to have no ancestors in common, at least up to the grandparental generation.</p></div></div><div class="section" id="abs1-3" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Results:</h3><div class="para"><p>The group selected through FS showed a greater gene diversity, which was confirmed by both network and haplogroup analysis. Among the shared haplogroups, we find clear differences in their frequencies. Sampling through grandparents criterion showed essentially the same haplogroups found in Sardinia, and with similar frequencies. Interesting results came from genetic tree. The FS sampling clustered with Northern African populations and it is located very far from Italian and Sardinian populations, whereas the grandparents criterion sampling clustered with Italian populations and it is located close to the other Sardinian populations.</p></div></div><div class="section" id="abs1-4" xmlns="http://www.w3.org/1999/xhtml"><h3 xhtml="http://www.w3.org/1999/xhtml" xmlns="http://purl.org/rss/1.0/">Conclusions:</h3><div class="para"><p>Results showed that different sampling strategies can lead to contrasting results. As sampling through grandparents criterion is influenced by recent gene flow, we hypothesize that the difference observed with the two sampling strategies is due to the merging of Carloforte with Sardinian populations. Am. J. Hum. Biol., 2012. © 2012 Wiley Periodicals, Inc.</p></div></div>]]></content:encoded><description>Objectives:Sampling strategies are crucial issues in population genetics and anthropological studies. The sampling choice is related to the research question and the type of markers used. In this research, we compared two different sampling strategies in the Sardinian linguistic isolate of Carloforte (Italy).Methods:A first sampling (N = 49) was carried out through grandparents criterion: individuals selected for the study were born and resident in Carloforte, and unrelated for at least three generations. A second sampling (N = 50) was based on founders surnames (FS): selected participants were proved to be descendants of the village founders, and to have no ancestors in common, at least up to the grandparental generation.Results:The group selected through FS showed a greater gene diversity, which was confirmed by both network and haplogroup analysis. Among the shared haplogroups, we find clear differences in their frequencies. Sampling through grandparents criterion showed essentially the same haplogroups found in Sardinia, and with similar frequencies. Interesting results came from genetic tree. The FS sampling clustered with Northern African populations and it is located very far from Italian and Sardinian populations, whereas the grandparents criterion sampling clustered with Italian populations and it is located close to the other Sardinian populations.Conclusions:Results showed that different sampling strategies can lead to contrasting results. As sampling through grandparents criterion is influenced by recent gene flow, we hypothesize that the difference observed with the two sampling strategies is due to the merging of Carloforte with Sardinian populations. Am. J. Hum. Biol., 2012. © 2012 Wiley Periodicals, Inc.</description></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22225" xmlns="http://purl.org/rss/1.0/"><title>Book review: Disease maps: Epidemics on the ground</title><link>http://dx.doi.org/10.1002%2Fajhb.22225</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Book review: Disease maps: Epidemics on the ground</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Lisa Sattenspiel</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22225</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/">10.1002/ajhb.22225</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22225</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Book Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">195</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">195</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22226" xmlns="http://purl.org/rss/1.0/"><title>Book review: Work Meets Life: Exploring the Integrative Study of Work in Living Systems</title><link>http://dx.doi.org/10.1002%2Fajhb.22226</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Book review: Work Meets Life: Exploring the Integrative Study of Work in Living Systems</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Katharine N. Farrell</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22226</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/">10.1002/ajhb.22226</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22226</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Book Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">196</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">197</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22227" xmlns="http://purl.org/rss/1.0/"><title>Book review: Plasticity, Robustness, Development and Evolution</title><link>http://dx.doi.org/10.1002%2Fajhb.22227</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Book review: Plasticity, Robustness, Development and Evolution</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Matthew Mcintyre</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22227</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/">10.1002/ajhb.22227</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22227</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Book Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">197</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">198</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22228" xmlns="http://purl.org/rss/1.0/"><title>Book review: The Evolution of Anisogamy: A Fundamental Phenomenon Underlying Sexual Selection</title><link>http://dx.doi.org/10.1002%2Fajhb.22228</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Book review: The Evolution of Anisogamy: A Fundamental Phenomenon Underlying Sexual Selection</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Lawrence Ian Reed</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22228</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/">10.1002/ajhb.22228</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22228</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Book Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">198</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">199</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22229" xmlns="http://purl.org/rss/1.0/"><title>Book review: The Major Transitions in Evolution Revisited</title><link>http://dx.doi.org/10.1002%2Fajhb.22229</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Book review: The Major Transitions in Evolution Revisited</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jeffrey S. Levinton</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22229</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/">10.1002/ajhb.22229</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22229</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Book Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">199</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">200</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22230" xmlns="http://purl.org/rss/1.0/"><title>37th Annual Meeting: Human Biology Association</title><link>http://dx.doi.org/10.1002%2Fajhb.22230</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">37th Annual Meeting: Human Biology Association</dc:title><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22230</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/">10.1002/ajhb.22230</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22230</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Meeting</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">201</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">252</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://dx.doi.org/10.1002%2Fajhb.22242" xmlns="http://purl.org/rss/1.0/"><title>Human biology association archives at the smithsonian institution national anthropological archives</title><link>http://dx.doi.org/10.1002%2Fajhb.22242</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Human biology association archives at the smithsonian institution national anthropological archives</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Michael A. Little</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Gary D. James</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ralph M. Garruto</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/ajhb.22242</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/">10.1002/ajhb.22242</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1002%2Fajhb.22242</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Archives</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">253</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">256</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item></rdf:RDF>
