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<title>American Journal of Clinical Nutrition current issue</title>
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<prism:eIssn>1938-3207</prism:eIssn>
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<title>American Journal of Clinical Nutrition</title>
<url>http://www.ajcn.org/icons/banner/title.gif</url>
<link>http://www.ajcn.org</link>
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<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/1?rss=1">
<title><![CDATA[[Perspective] Food sources of nitrates and nitrites: the physiologic context for potential health benefits]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/1?rss=1</link>
<description><![CDATA[
<p>The presence of nitrates and nitrites in food is associated with an increased risk of gastrointestinal cancer and, in infants, methemoglobinemia. Despite the physiologic roles for nitrate and nitrite in vascular and immune function, consideration of food sources of nitrates and nitrites as healthful dietary components has received little attention. Approximately 80% of dietary nitrates are derived from vegetable consumption; sources of nitrites include vegetables, fruit, and processed meats. Nitrites are produced endogenously through the oxidation of nitric oxide and through a reduction of nitrate by commensal bacteria in the mouth and gastrointestinal tract. As such, the dietary provision of nitrates and nitrites from vegetables and fruit may contribute to the blood pressure&ndash;lowering effects of the Dietary Approaches to Stop Hypertension (DASH) diet. We quantified nitrate and nitrite concentrations by HPLC in a convenience sample of foods. Incorporating these values into 2 hypothetical dietary patterns that emphasize high-nitrate or low-nitrate vegetable and fruit choices based on the DASH diet, we found that nitrate concentrations in these 2 patterns vary from 174 to 1222 mg. The hypothetical high-nitrate DASH diet pattern exceeds the World Health Organization's Acceptable Daily Intake for nitrate by 550% for a 60-kg adult. These data call into question the rationale for recommendations to limit nitrate and nitrite consumption from plant foods; a comprehensive reevaluation of the health effects of food sources of nitrates and nitrites is appropriate. The strength of the evidence linking the consumption of nitrate- and nitrite-containing plant foods to beneficial health effects supports the consideration of these compounds as nutrients.</p>
]]></description>
<dc:creator><![CDATA[Hord, N. G, Tang, Y., Bryan, N. S]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2008.27131</dc:identifier>
<dc:title><![CDATA[[Perspective] Food sources of nitrates and nitrites: the physiologic context for potential health benefits]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>10</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>1</prism:startingPage>
<prism:section>Perspective</prism:section>
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<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/11?rss=1">
<title><![CDATA[[Editorials] Nitrate in foods: harmful or healthy?]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/11?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Katan, M. B]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.28014</dc:identifier>
<dc:title><![CDATA[[Editorials] Nitrate in foods: harmful or healthy?]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>12</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>11</prism:startingPage>
<prism:section>Editorials</prism:section>
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<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/13?rss=1">
<title><![CDATA[[Editorials] Adherence to dietary guidelines: benefits on atherosclerosis progression]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/13?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kris-Etherton, P. M]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.28074</dc:identifier>
<dc:title><![CDATA[[Editorials] Adherence to dietary guidelines: benefits on atherosclerosis progression]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>14</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>13</prism:startingPage>
<prism:section>Editorials</prism:section>
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<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/15?rss=1">
<title><![CDATA[[Obesity and eating disorders] Vitamin status after bariatric surgery: a randomized study of gastric bypass and duodenal switch]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/15?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Bariatric surgery is widely performed to induce weight loss.</p>
<p><b>Objective:</b> The objective was to examine changes in vitamin status after 2 bariatric surgical techniques.</p>
<p><b>Design:</b> A randomized controlled trial was conducted in 2 Scandinavian hospitals. The subjects were 60 superobese patients [body mass index (BMI; in kg/m<sup>2</sup>): 50&ndash;60]. The surgical interventions were either laparoscopic Roux-en-Y gastric bypass or laparoscopic biliopancreatic diversion with duodenal switch. All patients received multivitamins, iron, calcium, and vitamin D supplements. Gastric bypass patients also received a vitamin B-12 substitute. The patients were examined before surgery and 6 wk, 6 mo, and 1 y after surgery.</p>
<p><b>Results:</b> Of 60 surgically treated patients, 59 completed the follow-up. After surgery, duodenal switch patients had lower mean vitamin A and 25-hydroxyvitamin D concentrations and a steeper decline in thiamine concentrations than did the gastric bypass patients. Other vitamins (riboflavin, vitamin B-6, vitamin C, and vitamin E adjusted for serum lipids) did not change differently in the surgical groups, and concentrations were either stable or increased. Furthermore, duodenal switch patients had lower hemoglobin and total cholesterol concentrations and a lower BMI (mean reduction: 41% compared with 30%) than did gastric bypass patients 1 y after surgery. Additional dietary supplement use was more frequent among duodenal switch patients (55%) than among gastric bypass patients (26%).</p>
<p><b>Conclusions:</b> Compared with gastric bypass, duodenal switch may be associated with a greater risk of vitamin A and D deficiencies in the first year after surgery and of thiamine deficiency in the initial months after surgery. Patients who undergo these 2 surgical interventions may require different monitoring and supplementation regimens in the first year after surgery. This trial was registered at clinicaltrials.gov as NCT00327912.</p>
]]></description>
<dc:creator><![CDATA[Aasheim, E. T, Bjorkman, S., Sovik, T. T, Engstrom, M., Hanvold, S. E, Mala, T., Olbers, T., Bohmer, T.]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27583</dc:identifier>
<dc:title><![CDATA[[Obesity and eating disorders] Vitamin status after bariatric surgery: a randomized study of gastric bypass and duodenal switch]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>22</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>15</prism:startingPage>
<prism:section>Obesity and eating disorders</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/23?rss=1">
<title><![CDATA[[Obesity and eating disorders] Long-term effects of a very-low-carbohydrate weight loss diet compared with an isocaloric low-fat diet after 12 mo]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/23?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Long-term weight loss and cardiometabolic effects of a very-low-carbohydrate, high-saturated-fat diet (LC) and a high-carbohydrate, low-fat diet (LF) have not been evaluated under isocaloric conditions.</p>
<p><b>Objective:</b> The objective was to compare an energy-controlled LC diet with an LF diet at 1 y.</p>
<p><b>Design:</b> Men and women (<I>n</I> = 118) with abdominal obesity and at least one additional metabolic syndrome risk factor were randomly assigned to either an energy-restricted (6&ndash;7 MJ) LC diet (4%, 35%, and 61% of energy as carbohydrate, protein, and fat, respectively) or an isocaloric LF diet (46%, 24%, and 30% of energy as carbohydrate, protein, and fat, respectively) for 1 y. Weight, body composition, and cardiometabolic risk markers were assessed.</p>
<p><b>Results:</b> Sixty-nine participants (59%) completed the trial: 33 in the LC group and 36 in the LF group. Both groups lost similar amounts of weight (LC: &ndash;14.5 &plusmn; 1.7 kg; LF: &ndash;11.5 &plusmn; 1.2 kg; <I>P</I> = 0.14, time <FONT FACE="arial,helvetica">x</FONT> diet) and body fat (LC: &ndash;11.3 &plusmn; 1.5 kg; LF: &ndash;9.4 &plusmn; 1.2 kg; <I>P</I> = 0.30). Blood pressure, fasting glucose, insulin, insulin resistance, and C-reactive protein decreased independently of diet composition. Compared with the LF group, the LC group had greater decreases in triglycerides (&ndash;0.36 &plusmn; 0.15 mmol/L; 95% CI: &ndash;0.67, &ndash;0.05 mmol/L; <I>P</I> = 0.011), increases in HDL cholesterol (0.23 &plusmn; 0.09 mmol/L; 95% CI: 0.06, 0.40 mmol/L; <I>P</I> = 0.018) and LDL cholesterol (0.6 &plusmn; 0.2 mmol/L; 95% CI: 0.2, 1.0 mmol/L; <I>P</I> = 0.001), and a greater but nonsignificant increase in apolipoprotein B (0.08 &plusmn; 0.04 g/L; 95% CI: &ndash;0.004, 0.171 g/L; <I>P</I> = 0.17).</p>
<p><b>Conclusions:</b> Under planned isoenergetic conditions, as expected, both dietary patterns resulted in similar weight loss and changes in body composition. The LC diet may offer clinical benefits to obese persons with insulin resistance. However, the increase in LDL cholesterol with the LC diet suggests that this measure should be monitored. This trial was registered with the Australian New Zealand Clinical Trials Registry at <inter-ref locator="http://www.anzctr.org.au" locator-type="url">http://www.anzctr.org.au</inter-ref> as ACTR 12606000203550.</p>
]]></description>
<dc:creator><![CDATA[Brinkworth, G. D, Noakes, M., Buckley, J. D, Keogh, J. B, Clifton, P. M]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2008.27326</dc:identifier>
<dc:title><![CDATA[[Obesity and eating disorders] Long-term effects of a very-low-carbohydrate weight loss diet compared with an isocaloric low-fat diet after 12 mo]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>32</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>23</prism:startingPage>
<prism:section>Obesity and eating disorders</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/33?rss=1">
<title><![CDATA[[Obesity and eating disorders] Dieting, restraint, and disinhibition predict women's weight change over 6 y]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/33?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Although disinhibited eating is positively associated with higher weight in women, it is not known whether restrained eating and dieting moderate the influence of disinhibited eating on weight change.</p>
<p><b>Objective:</b> The objective was to investigate over 6 y the interactive effects of restrained and disinhibited eating and self-reported dieting to lose weight as predictors of weight gain in women.</p>
<p><b>Design:</b> Data were collected from non-Hispanic white women (<I>n</I> = 163) every 2 y. Height and weight were measured in triplicate. Dietary restraint and disinhibition were assessed by using the Eating Inventory. Participants were also asked if they were "currently dieting to lose weight." Multilevel modeling was used to examine change in weight as a function of time-invariant and time-varying predictors, including dietary restraint, dietary disinhibition, and self-reported dieting.</p>
<p><b>Results:</b> After covariates were adjusted for, growth curve models showed that within-person increases in restraint over time were associated with concurrent decreases in weight and that higher levels of restraint moderated the positive association between dietary disinhibition and weight. Women who reported dieting at study entry were heavier at study entry and gained more weight over time than did nondieters. Finally, a significant interaction between restraint, disinhibition, and dieting showed that restraint moderated the effect of disinhibition on weight differently in nondieters than in dieters.</p>
<p><b>Conclusions:</b> Increasing levels of dietary restraint may be beneficial in moderating weight by attenuating the positive association between disinhibition and weight in dieting women. An understanding of weight and weight change requires examination of the interactive effects of restraint, disinhibition, and dieting.</p>
]]></description>
<dc:creator><![CDATA[Savage, J. S, Hoffman, L., Birch, L. L]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2008.26558</dc:identifier>
<dc:title><![CDATA[[Obesity and eating disorders] Dieting, restraint, and disinhibition predict women's weight change over 6 y]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>40</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>33</prism:startingPage>
<prism:section>Obesity and eating disorders</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/41?rss=1">
<title><![CDATA[[Lipids] Differential effects of protein quality on postprandial lipemia in response to a fat-rich meal in type 2 diabetes: comparison of whey, casein, gluten, and cod protein]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/41?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Enhanced and prolonged postprandial triglyceride responses involve increased cardiovascular disease risk in type 2 diabetes. Dietary fat and carbohydrates profoundly influence postprandial hypertriglyceridemia, whereas little information exists on the effect of proteins.</p>
<p><b>Objective:</b> The objective was to compare the effects of the proteins casein, whey, cod, and gluten on postprandial lipid and incretin responses to a high-fat meal in persons with type 2 diabetes.</p>
<p><b>Design:</b> A crossover study was conducted in 12 patients with type 2 diabetes. Blood samples were collected over 8 h after ingestion of a test meal containing 100 g butter and 45 g carbohydrate in combination with 45 g casein (Cas-meal), whey (Whe-meal), cod (Cod-meal), or gluten (Glu-meal). We measured plasma concentrations of triglycerides, retinyl palmitate (RP), free fatty acids, insulin, glucose, glucagon, glucagon-like peptide 1, and glucose-dependent insulinotropic peptide.</p>
<p><b>Results:</b> The incremental area under the curve for triglyceride was significantly lower after the Whe-meal than after the other meals. The RP response was lower after the Whe-meal than after the Cas-meal and Cod-meal in the chylomicron-rich fraction and higher after the Whe-meal than after Cod- and Glu-meals in the chylomicron-poor fraction. Free fatty acids were most pronouncedly suppressed after the Whe-meal. The glucose response was lower after the Whe-meal than after the other meals, whereas no significant differences were found in insulin, glucagon, glucagon-like peptide 1, and glucose-dependent insulinotropic peptide responses.</p>
<p><b>Conclusion:</b> The data suggest that as a supplement to a fat-rich meal in patients with type 2 diabetes, whey protein seems to outperform other proteins in terms of postprandial lipemia improvement, possibly because of the formation of fewer chylomicrons or increased clearance of chylomicrons. The trial was registered at clinicaltrials.gov as NCT00817973.</p>
]]></description>
<dc:creator><![CDATA[Mortensen, L. S, Hartvigsen, M. L, Brader, L. J, Astrup, A., Schrezenmeir, J., Holst, J. J, Thomsen, C., Hermansen, K.]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2008.27281</dc:identifier>
<dc:title><![CDATA[[Lipids] Differential effects of protein quality on postprandial lipemia in response to a fat-rich meal in type 2 diabetes: comparison of whey, casein, gluten, and cod protein]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>48</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>41</prism:startingPage>
<prism:section>Lipids</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/49?rss=1">
<title><![CDATA[[Lipids] Association of serum n-6 and n-3 polyunsaturated fatty acids with lipids in 3 populations of middle-aged men]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/49?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> The association of serum polyunsaturated fatty acids (PUFAs) with lipids in different populations is not known.</p>
<p><b>Objective:</b> Our aim was to examine the association of serum n&ndash;6 (omega-6) or n&ndash;3 (omega-3) PUFAs with triglycerides or HDL-cholesterol concentrations in 261 white, 285 Japanese, and 212 Japanese American men aged 40&ndash;49 y.</p>
<p><b>Design:</b> We used a population-based cross-sectional study. Of the original sample (<I>n</I> = 926), those taking lipid-lowering medications or who had diabetes (<I>n</I> = 168) were excluded. Serum fatty acids were analyzed by capillary gas-liquid chromatography. Multiple regression models as a function of tertile groups of each PUFA were used.</p>
<p><b>Results:</b> Serum n&ndash;6 PUFAs were significantly inversely associated with triglycerides across populations after adjustment for age, body mass index, pack-years of smoking, and ethanol consumption [<I>&beta;</I> = &ndash;0.39 (<I>P</I> &lt; 0.001), &ndash;0.38 (<I>P</I> &lt; 0.001), and &ndash;0.33 (<I>P</I> &lt; 0.001) in whites, Japanese, and Japanese Americans, respectively]. Marine n&ndash;3 PUFAs were significantly inversely associated with triglycerides across populations [<I>&beta;</I> = &ndash;0.15 (<I>P</I> &lt; 0.001), &ndash;0.22 (<I>P</I> &lt; 0.001), and &ndash;0.13 (<I>P</I> &lt; 0.001) in whites, Japanese, and Japanese Americans, respectively]. n&ndash;6 PUFAs were significantly positively associated with HDL cholesterol in whites (<I>&beta;</I> = 4.49, <I>P</I> &lt; 0.001) and Japanese (<I>&beta;</I> = 3.73, <I>P</I> &lt; 0.01). Marine n&ndash;3 PUFAs were significantly positively associated with HDL cholesterol in Japanese (<I>&beta;</I> = 2.15, <I>P</I> &lt; 0.05), and eicosapentaenoic acid was significantly positively associated with HDL cholesterol in whites (<I>&beta;</I> = 2.68, <I>P</I> &lt; 0.01).</p>
<p><b>Conclusion:</b> Serum n&ndash;6 and n&ndash;3 PUFAs are inversely associated with triglycerides across populations.</p>
]]></description>
<dc:creator><![CDATA[Motoyama, K. R, Curb, J D., Kadowaki, T., El-Saed, A., Abbott, R. D, Okamura, T., Evans, R. W, Nakamura, Y., Sutton-Tyrrell, K., Rodriquez, B. L, Kadota, A., Edmundowicz, D., Willcox, B. J, Choo, J., Katsumi, N., Otake, T., Kadowaki, S., Kuller, L. H, Ueshima, H., Sekikawa, A.]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2008.26761</dc:identifier>
<dc:title><![CDATA[[Lipids] Association of serum n-6 and n-3 polyunsaturated fatty acids with lipids in 3 populations of middle-aged men]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>55</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>49</prism:startingPage>
<prism:section>Lipids</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/56?rss=1">
<title><![CDATA[[Cardiovascular disease risk] Effects of walnut consumption on blood lipids and other cardiovascular risk factors: a meta-analysis and systematic review]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/56?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Consumption of nuts has been associated with a decreased risk of cardiovascular disease events and death. Walnuts in particular have a unique profile: they are rich in polyunsaturated fatty acids, which may improve blood lipids and other cardiovascular disease risk factors.</p>
<p><b>Objectives:</b> We aimed to conduct a literature review and a meta-analysis to combine the results from several trials and to estimate the effect of walnuts on blood lipids.</p>
<p><b>Design:</b> Literature databases were searched for published trials that compared a specifically walnut-enhanced diet with a control diet. We conducted a random-effects meta-analysis of weighted mean differences (WMDs) of lipid outcomes.</p>
<p><b>Results:</b> Thirteen studies representing 365 participants were included in the analysis. Diets lasted 4&ndash;24 wk with walnuts providing 10&ndash;24% of total calories. When compared with control diets, diets supplemented with walnuts resulted in a significantly greater decrease in total cholesterol and in LDL-cholesterol concentrations (total cholesterol: WMD = &ndash;10.3 mg/dL, <I>P</I> &lt; 0.001; LDL cholesterol: WMD = &ndash;9.2 mg/dL, <I>P</I> &lt; 0.001). HDL cholesterol and triglycerides were not significantly affected by walnut diets more than with control diets (HDL cholesterol: WMD = &ndash;0.2, <I>P</I> = 0.8; triglycerides: WMD = &ndash;3.9, <I>P</I> = 0.3). Other results reported in the trials indicated that walnuts provided significant benefits for certain antioxidant capacity and inflammatory markers and had no adverse effects on body weight [body mass index (kg/m<sup>2</sup>): WMD = &ndash;0.4, <I>P</I> = 0.5; weight (kg): WMD = &ndash;0.05, <I>P</I> = 0.97].</p>
<p><b>Conclusions:</b> Overall, high-walnut-enriched diets significantly decreased total and LDL cholesterol for the duration of the short-term trials. Larger and longer-term trials are needed to address the effects of walnut consumption on cardiovascular risk and body weight.</p>
]]></description>
<dc:creator><![CDATA[Banel, D. K, Hu, F. B]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27457</dc:identifier>
<dc:title><![CDATA[[Cardiovascular disease risk] Effects of walnut consumption on blood lipids and other cardiovascular risk factors: a meta-analysis and systematic review]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>63</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>56</prism:startingPage>
<prism:section>Cardiovascular disease risk</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/64?rss=1">
<title><![CDATA[[Nutritional status, dietary intake, and body composition] Adiposity and insulin resistance in nondiabetic hemodialysis patients: effects of high energy supplementation]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/64?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> In contrast to the general population, a higher body mass index is associated with better survival among hemodialysis patients. Theoretically, high energy supplementation in these patients ought to lead to weight gain over time, but the benefits of this strategy are unclear.</p>
<p><b>Objective:</b> The objective was to assess whether high energy supplementation in nondiabetic hemodialysis patients might adversely affect insulin resistance&mdash;a known risk factor for cardiovascular disease.</p>
<p><b>Design:</b> We first investigated the association between body fat mass and insulin resistance (homeostasis model assessment of insulin resistance; HOMA-IR) in nondiabetic hemodialysis patients in a cross-sectional analysis (study 1). Of the 106 individuals studied, 55 were randomly assigned to either high energy supplementation (an extra 475 kcal/d; <I>n</I> = 28) or not (<I>n</I> = 27) for 12 wk to assess prospective changes in body fat mass and insulin resistance (study 2).</p>
<p><b>Results:</b> In study 1, body fat mass (<I>P</I> &lt; 0.05) and C-reactive protein (CRP) (<I>P</I> &lt; 0.05) each contributed independently to HOMA-IR. In study 2, 41 patients completed the study. The 20 patients who received high energy supplementation had a significantly greater increase in body fat mass (<I>P</I> &lt; 0.05), CRP (<I>P</I> &lt; 0.05), and HOMA-IR (<I>P</I> &lt; 0.001) than did the 21 controls.</p>
<p><b>Conclusions:</b> Body fat mass and CRP are primary determinants of insulin resistance in nondiabetic hemodialysis patients. High energy supplementation, because it increases adiposity and inflammation, exacerbates insulin resistance. A long-term study is needed to clarify the metabolic effects of high energy supplementation on cardiovascular disease outcomes in hemodialysis patients.</p>
]]></description>
<dc:creator><![CDATA[Hung, S.-C., Tarng, D.-C.]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27438</dc:identifier>
<dc:title><![CDATA[[Nutritional status, dietary intake, and body composition] Adiposity and insulin resistance in nondiabetic hemodialysis patients: effects of high energy supplementation]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>69</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>64</prism:startingPage>
<prism:section>Nutritional status, dietary intake, and body composition</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/70?rss=1">
<title><![CDATA[[Nutritional status, dietary intake, and body composition] Skim milk compared with a fruit drink acutely reduces appetite and energy intake in overweight men and women]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/70?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Several studies show that proteins, including whey and casein, are more satiating than carbohydrates. It follows that skim milk would be more satiating than sugar-rich beverages. However, this has yet to be shown.</p>
<p><b>Objective:</b> The objective was to investigate the effects of drinking skim milk in comparison with a fruit drink at breakfast on self-reported postmeal satiety and energy intake at lunch.</p>
<p><b>Design:</b> In a randomized crossover trial, 34 overweight women (<I>n</I> = 21) and men (<I>n</I> = 13) attended 2 sessions 1 wk apart. At each session, participants consumed a fixed-energy breakfast together with either 600 mL skim milk (25 g protein, 36 g lactose, &lt;1 g fat; 1062 kJ) or 600 mL fruit drink (&lt;1 g protein, 63 g sugar, &lt;1 g fat; 1062 kJ). Participants provided satiety ratings throughout the morning. Four hours after breakfast they consumed an ad libitum lunch, and energy intake was assessed.</p>
<p><b>Results:</b> Participants consumed significantly less energy at lunch after consuming skim milk (mean: 2432 kJ; 95% CI: 2160, 2704 kJ) than after consuming the fruit drink (mean: 2658 kJ; 95% CI: 2386, 2930 kJ), with a mean difference of 8.5% (<I>P</I> &lt; 0.05). In addition, self-reports of satiety were higher throughout the morning after consumption of skim milk than after consumption of the fruit drink (<I>P</I> &lt; 0.05) with the differences becoming larger over the 4 h (<I>P</I> &lt; 0.05).</p>
<p><b>Conclusion:</b> Consumption of skim milk, in comparison with a fruit drink, leads to increased perceptions of satiety and to decreased energy intake at a subsequent meal. This trial was registered with the Australian New Zealand Clinical Trials Registry at www.anzctr.org.au as ACTRN12608000510347.</p>
]]></description>
<dc:creator><![CDATA[Dove, E. R, Hodgson, J. M, Puddey, I. B, Beilin, L. J, Lee, Y. P, Mori, T. A]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2008.27411</dc:identifier>
<dc:title><![CDATA[[Nutritional status, dietary intake, and body composition] Skim milk compared with a fruit drink acutely reduces appetite and energy intake in overweight men and women]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>75</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>70</prism:startingPage>
<prism:section>Nutritional status, dietary intake, and body composition</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/76?rss=1">
<title><![CDATA[[Nutritional status, dietary intake, and body composition] Iron status of breastfed infants is improved equally by medicinal iron and iron-fortified cereal]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/76?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Although uncommon, iron deficiency (ID) occurs in breastfed infants. The regular provision of iron may prevent ID.</p>
<p><b>Objective:</b> The objective was to test the feasibility and effectiveness of 2 modalities of providing iron (medicinal iron or iron-fortified cereal) to breastfed infants. The study tested the hypothesis that regular provision of iron improves iron status of breastfed infants without adverse effects.</p>
<p><b>Design:</b> In this prospective, randomized, open-label trial, breastfed infants received on a regular basis either medicinal iron (<I>n</I> = 48) or an iron-fortified fruit-cereal combination (<I>n</I> = 45) from 4 to 9 mo or no intervention (control group; <I>n</I> = 59). The interventions provided 7.0&ndash;7.5 mg ferrous sulfate/d. Infants were enrolled at 1 mo and were followed to 2 y. Iron-status indicators were determined periodically, stool characteristics were recorded, and growth was monitored.</p>
<p><b>Results:</b> The regular provision of iron led to improved iron status during and for some months after the intervention. Both sources of iron were about equally effective. Iron affected stool color but had no effect on feeding-related behavior. However, medicinal iron was associated with a small but significant reduction in length gain and a trend toward reduced weight gain. ID anemia was observed in 4 infants (2.3%), most of whom had a low birth iron endowment. Mild ID was common in the second year of life.</p>
<p><b>Conclusions:</b> Regular provision of medicinal iron or iron-fortified cereal improves the iron status of breastfed infants and may prevent ID. Both modalities are equally effective, but medicinal iron leads to somewhat reduced growth. This trial was registered at <inter-ref locator="clinicaltrials.gov" locator-type="url">clinicaltrials.gov</inter-ref> as NCT00760890.</p>
]]></description>
<dc:creator><![CDATA[Ziegler, E. E, Nelson, S. E, Jeter, J. M]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2008.27350</dc:identifier>
<dc:title><![CDATA[[Nutritional status, dietary intake, and body composition] Iron status of breastfed infants is improved equally by medicinal iron and iron-fortified cereal]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>87</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>76</prism:startingPage>
<prism:section>Nutritional status, dietary intake, and body composition</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/88?rss=1">
<title><![CDATA[[Carbohydrate metabolism and diabetes] Dairy and industrial sources of trans fat do not impair peripheral insulin sensitivity in overweight women]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/88?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> The 2 major dietary sources of <I>trans</I> fatty acids (TFAs) are partially hydrogenated oils and ruminant-derived products. Epidemiologic data suggest that chronic consumption of industrial sources of TFAs could be damaging to insulin sensitivity, but intervention studies on this issue have remained inconclusive.</p>
<p><b>Objective:</b> The trial was designed to compare the effects of dairy compared with industrial sources of TFAs on insulin sensitivity in overweight women.</p>
<p><b>Design:</b> Sixty-three healthy women with abdominal obesity [waist circumference &gt;88 cm and a body mass index (in kg/m<sup>2</sup>) &gt;28] were recruited. After a run-in period, the volunteers were randomly assigned to consume 1 of 3 four-week diets: 60 g low-TFA lipids/d (0.54 g/d; <I>n</I> = 21), ruminant TFA&ndash;rich lipids (4.86 g/d; <I>n</I> = 21), or industrial TFA&ndash;rich lipids (5.58 g/d; <I>n</I> = 21). Changes in peripheral insulin sensitivity were assessed by using hyperinsulinemic-euglycemic clamps.</p>
<p><b>Results:</b> After the intervention period, fasting glycemia and insulinemia and insulin sensitivity were not significantly modified in either group (<I>P</I> &gt; 0.05).</p>
<p><b>Conclusions:</b> These data indicate that consumption of dairy- and industrial-source TFAs for 4 wk at nutritional levels do not impair peripheral insulin sensitivity in insulin-resistant women. Our study may not preassess the effects of TFAs in normal insulin-sensitive individuals. This trial was registered at clinicaltrials.gov as NCT00617435.</p>
]]></description>
<dc:creator><![CDATA[Tardy, A.-L., Lambert-Porcheron, S., Malpuech-Brugere, C., Giraudet, C., Rigaudiere, J.-P., Laillet, B., LeRuyet, P., Peyraud, J.-L., Boirie, Y., Laville, M., Michalski, M.-C., Chardigny, J.-M., Morio, B.]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27515</dc:identifier>
<dc:title><![CDATA[[Carbohydrate metabolism and diabetes] Dairy and industrial sources of trans fat do not impair peripheral insulin sensitivity in overweight women]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>94</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>88</prism:startingPage>
<prism:section>Carbohydrate metabolism and diabetes</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/95?rss=1">
<title><![CDATA[[Energy and protein metabolism] Enteral administration of alanyl-[2-15N]glutamine contributes more to the de novo synthesis of arginine than does intravenous infusion of the dipeptide in humans]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/95?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> We previously confirmed in humans the existence of a pathway of glutamine into citrulline and arginine, which is preferentially stimulated by luminally provided glutamine. However, because glutamine is unstable, we tested this pathway with a stable dipeptide of glutamine.</p>
<p><b>Objectives:</b> The objectives were to explore whether alanyl-glutamine contributes to the synthesis of arginine in humans and whether this depends on the route of administration.</p>
<p><b>Design:</b> The study was conducted under postabsorptive conditions during surgery. Sixteen patients received alanyl-[2-<sup>15</sup>N]glutamine enterally or intravenously together with intravenously administered stable-isotope tracers of citrulline and arginine. Blood was collected from an artery, the portal vein, a hepatic vein, and the right renal vein. Arterial and venous enrichments and (tracer) net balances of alanyl-glutamine and glutamine, citrulline, and arginine across the portal-drained viscera, liver, and kidneys were determined. Parametric tests were used to test results (mean &plusmn; SEM). <I>P</I> &lt; 0.05 was considered significant.</p>
<p><b>Results:</b> Twice as much exogenous glutamine was used for the synthesis of citrulline when alanyl-glutamine was provided enterally (5.9 &plusmn; 0.6%) than when provided intravenously (2.8 &plusmn; 0.3%) (<I>P</I> &lt; 0.01). Consequently, twice as much exogenous glutamine was used for the synthesis of arginine when alanyl-glutamine was provided enterally (5 &plusmn; 0.7%) than when provided intravenously (2.4 &plusmn; 0.2%) (<I>P</I> &lt; 0.01). However, results at the organ level did not explain the differences due to route of administration.</p>
<p><b>Conclusions:</b> Alanyl-glutamine contributes to the de novo synthesis of arginine, especially when provided enterally. A stable-isotope study using a therapeutic dose of alanyl-glutamine is needed to investigate the clinical implications of this finding.</p>
]]></description>
<dc:creator><![CDATA[Ligthart-Melis, G. C, van de Poll, M. C., Vermeulen, M. A., Boelens, P. G, van den Tol, M P., van Schaik, C., De Bandt, J.-P., Deutz, N. E., Dejong, C. H., van Leeuwen, P. A.]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2008.26399</dc:identifier>
<dc:title><![CDATA[[Energy and protein metabolism] Enteral administration of alanyl-[2-15N]glutamine contributes more to the de novo synthesis of arginine than does intravenous infusion of the dipeptide in humans]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>105</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>95</prism:startingPage>
<prism:section>Energy and protein metabolism</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/106?rss=1">
<title><![CDATA[[Energy and protein metabolism] Ingestion of a protein hydrolysate is accompanied by an accelerated in vivo digestion and absorption rate when compared with its intact protein]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/106?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> It has been suggested that a protein hydrolysate, as opposed to its intact protein, is more easily digested and absorbed from the gut, which results in greater plasma amino acid availability and a greater muscle protein synthetic response.</p>
<p><b>Objective:</b> We aimed to compare dietary protein digestion and absorption kinetics and the subsequent muscle protein synthetic response to the ingestion of a single bolus of protein hydrolysate compared with its intact protein in vivo in humans.</p>
<p><b>Design:</b> Ten elderly men (mean &plusmn; SEM age: 64 &plusmn; 1 y) were randomly assigned to a crossover experiment that involved 2 treatments in which the subjects consumed a 35-g bolus of specifically produced <scp>l</scp>-[1-<sup>13</sup>C]phenylalanine-labeled intact casein (CAS) or hydrolyzed casein (CASH). Blood and muscle-tissue samples were collected to assess the appearance rate of dietary protein&ndash;derived phenylalanine in the circulation and subsequent muscle protein fractional synthetic rate over a 6-h postprandial period.</p>
<p><b>Results:</b> The mean (&plusmn;SEM) exogenous phenylalanine appearance rate was 27 &plusmn; 6% higher after ingestion of CASH than after ingestion of CAS (<I>P</I> &lt; 0.001). Splanchnic extraction was significantly lower in CASH compared with CAS treatment (<I>P</I> &lt; 0.01). Plasma amino acid concentrations increased to a greater extent (25&ndash;50%) after the ingestion of CASH than after the ingestion of CAS (<I>P</I> &lt; 0.01). Muscle protein synthesis rates averaged 0.054 &plusmn; 0.004% and 0.068 &plusmn; 0.006%/h in the CAS and CASH treatments, respectively (<I>P</I> = 0.10).</p>
<p><b>Conclusions:</b> Ingestion of a protein hydrolysate, as opposed to its intact protein, accelerates protein digestion and absorption from the gut, augments postprandial amino acid availability, and tends to increase the incorporation rate of dietary amino acids into skeletal muscle protein.</p>
]]></description>
<dc:creator><![CDATA[Koopman, R., Crombach, N., Gijsen, A. P, Walrand, S., Fauquant, J., Kies, A. K, Lemosquet, S., Saris, W. H., Boirie, Y., van Loon, L. J.]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27474</dc:identifier>
<dc:title><![CDATA[[Energy and protein metabolism] Ingestion of a protein hydrolysate is accompanied by an accelerated in vivo digestion and absorption rate when compared with its intact protein]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>115</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>106</prism:startingPage>
<prism:section>Energy and protein metabolism</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/116?rss=1">
<title><![CDATA[[Vitamins, minerals, and phytochemicals] Folate is absorbed across the colon of adults: evidence from cecal infusion of 13C-labeled [6S]-5-formyltetrahydrofolic acid]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/116?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Folate deficiency increases the risk of several human diseases. Likewise, high intakes of folate, particularly synthetic folic acid intake, may be associated with adverse health outcomes in humans. A more comprehensive understanding of the "input side" of folate nutrition may help to set dietary recommendations that strike the right balance between health benefits and risks. It is well known that the microflora in the colon produce large quantities of folate that approach or exceed recommended dietary intakes; however, there is no direct evidence of the bioavailability of this pool in humans.</p>
<p><b>Objective:</b> The objective was to determine whether, and to what extent, the natural folate vitamer 5-formyltetrahydrofolic acid is absorbed across the intact colon of humans.</p>
<p><b>Design:</b> During screening colonoscopy, 684 nmol (320 <I>&micro;</I>g) [<sup>13</sup>C]glutamyl-5-formyltetrahydrofolic acid was infused directly into the cecum of 6 healthy adults. Three or more weeks later, each subject received an intravenous injection of the same compound (172 nmol). Blood samples were collected before and after each treatment. The ratio of labeled to unlabeled folates was determined in plasma by tandem mass spectrometry.</p>
<p><b>Results:</b> The apparent rate of folate absorption across the colon of a bolus dose of [<sup>13</sup>C]5-formyltetrahydrofolic acid infused into the cecum was 0.6 &plusmn; 0.2 nmol/h, as determined by the appearance of [<sup>13</sup>C<SUB>5</SUB>]5-methyltetrahydrofolic acid in plasma. In comparison, the rate of appearance of [<sup>13</sup>C<SUB>5</SUB>]5-methyltetrahydrofolic acid after an intravenous injection of [<sup>13</sup>C<SUB>5</SUB>]5-formyltetrahydrofolate was 7 &plusmn; 1.2 nmol/h.</p>
<p><b>Conclusion:</b> Physiologic doses of natural folate are absorbed across the intact colon in humans.</p>
]]></description>
<dc:creator><![CDATA[Aufreiter, S., Gregory, J. F, Pfeiffer, C. M, Fazili, Z., Kim, Y.-I., Marcon, N., Kamalaporn, P., Pencharz, P. B, O'Connor, D. L]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2008.27345</dc:identifier>
<dc:title><![CDATA[[Vitamins, minerals, and phytochemicals] Folate is absorbed across the colon of adults: evidence from cecal infusion of 13C-labeled [6S]-5-formyltetrahydrofolic acid]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>123</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>116</prism:startingPage>
<prism:section>Vitamins, minerals, and phytochemicals</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/124?rss=1">
<title><![CDATA[[Vitamins, minerals, and phytochemicals] Randomized, double-blind, placebo-controlled trial of iron supplementation in female soldiers during military training: effects on iron status, physical performance, and mood]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/124?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Decrements in iron status have been reported in female soldiers during military training. Diminished iron status adversely affects physical and cognitive performance.</p>
<p><b>Objective:</b> We wanted to determine whether iron supplementation could prevent decrements in iron status and improve measures of physical performance and cognitive status in female soldiers during basic combat training (BCT).</p>
<p><b>Design:</b> In this 8-wk randomized, double-blind, placebo-controlled trial, soldier volunteers (<I>n</I> = 219) were provided with capsules containing either 100 mg ferrous sulfate or a placebo. Iron status indicator assays were performed pre- and post-BCT. Two-mile running time was assessed post-BCT; mood was assessed by using the Profile of Mood States questionnaire pre- and post-BCT.</p>
<p><b>Results:</b> The BCT course affected iron status: red blood cell distribution width and soluble transferrin receptor were elevated (<I>P</I> &lt; 0.05), and serum ferritin was lowered (<I>P</I> &lt; 0.05) post-BCT. Iron supplementation attenuated the decrement in iron status; group-by-time interactions (<I>P</I> &lt; 0.01) were observed for serum ferritin and soluble transferrin receptor. Iron supplementation resulted in improved (<I>P</I> &lt; 0.05) vigor scores on the Profile of Mood States post-BCT and in faster running time (<I>P</I> &lt; 0.05) in volunteers reporting to BCT with iron deficiency anemia.</p>
<p><b>Conclusions:</b> Iron status is affected by BCT, and iron supplementation attenuates the decrement in indicators of iron status in female soldiers. Furthermore, iron supplementation may prove to be beneficial for mood and physical performance during the training period. Future efforts should identify and treat female soldiers or athletes who begin training regimens with iron deficiency or iron deficiency anemia.</p>
]]></description>
<dc:creator><![CDATA[McClung, J. P, Karl, J P., Cable, S. J, Williams, K. W, Nindl, B. C, Young, A. J, Lieberman, H. R]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27774</dc:identifier>
<dc:title><![CDATA[[Vitamins, minerals, and phytochemicals] Randomized, double-blind, placebo-controlled trial of iron supplementation in female soldiers during military training: effects on iron status, physical performance, and mood]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>131</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>124</prism:startingPage>
<prism:section>Vitamins, minerals, and phytochemicals</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/132?rss=1">
<title><![CDATA[[Vitamins, minerals, and phytochemicals] Antenatal supplementation with folic acid + iron + zinc improves linear growth and reduces peripheral adiposity in school-age children in rural Nepal]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/132?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> We previously reported that a randomized controlled trial of antenatal micronutrient supplements in rural Nepal decreased the risk of low birth weight by 15%.</p>
<p><b>Objective:</b> The objective was to examine the effects of micronutrient supplementation on growth and body composition in children of supplemented mothers through school age.</p>
<p><b>Design:</b> Mothers received 1 of 5 micronutrient supplements daily: folic acid, folic acid + iron, folic acid + iron + zinc, multiple micronutrients, or a control. All of the supplements contained vitamin A. Children born during this trial were revisited at age 6&ndash;8 y to measure height, weight, midupper arm circumference, waist circumference, and triceps and subscapular skinfold thicknesses. Arm fat and muscle area were estimated by using standard formulas, and height-for-age, weight-for-age, and body mass index&ndash;for-age <I>z</I> scores were calculated by using the World Health Organization growth standard.</p>
<p><b>Results:</b> Of the 3771 surviving children, 3324 were revisited and consented to anthropometric measurements. Maternal supplementation with folic acid + iron + zinc resulted in an increase in mean height (0.64 cm; 95% CI: 0.04, 1.25) and a reduction in mean triceps skinfold thickness (&ndash;0.25 mm; 95% CI: &ndash;0.44, &ndash;0.06), subscapular skinfold thickness (&ndash;0.20 mm; 95% CI: &ndash;0.33, &ndash;0.06), and arm fat area (&ndash;0.18 cm<sup>2</sup>; &ndash;0.34, &ndash;0.01). No significant differences were found between groups in mean weight or body mass index&ndash;for-age <I>z</I> scores, waist circumference, or arm muscle area. Other micronutrient combinations including a multiple micronutrient formulation failed to show a growth benefit.</p>
<p><b>Conclusion:</b> Antenatal supplementation with zinc may benefit child growth, particularly in areas where a deficiency of this nutrient is common.</p>
]]></description>
<dc:creator><![CDATA[Stewart, C. P, Christian, P., LeClerq, S. C, West, K. P, Khatry, S. K]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2008.27368</dc:identifier>
<dc:title><![CDATA[[Vitamins, minerals, and phytochemicals] Antenatal supplementation with folic acid + iron + zinc improves linear growth and reduces peripheral adiposity in school-age children in rural Nepal]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>140</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>132</prism:startingPage>
<prism:section>Vitamins, minerals, and phytochemicals</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/141?rss=1">
<title><![CDATA[[Pregnancy and lactation] Micronutrient supplementation affects maternal-infant feeding interactions and maternal distress in Bangladesh]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/141?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Good maternal-infant interaction is essential for optimal infant growth, health, and development. Although micronutrient malnutrition has been associated with poorer interaction, the effects of maternal micronutrient supplementation on interaction are unknown.</p>
<p><b>Objectives:</b> We examined differences in maternal-infant feeding interaction between 3 maternal pre- and postpartum micronutrient supplementation groups that differed in iron dose and inclusion of multiple micronutrients and determined whether any differences observed were mediated by maternal distress.</p>
<p><b>Design:</b> A cohort of 180 pregnant women was selected from 3300 women in the randomized controlled trial Maternal Infant Nutritional Interventions Matlab, which was conducted in Matlab, Bangladesh. At 8 wk of gestation, women were randomly assigned to 1 of 3 groups to receive a daily supplement of micronutrients (14 wk gestation to 12 wk postpartum): 60 or 30 mg Fe each with 400 &micro;g folic acid or multiple micronutrients (MuMS; 30 mg Fe, 400 &micro;g folic acid, and other micronutrients). A maternal-infant feeding interaction was observed in the home when infants were 3.4&ndash;4.0 mo of age, and maternal distress was assessed.</p>
<p><b>Results:</b> Compared with 30 mg Fe, 60 mg Fe decreased the quality of maternal-infant feeding interaction by 10%. Compared with 30 mg Fe, MuMS did not improve interaction but reduced maternal early postpartum distress. Distress did not mediate the effects of micronutrient supplementation on interaction.</p>
<p><b>Conclusion:</b> For pregnant and postpartum women, micronutrient supplementation should be based on both nutritional variables (eg, iron status) and functional outcomes (eg, maternal-infant interaction and maternal distress).</p>
]]></description>
<dc:creator><![CDATA[Frith, A. L, Naved, R. T, Ekstrom, E.-C., Rasmussen, K. M, Frongillo, E. A]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2008.26817</dc:identifier>
<dc:title><![CDATA[[Pregnancy and lactation] Micronutrient supplementation affects maternal-infant feeding interactions and maternal distress in Bangladesh]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>148</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>141</prism:startingPage>
<prism:section>Pregnancy and lactation</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/149?rss=1">
<title><![CDATA[[Pregnancy and lactation] Fish and long-chain n-3 polyunsaturated fatty acid intakes during pregnancy and risk of postpartum depression: a prospective study based on a large national birth cohort]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/149?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Mothers may be reluctant to receive medical treatment of postpartum depression (PPD), despite the detrimental consequences the disorder can impose on mother and child. Research on alternative methods of prevention and treatment of PPD is warranted. Previous studies have suggested that long-chain n&ndash;3 polyunsaturated fatty acids (PUFAs) might have a beneficial effect on depression.</p>
<p><b>Objective:</b> The objective was to explore the association between intake of fish and n&ndash;3 PUFAs during pregnancy and PPD in the Danish National Birth Cohort (DNBC).</p>
<p><b>Design:</b> Exposure information from the DNBC was linked to the Danish patient and prescription registries for data on clinically identified cases of depression up to 1 y postpartum. Intake of fish and n&ndash;3 PUFAs was assessed in midpregnancy with a food-frequency questionnaire. Admission to the hospital for PPD (PPD-admission) and prescription of antidepressants (PPD-prescription) were treated as separate outcomes. A total of 54,202 women were included in the present study sample.</p>
<p><b>Results:</b> Rates of depression were 0.3% (PPD-admission) and 1.6% (PPD-prescription). No association was observed between fish intake and risk of PPD-admission [crude odds ratio of 1.01 (95% CI: 0.52, 1.97) and adjusted odds ratio of 0.82 (95% CI: 0.42, 1.64)], whereas a higher risk of PPD-prescription was found for the lowest compared with the highest fish intake group [crude odds ratio of 1.61 (95% CI: 1.26, 2.06) and adjusted odds ratio of 1.46 (95% CI: 1.12, 1.90)]. No association was observed with respect to n&ndash;3 PUFA intake.</p>
<p><b>Conclusion:</b> Overall, our data from a large prospective cohort linked with high-quality registers showed little evidence to support an association between intake of fish or n&ndash;3 PUFAs and PPD.</p>
]]></description>
<dc:creator><![CDATA[Strom, M., Mortensen, E. L, Halldorsson, T. I, Thorsdottir, I., Olsen, S. F]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27552</dc:identifier>
<dc:title><![CDATA[[Pregnancy and lactation] Fish and long-chain n-3 polyunsaturated fatty acid intakes during pregnancy and risk of postpartum depression: a prospective study based on a large national birth cohort]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>155</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>149</prism:startingPage>
<prism:section>Pregnancy and lactation</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/156?rss=1">
<title><![CDATA[[Growth, development, and pediatrics] Insulin-like growth factor I concentrations in infancy predict differential gains in body length and adiposity: the Cambridge Baby Growth Study]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/156?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Formula milk&ndash;fed infants show faster rates of growth and weight gain than do breastfed infants, and they have higher concentrations of insulin-like growth factor I (IGF-I).</p>
<p><b>Objective:</b> Our objective was to determine the influence of IGF-I concentrations on gains in weight, length, body mass index (BMI), and adiposity in the first year of life.</p>
<p><b>Design:</b> IGF-I concentrations were measured in 953 capillary blood samples from 675 unselected infants at ages 3 and 12 mo. These infants were born between 2002 and 2008 in one center and were participating in a prospective longitudinal birth cohort. Weight, length, and 4 skinfold thicknesses as an indicator of adiposity were measured at ages 0, 3, and 12 mo. Analyses were adjusted for age and sex.</p>
<p><b>Results:</b> Infants who were formula milk&ndash;fed had higher IGF-I concentrations at 3 mo, and they showed greater gains in weight, length, BMI, and adiposity between age 3 and 12 mo. IGF-I concentrations at 3 mo were unrelated to subsequent overall weight gain (<I>P</I> = 0.5). However, higher IGF-I concentrations at age 3 mo predicted greater subsequent gains in body length (<I>P</I> &lt; 0.001 and <I>P</I> = 0.007 in formula milk&ndash;fed and breastfed infants, respectively) and slower gains in BMI (<I>P</I> &lt; 0.001 and <I>P</I> = 0.004, respectively) and adiposity (<I>P</I> = 0.03 and <I>P</I> = 0.003, respectively).</p>
<p><b>Conclusions:</b> Our findings support a key role for IGF-I in the partitioning of overall infant weight gain into statural growth compared with adiposity. In formula milk&ndash;fed infants, higher IGF-I concentrations may lead to faster gains in length; however, other mechanisms likely explain their faster gains in weight, BMI, and adiposity.</p>
]]></description>
<dc:creator><![CDATA[Ong, K. K, Langkamp, M., Ranke, M. B, Whitehead, K., Hughes, I. A, Acerini, C. L, Dunger, D. B]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2008.27408</dc:identifier>
<dc:title><![CDATA[[Growth, development, and pediatrics] Insulin-like growth factor I concentrations in infancy predict differential gains in body length and adiposity: the Cambridge Baby Growth Study]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>161</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>156</prism:startingPage>
<prism:section>Growth, development, and pediatrics</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/162?rss=1">
<title><![CDATA[[Cancer] Longitudinal study of serum carotenoid, retinol, and tocopherol concentrations in relation to breast cancer risk among postmenopausal women]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/162?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Prospective studies have examined the association of serum and plasma carotenoids and micronutrients and breast cancer; however, to date, studies have only assessed exposure at one point in time.</p>
<p><b>Objective:</b> This study analyzed baseline and repeated serum measurements of carotenoids, retinol, and tocopherols to assess their associations with postmenopausal breast cancer risk.</p>
<p><b>Design:</b> Serum concentrations of <I></I>-carotene, <I>&beta;</I>-carotene, <I>&beta;</I>-cryptoxanthin, lycopene, lutein + zeaxanthin, retinol, <I></I>-tocopherol, and <I></I>-tocopherol were measured in a 6% sample of women in the Women's Health Initiative clinical trials at baseline and at years 1, 3, and 6 and in a 1% sample of women in the observational study at baseline and at year 3. The association of baseline compounds and breast cancer risk was estimated by Cox proportional hazards models. In addition, repeated measurements were analyzed as time-dependent covariates. Of 5450 women with baseline measurements, 190 incident cases of breast cancer were ascertained over a median of 8.0 y of follow-up.</p>
<p><b>Results:</b> After multivariable adjustment, risk of invasive breast cancer was inversely associated with baseline serum <I></I>-carotene concentrations (hazard ratio for highest compared with the lowest tertile: 0.55; 95% CI: 0.34, 0.90; <I>P</I> = 0.02) and positively associated with baseline lycopene (hazard ratio: 1.47; 95% CI: 0.98, 2.22; <I>P</I> = 0.06). Analysis of repeated measurements indicated that <I></I>-carotene and <I>&beta;</I>-carotene were inversely associated with breast cancer and that <I></I>-tocopherol was associated with increased risk.</p>
<p><b>Conclusions:</b> The present study, which was the first to assess repeated measurements of serum carotenoids and micronutrients in relation to breast cancer, adds to the evidence of an inverse association of specific carotenoids with breast cancer. The positive associations observed for lycopene and <I></I>-tocopherol require confirmation. This trial was registered at clinicaltrials.gov as NCT00000611.</p>
]]></description>
<dc:creator><![CDATA[Kabat, G. C, Kim, M., Adams-Campbell, L. L, Caan, B. J, Chlebowski, R. T, Neuhouser, M. L, Shikany, J. M, Rohan, T. E]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27568</dc:identifier>
<dc:title><![CDATA[[Cancer] Longitudinal study of serum carotenoid, retinol, and tocopherol concentrations in relation to breast cancer risk among postmenopausal women]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>169</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>162</prism:startingPage>
<prism:section>Cancer</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/170?rss=1">
<title><![CDATA[[Aging] Dietary intake of fish and omega-3 fatty acids in relation to long-term dementia risk]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/170?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Greater fish and omega-3 (n&ndash;3) polyunsaturated fatty acid (PUFA) intake may reduce dementia risk; however, previous studies have reported conflicting results, which were largely based on short-term follow-up.</p>
<p><b>Objective:</b> The objective was to study the dietary consumption of fish and omega-3 PUFAs in relation to long-term dementia risk.</p>
<p><b>Design:</b> We studied 5395 participants aged &ge;55 y in the Rotterdam Study who were free of dementia and reported dietary information at baseline. We used age- and sex-adjusted Cox proportional hazard and multivariate-adjusted models to evaluate the relative risk of dementia and Alzheimer disease (AD) across categories of typical fish intake (none, low, and high) and fish type consumed (none, lean, and fatty). We also evaluated dementia and AD risk across tertiles of omega-3 PUFA intake, specifically, total long-chain omega-3 fatty acids: eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA), <I></I>-linolenic acid, and EPA and DHA individually.</p>
<p><b>Results:</b> During an average follow-up of 9.6 y, dementia developed in 465 participants (365 with a diagnosis of AD). In multivariate-adjusted models, total fish intake was unrelated to dementia risk (<I>P</I> for trend = 0.7). Compared with participants who typically ate no fish, those with a high fish intake had a similar dementia risk (hazard ratio: 0.95; 95% CI: 0.76, 1.19), as did those who typically ate fatty fish (hazard ratio: 0.98; 95% CI: 0.77, 1.24). Dietary intakes of omega-3 PUFAs were also not associated with dementia risk, and the results were similar when we considered AD specifically.</p>
<p><b>Conclusion:</b> In this Dutch cohort, who had a moderate consumption of fish and omega-3 PUFAs, these dietary factors do not appear to be associated with long-term dementia risk.</p>
]]></description>
<dc:creator><![CDATA[Devore, E. E, Grodstein, F., van Rooij, F. J., Hofman, A., Rosner, B., Stampfer, M. J, Witteman, J. C., Breteler, M. M.]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2008.27037</dc:identifier>
<dc:title><![CDATA[[Aging] Dietary intake of fish and omega-3 fatty acids in relation to long-term dementia risk]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>176</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>170</prism:startingPage>
<prism:section>Aging</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/177?rss=1">
<title><![CDATA[[Aging] Dietary screening tool identifies nutritional risk in older adults]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/177?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> No rapid methods exist for screening overall dietary intakes in older adults.</p>
<p><b>Objective:</b> The purpose of this study was to develop and evaluate a scoring system for a diet screening tool to identify nutritional risk in community-dwelling older adults.</p>
<p><b>Design:</b> This cross-sectional study in older adults (<I>n</I> = 204) who reside in rural areas examined nutrition status by using an in-person interview, biochemical measures, and four 24-h recalls that included the use of dietary supplements.</p>
<p><b>Results:</b> The dietary screening tool was able to characterize 3 levels of nutritional risk: at risk, possible risk, and not at risk. Individuals classified as at nutritional risk had significantly lower indicators of diet quality (Healthy Eating Index and Mean Adequacy Ratio) and intakes of protein, most micronutrients, dietary fiber, fruit, and vegetables. The at-risk group had higher intakes of fats and oils and refined grains. The at-risk group also had the lowest serum vitamin B-12, folate, <I>&beta;</I>-cryptoxanthin, lutein, and zeaxanthin concentrations. The not-at-nutritional-risk group had significantly higher lycopene and <I>&beta;</I>-carotene and lower homocysteine and methylmalonic acid concentrations.</p>
<p><b>Conclusion:</b> The dietary screening tool is a simple and practical tool that can help to detect nutritional risk in older adults.</p>
]]></description>
<dc:creator><![CDATA[Bailey, R. L, Miller, P. E, Mitchell, D. C, Hartman, T. J, Lawrence, F. R, Sempos, C. T, Smiciklas-Wright, H.]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2008.27268</dc:identifier>
<dc:title><![CDATA[[Aging] Dietary screening tool identifies nutritional risk in older adults]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>183</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>177</prism:startingPage>
<prism:section>Aging</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/184?rss=1">
<title><![CDATA[[Aging] Omega-3 fatty acids and risk of dementia: the Canadian Study of Health and Aging]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/184?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Omega-3 polyunsaturated fatty acids (n&ndash;3 PUFAs) may protect against dementia, although epidemiologic studies have yielded inconclusive results. Fish is the main dietary source of n&ndash;3 PUFAs and is sometimes contaminated with mercury. This neurotoxicant may modify the association with dementia.</p>
<p><b>Objective:</b> We evaluated the association of erythrocyte membrane total n&ndash;3 PUFAs, docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), and blood mercury with the incidence of dementia and Alzheimer disease (AD) in the Canadian Study of Health and Aging (CSHA) with adjustment for confounders including apolipoprotein E <I></I>4 (<I>APOE 4</I>) status.</p>
<p><b>Design:</b> The CSHA is a cohort study of a representative sample of persons aged &ge;65 y, conducted from 1991 to 2002. A subsample of 663 nondemented CSHA subjects with a complete clinical examination, blood samples, and follow-up information was eligible for prospective analyses on laboratory measurements. Of these, 149 were incident cases of dementia, including 105 with AD.</p>
<p><b>Results:</b> In adjusted Cox regression models with age as the time scale, there were no associations between total n&ndash;3 PUFAs, DHA, or EPA and dementia or AD. In contrast, a mercury concentration in the highest quartile was associated with a reduced risk of dementia (hazard ratio: 0.53; 95% CI: 0.33, 0.88). However, significant risk reductions were limited to subjects with concentrations of both n&ndash;3 PUFAs and mercury that were above the median. There was no modification of risk by <I>APOE 4</I> status.</p>
<p><b>Conclusions:</b> No associations between n&ndash;3 PUFAs and dementia or AD were found. The results regarding mercury may indicate a spurious association.</p>
]]></description>
<dc:creator><![CDATA[Kroger, E., Verreault, R., Carmichael, P.-H., Lindsay, J., Julien, P., Dewailly, E., Ayotte, P., Laurin, D.]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2008.26987</dc:identifier>
<dc:title><![CDATA[[Aging] Omega-3 fatty acids and risk of dementia: the Canadian Study of Health and Aging]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>192</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>184</prism:startingPage>
<prism:section>Aging</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/193?rss=1">
<title><![CDATA[[Nutritional epidemiology and public health] Adherence to 2005 Dietary Guidelines for Americans is associated with a reduced progression of coronary artery atherosclerosis in women with established coronary artery disease]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/193?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> A premise of the 2005 <I>Dietary Guidelines for Americans</I> (DGA) is chronic disease prevention.</p>
<p><b>Objective:</b> The goal was to determine whether a diet meeting the DGA is associated with less atherosclerotic lesion progression.</p>
<p><b>Design:</b> We used the data from 224 postmenopausal women with established coronary artery disease enrolled in the Estrogen Replacement and Atherosclerosis Study. Atherosclerosis progression was defined by repeated measures of quantitative angiography over a 3-y period. Adherence to the key DGA recommendations was measured by using the DGA Adherence Index (DGAI; possible range: 0&ndash;20), with each component weighted equally, and the modified DGAI score (wDGAI; possible range: &ndash;0.19&ndash;0.51), with each component weighted based on its relation to atherosclerosis progression. Mixed-model regression analyses were performed to assess the association between diet and atherosclerosis progression.</p>
<p><b>Results:</b> No women consumed a diet meeting all of the DGA recommendations. The mean (range) of the DGAI score was 14.1 (8.0&ndash;19.0). DGAI was not associated with atherosclerosis progression (<I>P</I> = 0.44), whereas wDGAI was inversely associated; a 1-SD difference in wDGAI was related to 0.049-mm less narrowing of the coronary arteries (SE = 0.017, <I>P</I> = 0.004).</p>
<p><b>Conclusions:</b> In postmenopausal women with established heart disease, under the assumption that all DGA recommendations are similarly effective, overall adherence was not associated with atherosclerosis progression. However, assigning differential weights to the DGA recommendations, the adherence was significantly associated with slower atherosclerosis progression. Assuming equity of associations between all dietary recommendations and disease outcomes is a limitation in accurately examining the effectiveness of the DGA.</p>
]]></description>
<dc:creator><![CDATA[Imamura, F., Jacques, P. F, Herrington, D. M, Dallal, G. E, Lichtenstein, A. H]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27576</dc:identifier>
<dc:title><![CDATA[[Nutritional epidemiology and public health] Adherence to 2005 Dietary Guidelines for Americans is associated with a reduced progression of coronary artery atherosclerosis in women with established coronary artery disease]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>201</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>193</prism:startingPage>
<prism:section>Nutritional epidemiology and public health</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/202?rss=1">
<title><![CDATA[[Nutritional epidemiology and public health] Fruit and vegetable intakes and subsequent changes in body weight in European populations: results from the project on Diet, Obesity, and Genes (DiOGenes)]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/202?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> High fruit and vegetable intakes may limit weight gain, particularly in susceptible persons, such as those who stop smoking.</p>
<p><b>Objective:</b> The objective was to assess the association of fruit and vegetable intake with subsequent weight change in a large-scale prospective study.</p>
<p><b>Design:</b> The data used were from 89,432 men and women from 5 countries participating in the European Prospective Investigation into Cancer and Nutrition (EPIC). The association between fruit and vegetable intake and weight change after a mean follow-up of 6.5 y was assessed by linear regression. Polytomous logistic regression was used to evaluate whether fruit and vegetable intake relates to weight gain, weight loss, or both.</p>
<p><b>Results:</b> Per 100-g intake of fruit and vegetables, weight change was &ndash;14 g/y (95% CI: &ndash;19, &ndash;9 g/y). In those who stopped smoking during follow-up, this value was &ndash;37 g/y (95% CI: &ndash;58, &ndash;15 g/y; <I>P</I> for interaction &lt; 0.0001). When weight gain and loss were analyzed separately per 100-g intake of fruit and vegetables in a combined model, the odds ratios (95% CIs) were 0.97 (0.95, 0.98) for weight gain &ge;0.5 and &lt;1 kg/y, 0.94 (0.92, 0.96) for weight gain &ge;1 kg/y, and 0.97 (0.95, 0.99) for weight loss &ge;0.5 kg/y. In those who stopped smoking during follow-up, the odds ratios (95% CIs) were 0.93 (0.88, 0.99), 0.87 (0.81, 0.92), and 0.97 (0.88, 1.07), respectively (<I>P</I> for interaction &lt; 0.0001).</p>
<p><b>Conclusions:</b> Fruit and vegetable intake relates significantly, albeit weakly inversely, to weight change. For persons who stop smoking, high fruit and vegetable intakes may be recommended to reduce the risk of weight gain.</p>
]]></description>
<dc:creator><![CDATA[Buijsse, B., Feskens, E. J., Schulze, M. B, Forouhi, N. G, Wareham, N. J, Sharp, S., Palli, D., Tognon, G., Halkjaer, J., Tjonneland, A., Jakobsen, M. U, Overvad, K., van der A, D. L, Du, H., Sorensen, T. I., Boeing, H.]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2008.27394</dc:identifier>
<dc:title><![CDATA[[Nutritional epidemiology and public health] Fruit and vegetable intakes and subsequent changes in body weight in European populations: results from the project on Diet, Obesity, and Genes (DiOGenes)]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>209</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>202</prism:startingPage>
<prism:section>Nutritional epidemiology and public health</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/210?rss=1">
<title><![CDATA[[Nutritional epidemiology and public health] Relation of body mass index and skinfold thicknesses to cardiovascular disease risk factors in children: the Bogalusa Heart Study]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/210?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Adverse levels of cardiovascular disease (CVD) risk factors are related to skinfold thicknesses and body mass index (BMI) among children, but the relative strengths of these associations are unknown.</p>
<p><b>Objective:</b> The objective was to determine whether the sum of the triceps and subscapular skinfold thicknesses (SF sum) is more strongly related to levels of 6 risk factors (triglycerides, LDL and HDL cholesterol, insulin, and systolic and diastolic blood pressure) than is BMI.</p>
<p><b>Design:</b> Cross-sectional analyses of schoolchildren examined in the Bogalusa Heart Study from 1981 to 1994 (<I>n</I> = 6866) were conducted. A risk factor summary index was derived by using principal components analysis.</p>
<p><b>Results:</b> After race, sex, study period, and age were controlled for, almost all comparisons indicated that BMI was more strongly related to risk factor levels than was the SF sum. Although the differences were generally small, many were statistically significant. Associations with the risk factor summary, for example, were <I>r</I> = 0.50 for BMI and <I>r</I> = 0.47 for SF sum (<I>P</I> &lt; 0.001 for difference). Furthermore, an adverse risk factor summary was observed among 62% of the children with the highest (upper 5%) BMI levels but among only 54% of children with the highest SF sum levels.</p>
<p><b>Conclusions:</b> BMI is at least as accurate as SF sum in identifying children and adolescents who are at metabolic risk. Because of the training and errors associated with skinfold-thickness measurements, the advantages of BMI should be considered in the design and interpretation of clinical and epidemiologic studies.</p>
]]></description>
<dc:creator><![CDATA[Freedman, D. S, Katzmarzyk, P. T, Dietz, W. H, Srinivasan, S. R, Berenson, G. S]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27525</dc:identifier>
<dc:title><![CDATA[[Nutritional epidemiology and public health] Relation of body mass index and skinfold thicknesses to cardiovascular disease risk factors in children: the Bogalusa Heart Study]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>216</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>210</prism:startingPage>
<prism:section>Nutritional epidemiology and public health</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/217?rss=1">
<title><![CDATA[[Nutritional epidemiology and public health] Assessment of the relative dose-response test based on serum retinol-binding protein instead of serum retinol in determining low hepatic vitamin A stores]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/217?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> The relative dose-response (RDR) test, which measures the percentage of change in serum retinol concentration in response to an oral vitamin A (VA) dose, is a functional reference method to assess low hepatic VA stores. However, problems due to the relative instability of retinol, which is measured in the traditional RDR test, could be circumvented if retinol-binding protein (RBP), a more stable marker of VA, could be measured instead of retinol to provide the RDR value.</p>
<p><b>Objective:</b> The objective was to compare classification of VA status assessed by retinol-RDR with that assessed by using RBP-RDR.</p>
<p><b>Design:</b> With the use of serum samples from 57 lactating women in northern Kenya collected in August-September 2006, we assessed the accuracy of RBP-RDR in predicting low hepatic VA stores through receiver operator characteristic (ROC) analysis using retinol-RDR values as the gold standard. By using regression analysis, we explored the effects of <I>1</I>) body mass index (BMI) on RBP-RDR performance and <I>2</I>) the oral VA dose on the retinol-RBP molar ratio.</p>
<p><b>Results:</b> The classificatory accuracy of RBP-RDR was low to moderate (<I>n</I> = 50; ROC area: 0.56&ndash;0.72) depending on the cutoffs used. RBP-RDR systematically overestimated VA deficiency with higher BMI, although it was superior to a single measurement of serum retinol. The discrepancy between RBP-RDR and retinol-RDR appears to originate in a retinol concentration&ndash;dependent alteration of the retinol-RBP molar ratio triggered by the oral dose.</p>
<p><b>Conclusions:</b> RBP-RDR has the potential to serve as a moderately accurate surrogate measure of retinol-RDR if the variation associated with BMI is understood and adjusted. Further studies should clarify the dynamics of the retinol-RBP molar ratio and its link to RBP-RDR performance.</p>
]]></description>
<dc:creator><![CDATA[Fujita, M., Brindle, E., Rocha, A., Shell-Duncan, B., Ndemwa, P., O'Connor, K. A]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27569</dc:identifier>
<dc:title><![CDATA[[Nutritional epidemiology and public health] Assessment of the relative dose-response test based on serum retinol-binding protein instead of serum retinol in determining low hepatic vitamin A stores]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>224</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>217</prism:startingPage>
<prism:section>Nutritional epidemiology and public health</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/225?rss=1">
<title><![CDATA[[Gene-nutrient interactions] Mortality in HIV infection is independently predicted by host iron status and SLC11A1 and HP genotypes, with new evidence of a gene-nutrient interaction]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/225?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Iron-related genes and iron status may independently contribute to variable HIV outcomes. The nature of the biologically plausible gene-nutrient interaction remains unknown.</p>
<p><b>Objectives:</b> The objectives were to investigate whether iron-related genotypes and clinically abnormal iron status independently predict mortality in HIV and whether a gene-nutrient interaction exists.</p>
<p><b>Design:</b> Baseline plasma, DNA, and clinical data were obtained from 1362 HIV-seropositive Gambian adults followed for 11.5 y to ascertain all-cause mortality. Iron status was estimated on the basis of plasma iron, soluble transferrin receptor (sTfR), ferritin, transferrin, transferrin index, and log(sTfR/ferritin). One haptoglobin (<I>HP</I>) and 5 <I>SLC11A1</I> (<I>NRAMP1</I>) polymorphisms were genotyped.</p>
<p><b>Results:</b> <I>SLC11A1</I>-<I>SLC3</I> and <I>CAAA</I> polymorphisms were the best independent genetic predictors of mortality [adjusted mortality rate ratio (95% CI)]: <I>SLC3:G/C</I> = 0.59 (95% CI: 0.45, 0.85), <I>CAAA:del/ins</I> = 1.51 (95% CI: 1.10, 2.07). In an adjusted model that included all polymorphisms, <I>SLC1:199/199</I>, <I>SLC1:other/other</I>, <I>SLC6a:A/A</I>, and <I>CAAA:del/ins</I> were associated with significantly greater mortality, whereas Hp 2&ndash;1 and <I>SLC3:G/C</I> were protective. In unadjusted analyses, all biomarker concentrations were significantly associated with mortality. In an extension of previous findings, both low and elevated iron states were associated with mortality, but the nature of the risk was variable, with linear, inversely linear, and U-shaped associations depending on the biomarker. Mortality was significantly lower in HIV-2 than in HIV-1 infection in the presence of abnormal (low or elevated) iron status. A gene-iron interaction was detected (likelihood-ratio test <I>P</I> = 0.018); however, subject numbers restricted category-specific interpretation.</p>
<p><b>Conclusions:</b> Iron-related genes, iron status, and their interaction predict mortality in HIV. These findings illustrate the complexity and uncertainty surrounding best practice for managing abnormal iron status and anemia during HIV infection and in regions with a high risk of infection.</p>
]]></description>
<dc:creator><![CDATA[McDermid, J. M, van der Loeff, M. F S., Jaye, A., Hennig, B. J, Bates, C., Todd, J., Sirugo, G., Hill, A. V, Whittle, H. C, Prentice, A. M]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27709</dc:identifier>
<dc:title><![CDATA[[Gene-nutrient interactions] Mortality in HIV infection is independently predicted by host iron status and SLC11A1 and HP genotypes, with new evidence of a gene-nutrient interaction]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>233</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>225</prism:startingPage>
<prism:section>Gene-nutrient interactions</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/234?rss=1">
<title><![CDATA[[Bone metabolism] Soy proteins and isoflavones affect bone mineral density in older women: a randomized controlled trial]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/234?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Soy foods contain several components (isoflavones and amino acids) that potentially affect bone. Few long-term, large clinical trials of soy as a means of improving bone mineral density (BMD) in late postmenopausal women have been conducted.</p>
<p><b>Objective:</b> Our goal was to evaluate the long-term effect of dietary soy protein and/or soy isoflavone consumption on skeletal health in late postmenopausal women.</p>
<p><b>Design:</b> We conducted a randomized, double-blind, placebo-controlled clinical trial in 131 healthy ambulatory women aged &gt;60 y. Ninety-seven women completed the trial. After a 1-mo baseline period, subjects were randomly assigned into 1 of 4 intervention groups: soy protein (18 g) + isoflavone tablets (105 mg isoflavone aglycone equivalents), soy protein + placebo tablets, control protein + isoflavone tablets, and control protein + placebo tablets.</p>
<p><b>Results:</b> Consumption of protein powder and isoflavone pills did not differ between groups, and compliance with the study powder and pills was 80&ndash;90%. No significant differences in BMD were observed between groups from baseline to 1 y after the intervention or in BMD change between equol and non-equol producers. However, there were significant negative correlations between total dietary protein (per kg) and markers of bone turnover (<I>P</I> &lt; 0.05).</p>
<p><b>Conclusions:</b> Because soy protein and isoflavones (either alone or together) did not affect BMD, they should not be considered as effective interventions for preserving skeletal health in older women. The negative correlation between dietary protein and bone turnover suggests that increasing protein intakes may suppress skeletal turnover. This trial was registered at clinicaltrials.gov as NCT00668447.</p>
]]></description>
<dc:creator><![CDATA[Kenny, A. M, Mangano, K. M, Abourizk, R. H, Bruno, R. S, Anamani, D. E, Kleppinger, A., Walsh, S. J, Prestwood, K. M, Kerstetter, J. E]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27600</dc:identifier>
<dc:title><![CDATA[[Bone metabolism] Soy proteins and isoflavones affect bone mineral density in older women: a randomized controlled trial]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>242</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>234</prism:startingPage>
<prism:section>Bone metabolism</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/243?rss=1">
<title><![CDATA[[Letters to the Editor] Glycemic index in overweight development: distinguishing limited evidence from limits in evidence]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/243?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Buyken, A. E, Gunther, A. L., Barclay, A., Brand-Miller, J., Schulze, M. B]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27742</dc:identifier>
<dc:title><![CDATA[[Letters to the Editor] Glycemic index in overweight development: distinguishing limited evidence from limits in evidence]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>244</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>243</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/244?rss=1">
<title><![CDATA[[Letters to the Editor] Reply to AE Buyken et al]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/244?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Mendez, M. A, Schroder, H.]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27890</dc:identifier>
<dc:title><![CDATA[[Letters to the Editor] Reply to AE Buyken et al]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>246</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>244</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/246?rss=1">
<title><![CDATA[[Letters to the Editor] Fortification of salt with iodine and iron in India]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/246?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Shankar, S. R., Mathew, A. C, Sivamani, M, Banu, M S., Idupuganti, A A.]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27857</dc:identifier>
<dc:title><![CDATA[[Letters to the Editor] Fortification of salt with iodine and iron in India]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>246</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>246</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/246-a?rss=1">
<title><![CDATA[[Letters to the Editor] Reply to SLR Shankar et al]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/246-a?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Andersson, M., Hurrell, R. F, Zimmermann, M. B, Thankachan, P., Muthayya, S., Kurpad, A. V, Goud, R. B]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27979</dc:identifier>
<dc:title><![CDATA[[Letters to the Editor] Reply to SLR Shankar et al]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>247</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>246</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/248?rss=1">
<title><![CDATA[[Errata] Erratum]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/248?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27932</dc:identifier>
<dc:title><![CDATA[[Errata] Erratum]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>248</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>248</prism:startingPage>
<prism:section>Errata</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/248-a?rss=1">
<title><![CDATA[[Errata] Erratum]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/248-a?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27933</dc:identifier>
<dc:title><![CDATA[[Errata] Erratum]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>248</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>248</prism:startingPage>
<prism:section>Errata</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/248-b?rss=1">
<title><![CDATA[[Errata] Erratum]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/248-b?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27937</dc:identifier>
<dc:title><![CDATA[[Errata] Erratum]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>248</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>248</prism:startingPage>
<prism:section>Errata</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/1/248-c?rss=1">
<title><![CDATA[[Errata] Erratum]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/1/248-c?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27994</dc:identifier>
<dc:title><![CDATA[[Errata] Erratum]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>248</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>248</prism:startingPage>
<prism:section>Errata</prism:section>
</item>

</rdf:RDF>