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	<title>CiteULike: omalbam's diet</title>
	<description>CiteULike: omalbam's diet</description>


	<link>http://www.citeulike.org/user/omalbam/tag/diet</link>
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<item rdf:about="http://www.citeulike.org/user/omalbam/article/3014975">
    <title>Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet</title>
    <link>http://www.citeulike.org/user/omalbam/article/3014975</link>
    <description>&lt;i&gt;N Engl J Med, Vol. 359, No. 3. (17 July 2008), pp. 229-241.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Background Trials comparing the effectiveness and safety of weight-loss diets are frequently limited by short follow-up times and high dropout rates. Methods In this 2-year trial, we randomly assigned 322 moderately obese subjects (mean age, 52 years; mean body-mass index [the weight in kilograms divided by the square of the height in meters], 31; male sex, 86%) to one of three diets: low-fat, restricted-calorie; Mediterranean, restricted-calorie; or low-carbohydrate, non-restricted-calorie. Results The rate of adherence to a study diet was 95.4% at 1 year and 84.6% at 2 years. The Mediterranean-diet group consumed the largest amounts of dietary fiber and had the highest ratio of monounsaturated to saturated fat (P&#60;0.05 for all comparisons among treatment groups). The low-carbohydrate group consumed the smallest amount of carbohydrates and the largest amounts of fat, protein, and cholesterol and had the highest percentage of participants with detectable urinary ketones (P&#60;0.05 for all comparisons among treatment groups). The mean weight loss was 2.9 kg for the low-fat group, 4.4 kg for the Mediterranean-diet group, and 4.7 kg for the low-carbohydrate group (P&#60;0.001 for the interaction between diet group and time); among the 272 participants who completed the intervention, the mean weight losses were 3.3 kg, 4.6 kg, and 5.5 kg, respectively. The relative reduction in the ratio of total cholesterol to high-density lipoprotein cholesterol was 20% in the low-carbohydrate group and 12% in the low-fat group (P=0.01). Among the 36 subjects with diabetes, changes in fasting plasma glucose and insulin levels were more favorable among those assigned to the Mediterranean diet than among those assigned to the low-fat diet (P&#60;0.001 for the interaction among diabetes and Mediterranean diet and time with respect to fasting glucose levels). Conclusions Mediterranean and low-carbohydrate diets may be effective alternatives to low-fat diets. The more favorable effects on lipids (with the low-carbohydrate diet) and on glycemic control (with the Mediterranean diet) suggest that personal preferences and metabolic considerations might inform individualized tailoring of dietary interventions. (ClinicalTrials.gov number, NCT00160108 .) 10.1056/NEJMoa0708681</description>
    <dc:title>Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet</dc:title>

    <dc:creator>Iris Shai</dc:creator>
    <dc:creator>Dan Schwarzfuchs</dc:creator>
    <dc:creator>Yaakov Henkin</dc:creator>
    <dc:creator>Danit Shahar</dc:creator>
    <dc:creator>Shula Witkow</dc:creator>
    <dc:creator>Ilana Greenberg</dc:creator>
    <dc:creator>Rachel Golan</dc:creator>
    <dc:creator>Drora Fraser</dc:creator>
    <dc:creator>Arkady Bolotin</dc:creator>
    <dc:creator>Hilel Vardi</dc:creator>
    <dc:creator>Osnat Tangi-Rozental</dc:creator>
    <dc:creator>Rachel Zuk-Ramot</dc:creator>
    <dc:creator>Benjamin Sarusi</dc:creator>
    <dc:creator>Dov Brickner</dc:creator>
    <dc:creator>Ziva Schwartz</dc:creator>
    <dc:creator>Einat Sheiner</dc:creator>
    <dc:creator>Rachel Marko</dc:creator>
    <dc:creator>Esther Katorza</dc:creator>
    <dc:creator>Joachim Thiery</dc:creator>
    <dc:creator>Georg Fiedler</dc:creator>
    <dc:creator>Matthias Bluher</dc:creator>
    <dc:creator>Michael Stumvoll</dc:creator>
    <dc:creator>Meir Stampfer</dc:creator>
    <dc:creator>The</dc:creator>
    <dc:identifier>doi:10.1056/NEJMoa0708681</dc:identifier>
    <dc:source>N Engl J Med, Vol. 359, No. 3. (17 July 2008), pp. 229-241.</dc:source>
    <dc:date>2008-07-17T16:07:15-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>N Engl J Med</prism:publicationName>
    <prism:volume>359</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>229</prism:startingPage>
    <prism:endingPage>241</prism:endingPage>
    <prism:category>diet</prism:category>
    <prism:category>dietaryfiber</prism:category>
    <prism:category>glycemic-load</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2762781">
    <title>Whole Grain Consumption and Body Mass Index in Adult Women: An Analysis of NHANES 1999-2000 and the USDA Pyramid Servings Database</title>
    <link>http://www.citeulike.org/user/omalbam/article/2762781</link>
    <description>&lt;i&gt;J Am Coll Nutr, Vol. 27, No. 1. (1 February 2008), pp. 80-87.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Objective: To examine the relationship between whole grain consumption and body mass index (BMI) in a sample of American adult women. Methods: Dietary intake data from the National Health and Nutrition Examination Survey 1999-2000 were linked to the USDA Pyramid Servings Database. Women 19 years of age and older (n = 2,092) were classified into groups based on their average whole grain (WG) intake: 0 servings, more than 0 but less than 1 serving, and [&#8805;]1 servings per day. Within these classifications, mean BMI, mean waist circumference and percent overweight/obese (BMI [&#8805;] 25) were identified as primary dependent variables. Regression and logistic regression analyses were used to assess associations between BMI, waist circumference and percent of the population overweight/obese (BMI [&#8805;]25) and WG consumption. Results: Women consuming at least one serving of WG had a significantly lower mean BMI and waist circumference than women with no WG consumption (p &#60; 0.05). Multiple regression analysis showed a significant inverse relationship between BMI and whole grain intake after adjustment for age, energy intake, dietary fiber and alcohol intake (p = 0.004). This effect was mildly attenuated but remained significant after further adjustment for level of physical activity, smoking status, ethnicity and education (p = 0.018). The odds ratio for having a BMI [&#8805;] 25 was 1.47 (95% CI 1.12-1.94; p for trend 0.013) for women consuming no WG compared to those consuming at least one serving, after adjustment for all covariates. Conclusions: These data support other research suggesting increased WG intake may contribute to a healthy body weight in adult women.</description>
    <dc:title>Whole Grain Consumption and Body Mass Index in Adult Women: An Analysis of NHANES 1999-2000 and the USDA Pyramid Servings Database</dc:title>

    <dc:creator>Carolyn Good</dc:creator>
    <dc:creator>Norton Holschuh</dc:creator>
    <dc:creator>Ann Albertson</dc:creator>
    <dc:creator>Alison Eldridge</dc:creator>
    <dc:source>J Am Coll Nutr, Vol. 27, No. 1. (1 February 2008), pp. 80-87.</dc:source>
    <dc:date>2008-05-06T19:57:55-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>J Am Coll Nutr</prism:publicationName>
    <prism:volume>27</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>80</prism:startingPage>
    <prism:endingPage>87</prism:endingPage>
    <prism:category>diet</prism:category>
    <prism:category>dietaryfiber</prism:category>
    <prism:category>obesity</prism:category>
    <prism:category>risk</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2762736">
    <title>The Effects of 6-Week Low Glycemic Load Diet Based on Low Glycemic Index Foods in Overweight/Obese Children - Pilot Study</title>
    <link>http://www.citeulike.org/user/omalbam/article/2762736</link>
    <description>&lt;i&gt;J Am Coll Nutr, Vol. 27, No. 1. (1 February 2008), pp. 12-21.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Objective: To evaluate the effectiveness of a 6-week low Glycemic Load (GL) diet intervention based on low Glycemic Index (GI) foods on body weight, body composition, metabolic risk factors and satiety in overweight/obese pre-pubertal children. Methods: Following a pediatric examination 8 healthy, average age 11 year old, Caucasian, pre-pubertal overweight/obese (BMI = 24, 7 +/- 3.8 kg/m2) children participated in the study. The Low GL diet intervention was based on the replacement of at least 50% of the high GI foods with Low-GI foods. The children with one of their parents participated in weekly nutrition consultations. Body composition, fasting glucose, insulin, cholesterol and triglyceride were measured before and after the study. Dietary changes were made based on weekly 4-day food-diaries. Results: Despite no change in body weight, there was a significant (p &#60; 0.05) reduction in % body fat (29.4 +/- 4.2 vs. 25.4 +/- 5.3), Waist-to-Hip Ratio (WHR 0.87 +/- 0.053 vs. 0.86 +/- 0.05), decrease in self-reported hunger level (4.37 +/- 0.74 vs. 1.75 +/- 0.75) and the total number of risk factors (28 vs. 15). There was a strong negative correlation between fasting glucose and insulin levels at baseline and in the magnitude of change after the study (r = -0.93 and r = -0.85 respectively; p &#60; 0.01). Conclusions: A 6 week study demonstrated the practicality and effectiveness of this Low GL dietary approach. Despite of the unchanged body weight, Low GL diet consultations positively modified body fat content and cardiovascular risk factors in overweight or obese children.</description>
    <dc:title>The Effects of 6-Week Low Glycemic Load Diet Based on Low Glycemic Index Foods in Overweight/Obese Children - Pilot Study</dc:title>

    <dc:creator>Zsuzsanna Fajcsak</dc:creator>
    <dc:creator>Anita Gabor</dc:creator>
    <dc:creator>Victoria Kovacs</dc:creator>
    <dc:creator>Eva Martos</dc:creator>
    <dc:source>J Am Coll Nutr, Vol. 27, No. 1. (1 February 2008), pp. 12-21.</dc:source>
    <dc:date>2008-05-06T19:53:40-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>J Am Coll Nutr</prism:publicationName>
    <prism:volume>27</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>12</prism:startingPage>
    <prism:endingPage>21</prism:endingPage>
    <prism:category>diet</prism:category>
    <prism:category>glycemic-load</prism:category>
    <prism:category>therapy</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2638365">
    <title>Dietary intake and the development of the metabolic syndrome: the Atherosclerosis Risk in Communities study.</title>
    <link>http://www.citeulike.org/user/omalbam/article/2638365</link>
    <description>&lt;i&gt;Circulation, Vol. 117, No. 6. (12 February 2008), pp. 754-761.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: The role of diet in the origin of metabolic syndrome (MetSyn) is not well understood; thus, we sought to evaluate the relationship between incident MetSyn and dietary intake using prospective data from 9514 participants (age, 45 to 64 years) enrolled in the Atherosclerosis Risk in Communities (ARIC) study. METHODS AND RESULTS: Dietary intake was assessed at baseline via a 66-item food frequency questionnaire. We used principal-components analysis to derive &#34;Western&#34; and &#34;prudent&#34; dietary patterns from 32 food groups and evaluated 10 food groups used in previous studies of the ARIC cohort. MetSyn was defined by American Heart Association guidelines. Proportional-hazards regression was used. Over 9 years of follow-up, 3782 incident cases of MetSyn were identified. After adjustment for demographic factors, smoking, physical activity, and energy intake, consumption of a Western dietary pattern (P(trend)=0.03) was adversely associated with incident MetSyn. After further adjustment for intake of meat, dairy, fruits and vegetables, refined grains, and whole grains, analysis of individual food groups revealed that meat (P(trend)&#60;0.001), fried foods (P(trend)=0.02), and diet soda (P(trend)=&#60; 0.001) also were adversely associated with incident MetSyn, whereas dairy consumption (P(trend)=0.006) was beneficial. No associations were observed between incident MetSyn and a prudent dietary pattern or intakes of whole grains, refined grains, fruits and vegetables, nuts, coffee, or sweetened beverages. CONCLUSIONS: These prospective findings suggest that consumption of a Western dietary pattern, meat, and fried foods promotes the incidence of MetSyn, whereas dairy consumption provides some protection. The diet soda association was not hypothesized and deserves further study.</description>
    <dc:title>Dietary intake and the development of the metabolic syndrome: the Atherosclerosis Risk in Communities study.</dc:title>

    <dc:creator>PL Lutsey</dc:creator>
    <dc:creator>LM Steffen</dc:creator>
    <dc:creator>J Stevens</dc:creator>
    <dc:identifier>doi:10.1161/CIRCULATIONAHA.107.716159</dc:identifier>
    <dc:source>Circulation, Vol. 117, No. 6. (12 February 2008), pp. 754-761.</dc:source>
    <dc:date>2008-04-07T17:53:31-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Circulation</prism:publicationName>
    <prism:issn>1524-4539</prism:issn>
    <prism:volume>117</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>754</prism:startingPage>
    <prism:endingPage>761</prism:endingPage>
    <prism:category>diet</prism:category>
    <prism:category>dietaryfiber</prism:category>
    <prism:category>metabolic-syndrome</prism:category>
    <prism:category>risk</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2638362">
    <title>Comparison of strategies for sustaining weight loss: the weight loss maintenance randomized controlled trial.</title>
    <link>http://www.citeulike.org/user/omalbam/article/2638362</link>
    <description>&lt;i&gt;JAMA : the journal of the American Medical Association, Vol. 299, No. 10. (12 March 2008), pp. 1139-1148.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;CONTEXT: Behavioral weight loss interventions achieve short-term success, but re-gain is common. OBJECTIVE: To compare 2 weight loss maintenance interventions with a self-directed control group. DESIGN, SETTING, AND PARTICIPANTS: Two-phase trial in which 1032 overweight or obese adults (38% African American, 63% women) with hypertension, dyslipidemia, or both who had lost at least 4 kg during a 6-month weight loss program (phase 1) were randomized to a weight-loss maintenance intervention (phase 2). Enrollment at 4 academic centers occurred August 2003-July 2004 and randomization, February-December 2004. Data collection was completed in June 2007. INTERVENTIONS: After the phase 1 weight-loss program, participants were randomized to one of the following groups for 30 months: monthly personal contact, unlimited access to an interactive technology-based intervention, or self-directed control. Main Outcome Changes in weight from randomization. RESULTS: Mean entry weight was 96.7 kg. During the initial 6-month program, mean weight loss was 8.5 kg. After randomization, weight regain occurred. Participants in the personal-contact group regained less weight (4.0 kg) than those in the self-directed group (5.5 kg; mean difference at 30 months, -1.5 kg; 95% confidence interval [CI], -2.4 to -0.6 kg; P = .001). At 30 months, weight regain did not differ between the interactive technology-based (5.2 kg) and self-directed groups (5.5 kg; mean difference -0.3 kg; 95% CI, -1.2 to 0.6 kg; P = .51); however, weight regain was lower in the interactive technology-based than in the self-directed group at 18 months (mean difference, -1.1 kg; 95% CI, -1.9 to -0.4 kg; P = .003) and at 24 months (mean difference, -0.9 kg; 95% CI, -1.7 to -0.02 kg; P = .04). At 30 months, the difference between the personal-contact and interactive technology-based group was -1.2 kg (95% CI -2.1 to -0.3; P = .008). Effects did not differ significantly by sex, race, age, and body mass index subgroups. Overall, 71% of study participants remained below entry weight. CONCLUSIONS: The majority of individuals who successfully completed an initial behavioral weight loss program maintained a weight below their initial level. Monthly brief personal contact provided modest benefit in sustaining weight loss, whereas an interactive technology-based intervention provided early but transient benefit. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00054925.</description>
    <dc:title>Comparison of strategies for sustaining weight loss: the weight loss maintenance randomized controlled trial.</dc:title>

    <dc:creator>LP Svetkey</dc:creator>
    <dc:creator>VJ Stevens</dc:creator>
    <dc:creator>PJ Brantley</dc:creator>
    <dc:creator>LJ Appel</dc:creator>
    <dc:creator>JF Hollis</dc:creator>
    <dc:creator>CM Loria</dc:creator>
    <dc:creator>WM Vollmer</dc:creator>
    <dc:creator>CM Gullion</dc:creator>
    <dc:creator>K Funk</dc:creator>
    <dc:creator>P Smith</dc:creator>
    <dc:creator>C Samuel-Hodge</dc:creator>
    <dc:creator>V Myers</dc:creator>
    <dc:creator>LF Lien</dc:creator>
    <dc:creator>D Laferriere</dc:creator>
    <dc:creator>B Kennedy</dc:creator>
    <dc:creator>GJ Jerome</dc:creator>
    <dc:creator>F Heinith</dc:creator>
    <dc:creator>DW Harsha</dc:creator>
    <dc:creator>P Evans</dc:creator>
    <dc:creator>TP Erlinger</dc:creator>
    <dc:creator>AT Dalcin</dc:creator>
    <dc:creator>J Coughlin</dc:creator>
    <dc:creator>J Charleston</dc:creator>
    <dc:creator>CM Champagne</dc:creator>
    <dc:creator>A Bauck</dc:creator>
    <dc:creator>JD Ard</dc:creator>
    <dc:creator>K Aicher</dc:creator>
    <dc:creator></dc:creator>
    <dc:identifier>doi:10.1001/jama.299.10.1139</dc:identifier>
    <dc:source>JAMA : the journal of the American Medical Association, Vol. 299, No. 10. (12 March 2008), pp. 1139-1148.</dc:source>
    <dc:date>2008-04-07T17:50:47-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>JAMA : the journal of the American Medical Association</prism:publicationName>
    <prism:issn>1538-3598</prism:issn>
    <prism:volume>299</prism:volume>
    <prism:number>10</prism:number>
    <prism:startingPage>1139</prism:startingPage>
    <prism:endingPage>1148</prism:endingPage>
    <prism:category>diet</prism:category>
    <prism:category>obesity</prism:category>
    <prism:category>rct</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2515496">
    <title>Whole grain foods for the prevention of type 2 diabetes mellitus.</title>
    <link>http://www.citeulike.org/user/omalbam/article/2515496</link>
    <description>&lt;i&gt;Cochrane Database Syst Rev, No. 1. (2008)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: Diet as one aspect of lifestyle is thought to be one of the modifiable risk factors for the development of type 2 diabetes mellitus (T2DM). Information is needed as to which components of the diet could be protective for this disease. OBJECTIVES: To asses the effects of whole-grain foods for the prevention of T2DM. SEARCH STRATEGY: We searched CENTRAL, MEDLINE, EMBASE, CINAHL and AMED. SELECTION CRITERIA: We selected cohort studies with a minimum duration of five years that assessed the association between intake of whole-grain foods or cereal fibre and incidence of T2DM. Randomised controlled trials lasting at least six weeks were selected that assessed the effect of a diet rich in whole-grain foods compared to a diet rich in refined grain foods on T2DM and its major risk factors. DATA COLLECTION AND ANALYSIS: Two authors independently selected the studies, assessed study quality and extracted data. Data of studies were not pooled because of methodological diversity. MAIN RESULTS: One randomised controlled trial and eleven prospective cohort studies were identified. The randomised controlled trial, which was of low methodological quality, reported the change in insulin sensitivity in 12 obese hyperinsulinemic participants after six-week long interventions. Intake of whole grain foods resulted in a slight improvement of insulin sensitivity and no adverse effects. Patient satisfaction, health related quality of life, total mortality and morbidity was not reported.Four of the eleven cohort studies measured cereal fibre intake, three studies whole grain intake and two studies both. Two studies measured the change in whole grain food intake and one of them also change in cereal fibre intake. The incidence of T2DM was assessed in nine studies and changes in weight gain in two studies. The prospective studies consistently showed a reduced risk for high intake of whole grain foods (27% to 30%) or cereal fibre (28% to 37%) on the development of T2DM. AUTHORS' CONCLUSIONS: The evidence from only prospective cohort trials is considered to be too weak to be able to draw a definite conclusion about the preventive effect of whole grain foods on the development of T2DM. Properly designed long-term randomised controlled trials are needed. To facilitate this, further mechanistic research should focus on finding a set of relevant intermediate endpoints for T2DM and on identifying genetic subgroups of the population at risk that are most susceptible to dietary intervention.</description>
    <dc:title>Whole grain foods for the prevention of type 2 diabetes mellitus.</dc:title>

    <dc:creator>M Priebe</dc:creator>
    <dc:creator>J van Binsbergen</dc:creator>
    <dc:creator>R de Vos</dc:creator>
    <dc:creator>R Vonk</dc:creator>
    <dc:identifier>doi:10.1002/14651858.CD006061.pub2</dc:identifier>
    <dc:source>Cochrane Database Syst Rev, No. 1. (2008)</dc:source>
    <dc:date>2008-03-11T16:06:05-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Cochrane Database Syst Rev</prism:publicationName>
    <prism:issn>1469-493X</prism:issn>
    <prism:number>1</prism:number>
    <prism:category>diabetes</prism:category>
    <prism:category>diet</prism:category>
    <prism:category>dietaryfiber</prism:category>
    <prism:category>insulinresistance</prism:category>
    <prism:category>risk</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2465814">
    <title>ChREBP, but not LXRs, is required for the induction of glucose-regulated genes in mouse liver</title>
    <link>http://www.citeulike.org/user/omalbam/article/2465814</link>
    <description>&lt;i&gt;J. Clin Invest, Vol. 118, No. 3. (March 2008), pp. 956-964.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The transcription factor carbohydrate-responsive element–binding protein (ChREBP) has emerged as a central regulator of lipid synthesis in liver because it is required for glucose-induced expression of the glycolytic enzyme liver–pyruvate kinase (L-PK) and acts in synergy with SREBP to induce lipogenic genes such as acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS). Liver X receptors (LXRs) are also important regulators of the lipogenic pathway, and the recent finding that ChREBP is a direct target of LXRs and that glucose itself can bind and activate LXRs prompted us to study the role of LXRs in the induction of glucose-regulated genes in liver. Using an LXR agonist in wild-type mice, we found that LXR stimulation did not promote ChREBP phosphorylation or nuclear localization in the absence of an increased intrahepatic glucose flux. Furthermore, the induction of ChREBP, L-PK, and ACC by glucose or high-carbohydrate diet was similar in LXRα/β knockout compared with wild-type mice, suggesting that the activation of these genes by glucose occurs by an LXR-independent mechanism. We used fluorescence resonance energy transfer analysis to demonstrate that glucose failed to promote the interaction of LXRα/β with specific cofactors. Finally, siRNA silencing of ChREBP in LXRα/β knockout hepatocytes abrogated glucose-induced expression of L-PK and ACC, further demonstrating the central role of ChREBP in glucose signaling. Taken together, our results demonstrate that glucose is required for ChREBP functional activity and that LXRs are not necessary for the induction of glucose-regulated genes in liver.</description>
    <dc:title>ChREBP, but not LXRs, is required for the induction of glucose-regulated genes in mouse liver</dc:title>

    <dc:source>J. Clin Invest, Vol. 118, No. 3. (March 2008), pp. 956-964.</dc:source>
    <dc:date>2008-03-04T17:01:41-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>J. Clin Invest</prism:publicationName>
    <prism:volume>118</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>956</prism:startingPage>
    <prism:endingPage>964</prism:endingPage>
    <prism:category>diet</prism:category>
    <prism:category>molecular</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2389303">
    <title>Low-carbohydrate-diet score and risk of type 2 diabetes in women</title>
    <link>http://www.citeulike.org/user/omalbam/article/2389303</link>
    <description>&lt;i&gt;Am J Clin Nutr, Vol. 87, No. 2. (1 February 2008), pp. 339-346.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Background: Low-carbohydrate weight-loss diets remain popular; however, the long-term effects of these diets are not known. Objective: The objective was to examine the association between low-carbohydrate-diet score and risk of type 2 diabetes Design: We prospectively examined the association between low-carbohydrate-diet score (based on percentage of energy as carbohydrate, fat, and protein) and risk of diabetes among 85 059 women in the Nurses' Health Study. Results: During 20 y of follow-up, we documented 4670 cases of type 2 diabetes. The multivariate relative risk (RR) of diabetes, after adjustment for body mass index and other covariates, in a comparison of the highest decile of low-carbohydrate-diet score with the lowest was 0.90 (95% CI: 0.78, 1.04; P for trend = 0.26). The multivariate RR for the comparison of extreme deciles of low-carbohydrate-diet score based on total carbohydrate, animal protein, and animal fat was 0.99 (95% CI: 0.85, 1.16; P for trend = 1.0), whereas the RR for a low-carbohydrate-diet score based on total carbohydrate, vegetable protein, and vegetable fat was 0.82 (95% CI: 0.71, 0.94; P for trend = 0.001). A higher dietary glycemic load was strongly associated with an increased risk of diabetes in a comparison of extreme deciles (RR: 2.47; 95% CI: 1.75, 3.47; P for trend &#60; 0.0001)). A higher carbohydrate consumption was also associated with an increased risk of diabetes in a comparison of extreme deciles (RR: 1.26; 95% CI: 1.07, 1.49; P for trend = 0.003). Conclusion: These data suggest that diets lower in carbohydrate and higher in fat and protein do not increase the risk of type 2 diabetes in women. In fact, diets rich in vegetable sources of fat and protein may modestly reduce the risk of diabetes.</description>
    <dc:title>Low-carbohydrate-diet score and risk of type 2 diabetes in women</dc:title>

    <dc:creator>Thomas Halton</dc:creator>
    <dc:creator>Simin Liu</dc:creator>
    <dc:creator>Joann Manson</dc:creator>
    <dc:creator>Frank Hu</dc:creator>
    <dc:source>Am J Clin Nutr, Vol. 87, No. 2. (1 February 2008), pp. 339-346.</dc:source>
    <dc:date>2008-02-16T23:29:17-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Am J Clin Nutr</prism:publicationName>
    <prism:volume>87</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>339</prism:startingPage>
    <prism:endingPage>346</prism:endingPage>
    <prism:category>diabetes</prism:category>
    <prism:category>diet</prism:category>
    <prism:category>glycemiapp</prism:category>
    <prism:category>risk</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2349240">
    <title>The Canadian Trial of Carbohydrates in Diabetes (CCD), a 1-y controlled trial of low-glycemic-index dietary carbohydrate in type 2 diabetes: no effect on glycated hemoglobin but reduction in C-reactive protein.</title>
    <link>http://www.citeulike.org/user/omalbam/article/2349240</link>
    <description>&lt;i&gt;Am J Clin Nutr, Vol. 87, No. 1. (January 2008), pp. 114-125.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: The optimal source and amount of dietary carbohydrate for managing type 2 diabetes (T2DM) are unknown. OBJECTIVE: We aimed to compare the effects of altering the glycemic index or the amount of carbohydrate on glycated hemoglobin (HbA(1c)), plasma glucose, lipids, and C-reactive protein (CRP) in T2DM patients. DESIGN: Subjects with T2DM managed by diet alone (n = 162) were randomly assigned to receive high-carbohydrate, high-glycemic-index (high-GI), high-carbohydrate, low-glycemic-index (low-GI), or low-carbohydrate, high-monounsaturated-fat (low-CHO) diets for 1 y. RESULTS: The high-GI, low-GI, and low-CHO diets contained, respectively, 47%, 52%, and 39% of energy as carbohydrate and 31%, 27%, and 40% of energy as fat; they had GIs of 63, 55, and 59, respectively. Body weight and HbA(1c) did not differ significantly between diets. Fasting glucose was higher (P = 0.041), but 2-h postload glucose was lower (P = 0.010) after 12 mo of the low-GI diet. With the low-GI diet, overall mean triacylglycerol was 12% higher and HDL cholesterol 4% lower than with the low-CHO diet (P &#60; 0.05), but the difference in the ratio of total to HDL cholesterol disappeared by 6 mo (time x diet interaction, P = 0.044). Overall mean CRP with the low-GI diet, 1.95 mg/L, was 30% less than that with the high-GI diet, 2.75 mg/L (P = 0.0078); the concentration with the low-CHO diet, 2.35 mg/L, was intermediate. CONCLUSIONS: In subjects with T2DM managed by diet alone with optimal glycemic control, long-term HbA(1c) was not affected by altering the GI or the amount of dietary carbohydrate. Differences in total:HDL cholesterol among diets had disappeared by 6 mo. However, because of sustained reductions in postprandial glucose and CRP, a low-GI diet may be preferred for the dietary management of T2DM.</description>
    <dc:title>The Canadian Trial of Carbohydrates in Diabetes (CCD), a 1-y controlled trial of low-glycemic-index dietary carbohydrate in type 2 diabetes: no effect on glycated hemoglobin but reduction in C-reactive protein.</dc:title>

    <dc:creator>TM Wolever</dc:creator>
    <dc:creator>AL Gibbs</dc:creator>
    <dc:creator>C Mehling</dc:creator>
    <dc:creator>JL Chiasson</dc:creator>
    <dc:creator>PW Connelly</dc:creator>
    <dc:creator>RG Josse</dc:creator>
    <dc:creator>LA Leiter</dc:creator>
    <dc:creator>P Maheux</dc:creator>
    <dc:creator>R Rabasa-Lhoret</dc:creator>
    <dc:creator>NW Rodger</dc:creator>
    <dc:creator>EA Ryan</dc:creator>
    <dc:source>Am J Clin Nutr, Vol. 87, No. 1. (January 2008), pp. 114-125.</dc:source>
    <dc:date>2008-02-07T14:24:03-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Am J Clin Nutr</prism:publicationName>
    <prism:issn>0002-9165</prism:issn>
    <prism:volume>87</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>114</prism:startingPage>
    <prism:endingPage>125</prism:endingPage>
    <prism:category>crp</prism:category>
    <prism:category>diabetes</prism:category>
    <prism:category>diet</prism:category>
    <prism:category>glycemiapp</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/1453710">
    <title>Purine-rich foods, dairy and protein intake, and the risk of gout in men.</title>
    <link>http://www.citeulike.org/user/omalbam/article/1453710</link>
    <description>&lt;i&gt;N Engl J Med, Vol. 350, No. 11. (11 March 2004), pp. 1093-1103.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: Various purine-rich foods and high protein intake have long been thought to be risk factors for gout. Similarly, the possibility that the consumption of dairy products has a role in protecting against gout has been raised by metabolic studies. We prospectively investigated the association of these dietary factors with new cases of gout. METHODS: Over a 12-year period, we prospectively examined the relationship between purported dietary risk factors and new cases of gout among 47,150 men who had no history of gout at base line. We used a supplementary questionnaire to ascertain whether participants met the American College of Rheumatology survey criteria for gout. Diet was assessed every four years by means of a food-frequency questionnaire. RESULTS: During the 12 years of the study, we documented 730 confirmed new cases of gout. The multivariate relative risk of gout among men in the highest quintile of meat intake, as compared with those in the lowest quintile, was 1.41 (95 percent confidence interval, 1.07 to 1.86; P for trend = 0.02), and the corresponding relative risk associated with seafood intake was 1.51 (95 percent confidence interval, 1.17 to 1.95; P for trend = 0.02). In contrast, the incidence of gout decreased with increasing intake of dairy products; the multivariate relative risk among men in the highest quintile, as compared with those in the lowest quintile, was 0.56 (95 percent confidence interval, 0.42 to 0.74; P for trend &#60;0.001). The level of consumption of purine-rich vegetables and the total protein intake were not associated with an increased risk of gout. CONCLUSIONS: Higher levels of meat and seafood consumption are associated with an increased risk of gout, whereas a higher level of consumption of dairy products is associated with a decreased risk. Moderate intake of purine-rich vegetables or protein is not associated with an increased risk of gout.</description>
    <dc:title>Purine-rich foods, dairy and protein intake, and the risk of gout in men.</dc:title>

    <dc:creator>HK Choi</dc:creator>
    <dc:creator>K Atkinson</dc:creator>
    <dc:creator>EW Karlson</dc:creator>
    <dc:creator>W Willett</dc:creator>
    <dc:creator>G Curhan</dc:creator>
    <dc:identifier>doi:10.1056/NEJMoa035700</dc:identifier>
    <dc:source>N Engl J Med, Vol. 350, No. 11. (11 March 2004), pp. 1093-1103.</dc:source>
    <dc:date>2007-07-13T09:51:55-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>N Engl J Med</prism:publicationName>
    <prism:issn>1533-4406</prism:issn>
    <prism:volume>350</prism:volume>
    <prism:number>11</prism:number>
    <prism:startingPage>1093</prism:startingPage>
    <prism:endingPage>1103</prism:endingPage>
    <prism:category>diet</prism:category>
    <prism:category>metabolism</prism:category>
    <prism:category>risk</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2328068">
    <title>Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study</title>
    <link>http://www.citeulike.org/user/omalbam/article/2328068</link>
    <description>&lt;i&gt;BMJ (31 January 2008), bmj.39449.819271.BE.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Objective To examine the relation between intake of sugar sweetened soft drinks and fructose and the risk of incident gout in men. Design Prospective cohort over 12 years. Setting Health professionals follow-up study. Participants 46 393 men with no history of gout at baseline who provided information on intake of soft drinks and fructose through validated food frequency questionnaires. Main outcome measure Incident cases of gout meeting the American College of Rheumatology survey criteria for gout. Results During the 12 years of follow-up 755 confirmed incident cases of gout were reported. Increasing intake of sugar sweetened soft drinks was associated with an increasing risk of gout. Compared with consumption of less than one serving of sugar sweetened soft drinks a month the multivariate relative risk of gout for 5-6 servings a week was 1.29 (95% confidence interval 1.00 to 1.68), for one serving a day was 1.45 (1.02 to 2.08), and for two or more servings a day was 1.85 (1.08 to 3.16; P for trend=0.002). Diet soft drinks were not associated with risk of gout (P for trend=0.99). The multivariate relative risk of gout according to increasing fifths of fructose intake were 1.00, 1.29, 1.41, 1.84, and 2.02 (1.49 to 2.75; P for trend &#60;0.001). Other major contributors to fructose intake such as total fruit juice or fructose rich fruits (apples and oranges) were also associated with a higher risk of gout (P values for trend &#60;0.05). Conclusions Prospective data suggest that consumption of sugar sweetened soft drinks and fructose is strongly associated with an increased risk of gout in men. Furthermore, fructose rich fruits and fruit juices may also increase the risk. Diet soft drinks were not associated with the risk of gout. 10.1136/bmj.39449.819271.BE</description>
    <dc:title>Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study</dc:title>

    <dc:creator>Hyon Choi</dc:creator>
    <dc:creator>Gary Curhan</dc:creator>
    <dc:identifier>doi:10.1136/bmj.39449.819271.BE</dc:identifier>
    <dc:source>BMJ (31 January 2008), bmj.39449.819271.BE.</dc:source>
    <dc:date>2008-02-04T03:45:23-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>BMJ</prism:publicationName>
    <prism:startingPage>bmj.39449.819271.BE</prism:startingPage>
    <prism:category>diet</prism:category>
    <prism:category>foodsfunctional</prism:category>
    <prism:category>metabolism</prism:category>
    <prism:category>risk</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2330323">
    <title>Prospective study of dietary carbohydrates, glycemic index, glycemic load, and incidence of type 2 diabetes mellitus in middle-aged Chinese women.</title>
    <link>http://www.citeulike.org/user/omalbam/article/2330323</link>
    <description>&lt;i&gt;Arch Intern Med, Vol. 167, No. 21. (26 November 2007), pp. 2310-2316.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: Much uncertainty exists about the role of dietary glycemic index and glycemic load in the development of type 2 diabetes mellitus, especially in populations that traditionally subsist on a diet high in carbohydrates. METHODS: We observed a cohort of 64,227 Chinese women with no history of diabetes or other chronic disease at baseline for 4.6 years. In-person interviews were conducted to collect data on dietary habits, physical activity, and other relevant information using a validated questionnaire. Incident diabetes cases were identified via in-person follow-up. Associations between dietary carbohydrate intake, glycemic index, and glycemic load and diabetes incidence were evaluated using multivariable Cox proportional hazards models. RESULTS: We identified 1,608 incident cases of type 2 diabetes mellitus in 297,755 person-years of follow-up. Dietary carbohydrate intake and consumption of rice were positively associated with risk of developing type 2 diabetes mellitus. The multivariable-adjusted estimates of relative risk comparing the highest vs the lowest quintiles of intake were 1.28 (95% confidence interval, 1.09-1.50) for carbohydrates and 1.78 (95% confidence interval, 1.48-2.15) for rice. The relative risk for increasing quintiles of intake was 1.00, 1.04, 1.02, 1.09, and 1.21 (95% confidence interval, 1.03-1.43) for dietary glycemic index and 1.00, 1.06, 0.97, 1.23, and 1.34 (95% confidence interval, 1.13-1.58) for dietary glycemic load. CONCLUSION: High intake of foods with a high glycemic index and glycemic load, especially rice, the main carbohydrate-contributing food in this population, may increase the risk of type 2 diabetes mellitus in Chinese women.</description>
    <dc:title>Prospective study of dietary carbohydrates, glycemic index, glycemic load, and incidence of type 2 diabetes mellitus in middle-aged Chinese women.</dc:title>

    <dc:creator>R Villegas</dc:creator>
    <dc:creator>S Liu</dc:creator>
    <dc:creator>YT Gao</dc:creator>
    <dc:creator>G Yang</dc:creator>
    <dc:creator>H Li</dc:creator>
    <dc:creator>W Zheng</dc:creator>
    <dc:creator>XO Shu</dc:creator>
    <dc:identifier>doi:10.1001/archinte.167.21.2310</dc:identifier>
    <dc:source>Arch Intern Med, Vol. 167, No. 21. (26 November 2007), pp. 2310-2316.</dc:source>
    <dc:date>2008-02-04T18:47:02-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Arch Intern Med</prism:publicationName>
    <prism:issn>0003-9926</prism:issn>
    <prism:volume>167</prism:volume>
    <prism:number>21</prism:number>
    <prism:startingPage>2310</prism:startingPage>
    <prism:endingPage>2316</prism:endingPage>
    <prism:category>diabetes</prism:category>
    <prism:category>diet</prism:category>
    <prism:category>risk</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/1604513">
    <title>Effect of 6-month calorie restriction on biomarkers of longevity, metabolic adaptation, and oxidative stress in overweight individuals: a randomized controlled trial.</title>
    <link>http://www.citeulike.org/user/omalbam/article/1604513</link>
    <description>&lt;i&gt;JAMA, Vol. 295, No. 13. (5 April 2006), pp. 1539-1548.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;CONTEXT: Prolonged calorie restriction increases life span in rodents. Whether prolonged calorie restriction affects biomarkers of longevity or markers of oxidative stress, or reduces metabolic rate beyond that expected from reduced metabolic mass, has not been investigated in humans. OBJECTIVE: To examine the effects of 6 months of calorie restriction, with or without exercise, in overweight, nonobese (body mass index, 25 to &#60;30) men and women. DESIGN, SETTING, AND PARTICIPANTS: Randomized controlled trial of healthy, sedentary men and women (N = 48) conducted between March 2002 and August 2004 at a research center in Baton Rouge, La. INTERVENTION: Participants were randomized to 1 of 4 groups for 6 months: control (weight maintenance diet); calorie restriction (25% calorie restriction of baseline energy requirements); calorie restriction with exercise (12.5% calorie restriction plus 12.5% increase in energy expenditure by structured exercise); very low-calorie diet (890 kcal/d until 15% weight reduction, followed by a weight maintenance diet). MAIN OUTCOME MEASURES: Body composition; dehydroepiandrosterone sulfate (DHEAS), glucose, and insulin levels; protein carbonyls; DNA damage; 24-hour energy expenditure; and core body temperature. RESULTS: Mean (SEM) weight change at 6 months in the 4 groups was as follows: controls, -1.0% (1.1%); calorie restriction, -10.4% (0.9%); calorie restriction with exercise, -10.0% (0.8%); and very low-calorie diet, -13.9% (0.7%). At 6 months, fasting insulin levels were significantly reduced from baseline in the intervention groups (all P&#60;.01), whereas DHEAS and glucose levels were unchanged. Core body temperature was reduced in the calorie restriction and calorie restriction with exercise groups (both P&#60;.05). After adjustment for changes in body composition, sedentary 24-hour energy expenditure was unchanged in controls, but decreased in the calorie restriction (-135 kcal/d [42 kcal/d]), calorie restriction with exercise (-117 kcal/d [52 kcal/d]), and very low-calorie diet (-125 kcal/d [35 kcal/d]) groups (all P&#60;.008). These &#34;metabolic adaptations&#34; (~ 6% more than expected based on loss of metabolic mass) were statistically different from controls (P&#60;.05). Protein carbonyl concentrations were not changed from baseline to month 6 in any group, whereas DNA damage was also reduced from baseline in all intervention groups (P &#60;.005). CONCLUSIONS: Our findings suggest that 2 biomarkers of longevity (fasting insulin level and body temperature) are decreased by prolonged calorie restriction in humans and support the theory that metabolic rate is reduced beyond the level expected from reduced metabolic body mass. Studies of longer duration are required to determine if calorie restriction attenuates the aging process in humans. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT00099151.</description>
    <dc:title>Effect of 6-month calorie restriction on biomarkers of longevity, metabolic adaptation, and oxidative stress in overweight individuals: a randomized controlled trial.</dc:title>

    <dc:creator>LK Heilbronn</dc:creator>
    <dc:creator>L de Jonge</dc:creator>
    <dc:creator>MI Frisard</dc:creator>
    <dc:creator>JP DeLany</dc:creator>
    <dc:creator>DE Larson-Meyer</dc:creator>
    <dc:creator>J Rood</dc:creator>
    <dc:creator>T Nguyen</dc:creator>
    <dc:creator>CK Martin</dc:creator>
    <dc:creator>J Volaufova</dc:creator>
    <dc:creator>MM Most</dc:creator>
    <dc:creator>FL Greenway</dc:creator>
    <dc:creator>SR Smith</dc:creator>
    <dc:creator>WA Deutsch</dc:creator>
    <dc:creator>DA Williamson</dc:creator>
    <dc:creator>E Ravussin</dc:creator>
    <dc:creator></dc:creator>
    <dc:identifier>doi:10.1001/jama.295.13.1539</dc:identifier>
    <dc:source>JAMA, Vol. 295, No. 13. (5 April 2006), pp. 1539-1548.</dc:source>
    <dc:date>2007-08-29T10:03:01-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>JAMA</prism:publicationName>
    <prism:issn>1538-3598</prism:issn>
    <prism:volume>295</prism:volume>
    <prism:number>13</prism:number>
    <prism:startingPage>1539</prism:startingPage>
    <prism:endingPage>1548</prism:endingPage>
    <prism:category>aging</prism:category>
    <prism:category>diet</prism:category>
    <prism:category>insulinresistance</prism:category>
    <prism:category>metabolism</prism:category>
    <prism:category>obesity</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2285958">
    <title>Loss of 50% of excess weight using a very low energy diet improves insulin-stimulated glucose disposal and skeletal muscle insulin signalling in obese insulin-treated type 2 diabetic patients</title>
    <link>http://www.citeulike.org/user/omalbam/article/2285958</link>
    <description>&lt;i&gt;Diabetologia, Vol. 51, No. 2. (1 February 2008), pp. 309-319.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Abstract Aims/hypothesis&#160;&#160;Both energy restriction (ER) per se and weight loss improve glucose metabolism in obese insulin-treated type 2 diabetic patients. Short-term ER decreases basal endogenous glucose production (EGP) but not glucose disposal. In contrast the blood glucose-lowering mechanism of long-term ER with substantial weight loss has not been fully elucidated. The aim of this study was to investigate the effect of loss of 50% of excess weight [50% excess weight reduction (EWR)] on EGP, whole-body insulin sensitivity and the disturbed myocellular insulin-signalling pathway in ten obese insulin-treated type 2 diabetic patients. Methods&#160;&#160;A euglycaemic–hyperinsulinaemic clamp with stable isotopes ([6,6-2H2]glucose and [2H5]glycerol) combined with skeletal muscle biopsies was performed during a very low energy diet (VLED; 1,883&#160;kJ/day) on day&#160;2 and again after 50% EWR. Oral blood glucose-lowering agents and insulin were discontinued 3&#160;weeks prior to the VLED and at the start of the VLED, respectively. Results&#160;&#160;Loss of 50% EWR (20.3 ± 2.2 kg from day&#160;2 to day of 50% EWR) normalised basal EGP and improved insulin sensitivity, especially insulin-stimulated glucose disposal (18.8 ± 2.0 to 39.1 ± 2.8&#160;μmol kg fat-free mass−1 min−1, p = 0.001). The latter was accompanied by improved insulin signalling at the level of the recently discovered protein kinase B/Akt substrates AS160 and PRAS40 along with a decrease in intramyocellular lipid (IMCL) content. Conclusions/interpretation&#160;&#160;Considerable weight loss in obese, insulin-treated type 2 diabetic patients normalises basal EGP and improves insulin sensitivity resulting from an improvement in insulin signal transduction in skeletal muscle. The decrease in IMCL might contribute to this effect.</description>
    <dc:title>Loss of 50% of excess weight using a very low energy diet improves insulin-stimulated glucose disposal and skeletal muscle insulin signalling in obese insulin-treated type 2 diabetic patients</dc:title>

    <dc:creator>I Jazet</dc:creator>
    <dc:creator>G Schaart</dc:creator>
    <dc:creator>A Gastaldelli</dc:creator>
    <dc:creator>E Ferrannini</dc:creator>
    <dc:creator>M Hesselink</dc:creator>
    <dc:creator>P Schrauwen</dc:creator>
    <dc:creator>J Romijn</dc:creator>
    <dc:creator>J Maassen</dc:creator>
    <dc:creator>H Pijl</dc:creator>
    <dc:creator>D Ouwens</dc:creator>
    <dc:creator>A Meinders</dc:creator>
    <dc:identifier>doi:10.1007/s00125-007-0862-2</dc:identifier>
    <dc:source>Diabetologia, Vol. 51, No. 2. (1 February 2008), pp. 309-319.</dc:source>
    <dc:date>2008-01-24T20:50:41-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Diabetologia</prism:publicationName>
    <prism:volume>51</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>309</prism:startingPage>
    <prism:endingPage>319</prism:endingPage>
    <prism:category>diabetes</prism:category>
    <prism:category>diet</prism:category>
    <prism:category>insulinresistance</prism:category>
    <prism:category>obesity</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2280722">
    <title>Effect of dairy calcium or supplementary calcium intake on postprandial fat metabolism, appetite, and subsequent energy intake</title>
    <link>http://www.citeulike.org/user/omalbam/article/2280722</link>
    <description>&lt;i&gt;Am J Clin Nutr, Vol. 85, No. 3. (1 March 2007), pp. 678-687.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Background: High calcium intake has been shown to increase fecal fat excretion. Objective: Our aim was to examine whether a high calcium intake from dairy products or from supplements affects postprandial fat metabolism and appetite through fat malabsorption. Design: Four different isocaloric meals were tested in 18 subjects according to a randomized crossover design. The test meals contained high (HC meal: 172 mg/MJ), medium (MC meal: 84 mg/MJ), or low (LC meal: 15 mg/MJ) amounts of calcium from dairy products or a high amount of calcium given as a calcium carbonate supplement (Suppl meal: 183 mg/MJ). Concentrations of plasma total triacylglycerol, chylomicron triacylglycerol, serum total cholesterol, HDL cholesterol, cholecystokinin, glucagon-like peptide 1, ghrelin, peptide YY, glucose, and insulin and appetite sensation were measured before and at regular intervals until 420 min postprandially. Results: Dairy calcium significantly diminished the postprandial lipid response. The baseline adjusted area under the curve for chylomicron triacylglycerol was approx17% lower after the MC meal (P = 0.02) and approx19% lower after the HC meal (P = 0.007) than after the LC meal and approx15% lower after the MC meal (P = 0.0495) and approx17% lower after the HC meal (P = 0.02) than after the Suppl meal. No consistent effects of calcium on appetite sensation, or on energy intake at the subsequent meal, or on the postprandial responses of cholecystokinin, glucagon-like peptide 1, ghrelin, peptide YY, insulin, or glucose were observed. Conclusions: Increased calcium intakes from dairy products attenuate postprandial lipidemia, most probably because of reduced fat absorption, whereas supplementary calcium carbonate does not exert such an effect. This may be due to differences in the chemical form of calcium or to cofactors in dairy products. Calcium did not affect appetite sensation, glucose metabolism, or gut hormone secretion.</description>
    <dc:title>Effect of dairy calcium or supplementary calcium intake on postprandial fat metabolism, appetite, and subsequent energy intake</dc:title>

    <dc:creator>Janne Lorenzen</dc:creator>
    <dc:creator>Sanne Nielsen</dc:creator>
    <dc:creator>Jens Holst</dc:creator>
    <dc:creator>Inge Tetens</dc:creator>
    <dc:creator>Jens Rehfeld</dc:creator>
    <dc:creator>Arne Astrup</dc:creator>
    <dc:source>Am J Clin Nutr, Vol. 85, No. 3. (1 March 2007), pp. 678-687.</dc:source>
    <dc:date>2008-01-23T14:09:21-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Am J Clin Nutr</prism:publicationName>
    <prism:volume>85</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>678</prism:startingPage>
    <prism:endingPage>687</prism:endingPage>
    <prism:category>calcium</prism:category>
    <prism:category>diet</prism:category>
    <prism:category>hplp</prism:category>
    <prism:category>physiology</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2232701">
    <title>The science behind dietary omega-3 fatty acids</title>
    <link>http://www.citeulike.org/user/omalbam/article/2232701</link>
    <description>&lt;i&gt;CMAJ, Vol. 178, No. 2. (15 January 2008), pp. 177-180.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;10.1503/cmaj.071356</description>
    <dc:title>The science behind dietary omega-3 fatty acids</dc:title>

    <dc:creator>Marc Surette</dc:creator>
    <dc:identifier>doi:10.1503/cmaj.071356</dc:identifier>
    <dc:source>CMAJ, Vol. 178, No. 2. (15 January 2008), pp. 177-180.</dc:source>
    <dc:date>2008-01-15T00:53:52-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>CMAJ</prism:publicationName>
    <prism:volume>178</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>177</prism:startingPage>
    <prism:endingPage>180</prism:endingPage>
    <prism:category>diet</prism:category>
    <prism:category>foodsfunctional</prism:category>
    <prism:category>metabolism</prism:category>
    <prism:category>physiology</prism:category>
    <prism:category>w3</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2232660">
    <title>Fish oil and omega-3 fatty acids</title>
    <link>http://www.citeulike.org/user/omalbam/article/2232660</link>
    <description>&lt;i&gt;CMAJ, Vol. 178, No. 2. (15 January 2008), 150.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;10.1503/cmaj.071754</description>
    <dc:title>Fish oil and omega-3 fatty acids</dc:title>

    <dc:creator>David Jenkins</dc:creator>
    <dc:creator>Andrea Josse</dc:creator>
    <dc:identifier>doi:10.1503/cmaj.071754</dc:identifier>
    <dc:source>CMAJ, Vol. 178, No. 2. (15 January 2008), 150.</dc:source>
    <dc:date>2008-01-15T00:39:20-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>CMAJ</prism:publicationName>
    <prism:volume>178</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>150</prism:startingPage>
    <prism:category>diet</prism:category>
    <prism:category>foodsfunctional</prism:category>
    <prism:category>w3</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2214801">
    <title>Nutrition recommendations and interventions for diabetes: a position statement of the American Diabetes Association.</title>
    <link>http://www.citeulike.org/user/omalbam/article/2214801</link>
    <description>&lt;i&gt;Diabetes Care, Vol. 31 Suppl 1 (January 2008)&lt;/i&gt;</description>
    <dc:title>Nutrition recommendations and interventions for diabetes: a position statement of the American Diabetes Association.</dc:title>

    <dc:creator></dc:creator>
    <dc:creator>JP Bantle</dc:creator>
    <dc:creator>J Wylie-Rosett</dc:creator>
    <dc:creator>AL Albright</dc:creator>
    <dc:creator>CM Apovian</dc:creator>
    <dc:creator>NG Clark</dc:creator>
    <dc:creator>MJ Franz</dc:creator>
    <dc:creator>BJ Hoogwerf</dc:creator>
    <dc:creator>AH Lichtenstein</dc:creator>
    <dc:creator>E Mayer-Davis</dc:creator>
    <dc:creator>AD Mooradian</dc:creator>
    <dc:creator>ML Wheeler</dc:creator>
    <dc:identifier>doi:10.2337/dc08-S061</dc:identifier>
    <dc:source>Diabetes Care, Vol. 31 Suppl 1 (January 2008)</dc:source>
    <dc:date>2008-01-10T15:28:49-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Diabetes Care</prism:publicationName>
    <prism:issn>1935-5548</prism:issn>
    <prism:volume>31 Suppl 1</prism:volume>
    <prism:category>diabetes</prism:category>
    <prism:category>diet</prism:category>
    <prism:category>guidelines</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2214634">
    <title>Acute Effect of Poly-gamma-Glutamic Acid on Calcium Absorption in Post-Menopausal Women</title>
    <link>http://www.citeulike.org/user/omalbam/article/2214634</link>
    <description>&lt;i&gt;J Am Coll Nutr, Vol. 26, No. 6. (1 December 2007), pp. 645-649.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Objective: Poly-gamma-glutamic acid (PGA) increases calcium (Ca) solubility in vitro and in vivo, and is associated with reduced bone loss in post-menopausal Japanese women. This study is the first to examine the effect of PGA on Ca absorption in humans. Methods: A single-blind, randomized, crossover study with a 34 week wash-out was performed to determine the effect of PGA (80.6% glutamic acids) on Ca absorption measured by the double stable isotope method. Twenty-four healthy, non-smoking, postmenopausal women (mean age: 56.4 +/- SE 0.9) were given 200 g of orange juice containing 200 mg Ca as Ca-44 enriched CaCO3, with or without 60 mg of PGA, after an overnight fast. The two tests were separated by 34 weeks. An intravenous injection of Ca-42 (CaCl2 solution) was given 30 min after consuming the drink and a complete urine collection carried out from 2448 h post-dosing. Ca absorption was calculated from the Ca isotope ratios measured by thermal ionization quadrupole mass spectrometry (TIQMS). Results: Mean Ca absorption with PGA was significantly higher (P &#60; 0.01) than without PGA, 39.1 (SE 1.6) % and 34.6 (SE 1.9) %, respectively. The effect of PGA on increasing Ca absorption was more marked in a sub-group of subjects whose baseline Ca absorption (without PGA) was lower than the population mean value. Conclusion: Postmenopausal women who received a single dose of PGA increased their intestinal Ca absorption particularly those individuals with lower basal absorptive capacity.</description>
    <dc:title>Acute Effect of Poly-gamma-Glutamic Acid on Calcium Absorption in Post-Menopausal Women</dc:title>

    <dc:creator>Hiroyuki Tanimoto</dc:creator>
    <dc:creator>Tom Fox</dc:creator>
    <dc:creator>John Eagles</dc:creator>
    <dc:creator>Hitoshi Satoh</dc:creator>
    <dc:creator>Hiroko Nozawa</dc:creator>
    <dc:creator>Atsushi Okiyama</dc:creator>
    <dc:creator>Yasushi Morinaga</dc:creator>
    <dc:creator>Susan Fairweather-Tait</dc:creator>
    <dc:source>J Am Coll Nutr, Vol. 26, No. 6. (1 December 2007), pp. 645-649.</dc:source>
    <dc:date>2008-01-10T14:47:10-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>J Am Coll Nutr</prism:publicationName>
    <prism:volume>26</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>645</prism:startingPage>
    <prism:endingPage>649</prism:endingPage>
    <prism:category>diet</prism:category>
    <prism:category>foodsfunctional</prism:category>
    <prism:category>mineral</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2214613">
    <title>Beta-Glucan from Two Sources of Oat Concentrates Affect Postprandial Glycemia in Relation to the Level of Viscosity</title>
    <link>http://www.citeulike.org/user/omalbam/article/2214613</link>
    <description>&lt;i&gt;J Am Coll Nutr, Vol. 26, No. 6. (1 December 2007), pp. 639-644.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Objective: Soluble dietary fiber has been shown to attenuate the postprandial rise in blood glucose levels and reduce the risk of type 2 diabetes and cardiovascular disease. This effect seems to be related to its rheological properties including viscosity. We examined the intra-fiber variability between two different processing methods of concentrating -glucan from oats (aqueous vs. enzymatic) in relation to the level of viscosity of -glucan and its effect on postprandial glycemia in healthy individuals. Design: In an acute, randomized, double-blind, crossover study, 11 healthy subjects (gender: 5M:6F; age: 34 +/- 5 years; BMI: 23 +/- 0.8 kg/m2) were randomly assigned, on three separate occasions, to consume one of three fiber-matched treatments along with a 75g oral glucose drink. The enzymatically processed -glucan (Oat-A) differed from -glucan processed through the aqueous method (Oat-B) solely with regard to viscosity. Finger-prick capillary blood samples were obtained at fasting and at 15, 30, 45, 60, 90 and 120 min after the start of the test drink. The viscosities of the fiber drinks were determined (Paar Physica UDS200 viscometer). Results: Rheological measurements demonstrated that Oat-A had a significantly higher viscosity than Oat-B and control at 5, 15, 30, 60, and 120 min (p &#60; 0.001). The incremental area under the glucose curve (AUC) on Oat-A was 19.6% and 17% lower than that of Oat-B and control, respectively (p &#60; 0.01). Conclusions: This study shows that processing oat -glucan through enzymatic, rather than by aqueous methods, preserves the viscosity and improves postprandial glycemic control.</description>
    <dc:title>Beta-Glucan from Two Sources of Oat Concentrates Affect Postprandial Glycemia in Relation to the Level of Viscosity</dc:title>

    <dc:creator>Shirin Panahi</dc:creator>
    <dc:creator>Adish Ezatagha</dc:creator>
    <dc:creator>Feral Temelli</dc:creator>
    <dc:creator>Thavaratnam Vasanthan</dc:creator>
    <dc:creator>Vladimir Vuksan</dc:creator>
    <dc:source>J Am Coll Nutr, Vol. 26, No. 6. (1 December 2007), pp. 639-644.</dc:source>
    <dc:date>2008-01-10T14:37:51-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>J Am Coll Nutr</prism:publicationName>
    <prism:volume>26</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>639</prism:startingPage>
    <prism:endingPage>644</prism:endingPage>
    <prism:category>diet</prism:category>
    <prism:category>dietaryfiber</prism:category>
    <prism:category>glycemiapp</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2205765">
    <title>Very low protein diet supplemented with ketoanalogs improves blood pressure control in chronic kidney disease.</title>
    <link>http://www.citeulike.org/user/omalbam/article/2205765</link>
    <description>&lt;i&gt;Kidney Int, Vol. 71, No. 3. (February 2007), pp. 245-251.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Blood pressure (BP) is hardly controlled in chronic kidney disease (CKD). We compared the effect of very low protein diet (VLPD) supplemented with ketoanalogs of essential amino acids (0.35 g/kg/day), low protein diet (LPD, 0.60 g/kg/day), and free diet (FD) on BP in patients with CKD stages 4 and 5. Vegetable proteins were higher in VLPD (66%) than in LPD (48%). LPD was prescribed to 110 consecutive patients; after run-in, they were invited to start VLPD. Thirty subjects accepted; 57 decided to continue LPD; 23 refused either diet (FD group). At baseline, protein intake (g/kg/day) was 0.79+/-0.09 in VLPD, 0.78+/-0.11 in LPD, and 1.11+/-0.18 in FD (P&#60;0.0001). After 6 months, protein intake was lower in VLPD than LPD and FD (0.54+/-0.11, 0.78+/-0.10, and 1.04+/-0.21 g/kg/day, respectively; P&#60;0.0001). BP diminished only in VLPD, from 143+/-19/84+/-10 to 128+/-16/78+/-7 mm Hg (P&#60;0.0001), despite reduction of antihypertensive drugs (from 2.6+/-1.1 to 1.8+/-1.2; P&#60;0.001). Urinary urea excretion directly correlated with urinary sodium excretion, which diminished in VLPD (from 181+/-32 to 131+/-36 mEq/day; P&#60;0.001). At multiple regression analysis (R2=0.270, P&#60;0.0001), BP results independently related to urinary sodium excretion (P=0.023) and VLPD prescription (P=0.003), but not to the level of protein intake. Thus, in moderate to advanced CKD, VLPD has an antihypertensive effect likely due to reduction of salt intake, type of proteins, and ketoanalogs supplementation, independent of actual protein intake.</description>
    <dc:title>Very low protein diet supplemented with ketoanalogs improves blood pressure control in chronic kidney disease.</dc:title>

    <dc:creator>V Bellizzi</dc:creator>
    <dc:creator>BR Di Iorio</dc:creator>
    <dc:creator>L De Nicola</dc:creator>
    <dc:creator>R Minutolo</dc:creator>
    <dc:creator>P Zamboli</dc:creator>
    <dc:creator>P Trucillo</dc:creator>
    <dc:creator>F Catapano</dc:creator>
    <dc:creator>C Cristofano</dc:creator>
    <dc:creator>L Scalfi</dc:creator>
    <dc:creator>G Conte</dc:creator>
    <dc:creator></dc:creator>
    <dc:identifier>doi:10.1038/sj.ki.5001955</dc:identifier>
    <dc:source>Kidney Int, Vol. 71, No. 3. (February 2007), pp. 245-251.</dc:source>
    <dc:date>2008-01-08T00:32:49-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Kidney Int</prism:publicationName>
    <prism:issn>0085-2538</prism:issn>
    <prism:volume>71</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>245</prism:startingPage>
    <prism:endingPage>251</prism:endingPage>
    <prism:category>diet</prism:category>
    <prism:category>renal</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2205272">
    <title>Effects of low habitual cocoa intake on blood pressure and bioactive nitric oxide: a randomized controlled trial.</title>
    <link>http://www.citeulike.org/user/omalbam/article/2205272</link>
    <description>&lt;i&gt;JAMA, Vol. 298, No. 1. (4 July 2007), pp. 49-60.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;CONTEXT: Regular intake of cocoa-containing foods is linked to lower cardiovascular mortality in observational studies. Short-term interventions of at most 2 weeks indicate that high doses of cocoa can improve endothelial function and reduce blood pressure (BP) due to the action of the cocoa polyphenols, but the clinical effect of low habitual cocoa intake on BP and the underlying BP-lowering mechanisms are unclear. OBJECTIVE: To determine effects of low doses of polyphenol-rich dark chocolate on BP. DESIGN, SETTING, AND PARTICIPANTS: Randomized, controlled, investigator-blinded, parallel-group trial involving 44 adults aged 56 through 73 years (24 women, 20 men) with untreated upper-range prehypertension or stage 1 hypertension without concomitant risk factors. The trial was conducted at a primary care clinic in Germany between January 2005 and December 2006. INTERVENTION: Participants were randomly assigned to receive for 18 weeks either 6.3 g (30 kcal) per day of dark chocolate containing 30 mg of polyphenols or matching polyphenol-free white chocolate. MAIN OUTCOME MEASURES: Primary outcome measure was the change in BP after 18 weeks. Secondary outcome measures were changes in plasma markers of vasodilative nitric oxide (S-nitrosoglutathione) and oxidative stress (8-isoprostane), and bioavailability of cocoa polyphenols. RESULTS: From baseline to 18 weeks, dark chocolate intake reduced mean (SD) systolic BP by -2.9 (1.6) mm Hg (P &#60; .001) and diastolic BP by -1.9 (1.0) mm Hg (P &#60; .001) without changes in body weight, plasma levels of lipids, glucose, and 8-isoprostane. Hypertension prevalence declined from 86% to 68%. The BP decrease was accompanied by a sustained increase of S-nitrosoglutathione by 0.23 (0.12) nmol/L (P &#60; .001), and a dark chocolate dose resulted in the appearance of cocoa phenols in plasma. White chocolate intake caused no changes in BP or plasma biomarkers. CONCLUSIONS: Data in this relatively small sample of otherwise healthy individuals with above-optimal BP indicate that inclusion of small amounts of polyphenol-rich dark chocolate as part of a usual diet efficiently reduced BP and improved formation of vasodilative nitric oxide. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00421499.</description>
    <dc:title>Effects of low habitual cocoa intake on blood pressure and bioactive nitric oxide: a randomized controlled trial.</dc:title>

    <dc:creator>D Taubert</dc:creator>
    <dc:creator>R Roesen</dc:creator>
    <dc:creator>C Lehmann</dc:creator>
    <dc:creator>N Jung</dc:creator>
    <dc:creator>E Schömig</dc:creator>
    <dc:identifier>doi:10.1001/jama.298.1.49</dc:identifier>
    <dc:source>JAMA, Vol. 298, No. 1. (4 July 2007), pp. 49-60.</dc:source>
    <dc:date>2008-01-07T22:34:03-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>JAMA</prism:publicationName>
    <prism:issn>1538-3598</prism:issn>
    <prism:volume>298</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>49</prism:startingPage>
    <prism:endingPage>60</prism:endingPage>
    <prism:category>diet</prism:category>
    <prism:category>vasculardisease</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/1617497">
    <title>High dietary glycemic load and glycemic index increase risk of cardiovascular disease among middle-aged women: a population-based follow-up study.</title>
    <link>http://www.citeulike.org/user/omalbam/article/1617497</link>
    <description>&lt;i&gt;J Am Coll Cardiol, Vol. 50, No. 1. (3 July 2007), pp. 14-21.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;OBJECTIVES: The goal of this work was to assess whether high dietary glycemic load and glycemic index are associated with an increased risk of cardiovascular disease (CVD). BACKGROUND: The associations of dietary glycemic index and glycemic load with risk of CVD are not well established, particularly in populations consuming modest glycemic load diets. Moreover, risk may differ between lean and overweight subjects. METHODS: Associations of glycemic index and glycemic load with incident CVD were examined in a prospective cohort of 15,714 Dutch women age 49 to 70 years without diabetes or CVD. Dietary glycemic index and glycemic load were calculated using the glycemic index, carbohydrate content, and frequency of intake of individual foods. RESULTS: During 9 +/- 2 years of follow-up, 556 cases of coronary heart disease (CHD) and 243 cases of cerebrovascular accident (CVA) occurred. Dietary glycemic load (mean = 100; SD = 17) was associated with increased risk of CVD, adjusted for CVD risk factors and dietary variables, with a hazard ratio (HR) for the highest against lowest quartile of 1.47 (95% confidence interval [CI] 1.04 to 2.09; p(trend) = 0.03). Similar results were observed for dietary glycemic index with a corresponding HR of 1.33 (95% CI 1.07 to 1.67; p(trend) = 0.02). Glycemic load tended to be associated with both CHD (HR 1.44; 95% CI 0.95 to 2.19; p(trend) = 0.14) and CVA (HR 1.55; 95% CI 0.81 to 2.97; p(trend) = 0.10), but glycemic index only with CHD (HR 1.44; 95% CI 1.10 to 1.89; p(trend) = 0.01). Among overweight women (body mass index &#62;25 kg/m2), glycemic load was associated with CVD (1.78; 95% CI 1.11 to 2.85; p(trend) = 0.04), but not among normal weight women (p(interaction) = 0.19). Body mass index did not modify the association of glycemic index with CVD. CONCLUSIONS: Among women consuming modest glycemic load diets, high dietary glycemic load and glycemic index increase the risk of CVD, particularly for overweight women.</description>
    <dc:title>High dietary glycemic load and glycemic index increase risk of cardiovascular disease among middle-aged women: a population-based follow-up study.</dc:title>

    <dc:creator>JW Beulens</dc:creator>
    <dc:creator>LM de Bruijne</dc:creator>
    <dc:creator>RP Stolk</dc:creator>
    <dc:creator>PH Peeters</dc:creator>
    <dc:creator>ML Bots</dc:creator>
    <dc:creator>DE Grobbee</dc:creator>
    <dc:creator>YT van der Schouw</dc:creator>
    <dc:identifier>doi:10.1016/j.jacc.2007.02.068</dc:identifier>
    <dc:source>J Am Coll Cardiol, Vol. 50, No. 1. (3 July 2007), pp. 14-21.</dc:source>
    <dc:date>2007-09-04T06:30:50-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>J Am Coll Cardiol</prism:publicationName>
    <prism:issn>1558-3597</prism:issn>
    <prism:volume>50</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>14</prism:startingPage>
    <prism:endingPage>21</prism:endingPage>
    <prism:category>chd</prism:category>
    <prism:category>diet</prism:category>
</item>



</rdf:RDF>

