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Journal Cover The Lancet Diabetes and Endocrinology
  [SJR: 6.919]   [H-I: 27]   [128 followers]  Follow
    
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   ISSN (Online) 2213-8587
   Published by Elsevier Homepage  [3043 journals]
  • Looking again at the Look AHEAD study
    • Authors: Edward W Gregg; Rena Wing
      Pages: 763 - 764
      Abstract: Publication date: October 2017
      Source:The Lancet Diabetes & Endocrinology, Volume 5, Issue 10
      Author(s): Edward W Gregg, Rena Wing


      PubDate: 2017-09-23T08:20:04Z
      DOI: 10.1016/s2213-8587(17)30238-3
       
  • Changing ethical and legal norms in the management of differences of sex
           development
    • Authors: Maayan Sudai
      Pages: 764 - 766
      Abstract: Publication date: October 2017
      Source:The Lancet Diabetes & Endocrinology, Volume 5, Issue 10
      Author(s): Maayan Sudai


      PubDate: 2017-09-23T08:20:04Z
      DOI: 10.1016/s2213-8587(17)30043-8
       
  • Denosumab treatment in postmenopausal women with osteoporosis
    • Authors: Yu Zhang; Rongrui Tang
      First page: 767
      Abstract: Publication date: October 2017
      Source:The Lancet Diabetes & Endocrinology, Volume 5, Issue 10
      Author(s): Yu Zhang, Rongrui Tang


      PubDate: 2017-09-23T08:20:04Z
      DOI: 10.1016/s2213-8587(17)30286-3
       
  • Denosumab treatment in postmenopausal women with osteoporosis
    • Authors: Paul de Boissieu; Thierry Trenque
      Pages: 767 - 768
      Abstract: Publication date: October 2017
      Source:The Lancet Diabetes & Endocrinology, Volume 5, Issue 10
      Author(s): Paul de Boissieu, Thierry Trenque


      PubDate: 2017-09-23T08:20:04Z
      DOI: 10.1016/s2213-8587(17)30287-5
       
  • Denosumab treatment in postmenopausal women with osteoporosis –
           Authors' reply
    • Authors: Henry G Bone; Rachel B Wagman; Nicola Pannacciulli; Socrates Papapoulos
      Pages: 768 - 769
      Abstract: Publication date: October 2017
      Source:The Lancet Diabetes & Endocrinology, Volume 5, Issue 10
      Author(s): Henry G Bone, Rachel B Wagman, Nicola Pannacciulli, Socrates Papapoulos


      PubDate: 2017-09-23T08:20:04Z
      DOI: 10.1016/s2213-8587(17)30288-7
       
  • Disentangling the association between diabetes and bone disease
    • Authors: Katrine Hygum; Bente Lomholt Langdahl; Jakob Starup-Linde
      First page: 769
      Abstract: Publication date: October 2017
      Source:The Lancet Diabetes & Endocrinology, Volume 5, Issue 10
      Author(s): Katrine Hygum, Bente Lomholt Langdahl, Jakob Starup-Linde


      PubDate: 2017-09-23T08:20:04Z
      DOI: 10.1016/s2213-8587(17)30289-9
       
  • Disentangling the association between diabetes and bone disease –
           Authors' reply
    • Authors: Vikram V Shanbhogue; Stinus Hansen; Morten Frost; Kim Brixen; Anne P Hermann
      Pages: 769 - 770
      Abstract: Publication date: October 2017
      Source:The Lancet Diabetes & Endocrinology, Volume 5, Issue 10
      Author(s): Vikram V Shanbhogue, Stinus Hansen, Morten Frost, Kim Brixen, Anne P Hermann


      PubDate: 2017-09-23T08:20:04Z
      DOI: 10.1016/s2213-8587(17)30290-5
       
  • Alafia Samuels: fast-food watchdog in the Caribbean
    • Authors: Ray Cavanaugh
      First page: 772
      Abstract: Publication date: October 2017
      Source:The Lancet Diabetes & Endocrinology, Volume 5, Issue 10
      Author(s): Ray Cavanaugh


      PubDate: 2017-09-23T08:20:04Z
      DOI: 10.1016/s2213-8587(16)30312-6
       
  • The politics of health inequalities
    • Authors: Talha Khan Burki
      First page: 773
      Abstract: Publication date: October 2017
      Source:The Lancet Diabetes & Endocrinology, Volume 5, Issue 10
      Author(s): Talha Khan Burki


      PubDate: 2017-09-23T08:20:04Z
      DOI: 10.1016/s2213-8587(17)30062-1
       
  • Targeting weight loss interventions to reduce cardiovascular complications
           of type 2 diabetes: a machine learning-based post-hoc analysis of
           heterogeneous treatment effects in the Look AHEAD trial
    • Authors: Aaron Baum; Joseph Scarpa; Emilie Bruzelius; Ronald Tamler; Sanjay Basu; James Faghmous
      Pages: 808 - 815
      Abstract: Publication date: October 2017
      Source:The Lancet Diabetes & Endocrinology, Volume 5, Issue 10
      Author(s): Aaron Baum, Joseph Scarpa, Emilie Bruzelius, Ronald Tamler, Sanjay Basu, James Faghmous
      Background The Action for Health in Diabetes (Look AHEAD) trial investigated whether long-term cardiovascular disease morbidity and mortality could be reduced through a weight loss intervention among people with type 2 diabetes. Despite finding no significant reduction in cardiovascular events on average, it is possible that some subpopulations might have derived benefit. In this post-hoc analysis, we test the hypothesis that the overall neutral average treatment effect in the trial masked important heterogeneous treatment effects (HTEs) from intensive weight loss interventions. Methods We used causal forest modelling, which identifies HTEs, using a random half of the trial data (the training set). We applied Cox proportional hazards models to test the potential HTEs on the remaining half of the data (the testing set). The analysis was deemed exempt from review by the Columbia University Institutional Review Board, Protocol ID# AAAO3003. Findings Between Aug 22, 2001, and April 30, 2004, 5145 patients with type 2 diabetes were enrolled in the Look AHEAD randomised controlled trial, of whom 4901 were included in the The National Institute of Diabetes and Digestive and Kidney Diseases Repository and included in our analyses: 2450 for model development and 2451 in the testing dataset. Baseline HbA1c and self-reported general health distinguished participants who differentially benefited from the intervention. Cox models for the primary composite cardiovascular outcome revealed a number needed to treat of 28·9 to prevent 1 event over 9·6 years among participants with HbA1c 6·8% or higher, or both HbA1c less than 6·8% and Short Form Health Survey (SF-36) general health score of 48 or more (2101 [86%] of 2451 participants in the testing dataset; 167 [16%] of 1046 primary outcome events for intervention vs 205 [19%] of 1055 for control, absolute risk reduction of 3·46%, 95% CI 0·21–6·73%, p=0·038) By contrast, participants with HbA1c less than 6·8% and baseline SF-36 general health score of less than 48 (350 [14%] of 2451 participants in the testing data; 27 [16%] of 171 primary outcome events for intervention vs 15 [8%] of 179 primary outcome events for control) had an absolute risk increase of the primary outcome of 7·41% (0·60 to 14·22, p=0·003). Interpretation Look AHEAD participants with moderately or poorly controlled diabetes (HbA1c 6·8% or higher) and subjects with well controlled diabetes (HbA1c less than 6·8%) and good self-reported health (85% of the overall study population) averted cardiovascular events from a behavioural intervention aimed at weight loss. However, 15% of participants with well controlled diabetes and poor self-reported general health experienced negative effects that rendered the overall study outcome neutral. HbA1c and a short questionnaire on general health might identify people with type 2 diabetes likely to derive benefit from an intensive lifestyle intervention aimed at weight loss. Funding None.

      PubDate: 2017-09-23T08:20:04Z
      DOI: 10.1016/s2213-8587(17)30176-6
       
  • Puberty suppression in transgender children and adolescents
    • Authors: Simone Mahfouda; Julia K Moore; Aris Siafarikas; Florian D Zepf; Ashleigh Lin
      Pages: 816 - 826
      Abstract: Publication date: October 2017
      Source:The Lancet Diabetes & Endocrinology, Volume 5, Issue 10
      Author(s): Simone Mahfouda, Julia K Moore, Aris Siafarikas, Florian D Zepf, Ashleigh Lin
      The World Professional Association for Transgender Health's standards of care recommend suspending puberty, preferably with the use of gonadotropin-releasing hormone agonists, in certain gender non-conforming minors (aged under 18 years) who have undergone a psychiatric assessment and have reached at least Tanner stage II of puberty. This approach seeks to lessen the discordance between assigned natal sex and gender identity by temporarily halting the development of secondary sexual characteristics, essentially widening the temporal window for gender clarification. Despite promising preliminary evidence on the clinical utility of this approach, there is a dearth of research to inform evidence-based practice. In view of these challenges, we review the available empirical evidence on the cognitive, physical, and surgical implications of puberty suppression in gender-incongruent children and adolescents. We also explore the historical underpinnings and clinical impetus for suspending puberty in this population, and propose key research priorities.

      PubDate: 2017-09-23T08:20:04Z
      DOI: 10.1016/s2213-8587(17)30099-2
       
  • Bone disease in diabetes: another manifestation of microvascular
           disease'
    • Authors: Vikram V Shanbhogue; Stinus Hansen; Morten Frost; Kim Brixen; Anne P Hermann
      Pages: 827 - 838
      Abstract: Publication date: October 2017
      Source:The Lancet Diabetes & Endocrinology, Volume 5, Issue 10
      Author(s): Vikram V Shanbhogue, Stinus Hansen, Morten Frost, Kim Brixen, Anne P Hermann
      Type 1 and type 2 diabetes are generally accepted to be associated with increased bone fracture risk. However, the pathophysiological mechanisms of diabetic bone disease are poorly understood, and whether the associated increased skeletal fragility is a comorbidity or a complication of diabetes remains under debate. Although there is some indication of a direct deleterious effect of microangiopathy on bone, the evidence is open to question, and whether diabetic osteopathy can be classified as a chronic, microvascular complication of diabetes remains uncertain. Here, we review the current knowledge of potential contributory factors to diabetic bone disease, particularly the association between diabetic microangiopathy and bone mineral density, bone structure, and bone turnover. Additionally, we discuss and propose a pathophysiological model of the effects of diabetic microvascular disease on bone, and examine the progression of bone disease alongside the evolution of diabetes.

      PubDate: 2017-09-23T08:20:04Z
      DOI: 10.1016/s2213-8587(17)30134-1
       
  • Sugar: the prime suspect in poor health
    • Authors: Talha Khan Burki
      First page: 17
      Abstract: Publication date: Available online 4 October 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Talha Khan Burki


      PubDate: 2017-10-08T15:11:45Z
      DOI: 10.1016/s2213-8587(16)30083-3
       
  • Correction to Lancet Diabetes Endocrinol 2017; published online Sept 29.
           http://dx.doi.org/10.1016/S2213-8587(17)30239-5
    • Abstract: Publication date: Available online 20 October 2017
      Source:The Lancet Diabetes & Endocrinology


      PubDate: 2017-10-21T15:34:53Z
       
  • Interventions to prevent global childhood overweight and obesity: a
           systematic review
    • Authors: Sara Bleich; Kelsey Vercammen Laura Zatz Johannah Frelier Cara Ebbeling
      Abstract: Publication date: Available online 20 October 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Sara N Bleich, Kelsey A Vercammen, Laura Y Zatz, Johannah M Frelier, Cara B Ebbeling, Anna Peeters
      In view of the prevalence, health consequences, and costs of childhood obesity, there has been substantial interest in identifying effective interventions to prevent excess weight gain in young people. In this systematic review, we expand on previous reviews of obesity prevention interventions by including recent studies (until May 23, 2017) from all parts of the world. We searched MEDLINE, Embase, CINAHL Plus, Web of Science, CAB s, and PAIS Index and included randomised controlled trials, quasi-experimental studies, or natural experiments with: (1) a control group; (2) minimum follow-up of 12 months for community-based and home-based interventions or 6 months for school-based and preschool-based interventions; and (3) a primary outcome of BMI, BMI Z score, BMI percentile, body fat percentage, skinfold thickness, waist circumference, or prevalence of overweight or obesity. School-based interventions with combined diet and physical activity components and a home element (n=41) had greatest effectiveness; evidence in support of the effect of preschool-based (n=6), community-based (n=7), and home-based (n=2) interventions was limited by a paucity of studies and heterogeneity in study design. The effectiveness of school-based interventions that combined diet and physical activity components suggests that they hold promise for childhood obesity prevention worldwide. More research with rigorous evaluation and consistent reporting is needed in non-school settings and in combinations of settings.

      PubDate: 2017-10-21T15:34:53Z
       
  • Bone and mineral disorders in chronic kidney disease: implications for
           cardiovascular health and ageing in the general population
    • Authors: Adrian Covic; Marc Vervloet; Ziad A Massy; Pablo Ureña Torres; David Goldsmith; Vincent Brandenburg; Sandro Mazzaferro; Pieter Evenepoel; Jordi Bover; Mugurel Apetrii; Mario Cozzolino
      Abstract: Publication date: Available online 16 October 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Adrian Covic, Marc Vervloet, Ziad A Massy, Pablo Ureña Torres, David Goldsmith, Vincent Brandenburg, Sandro Mazzaferro, Pieter Evenepoel, Jordi Bover, Mugurel Apetrii, Mario Cozzolino
      The patient with chronic kidney disease (CKD) represents an extreme model for arteriosclerosis, vascular calcification, and bone disorders, all of which are also associated with ageing in the general population. These pathological features are also relevant to other common chronic health disorders such as diabetes, and chronic inflammatory and cardiovascular diseases. Although management and interventions for these major risk factors are now incorporated into most public health guidelines (eg, smoking cessation and control of bodyweight and blood pressure, as well as glucose and cholesterol concentrations), some residual cardiovascular risk is not reduced by implementation of these interventions. CKD should be regarded as an atypical disease in which both traditional and novel cardiovascular risk factors have effects on outcomes. But CKD can also be viewed conceptually as an accelerator of traditional cardiovascular risk factors. Findings from research into mineral bone disorder associated with CKD (CKD–MBD) could help the medical community to better understand the vascular actions of certain molecules, such as phosphates, fibroblast growth factor 23, parathyroid hormone, sclerostin, or vitamin D and their relevance to the management of different pathologies in the general population. Importantly, these components, which are recognised in nephrology, could help to explain residual risk of cardiovascular events in the general population. Thus, achieving a better understanding of CKD–MBDs could provide substantial insight into future treatments for arteriosclerosis and osteoporosis, which are strongly associated with ageing and morbidity in the general population.

      PubDate: 2017-10-21T15:34:53Z
      DOI: 10.1016/s2213-8587(17)30310-8
       
  • Research in brief
    • Authors: Seema Kang
      Abstract: Publication date: Available online 12 October 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Seema Kang


      PubDate: 2017-10-14T15:06:22Z
      DOI: 10.1016/s2213-8587(17)30337-6
       
  • Linoleic acid and risk of type 2 diabetes
    • Authors: Gabriele Riccardi
      Abstract: Publication date: Available online 12 October 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Gabriele Riccardi


      PubDate: 2017-10-14T15:06:22Z
      DOI: 10.1016/s2213-8587(17)30322-4
       
  • Is the new treatment for Cushing's disease too sweet'
    • Authors: Ashley Grossman
      Abstract: Publication date: Available online 12 October 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Ashley Grossman


      PubDate: 2017-10-14T15:06:22Z
      DOI: 10.1016/s2213-8587(17)30341-8
       
  • Omega-6 fatty acid biomarkers and incident type 2 diabetes: pooled
           analysis of individual-level data for 39 740 adults from 20 prospective
           cohort studies
    • Authors: Jason H Y Wu; Matti Marklund; Fumiaki Imamura; Nathan Tintle; Andres V Ardisson Korat; Janette de Goede; Xia Zhou; Wei-Sin Yang; Marcia C de Oliveira Otto; Janine Kröger; Waqas Qureshi; Jyrki K Virtanen; Julie K Bassett; Alexis C Frazier-Wood; Maria Lankinen; Rachel A Murphy; Kalina Rajaobelina; Liana C Del Gobbo; Nita G Forouhi; Robert Luben; Kay-Tee Khaw; Nick Wareham; Anya Kalsbeek; Jenna Veenstra; Juhua Luo; Frank B Hu; Hung-Ju Lin; David S Siscovick; Heiner Boeing; Tzu-An Chen; Brian Steffen; Lyn M Steffen; Allison Hodge; Gudny Eriksdottir; Albert V Smith; Vilmunder Gudnason; Tamara B Harris; Ingeborg A Brouwer; Claudine Berr; Catherine Helmer; Cecilia Samieri; Markku Laakso; Michael Y Tsai; Graham G Giles; Tarja Nurmi; Lynne Wagenknecht; Matthias B Schulze; Rozenn N Lemaitre; Kuo-Liong Chien; Sabita S Soedamah-Muthu; Johanna M Geleijnse; Qi Sun; William S Harris; Lars Lind; Johan Ärnlöv; Ulf Riserus; Renata Micha; Dariush Mozaffarian
      Abstract: Publication date: Available online 12 October 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Jason H Y Wu, Matti Marklund, Fumiaki Imamura, Nathan Tintle, Andres V Ardisson Korat, Janette de Goede, Xia Zhou, Wei-Sin Yang, Marcia C de Oliveira Otto, Janine Kröger, Waqas Qureshi, Jyrki K Virtanen, Julie K Bassett, Alexis C Frazier-Wood, Maria Lankinen, Rachel A Murphy, Kalina Rajaobelina, Liana C Del Gobbo, Nita G Forouhi, Robert Luben, Kay-Tee Khaw, Nick Wareham, Anya Kalsbeek, Jenna Veenstra, Juhua Luo, Frank B Hu, Hung-Ju Lin, David S Siscovick, Heiner Boeing, Tzu-An Chen, Brian Steffen, Lyn M Steffen, Allison Hodge, Gudny Eriksdottir, Albert V Smith, Vilmunder Gudnason, Tamara B Harris, Ingeborg A Brouwer, Claudine Berr, Catherine Helmer, Cecilia Samieri, Markku Laakso, Michael Y Tsai, Graham G Giles, Tarja Nurmi, Lynne Wagenknecht, Matthias B Schulze, Rozenn N Lemaitre, Kuo-Liong Chien, Sabita S Soedamah-Muthu, Johanna M Geleijnse, Qi Sun, William S Harris, Lars Lind, Johan Ärnlöv, Ulf Riserus, Renata Micha, Dariush Mozaffarian
      Background The metabolic effects of omega-6 polyunsaturated fatty acids (PUFAs) remain contentious, and little evidence is available regarding their potential role in primary prevention of type 2 diabetes. We aimed to assess the associations of linoleic acid and arachidonic acid biomarkers with incident type 2 diabetes. Methods We did a pooled analysis of new, harmonised, individual-level analyses for the biomarkers linoleic acid and its metabolite arachidonic acid and incident type 2 diabetes. We analysed data from 20 prospective cohort studies from ten countries (Iceland, the Netherlands, the USA, Taiwan, the UK, Germany, Finland, Australia, Sweden, and France), with biomarkers sampled between 1970 and 2010. Participants included in the analyses were aged 18 years or older and had data available for linoleic acid and arachidonic acid biomarkers at baseline. We excluded participants with type 2 diabetes at baseline. The main outcome was the association between omega-6 PUFA biomarkers and incident type 2 diabetes. We assessed the relative risk of type 2 diabetes prospectively for each cohort and lipid compartment separately using a prespecified analytic plan for exposures, covariates, effect modifiers, and analysis, and the findings were then pooled using inverse-variance weighted meta-analysis. Findings Participants were 39 740 adults, aged (range of cohort means) 49–76 years with a BMI (range of cohort means) of 23·3–28·4 kg/m2, who did not have type 2 diabetes at baseline. During a follow-up of 366 073 person-years, we identified 4347 cases of incident type 2 diabetes. In multivariable-adjusted pooled analyses, higher proportions of linoleic acid biomarkers as percentages of total fatty acid were associated with a lower risk of type 2 diabetes overall (risk ratio [RR] per interquintile range 0·65, 95% CI 0·60–0·72, p<0·0001; I 2=53·9%, pheterogeneity=0·002). The associations between linoleic acid biomarkers and type 2 diabetes were generally similar in different lipid compartments, including phospholipids, plasma, cholesterol esters, and adipose tissue. Levels of arachidonic acid biomarker were not significantly associated with type 2 diabetes risk overall (RR per interquintile range 0·96, 95% CI 0·88–1·05; p=0·38; I 2=63·0%, pheterogeneity<0·0001). The associations between linoleic acid and arachidonic acid biomarkers and the risk of type 2 diabetes were not significantly modified by any prespecified potential sources of heterogeneity (ie, age, BMI, sex, race, aspirin use, omega-3 PUFA levels, or variants of the FADS gene; all pheterogeneity≥0·13). Interpretation Findings suggest that linoleic acid has long-term benefits for the prevention of type 2 diabetes and that arachidonic acid is not harmful. Funding Funders are shown in the appendix.

      PubDate: 2017-10-14T15:06:22Z
      DOI: 10.1016/s2213-8587(17)30307-8
       
  • Improving the clinical impact of randomised trials in thyroidology
    • Authors: Tim I M Korevaar; Layal Chaker; Robin P Peeters
      Abstract: Publication date: Available online 10 October 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Tim I M Korevaar, Layal Chaker, Robin P Peeters


      PubDate: 2017-10-14T15:06:22Z
      DOI: 10.1016/s2213-8587(17)30316-9
       
  • Effect of iodine supplementation in pregnant women on child
           neurodevelopment: a randomised, double-blind, placebo-controlled trial
    • Authors: Sueppong Gowachirapant; Nidhi Jaiswal; Alida Melse-Boonstra; Valeria Galetti; Sara Stinca; Ian Mackenzie; Susan Thomas; Tinku Thomas; Pattanee Winichagoon; Krishnamachari Srinivasan; Michael B Zimmermann
      Abstract: Publication date: Available online 10 October 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Sueppong Gowachirapant, Nidhi Jaiswal, Alida Melse-Boonstra, Valeria Galetti, Sara Stinca, Ian Mackenzie, Susan Thomas, Tinku Thomas, Pattanee Winichagoon, Krishnamachari Srinivasan, Michael B Zimmermann
      Background Iodine deficiency during pregnancy might be associated with reduced intelligence quotient (IQ) score in offspring. We assessed the effect of iodine supplementation in mildly iodine-deficient pregnant women on neurodevelopment of their offspring in areas where schoolchildren were iodine sufficient. Methods In this randomised, placebo-controlled trial, pregnant women in Bangalore, India, and Bangkok, Thailand, were randomly assigned (1:1) to receive 200 μg iodine orally once a day or placebo until delivery. Randomisation was done with a computer-generated sequence and stratified by site. Co-primary outcomes were verbal and performance IQ scores on the Wechsler Preschool and Primary Scale of Intelligence Third Edition (WPPSI-III) and the global executive composite score from the Behaviour Rating Inventory of Executive Function-Preschool Version (BRIEF-P) in the children at age 5–6 years. The trial was double-blinded; some unmasking took place at age 2 years for an interim analysis, but participants and nearly all investigators remained masked to group assignment until age 5–6 years. Analysis was by intention to treat using mixed-effects models. This trial is registered with ClinicalTrials.gov, number NCT00791466. Findings Between Nov 18, 2008, and March 12, 2011, 832 women entered the trial at a mean gestational age of 10·7 weeks (SD 2·7); median urinary iodine concentration was 131 μg/L (IQR 81–213). Mean compliance with supplementation was 87%, assessed by monthly tablet counts. 313 children (iodine group, n=159; placebo group, n=154) were analysed for verbal and performance IQ with WPPSI-III and 315 (iodine group, n=159; placebo group, n=156) for overall executive function with BRIEF-P. Mean WPPSI-III scores for verbal IQ were 89·5 (SD 9·8) in the iodine group and 90·2 (9·8) in the placebo group (difference −0·7, 95% CI −2·9 to 1·5; p=0·77), and for performance IQ were 97·5 (12·5) in the iodine group and 99·1 (13·4) in the placebo group (difference −1·6, −4·5 to 1·3; p=0·44). The mean BRIEF-P global executive composite score was 90·6 (26·2) in the iodine group and 91·5 (27·0) in the placebo group (difference −0·9, −6·8 to 5·0; p=0·74). The frequency of adverse events did not differ between groups during gestation or at delivery: 24 women in the iodine group and 28 in the placebo group reported adverse events (iodine group: abortion, n=20; blighted ovum, and n=2; intrauterine death, n=2; placebo group: abortion, n=22; blighted ovum, n=1; intrauterine death, n=2; early neonatal death, n=1; and neonatal death, n=2). Interpretation Daily iodine supplementation in mildly iodine-deficient pregnant women had no effect on child neurodevelopment at age 5–6 years. Funding Swiss National Science Foundation, Nestlé Foundation, Wageningen University and Research, and ETH Zurich.

      PubDate: 2017-10-14T15:06:22Z
      DOI: 10.1016/s2213-8587(17)30332-7
       
  • Iodine supplementation in pregnancy in mildly deficient regions
    • Authors: Sarah C Bath
      Abstract: Publication date: Available online 10 October 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Sarah C Bath


      PubDate: 2017-10-14T15:06:22Z
      DOI: 10.1016/s2213-8587(17)30331-5
       
  • SGLT2 inhibitors: hypotheses on the mechanism of cardiovascular protection
    • Authors: Robert M Bell; Derek M Yellon
      Abstract: Publication date: Available online 10 October 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Robert M Bell, Derek M Yellon


      PubDate: 2017-10-14T15:06:22Z
      DOI: 10.1016/s2213-8587(17)30314-5
       
  • Clinical inertia versus overtreatment in glycaemic management
    • Authors: Kamlesh Khunti; Melanie J Davies
      Abstract: Publication date: Available online 9 October 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Kamlesh Khunti, Melanie J Davies


      PubDate: 2017-10-14T15:06:22Z
      DOI: 10.1016/s2213-8587(17)30339-x
       
  • Diabetes structured self-management education programmes: a narrative
           review and current innovations
    • Authors: Sudesna Chatterjee; Melanie J Davies; Simon Heller; Jane Speight; Frank J Snoek; Kamlesh Khunti
      Abstract: Publication date: Available online 29 September 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Sudesna Chatterjee, Melanie J Davies, Simon Heller, Jane Speight, Frank J Snoek, Kamlesh Khunti
      Both type 1 and type 2 diabetes are associated with long-term complications that can be prevented or delayed by intensive glycaemic management. People who are empowered and skilled to self-manage their diabetes have improved health outcomes. Over the past 20 years, diabetes self-management education programmes have been shown to be efficacious and cost-effective in promotion and facilitation of self-management, with improvements in patients' knowledge, skills, and motivation leading to improved biomedical, behavioural, and psychosocial outcomes. Diabetes self-management education programmes, developed robustly with an evidence-based structured curriculum, vary in their method of delivery, content, and use of technology, person-centred philosophy, and specific aims. They are delivered by trained educators, and monitored for quality by independent assessors and routine audit. Self-management education should be tailored to specific populations, taking into consideration the type of diabetes, and ethnic, social, cognitive, literacy, and cultural factors. Ways to improve access to and uptake of diabetes self-management programmes are needed globally.

      PubDate: 2017-09-30T14:28:02Z
      DOI: 10.1016/s2213-8587(17)30239-5
       
  • Fat: so much more than just fat
    • Authors: Robert Stirrups
      Abstract: Publication date: Available online 22 September 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Robert Stirrups


      PubDate: 2017-09-23T08:20:04Z
       
  • Correction to Lancet Diabetes Endocrinol 2016; 4: 756–65
    • Abstract: Publication date: Available online 22 September 2017
      Source:The Lancet Diabetes & Endocrinology


      PubDate: 2017-09-23T08:20:04Z
       
  • Bollywood's dialogue with diabetes: sweet and subtle
    • Authors: Sanghamitra Pati
      Abstract: Publication date: Available online 22 September 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Sanghamitra Pati


      PubDate: 2017-09-23T08:20:04Z
      DOI: 10.1016/s2213-8587(17)30329-7
       
  • PCSK9 inhibition and type 2 diabetes
    • Authors: Luca A Lotta; Simon J Griffin
      Abstract: Publication date: Available online 15 September 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Luca A Lotta, Simon J Griffin


      PubDate: 2017-09-18T05:54:12Z
      DOI: 10.1016/s2213-8587(17)30321-2
       
  • Cardiovascular safety and efficacy of the PCSK9 inhibitor evolocumab in
           patients with and without diabetes and the effect of evolocumab on
           glycaemia and risk of new-onset diabetes: a prespecified analysis of the
           FOURIER randomised controlled trial
    • Authors: Marc S Sabatine; Lawrence A Leiter; Stephen D Wiviott; Robert P Giugliano; Prakash Deedwania; Gaetano M De Ferrari; Sabina A Murphy; Julia F Kuder; Ioanna Gouni-Berthold; Basil S Lewis; Yehuda Handelsman; Armando Lira Pineda; Narimon Honarpour; Anthony C Keech; Peter S Sever; Terje R Pedersen
      Abstract: Publication date: Available online 15 September 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Marc S Sabatine, Lawrence A Leiter, Stephen D Wiviott, Robert P Giugliano, Prakash Deedwania, Gaetano M De Ferrari, Sabina A Murphy, Julia F Kuder, Ioanna Gouni-Berthold, Basil S Lewis, Yehuda Handelsman, Armando Lira Pineda, Narimon Honarpour, Anthony C Keech, Peter S Sever, Terje R Pedersen
      Background The proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor evolocumab reduced LDL cholesterol and cardiovascular events in the FOURIER trial. In this prespecified analysis of FOURIER, we investigated the efficacy and safety of evolocumab by diabetes status and the effect of evolocumab on glycaemia and risk of developing diabetes. Methods FOURIER was a randomised trial of evolocumab (140 mg every 2 weeks or 420 mg once per month) versus placebo in 27 564 patients with atherosclerotic disease who were on statin therapy, followed up for a median of 2·2 years. In this prespecified analysis, we investigated the effect of evolocumab on cardiovascular events by diabetes status at baseline, defined on the basis of patient history, clinical events committee review of medical records, or baseline HbA1c of 6·5% (48 mmol/mol) or greater or fasting plasma glucose (FPG) of 7·0 mmol/L or greater. The primary endpoint was a composite of cardiovascular death, myocardial infarction, stroke, hospital admission for unstable angina, or coronary revascularisation. The key secondary endpoint was a composite of cardiovascular death, myocardial infarction, or stroke. We also assessed the effect of evolocumab on glycaemia, and on the risk of new-onset diabetes among patients without diabetes at baseline. HbA1c was measured at baseline then every 24 weeks and FPG was measured at baseline, week 12, week 24, and every 24 weeks thereafter, and potential cases of new-onset diabetes were adjudicated centrally. In a post-hoc analysis, we also investigated the effects on glycaemia and diabetes risk in patients with prediabetes (HbA1c 5·7–6·4% [39–46 mmol/mol] or FPG 5·6–6·9 mmol/L) at baseline. FOURIER is registered with ClinicalTrials.gov, number NCT01764633. Findings At study baseline, 11 031 patients (40%) had diabetes and 16 533 (60%) did not have diabetes (of whom 10 344 had prediabetes and 6189 had normoglycaemia). Evolocumab significantly reduced cardiovascular outcomes consistently in patients with and without diabetes at baseline. For the primary composite endpoint, the hazard ratios (HRs) were 0·83 (95% CI 0·75–0·93; p=0·0008) for patients with diabetes and 0·87 (0·79–0·96; p=0·0052) for patients without diabetes (pinteraction=0·60). For the key secondary endpoint, the HRs were 0·82 (0·72–0·93; p=0·0021) for those with diabetes and 0·78 (0·69–0·89; p=0·0002) for those without diabetes (pinteraction=0·65). Evolocumab did not increase the risk of new-onset diabetes in patients without diabetes at baseline (HR 1·05, 0·94–1·17), including in those with prediabetes (HR 1·00, 0·89–1·13). Levels of HbA1c and FPG were similar between the evolocumab and placebo groups over time in patients with diabetes, prediabetes, or normoglycaemia. Among patients with diabetes at baseline, the proportions of patients with adverse events were 78·5% (4327 of 5513 patients) in the evolocumab group and 78·3% (4307 of 5502 patients) in the placebo group; among patients without diabetes at baseline, the proportions with adverse events were 76·8% (6337 of 8256 patients) in the evolocumab group and 76·8% (6337 of 8254 patients) in the placebo group. Interpretation PCSK9 inhibition with evolocumab significantly reduced cardiovascular risk in patients with and without diabetes. Evolocumab did not increase the risk of new-onset diabetes, nor did it worsen glycaemia. These data suggest evolocumab use in patients with atherosclerotic disease is efficacious and safe in patients with and without diabetes. Funding Amgen.
      PubDate: 2017-09-18T05:54:12Z
      DOI: 10.1016/s2213-8587(17)30313-3
       
  • SGLT2 inhibitors in type 1 diabetes: knocked down, but up again'
    • Authors: John R Petrie
      Abstract: Publication date: Available online 14 September 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): John R Petrie


      PubDate: 2017-09-18T05:54:12Z
      DOI: 10.1016/s2213-8587(17)30315-7
       
  • Precision medicine: diagnosis and management of obesity
    • Authors: Gema Frühbeck; Dimitrios N Kiortsis; Victoria Catalán
      Abstract: Publication date: Available online 14 September 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Gema Frühbeck, Dimitrios N Kiortsis, Victoria Catalán


      PubDate: 2017-09-18T05:54:12Z
      DOI: 10.1016/s2213-8587(17)30312-1
       
  • Progress and challenges in anti-obesity pharmacotherapy
    • Authors: Daniel H Bessesen; Luc F Van Gaal
      Abstract: Publication date: Available online 14 September 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Daniel H Bessesen, Luc F Van Gaal
      Obesity is a serious and growing worldwide health challenge. Healthy lifestyle choices are the foundation of obesity treatment. However, weight loss can lead to physiological adaptations that promote weight regain. As a result, lifestyle treatment alone typically produces only modest weight loss that is difficult to sustain. In other metabolic diseases, pharmacotherapy is an accepted adjunct to lifestyle. Several anti-obesity drugs have been approved in the USA, European Union, Australia, and Japan including sympathomimetics, pancreatic lipase inhibitors, GABAA receptor activators, a serotonin 2C receptor agonist, opioid antagonist, dopamine–norepinephrine reuptake inhibitor, and glucagon-like peptide-1 (GLP-1) receptor agonists. These drugs vary in their efficacy and side-effect profiles but all provide greater weight loss than do lifestyle changes alone. Even though obesity is widespread and associated with adverse health consequences, and anti-obesity drugs can help people to lose weight, very few patients use these drugs partly because of concerns about safety and efficacy, but also because of inadequate health insurance coverage. Despite great advances in our understanding of the biology of weight regulation, many clinicians still believe that patients with obesity should have the willpower to eat less. The tendency to hold the patient with obesity responsible for their condition can be a barrier to greater acceptance of anti-obesity drugs as appropriate options for treatment. Physicians should be comfortable discussing the risks and benefits of these drugs, and health insurance companies should provide reasonable coverage for their use in patients who are most likely to benefit. Although few promising anti-obesity medications are in the drug-development pipeline, the most promising drugs are novel molecules that are co-agonists for multiple gut hormones including GLP-1, glucagon, and gastric inhibitory peptide.

      PubDate: 2017-09-18T05:54:12Z
      DOI: 10.1016/s2213-8587(17)30236-x
       
  • Metabolically healthy obesity: the low-hanging fruit in obesity
           treatment'
    • Authors: Norbert Stefan; Hans-Ulrich Häring; Matthias B Schulze
      Abstract: Publication date: Available online 14 September 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Norbert Stefan, Hans-Ulrich Häring, Matthias B Schulze
      Obesity increases the risk of several other chronic diseases and, because of its epidemic proportions, has become a major public health problem worldwide. Alarmingly, a lower proportion of adults have tried to lose weight during the past decade than during the mid-1980s to 1990s. The first-line treatment option for obesity is lifestyle intervention. Although this approach can decrease fat mass in the short term, these beneficial effects typically do not persist. If a large amount of weight loss is not an easily achievable goal, other goals that might motivate people with obesity to adopt a healthy lifestyle should be considered. In this setting, the concept of metabolically healthy obesity is useful. Accumulating evidence suggests that, although the risk of all-cause mortality and cardiovascular events might be higher in people with metabolically healthy obesity compared with metabolically healthy people of a normal weight, the risk is substantially lower than in individuals with metabolically unhealthy obesity. Therefore, every person with obesity should be motivated to achieve a normal weight in the long term, but more moderate weight loss sufficient for the transition from metabolically unhealthy obesity to metabolically healthy obesity might also lower the risk of adverse outcomes. However, how much weight needs to be lost for this transition to occur is under debate. This transition might be supported by lifestyle factors—such as the Mediterranean diet—that affect cardiovascular risk, independent of body fat. In this Series paper, we summarise available information about the concept of metabolically healthy obesity, highlight gaps in research, and discuss how this concept can be implemented in clinical care.

      PubDate: 2017-09-18T05:54:12Z
      DOI: 10.1016/s2213-8587(17)30292-9
       
  • Genetics of obesity: what genetic association studies have taught us about
           the biology of obesity and its complications
    • Authors: Mark O Goodarzi
      Abstract: Publication date: Available online 14 September 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Mark O Goodarzi
      Genome-wide association studies (GWAS) for BMI, waist-to-hip ratio, and other adiposity traits have identified more than 300 single-nucleotide polymorphisms (SNPs). Although there is reason to hope that these discoveries will eventually lead to new preventive and therapeutic agents for obesity, this will take time because such developments require detailed mechanistic understanding of how an SNP influences phenotype (and this information is largely unavailable). Fortunately, absence of functional information has not prevented GWAS findings from providing insights into the biology of obesity. Genes near loci regulating total body mass are enriched for expression in the CNS, whereas genes for fat distribution are enriched in adipose tissue itself. Gene by environment and lifestyle interaction analyses have revealed that our increasingly obesogenic environment might be amplifying genetic risk for obesity, yet those at highest risk could mitigate this risk by increasing physical activity and possibly by avoiding specific dietary components. GWAS findings have also been used in mendelian randomisation analyses probing the causal association between obesity and its many putative complications. In supporting a causal association of obesity with diabetes, coronary heart disease, specific cancers, and other conditions, these analyses have clinical relevance in identifying which outcomes could be preventable through weight loss interventions.

      PubDate: 2017-09-18T05:54:12Z
      DOI: 10.1016/s2213-8587(17)30200-0
       
  • Pioglitazone versus sulfonylureas: cardiovascular outcomes with older
           diabetes drugs
    • Authors: Vivian A Fonseca; Dragana Lovre
      Abstract: Publication date: Available online 13 September 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Vivian A Fonseca, Dragana Lovre


      PubDate: 2017-09-18T05:54:12Z
      DOI: 10.1016/s2213-8587(17)30320-0
       
  • Break point instead of ACE: acarbose, post-load glycaemic excursions, and
           cardiovascular events
    • Authors: Michael A Nauck; Juris J Meier
      Abstract: Publication date: Available online 13 September 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Michael A Nauck, Juris J Meier


      PubDate: 2017-09-18T05:54:12Z
      DOI: 10.1016/s2213-8587(17)30318-2
       
  • South Asian floods and Hurricane Harvey: diabetes in crisis
    • Authors: The Lancet Diabetes & Endocrinology
      Abstract: Publication date: Available online 6 September 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): The Lancet Diabetes & Endocrinology


      PubDate: 2017-09-11T05:40:38Z
      DOI: 10.1016/s2213-8587(17)30291-7
       
  • Is atrial fibrillation another manifestation of organ damage in
           diabetes'
    • Authors: Kazuo Miyazawa; Gregory Y H Lip
      Abstract: Publication date: Available online 30 August 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Kazuo Miyazawa, Gregory Y H Lip


      PubDate: 2017-09-06T05:22:50Z
      DOI: 10.1016/s2213-8587(17)30282-6
       
  • Macronutrients and cardiovascular risk in a global context
    • Authors: Nita G Forouhi; Naveed Sattar; Fumiaki Imamura
      Abstract: Publication date: Available online 29 August 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Nita G Forouhi, Naveed Sattar, Fumiaki Imamura


      PubDate: 2017-09-06T05:22:50Z
      DOI: 10.1016/s2213-8587(17)30285-1
       
  • Research misconduct and the INTERGROWTH-21st study
    • Authors: Lawrence D Platt; Torvid Kiserud; Marshall Lindheimer
      Abstract: Publication date: Available online 23 August 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Lawrence D Platt, Torvid Kiserud, Marshall Lindheimer


      PubDate: 2017-08-28T12:20:18Z
      DOI: 10.1016/s0140-6736(17)31365-x
       
  • New risk equations for complications of type 2 diabetes are welcome, but a
           broader perspective is needed
    • Authors: Coen D A Stehouwer
      Abstract: Publication date: Available online 10 August 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Coen D A Stehouwer


      PubDate: 2017-08-17T15:59:04Z
      DOI: 10.1016/s2213-8587(17)30232-2
       
  • Development and validation of Risk Equations for Complications Of type 2
           Diabetes (RECODe) using individual participant data from randomised trials
           
    • Authors: Sanjay Basu; Jeremy B Sussman; Seth A Berkowitz; Rodney A Hayward; John S Yudkin
      Abstract: Publication date: Available online 10 August 2017
      Source:The Lancet Diabetes & Endocrinology
      Author(s): Sanjay Basu, Jeremy B Sussman, Seth A Berkowitz, Rodney A Hayward, John S Yudkin
      Background In view of substantial mis-estimation of risks of diabetes complications using existing equations, we sought to develop updated Risk Equations for Complications Of type 2 Diabetes (RECODe). Methods To develop and validate these risk equations, we used data from the Action to Control Cardiovascular Risk in Diabetes study (ACCORD, n=9635; 2001–09) and validated the equations for microvascular events using data from the Diabetes Prevention Program Outcomes Study (DPPOS, n=1018; 1996–2001), and for cardiovascular events using data from the Action for Health in Diabetes (Look AHEAD, n=4760; 2001–12). Microvascular outcomes were nephropathy, retinopathy, and neuropathy. Cardiovascular outcomes were myocardial infarction, stroke, congestive heart failure, and cardiovascular mortality. We also included all-cause mortality as an outcome. We used a cross-validating machine learning method to select predictor variables from demographic characteristics, clinical variables, comorbidities, medications, and biomarkers into Cox proportional hazards models for each outcome. The new equations were compared to older risk equations by assessing model discrimination, calibration, and the net reclassification index. Findings All equations had moderate internal and external discrimination (C-statistics 0·55–0·84 internally, 0·57–0·79 externally) and high internal and external calibration (slopes 0·71–1·31 between observed and estimated risk). Our equations had better discrimination and calibration than the UK Prospective Diabetes Study Outcomes Model 2 (for microvascular and cardiovascular outcomes, C-statistics 0·54–0·62, slopes 0·06–1·12) and the American College of Cardiology/American Heart Association Pooled Cohort Equations (for fatal or non-fatal myocardial infarction or stroke, C-statistics 0·61–0·66, slopes 0·30–0·39). Interpretation RECODe might improve estimation of risk of complications for patients with type 2 diabetes. Funding National Institute for Diabetes and Digestive and Kidney Disease, National Heart, Lung and Blood Institute, and National Institute on Minority Health and Health Disparities, National Institutes of Health, and US Department of Veterans Affairs.

      PubDate: 2017-08-17T15:59:04Z
      DOI: 10.1016/s2213-8587(17)30221-8
       
 
 
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