Skip header and navigation

Refine By

15 records – page 1 of 2.

Associations between physical activity and fat mass in adolescents: the Stockholm Weight Development Study.

https://arctichealth.org/en/permalink/ahliterature49632
Source
Am J Clin Nutr. 2005 Feb;81(2):355-60
Publication Type
Article
Date
Feb-2005
Author
Ulf Ekelund
Martin Neovius
Yvonné Linné
Søren Brage
Nicholas J Wareham
Stephan Rössner
Author Affiliation
Medical Research Council Epidemiology Unit, Cambridge, United Kingdom. ue202@medschl.cam.ac.uk
Source
Am J Clin Nutr. 2005 Feb;81(2):355-60
Date
Feb-2005
Language
English
Publication Type
Article
Keywords
Adipose Tissue - metabolism
Adolescent
Anthropometry
Body Composition - physiology
Cohort Studies
Cross-Sectional Studies
Energy Metabolism - genetics - physiology
Exercise - physiology
Female
Humans
Longitudinal Studies
Male
Middle Aged
Mothers
Obesity - epidemiology - etiology - metabolism
Plethysmography, Whole Body - methods
Questionnaires
Research Support, Non-U.S. Gov't
Self Disclosure
Sex Factors
Socioeconomic Factors
Sweden - epidemiology
Abstract
BACKGROUND: Obesity is multifactorial. However, the accumulation of fat mass (FM) is proposed to be due to a positive energy balance, which may be caused by reduced physical activity (PA). OBJECTIVE: The objectives of the study were to describe the independent associations between PA and FM in adolescents and to describe the intergenerational association of FM between mothers and their offspring. DESIGN: We conducted a cross-sectional study in 445 (190 M, 255 F) 17-y-old adolescents and their mothers. PA was assessed with a self-reported questionnaire and validated by comparison with accelerometric data in a subsample of the cohort. Body composition was measured by using air-displacement plethysmography. RESULTS: Males were significantly more active than were females (P
Notes
Comment In: Am J Clin Nutr. 2005 Feb;81(2):337-815699218
PubMed ID
15699221 View in PubMed
Less detail

Change in cardiovascular risk factors following early diagnosis of type 2 diabetes: a cohort analysis of a cluster-randomised trial.

https://arctichealth.org/en/permalink/ahliterature266383
Source
Br J Gen Pract. 2014 Apr;64(621):e208-16
Publication Type
Article
Date
Apr-2014
Author
James A Black
Stephen J Sharp
Nicholas J Wareham
Annelli Sandbæk
Guy E H M Rutten
Torsten Lauritzen
Kamlesh Khunti
Melanie J Davies
Knut Borch-Johnsen
Simon J Griffin
Rebecca K Simmons
Source
Br J Gen Pract. 2014 Apr;64(621):e208-16
Date
Apr-2014
Language
English
Publication Type
Article
Keywords
Biological Markers - blood
Body mass index
Cardiovascular Diseases - blood - prevention & control
Cholesterol, HDL - blood
Cluster analysis
Cohort Studies
Creatinine - blood
Denmark
Diabetes Mellitus, Type 2 - blood - diagnosis - drug therapy
Early Diagnosis
England
Female
Follow-Up Studies
Hemoglobin A, Glycosylated - metabolism
Humans
Hypoglycemic agents - therapeutic use
Male
Middle Aged
Netherlands
Questionnaires
Risk assessment
Risk factors
Serum Albumin - metabolism
Triglycerides - blood
Abstract
There is little evidence to inform the targeted treatment of individuals found early in the diabetes disease trajectory.
To describe cardiovascular disease (CVD) risk profiles and treatment of individual CVD risk factors by modelled CVD risk at diagnosis; changes in treatment, modelled CVD risk, and CVD risk factors in the 5 years following diagnosis; and how these are patterned by socioeconomic status.
Cohort analysis of a cluster-randomised trial (ADDITION-Europe) in general practices in Denmark, England, and the Netherlands.
A total of 2418 individuals with screen-detected diabetes were divided into quartiles of modelled 10-year CVD risk at diagnosis. Changes in treatment, modelled CVD risk, and CVD risk factors were assessed at 5 years.
The largest reductions in risk factors and modelled CVD risk were seen in participants who were in the highest quartile of modelled risk at baseline, suggesting that treatment was offered appropriately. Participants in the lowest quartile of risk at baseline had very similar levels of modelled CVD risk at 5 years and showed the least variation in change in modelled risk. No association was found between socioeconomic status and changes in CVD risk factors, suggesting that treatment was equitable.
Diabetes management requires setting of individualised attainable targets. This analysis provides a reference point for patients, clinicians, and policymakers when considering goals for changes in risk factors early in the course of the disease that account for the diverse cardiometabolic profile present in individuals who are newly diagnosed with type 2 diabetes.
Notes
Cites: BMJ. 1998 Sep 12;317(7160):703-139732337
Cites: BMJ. 1998 Jan 10;316(7125):100-59462313
Cites: Lancet. 1999 Feb 20;353(9153):617-2210030326
Cites: Diabetologia. 2004 Oct;47(10):1747-5915517152
Cites: Heart. 2005 Dec;91 Suppl 5:v1-5216365341
Cites: Metabolism. 2006 May;55(5 Suppl 1):S2-516631806
Cites: Stat Med. 2007 Jan 30;26(2):443-5716526009
Cites: Diabet Med. 2007 Dec;24(12):1436-4117971182
Cites: Diabetes Care. 2008 Feb;31 Suppl 2:S222-518227489
Cites: N Engl J Med. 2008 Feb 7;358(6):580-9118256393
Cites: BMJ. 2008 Mar 1;336(7642):491-518276664
Cites: Diabetologia. 2008 Nov;51(11):1971-918779946
Cites: Br J Gen Pract. 2009 Jan;59(558):43-819105915
Cites: BMC Public Health. 2009;9:13619435491
Cites: Diabetologia. 2009 Oct;52(10):2001-1419629430
Cites: Trials. 2010;11:1620170482
Cites: Diabetologia. 2011 Feb;54(2):264-7021076956
Cites: Lancet. 2011 Jul 9;378(9786):156-6721705063
Cites: BMJ. 2012;344:e233322539172
Cites: Br J Gen Pract. 2012 Jun;62(599):e396-40222687231
Cites: Prim Care Diabetes. 2012 Oct;6(3):193-20022595031
Cites: Ugeskr Laeger. 2012 Sep 10;174(37):2159-6222971297
Cites: Diabet Med. 2012 Oct;29(10):1237-5222553954
Cites: Int J Behav Med. 2012 Dec;19(4):403-8823093473
Cites: Diabetes Care. 2013 Jan;36 Suppl 1:S11-6623264422
Cites: Diabetologia. 2013 Jun;56(6):1272-8123494447
Cites: Lancet. 2000 Jan 22;355(9200):253-910675071
Cites: Int J Obes Relat Metab Disord. 2000 Sep;24 Suppl 3:S6-1111063279
Cites: Diabetes Care. 2001 Jul;24(7):1167-7411423497
Cites: Lancet. 2004 Mar 6;363(9411):757-6715016485
Cites: Fam Pract. 1995 Jun;12(2):184-927589943
Cites: Diabetes Care. 1997 Apr;20(4):614-209096989
Cites: Med Care. 1997 Nov;35(11):1095-1089366889
Cites: Lancet. 1998 Sep 12;352(9131):837-539742976
PubMed ID
24686885 View in PubMed
Less detail

Common genetic determinants of vitamin D insufficiency: a genome-wide association study.

https://arctichealth.org/en/permalink/ahliterature142930
Source
Lancet. 2010 Jul 17;376(9736):180-8
Publication Type
Article
Date
Jul-17-2010
Author
Thomas J Wang
Feng Zhang
J Brent Richards
Bryan Kestenbaum
Joyce B van Meurs
Diane Berry
Douglas P Kiel
Elizabeth A Streeten
Claes Ohlsson
Daniel L Koller
Leena Peltonen
Jason D Cooper
Paul F O'Reilly
Denise K Houston
Nicole L Glazer
Liesbeth Vandenput
Munro Peacock
Julia Shi
Fernando Rivadeneira
Mark I McCarthy
Pouta Anneli
Ian H de Boer
Massimo Mangino
Bernet Kato
Deborah J Smyth
Sarah L Booth
Paul F Jacques
Greg L Burke
Mark Goodarzi
Ching-Lung Cheung
Myles Wolf
Kenneth Rice
David Goltzman
Nick Hidiroglou
Martin Ladouceur
Nicholas J Wareham
Lynne J Hocking
Deborah Hart
Nigel K Arden
Cyrus Cooper
Suneil Malik
William D Fraser
Anna-Liisa Hartikainen
Guangju Zhai
Helen M Macdonald
Nita G Forouhi
Ruth J F Loos
David M Reid
Alan Hakim
Elaine Dennison
Yongmei Liu
Chris Power
Helen E Stevens
Laitinen Jaana
Ramachandran S Vasan
Nicole Soranzo
Jörg Bojunga
Bruce M Psaty
Mattias Lorentzon
Tatiana Foroud
Tamara B Harris
Albert Hofman
John-Olov Jansson
Jane A Cauley
Andre G Uitterlinden
Quince Gibson
Marjo-Riitta Järvelin
David Karasik
David S Siscovick
Michael J Econs
Stephen B Kritchevsky
Jose C Florez
John A Todd
Josee Dupuis
Elina Hyppönen
Timothy D Spector
Author Affiliation
Division of Cardiology, Department of Medicine, Massachusetts General Hospital, Boston, MA 02114, USA. tjwang@partners.org
Source
Lancet. 2010 Jul 17;376(9736):180-8
Date
Jul-17-2010
Language
English
Publication Type
Article
Keywords
Canada
Chromosomes, Human, Pair 11
Chromosomes, Human, Pair 4
Cohort Studies
Dietary Supplements
Europe
European Continental Ancestry Group - genetics
Genetic Predisposition to Disease
Genome-Wide Association Study
Heterozygote
Homozygote
Humans
Immunoassay
International Cooperation
Linkage Disequilibrium
Polymorphism, Single Nucleotide
Seasons
United States
Vitamin D - analogs & derivatives - blood - genetics
Vitamin D Deficiency - blood - genetics - prevention & control
Abstract
Vitamin D is crucial for maintenance of musculoskeletal health, and might also have a role in extraskeletal tissues. Determinants of circulating 25-hydroxyvitamin D concentrations include sun exposure and diet, but high heritability suggests that genetic factors could also play a part. We aimed to identify common genetic variants affecting vitamin D concentrations and risk of insufficiency.
We undertook a genome-wide association study of 25-hydroxyvitamin D concentrations in 33 996 individuals of European descent from 15 cohorts. Five epidemiological cohorts were designated as discovery cohorts (n=16 125), five as in-silico replication cohorts (n=9367), and five as de-novo replication cohorts (n=8504). 25-hydroxyvitamin D concentrations were measured by radioimmunoassay, chemiluminescent assay, ELISA, or mass spectrometry. Vitamin D insufficiency was defined as concentrations lower than 75 nmol/L or 50 nmol/L. We combined results of genome-wide analyses across cohorts using Z-score-weighted meta-analysis. Genotype scores were constructed for confirmed variants.
Variants at three loci reached genome-wide significance in discovery cohorts for association with 25-hydroxyvitamin D concentrations, and were confirmed in replication cohorts: 4p12 (overall p=1.9x10(-109) for rs2282679, in GC); 11q12 (p=2.1x10(-27) for rs12785878, near DHCR7); and 11p15 (p=3.3x10(-20) for rs10741657, near CYP2R1). Variants at an additional locus (20q13, CYP24A1) were genome-wide significant in the pooled sample (p=6.0x10(-10) for rs6013897). Participants with a genotype score (combining the three confirmed variants) in the highest quartile were at increased risk of having 25-hydroxyvitamin D concentrations lower than 75 nmol/L (OR 2.47, 95% CI 2.20-2.78, p=2.3x10(-48)) or lower than 50 nmol/L (1.92, 1.70-2.16, p=1.0x10(-26)) compared with those in the lowest quartile.
Variants near genes involved in cholesterol synthesis, hydroxylation, and vitamin D transport affect vitamin D status. Genetic variation at these loci identifies individuals who have substantially raised risk of vitamin D insufficiency.
Full funding sources listed at end of paper (see Acknowledgments).
Notes
Cites: Am J Hum Genet. 2008 Apr;82(4):849-5818387595
Cites: Clin Chim Acta. 2006 Oct;372(1-2):33-4216697362
Cites: J Clin Endocrinol Metab. 2007 Dec;92(12):4615-2217726070
Cites: Diabetes Metab Res Rev. 2007 Nov;23(8):631-617607662
Cites: Am J Hum Genet. 2007 Nov;81(5):913-2617924335
Cites: J Bone Miner Res. 2001 Feb;16(2):371-811204437
Cites: Lancet. 2001 Nov 3;358(9292):1500-311705562
Cites: J Clin Invest. 2002 Sep;110(6):715-2412235098
Cites: Proc Natl Acad Sci U S A. 2004 May 18;101(20):7711-515128933
Cites: Lancet. 1989 Nov 18;2(8673):1176-82572900
Cites: Clin Chem. 1992 Sep;38(9):1796-8011526017
Cites: N Engl J Med. 1994 Jan 13;330(2):107-138259166
Cites: J Natl Cancer Inst. 1996 Oct 2;88(19):1375-828827015
Cites: Am J Clin Nutr. 2008 Aug;88(2):541S-544S18689398
Cites: Circulation. 2008 Jan 29;117(4):503-1118180395
Cites: Nat Genet. 2006 Feb;38(2):209-1316415888
Cites: Calcif Tissue Int. 2005 Jul;77(1):15-2215868280
Cites: J Inherit Metab Dis. 2005;28(1):69-8015702407
Cites: Arch Intern Med. 2008 Jun 9;168(11):1174-8018541825
Cites: Arch Dis Child. 2008 Jun;93(6):512-718339654
Cites: Arch Intern Med. 2007 Sep 10;167(16):1730-717846391
Cites: N Engl J Med. 2007 Jul 19;357(3):266-8117634462
Cites: J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):799-80217236760
Cites: Genet Epidemiol. 2008 May;32(4):381-518348202
Cites: Cancer Epidemiol Biomarkers Prev. 1999 May;8(5):399-40610350434
Cites: J Clin Endocrinol Metab. 2008 Sep;93(9):3381-818593774
Cites: Endocr Rev. 2008 Oct;29(6):726-7618694980
Cites: Am J Clin Nutr. 2009 Feb;89(2):634-4019116321
Cites: Eur J Clin Nutr. 2009 Apr;63(4):458-6418030310
Cites: Carcinogenesis. 2009 May;30(5):769-7619255064
Cites: BMJ. 2009;339:b369219797342
Cites: Thorax. 2010 Mar;65(3):215-2019996341
Cites: Ann Hum Genet. 1999 Sep;63(Pt 5):429-3910735584
Comment In: Lancet. 2010 Jul 17;376(9736):14220638551
Comment In: Lancet. 2010 Jul 17;376(9736):148-920541253
Comment In: Lancet. 2010 Oct 16;376(9749):130120951890
Comment On: Lancet. 2010 Jul 17;376(9736):14220638551
PubMed ID
20541252 View in PubMed
Less detail

Criterion-related validity of the last 7-day, short form of the International Physical Activity Questionnaire in Swedish adults.

https://arctichealth.org/en/permalink/ahliterature51744
Source
Public Health Nutr. 2006 Apr;9(2):258-65
Publication Type
Article
Date
Apr-2006
Author
Ulf Ekelund
Hanna Sepp
Sören Brage
Wulf Becker
Rupert Jakes
Mark Hennings
Nicholas J Wareham
Author Affiliation
National Food Administration, Uppsala, Sweden.
Source
Public Health Nutr. 2006 Apr;9(2):258-65
Date
Apr-2006
Language
English
Publication Type
Article
Abstract
Objective To examine the validity of the short, last 7-day, self-administered form of the International Physical Activity Questionnaire (IPAQ).Design All subjects wore an accelerometer for seven consecutive days and completed the IPAQ questionnaire on the eighth day. Criterion validity was assessed by linear regression analysis and by modified Bland-Altman analysis. Specificity and sensitivity were calculated for classifying respondents according to the physical activity guidelines of the American College of Sports Medicine/Centers for Disease Control and Prevention.Setting Workplaces in Uppsala, Sweden.Subjects One hundred and eighty-five (87 males) participants, aged 20 to 69 years.Results Total self-reported physical activity (PA) (MET-min day(-1)) was significantly correlated with average intensity of activity (counts min(-1)) from accelerometry (r=0.34, P
PubMed ID
16571181 View in PubMed
Less detail

Early Detection and Treatment of Type 2 Diabetes Reduce Cardiovascular Morbidity and Mortality: A Simulation of the Results of the Anglo-Danish-Dutch Study of Intensive Treatment in People With Screen-Detected Diabetes in Primary Care (ADDITION-Europe).

https://arctichealth.org/en/permalink/ahliterature270214
Source
Diabetes Care. 2015 Aug;38(8):1449-55
Publication Type
Article
Date
Aug-2015
Author
William H Herman
Wen Ye
Simon J Griffin
Rebecca K Simmons
Melanie J Davies
Kamlesh Khunti
Guy E H M Rutten
Annelli Sandbaek
Torsten Lauritzen
Knut Borch-Johnsen
Morton B Brown
Nicholas J Wareham
Source
Diabetes Care. 2015 Aug;38(8):1449-55
Date
Aug-2015
Language
English
Publication Type
Article
Keywords
Adult
Aged
Blood Glucose - metabolism
Blood Pressure - physiology
Cholesterol - blood
Computer simulation
Critical Care
Denmark - epidemiology
Diabetes Mellitus, Type 2 - mortality - prevention & control
Diabetic Angiopathies - mortality - prevention & control
Early Diagnosis
Female
Great Britain - epidemiology
Humans
Mass Screening - methods
Middle Aged
Netherlands - epidemiology
Primary Health Care
Risk factors
Abstract
To estimate the benefits of screening and early treatment of type 2 diabetes compared with no screening and late treatment using a simulation model with data from the ADDITION-Europe study.
We used the Michigan Model, a validated computer simulation model, and data from the ADDITION-Europe study to estimate the absolute risk of cardiovascular outcomes and the relative risk reduction associated with screening and intensive treatment, screening and routine treatment, and no screening with a 3- or 6-year delay in the diagnosis and routine treatment of diabetes and cardiovascular risk factors.
When the computer simulation model was programmed with the baseline demographic and clinical characteristics of the ADDITION-Europe population, it accurately predicted the empiric results of the trial. The simulated absolute risk reduction and relative risk reduction were substantially greater at 5 years with screening, early diagnosis, and routine treatment compared with scenarios in which there was a 3-year (3.3% absolute risk reduction [ARR], 29% relative risk reduction [RRR]) or a 6-year (4.9% ARR, 38% RRR) delay in diagnosis and routine treatment of diabetes and cardiovascular risk factors.
Major benefits are likely to accrue from the early diagnosis and treatment of glycemia and cardiovascular risk factors in type 2 diabetes. The intensity of glucose, blood pressure, and cholesterol treatment after diagnosis is less important than the time of its initiation. Screening for type 2 diabetes to reduce the lead time between diabetes onset and clinical diagnosis and to allow for prompt multifactorial treatment is warranted.
Notes
Cites: Diabetes Care. 2000 Oct;23(10):1563-8011023153
Cites: Lancet. 2010 Apr 17;375(9723):1365-7420356621
Cites: Diabet Med. 1996 Apr;13(4):337-409162609
Cites: Diabetologia. 2004 Oct;47(10):1747-5915517152
Cites: BMJ. 2007 Sep 8;335(7618):48617761995
Cites: BMJ. 2008 May 24;336(7654):1180-518426840
Cites: Diabetologia. 2008 Jul;51(7):1127-3418443762
Cites: BMJ. 2009;339:b453519948642
Cites: Int J Obes Relat Metab Disord. 2000 Sep;24 Suppl 3:S6-1111063279
Cites: Lancet. 2011 Jul 9;378(9786):156-6721705063
Cites: Diabetologia. 2012 Jun;55(6):1651-922237689
Cites: Diabetes Care. 2014 Jun;37(6):1668-7424705614
Cites: Diabetes Care. 1992 Jul;15(7):815-91516497
Comment In: Diabetes Care. 2015 Aug;38(8):1399-40126207050
PubMed ID
25986661 View in PubMed
Less detail

Effect of early intensive multifactorial therapy on 5-year cardiovascular outcomes in individuals with type 2 diabetes detected by screening (ADDITION-Europe): a cluster-randomised trial.

https://arctichealth.org/en/permalink/ahliterature133438
Source
Lancet. 2011 Jul 9;378(9786):156-67
Publication Type
Article
Date
Jul-9-2011
Author
Simon J Griffin
Knut Borch-Johnsen
Melanie J Davies
Kamlesh Khunti
Guy E H M Rutten
Annelli Sandbæk
Stephen J Sharp
Rebecca K Simmons
Maureen van den Donk
Nicholas J Wareham
Torsten Lauritzen
Author Affiliation
MRC Epidemiology Unit, Institute of Metabolic Science, Cambridge, UK. simon.griffin@mrc-epid.cam.ac.uk
Source
Lancet. 2011 Jul 9;378(9786):156-67
Date
Jul-9-2011
Language
English
Publication Type
Article
Keywords
Aged
Cluster analysis
Denmark - epidemiology
Diabetes Mellitus, Type 2 - diagnosis - drug therapy - mortality - therapy
Diabetic Angiopathies - mortality - prevention & control
Female
Great Britain - epidemiology
Humans
Hypoglycemic agents - therapeutic use
Intention to Treat Analysis
Male
Mass Screening
Middle Aged
Netherlands - epidemiology
Outcome Assessment (Health Care)
Risk factors
Abstract
Intensive treatment of multiple cardiovascular risk factors can halve mortality among people with established type 2 diabetes. We investigated the effect of early multifactorial treatment after diagnosis by screening.
In a pragmatic, cluster-randomised, parallel-group trial done in Denmark, the Netherlands, and the UK, 343 general practices were randomly assigned screening of registered patients aged 40-69 years without known diabetes followed by routine care of diabetes or screening followed by intensive treatment of multiple risk factors. The primary endpoint was first cardiovascular event, including cardiovascular mortality and morbidity, revascularisation, and non-traumatic amputation within 5 years. Patients and staff assessing outcomes were unaware of the practice's study group assignment. Analysis was done by intention to treat. This study is registered with ClinicalTrials.gov, number NCT00237549.
Primary endpoint data were available for 3055 (99
9%) of 3057 screen-detected patients. The mean age was 60
3 (SD 6
9) years and the mean duration of follow-up was 5
3 (SD 1
6) years. Improvements in cardiovascular risk factors (HbA(1c) and cholesterol concentrations and blood pressure) were slightly but significantly better in the intensive treatment group. The incidence of first cardiovascular event was 7
2% (13
5 per 1000 person-years) in the intensive treatment group and 8
5% (15
9 per 1000 person-years) in the routine care group (hazard ratio 0
83, 95% CI 0
65-1
05), and of all-cause mortality 6
2% (11
6 per 1000 person-years) and 6
7% (12
5 per 1000 person-years; 0
91, 0
69-1
21), respectively.
An intervention to promote early intensive management of patients with type 2 diabetes was associated with a small, non-significant reduction in the incidence of cardiovascular events and death.
National Health Service Denmark, Danish Council for Strategic Research, Danish Research Foundation for General Practice, Danish Centre for Evaluation and Health Technology Assessment, Danish National Board of Health, Danish Medical Research Council, Aarhus University Research Foundation, Wellcome Trust, UK Medical Research Council, UK NIHR Health Technology Assessment Programme, UK National Health Service R&D, UK National Institute for Health Research, Julius Center for Health Sciences and Primary Care, University Medical Center, Utrecht, Novo Nordisk, Astra, Pfizer, GlaxoSmithKline, Servier, HemoCue, Merck.
Notes
Cites: Eur J Clin Invest. 2002 Dec;32(12):924-3012534452
Cites: N Engl J Med. 2003 Jan 30;348(5):383-9312556541
Cites: Lancet. 2003 Jun 14;361(9374):2005-1612814710
Cites: Diabetes Care. 2003 Aug;26(8):2335-4012882858
Cites: Diabetes Care. 2004 Mar;27(3):727-3314988293
Cites: Diabetes Care. 1992 Jul;15(7):815-91516497
Cites: Diabetes. 1995 Nov;44(11):1249-587589820
Cites: Diabetes Care. 1997 Apr;20(4):491-69096967
Cites: Diabetes Care. 1997 Apr;20(4):614-209096989
Cites: BMJ. 1998 Sep 12;317(7160):703-139732337
Cites: Lancet. 1998 Sep 12;352(9131):837-539742976
Cites: Stat Med. 1999 Mar 30;18(6):695-70610204198
Cites: Stat Med. 2005 Apr 15;24(7):993-100715570623
Cites: Diabetologia. 2006 Jul;49(7):1536-4416752172
Cites: Lancet. 2010 Apr 17;375(9723):1365-7420356621
Cites: Diabet Med. 2010 Sep;27(9):995-100320722672
Cites: BMJ. 2007 Sep 8;335(7618):48617761995
Cites: N Engl J Med. 2006 Jul 27;355(4):375-8416870916
Cites: N Engl J Med. 2008 Feb 7;358(6):580-9118256393
Cites: BMJ. 2008 Mar 1;336(7642):491-518276664
Cites: Diabetologia. 2008 Jul;51(7):1127-3418443762
Cites: N Engl J Med. 2008 Oct 9;359(15):1577-8918784090
Cites: Diabetologia. 2008 Dec;51(12):2187-9618815769
Cites: Br J Gen Pract. 2009 Jan;59(558):43-819105915
Cites: Lancet. 2009 May 23;373(9677):1765-7219465231
Cites: Lancet. 2000 Jan 22;355(9200):253-910675071
Cites: BMC Public Health. 2009;9:13619435491
Cites: Trials. 2010;11:1620170482
Cites: Qual Life Res. 2010 May;19(4):509-1320155327
Cites: Diabetes Metab Res Rev. 2000 May-Jun;16(3):164-7110867715
Cites: Int J Obes Relat Metab Disord. 2000 Sep;24 Suppl 3:S6-1111063279
Cites: BMJ. 2001 Apr 21;322(7292):986-811312236
Cites: BMJ. 2001 Oct 27;323(7319):970-511679387
Comment In: Lancet. 2011 Jul 9;378(9786):106-821705070
Comment In: Lancet. 2012 Jan 28;379(9813):313; author reply 313-422284655
Erratum In: Lancet. 2012 Mar 3;379(9818):804
PubMed ID
21705063 View in PubMed
Less detail

Effect of early multifactorial therapy compared with routine care on microvascular outcomes at 5 years in people with screen-detected diabetes: a randomized controlled trial: the ADDITION-Europe Study.

https://arctichealth.org/en/permalink/ahliterature258858
Source
Diabetes Care. 2014 Jul;37(7):2015-23
Publication Type
Article
Date
Jul-2014
Author
Annelli Sandbæk
Simon J Griffin
Stephen J Sharp
Rebecca K Simmons
Knut Borch-Johnsen
Guy E H M Rutten
Maureen van den Donk
Nicholas J Wareham
Torsten Lauritzen
Melanie J Davies
Kamlesh Khunti
Source
Diabetes Care. 2014 Jul;37(7):2015-23
Date
Jul-2014
Language
English
Publication Type
Article
Keywords
Adult
Aged
Cluster analysis
Denmark - epidemiology
Diabetes Mellitus, Type 2 - complications - therapy
Diabetic Angiopathies - epidemiology
Diabetic Neuropathies - epidemiology
Female
Follow-Up Studies
General Practice - methods
Great Britain - epidemiology
Humans
Male
Mass Screening - methods
Middle Aged
Netherlands - epidemiology
Primary Health Care - methods
Questionnaires
Secondary Prevention
Abstract
To determine the benefit of multifactorial treatment on microvascular complications among people with type 2 diabetes detected by screening.
This study was a multicenter cluster randomized controlled trial in primary care with randomization at the practice level. In four centers in Denmark; Cambridge, U.K.; the Netherlands; and Leicester, U.K., 343 general practices participated in the trial. Eligible for follow-up were 2,861 of the 3,057 people with diabetes detected by screening included in the original trial. Biomedical data on nephropathy were collected in 2,710 (94.7%) participants, retinal photos in 2,190 (76.6%), and questionnaire data on peripheral neuropathy in 2,312 (80.9%). The prespecified microvascular end points were analyzed by intention to treat. Results from the four centers were pooled using fixed-effects meta-analysis.
Five years after diagnosis, any kind of albuminuria was present in 22.7% of participants in the intensive treatment (IT) group and in 24.4% in the routine care (RC) group (odds ratio 0.87 [95% CI 0.72-1.07]). Retinopathy was present in 10.2% of the IT group and 12.1% of the RC group (0.84 [0.64-1.10]), and severe retinopathy was present in one patient in the IT group and seven in the RC group. Neuropathy was present in 4.9% and 5.9% (0.95 [0.68-1.34]), respectively. Estimated glomerular filtration rate increased between baseline and follow-up in both groups (4.31 and 6.44 mL/min, respectively).
Compared with RC, an intervention to promote target-driven, intensive management of patients with type 2 diabetes detected by screening was not associated with significant reductions in the frequency of microvascular events at 5 years.
PubMed ID
24784827 View in PubMed
Less detail

Features of the metabolic syndrome are associated with objectively measured physical activity and fitness in Danish children: the European Youth Heart Study (EYHS).

https://arctichealth.org/en/permalink/ahliterature30168
Source
Diabetes Care. 2004 Sep;27(9):2141-8
Publication Type
Article
Date
Sep-2004
Author
Søren Brage
Niels Wedderkopp
Ulf Ekelund
Paul W Franks
Nicholas J Wareham
Lars Bo Andersen
Karsten Froberg
Author Affiliation
Institute of Sport & Health Biomechanics, University of Southern Denmark, Odense. sb400@medschl.cam.ac.uk
Source
Diabetes Care. 2004 Sep;27(9):2141-8
Date
Sep-2004
Language
English
Publication Type
Article
Keywords
Blood pressure
Child
Cross-Sectional Studies
Denmark - epidemiology
Exercise
Female
Humans
Male
Metabolic Syndrome X - epidemiology - physiopathology
Physical Examination
Physical Fitness
Research Support, Non-U.S. Gov't
Risk factors
Abstract
OBJECTIVE: Features of the metabolic syndrome are becoming increasingly evident in children. Decreased physical activity is likely to be an important etiological factor, as shown previously for subjective measures of physical activity in selected groups. The purpose of this study was to examine the relationship between the metabolic syndrome and objectively measured physical activity and whether fitness modified this relationship. RESEARCH DESIGN AND METHODS: A total of 589 Danish children (310 girls, 279 boys, mean [+/-SD] age 9.6 +/- 0.44 years, mean weight 33.6 +/- 6.4 kg, mean height 1.39 +/- 0.06 m) were randomly selected. Physical activity was measured with the uni-axial Computer Science & Applications accelerometer (MTI actigraph) worn at the hip for at least 3 days (>/=10 h/day) and fitness with a maximal bike test. As outcomes, we measured sitting systolic and diastolic blood pressure, degree of adiposity (sum of four skinfolds), and, finally, insulin, glucose, triglicerides, and HDL cholesterol in fasting blood samples. The outcome variables were statistically normalized and expressed as the number of SDs from the mean. (i.e., Z scores). A metabolic syndrome risk score was computed as the mean of these Z scores. Multiple linear regression was used to test the association between physical activity and metabolic risk, adjusted primarily for age, sex, sexual maturation, ethnicity, parental smoking, socioeconomic factors, and the Computer Science & Applications unit, as well as for fitness. Robust SEs were computed by clustering on school. RESULTS: All children were in the nondiabetic range of fasting glucose. Metabolic risk was inversely related to physical activity (P = 0.008). The relationship was weakened after adjustment for fitness, but there was a significantly positive interaction between physical activity and fitness. CONCLUSIONS: Physical activity is inversely associated with metabolic risk, independently of potential confounders. The interaction between physical activity and fitness suggests that the potential beneficial effect of activity may be greatest in children with lower cardiorespiratory fitness.
PubMed ID
15333475 View in PubMed
Less detail

Food composition of the diet in relation to changes in waist circumference adjusted for body mass index.

https://arctichealth.org/en/permalink/ahliterature131961
Source
PLoS One. 2011;6(8):e23384
Publication Type
Article
Date
2011
Author
Dora Romaguera
Lars Ã?ngquist
Huaidong Du
Marianne Uhre Jakobsen
Nita G Forouhi
Jytte Halkjær
Edith J M Feskens
Daphne L van der A
Giovanna Masala
Annika Steffen
Domenico Palli
Nicholas J Wareham
Kim Overvad
Anne Tjønneland
Heiner Boeing
Elio Riboli
Thorkild I Sørensen
Author Affiliation
Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, United Kingdom. d.romaguera-bosch@imperial.ac.uk
Source
PLoS One. 2011;6(8):e23384
Date
2011
Language
English
Publication Type
Article
Keywords
Abdominal Fat - metabolism
Adiposity - physiology
Adult
Aged
Body Composition - physiology
Body mass index
Dairy Products
Denmark
Diet
Female
Food
Fruit
Germany
Glycemic Index
Great Britain
Humans
Italy
Linear Models
Male
Meat
Middle Aged
Netherlands
Waist Circumference - physiology
Abstract
Dietary factors such as low energy density and low glycemic index were associated with a lower gain in abdominal adiposity. A better understanding of which food groups/items contribute to these associations is necessary.
To ascertain the association of food groups/items consumption on prospective annual changes in "waist circumference for a given BMI" (WC(BMI)), a proxy for abdominal adiposity.
We analyzed data from 48,631 men and women from 5 countries participating in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Anthropometric measurements were obtained at baseline and after a median follow-up time of 5.5 years. WC(BMI) was defined as the residuals of waist circumference regressed on BMI, and annual change in WC(BMI) (?WC(BMI), cm/y) was defined as the difference between residuals at follow-up and baseline, divided by follow-up time. The association between food groups/items and ?WC(BMI) was modelled using centre-specific adjusted linear regression, and random-effects meta-analyses to obtain pooled estimates.
Higher fruit and dairy products consumption was associated with a lower gain in WC(BMI) whereas the consumption of white bread, processed meat, margarine, and soft drinks was positively associated with ?WC(BMI). When these six food groups/items were analyzed in combination using a summary score, those in the highest quartile of the score--indicating a more favourable dietary pattern--showed a ?WC(BMI) of -0.11 (95% CI -0.09 to -0.14) cm/y compared to those in the lowest quartile.
A dietary pattern high in fruit and dairy and low in white bread, processed meat, margarine, and soft drinks may help to prevent abdominal fat accumulation.
Notes
Cites: Int J Obes (Lond). 2005 Jul;29(7):778-8415917857
Cites: J Nutr. 2005 Sep;135(9):2263-7016140909
Cites: Diabetes Care. 2005 Dec;28(12):2823-3116306540
Cites: Am J Clin Nutr. 2006 Feb;83(2):284-9016469985
Cites: Eur J Clin Nutr. 2007 Sep;61(9):1037-5617375121
Cites: Arch Intern Med. 2008 Apr 14;168(7):713-2018413553
Cites: Obesity (Silver Spring). 2008 Jul;16(7):1693-718451775
Cites: Am J Clin Nutr. 2008 Nov;88(5):1248-5518996859
Cites: N Engl J Med. 2008 Nov 13;359(20):2105-2019005195
Cites: PLoS One. 2009;4(4):e533919396357
Cites: J Nutr. 2009 Oct;139(10):1950-519726588
Cites: Int J Obes (Lond). 2009 Nov;33(11):1280-819704411
Cites: Am J Clin Nutr. 2009 Dec;90(6):1632-4119828709
Cites: Am J Clin Nutr. 2010 Feb;91(2):329-3620016015
Cites: Public Health Nutr. 2010 Jun;13(6):797-80519772691
Cites: PLoS One. 2010;5(7):e1158820644647
Cites: PLoS One. 2010;5(9). pii: e13097. doi: 10.1371/journal.pone.001309720927346
Cites: Am J Clin Nutr. 2010 Nov;92(5):1017-2220810979
Cites: Am J Clin Nutr. 2010 Nov;92(5):1165-7120881074
Cites: Obesity (Silver Spring). 2010 Nov;18(11):2101-420203630
Cites: Am J Clin Nutr. 2010 Dec;92(6):1429-3521097651
Cites: Diabetes Care. 2011 Jan;34(1):55-720843978
Cites: Int J Obes Relat Metab Disord. 2000 Jan;24(1):60-910702752
Cites: N Engl J Med. 2001 Jan 4;344(1):3-1011136953
Cites: J Hum Hypertens. 2001 May;15(5):307-1211378832
Cites: Am J Clin Nutr. 2001 Jul;74(1):80-911451721
Cites: Am J Clin Nutr. 2002 Apr;75(4):683-811916754
Cites: Public Health Nutr. 2002 Dec;5(6B):1113-2412639222
Cites: Public Health Nutr. 2002 Dec;5(6B):1147-6212639224
Cites: Am J Clin Nutr. 2003 Jun;77(6):1417-2512791618
Cites: Public Health Nutr. 2003 Jun;6(4):407-1312795830
Cites: Obes Res. 2003 Jul;11(7):895-90312855760
Cites: N Engl J Med. 1997 Apr 17;336(16):1117-249099655
Cites: Int J Epidemiol. 1997;26 Suppl 1:S15-259126530
Cites: Int J Epidemiol. 1998 Jun;27(3):422-309698130
Cites: Br J Nutr. 2004 Oct;92(4):735-4815522143
PubMed ID
21858094 View in PubMed
Less detail

Genetic Predisposition to an Impaired Metabolism of the Branched-Chain Amino Acids and Risk of Type 2 Diabetes: A Mendelian Randomisation Analysis.

https://arctichealth.org/en/permalink/ahliterature282592
Source
PLoS Med. 2016 Nov;13(11):e1002179
Publication Type
Article
Date
Nov-2016
Author
Luca A Lotta
Robert A Scott
Stephen J Sharp
Stephen Burgess
Jian'an Luan
Therese Tillin
Amand F Schmidt
Fumiaki Imamura
Isobel D Stewart
John R B Perry
Luke Marney
Albert Koulman
Edward D Karoly
Nita G Forouhi
Rasmus J O Sjögren
Erik Näslund
Juleen R Zierath
Anna Krook
David B Savage
Julian L Griffin
Nishi Chaturvedi
Aroon D Hingorani
Kay-Tee Khaw
Inês Barroso
Mark I McCarthy
Stephen O'Rahilly
Nicholas J Wareham
Claudia Langenberg
Source
PLoS Med. 2016 Nov;13(11):e1002179
Date
Nov-2016
Language
English
Publication Type
Article
Keywords
Adult
Aged
Amino Acids, Branched-Chain - metabolism
Diabetes Mellitus, Type 2 - genetics - metabolism - physiopathology
Genetic Predisposition to Disease
Genome-Wide Association Study
Humans
Male
Mendelian Randomization Analysis
Middle Aged
Prospective Studies
Risk factors
Sweden
Young Adult
Abstract
Higher circulating levels of the branched-chain amino acids (BCAAs; i.e., isoleucine, leucine, and valine) are strongly associated with higher type 2 diabetes risk, but it is not known whether this association is causal. We undertook large-scale human genetic analyses to address this question.
Genome-wide studies of BCAA levels in 16,596 individuals revealed five genomic regions associated at genome-wide levels of significance (p
Notes
Cites: Hum Mutat. 2013 Feb;34(2):355-6223086801
Cites: Diabetologia. 2015 Oct;58(10):2324-3526254576
Cites: Bioinformatics. 2008 Dec 15;24(24):2938-918974171
Cites: Nat Genet. 2013 Nov;45(11):1274-8324097068
Cites: Diabetes. 2013 Aug;62(8):2689-9823382451
Cites: Nat Genet. 2015 Dec;47(12):1385-9226523775
Cites: N Engl J Med. 1969 Oct 9;281(15):811-65809519
Cites: Circ Cardiovasc Genet. 2015 Feb;8(1):192-20625691689
Cites: PLoS Med. 2014 Dec 09;11(12):e100176525490400
Cites: Nature. 2016 Jul 21;535(7612):376-8127409811
Cites: N Engl J Med. 2014 Nov 27;371(22):2072-8225390462
Cites: Hum Mol Genet. 2009 Nov 1;18(21):4081-819643913
Cites: Cell Metab. 2009 Apr;9(4):311-2619356713
Cites: Nat Rev Endocrinol. 2014 Dec;10(12):723-3625287287
Cites: Cell Metab. 2014 Nov 4;20(5):898-90925307860
Cites: Science. 2013 Sep 6;341(6150):124121424009397
Cites: Lancet. 2012 Mar 31;379(9822):1173-422463865
Cites: Hum Mol Genet. 2011 Feb 15;20(4):631-4021098507
Cites: Diabetes. 2010 Feb;59(2):448-5919903739
Cites: Cell Metab. 2012 Jul 3;16(1):122-3422768844
Cites: Br J Cancer. 1999 Jul;80 Suppl 1:95-10310466767
Cites: JAMA. 2016 Oct 4;316(13):1383-139127701660
Cites: Diabetes. 2015 Jan;64(1):49-5925071024
Cites: Mol Syst Biol. 2008;4:21418682704
Cites: Nat Genet. 2012 Jan 29;44(3):269-7622286219
Cites: Diabetes. 1964 Sep-Oct;13:451-6114208234
Cites: Bioinformatics. 2010 Sep 1;26(17):2190-120616382
Cites: Proc Natl Acad Sci U S A. 2013 Jun 11;110(24):9728-3323716694
Cites: Diabetes Care. 2014 Dec;37(12):3150-625315204
Cites: J Clin Invest. 2009 Jun;119(6):1678-8719411760
Cites: J Am Coll Cardiol. 2015 Apr 21;65(15):1552-6125770315
Cites: Nat Rev Genet. 2010 Jul;11(7):499-51120517342
Cites: Rom J Intern Med. 1994 Jan-Mar;32(1):57-618081313
Cites: Stat Med. 2016 May 20;35(11):1880-90626661904
Cites: Mol Genet Metab. 2014 Sep-Oct;113(1-2):131-525042691
Cites: Nat Genet. 2015 Nov;47(11):1236-4126414676
Cites: N Engl J Med. 2006 Mar 23;354(12 ):1264-7216554528
Cites: Nature. 1975 Apr 10;254(5500):529-301121328
Cites: Lancet. 2012 Aug 11;380(9841):572-8022607825
Cites: Diabetes. 2013 Feb;62(2):639-4823043162
Cites: Nat Genet. 2014 Jun;46(6):543-5024816252
Cites: J Clin Invest. 2011 Apr;121(4):1402-1121403394
Cites: Cell Metab. 2013 Jul 2;18(1):130-4323823483
Cites: Nat Genet. 2012 May 13;44(6):659-6922581228
Cites: Nat Genet. 2012 Sep;44(9):991-100522885924
Cites: Nature. 2015 Feb 12;518(7538):187-9625673412
Cites: Sci Transl Med. 2016 Jun 1;8(341):341ra7627252175
Cites: Circulation. 2013 Mar 26;127(12 ):1283-923446828
Cites: Nat Med. 2011 Apr;17(4):448-5321423183
Cites: Diabetes. 2011 Mar;60(3):918-2421270237
Cites: Bioinformatics. 2017 Jan 15;33(2):272-27927663502
Cites: Structure. 2004 Dec;12(12):2185-9615576032
Cites: Hepatol Int. 2013 Jun;7(2):577-8526201790
Cites: J Clin Endocrinol Metab. 2015 Mar;100(3):E463-825423564
Cites: Diabetes. 2007 Nov;56(11):2722-3117682092
Cites: Mol Syst Biol. 2012;8:61523010998
Cites: Cancer Res. 2004 Aug 1;64(15):5245-5015289330
Cites: Diabetologia. 2011 Sep;54(9):2272-8221717116
Cites: Genet Epidemiol. 2013 Nov;37(7):658-6524114802
Cites: Nature. 2015 Feb 12;518(7538):197-20625673413
Cites: Nat Genet. 2012 Sep;44(9):981-9022885922
Cites: Diabetes. 2013 Dec;62(12):4270-623884885
Cites: J Biol Chem. 1994 Jul 15;269(28):18583-78034607
Cites: PLoS Med. 2015 Jun 16;12(6):e1001841; discussion e100184126079503
Cites: Diabetes. 2014 Dec;63(12):4378-8724947364
Cites: Diabetologia. 2015 May;58(5):968-7925693751
Cites: Cell Metab. 2012 May 2;15(5):606-1422560213
Cites: Int J Epidemiol. 2003 Feb;32(1):1-2212689998
Cites: J Natl Cancer Inst. 2015 Jul 01;107(9):null26134033
Cites: J Biol Chem. 2014 Jul 25;289(30):20583-9324895126
PubMed ID
27898682 View in PubMed
Less detail

15 records – page 1 of 2.