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Adipose tissue density, a novel biomarker predicting mortality risk in older adults.

https://arctichealth.org/en/permalink/ahliterature113601
Source
J Gerontol A Biol Sci Med Sci. 2014 Jan;69(1):109-17
Publication Type
Article
Date
Jan-2014
Author
Rachel A Murphy
Thomas C Register
Carol A Shively
J Jeffrey Carr
Yaorong Ge
Marta E Heilbrun
Steven R Cummings
Annemarie Koster
Michael C Nevitt
Suzanne Satterfield
Frances A Tylvasky
Elsa S Strotmeyer
Anne B Newman
Eleanor M Simonsick
Ann Scherzinger
Bret H Goodpaster
Lenore J Launer
Gudny Eiriksdottir
Sigurdur Sigurdsson
Gunnar Sigurdsson
Vilmundur Gudnason
Thomas F Lang
Stephen B Kritchevsky
Tamara B Harris
Author Affiliation
Laboratory of Population Science, National Institute on Aging, 7201 Wisconsin Ave, 3C-309 Bethesda, MD 20814. rachel.murphy@nih.gov.
Source
J Gerontol A Biol Sci Med Sci. 2014 Jan;69(1):109-17
Date
Jan-2014
Language
English
Publication Type
Article
Keywords
Absorptiometry, Photon
Adiponectin - metabolism
Adipose Tissue - metabolism - radiography
Aged
Aged, 80 and over
Aging - physiology
Animals
Biological Markers - metabolism
Body mass index
Female
Follow-Up Studies
Humans
Leptin - metabolism
Macaca fascicularis
Male
Obesity - metabolism - mortality - radiography
Prognosis
Prospective Studies
Risk factors
Survival Rate - trends
Abstract
Knowledge of adipose composition in relation to mortality may help delineate inconsistent relationships between obesity and mortality in old age. We evaluated relationships between abdominal visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) density, mortality, biomarkers, and characteristics.
VAT and SAT density were determined from computed tomography scans in persons aged 65 and older, Health ABC (n = 2,735) and AGES-Reykjavik (n = 5,131), and 24 nonhuman primates (NHPs). Associations between adipose density and mortality (4-13 years follow-up) were assessed with Cox proportional hazards models. In NHPs, adipose density was related to serum markers and tissue characteristics.
Higher density adipose tissue was associated with mortality in both studies with adjustment for risk factors including adipose area, total fat, and body mass index. In women, hazard ratio and 95% CI for the densest quintile (Q5) versus least dense (Q1) for VAT density were 1.95 (1.36-2.80; Health ABC) and 1.88 (1.31-2.69; AGES-Reykjavik) and for SAT density, 1.76 (1.35-2.28; Health ABC) and 1.56 (1.15-2.11; AGES-Reykjavik). In men, VAT density was associated with mortality in Health ABC, 1.52 (1.12-2.08), whereas SAT density was associated with mortality in both Health ABC, 1.58 (1.21-2.07), and AGES-Reykjavik, 1.43 (1.07-1.91). Higher density adipose tissue was associated with smaller adipocytes in NHPs. There were no consistent associations with inflammation in any group. Higher density adipose tissue was associated with lower serum leptin in Health ABC and NHPs, lower leptin mRNA expression in NHPs, and higher serum adiponectin in Health ABC and NHPs.
VAT and SAT density provide a unique marker of mortality risk that does not appear to be inflammation related.
PubMed ID
23707956 View in PubMed
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Adipose Tissue, Muscle, and Function: Potential Mediators of Associations Between Body Weight and Mortality in Older Adults With Type 2 Diabetes.

https://arctichealth.org/en/permalink/ahliterature257280
Source
Diabetes Care. 2014 Oct 14;
Publication Type
Article
Date
Oct-14-2014
Author
Rachel A Murphy
Ilse Reinders
Melissa E Garcia
Gudny Eiriksdottir
Lenore J Launer
Rafn Benediktsson
Vilmundur Gudnason
Palmi V Jonsson
Tamara B Harris
Author Affiliation
Laboratory of Epidemiology and Population Sciences, National Institute on Aging, Bethesda, MD rachel.murphy@nih.gov.
Source
Diabetes Care. 2014 Oct 14;
Date
Oct-14-2014
Language
English
Publication Type
Article
Abstract
Studies in type 2 diabetes report both increased mortality for normal weight and no evidence of an obesity paradox. We aimed to examine whether adipose tissue, muscle size, and physical function, which are known to vary by weight, mediate associations between BMI and mortality.
The AGES-Reykjavik cohort comprised participants aged 66-96 years with diabetes defined by fasting glucose, medications, or self-report. BMI was determined from measured height and weight and classified as normal (18.5-24.9 kg/m(2), n = 117), overweight (25.0-29.9 kg/m(2), n = 293, referent group) or obese (=30.0 kg/m(2), n = 227). Thigh muscle area and intermuscular, visceral, and subcutaneous adipose tissues were assessed with computed tomography. Function was assessed from gait speed and knee extensor strength. Hazard ratios (HRs) and 95% CIs were estimated by Cox proportional hazards regression adjusted for demographics and diabetes-related risk factors.
The median follow-up was 6.66 years, and there were 85, 59, and 44 deaths among normal weight, overweight, and obese participants, respectively. There was no mortality risk for obese participants and an increased risk among normal weight compared with overweight participants (HR 1.72 [95% CI 1.12-2.64]). Associations remained with adjustment for adipose tissues and knee extensor strength; however, mortality risk for normal weight was attenuated following adjustment for thigh muscle (HR 1.36 [95% CI 0.87-2.11]) and gait speed (HR 1.44 [95% CI 0.91-2.27]). Linear regression confirmed with bootstrapping indicated that thigh muscle size mediated 46% of the relationship between normal weight and mortality.
Normal weight participants had elevated mortality risk compared with overweight participants. This paradoxical association was mediated in part by muscle size.
PubMed ID
25315206 View in PubMed
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Age-related macular degeneration and mortality in community-dwelling elders: the age, gene/environment susceptibility Reykjavik study.

https://arctichealth.org/en/permalink/ahliterature261803
Source
Ophthalmology. 2015 Feb;122(2):382-90
Publication Type
Article
Date
Feb-2015
Author
Diana E Fisher
Fridbert Jonasson
Gudny Eiriksdottir
Sigurdur Sigurdsson
Ronald Klein
Lenore J Launer
Vilmundur Gudnason
Mary Frances Cotch
Source
Ophthalmology. 2015 Feb;122(2):382-90
Date
Feb-2015
Language
English
Publication Type
Article
Keywords
Age Factors
Aged
Aged, 80 and over
Cause of Death
Cohort Studies
Disease Susceptibility
Female
Follow-Up Studies
Gene-Environment Interaction
Humans
Iceland - epidemiology
Incidence
Macular Degeneration - mortality
Male
Proportional Hazards Models
Prospective Studies
Risk factors
Abstract
To investigate the association between age-related macular degeneration (AMD) and mortality in older persons.
Population-based prospective cohort study.
Participants 67 to 96 years of age (43.1% male) enrolled between 2002 and 2006 in the Age, Gene/Environment Susceptibility-Reykjavik Study.
Retinal photographs of the macula were acquired digitally and evaluated for the presence of AMD lesions using the Wisconsin Age-Related Maculopathy grading scheme. Mortality was assessed prospectively through 2013 with cause of death available through 2009. The association between AMD and death, resulting from any cause and specifically cardiovascular disease (CVD), was examined using Cox proportional hazards regression with age as the time scale, adjusted for significant risk factors and comorbid conditions. To address a violation in the proportional hazards assumption, analyses were stratified into 2 groups based on the mean age at death (83 years).
Mortality resulting from all causes and CVD.
Among 4910 participants, after a median follow-up of 8.6 years, 1742 died (35.5%), of whom 614 (35.2%) had signs of AMD at baseline. Cardiovascular disease was the cause of death for 357 people who died before the end of 2009, of whom 144 (40%) had AMD (101 with early disease and 43 with late disease). After considering covariates, including comorbid conditions, having early AMD at any age or having late AMD in individuals younger than 83 years (n = 4179) were not associated with all-cause or CVD mortality. In individuals 83 years of age and older (n = 731), late AMD was associated significantly with increased risk of all-cause mortality (hazard ratio [HR], 1.76; 95% confidence interval [CI], 1.20-2.57) and CVD-related mortality (HR, 2.37; 95% CI, 1.41-3.98). In addition to having AMD, older individuals who died were more likely to be male and to have low body mass index, impaired cognition, and microalbuminuria.
Competing risk factors and concomitant conditions are important in determining mortality risk resulting from AMD. Individuals with early AMD are not more likely to die than peers of comparable age. Late AMD becomes a predictor of mortality by the mid-octogenarian years.
Notes
Cites: Arch Ophthalmol. 2000 Mar;118(3):351-810721957
Cites: Arch Ophthalmol. 2001 Oct;119(10):1455-6211594944
Cites: Eur Heart J. 2003 Jun;24(11):987-100312788299
Cites: Arch Ophthalmol. 2003 Jun;121(6):785-9212796248
Cites: Ophthalmology. 2003 Jul;110(7):1292-612867381
Cites: Arch Ophthalmol. 2004 May;122(5):716-2615136320
Cites: Ophthalmology. 1991 Jul;98(7):1128-341843453
Cites: Arch Ophthalmol. 1992 Dec;110(12):1701-81281403
Cites: Ophthalmology. 1993 Mar;100(3):406-148460013
Cites: Arch Ophthalmol. 1995 Mar;113(3):333-97887847
Cites: Am J Epidemiol. 1995 Aug 15;142(4):404-97625405
Cites: JAMA. 1996 Oct 9;276(14):1141-68827966
Cites: Arch Ophthalmol. 1998 May;116(5):583-79596493
Cites: Arch Ophthalmol. 2004 Nov;122(11):1642-615534124
Cites: Ophthalmology. 2005 Feb;112(2):305-1215691568
Cites: Arch Ophthalmol. 2005 Oct;123(10):1397-40316219731
Cites: Arch Ophthalmol. 2006 Feb;124(2):243-916476894
Cites: Ophthalmology. 2006 Mar;113(3):373-8016513455
Cites: Ophthalmology. 2007 Jan;114(1):86-9117198851
Cites: Am J Epidemiol. 2007 May 1;165(9):1076-8717351290
Cites: Arch Ophthalmol. 2007 Jul;125(7):917-2417620571
Cites: Br J Ophthalmol. 2008 Apr;92(4):509-1218310310
Cites: Am J Epidemiol. 2008 Nov 15;168(10):1132-918836152
Cites: Exp Gerontol. 2009 Apr;44(4):297-919000922
Cites: Ophthalmology. 2009 Apr;116(4):732-819195709
Cites: Ophthalmology. 2011 May;118(5):825-3021126770
Cites: Arch Ophthalmol. 2012 Sep;130(9):1169-7622965593
Cites: Hum Mol Genet. 2012 Dec 1;21(23):5229-3622936692
Cites: Age Ageing. 2014 Jan;43(1):69-7623996030
Cites: Ophthalmology. 2014 Sep;121(9):1766-7224768241
PubMed ID
25264026 View in PubMed
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The AGES-Reykjavik study atlases: Non-linear multi-spectral template and atlases for studies of the ageing brain.

https://arctichealth.org/en/permalink/ahliterature282555
Source
Med Image Anal. 2017 May 06;39:133-144
Publication Type
Article
Date
May-06-2017
Author
Lars Forsberg
Sigurdur Sigurdsson
Jesper Fredriksson
Asdis Egilsdottir
Bryndis Oskarsdottir
Olafur Kjartansson
Mark A van Buchem
Lenore J Launer
Vilmundur Gudnason
Alex Zijdenbos
Source
Med Image Anal. 2017 May 06;39:133-144
Date
May-06-2017
Language
English
Publication Type
Article
Abstract
Quantitative analyses of brain structures from Magnetic Resonance (MR) image data are often performed using automatic segmentation algorithms. Many of these algorithms rely on templates and atlases in a common coordinate space. Most freely available brain atlases are generated from relatively young individuals and not always derived from well-defined cohort studies. In this paper, we introduce a publicly available multi-spectral template with corresponding tissue probability atlases and regional atlases, optimised to use in studies of ageing cohorts (mean age 75 ± 5 years). Furthermore, we provide validation data from a regional segmentation pipeline to assure the integrity of the dataset.
PubMed ID
28501699 View in PubMed
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The AGES-Reykjavik study atlases: Non-linear multi-spectral template and atlases for studies of the ageing brain.

https://arctichealth.org/en/permalink/ahliterature292006
Source
Med Image Anal. 2017 Jul; 39:133-144
Publication Type
Journal Article
Date
Jul-2017
Author
Lars Forsberg
Sigurdur Sigurdsson
Jesper Fredriksson
Asdis Egilsdottir
Bryndis Oskarsdottir
Olafur Kjartansson
Mark A van Buchem
Lenore J Launer
Vilmundur Gudnason
Alex Zijdenbos
Author Affiliation
The Icelandic Heart Association, Kopavogur, Iceland; Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden. Electronic address: larsef@me.com.
Source
Med Image Anal. 2017 Jul; 39:133-144
Date
Jul-2017
Language
English
Publication Type
Journal Article
Keywords
Aged
Aging
Algorithms
Anatomy, Artistic
Atlases as Topic
Brain - diagnostic imaging
Female
Humans
Image Processing, Computer-Assisted - methods
Magnetic Resonance Imaging - methods
Male
Abstract
Quantitative analyses of brain structures from Magnetic Resonance (MR) image data are often performed using automatic segmentation algorithms. Many of these algorithms rely on templates and atlases in a common coordinate space. Most freely available brain atlases are generated from relatively young individuals and not always derived from well-defined cohort studies. In this paper, we introduce a publicly available multi-spectral template with corresponding tissue probability atlases and regional atlases, optimised to use in studies of ageing cohorts (mean age 75 ± 5 years). Furthermore, we provide validation data from a regional segmentation pipeline to assure the integrity of the dataset.
Notes
Cites: Neuroimage. 2010 Feb 1;49(3):2352-65 PMID 19857578
Cites: Neuroimage. 2004;23 Suppl 1:S208-19 PMID 15501092
Cites: Stroke. 2008 Apr;39(4):1134-41 PMID 18323507
Cites: J Cereb Blood Flow Metab. 1990 Jul;10 (4):443-57 PMID 2347878
Cites: Neuron. 2002 Jan 31;33(3):341-55 PMID 11832223
Cites: Neuroimage. 2008 Feb 1;39(3):1064-80 PMID 18037310
Cites: Neuroimage. 1997 Oct;6(3):209-17 PMID 9344825
Cites: NMR Biomed. 2015 Apr;28(4):468-85 PMID 25802212
Cites: Neuroimage. 2006 Oct 15;33(1):115-26 PMID 16860573
Cites: Neuroimage. 2011 Jan 1;54(1):313-27 PMID 20656036
Cites: Neuroimage. 2009 Jul 1;46(3):726-38 PMID 19245840
Cites: Neuroimage. 2001 Jul;14(1 Pt 1):21-36 PMID 11525331
Cites: J Comput Assist Tomogr. 1994 Mar-Apr;18(2):192-205 PMID 8126267
Cites: IEEE Trans Med Imaging. 2007 Apr;26(4):479-86 PMID 17427735
Cites: Image Vis Comput. 2001 Jan 1;19(1-2):3-24 PMID 19890483
Cites: Neuroimage. 2005 Jul 15;26(4):1009-18 PMID 15908234
Cites: Comput Methods Programs Biomed. 2011 Dec;104(3):e158-77 PMID 21871688
Cites: IEEE Trans Med Imaging. 2002 Oct;21(10):1280-91 PMID 12585710
Cites: Ann N Y Acad Sci. 2002 Nov;977:141-8 PMID 12480744
Cites: Neuroimage. 1995 Jun;2(2):89-101 PMID 9343592
Cites: Neuroimage. 2007 Apr 1;35(2):686-97 PMID 17320415
Cites: Neuroimage. 2002 Jan;15(1):273-89 PMID 11771995
Cites: Hum Brain Mapp. 2002 Nov;17(3):143-55 PMID 12391568
Cites: IEEE Trans Med Imaging. 2009 Aug;28(8):1266-77 PMID 19228554
Cites: Inf Process Med Imaging. 2001;2082:488-501 PMID 21218175
Cites: Philos Trans R Soc Lond B Biol Sci. 2001 Aug 29;356(1412):1293-322 PMID 11545704
Cites: Clin Chem. 1974 Dec;20(12):1535-42 PMID 4430131
Cites: Biometrics. 1996 Dec;52(4):1195-203 PMID 8962450
Cites: Neuroimage. 2012 Feb 15;59(4):3862-3870 PMID 22119006
Cites: Hum Brain Mapp. 1994;1(3):173-84 PMID 24578038
Cites: Clin Neuroradiol. 2016 Dec;26(4):423-430 PMID 25791203
PubMed ID
28501699 View in PubMed
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The AGES-Reykjavik Study suggests that change in kidney measures is associated with subclinical brain pathology in older community-dwelling persons.

https://arctichealth.org/en/permalink/ahliterature292670
Source
Kidney Int. 2018 Jun 27; :
Publication Type
Journal Article
Date
Jun-27-2018
Author
Sanaz Sedaghat
Jie Ding
Gudny Eiriksdottir
Mark A van Buchem
Sigurdur Sigurdsson
M Arfan Ikram
Osorio Meirelles
Vilmundur Gudnason
Andrew S Levey
Lenore J Launer
Author Affiliation
Department of Epidemiology, Erasmus University Medical Center, Rotterdam, The Netherlands; Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Source
Kidney Int. 2018 Jun 27; :
Date
Jun-27-2018
Language
English
Publication Type
Journal Article
Abstract
Decreased glomerular filtration rate (GFR) and albuminuria may be accompanied by brain pathology. Here we investigated whether changes in these kidney measures are linked to development of new MRI-detected infarcts and microbleeds, and progression of white matter hyperintensity volume. The study included 2671 participants from the population-based AGES-Reykjavik Study (mean age 75, 58.7% women). GFR was estimated from serum creatinine, and albuminuria was assessed by urinary albumin-to-creatinine ratio. Brain MRI was acquired at baseline (2002-2006) and 5 years later (2007-2011). New MRI-detected infarcts and microbleeds were counted on the follow-up scans. White matter hyperintensity progression was estimated as percent change in white matter hyperintensity volumes between the two exams. Participants with a large eGFR decline (over 3 ml/min per 1.73m2 per year) had more incident subcortical infarcts (odds ratio 1.53; 95% confidence interval 1.05, 2.22), and more marked progression of white matter hyperintensity volume (difference: 8%; 95% confidence interval: 4%, 12%), compared to participants without a large decline. Participants with incident albuminuria (over 30 mg/g) had 21% more white matter hyperintensity volume progression (95% confidence interval: 14%, 29%) and 1.86 higher odds of developing new deep microbleeds (95% confidence interval 1.16, 2.98), compared to participants without incident albuminuria. The findings were independent of cardiovascular risk factors. Changes in kidney measures were not associated with occurrence of cortical infarcts. Thus, larger changes in eGFR and albuminuria are associated with increased risk for developing manifestations of cerebral small vessel disease. Individuals with larger changes in these kidney measures should be considered as a high risk population for accelerated brain pathology.
PubMed ID
29960746 View in PubMed
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The AGES-Reykjavik Study suggests that change in kidney measures is associated with subclinical brain pathology in older community-dwelling persons.

https://arctichealth.org/en/permalink/ahliterature300494
Source
Kidney Int. 2018 09; 94(3):608-615
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Date
09-2018
Author
Sanaz Sedaghat
Jie Ding
Gudny Eiriksdottir
Mark A van Buchem
Sigurdur Sigurdsson
M Arfan Ikram
Osorio Meirelles
Vilmundur Gudnason
Andrew S Levey
Lenore J Launer
Author Affiliation
Department of Epidemiology, Erasmus University Medical Center, Rotterdam, The Netherlands; Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Source
Kidney Int. 2018 09; 94(3):608-615
Date
09-2018
Language
English
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Keywords
Aged
Albuminuria - physiopathology - urine
Cerebral Small Vessel Diseases - diagnosis - epidemiology
Creatinine - urine
Disease Progression
Female
Follow-Up Studies
Glomerular Filtration Rate - physiology
Humans
Incidence
Independent living
Kidney - physiopathology
Magnetic Resonance Imaging
Male
Prospective Studies
Renal Insufficiency, Chronic - physiopathology - urine
Risk factors
Serum Albumin
White Matter - diagnostic imaging - pathology
Abstract
Decreased glomerular filtration rate (GFR) and albuminuria may be accompanied by brain pathology. Here we investigated whether changes in these kidney measures are linked to development of new MRI-detected infarcts and microbleeds, and progression of white matter hyperintensity volume. The study included 2671 participants from the population-based AGES-Reykjavik Study (mean age 75, 58.7% women). GFR was estimated from serum creatinine, and albuminuria was assessed by urinary albumin-to-creatinine ratio. Brain MRI was acquired at baseline (2002-2006) and 5 years later (2007-2011). New MRI-detected infarcts and microbleeds were counted on the follow-up scans. White matter hyperintensity progression was estimated as percent change in white matter hyperintensity volumes between the two exams. Participants with a large eGFR decline (over 3 ml/min/1.73m2 per year) had more incident subcortical infarcts (odds ratio 1.53; 95% confidence interval 1.05, 2.22), and more marked progression of white matter hyperintensity volume (difference: 8%; 95% confidence interval: 4%, 12%), compared to participants without a large decline. Participants with incident albuminuria (over 30 mg/g) had 21% more white matter hyperintensity volume progression (95% confidence interval: 14%, 29%) and 1.86 higher odds of developing new deep microbleeds (95% confidence interval 1.16, 2.98), compared to participants without incident albuminuria. The findings were independent of cardiovascular risk factors. Changes in kidney measures were not associated with occurrence of cortical infarcts. Thus, larger changes in eGFR and albuminuria are associated with increased risk for developing manifestations of cerebral small vessel disease. Individuals with larger changes in these kidney measures should be considered as a high risk population for accelerated brain pathology.
PubMed ID
29960746 View in PubMed
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Airflow obstruction, atherosclerosis and cardiovascular risk factors in the AGES Reykjavik study.

https://arctichealth.org/en/permalink/ahliterature275323
Source
Atherosclerosis. 2016 Jul 28;252:122-127
Publication Type
Article
Date
Jul-28-2016
Author
Gunnar Gudmundsson
Olof Birna Margretardottir
Martin Ingi Sigurdsson
Tamara B Harris
Lenore J Launer
Sigurdur Sigurdsson
Orn Olafsson
Thor Aspelund
Vilmundur Gudnason
Source
Atherosclerosis. 2016 Jul 28;252:122-127
Date
Jul-28-2016
Language
English
Publication Type
Article
Abstract
Airflow limitation, i.e. reduced forced expiratory volume in 1-s (FEV1), is associated with increased prevalence of atherosclerosis, however, causal mechanisms remain elusive. The objective of the study was to determine if the association between airflow obstruction and markers of atherosclerosis is mediated by systemic inflammation.
1154 subjects from the longitudinal AGES Reykjavik study were included. Population characteristics, systemic inflammation markers from blood (white blood cell counts (WBC) and level of C-reactive protein (CRP)) were compared between patients with and without airflow limitation defined by reduced FEV1 on spirometry. Atherosclerosis burden was quantified by measurements of coronary artery calcium, aortic arch and distal aortic calcification in addition to carotid intimal media thickness (CIMT).
Subjects were split into four groups according to smoking status and whether airflow limitation was present. There was a higher overall burden of atherosclerosis in ever-smokers compared to never-smokers, and in individuals with airflow obstruction compared to individuals without airflow obstruction. After adjusting for population characteristics, Framingham cardiovascular risk factors and markers of systemic inflammation (WBC and CRP), there was a significantly increased aortic arch and distal aorta calcification and higher CIMT measurement in individuals with airflow obstruction compared to individuals without airflow obstruction. After adjusting for population characteristics, Framingham cardiovascular risk factors and markers of systemic inflammation (WBC and CRP), there was a significantly increased aortic arch and distal aorta calcification and higher CIMT measurement in individuals with airflow obstruction compared to individuals without airflow obstruction.
Systemic inflammation (WBC and CRP) does not appear to mediate the association between airflow limitation and atherosclerosis. Only airflow limitation and not systemic inflammation (WBC and CRP) appears to be an independent predictor of atherosclerosis.
PubMed ID
27522264 View in PubMed
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The alcohol paradox: light-to-moderate alcohol consumption, cognitive function, and brain volume.

https://arctichealth.org/en/permalink/ahliterature259852
Source
J Gerontol A Biol Sci Med Sci. 2014 Dec;69(12):1528-35
Publication Type
Article
Date
Dec-2014
Author
Benjamin J K Davis
Jean-Sebastian Vidal
Melissa Garcia
Thor Aspelund
Mark A van Buchem
Maria K Jonsdottir
Sigurdur Sigurdsson
Tamara B Harris
Vilmundur Gudnason
Lenore J Launer
Source
J Gerontol A Biol Sci Med Sci. 2014 Dec;69(12):1528-35
Date
Dec-2014
Language
English
Publication Type
Article
Keywords
Aged
Aging
Alcohol Drinking - epidemiology - physiopathology - psychology
Brain - pathology
Cognition Disorders - diagnosis - epidemiology - psychology
Disease Progression
Female
Follow-Up Studies
Humans
Iceland - epidemiology
Incidence
Magnetic Resonance Imaging
Male
Neuropsychological Tests
Prevalence
Prognosis
Questionnaires
Retrospective Studies
Risk factors
Abstract
Studies of older persons show consumption of light-to-moderate amounts of alcohol is positively associated with cognitive function and, separately, is negatively associated with total brain volume (TBV). This is paradoxical as generally, cognitive function is positively associated with TBV. We examined the relationships of TBV, global cognitive function (GCF), and alcohol consumption in a population-based cohort of 3,363 men and women (b. 1907-1935) participating in the Age Gene/Environment Susceptibility-Reykjavik Study (2002-2006) and who were free of dementia or mild cognitive impairment
Drinking status (never, former, and current) and current amount of alcohol consumed were assessed by questionnaire. GCF is a composite score derived from a battery of cognitive tests. TBV, standardized to head size, is estimated quantitatively from brain magnetic resonance imaging.
Among women and not men, adjusting for demographic and cardiovascular risk factors, current drinkers had significantly higher GCF scores than abstainers and former drinkers (p
PubMed ID
24994845 View in PubMed
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Allometric scaling of brain regions to intra-cranial volume: An epidemiological MRI study.

https://arctichealth.org/en/permalink/ahliterature275481
Source
Hum Brain Mapp. 2016 Aug 25;
Publication Type
Article
Date
Aug-25-2016
Author
Laura W de Jong
Jean-Sébastien Vidal
Lars E Forsberg
Alex P Zijdenbos
Thaddeus Haight
Sigurdur Sigurdsson
Vilmundur Gudnason
Mark A van Buchem
Lenore J Launer
Source
Hum Brain Mapp. 2016 Aug 25;
Date
Aug-25-2016
Language
English
Publication Type
Article
Abstract
There is growing evidence that sub-structures of the brain scale allometrically to total brain size, that is, in a non-proportional and non-linear way. Here, scaling of different volumes of interest (VOI) to intra-cranial volume (ICV) was examined. It was assessed whether scaling was allometric or isometric and whether scaling coefficients significantly differed from each other. We also tested to what extent allometric scaling of VOI was introduced by the automated segmentation technique. Furthermore, reproducibility of allometric scaling was studied different age groups and study populations. Study samples included samples of cognitively healthy adults from the community-based Age Gene/Environment Susceptibility-Reykjavik Study (AGES-Reykjavik Study) (N?=?3,883), the Coronary Artery Risk Development in Young Adults Study (CARDIA) (N =709), and the Alzheimer's Disease Neuroimaging Initiative (ADNI) (N?=?180). Data encompassed participants with different age, ethnicity, risk factor profile, and ICV and VOI obtained with different automated MRI segmentation techniques. Our analysis showed that (1) allometric scaling is a trait of all parts of the brain, (2) scaling of neo-cortical white matter, neo-cortical gray matter, and deep gray matter structures including the cerebellum are significantly different from each other, and (3) allometric scaling of brain structures cannot solely be explained by age-associated atrophy, sex, ethnicity, or a systematic bias from study-specific segmentation algorithm, but appears to be a true feature of brain geometry. Hum Brain Mapp, 2016. © 2016 Wiley Periodicals, Inc.
PubMed ID
27557999 View in PubMed
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124 records – page 1 of 13.