Skip header and navigation

Refine By

62 records – page 1 of 7.

Age, Gene/Environment Susceptibility-Reykjavik Study: multidisciplinary applied phenomics.

https://arctichealth.org/en/permalink/ahliterature78517
Source
Am J Epidemiol. 2007 May 1;165(9):1076-87
Publication Type
Article
Date
May-1-2007
Author
Harris Tamara B
Launer Lenore J
Eiriksdottir Gudny
Kjartansson Olafur
Jonsson Palmi V
Sigurdsson Gunnar
Thorgeirsson Gudmundur
Aspelund Thor
Garcia Melissa E
Cotch Mary Frances
Hoffman Howard J
Gudnason Vilmundur
Author Affiliation
Laboratory of Epidemiology, Demography, and Biometry, Intramural Research Program, National Institute on Aging, Bethesda, MD 20892-9205, USA. Harris99@mail.nih.gov
Source
Am J Epidemiol. 2007 May 1;165(9):1076-87
Date
May-1-2007
Language
English
Publication Type
Article
Keywords
Age Factors
Aged
Aged, 80 and over
Aging - genetics - pathology
Body Composition
Cardiovascular Diseases - epidemiology - genetics
Chronic Disease
Dementia - epidemiology - genetics
Disease Susceptibility
Environment
Female
Genotype
Geriatrics
Health Status Indicators
Humans
Iceland - epidemiology
Male
Osteoporosis - epidemiology - genetics
Phenotype
Questionnaires
Risk Assessment - methods
Risk factors
Variation (Genetics)
Abstract
In anticipation of the sequencing of the human genome and description of the human proteome, the Age, Gene/Environment Susceptibility-Reykjavik Study (AGES-Reykjavik) was initiated in 2002. AGES-Reykjavik was designed to examine risk factors, including genetic susceptibility and gene/environment interaction, in relation to disease and disability in old age. The study is multidisciplinary, providing detailed phenotypes related to the cardiovascular, neurocognitive (including sensory), and musculoskeletal systems, and to body composition and metabolic regulation. Relevant quantitative traits, subclinical indicators of disease, and medical diagnoses are identified by using biomarkers, imaging, and other physiologic indicators. The AGES-Reykjavik sample is drawn from an established population-based cohort, the Reykjavik Study. This cohort of men and women born between 1907 and 1935 has been followed in Iceland since 1967 by the Icelandic Heart Association. The AGES-Reykjavik cohort, with cardiovascular risk factor assessments earlier in life and detailed late-life phenotypes of quantitative traits, will create a comprehensive study of aging nested in a relatively genetically homogeneous older population. This approach should facilitate identification of genetic factors that contribute to healthy aging as well as the chronic conditions common in old age.
PubMed ID
17351290 View in PubMed
Less detail

Assessing the association of the HNF1A G319S variant with C-reactive protein in Aboriginal Canadians: a population-based epidemiological study.

https://arctichealth.org/en/permalink/ahliterature141499
Source
Cardiovasc Diabetol. 2010;9:39
Publication Type
Article
Date
2010
Author
Sylvia H Ley
Robert A Hegele
Philip W Connelly
Stewart B Harris
Mary Mamakeesick
Henian Cao
Joel Gittelsohn
Ravi Retnakaran
Bernard Zinman
Anthony J Hanley
Author Affiliation
Department of Nutritional Sciences, University of Toronto, Toronto, Canada.
Source
Cardiovasc Diabetol. 2010;9:39
Date
2010
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
C-Reactive Protein - metabolism
Canada - epidemiology
Cardiovascular Diseases - epidemiology - genetics - immunology
Child
Diabetes Mellitus, Type 2 - epidemiology - genetics - immunology
Female
Genotype
Hepatocyte Nuclear Factor 1-alpha - genetics
Humans
Indians, North American - genetics - statistics & numerical data
Inflammation - epidemiology - genetics - metabolism
Male
Middle Aged
Prevalence
Risk factors
Young Adult
Abstract
C-reactive protein (CRP), a biomarker of inflammation, has been associated with increased risk of developing cardiovascular disease. Common variants of the hepatocyte nuclear factor 1A (HNF1A) gene encoding HNF-1alpha have been associated with plasma CRP in predominantly European Caucasian samples. HNF1A might therefore have an impact on vascular disease and diabetes risk that is mediated by CRP. In an Aboriginal Canadian population, a private polymorphism, HNF1A G319S, was associated with increased prevalence of type 2 diabetes. However, it has not been investigated whether this association is mediated by CRP. We aimed to investigate whether CRP was mediating the association between HNF1A G319S and type 2 diabetes in an Aboriginal Canadian population with a high prevalence of diabetes.
A total of 718 individuals who participated in a diabetes prevalence and risk factor survey were included in the current analysis. Participants were genotyped for HNF1A G319S. Fasting plasma samples were analyzed for CRP. Fasting plasma glucose and a 75-g oral glucose tolerance test were obtained to determine type 2 diabetes.
The prevalence rate of type 2 diabetes was 17.4% (125/718) using the 1999 World Health Organization definition and was higher among S319 allele carriers compared to G/G homozygotes (p
Notes
Cites: J Mol Endocrinol. 2001 Aug;27(1):11-2911463573
Cites: Am J Hum Genet. 2008 May;82(5):1193-20118439552
Cites: N Engl J Med. 2001 Sep 27;345(13):971-8011575290
Cites: Proc Natl Acad Sci U S A. 2002 Apr 2;99(7):4614-911904371
Cites: Circulation. 2003 Jan 28;107(3):499-51112551878
Cites: Int J Obes Relat Metab Disord. 2003 Mar;27(3):347-5412629562
Cites: Diabetes Care. 2003 Jun;26(6):1745-5112766104
Cites: Diabetes. 2003 Jul;52(7):1799-80512829649
Cites: Diabetes. 2008 Jul;57(7):1978-8218586913
Cites: Diabetes Care. 2008 Jul;31(7):1410-518339973
Cites: J Intern Med. 2008 Oct;264(4):295-31418823504
Cites: Cardiovasc Diabetol. 2009;8:2819490620
Cites: JAMA. 2009 Jul 1;302(1):37-4819567438
Cites: JAMA. 2001 Jul 18;286(3):327-3411466099
Cites: N Engl J Med. 2004 Apr 1;350(14):1387-9715070788
Cites: Diabetologia. 1985 Jul;28(7):412-93899825
Cites: EMBO J. 1990 Dec;9(13):4467-752265613
Cites: Biochemistry. 1996 Jul 16;35(28):9060-88703909
Cites: Nature. 1996 Dec 5;384(6608):455-88945470
Cites: Diabetes Care. 1997 Feb;20(2):185-79118771
Cites: Hum Mol Genet. 1997 Apr;6(4):583-69097962
Cites: J Clin Endocrinol Metab. 1999 Mar;84(3):1077-8210084598
Cites: J Clin Invest. 2005 May;115(5):1111-915864338
Cites: Hum Mutat. 2006 Sep;27(9):854-6916917892
Cites: Diabetes. 2007 Feb;56(2):513-717259399
Cites: Arch Intern Med. 2007 Aug 13-27;167(15):1676-8517698692
Cites: J Immunol. 2008 Mar 1;180(5):3492-50118292576
Cites: Am J Hum Genet. 2008 May;82(5):1185-9218439548
Cites: Cardiovasc Diabetol. 2009;8:6320003313
PubMed ID
20716378 View in PubMed
Less detail

The association between cigarette smoking and carotid intima-media thickness is influenced by the -930A/G CYBA gene polymorphism: the Cardiovascular Risk in Young Finns Study.

https://arctichealth.org/en/permalink/ahliterature153088
Source
Am J Hypertens. 2009 Mar;22(3):281-7
Publication Type
Article
Date
Mar-2009
Author
Fan M
Raitakari OT
Kähönen M
Juonala M
Hutri-Kähönen N
Pörsti I
Viikari J
Lehtimäki T
Author Affiliation
Laboratory of Atherosclerosis Genetics, Department of Clinical Chemistry, Tampere University Hospital, University of Tampere, Tampere, Finland. meng.fan@uta.fi
Source
Am J Hypertens. 2009 Mar;22(3):281-7
Date
Mar-2009
Language
English
Publication Type
Article
Keywords
Adult
Atherosclerosis - genetics - pathology
Cardiovascular Diseases - epidemiology - genetics - pathology
Carotid Arteries - pathology
DNA - genetics - isolation & purification
Female
Finland - epidemiology
Gene Frequency
Genotype
Humans
Male
NADPH Oxidase - genetics
Polymorphism, Genetic - genetics
Risk factors
Smoking - epidemiology - genetics - pathology
Young Adult
Abstract
Smoking-induced damage to the cardiovascular system has been shown in many studies; however, the degree of damage varies from individual to individual. We hypothesized that the -930A/G CYBA gene polymorphism in the NADPH oxidase influences the association between cigarette smoking and carotid intima-media thickness (IMT) in young healthy adults.
Cross-sectional data obtained in 2001 for the Cardiovascular Risk in Young Finns Study were used. IMT was measured with ultrasound. The genotyping was performed using a 5'-nuclease assay. A linear regression model was used to test whether the interaction between smoking and the genotypes was associated with IMT. The magnitude of the interaction effect was further examined by performing a stratified analysis according to smoking habits.
In the entire population, the mean and maxima IMT were higher in smokers than nonsmokers (P = 0.005 and 0.008, respectively). The differences were most significant in subjects with the GG genotype, borderline significant for the GA genotype, and nonsignificant for the AA genotype. The interaction of genotypes with smoking was associated with mean and maximal IMT (P = 0.042 and 0.022). Among smokers, subjects with the GG genotype had a higher mean and maximal IMT compared with carriers of the A allele (P = 0.021 and 0.012). In contrast, the mean and maximal IMT were lower for G allele carriers than subjects with the AA genotype among nonsmokers (P = 0.022 and 0.026). All results had been adjusted for potential risk factors related to IMT.
The -930A/G polymorphism modifies the association between cigarette smoking and IMT in young healthy adults.
PubMed ID
19151692 View in PubMed
Less detail

Association between the G protein ß3 subunit C825T polymorphism and the occurrence of cardiovascular disease in hypertensives: The Nord-Trøndelag Health Study (HUNT).

https://arctichealth.org/en/permalink/ahliterature142941
Source
Am J Hypertens. 2010 Oct;23(10):1121-7
Publication Type
Article
Date
Oct-2010
Author
Oddgeir L Holmen
Solfrid Romundstad
Oyvind Melien
Author Affiliation
HUNT Research Centre, Department of Public Health and General Practice, Norwegian University of Science and Technology, Levanger, Norway. oddgeir.lingaas.holmen@gmail.com
Source
Am J Hypertens. 2010 Oct;23(10):1121-7
Date
Oct-2010
Language
English
Publication Type
Article
Keywords
Aged
Alleles
Antihypertensive Agents - therapeutic use
Blood Pressure - physiology
Cardiovascular Diseases - epidemiology - genetics
DNA - genetics
Female
Genetic Association Studies
Genotype
Heterotrimeric GTP-Binding Proteins - genetics
Humans
Hypertension - drug therapy - epidemiology - genetics
Logistic Models
Male
Middle Aged
Norway - epidemiology
Polymorphism, Genetic - genetics
Reverse Transcriptase Polymerase Chain Reaction
Abstract
Several studies examining the C825T polymorphism of the G protein ß3 subunit (GNB3) have shown inconsistent results regarding susceptibility to hypertension. With twice the length of earlier studies, the aim of our study was to further investigate this association with a cross-sectional design over an 11.5-year follow-up period in a Norwegian population.
Two randomized selected population samples from the Nord-Trøndelag Health Study 1995-1997 (HUNT 2) were genotyped. One sample included individuals reporting use of antihypertensive medication (n = 969), and the other did not report use of antihypertensive medication, cardiovascular disease (CVD), or diabetes (n = 1,867). Of those genotyped, 2,254 participants (79.5%) also attended HUNT 1 in 1984-1986.
There was no significant higher prevalence of hypertension (blood pressure =140/90 mm Hg and/or antihypertensive medication) in T-allele carriers than in C allele carriers. However, TT homozygous men with treated hypertension showed statistical significant association with self-reported CVD compared to the CC genotype (odds ratio (OR) 3.19, P = 0.001). No statistical significant association between hypertension and the C825T polymorphism was found during the follow-up.
No association was found between the C285T polymorphism of the GNB3 and hypertension. However, CVD was more common among treated hypertensive men with the TT genotype compared to men with the CC genotype. Thus, further studies are needed to explore whether this finding could be caused by other mechanisms than elevated blood pressure.
PubMed ID
20539277 View in PubMed
Less detail

The association of ADH and ALDH gene variants with alcohol drinking habits and cardiovascular disease risk factors.

https://arctichealth.org/en/permalink/ahliterature92098
Source
Alcohol Clin Exp Res. 2008 Nov;32(11):1984-91
Publication Type
Article
Date
Nov-2008
Author
Husemoen Lise Lotte Nystrup
Fenger Mogens
Friedrich Nele
Tolstrup Janne Schurmann
Beenfeldt Fredriksen Stine
Linneberg Allan
Author Affiliation
Research Centre for Prevention and Health, Glostrup Hospital, Glostrup, Denmark. lloh@glo.regionh.dk
Source
Alcohol Clin Exp Res. 2008 Nov;32(11):1984-91
Date
Nov-2008
Language
English
Publication Type
Article
Keywords
Adult
Alcohol Dehydrogenase - genetics
Alcohol Drinking - genetics - metabolism
Aldehyde Dehydrogenase - genetics
Blood Pressure - genetics
Cardiovascular Diseases - epidemiology - genetics - metabolism
Case-Control Studies
Denmark
Ethanol - metabolism
European Continental Ancestry Group - genetics
Female
Genetic Variation - genetics
Habits
Health Surveys
Humans
Male
Middle Aged
Polymorphism, Single Nucleotide - genetics
Risk factors
Abstract
BACKGROUND: Genetic variation in ethanol metabolism may have an influence on both alcohol drinking habits and the susceptibility to health effects of alcohol drinking. Such influences are likely to bias exposure-disease associations in epidemiologic studies of health effects of alcohol drinking. In a Caucasian population, we examined the association of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) genetic variants with alcohol drinking habits, biomarkers of alcohol exposure, and risk factors for cardiovascular disease. METHODS: The study population consisted of 1,216 Danish men and women aged 15-77 years participating in a health examination in 1998. The health examination included a self-administered questionnaire (alcohol drinking habits), a physical examination (blood pressure), and various blood tests [alanine aminotransferase (ALAT), erythrocyte mean corpuscular volume (E-MCV), and lipids]. ADH and ALDH gene variants were determined by standard techniques. Data were analyzed by regression analyses adjusted for relevant confounders. RESULTS: Self-reported alcohol drinking was significantly associated with increasing levels of ALAT, E-MCV, high-density lipoprotein cholesterol, and blood pressure. The ALDH1b ala69val variant was associated with nondrinking and total alcohol intake. The ALDH2 promoter variant was associated with binge-drinking, and the ALDH1b1 ala69val polymorphism was associated with diastolic blood pressure. We did not find any statistically significant interactions between any of the gene variants and alcohol consumption in relation to the various outcomes. CONCLUSIONS: In this Caucasian population sample, we found evidence to support that genetic variation in ethanol metabolism may influence drinking habits, but no statistically significant gene-environment interactions. More large-scale epidemiologic studies are needed to confirm theses results and to further investigate genetic susceptibility to the effects of alcohol drinking.
PubMed ID
18782342 View in PubMed
Less detail

Association of the FTO gene variant (rs9939609) with cardiovascular disease in men with abnormal glucose metabolism--the Finnish Diabetes Prevention Study.

https://arctichealth.org/en/permalink/ahliterature144157
Source
Nutr Metab Cardiovasc Dis. 2011 Sep;21(9):691-8
Publication Type
Article
Date
Sep-2011
Author
Lappalainen T
Kolehmainen M
Schwab US
Tolppanen AM
Stancáková A
Lindström J
Eriksson JG
Keinänen-Kiukaanniemi S
Aunola S
Ilanne-Parikka P
Herder C
Koenig W
Gylling H
Kolb H
Tuomilehto J
Kuusisto J
Uusitupa M
Author Affiliation
School of Public Health and Clinical Nutrition, Department of Clinical Nutrition and Food and Health Research Centre, University of Kuopio, Kuopio, Finland. tiina.lappalainen@uef.fi
Source
Nutr Metab Cardiovasc Dis. 2011 Sep;21(9):691-8
Date
Sep-2011
Language
English
Publication Type
Article
Keywords
Aged
Blood Glucose - analysis - metabolism
C-Reactive Protein - analysis
Cardiovascular Diseases - epidemiology - genetics - pathology
Cross-Sectional Studies
Female
Finland - epidemiology
Follow-Up Studies
Genotype
Glucose Intolerance - genetics
Humans
Male
Middle Aged
Polymorphism, Single Nucleotide
Proteins - genetics - metabolism
Risk factors
Abstract
The common single nucleotide polymorphism (SNP) in the FTO (fat mass and obesity associated) gene has been consistently associated with an increased risk of obesity. We investigated whether the SNP rs9939609 (T/A) of the FTO is associated with risk factors of cardiovascular diseases (CVD), including serum levels of C - reactive protein (CRP), the chemokine RANTES (Regulated on Activation, Normal T Cell Expressed and Secreted; CCL5), and serum and lipoprotein lipids in the Finnish Diabetes Prevention Study (DPS). Furthermore, we examined whether the rs9939609 increased the CVD risk in the DPS and if these results could be replicated in a larger cross-sectional population-based random sample of Finnish men (the METSIM).
In the DPS, altogether 490 (BMI=25kg/m(2)) subjects with impaired glucose tolerance were genotyped for rs9939609. Cardiovascular morbidity and mortality data were collected during the median follow-up of 10.2 years. The replication study was a population-based cross-sectional study of 6214 men. In the DPS, the AA genotype of rs9939609 was associated, independently of BMI, with increased RANTES (p=0.002) and decreased HDL cholesterol concentrations (p=0.007) in men. During the follow-up, the AA genotype was associated with an adjusted 2.09-fold risk (95% CI 1.17-3.73, p=0.013) of CVD in men. In the METSIM Study, the association with a history of myocardial infarction was replicated in the subgroup of men with type 2 diabetes.
We suggest that the variation in the FTO gene may contribute to the development of CVD in men with an abnormal glucose metabolism.
PubMed ID
20400278 View in PubMed
Less detail

Associations between USF1 gene variants and cardiovascular risk factors in the Quebec Family Study.

https://arctichealth.org/en/permalink/ahliterature165080
Source
Clin Genet. 2007 Mar;71(3):245-53
Publication Type
Article
Date
Mar-2007
Author
A C Choquette
L. Bouchard
A. Houde
C. Bouchard
L. Pérusse
M-C Vohl
Author Affiliation
Lipid Research Center, CHUQ, CHUL, Quebec, Canada.
Source
Clin Genet. 2007 Mar;71(3):245-53
Date
Mar-2007
Language
English
Publication Type
Article
Keywords
Adult
Apolipoproteins B - blood
Body mass index
Cardiovascular Diseases - epidemiology - genetics
Cohort Studies
Female
Gene Frequency
Genetic Predisposition to Disease
Genetic Variation
Genotype
Humans
Lipoproteins, LDL - blood
Male
Middle Aged
Phenotype
Polymorphism, Genetic
Quebec
Risk factors
Upstream Stimulatory Factors - genetics
Abstract
Cardiovascular (CVD) risk factors are under the influence of environmental and genetic factors. Human upstream transcription factor 1 gene (USF1) encodes for a transcription factor, which modulates the expression of genes involved in lipid and carbohydrate metabolic pathways. The aim of this study was to test the hypothesis that USF1 gene variants are associated with CVD risk factors in the Quebec Family Study (QFS). USF1 has been sequenced in 20 QFS subjects with high plasma apolipoprotein B100 (APOB) levels (>1.14 g/l) and small, dense low-density lipoprotein (LDL) particles (> or =250.7 Angstroms and A, and exon 11 c.*187 C>T) as well as the c.-56 A>G polymorphism, were genotyped and analyzed in 760 subjects from QFS. Association studies showed that women with c.561-100 A/A and c.*187 T/T genotypes had more favorable adiposity indices (
PubMed ID
17309647 View in PubMed
Less detail

Cardiovascular consequences of a polygenetic component of blood pressure in an urban-based longitudinal study: the Malmö diet and cancer.

https://arctichealth.org/en/permalink/ahliterature262787
Source
J Hypertens. 2014 Jul;32(7):1424-8; discussion 1428
Publication Type
Article
Date
Jul-2014
Author
Cristiano Fava
Therese Ohlsson
Marketa Sjögren
Angela Tagetti
Peter Almgren
Gunnar Engström
Peter Nilsson
Bo Hedblad
Pietro Minuz
Olle Melander
Source
J Hypertens. 2014 Jul;32(7):1424-8; discussion 1428
Date
Jul-2014
Language
English
Publication Type
Article
Keywords
Adult
Aged
Blood Pressure - genetics
Cardiovascular Diseases - epidemiology - genetics - mortality
Cohort Studies
Diet
Female
Genetic Predisposition to Disease
Humans
Incidence
Kaplan-Meier Estimate
Longitudinal Studies
Male
Middle Aged
Neoplasms - etiology
Polymorphism, Single Nucleotide
Risk factors
Sweden - epidemiology
Urban Population
Abstract
A recently published genome wide association study identified 29 single nucleotide polymorphisms (SNPs) influencing blood pressure (BP). Case-control studies suggest that a genetic risk score (GRS) based on these 29 SNPs affect the risk of cardiovascular disease (CVD), but its role for CVD at population level is unknown. Here, we prospectively evaluate the impact of this polygenetic BP component on CVD morbidity and mortality in a large urban-based middle-aged population.
The 29 previously BP associated SNPs were genotyped in the Swedish Malmö Diet and Cancer Study; (n = 27,003 with at least 24 valid SNPs). The number of BP elevating alleles of each SNPs, weighted by their effect size in the discovery studies, was summed into a BP-GRS.
Using regression models, we found significant associations of the BP-GRS, cross-sectionally, with BP and hypertension prevalence, prospectively, with incident cardiovascular morbidity and mortality during 14.2 ± 3.2 years of follow-up. After adjustment for traditional cardiovascular risk factors (TRF), including hypertension, the BP-GRS remained significantly associated only with CVDs [in terms of strokes and coronary artery disease; hazard ratio 1.15; 95% confidence interval (CI) 1.06-1.24 comparing the third vs. first tertile; P = 0.003]. Calibration, discrimination and reclassification analyses did not show a meaningful increment in prediction using the BP-GRS in addition to the model encompassing only the TRF.
The polygenetic component of BP influences risk of cardiovascular morbidity and mortality. However, the effect size is small and unlikely to be useful for prediction at the population level.
Notes
Comment In: J Hypertens. 2014 Jul;32(7):1395-624984173
PubMed ID
24879493 View in PubMed
Less detail

Cardiovascular diseases and risk of hip fracture.

https://arctichealth.org/en/permalink/ahliterature94958
Source
JAMA. 2009 Oct 21;302(15):1666-73
Publication Type
Article
Date
Oct-21-2009
Author
Sennerby Ulf
Melhus Håkan
Gedeborg Rolf
Byberg Liisa
Garmo Hans
Ahlbom Anders
Pedersen Nancy L
Michaëlsson Karl
Author Affiliation
Department of Surgical Sciences, Section of Orthopaedics, Uppsala University, SE-751 85 Uppsala, Sweden.
Source
JAMA. 2009 Oct 21;302(15):1666-73
Date
Oct-21-2009
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Cardiovascular Diseases - epidemiology - genetics
Diseases in Twins - epidemiology - genetics
Female
Genetic Predisposition to Disease
Hip Fractures - epidemiology - genetics
Humans
Kaplan-Meiers Estimate
Life Style
Male
Middle Aged
Osteoporosis - epidemiology - genetics
Proportional Hazards Models
Registries
Risk
Sweden
Twins
Abstract
CONTEXT: Recent studies indicate common etiologies for cardiovascular disease (CVD) and osteoporotic fractures. OBJECTIVES: To examine the relation between CVD and risk of hip fracture in twins and evaluate the relative importance of genetics and lifestyle factors in this association. DESIGN, SETTING, AND PARTICIPANTS: A cohort of all 31,936 Swedish twins born from 1914-1944 was followed up from the age of 50 years. The National Patient Registry identified twins with CVDs and fractures from 1964 through 2005. Time-dependent exposures using Cox proportional hazard regression models were evaluated. MAIN OUTCOME MEASURE: Time to hip fracture after diagnosis of CVD. RESULTS: The crude absolute rate of hip fractures was 12.6 per 1000 person-years after a diagnosis of heart failure, 12.6 per 1000 person-years after a stroke, 6.6 per 1000 person-years after a diagnosis of peripheral atherosclerosis, and 5.2 per 1000 person-years after a diagnosis of ischemic heart disease compared with 1.2 per 1000 person-years for those without a CVD diagnosis. The multivariable-adjusted hazard ratio (HR) of hip fracture after a diagnosis of heart failure was 4.40 (95% confidence interval [CI], 3.43-5.63); after a stroke, the HR was 5.09 (95% CI, 4.18-6.20); after a diagnosis of peripheral atherosclerosis, the HR was 3.20 (95% CI, 2.28-4.50); and after an ischemic heart disease event, the HR was 2.32 (95% CI, 1.91-2.84). Identical twins without heart failure and stroke also had, after their co-twins had been exposed to these respective diseases, an increased rate of hip fracture. These sibling twins pseudoexposed for heart failure had a multivariable-adjusted HR of 3.74 (95% CI, 1.97-7.10) for hip fracture, whereas pseudoexposure for stroke had an HR of 2.29 (95% CI, 1.20-4.35). CONCLUSIONS: A diagnosis of CVD was significantly associated with risk of subsequent hip fracture. Increased risks in co-twins without an index diagnosis suggest genetic factors in the association between CVD and osteoporotic fractures.
PubMed ID
19843901 View in PubMed
Less detail

Cardiovascular risk factors and Alzheimer's disease: a genetic association study in a population aged 85 or over.

https://arctichealth.org/en/permalink/ahliterature197031
Source
Neurosci Lett. 2000 Oct 13;292(3):195-8
Publication Type
Article
Date
Oct-13-2000
Author
L. Myllykangas
T. Polvikoski
R. Sulkava
A. Verkkoniemi
P. Tienari
L. Niinistö
K. Kontula
J. Hardy
M. Haltia
J. Pérez-Tur
Author Affiliation
Neurogenetics Laboratory, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, FL 32224, USA. liisa.myllykangas@helsinki.fi
Source
Neurosci Lett. 2000 Oct 13;292(3):195-8
Date
Oct-13-2000
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Alleles
Alzheimer Disease - epidemiology - genetics
Apolipoproteins E - genetics
Cardiovascular Diseases - epidemiology - genetics
Cohort Studies
Comorbidity
Female
Finland - epidemiology
Genetic Linkage
Genetic Testing
Genotype
Humans
Lipoprotein Lipase - genetics
Low Density Lipoprotein Receptor-Related Protein-1
Male
Peptidyl-Dipeptidase A - genetics
Polymorphism, Genetic - genetics
Receptors, Immunologic - genetics
Risk factors
Abstract
Increasing evidence suggests a relation between vascular disorders and late-onset Alzheimer's disease (AD). We performed an association analysis of low-density lipoprotein receptor-related protein (LRP), lipoprotein lipase (LPL), and angiotensin converting enzyme (ACE) genes, known to be involved in vascular disorders, and AD. Genotyping was carried out in 113 patients with clinically defined Alzheimer's disease (NINCDS-ADRDA criteria) and 203 non-demented controls in a prospective, population-based study of people aged 85 years or over (Vantaa 85+ Study). Corresponding analysis was performed on 121 neuropathologically verified AD patients (CERAD criteria) and 75 controls derived from the same study population. We did not find significant associations between the polymorphisms studied and AD. However, analysis of the LPL polymorphism showed a weak trend (uncorrected P-value 0.095) towards protection against neuropathologically defined AD. Our study is based on very elderly Finns. Therefore, further studies are warranted in other populations.
PubMed ID
11018310 View in PubMed
Less detail

62 records – page 1 of 7.