Skip header and navigation

Refine By

125 records – page 1 of 13.

ß2 -adrenergic receptor Thr164IIe polymorphism, blood pressure and ischaemic heart disease in 66?750 individuals.

https://arctichealth.org/en/permalink/ahliterature131722
Source
J Intern Med. 2012 Mar;271(3):305-14
Publication Type
Article
Date
Mar-2012
Author
M. Thomsen
M. Dahl
A. Tybjaerg-Hansen
B G Nordestgaard
Author Affiliation
Department of Clinical Biochemistry, Herlev Hospital, Copenhagen University Hospital, Copenhagen, Denmark.
Source
J Intern Med. 2012 Mar;271(3):305-14
Date
Mar-2012
Language
English
Publication Type
Article
Keywords
Aged
Blood Pressure - genetics
Cross-Sectional Studies
Denmark
Female
Genetic Predisposition to Disease - genetics
Genotype
Humans
Hypertension - genetics
Male
Middle Aged
Muscle, Skeletal
Myocardial Ischemia - genetics
Myocytes, Smooth Muscle
Polymorphism, Single Nucleotide
Prospective Studies
Questionnaires
Receptors, Adrenergic, beta-2 - genetics
Sex Factors
Abstract
The ß(2) -adrenergic receptor (ADRB2) is located on smooth muscle cells and is an important regulator of smooth muscle tone. The Thr164Ile polymorphism (rs1800888) in the ADRB2 gene is rare but has profound functional consequences on receptor function and could cause lifelong elevated smooth muscle tone. We tested the hypothesis that Thr164Ile is associated with increased blood pressure, increased frequency of hypertension and increased risk of cardiovascular disease (CVD).
A total of 66 750 individuals from two large Danish general population studies were genotyped, and 1943 Thr164Ile heterozygotes and 16 homozygotes were identified.
Thr164Ile genotype was associated with increased systolic and diastolic blood pressure in women (trend: P = 0.04 and 0.02): systolic and diastolic blood pressure increased by 5% and 2%, respectively, in female homozygotes compared with female noncarriers. All female Thr164Ile homozygotes had hypertension compared with 58% of female heterozygotes and 54% of female noncarriers (chi-square: P = 0.001). Female Thr164Ile homozygotes and heterozygotes had odds ratios for ischaemic heart disease (IHD) of 2.93 (0.56-15.5) and 1.28 (1.03-1.61), respectively, compared with female noncarriers (trend: P = 0.007). These differences were not observed in men. Furthermore, Gly16Arg (rs1042713) and Gln27Glu (rs1042714) in the ADRB2 gene were not associated with blood pressure, hypertension or CVD either in the population overall or in women and men separately.
ADRB2 Thr164Ile is associated with increased blood pressure, increased frequency of hypertension and increased risk of IHD amongst women in the general population. These findings, particularly for homozygotes, are novel.
PubMed ID
21883537 View in PubMed
Less detail

Adipose tissue PCB levels and CYP1B1 and COMT genotypes in relation to breast cancer risk in postmenopausal Danish women.

https://arctichealth.org/en/permalink/ahliterature258362
Source
Int J Environ Health Res. 2014;24(3):256-68
Publication Type
Article
Date
2014
Author
Elvira V Bräuner
Steffen Loft
Anja Wellejus
Herman Autrup
Anne Tjønneland
Ole Raaschou-Nielsen
Author Affiliation
a Danish Building Research Institute, Construction and Health, Aalborg University , Copenhagen , Denmark .
Source
Int J Environ Health Res. 2014;24(3):256-68
Date
2014
Language
English
Publication Type
Article
Keywords
Adipose Tissue - metabolism
Aryl Hydrocarbon Hydroxylases - genetics
Breast Neoplasms - chemically induced - enzymology - genetics
Case-Control Studies
Catechol O-Methyltransferase - genetics
Data Interpretation, Statistical
Denmark
Female
Genotype
Hormone Replacement Therapy
Humans
Middle Aged
Polychlorinated Biphenyls - analysis - pharmacokinetics - toxicity
Polymorphism, Single Nucleotide
Postmenopause - metabolism
Prospective Studies
Risk
Abstract
Exposure to PCBs may be an etiologic factor for breast cancer. The cytochrome P450 1B1 (CYP1B1) and catechol-O-methyltransferase (COMT) enzymes are involved in estrogen metabolism and PCB metabolism, both of which may relate to breast cancer susceptibility. Polymorphisms in genes regulating these enzymes control efficiency. Our objective was to assess whether CYP1B1 and COMT gene polymorphisms modulate the effect of PCBs in breast cancer risk, among postmenopausal Danish women. Neither CYP1B1 Leu432Val polymorphisms nor adipose tissue PCBs were independently associated with breast cancer risk. When assessing the independent effect of the COMT Val158Met polymorphism, we observed reduced risk for breast cancer amongst hormone replacement therapy using women who were homozygous carriers of the variant allele compared with those carrying the wild-type variant (RR?=?0.41; 95% CI: 0.29-0.89). We found no statistically significant interactions between any of the PCB groups and CYP1B1 or COMT polymorphisms on the risk of breast cancer.
PubMed ID
23869875 View in PubMed
Less detail

An association of AKT1 gene polymorphism with antidepressant treatment response.

https://arctichealth.org/en/permalink/ahliterature282865
Source
World J Biol Psychiatry. 2016 Apr;17(3):239-42
Publication Type
Article
Date
Apr-2016
Author
Innokentiy S Losenkov
Natalya M Vyalova
German G Simutkin
Nikolay A Bokhan
Svetlana A Ivanova
Source
World J Biol Psychiatry. 2016 Apr;17(3):239-42
Date
Apr-2016
Language
English
Publication Type
Article
Keywords
Adult
Antidepressive Agents - therapeutic use
Case-Control Studies
Depressive Disorder - drug therapy - genetics
European Continental Ancestry Group - genetics
Female
Gene Frequency
Genetic Predisposition to Disease
Humans
Male
Middle Aged
Polymorphism, Single Nucleotide
Prospective Studies
Proto-Oncogene Proteins c-akt - genetics
Siberia
Abstract
Nowadays it is considered that protein kinase Akt1 could be involved in pathogenesis of affective disorders. We have examined whether AKT1 gene polymorphisms are associated with antidepressant treatment response.
The study included 106 Caucasian patients with depressive disorders from Siberia and 103 healthy control donors. The frequencies of single nucleotide polymorphisms rs1130214 and rs3730358 of AKT1 gene were examined.
A comparison of genotypic or allelic frequencies between the groups of healthy donors and depressive patients showed no statistically significant difference. No association between the polymorphisms under study and the scores according to Hamilton Depression Rating Scale 17 was found. However, an association between treatment response assessed by the Clinical Global Impression - Improvement scale and rs1130214 polymorphism was observed.
AKT1 gene polymorphism rs1130214 is associated with antidepressant treatment response in patients with depressive disorders.
PubMed ID
26515520 View in PubMed
Less detail

Association of environmental and genetic factors and gene-environment interactions with risk of developing rheumatoid arthritis.

https://arctichealth.org/en/permalink/ahliterature115564
Source
Arthritis Care Res (Hoboken). 2013 Jul;65(7):1147-56
Publication Type
Article
Date
Jul-2013
Author
Elizabeth W Karlson
Bo Ding
Brendan T Keenan
Katherine Liao
Karen H Costenbader
Lars Klareskog
Lars Alfredsson
Lori B Chibnik
Author Affiliation
Brigham and Women's Hospital, Boston, Massachusetts 02115, USA. ekarlson@partners.org
Source
Arthritis Care Res (Hoboken). 2013 Jul;65(7):1147-56
Date
Jul-2013
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age Factors
Aged
Alcohol Drinking
Area Under Curve
Arthritis, Rheumatoid - blood - diagnosis - genetics - immunology
Autoantibodies - blood
Case-Control Studies
Chi-Square Distribution
Educational Status
Female
Gene-Environment Interaction
Genetic Predisposition to Disease
HLA Antigens - genetics - immunology
Humans
Logistic Models
Male
Middle Aged
Odds Ratio
Parity
Peptides, Cyclic - immunology
Polymorphism, Single Nucleotide
Pregnancy
Prospective Studies
ROC Curve
Risk assessment
Risk factors
Smoking - adverse effects
Sweden
United States
Young Adult
Abstract
We developed rheumatoid arthritis (RA) risk models based on validated environmental factors (E), genetic risk scores (GRS), and gene-environment interactions (GEI) to identify factors that can improve accuracy and reclassification.
Models including E, GRS, and GEI were developed among 317 white seropositive RA cases and 551 controls from the Nurses' Health Studies (NHS) and validated in 987 white anti-citrullinated protein antibody-positive cases and 958 controls from the Swedish Epidemiologic Investigation of Rheumatoid Arthritis (EIRA), stratified by sex. Primary analyses included age, smoking, alcohol, parity, weighted GRS using 31 non-HLA alleles and 8 HLA-DRB1 alleles, and the HLA × smoking interaction. Expanded models included reproductive, geographic, and occupational factors and additional GEI terms. Hierarchical models were compared for discriminative accuracy using the area under the receiver operating characteristic curve (AUC) and reclassification using the integrated discrimination improvement (IDI) and the continuous net reclassification improvement.
The mean age at RA diagnosis was 56 years in the NHS and 51 years in the EIRA. Primary models produced AUCs of 0.716 in the NHS, 0.716 in women in the EIRA, and 0.756 in men in the EIRA. Expanded models produced improvements in discrimination with AUCs of 0.738 in the NHS, 0.724 in women in the EIRA, and 0.769 in men in the EIRA. Models including genetic factors (G) or G + GEI improved reclassification over E models; the full E + G + GEI model provided the optimal predictive ability by IDI analyses.
We have developed comprehensive RA risk models incorporating E, G, and GEI that have improved the discriminative accuracy for RA. Further work developing and assessing highly specific prediction models in prospective cohorts is still needed to inform primary RA prevention trials.
Notes
Cites: Ann Rheum Dis. 2010 Mar;69(3):503-919825849
Cites: Ann Rheum Dis. 2010 Jun;69(6):1077-8520233754
Cites: Nat Genet. 2010 Jun;42(6):508-1420453842
Cites: Rheum Dis Clin North Am. 2010 May;36(2):213-4120510231
Cites: Environ Health Perspect. 2010 Jul;118(7):957-6120338859
Cites: Arthritis Rheum. 2010 Nov;62(11):3196-21020597111
Cites: Diabetes Care. 2011 Jan;34(1):121-520889853
Cites: Stat Med. 2011 Jan 15;30(1):11-2121204120
Cites: Genet Med. 2011 May;13(5):453-621502867
Cites: Curr Diab Rep. 2011 Dec;11(6):511-821947855
Cites: Ann Rheum Dis. 2012 Mar;71(3):378-8121972241
Cites: Rheumatology (Oxford). 2012 Mar;51(3):499-51222120459
Cites: PLoS One. 2012;7(5):e3529622662108
Cites: Am J Hum Genet. 2012 Jun 8;90(6):962-7222633398
Cites: Epidemiology. 1994 Sep;5(5):525-327986867
Cites: Ann Epidemiol. 1995 Jul;5(4):297-3028520712
Cites: Am J Epidemiol. 1996 Jul 1;144(1):1-148659479
Cites: Ann Rheum Dis. 1996 Feb;55(2):94-88712873
Cites: Arthritis Rheum. 1997 Nov;40(11):1955-619365083
Cites: JAMA. 1998 Feb 11;279(6):445-99466637
Cites: Arthritis Rheum. 1999 Mar;42(3):415-2010088762
Cites: Arthritis Rheum. 2004 Nov;50(11):3458-6715529351
Cites: Ann Rheum Dis. 2005 Apr;64(4):582-615319232
Cites: Ann Rheum Dis. 2005 Nov;64(11):1588-9415843455
Cites: Arthritis Res Ther. 2005;7(6):R1296-30316277683
Cites: Arthritis Rheum. 2006 Jan;54(1):38-4616385494
Cites: PLoS Med. 2006 Feb;3(2):e114; author reply e12716492078
Cites: Am J Med. 2006 Jun;119(6):503.e1-916750964
Cites: J Rheumatol. 2006 Jun;33(6):1069-7416622905
Cites: Curr Opin Rheumatol. 2007 Jan;19(1):49-5417143096
Cites: Arthritis Res Ther. 2006;8(4):R13316872514
Cites: JAMA. 2007 Feb 14;297(6):611-917299196
Cites: Circulation. 2007 Feb 20;115(7):928-3517309939
Cites: Arthritis Rheum. 2007 May;56(5):1424-3217469099
Cites: N Engl J Med. 2007 Sep 6;357(10):977-8617804842
Cites: N Engl J Med. 2007 Sep 20;357(12):1199-20917804836
Cites: Nat Genet. 2007 Dec;39(12):1477-8217982456
Cites: Environ Health Perspect. 2009 Jul;117(7):1065-919654914
Cites: Nat Genet. 2009 Dec;41(12):1313-819898481
Cites: Ann Rheum Dis. 2010 Jan;69(1):54-6019151010
Cites: Clin Chem. 2008 Jan;54(1):17-2318024533
Cites: Stat Med. 2008 Jan 30;27(2):157-72; discussion 207-1217569110
Cites: Arthritis Rheum. 2008 Mar 15;59(3):302-1018311749
Cites: PLoS Genet. 2008 Apr;4(4):e100002418437207
Cites: Arch Intern Med. 2008 Aug 11;168(15):1664-7018695080
Cites: Nat Genet. 2008 Oct;40(10):1216-2318794853
Cites: Diabetes Care. 2008 Oct;31(10):2056-6118689695
Cites: N Engl J Med. 2008 Nov 20;359(21):2208-1919020323
Cites: N Engl J Med. 2008 Nov 20;359(21):2220-3219020324
Cites: Nat Genet. 2009 Jan;41(1):47-5519060911
Cites: Ann Rheum Dis. 2009 Feb;68(2):222-718535114
Cites: Ann Intern Med. 2009 Jan 20;150(2):65-7219153409
Cites: J Rheumatol. 2002 Feb;29(2):246-5411838841
Cites: Am J Med. 2002 Apr 15;112(6):465-7111959057
Cites: J Gend Specif Med. 2002 Mar-Apr;5(2):27-3711974672
Cites: Ann Rheum Dis. 2003 Sep;62(9):835-4112922955
Cites: Arthritis Rheum. 2003 Oct;48(10):2741-914558078
Cites: J Rheumatol. 2004 Feb;31(2):207-1314760786
Cites: Arthritis Rheum. 2004 Feb;50(2):380-614872479
Cites: Am J Epidemiol. 2004 May 1;159(9):882-9015105181
Cites: Am J Hum Genet. 2004 Aug;75(2):330-715208781
Cites: Arthritis Rheum. 2004 Oct;50(10):3085-9215476204
Cites: Scand J Rheumatol. 2004;33(5):300-615513677
Cites: Am J Epidemiol. 1982 Jan;115(1):92-1067055134
Cites: Thorax. 1986 Aug;41(8):596-6013787543
Cites: Br J Rheumatol. 1989;28 Suppl 1:13-7; discussion 18-232819343
Cites: N Engl J Med. 1990 Jun 7;322(23):1635-412288563
Cites: Arthritis Rheum. 1990 Jun;33(6):782-92363734
Cites: J Clin Epidemiol. 1990;43(11):1221-302147033
Cites: Ann Rheum Dis. 1990 Dec;49(12):980-22270970
Cites: Arthritis Rheum. 2009 Mar;60(3):641-5219248103
Cites: Ann Rheum Dis. 2009 Apr;68(4):526-3018477739
Cites: J Rheumatol. 2009 Apr;36(4):706-1119228654
Cites: Ann Rheum Dis. 2010 Jan;69(1):70-8119174392
Cites: BMJ. 2010;340:b483820075150
Cites: Arthritis Rheum. 2010 Feb;62(2):383-9120112361
PubMed ID
23495093 View in PubMed
Less detail

Association of mannose-binding lectin polymorphisms with sepsis and fatal outcome, in patients with systemic inflammatory response syndrome.

https://arctichealth.org/en/permalink/ahliterature183051
Source
J Infect Dis. 2003 Nov 1;188(9):1394-403
Publication Type
Article
Date
Nov-1-2003
Author
Peter Garred
Jens J Strøm
Lars Quist
Ellen Taaning
Hans O Madsen
Author Affiliation
Department of Clinical Immunology, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark. Garred@post5.tele.dk.
Source
J Infect Dis. 2003 Nov 1;188(9):1394-403
Date
Nov-1-2003
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Aged, 80 and over
Alleles
DNA - chemistry - genetics
Denmark - epidemiology
Female
Genetic Predisposition to Disease
Genetic Variation - genetics
Humans
Male
Mannose-Binding Lectin - genetics
Middle Aged
Polymerase Chain Reaction
Polymorphism, Single Nucleotide
Prospective Studies
Sequence Analysis, DNA
Survival Rate
Systemic Inflammatory Response Syndrome - genetics - mortality
Abstract
Genetic factors may predispose critically ill patients to increased risk of developing sepsis. Mannose-binding lectin (MBL) is an important factor in innate immune defense. We investigated whether MBL gene polymorphisms causing low levels of MBL are associated with the development and progression of sepsis in adult patients in intensive care units. In 272 prospectively monitored patients with systemic inflammatory response syndrome, different MBL genotypes were compared, with respect to microbiology, sepsis development, and survival. The presence of MBL variant alleles was associated with the development of sepsis, severe sepsis, and septic shock. An increased risk of fatal outcome was observed in patients carrying variant alleles. These data show that MBL insufficiency plays an important role in the susceptibility of critically ill patients to the development and progression of sepsis and confers a substantial risk of fatal outcome.
PubMed ID
14593599 View in PubMed
Less detail

Association of the LINGO2-related SNP rs10968576 with body mass in a cohort of elderly Swedes.

https://arctichealth.org/en/permalink/ahliterature267388
Source
Mol Genet Genomics. 2015 Aug;290(4):1485-91
Publication Type
Article
Date
Aug-2015
Author
Mathias Rask-Andersen
Markus Sällman Almén
Lars Lind
Helgi B Schiöth
Source
Mol Genet Genomics. 2015 Aug;290(4):1485-91
Date
Aug-2015
Language
English
Publication Type
Article
Keywords
Adiposity - genetics
Aged
Aged, 80 and over
Body mass index
Female
Gene Frequency
Genotype
Humans
Introns - genetics
Linkage Disequilibrium
Male
Polymorphism, Single Nucleotide
Prospective Studies
Sweden
Abstract
Genome-wide association studies (GWAS) have identified common genetic factors influencing body mass as well as body adiposity. The functional implications of these loci are currently under investigation. Intense scrutiny of the body mass-associated FTO locus revealed age-specific effects, or a weakened effect in elderly populations. In this study, we aimed to determine the effects of single nucleotide polymorphisms (SNPs) representing 35 GWAS-identified body mass- and adiposity-associated genetic loci. In our analysis, 949 participants of the Prospective Investigation of the Vasculature in Uppsala Seniors cohort were included. All participants were born between 1920 and 1924. Data were available for 474 male and 475 female participants at age 70 and 380 male and 390 female participants at age 75. Genetic associations with BMI and change in BMI from age 70 to 75 were analyzed. In our analysis, rs10968576, an intronic SNP within the LINGO2 (LERN3, LRRN6C) gene, was associated with body mass in a cross section of elderly Swedes at age 70. This is the first study to replicate the association of a LINGO2-related genetic variant with body mass in an independent cohort of elderly citizens.
PubMed ID
25711307 View in PubMed
Less detail

Associations of markers in 11 obesity candidate genes with maximal weight loss and weight regain in the SOS bariatric surgery cases.

https://arctichealth.org/en/permalink/ahliterature141350
Source
Int J Obes (Lond). 2011 May;35(5):676-83
Publication Type
Article
Date
May-2011
Author
M A Sarzynski
P. Jacobson
T. Rankinen
B. Carlsson
L. Sjöström
C. Bouchard
L M S Carlsson
Author Affiliation
Human Genomics Laboratory, Pennington Biomedical Research Center, Baton Rouge, LA, USA.
Source
Int J Obes (Lond). 2011 May;35(5):676-83
Date
May-2011
Language
English
Publication Type
Article
Keywords
Adult
Bariatric Surgery - methods
Female
Genetic Association Studies
Genetic Markers - genetics
Genetic Variation
Humans
Male
Middle Aged
Obesity, Morbid - genetics - metabolism - surgery
Polymorphism, Single Nucleotide - genetics
Prospective Studies
Sweden
Weight Gain - genetics
Weight Loss - genetics
Abstract
To test whether DNA sequence variation in 11 obesity genes is associated with maximum weight loss and weight regain over 6 years of follow-up in bariatric surgery patients of the Swedish obese subjects (SOS) intervention study.
A total of 1443 subjects were available for analysis (vertical banded gastroplasty: n = 966, banding: n = 293 and gastric bypass: n = 184). Single-nucleotide polymorphisms (SNPs) from the following 11 genes were included: ADIPOQ, BDNF, FTO, GNB3, LEP, LEPR, MC4R, NR3C1, PPARG, PPARGC1A and TNF. General linear models were used to analyze associations between the SNPs and maximum weight loss and weight regain.
The average maximum weight loss was 33.7 kg (s.d. 13.3; min -95.5 kg, max +2.0 kg), which was reached 2.2 (s.d. 1.6) years after the surgery. Subjects regained approximately 12 kg (range 0.0-51.4 kg) by year 6. After correcting for multiple testing, the FTO SNP rs16945088 remained significantly associated with maximum weight loss (P = 0.0002), as minor allele carriers lost approximately 3 kg less compared with common allele homozygotes. This association was particularly evident in the banding surgery patients (P
Notes
Erratum In: Int J Obes (Lond). 2012 Jul;36(7):1016
PubMed ID
20733583 View in PubMed
Less detail

Blood lipid genetic scores, the HMGCR gene and cancer risk: a Mendelian randomization study.

https://arctichealth.org/en/permalink/ahliterature298643
Source
Int J Epidemiol. 2018 04 01; 47(2):495-505
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Date
04-01-2018
Author
Marju Orho-Melander
George Hindy
Signe Borgquist
Christina-Alexandra Schulz
Jonas Manjer
Olle Melander
Tanja Stocks
Author Affiliation
Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.
Source
Int J Epidemiol. 2018 04 01; 47(2):495-505
Date
04-01-2018
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Adult
Aged
Female
Humans
Hydroxymethylglutaryl CoA Reductases - genetics
Logistic Models
Male
Mendelian Randomization Analysis
Middle Aged
Neoplasms - blood - genetics
Polymorphism, Single Nucleotide
Prospective Studies
Risk assessment
Risk factors
Sweden
Triglycerides - blood
Abstract
It is unclear whether there are causal associations between blood lipids, statin use and cancer risks. Under certain assumptions, Mendelian randomization analysis of a genetic marker for an exposure eliminates reverse causation and confounding.
We applied Mendelian randomization analysis to genetic scores, comprising 26-41 single-nucleotide polymorphisms (SNPs), as instrumental variables (IVs) for triglycerides and low- and high-density lipoprotein cholesterol (LDLC, HDLC), using a prospective cohort of 26?904 individuals in which there were 6607 incident cancers. We also investigated cancer risk for a SNP (rs12916) in the gene encoding hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), the targeted enzyme in statin treatment. We used logistic regression and SNP pleiotropy-adjusted analyses to estimate the odds ratio per standard deviation (OR).
The OR for the triglyceride IV as a predictor of any cancer was 0.91 [95% confidence interval (CI): 0.80-1.03] unadjusted, and 0.87 (95% CI: 0.78-0.95) from the pleiotropy-adjusted analysis. For the HMGCR rs12916 per LDLC-lowering T-allele, the OR was 1.09 (95% CI: 1.01-1.18) for prostate cancer and 0.89 (95% CI: 0.82-0.96) for breast cancer. The LDLC IV was not associated with prostate cancer or breast cancer. There were no associations between IVs and cancers of the lung, colon or bladder.
Under the assumptions of Mendelian randomization, there is a causal and negative association between serum triglycerides and risk of any cancer. Further, the HMGCR genetic variant might be associated with risks of prostate and breast cancers but the biological mechanisms behind these findings are unclear, as the LDLC IV was not associated with these cancers.
PubMed ID
29165714 View in PubMed
Less detail

A blood pressure genetic risk score is a significant predictor of incident cardiovascular events in 32,669 individuals.

https://arctichealth.org/en/permalink/ahliterature115422
Source
Hypertension. 2013 May;61(5):987-94
Publication Type
Article
Date
May-2013
Author
Aki S Havulinna
Johannes Kettunen
Olavi Ukkola
Clive Osmond
Johan G Eriksson
Y Antero Kesäniemi
Antti Jula
Leena Peltonen
Kimmo Kontula
Veikko Salomaa
Christopher Newton-Cheh
Author Affiliation
Department of Chronic Disease Prevention, National Institute for Health and Welfare, Helsinki, Finland.
Source
Hypertension. 2013 May;61(5):987-94
Date
May-2013
Language
English
Publication Type
Article
Keywords
Adult
Blood Pressure - genetics
Cardiovascular Diseases - epidemiology - ethnology - genetics
Cohort Studies
Cross-Sectional Studies
Female
Finland - epidemiology
Follow-Up Studies
Genome-Wide Association Study
Genotype
Humans
Hypertension - genetics
Incidence
Longitudinal Studies
Male
Middle Aged
Polymorphism, Single Nucleotide - genetics
Prospective Studies
Retrospective Studies
Risk factors
Abstract
Recent genome-wide association studies have identified genetic variants associated with blood pressure (BP). We investigated whether genetic risk scores (GRSs) constructed of these variants would predict incident cardiovascular disease (CVD) events. We genotyped 32 common single nucleotide polymorphisms in several Finnish cohorts, with up to 32,669 individuals after exclusion of prevalent CVD cases. The median follow-up was 9.8 years, during which 2295 incident CVD events occurred. We created GRSs separately for systolic BP and diastolic BP by multiplying the risk allele count of each single nucleotide polymorphism by the effect size estimated in published genome-wide association studies. We performed Cox regression analyses with and without adjustment for clinical factors, including BP at baseline in each cohort. The results were combined by inverse variance-weighted fixed-effects meta-analysis. The GRSs were strongly associated with systolic BP and diastolic BP, and baseline hypertension (all P
Notes
Cites: Nat Genet. 2009 Jun;41(6):677-8719430479
Cites: Nat Genet. 2009 Jun;41(6):666-7619430483
Cites: PLoS Genet. 2010 Oct;6(10):e100117721082022
Cites: Stat Med. 2011 Jan 15;30(1):11-2121204120
Cites: Hypertension. 2011 May;57(5):903-1021444836
Cites: Nature. 2011 Oct 6;478(7367):103-921909115
Cites: Hypertension. 2011 Dec;58(6):1079-8522025373
Cites: Int J Epidemiol. 2010 Apr;39(2):504-1819959603
Cites: Hypertension. 2000 Oct;36(4):477-8311040222
Cites: Stat Med. 2002 Jun 15;21(11):1539-5812111919
Cites: Nat Genet. 2003 Feb;33(2):177-8212524541
Cites: JAMA. 2003 May 21;289(19):2560-7212748199
Cites: Lancet. 1990 Mar 31;335(8692):765-741969518
Cites: Lancet. 1990 Apr 7;335(8693):827-381969567
Cites: Hypertension. 1996 Dec;28(6):1070-58952598
Cites: Stat Med. 1997 May 15;16(9):965-809160492
Cites: Eur J Cardiovasc Prev Rehabil. 2005 Apr;12(2):132-715785298
Cites: Stat Med. 2005 Oct 15;24(19):2911-3516152135
Cites: N Engl J Med. 2005 Oct 27;353(17):1802-916251536
Cites: Eur J Cardiovasc Prev Rehabil. 2007 Jun;14(3):380-517568236
Cites: Stat Med. 2008 Jan 30;27(2):157-72; discussion 207-1217569110
Cites: Lancet. 2010 Mar 13;375(9718):895-90520226988
Comment In: Hypertension. 2013 May;61(5):961-323509079
PubMed ID
23509078 View in PubMed
Less detail

Body mass index and depressive symptoms: instrumental-variables regression with genetic risk score.

https://arctichealth.org/en/permalink/ahliterature268632
Source
Genes Brain Behav. 2012 Nov;11(8):942-8
Publication Type
Article
Date
Nov-2012
Author
M. Jokela
M. Elovainio
L. Keltikangas-Järvinen
G D Batty
M. Hintsanen
I. Seppälä
M. Kähönen
J S Viikari
O T Raitakari
T. Lehtimäki
M. Kivimäki
Source
Genes Brain Behav. 2012 Nov;11(8):942-8
Date
Nov-2012
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Body mass index
Body Weight - genetics
Cohort Studies
Depressive Disorder - genetics
Female
Finland
Genetic Markers - genetics
Genetic Predisposition to Disease - genetics
Humans
Male
Mendelian Randomization Analysis
Obesity - genetics
Phenotype
Polymorphism, Single Nucleotide - genetics
Prospective Studies
Abstract
The causal role of obesity in the development of depression remains uncertain. We applied instrumental-variables regression (Mendelian randomization) to examine the association of adolescent and adult body mass index (BMI) with adult depressive symptoms. Participants were from the Young Finns prospective cohort study (n?=?1731 persons, 2844 person-observations), with repeated measurements of BMI and depressive symptoms (modified Beck's Depression Inventory). Genetic risk score of 31 single nucleotide polymorphisms previously identified as robust genetic markers of body weight was used as a proxy for variation in BMI. In standard linear regression analysis, higher adult depressive symptoms were predicted by higher adolescent BMI (B?=?0.33, CI?=?0.06-0.60, P?=?0.017) and adult BMI (B?=?0.47, CI?=?0.32-0.63, P?
PubMed ID
22958333 View in PubMed
Less detail

125 records – page 1 of 13.