Skip header and navigation

Refine By

98 records – page 1 of 10.

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

24-h ambulatory blood pressure is linked to chromosome 18q21-22 and genetic variation of NEDD4L associates with cross-sectional and longitudinal blood pressure in Swedes.

https://arctichealth.org/en/permalink/ahliterature81774
Source
Kidney Int. 2006 Aug;70(3):562-9
Publication Type
Article
Date
Aug-2006
Author
Fava C.
von Wowern F.
Berglund G.
Carlson J.
Hedblad B.
Rosberg L.
Burri P.
Almgren P.
Melander O.
Author Affiliation
Department of Clinical Sciences, University Hospital MAS, Malmö, Sweden.
Source
Kidney Int. 2006 Aug;70(3):562-9
Date
Aug-2006
Language
English
Publication Type
Article
Keywords
Adult
Alternative Splicing
Antihypertensive Agents - therapeutic use
Blood Pressure - genetics
Blood Pressure Monitoring, Ambulatory
Chromosomes, Human, Pair 18
Circadian Rhythm
Cross-Sectional Studies
Female
Genetic Predisposition to Disease - epidemiology
Genotype
Humans
Hypertension - drug therapy - epidemiology - genetics
Insulin - blood
Linkage (Genetics)
Longitudinal Studies
Male
Middle Aged
Phenotype
Polymorphism, Single Nucleotide
Risk factors
Sweden - epidemiology
Ubiquitin-Protein Ligases - genetics
Variation (Genetics)
Abstract
Numerous linkage studies have indicated chromosome 18q21-22 as a locus of importance for blood pressure regulation. This locus harbors the neural precursor cell expressed developmentally downregulated 4-like (NEDD4L) gene, which is instrumental for the regulation of the amiloride-sensitive epithelial sodium channel (ENaC). In a linkage study of 16 markers (including two single nucleotide polymorphism markers located within the NEDD4L gene) on chromosome 18 between 70-104 cM and ambulatory blood pressure (ABP), in 118 families, the strongest evidence of linkage was found for 24 h and day-time systolic ABP at the NEDD4L locus (82.25 cM) (P=0.0014). In a large population sample (n=4001), we subsequently showed that a NEDD4L gene variant (rs4149601), which by alternative splicing leads to varying expression of a functionally crucial C2 domain, was associated with diastolic blood pressure (DBP) (P=0.03) and DBP progression over time (P=0.04). A genotype combination of the rs4149601 and an intronic NEDD4L marker (rs2288774) was associated with systolic blood pressure (SBP) (P=0.01), DBP (P=0.04), and progression of both SBP (P=0.03) and DBP (P=0.05) over time. A quantitative transmission disequilibrium test in the family material of the rs4149601 supported this NEDD4L variant as being at least partially causative of the linkage result. In conclusion, our findings suggest that the chromosome 18 linkage peak at 82.25 cM is explained by genetic NEDD4L variation affecting cross-sectional and longitudinal blood pressure, possibly as a consequence of altered NEDD4L interaction with ENaC.
PubMed ID
16788695 View in PubMed
Less detail

The ADD1 G460W polymorphism is not associated with variation in blood pressure in Canadian Oji-Cree.

https://arctichealth.org/en/permalink/ahliterature201292
Source
J Hum Genet. 1999;44(4):225-9
Publication Type
Article
Date
1999
Author
C P Busch
S B Harris
A J Hanley
B. Zinman
R A Hegele
Author Affiliation
John P. Robarts Research Institute, University of Western Ontario, London, Canada.
Source
J Hum Genet. 1999;44(4):225-9
Date
1999
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Alleles
Analysis of Variance
Blood Pressure - genetics
CCAAT-Enhancer-Binding Proteins
Canada
Child
DNA-Binding Proteins - genetics
Female
Genetic Variation
Genotype
Humans
Indians, North American
Male
Middle Aged
Nuclear Proteins - genetics
Polymorphism, Genetic
Sterol Regulatory Element Binding Protein 1
Transcription Factors
Abstract
Since adducin modulates cellular sodium retention, its follows that ADD1, which encodes the alpha-subunit of adducin, is an attractive candidate gene for blood pressure variation. Association studies examining the relationship between polymorphism at ADD1 codon 460 (G460W) and both hypertension and blood pressure, which were performed in a variety of human population samples derived from different genetic backgrounds, have given inconsistent results. We examined the association between the ADD1 G460W polymorphism and variation in blood pressure in a sample of non-diabetic, largely normotensive Canadian Oji-Cree from an isolated community in Northern Ontario. Among 481 Oji-Cree subjects, we measured blood pressure and related clinical phenotypes and determined genotypes of ADD1 G460W. We observed an allele frequency of 0.08 for the ADD1 W460 variant, which is among the lowest so far observed in human populations. We found significant associations between variation in both systolic and diastolic blood pressure and gender, age, body mass index (BMI), and treatment for hypertension. However, we found no association between the ADD1 W460 allele and increased blood pressure, nor did we observe a higher frequency of the W460 allele in a hypertensive subgroup compared with normotensive subjects. While the low sample frequency of ADD1 W460 is consistent with the low sample prevalence of hypertension, the absence of a specific association with both blood pressure and hypertension suggests that the ADD1 W460 variant is not an important determinant of blood pressure among individuals of this genetic background.
PubMed ID
10429360 View in PubMed
Less detail

AGT M235T and ACE ID polymorphisms and exercise blood pressure in the HERITAGE Family Study.

https://arctichealth.org/en/permalink/ahliterature197889
Source
Am J Physiol Heart Circ Physiol. 2000 Jul;279(1):H368-74
Publication Type
Article
Date
Jul-2000
Author
T. Rankinen
J. Gagnon
L. Pérusse
Y C Chagnon
T. Rice
A S Leon
J S Skinner
J H Wilmore
D C Rao
C. Bouchard
Author Affiliation
Pennington Biomedical Research Center, Human Genomics Laboratory, Baton Rouge, Louisiana 70808, USA.
Source
Am J Physiol Heart Circ Physiol. 2000 Jul;279(1):H368-74
Date
Jul-2000
Language
English
Publication Type
Article
Keywords
Adult
Amino Acid Substitution
Angiotensinogen - genetics
Blood Pressure - genetics - physiology
Canada
Cohort Studies
DNA Transposable Elements
Diastole
European Continental Ancestry Group
Exercise - physiology
Female
Genotype
Humans
Male
Oxygen consumption
Peptidyl-Dipeptidase A - genetics
Physical Exertion - physiology
Polymorphism, Genetic
Sequence Deletion
Sex Characteristics
Systole
United States
Abstract
We investigated the association between angiotensinogen (AGT) and angiotensin-converting enzyme (ACE) gene polymorphisms and exercise training responses of resting and exercise blood pressure (BP). BP at rest and during submaximal (50 watts) and maximal exercise tests was measured before and after 20 wk of endurance training in 476 sedentary normotensive Caucasian subjects from 99 families. AGT M235T and ACE insertion/deletion polymorphisms were typed with PCR-based methods. Men carrying the AGT MM and MT genotypes showed 3. 7 +/- 0.6 and 3.2 +/- 0.5 (SE) mmHg reductions, respectively, in diastolic BP at 50 watts (DBP(50)), whereas, in the TT homozygotes, the decrease was 0.4 +/- 1.0 mmHg (P = 0.016 for trend, adjusted for age, body mass index, and baseline DBP(50)). Men with the ACE DD genotype showed a slightly greater decrease in DBP(50) (4.4 +/- 0.6 mmHg) than the II and ID genotypes (2.8 +/- 0.7 and 2.4 +/- 0.5 mmHg, respectively, P = 0.050). Furthermore, a significant (P = 0.022) interaction effect between the AGT and ACE genes was noted for DBP(50); the AGT TT homozygotes carrying the ACE D allele showed no response to training. Men with the AGT TT genotype had greater (P = 0.007) diastolic BP (DBP) response to acute maximal exercise at baseline. However, the difference disappeared after the training period. No associations were found in women. These data suggest that, in men, the genetic variation in the AGT locus modifies the responsiveness of submaximal exercise DBP to endurance training, and interactions between the AGT and ACE loci can alter this response.
PubMed ID
10899077 View in PubMed
Less detail

Angiotensin converting enzyme gene insertion/deletion polymorphism, angiotensinogen gene polymorphisms, family history of hypertension, and childhood blood pressure.

https://arctichealth.org/en/permalink/ahliterature33126
Source
Am J Hypertens. 1999 Sep;12(9 Pt 1):858-66
Publication Type
Article
Date
Sep-1999
Author
L. Taittonen
M. Uhari
K. Kontula
K. Kainulainen
H. Miettinen
J. Turtinen
M. Nuutinen
Author Affiliation
Department of Pediatrics, University of Oulu, Finland.
Source
Am J Hypertens. 1999 Sep;12(9 Pt 1):858-66
Date
Sep-1999
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Angiotensinogen - genetics
Blood Pressure - genetics
Child
Child, Preschool
Comparative Study
DNA - analysis
DNA Primers - chemistry
DNA Transposable Elements - genetics
Female
Follow-Up Studies
Gene Deletion
Genetic Code
Genetic markers
Genetic Predisposition to Disease
Genotype
Humans
Hypertension - blood - genetics
Male
Minisatellite Repeats
Peptidyl-Dipeptidase A - genetics
Polymerase Chain Reaction
Polymorphism, Genetic
Research Support, Non-U.S. Gov't
Retrospective Studies
Abstract
Earlier epidemiologic studies have yielded inconsistent results on the extent and timing of the blood pressure (BP) increase in offspring of hypertensive parents. We hypothesized that a familial influence on the BP of the offspring exists from birth on, but becomes significant only later in childhood. We studied the influence of familial occurrence of hypertension on the BP of 3596 children aged 6 to 18 years during a 6-year follow-up. In addition, we examined the possible associations of BP variations with polymorphisms of two candidate genes for hypertension, ie, those coding for the angiotensin converting enzyme (ACE) and those coding for angiotensinogen. A positive family history of hypertension was reflected as the occurrence of higher systolic BP values from the age of 9 years and upward among the females and from the age of 12 years and upward among the males. The mean differences in BP varied from 3.2 to 5.8 mm Hg (systolic) and 2.1 to 5.9 mm Hg (diastolic) between the female offspring of normotensive and hypertensive parents and grandparents. The systolic BP values were significantly higher among females with a hypertensive history in two generations in comparison with females from normotensive families. Among the male offspring of hypertensive and normotensive families, the BP differences were inconsistent. The deletion/deletion males had higher systolic BP values than those with other ACE genotypes. In contrast, variation at the angiotensinogen gene locus was not significantly associated with BP. We conclude that parental history of hypertension is a risk factor for high blood pressure among the offspring from the ages of 9 to 12 years and upward, and hypertension within two generations may enhance this effect. Although the common genetic variation of ACE may influence blood pressure in male children and adolescents, our data do not suggest a role for the common variation of the angiotensinogen gene as a BP regulator during childhood.
PubMed ID
10509542 View in PubMed
Less detail

Angiotensinogen gene variation associated with variation in blood pressure in aboriginal Canadians.

https://arctichealth.org/en/permalink/ahliterature208619
Source
Hypertension. 1997 May;29(5):1073-7
Publication Type
Article
Date
May-1997
Author
R A Hegele
S B Harris
A J Hanley
F. Sun
P W Connelly
B. Zinman
Author Affiliation
St Michael's Hospital Health Sciences Research Centre, Toronto, Ontario, Canada. robert.hegele@utoronto.ca
Source
Hypertension. 1997 May;29(5):1073-7
Date
May-1997
Language
English
Publication Type
Article
Keywords
Adult
Age Factors
American Native Continental Ancestry Group
Angiotensinogen - genetics
Blood Pressure - genetics
Body Weight
Canada - ethnology
Female
Humans
Hypertension - ethnology - genetics
Male
Abstract
We measured blood pressure and related clinical phenotypes in 497 adult native Canadians from an isolated community in Northern Ontario. We analyzed their DNA for genotypes of angiotensinogen. We found that the frequency of the T235 variant of the angiotensinogen gene was 0.89 in this sample. This variant was associated with a significantly increased systolic pressure but not diastolic pressure. We also found that sex and body mass were each highly significantly associated with variation in both systolic and diastolic pressures. We found a significant association between age and variation in systolic pressure but not diastolic pressure. We also found a highly significant association between plasma apolipoprotein B concentration and variation in diastolic pressure but not systolic pressure. The high frequency of the angiotensinogen T235 variant suggests that subjects in this young, essentially normotensive population might be predisposed to hypertension, which may become more apparent in the presence of secondary factors.
PubMed ID
9149668 View in PubMed
Less detail

[Association analysis of gene polymorphism in alcohol metabolizing enzymes with risk for coronary atherosclerosis].

https://arctichealth.org/en/permalink/ahliterature163692
Source
Genetika. 2007 Mar;43(3):409-16
Publication Type
Article
Date
Mar-2007
Author
A V Marusin
V A Stepanov
M G Spiridonova
V A Khar'kov
Ia R Pel's
V P Puzyrev
Source
Genetika. 2007 Mar;43(3):409-16
Date
Mar-2007
Language
Russian
Publication Type
Article
Keywords
Adult
Aged
Alcohol Dehydrogenase - genetics
Alleles
Blood Pressure - genetics
Case-Control Studies
Coronary Artery Disease - genetics
Cytochrome P-450 CYP2E1 - genetics
Ethanol - metabolism
Female
Gene Frequency
Genetic Predisposition to Disease
Humans
Linkage Disequilibrium
Male
Middle Aged
Polymorphism, Genetic
Risk
Russia
Abstract
The allele and genotype distribution of two alcohol dehydrogenase genes ADH1B (exon 3 polymorphism A/G (47His)), ADH7 (intron 5 polymorphism G/C) and cytochrome P450 2E1 gene (CYP2E1; 5'-flanking region G/C and intron 6 T/A polymorphisms) were examined in Russian (Tomsk, n = 125) healthy population and in coronary atherosclerosis patients (CA, n = 92). The genotype frequencies followed the Hardy-Weinberg equilibrium and the alleles were in linkage equilibrium or gametic equilibrium in the control sample. Only two CYP2E1 gene polymorphisms were in linkage disequilibrium. The frequencies of the derived alleles at ADH1B (*G (+MslI) allele), CYP2E1 (**C2 (+PstI) allele) and CYP2E1 (*C (-Dra I)2 allele) were 8.48 +/- 1.86%; 1.20 +/- 0.69% and 10.00 +/- 1.90%, respectively. The 2ADH7 gene polymorphism showed a high level of heterozygosity; the frequency of the ADH7*C (-Sty I) allele was 44.58 +/- 3.21%. A significantly higher frequency of CYP2E1 (*C2 (+Pst I)) allele has been revealed in the CA group (P = 0.043; OR = 4.23; 95% CI 1.03-20.01). The tendency to significant effect of A1A2 genotype in ADH1B Msl 1 polymorphism was observed for systolic blood pressure in the control group (P = 0.068). The statistically significant two-way interaction effects of ADH7 StyI and CYP2E1 DraI on diastolic blood pressure (P = 0.029) and on the serum high density lipoprotein level (P = 0,042) were also revealed. Association of A1A2 genotype in ADHIB Msl I polymorphism with reduced amount in a serum of a very low density lipoprotein level (P = 0.045) have also been shown. This may result from multifunctional activity of alcohol metabolizing enzymes and their involvement in many metabolic and free radical reactions in the body.
PubMed ID
17486761 View in PubMed
Less detail

Association between AGT codon 235 polymorphism and variation in serum concentrations of creatinine and urea in Canadian Oji-Cree.

https://arctichealth.org/en/permalink/ahliterature201134
Source
Clin Genet. 1999 Jun;55(6):438-43
Publication Type
Article
Date
Jun-1999
Author
R A Hegele
S B Harris
A J Hanley
B. Zinman
Author Affiliation
Blackburn Cardiovascular Genetics Laboratory, Robarts Research Institute, London, Ontario, Canada. robert.hegele@rri.on.ca
Source
Clin Genet. 1999 Jun;55(6):438-43
Date
Jun-1999
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Alleles
American Native Continental Ancestry Group - genetics
Angiotensinogen - genetics
Blood Pressure - genetics
Canada
Child
Codon
Creatinine - blood
Female
Gene Frequency
Genotype
Humans
Kidney Function Tests
Male
Middle Aged
Phenotype
Polymorphism, Genetic
Urea - blood
Abstract
Finding the genetic determinants of intermediate quantitative traits, such as serum creatinine and urea, might aid in finding the determinants of disease phenotypes, such as renal failure, that are, in part, defined according to threshold values imposed upon such traits. We evaluated the association between common variation in the gene encoding angiotensinogen, AGT, and the serum concentrations of creatinine and urea in non-diabetic Canadian Oji-Cree. We determined genotypes of the AGT codon 235 polymorphism among 502 non-diabetic Oji-Cree. We used multivariate analysis of variance to identify significant determinants of variation in serum concentrations of creatinine and urea and of systolic and diastolic blood pressure. We found significant associations between the AGT codon 235 genotype and serum concentrations of creatinine and urea (p = 0.017 and 0.049, respectively) and systolic blood pressure (p = 0.041). Compared with subjects with the other two genotypes, homozygotes for AGT T235/T235 had significantly lower serum concentrations of creatinine and urea and significantly higher mean systolic blood pressure. The findings suggest that the AGT T235 allele is a determinant of intermediate traits related to renal function in these aboriginal Canadians.
PubMed ID
10450860 View in PubMed
Less detail

Association between ghrelin gene variations and blood pressure in subjects with impaired glucose tolerance.

https://arctichealth.org/en/permalink/ahliterature167684
Source
Am J Hypertens. 2006 Sep;19(9):920-6
Publication Type
Article
Date
Sep-2006
Author
Ursula Mager
Marjukka Kolehmainen
Jaana Lindström
Johan G Eriksson
Timo T Valle
Helena Hämäläinen
Pirjo Ilanne-Parikka
Sirkka Keinänen-Kiukaanniemi
Jaakko O Tuomilehto
Leena Pulkkinen
Matti I Uusitupa
Author Affiliation
Department of Public Health and Clinical Nutrition and Food and Health Research Centre, University of Kuopio, Kuopio, Finland. ursula.mager@uku.fi
Source
Am J Hypertens. 2006 Sep;19(9):920-6
Date
Sep-2006
Language
English
Publication Type
Article
Keywords
Adult
Aged
Analysis of Variance
Blood Pressure - genetics
Female
Finland
Follow-Up Studies
Gene Frequency
Genetic Predisposition to Disease
Genotype
Ghrelin
Glucose Intolerance - genetics - physiopathology
Humans
Hypertension - genetics - physiopathology
Longitudinal Studies
Male
Middle Aged
Peptide Hormones - genetics
Phenotype
Polymorphism, Restriction Fragment Length
Polymorphism, Single Nucleotide - genetics
Promoter Regions, Genetic - genetics
Abstract
Ghrelin is a gut-brain hormone, which stimulates food intake and controls energy balance. Recently, it has been shown that ghrelin may also play a role in the regulation of blood pressure (BP) by acting at the sympathetic nervous system. In the present study we genotyped six variants of the ghrelin gene and its promoter, and tested whether these single nucleotide polymorphisms (SNPs) were associated with BP levels in participants of the Finnish Diabetes Prevention Study.
The Finnish Diabetes Prevention Study was a longitudinal study where 522 subjects with impaired glucose tolerance were randomized into either an intervention or control group. DNA was available from 507 subjects (mean body mass index [BMI] 31.2+/-4.5 kg/m2, age 55+/-7 years). All six SNPs were screened by the restriction fragment length polymorphism method.
Subjects with the most common genotype combination of the following four SNPs, -604G/A, -501A/C, Leu72Met, and Gln90Leu, had the lowest systolic (131+/-11 v 137+/-13 mm Hg, P=.003) and diastolic BP levels (79+/-7 v 83+/-7 mm Hg, P=.004) at the baseline of the study and during 3 years of follow-up compared to all other genotypes. Adjustments for age, gender, antihypertensive medication, BMI, waist circumference, and alcohol intake did not change this association.
Several ghrelin gene variations were associated with BP levels in subjects with impaired glucose tolerance.
PubMed ID
16942934 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

98 records – page 1 of 10.