Genetic Epidemiology, Translational Neurogenomics, Psychiatric Genetics and Statistical Genetics Laboratories investigate the pattern of disease in families, particularly identical and non-identical twins, to assess the relative importance of genes and environment in a variety of important health problems.
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PMID
12658118
TITLE
ADH genotype does not modify the effects of alcohol on high-density lipoprotein.
ABSTRACT
BACKGROUND NlmCategory: BACKGROUND
Alcohol consumption has beneficial effects on mortality which are mainly due to reduction in cardiovascular disease. These are believed to be due, at least in part, to the increase in plasma high-density lipoprotein (HDL) which is associated with alcohol consumption. It has been proposed that ADH3 genotype modifies the relationships between alcohol intake and cardiovascular disease by altering the HDL response to alcohol. The aim of this paper was to test for effects of ADH2 and ADH3 genotypes on the response of HDL components to habitual alcohol consumption.
METHODS NlmCategory: METHODS
Adult male and female subjects were genotyped for ADH2 and ADH3; and plasma HDL cholesterol, apolipoprotein A-I, and apolipoprotein A-II were measured. Nine hundred one subjects had both ADH2 and ADH3 genotypes and HDL cholesterol results, while 753 had both genotypes and all three lipid results. The effect of alcohol intake on the three measured HDL components, and a factor score derived from them, was estimated for each of the ADH2 and ADH3 genotype groups.
RESULTS NlmCategory: RESULTS
All the measured components of HDL increased with increasing alcohol consumption over the range of intakes studied, 0-4 drinks per day. There were no significant interactions between alcohol consumption and ADH2 or ADH3 genotypes.
CONCLUSIONS NlmCategory: CONCLUSIONS
The concept that alcohol dehydrogenase genotype and alcohol metabolic rate modify the effects of alcohol on plasma HDL concentration is not supported by our results.
DATE PUBLISHED
2003 Mar
HISTORY
PUBSTATUS PUBSTATUSDATE
pubmed 2003/03/27 05:00
medline 2003/09/25 05:00
entrez 2003/03/27 05:00
AUTHORS
NAME COLLECTIVENAME LASTNAME FORENAME INITIALS AFFILIATION AFFILIATIONINFO
Whitfield JB Whitfield John B JB Department of Clinical Biochemistry, Royal Prince Alfred Hospital, Camperdown NSW 2050, Australia. John.Whitfield@email.cs.nsw.gov.au
O'Brien ME O'Brien Martin E ME
Nightingale BN Nightingale Brian N BN
Zhu G Zhu Gu G
Heath AC Heath Andrew C AC
Martin NG Martin Nicholas G NG
INVESTIGATORS
JOURNAL
VOLUME: 27
ISSUE: 3
TITLE: Alcoholism, clinical and experimental research
ISOABBREVIATION: Alcohol. Clin. Exp. Res.
YEAR: 2003
MONTH: Mar
DAY:
MEDLINEDATE:
SEASON:
CITEDMEDIUM: Print
ISSN: 0145-6008
ISSNTYPE: Print
MEDLINE JOURNAL
MEDLINETA: Alcohol Clin Exp Res
COUNTRY: England
ISSNLINKING: 0145-6008
NLMUNIQUEID: 7707242
PUBLICATION TYPE
PUBLICATIONTYPE TEXT
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Twin Study
COMMENTS AND CORRECTIONS
GRANTS
GRANTID AGENCY COUNTRY
AA013321 NIAAA NIH HHS United States
AA013326 NIAAA NIH HHS United States
AA07535 NIAAA NIH HHS United States
AA119981 NIAAA NIH HHS United States
GENERAL NOTE
KEYWORDS
MESH HEADINGS
DESCRIPTORNAME QUALIFIERNAME
Adult
Aged
Aged, 80 and over
Alcohol Dehydrogenase genetics
Alcohol Drinking genetics
Chi-Square Distribution genetics
Cholesterol, HDL genetics
Female genetics
Genotype genetics
Humans genetics
Male genetics
Middle Aged genetics
Polymorphism, Genetic genetics
SUPPLEMENTARY MESH
GENE SYMBOLS
CHEMICALS
REGISTRYNUMBER NAMEOFSUBSTANCE
0 Cholesterol, HDL
EC 1.1.1.1 ADH1C protein, human
EC 1.1.1.1 Alcohol Dehydrogenase
OTHER ID's