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Interaction of apol...
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Gustavsson, Jaana,1974Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för samhällsmedicin och folkhälsa,Institute of Medicine, School of Public Health and Community Medicine
(author)
Interaction of apolipoprotein E genotype with smoking and physical inactivity on coronary heart disease risk in men and women.
- Article/chapterEnglish2012
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LIBRIS-ID:oai:gup.ub.gu.se/149716
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https://gup.ub.gu.se/publication/149716URI
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https://doi.org/10.1016/j.atherosclerosis.2011.10.011DOI
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http://kipublications.ki.se/Default.aspx?queryparsed=id:123873682URI
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
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OBJECTIVE: Apolipoprotein E genotype (APOE) polymorphism affects lipid levels and coronary heart disease (CHD) risk. However, these associations may be modified by lifestyle factors. Therefore, we studied whether smoking, physical inactivity or overweight interact with APOE on cholesterol levels and CHD risk. METHODS: Combining two Swedish case-control studies yielded 1735 CHD cases and 4654 population controls (3747 men, 2642 women). Self-reported questionnaire lifestyle data included smoking (ever [current or former regular] or never) and physical inactivity (mainly sitting leisure time). We obtained LDL cholesterol levels and APOE genotypes. CHD risk was modelled using logistic regression to obtain odds ratios (ORs) and 95% confidence intervals (CIs), adjusted for relevant covariates. RESULTS: Smoking interacted with APOE on CHD risk; adjusted ORs for ever versus never smoking were 1.45 (95% CI 1.00-2.10) in ɛ2 carriers, 2.25 (95% CI 1.90-2.68) in ɛ3 homozygotes and 2.37 (95% CI 1.85-3.04) in ɛ4 carriers. Female ɛ4 carriers had OR 3.62 (95% CI 2.32-5.63). The adjusted ORs for physical inactivity were 1.09 (95% CI 0.73-1.61), 1.34 (95% CI 1.12-1.61), and 1.79 (95% CI 1.38-2.30) in ɛ2, ɛ3ɛ3 and ɛ4 groups, respectively. No interaction was seen between overweight and APOE for CHD risk, or between any lifestyle factor and APOE for LDL cholesterol levels. CONCLUSION: The APOE ɛ2 allele counteracted CHD risk from smoking in both genders, while the ɛ4 allele was seen to potentiate this risk mainly in women. Similar ɛ2 protection and ɛ4 potentiation was suggested for CHD risk from physical inactivity.
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Mehlig, Kirsten,1964Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för samhällsmedicin och folkhälsa,Institute of Medicine, School of Public Health and Community Medicine(Swepub:gu)xmehki
(author)
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Leander, KarinKarolinska Institutet
(author)
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Strandhagen, Elisabeth,1960Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för samhällsmedicin och folkhälsa,Institute of Medicine, School of Public Health and Community Medicine(Swepub:gu)xstrel
(author)
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Björck, Lena,1959Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Institute of Medicine, Department of Molecular and Clinical Medicine(Swepub:gu)xblend
(author)
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Thelle, Dag,1942
(author)
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Lissner, Lauren,1956Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för samhällsmedicin och folkhälsa,Institute of Medicine, School of Public Health and Community Medicine(Swepub:gu)xlisla
(author)
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Nyberg, Fredrik,1961Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för samhällsmedicin och folkhälsa,Institute of Medicine, School of Public Health and Community Medicine(Swepub:gu)xnybef
(author)
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Blennow, K
(author)
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Zetterberg, H
(author)
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Göteborgs universitetInstitutionen för medicin, avdelningen för samhällsmedicin och folkhälsa
(creator_code:org_t)
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In:Atherosclerosis: Elsevier BV220:2, s. 486-4921879-14840021-9150
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Atherosclerosis
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