Publication Detail
The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Interaction of apolipoprotein E genotype with smoking and physical inactivity on coronary heart disease risk in men and women.
Jaana Gustavsson; Kirsten Mehlig; Karin Leander; Elisabeth Strandhagen; Lena Björck; Dag S Thelle; Lauren Lissner; Kaj Blennow; Henrik Zetterberg; Fredrik Nyberg (Profiled Author: Blennow, Kaj)
Department of Public Health and Community Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Sweden. jaana.gustavsson@amm.gu.se
Atherosclerosis 2012;220(2):486-92.
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.
Scientific Context
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
Related Grants
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1.
Mayeux, Richard P
GENETIC EPIDEMIOLOGY OF ALZHEIMERS DISEASE IN HISPANICS
1 December 1998 - 31 January 2004
NATIONAL INSTITUTE ON AGING
Total Funding: $ 5,549,515
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2.
Mayeux, Richard P
GENETIC EPIDEMIOLOGY OF AGING IN A MULTIETHNIC COMMUNITY
30 September 2000 - 31 July 2003
NATIONAL INSTITUTE ON AGING
Total Funding: $ 2,268,838
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3.
Smith, Mark A
METABOLIC ABNORMALITIES IN ALZHEIMER DISEASE
1 May 1999 - 30 April 2006
NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
Total Funding: $ 750,386
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Journal of Alzheimer's disease : JAD 2011;24(3):587-97. -
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1994M S Tsai; E G Tangalos; R C Petersen; G E Smith; D J Schaid; E Kokmen; R J Ivnik; S N Thibodeau
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2000Y Du; R C Dodel; B J Eastwood; K R Bales; F Gao; F Lohmüller; U Müller; A Kurz; R Zimmer; R M Evans; et al.
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