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Interaction of apolipoprotein E genotype with smoking and physical inactivity on coronary heart disease risk in men and women.

Artikel i vetenskaplig tidskrift
Författare Jaana Gustavsson
Kirsten Mehlig
Karin Leander
Elisabeth Strandhagen
Lena Björck
Dag Thelle
Lauren Lissner
Fredrik Nyberg
Publicerad i Atherosclerosis
Volym 220
Nummer/häfte 2
Sidor 486–492
ISSN 1879-1484
Publiceringsår 2012
Publicerad vid Institutionen för medicin, avdelningen för samhällsmedicin och folkhälsa
Institutionen för medicin, avdelningen för molekylär och klinisk medicin
Sidor 486–492
Språk en
Länkar dx.doi.org/10.1016/j.atherosclerosi...
Ämnesord gene-environment interaction, Apolipoprotein E polymorphism, smoking, physical activity
Ämneskategorier Folkhälsomedicinska forskningsområden

Sammanfattning

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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