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Göteborgs universitets publikationer

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

Författare och institution:
Jaana Gustavsson (Institutionen för medicin, avdelningen för samhällsmedicin och folkhälsa); Kirsten Mehlig (Institutionen för medicin, avdelningen för samhällsmedicin och folkhälsa); Karin Leander (-); Elisabeth Strandhagen (Institutionen för medicin, avdelningen för samhällsmedicin och folkhälsa); Lena Björck (Institutionen för medicin, avdelningen för molekylär och klinisk medicin); Dag Thelle (-); Lauren Lissner (Institutionen för medicin, avdelningen för samhällsmedicin och folkhälsa); Fredrik Nyberg (Institutionen för medicin, avdelningen för samhällsmedicin och folkhälsa)
Publicerad i:
Atherosclerosis, 220 ( 2 ) s. 486–492
ISSN:
1879-1484
Publikationstyp:
Artikel, refereegranskad vetenskaplig
Publiceringsår:
2012
Språk:
engelska
Fulltextlänk:
Sammanfattning (abstract):
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.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
MEDICIN OCH HÄLSOVETENSKAP ->
Hälsovetenskaper ->
Folkhälsovetenskap, global hälsa, socialmedicin och epidemiologi ->
Folkhälsomedicinska forskningsområden
Nyckelord:
gene-environment interaction, Apolipoprotein E polymorphism, smoking, physical activity
Postens nummer:
149716
Posten skapad:
2011-12-07 11:15
Posten ändrad:
2016-06-10 11:57

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