High intakes of trans monounsaturated fatty acids taken for 2 weeks do not influence procoagulant and fibrinolytic risk markers for CHD in young healthy men.
Dietary trans fatty acids are associated with increased risk of CHD. We hypothesized that the changes in plasma lipids associated with a high intake of trans fatty acids would cause adverse effects on procoagulant and fibrinolytic activities. A randomized crossover controlled feeding study was conducted in twenty-nine men. A trans-rich diet supplying 10 % energy as trans- 18:1 was compared with diets in which the trans fatty acids were replaced either with carbohydrate or oleate; each diet was taken for 2 weeks in random order. Fasting fibrinogen and d-dimer concentrations and factor VII coagulant, plasminogen activator inhibitor type 1 and tissue plasminogen activator did not differ between diets. Postprandially, tissue plasminogen activator activity increased and plasminogen activator inhibitor type 1 activity decreased on all diets. Factor VIIc increased postprandially by 15 and 17 % on the trans and oleate diets respectively, compared with an 11 % increase on the carbohydrate diet; the mean difference between oleate and carbohydrate diets was 6 (95 % CI 0.2, 11.9) %. The LDL-cholesterol:HDL-cholesterol and apolipoprotein B : apolipoprotein A-I ratios increased by 13 (95 % CI 5.7, 21.8) and 10 (95 % CI 3.1, 17.2) % respectively on the trans diet compared with the oleate diet and by 6 (95 % CI 0.1,12.7) and 7 (95 % CI 0, 13.5) % respectively compared with the carbohydrate diet. Plasma HDL2-cholesterol concentration was 18 (95 % CI 0.7, 35.9) % lower on the trans diet compared with the oleate diet. The results confirm adverse effects of trans fatty acids on HDL-cholesterol concentrations, but suggest that trans fatty acids do not have any specific effects on known haemostatic risk markers for cardiovascular disease in healthy young men in the short-term.
Sanders
Thomas A B
TA
Nutrition Food and Health Research Centre, King's College London, Franklin-Wilkins Building, 150 Stamford Street, London, SE1 9NN, UK. Tom.Sanders@kcl.ac.uk
Oakley
Francesca R
FR
Crook
David
D
Cooper
Jackie A
JA
Miller
George J
GJ
D000293:Adolescent; D000328:Adult; D000704:Analysis of Variance; D001054:Apolipoproteins A / Q000032:analysis; D001055:Apolipoproteins B / Q000032:analysis; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation / Q000187:drug effects*; D002784:Cholesterol / Q000097:blood; D003327:Coronary Disease / Q000097:blood / Q000209:etiology*; D018592:Cross-Over Studies; D004040:Dietary Carbohydrates / Q000494:pharmacology; D005167:Factor VII / Q000032:analysis; D005227:Fatty Acids / Q000494:pharmacology*; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005340:Fibrinogen / Q000032:analysis; D005342:Fibrinolysis; D006801:Humans; D008297:Male; D019301:Oleic Acid / Q000494:pharmacology; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D019518:Postprandial Period; D012307:Risk Factors; D013237:Stereoisomerism; D010959:Tissue Plasminogen Activator / Q000097:blood
D001054:Apolipoproteins A; D001055:Apolipoproteins B; D015415:Biomarkers; D004040:Dietary Carbohydrates; D005227:Fatty Acids; D005338:Fibrin Fibrinogen Degradation Products; D017395:Plasminogen Activator Inhibitor 1; C036309:fibrin fragment D; D019301:Oleic Acid; D005167:Factor VII; D005340:Fibrinogen; D002784:Cholesterol; D010959:Tissue Plasminogen Activator