The effects of vitamin C on the haemostatic system / Deirdré Loots

• Main Author: Loots, Deirdré
• Published: North-West University 2009
• Subjects: Haemostasis; Haemostatic factors; Fibrin network structure; Cardiovascular disease; Atherosclerosis; Inflammation; Vitamin C; Antioxidants
• Online Access: http://hdl.handle.net/10394/207

Motivation: Cardiovascular disease (CVD) is one of the leading causes of mortality and morbidity in South Africa and worldwide. Dyslipidaemia and an increased coagulation state contribute to the development of CVD. The quality of fibrin network structure (FNS) may also contribute to the risk for CVD and thrombosis. Changes in fibrinogen concentration directly affect FNS. Management of these risk factors is important and dietary intervention forms an essential part of this management program. An increased intake of vitamin C can lead to a decreased susceptibility to infection and subsequently to decreased levels of haemostatic factors (that give rise to an anti-thrombotic state) and thus reduction in CVD and mortality. Furthermore, vitamin C may prove to be beneficial by increasing the pro-fibrinolytx activities of FNS (formation of thick fibrin fibers and more lysable clots) that could result in a reduction in atherosclerosis and subsequent CVD. Obiective: To investigate the effects of FoodState Vitamin C complex supplementation on haemostatic factors, FNS, serum lipids and lipoprotein (a) (Lp(a)) in hyperlipideamic adults. Methods: Thirty free-living hiperlipidaemic volunteers from the Lipid Clinic, Potchefstroom University for Christian Higher Education (CHE), participated in this randomised placebo controlled double blind crossover study. The subjects were randomly divided into two groups (A or B). After a run-in period of 4 weeks during which the subjects excluded all vitamin supplements, Group A received 2 tablets/day of FoodState Vitamin C complex (500mg vitamin C, 600mg magnesium food complex, 900mg vitamin B complex and 160mg bioflavonoids) and Group B received 2 tablets/day of placebo, for at least 8 weeks. A washout period of 8 weeks followed after which the treatments were crossed-over for a further 8 weeks. Fasting blood samples were drawn 8 times (two samples, one week apart at the beginning and end of each treatment). Results: FoodState Vitamin C complex supplementation did not significantly influence the levels of plasma fibrinogen, plasminogen activator inhibitor 1 activity (PAI-I act), tissue plasminogen activator antigen (tPA ag) or d-dimer. Serum lipids and Lp(a) were also not affected. Median plasmin-antiplasmin complex (PAP) and thrombin-antithrombin complex (TAT) levels, which are markers of plasmin (initiate fibrinolysis) and thrombin (initiate coagulation) generation respectively, were both significantly decreased compared to placebo (PAP: 4.05[-23.39, -0.231% vs 1.81[-8.95, 8.091%; TAT: -5.81[-18,47, 0.391% vs 0.12[-8.03, 13.51%). FoodState Vitamin C complex beneficially affected FNS by significantly increasing compaction (49.95[47.55,53.70]% to 51.85[48.55,56.65]%). Conclusion: The decreases in TAT and PAP are possibly an indication that the FoodState Vitamin C complex decreased the initiation of haemostasis, which in turn led to a compensatory reduction in fibrinolysis. FoodState Vitamin C complex may, therefore be protective of cardiovascular disease by causing a new reduced steady state of hemostatic balance and more lysable clots (increased compaction). === Thesis (M.Sc. (Nutrition))--North-West University, Potchefstroom Campus, 2004.