|dc.description.abstract||Motivation: Cardiovascular heart disease (CVD) is the leading cause of death worldwide. Risk markers for CVD include, amongst others, the haemostatic factors tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor type 1 (PAI-1), factor VII (FVII) and fibrinogen and more recently, C-reactive protein (CRP), a sensitive marker of inflammation. Epidemiological studies have demonstrated an inverse association between dietary fibre (DF) consumption and risk factors for CVD and CVD prevalence. Some research indicates that this protection may be related to favourable changes in the haemostatic profile and inflammatory markers. This is applicable for the consumption of total DF, as well as soluble and insoluble fibre. However, clinical intervention trials report conflicting data on the effects of DF on t-PA, PAI-1, FVII, fibrinogen and CRP. In addition, available literature is not clear on the mechanisms through which DF may have favourable effects.
Objective: The main objective of this study was to review the results of randomised controlled trials systematically on the effects of DF on the above-mentioned selected haemostatic variables and CRP in healthy adults and subjects with hypertriglyceridaemia and the metabolic syndrome.
Methods: Human adult intervention trials, at least two weeks in duration, with an increased and measurable consumption of DF were included. Electronic databases were searched from the earliest record to May/July 2006 and supplemented by crosschecking reference lists of relevant publications. From the literature search, two reviewers identified studies that were rated for quality based on the published methodology. No formal statistical analysis was performed due to the large differences in the study designs of the dietary intervention trials. The primary outcome measures were percentage changes between intervention and control groups, or baseline to end comparisons for t-PA, PAI-1, FVII, fibrinogen and CRP.
Results t-PA activity increased significantly (14-167%) over the short and long-term following increased fibre intakes. PAI-1 activity decreased significantly between 15-57% over periods ranging from two to six weeks. These favourable changes in t-PA and PAI-1 occurred in healthy, hypertriglyceridaemic and metabolic syndrome subjects following consumption of diets containing ≥3.3 g/MJ DF and ≥4.5 g/MJ DF respectively.
Mechanisms through which DF may affect t-PA and PAI-1 include its lowering effect on insulinaemic and glycaemic responses, decreasing triglycerides which are a precursor of very-low-density lipoproteins, fermentation of DF to short-chain fatty acids, which may reduce free fatty acid concentrations, as well as the role of DF in promoting weight loss.
High DF intakes did not have a significant effect on fibrinogen concentrations possibly because of relatively little weight loss, too low DF dosages and maintaining a good nutritional status. Inadequate study designs deterred from meaningful conclusions.
Significant decreases in FVll coagulant activity (6-16%) were observed with DF intakes
of ≥3.3 g/MJ and concomitant decreased saturated fat intakes and weight loss in
healthy and hypertriglyceridaemic subjects. Confounding factors include weight loss
and a simultaneous decreased intake of saturated fats. The type of fibre seems to play
a role as well. Mechanisms through which DF may reduce FVll concentrations include
its effects on triglyceride-rich lipoproteins, insulin and weight loss.
Increased DF consumption with dosages ranging between 3.3-7.8 g/MJ were followed by significantly lower CRP concentrations (25-54%), however, simultaneous weight loss and altered fatty acid intakes were also present in all the studies. Mechanisms are inconclusive but may involve the effect of DF on weight loss, insulin, glucose, adiponectin, interleukin-6, free fatty acids and triglycerides. Conclusions: Epidemiological evidence indicates an association between DF and the CVD risk factors t-PA, PAI-1, FVII, fibrinogen and CRP. In general, the risk of CVD may improve with high-fibre intakes as indicated by the favourable changes in some of the parameters.
However, simultaneous reduced fat intakes and weight loss presented difficulties in separating out the effects of specific components. Furthermore, DF is consumed in a variety of different forms and different dosages that may have different effects. Overall, the study designs used in the intervention trials prevented significant conclusions. DF did, however, play a role in modifying t-PA, PAI-1, FVII and CRP. Potential effects on fibrinogen were not quantifiable.
Recommendations: The results from this investigation provide the motivation for additional controlled clinical research to establish the effect and mechanisms of DF on haemostatic variables and CRP. A critical aspect of future studies would be to set up suitable protocols. The amount of subjects, duration of the trials, confounding factors such as weight loss and altered fat intakes and differentiation between types and dosage of DF are important. DF supplemental studies are recommended as they may be the most suitable method to reach meaningful conclusions.||