British Journal of Nutrition

Research Article

Functional food science and the cardiovascular system

G. Hornstraa1 c1, C. A. Bartha2, C. Gallia3, R. P. Mensinka4, M. Mutanena5, R. A. Riemersmaa6, M. Roberfroida7, K. Salminena8, G. Vansanta9 and P. M. Verschurena10

a1 Department of Human Biology, Maastricht University, PO Box 616, NL-6200 MD, Maastricht, The Netherlands

a2 German Institute for Human Nutrition, Stiftung des Öffentlichen Rechts, Arthur-Scheunert-Allee 114–116, D–14558 Bergholz-Rehbrüicke, Germany

a3 Institute of Pharmacological Sciences, University of Milano, Via Balzaretti 9, I-20133 Milan, Italy

a4 Nutrition Research Centre, Department of Human Biology, Maastricht University, PO Box 616, NL-6200 MD, Maastricht, The Netherlands

a5 Department of Applied Chemistry and Microbiology, University of Helsinki, PO Box 27, SF-00014 Helsinki, Finland

a6 Cardiovascular Research Unit, Hugh Robinson Building, University of Edinburgh, George Square, Edinburgh EW8 9XF, UK

a7 UCL, Ecole de Pharmacie, Tour Van Helmont, Avenue E. Mounier, B-1200 Brussels, Belgium

a8 Research and Development, Valio Ltd, PB 390, SF-00101 Helsinki, Finland

a9 Laboratory voor Experimentele geneeskunde endocrinologie (LEGENDO), Katholieke Universiteit Leuven, Gasthuisberg, B-3000 Leuven, Belgium

a10 Unilever Research Laboratoly, Olivier van Noortlaan 120, NL-3133 AT Vlaardingen, The Netherlands


Cardiovascular disease has a multifactorial aetiology, as is illustrated by the existence of numerous risk indicators, many of which can be influenced by dietary means. It should be recalled, however, that only after a cause-and-effect relationship has been established between the disease and a given risk indicator (called a risk factor in that case), can modifying this factor be expected to affect disease morbidity and mortality. In this paper, effects of diet on cardiovascular risk are reviewed, with special emphasis on modification of the plasma lipoprotein profile and of hypertension. In addition, dietary influences on arterial thrombotic processes, immunological interactions, insulin resistance and hyperhomocysteinaemia are discussed. Diet-ary lipids are able to affect lipoprotein metabolism in a significant way, thereby modifying the risk of cardiovascular disease. However, more research is required concerning the possible interactions between the various dietary fatty acids, and between fatty acids and dietary cholesterol. In addition, more studies are needed with respect to the possible importance of the postprandial state. Although in the aetiology of hypertension the genetic component is definitely stronger than environmental factors, some benefit in terms of the development and coronary complications of atherosclerosis in hypertensive patients can be expected from fatty acids such as α-linolenic acid, eicosapentaenoic acid and docosahexaenoic acid. This particularly holds for those subjects where the hypertensive mechanism involves the formation of thromboxane A2 and/or α1-adrenergic activities. However, large-scale trials are required to test this contention. Certain aspects of blood platelet function, blood coagulability, and fibrinolytic activity are associated with cardiovascular risk, but causality has been insufficiently proven. Nonetheless, well-designed intervention studies should be initiated to further evaluate such promising dietary components as the various n−3 and n−6 fatty acids and their combination, antioxidants, fibre, etc. for their effect on processes participating in arterial thrombus formation. Long-chain polyenes of the n−3 family and antioxidants can modify the activity of immunocompetent cells, but we are at an early stage of examining the role of immune function on the development of atherosclerotic plaques. Actually, there is little, if any, evidence that dietary modulation of immune system responses of cells participating in atherogenesis exerts beneficial effects. Although it seems feasible to modulate insulin sensitivity and subsequent cardiovascular risk factors by decreasing the total amount of dietary fat and increasing the proportion of polyunsaturated fatty acids, additional studies on the efficacy of specific fatty acids, dietary fibre, and low-energy diets, as well as on the mechanisms involved are required to understand the real function of these dietary components. Finally, dietary supplements containing folate and vitamins B6 and/or B12 should be tested for their potential to reduce cardiovascular risk by lowering the plasma level of homocysteine.


c1 *Dr G. Homstra, fax +31 43 367 0976, email G. Homstra@HB.Unimaas.NL