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Functional food science and the cardiovascular system

Published online by Cambridge University Press:  09 March 2007

G. Hornstra ,
C. A. Barth ,
C. Galli ,
R. P. Mensink ,
M. Mutanen ,
R. A. Riemersma ,
M. Roberfroid ,
K. Salminen ,
G. Vansant  and
P. M. Verschuren
G. Hornstra*
Affiliation:
Department of Human Biology, Maastricht University, PO Box 616, NL-6200 MD, Maastricht, The Netherlands
C. A. Barth
Affiliation:
German Institute for Human Nutrition, Stiftung des Öffentlichen Rechts, Arthur-Scheunert-Allee 114–116, D–14558 Bergholz-Rehbrüicke, Germany
C. Galli
Affiliation:
Institute of Pharmacological Sciences, University of Milano, Via Balzaretti 9, I-20133 Milan, Italy
R. P. Mensink
Affiliation:
Nutrition Research Centre, Department of Human Biology, Maastricht University, PO Box 616, NL-6200 MD, Maastricht, The Netherlands
M. Mutanen
Affiliation:
Department of Applied Chemistry and Microbiology, University of Helsinki, PO Box 27, SF-00014 Helsinki, Finland
R. A. Riemersma
Affiliation:
Cardiovascular Research Unit, Hugh Robinson Building, University of Edinburgh, George Square, Edinburgh EW8 9XF, UK
M. Roberfroid
Affiliation:
UCL, Ecole de Pharmacie, Tour Van Helmont, Avenue E. Mounier, B-1200 Brussels, Belgium
K. Salminen
Affiliation:
Research and Development, Valio Ltd, PB 390, SF-00101 Helsinki, Finland
G. Vansant
Affiliation:
Laboratory voor Experimentele geneeskunde endocrinologie (LEGENDO), Katholieke Universiteit Leuven, Gasthuisberg, B-3000 Leuven, Belgium
P. M. Verschuren
Affiliation:
Unilever Research Laboratoly, Olivier van Noortlaan 120, NL-3133 AT Vlaardingen, The Netherlands
*
*Dr G. Homstra, fax +31 43 367 0976, email G. [email protected]
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Abstract

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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.

Type
Research Article
Information
British Journal of Nutrition , Volume 80 , Issue S1 , August 1998 , pp. S113 - S146
Copyright
Copyright © The Nutrition Society 1998

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