Hypertension prevention: from nutrients to (fortified) foods to dietary patterns. Focus on fatty acids

Abstract

A Grynberg INRA-Paris 11 UMR1154, Nutrition Lipidique et Re´gulation Fonctionnelle du Coeur et des Vaisseaux, Facultede Pharmacie, Châtenay-Malabry, FranceDiet affects significantly the incidence and severity of cardiovascular diseases and fatty acid intake, in its qualitative as well as quantitative aspects, and influences several risk factors including cholesterol (total, LDL and HDL), triglycerides, platelet aggregation and blood pressure, as evidenced in the 2001 WHO report. This review focuses on the qualitative concern of lipid intake, the various classes of fatty acids of the lipid fraction of the diet, saturated, monounsaturated and polyunsaturated, and their effects on blood pressure. Saturated fat have a bad file and several experimental studies in the rat showed a progressive increase in blood pressure in response to a highly saturated diet. Moreover, a highly saturated diet during gestation led to offspring which, when adults, presented a genderrelated hypertension. The mechanism of this effect may be related to the polyunsaturated/saturated ratio (p/s). During the past 20 years, trans fatty acids have been suspected of deleterious health effects, but the investigations have shown that these fatty acids display a biological behaviour close to that of saturated fatty acids (SFA). Moreover, epidemiological investigations did not confirm the relationship between trans fatty acids and cardiovascular pathology. Polyunsaturated fatty acids have been shown to exert a positive action on hypertension. This effect could be attributed to the alteration of the p/s, but mainly to the x3 polyunsaturated fatty acids (PUFAs). The comparison of several animal models led to the conclusion that long-chain x3 PUFAs (eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)) can prevent the increase in blood pressure and reduce established hypertension, but the efficient dose remains an object of discussion. Moreover, the two long-chain x3 PUFAs, EPA and DHA, display specific effects, which vary with the aetiology of hypertension, because their mechanism of action is different. DHA acts on both blood pressure and heart function (heart rate and ECG) and interferes with the adrenergic function. Conversely, EPA, which is not incorporated in cardiac phospholipids, has no effect on the heart and its mechanism of action is largely unknown. Although it is accepted by the scientific community that the intake of EPA and DHA needs to be increased, we will have to discover new ways to do it, since marine products are the main source of these fatty acids, and this source is not inexhaustible.

Docosahexaenoic Acid, but Not Eicosapentaenoic Acid, Supplementation Reduces Vulnerability to Atrial Fibrillation

“…25,28 Other observed differences in DHA and EPA activity that may explain our observations include the ability of DHA, but not EPA, to block certain cardiac ion channels, especially repolarizing potassium channels or membraneincorporated DHA-mediated inhibition of cardiac adrenergic stimulation. 11,29 Although these effects have been observed by others, we did not observe a PUFA effect on repolarization. A key to understanding the mechanism of the DHA effect may lie in the observation that DHA lowered the burden of persistent AF but not AF induction.…”

The effect of dietary fat on the fatty acid composition and cholesterol content of Hy-line and Warren hen eggs

“…A fish oil diet produced lower 18:1 n-9 levels in microsomal membrane lipids than a beef tallow diet. Linoleic acid is converted into arachidonic acid by desaturases and elongases (Grynberg, 2005). Present results suggest that the increased level of unsaturation and the higher n-3 PUFA levels in the added fat decreased the conversion of linoleic acid into arachidonic acid in eggs, particularly during the AF-SO period.…”

Polyunsaturated fatty acids: From diet to binding to ppars and other nuclear receptors

“…The nuclear actions of PUFAs is established in liver cells (Jump et al, 2005), in pancreas (Manco et al, 2004), immune system (Calder, 2003), brain (Uauy and Calderon, 2003), adipose tissue (Al-Hasani and Joost, 2005) and heart (Vanden Heuvel, 2004), and the possibility of counteracting human diseases by dietary FAs, particularly n-3 PUFAs, has been largely investigated, although their therapeutic effects are still unclear (De Caterina et al, 2006;Engler and Engler, 2006;Hooper et al, 2006;Lombardo and Chicco, 2006;Grynberg, 2005;Mills et al, 2005;Rodriguez-Cruz et al, 2005;Sekiya et al, 2003). It is important to remember that the effects of PUFAs are due to changes in membrane FA composition and subsequent alterations in hormonal signalling, as well as to their direct, membrane independent influence on molecular events that govern gene expression.…”