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• W2326747927 abstract "The meta-analysis on the effects of increased dietary fibre on blood pressure (BP), published in this issue of the Journal of Hypertension[1], calls for renovated attention on one of the many aspects of our dietary habits deemed to be relevant for cardiovascular prevention. Although Evans’ work is not the first comprehensive assessment of the possible relationship between increased fibre intake and BP, the 10 years that have elapsed since the two previous systematic reviews [2,3] on the same subject have seen the publication of several new reports that allowed Evans et al. to carry a more in-depth evaluation and, in particular, to try and dissect out the effects of different types of fibre in addition to their overall impact on BP. One merit of the review is that it is exclusively based on the analysis of randomized controlled trials, most of which rated as good or very good quality, whereas previous evidence suggesting that larger habitual consumption of dietary fibre is beneficial for human health, by reducing the risk of obesity, type 2 diabetes, hypertension and their cardiovascular complications, has mainly come from observational studies [4–8]. The most novel content of Evans’ work is the evidence in favour of a particularly beneficial effect on BP of β-glucans, a variety of soluble dietary fibre abundant in oats and barley-rich foods, whereas the authors found little or no statistical evidence of the BP impact of other types of dietary fibre. A strength of the study is that in all the five trials included in the meta-analysis, β-glucans were provided as oat bran, oat meals or directly as oat β-glucan-soluble powder in substitution for wheat-based products used as control; thus, it seems unlikely that the observed effect of the intervention could be attributable to other concomitant dietary changes. It also seems unlikely that body weight reduction induced by higher fibre intake during the intervention may have played a major role because in the three (out of five) studies reporting weight changes, the variations were actually minor. Furthermore, in the other studies included in the meta-analysis, which tested the effects of different fibres (pectins, mannans, etc.), similar or even greater body weight losses were not associated with the beneficial effects on BP. Three of the five studies featuring higher intake of oat meals and β-glucans recruited individuals with BP in the high–normal range or having grade 1 hypertension, which may have theoretically made it easier to appreciate a BP-lowering effect of these substances; however, a favourable BP response was detected in only two of these three studies and, in addition, it was detected also in one of the two trials involving only normotensive individuals [1]. Indeed, two studies not included in Evans’ systematic review reported an impact of oat consumption on BP. In a pilot study by Keenan et al.[9], SBP and DBP were both reduced after whole oat cereal intake for 6 weeks. In another study on drug-treated hypertensive patients, the consumption of oat cereal meals lead to a significant reduction in their need for antihypertensive medication compared with the control group [10]. A puzzling question is of course through which possible mechanisms do β-glucans or other components of oat-rich products favour a decrease in BP. At least three potential mechanisms may be envisaged: one or more pathways related to an overall improvement in glucose metabolism, an anti-inflammatory and/or antioxidant effect and an effect mediated by a reduction in plasma lipids. As the first possibility, β-glucans are known to delay gastric emptying, increase the viscosity of gastrointestinal content and increase satiety. The increased viscosity of the gastrointestinal content reduces food transit time and slows glucose absorption, thus diminishing the postprandial glucose and insulin responses [11]. A similar mechanism was operating in the Study to Prevent Non-Insulin-Dependent Diabetes Mellitus, involving individuals with impaired glucose tolerance who were assigned to treatment with either the oligosaccharide acarbose or the placebo. Treatment with acarbose was shown to reduce postprandial glucose and insulin responses by slowing starch digestion and delaying glucose absorption, and was associated with a significantly lower incidence of hypertension and evidence of carotid atherosclerosis over 3.3 years compared with control treatment [12]. Although there is no direct experimental evidence of the beneficial effects of β-glucan consumption on insulin resistance, lower postprandial insulin levels may conceivably affect BP, given the direct influence of hyperinsulinaemia on renal sodium reabsorption and sympathetic tone [13,14]. It is true that in addition to β-glucans, other viscous fibres also, for example, guar and mannan, used in some of the trials included in Evans’ meta-analysis, have shown a reduction in postprandial blood glucose response and insulin levels – albeit with some variation in the data reported; it remains obscure why no apparent effect on BP could be detected in those studies. Evidence from both experimental and clinical studies strongly suggests that one or more oat components may exert anti-inflammatory and antioxidant activity, which in turn may have an impact on endothelial function [15]. These include tocopherols, phenolic compounds (namely, the oat-specific polyphenols avenanthramides), phytic acids, sterols and flavonoids [16]. Of practical interest is that most of the antioxidant activities associated with oats seem to be resistant to heat treatment and thus likely to survive the commonly applied industrial processing treatments [17]. The phenolic components avenanthramides also exhibit anti-inflammatory properties through inhibition of nuclear factor κB signalling [18]. Only few clinical studies, however, have investigated the possible effect of oats on systemic inflammation. Some of them found no effect, possibly because of the use of chemical treatments susceptible to induce the loss of the active phenolic substances [19,20]. In a study in low-density lipoprotein (LDL) receptor-deficient mice fed oat bran, it was found that the levels of the inflammation-related plasma proteins fibrinogen and soluble vascular cell adhesion molecule-1 and the expression of the vascular cell adhesion molecule-1 in the aortic wall were consistently reduced [21]. In this study, however, a substantial reduction in plasma cholesterol also occurred as an effect of higher oat bran intake, a response capable to hamper the inflammatory activity per se[22]; this makes it difficult to discriminate between a direct or a secondary effect of oat consumption. Nevertheless, these results are in keeping with another in-vitro study on human endothelial cells showing that avenanthramides isolated from oat were able to reduce the interleukin-1-induced expression of several adhesion molecules, concomitantly reducing monocyte attachment to the cells and lowering interleukin secretion [23]. The oat phenolic compounds and flavonoids are also thought to exert an antioxidant action by scavenging reactive oxygen and nitrogen species and chelating transition minerals. In in-vitro studies, tocopherols were incorporated into low-density lipoproteins and protected them from oxidative agents [24]. Avenanthramides exert direct antioxidative effects and seem to be capable to stimulate the human body scavenging system in animals [25,26] and humans [27]. Both low-grade systemic inflammation and increased oxidative stress inhibit nitric oxide production and contribute to endothelial dysfunction. Thus, the reports in the literature suggesting that oats could favourably influence endothelial function are not surprising [28,29]. Specifically, these studies support the concept that oat components, by affecting the expression of endothelial nitric oxide synthase (eNOS), could increase the production of nitric oxide, thereby contrasting the negative effects of certain postprandial events such as excess insulin release, production of oxygen-free radicals and generation of triglyceride-rich lipoprotein particles – all contributing to endothelial dysfunction and possibly resulting in vasoconstriction and increased BP [30]. In this respect, Katz et al. [29,31] reported that long-term elevated oat consumption effectively opposes the failure in endothelial function following a high-fat meal in both normal weight and overweight individuals. A third mechanism whereby oat and, in particular, β-glucan intake might improve BP levels may be traced to their LDL-cholesterol-lowering action, clearly demonstrated by Brown et al.[32] in their meta-analysis; nevertheless, it might be argued that this effect is common to other types of viscous fibres such as guar, pectin or psyllium, the consumption of which was not associated with lower BP levels in Evans’ study. A seminal work by Nickenig et al.[33] revealed a significant upregulation of the angiotensin-I receptor gene expression by LDL in vascular smooth muscle cells, ultimately leading to an elevated functional response of vascular smooth muscle cells to angiotensin II stimulation, which could conceivably affect BP [33]. On the contrary, treatment of hypercholesterolaemia with statins has been associated with small but significantly lower BP levels [34]. Moreover, in two specular intervention trials of the metabolic and vascular effects of changes in dietary fat intake in normal volunteers, changes in either direction of total and LDL-cholesterol were consistently paralleled by BP changes in the same direction [35,36]. In conclusion, based on the evidence available from the clinical and experimental studies so far available, it is not possible to definitely confirm or exclude any of the above-mentioned potential mechanisms nor is it possible to discriminate if and to what extent the decrease in BP observed upon increased oat-based products intake is attributable to any one of the various oat compounds, including β-glucans. Evans et al. noted that, although advice on increasing fruit and vegetable consumption is included in the European Society of Hypertension/European Society of Cardiology (ESC/ESH) Guidelines for the Management of Arterial Hypertension [37], no advice is given for fibre consumption. A large habitual fibre intake has recognized merits in particular with regard to prevention of obesity and type 2 diabetes and, as such, is recommended in most nutritional guidelines, including the European Guidelines on Cardiovascular Disease Prevention in Clinical Practice [38]. Evans’ updated review of the evidence about fibre intake and BP does not bring further substantial support to larger fibre intake as an effective means for reducing BP. It nevertheless may focus the attention of scientists and health operators active in the nutritional field on the properties of β-glucans and, in general, of oat and possibly barley-rich foods. These foods are relatively popular in the framework of the so-called Western and Nordic diets whereas they are not prevalent within the Mediterranean dietary model. On practical grounds, although definitive conclusions on their specific value cannot be drawn, a reasonable increase in their consumption, where particularly low, promises to do more good than harm. ACKNOWLEDGEMENTS Conflicts of interest There are no conflicts of interest." @default.
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• W2326747927 title "Fibre intake and blood pressure" @default.
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• W2326747927 cites W1996935661 @default.
• W2326747927 cites W1999031655 @default.
• W2326747927 cites W1999878913 @default.
• W2326747927 cites W2016757269 @default.
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