Acute Effects of Nutritive and Non-Nutritive Sweeteners On
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nutrients Review Acute Effects of Nutritive and Non-Nutritive Sweeteners on Postprandial Blood Pressure Hung Pham 1, Liza K. Phillips 1,2 and Karen L. Jones 1,2,* 1 NHMRC Centre of Research Excellence in Translating Nutritional Science to Good Health, Adelaide Medical School, The University of Adelaide, Adelaide, SA 5000, Australia 2 Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide, SA 5000, Australia * Correspondence: [email protected]; Tel.: +61-8-8313-7821 Received: 24 June 2019; Accepted: 20 July 2019; Published: 25 July 2019 Abstract: Postprandial hypotension (PPH) is under-recognised, but common, particularly in the elderly, and is of clear clinical importance due to both the independent association between PPH and an increase in mortality and lack of effective management for this condition. Following health concerns surrounding excessive consumption of sugar, there has been a trend in the use of low- or non-nutritive sweeteners as an alternative. Due to the lack of literature in this area, we conducted a systematic search to identify studies relevant to the effects of different types of sweeteners on postprandial blood pressure (BP). The BP response to ingestion of sweeteners is generally unaffected in healthy young subjects, however in elderly subjects, glucose induces the greatest decrease in postprandial BP, while the response to sucrose is less pronounced. The limited studies investigating other nutritive and non-nutritive sweeteners have demonstrated minimal or no effect on postprandial BP. Dietary modification by replacing high nutritive sweeteners (glucose, fructose, and sucrose) with low nutritive (d-xylose, xylitol, erythritol, maltose, maltodextrin, and tagatose) and non-nutritive sweeteners may be a simple and effective management strategy for PPH. Keywords: postprandial hypotension; nutritive sweeteners; non-nutritive sweeteners; glucose; fructose; sucrose; d-xylose; xylitol; erythritol; maltose; maltodextrin; tagatose 1. Introduction The consumption of nutritive sweeteners has dramatically increased worldwide due to increasing urbanisation and beverage promotion [1]. Nutritive sweeteners commonly found in foods and beverages include glucose, fructose and sucrose [2,3]. More recently, some other sweeteners like d-xylose, xylitol, erythritol, maltose, maltodextrin, stevia and tagatose with lower energy have been used [2,3]. There has been a long history of debate as to the detrimental health effects of sucrose, glucose, and more recently, fructose, particularly when consumed in excess. The effects of both nutritive and non-nutritive sweeteners on cardiovascular risk factors, including blood pressure (BP), have been extensively investigated, however, less is known about their specific effects in the postprandial state. Postprandial hypotension (PPH), a fall in systolic BP (SBP) 20 mmHg after a meal, is now recognized ≥ as a frequent and important clinical problem, with a reported prevalence of 24–48% in the healthy elderly [4]. PPH is particularly common in conditions associated with autonomic dysfunction e.g., in type 2 diabetes mellitus (T2DM) (~40%) [4,5] and Parkinson’s disease (PD) (40–100%) [4,5]. Patients with PPH are at increased risk of syncope and falls [6], and importantly the presence of PPH has been established as an independent predictor of increased mortality [7]. In a cohort study of 401 elderly ambulatory hypertensive subjects, 292 (72.8%) were found to have PPH, and over a 4 year period, 34 died from cardiovascular disease; the post-breakfast BP fall was the strongest predictor of mortality in this cohort [8]. In a 29-month prospective study of 499 nursing home residents, the maximum Nutrients 2019, 11, 1717; doi:10.3390/nu11081717 www.mdpi.com/journal/nutrients NutrientsNutrients2019 2019,,11 11,, 1717 1717 2 ofof 2928 subsequent falls, syncope, new cardiovascular events (myocardial infarction and stroke) and total fallmortality in postprandial [9]. 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PPH, The these postprandial compensatory fall in responses BP is greater are inadequate when gastric [5]. emptying The postprandial is more fallrapid in BP[11–13], is greater whereas when gastric gastric distension emptying isattenuates more rapid the [11 fall–13 in], whereasBP in both gastric healthy distension youngattenuates and older theparticipants fall in BP [11–13]. in both healthyThe macronutrient young and older composition participants of the [11 meal–13]. is The also macronutrient an important compositiondeterminant ofof thepostprandial meal is also BP, an with important carbohydrate determinant inducing of postprandial an earlier fall BP, in withBP compared carbohydrate with inducingprotein and an earlierfat [14] fall(Figure in BP 1). compared The interaction with protein between and nutrients fat [14] (Figureand the1 ).small The intestine interaction stimulates between the nutrients secretion and of the the smallincretin intestine hormones, stimulates glucagon-like the secretion ofpeptide-1 the incretin (GLP-1) hormones, from glucagon-like L-cells and peptide-1 glucose-dependent (GLP-1) from L-cellsinsulinotropic and glucose-dependent polypeptide (GIP) insulinotropic from K-cells polypeptide [15]. GLP-1 (GIP) stimulates from K-cells insulin [15]. secretion, GLP-1 stimulates inhibits insulinglucagon secretion, secretion inhibits and slows glucagon gastric secretion emptying and [16,17]. slows Acute gastric infusion emptying of [GLP-116,17]. has Acute been infusion shown ofto GLP-1attenuate has the been fall shown in BP to and attenuate increases the fallSMA in blood BP and flow increases following SMA oral blood [16] flow or followingintraduodenal oral [(ID)16] orglucose intraduodenal [16,18]. In (ID) contrast, glucose exogenous [16,18]. InGIP contrast, has been exogenous shown to GIPincrease has beenthe rate shown of gastric to increase emptying the rate[19], of although gastric results emptying have [19 been], although conflicting results [20] an haved there been have conflicting been no [ studies20] and directly there have investigating been no studiesthe effect directly of GIP investigating on postprandial the eff ectBP. of A GIP reductio on postprandialn in BP is BP.not A observed reduction following in BP is not intravenous observed followingadministration intravenous of glucose administration [21], which of glucoseis a substantia [21], whichl stimulus is a substantial to insulin stimulus secretion, to insulin suggesting secretion, that suggestinginsulin by thatitself insulin if not byan itselfimportant if not anmediator important of PPH. mediator Furthermore, of PPH. Furthermore, PPH is seen PPH in the is seenabsence in the of absenceinsulin secretion of insulin i.e., secretion in those i.e., with in those type with1 diabetes type 1[22]. diabetes [22]. FigureFigure 1.1. 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