Perspective: Cardiovascular Responses to Sugar-Sweetened Beverages in Humans: A Narrative Review with Potential Hemodynamic Mechanisms

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Abstract

<p id="d7503262e118">Cardiovascular diseases are still the primary cause of mortality worldwide, with high blood pressure and type 2 diabetes as major promoters. Over the past 3 decades, almost in parallel with the rise in cardiovascular disease incidence, the consumption of sugar-sweetened beverages (SSBs) has increased. In this context, SSBs are potential contributors to weight gain and increase the risk for elevations in blood pressure, type 2 diabetes, coronary heart disease, and stroke. Nevertheless, the mechanisms underlying the cardiovascular and metabolic responses to SSBs, in particular on blood pressure, are poorly understood. We discuss and propose potential mechanisms underlying differential effects of sugars on postprandial blood pressure regulation; provide evidence for additional molecular contributors, i.e., fibroblast growth factor 21, towards sugar-induced cardiovascular responses; and discuss potential cardiovascular neutral sugars. Furthermore, we explore whether pre-existing glucose intolerance in humans exacerbates the cardiovascular responses to SSBs, thus potentially aggravating the cardiovascular risk in already-susceptible individuals. </p>

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Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.

Kimber L. Stanhope, Jean Schwarz, Nancy Keim … (2009)

Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.

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Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity.

George Bray, Samara Joy Nielsen, Barry M. Popkin (2004)

Obesity is a major epidemic, but its causes are still unclear. In this article, we investigate the relation between the intake of high-fructose corn syrup (HFCS) and the development of obesity. We analyzed food consumption patterns by using US Department of Agriculture food consumption tables from 1967 to 2000. The consumption of HFCS increased > 1000% between 1970 and 1990, far exceeding the changes in intake of any other food or food group. HFCS now represents > 40% of caloric sweeteners added to foods and beverages and is the sole caloric sweetener in soft drinks in the United States. Our most conservative estimate of the consumption of HFCS indicates a daily average of 132 kcal for all Americans aged > or = 2 y, and the top 20% of consumers of caloric sweeteners ingest 316 kcal from HFCS/d. The increased use of HFCS in the United States mirrors the rapid increase in obesity. The digestion, absorption, and metabolism of fructose differ from those of glucose. Hepatic metabolism of fructose favors de novo lipogenesis. In addition, unlike glucose, fructose does not stimulate insulin secretion or enhance leptin production. Because insulin and leptin act as key afferent signals in the regulation of food intake and body weight, this suggests that dietary fructose may contribute to increased energy intake and weight gain. Furthermore, calorically sweetened beverages may enhance caloric overconsumption. Thus, the increase in consumption of HFCS has a temporal relation to the epidemic of obesity, and the overconsumption of HFCS in calorically sweetened beverages may play a role in the epidemic of obesity.

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Consumption of sugar sweetened beverages, artificially sweetened beverages, and fruit juice and incidence of type 2 diabetes: systematic review, meta-analysis, and estimation of population attributable fraction

Fumiaki Imamura, Laura O’Connor, Zheng Ye … (2015)

Objectives To examine the prospective associations between consumption of sugar sweetened beverages, artificially sweetened beverages, and fruit juice with type 2 diabetes before and after adjustment for adiposity, and to estimate the population attributable fraction for type 2 diabetes from consumption of sugar sweetened beverages in the United States and United Kingdom. Design Systematic review and meta-analysis. Data sources and eligibility PubMed, Embase, Ovid, and Web of Knowledge for prospective studies of adults without diabetes, published until February 2014. The population attributable fraction was estimated in national surveys in the USA, 2009-10 (n=4729 representing 189.1 million adults without diabetes) and the UK, 2008-12 (n=1932 representing 44.7 million). Synthesis methods Random effects meta-analysis and survey analysis for population attributable fraction associated with consumption of sugar sweetened beverages. Results Prespecified information was extracted from 17 cohorts (38 253 cases/10 126 754 person years). Higher consumption of sugar sweetened beverages was associated with a greater incidence of type 2 diabetes, by 18% per one serving/day (95% confidence interval 9% to 28%, I2 for heterogeneity=89%) and 13% (6% to 21%, I2=79%) before and after adjustment for adiposity; for artificially sweetened beverages, 25% (18% to 33%, I2=70%) and 8% (2% to 15%, I2=64%); and for fruit juice, 5% (−1% to 11%, I2=58%) and 7% (1% to 14%, I2=51%). Potential sources of heterogeneity or bias were not evident for sugar sweetened beverages. For artificially sweetened beverages, publication bias and residual confounding were indicated. For fruit juice the finding was non-significant in studies ascertaining type 2 diabetes objectively (P for heterogeneity=0.008). Under specified assumptions for population attributable fraction, of 20.9 million events of type 2 diabetes predicted to occur over 10 years in the USA (absolute event rate 11.0%), 1.8 million would be attributable to consumption of sugar sweetened beverages (population attributable fraction 8.7%, 95% confidence interval 3.9% to 12.9%); and of 2.6 million events in the UK (absolute event rate 5.8%), 79 000 would be attributable to consumption of sugar sweetened beverages (population attributable fraction 3.6%, 1.7% to 5.6%). Conclusions Habitual consumption of sugar sweetened beverages was associated with a greater incidence of type 2 diabetes, independently of adiposity. Although artificially sweetened beverages and fruit juice also showd positive associations with incidence of type 2 diabetes, the findings were likely to involve bias. None the less, both artificially sweetened beverages and fruit juice were unlikely to be healthy alternatives to sugar sweetened beverages for the prevention of type 2 diabetes. Under assumption of causality, consumption of sugar sweetened beverages over years may be related to a substantial number of cases of new onset diabetes.

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Author and article information

Journal

Title: Advances in Nutrition

Publisher: Oxford University Press (OUP)

ISSN (Print): 2161-8313

ISSN (Electronic): 2156-5376

Publication date Created: March 2018

Publication date Created: March 01 2018

Publication date Created: April 11 2018

Publication date Other: March 2018

Publication date (Print): March 01 2018

Publication date (Electronic): April 11 2018

Volume: 9

Issue: 2

Pages: 70-77

Affiliations

[1 ]Department of Medicine/Physiology, University of Fribourg, Fribourg, Switzerland

Article

DOI: 10.1093/advances/nmx023

PMC ID: 5916433

PubMed ID: 29659691

SO-VID: 5aec8079-5d62-4473-b79c-fa0e9f22bcf2

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Perspective: Cardiovascular Responses to Sugar-Sweetened Beverages in Humans: A Narrative Review with Potential Hemodynamic Mechanisms

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Most cited references 59

Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.

Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity.

Consumption of sugar sweetened beverages, artificially sweetened beverages, and fruit juice and incidence of type 2 diabetes: systematic review, meta-analysis, and estimation of population attributable fraction

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