Non-caloric sweeteners Beyond sweetness

Article Sidebar

PDF (Spanish)
Published: 2016-06-30
DOI: https://doi.org/10.51987/Rev.Hosp.Ital.B.Aires.v36i2.679
Keywords:
non-caloric sweeteners, non-nutritive sweeteners, insulin resistance, microbiota, body weight, obesity, diabetes, aspartame, saccharin, acesulfame, sweetness, non-communicable diseases, nutritional transition

Main Article Content

Julio C. Montero
Sociedad Argentina de Obesidad y Trastornos Alimentarios (SAOTA)

Abstract

Non-caloric sweeteners (NCS), are widely used by people of all ages, from age 2. In addition to its intentional introduction by users, a massive incorporation is added by their manufacturers to numerous foods which is usually unnoticed, and since their sweetness increases the consumption of products that contain them. However, recent information on effects beyond the sweetness, such as its metabolic and endocrine changes, are associated with the so-called noncommunicable diseases of nutritional transition

Downloads

Download data is not yet available.

Article Details

Issue

Vol. 36 No. 2 (2016): Revista del Hospital Italiano de Buenos Aires

Section

Update and advances in research
Creative Commons License

This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.

How to Cite

1.
Montero JC. Non-caloric sweeteners: Beyond sweetness. Rev Hosp Ital B.Aires [Internet]. 2016 Jun. 30 [cited 2026 Jul. 6];36(2):63-7. Available from: https://ojs.hospitalitaliano.org.ar/index.php/revistahi/article/view/679

References

Peciña S, Smith KS, Berridge KC. Hedonic hot spots in the brain. Neuroscientist. 2006;12(6):500-11. DOI: https://doi.org/10.1177/1073858406293154

Beauchamp GK, Mennella JA. Early flavor learning and its impact on later feeding behavior. J Pediatr Gastroenterol Nutr. 2009;48 Suppl 1:S25-30. DOI: https://doi.org/10.1097/MPG.0b013e31819774a5

Desor JA, Beauchamp GK. Longitudinal changes in sweet preferences in humans. Physiol Behav. 1987;39(5):639-41. DOI: https://doi.org/10.1016/0031-9384(87)90166-1

American Diabetes Association. Standards of medical care in diabetes--2012. Diabetes Care. 2012;35 Suppl 1:S11-63. DOI: https://doi.org/10.2337/dc12-s011

Gardner C, Wylie-Rosett J, Gidding SS, et al. Nonnutritive sweeteners: current use and health perspectives: a scientific statement from the American Heart Association and the American Diabetes Association. Diabetes Care. 2012;35(8):1798-808. DOI: https://doi.org/10.2337/dc12-9002

Calorie Control Council 2007. Calorie Control Council. (2007, Fall). Saccharin: Howsweet it is. Retrieved April 23, 2008, from www.saccharin.org/facts_policy.html.

Sylvetsky AC, Welsh JA, Brown RJ, et al. Low-calorie sweetener consumption is increasing in the United States. Am J Clin Nutr. 2012;96(3):640-6. DOI: https://doi.org/10.3945/ajcn.112.034751

Roberts A, Renwick AG, Sims J, et al. Sucralose metabolism and pharmacokinetics in man. Food Chem Toxicol. 2000;38 Suppl 2:S31-41. DOI: https://doi.org/10.1016/S0278-6915(00)00026-0

Byard JL, Goldberg L. The metabolism of saccharin in laboratory animals. Food Cosmet Toxicol. 1973;11(3):391-402. DOI: https://doi.org/10.1016/0015-6264(73)90005-9

Brown RJ, de Banate MA, Rother KI. Artificial sweeteners: a systematic review of metabolic effects in youth. Int J Pediatr Obes. 2010;5(4):305-12 DOI: https://doi.org/10.3109/17477160903497027

Zhang GH, Chen ML, Liu SS, et al. Effects of Mother’s Dietary Exposure to Acesulfame-K in Pregnancy or Lactation on the Adult Offspring’s Sweet Preference. Chem Senses. 2011. DOI: https://doi.org/10.1093/chemse/bjr050

Bucher HU, Baumgartner R, Bucher N, et al. Artificial sweetener reduces nociceptive reaction in term newborn infants. Early Hum Dev. 2000 Jul;59(1):51-60. DOI: https://doi.org/10.1016/S0378-3782(00)00085-2

Swithers SE, Baker CR, Davidson TL. General and persistent effects of high-intensity sweeteners on body weight gain and caloric compensation in rats. Behav Neurosci. 2009;123(4):772-80. DOI: https://doi.org/10.1037/a0016139

Swithers SE. Artificial sweeteners produce the counterintuitive effect of inducing metabolic derangements. Trends Endocrinol Metab. 2013;24(9):431-41. DOI: https://doi.org/10.1016/j.tem.2013.05.005

Barclay AW, Brand-Miller J. The Australian paradox: a substantial decline in sugars intake over the same timeframe that overweight and obesity have increased. Nutrients. 2011;3(4):491-504 DOI: https://doi.org/10.3390/nu3040491

Dhingra R, Sullivan L, Jacques PF, et al. Soft drink consumption and risk of developing cardiometabolic risk factors and the metabolic syndrome in middle-aged adults in the community. Circulation. 2007;116(5):480-8. DOI: https://doi.org/10.1161/CIRCULATIONAHA.107.689935

Nettleton JA, Lutsey PL, Wang Y, et al. Diet soda intake and risk of incident metabolic syndrome and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA). Diabetes Care. 2009;32(4):688-94. DOI: https://doi.org/10.2337/dc08-1799

Brown RJ, Walter M, Rother KI. Ingestion of diet soda before a glucose load augments glucagon-like peptide-1 secretion. Diabetes Care. 2009;32(12):2184-6. DOI: https://doi.org/10.2337/dc09-1185

Yang Q. Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings: Neuroscience 2010. Yale J Biol Med. 2010;83(2):101-8.

Whitehouse CR, Boullata J, McCauley LA. The potential toxicity of artificial sweeteners. AAOHN J. 2008;56(6):251-9; quiz 260-1. DOI: https://doi.org/10.1177/216507990805600604

Rycerz K, Jaworska-Adamu JE. Effects of aspartame metabolites on astrocytes and neurons. Folia Neuropathol. 2013;51(1):10-7. DOI: https://doi.org/10.5114/fn.2013.34191

Rolls BJ. Effects of intense sweeteners on hunger, food intake, and body weight: a review. Am J Clin Nutr. 1991;53(4):872-8. DOI: https://doi.org/10.1093/ajcn/53.4.872

Tandel KR. Sugar substitutes: Health controversy over perceived benefits. J Pharmacol Pharmacother. 2011;2(4):236-43. DOI: https://doi.org/10.4103/0976-500X.85936

Miller PE, Perez V. Low-calorie sweeteners and body weight and composition: a meta-analysis of randomized controlled trials and prospective cohort studies. Am J Clin Nutr. 2014;100(3):765-77. DOI: https://doi.org/10.3945/ajcn.113.082826

Blundell JE, Hill AJ. Paradoxical effects of an intense sweetener (aspartame) on appetite. Lancet. 1986;1(8489):1092-3. DOI: https://doi.org/10.1016/S0140-6736(86)91352-8

Pierce WD, Heth CD, Owczarczyk JC, et al. Overeating by young obesity-prone and lean rats caused by tastes associated with low energy foods. Obesity (Silver Spring). 2007;15(8):1969-79. DOI: https://doi.org/10.1038/oby.2007.235

Benton D. The plausibility of sugar addiction and its role in obesity and eating disorders. Clin Nutr. 2010;29(3):288-303. DOI: https://doi.org/10.1016/j.clnu.2009.12.001

Liem DG, de Graaf C. Sweet and sour preferences in young children and adults: role of repeated exposure. Physiol Behav. 2004;83(3):421-9. DOI: https://doi.org/10.1016/j.physbeh.2004.08.028

Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev. 2008;32(1):20-39 DOI: https://doi.org/10.1016/j.neubiorev.2007.04.019

Volkow ND, Wise RA. How can drug addiction help us understand obesity? Nat Neurosci. 2005;8(5):555-60. DOI: https://doi.org/10.1038/nn1452

Fortuna JL. Sweet preference, sugar addiction and the familial history of alcohol dependence: shared neural pathways and genes. J Psychoactive Drugs. 2010; 42(2):147-51. DOI: https://doi.org/10.1080/02791072.2010.10400687

Rada P, Avena NM, Hoebel BG.Daily bingeing on sugar repeatedly releases dopamine in the accumbens shell. Neuroscience. 2005;134(3):737-44. DOI: https://doi.org/10.1016/j.neuroscience.2005.04.043

Lenoir M, Serre F, Cantin L, Ahmed SH. Intense sweetness surpasses cocaine reward. PLoS One. 2007;2(8):e698. DOI: https://doi.org/10.1371/journal.pone.0000698

de Araujo IE, Oliveira-Maia AJ, Sotnikova TD, et al. Food reward in the absence of taste receptor signaling. Neuron. 2008;57(6):930-41. DOI: https://doi.org/10.1016/j.neuron.2008.01.032

Mattes R. Effects of aspartame and sucrose on hunger and energy intake in humans. Physiol Behav. 1990;47(6):1037-44. DOI: https://doi.org/10.1016/0031-9384(90)90350-D

Fowler SP, Williams K, Resendez RG, et al. Fueling the obesity epidemic? Artificially sweetened beverage use and long-term weight gain. Obesity (Silver Spring). 2008;16(8):1894-900. DOI: https://doi.org/10.1038/oby.2008.284

Stellman SD, Garfinkel L. Artificial sweetener use and one-year weight change among women. Prev Med. 1986;15(2):195-202. DOI: https://doi.org/10.1016/0091-7435(86)90089-7

Ebbeling CB, Feldman HA, Osganian SK, et al. Effects of decreasing sugar-sweetened beverage consumption on body weight in adolescents: a randomized, controlled pilot study. Pediatrics. 2006;117(3):673-80. DOI: https://doi.org/10.1542/peds.2005-0983

Williams CL, Strobino BA, Brotanek J. Weight control among obese adolescents: a pilot study. Int J Food Sci Nutr. 2007;58(3):217-30. DOI: https://doi.org/10.1080/09637480701198083

Suez J, Korem T, Zeevi D, et al. Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature. 2014;514(7521):181-6. DOI: https://doi.org/10.1038/nature13793

Palmnäs MS, Cowan TE, Bomhof MR, et al. Low-dose aspartame consumption differentially affects gut microbiota-host metabolic interactions in the diet-induced obese rat. PLoS One. 2014;9(10):e109841. DOI: https://doi.org/10.1371/journal.pone.0109841

Kimura I, Ozawa K, Inoue D, et al. The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43. Nat Commun. 2013;4:1829. DOI: https://doi.org/10.1038/ncomms2852

Larsson E, Tremaroli V, Lee YS, et al. Analysis of gut microbial regulation of host gene expression along the length of the gut and regulation of gut microbial ecology through MyD88. Gut. 2012;61(8):1124-31. DOI: https://doi.org/10.1136/gutjnl-2011-301104

MacFabe DF, Cain NE, Boon F, et al. Effects of the enteric bacterial metabolic product propionic acid on object-directed behavior, social behavior, cognition, and neuroinflammation in adolescent rats: Relevance to autism spectrum disorder. Behav Brain Res. 2011;217(1):47-54 DOI: https://doi.org/10.1016/j.bbr.2010.10.005

Foley KA, Ossenkopp KP, Kavaliers M, et al. Pre- and neonatal exposure to lipopolysaccharide or the enteric metabolite, propionic acid, alters development and behavior in adolescent rats in a sexually dimorphic manner. PLoS One. 2014;9(1):e87072. Conflictos de interés: el autor declara no tener conflictos de interés. DOI: https://doi.org/10.1371/journal.pone.0087072

Lee KJ, Tack J. Altered intestinal microbiota in irritable bowel syndrome. Neurogastroenterol Motil. 2010;22(5):493-8. DOI: https://doi.org/10.1111/j.1365-2982.2010.01482.x

Corkey BE. Banting lecture 2011: hyperinsulinemia: cause or consequence? Diabetes. 2012;61(1):4-13. DOI: https://doi.org/10.2337/db11-1483

Pories WJ, Dohm GL. Diabetes: have we got it all wrong? Hyperinsulinism as the culprit: surgery provides the evidence. Diabetes Care. 2012;35(12):2438-42. DOI: https://doi.org/10.2337/dc12-0684

Brown RJ, Rother KI. Non-nutritive sweeteners and their role in the gastrointestinal tract. J Clin Endocrinol Metab. 2012;97(8):2597-605. DOI: https://doi.org/10.1210/jc.2012-1475

Margolskee RF, Dyer J, Kokrashvili Z, et al. T1R3 and gustducin in gut sense sugars to regulate expression of Na+-glucose cotransporter 1. Proc Natl Acad Sci U S A. 2007;104(38):15075-80. DOI: https://doi.org/10.1073/pnas.0706678104

Mace OJ, Affleck J, Patel N, et al. Sweet taste receptors in rat small intestine stimulate glucose absorption through apical GLUT2. J Physiol. 2007;582(Pt 1):379-92. DOI: https://doi.org/10.1113/jphysiol.2007.130906

González J, Otero-Losada ME, Guerri-Guttenberg RA, Grana D, Milei J. Manifestaciones bioquimicas, ecocardiográficas y anatomopatológicas asociadas con el síndrome metabólico inducido por Coca-Cola en la rata. Rev Fed Arg Cardiol 2011;40(2):143-151.