SCIENTIFIC STUDIES

Cravings & Satiety Studies

Satiation signals begin to occur after a sufficient amount of food has been consumed, and satiation signals are what tells us to bring a meal to an end. Satiety starts at the end of a meal and results in the delay of the next meal, until the return of hunger signals. While satiation is primarily driven by the volume of food in the stomach, satiety is also driven by other factors, including the body’s ability to sense the nutrient content of food in the intestine. The brain detects chemical signals from a variety of gut hormones and neural signals from the intestine that regulate how full one feels or how hungry one feels. These signals are also impacted by a host of factors, like stomach fullness, rate of stomach content flow to the intestine, the concentration of glucose in the bloodstream, etc. The potential for low-calorie sweeteners to adversely affect satiety, however, is not supported by the scientific literature. While there have been a few studies suggesting effects based on results from cellular studies, it is import to know that cellular studies do not include, by their nature, the full regulatory control pathways for satiation and hunger that include the interplay of various and multiple signals.

Nonnutritive Sweeteners are not Supernormal Stimuli

Antenucci, R. G., & Hayes, J. E. (2014). Nonnutritive sweeteners are not supernormal stimuli. International Journal of Obesity. Find full text of the article: Nature.com;
Full Study;

This study aimed to investigate the perceived sweetness intensity of a variety of nutritive sweeteners and non-nutritive sweeteners (NNS) in a large cohort of untrained participants using contemporary psychophysical methods. It is alleged that NNS have a supernormal stimuli with regard to perceived sweetness intensity and therefore can lead to sweet cravings and/or overeating of sweets. The study, supported by the National Institutes for Health, evaluated the perceived sweetness intensity of various low calorie sweeteners and other sugar substitutes when compared to sugar. Researchers at Penn State University recruited 401 participants for four separate test groups. The age range of participants ranged from 18-64. The results showed that participants perceived the sweetness of sugar substitutes at lower concentrations than real sugar, but the intensity of these sensations was not sweeter than sugar. The researchers concluded that NNS are not supernormal stimuli with regard to perceived sweetness intensity and therefore the data do not support the claim that NNS overstimulate sweet taste receptors to produce hyper-intense sweet sensations.

Gastric Emptying and Incretin Hormone Release Study

Ma J, Bellon M, Wishart JM, et al. Effect of the artificial sweetener, sucralose, on gastric emptying and incretin hormone release in healthy subjects. Am J Physiol Gastrointest Liver Physiol. 2009;296(4): G735-739.

Study abstract: "The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), play an important role in glucose homeostasis in both health and diabetes. In mice, sucralose, an artificial sweetener, stimulates GLP-1 release via sweet taste receptors on enteroendocrine cells. We studied blood glucose, plasma levels of insulin, GLP-1, and GIP, and gastric emptying (by a breath test) in 7 healthy humans after intragastric infusions of 1) 50 g sucrose in water to a total volume of 500 ml (approximately 290 mosmol/l), 2) 80 mg sucralose in 500 ml normal saline (approximately 300 mosmol/l, 0.4 mM sucralose), 3) 800 mg sucralose in 500 ml normal saline (approximately 300 mosmol/l, 4 mM sucralose), and 4) 500 ml normal saline (approximately 300 mosmol/l), all labeled with 150 mg 13C-acetate. Blood glucose increased only in response to sucrose (P<0.05). GLP-1, GIP, and insulin also increased after sucrose (P=0.0001) but not after either load of sucralose or saline. Gastric emptying of sucrose was slower than that of saline (t50: 87.4+/-4.1 min vs. 74.7+/-3.2 min, P<0.005), whereas there were no differences in t50 between sucralose 0.4 mM (73.7+/-3.1 min) or 4 mM (76.7+/-3.1 min) and saline. We conclude that sucralose, delivered by intragastric infusion, does not stimulate insulin, GLP-1, or GIP release or slow gastric emptying in healthy humans."

Small Intestinal Glucose Absorption Study

Ma J, Chang J, Checklin HL, et al. Effect of the artificial sweetener, sucralose, on small intestinal glucose absorption in healthy human subjects. Br J Nutr. 2010;104(6): 803-806.

Study abstract: "It has been reported that the artificial sweetener, sucralose, stimulates glucose absorption in rodents by enhancing apical availability of the transporter GLUT2. We evaluated whether exposure of the proximal small intestine to sucralose affects glucose absorption and/or the glycaemic response to an intraduodenal (ID) glucose infusion in healthy human subjects. Ten healthy subjects were studied on two separate occasions in a single-blind, randomised order. Each subject received an ID infusion of sucralose (4 mM in 0.9% saline) or control (0.9% saline) at 4 ml/min for 150 min (T = - 30 to 120 min). After 30 min (T = 0), glucose (25%) and its non-metabolised analogue, 3-O-methylglucose (3-OMG; 2.5%), were co-infused intraduodenally (T = 0-120 min; 4.2 kJ/min (1 kcal/min)). Blood was sampled at frequent intervals. Blood glucose, plasma glucagon-like peptide-1 (GLP-1) and serum 3-OMG concentrations increased during ID glucose/3-OMG infusion (P < 0.005 for each). However, there were no differences in blood glucose, plasma GLP-1 or serum 3-OMG concentrations between sucralose and control infusions. In conclusion, sucralose does not appear to modify the rate of glucose absorption or the glycaemic or incretin response to ID glucose infusion when given acutely in healthy human subjects."

Gut Hormone Response and Appetite Study

Ford HE, Peters V, Martin NM, et al. Effects of oral ingestion of sucralose on gut hormone response and appetite in healthy normal-weight subjects. Eur J Clin Nutr. 2011;65(4):508-513.

This is a randomized, single-blind, crossover study in healthy subjects to investigate whether oral ingestion of sucralose could stimulate enteroendocrine L-cell release of the hormones GLP-1 and peptide YY (PYY), including measurement of appetite ratings and energy intake with a meal. The authors concluded that oral ingestion of sucralose at the dose tested (50 ml of sucralose in water [0.083% w/v] or about 5 times the sucralose concentration in a diet soft drink) "does not increase plasma GLP-1 or PYY concentrations and hence, does not reduce appetite in healthy subjects." They further concluded that "oral stimulation with sucralose had no effect on GLP-1, insulin or appetite."

Sweet-taste Receptors, Low-energy sweeteners, Glucose Absorption and Insulin Release Study

Renwick AG, Molinary SV. Sweet-taste receptors, low-energy sweeteners, glucose absorption and insulin release. Br J Nutr. 2010;104(10):1415-1420.

Study abstract: "The present review explores the interactions between sweeteners and enteroendocrine cells, and consequences for glucose absorption and insulin release. A combination of in vitro, in situ, molecular biology and clinical studies has formed the basis of our knowledge about the taste receptor proteins in the glucose-sensing enteroendocrine cells and the secretion of incretins by these cells. Low-energy (intense) sweeteners have been used as tools to define the role of intestinal sweet-taste receptors in glucose absorption. Recent studies using animal and human cell lines and knockout mice have shown that low-energy sweeteners can stimulate intestinal enteroendocrine cells to release glucagon-like peptide-1 and glucose-dependent insulinotropic peptide. These studies have given rise to major speculations that the ingestion of food and beverages containing low-energy sweeteners may act via these intestinal mechanisms to increase obesity and the metabolic syndrome due to a loss of equilibrium between taste receptor activation, nutrient assimilation and appetite. However, data from numerous publications on the effects of low-energy sweeteners on appetite, insulin and glucose levels, food intake and body weight have shown that there is no consistent evidence that low-energy sweeteners increase appetite or subsequent food intake, cause insulin release or affect blood pressure in normal subjects. Thus, the data from extensive in vivo studies in human subjects show that low-energy sweeteners do not have any of the adverse effects predicted by in vitro, in situ or knockout studies in animals."

Appetite and Food Intake and Their Putative Mechanisms Study

Mattes RD, Popkin BM. Nonnutritive sweetener consumption in humans: effects on appetite and food intake and their putative mechanisms. Am J Clin Nutr.
2009;89(1):1-14.

Mattes and Popkin reported their findings following a review of available literature on low-calorie sweetener use and utility in weight management strategies. Their review describes recent trends in the use of non-nutritive sweeteners and current knowledge of their effects on short-term appetite and food intake as well as longer-term energy balance and body weight. The authors report that the evidence suggests that, when non-nutritive sweeteners are used as substitutes for higher energy yielding sweeteners, they have the potential to aid in weight management. They also report that, with respect to energy intake, there is no substantive evidence of inherent liking for sweetness or non-nutritive sweetener- activation of reward systems is problematic.

Nutrient Selection in the Absence of Taste Receptor Signaling Study

Ren X, Ferreira JG, Zhou L, Shammah-Lagnado SJ, Yeckel CW, de Araujo IE. Nutrient selection in the absence of taste receptor signaling. J Neurosci. 2010;30:8012–8023.

Taste quality, particularly sweet taste, seems to be an important driver of food preference by stimulating dopamine (DA) release, which is a marker of "pleasure" sensation. The authors report on a series of experiments, using "sweet knock-out" mice that are unable to taste sweetness to test this concept. The researchers showed mice preferred glucose over the sweet-tasting amino acid, L-serine (which has the same caloric value as glucose but cannot be converted to glucose). The preference for, and higher intake of glucose was associated with a higher glucose oxidation rate. In a related experiment, normal (wild-type) mice were found to have robust DA release in response to glucose infusion that bypasses interaction with taste receptors. The results suggest that signals related to glucose oxidation drive preference selections for sweets, not sweet taste alone. This further implies that beverages and foods with lower glucose oxidation potential (e.g., a diet drink) would be comparatively less likely to cause increased cravings for sweets than beverages and foods with higher glucose oxidation potential (e.g., a full-calorie soda).


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