An interesting correlation that is noted is that artificial sweeteners are associated with obesity, with both forward causation (artificial sweeteners cause obesity) and backwards causation (obese people consume more artificial sweeteners to lose weight) proposed using trend data from NHANES (American survey). In order to satisfy the first proposal, it was then hypothesized that artificial sweeteners can increase appetite and lead to higher caloric consumption.
It should be noted that the above studies look at 'artifical sweeteners' and do not usually discriminate between the non-caloric sweeteners of aspartame, sucralose, saccarhin, acesulfame-potassium and neotame (for more recent data); although data that is conducted on isolated ingredients such a saccharin suggest this phenomena may not apply to just aspartame.
The Cephalic Phase or Anticipatory Phase of digestion is digestion that is stimulated not by food, but by the senses. In this context (for aspartame), it would be any digestive processes that are stimulated by the sensation of sweetness.
A reason this 'Phase' is under investigation is that carbohydrates tend to have an appetite suppressing effect, but sweetness of carbohydrates tends to act in opposition to this (Typically shown with the same amount of carbohydrate having a greater appetite suppression if not as sweet). Logically, taking the enhancing variable away from the suppressing variable should result in enhancement of appetite.
Insulin does not appear to be at all influenced by tasting aspartame or other non-nutritive sweeteners. Which is in accordance with the inability of aspartame to influence insulin secretion in healthy persons, diabetics and those with other various disease states.
Only carbohydrates and possibly saccharin appear to be able to influence insulin from Cephalic Phase senses whereas carbohydrates may do this via direct absorption into the blood via the mouth. Only one study has noted a decrease in blood glucose associated with 500mg aspartame, theoretically through a release in insulin.
One study noted no differences in growth hormone, cortisol, prolactin, or insulin after ingestion of 0.534g aspartame (about 1L of sweetened beverage) when aspartame was paired with a meal.
The satiety hormone CCK, and Glucagon-like Peptide 1 (GLP-1) are also unaffected after aspartame consumption. These hormones, if risen, suppress appetite.
As aspartame ingestion does not influence satiety hormones to a great deal, suppression may be through a slight serum increase in phenylalanine; a component of aspartame.
Few human studies have found increases in subjective (self-report) or demonstrated (eats more) appetite with aspartame. While in contrast, there are some studies which argue a suppression of appetite for aspartame exists. One study conducted in a metabolic ward where obese persons (n=8) were not subject to food restriction found that covert replacement of sugars with aspartame without notifying the subjects of anything resulted in 25% less energy intake (number is more complimenting than practical usage, since calories were removed to accommodate the inclusion of aspartame). This study also noted a nonsignificant increase in food consumption after aspartame was discontinued, and sucrose reinstated.
When investigating weight changes associated with aspartame, none are seen if other variables are controlled. These variables tend to be calories, as some studies have noted that if calories are kept equal that weight can be lost to an equal degree with both diet soda and regular soda. Intervening in a lifestyle using regular soda and replacing it with diet soda, with no dietary controls, does not appear to induce weight loss in normal weight individuals (although it did so in the heavier individuals). One Meta-Analysis concluded no significant effects of any common artificial sweetener on weight loss assuming calories are controlled, this analysis was conducted on youth.
When looking at the overall data, no convincing data exists to conclude that aspartame positively or negatively affects appetite. Based on the metabolic ward study and other interventions which stratify on body weight though, a case could be made for aspartame suppressing appetite in obese persons with little to no effect on normal weight persons (still somewhat lack of evidence for this claim though, small sample sizes and whatnot)
Although aspartame has been insufficiently linked to increasing appetite, saccharin has been somewhat linked to weight gain. One animal study using saccharin to simulate sweet taste without caloric input found blunted thermic responses to food and weight gain. It was noted earlier that practical dosages of saccharin might influence insulin secretion after taste sensation whereas normal doses of aspartame had no influence; the might is based on some research showing the opposite, no influence from saccharin.
(Common phrases used by users for this page include digestion of artificial sweeteners cephalic, components of saccharin, aspertame examine, aspertaine and cortisol, aspartame, Artificial sweeteners and apatite)