Sunday, August 9, 2009
Diet Drinks, Ups and Downs
Diet drinks are one of the mainstays of the low-carb community. Diet Coke, Diet Pepsi, Diet Rite and many more provide fairly palatable carb-free alternatives to sugar-laden soda pop.
Some low-carbers drink all sorts of diet drinks and claim they have no problems with them. Others state that diet drinks cause them to gain weight or cause them to stall in their weight-loss programs, almost as if they were drinking the full-sugar equivalents. One of the ways to look at this phenomenon is to see if diet drinks cause the release of insulin.
One possibility is that the sweet taste of the diet drinks causes a cephalic or first-phase insulin response. Two 1995 studies by Teff, Devine and Engelman had normal-weight men sip and spit solutions that contained either water, aspartame, saccharin, or sucrose. Blood was drawn before and at two-minute intervals after the solutions were tasted. They found no significant increase in plasma insulin, even though the men had tasted the sweetened solutions for as long as three minutes.
Another possibility is that the presence of a sweet taste in the gut causes the release of peptides, and these in turn increase the secretion of insulin as part of a second-phase insulin response. It has recently been found that there is a TR2+T1R3 sweet taste receptor in the intestinal endocrine cells of the gut. In 2007, Margolskee et al. demonstrated that sucralose (brand name, Splenda) could activate this receptor in dishes of intestinal endocrine cells and cause the release of two incretin hormones, GLP-1 and GIP. In a whole organism, the incretin hormones would be expected to promote the release of insulin.
In 2009, Jin Ma et al. tested this hypothesis by infusing 500 ml of various solutions into the stomachs of seven healthy humans. (Putting a solution directly into the stomach bypassed any possible cephalic insulin response.) The first solution contained 50 grams of sucrose in water. The remaining solutions were: normal saline, 80 mg of sucralose in normal saline, and 800 mg of sucralose in normal saline. Of the four solutions, only the sucrose solution caused an increase in blood glucose. And contrary to the findings expected from the intestinal endrocrine cell study, only the sucrose caused an increase in GLP-1, GIP and insulin. The saline and sucralose solutions had no effect. Fujita et al. saw similar results when diabetic Zucker rats were given gastric boluses of solutions of glucose, sucralose, saccharin, acesulfame potassium, and stevia. Only the glucose solution affected the blood glucose, and only the glucose solution
increased the plasma GLP-1 and GIP levels. The artifically-sweetened solutions had no effect.
To drink or not to drink? A recent review of the literature in the American Journal of Clinical Nutrition noted that the use of nonnutritive sweeteners has increased along with the increase in Body Mass Index (BMI) in the United States. However, the authors found that if this is a cause-and-effect relationship, most of the mechanisms by which it is postulated to occur cannot be supported by current evidence. As we can see from the studies cited above, it appears that increased first-phase or second-phase insulin secretion is probably not a good explanation for any gain in weight as a result of diet drinks. As always, research is ongoing, but for now it looks as if diet drinks can be consumed without undue worry about their effect on insulin secretion and an insulin-associated gain in weight.