|Drinking diet soda now and then is certainly not going to harm you.|
Against that background, it is nice to see that a recent study by researchers from the NIH, the US National Institutes of Health in Bethesda, did something no previous study has done (which only proves that the currently available real = experimental science on artificial sweeteners is insufficient). In said study, the authors "aimed to test acute metabolic effects of NNS in isolation (water or seltzer) and in diet sodas" (Sylvetsky. 2016).
|Table 1: Overview of the ingredients of the "real world" treatment with Diet Rite Cola™ and Diet Mountain Dew™ - the ingredients I highlighted in yellow may be responsible for their ill effect on insulin (see bottom line).|
- 355 mL caffeine-free Diet Rite Cola™, Diet Mountain Dew™, which contained 68 mg sucralose and 41 mg acesulfame-potassium (Diet Rite) and 18 mg sucralose, 18 mg acesulfame-potassium and 57 mg aspartame (Mountain Dew), respectively
- seltzer water with NNS (containing 68 mg sucralose and 41 mg acesulfame-potassium, equivalent to Diet Rite Cola™)
|Figure 1: Serial data from OGTTs. Active (a) glucagon-like-peptide 1 (GLP-1) and (b) gastric inhibitory|
peptide (GIP) response to the four different treatments (Sylvetsky. 2016)
- The diet sodas augment active GLP-1, while the sweetened seltzer has no effect on the GLP-1 response to the oral glucose test; with a sign. different between treatments (!)
- All four treatments left gastric emptying and satiety measures unaffected.
- All NNS treatments (Diet Rite, Mountain Dew and sweetened seltzer) increased the total amount of insulin that was produced after the oral glucose test, but this difference is (a) not statistically significant (p = 0.53; see Figure 3) and, more importantly, (b) so small that it is almost certainly physiological irrelevant - at least in the short run.
- None of the NNS treatments affected the subject's glucose levels significantly.
|Figure 2: The acute glucose, insulin and C-peptide levels didn't differ significantly (p < 0.05) at any point in the|
130 minutes after the ingestion of the four test drinks (Sylvetsky. 2016).
|Figure 3: Glucose, GLP-1 and insulin AUC in the post-absorptive period (Sylvetsky. 2016); a statistically significant treatment effect was only observed for GLP-1 in the Diet Rite group (p < 0.05).|
In view of the exorbitant amount of acesulfame-K (human equivalent: 16mg/kg) Liang et al. (1987b) had to inject right into the bloodstream of their rats to induce significant in vivo effects on insulin, it appears more than questionable, though, if the oral ingestion 18mg and 41mg of acesulfame-K could, in fact, be responsible for the non-significant increase in insulin observed in the study at hand - and that's in spite of the more recent revelation that acesulfame-K has a disproportionately potent effect on the sweet taste receptors (Dotson. 2008).
"[...] effect of Acesulfame K on insulin secretion [see Figure 4] was similar to that observed by injecting or infusing [both right into the cervical vein and thus bypassing any potential effects of digestion and/or the interaction with sweet receptors in the gut] the same doses of glucose (150 mg/kg) body weight for injection and 20 mg/kg body weight/min for infusion), except that no hyperglycemia was observed with Acesulfame K (Loang. 1987)
Figure 4: Effect of acesulfame-K on insulin in rats.
So, if it's not a specific sweetener, what is it that triggers the differences - esp. in GLP-1?
|Water or Diet Soda - What's the Better Diet Beverage? Study Confirms Fake Sweetness Promotes Weight & Waist Loss, Decreases Hunger, Blood Pressure, Cholesterol & Trigs | more|
The comparatively large, treatment effect on GLP-1, on the other hand, can't be ascribed solely to the interaction with sweet taste receptors. After all, there's a visible difference between the three NNS treatments, Diet Rite Cola™ (+12%), Diet Mountain Dew™ (+11%) and seltzer + NNS (+3%), with only Diet Rite Cola™ producing statistically significant and Diet Rite™ and Diet Mountain Dew™ potentially relevant increases of the incretin hormone GLP-1 (Waldrop. 2016).
- Dotson, Cedrick D., et al. "Bitter taste receptors influence glucose homeostasis." PloS one 3.12 (2008): e3974.
- Liang, Yin, et al. "The effect of artificial sweetener on insulin secretionII. Stimulation of insulin release from isolated rat islets by Acesulfame K (in vitro experiments)." Hormone and metabolic research 19.07 (1987a): 285-289.
- Liang, Yin, et al. "The Effect of Artificial Sweetener on Insulin Secretion 1. The Effect of Acesulfame K on Insulin Secretion in the Rat (Studies In Vivo)." Hormone and metabolic research 19.06 (1987b): 233-238.
- Malaisse, Willy J., et al. "Effects of artificial sweeteners on insulin release and cationic fluxes in rat pancreatic islets." Cellular signaling 10.10 (1998): 727-733.
- Sylvetsky, et al. "Hormonal responses to non-nutritive sweeteners in water and diet soda." Nutrition & Metabolism 13:71 (2016).
- Waldrop, Greer, et al. "Incretin-based Therapy in Type 2 Diabetes: An Evidence Based Systematic Review and Meta-analysis." Journal of Diabetes and its Complications (2016).