Guest blog by Mathieu Bouchard, Naturopath and ATP-Lab’s research and development team
For many years now, non nutritious sweeteners (or NNS) like aspartame, sucralose, stevia and acesulfame-K were thought to have an influence on insulin and insulin secretion.
The reality is a bit different.
This article will not discuss which is the best sweetener and how they can be detrimental or not for your overall health, but rather discuss how they interact with your system and cause the weight gain associated with the consumption of diet soda and other sweetener-laden foods (1,2) .
First, let’s take a look at the insulin hypothesis. For a couple of years now, many experts have believed that the insulin response to NNS was to blame for the weight gain and increase in food consumption. NNS like sucralose and stevia have been studied thoroughly and their impact on insulin is either inconclusive or really weak (3,5). Their action is not on insulin per se, but on the incretin hormone GLP-1.
GLP-1 is a hormone secreted by the intestinal L cells that will encourage insulin secretion and is known to assist the pancreas in managing the amount of insulin being released (4). Interestingly, aspartame doesn’t seem to have the same properties. Since sucralose and stevia* do not contain any significant calories , how can they stimulate the secretion of an hormone known to interact with food?
The actions of these NNS are mediated by the sweet taste receptors T1r2 and T1r3 (6,7,12). T1r3 taste receptor on the tongue is usually positive for GLP-1R, who is the receptor for GLP-1. Thus GLP-1 is also secreted by the tongue and is proposed to play a role in the “sweet taste” (9) being experienced. These receptors are also known to have a positive effect on incretin GLP-1 secretion. So if the effects on insulin secretion are minimal, what’s the big deal?
The main problem with NNS consumption is with the brain and the satiety effect .The mechanism that detects sweetness (taste) goes like this: as soon as a food touches the tongue, information about it is sent to the primary taste cortex. Then neurons in the primary taste cortex send projections to areas associated with the brain’s primary reward-pathway located in the dopaminergic midbrain, which will induce a release of dopamine, a neurotransmitter associated with reward and pleasure. The food reward system is essential for the control of food intake and controlling eating behavior.
The activation of T1r3 and Trmp5 (a cation channel that it is essential for transduction of bitter, sweet and umami tastes (13)) by NNS will be enough to activate a cascade of signals. The good news is that the reward center can be activated by calorie dense food too, as these receptors are not the sole mechanism of activation (14,15). Even though the NNS can activate a portion of the taste receptors, a phenomenon made even worse by occasional use, the problem is that they cannot reproduce the dopamine response associated with sucrose intake in the long run (16,17).
A study demonstrates that even though sucralose will be pleasant to the taste and can fool the conscious mind, the dopaminergic midbrain areas in relation to the behavioral reward response are not fooled so easily and do not activate as well with sucralose as they do with sucrose (16). The taste of sweetness is so potent that it is able to cause a reward response even greater then cocaine (18).
So the big picture is, sweetness is inherently pleasant (19). It is also related to a complex system of associations which includes the brain and the reward system. This system is responsible for producing sensory signals and information to inform the body and to allow it to produce the associated responses upon tasting of a certain food. This system originally contributed to the maintenance of energy balance but in the case of NNS, the absence of calories or dilution of calories will impair this complex system (20). Sweet taste and sugar might not be recognized for what they are and might be confused for the other.
So the problem with NNS seems caused more by a shift in behavior than a metabolic effect, but although a link has previously been established between obesity and the activation of the reward system, clear associations with NNS or artificial sweeteners consumption and alterations of the brain activity and obesity will require further studies on this topic are needed to get all the pieces of the puzzle. One example is the implication of other appetite controlling hormones like leptin will need to be elucidated to improve our comprehension of this phenomenon. Until then, moderation is the key and both sugar and NNS should be consumed sparingly, even more so in people who suffer from diabetes or obesity, as their appetite regulation hormones are already altered.
*Stevia is actually being studied as a way to help with postprandial hyperglycemia , which recent studies indicate is an important contributor to the development of insulin resistance and Type 2 diabete3,10.11.
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