Do Artificial Sweeteners Cause Insulin Release – Why Do People Care So Much?
The search for the answer has reached almost mythical status, and is most commonly asked by those following a low carbohydrate diet, such as the Atkins diet. Lets briefly look at the theory behind the Atkins diet, which is outlined but vastly oversimplified on the Atkins webpage. Very simply put, eating carbohydrates leads to increased sugar in the blood stream (from the breakdown of the carbohydrates) that triggers insulin to be released and allow the sugar to be taken in to cells. Some of this sugar is used for energy, but the rest is stored in cells or converted into fat. On a low carb diet, there are no carbohydrates to turn in to sugar so there is no ‘insulin response.’ The body still needs fuel though, and so one of the things it does to compensate is that it turns to breaking down eaten and stored fats for energy thereby promoting fat loss. Whether this is exactly as it seems or not and the validity behind all the claims is the subject of great debate, and for the purposes of the current article I’m going to steer clear of that and stick to the title question.
Sweetening a Low Carb Diet, Is It OK?
A very low-carb diet is a tough diet to follow, largely because it means no sugar, no cakes, no chocolates, no sweets, no bread, no rice etc. and due to this a logical solution appears to be the use of artificial sweeteners as a way of making the diet more tolerable. There is some concern however that these sweeteners may lead to the release of insulin, and therefore lead to weight gain or plateaus in weight loss by people using these. There are all sorts of opinions out there on this subject; literally hundreds of forum pages are filled with this, and for each person that says they are fine using the sweeteners on the diet, there is a person saying it ruined their diet! In the rest of this article we will review some of the available scientific evidence to see what is reliably known about the subject.
The Pancreas and Insulin Release – A Little More Detail
When you eat something, it is broken down into its basic nutrients in the gut. These nutrients are then used or stored in our cells, principally under the control of insulin. Cells in the pancreas make insulin, and have the responsibility of releasing the right amount of insulin at the right time. Although it is well known that glucose stimulates insulin release, a number of studies raised the intriguing possibility that these beta cells may in fact react to the sweet taste of food also. The cells in the pancreas are remarkably smart, they can literally sense the concentration of nutrients such as glucose in the blood as well as the presence of hormones that they respond to. They add all these signals together and this leads to a series of chemical reactions leading to insulin release known as the “triggering pathway”. Glucose is a very powerful stimulator of insulin secretion, and is almost twice as powerful at causing insulin release as some of the medications used by diabetics to stimulate insulin release. When we eat meals, there is also stimulation of insulin secretion by hormones that are released by the gut, the main one is called GLP (glucagon like peptide) and this way of stimulating insulin release is known as the “neurohormonal amplifying pathway”. These pathways are recognized but not entirely understood at a molecular level.
Some Laboratory Experiments Suggested That Artificial Sweeteners Cause Insulin Release
Some experiments has been performed that left several things unexplained however. Fructose, a sugar, had been shown to result in insulin release much more than expected. Artificial sweeteners such as saccharin, acesulfame and stevioside, in certain settings were seen to result in increased insulin secretion also, the studies having been done in rats. One group of researchers used the artificial sweetener sucralose and although they found that insulin release doubled in response in an experimental setting although this was very different to a real life setting.
One possible explanation for this was that the artificial sweetener molecules were interacting with unknown receptors in the pancreas cells, and some proposed that these might be the “sweet taste receptors.” Scientists are beginning to put together the story of taste receptors, but its still a work in progress.
Experimental Settings Aren’t Human Settings!
But do these taste receptors play a role in increasing insulin secretion? Ultimately none of the studies that have been able to dispel the traditional model of insulin release, which is governed by glucose levels and is independent of the sweet taste receptors. The role of artificial sweeteners activating sweet taste receptors leading to insulin release remains speculation. It’s important to remember that in experiments done in test tubes the concentrations of the drugs used to stimulate the pancreas cells are not comparable to that in the body. Although the levels of non-glucose sugars and artificial sweeteners are high in the blood surrounding the gut after ingesting them, the concentrations that reach the pancreas are much lower. It is also possible that artificial sweeteners and fructose increase insulin secretion through sweet taste like receptors in the gut, however the clinical studies performed to date don’t support this as seen below.
Human studies of the older artificial sweeteners – Saccharin, Aspartame and Acesulfame
Several studies have examined the effect of artificial sweeteners on ‘cephalic phase’ insulin release. This is the insulin release that occurs before food enters the stomach, so basically while being eaten and basically a response to factors such as taste and smell. In one study, sucrose and saccharin were found to result in increase in cephalic phase insulin release. However there were a small number of participants tested and some design flaws that make the results inconclusive. In contrast, in another study, no increase in insulin was seen in participants that tasted solutions sweetened with aspartame or saccharin. In a further well-designed study it was shown that the sucking of lozenges that were sweetened with aspartame had no effect on insulin release. Finally a study looked at the effect of drinking a solution that contained aspartame, acesulfame, cyclamate or saccharin. It was found that there was no effect of these sweeteners on early (cephalic) or late insulin release,
Human studies of the newer artificial sweeteners – Sucralose and Stevioside
A study performed in human volunteers demonstrated that infusions of sucralose in to the stomach had no effect on insulin levels or glucose. In another study, drinking a diet soda sweetened with sucralose had no significant effect on insulin levels a (a minor non-significant increase was noted). A study also demonstrated that the use of stevia did not increase insulin levels in healthy or obese participants.
Do Artificial Sweeteners Cause Insulin Release – What to make of all this?
Although artificial sweeteners have been shown to possibly increase insulin release in an experimental setting and suggested a role of taste receptors in this, the studies done in human participants did not show either the older or the newer artificial sweeteners to be associated with insulin release. Its important to remember however that none of these studies were done in patients in ketosis such as those on a low carb diet, so you could conclude that we simply don’t have good evidence either way, however currently there is no conclusive evidence that that artificial sweeteners are harmful to those on a low carb diet.
Nevertheless as is seen on the many forums on the subject, many low-carb dieters appear to feel that use of artificially sweetened products such as diet-sodas cause them to reach plateaus or limit success with the diet. It would appear the most logical way would be to eliminate them in the event of reaching a plateau and see if the results improved. At the end of the day artificial sweeteners are not a perfect substitute for sugar and have been associated with a variety of health and metabolic effects and so if used they should certainly be used in moderation.
Comments are purely for informational purposes and are not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Disclaimer