Tuesday, September 23, 2014

Artificial Sweeteners Cause Metabolic Disorders

For the diabetics, obese and weight conscious individuals artificial sweeteners (AS) are considered safe choice to help regulate the blood glucose level and manage body weight. Use of AS considered good choice to sweeten the drinks and deserts as opposed to the common table sugar mostly due to low amount or lack of calorie in them.  Because of the same reason many food and beverage companies market their “calorie free” “Lite” and “diet” drinks and food items to cater the need of various “calorie conscious” customers.

Image curtsy: huntnewsnu.com

Food and drug administration (FDA) of USA identifies some of these sweeteners as “high-intensity sweeteners” and regulates them as food additive, meaning that they must undergo premarket review and approval by FDA before it can be used in food.  Accordingly nearly six artificial sweeteners have been approved by FDA as food additives in the USA. These are saccharin, aspartame, acesulfame potassium (Ace-K), sucralose, neotame, and advantame. The agency considers these FDA approved AS safe for the general population in certain conditions of use1.  

The use of AS has become more common in general population due to reported ill effects of common sugar including sudden increase in blood sugar, tooth decay, weight gain, obesity, and an array of life style diseases such as hypertension, cardiovascular diseases, type 2 diabetes and dementia among others. The increased use of AS has propelled the scientists to examine the long-term effects of AS on humans.

In a recent study scientists have observed that use of AS may lead to the development of glucose intolerance (GI). GI is a hyperglycaemic state that is linked to insulin resistance and generally occurs in pre-diabetic individuals. AS induced glucose intolerance, scientists observed, develops due to alteration in the composition and function of the microorganism or microbiota that live in our intestine.

The group of scientists led by Jotham Suez2 found that when mice were fed AS, they showed altered GI and also their intestinal microbiota composition changed from that of normal mice not fed AS. Further, when the intestinal microbiota from AS consuming mice was transferred to germ- free mice they also showed altered GI and other metabolic defects. These defective metabolisms were abrogated by the use of antibiotics which is known to kill the intestinal bacteria suggesting that the effects were caused due to the changed intestinal microbiota. 

When scientists compared the bacterial population from glucose-fed verses AS-fed mice by genetic analysis, they found that not only the composition, but the functions of the bacteria also had changed in AS-fed mice. The bacteria from AS-fed mice intestine showed increased carbohydrate degrading mechanisms. This means that they can degrade even complex carbohydrates easily leading to elevated glucose levels that may contribute to GI.

The scientists also examined and compared the intestinal microbiota of AS consuming individuals with those who did not consume AS and found that AS consuming people had different bacterial population in their intestine which correlated with markers of obesity and GI. When they fed AS to the volunteers, they showed increased blood glucose levels as well as altered intestinal bacteria in just four days.

These scientific evidences clearly indicate that consumption of AS is associated with increased GI, risk of obesity related metabolic disorders and these changes are not direct but by altering the bacterial community in the intestine. Thus, a caution regarding the excessive use of AS as food additive needs reassessment and in-depth study before being approved for use by general population


References:
1. http://www.fda.gov/Food/IngredientsPackagingLabeling/FoodAdditivesIngredients/ucm397716.htm

2. Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Suez J, Korem T, Zeevi D, Zilberman-Schapira G, Thaiss CA, Maza O, Israeli D, Zmora N, Gilad S, Weinberger A, Kuperman Y, Harmelin A, Kolodkin-Gal I, Shapiro H, Halpern Z, Segal E, Elinav E. Nature. 2014 Sep 17. doi: 10.1038/nature13793