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.

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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

Gut microbes linked with obesity and weight gain!

If you are obese and wondering how did you accumulated all that weight, well you could blame it to the bacteria living in your gut.

A new research has shown that inbred germ-free mice quickly gained weight when given gut bacteria derived from obese human twins than those mice which received gut bacteria from the lean twins. Scientists tested at least four such human twin pairs-derived gut microbes in the mice which all received the same kind and amount of the food.

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The study suggests that the gut microbiota, which include plethora of microbes such as bacteria, fungi, archea living in the intestine, can affect the metabolism and thus weight gain.

Scientist know that humans and microbes live in close association with each other, so much so that in number our body harbors far more microbial cells, nearly 100 trillion, than our own cells, in the ratio of 1 to 10. Although these numbers may look frightening to a layman but they actually live in a mutually beneficial relations with our body.

Some of them live as commensals - living but not causing any harm, symbiotic –mutually helping each other and some of them may live as pathogens, causing harm such as well known pathogenic diseases.

It is therefore logical that if so many organisms are in or on us, they may also affect how we function as an organism, they should then also affect our metabolism, so to say.

And they do! It is known that any disturbances in our intestinal environment could lead to the growth of harmful microbes which may lead to chronic inflammatory diseases including obesity, metabolic disorders and infections.

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Scientist have shown earlier that an antibiotic-resistant gut bacteria, Clostridium difficile, known to affect and killing thousands in America, can be treated by transplanting microbiota from a healthy individual into an infected persons gut.

Scientists have also shown that the gut microbes also amend our immune system which helps us identify the foreign pathogens, antigens and harmful substances and eradicate them. The increasing cases of allergic and autoimmune disease in the developed countries are arguably believed to be related with disturbance in microbial habitat, our body, due to the hygienic living, leading to emergence of “hygiene hypothesis” to explain these increased incidences.

Previously, scientists have also experimentally shown that when the intestinal flora of the lean mice was given to the obese mice, they successfully controlled and decreased the body weight in obese mice. 

The study led by Jeffrey I. Gordon at Washington University in St. Louis, MO found that when mice with the lean microbiota were made to cohabitate with mice having obese microbiota much before they gained weight, and found that the populations of bacteria in the obese-type mice changed to those of their lean cage-mates, and that their weight did not increase as well. It is known that mice eat each other’s faeces, so this allowed the replacement of ‘obese’ microbiota, but this migration was unidirectional and microbiota from obese mice did not colonize in the lean mice gut.

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However, interestingly enough, scientist also discovered that besides this there is strong correlation between the diet we take and how the gut microbes behave. When the researchers fed the mice a low fat diet rich in fruit and vegetables, the gut microbes from lean mice migrated to those with the obese type. But, when a high-fat diet low in fruits and vegetable was fed to mice, the microbe transfer did not occur and obese-type mice went on to gain weight.

This and many other studies clearly indicate that our relationship with the microbes is very intricate and scientists are unraveling these intricacies slowly but steadily. However, a lot remains to be learnt about various other players including genetics, environment, diet and diseases in the interaction of microbes and our body which benefits as well as harm each other.