Artificial Sweeteners Make your Fatter
All right, you are a little overweight and want to slim down a touch. Instead of fully sugared soda, you decide to get just the zero calorie soda instead, sweetened with an artificial sweetener. You won’t gain weight, right? In fact, you can drink that all day long and not put on any pounds because you aren’t eating any calories. Right?
Increasingly we are aware that our behavior is driven by forces other than our conscious, advanced brain. In fact, it’s pretty well established that it’s hormones that drive our eating behavior. We used to say you got fat because you were a lazy slob and didn’t exercise enough, ergo – your personality is flawed and it’s your fault that you are fat. If that were true, you would lose weight when you ate less and exercised more. Well, that approach has failed. We now know that to lose weight you have to manage your hormones, most notably your insulin, which requires you changing the foods that make your secrete insulin. Insulin and leptin are the hormones that drive your eating, and your weight gain.
So what does this study show? Very interesting. This happened in mice, not humans (yet) but it raises a new principle that is an open door for further inquiry. Mice, fed water sweetened with sugar versus artificial sweetener were followed for a variety of metabolic effects. What Dr Suez found was startling. The artificial sweetener mice became glucose resistant, the first step to diabetes. The source of that resistance was in their gut bacteria, not in their own chemical structure. That wasn’t all the scientists did. With that finding, they found that they could prevent the effect by killing off the colonic bacteria by treating with antibiotics. Further, they could transfer the glucose resistance to germ free mice by doing a fecal transplant and giving the germ free mice the colonic bacteria that caused the glucose resistance in the first place. Finally, they identified the metabolic pathways that were altered in the bacteria that altered their host’s glucose tolerance, and found that those same pathways exist in humans.
Did you get that core idea? An alteration of gut bacteria caused glucose intolerance and insulin resistance. That’s diabetes, or the first step. The sequence is then as follows. When you are glucose intolerant, your insulin level rises. Insulin causes your fat cells to take up calories and your liver to make more fat. Those calories aren’t available for activity so the body feels hungry and eats more food. You gain weight. And the net effect was all started by changes in colonic bacteria, brought about by the artificial sweetener.
One more time, we have to run the sequence of events that leads to obesity. It’s exactly opposite to what the American Diabetes Association teaches when it says it’s your fault for eating too much. The too-much-food-theory is NOT primary cause, it’s a secondary effect. What is primary is eating the wrong food that causes hormonal responses. In this case, the hormonal response is actually metabolic changes in your gut bacteria. Your colon is not just a waste dump, but a vibrant, active organ that controls much of your metabolism.
The cool thing is that you can change your behavior. Stop using artificial sweeteners. Just stop. Stop. Quit. Drink Water.
WWW. What will work for me. Water. Tea. Sour flavors. Just no artificial sweeteners. (Stevia was not measured, and being based on a plant is an unknown quantity. I’m still using Stevia. Trying to make it less.)
- Mice that eat water sweetened with artificial sweeteners have no metabolic effect. T or F
Go to top of page and re-read this article. They became glucose intolerant
- When you are glucose intolerant, you gain weight. T or F
True. May be chicken or egg, but with high insulin, you more easily push calories into storage.
- The primary cause of the glucose resistance in these experimental mice was in their gut bacteria. T or F
- The glucose resistance could be transferred to other mice that had been grown in a perfectly germ free environment, simply by giving them a fecal germ transplant. T or F
- The same pathways that cause this glucose intolerance are present in humans, but not tested yet in humans. T or F