Artificial sweetener reporting leaves a bad taste in my mouth

Nutrition science reporting is filled withreams of bad suppositions, unsupported conclusions, and pseudoscience. Time and time again individual studies about dietary science are reported and disseminated as "The New Knowledge" about nutrition. Some studies have good science, some are propaganda, and some are opinions. Individually no matter how good or bad they are it is just a single study. Individual findings do not guide recommendations. Weight control is a complicated and individualized problem. There is no single factor or simple solution for obesity that has long lasting results in the industrialized world. The convoluted nature of dietary research breeds misunderstanding, confirmation bias, and herd like trends. In my opinion, most nutrition science reporting is just sensationalized exploitation to grab attention. Recent media frenzy focused on artificial sweeteners.Artificial sweeteners are the low hanging fruit of dietary pseudoscience/hysteria. There are strong anti-corporate, and anti-chemical themes to artificial sweetener reporting. Overall most claims about artificial sweetenersare ludicrous and unsubstantiated . Brian Dunning has done a wholeskeptoidepisode related to just aspartame(4127). This recent media blitz is more a misleading interpretation rather than hysterical fear mongering.

In the study"Glucose Utilization Rates Regulate Intake Levels of Artificial Sweeteners" the researchers have suggested that mice are not fooled by artificial sweeteners. That they prefer glucose solution to the artificial sweetener. This is truly not revolutionary research. The interesting part of this research is that giving mice a identical artificial sweetener solution did not lessen them wanting a true glucose solution.Mice were fed an artificial sweetener solution that is supposedly indistinguishable from a glucose solution. No matter how much they consumed of the artificial they still wanted the sugar solution and preferred it. Meaning even when a mouse has had a lot of what he thinks is sugar, he still wants more.

In my opinion, interesting but not groundbreaking nor predictive. Artificial sweeteners failing to relieve hunger in mice is not really a radical finding. I am not convinced that you can make an artificial solution that is indistinguishable from glucose solution. I can tell the difference between sugar and artificial sweeteners. Maybe mice are less demanding tasters. So I will give that a pass. The research does demonstrate mouse biochemical response to glucose ingestion and hypothalamic feedback mechanism. That is about the limit of the research's direct findings.

For some reason this has been widely reported as artificial sweeteners cause weight gain. Here is the convoluted pathway to that conclusion.

1. Mice did not want glucose solution any less no matter how much artificial sweeteners were fed to them.

2. people use artificial sweeteners to remove sugar cravings.

3. Therefore people will use artificial sweeteners but still want more and more sugar.

No, that is not a valid conclusion. That is literally a fallacy of the undistributed middle, a non-sequitur. Meaning there are many reasons why people want sugar/sweeteners. Here are a few missed premises. Mice are not people. The purpose of artificial sweetener is not a caloric replacement. Artificial Sweeteners do not increase or decrease hunger in humans. Dopamine response is not theonly factor that drives consumption of sugar.

Just plain poor reporting. They took an opinion from individuals not associated with the research, augmented by out of context comments by one of the researchers. All in attempt to produce a compelling, albeit false, narrative.

It is a broad and inaccurate comparison to say that artificial sweeteners are causative of obesity. I will try to break down the illogic of this nutrient house of cards.

1. Humans and mice have a similar stimulus response to food.

2. Humans use artificial sweeteners to curb sugar cravings.

3. Sugar cravings will not be curbed.

4. no matter how much artificial sweetener you consume sugar cravings will cause you to seek out the equivalent amount of sugar.

5. therefore artificial sweeteners will result in increasing sugar intake and thus obesity as a direct result.

I will take these in reverse order.

There is no evidence that intake of artificial sweeteners results in physiologically increasing hunger. Previous multiple lines of research shows no effect. This bit of research has nothing to do with that discussion.

It is accurate that artificial sweeteners are not a metabolically or psychologically equivalent to sugar. That is not purpose of using artificial sweeteners. The purpose is to make food taste sugar sweetened. The sweeteners do not produce the physiologic response of satiety. Iftaste bud stimuluscaused you to incorrectly interpret glucose levels in your blood you would have significant nutritional issues. If sweeteners provided calories you have a type of sugar not a sweetener.

You are not sweetening your coffee to give your self a filling meal. Most people don't eat raw teaspoons of sugar. Usually sugar is consumed as a component of food and drink. Replacing sugar with artificial sweeteners is done for flavor not nutritional composition. It is a flavoring agent not a nutrient. Sugar is a nutrient, albeit a poor one.

Artificial sweeteners are intended to sweeten food and drinks so you reduce or eliminate sugar in the ingredients. It is a subtle difference but a significant one. A specific craving for plain sugar is not a large dietary driving factor. We like the taste of fat, and sweet and to some extent salt. Evolutionary benefit of favoring those tastes is clear. Normally people don't sit down with a bag of granulated sugar and eat a couple cups of sugar. People like the taste of certain foods, often made with sugar.

Finally we humans have a very complicated response to food in general. Food choices and caloric intake are far more complicated than cravings for specific nutrients. Food choices are social, cultural and psychological in nature. This is not true for mice. It is totally false to draw a parallel between a mouse's dopamine response to food and assume a similar response in people.It is common in dietary pseudoscience to portray a single physiologic response to a nutrient as the most significant factor in weight control.Single nutrient focused diets are flim flam, deceptive and useless for long term weight control. IE: Atkins, paleo diet, south beach, et al...

In the interest of balance, artificial sweeteners do have a downside for weight control. People commonly overestimate the calories saved by using artificial sweeteners. Usually you will find them overeating. Overcoming the calories saved by removing the sugar. IE: You choose a diet soda instead of a beer. So you feel you can have an extra slice of pizza. The slice of pizza has 3 times the calories of that same beer. A losing exchange if you are trying to consume fewer calories. Additionally they grossly overestimate the caloric savings of reducing sugar. "I made these cupcakes with a zero calorie sweetener so I can eat six." Ignoring the calories from oil or wheat or butter.

Artificial sweeteners are very useful for avoiding calories where extra calories from sugar are unnecessary. That is all. Using artificial sweeteners as you primary calorie reduction method will have little effect. Unless you consume a great deal of food products that are mostly sugar. IE: sugared drinks. It can be part of strategy to avoid unnecessary calories and sustainable satiety patterns long term.

Reporting that artificial sweeteners are "making you fat" is lazy, harmful, and flat out wrong. A major issue in the information age is the pile of contradictory and useless information constantly being broadcast in print and on TV. Frustrated people can feel powerless and just give up even trying. Reports should be vetted and analysed with a minimum of science understanding. I hold out little hope that it will happen, but I can dream.

References:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2892765/

http://www.ncbi.nlm.nih.gov/pubmed/22709780

http://www.ncbi.nlm.nih.gov/pubmed/8451310