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Artificial Sweeteners – Is It Time To Sound The Alarm?


West Palm Beach, USA – April 12, 2011: Product shot of three different brands of zero calorie sweeteners: Sweet N Low in pink, Equal in blue, and Splenda in yellow. Each brand is an artificial sweetener used as a sugar substitute.

To cut calories yet keep the sweet taste, non-nutritive sweeteners (NNS) are a staple of some people’s diets. But the effect of NNS on weight loss still isn’t fully understood. Some studies pointing to a bit of weight loss, while others show a neutral effect or even weight gain. The effect is probably dependent on the specific person using the sweetener.
There is correlation between artificial sweeteners enhancing appetite[1][2] and increasing hunger[3]. This tends to increase food consumption[2][4][5] and lead to weight gain. We have known this since the 1980s. There are also connections between artificial sweetener intake and increased risk for metabolic syndrome [6][7][8][9]. But it could be correlational evidence. Those using the largest amounts of NNS may simply have a predisposition for overeating and weight gain.
Another school of thought is that sweet taste, in the absence of calories, is causing people to eat more food elsewhere in their diet. But how would this work? Researchers hypothesized that the physiological response to sweet taste may be coupled to the energy content of food. Disrupting this balance could wreak havoc on appetite control and energy homeostasis.[10] Although a promising idea that seemed to be consistent with evidence in animal models,[11][12][13] lack of any known mechanism kept the concept at the theoretical stage.
The connection between NNS and appetite has remained a mystery, until Wang et. al published a potential breakthrough in the Journal Cell Metabolism. (See issue 23 of ERD for a detailed analysis of this study)

Although they lack the calories of sugar, the impact of non-nutritive sweeteners on body weight isn’t understood. A recent study looked at the specific mechanisms that might play a role.

Delving into appetite mechanisms, using fruit flies

To examine the connection between NNS and weight gain, fruit flies were the go-to model. While this may seem to have questionable relevance to humans, fruit flies have some big advantages as an experimental model. They are easy to genetically manipulate, have short life-cycles, and are cheap to keep in the lab. Moreover, they have systems that sense the sweetness and caloric content of food. They also have some of the same insulin signaling and taste-reward pathways that are present in humans.[14]
The flies were fed a sucralose-sweetened diet for 5 days. This caused an increase in food intake. It returned to normal only after removal of sucralose from the diet. Sucralose also increased the sensitivity of these flies to sweet taste. This again was a reversible effect. To rule out the possibility that it was some property of sucralose, and not sweet taste in general that was causing this effect, the researchers used L-glucose, another non-caloric agent that tastes sweet to flies. L-glucose had the same effect as sucralose. This confirmed that sweet taste in and of itself was leading to increased food consumption. The sucralose-fed mice also exhibited impaired glucose homeostasis. They were also hyperactive and had fragmented sleep. These effects have been reported in humans in connection with aspartame, another NNS.[15]

Fruit flies fed sucralose showed a variety of negative effects, including increased food intake and altered glucose homeostasis.

Having demonstrated that sucralose increases appetite in the flies, a key question remained. Was the effect of sucralose on the flies due to sweet taste itself? Or due to an imbalance between sweet taste and the actual energy content of food?
To answer this question, experiments compared sucralose head-to head with regular table sugar (sucrose). Sucralose increased food intake. Sucrose, which also tasted sweet to the flies but contained calories, decreased food intake. This suggested that sucralose increased food intake by creating an imbalance between sweetness and calorie content. If this were the case, supplementing the sucralose fed flies with an additional agent that has calories, but no sweet taste, might restore the balance of sweetness vs. energy content. Thus negating the increase in appetite. This is precisely what happened. Researchers gave the sucralose group sorbitol. This is a sugar alcohol that contains calories but does not taste sweet to fruit flies.

Taken together, these results pointed to a conclusion. That decoupling sweet taste from energy intake increased appetite and food consumption. But what was the mechanism? The researchers found an answer through an extra series of experiments. They found that long-term ingestion of sucralose-sweetened food activated the enzyme AMPK in the neuronal system. This caused certain cells to produce NPF, a neuropeptide that promotes hunger. This same signaling pathway was activated by fasting. Indicating that the consumption of synthetically sweetened food created a sweet taste vs. energy imbalance. This mimicked the effects of fasting on the brain.
Experiments in mice mirrored results in the flies. 7 days of sucralose consumption in mice significantly increased food intake. This means that from flies to mammals, decoupling sweet taste from the energy content of food can induce a neuronal fasting response. This conspires to increase appetite and food consumption.

Experiments in flies and mice showed that sucralose can increase food intake, through creating an imbalance between sweet taste and energy intake.

So … is it time to sound the alarm on artificial sweeteners?

Evidence from the Wang et al study suggests that creating an imbalance between sweet taste and calorie influx is bad. It could weaken the ability of sweet taste to be perceived as energy intake. Instead triggering a contradictory fasting response that increases appetite.

In other words, it’s like “The Boy who Cried Wolf”. Chronic intake of non-nutritive sweeteners could create a bad situation. Where the brain no longer ‘believes’ that a sweet taste is connected to an influx of energy. If this occurs in humans, it raises a dire possibility. That those using lots of artificial sweeteners could be at risk for unintended weight gain.

This idea is in line with the earlier published studies connecting NNS intake to increased appetite and weight gain in humans. But it is a hard one to prove. The mechanism uncovered by Wang et al has yet to be validated in human subjects. The fact that this novel ‘neuronal fasting pathway’ that integrates hunger, sweetness, and the nutritional content of food is intact from fruit flies to mammals does suggest that it may be time to wave the caution flag where NNS are concerned (after all, humans are mammals!). It is important to emphasize, though, that human studies on NNS and appetite regulation have reported mixed results[16]. This suggests that some individuals may be more affected than others (if at all). And at this point we can only speculate. A Splenda or two in your daily coffee probably is not an issue. But we need to take a closer look at the effects of chronic, high-level NNS intake in certain populations. Especially those that may be more predisposed to obesity or metabolic dysfunction.

Decoupling sweet taste from the usual increase in calories, if it occurs with NNS use, may undermine the ability of some to control food intake. NNS-induced increases in appetite could go unnoticed, leading to unexplained weight gain over time.

Thanks to the good folks over at for this article. Here is a link to the original article that appeared there: 

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