Can Diet Soft Drinks Make You Fat?

D. Eric Walters, PhD


September 16, 2013

Are Artificial Sweeteners Linked to Obesity?

This question appeared frequently in the popular press this summer, when Susan E. Swithers, PhD, a professor of psychological sciences and a behavioral neuroscientist at Purdue University, published an opinion piece in Trends in Endocrinology & Metabolism titled "Artificial Sweeteners Produce the Counterintuitive Effect of Inducing Metabolic Derangements."[1]

Dr. Swithers' working hypothesis is that "consuming sweet-tasting but noncaloric or reduced-calorie food and beverages interferes with learned responses that normally contribute to glucose and energy homeostasis."[1] There is a clear correlation between obesity (expressed as change in overweight and obesity prevalence since 1962) and the change in per capita soda availability since 1962. This includes the consumption of both artificially sweetened beverages and sugar-sweetened beverages. It is interesting to note that from 1994 to 2000, consumption of sweetened beverages (both artificial and sugar) plateaued, while the overweight/obesity number climbed even more steeply.

What Do the Experimental Data Show?

Dr. Swithers examined 24 prospective cohort studies of artificially sweetened beverages and health outcomes. The risk for metabolic syndrome, type 2 diabetes, hypertension, and coronary heart disease increased with consumption of artificially sweetened beverages in many of these studies, with odds ratios ranging from 1.1 to 2.0 or hazard ratios ranging from 1.1 to 1.6. Of note, risks for these conditions also increased with consumption of sugar-sweetened beverages, with a similar range of hazard ratios.

Two intervention studies were also examined. The first, conducted in overweight and obese adults, involved replacing sugar-sweetened beverages with either water or artificially sweetened beverages.[2] Over a 6-month period, both groups lost a small but statistically significant amount of weight, and both groups had small but statistically significant decreases in systolic (but not diastolic) blood pressure. The water group had a small but statistically significant decrease in blood glucose, whereas blood glucose was essentially unchanged for the artificially sweetened beverage group.

In the second study, 641 children of normal weight, aged 4-11 years, were given either a sugar-sweetened or artificially sweetened beverage once a day for 18 months.[3] The group receiving the artificially sweetened beverage had reduced weight gain and fat accumulation, as measured by body mass index (BMI).

Other published studies have shown that:

1. There are sweet taste receptors throughout the small intestine[4] ;

2. Artificial sweeteners can increase the rate of absorption of glucose in the intestine, via trafficking of transporters[5]; and

3. Long-term (2 weeks) consumption of a high-sugar diet or of artificial sweeteners leads to an increase of glucose transporters in the intestine.[6] The latter effect was shown for sucralose, saccharin, and acesulfame K, but not for aspartame. Aspartame does not taste sweet to rats or mice, and even if it did, would likely be digested before it could exert a significant effect.

There are numerous animal and human studies published that have examined the effects of artificial sweeteners on insulin and incretin levels.[7,8,9,10] The incretins glucagon-like peptide-1 (GLP-1)and gastric inhibitory peptide (GIP) are gastrointestinal hormones that trigger insulin release and inhibit glucagon release. Most of these studies show little or no effect of artificial sweeteners on insulin and blood glucose levels, although effects on GLP-1 and GIP are sometimes seen.

Functional MRI (fMRI) studies show that the human brain can distinguish between sugars and artificial sweeteners.[11] This result would seem to undermine the hypothesis that artificial sweeteners confuse the body's link between sweetness and calories and lead to metabolic derangement. However, subsequent fMRI studies[12,13] suggest that in human subjects who routinely consume artificially sweetened beverages, there may be changes in brain response to sucrose or to artificial sweeteners in some regions, which could relate to ingestive behavior.

Interpreting the Data

Although Dr. Swithers focuses on the observation that consumption of artificially sweetened beverages correlates with risk for the metabolic syndrome, type 2 diabetes, hypertension, and coronary heart disease, the fact is that the correlation also exists with sugar-sweetened beverages. This argues against the premise of the article title.

It is obvious (and pointed out in Dr. Swithers' article) that correlation is not the same as causation. People who have type 2 diabetes or obesity may be more likely to consume artificially sweetened beverages. A few studies have tried to correct for this potential "reverse causation" by analyzing results separately for subjects with normal or high baseline BMI, but the results are mixed.

A further complication is the "permission" effect. When people know that they have consumed a noncaloric beverage, they may give themselves permission to compensate by overconsuming other foods. The calories saved by forgoing a 12-ounce can of sugar-sweetened soft drink (about 150) are almost insignificant when traded for a large order of french fries (about 500). And that's before you add ketchup, at 15 calories per tablespoon.


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