Repost: Noncaloric sweeteners might not be the solution either

July 7, 2010

It seems like an opportune moment to revisit this post, for some reason or other.


The American Heart Associations recommendation to cut down on dietary sugar is all over the news. Discussion of this by Isis the Scientist triggered a comment from Callinectes :

Someone reading this may therefore assume diet drinks with Aspartame, Splenda, etc. may be okay because it’s 0 calories and added “sugar”. Can anyone comment authoritatively on this? The way I see it, it’s still just empty calories and not very good for you when consumed regularly on a weekly or (heaven forbid) daily basis.

To which Isis responded:

One might argue that diet drinks still activate the “Hedonistic food pathways” in the brain (centers in the ventral tegmental area and nucleus accumbens) that lead us to associate reward with food intake, causing us to take in more energy-dense food… That said, I don’t know of any multi-variate studies comparing risk between sugar drinks, diet drinks,… let’s be clear that Aspartame and Splenda are zero calorie sweeteners, meaning they would technically not contribute to the AHA’s recommended daily intake.

I am reminded of what I think of as a reasonably provocative series of observation from Susan Swithers and Terry Davidson at Purdue.


One of their more recent takes on this story is found in the following paper:
A role for sweet taste: calorie predictive relations in energy regulation by rats.
Swithers SE, Davidson TL.
Behav Neurosci. 2008 Feb;122(1):161-73. [DOI]
Swithers08-Fig1.jpg
Fig1: Cumulative body weight gain across 5 weeks
exposure to sweet predictive, sweet nonpredictive,
or sweet predictive control diets.
Error bars represent standard error. *p  .05.
The model is reasonably simple to understand. They offer rats the opportunity to consume up to 30 g of plain yoghurt (0.6 kcal/g) in addition to their standardized lab chow, six days per week. On three of these days, the yoghurt is sweetened with either glucose (20% wt/wt; 1.2 kcal/g) or saccharin (0.3% wt/wt). A control group received the three glucose-sweetened yoghurt sessions but not the three unsweetened yoghurt sessions to equate caloric intake with the saccharine group. As we see from the first figure, the rats in the saccharin group (non-predictive) gain more weight than do the rats in the glucose group (predictive) or the control group. They also ended up with increased bodyfat assessed by dual energy x-ray absorptiometry. Yet, the groups did not differ in yoghurt intake, nor total caloric intake (chow + yoghurt).
Nevertheless, the second experiment suggested a disruption of feeding regulation may still be present, you just have to tease it out. In glucose-trained animals a brief pre-meal of palatable Ensure reduced subsequent chow intake relative to when no pre-meal was provided. In the saccharine-trained animals the pre-meal did not suppress later chow feeding. So perhaps the numerical increase in total caloric intake which was not found statistically reliable in the analysis of the long-term training was nevertheless driving part of the observed effect on bodyweight. [This is a reminder to always look at the data and not be driven by the tyranny of the statistical finding.]
The statistically reliable effect shown in the pre-feeding experiment, and the numerical increase in caloric intake during training, both suggest a behavioral disregulation with implications for human dieting. It may be that chronic intake of noncaloric beverages leaves people insensitive to normal compensatory mechanisms involved in eating. To make a long leap from the second experiment, that candybar you eat at 4pm may reduce the amount you eat at dinner at 6pm if you are a sugared soda drinker but not if you consume noncaloric soda.
The group has worked a bit on additional parts of the saccharine effect as well. In this particular paper, they looked at periprandial body temperature, which cited work indicates is triggered by sensory aspects of ingestion rather than caloric absorption. Figure 8 compares body temperature in the hour after yoghurt ingestion for the three sweetened condition days versus the three unsweetened condition days. The addition of glucose to the yoghurt drives a lasting elevation of body temperature that is not seen in the other conditions. Although this is equivocal (being tied to the extra caloric content) additional experiments showed that, for example, when given the same pre-meal detailed above, the non-predictive saccharine trained rats generated a lower body temperature response and less locomotor activity in the first 30 minutes. This would also tend to support their hypothesis of a disruption in the processes triggered by the orosensory properties of consuming palatable foodstuffs. Although I would wish to know a little more, the dumb interpretation is that an attenuation of both higher body temperature and activity following high-calorie food would have an undesirable effect when it comes to weight regulation.
Swithers08-Fig8.jpg
Fig 8. Changes in core body temperature over the first 60 min following yogurt presentation during sweet predictive (A) or sweet nonpredictive (B) training. Error bars represent standard error. *p  .05.

I’ll close by noting that another recent paper from the group extends the basic observation to an additional noncaloric sweetener (AceK) and base foodstuff (refried beans; Isis, I swear I am not making that up)
General and persistent effects of high-intensity sweeteners on body weight gain and caloric compensation in rats.
Swithers SE, Baker CR, Davidson TL.
Behav Neurosci. 2009 Aug;123(4):772-80. [DOI]
__
*Discl: I am professionally acquainted with at least one of the authors.
Swithers, S., & Davidson, T. (2008). A role for sweet taste: Calorie predictive relations in energy regulation by rats. Behavioral Neuroscience, 122 (1), 161-173 DOI: 10.1037/0735-7044.122.1.161
Swithers SE, Baker CR, & Davidson TL (2009). General and persistent effects of high-intensity sweeteners on body weight gain and caloric compensation in rats. Behavioral neuroscience, 123 (4), 772-80 PMID: 19634935

No Responses Yet to “Repost: Noncaloric sweeteners might not be the solution either”

  1. speedwell Says:

    Very interesting. As a diabetic (T2) who does not use aspartame, acesulfame potassium, or sucralose, I wonder if the effect also exists with a different class of sweeteners, the sugar alcohols. I use erythritol and xylitol about 30 and 70 percent of the time, respectively, and I have not, subjectively, noticed changes in my weight loss. On Metformin and l-theanine my satiety levels vary. (Metformin has a known mild “anorexic” effect, not to be confused with anorexia nervosa, and l-theanine works to reduce my “anxiety eating”.) But I have noticed cravings after having a diet Chick-Fil-A lemonade, which is sweetened with Splenda, and no cravings after having homemade lemonade made with the equivalent amount of lemon juice and a sugar alcohol.

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  2. speedwell Says:

    Still thinking about this. Do you know of any studies like this done specifically on individuals with insulin resistance or other blood glucose issues? Satiety and blood glucose measurements done on individuals maintaining normal glucose levels because they have an adequate insulin resistance frankly have little relevance to diabetics like me.

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  3. Ed Terry Says:

    After I gave up all sweeteners several months ago, a lot of foods that were sweet became too sweet. I have yet to find a biological explanation for this change in perception. I have found that I’ve lost all cravings for anything sweet.

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  4. FrauTech Says:

    The thing I see here is people are always trying to say “it’s calories in vs calories out”. Clearly not the case here.

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  5. otskeptic Says:

    These attempts to draw conclusions from secondary effects in a species as different physiologically and psychologically from humans as rats are a complete waste of time. I can’t believe that anyone is engaging in such sophistry.

    Like


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