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I was amused by this post at Paleo Velo. Here's a snippet:

[Another nail in the coffin] of the carbohydrate obesity thesis? Check out Stephen Guyenet’s latest post about a new study that finds that sugar has to be palatable to be fattening in mice. In other words, despite an increase in calories from sugar water, mice whose sugar receptor taste buds had been knocked out did not gain weight like normal mice. Whatever conclusions different people might draw from this study, I think it goes to show that, however fat gain and loss works, it is just a heckuva lot more complicated than the carbohydrate-insulin obesity thesis most recently popularized by Gary Taubes.

The Guyenet post, New Study Demonstrates that Sugar has to be Palatable to be Fattening in Mice, is here.

Dr. Anthony Sclafani's research group just published a study definitively demonstrating that high palatability, or pleasantness of taste, is required for sugar to be fattening in mice (1). Dr. John Glendinning was lead author. Dr. Sclafani's group has done a lot of excellent research over the years. Among other things, he's the person who invented the most fattening rodent diet in the world-- the 'cafeteria diet'-- composed of human junk food.

What do you think of this new line of research? Does it blow your mind? Can we screw with human brains to not taste sugary carbs so that we can all consume crap while staying lean?

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 I guess, but the only reason why you'd be able to 'consume crap while staying lean' is because of your near total lack of interest in consuming crap (because you can't taste it). So you can consume all the food that you want, so long as you don't want to consume any food. – David Moss Jun 15 at 8:17
It just goes to show that New York subway rats have figured out how to get the most rewarding food...follow the commuters and they'll throw you what you want... – thhq Jun 15 at 11:22
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 I was going to comment but then realised David Moss said everything I was going to in an even more concise way... – Michael Jun 15 at 11:38
Just because the mechanism elucidated by Atkins/Taubes/Eades is incorrect, doesn't mean that low(ish) carb diets aren't effective for weight loss. Protein blunts hunger and ketogenesis is anorectic. Simply google scholar "protein hunger" or "psmf" for plenty of evidence. Of course, not eating crap helps. – Dave S. Jun 15 at 13:20
The difficulty is that temptation is everywhere. It's cheap and easy. I can't tell you how many times I've heard "No time to cook tonight, do you want burgers, pizza or chinese?" – Dave S. Jun 15 at 13:23
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6 Answers

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As to your comments, but if you can't taste the sugar who is going to want to eat the crap? We eat crap cause it tastes good. Take away the taste and no one will want it.

The study is interesting though. What it has to do with taking down insulin theory but it's definitely interesting. I think it clearly helps support the idea of palatability playing a part in obesity.

(Stephan really needs to stay away from "d" words. Dominant. Definitive. Saying anything is "definitive" using one study is pretty silly.)

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Absence of other options, perhaps? I'd hate to be stuck in that situation, but ya never know – Matthius Jun 15 at 8:23
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 My father-in-law lost his taste for food (everything started tasting weird) after an operation. He lost a fair bit of weight, until he got his taste buds back. – Dave S. Jun 15 at 13:10
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Mice are mice, not people...although it is said that cats cannot taste sweet, but I know plenty of obese house cats

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 And, of course, cats are neither mice nor people, cats being vastly superior to both. Whenever anyone trots out animal studies, regardless of their nutritional perspective, I just roll my eyes and mumble 'whatever' under my breath. The only animal study relevant to me is my own N=1. – Alex Jun 15 at 11:49
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Not necessarily. Here's a comment from Guyenet's post:

"George Henderson said...

Do sweet taste receptors cause obesity by inducing insulin secretion? This paper seems to reconcile food reward with the insulin hypothesis:

Diabetes Metab J. 2011 Oct;35(5):451-7. Epub 2011 Oct 31. The Role of the Sweet Taste Receptor in Enteroendocrine Cells and Pancreatic β-Cells. Kojima I, Nakagawa Y. SourceLaboratory of Cell Physiology, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Japan.

Abstract The sweet taste receptor is expressed in taste cells located in taste buds of the tongue. This receptor senses sweet substances in the oral cavity, activates taste cells, and transmits the taste signals to adjacent neurons. The sweet taste receptor is a heterodimer of two G protein-coupled receptors, T1R2 and T1R3. Recent studies have shown that this receptor is also expressed in the extragustatory system, including the gastrointestinal tract, pancreatic β-cells, and glucose-responsive neurons in the brain. In the intestine, the sweet taste receptor regulates secretion of incretin hormones and glucose uptake from the lumen.In β-cells, activation of the sweet taste receptor leads to stimulation of insulin secretion. Collectively, the sweet taste receptor plays an important role in recognition and metabolism of energy sources in the body."

If sugar taste receptors were knocked-out on the taste-buds, they were knocked-out in the pancreas as well, which means no insulin response.

Also, rats overfed with a gastric feeding tube gain weight even though they can't taste any of their food:

http://www.ncbi.nlm.nih.gov/pubmed/17185893

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 Correct me if I'm wrong, but won't there still be a substantial insulin response once the sugar is registered in the digestive tract? I understand that sweet-receptors on the tongue account for part of the insulin response, but I was under the impression that the main response was due to uptake in the small intestine. – Matthius Jun 15 at 8:21
Excellent points, easily forgotten. Seems clear that this cannot just be 'reward'/palatability, but must involve lots of other physiological processes. – David Moss Jun 15 at 8:29
"The WT and Tas1r3 KO mice overconsumed the Polycose diet and became obese. The WT and Tas1r3 KO mice also overconsumed the Sucrose diet, but only the WT mice became obese. The Trpm5 KO mice, in contrast, showed little or no overeating on the Sucrose and Polycose diets, and gained slightly or significantly less weight than WT mice on these diets." - It would seem this study implies the opposite of what the authors concluded, that palatability has little to do with it and its insulin response (one non-weight gaining mouse group overconsumed the sucrose but did not gain weight) – Jamie Jun 15 at 12:01
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I thought the new post was fascinating. I don't think his intention is to say we should knock out human's taste receptors. Rather, he is trying to prove his setpoint/food reward theory. I agree with Shari above that he should be careful about claiming definitive off one study, but I do still think it's interesting.

I think the point is that (in theory) the perceived higher palability of the food, raised the bodyfat setpoint of the mice and made them store more fat (likely by burning less energy - slower metabolism and/or less activity) just as the theory would have predicted. It's very interesting, because the most common argument I've seen against his food reward theory is "yes, of course you gain fat on high reward foods because you eat more." But, in this case the tasteless mice and the regular mice at about the same amount of food, yet the regular mice gained more fat. I am a laymen and have not read the original research paper, so forgive me if I've misstated any details.

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When Seth Roberts tried his first experiments, and lost a lost of weight, he used fructose water. Sweet, like salt, bitter, and sour is an extremely simple taste and it doesn't signal very much by itself. You need a more sophisticated flavor and a consistent calorie payload to get a good flavor/calorie signal going. The set point begins to rise with the presence of strong signals and dependable calorie loads.

So, this has something to do with how the brain perceives and anticipates food, but it doesn't negate the idea that insulin or blood sugar is an issue. This is why I think people should adopt Seth Roberts flavor/calorie association (well, possibly flavor/physiological response because some flavors are very positive without any meaningful calorie payload) rather than using this palatability/food reward concept- Guyenet and others espouse. For some reason the latter hypothesis is encouraging people to make overstatements.

Some processed foods are still pretty bland. Skinless, boneless chicken breast tastes like cardboard. White bread is gross. There are people who eat starch of out the box. The food reward theory doesn't explain people with bland diets who are fat. The flavor/calorie association does, because it suggests the signal might be muted, but the reliability of the signal is extremely high, so the set point would move up. Meanwhile, insulin is still inside the body doing whatever it is doing, and things unarguably get worse when that system starts to break.

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This goes along nicely with the fact that livestock are fed stevia (a non-caloric but sweet supplement) to encourage greater weight gain. Something in the "sweet" is doing it. And I didn't read the study in question, but it's known that sweet taste generates insulin response regardless of the presence/absence of carbohydrates (the diet soda effect) - so I don't see how this would disprove the insulin hypothesis at all.

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Are they really? OMG! – HippiPaleo Jun 15 at 13:22
Stevia for weight gain, good to know. – HippiPaleo Jun 15 at 13:23

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