r/keto•
FromageOmage

Why does Keto allow artificial sweeteners?

I've been thinking about moving from Paleo to Keto which as most of you know is not a huge change but mostly just a change in mindset. May of the low-carb diets like Paleo warn against sweeteners both natural and artificial saying that even carb free sweeteners can spike insulin. Why does keto allow some where other programs don't?

Thanks!

Posted Oct 15, 2012, 4:24 AM UTC

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aczkasow•

Because there are sweeteners which do not take part in metabolism (just filtered directly to urine and sweat), therefore can't strike ones insulin.

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FromageOmageOP•

That is true on the metabolic level but many in the Paleo community believe that even when something is not providing any actual carbs, the body will still respond to the sweetness with an insulin spike. In my short search, I couldn't find anything specific to cite but I know it's a mantra the trainer at my gym harps on. I'll look for something in writing tomorrow when I'm more awake.

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goggeCONSISTENT COMMENTER•

Artificial sweeteners by themselves doesn't cause an insulin response in any studies I've seen, but it might be that people have conditioned themselves to get one from artificial sweeteners. So it's possible that some people might need to be careful around artificial sweeteners while "unlearning" the response, but for the vast majority there shouldn't be any insulin related issues.

Mark has a more thorough article, "Do Artificial Sweeteners Cause an Insulin Spike? ".

From another thread:


Seems like you can probably get an insulin response if you've conditioned yourself to it.

Cephalic phase responses can also be stimulated by Pavlovian conditioning; i.e. animals can learn to associate arbitrary sensory stimuli with the availability of food, and then will react as if the food itself has been perceived. For example, insulin secretion in anticipation of feeding can be associated with other environmental stimuli, such as time of day, sounds, visual cues, or tastes (e.g. Woods et al., 1977). Rats fed at a certain time everyday begin to secrete insulin time locked to a circadian clock (Woods et al., 1970; Dallman et al., 1993).

"Anticipatory physiological regulation in feeding biology: cephalic phase responses", Power ML, Schulkin J. Appetite. 2008 Mar-May;50(2-3):194-206. Epub 2007 Oct 24.

It's in animals, but skimming abstracts from other studies says the same for humans:

Reviews studies considering whether hyperinsulinemia and its resultant effects on adipose tissue mass can alter perceived hunger, taste, and food consumption.

...

They show that high acute levels of insulin can be produced by simply seeing and thinking about food and that individuals showing this response show a greater tendency toward weight gain in a food-abundant environment.

"Insulin levels, hunger, and food intake: an example of feedback loops in body weight regulation". Rodin J. Health Psychol. 1985;4(1):1-24. (no free source)

The conditioning should wear off after a while (or it might have already worn off) if you don't keep reinforcing it by eating when you get the urge. You have more stable blood sugar on Keto which helps with self control, which might add to why you have an easier time controlling it now.


And from yet another thread:


From what I can find it seems that you are right that sweeteners doesn't give an insulin response. Studies quoted are for Aspartame, Saccharin and Sucralose (Splenda).

Twelve normal subjects and 10 subjects with non-insulin-dependent diabetes mellitus were given, in random order at intervals of greater than or equal to 1 wk, three drinks of the same beverage: one unsweetened, one sweetened with 400 mg aspartame, and one sweetened with 135 mg saccharin. The amount of sweetener approximated that in 1 L of sugar-free soft drink. Plasma glucose, insulin, and glucagon were measured for 3 h after ingestion of the test beverage. Plasma glucose declined slightly throughout the test period, probably due to fasting, with no differences between the three treatments. Neither sweetener affected peak insulin levels in subjects with or without diabetes.

"Response to single dose of aspartame or saccharin by NIDDM patients".

Because large doses of phenylalanine stimulate prolactin secretion in man, we studied the acute effects of oral doses of aspartame (0.534 g, equivalent to the amount of aspartame in approximately 1 L beverage), aspartic acid (0.242 g), and phenylalanine (0.3 and 1.0 g) on serum prolactin and other hormones in normal humans. Prolactin was not stimulated by any of the aspartame meals, aspartic acid, or 0.3 g phenylalanine; a small rise in serum prolactin, similar to that produced by a high-protein mixed meal, followed ingestion of 1.0 g phenylalanine. Serum growth hormone showed no statistically significant changes in response to any of the experimental meals whereas cortisol and insulin fell slightly and glucose rose slightly during each of the meals. We conclude that these doses of aspartame do not alter secretion of prolactin, cortisol, growth hormone, or insulin in normal individuals.

"Aspartame and its constituent amino acids: effects on prolactin, cortisol, growth hormone, insulin, and glucose in normal humans". Emphasis added.

METHODS: Fasted subjects were studied on 4 study days in random order. Subjects consumed 50 ml of either water, sucralose (0.083% w/v), a non-sweet, glucose-polymer matched for sweetness with sucralose addition (50% w/v maltodextrin+0.083% sucralose) or a modified sham-feeding protocol (MSF=oral stimulation) of sucralose (0.083% w/v). Appetite ratings and plasma GLP-1, PYY, insulin and glucose were measured at regular time points for 120 min. At 120 min, energy intake at a buffet meal was measured. CONCLUSIONS: At this dose, oral ingestion of sucralose does not increase plasma GLP-1 or PYY concentrations and hence, does not reduce appetite in healthy subjects. Oral stimulation with sucralose had no effect on GLP-1, insulin or appetite.

"Effects of oral ingestion of sucralose on gut hormone response and appetite in healthy normal-weight subjects". Emphasis added.

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ashsimmonds/r/ketoscience and ketopedia.com - dig the science of keto•
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goggeCONSISTENT COMMENTER•

Pepsi max contains Acesulfame Potassium (Acesulfame K), which could give an insulin response (no good studies on this in humans that I can find). It might be a cephalic response, it might not be related to insulin at all. As the blood glucose levels remained constant it likely wasn't a direct insulin response, could be related to caffeine causing increased gluconeogenesis and the slight elevation of insulin to manage that response. Or it might just be random daily fluctuations.

Another question would also be "what's the actual consequence?". Does this impact anything? What about the insulin response from eating a piece meat? Andreas' opinion of optimal range for ketones seems to be around 1.5 to 3 mmol/L and the ketone levels was above 2 during the whole test.

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aczkasow•

Just revised Wiki, looks like some researches do conclude that artificial sweeteners could increase insulin level. However, insulin is not bad by itself, high blood sugar level is.

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SexBobomb24M, 6'5" CW: 266 SW: 310 SD: Sept 13 2012 GW 210•

Because keto is just a diet focused on attaining a result through a set metabolic reaction that sweeteners do not effect. There are no peer-reviewed documents supporting an insulin spike. You can keto however you want, there's no point in forcing a limitation into a diet that doesn't effect the mechanism of the diet. Similar to how some people will keto with meat and vitamins while others will keto vegan style and never need a suppliment. There's no reason to restrict something artificially outside of the context of the mechanism of the diet.

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[deleted]•

http://www.ncbi.nlm.nih.gov/pubmed/17495045?dopt=Abstract

Our observation that artificial sweeteners are nutritionally active, because they can signal to a functional taste reception system to increase sugar absorption during a meal, has wide implications for nutrient sensing and nutrition in the treatment of obesity and diabetes.

http://www.ncbi.nlm.nih.gov/pubmed/15667333?dopt=Abstract

In the small intestine, there is a highly coordinated expression of sweet taste receptors and gustducin, a G-protein implicated in intracellular taste signal transduction, throughout the gut. The potential involvement of these receptors in sugar sensing in the intestine will facilitate our understanding of intestinal nutrient sensing, with implications for better nutrition and health maintenance.

Basically there's a very notable lack of investigation into this matter currently, and that's because nobody wants to fund it. The above links though do show very tentatively that taste alone can trigger metabolic and hormonal reactions in mammals. I'm not aware of any completed trials with human subjects, but I do know that at least one is currently being undertaken.

None of this is conclusive, and the bottom line is that nobody knows anything. For my part, I don't find artificial sweeteners particularly enticing anyway, and so the decision for me is an easy one.

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FromageOmageOP•

Thanks for all the great feedback and providing the citations I was going to get to today! :)

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