These topics should get you started…
[One more]
Studies showing Sweeteners that Raise Insulin Levels?
Alecmcq
(Alec)
#13
I did a series of live tests for this if you’re interested…
And there were others…
AuntJane
(Jane Srygley)
#14
Thank you! I so appreciate all the input on this thread!
I would have to say I did my own “self experiment” 2 days ago. I’ve been counting calories very well but lately have not been so careful. I made 12 of these wonderful chocolate coconut protein things sweetened with stevia and erythritol.
2 days ago I ate 7 of them. I just couldn’t stop. They have nearly 7g of protein each and I guarantee you I could not eat 7 eggs in one sitting!
So whether or not they trigger blood sugar or insulin, they definitely trigger me from an addictive/overeating perspective. I am interested in the insulin connection though and why they are so addictive for me. Thanks again everyone 
CFLBob
(Central Florida Bob )
#15
That’s a real puzzle. Well, maybe the second puzzle behind insulin effects. I heard on one of the podcasts I listen to that one of the problems with the home insulin measurement meter development is that insulin is more pulsatile during the day than blood sugar. I gather it varies for reasons that aren’t completely known. That makes checking meters against other tests harder. Because of that, a single fasting insulin test isn’t as meaningful as we’d like.
The other effects in the body coming from the small intestine are puzzling to me. I notice other people talking about cravings. I have a tendency to crave sweets, but no sweetener I’ve tried makes me worse at that. I get careless about that with erythritol because it seems harmless. I will put a teaspoon in my tea, for example, and then lick the spoon. It’s just a little more than I was having already, after all.
I used to wisecrack at work when donuts came around that, “I’m allergic to donuts. They make me break out in fat”. If the only small intestine-mediated reaction to a food was that it made it harder to lose weight, how would you know other than eliminating everything and adding stuff back?
Digital_Dave
#16
Thanks, Carol. Actually thought I put it in ‘Show me the Science?’ … But was tired when I did it. 
Thanks for the links too. Will be checking them out when I get the chance.
I remember reading through these when you did them back in the day. 
We have actually talked about doing just this, but haven’t as of yet. I did purchase some of the Powdered Erythritol, but think they were sold out of the Brown Sugar Swerve at that time? But I will probably purchase some at one point or another. I like to experiment to see what works best as well. And like you, I don’t find that many of the ones I’ve tried affects me either? But again, I’m still prefer to keep them to a very limited use as well. The most I’ve been using lately is the Liquid Stevia for when I want to add some to Iced Tea. I drink it as is as well, but do like to mix it up and have some sweetened Tea at times too.
You’re quite welcomed and you’re not the only one as you can see. 
A lot of folks speak about these issues from time to time and it would be good to know indeed. … One of the things I’ve noticed, both on my own and reading others post, is that simply keeping sweet treats in the mix, whether Keto or not, simply keeps that sweet tooth around, so folks tend to keep wanting more. - I personally don’t do a lot of things, such as Fat-Bombs, etc. Not just for this purpose, but simply don’t desire them as much as I probably did before? But instead will just do a couple squares of 92% Ghirardelli Dark Chocolate with most meals. This is not overly sweet, and I think by consuming this on a semi-regular basis, may even help to keep the sweet-tooth as bay more-so then if I were doing sweeter things? Again, this may be conjecture on my part, but it does seem to be doing just this overall. :slight_smile
carolT
#17
I’m going to add a couple of things here re: gut incretins.
First, a post I wrote about how fructose acts on the GIP sensor to potentiate the insulin response to glucose while not being particularly troublesome when ingested by itself.
Some studies summarizing the role of incretin sensors in hunger regulation
A recent study showing how processed foods increase appetite and corresponding measurements of incretins. Small but highly controlled study: ultra-processed foods hijack health - 5/16/19 Journal of Cell Metabolism
carolT
#18
Just one more thing…
GIP and GLP-1 sensors work in opposition to each other regarding inflammation. GIP increases it, GLP-1 decreases it. I’m still formulating a post about this aspect of foods and incretins and how inflammation and the immune system are directly related to IR.
David_Stilley
(Full Metal KETO AF)
#19
You’re looking at glucose levels if you’re testing for a reaction, you can’t test insulin at home.
Erythritol seems to be the best,
You may still lose some weight using them but they definitely have an effect on your metabolism and insulin response.
atomicspacebunny
(Bunny)
#21
Looking at that chart, looks like a wolf in sheep’s clothing.
My personal rule of thumb, if it is a man-made substance don’t eat it, it will kill you much faster, eventually!
Simply put, the research on artificial sweeteners has too many wolves doing the research and not enough sheep?
David_Stilley
(Full Metal KETO AF)
#22
Erythritol is a naturally occurring substance found in many fruits and vegetables. It’s man made in the same respect that Morton Salt is man made, (manufactured actually). Erythritol is made by a bacteria digesting starch similar to the way xanthan gum and transglutaminase are made, not a man made substance. Technically I guess it’s a fermentation process. These compounds occur in nature.
atomicspacebunny
(Bunny)
#23
Here is the problem; you want to have a little minor spike in insulin from natural unfreed fructose (when encased in its natural form, such as in fruit and vegetables) that occurs in nature to tell your liver to not go into a constant state of gluconeogenesis because you want to increase your HOMA-IR insulin sensitivity not kill it off completely with a constant steady supply of glucose hence chronically elevated levels of insulin?
In other words excessive protein will constantly spike insulin however minor but constant and steady and eating natural sugars turns off or inhibits the gluconeogenesis via minor insulin secretions. And yes you still remain in ketosis! If your body needs glucose it is going to pull it from your glycogen storage, glycerol from fatty acids or lactate through the cori cycle so why would you want to supply it with the additional gluconeogenesis?
References:
[1] “…The scientific name is “physiologic insulin resistance” and it’s a good thing — unlike “pathologic insulin resistance.” As regular visitors will know from Dr. Jason Fung, Dr. Ted Naiman, and Ivor Cummins, the “pathologic” kind of insulin resistance is caused by higher and higher levels of insulin — hyperinsulinemia — trying to force glucose into over-stuffed cells. That insulin resistance is a prominent feature of type 2 diabetes, polycystic ovarian syndrome (PCOS) and other chronic conditions. So let’s call physiologic insulin resistance instead “adaptive glucose sparing,” a name that has been proposed by many to reduce the confusion. Dr. Ted Naiman describes it as muscles that are in “glucose refusal mode.” Prior to converting to the ketogenic diet, your muscles were the major sites to soak up and use glucose in the blood for energy. On the long-term keto diet, however, they now prefer fat as fuel. So the muscles are resisting the action of insulin to bring sugar into cells for energy, saying, in essence: “We don’t want or need your sugar anymore, so move it along.” Hence, the slightly elevated, but generally stable, glucose circulating in the blood. Where is that glucose coming from when you consume no sugar and only leafy veggie carbs in your diet? Your liver, through gluconeogenesis — the creation of glucose from non-carbohydrate sources such as lactate, glycerol, and glucogenic amino acids from proteins. It is a natural protective process that got homo sapiens through hundreds of thousands of years of feasts and famines. “There is no essential requirement for dietary carbohydrate because humans possess a robust capacity to adapt to low-carbohydrate availability,” says Dr. Jeff Volek. In the liver of a keto-adapted person, he notes: “ketone production increases dramatically to displace glucose as the brain’s primary energy source, while fatty acids supply the majority of energy for skeletal muscle. Glucose production from non-carbohydrate sources via gluconeogenesis supplies carbons for the few cells dependent on glycolysis [using sugar for energy.]” …” …More
[3] “…When the body once again enters the absorptive state after fasting, fats and proteins are digested and used to replenish fat and protein stores, whereas glucose is processed and used first to replenish the glycogen stores in the peripheral tissues, then in the liver. If the fast is not broken and starvation begins to set in, during the initial days, glucose produced from gluconeogenesis is still used by the brain and organs. After a few days, however, ketone bodies are created from fats and serve as the preferential fuel source for the heart and other organs, so that the brain can still use glucose. Once these stores are depleted, proteins will be catabolized first from the organs with fast turnover, such as the intestinal lining. Muscle will be spared to prevent the wasting of muscle tissue; however, these proteins will be used if alternative stores are not available. …More
[4] “…The major site of gluconeogenesis is the liver, with a small amount also taking place in the kidney. Little gluconeogenesis takes place in the brain, skeletal muscle, or heart muscle. Rather, gluconeogenesis in the liver and kidney helps to maintain the glucose level in the blood so that brain and muscle can extract sufficient glucose from it to meet their metabolic demands. Go to: 16.3.1. Gluconeogenesis Is Not a Reversal of Glycolysis: In glycolysis, glucose is converted into pyruvate; in gluconeogenesis, pyruvate is converted into glucose. However, gluconeogenesis is not a reversal of glycolysis. Several reactions must differ because the equilibrium of glycolysis lies far on the side of pyruvate formation. The actual Δ G for the formation of pyruvate from glucose is about -20 kcal mol-1 (-84 kJ mol-1) under typical cellular conditions. Most of the decrease in free energy in glycolysis takes place in the three essentially irreversible steps catalyzed by hexokinase, phosphofructokinase, and pyruvate kinase. …” …More
CFLBob
(Central Florida Bob )
#24
Right. Glucose is a proxy measurement for insulin. If you’re fasted, and doing your best to limit the experiment to one variable, which is how the test is setup, it’s reasonable to think that if your insulin goes up your blood glucose will go down in response, and maybe even vice versa. I expect the magnitude of that effect depends on the person and how insulin resistant they are, but it’s the only measurement I have. If that original experiment had the blood glucose to go along with the insulin tests you showed, I’d expect to see it mirror that insulin curve, going lower instead of higher.
I come from a background where people say, “half a measurement is better than none”. While I like that idea, just keep in mind it’s half a measurement and always be looking for a better way.
Which one? Erythritol? That’s a compound occurring in several places in nature. Wikipedia says it was first isolated in 1852, and in 1950 it was produced from blackstrap molasses. Today it’s produced by fermenting with yeast, like wine is “manufactured”. The yeast ferments glucose, just like the brewer’s yeast, but it produces something other than alcohol.
While I’m with you on avoiding man made foods, I find those definitions more complicated than it seems most people do. I don’t see extracting xylitol from birch bark as being “man made”; I see extracting a seed oil, hydrogenating it, and doing other things to it as man made. I don’t see much difference between extracting oil from an olive and extracting the xylitol from bark.
atomicspacebunny
(Bunny)
#25
Erythritol acting as if it were HFCS are not triggering insulin, I‘m wondering how that is natural?
atomicspacebunny
(Bunny)
#27
HFCS does not trigger insulin and in high amounts, the liver takes that type of sugar and stores it directly as visceral fat. If Erythritol is not triggering insulin then what is it doing?
CFLBob
(Central Florida Bob )
#28
I don’t know of evidence for erythritol having that effect. The articles on it I’ve seen are consistent that we can’t metabolize it. As for what it’s doing, it appears it’s passing through our bodies unchanged. FWIW, Wikipedia says
most erythritol is absorbed into the bloodstream in the small intestine, and then for the most part excreted unchanged in the urine. About 10% enters the colon
and
Erythritol has no effect on blood sugar or blood insulin levels
atomicspacebunny
(Bunny)
#29
I can just imagine the bioaccumulation damage that might doing to the gut flora microbiome to make one glucose intolerant leading to more hepatic insulin resistants rather than skeletal muscle insulin resistance.
CFLBob
(Central Florida Bob )
#30
It’s conceivable. Bacterial populations are quick to adapt to changes in their environment.
Everyone talks about how important gut flora is, but the paucity of actual hard science (RCTs) is depressing.
carolT
#31
GNG only kicks in when glucose needs can’t be met from the other methods, not in addition to it. Liver glycogen is depleted in ketosis, so not a source of glucose; muscle glycogen does not release glucose back into the blood stream, it saves it for muscles; the cori cycle is used when muscles are being worked at an intensity sufficient to produce lactic acid (the burn); glycerol is torn from fatty acids during beta oxidation of fatty acids, which is part of the Krebs (TCA) cycle requiring sufficient OAA. Inadequate OAA is prerequisite for ketosis and results in production of glucose from fat by a pathway outside of the Kerbs cycle.
You are not going to run out of adequate glucose for bodily functions by depleting liver glycogen and being in ketosis. GNG alone will create sufficient glucose to replenish muscle glycogen overnight as well as supply glucose to the brain and red blood cells.
Over production of glucose can be triggered by a skewed insulin/glucagon ratio or by the removal of ketones from the blood by insulin response to a substance like a non-nutritive sweetener or a protein bolus. If ketone production is suspended long enough, the brain will sense an energy shortage and demand more glucose to compensate, thus triggering GNG.
After several days of starvation [I prefer the term “carbohydrate fasting”], ketone bodies become the major source of fuel for the heart and other organs. As starvation continues, fatty acids and triglyceride stores are used to create ketones for the body. This prevents the continued breakdown of proteins that serve as carbon sources for gluconeogenesis. Once these stores are fully depleted, proteins from muscles are released and broken down for glucose synthesis. Overall survival is dependent on the amount of fat and protein stored in the body.More…