@AuntJane @CFLBob @daddyoh @adorfaru … As I mentioned earlier, I have moved this information to it’s own thread, as to not distract or take away from the ‘Centurians Thread’ … I too would like to see some science on this as well. But as I mentioned before, I do use Erythritol in making some things such as when I make Keto Cheese Cake. As well, I use some Liquid Stevia, (mostly in Iced Tea here & there) But I still try to limit sweeteners in general, but do think they have their place. Example, we also use Liquid Stevia to replace things like Brown Sugar, when making BBQ Sauce, or Stir Fry Meals.
Try the Swerve Brown Sugar blend. I got that for barbecue sauce and can almost eat it by the teaspoonful. Then I found my wife is the one in a crowd who gets GI reactions to it. None of the sugar alcohols bother me. I think they all bother her.
Very much this. We are all special little snowflakes, and the anecdotal evidence I’ve seen in Ketoland (multiple peeps consuming the same sweetened foodstuffs, then measuring/comparing their numbers thereafter) seems to bear that out. And then of course there’s the whole cast-iron-stomach folks v GI-distress-disaster-pants folks thing…
Moved it to Show Me the Science for ya. I’ll dig up some links.
Just like to add that not all the effects of sweeteners are glucose or insulin related. The sensors in the small intestine are connected to the brain via the vagus nerve, in addition to the pancreas etc. so even non-nutritive additives do something. Exactly what is a big grey fuzzy area and best left to individual subjective testing.
Some sweetener tests are conducted by adding the test substance to a meal (one with carbs in it). The action of some sweeteners on the intestinal sensors will increase the insulin response to glucose in the same meal.
These topics should get you started…
I did a series of live tests for this if you’re interested…
And there were others…
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
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?
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
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.
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
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.
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.
Xylitol is similar to fructose in response. Interesting!
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?
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.
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?
 “…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
 “…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
 “…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
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.
Erythritol acting as if it were HFCS are not triggering insulin, I‘m wondering how that is natural?
I don’t get the “acting as if it were HFCS”? Could you explain?
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?