Studies showing Sweeteners that Raise Insulin Levels?


(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?


(Full Metal Keto) #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. :cowboy_hat_face:


(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

[2] Insulin Resistance is Good?

[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


(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.


(Bunny) #25

Erythritol acting as if it were HFCS are not triggering insulin, I‘m wondering how that is natural?


(Bob ) #26

I don’t get the “acting as if it were HFCS”? Could you explain?


(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?


(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


(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.


(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.


#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…


#32

HFCS at the typical 50-50 fruc/gluc seen in common beverages will definitely spike insulin. 100% pure fructose in the absence of glucose from HFCS or other starches in the same meal would cause a minimal insulin release and be exported by the liver to adipose tissue if sufficient choline is supplied for the task. Insufficient choline = liver stores fat internally = bad.


(Jane Srygley) #33

Wouldn’t blood glucose going down depend directly on the amount of insulin sensitivity in an individual? So if I am very insulin INsensitive, my blood glucose might stay high on the same amount of whatever substance while someone else who is very insulin sensitive would not experience that effect.

This is why it’s rather frustrating to me because I’d really like to know the effects of artificially sweet foods on insulin itself rather than on blood glucose. I know that stevia and erythritol don’t effect blood glucose, but if they cause an insulin response independent of glucose (perhaps due to the body “expecting” glucose due to the sweet taste), that could be a problem and stall weight loss.


#34

I would say yes.
Someone who produces normal to low insulin might not see anything noticeable, but then that person is less likely for the lower insulin response to cause a problem too.


(Bob ) #35

That’s what I would expect to see, and what you say is close to what I said in the sentence after the one you quoted

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.

The test I mention isn’t my idea. You can find videos of people doing it on YouTube, and many mentions of it online in blogs and other people’s posts here on the forums. I did it during an extended fast so that it wasn’t even the tiniest interruption to life to fast for four or five hours before doing the test. Take a reading, drink the solution, set the timer for the next test.

I like the whole “quantified self” movement and cheap, easy experiments. That means I test myself. I’m fairly sure I’m one of the many people that erythritol doesn’t affect. I also believe that there are people it will affect and the conclusion that it doesn’t affect me might possibly change in the future.


(Jane Srygley) #36

I found a study!!! Insulin is released based on taste alone, which is what I feared and also what I hope will motivate me to stop all this sweet crap.


(Bob ) #37

Let me tell you throw out an alternative view of why that study doesn’t impress me. As always, it’s just the way I see it, your mileage may vary, don’t take my word, I’m not a doctor and any other disclaimer you can think of.

First off: rats. Not people.

Second off: I side with Jason Fung’s observation that our bodies aren’t stupid. My guess is that if you did this experiment on people who are not exposed to artificial sweeteners (AS) that you’ll get similar results. My hypothesis is that as we become exposed to AS, our bodies learn that “gee, I dumped all this insulin, lowered blood glucose in response, and now my glucose is low. I need to re-absorb some of that insulin.” At some point, our bodies learn that all sensations of sweetness are not followed by usable glucose, so they learn not to go through that cycle. Someone who has been using non-nutritive sweeteners for years will have a different response from people who haven’t - and exactly what they’ve been using matters. Most powdered AS blends have some carbohydrates in them and end up at 0.5 gram or less per teaspoon equivalent.

I have exactly zero evidence for that exact sequence happening, but think it could explain why some people seem to have big effects from AS and other people don’t. I would love to see someone do such a study.

What this has going for it, though, is that it unifies how the AS, which are a group of very different molecules, could act the same way when our bodies are chemical systems at the lowest level. It also reminds me of the observation that mechanical filling of our stomachs can prompt insulin release - a fully mechanical effect and not related to chemical action at all.

FWIW


(Jane Srygley) #38

That’s a logical hypothesis but I think it assumes a lot. I think our biology is way behind the times in terms of the typical western diet. If the body were that “smart,” why wouldn’t it just adapt to a high carb diet and not allow us to become obese and/or unhealthy? Why has Type 2 Diabetes become so common? Why does inflammation go down due to ketosis? Artificial and other concentrated sweeteners are a product of our modern diet. Yes erythritol is present in nature and so is stevia, but is it “natural” to consume it in the quantities some of us on the keto diet tend to use?

I am looking into the work of Dr Benjamin Bikman, who says that insulin itself is the problem and that if you give more insulin to a type 2 diabetic, s/he will “die sooner.” I find that pretty alarming! I think it’s interesting that just filling the stomach causes a rise in insulin and to me, that shows that it’s not as simple as reducing carbs alone. Dr. Bikman is a big fan of keto, incidentally.


(Bob ) #39

Could it be it’s actually getting “rewarded” with a high carb diet? An “embarrassment of riches” - too much food - is harder to deal with than the unrewarded preparation for carbs that never come?

We’re getting away from things that can be tested by experiment when we talk about justifications. It’s like the “thrifty gene hypothesis” that used to get talked about more than it does now. It said people got fat because we were programmed through ice ages and other threats to store fat whenever possible. The ones who wasted energy and didn’t store fat when times were good died when times were tough. Nice idea, but how can you test that? And then what do you do about it? (obviously, eat keto!)

I’m familiar with Dr. Bikman - at least in the sense that I’ve watched a few of his videos. From what I know, he’s right. As Dr. Fung said, “I can may you fat. I can make anyone fat. I just give you insulin”.


(Bunny) #40

That combination right their is what’s so bad about the whole thing (yuck!). Compared to test conditions where only HFCS is used and does not trigger insulin like its friend a/k/a artificial sweeteners.

The other processed sugar like table sugar or cane sugar mixed with beet sugar (refined/bleached) so it looks pretty and has all nutrients and now rare trace elements removed like vital minerals and some vitamins.

Here is a small list below (what is supposed to be in natural sugar but IS NOT when it is refined), now what happens when you go on a ketogenic diet; WHAT GETS DEPLETED?

  • Vitamin B6: 14% of the RDI.
  • Calcium: 8%of the RDI.
  • Potassium: 16% of the RDI.
  • Copper: 10% of the RDI.
  • Iron: 10% of the RDI.
  • Magnesium: 24% of the RDI.
  • Manganese: 30% of the RDI.
  • Selenium: 10% of the RDI.

The electrolytes that get depleted the fastest?

Is that not strange?

Would it be that refined sugar somehow or someway compensates for that loss when we are eating this processed or un-natural form of sugar and then when you go keto all that extra water (hydrostatic or dynamic pressure) suddenly gets flushed (water weight) from the body with some of the major but vital electrolytes?

Another thing, when insulin is triggered; guess what it is pushing into all your cells and internal organs (or trying to); ONLY 100% REFINED AND PROCESSED PURE SUGAR (composition of supplied sugars and glucose) without its accompanying sister or natural combinations in ratios of vitamins, trace elements (periodic table of elements) and minerals that are supposed to come with it (components and composition of insulin; inc. sulfur), as is the same with glucagon?