The Effect of Insulin on Our Own GLP-1 Production

[VirginiaEdie]

I just listened to a fascinating podcast given by Dr. Ben Bikman. In it he discusses how high insulin causes a decrease in GLP-1 production. The most interesting part is where he discusses a study in which the researchers tested the amount of GLP-1 that was produced after a fatty meal and after a high carb meal. There were two groups: those with a normal BMI and those who were obese.

After the fatty meal, both groups produced the same amount of GLP-1 postprandial, but after the high carb meal, the obese group produced almost no GLP-1. Without GLP-1, the gastric emptying doesn’t slow down, making people hungry again sooner. Dr. Bikman mentioned that insulin levels were not tested during the experiment, but there is a good chance that the members of the obese group were at the least, insulin resistant. With insulin already being increased, the spike from the carbs caused even more insulin to be released, resulting in no GLP-1 being produced.

When GLP-1s became a hot topic it seemed to me they were a medication that, in a way, mimicked what happens when we get into ketosis. I think it’s been known a long time that fatty foods take longer to leave the stomach than high carb, low fat foods. So… eating high fat, low carb, allows the body to secrete GLP-1, decreasing the rate of gastric emptying, allowing us to stay satiated longer.

This also makes me wonder about those who still have a hard time losing weight on keto. How long does it take for cells to heal from possibly years of insulin resistance? Maybe that’s why some people, particularly those with type 2 diabetes, have to eat almost no carb, because even a tiny bit of carbs spikes insulin enough to affect endogenous GLP-1 production?

How Insulin May Be Silencing Your GLP-1

[clackley]

I think that all makes a lot of sense and may answer a question that still seems unanswered which is why does GLP-1 not work for everyone? In the same way keto doesn’t work for everyone. It is a fact and it’s not that the person isn’t doing it right in the same way that taking a GLP- 1 isn’t being administered correctly.

I think it may be a case of a very damage system involving, primarily, insulin sensitivity. Some peoples bodies may be just that broken. I do understand that it is hard to reverse the resistance for many. I think I am one. I could never make it to my goal weight despite having done it about 7 years prior. During that time, I went back to high carbs in a very destructive way. I am living with the consequences now. I broke my insulin resistance that much further.

[ctviggen]

This area is complex. Ben Bikman also gave a short Instagram on this:

https://www.sciencedirect.com/science/article/abs/pii/S1043276026000925

This is a paper (behind a paywall unfortunately) where the group thinks the main way these GLP-1 receptor agonists work is by causing fat cells to release their stored energy. Like this:

I have a lot of respect for Ben Bikman, but I would REALLY like to see insulin. For instance, Georgia Ede is highly against dairy, believing it raises insulin too much. But if I drink milk with proteins, I am NOT HUNGRY for hours. If any rise in insulin is a problem, what is the problem?

I’d love to eat some dairy and have my insulin take over time, then compare that with eating, say, beef. Ideally, I think the calories, protein, and fat levels would be similar. My guess is that there would be no difference, but I cannot get this test done.

My problem with insulin is that it’s “hidden”. I’ve had a bunch of these tests done, and I’ve gotten results from 3.8 to 33.0 for “fasting” values (try to get 12 hours, but might be smaller, and these are in the morning – the few times I’ve gotten it in the afternoon, it’s been lower). My typical values are around 12, which still puts me as being “insulin resistant” (depending on your “expert”), after 13 years of keto.

How do I get my (fasting) insulin down? I don’t know.

To Edith’s point, it could be that some people are so insulin resistant that it’s an issue for a lot, including GLP-1. But if keto doesn’t resolve that, what does?

Edit: This is the main reason I’ve restarted longer-term fasting. I KNOW fasting reduces insulin, because I got insulin taken the first day of fasting and the last day (4.5 day fast), and the last day just said “<3.0”. That’s the lowest “fasting” insulin I’ve ever gotten.

What I don’t know is what happens after that. Say, days 1, 2, 3, … of eating? I have the theory that there’s actually a rebound effect where my fasting insulin goes way high. I believe the 33.0 I got was because of this (I had fasted 4.5 days not too long before this). But testing these theories is difficult because I have to go to a lab.

[clackley]

I have heard that insulin is difficult to measure and that the standards vary a lot. It is a clue into what is happening but how to ‘fix’ it (if it can be and if it would help) is a mystery I think.

[lfod14]

When GLP-1s became a hot topic it seemed to me they were a medication that, in a way, mimicked what happens when we get into ketosis. I think it’s been known a long time that fatty foods take longer to leave the stomach than high carb, low fat foods. So… eating high fat, low carb, allows the body to secrete GLP-1, decreasing the rate of gastric emptying, allowing us to stay satiated longer.

I WISH that applied to me! While it was much easier to fast when I did standard keto (wish I never fasted), I swear the fattier more delicious stuff made me want more just like sweets do to most people. Only thing that can keep me half OK is high protein. Still always hungry though!

Was taking Semaglutide for the last year or so, now just switched to Tirzapatide for (hopefully) more appetite control. I’d rather force eat my last meal or two everyday than my normal which is to eat everything I can get my hands on all day long.

Still keeping weight and BF% in check, but it’s miserable.