Study where exo ketones reduce l-alanine, which reduces blood sugar

(Bob M) #1

The idea behind the study:


The study:

If you take exogenous ketones, you reduce blood sugar, mainly through reduction of l-alanine. Who knew?

They think something similar happens normally: increasing ketones decreases l-alanine, thereby decreasing blood sugar.

I’ve been testing MCTs (medium-chain triglycerides, i.e., saturated fats), and they do seem to increase my BHB while decreasing my blood sugar. I assume through a similar mechanism as to what is in the study.

(Bacon is a many-splendoured thing) #2

This paragraph confused me:

On the contrary, in type 2 diabetes (T2D), excessive gluconeogenesis underlies hyperglycemia. Thus, one could predict that βHB, by inhibiting gluconeogenesis, could help manage hyperglycemia in T2D. Consistent with this hypothesis, ketogenic diets have been shown to effectively reverse T2D and, while most of the benefit of ketogenic diets in T2D likely comes from carbohydrate reduction, it is not yet clear to what degree βHB itself might play a supporting therapeutic role. In fact, in both animals and humans, exogenous βHB are alone sufficient to decrease blood glucose.

How does excessive gluconeogenesis occur in someone eating a high amount of carbohydrate? Surely the insulin response to the carb intake would inhibit gluconeogenesis. My understanding is that glucagon can cause runaway gluconeogenesis only in conditions of low insulin, which is the case only in the very late stages of untreated Type II diabetes, which in the earlier stages is a problem of hyperinsulinaemia, not hypoinsulinaemia.

Second, the processes of ketogenesis and gluconeogenesis are both stimulated by glucagon, no? Although, come to think of it, when the insulin/glucagon ratio is low, there are other factors besides insulin that regulate gluconeogenesis, so I suppose one of them could be β-hydroxybutyrate. I’d like to see a study of high-carb and keto-adapted subjects done, and see what the results are.

Third, β-hydroxybutyrate does not inhibit gluconeogenesis in Type I diabetes, since the diagnostic for diabetic ketoacidosis is hyperglycaemia combined with serum β-hydroxybutyrate > 10.0 mmol/dL. The authors of the paper don’t explain how that works, and I think it’s relevant.

I’m also wondering why the study focused only on β-hydroxybutyrate and ignored aceotacetate and acetone. It would be interesting to know what their role in all this is.

(LS Conway) #3

Everything I read says no. I am so confused. If making ketones, then why add more. Though I know people are having much success. From what I have seen though, these people are eating all the 1 carb tortillas and that kind of thing. H Ave seen expensive pee to this is amazing. I did buy some a while back. They kind of knocked me for a loop. Just felt weird. No idea why.

(Bacon is a many-splendoured thing) #4

It’s actually quite simple: Why would anyone want to stop eating a food that causes illness, when there’s a very expensive treatment to take, instead? That’s a much more exciting solution than something as low-tech as eating different food.

Besides, the profits on exogenous ketones contribute to the large annual bonuses of pharmaceutical company executives, whereas dietary changes do not.

(KM) #5

I agree with the profit-motive hypothesis, but it might actually be a question worth asking on its face. Why DO some people feel that way? I know someone who is trying to get T2D under control, but I’m realizing nearly every meal they eat is either inadvertently carby, like ordering ribs (slathered in barbecue sauce) at a restaurant instead of steak and calling it healthy eating because they skipped the potato, or loaded with artificial sweeteners, or both. They simply can’t seem to choose a meal that isn’t sweet one way or another. And so, Rybelsus steps in as a magical solution. I could be critical, it can seem in part willful ignorance, but why is the sweetness so so necessary for this person?