Eating to your blood glucose pre-meal hunger "trigger" measurement for body fat loss

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(Mark Rhodes) #21

@amber Is also not a proponent of the high protein model and she has written about it on multiple platforms. She and Kelly Hogan who is also an old school ZC eater discussed this recently here: https://youtu.be/Ye6hSm7-3BI Much of these discussion were pretty settled around 2013. It’s funny how money makers raise their specters. Here is a post from here blog from I think 2013. To my knowledge nothing here has been proven wrong: https://www.mostly-fat.com/ketotic-blog/2013/01/protein-gluconeogenesis-and-blood-sugar/

Another issue with this discussion on fat and obesity is that not all fat is for energy transport. Some of the LDL lipoproteins may be part of the immune system. I think Siobahn Huggins was the first person I recall to mention that they are tiny ambulances arriving at the crash scene and we blame the ambulances for the crash itself.

(Edith) #22

I wasn’t thinking that the inflammation causes the obesity and type 2 diabetes, that the inflammation results in the insulin resistance that then results in the obesity and type 2 diabetes.

"The concept of inflammation in relation to metabolic conditions, such as obesity and insulin resistance started with a seminal publication by Hotamisligil et al . in 1993, which demonstrated that adipocytes constitutively express the proinflammatory cytokine tumour necrosis factor-α (TNF-α) and that TNF-α expression in adipocytes of obese animals (ob/ob mouse, db/db mouse and fa/fa Zucker rat) is markedly increased [1]. Neutralisation of TNF-α by soluble TNF-α receptor also leads to a decrease in insulin resistance in these animals [1]. These observations provided the first link between an increase in the expression and the plasma concentration of a proinflammatory cytokine and insulin resistance."

Later in the paper, the authors write:
“There is also evidence that glucose intake induces acute oxidative stress and inflammation at the cellular and molecular level for a period of three hours 28, 29 and a mixed fast-food meal also causes similar responses for next four hours.”

They continue with:

“It is probable that the proinflammatory state of the obese is related to chronic excessive macronutrient intake. Indeed, increased concentrations of inflammation sensitive proteins, fibrinogen, ceruloplasmin, orosomucoid and x-antitrypsin, were predictive of future weight gain [31].”

Increased macronutrient intake was predictive of future weight gain. If there was already insulin resistance occurring, say… due to inflammation, that would be a cause to eat more.

(Bacon is a many-splendoured thing) #23

It may well be, but all the stuff I’ve encountered on my keto journey suggests the opposite, that it’s the insulin-resistance that causes the inflammation.

Alternatively, as Gary Taubes asserts, his reading of the science is that the causality is reversed. In other words, it’s being in weight-gain mode that causes the increased macronutrient intake. After all, we don’t blame the fact that teenagers grow taller and wider on the fact that they eat so much, because we understand that their hormones have put them in growth mode, and they are eating so much to fuel their growth. In other words, their growth is not the result of the energy imbalance; the imbalance is the result of their growth.

Taubes argues that fat-gain is a similar phenomenon, and that it is our hormones, most notably insulin, that put us in weight-gain mode and therefore cause the appetite that makes us “overeat.” I think he has a point, because looking at the situation that way seems to be more productive than “eat less, move more,” which doesn’t seem to be working very well. Certainly, in my case, paying attention to what I was eating, instead of to how much I was eating, allowed me to lose 80 lbs./36 kg without effort and without hunger. That’s my primary reason for thinking that Taubes, Phinney, Volek, Bikman, Ludwig, Feinman, and many others are on the right track.

I grant you, however, that the standard American diet is highly inflammatory for additional reasons besides chronically elevated insulin, so it’s not surprising that people might have difficulty disentangling the effects of chronically elevated serum glucose from those of unhealthy fat intake.

(Edith) #24

Sorry, having fun with the back and forth today.

Isn’t that what I wrote?

(Bacon is a many-splendoured thing) #25

I’m saying that it’s not the inflammation that causes the insulin resistance, it’s the excessive insulin resulting from the insulin-resistance that is causing the inflammation. I got side-tracked by thinking of Taubes’s example of how causality is difficult to get right, and was riffing on it, sorry. And of course, as I mentioned, the fact that there’s plenty of inflammation resulting from other factors in our diet besides high carb intake only confuses the issue further.

What I think I’m seeing is a pronounced tendency in research to avoid thinking of sugar and carbohydrate intake as a problem, so that it simply has to be something else that is causing all our woes.

(Michael) #26

I did extensive testing and confirmed on a carnivore diet that my blood sugars increased linearly with protein intake (with a very small slope/increase but consistent) which completely matches amber’s post and conclusions. While protein may not be cake, it isn’t nothing either, so it kind of bugs me when people use this quote and then dismiss protein instead of taking it into proper perspective. :+1:

(Mark Rhodes) #27

I lift heavy. I eat at tops 27% protein. My sugars vacillate between 90 & 115. Depends on the fat I take in and the exertion the day before.

Im getting really angry with folks like Bronson Dant telling people that it doesn’t matter
He hasnt reversed osteoporosis or heart disease. Ive had success with this. Nor will he address it when asked directly. People like him are about aesthetics.

(Richard Morris) #28

trust the aesthetic?

(Mark Rhodes) #29

Beginning of 2022 my cardiologist had me go on TRT because I’m low, under 200. But I’ve been low my whole life. Okee dokee. I gained about 4 more pounds. But my lipids went crazy & my Agatston Score which had been going down went up.

As Feldman said at the kitchen table “Has he seen you, why would he prescribe…” Because he’s a doctor. A good one but still has to do something to feel useful. I quit TRT and lipids reverted to my normal.

I do laugh when folks say so and so is taking anabolic steroids. “Really, which ones?” I mean you still have to do the work. This guy looked like a serious load of T, Dbol & Tren A&E. What? I’m as knowledgeable on gym “aids” as I am keto. Ive lived in serious iron gyms most of my life. But lying, well marketers & liars should always be highlighted.