Haidut On Insulin Sensitivity / Insulin Resistance

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Yeah, I guess it still holds in principle but the studies said something along the lines "FFA damage the ability to synthesize glycogen so sugar floats around, and not so much inability of cells to burn glucose". It's the organism's inability to store extra glucose in the liver. Pointing us once again back to the liver as central in insulin resistance and diabetes type II.

Insulin resistance is caused by elevated fatty acids (FFA)
 

Elchapchapchapo

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Free fatty acids (FFA) as the cause of insulin resistance
Free fatty acids (FFA) as the cause of insulin resistance

Yes, and the above studies hint at that - i.e. FFA raise inflammatory mediators, and it is the inflammatory mediators that probably trigger an actual "disease". So, elevated FFA cause elevated NF-kB and TNF-alpha, which will eventually cause some type of named disease (i.e. diabetes, CVD, etc) even in a lean person. You don't have to be obese to be insulin resistant, most long distance runners have some sort of insulin resistance (due to adaptation to burn fat) and they are all very "lean". They also look untypically old for their age. I posted a study a week ago showing that the only difference between aged and young cells is that aged cells cannot switch to burning glucose when challenged with a glucose load. The aged cells "insist" on burning fat even in the presence of elevated insulin. So, aging is a type of whole-body diabetes energetically speaking. Just like Alzheimer's is diabetes of the brain. Inflammation plays a key causative role in diabetes and in aging, as Peat has said many times. Without PUFA there can be no inflammation as PUFA is the only precursor to the inflammatory cytokines. If you cannot deplete PUFA then vitamin E, aspirin and caffeine are your friends as they block pretty much the entire inflammatory cascade.
 
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Losing excess body fat is the main factor in reversing insulin resistance. The FFA's come from one's own fat tissue.
 

Elchapchapchapo

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People who are obese and have insulin sensitivity have a problem with oxidating glucose, due to damage in the Krebs cycle. The damage itself is done by polyunsaturated fats (omega-6 and omega-3) damaging the mitochondria. Their cells only perform glycolysis, which is what cancer cells do as well. In order to recover a diabetic person back to health, you need something that kickstarts the full Krebs Cycle all over again and limits glycolysis. Niacinamide / Nicotinamide (a type of vitamin B3) is one such substance (aspirin is another). It helps the mitochondria recover. There have been cases where Type I diabetes has been reversed by niacinamide. I can't find the exact study, but here are some pointers.

Effect of nicotinamide on newly diagnosed type 1 diabetic children. - PubMed - NCBI

A randomized trial of nicotinamide and vitamin E in children with recent onset type 1 diabetes (IMDIAB IX). - PubMed - NCBI

-From Haidut on Reddit: What does cancer eat? Sugar, mostly. • r/science
 

Elchapchapchapo

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Pregnenolone For Obesity And Insulin Resistance
Pregnenolone For Obesity And Insulin Resistance

I wrote in another thread about the history of PCN, which is just a slightly modified proprietary pregnenolone. This study shows that a human equivalent dose of 3.5mg/kg prevented the obesity caused by high-fat diet. The duration of experiment was 7 weeks.
Other noteworthy findings were that pregnenolone improved insulin sensitivity, lowered blood glucose, and lipogenesis. All of these negative metabolic effects can also be caused by high cortisol. Given my other thread of PCN powerfully stimulating the thyroid, and considering that it is a cortisol antagonist, I think this anti-obesity, pro-metabolic effect is certainly to be expected.
Again, the other well-known cortisol antagonist DHEA has been also been shown to have these effects in animal models and in some human trials. However, given the DHEA estrogenicity in higher doses, pregnenolone may be a safer method.
Basically, Ray knows his stuff:)

Activation of Pregnane X Receptor by Pregnenolone 16 α-carbonitrile Prevents High-Fat Diet-Induced Obesity in AKR/J Mice
"...In this study, we demonstrate that activation of PXR by PCN prevented development of high-fat diet-induced obesity and relieved obesity-related insulin resistance and hepatic lipid accumulation (Figures 1, ,3,3, ,4).4). The beneficial effect of PCN treatment was achieved by inhibition of lipogenesis and gluconeogenesis in the liver (Figures 3E and and5)5) as well as inhibition of lipid uptake in liver and WAT (Figures 5c and and7c),7c), by enhanced lipolysis in adipose tissue (Figures 7C, 7F), and by increased peripheral fat mobilization and energy expenditure in BAT (Figure 8)."
 

ddjd

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My insulin is at 17. Is the something to be concerned about?
 

ddjd

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Losing excess body fat is the main factor in reversing insulin resistance. The FFA's come from one's own fat tissue.
but how does one lose fat or improve insulin sensitivity on a peat diet because we're constantly told to block lipolysis with niacinamide, aspirin etc.
it only works if you have zero fat to start with which most of us dont
 

Hazarlar

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but how does one lose fat or improve insulin sensitivity on a peat diet because we're constantly told to block lipolysis with niacinamide, aspirin etc.
it only works if you have zero fat to start with which most of us dont

*try very low fat diet (if you think you should follow "Peat Diet")

I personally would prefer to 1) restrict calories 2) eat twice a day 3) eat once a day 4) fast

Trying to burn sugar from wake up to sleep in unnatural for me.
 

Amarsh213

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What would you suggest as primary mechanisms for doing this? Referring to excess body fat.

Sprint 20meters 5-7 times, full speed. 3 minutes rest.

Trains the CP-ATP without any or minimal lactate/glycogen sacrificing. It's drastically increases metabolism, androgen, insulin sensitivity, leptin sensitivity, lowers cortisol
 

Lokzo

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Sprint 20meters 5-7 times, full speed. 3 minutes rest.

Trains the CP-ATP without any or minimal lactate/glycogen sacrificing. It's drastically increases metabolism, androgen, insulin sensitivity, leptin sensitivity, lowers cortisol
I'm loving the sound of this. Reminds me of my old days of trying to get "shredded".
 

Cirion

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Some what of a thread necro.

But what about the fact that plenty of "skinny" people have Type 2 DB as well?

I think it all comes back to Dr. Peat being right again about PUFA. You can have a lot of PUFA damage going on even if you're skinny. And be eating too low carb etc.

You have to lose weight the correct way (High carb, low PUFA). If one does that, THEN, I can see this point being correct.

Everything needs to be held in context. Weight loss alone doesn't fix a metabolism.
 

Kyle Bigman

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I have been getting very sleepy after meals and a high heart rate. I wonder if it's because I have been taking lots of b-vitamins, which reduce fat oxidation, but because my cells are not processing glucose well either, the sugar just remains in the bloodstream, causing all kinds of bad symptoms. is this a reasonable theory?
 

ddjd

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is insulin resistance closely related to HPA axis dysfunction?
 
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