Only Dietary Fat, Not Protein Or Sugar (sucrose), Drives Obesity

[Braveheart]

I’m currently experimenting with a much lower carb and higher fat diet, and I immediately lost 7 pounds. A huge amount. My belly has flattened out completely. And I feel better. The experience alone has taught me that I don’t need to go crazy with carbs. More = doesn’t equal better. But then, I’ve spent the last four years PUFA restricting, so maybe I’m in a position to do this without turning into a car crash (poor temps, etc). My temps are really good.

am experiencing the same

 

[Hans]

@benaoao
"uncontrolled fructose input through mtG3Pdh"

He later mentioned he made a mistake and that fructose doesn't drive more mtG3Pdh than glucose.

I do not agree with his entire theory, because it's not as simple as just low level signalling as he is saying.

 

[benaoao]

What else do you think is missing? The electron transport chain / Krebs cycle / mitochondrial respiration sure is crucial

Indeed, fructose in the absence of fats is quite far from being that huge inconvenience. Nothing new for us though

 

[Hans]

What else do you think is missing? The electron transport chain / Krebs cycle / mitochondrial respiration sure is crucial

Indeed, fructose in the absence of fats is quite far from being that huge inconvenience. Nothing new for us though

Yes, about 90% of ROS is produced in ETC, which makes it all the more likely for his theory to be true. But I've thought some about it. White adipose tissue doesn't contain a lot of mitochondria in comparison to brown adipose tissue and muscle; so how much insulin resistance is saturated fat causing white adipose tissue compared to the muscle. And if all tissue are insulin resistant, what happens with the glucose? Does it just float around in the system, until there is space for them to be taken up somewhere? Wouldn't this mean though that saturated fat will cause hyperglycemia for an extended period of time? And this is the opposite that we see in studies. PUFAs cause hyperglycemia and not SFAs.

He also says that PUFAs make the adipose tissue more insulin sensitive, which allows them to uptake more fats and glucose, thus creating obesity. This is true of course. And then only when the adipose tissue cannot hold anymore fat, does the fat begin to leak out into the circulation causing hyperlipidemia, inflammation, diabetes, etc.
So PUFAs would make you healthy in the short run, but diabetic in the long run. But this is not true. This happens before adipose tissue becomes too distended.
PUFA consumption increases lipolysis, thus allowing more free fatty acids to circulate in the blood, while not increasing insulin the same way SFAs do. Insulin also inhibits gluconeogenesis, so GNG will be more elevated when PUFAs are elevated instead of SFAs.

PUFAs cause obesity by increasing prostacyclin, PPARgamma, endocannibinoids, inflammation, slowing the metabolism, lowering energy expenditure, inhibiting thyroid function at every level, etc.

"cPGI2, besides its ability to activate adenyl cyclase, was also able to induce a transient increase in intracellular free calcium. This phenomenon was independent of cAMP production or inositol phospholipid breakdown and appeared to be mediated after binding to a single class of PGI2 receptor. The potential to generate simultaneously two synergistic intracellular signals allows us to ascribe to PGI2 a key and specific role in the differentiation of adipose precursor cells in vitro that would likely lead in vivo to the recruitment of "dormant" preadipocytes to become adipocytes." (s)

"lowered production of cyclic AMP may limit the formation of adipocytes, leading to hyperplasia to accommodate the fatty acid supply" (s)

"dietary LA increased tissue AA, and subsequently elevated 2-AG + 1-AG and AEA resulting in the development of diet-induced obesity." (s)

I really like his theory, although he mainly likes to look at low level signalling, while I feel that doesn't explain enough and that "higher level signalling" can't be ignored.

 

[benaoao]

Very helpful post, thank you.

I do like the rationale behind very low fat, and agree with you that PUFAs being superior (as he’s interpreting it) was his mistake indeed.

I’d err on the side of caution when it comes to mixing (saturated) fats and carbs unless already quite insulin sensitive, don’t your think? Although that’d be a matter of absolute amounts. If we’re generally low, I doubt that it matters that much. Plus Kitavans do coconut+yams no problem.

 

[Hans]

Very helpful post, thank you.

I do like the rationale behind very low fat, and agree with you that PUFAs being superior (as he’s interpreting it) was his mistake indeed.

I’d err on the side of caution when it comes to mixing (saturated) fats and carbs unless already quite insulin sensitive, don’t your think? Although that’d be a matter of absolute amounts. If we’re generally low, I doubt that it matters that much. Plus Kitavans do coconut+yams no problem.

I also like the rationale behind very low fat, yet some people don't do so well on it, but it's always a good experiment to do.

I think the more compromised someone is, the less fat they might have to eat to restore proper glucose oxidation. But after restoration, they probably won't do very good on a higher fat diet. Nutrition is very individualized.