Kindke's Scrap Notes: Circadian entrainment of metabolism
Warning!, sloppy and controversial post incoming!
My interest in the 23/1 intermittent fasting regime was piqued again recently after reading this link. Its about Ori Hofmekler's Warrior Diet, I read this book in the day, and although I did agree with it, the science has since come along more to support his ideas over the years. However I believe I can take his theory further and really get to the "liver" of the matter. I propose that Ori's theory is correct only in as so much as your circadian rhythm is aligned with the light/dark cycle.
My interest in the 23/1 intermittent fasting regime was piqued again recently after reading this link. Its about Ori Hofmekler's Warrior Diet, I read this book in the day, and although I did agree with it, the science has since come along more to support his ideas over the years. However I believe I can take his theory further and really get to the "liver" of the matter. I propose that Ori's theory is correct only in as so much as your circadian rhythm is aligned with the light/dark cycle.
If you maintain a circadian rhythm such that you sleep during the day and are awake at night, you should still be able to reap all the benefits of this 23/1, because the key point about the whole thing is really to fast during the hours following waking up, while your liver AMPK activity is high, and your liver is burning fat like crazy. Then, 9 hours or so after waking, when diurnal cortisol flatlines, liver AMPK activity starts to fall off, liver fatty acid oxidation slows, and this flips the switch that turns on hunger. You now have an approximately 4 hour window to get in your big daily meal. I say 4 hours instead of 8 hours because I dont advise eating a massive meal just before going to sleep.
Now I want to get more into the "liver" of the matter why Intermittent Fasting in general is oh so important .
First some important things to recall, hepatic fatty acid oxidation controls appetite. When hepatic fatty acid oxidation falls, hunger increases. I firmly believe that is NOT just a coincidence, but is actually part of the circadian rhythmic tone of food intake.
If you've been reading Peter's "Proton" series recently, you should know that fatty acid oxidation induces insulin resistance. High levels of fatty acid oxidation in the liver likely contribute to making it IR, especially upon first waking in the morning.
Next, the degree of PPARα activation in the liver is positively correlated with liver fatty acid oxidation. ( The paper in that post also suggests that PPARα activation may have the power to reverse fatty liver btw. )
I also went back to read the full text of this paper Lets ignore all the bullshit about high-fat-diet VS chow. I only want to look at the Ad Lib feeding vs IF aspect. The important graph from this paper imo, is this one....
Red line = IF mice, pink line = Ad Lib mice.
PPARα is a surrogate for liver fatty acid oxidation, we can safely say then that liver fat oxidation was substantially higher in the IF group. From the graph above we see that, after feeding in the IF group , PPARα shoots up then gradually declines until a few hours before feeding again. This essentially means that, all that time PPARα was elevated, hepatic fatty acid oxidation was increased and hunger was most likely diminished.
The decline in liver fatty acid oxidation before feeding is also important, because this would naturally make the liver more insulin sensitive. Exactly what we need before we cram food down our throats.
Fatty acid synthesis inhibits mitochondrial beta-oxidation. This right here, is the breaking of the CICO theory.
Malonyl-CoA, a product of ACC activity in the first step of fatty acid synthesis, allosterically inhibits mitochondrial carnitine palmitoyltransferase (CPT). CPT is essential for the transit of longchain fatty acids and acylcarnitine esters into the mitochondria for b-oxidation. Increased hepatic malonylcarnitine levels in FA mice, but not in FT mice (Figure S4B), are indicative of the specific disruption of fatty acid oxidation caused by impaired entry of fatty acids into the mitochondria.
And this.....
increased levels of the transcriptional repressor Rev-erba (Figure 2E) led to reduced expression of its direct target and a key lipogenic gene, fatty acid synthase
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Food intake and insulin stimulate fatty acid synthase. ( 1 ) , this blocks liver fat oxidation which in turn stimulates appetite. In order to overcome that increase in appetite, you need incretins from the food you just ate. The satiating affect from the incretins you get must be enough to offset the hunger stimulated by the drop in liver fat oxidation. This is a good reason why eating big and rarely wins, while eating small but often FAILS.
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It should be apparent by now that circadian entrainment of food intake is as vital as circadian entrainment of sleep. If I told you I didnt sleep straight 8 hours every night, but instead slept in 3 small bursts of 3 hours, would you think that was healthy? How good do you feel when you get a solid 9 hours of deep sleep. Compared to continuously waking up in the night and lying awake for 1-2 hours before returning to sleep.
The discontinuous sleep makes you feel like shit doesnt it?
So why is it then, when it comes to food, which is also dependent on circadian rhythmic
tone, that we insist on getting our calories in 3 small short bursts? i.e. breakfast, lunch,dinner? If getting our sleep in one large burst is healthy and makes us feel good, why wouldn't getting our daily calories all in one burst also be healthy? I.e. 23/1 Intermittent fasting.
( BTW yes I know the mice in the intermittent fasting study weren't doing 23/1, they were doing 16/8 , but as far as im concerned, the fact remains, eating at the SAME TIME everyday is as important as sleeping at the same time everyday. And dont randomly nibble on food, youll fuck up your circadian clock of ghrelin secretion leading to random hunger pangs, like randomly napping during the day can affect your sleep at night. Random nibbles also risks inhibition of liver fat oxidation while failing to generate necessary incretin secretion to keep you un-hungry, )
