Does the body require the release of adrenaline in order to release free fatty acids into the blood stream?
If this is the case does being on a ketogenic diet not raise stress hormones through the constant mobilisation of fat?
Being that cortisol is also necessary to regulate blood sugar levels… if blood sugar is low wouldn’t this mean a constant release of cortisol?
Berson and Yalow, in a study that Gary Taubes quotes frequently, state that for the fat cells to release fatty acids, “the only requirement is the negative stimulus of insulin deficiency.”
Oh ok thanks Paul i will check out that study. I always assumed from reading that stress hormones were required to signal to fat cells to release fuel
Epinephrine (adrenaline) is released from nerve endings and the adrenals, and acts directly on the liver to promote sugar production (via glycogenolysis). Epinephrine also promotes the breakdown and release of fat nutrients that travel to the liver and that are converted into sugar and ketones
https://dtc.ucsf.edu/types-of-diabetes/type2/understanding-type-2-diabetes/how-the-body-processes-sugar/blood-sugar-other-hormones/ taken from this website
So if we are constantly breaking down fats then we must require highs amounts of adrenaline?
Our ancestors broke down fats for a couple million years and we’re still here. On the other hand, agricultural carbohydrate has been around for only a few thousand years and look at all the issues.
So they must have also been eating carbohydrates in some form for millions of years since they were able to store fat to burn
Yes this is the important distinction I believe. Since we can store grains we had access to carbs year round instaed ox seasonal variation. This is the issue
Temporarily (usually 27 weeks or 6 months until metabolism re-adjusts to normal); adrenaline does become higher because of the lower carbohydrate intake from my personal experience, you just have to get over that metabolic hump (artificial metabolism withdrawal from high octane carbs/sugars) and back to what Mother Nature intended…
Footnotes:
[1] “…People are already adrenally fatigued and have too high cortisol levels. Adrenaline releases glucose into our bloodstream which halts using fat for fuel for the time being. Unless you’re completely adapted, you can’t utilize ketones at high intensities and will thus have to use glucose no matter what. …” …More
High Fructose Corn Syrup DOES NOT trigger/spike insulin but it does increase cortisol[1][2][3].
Additionally this substance (HFCS) punches holes in the intestinal walls creating a leaky gut leading to auto-immunity diseases (arthritis, diabetes, hashimoto’s etc.), histamine intolerances and food allergies.
Footnotes:
[1] **”…Few studies have measured cortisol levels of people on keto and the results are inconclusive. One study found that cortisol increased over time in subjects given a ketogenic diet with a low/inadequate sodium intake. Another study showed no change in cortisol after six weeks of a well-formulated ketogenic diet. …” …More
Abstract:
Traditionally, the leading hypothesis regarding the development of obesity involves caloric imbalance, whereby the amount of calories consumed exceeds the amount of calories burned which causes obesity.
Another hypothesis for why we get fat has surfaced in the last decade which is the idea that the overconsumption of added sugars and refined carbohydrates induce insulin resistance and high insulin levels causing obesity.
While insulin is a fat-storing hormone, this hypothesis does not explain visceral adiposity, or why certain people are found to have fat stored in and around their organs.
We propose a new mechanism for body fattening, particular visceral adiposity. This hypothesis involves the overconsumption of fructose, which leads to inflammation in all cells that metabolize it rapidly.
When fructose is metabolized in subcutaneous adipocytes, the subsequent inflammation leads to an increase in intracellular cortisol in order to help squelch the inflammation.
Unfortunately, the increase in intracellular cortisol leads to an increased flux of fatty acids out of the subcutaneous adipocytes allowing more substrate for fat storage into visceral fat tissue. Moreover fructose-induced inflammation in the liver also leads to increased intracellular cortisol via an upregulation of 11-B hydroxysteroid dehydrogenase type 1 causing increased fat storage in the liver (i.e., fatty liver).
In essence, the fructose-induced inflammatory cortisol response causes “thin on the outside, fat on the inside” (TOFI). Furthermore, fructose in the brain, either from fructose uptake via the blood brain barrier or endogenous formation from glucose via the polyol pathway stimulates an increased release of cortisol causing hepatic gluconeogenesis leading to overall insulin resistance and further body fattening.
This review paper will discuss in detail the hypothesis that fructose-induced inflammation and cortisol activation causes visceral adiposity. …More
[4] “…Insulin is not the problem, I personally would be worried about the amount of Carnitine and Choline in my diet and are what help the ketogenic diet or even a high carb diet[1][2] (believe it or not?) burn up the visceral adipose fat VAT (what is causing the problem to begin with?) around the internal organs i.e. liver, pancreas; what really happens is little tiny particles of fat tissue become microscopically deposited or embedded specifically into the liver and pancreas tissue, in other words becomes part of it, not just around it? Thanks to High Fructose Corn Syrup HFCS? …” …More
Why would one have to eat carbs to store fat? The hunt was successful and the tribe feasts for a week on the fat/protein of a 5K pound mammoth. I don’t think those fat adapted metabolisms failed to store the (currently) unneeded fat just because there was no salad on the side.
Granted they also ate the contents of the stomach and intestines the first day, and got some nice vitamins and minerals from it. But that would have been doodly squat overall.
im not saying that one would have to but obviously fruit is far more lipogenic than protein you just cant dispute that. if i was looking to put on a lot of weight in fat in order to survive winter. like a bear i would be eating fruit with my meat.
you cant chuck the baby out eith the bath water. carbs like it or not have allowed us to survive in truly harsh climates. maybe you could argue natural selection because nature doesnt really give a shit if you live past your first chance to reproduce.
we seem to have this romantic idea of grok killing willing deer every day and being this ripped and healthy specimin. our ancestors rarely lived past 40. being mauled to death by animals, wars and starvation was usually far mor important than macros. what did our ancestors eat/? whatever they could get their hands on to avoid them starving to death
I haven’t seen any data to suggest that adrenaline is involved in either lipolysis (the breakdown of triglycerides into fatty acids and glycerol) or fatty-acid metabolism.
The question of how much carbohydrate our ancestors ate is a vexed one. They undoubtedly ate some, since we evolved from herbivores and have not lost the ability to metabolise carbohydrate. Carbon analyses of hunter-gatherer bones, however, suggest that they can’t have eaten very much plant matter, or the ratio of carbon isotopes in their bones would be different. There is also a noticeable reduction in average height and increase in diseased bones that coincides with the introduction of agriculture and the switch to a diet higher in plant matter. Dr. Mike Eades gave this fascinating lecture a couple of years ago:
We actually don’t have to guess about survival in harsh climates. We have Villjamur Stefansson’s accounts of his two decades living amoung the Inuit during the early the 20th century, including My life with the Eskimos (1913), The friendly Arctic (1921) and many more (he was a prolific writer!). He wrote about his later experiments with lo/no-carb diets in Not by Bread Alone (1946) and The Fat of the Land (1956) which expanded upon Not by Bread Alone. Ancel Keys obviously never heard of him or pretended not to have.
Other than whatever might be the latest stomach contents of the seal or whale killed by successful hunters, the Inuit consumed zero carbs because there were no carbs to consume at any time of the year. They thrived on their diet as did Stefansson once he adapted to it.
It was only after adopting the standard carb-based diet of so-called modern life did the Inuit begin to suffer from all the common metabolic diseases.
Thank you for posting this link!
By the way Rob Grantham, Eades addresses your ‘rarely lived past 40’ in the first Q/A response. In fact, our ancestors lived as long as we do.
This is interesting. If I understand correctly if you are not fat adapted or even if you are? When switching between fuels there is an adrenaline shot?
I ask this because on several podcast I’ve seen people suggesting to eat more carbs at night to build up some glycogen for the night. Dave aspry suggested a teaspoon of honey before bed.
A guy on his show said sleeping issues on keto are due to glycogen stores running low and your body giving a shot of adrenaline.
It’s the HPA-Axis that’s being engaged, that is basically your survival mode (flight-fight-response) being switched to the on position (your hungry and now your hunting and scavenging for food, you don’t need sleep) but after awhile it is kind of like lifting weights to failure and then you get adrenal fatigue because glycogen stores are running low. But usually it goes away and returns too normal after 6 months (your now fat adapted) and things return to normal once fat adapted. Basically your body stops freaking out when you hit that 27 week mark or sooner and says “hey I’m ok!” It is a transitionary process that is not well understood.
I could see how the shot of honey could help alleviate the symptoms also! Eating Honey before bed while adapting to a ketogenic diet could also be viewed through the lense of hormetic adaption.
Here is the thing to be aware of also; if your metabolically fit you usually deplete glycogen storage and go into ketosis anyway on a high carb diet when you go to sleep, but when your body stops doing that (burning too much sugar for too long a time), it means your becoming insulin resistant and becoming diabetic.
This one is right up your alley @atomicspacebunny. Have you read this? It dovetails nicely with the booty-centric metabolic syndrome hypothesis (that probably deserves a better name at this point). All about the intermuscular fat. Even more interesting was a recent article on epinephrine catabolism by macrophages discovered in the obese & elderly. I lost the link, but it ties back to intermuscular fat and insulin resistance as well.
Super interesting stuff. I might start adding squats in addition to leg presses at this rate… 
This was helpful I at least now I know why. I’ve been IF/keto for months and very close to my maintenance weight. It had seemed like to me I was seeing correlation of high BP and Ketones in the morning…sort of. Been playing with all the normal things. Electrolytes coffee etc
I have been trying including more carbish things in the evening that seemed to work. To be honest I hadn’t heard this anywhere.
So seems like in summary it is possible when fat adapting or after when switching fuels you can see this rise in adrenaline
The guy on bulletproof radio recommended progesterone cream
Thanks
I was reading study that examined the walking gate of mice fed a high fat diet compared to humans on a tread mill and they discovered something quite remarkable, in that they noticed that high fat diet (what’s in that mouse chow?) or the fats from the diet attached (bio-accumulated) itself to the gluteus maximus first then all the other muscle health and lypolytic activity followed and the hypothesis was it would even be more so in humans?
Looking at the research you cited below I suspect tyrosine pathway has a lot to do with this.
”…Conclusions: The lipolytic activity of SM is increased by endogenous catecholamines in vivo and appears to be more responsive to epinephrine than norepinephrine stimulation. …” …More
Footnotes:
image link[1] “…tyrosine metabolic pathway + Those metabolic reactions involved in the synthesis, utilization and/or degradation of tyrosine - a non-essential amino acid produced from phenylalanine (an amino acid widely distributed by plant protein) and precursor of thyroid hormones, catecholamines and melanin. …” …More
[2] “…Ingested iodide is trapped in the thyroid, oxidized, and bound to tyrosine to form iodotyrosines…” …More
[3] “…Phenylalanine is an amino acid, a “building block” of protein. There are three forms of phenylalanine: D-phenylalanine, L-phenylalanine, and the mix made in the laboratory called DL-phenylalanine. D-phenylalanine is not an essential amino acid. Its role in people is not currently understood. …” …More
[4] “…The thyroid hormones triiodothyronine (T3) and thyroxine (T4) help regulate growth and metabolism in the body. …Supplementing with tyrosine may influence these hormones (36). …” …More
