I blogged a few days ago about restricting protein, consuming more 2:1: meals (read: aiming for a goal of an 82% fat diet) primarily for emotional/neurological benefits. I had no delusions this would make me slimmer, I fully expected if any change at all I was likely to develop a worse body composition from reducing my protein intake and increasing dietary fat. While the very high fat keto diet is likely palliative for obesity relative to a high carb mixed diet, after experimentation over the years I have observed the meat based carb restricted diet is best for obesity. Basically, atkins and low carb paleo diets are the ideal for weight/fitness explicitly because of their very high protein content. These diets are being misrepresented as "high fat diets" , which is unfortunate as the reason the diets work is a very high protein concentration relative to energy density. E.g. a meal of steak and a few sprigs of broccoli derives a LOT of protein per calorie relative to any other type of meal. While these meat based atkins meals are certainly high fat relative to a low fat diet or a standard diet, they are actually substantially lower in fat than any true ketogenic diet. This is an important distinction as there is so much confusion of how these diets are helping obesity; the ketosis appears mostly incidental to what is a protein based insulin suppressive diet. The ketosis occurs from spontaneous under eating secondary to this, and it will NOT occur if protein is consumed sufficiently to maintain wt.
However, the good news is a very mildly ketogenic atkins diet is still useful for epilepsy and many conditions that respond to keto because a ketosis is produced by the low carbohydrate content, as well as the fact many people spontaneously fast + restrict energy when consuming protein in the context of low carbs.
Anyway, for the sake of this informal experiment, I restricted my protein to about 50-60 grams, and consumed a whole lot more fat.
Very quickly I began observing fuschia and purple pee, whereas eating meat my pee is always trace, maybe small .
Pee began looking like this all the time...
This color or darker! PeE SeLfIe!
In addition to an obvious increase in pee pee ketones, my blood sugar readings were always 60s, 70s, even after eating. I was basically chronically hypoglycemic, which in my experience is the only way I will see a measurable ketosis these days, in the dead of a lazy fatass chair bound winter. In other words if my blood ketones and pee is going to get above 1, I need to do something, SOMETHING that depletes blood sugar. Here are a list of such things:
Fasting
Exercising, either walking, running, or lifting heavy stuff
Cold exposure, both formal cold therapy as well as just being in a jersey winter hell
Not eating "keto carnivore" meat proteins which turns into glucose quite evidently from this experiment.
Now in the summer time when my metabolism is less terrible, I can have a stronger ketone along with a higher blood sugar which represents a higher metabolic rate. This is not the case in winter when I am chronically fatiged almost in a hibernation like state from SNS suppression. Anyway!
The point is if I want my blood ketones to get above 1, I need to markedly lower my blood glucose somehow. I don't mean lower it from 90 to 80 ...but lower it from like, 80 to 60. In this case/most recent experiment, I restricted my protein intake to near deficiency levels in order to induce a stronger peripheral ketosis. The protein restriction eliminated glucose, which forced my body to supply more ketones for energy. Please note I am not advocating this is necessary for ANYONE and I experienced many unpleasant side effects from protein restriction.
My nails began to grow slowly
My skin quality went to shit
Eventually my appetite became higher, although evil female hormones may have contributed to this (Progesterone sucks)
Emotionally I felt a lot better and I had no PMS symptoms as I ordinarily would which is quite remarkable, however!
In general I would not recommend lowering protein to 1g/kg, it was just an obvious physical health fail.
The original motivation for my keto diet experiment was observing during flu illness, my kratom was not as effective as controlling CNS stuff, although increasing my keto *was* effective. Since discovering kratom months ago I have observed I can weakly defile keto with protein based meals and feel no worse than a fasting state for the first time in my key tow life. While I had the flu, this was not true, kratom seemed to be a lot less effective in general. (Note: my flu has entirely resolved and everything is back to baseline, fortunately).
I observed if I was "more keto", I was less interested in kratom in general, did not "need" kratom as much because the greater CNS ketosis seemed to replace the effects of the kratom. This is inverse of the idea that when I am "more keto", kratom is much more inhibitory/sedating than when I am very weakly keto (for example, after eating a lot of meat while sedentary). So, if kratom is not working as well, greater ketosis + kratom can help fill the gaps, correct? Correct.
Anyway, things have resolved, kratom appears to be working more typically again, and I have resumed my protein addict lifestyle inhaling 100+ grams of protein on occasion. I now typically eat meat multiple times a day, pork rinds, the whole deal ;) . As expected , my pee pee ketosis has returned to trace-small at almost any given time. In addition my blood sugar values are more typically elevated again (they are not high, but they are no longer 50-60-70 as before).
This experiment has once again demonstrated the following:
Meat is a ketogenic penalty. The more meat you consume, the weaker your peripheral keto will be.
I suspect adaptation to a low carb / higher protein diet involves superior blood glucose conversion from proteins, an entirely reasonable assumption. While it is true ketosis may spare protein loss in starvation, this is not mutually exclusive with enhanced blood glucose synthesis from proteins if excessive in a carbohydrate restricted high meat diet. In other words, as one eats a very high meat/protein diet, one becomes very good at creating blood glucose (and ketones) from amino acids to fuel the body.
A parallel example would be the ketosis of starvation slowing total rate of fat oxidation, but increasing percent of energy from fat substantially relative to the fed state. Starvation involves a profoundly depressed metabolism, a suppression of fat oxidation, with a steep drop in the RQ representing almost total dependence on fats for energy as expected. Suppressing fat oxidation while increasing the % of energy from fat is not mutually exclusive, just as sparing protein waste while increasing glucose from excess protein is also not mutually exclusive.
Again, all of this is irrelevant for weight and fitness pretty much and the evidence is rather clear a high % of protein seems to inhibit appetite and superior prevents muscle/lean tissue loss while in negative energy balance.
I would also like to have a discussion of keto adaption, as I feel much of what I experience WRT low ketones even on a very high fat diet can be explained by this.
First, what is "keto adaption"? It's a popular buzz word in the keto circles and it seems to be defined different ways.
One idea is keto-adaption represents the lack of "wasting" of ketones. As a person becomes more adept at using them, they waste less in the urine. I believe The Bear developed this definition. The ketones disappear from urine when the dieter becomes so good at using ketones, the strips then become negative due to lack of waste spilliage. I believe this definition is approaching true but the mechanism is wrong.
All evidence suggests ketones are glucose-like and exists primarily to replace glucose; therefore, ketosis will be highest in the most glucose-dependent people when temporarily deprived of it. (examples: children on keto diets, who routinely get ketones of 4+ due to huge metabolically intensive brains, a fasting vegan who easily becomes very keto; in general, ketones in the blood match lack of carbs/glucose in the diet for people who are glucose based). Contrary to the idea that ketones require "adaption" for use, ketones are a quick source of energy to replace glucose similar to alcohol, which is precisely why they meet this need so well. Ketones do NOT require adaption to use for energy at all. The idea that ketosis becomes lower due to "superior use of ketones" seems therefore quite unlikely.
Another , more scientifically supported concept is that with an extended period of time on a very low carb ketogenic diet, the body becomes increasingly adept at using FFA directly for energy in most tissues (vs glucose + ketones as in the earlier stages of a LC diet). FFA directly enter the mitochondria for oxidation, which spares energy waste vs the relatively more wasteful ketogenesis. The ketosis is a temporary surrogate for glucose when one is dropping carbohydrate temporarily or totally starved of ANY food.
However, with time on a ketogenic diet, FFA are oxidized more readily. The ketones in the blood drop due to negative feedback; with a higher influx of FFA entering the mitochondria, superoxide is generated to induce insulin resistance; the rise in insulin resistance from such a high rate of fat oxdiation trivially inhibits further ketogenesis. Basically, the ketones are not needed, because the mitochondria are loaded with fatty acid goodness ;). A high level of ketones are no longer necessary as you are now fat adapted.
In contrast to the idea ketones drop because of super-efficiency using them, the FFA-based perspective would posit ketones drop as a reaction to superior use of fatty acids, which inhibit ketogenesis via IR related negative feedback. I think the latter idea is way closer to the mark.
The tissues which cannot use FFA directly for energy such as the brain are a bit different. Well, everything is a bit different in the brain ;) In the brain of a fat adapted person, there is a big upregulation of FFA transport and astrocytes convert FFA to ketones, which spares glucose and also raises lactate which provides plenty of ATP for the neurons, way more superior in fact to a glucose based. In a fat adapted state, perhiperhal ketones might be low as most of our cells can use FFA for energy; in the brain it is likely a high level of ketosis is maintained behind the BBB. We are unable to perceive this with a fingerstick reading, however.
As an evidencing argument, the nature of fat adaption was expressed rather well in woo during my protein restriction experiment. I was quite energetic, thinking perfectly fine with a fingerstick of 48, and blood ketones of 1.3. There is no way for blood ketones of 1.3 to cover that much glycopenia, but apparently my brain was just humming along quite nicely in spite of this seemingly *massive* energy deficiency. I was jumping, running, perfect woo! No issues!
I had no glucose, I had very few ketones. I should have been barely conscious. Why was I not passing out, wavering in and out of consciousness the way I was when my glucose crashed to 44 after slamming a 50g dextrose solution?
What my meters could not tell me was the fact my entire body was oxidizing FFA directly, not ketones or glucose as much as a recently inducted atkins dieter.
What my metmer also could not tell me is that my brain is keto adapted, transports lots of FFA into it, to churn out ketones that create tons of ATP and lactate to feed my neurons.
A person newer to the low carb diet who was not fat adapted would likely be very symptomatic with those numbers. I was not, because I run live and breath on FFA after 12 yrs.
Further evidence to support FFA = life fuel is when I take ketone salts can induce a hypgoglycemic like condition in spite of masking the energy paucity on meters. About 20 minutes after consuming ketone salts, I experience a crash of energy and massive hunger similar to hypoglycemia in spite of extremely high serum ketones and normal blood glucose. This would be the total OPPOSITE condition of perfect energy while fasting with a glucose 48/ketone 1.3.
What occurs is also opposite.
What cannot be seen (and explaining my symtpoms) is the ketone-induced insulin secretion that suppresses my FFAs, leading to a perception of hunger and energy crash once it occurs. There is no way to explain the symptoms as my meters will look great: sugar will be 70, ketones will be 2-3...but inside I feel frail, weak, ravenous. This occurs because the exogenous ketone salts have disrupted my ketogenic diet, disrupted my lipolysis homeostasis which has an end point of FFA suppression and energy deficit. The symptoms are hunger and an energy crash, but there is no evidence of it on meters as my meters do not measure FFA.
These two anecdotes only make sense if we assume I am FAT ADAPTED.
Every aspect of my observed physiology suggests I am a lean(ish), mean, FATTY ACID burning machine. Ketones ? Meh. Who cares.
Like I said. Glucose of 40. Ketones of 1. I'm fine! I'm BETTER than fine!
Suppress my FFA, though, and this is my hypoglycemia. Trembly, ravenous, but there is no explanation on my ketone salt adulterated meter of why I am experiencing such symptoms.
TL;DR:
Protein is an important source of blood sugar.
Restricting protein depletes blood sugar which forces ketones higher to compensate
Keto adaption is likely adaption to more efficient use of FFA for energy, ketones drop due to attending IR and autoinhibition of ketogenesis
Ketones may also drop if eating lots of meat/protein which clearly provokes blood glucose
None of this means anything if internested in fitness and weight loss, of which a protein based diet is clearly superior.
Even for CNS issues, an atkins diet is "good enough" most of the time.