This is what I would like to find out. You would think that if one is eating 70 or 75% of calories from fat for an extended period of time that they would be burning fat for fuel a majority of the time, but I think there are other confounding factors. For example, cortisol or the presence of an immune response could create a demand for glucose. I would like to know if itās possible for gluconeogenesis to create enough glucose to cause the body to switch itās main fuel source to carbohydrates even in the absence of dietary carbs. I donāt have any evidence of this, and maybe Iām misunderstanding something, but I think it might be possible. It would be really interesting if, for example, I were to try this product and find that despite eating less than 20 grams of carbs per day my RER was closer to 1.0 than .7 or .8 while being sick with a cold, for example, or after eating something that caused an inflammatory response.
Lumen - let the conversation begin š
Anything is possible. All the research Iāve read and my own n=1 supports what I said above, but I didnāt mean to suggest that universal.
It sounds like at least part of your n=1 might support my hypothesis 
Iām mostly kidding because I obviously donāt know the whole story, but I suspect it is possible for your RER to be over .8 while 80 hours into a fast. Everyone talks about autophagy during fasting, so you could be turning old proteins into glucose to provide some energy for your brain and red blood cells. Certain hormones like human growth hormone go up during fasting and I think this might also create a demand for glucose.
Exercise can also cause your body to use glucose. If our evolutionary ancestors had to outrun a saber toothed tiger, theyād have a jolt of cortisol and glucose to give them quick energy to run away. I assume they would use the glycogen in their muscles first, but then the extra glucose that had been created would go into the muscles to replace that loss. Often today when people experiences stress it is more chronic and doesnāt necessarily involve physically running for oneās life, so glucose is not depleted.
As much as I think keto is a great way to heal oneās metabolism, I still have questions and the more n=1ās the better. I just think we should be careful that the cognitive dissonance that weāre all susceptible to doesnāt get the better of us 
RER or RQ is something they track closely during fasting studies. They use $$$ metabolic carts for this purpose. The RQ of a fasting subject is around ~0.7 after the first couple days, and it stays that way until fasting ceases regardless of whether itās a few days or a few months. Every study done has had exactly the same result.
That said, there are exceptions due to genetic abnormalities but itās pretty rare. One example is that fasting is lethal for most inuit and other folks indigeonus to the artic circle. They die very quickly if they donāt have food. Read the article, itās kind of fascinating!
That video was super interesting! I vaguely remember hearing about this genetic variation in Inuit populations and I liked the deep dive. Iām not sure how much evidence there is to back up Chrisās conclusion, though. Sounded like his theory was that Inuit populations developed this impaired ability to create ketones because of the threat of ketoacidosis. I think itās just as likely that being in a constant state of ketosis might have made it hard to hold on to body fat, which would be bad in such a cold environment. I also think Inuit peoples must have been able to get enough glycogen from organ/muscle meat to keep their brain fueled, hence less need for ketones as fuel. Otherwise, if gluconeogensis and ketogenesis were both impaired, how would they feed their brains on a mostly meat diet?
I couldnāt find the studies you were referring to regarding fasting RER/RQ, but would be interested to see them!
The āarctic variant of cpt1aā take away: ketones are a byproduct of fat metabolism not the most important thing. Fat burning and fat adaptation are the most important things. We already know this. Defining āketosisā as the production of ketones may not be applicable in this specific situation. These people are predominantly burning fat, not glucose. Because they do not have carbs to eat. They are producing sufficient glucose via gluconeogenesis. So Masterjohnās conclusion is a non sequiter. It also illustrates why āchasing ketonesā is a waste of time. The most important thing is fat burn (which hopefully the Lumen will help determine under all circumstances). When Masterjohn claims that our ancestors were not in ketosis most of the time, he has to explain what exactly they ate as an alternative to fat/protein. Plants of the Pleistocene were mostly indigestible cellulose and thus were not a viable alternative.
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What if, as I often do, you eat a higher percentage of protein (oh the horror!) rather than fat. That is, a āhighā protein, ālow(er)ā fat diet? And then compare that with lower protein, higher fat? If the same RER is achieved, does this mean Iām burning more body fat while eating lower fat?
Even now, the Sami people (if they adhere to tradition) eat mainly reindeer, and only eat berries and roots for a short period, to fatten up for the winter. The vast majority of time, they will be in ketosis.
Iām also wondering about the effect of protein/amino acid oxidation on RER. For that matter, also ethanol. This might be relevant to carbs, amino and fatty acids:
Apparently, ethanol does not oxidize to CO2 but to aldehyde and H2O. If so then it would not affect RER. Yet, I find that hard to accept. Something must happen to RER when youāre consuming ethanol. Maybe? Another question that Lumen may answer.
One thing that stood out in looking through that study was this: āMcCloy et al. (McCloy et al., 2004) found the cumulative oxidation of exogenous oleate and linolenate in humans to be 62% higher than exogenous linoleic acid.ā This doesnāt have anything to do with protein, but seems to further support what we already know about linoleic acid - that itās bad, oxidizes slower than other fats, and probably stays around in the body longer.
My primary interest in Lumen would be to figure out if and when my body is producing amounts of endogenous glucose that are enough to trigger an insulin response that could switch me from burning fat to burning glucose. I think many here would agree that if they were to eat 60 grams of carbs that could trigger enough of an insulin response to switch their body from burning fat to glucose. I donāt have any real proof of this, but Iām fairly certain that the body can create at least 60 grams of endogenous glucose in a day and probably much more. Why would the body do this if it has plenty of fat to burn? One reason could be in response to inflammation. Itās my understanding that an inflammatory response creates a demand for glucose. I have been obsessed with this topic because I think that having a better understanding of how certain immune responses affect metabolism could help answer a lot of my questions. For example, why do people with type 2 diabetes produce 3x more glucose than non-diabetic people? Why does 20 grams of carbs seem to be the limit when the brain requires probably around 40 grams per day even in ketosis? Is overeating carbs for an extended period of time really the main underlying cause of insulin resistance?
I think that makes a lot of sense!
OMG you still havenāt gotten that yet???
What is RER?
@jennasaurus good questions!
I heard a discussion where the two people were theorizing that glucagon and not insulin was supposed to be the bodyās blood sugar control system. The reason weāre using insulin is because weāre eating too many carbs. So, if diabetics can produce glucagon but not insulin, glucagonās job is to raise blood sugar. Without a counteracting effect from insulin, you get higher blood sugar.
No one really knows whether 20 grams is a limit. I donāt count, but there are days I know get over 20 grams yet am still in ketosis. It depends on exercise, etc. I think 20 is used because if you overshoot, you should still be in ketosis. If you use 50 (which some people consider the actual limit), itās easy to overshoot.
As for overeating carbs, it could be. But PUFAs have an effect, too. The term āinsulin resistanceā is a poorly defined term. The primary drivers of āinsulin resistanceā are the liver and pancreas. But the fat cells themselves can be insulin resistant or insulin sensitive. And those have an effect on the body too.
Concerning this, see this conversation at Hyperlipid:
He thinks if you eat super high carb, low fat, thereās no issue. If you eat super low carb, high fat, thereās no issue. But thereās a range with carbs + fat thatās an issue.
I think this is why thereās a move to saying hyperinsulinemia - āhigh insulin in the bloodā - instead of insulin resistance. As you were saying over in your thread on your N=1 on trying higher levels of fat, there are times we want insulin resistance. In that case, we want our fat cells to be resistant to insulin to keep them from storing more fat.
And also in the morning, weāre āinsulin resistantā to allow blood sugar to go up. (Though some define this time as being āinsulin sensitiveā, but free fatty acids are high, counteracting that.) Thatās why āinsulin resistanceā is tough to define: It has too many faces.
I think the theory that different fats affect fat cells differently is an interesting one.
Hate to interrupt the discussion but this started six months ago I was hoping to see some results
So was I! Hopefully soon.
Hmmā¦Ted Naiman got his alreadyā¦and hates it. Says he canāt calibrate it due to the rigid rules it has for calibration.
Bummer! Still awaiting mine.