Moot point but the two do go hand in glove. The general feeling here is that, for reasons of natural satiety and the fact that fat-laden meals are more calorie dense, it is more fun to eat your meals in 1-2 sittings while not feeling hungry in between.
16/8 and related protocols is very popular among the keto community. Whether they are efficient for building muscle is another question.
I have generally read of this glucose sparing phenomenon referred to as “physiological insulin resistance” but as it has been presented to me, it is a sign that the brain and glucose dependent tissues are still dependent on glucose and not working optimally on ketones. The mechanism was that the cells were fat loaded and also had their glycolytic enzyme synthesis downregulated. The issue is that physiological insulin resistance tends to start at under about 45% carbs. (you can fail a glucose tolerance test if you don’t eat 45% carbs for 3 days and the test is considered to be invalid in that case). 45%+ carb diets tend to produce fasting blood sugar in the 80s. Isocaloric down to about 20% carbs tend to produce fasting levels in the 90s. Down below 20%, the fasting level rises even higher, up to 100-125, but the lowest health hazard ratios of all groups occurs with a fasting blood sugar of 90-99 IF the individual is not on a high carb diet which should push fasting blood sugar even lower. I know keto dieters though who eat low-ish protein and get A1Cs in the mid 4’s and fasting blood sugar in the 68-80 range. Ketones are considered to be brain protective and actually prevent harms of mild low blood sugar such as in the 60s.
So while I would not take a fasting blood sugar of 100-110 to be pathological, or a sign of developing diabetes, but rather that you may have ketones but still be making a lot of glucose from protein, and the brain may still be using glucose. I would ask this: If you eat 200 grams of protein in a day, what is the metabolic fate of that protein, or the protein that it replaces in the process of protein turnover. What happens to the pieces once the nitrogen has been eliminated from the body. I think that the ONLY explanation is that transamination creates glutamine which gets transformed into glucose and urea or ammonia, though I will have to research the pathway. I am asking for you to basically trace the path of the amino acids through the body until the nitrogen is eliminated and ask "what products HAD to be built as the nitrogen traveled that path.
I think this is largely emerging science regarding ketones, physiological insulin resistance, etc. so I don’t know answers, just some qualified facts. I do know that when I spent time in ketosis on <40 grams of carbs AND <120 grams of protein, my fasting blood sugar was in the 70s, while on an isocaloric diet it is in the 90s, but I was also largely below maintenance calories when I was in ketosis. I also woke up with the lowest ketone levels 0.3-0.5 which rose over the day, but my morning glucose was low. Cortisol can raise morning glucose (“dawn effect”) but I think a ketogenic diet should largely block the dawn effect. I am totally fine with a fasting blood sugar of 90-100 on a 25% carb diet, but I would not want to have a fasting blood sugar of 90-100 with 1.1 ketones which would represent a high level of total blood energetics. I have read keto authors suggest that if combined blood glucose+ketones in mmol/dL goes up then you are falling out of the keto adapted state and undergoing gluconeogenesis, and that it is comparable in harms to having that combined level as a fasting BG. Example, 5.5 BG and 1.1 BKet would be as damaging as a 6.6 BG with trace ketones.
I will add that in addition, insulin dependent individuals tend to experience a need for a very stable basal insulin level when they consume 100-150 grams of carbs a day, but start to have erratic basal blood sugar rises when they go under 100 grams a day, presumed to be from gluconeogenesis kicking in sporadically. They tend to have basal needs smooth out again if they move into ketosis with moderate protein. The most erratic basal needs occur in the transitional zone from “glucose to match glucose dependent tissue” levels and ketosis. You may have seen some videos from Dr. Bernstein, an insulin dependent man who became a doctor and promotes a ketogenic diet who has had A1Cs as low as 4.2. Now it is possible that he is overdelivering insulin.