This is where we need to separate mTOR and IGF-1 activation from chronic mTOR and IGF-1 activation.
Elevated insulin after a meal isn’t bad at all… it’s vital. What is bad is chronically elevated insulin.
My suspicion is keeping these things pulsatile instead of chronically high makes a lot more impact than trying to keep them chronically depressed.
That’s not enough protein to create gluconeogenesis (immediately) or conversion of non-carbohydrate carbon substrates such as lactate, glycerol, and glucogenic amino acids into glucose (immediately), your only going to spike glucagon with that amount and depending on how frequently you eat meat in timed sequences in contrast to amount eaten? The window of time for this phase to take place is very broad (two to ten days) if you eat enough meat to cancel out glucagon with lots of glucose and kick-in insulin days or a week later? Why protein cycling is very very important if your trying to burn fat in contrast to intermittent fasting ratios? That conversionary or timing turnover process drives people insane!
Thinking fat or protein does not turn into glucose eventually or never will is like thinking you can drive your car without a steering wheel?
If your liver decides your brain needs a little glucose it will trickle a little of that gluconeogenic glucose (rather than ketone fatty acids) to the brain like a battery on a circuit board to a CMOS chip!
Why eating meat & fat is so awesome!
Examples:
- SCALE DOES NOT BUDGE (plateau/stall)?
- INSULIN WAS SPIKED (fat cells were replenished {after being broken down into ketones} and stored for energy or like a snake swallowing its own tale; looping effect)?
- “…The reason you want to under-eat protein on some days of the week is similar to why you want to start intermittent fasting – it comes back to the dance between glucagon and insulin. Lowered protein intake means lowered insulin levels and higher glucagon. …” - Naomi Whittel
-VS.-
- IMMEDIATE GLUCOSE UPTAKE:===>CARBOHYDRATES====>CARBOHYDRATES SHOW UP ON GLUCOSE METER IMMEDIATELY OR WITHIN A CLOSE TIME FRAME THEREAFTER?
The raising of blood sugar from protein is demand driven. But the conversion of protein into carbohydrate is also supply driven.
We catabolize excess protein. How that happens depends on the specific amino acids. Several, for example glycine, are broken down into pyruvate. If ATP is low pyruvate from amino acids is oxidized exactly the same as pyruvate from glucose. If ATP is high pyruvate is converted to glucose.
There are other gluconeogenic (glucose precursors) breakdown products of amino acids such as α-ketoglutarate, succinyl-CoA, fumarate, and oxaloacetate. There are also a couple ketogenic breakdown products acetyl-CoA and acetoacetate and the net effect of consuming protein is roughly half as anti-ketogenic as consuming carbs.
Good explanation, Todd - thank you. I would guess that the speed of lipid synthesis from the additional glucose (created, as you say, by protein degradation when ATP levels are high) weighs on the blood glucose number - it may be an individual thing, and also related to the amount of insulin in response to eating the protein, an amount said to be considerably higher in Type 2 diabetics.
If we necessarily end up with glucose from breaking protein down, then it matters how fast the body clears that glucose - we do see some apparent wide variation among individuals.
Another thing to consider is eating protein raises insulin which drives amino acids into muscle. If the muscle has been used hard a lot of amino acids can be used for repair and growth. Even with minimal use surplus amino acids stimulate a little growth and can help sustain higher muscle mass. But the excess not used for growth get catabolized for energy. Glucose produced in the muscle can’t get released into the blood as muscle lacks the enzyme glucose-6-phosphatase needed for glucose export.
Wow a lot of sciencey stuff…
Let’s see if I under stand you all…
Eat a low carbohydrate, moderate protein, high fat diet in a time restricted eating window for optimal health YMMV 
Actually, if you’re keto and IF, you don’t have the usual sugar burner’s liver glycogen stores. (and you know the muscle glycogen can’t be exported) There’s always a trickle of glucose being made from FFA beta oxidation from the glycerol backbone of the triglyceride, but I’d think our demand would be higher and the glycemic amino acids in the labile pool would look tempting after a while, especially if you regularly work-out.
Thought I would mention why some people who eat meat and fat very frequently on the LCHF (ketogenic) diet and lose weight (burn fat) like it’s nothing (no problems?) and I think the reason for this is, is our individual metabolic ability to oxidize glucose in contrast to perhaps age (not sold on that concept at the moment)?
Figure 6. (above) ”… Metabolites that changed between young and old are indicated in bold; representative metabolites data from the muscle and liver are shown in the left and right margin respectively. …” …More
Well that sucks for old mice. 
Can we get him to do the study in insulin resistant and sensitive people, both carb burners and fat adapted, young and old, athletes and couch potatoes?
Actually, I have seen a couple of his talks where he discusses this, in detail, with an excellent understanding, so I think you are assuming that he is ignorant. Where in fact he is actually very knowledgeable and experienced, having studied this subject for decades, in the lab and with patients and athletes.
I’m thinking of one video in particular where he is talking about how unimportant ketone numbers are, and how pointless it is trying to score higher ketone readings, since ketosis is ketosis and the reading is no measure at all of how efficient your body is at actually using ketones. Sorry, don’t have the vid link handy. It is the one where he reminisces about formulating a keto diet for the record breaking rowing team. 
This is all true but Phinney still talks about protein raising insulin, aka being problematic. Which is only half of the situation, since it also raises glucagon, which is something carbs don’t do. I have not heard him speak on the whole insulin/glucagon ratio thing, which admittedly is pretty novel to most people following the keto diet and has been brought to more peoples’ attention by Ben Bikman.
Phinney’s a smart dude that I still don’t think gets the protein question completely right.
Besides mice! You know what is really interesting, is Japan, they have a long list (or longest list in the world?) of centenarians but one thing that really sticks out is portion size of food not just the quality of food and the soil quality is probably better their than any other place in the world right now, that may explain the longevity and of course you have the Japanese potato full of organic hyaluronic acid (also in bone broth) or the molecular glue (no leaky gut) of the body and green tea etc.
But that portion size thing really sticks out in contrast to centenarians (with no health problems); when I look at serving or portion sizes per-meal, per-culture (looks similar to keto?), just one of those things that make you go hmm?
Then you see vegans of the Seventh Day Adventist sect with quite a few centenarians and I am thinking if all your eating is veggies, your not going to be eating a lot of it because it would get boring after sometime?
As long as you’re operating on a caloric deficit, and keep sugar and starch low, you’ll engage those longevity genes. Who’s to say how long you can subsist?
I just object, as an American, to having the SDA dictate through their policy making puppets nutritional morality.
I see where you are going with the portion size thing, but if I look at the way my parents’ eating has changed over the years (they are now both in their 80s) their portion sizes have drifted downwards for around 20 years. More likely linked to age, activity levels and appetite, rather than a lifelong policy of small portions.
They have always eaten nutritiously, with good quality non-processed foods, and I am glad to say that they are still doing so, whereas many of their contemporaries don’t bother to cook any more and eat easy processed foods, and replace meals with toast or tea and biscuits - which eventually causes malnutrition.
I didn’t know there was any actual research on what I was thinking about but lo & behold there is…lol
Some research on the subject:
- ”…It turns out that calorie control not only works in the Battle of the Bulge, but also can help to extend your life. As a matter of fact, in the European Journal of Clinical Nutrition , Dr. G.S. Roth and colleagues at the National Institute on Ageing in Baltimore make it absolutely clear. “Dietary energy restriction is the only proven method for extending the lifespan and slowing aging in mammals, while maintaining health and vitality.” The equation - less food equals a longer healthier life - has been known for over 60 years now (in mice), although researchers have just begun translating these findings to primates like us. …” - Dr. Will Clower
- PERMANENTLY cutting the daily calories you consume may turn out to have a profound effect on your future life, according to some tantalising scientific studies. …More
- The Secret to Queen Elizabeth’s Longevity “… Queen Elizabeth sticks to small portion sizes, preferring four light meals instead of three larger ones …”’
- “… For the Japanese, hara hachi bunme or hara hachi bu, eating until they’re 80 percent full, is a traditional dietary control that achieves good health and longevity …” …More
- Living to 100: Sardinia’s secret to longevity: In “The Blue Zones Solutions,” author Dan Buettner writes about the Italian island of Sardinia, where people frequently lead unusually long and healthy lives. NBC senior investigative correspondent Cynthia McFadden reports.
I’m just listening to Peter Attia talking about this now. According to him, broadly speaking… general daily calory reduction can reduce the risk of cancers and cardiovascular disease, but into old age the loss of muscle mass which is associated with low caloric levels could be attributable for other older generation mortality causes such as falling and motor-neuron diseases.
