Peter Attia· MD
of the healing process glucose is is instrumental for self proliferation W healing and part of is lactate too as a byproduct in singular molecule but um but we see that um um and this is a study that we published looking indirectly a methodology to look at glycogen and we did it with a with a it's it's a pilot study we did with the ICU patients they don't have glycogen and it makes all the sense in the world because if you enter ICU first of all normally sorry when you say they don't have glycogen you mean liver glycogen muscle glycogen are depleted by how much and and depleted to what level yeah so let's say that let's say that you have 500 grams you know of of of glycogen um if you have a full High carbohy diet so that might not be the case of someone entering the ICU first because they might not be elite athletes or they might have maybe 300 grams or they might not have that adaptation to home more glycogen so let's say they have 300 grams or so uh and then uh by the time they get into that condition the body uses about three times the glucose at rest now an athlete uh use that same glucose but a higher intensities but only for a reduced amount of time 2 hours 3 hours for hours whereas the ICU patient is 24/7 right So eventually the body is going to run out of glycogen in the muscle or it's going to be under huge stress so the body has evolutionary mechanisms this is a wonderful machine and it needs to continue so it increases um another route which is uh glutaminolysis so glutamine is an excellent source of fuel it enters directly the mitochondria um we have seen in in in in the publication that we're going to show um now that um when we publish it is that when we when we uh inject mitochondria with h with glutamate uh it's incredibly well oxidized and what's the source of of glutamate in these ICU patients are they breaking down muscle exactly so this is this is where CIA comes into place we know that pretty much every single ICU patient becomes um CTIC or suffers from muscle muscle waste and this is the syndrome right post IU muscle waste syndrome um and this is where like where why do they get CTIC or catabolic right and and and why they overexpress tremendously levels of glutamine because they need it for either uh enter the the CP cycle for energy or for glucono Genesis so this is one of the things that uh we learn a lot from ICU these ICU patients they have hypoglycemia right yet they're not given them usually because they have hypoglycemia it's true too that in the acute ICU phase they also have insulin resistance right but obviously this hyperglycemia and ICU doctors historically have seen this it's like whoa this patient has hyperglycemia of the chart so obviously we're not going to give them IVs of FIA of glucose we're going to give more protein and glucose I mean and FAS and in fact glutamine has shown that increased survival rate in these patients right uh but where is this hyper glycemia is coming from when you do not have glycogen it comes probably from proteolysis right where you break down protein from your muscles to release glutamine but I mean I think we could we would only know that if we understood hepatic glucose stores because regardless of how much glycogen is in the muscle it's never going to make its way into circulation because the muscle can't fully def phosphorated so do we have a sense of what the hepatic glycogen content is cuz I can't imagine the body would ever let anything compromise that given that if the liver can't produce glucose continuously the brain dies so it might be that this is true true and unrelated right it could be that the the muscles are depleting glycogen because of high utilization but the liver through glucan Genesis has plenty of glucose that's what's making it into the circulation because of hypercortisolemia because of other acute phase reactants and so we have hypoglycemia but it's all being mediated by the liver which has no trouble maintaining glycogen levels and again from an evolutionary perspective you much rather air on the side of hyperglycemia than hypoglycemia under period of stress absolutely and is and is necessarily and that's I think what's the source of that gluconeogenesis right so it's probably glutaminolysis right coming from the muscle so this is what um this is my hypothesis right that those muscles they eat themselves to feed themselves or to feed the rest of the body right this is why so it would suggest that exercising ICU patients would be important right so getting some loadbearing resistance even of course they're in a bed but you know sort of moving their extremities against a load supplementing with amino acids absolutely could actually improve outcomes absolutely there's there a lot of research in this area my colleague uh Paul wh Meer who used to work here with me at the University now he's in Duke he's doing a lot of research and uh and practical work with that but with the with this is like uh yeah this hypoglycemia probably comes from glucono Genesis um uh and again this is this is what to to going back to where we started um um yeah could be that there's a lot of um glutamine released you know when you're also in know keto acidos State as well especially in the first phases of that right we know cortisol is very high at first the same thing that we see in ICU patients that that the two main parameters that are predict predictors of mortality at the ICU is a hypercortisolemia high cortisol levels and high lactate levels right they both are completely related right anyways um um yeah I think this is this is fascinating there this a great model to understand um metabolism stress metabolism of these patients in the ICU patients and and that's the other thing too once once you exercise and this is a very important concept for people with type two diabetes with type one