Peter Attia· MD
and and and here is one of the that is an interesting point because the question is if we're trying to change the serum saturated fats into something else okay i mean the body is obviously doing that one would have to wonder is that a protection mechanism why do we want to do that i i yeah to me that's a great question sarah it seems counter-intuitive if i'm going to be obvious because we would think that a saturated fat is much safer it's inert there's no chance a reactive oxygen species can be formed out of it why is it our body even if we wanted to export fat from the liver which we could argue all the reasons that's not a great idea why would we go to the trouble of this conversion all right well let's go through it really quick and then get to answering that question because i think it's really important and really sheds light on why we need to be paying more attention to the all-important poa and of course the precursors and and enzymes that act in its creation so let's go through if you will this cartoon that i know looks really busy initially but let me just kind of run through it starting here in the intestine and remember you know we'll start off by saying our focus in health care and in nutrition recommendations for so long has been low fat low fat more carbohydrates higher carbohydrates well let's take a look in the intestine at those carbohydrates changing the focus for a minute so they come in rapidly absorbed carbohydrates or even our slowly absorbed carbohydrates our starches okay um and what happens when they come in right as glucose that feeds in again through glut2 into the pancreas pushing out more insulin insulin then feeds into the liver and what we get here okay is going through it a big big part of this is srebp-1 okay and i don't know if we need to get that technical but we'll lead here to that enzyme we were talking about the scd-1 or sterile coa uh saturates a desaturate increasing okay very important and it comes about through other means as well fructose coming in through glute 5 or glucose coming directly into the liver through glut2 they're all feeding into this by slightly different mechanisms to increase this scd1 now we're going to look more at the process in a different way so we have increased hepatic first of all saturated fat okay here's our 16 0 the saturated fat all right uh increase hepatic levels of this what gets turned on as from the past cartoon we get that scd-1 activity increasing that leads to this increase in poa all right coming down here what's the end gain here increased vldl all right same thing over here looking at it different we see again scd-1 if it's blocked we won't see that all right we'll see a decrease in vldl and this again has to do if this scd enzyme is blocked we're going to have an increase in the saturate a decrease in our poa okay but again what we have when we're consuming the high carbohydrates even if they're the again more refined carbohydrates or the less rapidly absorbed carbohydrates this is the path that we wind up going on 16 1 is our 16 0 saturated fat is elevated and it turns on this cascade leading to increase in vldl