ATP, Obesity, Peru discussed on The Peter Attia Drive


The two look alike but when fructose is metabolized there's this process that causes the energy in the south to fall fall before it goes up so normally when you eat a calorie when you eat any kind of nutrient we use it to make energy. That's what we do but when you eat eight fructose the energy in the south false before it goes up it's the only nutrient that lowers energy in the south. Seem more what you mean by that. So we're talking about a cell in the liver for example. Yes I'm talking about the cells that metabolize the fructose okay. So we'll contrast it with Glucose so with glucose enters a cell it gets turned into Peru vate and ultimately. ATP is made so you're saying total energy goes up as a result of metabolising that glucose. So whenever you metabolize any kind of calorie any kind of food eat food you're going to metabolize it to make energy. That's what we do. We try to break down the food and we use it to make energy that energy is called. ATP ATP is the currency in our body that we a US to make us run walk. Think talk everything so the peace pretty critical but to make. ATP You have to spend a little of it to make it so the process of breaking down metabolising food or glucose or fructose or requires spending a little bit of ATP before you make it well what happens is when you metabolize glucose you do oh spend some ATP but the body has a system whereby feeds back to stop the process before any significant ATP ATP depletion occurs so for example. There's an enzyme called phosphor fructose kindness. That's used in glucose metabolism if ATP LEVELS LEVELS FALL THAT ENZYME GETS turned off to stop glucose metabolism to allow ATP levels to come back up but when fructose else's metabolize the enzyme that metabolize. Fructose is called fructose kindness. And when that metabolize fructose it consumes the. ATP IN AN UNREGULATED WAY. So if the SAL sees a Lotta fructose the P. levels can plummet by forty or fifty percent percent in the cell and that signals a huge number of effects throughout the body. It's like a mayday signal. It says we're under attack. We're running out of energy and switches the animal into a condition in which they're trying to preserve their energy so they reduce their metabolism a reduce their expenditure arresting the energy expenditure. They shot the energy that they're eating. The calories salaries are eating into fat and glycogen as opposed to making more. ATP They're trying to protect the body by putting you into a system where you try to store fuel it triggers hunger and thirst. That makes you wanNA eat more so you eat more to restore the energy but at expense that you're shutting much of it into fat and into fuel storage so fructose turns out to be used by animals as a mechanism to store fat. Normally animals will regulate their weight beautifully. They just maintain their weight. Normally if you take an animal and you put a tube down its throat and give it extra food to make a gain weight if you take the tube out the animal go right back to its normal weight if you start an animal and so it's below its normal. Wait and then you let it just eat. It will eat back to its regular weight but when it wants to gain fat it will do so usually through mechanism that involves fructose fructose. So what they do is they like a hibernating. Animal will start eating a lot of fruit in the fall to increase. Its weight and increase induces uses insulin. Resistance it gets hungry drops its metabolism. So that most of the energy at each goes into fat and same thing with the long distance migrating grading bird. They'll start eating fruit to get the fructose. And so this is a very common patter and it's driven by that. ATP EP depletion and this is distinct or in parallel of course to this year case mutation so they can you separate these two phenomenon in other words if you can and restore your a case to the non mutated version do you still have this problem around the ATP depletion yeah so the ATP depletion triggers a series of reactions and what happens with the key one is not only does ATP decrease in the SAL but intracellular intracellular phosphate also falls on that activates an enzyme called amp the anthonys that converts the broken down product of ATP pitches amp and it converts it to uric acid and that process has multiple steps. And we know that that whole pathways involved in the generation and stimulation of fat diet. Insulin resistance fatty liver elevations in blood pressure a variety of effects. The facts and that pathway is what seems to be critical for inducing obesity from sugar. Let's go through that again because that what you sort of talked about at the very end is effectively. The thesis of your book the Fat Switch. You explain what. ATP is a denizen Tri Phosphate in the tea. Of course dancer try or three phosphates. It's the liberation of a phosphate. That is the production of energy. So when you need to breathe you need to move when you need to do anything you have to turn a tee pee into a DP so the chemical reaction is dancing. TRIPHOSPHATE becomes a dennison. Di Phosphate one phosphate escapes. And that's what gives us the energy. Now that can happen again. A DP can lose lose one of its two remaining phosphates and become a. m. p. identifying mono phosphate which you said after is the really critical critical article piece of this. which is when you have a molecule of identity mono phosphate it stands at a proverbial fork in the road? It can either go down a path that is driven by something called a. m. p. k. or amp kind is or can go down the pathway of amp de now. Let's go back to this point because I again. It seems everything comes down to that choice. What happens if amp goes down the am PK pathway versus the amp deep? Pathway yeah so if it goes down the amp K.. Pathway it actually is burning energy. It's burning fat. It does a lot of really positive things if it goes down the aim PD. Pathway it goes down a fat storage urge pathway. So it's their exact kind of opposites. amp if you stimulate. It will cause insulin resistance and eventually diabetes whereas if few stimulate amp K.. You can actually use that. Med Forman to actually treat diabetes so that fork is critical. And what drives that switch. Is the fall in interest siler phosphate. And the reason that phosphate falls is because it's taken up in the fructose one phosphate are taken up by fructose. So so the fructose gets phosphor elated by the ATP and it becomes fructose one phosphate. That's equestrian phosphate and there. Is this process where both. ATP EP levels fall and interstellar phosphate falls in that triggers this aim PD pathway. And if we interrupt the pathway we can black a lot of metabolic effects do other animals also have this phenomenon. Oh yeah no we can show this. We actually showed it in hibernating squirrels so when a squirrel girl wants to gain weight it will activate the pathway for am PD when it's hibernating burning fat it activates the P K pathway athlete. I got it so even though humans are most close descendants in primates have the euro case mutation this ability to toggle goal between amp K.. And Ham PD is unique to any species that has the potential to gain weight and wants to use it to their advantage. I'll absolutely part of the pathway through which aim PD is working involves the generation of uric acid. So we know that the uric acid when it's going up inside the cell is doing all kinds of via logic effects in the aim. PD driving that there may be other things. Besides the uric acid so the hummingbird the squirrel can still store fat. They just don't get the bump in uric acid that comes with it because they don't have the euro case mutation. Well actually the Hummingbird does have the your case mutation or yeah. I don't know my evolution so breads HAB reply. Forget it it off. Yeah reptiles the case mutation even dinosaurs had the you're chasing sue the dinosaur tyrannosaurus rex. Actually she had got. I mean that's got to be. Why Renaissance Rex with so ordering because if you think of this is not rex? Great Toe I mean. That would be infuriating memory. Bronx Out there I think so. He's eating the broncos. Sorry sorry to get back into the minutia of this but I it's important. You still have to formulate glucose during its metabolism awesome. Why is it that the phosphorylation of Glucose during its metabolism to Peru doesn't result in a strong enough drop in intracellular phosphate to cause the same problem because has reaction stops whenever there's The phosphate and ATP levels start dropping a little bit about auto regulatory thing with the regulatory thing with the enzyme stops functioning it's inhibited and then allows the ATP levels stay normal so here's a really cool foul up of this and added. Sugar is much more likely to cause obesity if you drink it rather than if you eat it and the reason for that is. Is that when you drink a drink. That has fructose in it. We tended drink a lot in a short period of time. So if you have a soft drink you can drink now. Why does it have a lot of sugar? But we tend to drink it fast and so the concentration of fructose turns out to be high when it gets to the liver and it's the concentration that triggers this reaction so if the concentration of fructose is really low the ATP Pete Depletion may not be significant to drive dramatic metabolic effects but if the concentration fructose is really high. Then you're GONNA get a big big metabolic effect so eating like a candy bar where it's coming with lots of fat. Lots of glucose lots of all sorts of things lots of protein gene. You know if it's like a snickers bar in its got nuts or whatever even if it's the same amount of fructose even if you're talking about twenty five grams of fructose versus twenty five grams of fructose. There's you would drink very quickly. You're saying equal amounts of fructose can produce a different effect if both the speed and the concentration with which they arrive at deliver liver are different. Yeah it's the amount it's the speed and it's ultimately how rapidly it's absorbed so if you drink something if you take a lot of fructose like I mean candy is very concentrated fructose. I mean if you eat that for example Empty stomach that will be absorbed faster than you eat it with oatmeal. L. Or something. You know where there's five or and so forth and so the speed of absorption the makes a difference so for example if I was working for a High Fructose Corn Syrup Company and I wanted to prove that a soft drink wasn't bad. I could do a study where I would give the soft drinks. It's two people but I would give it over. You're only allowed to make a tiny sip every ten minutes. So takes you three hours to drink soft drink in that case the amount even though you drinking a lot the concentration may never be never let the phosphate depletion get significant difficult enough in magnitude that it really triggers amp. Yes that's it you know. It's really interesting. I think of all the sugar. The PRO sugar studies. I've read they are funded by the sugar industry. I don't think I've ever dug into the methodology to look at factors like that specifically. Well the other issue is thank you. Just take a single dose of fructose. Most of the metabolic effects are best. Seen like in the first four hours following the ingestion so the triglycerides strides go up and the uric acid goes up. The blood pressure goes up. But if you just do a single dose study if you then look the following morning or or the effects of now kinda come back down then you can't really show it in a lot of these studies. They design it that way so they say a high. Fructose doesn't raise uric eric acid but we measured it after fasting overnight but the surgeon uric acid occurred earlier. So that's the common trick so all these things you're talking about with. Fructose seem to fit almost directly into the five characteristics of Metabolic Syndrome which are elevated glucose. So that insulin resistance we'd be manifested is elevated glucose elevated blood pressure elevated waist waist circumference of storage fat elevated triglycerides. What you just said and the only one we didn't address is low? HDL L. Cholesterol which is the fifth finding that now. Of course three out of those five or sufficient to put you in the category but fructose does all five. What is the mechanism by? So you've already ready described the mechanism by which it does three of them we alluded loosely to how it raises triglycerides. But I'd like to talk about that more and then of course I'd like to hear how it lowers. HDL cholesterol draw. Okay so the uric. Acid generated by fructose has a very pronounced effect to stimulate oxidative stress. US in the Mitochondria and fructose also generates lactate big time in the lactate also has effects on my country's you learned from Dr Under Similan talk and in addition fructose preferentially decreases Mina conrail function and stimulates glycolysis Colossus. And so all those things. 'cause you get this big oxidative stress to the monarch Andrea and there's an enzyme in the mighty Qendra that drives his fat oxidation called. No Coy Hydra tastes..

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