Dr. Benjamin Bikman - 'Ketones: The Metabolic Advantage'

thank you thanks so much I'm delighted to be back Jeff and rod thanks again for the invitation for me two years ago this is where I took my first steps into the low carb community and I've enjoyed it I you probably know I don't attend or present at many of these kinds of meetings it's because I'm a father of young kids and being with them is and giving my wife a break is priority number one but here I am so you're my next priority this time I am delighted to be here I'm glad to follow Zoey in particular because most of you are too polite to get up and leave and you all wanted to hear her now it's time for me again thanks for being here I'm delighted to be invited in a way I'm coming back to what I started with two years ago not in a way I am I'm and so let's just get started in the end I'm going to impress upon you how ketones are eliciting such a unique change in mitochondria across two distinct cell types overall creating what I would consider to be a metabolic advantage here are my disclosures involved in educating and supplementing now let's get into it last time two years ago when I presented I didn't mention these academic ancestors that were really a motivation and inspiration to me in particular Elliot Joslin but Joslin and Benedict diabetes and the metabolism metabolism scientist came together to ask the question to what degree is metabolism or metabolic rate changed from healthy versus type 1 diabetics and please note the year this was before insulin was used as a therapy in type 1 diabetes what they found was that the people with type 1 diabetes had significantly higher metabolic rates this one finding started me asking the questions that I presented two years ago and I'm now following up and showing you kind of the data to finish the story it started with them since then I've found more data that supports this general pair of I'm that insulin is relevant for metabolic health in particular 70 years after Joslin and Benedict study Shri Nair while studying in the UK published this paper so in type 1 diabetics so first of all let's note that they noticed type 1 diabetics had a higher than expected metabolic rate based on their body size which is the main driver of metabolic rate they had a metabolic rate that was about 300 calories per day higher than it should have been interestingly when they gave them insulin the metabolic rate dropped to where they expected it went down about 300 calories per day in the end it was a difference in metabolic rate of around 15 or more percent so insulin this hormone that many of us implicate in being causal or at least very meaningful and significant with adipocyte size and obesity by extension is having an obvious effect on metabolism romantic Andreea function and moreover they detected this very rapidly in real time they found when they administered the insulin to the type 1 diabetics within just minutes they could start to detect this reduction in metabolic rate insulin was slowing things down now there's a lot more they looked at it's actually a very neat paper and there's the reference if you're curious so all of this was floating in my mind two years ago and I presented my very first low carb community talk which again is so delightful it is uncommon for a scientist to get up in front of people and have them clap with enthusiasm usually it's a bunch of it's 20 other scientists who don't really care they just want to make sure they just don't want you to get the next funding that they're trying to get nevertheless I presented this paradigm where obesity could be explained by either a purely caloric accounting or rather a balance of hormones promoting catabolic or anabolic processes while both of these are certainly relevant the laws of thermodynamics need to be considered what I submitted to you was that the endocrine theory actually encompasses and accounts for the caloric theory insofar as when the main anabolic obesity promoting hormone insulin is down the body has entered such a state that beta oxidation of the fats and I'll come back to this in a bit is so high that we now have ketogenesis and ketones are creating this particularly unique metabolic milieu where the cells of the body are more inclined to just spend energy in the form of increased metabolic rate and in the form of wasting remember anytime you're detecting ketones in your breath or in your urine those ketones are little pieces of fat that otherwise would have had to be accounted for and now they've simply left the body so that's it's slight that's not a lot of calories but it nevertheless needs to be considered a night I don't believe it always is nevertheless this is this was the general conclusion two years ago with a little bit of preliminary data to support it now we'll finish the story pretty much so I probably won't ever talk about this stuff again now let's look at the body so within all of us we are interested in metabolic rate and in a way metabolic rate represents a fire it's a flame there it is giving life animation and even yes heat to our to our warm blooded bodies this heat this little fire is the consequence of multiple reactions Happel countless reactions happening in the body and all of these chemical reactions can be lumped into one of two general processes they are either promoting the growth of molecules using energy to grow things those are the anabolic reactions or it's taking these big molecules and breaking them down and getting energy from it to do something else so the catabolic reactions at is at its purest definition this is metabolism despite and the way even I may sometimes use the term if we're talking about metabolism we are strictly speaking talking about the sum of all anabolic and all catabolic reactions now if there's a fire in our bodies this metabolic fire how do we fuel the fire well that of course comes from the foods we eat our three macronutrients now I'm presenting these up here as if they're all equal when it comes to fuel but they are not as you know carbohydrate and fat are in fact fuel protein I think it is not justified to consider protein of fuel because it is only used as a fuel very acutely as David Ludwig showed earlier in transition on the low carbohydrate diet or even fasting assuming the person has an effect to rely on for the production of ketones or in true end stage starvation otherwise protein is miniscule when it comes to its contribution to energy so we will look at protein as a builder and thus we won't consider it I'm not going to consider it fuel so let's just drop it we're decide it being very important we're gonna stick with fuel for now and we're looking at the whole body but in order to talk about metabolic function we have to zoom in a little bit and of course we come to the so called powerhouse of the cell and that's the mitochondria so the mitochondria are the organelles within the cell that are taking fuel with a little help from oxygen because in a way this kind of is like a combustion event it is burning these nutrients we have to have oxygen and now in the presence of oxygen we the mitochondria are using their catabolized these these nutrients this nutrient energy in the process as a result of any chemical reaction we always get a little bit of heat so I'm going I'm going to denote that and I'll come back to that idea but the mitochondria are better than a normal campfire they are they aren't just producing Heat they're clever enough to actually get something productive out of it and that productive thing that I want you to keep in mind is the production of a molecule called ATP you've likely heard of it but just to create a common definition for the sake of my talk AP P represents cellular or chemical currency we often say that we we professors teaching our undergraduate students and because I've missed class stall a week you're my undergraduates for today it's not an insult I hope but nevertheless the the ATP is this is what the cell actually uses to get work done it will use ATP for example to relax the muscle and when the muscle is contracting and relaxing that's a phenomenon known as crossbridge cycling at the microscopic level and we need ATP to do that neurons in the brain and nervous system will use ATP to maintain the appropriate shifting or flux of electrolytes for the sake of conducting an impulse across the length of a neuron and many many more things suffice it to say the cell will use ATP to get something done which I'm just going to define right here as work so the production of ATP represents a cell being productive now with all this in mind let's shift the paradigm a little bit to enable me to present another concept so the mitochondria is interested or are interested in producing ATP this evidence of it being productive and earning its keep within the cell if you will this of course requires fuel and so we'll bring up again fat and carbohydrate and the relevance of oxygen in these and these points throughout these reactions and then the mitochondria will catabolized the nutrient energy producing the chemical energy normally or on occasion this will happen in in what we could consider an ideal balance or an ideal ratio in other words the mitochondria are only using as much energy in the form of fat and carbohydrate as is needed to produce the chemical energy in the form of ATP so essentially we would say it's happening at a one-to-one ratio it's only using as much energy as it needs now here's the first important point in this state we would consider the mitochondria as being coupled now this isn't some honeymoon advice I mean again we're taking the chemical energy and it is tightly coupled to how much the nutrient energy is only being used to the agree that the cell or the mitochondria is producing ATP this chemical workable functional energy that the cell can use to get some work done so we'll say that's happening in a coupled state in this arbitrarily set one-to-one ratio oh and of course in the process it's so efficient that there's relatively little heat in other words I'm just mentioning heat as a sign of of waste because heat is evidence of a chemical inefficiency at the level of the chemical reaction now let's shift it a little bit in this same paradigm we could have the mitochondria working in such a way that it's using relatively too much carbohydrate and fat and it's getting relatively less ATP being produced of course that nutrient energy that's being catabolized if it's not being yoked or coupled to the production of ATP it's going to be producing more waste in the form of say an exaggerated heat emission from the chemical reaction but in this case because we're using relatively more nutrient and getting relatively less ATP we've we've uncoupled that process the cell is using more energy than it actually needs and so again uncoupled will be that would be the state in this relative imbalance where we're using more nutrient energy than we're producing chemical energy so to wrap this general point up let's superimpose the two concepts the mitochondria are using nutrient energy in either a very coupled way in other words it is yoked to the production of ATP it's somewhat demand-driven it's only using as much as it needs or the mitochondria are being very wasteful and they're using more nutrient energy than needed for the sake of chemical energy so to put it another way and very explicitly in a coupled state the mitochondria are using energy very sparingly or very efficiently in an uncoupled state it is inefficient and it's using the energy quite liberally all right now because I teach undergraduates and my lectures are always two hours long to find ways to keep the students engaged and I'm constantly fighting with Facebook and Instagram so that's all actually I find that's a balance of a little bit of irreverent humor a little like what Zooey utilized earlier too with very with great finesse but also with analogy so here's my analogy let's look at the mitochondria as an engine and because and then we don't feed an engine with carbohydrate and fat we feed it with gasoline or diesel which I'll just call fuel and the engine doesn't produce ATP it of course just produces work which I'll convey with these gears because the engine is promoting the it's moving gears moving axles moving wheels and so those little axles will be evident so those gears will be evidence of the engine actually moving the car now in my car which is a 20 year old five-speed manual transmission Subaru Outback I see the RPMs in the speed and because I have a clutch I can really readily control these two things anyone who drives a stick shift knows what I'm talking about in fact so few students drive it and when I park on campus I don't even lock my doors they couldn't they couldn't steal it if they tried they'd be pushing it anyway so here's the general paradigm that I'll use to to convey this idea and then we'll come back I promise to the relevance of ketones we are getting there this is just my long-winded introduction but hope but hopefully for a point so ideally as I am pressing down on the gas pedal in my car my foot is off the clutch now I'm in gear and I see a subsequent and relative increase in the speed of the car in other words as I'm pushing the fuel into the engine to be combusted I'm getting work out of it and so the gears are spinning the axles are spinning the wheels are going and I'm in other words it's working very well and I'm not wasting my fuel in the form of heat production and so in this particular situation or I'm just pressing on the gas and my other foot is off the clutch we would say that the engine is only burning what it needs for me to start moving the car thus in this state where rpm and speed are relatively matched the engine is coupled if you will now in contrast to the student who would try to steal my car they don't know how to drive a stick stiff of manual transmission so they're pressing on the gas pedal and yet they don't know to lift their foot all the way off the clutch they are riding the clutch so to speak and so the actual amount of speed or movement or work that the student is getting out of the engine is pretty low the car is not really moving and in this case of course as I'm indicating there's not much work going on but the fuel is still being used because they're pressing down on the gas pedal and that's being manifest in this inefficient production of heat so in this case the engine is using more energy or more fuel than it needs in order to get the work done so the engine is uncoupled under the hands of this novice driver now I'm not a car guy at all despite my affection for my very old beat-up Subaru which I plan on making my daughter's first car so in this case let's go back to the body and because we're going back to the body let's stop talking about fuel in a generic sense and let's talk about one in particular and that is fat and again let's just keep shifting the analogy back to being relevant and so we'll drop the RPM and speed and now we're going to talk about oxygen use as evidence of fuel use the rate at which somatic Andreea are working because of mitochondria are working they are using oxygen and then we'll look at the production of ATP the productive aspect of what the mitochondria are trying to do now in this case as you know this audience knows better than most if fat catabolism or fat use is very high for very long we begin to produce these small little molecules called ketones interestingly when someone is an active ketogenesis and thus ketosis or getting to what we would define classically as ketosis that production of ketones accounts for almost half of all of the oxidation of fats so someone's burning fat like gangbusters so to speak almost half of that is actually going to the production of ketones a pretty meaningful amount of course this can only happen when insulin is low and in fact that is what got me involved in ketones in the first place a few years ago I'm an insulin guy at my core but you can't really separate the ketones from the insulin well nowadays we do with supplements but those two things are inversely related and of course the gist of it the biochemistry in a very simple way is that as fat is low the oxidation or the burning of sorry as insulin is low the burning of fat is so high that you start to accumulate a lot of acetyl co a an acetyl co a represents this very relevant kind of branch point in biochemistry where can go all kinds of different ways because insulin is low it cannot go to Lippo genesis and be used to create fat also because there's so much acetyl co a it inhibits its own entry into the citrate cycle I bet many of you are actually understanding everything I'm saying and so I think you probably are I don't mean that in a cheeky way but it can't be catabolized in the citrate cycle which means no gluconeogenesis and no more energy production there's only one Avenue left and of course that's ketogenesis so nevertheless that was a bit of a tangent now all of this has been introduction finally you're thinking professor let's get on with it I will so now let's look into the data that my lab is generated where we've been exploring the effects on of my tone of ketones on adipocyte mitochondria and muscle mitochondria particularly skeletal muscle interestingly we also recently have some incredible data from brain tissue but I'm not going to show that this time now maybe next time it's just there's not enough time and too much to talk about so let's talk about the muscle first in the case of the muscle this is a I'm going to base these data on paper we published from my lab last year where we found let's look at a few things and I'm not going to show you all of it although I would submit it's all quite relevant to this conversation first of all we found in Figure a we're just looking at the rate at which the the muscle cells are using oxygen and you'll see in the ketone treated cells the muscle cells are are using a little more normal not a lot but it was significant it's a slight increase in oxygen consumption very importantly we also measured something called the respiratory control ratio that's the figure at the bottom that's a general indicator of mitochondrial fitness or health in other words how well are the mitochondria are responding to what we're doing in a fashion that we're expecting and what we see is that these mitochondria actually a little more responsive in other words they're a little healthier based on this one particular metric also this one's important we see in Figure D ATP production is trending upwards importantly and I'll come back to this when we get to the adipose UM data in a minute in Figure II you'll see that the p2o ratio this is an indicator of how much ATP is being produced per unit oxygen consumed in other words how efficient is it being or in other words how coupled are the mitochondria and we actually see that there's this upward trend not statistically significant but it's certainly not less when the muscle cells were treated with ketones there is at least a fully maintained coupled state what's interesting when we look at the bottom figures the mitochondria are actually producing less what we could call exhaust there's less h2o2 production which is one of the main reactive oxygen species that are generated so when people talk about oxidative stress when anyone talks about the relevance of of fats being oxidized and causing atherosclerosis we actually more accurately say the fats are per oxidized because of what hydrogen peroxide is doing so it's a very powerful very relevant reactive oxygen species and there's less of it when the muscle cells are fed ketones as a fuel now the general conclusions then on this one particular section what are ketones doing to muscle with regards to mitochondrial function and even a little beyond not much change in the rate at which it's using oxygen the respiratory control ratio suggests a slight but significant increase in overall mitochondrial health I didn't take the time to show you this but we found also that ketone fed muscle cells were more what we call viable they grew better and were more resistant to injury so they were a little more robust a little tougher if you will which is a good thing for any cell in muscle cells in particular they had reduct reduced production of reactive oxygen species in the form of h2o to that primary Ross molecule and then lastly we found a maintained and even a trend for increased ATP production so if we look specifically at the content from the from the perspective of the mitochondria we see that it's using a lot of oxygen the mitochondria are pressing down on the gas as readily as they want to and they're getting a lot of activity out of it it's working so the mitochondria are as productive as you would expect as it is ramping up its use of fuel so what that means again in this case the mitochondria in the muscle cell when fed ketones are exposed to ketones are very well coupled they are using the energy they need and for a tissue cell that has a high energetic need and yet not a lot of storage in itself as energy it is that is I would submit to you a pretty clever use of ketones or or a clever response to ketones to be very efficient and prudent with the use of energy in a tissue that has such a high workload and demand and expectation and yet so little actual energy stored of course it can take in energy very readily now is this relevant I'll do this with the adipose data as well but I submit that it is this study from several years ago looking at people in a ketogenic diet found an increase in lean body mass some of which of course was muscle you aren't gaining muscle if muscle cells are wasting energy as anyone knows that anabolic reaction of building muscle mass is extremely expensive energetically speaking and moreover this could be evidence not only of very well tightly coupled mitochondria but also the fact that the ketones as I mentioned we found are helping the muscle cells be a little more robust and resistant to injury so this increase in lean body mass could also be a flexion of the muscle cells themselves simply being a little tougher than they were before another study done by published by preeminent ketone scientists in the UK and you've all seen this study they found that actual exercise production was better when the athletes were fed relatively less glucose and relatively more ketones so again a potential evidence suggesting irrelevance to what I was showing you that ketones are a good fuel for the mitochondria perhaps because or for the muscle cell because of what the ketones are doing to the mitochondria helping them work in a more tightly coupled state in other words using nutrient energy insofar as it needs chemical energy okay now let's look before we leave the muscle behind let's look at the heart muscle which for you right now not me cuz I'm up and I'm animated for you your heart is the main caloric demander when it comes to muscle of course the liver in the brain are higher than the heart but the heart is still very relevant with regards to muscle this study published a few years ago by some legends Chuck hopple in particular being a heart mitochondria guy they found that the the failing heart so in heart failure the heart starts to rely more on ketones a follow-up to this found that the failing heart as it was relying more on ketones actually increased its production of ATP that's what that figures showing as the ATP as the ketone had two levels of ketone and the heart failure situation attack you could see that the ATP production went up as the ketones went up and so the ketones at the heart are improving ATP production it wasn't enough to rescue the heart failure in this model but it still was sufficient the ketones did increase ATP production I believe that is again evidence of ketones helping the matoke Andreea be more tightly coupled and again that means using nutrient energy more efficiently in the production of chemical energy ATP all right now let's leave the muscle behind and get into the fat cells I need to admit or present this as well that same some of the same people from the UK ketone preeminent group found that ketones helped brown fat be a little more uncoupled that's the gist of this particular figure and they were looking at uncoupling protein 1 or UCP 1 now if this is kind of unfamiliar brown fat white fat I'm not going to take the time to talk about it because I will assume that you are like my students and you've done your homework before coming if it is new to you then I beg your pardon I'm not going to take the time but I'm Jeff and rod posted my lecture from two years ago and it's readily available on YouTube so you could check that out for understanding the difference between brown fat and white fed but very briefly brown fat has a lot of mitochondria that are very uncoupled white fat has very little mitochondria that are very tightly coupled only using energy when it needs to ok so this is just some background showing that before I ever started talking about this there were others who are talking about it probably much more lucidly and with a much more beautiful accent but by the way the Canadian group why are you ignoring one of your own just because I don't I've lost my Canadian accent man I'm I'm a little upset all right I don't have a man without a home I guess alright anyway so let's now look at the rodent work that we did and then I'll move into the human work making it supremely relevant I promise here we were looking at white adipose tissue the the prototypical in fact the the type the fat on there on the rat and in the mouse it's the same it's this small little pocket of subcutaneous fat rodents don't have a lot of subcutaneous fat like like we do and of course there's an ethnic kind of disparity among humans but generally as people are getting fat a lot of that is subcutaneous fat which is generally pretty healthy so I always joke as my students if the jiggles it's good it might not look good but it's healthier than the alternative so briefly what we see here and we are looking at the white adipose tissue w80 the o2 flux the amount of oxygen the adipose tissue was taking you can see them in those blue bars the ketone diet animals their oxygen consumption was significantly higher in other words this white adipose tissue that importantly has the capability to act a little bit more like brown adipose what's called it it becomes beige it's not quite brown but it's not quite white anymore it's a little in the middle it's behaving a little more in an uncoupled fashion so the mitochondria are wasting energy more and that's reflected in that observation it's using significantly more mitochondria oxygen in other words it's using its fuel much more readily importantly we do not see a relative increase in ATP production so that bottom figure really tells the story the amount of ATP produced per unit oxygen consumed the pto ratio drops significantly strong evidence that ketones are causing this white adipose tissue to become more uncoupled and we see very relevant changes in gene expression that would be mediating causing in other words these mitochondrial changes increasing the number of mitochondria in to the end the degree to which they are uncoupled now in humans what we've done that print this is still unpublished but but getting more and more solid all the time we have humans coming in in two groups weight stable adhering to standard diet and no detectable ketones from a blood ketone monitor or in obvious ketosis detected and measured quantified we've done two things to these people we measure resting energy expenditure under a metabolic a little hood like a space helmet they wear and we just track the gas exchange with oxygen and co2 that gives us something called in.we that's indirect calorimetry which we're using as our marker of resting energy expenditure and then we're also pulling fat biopsies from their bellies the subcutaneous abdominal fat so let's look at the adipose biopsy data first we firstly see in this very condensed simplified version of looking at oxygen use a significant increase in the amount of oxygen consumed in the fat tissue of humans that are in ketosis so very clear definitive evidence that these mitochondria in these fat cells are more active now when we look at the ATP production in particular the amount of ATP being produced per unit oxygen consumed again what we define as the pto ratio or how we measure the pedo ratio it is almost half so these mitochondria are half as coupled or in other words twice as uncoupled as the mitochondria are in the fat cells from the people eating the standard diet in other words the mitochondria in the fat cells of the people adhering to a ketogenic diet people that are in ketosis whose fat cells are seeing ketones it is causing mitochondrial uncoupling and we don't have the gene data yet and that's on the way now with resting energy expenditure we did not detect a significant change in energy expenditure across our patients however when we split it up by age we saw something in fact it was significant there was a slight but significant increase in resting energy expenditure in the older subjects and I that's myself included so I can use that term without offending anyone so in the older subjects compared to the younger college-aged in particular subjects we saw the difference ketones are doing something in the older people fat tissue that they weren't doing or a whole body level I should say that wasn't obvious at the whole body level of the younger subjects so in this case as we conclude this section we see that the ketones are dramatically increasing oxygen consumption in the mitochondria of fat cells meaning the mitochondria are much more active they're very healthy still there's nothing clearly wrong with them however they are making much less ATP definitive on undeniable evidence of the fact that these mitochondria are more uncoupled so they're wasting energy and then in the end this increased degree of wasting energy in the form of just heat this could explain the differences we see in resting energy expenditure so in this case the mitochondria in the fat cells with ketones they are pushing the foot under pushing the gas pedal so the oxygen consumption is ramped up and there's not a relative increase in obvious work or productivity and so these mitochondria are as you of course know already very uncoupled now what's the relevance here I submit again there is a lot of relevance this study published by people who don't like this kind of conversation nevertheless provided pretty wonderful supporting evidence to find that in this extremely tightly controlled environment people that were in ketosis despite eating the exact same amount of calories had a slight yet significant increase in metabolic rate another study and Dave Ludwig showed these data earlier now he would be the first to say in his study these people were not in what would classically be defined as ketosis but nevertheless they found that in the group with the most tightly controlled carbohydrate consumption or I should say least amount they had the highest metabolic rate some degree of uncoupling may explain some of what we're seeing and that may explain why people in a ketotic or a ketogenic diet keep a katatak state don't have to try to account for calories quite as precisely as someone who's not in ketosis there is obviously a little more wiggle room and again it could come down to the level of the mitochondria and whether the medic Andreea are coupled or uncoupled and in fact very briefly when I heard David Ludwig's talk this morning and I consider this kind of a nice follow-up to his I have mentioned two years ago data that I only showed a little bit but when insulin is very high ketones are low of course because of the inhibition of beta oxidation and the very powerful inhibition at every step of ketogenesis that insulin elicits ketones are wiped out in this we published a paper last year we find that in animals when we induce hyperinsulinemia resting metabolic rate is down particularly in the dark cycle which is when they're more active because they are nocturnal we see that when we look at these specific fat depots peri renal which is visceral white fat subcutaneous which is the fat that can shift into more beige like or the prototypical brown fat which on the animal is inter scapular on humans it's kind of all around the thoracic area we see that those fat depots that can be a little more uncoupled became less uncoupled in other words more tightly coupled when insulin was elevated so insulin was making brown fat which wants to waste energy or fat that can kind of be hay like brown fat act more like white fat it was making it be more tightly coupled in other words wasting very little energy and we supported this or this finding was supported by biochemistry looking at actual protein levels so in conclusion the data find collectively that ketones are inducing a mitochondrial uncoupling in fat cells the fat cells are using nutrient energy but not really getting productive chemical energy out of it so again it is uncoupled those two processes in contrast ketones are actually maintaining if not improving the coupled status of the mitochondria in muscle cells so one way to generally look at this in conclusion and reflective of my love of alliteration and making sure my students can always remember some key point ketones are inducing the state of affluent adipose tissue in other words it is wealthy and it is very liberal with the wealth in contrast it's inducing this state of Mies early muscles so the muscles are more reluctant to give away their energy they're only using what they need altogether I believe this creates a situation where ketones given the different effects of the mitochondria in fat cells versus muscle cells what we could consider a metabolic advantage thanks for listening if you have any questions I would look forward to getting them thank you very much [Applause]

Channel: Low Carb Down Under

Views: 248,759

Rating: 4.9005814 out of 5

Keywords: Low Carb Down Under, LCDU, www.lowcarbdownunder.com.au, Low Carb Denver 2019, #LowCarbDenver, Ketones, Ketogenic Diet, Brown Fat, White Fat, Ben Bikman, Insulin, mitochondria, Fat Metabolism, mitochondrial changes, metabolic advantage, nutritional ketosis, LCHF, Low Carb High Fat

Id: cCJS2m92KwI

Length: 37min 37sec (2257 seconds)

Published: Thu Mar 28 2019

Reddit Comments

[u/unibball]

Makes sense. If you are gorging on fruit and starch to get fat for winter, you would not want to waste any of that energy, so your metabolic rate goes down. Eat carbs year 'round, get fat... there you go. Sure, it may be just 15%, but 50 pounds over 20 years can be explained by about 20 calories a day, either less burned or more consumed.

I'm glad he's a teacher.

[u/Ricosss]

Great talk. I do would love to know the difference though when it comes to glucose sparing. As you transition to a high fat diet, ketones become a fuel for the muscle cells. But as you get long term adapted, I believe your muscle cells start to rely more on fat directly, also sparing ketones. How much abundance of acetyl-Coa is there going to be when everything runs efficiently on fat? Glucose sparing at its highest are we still producing a lot of ketones? Meaning > 1.5mmol Linked to this is VLDL secretion which is very low showing evidence of little availability of fat in the liver thus also not enough fat to produce a high amount of ketones?

[u/OwlyFox]

/u/sanpilou