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The Metabolism Reset Diet | How To Improve Blood Sugar, Inflammation And Lose Weight In 28 Days With Dr. Alan Christianson

The Metabolism Reset Diet | How to improve blood sugar, inflammation and lose weight in 28 days with Dr. Alan Christianson coverIn this podcast, I am speaking with my good friend Dr. Alan Christianson – a New York Times Bestselling author and naturopathic doctor who specializes in natural endocrinology – about his latest book The Metabolism Reset Diet and how to improve blood sugar, reduce inflammation and lose weight in only 28 days.

In this podcast, Dr. Christianson will cover

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The Metabolism Reset Diet | How to Improve Blood Sugar, Inflammation and Lose Weight in 28 Days with Dr. Alan Christianson – Transcript

Ari Witten: Everyone, welcome back to the Energy Blueprint Podcast. I’m your host Ari Whitten. And today I have with me for the, I believe, fourth time. I think that we’re setting new records. My good friend, Doctor Alan Christianson, who is a New York Times bestselling author and naturopathic medical doctor who specializes in natural endocrinology. If you’ve heard the previous podcast, you know that I have an enormous amount of respect for him. He’s one of the highest integrity health professionals who’s really bringing – who doesn’t go along with the fads and really brings an evidence-based look to pretty much all the topics that he talks about. So, I am excited to bring you for a record fourth time, doctor Alan Christianson. Welcome back to the show, my friend.

Dr. Alan Christianson: That is awesome. I’m just jazzed to be here with you, Ari. Thank you so much.

Ari Whitten:  Yeah. So, you have a new book. It’s awesome. The Metabolism Reset Diet. I believe I even wrote a review for it.

Dr. Alan Christianson: You did. You’re a lot of the inspiration for it too, for sure.

The importance of resetting the metabolism

Ari Whitten:  Oh, thank you. Well thanks. That’s nice to hear. Thanks for the kind words, but I think you’re giving too much credit. This is pretty novel information and most of it is not things that I’ve talked about, but it’s awesome work. And we’re talking about resetting the metabolism and a big focus of this book is the liver. So, give us a sort of 30,000 foot view of what we’re talking about when we’re talking about resetting the metabolism and why the liver matters – why you’ve kind of centered on the liver as being of central importance. Because most people think of the liver a sort of being there for detoxifying our blood. They don’t necessarily connect it with fat loss or resetting our metabolism. So, what’s the big picture there and the sort of framework for your new book?

Dr. Alan Christianson: I will. Before that, the part that you deserve credit for is that we had a conversation about this topic and the micro workouts idea came from you. This included some movement to keep the muscles activated during a time of temporary fuel restrictions.

Ari Whitten:  Yes. Yeah. It’s funny, I was listening to another interview that you did with our buddy Pedram and I heard you mentioned the micro workouts and I was like, Huh, I remember talking to him about that. I wonder if he got that from me, or if you start sort of stumbled across the idea somewhere else.

Dr. Alan Christianson: No, I thought it was awesome.

Ari Whitten:  Sweet. Yeah. Well thank you.

Dr. Alan Christianson: So yeah, the liver, you know, the best analogy I’ve thought of is that the body gets too much fuel and it stores it in various places, and some places are more harmful than others. I’ve seen these like lawn fountains – growing up in the Midwest – fountains where the water fills a bucket on top and then that fills a bowl, that fills a bowl. You know, when it wasn’t freezing outside, they looked pretty cool when they were working, but the body does that with its fuel. The first place that any extra fuel goes to would be muscle mass. You know, muscle tissue gets first priority. If the muscle doesn’t want it, can’t take it anymore, then we think about subcutaneous fat, then we think about visceral fat and then we think about liver tissue. And when the liver can’t take anymore, the sad thing is it’s the human equivalent of Foie Gras. You know, you have animals that are force fed, their livers get fatty, and they change their physical properties. And it happens to us by a large matter of degree and there’s disease states, but it’s not so much like you’re perfect, and now there’s a problem. It’s this big continuum. And the problem with accumulating too much fat in the liver is that you make a tour of the body loses the capacity to effectively burn fat in the liver. We can talk more about how that works, but yeah.

The liver’s role in glycogen storage

Ari Whitten:  Very, very nice. So the liver… there’s two different things we’re talking about here when we’re talking about liver storage of fuel. One is liver glycogen and the other one is a fatty liver or like fat sort of…

Dr. Alan Christianson: Triglycerides

Ari Whitten:  Triglycerides overflowing in the liver. So, first let’s kind of step back and just talk about sort of the liver’s role in glycogen storage. And I mean before we sort of get into the fatty liver, but what’s the liver involved in as sort of on a basic level as far as storing energy for later use?

Dr. Alan Christianson: You know, a pretty cool thing. Our bodies are always needing energy, but we’re only consuming it during distinct windows of time. And so, the liver is the main place that holds that excess and then releases it as we need it. And in this context, relative to glycogen, we can think about glucose. You know, we’re consuming carbohydrate or we break down muscle tissue, but we always have to have glucose in our bloodstream. And when things work well, the liver takes it and it stacks it in. You know, steel belted radials? You’ve got threads that wraparound threads that make braids that wrap around more threads. So, it’s kind of like that. It’s a lot like what starch is in plants, but it’s like an animal version starch and that’s our glycogen. So, the liver housed somewhere around enough to power us completely for 90 minutes, but in normal metabolism, we’re using a little bit of that, plus some triglycerides and we can keep our blood sugar stable between meals. And so, any glucose that’s more than we need in the moment it goes there. And then in between meals it comes out of there. And we see this for example, like when we define diabetes. One of the ways is by morning fasting blood sugar that’s greater than 126. And assuming someone’s not sleep eating, which is rare, but it happens. But assuming that’s not case, that’s not the body responding badly to a carbohydrate rich meal, that’s not oatmeal spiking blood sugar. You know, that’s the liver pouring this stuff out. The blood sugar drops off and we’re not eating. And the body says, Hey, I need some more. And if the liver is overloaded, I guess it’s like when your suitcase is so stuffed the zipper’s broken. You know, when the liver is overloaded, you ask him for some glucose and it’s like, Blah! Here’s a ton.

The liver’s role in fat gain

Ari Whitten:  Okay. So, liver’s there to store fuel during the periods that we don’t need it. Sorry, during the periods that we’re not eating and that we need to be releasing fuel to burn it. But there’s also this other thing that if we’re chronically overloaded with energy coming into the system, that the liver eventually gets fatty and starts to accumulate fat. Now, why have you centered on that process as sort of such a critical factor in this overall mix of why people are getting fat and, and how to lose fat. Why is that the critical step of this whole process of fat gain?

Dr. Alan Christianson: You know, it came onto me as an insight. It was reading a long paper about the, the chemistry, the pathophysiology behind fatty liver and how it ties to diabetes. And they were showing pictomicrographs of hepatocytes, of liver cells. And you can see these liver cells and physically the triglycerides have compressed and crowded out the nucleus, which is the DNA, the mitochondria, but it’s also crushed out the glycogen storage vesicles. So, here’s what that really means to make this make sense for people. Imagine that – this is a funny analogy to use with you – imagine that you want to stay warm at night when you’re camping. *Laughing

Ari Whitten:  I think we have to do the 30 second quick backstory.

Dr. Alan Christianson: Oh, you could let them wonder!

Ari Whitten:  So, Alan and I did a backpacking trip to the Grand Canyon. What was about a year ago, year and a half ago? And of all things to forget during, I think it was what, November or something? We were there during winter.

Dr. Alan Christianson: About twenty degrees at night. It was cold.

Ari Whitten:  Yeah. Of all things to forget, I forgot my sleeping bag. So, I ended up, we ended up having to rig… I was sleeping in just my clothing, like all the clothing that I had packed. And then one of your, what do you call them? Those sort of life-saving, what do they call them?

Dr. Alan Christianson: The liners. The sleeping bag liner and whatever stuff we brought.

Ari Whitten:  It was the liner and then one of those sort of lifesaving things like reflective…

Dr. Alan Christianson: Space blankets.

Ari Whitten:  There you go. So that was it. It was a sleeping bag liner and the space blanket to sleep in on some nights that were below freezing. But yeah, anyway, sorry for the digression.

Dr. Alan Christianson: Back to the analogy. In a perfect scenario, you’d have some logs to burn. It would keep you warm all night. Right? And the thing about logs is they’re dense, they go for a long time to give tons of fuel, but you can’t just drop a match on and have them burn. You need some kindling to get them going. So, when the liver is breaking down fat for energy, we call that process beta oxidation. Beta oxidation is burning the triglyceride as logs but using glycogen as kindling. In this compression state and all this overflow of triglyceride, there’s not enough glycogen to spark up the logs. So, that’s how it gets stuck. The paradox is: the body is deficit of energy, but there’s an overload of fuel that it can’t tap into. And there still are times to where you know, every time we have a meal, in that moment we’ve got more fuel that we need. So, even if we’re not consuming more than we need for the day in that moment, we don’t eat all of it right then and there. Each little feeding time fuel can come in because you can almost always make more triglyceride, but you can’t get it out. It becomes a one-way thing. And even though your total food intake may not be in excess of what your day’s needs are, because each feeding window you can’t retrieve as much as went in. This thing keeps on cycling.

Ari Whitten:  And in the process, we accumulate body fat.

Dr. Alan Christianson: And body fat and the whole overflowing buckets. The final stage of this, this is bizarre, but I read some papers showing how the more inflammation that your visceral fat can make, the safer you are from the complications of over fuel.

Ari Whitten:  That’s interesting. Why do you think so?

Dr. Alan Christianson: The inflammation is also part of a fibrinolytic response in which the visceral fat is growing new cells and expanding upon, remodeling existing cells. As long as you can gain more fat and keep it somewhere safer, it’s not overloading liver cells, but that final bowl and the visceral fat can’t inflame and can’t take on anymore, then we’re seeing an overflow inside the liver and inside the organs. And that’s when the whole pathology starts up.

Ari Whitten:  Probably also chronically into the bloodstream.

Dr. Alan Christianson: Exactly. When the liver gets all filled up, that’s another suitcase with a broken zipper and, you want to take out one sock and the whole thing explodes all over there. And the, and edge of the gate, where you’re trying to sneak the one thing out.

Ari Whitten:  Okay. So this is a novel paradigm I think for most people. The typical paradigms that most people are going to be familiar with when it comes to talk of fat gain and fat loss are, you know, the calories in, calories out model, which has been around for a long time. Everybody’s pretty familiar with that model, even though they, most people don’t understand the nuances of it. And then, there was the idea that hey, fat makes you fat, you know, fat is uniquely fattening. We had sort of the low fat movement for a period of time and then, you know, off and on through various periods starting with Atkins and then still into the two thousands and more recently with the Keto Movement, we’ve had these trends with people popularizing the idea that carbs and insulin are uniquely fattening things and sort of if you just avoid carbs and insulin, then you can lose fat by putting your body into a low insulin state. So, how does your paradigm situate within those sorts of contexts that most people will be familiar with?

Dr. Alan Christianson: You know, what, they can all be true in contexts. You know, in any case, if you’re overloading any version of fuel and the fuel, I talk about just being carbs, fats, even ketones or alcohol and biochemically, they’re all providers of oxaloacetate. And if the body’s supply of oxaloacetate exceeds its capacity to utilize it, it’s treated as fuel. So in any case that can be partially true, but in the liver it’s a little different. Anywhere in the body you can form triglyceride or adipose tissue out of any substrate which… Our liver – inside of it, fat comes in three places only and one of the big ones is that bucket overflow thing that was talking about, so it spilled over from visceral fat. To be really precise there was also a spillover from subcutaneous, but for the model, most of it tries to stay there so you can spill over from subcutaneous or visceral fat straight into the bloodstream, right into the liver, that’s one. The other one is dietary fat, so we consume fat portal veins straight to liver, so it’s right there. There’s no conversion required. The last one is called de novo lipogenesis, and that’s converting carbohydrate into fat. That one doesn’t really work very well so you can overeat carbs and grow body fat and that body fat can spill into your liver, but the carbs don’t really directly make that more than in the most extreme scenario is about four to six grams per day, which even on a low fat diet is almost minimal compared to what you’d be consuming in the diet.

Ari Whitten:  But ultimately when we’re talking about caloric… when we’re talking about calorie excess or fuel excess it ends up not really mattering whether the fuel came mostly… If you are overeating and you are eat- overeating a with a predominantly fat-based diet versus a predominantly carb-based diet, is there any difference based on your analysis of the research, is there any difference in actual outcome in terms of the amount of fat gain?

Dr. Alan Christianson: No. And even ketone supplements, the same problems apply. Ketones also convert back to triglycerides, liver can’t burn ketones. You know, one, one case in point that shocks people is, I’ve had a lot of questions come up about, you know, fructose in fruit being dangerous with fatty liver. So, there’ve been human studies on exactly that and how fruit affects fatty liver syndrome. And what they’ve shown is that you can take, I’m sorry, there’ve been some animal studies on fructose, and human studies on fruit. The human studies on fruit. Show just no impact on fatty liver were just nothing. The animal studies on processed fructose show that you can take rats that are given their full day supply of rat chow and now you can tag on 20% more in the source of pure fructose. Those rats would get fatty liver plain as day, but you take the same rats and take away 20% of their rat chow and give them that difference on ructose. There’s no more fatty liver or you take those rats and full day of their rat chow plus 10% extra of, of palmitic acid, a saturated fat, same thing, major fatty liver, but it’s all, it’s only at that excess. It’s not that there’s any food that’s inherently harmful for the liver. It’s that the fuel overload is what causes all of this.

Ari Whitten:  Okay, so to rephrase that, basically everything becomes toxic when you’re in a caloric excess. And it doesn’t really matter whether the excess came from carbs or fats or it doesn’t really matter sort of what, whatever the macro nutrient breakdown was, the calorie excess part is what makes whatever toxic.

Dr. Alan Christianson: No, the term calorie, I always just hear so many people just shut down and not always for reasons that have to be there. But you know, in terms of practicalities, protein lumped into the calorie bucket. But it does work differently in terms of its satiety effects its effects upon liver function and body composition. So yeah, that’s why I’m always like resisting the calorie terms much because protein resistant starch fibers, they fall on the same rubric. But in terms of practical applications, they do play out differently. But overall, yeah, when there’s too much and stuff, that’s when it goes wrong. So you have great, great summary.

Ari Whitten:  So I know you’re trying to avoid the word calorie. However…

Dr. Alan Christianson: It’s a great word. I just wanted to throw that nuance.

Ari Whitten:  No, no, no. I, I totally agree with why you’re doing it because the, the source of the calories in calories out paradigm has been contaminated with a lot of people who have tried to present very magical mystical fat loss solutions and have said, you know, basically something to the effect that the sort of traditional marketing approach is like, Hey, you know, if you’ve tried to lose weight and you know, by just restricting your calorie intake and burning more calories and it hasn’t worked out, that’s because calories don’t really matter.

Dr. Alan Christianson: Right.

Ari Whitten:  It’s this other thing. Okay. And there’s been lots and lots of variations of that theme. Just to be clear, and I know you’re preferring the word fuel, but just to be clear, do you think calories matter or… I’ll just state it, I was trying to find a more nuanced way of stating it very directly. Do you think that calories matter, or that it’s just the hormonal state that the body’s in that that matters?

Dr. Alan Christianson: In terms of scale, weight, they matter completely and there they’re… the thing is that people have asked me in strong man arguments against calories saying things like: You can perfectly predict your calorie needs. You could perfectly measure the calorie needs. Calorie counting is the best way to go for most people. And none of those things are true. You know, and foods don’t always have what they have labeled as their calorie content. There’s all sorts of agencies that are completely valid, but I think a lot about the idea of scale weight versus like long-term waist reduction. And that’s where it gets only calories. You can always achieve the scale goal. But if you think more about fuel and protein as being distinct things, fuel protein, RS fibers, then you have better success on the waste loss, on the lasting reduction of body waste. And that’s more of what I’m shooting for.

Ari Whitten:  Okay, what is the distinction there to make that even more clear to people? The distinction is between pounds of weight loss on the scale versus actual fat loss, which is what we’re really after. And so why does, specifically, I know you’re, I understand what you’re getting at, but just specifically kind of spell it out, why does just talking about things in terms of calories and assuming that all forms of calories are equal calories, why does that lead to problems when it comes to this distinction between weight loss versus fat loss?

Dr. Alan Christianson: Well, a pitfall of someone who’s solely focusing upon calories. They may be dropping a lot of lean body mass as they’re losing body weight and that’s easy to do if you’re… That’s the thing is that your fuel requirements, your body’s intake of energy sources, the carbs and fats primarily, you can skimp on that. I mean you can compromise on and you can be flexible with it, but your protein needs, you can, you can skimp on those too, but you’re going to make up for that with your muscle tissue. Your body still needs it on any given day. And how you compensate for that is just nonnegotiable and the drawback is when you are surrendering muscle tissue to keep meeting that need, your scale weight may go down, but you won’t be in a healthier place and you’re getting set up to have this whole rebound event occur afterward.

The importance of metabolic flexibility

Ari Whitten:  Interesting. When it comes to losing fat and reprogramming our metabolism, this is, this book is after all called the metabolism reset. One of the things that you talk about a lot is metabolic flexibility. So, what is that and how does that figure into all of these things that we’ve been talking about so far?

Dr. Alan Christianson: You know a funny thing happens when you write a book. It takes about two years before your concept gets out. I had this happen with the last book about carb cycling. My time the book came out, it was being used in a different context. It happened to this one too. So, a lot of books talk about metabolic flexibility and how in terms of being able to freely burn fats or carbs and cool idea, but I was talking more about having some latitude. By latitude, there’s never a day in which we exactly mirror our fuel requirements to our food intake. And the healthier we are, the more we have safe places to hold onto that, like the muscle tissue and safely store back in the liver for later use. And that’s a flexible metabolism. You know your body can have some overage and not have bad consequences in terms of weight or blood sugar, or inflammation. And you can also have some underage on some day and not have your energy tank. So that’s a flexible metabolism. You can have a little more, a little less and you’ll always have the extremes that could throw you off. But how far those extremes, and when someone’s like on a tight rope between too much makes them feel awful, too little, makes them feel awful. They have no flexibility anymore. And so, this is the trick is to regain that leeway again.

Ari Whitten:  So that we are able to maintain stable energy levels and also just fuel burning, sort of stability during the times we’re eating or not eating.

Dr. Alan Christianson: The most exciting feedback I get from the program – there’s two that light me up the most – and one of them is, I’ve done this now, months had gone by and what’s happened is that what I did before, the reasonably healthy diet I did before now is able to maintain my weight. Whereas before it would not, I would keep on going up. So that’s what lights me up is someone can change in a way to where they can do 80, 90% of things where they know they should and have good results from that. Because everyone knows people that do maybe 60% of what they should and seem to get better results. So, that’s the trick is how can you make it to your body can make up that difference again.

Practical ways you can fix your liver

Ari Whitten:  Yeah. When it comes to fixing our livers’ function, and rebuilding in this metabolic flexibility, what are some of the practical steps that people can take in that direction?

Dr. Alan Christianson: So, I did a 28-day program. We did some trials on that, and then we really pulled it down to keeping a low amount of fuel, having an adequate amount of protein, having it not require a lot of thought processes or decisions. Then also using some food categories that uniquely support various liver pathways. And the funny thing is that as important as it is to lose organ fat and visceral fat, it’s also a big stressor on the body. And it’s easy to have that create a large load of uric acid or purines or other metabolites that are stress on the system. So, we wanted it to work in ways to where it wasn’t traumatic, and it was not apt to cause symptoms or complications and people could have just lasting results from that.

Ari Whitten:  Interesting. So, can you talk about a little bit of what… When are we talking about a low fuel diet, how do we accomplish that? Is that a matter of calorie counting or are you modulating which foods people can eat? Are you saying, hey, eat this percentage of your diet as fats and this percentage as carbs or keep carbs under a hundred grams a day, or keep the fat under a hundred grams a day or something like that? What’s the method that you take to reduce fuel intake?

Dr. Alan Christianson: So the program, I set it up to where there’s one evening meal and I give parameters on here’s what you want for lean protein, here’s some good options, here’s amounts, here’s what you want for healthy carbs, here’s good fats, here’s lots of veggies to have tons of, and all those things. There’s some good examples of that. Here’s amounts. So, someone can certainly assemble as they wish. And we made a lot of awesome recipes so you can just do the recipes and call it good. So that’s the evening meal. And then there’s breakfast and lunch. And the simplest iteration of that is you make up a giant shake for breakfast, make twice what you need, have half of that for lunch and here’s what you want to go into that. And the cool thing about the shakes is that there an easy way to get good amounts of protein without a lot of extra carbs or fats and also easy and automated. And then the last thing we included was if, especially during the first few days of phasing into this, you’re feeling too hungry, you’re munchie or something. Here’s some great ways you can make unlimited snacks out of raw or cooked vegetables to fill in those gaps. So, yeah, we gave quantities and foods to choose from for all those meals and recipes people can just follow. So not so much you weigh or measure grams or count calories, but just this for breakfast and lunch and do dinner like that.

Ari Whitten:  Is there any specific macronutrient ratio that you’re asking people to adhere to? Like as far as the carb to fat ratio, do you favor a low carb approach or a moderate carb approach or higher fat, lower fat approach? And sort of along with that question, what is your take on the popularity of the Keto movement right now?

Dr. Alan Christianson: The first one, I’m not so much saying you’ve got to track macros or be certain target. If someone is on the program, following it per the guidelines, they’ll end up with probably about 35% protein calories and about 40 to 45% carb and the remainder from fat. It’ll come somewhere close to that, but there’s some leeway of several percentage points by each of those. As to the Keto one, you know, it’s kind of a thing to where at the way it’s talked about to where this is how your body burns fat, if you eat fat, you burn fat. A lot of those tropes seem to be intuitive, but it’s just not how biochemistry works. You know, it’s, it’s really the antithesis. I talked before about the whole logs we had in our camping thing, but the logs and the kindling, you know, and the beta oxidation. So, the antithesis of that is ketogenesis, you know, when you cannot run beta oxidation, you’re making all that stuff into ketones. The analogy I’ve thought of with that is the problem.

Let’s say you’re filling your car and the pump doesn’t stop, the gas is overflowing, and this is like the liver with too much fuel. Well, if you swap out unleaded for diesel and turn on, it’s the same problem and that’s all ketogenesis is. It’s that you’re converting fat into ketones through another kind of fuel. They’re not a get out of jail free card they’re another version of fuel and they’ll make the rounds of your body. If you don’t have the capacity to burn them or store them, they’re going to go right into triglycerides and go stop right back in the liver. There’s no difference or benefit that way. And it’s actually some downside because the liver is the only organ that cannot burn ketones for fuel. If it’s in a state of fuel overload, but it’s now nutrient deprived, it can’t deal with that effectively. And I guess that’s a parallel between someone that has liver issues. The same thing that can be a pitfall about overt fasting is that you’ve got a fuel deficit, which is cool, but you’ve got no amino acids in no micronutrients or phytonutrients to support liver function. So your liver is working even harder than it would be during normal life, but it has fewer resources in which to keep up with all that.

Ari Whitten:  So, with that in mind, do you want to elaborate on your, your take on fasting? Is that something that you’re universally opposed to or only in specific contexts that you think fasting is not a good idea?

Dr. Alan Christianson: Well, if someone’s goal is really waist loss, if they’re somewhere in this continuum of fatty liver and liver congestion, there’s a good chance of that being counterproductive for them. You still require amino acids. So your body has to borrow from lean body mass for that. In terms of it being something that there’s hypothesis about longevity changes, you know, we’ll see. I haven’t really seen data that’s maybe compelled me to think that there’s long-term benefits that way. There might be. We’ve got some short term metrics. There’s, there’s also ideas about psychological, spiritual benefits that are I think, really strong and very culturally based and historically based, but yeah, for someone who’s had this whole overload issue, it could go the wrong way for them.

Ari Whitten:  Interesting. What about the role of glycogen depletion from the liver? I’ll sort of explain my thinking on this topic and you can tell me whether you agree, or you think something different. The way I look at it is if you look at the standard American diet-eating non-health conscious person who’s sedentary, eating lots of junk food, is obese, they’re in a state of constant glycogen fullness basically. You know, arguably they’re going to get to a point where the liver becomes fatty and then it’s actually crowding out the glycogen. Let’s just imagine that they’re in a scenario that their liver still has the capacity to store glycogen. They’re chronically basically full on glycogen and that’s leading to basically this overflow mechanism and then excess body fat gain. Is the sort of optimal place to operate from to be halfway full in your liver glycogen stores or is it to be like totally empty in your liver glycogen stores or near full, and to be in this balance between like, hey, you’re regularly emptying out or at least partially emptying out your glycogen stores in your liver and then refilling when you eat and then emptying them out again through physical activity and periods in between meals and then refilling and that sort of thing? Do you get what I’m saying? Like sort of what’s the default level of glycogen fullness in the liver that you think would be most optimal?

Dr. Alan Christianson: Yeah, in terms of percent or numbers, I’m not sure if I wouldn’t know an answer or if that exists. But in general, the whole crowding issue is a real thing that does block beta oxidation. One thing is that glycogen storage is highly limited. You know, there’s just not… Glycogen is a lot less dense. If we want to draw the analogy out further the kindling takes up a ton of room and the logs take up less space per energy density. There’s very little limit. A healthy liver is probably somewhere around 1 to 2% triglycerides by weight. But when we’re above five, we call that fatty liver and people can hit 10 to 15%. So, the sky is the limit pretty much for triglycerides. With glycogen, we’ve got the capacity to store around – trying to get my numbers correct here – it’s about two or three hundred grams and that’s about it. So, if we could store more, like I did a marathon recently, I wish I could pack a lot more glycogen in there. Physiologically there’s just not a lot of room in that suitcase and the average person in that continuum, their problem is a deficit of that. I think for general health all the points are well taken that it’d be great to load and unload that and have, you know, long exercise here and there. Many people who are in this stuck state, their core issue is they lack the quantity needed to adequately utilize the triglycerides. That’s where they get into that stuck pattern. Glycogen overload is not so much a thing, again – and for endurance athletes, we wish it could be – but really you can’t do that.

Ari Whitten:  Let’s take someone like you or me that is lean and very physically active. If you could do, like if you had x-ray vision into our livers over the course of the day, what’s going on with glycogen status?

Dr. Alan Christianson: For sure it’s ebbing and flowing. Between meals, after meals, assuming someone’s consuming carbohydrate. Yeah. You’re always replenishing and drawing out and there’s the glycogen in the liver. There’s a lot of parallel between that and skeletal muscle glycogen and then circulating blood glycogen. It does take some time. You’ll often utilize what’s in the muscles first. And so it may be a bit of more activity before you do start significantly tapping into your stores. But for sure with long hard bouts of effort, you can dwindle them down pretty significantly.

Why we have a fuel overflow

Ari Whitten:  Interesting. So, I want to zoom back out for a moment and talk about some of the factors that are leading to this overflow process, this sort of fuel overload in the first place. How do you conceptualize that? Why – and maybe I’ll phrase this differently – Why have there been obesity epidemics in the modern world in specifically westernized countries as soon as they, you know, adopt a more modern way of life and a more modern, westernized diet? What are the factors? Previously we talked about this sort of overload of fuels, but what’s driving that over consumption of fuel in the first place?

Dr. Alan Christianson: Yeah, so two separate things. So how it works mechanistically is different from the factors behind it and the factors behind it are many. I think some things we can clearly state is that it’s not solely, genetics is not solely behavioral. It’s not solely food. I’ve even seen data arguing that processed food is not a perfect predictor. Areas that have more processed food don’t always have the same parallels in obesity. So, I don’t think we have clear answers on all of it yet. There’s talk about infectious vectors being variables as well. There’s talk about correlations with work schedules, like people being on shift work and globalization being a big instigator of when the peak came up. Something hit us in the mid-eighties and there’s talking about obesogenic chemicals that are changing epigenetic expression. And I think there’s a few of these things that one could ignore as being ultimate drivers of that. But willpower is not a good explanation. We didn’t suddenly lose that in one fell swoop in, you know, New Year’s Eve, 1984, that doesn’t seem recognizable.

Ari Whitten:  The cause of the obesity epidemic wasn’t that all of our ancestors have been counting calories and then, hey, you know, back in 1970 we all stopped counting calories.

Dr. Alan Christianson: Yeah. That’s not a likely hypothesis, but in terms of how it plays out, I guess there’s like three ways I think of that. One of which is that there’s just a plain old fuel excess. And the other one is that back to that bucket analogy, the buckets can be bigger or smaller and they can be more or less receptive. So, a big variable there is the muscle mass. You know the more space there is, the more receptive it is, the hungrier it is. That’s a positive variable. Making the body have more ways to dispose if you will and utilize it safely. And then the third part is down at a molecular level is that pilot light on. And there we think about things like the endoplasmic reticulum, mitochondrial function, micronutrient status, the obesogenic chemicals we’re exposed to. And then also things like the HPA axis and that one I would argue doesn’t affect so much the total fuel status, but it does certainly affect allocation. There’s data arguing that if your HPA axis is dysregulated, you’ll convert – and this is your liver’s thing too. Your liver actively converts more weak cortisone into more strong cortisol. And that will prioritize fuel being redirected away from muscle mass down towards visceral fat. So, it’s still the same thermodynamics and same grams you’re working with. The body composition can change from that. So yeah, fuel available fuel utilization, and then how well fuel’s being burned are the main three variables that were worked together in some combination.

The role of insulin resistance

Ari Whitten:  Right. You mentioned in passing earlier insulin resistance. It is a common conception among a lot of people that insulin resistance is just caused by the body producing lots of insulin regularly and having insulin spikes from eating carbohydrates, sort of the thinking is often carbs boost insulin. if you boost insulin a lot, then you get insulin resistance.

Dr. Alan Christianson: And then fat grows…

Ari Whitten:  Right. What is your take on the real causes of insulin resistance?

Dr. Alan Christianson: You know, it’s fascinating stuff and some of the short perspectives are that insulin is really a symptom and the resistance is a safety mechanism. You know, I think without one, you’ve got… I can see sky harbor airport and if there was a busy day and the planes couldn’t land, the traffic control, would have them stay in a pattern above the airport. All insulin resistance is, is your body saying, look, these cells don’t need more fuel right now. Let’s keep that in play. And yes, it’s harmful to have all these fuel substrates, the glucose, the ketones, the triglycerides, it’s harmful to have those above parameters in circulation. It would be worse to have them go inside the cells and fry the machinery and make things just breakdown. So, it’s a protective mechanism. A couple of wild things that I’ve seen too, back to the, the model that you put up. The old thought was really just that, that we would mind our own business, but if we were a haphazard enough to eat oatmeal in the morning, we would spike our blood sugar. That would form fat, that would make insulin resistance, and enough times we would get sick. And what we’ve learned now is that the body doesn’t need insulin to uptake glucose. It may make the process a little easier, but it works just fine without it. And they’ve done this in animal studies. You can take animals and have no insulin whatsoever and unless their liver is going to over respond to a compound called glucagon, which is like the opposite signal, unless they’re liver over-responds to glucagon, animals with no insulin don’t have high blood sugar, they have like no diabetes at all. So, what we’ve seen too along those lines, we used to think that yeah, your blood sugar after meals, I talked before about how morning blood sugar was your liver leaking out. Well, we always thought that after a meal you would eat carbs, good or bad carbs and you would spike your sugar and that’s why your sugar was high. Now, in research they can differentiate the sugar that your liver made from the sugar that came from your diet. You know, the idea is that even good carbs contain glucose. They spike the blood sugar. So, what they’ve shown is that in people that are in the diabetes continuum, probably upwards of 80, 85% this, it’s called Postprandial hyperglycemia. The bulk of their blood sugar elevations after a meal don’t come from the meal. You know, some of it does, but the bulk of it is with the body itself is making. So, all those old models, they seem really simple and intuitive, but the body oftentimes defies what makes sense at a first glance.

Ari Whitten:  So, two questions. First, why is the body making lots of sugar after eating?

Dr. Alan Christianson: So, this is the same thing. You’ve gotten more fuel coming in and the liver’s like seriously, where am I going to put this? You know, all right, I’ve got to drop some ballast. I got to throw this out in some way to try to make room. And there was a lot.

Ari Whitten:  So, it’s just throwing off it’s stored glucose or glycogen? In favor of taking in the new surge?

Dr. Alan Christianson: Well, when you look closely, there’s also triglyceride elevations as well. And they parallel that. If you were to completely starve all carbohydrate intake, you can still see glucose elevations. But you’ll also see more triglyceride elevations. They’re just different fuel types and they’re both signs of there being fuel overload, and they’re both harmful when they’re outside of their desired ranges in the bloodstream.

Ari Whitten:  Gotcha. So having said that, it’s not just consuming carbs that’s causing insulin resistance. What is the sort of… How do you conceptualize the top cause or, or the top three causes of insulin resistance?

Dr. Alan Christianson: It’s ultimately fuel overload. It’s the body intentionally restricting the influx of substrate across the cell membrane for good reason. The body has so many ways that it regulates energy balance, and this is just one of those tools.

Ari Whitten:  Gotcha. You mentioned obesogens, obesogenic chemicals in the environment in passing a couple times earlier. What is your take on how that fits into this model of fuel overload? I guess too, that’s a two-part question. One is, do you believe that obesogens, are a contributor to fat gain? And the second part is what’s the mechanism and how does it relate to the concepts you’ve explained so far as far as fuel overload?

Dr. Alan Christianson: I love that you said fat gain and not weight gain because weight gain would have been a hard one. Because for thermodynamics you need more building blocks to have more mass. It’s got to come from somewhere. But in terms of fat gain I mentioned before briefly about the idea of stress hormones causing a repartitioning of fuels where fuel goes to some places more than others. There’s data saying that chemicals… I’ve seen data about BPA and also lead. They can shift the liver’s regulation of cortisol to cortisone. A big picture concept is that your glands, the same way that our energy or energy intake never perfectly parallels our immediate energy needs. Our liver sorts all that out. It’s the same way for hormones. You know your adrenals, your thyroid, by and large, they make a lot more hormone than you’ll ever need and most of it’s made in inactive states and it’s often made at random pulses throughout the day, but your liver is holding a lot of that and converting them into the more active states and doing so per what your needs are like in that moment. And chemicals can disrupt that. So, there’s good data saying that there’s an enzyme called 11 beta hydroxysteroid dehydrogenase that shifts weak cortisone to strong cortisol, and you can leave that enzyme stuck in the on mode when you’ve got a lot of lead circulating in your body or if you’ve got a lot of plastic byproduct in your system. So that that’s one way that it can be a factor.

Ari Whitten:  And then by having excess cortisol in the system that’s going to contribute to fat storage?

Dr. Alan Christianson: Yup. That’ll repartition the fuel towards visceral fat and away from skeletal muscle. So that can affect the body composition and the fat storage.

Ari Whitten:  Is a primary mechanism through insulin resistance there?

Dr. Alan Christianson: It’s changing which tissues are more responsive to insulin, more sensitive and which are more resistant to it.

The difference between different types of calories

Ari Whitten:  Gotcha. Excellent. I want to cover nuances of calories because this is a point that you emphasized in your book that we talked about briefly earlier. So why are not all calories the same and why do you make a distinction between certain types of foods in terms of, you know, whatever their calorie content is being different from actual outcomes?

Dr. Alan Christianson: Well, I guess the main thing here is just the differences between protein versus fuel and how that affects satiety and basal metabolic rate and body composition longer term. So that’s one. The other big one involves how resistant starch acts in the body. So a fair number of foods contain this compound, which is neither carbohydrate and neither fiber, but it’s somewhere in between kind of the best of both worlds. And it’s not calorically empty. There is a calorie load we get from that, but it’s different in the sense that our, some of our better types of bacteria, they eat it first and we get some of their leftovers. We get it really slowly and we get it over a long period of time. And there’s also effects that it has on changing short chain fatty acids and it’s pretty wild. For a while we thought that the gut flora and the integrity of the gut lining could influence the liver. You get leaky gut – bad things would hurt your liver. Now, a lot of data is suggesting that that was the opposite. That was like the opposite relationship. That based upon the properties of our bile and some of the chemical nuances of our bile, that would be one of the big drivers of gut permeability and also one of the big regulators of our gut flora.

Ari Whitten:  So, the… Liver health regulating gut permeability?

Dr. Alan Christianson: Yeah. As opposed to vice versa. And I’m sure there’s examples of both, but there’s a lot of emerging data saying that it’s more so the liver effecting affecting that. And in terms of the big picture concept too, the gut is still outside the body. You know, what we swallow is not so much in, us, it’s not in our bloodstream, it’s not interacting with our organs. But once it does, you know, the first thing it does is it primarily crosses the small intestine lining and hits the portal vasculature and goes straight to your liver. So that’s supportive entry and this is where the outside really meets the inside. And there’s regulatory cells called Kupffer cells that are unique liver immune cells and they are, you know, checking the wind and seeing what the conditions are like outside and seeing how the immune system should behave. You know, whether it needs to be vigilant and hyper responsive or whether it could be more of a relaxing, reparative mode. So, the liver has a central role in many of those facets of health.

Ari Whitten:  When a lot of people think of liver health, they think predominantly of detoxification and they might think of things like dandelion root and burdock root and milk thistle and things like that. The context that you’re talking about, the function of the liver here is obviously pretty distinct from just a pure role in detoxification, but do, I’m just curious, do you think any of those sorts of herbal supports for liver function have any role or any benefit in the kinds of contexts that you’re talking about as far as fat loss?

Dr. Alan Christianson: In these contexts, for fat loss per se, they don’t so much change the process. There is data saying that if one is chronically in an inflammatory state, then some things like gamma tocopherols or you’ve mentioned milk thistle the salivum extracts, there are things that could attenuate that free radical damage. But I guess I thought about that like let’s say that, I don’t know, you were forced to march on some coals and maybe Tony Robbins wasn’t there, and your feet weren’t going to be safe and you could put on thicker shoes, maybe you wouldn’t burn quite as fast. That’s how I think about some of those protective agents. Yeah. But the thing is, you don’t want to go walk on those coals. And the ultimate driver of the inflammation is just that fuel overload. And it’s bizarre because I really had a chance to get a sense of how, what are the relative effects of various inflammatory causes, whether it’s, you know, chronic infections or autoimmunity or whatever. And seriously the biggest driver is the whole fuel overload. You know, once that’s there, then the body is in this proinflammatory state, the adipokines are the biggest drivers of that. So, these things certainly are fine. They’re fun things to throw in the diet. They’re nice foods. Yeah, if you’re walking on coals, thick shoes would be nice, but you could just not walk on coals and that’s the idea of like getting the junk out.

The difference between fast and slow fat loss

Ari Whitten:  Gotcha. I have a couple more questions for you. One is the distinction between fat loss, fast fat loss and slow fat loss. The common thinking for a long time on that issue has been slow and steady wins the race, sort of if you do things in a more prolonged steady pace rather than just going on a diet for 30 days, that, that will lead to better outcomes. And I think there’s… I’ll say that I’m familiar with the research that’s come out, which I want you to speak to, but I think there’s a grain of truth in the slow and steady aspect in just the sense that a lot of the people who are trying to do things the fast way are people who are not operating with a long term thought process in place. They’re operating with, I’m going to go on this 30-day or 60-day diet, lose 20 pounds, and then I get to go back to eating all the things that I used to eat. Instead of where like a healthy fast fat loss approach, which would be, I’m going to do this rapid fat loss protocol for whatever, let’s say 28 days or 60 days. And then I’m going to, then I’m not going to go back to my old habits. I’m going to go on a maintenance protocol and still continue with healthy diet and lifestyle behaviors. With that in mind, so that’s sort of separating out that confounding variable about just like people with very bad mentality going into this weight loss approach. What are the outcome differences in terms of a short term or fast versus slow weight loss diets?

Dr. Alan Christianson:  No. Great question and great framing for sure with those considerations are super important. The other thing I would throw in, there was a distinction between doing it in a way to where you’re primarily losing fat versus losing a lot of muscle tissue. So, if someone is doing just caloric restriction and maybe they’re training hard and eating a ton less food and putting no more thought into it, they may be better off doing that more gradually. They may have less loss of muscle mass. If they do that very aggressively, they may have even more apt to rebound. But there is a large body of data saying that if things are done in ways that spare the lean mass and I would argue to support liver function, that they may see better effects long term if they do get some rapid loss early along. And a cool way someone we can see when it’s working too is the proportionality between waist loss and weight loss. You know a lot of data suggests that adults, women may have between 6 to 10 pounds of weight loss per pound of waste loss, and that can be a sign of there being a lot of loss of muscle mass along the way. So, what we commonly seen in the last month, we’ve had thousand people go through the challenge. We’re averaging about two to three pounds of weight loss per inch of waist loss in many people, it’s one to two are very close to that. So that’s exciting when someone’s saying I’m only down seven pounds, we’re down three and a half inches. That’s awesome. You’re a healthier person now from that.

Ari Whitten:  So, this protocol is a 28-day protocol. What do you recommend for people after that? How do you transition them into a sustainable approach that’s going to keep the fat off?

Dr. Alan Christianson: You know, that part I talk a fair amount about, it’s not too complicated or too counter intuitive. I really believe that when someone has a successful transition, their body can take care of a lot of that. I encourage them to maintain, to really regain a high amount of healthy exercise and do it in a way to where they’ve got time off. They’re recovering, they’re mixing it up. Also, I encouraged a lot of straight forward stuff on processed foods. One thing that I think is distinct is I put a lot of thought into types of fibers. You know, like 17 types of fibers and people often get, I think far too restrictive and just cutting out a lot of food categories and there’s negative pitfalls in micronutrient status, but also in microbiome from that. So, consuming a broader variety of foods, getting a better sense about their own levels of satiety, you know, still maintaining healthy protein intakes. Still putting a lot of emphasis on resistant starch. But I didn’t get to a micro-managing on the maintenance because I do think with some broad stroke ideas and with a healthy restart of their systems that they can do well from that.

What to do when you are addicted to food

Ari Whitten:  Yeah. Another question. What do you… Do you have any thoughts on people who are addicted to processed foods or addicted to sugar and are binge eaters? Do they, have you found that they do well with this approach or that they have problems with it? Do you have any unique tips for that sort of segment of the population?

Dr. Alan Christianson: You know, for sure. And definitely a distinct category and there’s no one approach with the best fit for everyone. Some people from those categories have enjoyed the structure of the whole process and like the idea that there’s prescribed quantities and they found it simple that there’s fewer decisions to make. You know? So, there’s a lot of data about the pitfalls of decision fatigue and I’ve seen data arguing that a diet, if diet A involves a more radical change in total food intake, but there’s not a lot of moving parts, whereas diet B may be a more minor reduction, but there’s like 50 rules to keep in mind. You know, diet A is easier to do longer term. So that’s one idea around just a couple shakes. So it makes it very simple for people. So that that’s been a helpful thing. But for sure there are populations that have to think hard about what the habits are and in some cases to also I found that if they are changing more things at once, so you mentioned about like sugar for example. I do encourage them to 28 days for sugar, caffeine, alcohol to stop those things. And the funny thing is that the more that freaks someone out, the more it’s probably going to help them when they do it. And sometimes too, by making those changes at once and also having resistance starts to keep blood sugar stable, it’s often easier than doing it by trying to reduce one of those things for example.

Ari Whitten:  So, you mentioned caffeine a second ago, am I right? Why do you have them eliminate caffeine?

Dr. Alan Christianson: So, there’s a couple of liver pathways and the basic idea is that you’re loosening junk up, you’re packaging it to send it out. And the first part we call it phase one, caffeine is a real strong driver of phase one. And in the past, I would test a lot of people who would give them a tiny amount of caffeine, aspirin and Tylenol and then watch all the byproducts it would make how much and how soon and many that would have these propensities towards a poor metabolism would also have a highly exaggerated phase one response. So, eliminating caffeine for a while can lower and reregulate that phase one to phase two ratio. So we can make detoxification that occurred more smoothly. People also notice that, you know, sleep is a big part of this. I encourage sleep binges and there’s a lot of folks to where they’ve not cleared a caffeine backlog. So it’s a funny thing, but it really only takes somewhere like six and 12 hours to move caffeine through your body. But what you don’t hear about is that when it’s gone, what is next? What have you made it into? And there’s secondary compounds like the bromates that are not really caffeine, but they’re no different and they’re still having the same effects and people can often hit a place in adulthood. There’s a thing called hepatopause where our liver gets slower each decade at converting caffeine and eliminating it. And people can often hit a threshold to where it takes them more than 24 hours to go from caffeine to water, counting all the steps. And if you think about that, if you’re ingesting it every 24 hours and takes more than that to get it out, you’ve got a chronic level throughout the day. Throughout the night too. So someone’s not had a break for a little while. It’s a healthy thing to do.

The power of micro workouts

Ari Whitten:  Gotcha. I’ve saved the best for last, which is my little contribution to your micro workouts. So, talk to me about why micro workouts, what are they how do they figure in your protocol and why do they matter?

Dr. Alan Christianson: For sure. So one thing that’s counterintuitive also about the protocols, in fact that I do really limit exercise. You know, I love it. It’s the best thing in the world for your long-term health but during this reset process, it can work against the goal of rebuilding glycogen and can also raise stress hormones during the food reduction stage and can suppress metabolism, can raise reverse T3 levels. So, I greatly limited that and yeah, personal of our conversations the first week I think is somewhat indifferent as to whether that’s there or not. And there’s clear data saying that if you’re more than six weeks out to fuel restriction, metabolism can slow. But if you’re within about four weeks, so that that remaining time, I encourage brief bouts of, not strenuous but vigorous activity. So, you’re keeping the muscle tissue engaged and some perks about that. What I’ve seen is that people are more apt to finish it up and say they’ve not really lost any of their basal level of fitness. I think it’s also healthy in a sense of you’ve still got a placeholder for exercise throughout your day, so there’s still a time that’s set aside for that, so you don’t lose that relationship with it. And I think it’s a good thing in terms of just maintaining some endorphins in circulation as well. Yeah, we do very brief high intensity interval training sessions of about three to five minutes and also alternating those in days with brief calisthenic programs that you know, some basic multi-joint movements to cover the whole body. And then some parameters for optional gentle stretching, some light locks. But yeah, keeping it to those things during the program.

The Metabolism Reset Diet – What you can expect in 28 days

Ari Whitten:  Excellent. Love it. So, I want to recommend to everybody listening to go out and get this book The Metabolism Reset Diet. You can get it on Amazon. Dr. Christianson, what can people expect with this 28-day protocol? What kinds of results have you seen in the people going through your challenge? And what can people anticipate if they do this?

Dr. Alan Christianson: You know, a couple of framing expectations that want to put out. Please do expect it to be a change. Please do expect it to be some ideas that are for a purpose and are not necessarily things that you need to do forever and not even intended to do forever. And please do expect the first couple of days can be a transition. You can be hungry, it can be difficult. You know, no bones about that. I’ve worked hard to make it pretty smooth and easy, but it does take some effort for that transition part. Most find that after those first few days, they’ve got some momentum going. It’s pretty automated. They’ve often noticed that cravings and hunger are pretty manageable and smooth for them. Some of the things I really, the first iteration of this was for reversing diabetes. So, we totally expect to see blood sugar improvement. That’s common cholesterol, triglycerides, the waist loss is exciting. Something else that I’ve seen more now that larger groups of people have gone through this has been a big plummet in inflammatory reactions and I alluded to that a bit earlier, but we’ve had so many people talk about their chronic Epstein Barr or their rheumatoid arthritis or their autoimmune thyroid disease or all these things that you wouldn’t think dropping a few inches from the belly would really reverse. Now that I’m getting how this works and what are the biggest drivers of the inflammation, like, oh wow, that makes sense. So yeah, just some awesome changes like that.

Ari Whitten:  Yeah. Beautiful. Well, again, everybody, go get this book, The Metabolism Reset Diet. It’s awesome. I highly, highly recommend it. Dr. Christianson, thank you so much for coming on the show and thank you for breaking records of podcast appearances.

Dr. Alan Christianson: Number Four!

Ari Whitten:  On that note, you just ran a marathon, what, a week ago? Two weeks ago? Something like that.

Dr. Alan Christianson: Dude, I did. Thank you so much. A week ago, from this last Saturday.

Ari Whitten:  And you did it, what in close to three hours?

Dr. Alan Christianson: Three fifteen.

Ari Whitten:  Yeah. Amazing. That’s like, something like three hours faster than I could have done it, because I would have just stopped after mile two. I don’t do endurance stuff. I like only… I love physical activity, but I like it when it lasts, you know, no more than a few minutes.

Dr. Alan Christianson: If it was picking up a refrigerator and running with it, you’d go somewhere, and I wouldn’t even move.

Ari Whitten:  I would challenge you to race carrying a large stone or refrigerator over the course of a hundred feet, but I will not be doing any kind of anything that’s over a mile. Well, thanks again, Dr. Christianson it’s such a pleasure to have you on as always. And I hope to catch up with you very soon again, and I hope we can do another backpacking trip sometime soon where I can hopefully not freeze to death.

Dr. Alan Christianson: Let’s do it. I’ll be game.

Ari Whitten:  All right.

The Metabolism Reset Diet | How to Improve Blood Sugar, Inflammation and Lose Weight in 28 Days with Dr. Alan Christianson – Show Notes

The importance of resetting the metabolism (1:11)
The liver’s role in glycogen storage (4:00)
The liver’s role in fat gain (6:20)
The importance of metabolic flexibility (19:37)
Practical ways you can fix your liver (22:07)
Why we have a fuel overflow (32:25)
The role of insulin resistance (35:45)
The difference between different types of calories (42:20)
The difference between fast and slow fat loss (46:45)
What to do when you are addicted to food (51:20)
The power of micro workouts (51:50)
The Metabolism Reset Diet – What you can expect in 28 days (56:50)

Links

Separating myths from science on functional medicine testing, lectins, homeopathy, muscle testing and more with Alan Christianson
Listen in to my latest podcast with Dr. Christianson where we are separating the myths from science on a lot of different topics.

 

 

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