Theresa Piela  0:00  
Welcome to the bio energetic view. I'm your host, Theresa piela, joined, as always, by Jay Feldman and Mike Fave today, we're going to be talking about how evil fruit is, putting NAD plus into context and closing out the show with a Q and A so thanks to you guys. I didn't, I don't hear about any of these, these Doctor influencers. But now I've heard of Doctor buzz, and I feel like I've been getting so many ads for the sardine diet. But, yeah, I mean, that's, that's her legacy at this point.

Jay Feldman  0:34  
And, well, you can mostly listeners. I mean, most of these are, are sent in by listeners, Mike and I don't normally come across these things as much, but yeah, we appreciate people sending these things in and exposing us

Theresa Piela  0:46  
to what's out there. All right. Well, thank you listeners. Thank you Mike and Jay. I get a good a good cultural experience things I miss out on living in the country. But yeah, I think this, this clip is is interesting because it's kind of like the it's a dominant thread that keeps being pushed, especially on like Instagram and Facebook and YouTube, about how dangerous and how evil fruit is. So let's, let's hear what Dr baz has to say.

Dr Boz  1:19  
Grapes are the worst fruit you could ever eat. Fruit has been sold to us as healthy and nourishing, even by people who used to be carnivore, but the opposite is true. Fruit is clearly beneficial for the human body. It's very hard to make an argument that fruit is harmful. Last night, my husband and I left work and went to the sauna. My blood sugar leaving the sauna was 78 on the way home, we stopped by the grocery store and grab some ribs, and he picked up a healthy snack. Guess what? Whole Food, unprocessed, healthy snack, shot my blood sugar up to 225 grapes. The worst part is I know that for every minute my blood sugar is that high, my brain is making a few tau proteins, the mechanism behind dementia. On top of that, I know that the excess glucose in my circulation will be converted to fructose, which is preparing my body for winter and to store fat. Fruit is evil,

Theresa Piela  2:18  
the intensity of her delivery. I watched it a few times. Every single time, I'm just a little bit shaken. Anyways, Mike, so

taking Dr Boz's advice, it would be best to, you know, go to the sauna and then, you know, go straight into your keto snacks, correct, just for health. 178, feeling good, feeling great.

Mike Fave  2:43  
Yeah, this is, I think, well, a she's shots fired at Paul. You know, she's, she threw some shade there at Paul with, you know, previous carnivore influencers saying that fruit is healthy. I think that Dr Boz's take here is less an indication that fruit is evil, and it's more of an indication that Dr Boz is insulin resistant. And now, whether that's a pathological insulin resistance or physiologic insulin resistance, which is likely the latter, she is not. She doesn't tolerate carbohydrate very well, so, and I think that this is a function of her being on a ketogenic diet and forcing fatty acid oxidation, and then, which drives a peripheral instrument, insulin resistance, and then also her pancreatic production of insulin, because she doesn't eat carbohydrates on a consistent basis, is going to be altered. So, yeah, when you are on a diet like this, you're doing keto, you're fasting, you're forcing fat oxidation, you don't have carbohydrate exposure. What's going to happen when you start eating carbs is you're going to have a rapid rise in your blood glucose levels, and it's going to take longer time to actually clear those blood that blood glucose. So I think this, this is basically if she continued to eat carbs over time, assuming she's not type two diabetic, and there's not dysfunction in her ability to process carbohydrate as a as an energy substrate, or problems with her pancreas, then essentially what I think she would be able to not see this happen long term. So I think she doesn't fully understand the mechanisms in terms of what's going on that drives metabolic dysfunction, or how running fatty, high fat diet and oxidizing fats can actually drive in some resistance. But this is a clear example this. I also think it's weird that she tried to pick her one her like, one specific example like her N equals one experiment on one time consumption of grapes to use it as a, I guess, a resource or or a citation for that grapes are evil. So that's my first take there on the overarching context. Now, then she makes, she goes in to make some very specific points that I think these are also pretty strong exaggerations and an indication of a lack of understanding of the underlying physiology. So the first one she talks about is that her high blood glucose level will drive tau protein formation. So just for context, for listeners, tau proteins are involved, or are said to be involved, in the pathology of Alzheimer's disease. So basically, you get an accumulation of amyloid beta and tau proteins which impair neuronal function and neuro neuronal energy metabolism, and so the accumulation needs is a hallmark of this. Now inside the research, what you typically see is an association with states like type two diabetes, insulin resistance, obesity and overarching metabolic dysfunction as a driver of tau accumulation and also amyloid beta accumulation. So Dr baz is assuming that if her blood glucose goes high one time that she's forming tau proteins. But it's pretty clear from the literature that the problem in these states is an impaired ability to use carbohydrate. It's not necessary that carbohydrate or glucose itself, directly drives tau protein formation or amyloid beta protein formation. What more happens is that when the brain is having energetic failure or metabolic dysfunction, you have a hyper accumulation of these proteins over time of the lack of breakdown, and then that's that's that is the pathology in and of itself. And so there's actually animal models that they take rats are mice, and they humanize them so that they have similar pathology to Alzheimer's disease with tau accumulation. There's multiple models. Some are amyloid beta, some are tau accumulation, and what they actually find is that if they block glucose metabolism in these animals by giving them two deoxy glucose, which is an analog of glucose that cannot be metabolized effectively, they actually find it worsens tau accumulation, which is indicating actually that the problem is not that you are having glucose, it's that you are not taking glucose and effectively metabolizing it, which is, again, this is central to the pro metabolic argument and the pro metabolic perspective, that the problem is not glucose as a substrate, The problem is the inability to effectively oxidize glucose in in through the Krebs cycle and the electron transport chain to produce energy. And these, these, a lot of these disease states, all of the, almost all of these disease states have this as a characteristic central piece, particularly the long term chronic health states in that in different metabolic diseases, which Alzheimer's and dementia are basically an offshoot of that or leg of that process. So you know, that kind of this idea that if you have a glucose spike, that you're just driving tau protein formation, I don't think is 100% correct. I think it's an exaggeration, extrapolation that isn't borne out necessarily in the research. So there's this. And then the last piece that she she goes into is she talks about, she says that glucose will be converted into fructose, and then the fructose will then be stored as fat. This is actually in physiologically incorrect. So if we look at the fate of glucose, most ingested glucose is actually directly converted to energy through oxidation or non oxidative pathways. So the oxidative pathway is running through Krebs cycle and an electron transport chain. Non oxidative pathway is running through glycolysis, and then the other portion of that is stored as glycogen. So the vast majority of glucose is not converted into fructose. Now some glucose can be converted into fructose, and this you tend to see, again, in pathologic states where glucose isn't being used effectively, you get a backlog of glucose through the glycolytic pathway, and then it gets shunted towards the polyol pathway, where it gets converted to fructose. Now one thing that is important to mention here is that if you are insulin sensitive, and when you consume carbohydrates and the cells effectively respond to insulin, the normal conversion of glucose of fructose is heavily curtailed. It's minimized to a very large extent, because glucose up regulates all of the major enzymes through the glycolytic pathway that drive the or insulin up regulates all the enzymes in the glycolytic pathway that drive glucose into pyruvate to move it into the Krebs cycle. So it's in states of metabolic dysfunction with an impaired ability to respond to insulin because of issues inside the cell and inside the mitochondria and inside the insulin signaling cascade that you then see a backlog towards the polyol pathway with conversion of fructose, not necessarily just you have glucose, you eat it, and it gets converted to fructose, and then fructose just gets converted to fat, not to mention that fructose doesn't just get converted to fat. And Jay and I have covered this in other podcasts, where the vast majority of fructose doesn't actually wind up in de novo lipogenesis, which is the production of fat from carbohydrates. It winds up going either conversion to lactate energy back to glucose or to glycogen. So it's just like basically this short indicates, at least to me, that Dr Boz doesn't fundamentally understand the different metabolic pathways and understand what's going on in the states of insulin resistance. It's just kind of a fear mongering post that tries to say. That if you have glucose, if if you eat glucose, you get tau protein formation, which is creates cognitive dysfunction, or it converts to fructose, which then creates fat storage. And that's not really how things work when you start to get into the weeds of the physiologic pathways.

Theresa Piela  10:17  
I think it's interesting, too, that she didn't mention that after being in the sauna, something in her was craving sugar, like, if she's on a ketogenic, sardine based diet, but she's at the store, and you know, something wisely in her body is saying, please get some grapes. And like you were saying, Mike, then she takes this one experience and extrapolate to why it's so dangerous, kind of ignoring what deeper dysfunction is going on in her body. And, you know, the stress state she was likely in leaving the sauna, I'm guessing, you know, incredibly low blood sugar, high stress hormones, and just kind of that ravenous state where the body is desperate for some kind of stability. Jay, what would you like to add to her, her scary video,

Jay Feldman  11:05  
yeah, I mean, I think you guys both touched on again, just this overarching hyperbole, right, this extreme exaggeration, and then a lot of fear mongering with it. And I want to go back through and continue to break down some of the specifics there, like Mike did with some of those mechanisms and mentioned a couple other points, but in a broad sense, this is not what we need in the health world, like in the online health space, we don't need more of this on social media like this isn't helping anybody. This isn't helping us get closer to truth. It's not actually helping people improve their health in any way, obviously, and even if we thought that grapes weren't an ideal food, this is still, I think, just a there's everything wrong with social media nowadays, and just adds to the division, the tribalism, just Everything that we don't need right now, any further causes people to to have like this, you know, intense fear when they're doing things. And obviously she ate the grapes, so I don't even know if she fully believes what she's saying here. Like, does she actually think that she's causing, like, permanent damage that she's not going to recover from? And she just thought that was worth it for this post, or is she exaggerating? Further than what she knows is the truth, considering that she ate the grapes herself. And I don't think this is the only video where she's, like, showed her CGM and that, you know, she's had glucose spikes and and showing this obvious sense and resistance so, and it reminds me a lot of glucose Goddess, and we talked about her a couple times where. And there's a number of people who do this where they show their glucose responses to foods and say, Hey, I had a glucose spike to this that's higher than optimal, so don't eat it. We've talked about this before. It's like, just because you're insulin resistant or because you're dealing with some issue doesn't mean that this food is a problem for everybody. And obviously there's so much more that goes into it. And there's a lot of issues with just looking at a CGM and saying, I had a spike, so don't eat this anymore. Nor this was bad. And that adds to all of this fear, and that adds to to stress in a way that I don't think is productive for virtually anybody. So wanted to kind of start there. If you're dealing with low energy symptoms like chronic cravings and hunger, low energy and fatigue, joint pain, weight gain, digestive symptoms like bloating or issues with motility, brain fog, poor sleep or insomnia, hormonal imbalances or various low energy, chronic health conditions, like autoimmune conditions, high blood pressure, insulin resistance and on From there that head over to J Feldman, wellness.com/energy, where you can sign up for the free energy balance mini course. In this mini course, I'll walk you through the best diet, exercise and lifestyle strategies to resolve these low energy symptoms and chronic health issues. These strategies are all centered around how you can maximize your cellular energy to resolve these issues. So again, to sign up for that free energy balance mini course. Head over to J Feldman wellness.com/energy, but yeah, breaking down some of the claims she made, and maybe kind of working backwards, so it's fresher, you know, talking about, I think it was really ironic to talk about, and it shows, again, misunderstanding and I think just reductionism when it comes to these pathways to talk about all this fear around the excess glucose being converted to fructose, which, as you said, Mike, is an extremely minor pathway, unless there's major insulin resistance going on and major metabolic issues, but a super minor pathway, and not even mentioning the fructose that's already in the grapes, like you're getting way more fructose from the grapes than you're getting converted from glucose through the polyol pathway. And again, it's like this pathway is bad. This is, I heard Robert Lustig talk about it, and so that's the problem here. And again, just like no overarching conception of of what's going on here. And then, of course, adding on to that, as you said, Mike, the fact that the fructose itself is not an issue. When we consume fructose, we utilize it in. Incredibly well. We convert it to glycogen, we convert it to energy, we convert it to glucose and lactate to send out for the rest of the body to utilize, which, by the way, you're going to have way more fructose conversion to glucose than you ever would glucose to fructose. But all that aside, the amount that goes to de novo lipogenesis for fat production is extremely minimal, and also is far less than the amount of stored fat you would get from the amount of fat in the food that you ate, which in this case being ribs from the grocery store, I'm assuming, are also really high in PUFA, if we're just talking about all of the potential problems with this meal. So yeah, I wanted to touch on that on the fructose side, as you mentioned, Mike, seeing this sort of glucose spike is just a sign of physiological insulin resistance. And speaking of the fear mongering here, I know so many people who are on low carb diets, and you know, they've slowly made the transition toward utilizing carbs more, and they're feeling so much better and everything. But what they say is that early on, they had all this fear because they were using a CGM on their low carb ketogenic diet, and then they noticed, anytime they ate something like fruit, they had this big spike, and it reinforced that that was bad for them and causing issues. And without explaining that, that's a normal physiological response when your body hasn't consumed carbohydrates in a long time, changes the perception there. And that's, again, talking about the kind of hyperbole here, missing that is adding to fear, as opposed to just explaining the normal physiology. Because when you're on a ketogenic diet, and in her case, also a really low calorie diet, she has another post that maybe we'll do at some point, talking about what she eats in a day. And it was nothing. There's like, you know, a couple cans of sardines and some some meat, and it was kind of it. But in any case, all those things drive this physiological insulin resistance, which is an adaptive mechanism. Again, it's not pathologic, which is important to note, but also it's temporary. It's just because you're not consuming the carbs, and after a couple days of consuming more carbohydrates, you see this blood sugar response lessen. It doesn't go away like it'll still be higher than optimal, because it takes some time for kind of full adaptation of the mitochondrial enzymes and the hormones and everything and digestion. I mean, there's so many factors that take a little bit of time to adapt, but it's a temporary normal response to a very low carb diet. It's not a pathological response, and it doesn't mean that grapes are causing high blood sugar in someone who's not in that state, and it doesn't mean that they're causing insulin. Causing insulin resistance either. So yeah, just really important to highlight that, since that wasn't something that she discussed at all, and then then we have this fear mongering about the blood sugar spike itself. And oftentimes we'll hear in terms of glycation, or we'll hear it in terms of some sort of oxidative damage to the blood vessels or something like that. But here we're getting this fear around the tau protein and Alzheimer's. And you know, Mike, you mentioned a couple of really important things here, which are that in like the states where we're seeing accumulated beta amyloid and tau proteins, reduced glucose utilization is a key, key feature, and another way of saying that is when your brain is using more glucose, there's more glucose uptake and more glucose metabolism. There's less tau protein and less amyloid beta accumulation. When there's less glucose uptake in the brain and less utilization, that's when you see more of those problems, and you actually see the pathology of Alzheimer's disease. So it's really the opposite of what's being suggested here, and definitely very far from the underlying state, which you know, what you do see in that pathology is poor glucose utilization, which then leads to reduced uptake and reduced utilization, and low energy and the chronic issues with that. So we do want to make sure that we're not consuming, you know, carbs, without considering how we're utilizing them and supporting our energy production, supporting our mitochondria like that's all important. But again, it's not the carbs that are the issue, as you touched on. And the other thing is, I think maybe where she's getting this from is there are some studies looking at acute hyperglycemia, so acute moments of high blood sugar, and they show increased amounts of amyloid beta in the interstitial fluid in the brain. And that might be misconstrued or misinterpreted as an increase in production of amyloid beta from hyperglycemia that she's saying is going to happen every minute that her blood sugar is elevated. But the reality in those cases is there's not actually an increase in total amount of amyloid beta. It's just being released from the neurons into the interstitial fluid where they're measuring the amount of amyloid beta. But they even note in some of those studies that when they look at the total amount, there's no increase. It's just a movement from one area to another. And so maybe there's a misinterpretation there. I haven't, you know, looked at that much in the low carb space, if, that's if those are some studies that are being cited. And that's where she got this from, like listening to someone who who is citing that and saying that any moment that your blood sugar's too high is going to cause increased tau protein production, or amyloid beta. But there's. There's no evidence or physiological support for that. Again, not to say that having chronic spikes in the two hundreds is ideal, but that's so separated from what's actually going

Mike Fave  20:12  
on here. And I think one thing that I want to highlight that you mentioned Jay has something to highlight in the research, is that a fundamental feature of Alzheimer's disease is an inability to oxidize glucose effectively, and it's brain hypo metabolism. So it's not it the question of like, what causes that is something that they're still trying to determine. But the fundamental defects are energetic defects inside the neurons, where the cells cannot use glucose effectively, and for most for a large variety of cognitive disorders and cognitive dysfunction. That is a key feature, even in mood disorders. Are looking at this now, right? That was the whole what was the guy's name, he had the this hypothesis, and he put positions for a ketogenic diet. Chris Palmer. Chris Palmer, that was, like his central hypothesis, something that Dr Pete has talked about extensively, like decades before that. But even when you look in most of the studies specifically talk about brain hypo metabolism. And I've had a couple of clients where their parent I was helping them organize some of the dietary structure and stuff with their parents who had dementia and Alzheimer's disease. And when you look and there's on the scans that they do, they indicate a Hypo metabolic brain state and atrophy of those areas with a lack of energy production. So it's, again, like the fundamental problem with the vast majority of disease states. There's some specifics right in different areas, but it's a breakdown in energy production in these particular tissues. And the high blood glucose readings that we see in the high insulin levels and stuff like this is a consequence of the breakdown of metabolism, the cells are unable to effectively respond, take up to insulin and then take up the carbohydrate and then use it effectively. So it's this, it's you get this backwards extrapolation of, well, anytime my blood glucose is high, I'm causing these problems without fundamentally understanding the pathology that's occurring down at the cellular level, that's driving the process. And then these things that we're seeing in the blood are a feature of that, or a symptom of that, right? Because everything we're seeing in the blood, these markers that we're seeing in the blood, you have the liver, which is taking substrate up from the GI tract, and an adjusting output of fuel sources into the bloodstream that are going to the tissues, and then the tissues are using that substrate, using those fuel sources. So when we're looking at the blood, we're really trying to understand what's happening at these other points. Why are these markers backing up, instead of just saying, Oh, this is high, so it causes that. It the it's a the the order of understanding is flipped, and we need to really understand what's going on at the tissue level, and then what's going on at the the liver, pancreas, gut level, and to understand what's going on. Now think if you have high blood glucose spikes continuously, you and certain you have high free fatty acids and high amounts of polyunsaturated fatty acids and oxidized lipids in floating around the bloodstream, etc, that can also damage the blood vessels, and then over time, you can get derangement and delivery of fuel sources to the tissues. So that can also happen. But the some of the early problems, or like some of the fundamental problems, is problems directly at the cellular level, or problems of things coming into the diet, or regulation around the liver and stuff like this, and then the bloodstream is just as is the in between state. So I think it's important to always keep that context in mind when we're trying to when we're trying to understand the disease processes and then work from understanding you have these three, not that these are the most important overall, but you have these three different contexts with which you're trying to understand where things are going on. Instead of, oh, blood marker, then this. It's like, this is just one contextual area in the overarching picture. So I think that's important. I think it's important for people who are in the low carb camp and trying to use this metric to understand the context in which they're existing. If you are running fatty ass as your primary fuel source, you are going to be insulin resistant physiologically, right? And so your ability to respond to carbohydrate is going to be impaired, and respond to insulin is going to be impaired. And there's a lot of shifts that have to occur. You have to shift what's going on metabolically in the cell. This is where we talk about Randall cycle mechanisms. On top of that, you have to shift what's going on in terms of the hormonal regulation that overlays that between insulin and between glucagon and between free fatty acid release. And then you have shifts that go on at the liver, and then shifts that go on at the gut. So it's not as easy as 123, there we go. I switch back into carbs, just like when you switch from having carbs to going into keto. You know, we don't really know what the timelines are, if you look in the comment section, because in the research, it says there's about a three week time frame where you have the elevated stress hormones before this body kind of adapts in the Keto but now we're saying it takes months and years to fully adapt to the ketogenic state. But fundamentally, at least, if we look at a three week timeframe, there is this amount of time for the body to switch over these systems and be able to get into the process of primarily oxidizing fatty acids without the exposure to glucose. And when you're coming back from. Carbs is the same thing. So for Dr baz, my recommendation would be to to use whole food fruit sources. Maybe grapes are a little bit more rapidly digesting, have a faster hit on the system than some of the other sources, like berries or something like this, or some of the citrus fruits. But fundamentally, to use those sources progressively, add them in over time, and then watch how our CGM changes throughout that process, instead of using a one marker in this particular or this one example in this particular context to make a point, because it's not really a realistic point, especially if you understand the mechanisms at play. So it's like this is basically an illustration of somebody who doesn't understand the underlying physiology trying to make this bold point with a singular intervention, and an N equals one case. And if she understood the broader context, she would know that as she started to add in carbs and decrease her fat content, her response to these foods over time, assuming she doesn't have severe metabolic dysfunction, would shift back, and she would find that grapes wouldn't really hit her blood sugar that hard. So that's the that, and that's, the question that people that I'm working with are always asking me. It's like, is, you know, what's gonna happen my blood sugar? Where these the values come down? It's like, yes, it takes a little bit of time, and there's things we can do in the meantime to get things back under control.

Theresa Piela  26:13  
Yeah, I'm thinking too, if she had her sardines after the sauna and then had a handful of grapes and maybe tracked that for a couple of weeks, and was also paying attention to how she felt. That would be a more interesting report, I think. But Jay, kind of like you were saying, it seems like she's not fully convinced that the approach she's she's talking about is actually the right way, if her, if she's literally craving grapes and, you know, loses control at the grocery store and can't hold out till her rib dinner, like there's something, there's something there that she's not able to say yet, she boomerangs back and says, Well, you know, that didn't work because of this one, this one off data point. But, yeah, it's just interesting. And the fear, like you both mentioned, it's not helpful, because you're working with people that are terrified, and we know that in a terrified state, we can't progress, we can't stay curious, and, you know, actually pay attention to what's going to happen over the course of a month, not just one experience where the body is clearly still recovering, adapting, repairing from the damage of these of these diets that have gained so much popularity. But anyways, do either of you have anything else to add to this video? Any, any Jay?

Speaker 2  27:28  
Do you have any advice for Dr baz if she watches this well?

Jay Feldman  27:32  
I mean, I think the, I think I would continue slowly adding in carbs. Whole fruits are good option. Mike talked through a few, you know, few you know, few different options, whole fruits, whole fruit vegetables, that could go well. And so, I mean, I've, I see, like, kind of two categories of clients. There's one set where they want to have the CGM, they want to have the data, they want to track it over time, and they're able to look at it kind of objectively, and it doesn't, it doesn't drive all the fear. And, you know, it can be a helpful tool. And then I would say a larger subset, either if they have the CGM and they see any spikes, it's going to really stress them out and going to lead to them backtracking, or they just aren't that concerned with wanting to see the data over time. They just want to feel better. And in that case, I often say, Don't worry about looking at your blood sugar in the first few weeks. Obviously, let's pay attention. Obviously, let's pay attention to how you feel. And if you eat a meal that has a ton of quick digesting carbs and you don't feel good after, we'll make some changes. But that's, I would say, pretty rare anyway. And I would say, use your symptoms. Use how you feel. Listen to that hunger and cravings, because they're telling you something. And with time, we'll see that improve. And then if we want to check on a CGM a little bit later, and obviously, you know, keep an eye on blood work and everything we can do that after a little while having that adaptation. So, I mean, either way, I don't know which one would be a better fit for Dr Bos, but it sounds like, sounds like there was a lot of fear. What's that?

Mike Fave  28:56  
Mike? Sounds like the latter option would probably

Jay Feldman  28:59  
that's, yeah, because of the, because of the fear with the blood sugar spikes. And, you know, I've talked with practitioners as well, like, you know, on their podcasts, or as clients or in my programs, who, sometimes they are the ones who have the most fear because they've learned so much they've been so inundated with these perspectives. And so sometimes there's a lot of relief and kind of letting go and trusting the process a little bit and just giving it a bit of time. So yeah, maybe that would be the best route here. But yeah, I mean, that would be my, my Broad Thoughts. And of course, one thing, and I don't want to go into all of the ins and outs of things to consider when it comes to adding carbs in, but there's a lot of adaptation that occurs the gut, and digestion is a big part of it. And so sometimes we have to be careful with careful with adding in a lot of fermentable carbs or microbiomes typically not used to that when we've been on a low carb or ketogenic diet. So if you were to just add in a bunch of apples, maybe your blood sugar wouldn't spike as high, but you might end up with bloating and gas and other symptoms like some other carnivore influencers have. On, and then, kind of like they see a high blood sugar spike, and they stop while they eat some apples and have bloating and gas, and so they stop. And the reality is that they're probably just not as familiar with the ins and outs there. I mean, they haven't had carbs in decades. So understanding that a little bit, being careful with the fermentable carbs very slowly increasing, are all important to

Theresa Piela  30:21  
consider wise wise words. All right, let's move on to our next interesting clip, another, another influencer that's brand new to me, Richard Smith. I was looking at some of his keto Pro Products. Do you guys remember getting really excited about all of the Keto snacks when we were so deprived and so desperate for sugar, and they had like, keto cups and keto bars. I don't know if you let yourself eat those, but it brought me back to the days of trying to survive on low carb. And you know something about those, those snacks really, really looked enticing.

Mike Fave  30:57  
Yeah, I don't think that the Keto snacks existed when we first were doing keto, so early into the game. So, yeah, I started keto in high school.

Theresa Piela  31:09  
Whoa, yeah. Okay, so you were before the wave of all of the, like, snack cups and like fat

Mike Fave  31:14  
bombs and, I mean, keto is still super fringe, and a lot of people it was like, you know, Paleo was starting to come around, and that pushed into keto. And the Keto snacks was Jay putting on his Baker outfit and making us like keto treats with coconut flour as the vase and stuff like this. That was and that was us in college. So there wasn't really treats. It was like we were trying to figure out unique ways to keep the carbohydrate intake super low, and then, like, exercise a crap ton before we ate them, so that we could still, like, we'd burn through all of our glycogen, and then ideally, we'd repeat our glycogen but we wouldn't actually, like, impact our blood glucose regulation too much, and we could easily get back into ketosis and all this type of stuff. Yeah.

Jay Feldman  31:59  
And then even that was really toward the end of our keto days, like when we were really slowly, you know, starting to add in some carbs, or just on the workout days, we'd have a bit more, you know, we were kind of on our transition out. But before that, I mean, like the Keto snack, I remember, like, adding avocado to my meals, you know, when I started doing that, that was, like, some way to mix it up. You know, instead of just the the really fatty ground meat and some cooked vegetables. And, you know, pouring olive oil or butter on top. Yeah. So, yeah, those the it

Mike Fave  32:26  
was berries too, yeah.

Jay Feldman  32:28  
But again, the batteries were towards the, I mean, there was, we went years without eating any fruit or anything the berries. Was true. Again, I

Theresa Piela  32:34  
transitioned out and only six berries, right? Like six blueberries, Max.

Mike Fave  32:41  
You start. If you're on keto, and you start eating blueberries, like, there has to be some pictures of us in college sitting on the couch, like with our faces blue and our hands blue because we pulled out the five pound bag of blueberries that our other roommate had bought from Costco, and we just ate the whole thing. But again, this, this also was later in the early stages of keto, I was counting the amount of carbs that I had coming in from green vegetables. So, like, how much? Because I would eat a lot of green vegetables to hit my micros that before I did, like, a much lower fiber setup, and then it's like, Okay, I can't go over this amount of spinach and and kale, because if I do, like, I'm going to get my carb intake too close to the limit, um, because I was still trying to hit my potassium and hit all this without taking supplements and stuff like that. So I was doing a lot of veggies and, yeah, it was just basically the diet was like meat and meat and fat and eggs.

Theresa Piela  33:34  
That was, it wasn't keto treats, not Yeah, you couldn't. You could have started your own business, but Richard Smith beat you to it, missed opportunity. So yeah, I'd love to dive into this and kind of break down what he's saying. For people, I feel like in especially in the ray Pete world, people who are interested in more of, like a bio energetic approach, there has been a lot of talk about NAD plus for healthy aging, and even, you know, gut function, looking at how it declines and in really sickly, constipated rats and mice. But let's jump in with this and kind of see where he's trying to take it, what he's missing, if he got anything right,

Speaker 3  34:21  
when we use glucose through the electron transport chain, it costs the body four NAD plus in order to process one glucose molecule. When we process beta hydroxybutyrate, or ketones, it costs the body one now this is important because the level of NAD plus in the body is directly correlated with longevity. So we typically see people who age have less NAD that isn't strictly true. It is generally because people who live a standard lifestyle are constantly reducing this because of the amount of glucose they consume. But what we see in people who are living a ketogenic. Lifestyle, their NAD plus actually increases, or at least maintains. And the reason is that ketones increase this ratio. They increase NAD plus to NADH. So you can, you can live a ketogenic lifestyle. You can increase NAD by living a ketogenic lifestyle.

Unknown Speaker  35:17  
Okay, so

Theresa Piela  35:20  
Jada to jump into what he's saying. Is there any truth? And especially for people that are concerned about their NAD levels, they want to age well, they want to be able to poop when they're 90. What can we take from this? What can we leave behind?

Jay Feldman  35:35  
Yeah, well, I'm glad that you opened with that and kind of mentioned it prior. I mean, first and foremost, I think it's really good that we're talking about NAD plus to NADH ratios. I'm glad that we're having like we're getting into the biochemistry here, because I think we're getting closer to some of the important physiological implications of low carb diets versus higher carb diets, things that aren't often discussed. And I think we're getting steps closer to the truth in terms of the physiology and and the implications of it. And, you know, he's definitely spot on talking about how the NAD plus NADH ratio is highly correlated with health. And, you know, versus disease and aging, it's, it's really, really crucial, and it's basically a proxy for how well we're metabolizing fuel, and how well, we're producing energy, which, as we talked about in response to the last clip, is fundamental when it comes to health and disease and aging. And so the more that we're zooming in on that, I think the closer we're getting. So I think that that's great. Now, beyond that, the specifics that we're talking about here, there's, I would say, a lot that is missing the mark, just in terms of kind of the the basics of of utilizing NAD plus the conversion NADH, utilizing glucose versus ketones at the electron transport chain. Like there's, I think, some real fundamental issues here, and then the implications also, I think there's some, some large gaps. So just as a starting place, talking about this in terms of consuming entity Plus is a is problematic because it's giving you the idea that you have a certain amount of entity plus, and you, as you destroy it or utilize it, and then it's gone. That's going to lower your NAD plus to NADH ratio. And it's almost like there's not this recognition that NAD plus and NADH are constantly inter converting in a number of different metabolic pathways, and those are really important, and we have to understand what's going on in those in terms of how they regulate the NAD plus 10 ADH ratio. So it's not a situation where anything that just utilizes NAD plus, which really it's not consuming, it's converting a 10 ADH it's not like any pathway that does that necessarily means that it's going to lower than 80 plus 10 ADH ratio. There's a lot of different factors going into that. And then there's actual some some issues with the numbers brought up here. So he mentioned that when you're utilizing glucose to produce energy through the electron transport chain, it consumes four NAD plus. And again, I think there's a lot of misconceptions built into that one just on the numbering standpoint. In order to convert glucose to acetyl CoA, which we produce two acetyl CoA from one glucose, that's where we convert four NAD plus to NADH. So that happens after that, that acetyl CoA then has to make its way through the citric acid cycle, where you would then produce another three NADH. So you quote, unquote, consume. But even though it's not really an accurate way of saying it, but you convert three NAD plus NADH for every acetyl CoA going through, and then 1f ADH to 1f ADH two. So from an entire glucose molecule, if you're phrasing in the way of consumption, you would have the four NAD plus prior to acetyl CoA, then you would have the six NAD plus from the citric acid cycle. So you get a total of 10 conversions of NAD plus to NADH. And if that was all that happened, and we were looking at this in a vacuum, then yes, that would be true, that that would really decrease NAD plus NADH ratio. But it's really interesting, especially when you consider his phrasing, when he talks about producing energy at the electron transport chain, because in order to do that, you have to drop off electrons at the electron transport chain. From, in this case, we're talking about NADH, which is an electron carrier. And when NADH drops electrons off at the electron transport chain, it gets converted back to NAD plus as it drops off the electron and then loses the proton. And so in order to produce energy, like if you if we're just isolating NAD plus and NADH, and you are producing energy at the electron transport port chain from glucose, and you went all the way through. The net change is zero because you've converted 10 NAD plus, 10 ADH, and then 10 NADH back to NAD plus. And you essentially have a similar say. Situation when it comes to the ketones, I don't know if you named beta hydroxybutyrate directly, I think he did. But again, yeah, I think he did. Okay. So again, in the process of converting beta hydroxybutyrate to two acetyl CoA, it converts one NAD plus to NADH. Then you have all of the NAD plus conversion in the electron or, sorry, in the citric acid cycle, which, again, seemed like it was missed. So there we get another six conversions of NAD plus to NADH. So you would end up with seven NAD plus has been converted to seven NADH. And then to use those at the electron transport chain, you then have to convert them back to NAD plus, assuming everything is working with 100% efficiency. And so you would still have a net no change. So the reason why I'm going through all that, I mean, first off, the numbers were just not accurately representing the entire picture. And then the other being that the utilization of NAD plus, or the drop off of electrons onto NAD plus, is actually fundamental for producing energy, for producing ATP. It's not a bad thing to be converting NAD plus to NADH. You need that to happen. That's like without that, you have zero energy and you die. Like it's it's the fundamental thing. And it's not the fundamental thing that determines the NAD plus NADH ratio, the rate limiting factor there. The main thing that determines that conversion is how well we're dropping off NAD or electrons from NADH at the electron transport chain at complex one, and converting it back to NAD plus. And that's really where we want to focus. There are tons of things that can affect this, everything from pesticides to heavy metals to endotoxin to stress. There's tons of things that can interfere with this process and affect other aspects of the electron transport chain. So it's quite a an interconnected just complex web of things going on. But if all of those are the same, and we're just looking at metabolism of different fuels, like glucose versus ketones, the main determinant there is going to be the ratio between NADH and FADH two that gets produced from metabolizing either of those. And the greater the ratio of FADH two to NADH or the lower ratio of NADH to FADH two, the less efficiently you're going to be able to drop off electrons at complex one from NADH, and the more backlog you're going to have. Well, really, it's the other way around, the more backlog you're going to have because of the competition for ubiquinone between complex two and complex one, and so you have less efficient drop off of electrons at complex one. And so if we were just looking at that ratio, which, again, all else equal, is far more determinant of the NAD plus tan ADH ratio. Looking at glucose versus ketone metabolism, they're relatively similar in terms of their FADH to NADH ratio. But with glucose, it's going to be about 0.2 and with beta hydroxybutyrate, it'll be about 0.285

give or take. And so with that, the glucose metabolism actually leads to a lower ratio there, which is more optimal when it comes to drop off at complex one, and actually leads to a higher NAD plus 10 ADH ratio. So just looking at that in isolation and citing what he cited for the mechanisms we're off in a number of places, that isn't to mention a number of other things that are going on in the broader context when we're talking about a ketogenic diet. So for one, you're going to see far more fatty acid metabolism. And if we were just talking about NAD plus consumption, you get way more NAD plus consumption from a single fatty acid than you would for a ketone or glucose. But more importantly, you get a much higher FADH to NADH ratio. So if we were to put these in order, you would see that glucose has the lowest FADH to NADH ratio. Then we have ketones like beta hydroxybutyrate, and then we have fatty acids which have the highest FADH two to NADH ratio. And so with that in mind, you're actually going to see far less efficient mitochondrial respiration, far less efficient electron drop off of the electron transport chain, and a far lower NAD plus to NADH ratio with fatty acid metabolism. That being said, there's one other important piece to touch on here, when it comes to the impact of a low carb diet and this whole metabolic relationship with NAD plus to NADH ratio, which is the adaptive pathways. So when there are issues metabolically, when we have a low NAD plus 10 ADH ratio, we end up with a number of adaptive responses. Right? We see increased oxidative stress, increased inflammation, increased activity of these different adaptive proteins in order to deal with the sub optimal metabolic state. And so what we see as a result is an up regulation of of what's called the NAD salvage pathway, which resynthesizes nad so that you restore a proper NAD plus to NADH ratio. So when you look at fatty acid metabolism initial initially you'll see a very low NAD plus to NADH ratio, and that's because of the inherent metabolic inefficiency you then activate. Defensive pathways, and then you bring that NAD plus to NADH ratio back up, that's not a good thing. You don't want to be activating this pathway. It requires oxidative stress and metabolic inefficiency in the first place. But as a result, if you just look at that one snapshot a bit later, you will see a restoration of the NAD plus to NADH ratio. And that's part of what you see in the ketogenic diets. That's part of why in certain circumstances, you can see an increase in the NAD plus to NADH ratio. It's due to the triggering of these defensive pathways. And then alternatively, the other situation where you can see some benefits is if you have poor glucose metabolism. So again, with efficient glucose metabolism, you'll have a much higher NADH to FADH to ratio, which is much higher compared to ketones or fatty acids. But if you have impaired glucose metabolism, if you're not utilizing it well, then there's going to be a major shift in efficiency. And you will end up seeing issues all across the metabolic pathways, including a low NAD plus to NADH ratio. And then if you provide a fuel that can be used well, like a ketone, then you'll see some restoration. There. You'll see an improvement in the metabolic state, and you'll see that the NAD plus NADH ratio increases again. And so in situations like epilepsy, these are situations where you have impaired glucose metabolism, elevated lactate values, and impaired mitochondrial utilization of glucose. And then if you provide ketones, you tend to see improvements there. And that's not because of an inherent benefit of ketone metabolism over glucose metabolism. It's that we're able to provide an alternate fuel that can actually be metabolized well when the glucose can't be and so that's another situation where you'll see an increase in NAD plus 1088, ratio. But again, that's not relevant to kind of a healthy metabolism of glucose versus a healthy metabolism of ketones. And all that being said, the one last thing I want to mention is that ketone metabolism, in and of itself, is pretty efficient. I don't see an inherent issue with it when it comes to a low carb diet. I would say that the ketones themselves are not the problem. It's getting into a state that causes the production of ketones, which inherently require stress, and it's all of the up regulated fatty acid metabolism, which is far more inefficient than glucose metabolism, and that's really where we run into issues. If the whole body was running on ketones, you know, instead of fat that I would have much less of an issue to be a much less stressful state, assuming that we didn't have to go through the stress to, you know, get into the stressful state to be in a place to produce the ketones

Mike Fave  47:28  
in the first place. I wanted to add something that I think is something that's really important to talk about, that Jay mentioned, is that in impaired glucose metabolism, you actually have a shunting towards lactate, which is basically an attempt to the body to try to get and recycle NAD and NAD plus and produce some ATP. So when you have this metabolic dysfunction, and you drop ketones into that state, the ketones, when they're going to be oxidized, they have to run into the Kreb, cycle into the and then into the electron transport chain. Whereas, if glucose isn't working well, it's forced into this lactate pathway. So ketones are kind of a rescue option when you have this faulty metabolic state, and then, yeah, of course, they show benefit. And that that's where they show benefit, particularly in brain metabolic disorders, in states of epilepsy, where you see a high production of lactate. And something I want to point out here is that the papers, I assume, where Richard Smith is getting this stuff from, our papers discussing ketone metabolism in states of brain metabolic disorders. And the reason this is and this is ketogenic diet, in particular, in states of epilepsy or in seizure disorders, and the reason that this is important, specifically in brain metabolic disorders, is because the context in which these ketones are being produced and oxidized in these ketogenic diet is specifically in the central nervous system, because what happens is, when you don't have enough glucose coming in, the the body makes ketones kind of as a backup option, because the brain can't oxidize fatty acids. So what winds up happening is it starts to oxidize ketones. So we're what we're looking here, and seeing these improvements in people who have epilepsy or who have seizure disorders, is that their NAD plus NADH ratio is improved. They have a state of metabolic dysfunction when you provide ketones, because they're not using glucose well, and then you're providing a ketone that they can use Well, which oxidize much more closely to glucose than it does to two fatty acids. And further, again, this is in the central nervous system, because those ketones are directed towards the central nervous system at large, right? It's to replace glucose when you don't have adequate glucose coming in. So you don't have to force so much gluconeogenesis and shred through the the amino acid supply and the glycerol supply, lactate supply, etc. So you have this other backup there, which are the ketones, which can be generated from fatty acids, which we have an abundance amount of fat stored on our tissues. Even if we're relatively lean, you still have pounds of fat stored which is a good source of energy. So what we're really doing in this ketogenic diet state, in this context, is that we are providing we're forcing the rest of the body to run on fatty acids, which is fundamentally worse, from an NAD plus to NAD. H ratio because of the amount of F, A, D, H that's produced that alters electron transport chain function by over reduction. And then on top of that, there's way more NAD plus consumed by the fatty acids. If you look at one fatty acids consumption NAD Plus, we're going to frame it in this light, fatty acids are by far the worst of the three substrate in terms of NAD plus consumption and then regeneration through appropriate, appropriate recycling inside the electron transport chain. Not to mention that in ratio to ATP generation is also the worst because the uncoupling that gets produced. So if you're going to, if you're going to make an argument of I want to improve the NAD plus to NADH ratio based on this context that he's providing. It's not a ketogenic diet. It's supplying ketones directly into a state where you have metabolic dysfunction. So this is a because what happens is the NAD plus NADH ratio across the rest of body is going to be crap, and then the central nervous system is going to get some ketones, and then maybe you see some improvements there. If there's some energy metabolism disorder of the brain, like a seizure disorder. So fundamentally, it's like this is in the context of the central nervous system, where you see an improvement in that NAD plus NADH ratio, and the rest of the tissues that are primarily relying on fatty acid oxidation are going to have a worse ratio across the board. And maybe there's some adjustments because of the salvage pathway. But fundamentally, the way things are supposed to work is you're recycling it. Not having to sell. You're recycling the NADH is converted to NAD plus the electron transport chain, and then you reuse that NAD plus again. So I think this is this whole piece is like a very it's like, oh, look at what ketones do. And then, and then, based on what ketones do, we recommend a ketogenic diet. But it's like the argument in support of ketones basically invalidates the idea of running a ketogenic diet, because you can't sit there and say, Oh, we want this better NAD plus to NADH ratio, and we want less NAD plus consumption when it's like, okay, then you don't want to burn fats, period. You want to burn glucose and then supply ketones. So you would just take MCTs or take exogenous ketones. So like his whole argument invalidates his existing premise based on the mechanisms that he's discussing here, not to mention that the hormonal profile when you when you don't eat carbohydrates, even if you were, even if we want to split hairs, about, about cortisol, right? That is, oh, it only raises for three weeks, and, well, that mechanism that you guys cite about altered cortisol signaling like, that's not relevant. Okay, glucagon levels and then adrenaline levels, they're going to be higher, fundamentally. And glucagon, by itself, forces fatty acid oxidation. That's one of the primary things that it does, is it shifts what's going and it's through some of the same mechanisms that we see with the Randall cycle, but glucagon directly forces fatty acid oxidation. So the lack of carbohydrates itself selects for up regulated glucagon signaling, which then selects for increased fatty acid oxidation, which is worse for your NAD plus NADH ratio, fundamentally, not to mention some of the other hormones, impacts, and then on top of that, the uncoupling impact, which decreases ATP production. So you have an a worse NAD plus NADH ratio with less ATB produced. And maybe the brain gets some ketones. That's that would in a this dysregulated metabolic state is better. So it's just, it's not that he's wrong in his in in part of his assessment here, the numbers aren't fully correct because he's just looking at like one particular area of the Cascade. He's not looking at what's going on in the Krebs cycle, in terms of production of any DH in the Kreb cycle with ketones and glucose. He's just looking at the starting pathways glycolysis, and then the ketone production into acetyl CoA, or the ketones conversion into CoA, but it's the for when you look at the overarching picture, I think it's like very myopic and misses the point of what's going on inside the rest of the body. Doesn't recognize that this is specifically to ketones, largely inside the central nervous system, where they're selected for. And then it completely discounts the fact that the diet setup is forcing fat oxidation, which is worse from this context. So yeah, all together, when I'm looking at this, I think it's just there's like, it's the same thing where you get, like, a small amount of truth from a weird angle, and then it doesn't put the it's not in context. It's not in context of how things are actually working. So based on Richard Smith's argument, you could say that using exogenous ketones or medium chain triglyceride fats like you would get from coconut oil can have benefits for people who have metabolic disorders, particularly in the central nervous system and are not oxidizing glucose well to improve their NAD plus to NADH ratio. This is not an argument for a ketogenic diet, that's especially if you're looking at NAD plus and Ed ratio across the whole body, right? Yeah.

Theresa Piela  54:48  
Mike, really good reminder too, that we can derange things when we're zooming in way too closely, whereas if we're looking at, like you said, the whole cascade, or thinking long term thinking, what's happening in the. Body as a system, not just in the brain, you know, then starting to get a whole perspective, and it takes out the like, again, not to say this was fear based at all, but sometimes I feel like people watch videos like this, and they feel like they need to, you know, stop what they're doing and and shift everything to whatever this trend is of, you know, ketogenic diet versus, okay, what's, what's going to be the sustainable option if I actually want to live a long, healthy, beautiful life and increase my NAD plus levels, how can I actually do that in a way that's going to support the entire system? And for people that are curious about that, maybe they don't have epilepsy, and they, they, you know, they're on a predominantly carb based diet, and maybe they're getting plenty of niacinamide. Are there other ways that they can boost their NAD NAD plus levels? Jay, do you have any ideas there?

Jay Feldman  55:50  
Yeah, I mean, and it's really the ratio more than anything, which the reason why I say that is we don't want to necessarily. I mean, adding NAD plus does tend to have benefits, but it's not as much about like synthesizing more NAD plus. Rather, it's about fixing the metabolic issue that lowers the conversion of NADH back to NAD plus. That's really the fundamental thing that that gets interfered with with aging and and chronic disease. And as I was mentioning earlier, there are so many things that affect that some of the most common are going to be things like PUFA and the oxidative stress that results from them, and the inefficient mitochondrial respiration that results from them. Endotoxin is a huge one as well that directly interferes with the electron transport chain in a number of places. It will cause slower or less efficient NADH drop off, so you get less of the NAD plus more of that NADH. So it's really those fundamental things. I mean, nutrient deficiencies can be a big factor stress, which will drive fatty acid metabolism and lower the NAD plus to NADH ratio, just like we were just talking about, is a big factor, of course, a low carb diet as well, but it's really when we zoom in in this way. And you were talking about this a little bit. Theresa, how important it is to make sure we're zooming back out and not losing the full picture when we zoom in in this way, what we come to, more than anything, is that what we can see is that every single input in our environment is having an impact on how well we produce energy, how well our mitochondria are functioning, and as a result of that, the entity plus to NADH ratio, and it ends up being this through line that connects everything that's going on around us, from sunlight to stress to sleep to nutrition and the different chronic diseases that we're seeing. And on one hand, it doesn't necessarily, I think some people take this to say, Okay, well, then there's just a single pill or a single solution here, and that will help reverse all the health issues, as opposed to more of this recognition that there is a universal situation going on here, and we need to treat it as such, and we need to consider all of the different inputs that are playing a role here. And a low carb ketogenic diet is certainly not the only one, and and that's part of why people can have a lot of benefits on those diets, because they dramatically lower endotoxin. And if someone is poorly utilizing glucose, and you provide something like ketones or even fats that are that can be utilized better than glucose in certain circumstances, in certain states of mitochondrial dysfunction, you can see relief. You can see better ATP production, at least in the short term, you can have this net benefit, and then in the long term, start to see the kind of negatives creep in as a result of hammering the stress pathways and forcing inefficient mitochondrial respiration and a low NAD plus to NADH ratio, and trying to trigger all these adaptive pathways, which you can only do for so long. And that's where we start to get into the issue with the hormetic perspective. And I think that's kind of the natural transition here. So once you start to really look into what's going on metabolically on a low carb diet, and you start to realize, inherently there's an increase in ROS production and oxidative stress, inherently there's an increase in uncoupling, inherently there's a reduction in the NAD plus 10 ADH ratio. You then say, Oh, well, as a result of those things, you have these adaptive pathways. You have this NAD salvage pathway. You up regulate na MPT, so you increase the NAD plus NADH ratio. So this is actually a good thing. And we get into this hormetic argument where we basically see that whether it's caloric restriction or intermittent fasting or cold plunges or arsenic or cadmium or ionizing radiation, you have this damage, and then you have an adaptive response. So that must be good, because the adaptive response has some benefit, just like how we produce cortisol under stress, and cortisol is anti inflammatory. So that must be good. And I think that, I mean, hopefully this starts to transition into that, because then I think the transition after that is recognizing that that isn't actually physiologically accurate and not actually the way to improve health. And so I hope that this is kind of that next step there. It seems like it is that we're working our way down that that journey, and we will get to the point of recognizing the bioenergetic perspective, right? Recognizing. What, what we were just talking about Theresa with, with energy production being foundational and fundamental as the driver of health, and just recognizing that a low carb diet is antithetical to that it's not helpful there, as opposed to it being helpful. So, yeah, I think that's all I had to mention here.

Mike Fave  1:00:18  
Mike, anything else? Yeah, there's one point to I think that's really important to keep in mind here, is that the entity plus NADH ratio is an indicator. It's not necessarily the be all to end all that it like you want to optimize your entity plus NADH ratio because it indicates that you are moving electrons appropriately through the Krebs cycle and the electron transport chain to produce energy. You don't want to increase it just because of increasing it. And I think that's the problem that you that we get here, is that it's like, there's this focus on, oh, what are all the things I can do to and I'm not saying this for you Theresa, but this is like inside the bio hacking spheres, what are all the things I can do to increase my NAD plus NADH ratio? And it's just like this hyper focus on this individual marker. It's like a myopic focus on this individual marker, and with a lack of understanding of what it actually represents, because if you understand what it represents, then you wouldn't go about the ways that Jay just mentioned to increase it by increasing salvage pathways or inducing different pathways that create an antioxidant response after driving ROS or that are trying to help minimize an excessively reduced state. You're not trying to drive that process in the first place. The ideal process. And this is something that also comes directly from Dr Pete is and he says, when people ask him, it's like, you know, what's you know, what's the best diet? Or, like, how should I eat? And it's like, anything that improves your ability to flow energy through the mitochondria. And that's like, fundamentally, the NAD plus NADH ratio is an indicator of that. It's are you able to take your NADH and are you able to convert that and recycle that back to NAD plus? And the way that occurs is with the electron transport chain and ATP production working effectively. That's how that works. So it's a marker of this low, this process, this energy production process. It is not the be all, the be all to end all by itself alone. And I think that's where we get into these weird interpretations of things. Is you see like, Oh, if this marker is this and these part, like, for example, with insulin, right? Oh, well, insulin is low in when I don't have carbohydrates, and low insulin states are associated, or these insulin levels, or blood glucose levels, are associated with all these different disease processes. So then what we're going to say is, well, I don't want to have carbs because carbs raise my insulin. But the reason insulin is low in these health states, and why it's a good marker is because people are able to or are sensitive to insulin. So when they eat carbohydrates, they take up the carbohydrate, they turn it to energy. The cell internally takes up the insulin, degrades it, and then the insulin levels are low because the cells are responding effectively. So that's why, when we're talking about solutions to these problems, a cure for a high insulin state and insulin resistant state is the ability to eat carbohydrates, respond to insulin effectively and maintain normal insulin levels, not I suppress my insulin levels because I just don't eat carbs. So it's like this weird focus on the individual marker and without necessarily understanding the under the underlying context. And it's and it's weird too, because you have this in the low carb sphere, they try to have it both ways. Whereas, like, first your a 1c goes down, your fasting blood goes goes down. And this is an indicator that things are okay, things are working. Like, I'm in a better health state. And then when it gets then when things start to get worse, a 1c picks up, and fasting, blood goes, picks up. It's like, well, my insulin still looks good, and these markers don't matter anymore. And we're going to change the context, instead of trying to understand what's fundamentally going on physiologically, and why are these things adjusting in these different types of ways. So again, the overarching picture that we're looking for is, you take energy, or you Sorry, you take fuel, source of substrate, you convert it to energy effectively. And all of these other markers that we're looking at in between are indicators of this under arching or this overarching process. And if you understand things from that perspective, then things start to make a lot more sense, and you start to get, I think, a better picture of what we're shooting for, instead of this piecemeal approach to adjusting these individual markers. And I think right now, we're still stuck in this timeframe where it's piecemeal adjustment to these individual markers instead of underlying understanding of the physiology.

Theresa Piela  1:04:29  
Yeah, I've seen in the more like, biohacking space as well, where they're maybe on that low, low carb diet, and then they're trying to sell this, like nicotinamide riboside supplement or, you know, and like you're saying, they're hyper focusing and not seeing that there's a more systemic solution. But that's where we're at in the wellness world these days, I guess. Okay, to close out the show with a success story from been a there, 2574, they said, I've increased my. Carves, and my fasting blood sugar has gone from 5.6 to 5.2 I'm happy. I think I also had mild insulin resistance. Not sure about that at the moment. Need to do some more blood tests soon. But, uh, congrats to Binna there. I'm I'm glad that they're feeling happier and feeling better, which is probably the best test. Just you know, the felt experience of of more energy, more health, better moods, more creativity, everything that's indicating that the body's working well and feeling good everywhere, not just in one, one area. Okay, Mike, where can people find you?

Mike Fave  1:05:36  
They can find me here on bioenergetic view as well as an energy balance podcast, and they can find me on my YouTube channel. Mike fave, as well as my website. Mike fave.com,

Theresa Piela  1:05:46  
awesome. Jay, where can people track you down?

Jay Feldman  1:05:50  
Yeah, best place is to head over to my website. Jay Feldman, wellness.com, got tons of free resources. There links to podcasts and articles, and of course, here on my YouTube channel and social media as well,

Theresa Piela  1:06:02  
awesome, and you can find me at living roots wellness on Instagram, and then also my app and community called tapping with tea. And thanks everyone for tuning in and listening today, we will see you in the next one you.