Episode 146: Why All Calories Are Not Created Equal
This week on Geeky Magic, we debunk the myth that a calorie is a calorie. In this podcast, we discuss how this is incorrect as it does not account for many other important variables, such as Ghrelin, Leptin, Insulin, and Fructose. We discuss how energy is made, mitochondria, cell metabolism, and recommended lab tests. Join The Better! Community On Facebook. Get the show notes here.
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- 0:30 Introduction
- 3:05 Where And How Is Energy Made
- 11:07 Why It’s More Than Just Calories
- 20:16 Insulin, Mitochondria & Cell Metabolism
- 31:22 Self Assessment & Lab Tests
- 37:00 Conclusion
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Dr. Stephanie (00:31):
today I wanted to go on a geeky magic carpet ride on energy calories in versus calories out and the effect of sugar, the different types of sugar and insulin. And this is really, I've been watching a lot of influencers in the online space. And there just seems to be this ongoing sort of dogmatic argument around the idea that all that matters are calories. You have sort of that one camp where people will say the only thing that matters is the amount of calories that you take in. And on the other side, you know, it's the type of diet. It's the only the type of diet that matters. You know, if you're doing keto, that's the only thing that matters. Or if you're doing vegan, that's the only thing that matters or Mediterranean or whatever. And like most things, neither, neither camps are right, and neither camps are wrong.
Dr. Stephanie (01:29):
They there's parts of each of those arguments that are succinct and correct calories of course matter. Macronutrient composition of the diet of course matters. But I really want to give you more of a nuanced presentation around understanding energy production, because I think that a lot of women, when we get into our late, you know, we have children we're in our late thirties and our forties. And as we move into menopause, you all know that calories, like you could be eating the same diet and you start gaining weight and you don't know why. And I talked a little bit about the Addepar stat and the influence of chronic low grade inflammation in my book, the Betty body. So we go on a big you know, geeky magic carpet ride there, if you will. And I wanted to do it in this podcast as well.
Dr. Stephanie (02:25):
And I really wanted to, I think that you Bettys are such intelligent information seeking women and my community. And I just wanted to, I just wanted to nerd out with you a little bit. So here we go. We have show notes for this, of course which will be helpful and some links and resources that I'll talk about in terms of a list of what I call sneaky sugars, which are really sexy names for sugar, because most of us are not putting sugar into our everyday lives, but believe you me, hopefully by the end of this podcast, you will understand where some of your sugars may be coming from. So first let's just discuss some basic science, right? Where, and how is energy made? Where does it come from? So, you know, very simply energy comes from our body's ability to make that ATP, that adenosine triphosphate from precursors.
Dr. Stephanie (03:26):
So these are substrates and substrates basically come from two places outside the body and inside the body. So exogenous substrates are going to be our dietary carbohydrates, our fats, our proteins, and those are going to break down and we'll be able to use those as a substrate for ATP production. That is the precursor. That is energy. That is the currency that we all trade in every single day. So that's our exogenous substrate. We also have endogenous meaning that we can produce our own energy as well. So precursors for energy production are going to be glucose of free fatty acids, amino acids that we have stored, you know, throughout the body carbohydrates are stored as glycogen in the liver and in the muscle and in our adipose tissue and the fat cell we have triacylglycerides. And so that is the, the storage form of fat. So excess carbs, excess fat, excess, everything gets sort of loaded into this triglyceride.
Speaker 1 (04:36):
And of course in the apps,
Dr. Stephanie (04:38):
It's a food. So whether we are in a, you know, maybe we're in a fasted state or if you're working out fasted, we can draw from these stored sources. So we can draw from our liver and our muscle. We can draw from the fat, from the fat cell. And the other piece that I wanted to talk about here in terms of adipose tissue or fat, is there's a couple of different areas in the body where we store fat. So most of the sort of we'll call it harmless fat is our subcutaneous fat. And that's the stuff that we tend to hate the most because it's, you know, not necessarily visually appealing, you know, we all want to slim down our arms and our tummy and our bums. But this is not the fat that's really deadly there. The really deadly adipose tissue is where we find it when it is accumulating in an ectopic fashion. So when it is accumulating in the organs
Speaker 1 (05:38):
Dr. Stephanie (05:40):
In the liver, something that has been coined NAFA Aldi, or non-alcoholic fatty liver disease. So it used to be when you had a fatty liver, it was usually from excess consumption of alcohol, but now know that the population has really shifted and that, you know, I think the number is like 40 to 50% of Americans, if my numbers, right. Have some degree of NAFA, D some degree of fatty liver, and this is, and that's not just in the liver. We also see fatty pancreas. We see fatty fatty Oregon's, but the NAFA LD is really the big killer. So when we are storing ectopic fat is what I want to focus on a little bit today and how the influence of sugar and insulin. And of course, insulin is the response to sugar or glucose and other sugars, how that can be driving this process.
Dr. Stephanie (06:37):
So just before we get into there. So we were talking about basically you know, systems in the, in the body that influence those energetic capacity. So a lot of times women will say, God, like I used to have all this energy, I could work out, you know, I could, you know, go out and party all night and go to the, you know, and be able to get up for my classes the next day. That was totally me. And then something happens, you know, after childbirth is big, energetic expenditure of, you know, creating a life. And all of a sudden you're getting in bed by nine is a big luxury, right? So, you know, as we mentioned, you know, the things that are going to affect our ability to make energy is that substrate availability, right? So that's the first thing, how much precursor of energy we have, whether that's endogenous or exogenous.
Dr. Stephanie (07:24):
The other things that we want to take into consideration is hormonal regulation, right? So I mentioned this briefly with perimenopause, a lot of women will say, Hey, listen, I'm having the same calories, but my way to shifting something's wrong. So dysregulated hormones, and we see this not only in our sex hormones with estrogen and progesterone and testosterone, but we will also, we also want to be looking at insulin, for example, the pattern of insulin secretion in response to a rise in blood glucose, or, you know, on the, on the opposite. On the flip side of that, we might see glucagon what the response of glucagon is in response to a fall in blood glucose. So we want to look at our hormones that will affect our energy. And then the third piece in terms of what affects energy is enzymatic modification, right? So how quickly, or how slowly an enzyme is going to work.
Dr. Stephanie (08:17):
So this is based on genetics too, to some degree. So what, what snip you may have, or what polymorphism you may have of that particular gene that we're looking at, whatever gene we're looking at and also, you know, the S the structure of the enzyme, and then the concentration of the enzyme as well, because we'll see a change in concentration as any particular biological process is is happening. So very simply, you know, a major influencers of energy are going to be what you're eating or not eating, right? So substrate your hormones, which are determined largely by many lifestyle factors, right? So your stress levels, which we talked about last week sleep quality, exercise and activity levels, diets on exposure, lean body, mass muscle development, like all the things that are going to drive hormonal balance or imbalance, and then the genetic and epigenetic expression of enzymes.
Dr. Stephanie (09:17):
So that is how we influence our energetic capacity, our ability to produce energy. And of course, when we're producing energy, the most abundant way to do so is in these structures called the mitochondria. So this has, these have been referred to as like the battery packs of the cell, the powerhouses of the cell, these are it is a, they are not of human origin. They are bacterial in origin. So you might argue that we are, but a vesicle for our, you know, our mitochondria, these bacterial entities. And this happens, this really abundant way of producing energy is something called oxidative phosphorylation or Oxfam. For short, there are other ways that we can produce energy. We won't get into them today, but just, you know, for, for completeness, we want to talk about glycolysis. This can be aerobic or anaerobic. And in the anaerobic we see instead of [inaudible] you know, changing into a Colet, it gets converted to lactate. That is, you know, if you ever have, you know, been sprinting and you get that, like stitch in the side, that lactic, that's your lactic acid kind of building up like to gas. It also can be converted to pirate as well via the liver to produce, like, to produce more glucose as well.
Speaker 1 (10:40):
So stay with me,
Dr. Stephanie (10:43):
I promise I'm getting to a point. So I wanted to just sort of re I wanted to talk about sort of the baseline, like that's how energy happens. It's through this oxidative phosphorylation in the mitochondria, and then the things that are influencing it are what we're eating or not eating what our lifestyle is. It's going to influence our hormones and then the genetic and epigenetic expression
Speaker 1 (11:05):
Of our genes. Okay.
Dr. Stephanie (11:07):
So this is where it starts to get a little bit, well, the, the calorie, the only thing that matters is calories begins to fall apart because when we look at different types of substrates. So if we were to just look at, for example, the different types of sugars, and we'll talk about for the, you know, there's many types of sugars, galactose, sucrose, glucose, fructose for simplicity. We'll talk about glucose and fructose because glucose is the molecule of life, right? Every single human needs glucose. And even when we cannot get glucose in our, in our diet, our body is so dang smart that it has a gluconeogenic pathway, meaning it is just you know, we can produce new glucose on demand if we don't have the substrate availability. And that, you know, glucose is really assigned you know, four kilocalories per gram. So it was fructose, right?
Dr. Stephanie (12:06):
But these are two very different structures that have very different impacts on the body. So glucose is a six carbon ring. Fructose is a five carbon ring. And one of the things that we know about fructose, so you'll see fructose in just to give you some context here. Fructose is, is we see it in fruits, right? So there's some glucose and some fruit dose in, in fruits. But it's a lot of it is in processed food. So we'll see it in things like sodas and candy, and like the sweetened yogurt, not like the plain unsweetened fat, full fat yogurt, but like the blueberry bottom and the honey sweetened with honey and the vanilla flavored yogurt, store-bought salad, dressing, canned fruit baked any kind of baked goods, especially if they're bought from the store, cereals, granola, you know, any type of juice. And, you know, we can get into the problems of juice cause you like completely have removed the fiber, but juices are a big problem.
Dr. Stephanie (13:08):
Jams, jellies, sports drinks, Oh my God. Never ever drink. If you take one thing away from this podcast, throw away the sports drinks they are doing, absolutely nothing for you, ice cream sauces, condiments, that kind of thing. So this is where, you know, it's a lot of it is in these processed foods. And if you were to just say, well, fructose has the same caloric value as glucose. Like what's the big deal, yo. Well, there is a really big deal in terms of your satiety signaling. So when we think about the two main hormones around hunger and satiety are ghrelin and leptin, so grelin is like the gremlin. If you will, in your tummy that tells you, Hey, it's time to eat girl. And leptin is secreted from your adipose tissue, but picked up from some of the appetite regulation centers in the brain that says, girl, you're done now put the four down.
Dr. Stephanie (14:01):
Okay. So grelin when we have, when we consume glucose, okay. Grelin will go down. So we will, we will attenuate. We will lower our hunger. When we consume foods with glucose, the same is true for fatty acids that like for fats and proteins, however, when we consume fructose like those sports drinks and those flavored yogurts and those salads and those condiments, the gremlin signaling doesn't change. So when you consume a lot of fructose, your brain really doesn't know that you've eaten, right. So what happens? You end up consuming more calories. So of course, you know, you'll, you'll have this like bro science, these guys, and these these guys on the internet that will be like, Hey man. Yeah. If you have some more calories you'll gain weight. Well, yeah, no. Of course, if you're having foods that are filled with fructose, you're actually altering your satiety signals.
Dr. Stephanie (14:59):
So of course you're going to over consume calories, but the type of calorie matters, all carbohydrates are not equal. The same is true. So we we've talked about, you know, gremlin the same, you know, another piece two, this is also leptin. So we know leptin says, put the fork down. I talked about that in the Betty body, but leptin also has a direct impact on brain development and cognition, right? So fructose, wha you know, in it's inducing, you know, because it is driving up this insulin response and this hyperinsulinemia, it blocks leptin's ability to, to help neurons branch out and connect. Okay. So it can lead to cognitive deficits over time. It's basically like your, it is not allowing the neurons to hold hands and be friends. It is isolating them. It's like social isolation, right? That's, that's what happens under the influence of fructose.
Dr. Stephanie (15:58):
And the other thing is fructose inhibits of really important enzyme called brain derived neurotrophic factor. I've talked about this, we've talked about this lots and lots on the podcast and BDNF is the alphabet soup that we refer to as brain-derived neurotrophic factor. And that's like the miracle grow for your brain and fructose inhibits BDNF. So of course I, you know, I've said this in the book, I've said this on the pod, you want your, the one organ you want big is your brain, right. And fructose inhibits that. The other thing to consider when we are looking at the difference between glucose and fructose is something called the Mayard reaction. And this is basically the Browning effect. So if you were to you know, if you were to caramelize sugar, right, if you were to boil sugar over time, if you were to put white, you know, white sugar in with some water on a stove top over time that sugar would Brown, right?
Dr. Stephanie (16:55):
Fructose and glucose, like all sugars, Brown, they all undergo this Mayard reaction. But the difference is the speed with which this reaction happens. So glucose, we said as a six member ring structure, right? So it's more Abel and it does engage in the Mayard reaction, but it does so relative to fructose slower. So fructose, we said as a five member ring, so it is much easier to break apart. And so it will engage in the Mayard reaction seven times, times faster, seven times faster than glucose. So for all of my ladies who are vain, including myself, we want to avoid wrinkles. We want to avoid cataracts. We want to avoid all of these elements of aging, right? Like if were to look at, you know, the skin, for example, of a newborn, compared with a skin thinning of the skin of, you know, 70 or 80 year old, you can see that the mayor reaction has happened.
Dr. Stephanie (18:00):
You're going to see that fine lines and wrinkles, but the more fructose that you consume, the faster you are going to look more Haggard, and you're going to get more of those fine lines and wrinkles. So, you know, it's like buyer beware. If you, if you are okay with that, or you don't care about that, then that's fine. I bring it up because I am a vain woman and add those sprinkles. So the, and the other thing just when we're talking about brain health, of course, is that fructose really lights up reward centers in the brain, much stronger than glucose. So what we, what we know is that fructose activates the same air. It has the same neurochemical cascade that we see in cocaine, addicts, heroin addicts, nicotine alcohol. It is, it is much more he Dominic. And it can generate more of that reward seeking behavior, right?
Dr. Stephanie (18:57):
So once you get a hit, what do you want? You want another hit, right? And over time, of course we, we get habituation. Like it's going to require more and more and more of that substrate to get that same hit in those reward centers of the brain. So that's why I really sort of cringe. And I get a little bit of a nervous tick. When I, when I hear these people say, Oh, calories, the calorie doesn't matter. Does it? Like, it really does matter because we can see already. And I'm, you know, we're S we're going to wait into the insulin and what happens in the metabolism of energy in just a moment, but you can already see that even when you equate for calories, what we're seeing is already a change in behavior, right? A change in brain, a change in glycation and oxidative stress via the Mayard reaction, this increased aging.
Dr. Stephanie (19:47):
So yes, it's the same calories, but what ends up happening is you eat more calories because you don't feel full, which is kind of a, you know, it's a bit of a red herring for someone to be like, yeah, but it's like the calories weren't equal. The person ate more. And it's like, yeah, if they had, if they just had glucose, they, they, you know, if they weren't having some of these, you know, pro-inflammatory, anti-aging compounds and they wouldn't have had, they wouldn't have had this much calories to begin with. Okay. So I will now move on to insulin and really what happens inside the cell. And what happens when your mitochondria are not healthy, right? Again, really moving away from this idea that a calorie is not really a calorie. It's like what your body can do with those calories. That really matter.
Dr. Stephanie (20:33):
So a lot of people, and I see this really happening a lot now are really interested in blood glucose, right? So when we, you know, diabetics have to look at their blood glucose daily and also see this happening in a lot of them, even though I hate this word, but the biohacking space, we see the biohackers that they are wearing CGMs or these continuous glucose monitors to look at our response to foods and stress and sleep and workouts and stuff, all good data. And I am actually really excited. We have a couple of, I have an expert coming in on the podcast soon to talk about continuous blood glucose monitors. So this is really useful information, except a lot of times people will conflate blood glucose with blood insulin, and often, especially if there's any type of mitochondrial dysregulation it is they're unrelated to each other.
Dr. Stephanie (21:27):
And I know that, that sounds a little bit crazy. Like how can my blood glucose be unrelated? Like not be related to my insulin. I'm not saying that they're two separate entities. Blood glucose will drive up blood insulin, but it is the patterning of the insulin. Is there hyperinsulinemia, is there a, is there a dysregulated insulin or DIC response to the glucose? Right. And then what happens to the glucose? So I want to talk a little bit about what happens inside the cell. So we have glucose, we're going to assume that we have glucose here and not fructose because by the way, if you're having fructose your blood glucose doesn't change, right. So you can have a sports drink, have a CGM and be like, Hey, you know what? Like my blood sugar didn't raise. It's like, well, it did. It's just, your CGM is only looking at your glucose, not your fructose.
Dr. Stephanie (22:12):
So, and we'll talk about if you want to, if you want to sort of get a proxy for what your fructose levels might might be. We'll talk about that today as well, but let's talk about cell metabolism and what happens. So we have glucose, right? We're gonna assume that insulin rises, right? So insulin's job. This is the fed state hormone. It is the fat storage hormone, if you will. And th the idea is that insulin exists to take the sugar, to take the glucose out of the bloodstream, cause that can be lethal and put it into the cell so that the cell can either use it for burning, or it can use it to create you know, structural elements. So insulin works in tandem with three, we're going to call them other kinases. So they're enzymes and I'll use Dr. Robert Lustig's reference here.
Dr. Stephanie (23:10):
He calls them three checkpoints, right in the metabolism of glucose in the cell. And we have these three checkpoints. And when they're coordinated, right, you will get cell growth, right? When they are coordinated in, in one way, you'll get growth. Another way you'll get burning. So it's kind of two things. It's either you're burning the energy or you're growing, but when they become uncoordinated, you start to get traffic jams. The glucose is hanging out in the cell, but not really doing anything. And then this is when we start to develop some of these metabolic, this metabolic. So
Speaker 1 (23:46):
The first checkpoint, if you will is called P three kinase.
Dr. Stephanie (23:52):
So we have insulin is like, Hey, there's blood glucose. Let me bring it into the cell. PI three kinase or phosphatidyl. And [inaudible]
Speaker 1 (23:59):
All three kinase. If you want the full name, P
Dr. Stephanie (24:02):
See why we call it PI three kinase. So PI three kinase really determines. So insulin kind of knocks at the door of the cell. It's like, Hey girl, I got some glucose here for you. And PI three kinase is the hostess. She determines how
Speaker 1 (24:17):
Wide the door swings open. Right? So,
Dr. Stephanie (24:19):
So if we have, if PI three kinase is activated the door swings wide open, and we can get the
Speaker 1 (24:25):
Goes to flood the intracellular space, right? And of
Dr. Stephanie (24:29):
Course, lots of glucose means that now the cell
Speaker 1 (24:31):
Has fuel to power itself.
Dr. Stephanie (24:34):
When we actually look at cancer cells, a lot of cancer cells have very, very high levels of PI three kinase, and they actually don't have, you know, one
Speaker 1 (24:45):
Of the things that is sort of coming about in the literature
Dr. Stephanie (24:48):
Is that they don't need oxygen and they don't have a lot of mitochondria. Most of the mitochondria are kind of defunct, but they have a lot of their big, big glucose gobblers. So PI three kinase swings the door open
Speaker 1 (25:03):
To let glucose in. And then from that
Dr. Stephanie (25:06):
Point, we have glucose inside the cell. Now, where does it go? Okay. So if the cell is low on energy, right? So if you think about,
Speaker 1 (25:16):
You're looking at your, you know, your gas tank on your car, you have like an indicator that either is pointing up towards
Dr. Stephanie (25:23):
The F the full or the E is empty or somewhere in between. You know, if the cell is lower on energy, it is going to need to burn that glucose. So
Speaker 1 (25:34):
It can create more energy, so it can get more gas, right.
Dr. Stephanie (25:38):
And if it's high on energy, then it may not necessarily need
Speaker 1 (25:41):
To burn it. So
Dr. Stephanie (25:43):
This is like this third, the second checkpoint rather is amp kinase, adenosine, monophosphate kinase. And this is like the gas gauge, right? This is like the fuel gauge. It knows the difference. Your amp kinase knows the difference between when your cell is full and when your cell is empty. And just as a one more piece of kind of geeky, goodness, here is that amp kinase also can signal the creation of new mitochondria. Okay. So that's why we love in, you know, exercise and even you know, fasting this can, this can really amp up and P kinase is because it will make more mitochondria so that when we have a lot of glucose, then we can say, Oh, we have way more mitochondria to like push this glucose
Speaker 1 (26:30):
To be able to create more energy. So that is what an P kinase does.
Dr. Stephanie (26:36):
And, you know, we were talking a little bit about fatty liver, and this is kind of a, an important point in our metabolism. So, you know, inside the cell, when glucose is going through, you know, these metabolic steps is called glycolysis from glycolysis. It produces this kind of intermediate, right? So it's called [inaudible] acid and [inaudible] acid has one of two fates, right? It either goes to the mitochondria under the direction of amp kinase, right? If we have, if we don't have enough fuel, or if we have enough mitochondria and capacity to burn it,
Speaker 1 (27:16):
Right. Or if the,
Dr. Stephanie (27:20):
The mitochondria are busy or we have defunct mitochondria, or we don't have enough of them, then Piru Vic acid gets di that gets diverted to a process called de Novo lipogenesis DNL, which is basically new fat-making is basically what it, what it translates to. And it turns into, so it's either at this point, if you are making de Novo, lipogenesis, it is either exported from the liver as a triacylglycerol. So you'll have, you know, you'll have three fatty acids on this backbone of glycerol
Speaker 1 (27:53):
Or a very important ORM or your,
Dr. Stephanie (27:57):
Your liver hoards it. And this is how we start to get that NAFLD di that non-alcoholic fatty liver disease. So your mitochondrial health, and I'll get to that third checkpoint in just a minute, but it's worth noting here that it's important for your mitochondria to be healthy and to have a lot of them. And that is why movement and exercise is so important. And then transient, you know, intermittent fasting so important because you're going to goose up your Hampi kinase. You're going to amplify the, the activity of amp kinase. So that is going to help to turn on your mitochondria and also to birth new mitochondria. Okay. Last piece in the energy metabolism of the cell is the mammalian target of rapamycin or mTOR for short. So this is like when I think of mTOR, I think of the Roman emperor in the gladiator games, if you ever saw the movie gladiator and I'm blanking on the actor's name, but there was you know, the Roman emperor at the end of the games, he would stand up and he would either put his thumb up for the gladiator to live, or he would put his thumb down for the gladiator to die.
Dr. Stephanie (29:11):
And this is basically what M Tor does. So mTOR basically determines whether a cell is
Speaker 1 (29:19):
To live or die or just hang out, okay. It is a great
Dr. Stephanie (29:25):
Growth pathway. So having a high protein composition in your diet will activate M tour. And this is going to drive a lot of these structural elements to be built. So you'll see a lot of bodybuilders and people in the fitness space when they are consuming a high protein, they are often activating mTOR. And as you might guess, mTOR very sensitive to the diet. So very high carbohydrate, very high protein is going to activate that. And on the flip side, of course, caloric deprivation. So when you're restricting your calories or when you're fasting can reduce M tour, right? So it, it like the growth, like, you know, creating these structural elements in the cell. If it's a myosin, if it's a myocyte, you know, you're not building muscle. It now is just going to burn it for energy. So we see this in fasting, we see this in the ketogenic diet as well.
Dr. Stephanie (30:17):
And this leads to autophagy, which is just basically a cellular spring cleaning, where I always liken it to like Pac-Man. So when you look at it, you can tell that I like a lot of analogies, hopefully by this point, but Pac-Man is basically like going around eating all those little dots. And that's, that's basically what it's often DJs, you have these lysosomes, they kind of scavenge the, you know, and they eat up all this sort of like broken bits of nucleotide and sell bits and parts and kind of clean everything up. So these three enzymatic checkpoints, right? We have PI three kinase and B kinase
Speaker 1 (30:52):
And mTOR. These explain
Dr. Stephanie (30:55):
How the cell uses energy. So it's, we have to really begin to move away from this idea that it's only calories that matter because calories do matter, but they don't matter as much as what the cell does
Speaker 1 (31:09):
Was with the, with the calorie. Okay.
Dr. Stephanie (31:12):
So I wanted to want it to go over. I wanted to talk about that. I wanted to give you a couple of tools here, because I know that we're going on this, like really geeky magic carpet ride. I know you can handle it. You'll have, maybe you want to listen to this podcast a couple of times and take some notes. But one of the things that I like to give people tools with is if you want to, you know, give yourself a self analysis and say, okay, how am I actually doing, like, do I have high glycation? Do I have this you know, aging like accelerated aging, am I having too much fructose, you know, what's happening with my liver. There are a couple of tests that you can request from your doctor or your functional medicine provider. And they're pretty, and most of them are pretty standard.
Dr. Stephanie (31:59):
So if you want to look at your glycation, and this is what I was talking about before with like the Mayard reaction and with advanced aging and lots of you know, the, the the Browning effect, if you will, or the wrinkles and the cataracts and all that. One of one standard tests that you can get is hemoglobin a one C. So this is only going to look at your glucose. It doesn't evaluate fructose, which we'll talk about in a moment, but basically this hemoglobin A1C test is going to tell you your average level of blood sugar in the past two to three months. Okay. So this is really looking at hemoglobin. So labs will, you know, there's going to be a range, and this is also really important. Do not accept this from your doctor. Oh, it's normal. You want, you want the number?
Dr. Stephanie (32:50):
Okay. So labs will go anywhere from, you know, I guess it depends on where you are in the world, but 4.6 to 5.2, 5.2 would be, you know, that's a little high for me to be honest. I would love to see a hemoglobin A1C of 5.1 or below because even at 5.1, that's mapping out to an average blood sugar of about a hundred milligrams per deciliter, which in my opinion is already too high. So don't let your doctor say, Oh yeah, no, it's normal. Just because the number falls in between the standard deviation that their lab has given them, you want the number. Okay. So that's one, if you do the other thing that you can do to look at your fructose levels now there's no direct tests like you can't say to your doctor, Hey, can I get like you know some sort of fructose test, you can't do that, but you can indirectly look at some transferees is from your liver.
Dr. Stephanie (33:50):
So looking at some of the there's two that we'll talk about a S T N a L T. And the other thing that you can look at is uric acid. So let's talk about alt first. So alt alanine, amino, transferees, relative, like on most standard lab test. So this is not a specialty lab test either. This is you know, it's reasonably sensitive. It's, it's looking at measuring liver fat again, do not let your doctor say, Hey, it's normal. You want the number? Because in what we see now in terms of normal is like 35 40. You don't want it over 25. Okay. So your alt levels should be 25 or under, and then the other, so an alt I'll just say is also looking at more chronic. This is looking at more of a chronic metabolic assault, okay. Or lack thereof, a S T or aspartate aminotransferase res this is more of an acute measure of liver function.
Dr. Stephanie (34:54):
It's looking more at your mitochondria as well. AST levels will rise with if you've had alcohol, or even if you, if you take things like aspirin, like acetaminophen consumption can also Jack up your AST. And of course, like hepatitis things like that will also increase it as well. So you want, if your AST is elevated, you want to maybe go a little bit further and look at some other they're non-standard but like super easy to find, like, you'll you want to go and look for H G, G, T or gamma glutamyl transpeptidase. This is again like numbers over 35. This is where we see a problem. And you should probably, if your number comes back at over 35, you probably go and get an ultrasound to take a look at the quality of the liver. So these are gonna tell us indirectly, your fructose, if these are high, then you either have a acute or chronic liver assaults.
Dr. Stephanie (35:52):
We are probably seeing some degree of fatty liver accumulation. Vis-A-Vis excess fructose consumption. The other thing that you can look at is is uric acid. So I know that uric acid, for any of you that have that have ever heard of uric acid, we, we often associate it with gout, right? So we will often think of you know, the uric acid as as it increases, increases your risk for goat, but also fructose can only be metabolized in the liver and when you're fructose. And then when you consume fructose, it'll enter the liver. And then it has to be phosphorylated through this sort of complex pathway, but essentially your uric acid levels will also increase. So five milligrams per deciliter. You want your uric acid levels to be under that as well. Okay. So I've given you a couple of labs and a couple of thoughts on why a calorie is not just a calorie.
Dr. Stephanie (36:58):
It really does matter. What we do with that calorie carbs are not equivalent. All sugars are not created equal, and I hope that this can help you with some of your decisions. And when it comes to sugar, I mean, this is probably a separate podcast altogether, but it's not the devil that, you know, it's the devil that you don't know there. The food industry is very, very smart, and they will often change the word sugar. They have lots of sexy words for sugar, and I've put together a checklist for you if you're interested. So you can head over to hello, betty.club forward slash sugar. So that's H E L L O B E T T y.club forward slash sugar, S U G a R. And I've put together basically my list of sneaky sugars. Like it's like molasses and all these sexy words so that you can look on.
Dr. Stephanie (37:57):
So you can be better at reading your nutrition labels, and you can be more of a savvy consumer. So the checklist is there. It'll also be the link will also be in the show notes. And then just as a reminder is if any of the names on the nutrition label are any of these sneaky sugars, it should be a hard pass for you so that you can improve your mitochondrial function, your insulin, your blood glucose, and of course protecting your beautiful liver. So with that, I will bid you adieu, and I hope that you enjoyed this, and we will talk very soon.
Speaker 1 (38:37):
I hope you enjoyed today's episode for those of you who want to continue on this week's geeky magic carpet ride with me, visit better show.co forward slash show notes. You'll find research links, summary notes, musings that I prepared in preparation for the podcast. And I often throw in some of my best practices, bonuses, and links. All the juicy bits are in there for you.