Why 80% of Women Gain Weight in Menopause

Foreign. Of women will experience weight gain as they enter perimenopause and menopause. And what makes it even more insidious is it's often around our abdomen, underneath our muscle. And the actions that it took to get that body fat off that worked in our 20s and 30s often stop working. So in honor of the New year on Menopause mastery, I'm going to go through the exact activities it takes to help make metabolic change in your body to lose that additional body fat, specifically visceral fat around your abdominal area, but also to increase your metabolic fitness, which is one of the most important activities that you can do to improve your overall health. So today I'm going to go through some myths and some additional information, really going into the science to help you understand exactly what we need to know. So what we need to understand is there is a deep mechanistic activity that is happening during menopause due to the changes in hormones, specifically the loss of estradiol function from the ovaries, varying levels of progesterone, and then the standardized decline that happens over 20, 30 years of testosterone. And what happens is it often accelerates this metabolic dysfunction. And, and that connects to things like insulin resistance, prediabetes and diabetes and then the ensuing inflammatory activities that increase the concerns of longevity and health, like cardiovascular disease, diabetes risk and other inflammatory conditions. And what we're really going to talk about today is the order in which you do things. So sometimes we get told very simplified ways to make changes. Okay, let's go over the biggies that we've heard all 20, 25. Eat more protein, lift heavy weights, eat fiber. However, how you do those, when you do those, and in what order you do those, and additionally why you're doing them can make the difference as to whether these things actually help or hinder what you're doing. And that's what I'm covering today. So we're going to talk specifically about mitochondrial energetics, your powerhouses of your cells, what are they up to? How do they work? Where do the hormones play a role? Insulin signalings, how insulin and the production of insulin in your pancreas actually changes during perimenopause and menopause, particularly visceral fat. Biology. Yes, your fat has a biology and it has a very impactful metabolic activity and inflammatory activity that can in either improve things or make things worse. And we're going to talk specifically about the liver's interaction, particularly its ability to produce glucose inappropriately from non carbohydrate sources, and how that plays A role and how the loss of estrogen can drive that, particularly when other things are awry, like insulin resistance, pre diabetes or being overweight or obese. And we're going to discuss how hormone replacement therapy may fit into this role and how to utilize it properly. And the other thing that really, really gets me going, I know you guys, I get going on so many different things, is when people online, and particularly companies online, start promoting hormone replacement therapy as some sort of magic pill for weight loss and other things. It is part of the mechanism. Just like sleep, lifestyle, exercise, diet, all of those things play a role. But none of these things are magic bullets. So what I'm going to give you today is the actual science behind the order in which you do things, how to do it, and then what you want to do long term to really, really make your midlife your best ever. And so let's get started with the up upstream disruptions of menopause and the multiple metabolic shifts that occur during menopause. All right, so menopause causes disruption across multiple metabolic areas, right? Think of these as cells, systems. So mitochondrial function, your powerhouse and its ability to burn sugar and burn fat and produce energy. Insulin signaling, so insulin's activity at the cell and mitochondrial function, including GLUT4, which is the kind of slow roll mechanism to actually transport glucose once it's been put into the cell, into your powerhouse. And then we're also going to talk a lot about adipiconine. This is your adipocytes, your fat cells and the biology of fat cells, particularly menopause. You may not realize that your fat cells are busy, but they are massively busy. We're going to talk about energy metabolism and put together, pushing towards. So if we put all these things together, it's pushing towards insulin resistance, cardiometabolic disease and other things. So it's these multiple mechanisms that drive a lot of the changes that we see. And here's the thing that most people forget is that it depends how healthy you were prior to perimenopause. The more healthy you were when these changes start to occur, usually the easier it is to make change and make those metabolic engines run more efficiently. So what does this mean? So if you were, you know, part of what they call the skinny. Privileged, right? And I hate the word skinny, but if you were somebody that pretty much had good body composition, so you were on the thinner side, were able to maintain body composition without having to yo yo diet and other things, you are in a different metabolic camp going into perimenopause and menopause than somebody who maybe had to fight to maintain body composition or maybe they yo yo dieted, maybe they experienced all those things. My own experience, I have never been naturally thin and once I hit puberty, my body picked up body fat and there always felt like there was a struggle there. And so much of it was kind of the hormonal interplay between estrogens and insulin. But so I was somebody that always was challenged with it. And I spent periods of my life where I had gained weight, especially in kind of perimenopause. And that's where all of this research really came from. So I was in a different metabolic camp than somebody who maybe never really had weight problems. Things change in your body and we're going to cover that specifically. So if you've been overweight or obese, if you've been diabetic or pre diabetic, you are in a different camp. And so if you are in this camp, this episode is absolutely for you because your metabolic freedom is going to come from the order in which we talk about how to fix these things. All right, so let's talk about the first thing, right? Insulin signaling, skeletal muscle. Right? So insulin signaling, estrogen declines. Right? Estrogen declines as we enter into perimenopause and it directly impairs insulin sensitivity in the, what they call the peripheral tissue. So this is your muscle tissue, especially skeletal muscle. So these are the big groups, your hips, your thighs, your buttocks, your, your abdominal muscles, your back muscles. This is where insulin mediated glucose uptake is normally doing the heavy lifting. So let me say that again. In order for your body to burn carbohydrate glucose, appropriately, the majority of it is happening in your skeletal muscles. So if you're like I am and you spend an inordinate amount of time sitting on your butt because you're working all day, you are not burning a lot of your actual glucose through skeletal muscle activity. So inactivity is going to increase this. But perimenopause does a number on your ability for your skeletal muscles to use glucose. Decreases in estrogen affect a particular estrogen receptor. So we have estrogen receptor A and estrogen receptor B. Now both of these are important, so it's not like you want one and not the other. And all of your tissues have estrogen receptor A and estrogen receptor B. What's interesting is estrogen receptor A when it is properly estrogenized. So think of it as estrogen's. The key, the receptor, it goes in and clicks in when A gets properly stimulated not too much, not too little. We get better insulin sensitivity when we start to lose estrogen activity. Or it's wildly varied. What we see is insulin resistance and that is independent of changes in your body fat. So that is independent. So, so estrogen activity is going to change the alpha receptor of estrogen and its ability to stimulate muscle utilization of glucose. So the independent of adiposity or fat is really important because it implies that insulin resistance and its menopause related activity is not just about weight gain, it's actually direct. And during the menopause transition, this hypoestrogenic state is worsening insulin resistance at these big muscle groups and compounding increased adipose adipocyte activity. So increased fat building. Right? So not only are we not burning, but we're going to see an increase in, in adipose tissue, fat tissue, and that causes lean muscle mass reduction. All right, so skeletal muscle can't do its job and it's the estrogen receptor A that's the primary driver. So estrogen way too high drives insulin resistance, estrogen way too low drives significant estrogen resistance. And then so the skeletal muscle can't burn fat and sugar and it can't burn very efficiently. And we get cellular resistance and increased fat building and fat production. So when estrogen declines, we also get increased insulin production by pancreatic B cells. And so we see less disposal of glucose and use of insulin in the muscle and, and more insulin production by your pancreatic cells. Now this becomes problematic because that means you have more sugar outside the cell in the bloodstream hanging out, waiting to get burned. So why is that important if you have glucose sitting outside the cell waiting to get burned? Your body's not going to flip the switch and go, hey, I'm going to burn fat, right? It's a seesaw. We have to have, we have to have utilization work really well and we don't want a bunch of glucose sitting out in the street waiting to get burned. Now glute 4 is one of the transports that takes glucose. Once insulin is pushed it across the cell wall and helps transport to the mitochondria that translocation during menopause are limited. And this is, is part of the impaired insulin secretion and sensitivity. And it strongly suggests that glute 4 disruption is a trafficking mechanism that actually slows the ability of glute 4 to sort of take glucose to the powerhouse. So ultimately what happens is you can't get it into the powerhouse, your mitochondria. So what happens to a cell when I've got glucose sitting outside the mitochondria, not getting burned. It can get burned in the cytosol, right? And that produces lactic acid. And we got much less energy production. But the other thing is that starts to create sort of a cytotoxic, a glucotoxic situation inside the cell, and it becomes less capable of doing its job. So take home, message. Your transporter from taking it from insulin to take your glucose to the powerhouse gets impaired, and this starts to compound that metabolic effect of perimenopause. Now, our mitochondria, our powerhouses, our powerhouses do several things when it comes to fat. So fat is burned through an activity called beta oxidation. And, and that starts to slow down during perimenopause and menopause. Our ability to produce ATP, your actual energy molecule, has been turned down because of the mechanisms that are affected by glucose. But it also gets turned down to your ability to use fat through beta oxidation to create ATP. And we increase lipid synthesis. So that's a fancy way of saying lipids, I. E. Producing fat by the liver to be stored in your fat cells. So on the mitochondrial side, estradiol loss is associated with a downregulation with the genes that increase fat burning through beta oxidation, which. Which basically malfunctions the entire act of using excess free fatty acids for energy. So what does that mean if your body was successful in moving fat out of the fat cell, dumping it into the bloodstream to get burned, which requires glucose to not be sitting out in the bloodstream, at least not in high levels. There's always some glucose, but if we have a lot of glucose, our body is going to use that first. So even if fat is sitting in the bloodstream, it requires beta oxidation and epinephrine to get into the mitochondria. So EPI is the major driver of that activity. But the genes that then take it and say, cool, I'm going to take it to the powerhouse, the mitochondria, which is the only place fat can get burned and aren't doing their job very well. So we basically become less capable of producing energy, ATP from body fat, and we just can't produce that much. So instead of being a Lamborghini, we are now a 1987 Yugo. So we become very slowed. So if my goal before was I'm just going to cut a few calories, work out a little bit more, and burn fat on a cardio machine, I am basically trying to climb the Himalayas with a pickaxe and in, in a bathing Suit and running shoes. It's going to be real hard right now. So fatty acids are increased, but the systems that should burn them are decreased. Okay, so we, we've figured out that piece now. What happens next? Your energy expenditure drops, right? So your ability to make energy expenditure happen. Right? So energy is I can I use it, right? My muscle cells aren't using it. I'm not efficient at creating it. We also get visceral fat lipolysis, right? So all of a sudden the creation of fat cells in the abdomen underneath the muscle increases. That is directly related to the changes in estradiol. And then that stuff is very metabolically active, which we're getting ready to talk about. So visceral lipolysis rises, lipolysis is creating fat cells, ectopic fat increases. So we get again the fat increasing around the abdomen. So what happens is our waistline gets bigger, we get a little bit more of a muffin top. But what's driving it is not the jiggly bits on the outside. It's the fat that's in the inside under the muscle that is metabolically damaging and also risky because it increases our risk for diabetes and cardiovascular disease, cancer, inflammatory conditions. All right, so the main menopause transition is, is a decreased energy expenditure and basal metabolic rate. So basal metabolic rate is what you burn calorically sitting on the couch doing nothing. So let's say you might be at 1300 prior to menopause. What we see is a serious downgrading of that. Right? So it might go down to 1150. Right. It's all over the place. But here's where yo yo dieting, and particularly extreme dieting can make this worse. So what happens if you had been a yo yo dieter, or if you've spent a lot of time doing very restrictive dieting, is your body has slowed its metabolic rate to respond to long term caloric loss. Right? So these really extreme diets or even really extreme fasting regimens can often increase the metabolic derangement and a loss of metabolic rate, just in general. So if you have yo yo diet at a percentage of your life, you may be at a lower metabolic rate than what is expected affected. Some of the research shows when you start digging through it and, and again, a lot of the research was done on younger individuals. But prolonged protracted starvation situations, whether it's disordered eating or significant dieting, can slow metabolic rate by, you know, anywhere from 10 to 30%. 30% is often seen in your most obese individuals that it becomes sort of the metabolic effects of obesity. So we have a decreased energy expenditure and basal metabolic rate. And if we have reduced physical activity, this now is the like trifecta of doom, right? So I don't know about you, but I have to make serious effort to get out and exercise both weight training and, you know, cardiovascular training in order to keep my muscles able to use that fuel appropriately. So at the same time, right, energy expenditures down, we have decreased ability to burn any kind of fuel, and our metabolic rate is lower regardless of thyroid function. You could be taking truckloads of thyroid. Metabolic rate can still be disrupted. And if I'm low on physical activity, I'm going to have problems. Now, at the same time, we're producing more visceral fat and that triggers free fatty acid production. So making fat actually frees up free fatty acids to put them in the bloodstream, but then you can't get them into the mitochondria, so so they're just hanging out, which makes you more insulin resistant. One of the most insidious things you see in type 2 diabetes is in the bloodstream you will often see high glucose, and if you checked serum free fatty acids, I. E. The fat your body should be up to and burning, both are high. Now this may be confusing because you're like, how is glucose high and how is fat high in the bloodstream? It's because of this action, we get more fat lipolysis, we get more serum free fatty acids and, and that contributes to the metabolic derangement. So pre diabetes is a state of excess glucose and excess free fatty acids in the bloodstream, Neither of which are getting burned efficiently. So when we go to fix it, we have to fix that in order to do that. And it's not just eat more protein. Now your beta oxidation, so your ability to burn fat is also damaged. So those fatty acids can't be get metabolized and it leads to more fat accumulation and what we call lipotoxicity. Lipotoxicity is fat that's nasty, right? Think of it as angry fat making cytokines and, and, and being more toxic, creating more inflammatory response. This is what the adipiconines are, and they're inflammatory and there's hormonal interactions to these. So our visceral fat are tied to inflammatory signaling, right? Changes in these adipic, which is basically a cyto kind coming from a fat cell produces more visceral fat, triggers inflammation that contributes to insulin resistance, which contributes to more visceral fat production. And then you get the vicious cycle. It's also noted that visceral fat and subcutaneous fat during menopause. So the jiggly bits, the sub Q which is underneath your muscle, or I'm sorry, on top of your muscle, the jiggly bits on your hips and thighs also increase. And it's both of these are accompanied by elevated cytokines. And so we become chronically inflamed. The loss of estrogen drives chronic inflammation. And this is one of the major mechanisms of inflammation. It's the metabolic effect of the loss of estrogen that drives inflammatory cytokine production by the abdominal fat that drives the inflammatory response of medicine of menopause. That's one of the primary drivers. Then we get hormonal interactions, right? Our relative androgen excess and decreased sex hormone binding globulin because estrogen is down. So sex hormone binding globulin, known as shbg, is tied to your estradiol levels, so it tends to come down as estrogen levels. Both estradiol and estrone come down. Now, you may have low testosterone relative to what it was at 20, but your testosterone, your DHEA, your DHT, androstene Dione levels are high relative to your estrogen. Now, I need to say this again because there's a lot of people out there talking about testosterone replacement for women, and I am absolutely 100% on board. However, menopause is an estrogen deficiency stage state. And if you add testosterone and androgens like DHEA without supporting subsequent estrogen activity, you can drive more metabolic effect that might be messing with these system, these symptoms, right, These excess androgens relative to estrogen are associated with insulin resistance and all the things I talked about before and pre diabetes after menopause. Now this is an area that I want to talk about my own experience because I believe this is what was happening. Because when I started in my perimenopause journey in my late 30s, I knew I was progesterone deficient. I went on progesterone. It was not magic. It did not necessarily make me feel radically better. I definitely felt worse if I took it out. But I was still experiencing. I experienced like 35 pounds of weight gain after my tubal and ablation, right? I had an ablation in a tubal and that sort of disrupted all of my hormone production. I didn't realize it at the time. Again, you know, hindsight's 20 20, so, and, and so I was thrown into sort of an early perimenopause journey. So progesterone getting introduced was great, but it didn't fix Everything. So flash forward a couple years later. In my early 40s, this is when testosterone treatment really hits the market. I'm in Dallas. I live where all of the pellet companies are made. So Biot, Avexapel, Soda, Pelley, all of those companies are based in the Dallas Fort Worth area. So we have thousands of pellet providers here. Our clinic was one of the early adopters because we were already doing hormone replacement, and we wanted to be able to utilize this. This technique as well, adjusting the levels. So the provider I worked with was like, oh, you need testosterone? Because my libido was in the trash. They were like, you'll lose weight, you'll gain muscle, you'll lean out. So what happened? I got testosterone pellets. I did have a libido for the first time in a long time, and that was amazing. And I felt sharp mentally, but I literally gained 10 pounds in about a month and a half. Now, the argument was, oh, it was water weight gain, because the muscles are, you know, firming up and we're getting water weight gain. It'll go away in a couple months. You know, flash forward six, nine months later, it doesn't go away. And I'm having more difficulty with sort of insulin resistance and other things. And the reality was that is, I looked like I was estrogen dominant. I have always been estrogen dominant. My genetics are estrogen dominant. And there probably was times that I was estrogen dominant because I was in the bungee cord experience of estradiol and estrone, and my estrogen's kind of going up and down, but I had an ablation, so I couldn't tell. My androgens were high for sure on blood work. And depending on the day, my estrogen was either high or relatively normal, but my androgens were very high, right? And eventually I said, you know, after about a year and a half, I was like, whoa, I can't be on this. Like, I am five, three. So the 35 pounds I gained from kind of the metabolic shift of early perimenopause. The £10 I got from testosterone, I was like, I had to buy a whole new wardrobe. And I was demoralized. And so I quit the testosterone. It took me a while to lose that 10 pounds, because what was happening is I was having this metabolic effect of excess androgens relative to estrogen, depending on the day of the week in the month. But the overall effect, I believe today, is that my androgens were too high relative to my estrogen, even in perimenopause. And I had adequate progesterone, but that couldn't make up enough for it. So what I'm saying here is if you're in menopause and somebody gives you a bunch of testosterone and maybe even progesterone, but doesn't control for and manage the relationship between your testosterone and your estrogen, you may be driving this metabolic effect of insulin resistance, prediabetes and, and fat storage that is actually happening when we go through menopause naturally. And it's because they're actually treating with the wrong levels, because most of these companies that sell testosterone treatment believe more is better. They're ran by men. They have very masculine sort of ideas around testosterone therapy. And of course, anybody that gets a testosterone that used to be 20 and now they're 150, they have a sex drive for the first time and they feel great, and that's fabulous. But they may be experiencing metabolic changes because of that now. So here's the other hormone that plays a role. If my androgens are elevated relative to my estrogen, I become all of these metabolic things. And cortisol, Cortisol levels are going to be high relative to your sex hormones, estrogen and progesterone, specifically during menopause and perimenopause anyway. But if you add the normal stressors that we have raising teenagers, empty nesting, probably at the pinnacle of our career, possibly managing elder parents, maybe experiencing spousal issues because you're all these things are going on and you have new stressors in your life, the reality is cortisol and the ensuing metabolic effects of excess cortisol induces a thing called gluconeogenesis, which promotes insulin resistance. And gluconeogenesis is when your body takes amino acids from proteins and makes it into glucose in your liver that then gets mobilized into your bloodstream. Right. Remember, excess glucose will keep you from burning fat and your fats will be out in the bloodstream anyway. Gluconeogenesis is one of these mechanisms in which your body protectively enables you to be able to make glucose in a starvation state. So, for instance, let's say somebody went carnivore. Why is it a carnivore that only eats meat, literally only eats meat, can survive because your body has to have glucose, and your body will maintain an average glucose somewhere between 70 and 100, usually in your lower 80s, if you are on a carnivore diet. I'm not a fan, however, how. And it's because the body can take amino acids either from your muscles or from the foods that you eat, and it can produce glucose to keep your red blood cells alive. Your red blood cells cannot use fat as fuel. You must have glucose. And so your body can do that. And gluconeogenesis is the mechanism. Now here's where it becomes important. And I've talked about this before, but I have a ton of new listeners and I want to really cover this and in depth. Gluconeogenesis is elevated in a pre diabetic, insulin resistant, previously overweight or obese state. Right. So basically we see an excess of this activity, particularly if you've been overweight for a longer period of time or you have been, you know, let's say for a decade, because you've been fighting with insulin resistance and everything else. So impaired fasting glucose, which is called fasting hyperglycemia, results from excess glucose production, usually by elevated gluconeogenesis. So let's say you go to bed and your blood sugar is totally normal and you wake up, it's an 110, you didn't eat anything, you didn't sleepwalk to the kitchen, but somehow or another your glucose went up often. This is because our cortisol came up. Maybe we had a hot flash, maybe we didn't. But what causes it is elevated gluconeogenesis, the mechanism. And this can even occur when you have normal fasting glucose. So this gets missed all the time, right? So what I have seen anecdotally in our population, in our clinic is a lot of women come in, they're really contributing to their protein intake. They've had struggles with weight gain for quite a few years, and no matter what they do, they will wake up with slightly high fasting glucose. And they're like, I'm not eating carbs, but I can't burn anything. This is the mechanism. This is the mechanism. So it's important to understand that it can be increased significantly compared to normal controls. You know, if we look at research, so if somebody who is always thinner, right, didn't have metabolic derangement, never fought with their weight, never experienced what I experienced, their body's activity of gluconeogenesis is down regulated compared to somebody who's upregulated because they've been overweight. So this is endogenous glucose production in the liver, hepatic instructions that are the problem, that's creating an inability to lose weight despite doing all the right things. So if you have insulin resistance, impaired glucose utilization and gluconeogenesis, this is the major derangement that we see. And the the situation is it increases fat storage, decreases ATP production, decreases your ability to burn fat and to burn sugar appropriately. So this is independent, these are all independent of each other. So when they show up together, it's a trifecta and it can drive the risk towards metabolic syndrome and diabetes. So the more bmi. So if you look at the studies, they looked at bmi, body mass index, that's the height weight ratio. So the higher the BMI, right? So if your BMI is over 25, that starts to be overweight. If it's over 29, it's obese. Higher the BMI goes, the more this is occurring and it provides a striking comparison. So here's one of the studies. In obese, non diabetic individuals, Fractional gluconeogenesis averages 59%. So 59%. So think about that. 59% of what's happening is gluconeogenesis. If we look at lean controls, individuals who are not overweight, it's 29%. So total endogenous glucose production remains normal due to compensatory regulation and reduction of your ability to burn sugar. So what does that mean in somebody who's overweight? Gluconeogenesis is elevated compared to lean people because lean people are actually able to burn it. You cannot burn it. So this is a trifecta. So the reality is we have to fix the burning before we can fix the fueling. Because if you fix the fueling without the burning, you don't get the answer that you need. Now protein breakdown or catabolism also contributes to this mechanistically. Obesity related gluconeogenesis is linked to increased whole body protein breakdown. And this is, this is because we become more insulin resistant and it also is dependent on our amino acids, particularly leucine. So if we're not getting enough leucine, we see an increase in this muscle breakdown and what happens is we just basically produce more glucose from muscle protein, particularly if leucine levels, which is one of your primary amino acids that you must get in your diet. And we know that the higher the leucine level is, the more muscle protein synthesis. So your body's ability to take that protein and make muscle occurs. Right? So the big thing is, is when we have a greater supply of glucogenic amino acids, so most of your amino acids can increase, increase gluconeogenesis from the liver. So certain ones are more likely than others. This enhanced protein turnover may trigger preferential use of these, of these amino acids for glycogen and glucose. Production over muscle creation. Let me say that again. Your essential amino acids you're consuming in your protein foods, in the absence of appropriate leucine and appropriate muscle utilization of glucose and fat can trigger your body to use those amino acids from proteins to make glycogen and glucose at the liver instead of burning it. So this is really important. So we have this additive effect now, right? So now my liver says, cool, I'm going to make fat and I'm going to make glucose instead of actually burning it. If I also have some pre diabetic state where I'm seeing early fasting glucose levels that are high in the morning and hemoglobin A1C showing that it's, that it's likely high all the time now we're going to see a bigger, a bigger impact, right? So when we look at the metabolic costs of gluconeogenesis, right? So malfunctioning overproduction of glucose from amino acid substrates, in some studies that accounts for nearly 1/3 of resting energy expenditure in insulin resistant substance state. Right. Healthy people, it's less than 10%. What does that mean? So 1/3 would be 33%. So that means at night, when you're sleeping, 33% of all of your energy expenditure to manage your body and do all that other stuff is coming from your body producing glucose rather than your body burning fat, which is 100% what should be happening at night after a couple hours of sleep. And if your sleep is disrupted because of hot flashes, night sweats, insomnia, interrupted sleeping, progesterone deficiency, sleep apnea, upper airway resistance, excess cortisol, somebody who snores next to you, that is going to drive more of that, right? So the reality is, is when you should be burning fat, your liver is making glucose instead. And then eventually we start to see fasting glucose in the morning elevated. Now how do we fix it? Right, so here's the big take home message. We all know protein intake is important, we know exercise is important. And I'm going to hit the other third thing that I think is extremely important is fiber intake and then hydration. So why. Right, so exercise first. Why do I say it's really important to really dial in some energy burning before we really worry about getting our protein intake? All of us have heard it, you need 100 to 120 grams, 150 grams or more or less. Well, if you're an obese or overweight woman who's got this metabolic derangement, adding more protein just gives your body more substrate for it to be able to make more glucose. Right. So we need to have adequate, that doesn't mean stop eating protein, but we don't necessarily need to take our protein really high in the beginning. What we need is glucose disposal. And what does this is the right exercise. So when we look at the exercise we, we want to do two different things. We need to weight train. We need to do a combination of high intensity interval work and heavy load. Right. So high intensity intervals is keeping the heart rate up using more repetitions, multibody parts. We need to do that because it creates a, a better heart rate zone to improve glucose utilization and and mitochondrial biogenesis which is the production of new mitochondria. And then lifting heavy enables us to build stronger bone and increases muscle fibrillary activity. So fiber activity, making more muscle fibers, those combinations are very important. I would do four times a week of that type of exercise. You know, heavy lifting twice a week, break the body apart, lower body, upper body and then two other days where you're doing some interval intensity work with lower weight, higher repetition. Now that is not enough usually to make this happen. When we do that exercise though, it can increase muscle glucose use up to five fold in insulin resistant person. So this is why this is important. We can get that insulin resistance out of the way. And that mechanism of weight training can increase insulin's action up to 24 to 48 hours. Now women were closer to that 24 number. Men they get much closer to that 48 hour burn. So the long term adaptation, so our ability to adapt and start becoming a better glucose and fat burner requires exercise first. So we always have weight training. Now the other thing that's really important is we need to look at also increasing zone two exercise. Now this is the one nobody wants and we, we hear people talking online about oh you don't want to, you don't want to, you don't want to do cardio because you can't burn off a bad diet. True. However, zone two exercise, which is heart rate specific, which is where you take your, your current age, so 220 minus your current age and somewhere between, you know, 65% of your 220 minus your age is going to be your heart rate range. So for somebody my age it's going to be if you're metabolically more fit and you have some cardiovascular fitness, you might be closer to this like 134 range, maybe 125 heart rate. So what this means is it's often at a heart rate that is higher than what you can do walking. I don't care how fast you walk, you just can't get the heart rate up enough. But slower than what you would normally do on a cardio exercise, right? Because almost every cardio person will say, I'm not, I'm not feeling like I do enough. And zone two requires time, right? So zone two, you got to do it for at least, at least 40 minutes to really get benefit. What I do is I add one of those to two of those a week, and I get on my bike and I knock out time. My usual time is an hour and a half, hour and 15 minutes to two hours. I do them a lot on the weekend because that is something that I can fit into my schedule. But what that causes is muscle sensitivity, mitochondrial biogenesis. We make more and we become better at burning. It will not burn off muscle mass if you keep the heart rate in that zone two zone. If you use devices like Wahoo or your oura ring or other things like that, you can calculate your own zone too and individualize it to yourself. But if you go above that, you will burn muscle. Zone two will burn through glucose, will burn through glycogen, and then it will start to burn fat. That's why duration is important. It's going to take well over 20 minutes to do that. And in the beginning, if you're somebody who has all this metabolic derangement going on, your body's going to produce glucose first. It's not going to try and burn fat until it becomes better at it. And so when you have that longer duration at a heart rate that's lower than cardio, but not as low as walking, you become more efficient. And it works very, very well because again, between those two combinations, you're going to have a five fold increase use of glucose at the muscle tissue and it becomes more effective. So if you're weight training four days a week and you put in some of these zone twos at least once or twice a week, you're going to start to see movement. Now, you can still exercise. I exercise like walking, that is additional steps. That's movement, very important. But we need that other zone too. So unless you can get walking fast enough to get that heart rate up in that fat burning zone, which you probably can't, we got to throw something else in there now. Now we're getting to the one everybody wants to talk about protein and timing. If you add protein before you start getting better at glucose utilization, you're going to have issues, right? In most cases. Now, more is not Always better first. That's the take home message. So higher dietary protein intake, particularly rich in the branch chain amino acids, acids are associated with increased diabetes risk and increase insulin resistance through stimulating MTOR complex 1 hyperactivation. That's the mechanism, right? So in a metabolically healthy person, stimulating MTOR at the right time is awesome, right? In somebody deranged, it is not awesome, right? So at that point we become less metabolically active and we can't do it. So if I've started the exercise for like a month or two and then I start increasing my protein, I'm not going to stimulate mtor complex 1 in the same way. And it's because the amino acids basically get overloaded into gluconeogenesis and it contributes to insulin receptor activity degradation and reducing insulin mediated glucose uptake. So all those things start to malfunction. So we add protein and we start going towards that 120 grams per day because then my body can use it through muscle protein synthesis, right? So exercise first, then adding protein. And what the research shows is if I have the bigger chunk of protein intake in the morning, the first meal of the day and the last meal of the day, I'm going to get the best muscle protein synthesis as an, as a midlife woman. So don't drizzle it in with little tiny bits of protein. Protein throughout the day, get a big chunk at breakfast and a big chunk at dinner. Now the upside from this is once insulin sensitivity improves, gluconeogenesis is downregulated, we get protein being able to make muscle, right? And we start to become more efficient with fat burning and glucose burning at the same time. Because again, I want you to be able to burn both. I don't want you to have to cut carbohydrates from your diet, I don't want you to have to like eat ketogenic. I want you to be able to eat the right foods and have your body be a fat and glucose burning machine. So what's the practical timeline here? If we look at the American College of Sports Medicine, resistance training helps in insulin resistance. Adults results in about a 10 to 15% improvement in strength, lean muscle mass and insulin sensitivity when it's combined with aerobic activity. And it's superior when they're put together, not when they're one or the other. So we're going to see it and most of the time we see this metabolic improvement start at about 8 to 12 weeks. So like I said, if we do this for a week or two and then we're Pounding protein, we're not going to see the results. So you got to commit to doing the burn right and then worry about the protein intake. Ladies, if you're noticing more fine lines and wrinkles, it's not just about aging. It's about the loss of estrogen. And that affects our skin structure, making it drier, thinner, less firm. But here's the great news. I've created Bias Mastery Cream to help. This luxurious bioidentical estrogen cream supports your natural hydration and elasticity. It's packed with nourishing oils like olive jojoba, aloe and coconut. So it feels amazing and helps soften those lines and bring back that healthy glow. I've been using it, and let me tell you, my skin has never looked or felt bad better. It's smoother, more radiant, and those little cracks and creases are way less noticeable. If you're ready to give your skin some extra love, check out Buy Est Mastery on the Metabolic Blueprint website. And that's metabolicblueprint.com BiestMastery that's B I E S T Mastery. M A S T E R Y and your face will. Thank you. Okay, so we've talked about protein, we've talked about appropriate exercise and how to time those things to improve the metabolic activity. Now, the next one I'm going to talk about, most of you have probably heard me talk about it or other individuals talk about it, but it is the relationship of fiber to metabolic health. Now, dietary fiber is inversely correlated or associated with metabolic syndrome, obesity and cardiovascular risk, particularly in menopausal women. Basically saying, where we get a higher fiber intake, it improves body composition, reduces visceral fat, and we see better glycemic control and lower morbidity risks and mortality risks. So ultimately, fiber intake is really, really important. And the reason why it is so important in perimenopause and menopause is because of its impact on visceral fat. So in a randomized controlled trial of central adiposity, right? So weight gain, muffin top around the middle, particularly being driven by visceral fat. When they looked in postmenopausal women, they a central kind of European diet, so let's call it a standard, cleaner than American diet, but again, very, very carbohydrate rich, that was high in dietary fiber. So when they had a higher amount of dietary fiber, it reduced visceral fat levels by 24.6% over 16 weeks. Let me repeat that. So the higher dietary fiber intake of the diet reduced 24.6% of the visceral fat over 16 weeks. And this correlated directly with the fiber as a proportion of the dietary intake. So why is this important? So prospective data shows that for each 10 grams of fiber increase a day, we have an association with a 0.08 centimeter per year reduction in waist circumference. And then if we look at cereal fibers, so this is kind of interesting, so I'm going to piss off a bunch of anti grain people. Cereal fibers. So this is the stuff that's found in quinoa and brown rice and whole grains. Right. It was even stronger at a negative 0.10 centimeter per year. So ultimately the higher fiber count in the food is going to reduce your abdominal fat more clearly. So for the people that have been doing keto for forever, and maybe they're eating enough protein, they're getting in the protein, they're eating quite a bit of fat, and they're getting low, low glucose or low carbohydrate carbs, but they may not actually be getting the fiber count that they need. And that may be why they're not seeing the weight loss reduction, particularly the fat loss reduction in the abdominal area. Another study looked at postmenopausal African American women with obesity. And each unit increase in energy adjusted fiber intake is associated with a 0.10 unit decrease in metabolic syndrome score. So we also see a reduction in insulin resistance, metabolic syndrome, pre diabetes, fasting glucose levels, high high hemoglobin A1C metabolic syndrome. Right. So fiber intake is really important. And when women don't meet this fiber intake amount, what we see is they have a four fold higher odds of metabolic syndrome. Right. So four times, four times the amount of likelihood for metabolic syndrome. So higher fiber intake is also associated with lower mortality rates in women. And if the women that had the highest amount of fiber intake had a 15% lower all cause mortality and a 31% lower cardiovascular mortality risk compared to women with very low fiber intake. So if you're concerned about your longevity, and particularly those kinds of diseases that lead to long term morbidity and mortality, fiber is your friend. It also has a threshold nuance. So the protective effect is most pronounced above 7.9 grams per day. And each 5 grams increased below that threshold is associated with a 7% reduced risk. So what does that mean? So the average American gets lower than 8 grams. Right. So all the average Americans are in this risk factor. Every five gram that is increased from that threshold is going to increase the, the benefits through mortality. And those who have the most fiber benefit the most. So this is where this, the research even gets more interesting. So fiber intake from your foods, right, embedded with your foods. Why is fiber so important? Number one, it's wrapped around the carbohydrate molecule. The simplified sugars that get, that get, get broken away as you digest to be absorbed into the bloodstream. The fiber keeps it bound longer and makes it go to the large intestines where it is available to your microbiome. So the microbiome benefit from those complex carbohydrates and the fiber content that we cannot digest. So we see huge changes to your, your microbiome in a higher fiber diet that favors all, all cause improvement in health. So a higher fiber content improves that and improves short chain fatty acid production, particularly things like butyrate, which helps metabolism, it helps anti inflammatory. It even has studies indicating it can help with bone mineral density. Also, it changes the production and the enzyme activity of your microbiome and reduces things like beta glucuronidase, improves GLP1 production by the microbiome that actually help with that production. So overall fiber is beneficial. Fiber also binds to toxins coming out of the liver that are going to be slated to go out in the stool. So estroge, estrogenic compounds, xenoestrogens, a lot of your other toxins get bound in fiber. It also makes you more regular and helps your stools be softer and more bulky, especially when you consume enough water. Now, fiber is one of those things that you have to add slowly. So if you don't eat a lot of fiber, you have to go slow. And my preference is to eat it in foods, not supplement. There are several studies out there that looked at supplementation of dietary fibers like psyllium husk and other things in lieu of eating fibrous foods. They do not equate to each other. Now hear this. That does not mean that you can't use supplemental fiber to support what you're doing. But what it does mean is you cannot take 30 to 35 grams of dietary supplemental fiber in the form of supplements and get the same outcome as if you ate the vegetables and fruits, nuts and seeds and whole grains that are helpful. Right. Sorry. I. Believe me, if I could, you know, help you and give you a pill, it'd be great. But you got to eat it, right? So that means we have to eat a lot of those vegetables, a lot of those fruits, and appropriate levels of whole grain in its natural form, ideally where you get the fiber content. And fiber is really helpful. So if I've already added the exercise and I'm increasing my protein and I'm going to increase my fiber count to improve all the visceral fat activity, reduce inflammation, help my body produce more of the short chain fatty acids, and support my microbiome that supports my metabolism. Right. So that's really, really important. And then last but not least, on the dietary front, hydration. Hydration is very important to your body. Your body is mostly water. About 70% of your body is water, and it's kept in the muscle tissues. In the muscle tissues, water actually helps the metabolic activity. Right. So think of it this way. The solution to pollution is dilution. We need to have higher water intake to support all of the metabolic functions in the body. And then the body's better at excreting toxins through the kidneys, better at metabolizing fats and other things. It also changes a bunch of activities within the cell. This is Dr. Rick Johnson's work. He wrote a book called the Fat Switch, an amazing book. He's been published over 300 times. He was studying specifically uric acid and its relationship with salt sensitive hypertensive hypertension and obesity. And what he found was one of the mechanisms that humans have for survival is this enzyme called fructokinase, and the body's ability to raise uric acid inside, inside the powerhouse, the mitochondria, and basically turn down mitochondrial function in a starvation state. So what does that mean when we've been starving for a long period of time? Whether it's intentional or not, like inappropriate fasting, what happens is the body will raise uric acid inside the powerhouse, and the powerhouse will downregulate, so it produces less energy. So it's directly affecting mitochondrial energy production. And in lieu of producing ATP, we produce a lot more ampk. So what they found was hydration had an impact on that, and it was mitigated when you had enough hydration along the way. The other thing that they found is that most people select for this particular genetic activity, where in the blood glucose, under starvation states or dehydration states, the body can convert glucose into fructose. Fructose, which can preferentially get stored in the liver as glycogen and stored in the fat cells and act as a secondary fuel source and capacity to slow metabolic rate. So when you're chronically dehydrated, you're slowing your mitochondria, and you're also potentially turning on your body's ability to basically utilize glucose as a more primary fuel and manufacture fructose depending on your genetics. And let me tell you, 99% of us have that genetics. So the truth is, is it's still there. So hydration is really important. So that means drinking between meals and getting enough right when you first wake up, all the way through the end of the day and drinking it earlier so it doesn't interrupt your sleep. So that's vitally important. And water you add at the very beginning and all the time, yes, if you're sweating heavily, you might need electrolytes. But for the most part, if we're getting healthy foods, we're using our spices and things like that, we're probably going to get enough sodium and potassium and we can use, you know, salt freely if we're hydrated. Well, that was one of the other major things that Rick Johnson's work showed, was you could mitigate any impact of sodium on blood pressure if you diluted it enough with enough hydration. So we can increase our salt intake accordingly as needed and then add electrolytes as needed. Now, the last thing I want to talk about here is the use of hormone replacement therapy and the metabolic benefits, because this is important. So hormone replacement therapy has been shown to improve insulin sensitivity through the mechanisms of estradiol, both at the cell and the mitochondria. It reduces diabetes risk by affecting those areas and also reducing inflammatory cytokine activity by the adipose tissue. And hormone replacement therapy should be used, obviously for menopausal and perimenopausal symptoms, but there is a metabolic effect of hormones that if given while you're doing these other things, you're going to see an improvement. So estrogen alone and combined estrogen and progesterone therapy has been shown to reduce the risk for type 2 diabetes in postmenopausal women. We know it also reduces the risk for things like cardiovascular disease and cognition, particularly given early in the perimenopausal to menopausal journey. But when we look at particularly the Women's Health Initiative and some of the other trials, we saw reduced diabetes impact when women were on hormone therapy. The KEEPS findings showed transdermal estrogen, decreased fasting insulin and glucose versus placebo. Right. So in that KEEPS trial, looking at transdermal estrogen, which is what is used today, we saw improvement in fasting insulin and glucose compared to, you know, sham treatment. And we also have seen other studies look at insulin resistance and homa ir. Now, many of those were done with oral conjugated esty and estrogen, because many of these studies that were done 20 years ago because of the Women's Health Initiative. But the reality is hormone replacement therapy can absolutely improve your metabolic effects. But it's not a panacea for all of it. Right? It's part of the picture. You know, an HRT is recommended obviously for vasomotor symptoms, cardiovascular health, bone mineral density and cancer prevention and cognition prevention. And here's the deal. Formulations matter, right? Transdermal creams, patches, oils. We use oils most predominantly because they are all organic and bioidentical and transdermal estrogens can be given at low to moderate doses. And, and we see the benefits now when we look at the mechanistic reasons to do these things, the why behind the plan. Let me summarize those for you. What's the simplest mechanistic activities? Menopause shifts the insulin sensitivity, the mitochondrial ability to burn fat and glucose. It increases inflammatory cytokines and adipokine signaling which tells the body to store more fat and hormonal drivers like excess excess androgens relative to estrogen and progesterone. Lack of activation of estrogen receptor A and increased levels of cortisol and likely disruption to thyroid function can all cause elevated insulin resistance, hepatic glucose production through the activity of gluconeogenesis, fat storage, muffin top and a slowing of metabolic function. Meanwhile, insulin resistance, obesity and gluconeogenesis becomes the quantitatively dominant activity. Again, we can see sometimes 59% contribution compared to 29%. So nearly one third of your resting energy expenditure, particularly during sleep, will be going to glucose production and the use of glucose instead of fat. Fat burning happens while we're sleeping. It is through that mechanism that we see it decline. So I'm going to talk a lot more about sleep and other things coming up in the upcoming podcasts. But this is really important and this is why you might be doing all the right things and it's not working. So then the strategy, right, the strategy is exercise first because we have a mechanistic target to increase glucose disposal capacity. Insulin action, including a active acute five fold rise in muscle disposal of glucose within the first 24 to 48 hours. Women, we don't get the same benefit as men. It's closer to 24 hours then once that metabolic improvement occurs, often about 8 to 12 weeks out. So you got to suck it up and say it's okay. I'm going to keep doing this even though I, I, I'm waiting for some results. The results take a while. Then I'm going to increase my protein intake to about 1.6 to, to 2, 2 to 2.2 grams per kilogram a day. So for most women that's about 100, 150 if you're itty bitty, about 100 if you're, you know, you know, 5, 7, 5, 8 and above, you're probably at 150 grams per day for muscle protein synthesis, focusing on that breakfast and dinner most. And then finally fiber and water. Fiber doesn't just help. It supports visceral fat and, and reduction and mortality link statistics including a 26 point, I'm sorry, 24.6% reduced visceral fat reduction in 16 weeks in menopausal women and a reduction in metabolic syndrome. And we're going to slowly increase our fiber, shooting for a 30 to 35 gram a day dose in food. You can use a little bit to supplement it, but you're not going to take 35 grams of 35 grams of fiber a day is you don't get the same benefit. And then the last two steps is hydration. The solution to pollution is dilution, right? Getting hydration in there because it affects your metabolic rate, it affects the liver function, it affects the production of ATP and AMPK and mitochondrial function. And when we are chronically dehydrated, we raise uric acid inside the mitochondria, which turns on the starvation response and slows mitochondrial action. And the last possible thing is look at hormone replacement therapy. Every woman deserves that opportunity to explore hormone replacement therapy for you, whether you're in perimenopause or you think you might be, or you're in menopause or maybe even you're postmenopausal. The only contraindications there would be for a woman would be active current estrogen receptor positive breast cancer treatment and post treatment estrogen receptor and estrogen blocking drugs like letrozole or tamoxifen. We wouldn't couple hormone replacement therapy on top of that active uterine bleeding because we got to figure out what the uterine bleeding is for family history of breast cancer. Those kind of things are not a contraindication. Now if you're a good, you know, 10, 15, 20 years past menopause, topical forms of estrogen have not shown the clotting and cardiovascular risk that we saw with conjugated equine estrogen. Every woman deserves the opportunity to explore those hormones, even if you're 15, 20 years out. So the truth is your metabolism is affected by perimenopause and menopause. And the standard recommendations don't work with this approach, you're going to have the right answers. Now, as you've listened to this podcast, I'm going to include in the Show Notes a very easy takeaway document that you can use to start this process on your own, and you'll be able to work on it over the next two to three months as we go through the beginning of 2026 and see your body change without having to be at fighting with it. So I want to thank you for listening to Menopause Mastery, and then we'll be back with you next week with a little deeper dive in the other things that may help you with your process of improving body composition for 2026. Thanks.