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Learn: Menopause Impact On Metabolism & Diabetes

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Summary
  • Understand the intricate impact of hormonal changes during menopause on metabolism, diabetes risk, and complications
  • Learn about the role of insulin resistance and other key hormones in the development of type 2 diabetes during menopause
  • Gather practical steps to manage hormonal imbalances, improve diabetes, and address related issues like weight gain and osteoporosis
  • This video is part of the Reversing Type 2 Diabetes Summit
Transcript
Beverly Yates, ND

Hi, everyone. Welcome to the Reversing Type 2 Diabetes Summit. I am your host, Dr. Beverly Yates, ND, and I am delighted to interview today Betty Murray, who has expertise that is specific to these issues around reversing type 2 diabetes, hormonal management, weight, hormonal metabolism, and all of the things that come together. Betty, would you please introduce yourself to our audience?

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

Sure. I am Betty Murray. I am a clinical nutritionist and a PhD candidate. I have spent the last five or six years of my life really digging into the metabolism, specifically around women’s hormones and how the body really operates as we head through that transition to menopause and the impact those hormones have on mitochondrial function. I am also a practicing clinician, so I work with patients every day. I also own a very large integrative medical clinic, and I am certified by the Institute for Functional Medicine as a functional medicine practitioner. I am an O.G. in this town for a while.

 

Beverly Yates, ND

We are O.G.’s together. I hear you. That is great. Let us start off with a question to get us going on their journey. The audience really gets a picture of what the situation is and how they can recognize themselves and get some hope, inspiration, and clarity. What is the interaction that sex hormones play when they interact with insulin, weight gain, type 2 diabetes, and pre-diabetes?

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

Yes. It is interesting because if you look at a man and a woman, I think almost any time you get two of them together and let us say they are working on trying to lose weight, both of them say, Okay, I am going to give up all the processed stuff. Maybe I am giving up donuts, bagels, and sodas. For the most part, a man is going to lose weight more quickly. Statistically, it is just the way everything seems to go. There is a profound effect of our sex hormones, not only on what makes a woman a woman biologically. It is our hormone, estrogen. We have three of those that we make: estradiol, estriol, and estrone. Then we have another one called progesterone. It is the fluctuation of those hormones throughout the course of the month that causes the cycle. For anybody that is, what is that? Then men have testosterone, and women have a lot of testosterone. We have about 3 to 4 times the amount of testosterone. Then we do estrogen when our estrogen levels are at their highest. But men’s testosterone is significantly higher. Testosterone causes a larger growth spurt. We see more muscle mass. It has its own metabolic effects as well.

But for women, when we are fertile, healthy, and have balanced hormones, it is the act of estrogen being balanced that actually helps us maintain lean body mass. Let us say you are in your twenties or early thirties. That happens to be the case as women enter their late thirties and early forties and enter a period that we call perimenopause. It is that it can be anywhere. On average, it takes eight years. That means some people double that number; maybe they do not get a whole lot of experience with it. But really, that is the start of the change in these hormones that affect fertility. But in that perimenopausal state, one of the hormones, progesterone, starts to decline fairly quickly. It is, and it is why we see fertility issues in our late thirties and especially in our forties, because progesterone is really there to help progest and basically help the fetus grow.

With that decline in progesterone, what we see is a state where estrogen is still circulating at a normal level. It is starting, but it is still popping up very high. The second half of your cycle is often when women get more symptoms, including peri-menopausal symptoms, heavier periods, more PMS, and weepy, angry sleep problems. Those things start to appear because these hormones are shifting. In that time period, because estrogen is elevated, we can always be in a state where we are estrogen-dominant relative to these other hormones. There is an interplay between estrogen and insulin because insulin’s job obviously is to either shuttle glucose or sugar from the bloodstream into a muscle cell or other cell to burn immediately, or it is to store it as fat. Well, in our fat cells, we have the capacity to take testosterone and the androgen androstenedione, which are two of the male hormones that we would like to talk about. We have an enzyme called aromatase that can convert that into estrogen in the fat cells, so we can actually make estrogen out of our fat cells.

There is an intimate relationship between insulin and estrogen. So as we become androgen-dominant, we start to see more insulin resistance, meaning the muscle cells in particular become less capable of using glucose as their primary fuel. That’s the disposal vessel. So think of it this way: The muscles are going to be your big, burning engine. If they start to become resistant, and then you are a woman, that is because the hormones are changing behind it. We start to see weight gain, despite probably doing all the right things. I would say that’s my experience.

I hit 40, and everything fell apart. I was like, What is going on? What used to work great for me is not working anymore. A lot of it was this hormonal thing going on behind the scenes. When you are in that early stage of perimenopause, estrogen dominance will lead to it. Well, when we get into menopause, which is officially one day after one full year of no period, once you are in menopause, you are always in menopause. It is not something magical that happens and changes. Well, the loss of that estrogen also leads to insulin resistance and weight gain. It is about the Goldilocks story. You want it to be just right—not too much, not too little. Women have a unique metabolic situation where the change in their sex hormones is changing their metabolism truly and honestly at a cellular level. That is amazing.

 

Beverly Yates, ND

There is a lot of complexity there, but in some ways, it is simple. I think of our reproductive years as being the time when we have the potential to bring life into the world, and then when we shift to the other end of it, puberty turns that on. Menopause is now turning that off. of these things have to shift. I would imagine that at that time, when a woman is in perimenopause and approaching menopause—the end of her menstrual cycle—it would be really important for her to have a fantastic lifestyle and quality of life. It seems to me that she was far more vulnerable. If she has a lot of stress, then if she is struggling with poor sleep, maybe hot flashes, maybe too many worries or anxiety, and all these other factors that can come in, it seems that would be really unfair. What are your thoughts on that?

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

I agree. We pay these extraordinary expenses for having the ability to really bring another life to this planet. I think some of the things that we see, whether it is sleep deprivation or not, are truly, let’s put it this way, the things that lead to stress. Whether it is sleep, toxins, or this or that, our bodies, more so than even a man, are hardwired to see that change in stress chemistry. The increase of particularly prolonged stress and cortisol. Then what ultimately happens from that is that we have this increase in cortisol. How does the body interpret that? The body is going to interpret that situation as me starving on the Serengeti because all mammals, so all mammals on the planet, I do not care if it is a sperm whale, a monkey, an ape, or a human, the only time their cortisol is going to be high in the natural world is when they are starving. The cortisol message to the brain is that you need to forage outside of your normal foraging time because we need food. All of the things that stress us out as women and then the hormones changing behind it are driving a lot of this because our body is getting this biochemical message from our stress that says, Hey, you are starving on the Serengeti, which starvation response drives an insulin resistance response. It is a well; that is the thing about the disease. Diabetes is a natural response in our bodies. Broken perception at the cell level, in the powerhouse, and in the hormones.

 

Beverly Yates, ND

It is the powerhouse, the mitochondria.

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

Yes, 

 

Beverly Yates, ND

Yes.

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

Yes. Absolutely.

 

Beverly Yates, ND

It is so interesting. Thank you for laying it out so clearly and tying together those pieces, because I think a lot of times people are not aware of the connections and feel their body has betrayed them. So, women, we just want to be really clear. Your body is not broken; it has not betrayed you. It is responding to your situation.

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

Yes.  It thinks it is doing the right thing. The chemical messages our body is giving itself are these messages that are setting off these metabolic changes, and it thinks it is doing it. It just does not realize that it is not working the way it should.

 

Beverly Yates, ND

Then that leads us to our next question. Which is why other hormones become dysregulated with type 2 diabetes and pre-diabetes and are also dysregulated at the same time during perimenopause and menopause.

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

Yes. There are several hormones. We have hormones that handle satiety and hormones that handle gastric emptying and appetite regulation. If we think of these hormones as actually peptides, if we look at them and look at what the body’s really thinking about, these regulatory activities are happening, and we see that appetite regulation can be controlled by things like ghrelin and gastrin. These are all glucagon-like peptide 1, or GLP 1, which has become very popular. These gastric hormones become dysregulated because they are themselves dysregulated during diabetes. Let me back up and explain that. In diabetes, obviously, the start of it is going to be insulin resistance. The cells are no longer listening to the different tissues in the body, whether it is muscle, liver, or your brain. They get dysregulated and insulin-resistant at different levels. Muscles first, and then eventually the liver, which is usually the last to know. The liver is thinking that everything is working properly, and the liver is the one that is producing some of these hormones. When we become insulin resistant, all of a sudden the liver thinks things are okay, but the rest of the body is not.

We see things through gastric gastrin, which is a hormone produced by the stomach that primarily stimulates the secretion of gastric acid. The stuff that helps you break down your foods, like proteins. That changes even the passage of food from the stomach into the small intestines. gastric and get slowed down. We get a gastric slowdown, so your food sits here longer and you do not digest it as well. You can get heartburn. But it is also the stimulation of gastrin and another hormone called ghrelin that then says, Hey, I am full. They report back to the brain and say to the hypothalamus, We were good. I do not need it anymore. We get this message that we are not full because food is being slowed down. All of a sudden, ghrelin, which is the hunger hormone, is produced in the stomach, which stimulates appetite and promotes gastric emptying. If we get disconnected from that message, we may also be hungrier and have a greater inability for the body to actually digest and also manage blood sugar.

There’s also a hormone called motilin, which is produced in the small intestine and stimulates gastric motility. It moves what they call the migrating motor complex. Think of that as a mechanical thing. Your body goes through it. Know that about 90 minutes after you eat, it starts at the top. I think of this as a snake, and it squishes everything down, squishes all the food down, and moves it through the digestive tract, so the motility changes and we see different contractility. All of a sudden, you might get more digestive stuff, but the longer your digestion takes, the longer your carbohydrate content is sitting in the spine since passing through the small intestines, particularly if you are eating more processed foods that turn to sugar more quickly, the faster and easier it is for it to get into the bloodstream, hit your bloodstream, and be used. That means your ability for your blood sugar to come up after eating is going to increase more quickly than somebody who has better gastric hormone control. Then probably one of the other big ones that we hear a lot about now, because some of the medications for diabetes that are also very popular now for weight loss are hormones called glucagon-like peptide 1, or GLP 1. It is called an increase in hormone, and it is created by the small intestines. It is in response to nutrients, inhibits gastric emptying, and increases tone in the stomach, which moves the food to the small intestines. 

Well, I always thought it was really interesting that changing that hormone in particular all of a sudden led to weight loss, number one, and an improvement in diabetes. Because the food, again, is not moving from the stomach into the small intestines, where it can be mobilized into glucose as quickly, you have that same messaging thing going back and forth with the brain. Those drugs actually change gastric and digestive functions. They’re not directly working on insulin, per se. Those hormones change. As we go through estrogen replacement or estrogen depletion through menopause, we also see the impact of these hormones because they work together. But they can also be impaired. Then one of the other areas that is really important is the activity of gluconeogenesis. It is a big word that sounds really important. Gluconeogenesis is the process by which your body uses another form of fuel to make glucose. At any given time, our body is going to have, as an adult, about a teaspoon of sugar circulating. To be diabetic, one teaspoon now has to get up to about a teaspoon and a half, which I think is about right, Beverly?

 

Beverly Yates, ND

About right.

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

Yes. Teaspoon and a half. Everyone, put your thoughts aside for a moment and just check it out. If you drink a soda, it is going to be anywhere from 17 to 39, depending on the size of the teaspoons. The body is going to freak out if anything goes above that. The other thing is that we do not have to have a high carbohydrate content in order to survive in our diet. Now our bodies are made to use it. It is appropriate, but it is not an essential nutrient. We need proteins, and we need fats. What that means is that the body has the capacity to make glucose with other fuel sources when we do not have it, i.e., in a starvation state or something similar where food is not plentiful. In the liver, glucose can be made out of non-glucose ingredients. That is what your amino acids, proteins, and fat are made of. We can go to lipogenesis and create fat, and the body can then take it, make glucose out of it, and transport it into the bloodstream to get used. In my research, I found that I think this is what is happening to women who are perimenopausal or menopausal. I think this has been amplified. So there are some studies, particularly looking at animals, showing that as estrogen declines, gluconeogenesis, the act of producing glucose in the liver, is amplified. What that means is, is your body doing this instead of burning fat? Because if I am low-carb or fasting overnight, my body should be dipping into the fat stores, but instead it is going and creating its own glucose.

 

Beverly Yates, ND

This would explain why, at that moment in life, there is such a change in terms of the fatty deposition. It is just so unfair. This is a real thing, especially in an era where we tend to have more access to food, and if we are not mindful about what we eat, if it is not the best quality food, if it is not nutrient dense, if it is not filling, and if it often stimulates the desire for yet more calories, especially if we make the mistake of eating anything with artificial sweeteners and fake sugars, this is trouble. This is real trouble.

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

It is complete trouble. The take-home message for everybody is, Okay, that is super technical.  I will break it down very quickly. You could be eating really well, you could be doing those things, and maybe you are just starting on this journey, and your blood sugar may or may not be out of whack. Let us say you are pre-diabetic, and it does not look terrible. If you have some degree of insulin resistance—let us say you are pre-diabetic—you are probably going through gluconeogenesis. If you are a perimenopausal or menopausal woman, that is probably amplified. Even if you have removed some carbohydrates. Maybe you said, “Okay, I am cutting back on my breads, pastas, crackers, and cookies, and I am going to eat more of my healthy vegetables,” like broccoli, Brussels sprouts, and sweet potatoes. Maybe you are doing all that, but maybe you are not seeing things shift yet. It may be because your body is literally going behind the scenes and making glucose for you. I think this is also very tied. If we wrap this up and look at it, okay, this is a survival mechanism. This makes sure we can survive because red blood cells and the brain, but particularly red blood cells, must have glucose.

If we back it up and say, okay, 95% of us are usually stressed and we have elevated cortisol, probably at a significant time of the day, that is going to drive gluconeogenesis, that is going to drive the liver to do this. When we look at all the things that you recommend and the stuff we were talking about just a minute ago with lifestyle, we have to protect our sleep. We have to get good physical exercise to burn off that stress chemistry. We have to learn to say no. We have to do these things that help protect the body’s perception of what is going on so the hormones can respond appropriately. Because when we are in perimenopause and menopause, we have a less than stellar metabolism because our body is going into conservation.

 

Beverly Yates, ND

It makes total sense; the word no is a complete theme. Absolutely. Betty, a little bit earlier, when you talked, you brought up the topic of mitochondria. Would you share with us what the function is of the mitochondria that you referenced as a powerhouse before? I have a specific question to ask you about mitochondrial function as we continue to look at these issues that affect health and the development of blood sugar dysregulation.

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

Yes, mitochondria are known as the powerhouse of the cell, so depending on the type of cell you have, you may have thousands of little powerhouses in it, and other cells may have fewer. but they also produce things. But for this reason, the argument in this conversation will focus mostly on their powerhouse activities. Inside the powerhouse, we can burn different types of fuel, so we can burn glucose. Blood sugar, and we can burn fat. The most important thing about the mitochondria is that they must have oxygen. Think of it as a coal-burning power plant or a fire. You cannot light a fire without oxygen. Actually, the fastest way to put out a fire is to deprive it of oxygen. We have a coal-burning plant. It is going to start firing up. The more fuel we bring in, the faster and hotter it is going to get. The mitochondria are our biggest source of energy. Think of that as your high-pass sports car. If it is running perfectly and we are burning glucose really, really well, we’ll come out with about 36 molecules of the energy molecule called ATP.

Now we have the capacity to burn fuel outside of the powerhouse when we need to, in a squishy part of the cell out by the nucleus. Think of that as a little area outside the powerhouse. I should refer to it as the campfire. We have the capacity in the cytosol to make a little campfire and generate some heat. We can do that, but we cannot do it for very long because, in most cases, that campfire can be created and used in an aerobic condition where we have a lot of oxygen, but it is generally anaerobic. What that means to everybody is that we do not have enough oxygen. Our body is designed to do either one because there are times when we will need to use that campfire. I will give a really good example. If I am running up a flight of stairs as fast as I can, I am going to start huffing and puffing. When I get to that last step at the top, I am probably out of air. That is almost the worst breath you can take. When I get to the point where it is difficult to breathe and I am losing oxygen, my body has shifted the activity of burning into the campfire, and it uses glucose and another thing called phosphate creatine. You can only do that for a short period of time.

That is why you cannot sprint for 20 minutes. It is that you are going to burn through that really, really quickly, and it produces a ton of lactic acid. We cannot do that for very long, which is interesting because interval exercise causes you to flip back and forth between the powerhouse and the campfire, from the powerhouse to the campfire. It is that switching that tells your body to go make more mitochondrial biogenesis. Make them. But when I am out by the campfire, that is the equivalent of being in a four-banger Hyundai from 1984. Since it is just the reality of it, everybody that is older on this is like, Oh, totally. I remember those. So what it means is that as I produce four molecules of ATP in the campfire, I also produce 36 in the mitochondria. Mitochondrial function is vital to your body’s ability to make energy appropriately. Diabetes, to some degree, is also a mitochondrial problem. We were not getting glucose into the powerhouse we were supposed to because it was getting blocked because insulin is resistant at the receptor. Before that, we become glucose-toxic. It is because we shove too much coal into the plant and they cannot get it moving quickly enough. Mitochondria are really important, not only to produce energy but to be part of the entire picture.

 

Beverly Yates, ND

I think that it is an underlying piece that does not get explained around one of the key hallmark symptoms of diabetes. Really, any diabetes—type 2 diabetes, prediabetes, type 1.5 diabetes, type one diabetes, metabolic syndrome, PCOS, and often resistance—is an issue of fatigue or tiredness. Their mitochondrial powerhouse production is compromised, and this is part of what is going on. With this in mind, now you are talking about these key changes in mitochondrial function that can lead to diabetes and metabolic derangements along the way, particularly for women in menopause. What is going on here with this setup?

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

When we look at women’s mitochondria, obviously the mitochondria are slowing down. Your powerhouses are all at half-mast, and they are not quite as effective. Estrogen affects the mitochondria in several different ways. Estrogen has receptors on the mitochondrial wall. Estrogen actually enters a cell, goes into the powerhouse, and clicks in. Estrogen affects the signaling of several different pathways. One of them is the passive transport of glucose into the mitochondria, called the gloop for transport. Think of this as a game that we used to play as kids: Chutes and Ladders. So you get to the ladder, and you get to slide down the ladder. Well, think of it as that. Your ladder is not really tilted at a very high angle. The incline is just barely 7%, just enough to feel it but not enough to really get somewhere. That is the passive transport of glute, which is stimulated by estrogen. So when we lose estrogen, we cannot get glucose into mitochondrial activity either. We also see the signaling of actual muscle tissue. that the actual innervation of muscle tissue and fat tissue to mobilize fat is impaired. That is because, then, what am I trying to say? It is the activity of your nerves talking to your fat cells that stimulates epinephrine’s transport. Estrogen has an interaction there, too. It is why we get subcutaneous fat on the outside of our thighs, the jiggly bits that we do not have, and the innovation, the discussion to those tissues to mobilize the jiggly bits on the outside, the subcutaneous fat becomes impaired. So we also cannot get the fat out of the fat cell as efficiently.

But even more importantly, if we look at what is happening inside the cell, one of the mechanisms that is again a protective mechanism in the cell to allow the body to store fat actually came about millions of years ago when we moved from some transition from what looks like an ape to mankind. There was an ice age, and the apes that happened to be on the planet at that time, up until that point, really could not store body fat. They had to have a constant supply of food, and their food was all vegetable-based. It was mostly fruit. There was a change in an enzyme called urease. We were no longer capable of clearing uric acid out of our bodies, as most mammals can. It was this alteration in the urease enzyme that allowed our great ancestors to survive because, for the first time, they were able to store fat. Urease changes a molecule called uric acid. Uric acid is produced inside the cell, and it is a signaling mechanism inside the cell to also tell that powerhouse whether to amplify or decline in activity, and it is in relation to what is perceived as damage. things that contain RNA. RNA is part of your cellular mechanics and part of your cellular parts. If there is a lot of RNA being spilled inside the cell, there is some damage happening. For anybody thinking about it, maybe somebody pulled into the parking lot outside the site of the powerhouse and forgot to hit the brakes and hit the gas and banged into the wall. Now there is damage. So everybody goes, Oh, we have got to slow some production down because we have got to go fix the wall.

Uric acid is this cellular injury mechanism. What we know now, and it has been studied pretty heavily at this point, is that as uric acid rises inside the cell and makes the powerhouse slow down, our body then becomes more insulin-resistant, stores more fat, and allows us to act as if we were hibernating. This was found in hibernating animals like bears and squirrels. This is the mechanism by which they gain weight, so they can sleep for months on end through the winter and not die.  Uric acid is a hibernation response. What is interesting is that when you look at women, you go out and dig through the studies automatically. When we hit menopause, there seems to be this significant rise in uric acid levels when we look at bloodwork. Uric acid levels in the blood; a very easy lab test that your doctor can run can show whether uric acid levels climb. Most people think of uric acid for gout; it is associated with hypertension, cardiovascular disease, diabetes, metabolic syndrome, obesity, and all of those different things. The higher it goes, the more it is going to cause these problems. It is causative; it causes hypertension and diabetes. It is through this mechanism. Uric acid, as it elevates, becomes a surrogate marker for whether the powerhouse is up or not. Is it working? 

So what the research showed is that if it is over 4.2 on a serum test, that means that the so let us say it is a six, let us say somebody came back at a six, that means that you are a fat switch is on and your body thinks it needs to store, and it will do that with carbohydrate content, particularly fructose high fructose corn syrup, and it will do that with aged foods, alcohol, and sugar. But that is the big stuff that we see. A big change in our diets, particularly in the last 20–30 years, is the increase in high fructose corn syrup, corn sugar, and all the other names we have for it, because it is triggering this all the time. Well, as menopausal and perimenopausal women, we are already dealing with an amplification of that uric acid switch inside the cell, regardless of what we are consuming, which means we have less freedom within those food categories because we might be turning it on all the time.

 

Beverly Yates, ND

I can see that this becomes a trap for sure.

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

Absolutely. Yes.

 

Beverly Yates, ND

Okay, great. Thank you so much for that. Now that we have walked through these particular kinds of issues, they circle back a bit to what you had started to talk about with GLP-1 and some of these peptides and receptors. What about these current obesity drugs like semaglutide and liraglutide? They do provide people with amazing support, and for people who struggle with these things where something’s clearly broken, they are finally getting some practical support that is helpful. But then, of course, other people are using it inappropriately. That’s my opinion. Tell us, please, about these obesity drugs to make the tide and to his appetite. 

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

Yes. Semaglutide. I will say I am not the world’s biggest expert on these, but semaglutide is obviously designed as a diabetes drug. Is it what they call a GLP-1 receptor agonist? What it does is bind to receptors in the brain in the hypothalamus, which is your regulator. The hypothalamus takes information from your environment. It takes information from your senses and all your chemistry and starts making decisions about what needs to happen. It sets the appetite. It also talks to the pituitary, which is the conductor for the entire endocrine system. Between the two of them, they are picking up messages and figuring out, Hey, this is how the show is going to look. This is the look and feel. Is it a thriller? Is it a drama? Is it a comedy? The pituitary is going to tell the band how to play the orchestra. There is a lot of information there. Well, if we are taking a GLP-1 receptor and we have a binding there, it is going to talk to the hypothalamus, which regulates appetite. 

Both semaglutide and liraglutide are appetite suppressing through their mechanisms. In some cases, that is going to reduce and regulate appetite. We were going to probably eat less, and when you activate these receptors, it also affects the satiety mechanism. It feels like you are more satisfied. You reduce hunger, so you tend to eat less. Semaglutide also slows gastric emptying. That means, again, that you are going to have food sitting in your stomach longer. Are you going to feel fuller for longer? It is going to trigger ghrelin. We were going to get this message: Hey, the stomach is stretched; I am full, and then we were going to have food hit the small intestines as quickly as possible. We were going to have a slowing of the speed at which particular carbohydrate content can be made into sugar and mobilized into the blood, or, I will not say, broken down into its simple sugars.

The GLP-1 receptor agonists also regulate blood glucose levels by stimulating insulin secretion and, to some degree, suppressing a little bit of gluconeogenesis. But mostly, it is stimulating that insulin activity. It can help improve glucose control, which will lead to weight loss and, ideally, reduce insulin resistance. Then it has a little bit of an energy expenditure change where we see a little bit of an increase in fatty acid burn. The goal is to see if insulin comes down, we are more insulin-sensitive, and we eat less. I have less food available in the bloodstream in the form of carbohydrates. Ultimately, your body should be dipping into the tens of thousands of calories that we have sitting in our fat cells to burn them. It has to burn it in those mitochondria in the powerhouse. It needs oxygen. If you eat those drugs, you end up losing weight, for sure. Now, with semaglutide, what is interesting about that one is that because of its impact, particularly on gastric emptying, it has a pretty sizable issue with symptoms. In some of the studies, as many as 40% experienced digestive problems, nausea, GERD, and changes in bowel habits. And so it does result in weight loss because it has this multi-mechanism effect. It is a drug that can help with diabetes, which I am sure you could speak to much better than I can. But the side effects and the weight loss, to some degree, I think, even if you dig through the literature, are probably because you just do not want to eat because you do not feel good.

 

Beverly Yates, ND

There’s a tradeoff. If people are suffering or feeling miserable, if they are having the side effects along with the benefits, I think it is a mixed thing. But if that is the case, if they have tried everything else and this is what is working and they have symptoms that are tied to the issues with unregulated blood sugar and weight, it is a cost-benefit analysis for that person and their lived experience in their skin. It is a fascinating moment in human history, for sure.

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

Yes. The thing is, because I was very interested, I am always interested in biochemically how these things work and that there is appetite, which I think just got approved as Mounjaro.

 

Beverly Yates, ND

Yes.

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

Recently for weight loss. It is slightly different; it is a GLP-1 drug, but both of them have very similar mechanisms. The thing that I found interesting is that there is significant weight loss. I would say if somebody had to lose a lot of weight, let’s say they are diabetic or maybe they are on the thing, that definitely weight is contributing, that it definitely resulted in weight loss, and it was significant. But in many cases, as they took the drug out after that first year, there was less weight gain, but what was really interesting is that for people who want to use it for 10 to 20 pounds, it does not have the same positive effect as if somebody needed to lose 40, 50, 60, 70, or more. Meaning that it is probably a good solution for somebody if they are really struggling. They’ve tried everything else, and they are not losing weight to know that. But the thing is, it is expensive, and it is injectable. You have to take it over a long period of time. You have to slowly titrate up to some of the symptoms; if you go very slow, it increases the dose, and coming off of it is a very slow ride because there is a weight regain and a rebound weight gain.

But for the person who is trying to use this for a 20-pound weight loss, I want to get ready for the summer because it is bikini season. The weight regain potential is something that I think outweighs the use of that drug because, from the studies, it does not look like it is very effective and that there is a rebound weight gain. I do not think it is something that should be used as a routine. I am just going to do it every spring and drop that toe, and then I am good. I don’t know what you think, but I was a little cautious. If it looks too good to be true, it probably is.

 

Beverly Yates, ND

I agree with you on that. I think that those drugs should be for the people for whom they were designed and intended, where the strongest body of research is. For the ones that are for people with type 2 diabetes, absolutely. The ones who are obese and are not able to lose weight any other way, yes. I think for people who have just a few pounds to lose and are doing this almost as a sport or much more casually, it is not lifesaving for them. I just think it is the wrong approach. That speaks to, I think, a different set of issues. That’s my own personal and professional opinion about that.

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

Yes. Semaglutide, has slightly fewer symptoms, so because it has a slightly different mechanism than it seems to have, I would say I think it is going to be a better drug overall in that respect. But I think that there are so many other solutions that people can have if weight loss is their only goal. I said, I agree with you. I think, from a diabetes standpoint, it is a really, really good drug used in the population.

 

Beverly Yates, ND

Yes.  So far, the research is showing results in terms of rebound weight gain. If people were taking the drug as prescribed and they were using it for the correct reasons that they rebounded, weight gain would be about two-thirds. Let us say they need to lose 100 pounds, and then they go off of the drug for about 66 or 67 pounds and come back for a net loss of 33 pounds, just to make a clear, simple example, so I think in that case, perhaps it is buying people time, and they can correct some other things and maybe start to get some success. These things are complex and multifactorial today, as we’ll talk about in other sessions with other experts. Friends, just please understand that there is no one-size-fits-all approach that works for everyone 100% of the time. I wish it were that simple. In the 1950s, the advice was to eat less and move more. In this era, we really have to all, as health professionals, up our game. For people who have the problem, you really will have to insist that whoever you are working with can meet you where you are and help you get where you need to go.

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

Yes, well, the beauty of what you are doing here with this summit is that people are going to get information about the different medication choices and other things, but they are going to get so much more from you and all the other experts as well about dietary changes and lifestyle changes, even if they are using this medication. You’ve got to remember that the people who did these studies were probably not given any dietary supplements. It was, Hey, just go on this medication; do it, because they do not want any confounding variables. They do not want to add anything else that might make it more effective. We’re just going to do the drug. They were still eating the same things. Then, when they got off the medication, they went back to the same standard American diet, which is a diet guaranteed to cause metabolic derangement. People listening to this are going to learn so much about how to do things better. Even if they are using this drug to reverse diabetes, they are going to be so much better off, as what the research showed.

 

Beverly Yates, ND

Agree. With that in mind, let us get to our next topic, which is: what can someone do who is in transition to menopause? This is a woman. She is perimenopausal, and the actual end of the road in terms of the menstrual cycle is coming. She is clearly in transition—the menopause. If she is struggling with blood sugar control, she is struggling with diabetes. What can be done to help her fix some of those underlying causes?

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

Yes, a lot of it is going to follow, probably along with many of your other experts that are here. I think the first thing that we have to understand is that 88% of us are insulin resistant, and you can be insulin resistant and still be body normative, meaning that your BMI is perfectly fine. You are not overweight. That just means your cells, particularly muscle cells and different cells in your body, are not capable of using glucose properly. I think one of the most important things that people should do is move more. If our muscles are our primary target for glucose utilization, I want to put a bunch of fuel cells in my Tesla. I need to take the Tesla out for a ride. That means I need to move more. that, and that means that I need to do some interval training. I think I want to move back and forth between the powerhouse and the campfire. What is cool about interval and verse training is that they are different for each person. One person who is super athletic is going to be more intense than somebody else. You’re just looking for that. We need to do a little bit of that fuel switching and fire switching, but we also just need to move more. In general, I think people forget that we need to teach the cells in the muscles to be active.

What that really means is that we need to do some low- to moderate-intensity cardio, not cardio with heart rates above the fat-burning zone. Most people, when they do cardio, they overdo it. You cannot truly have a conversation with someone. You’re not burning fat. You have to be able to still have a conversation. But for most people, if you are in your forties or fifties, you are probably looking at a 120 to 130 heart rate; if you are deconditioned, maybe a little bit slower. But we just need to do that, and we need to do it in time. It is not really effective if you do not do it for at least an hour, which it is, and it is almost better to do it one day and say, Okay, I am going to do at least an hour one day. Teach your body that. then throw in these other exercise things so your muscles become sensitive because that is going to help you move glucose, and recognize that if you are a woman in perimenopause or menopause, you are going to probably have to amp it up a little bit more because your messengers from your nerve cells are not talking to your fat cells at the same level. Half of them went on break.

 

Beverly Yates, ND

Are you saying things change?

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

Yes, they do. Well, because I hear this all the time. I know there are metabolic things going on. If we were to look at bloodwork constantly, we could see that glucose is getting more sensitive and all that other stuff. Well, we get mad about the jiggly bits on our buttocks and thighs and her abdomen, but that is the subcutaneous fat. That’s the first and last off, and that is the stuff that is very hard to move. So you have got to think about when your body becomes more insulin-sensitive and you are more capable of burning fat because insulin is down, because it has got to come down in order for fat burning to come up if your muscles are a prime rib. There’s fat running through them, and then there is fat on the outside that you see. It has got to burn through all that fat and the muscle tissue first before it touches the subcutaneous fat. We get frustrated if we work out for three weeks and do not see a change in the way our pants fit. It is just, Hey, I have a burn injury to the prime rib, and then it is going to hit that subcutaneous fat on my body, and it’ll slowly burn off some of the booty. That we have. We have to hit a little harder. We began weight training. I bought a weight trainer. Ladies, I have a specialty in osteoporosis. You’ve got a weight problem. We’re going to protect our bones and our muscles.

 

Beverly Yates, ND

Here’s my kettlebell weight training. People do it.

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

They’ve got to do it. You cannot get bulky. You cannot get bulky. I promise you, it is impossible. Even if you answered almost yes. weight. Yes. The exercise is important. The other side of it is that we have to make sure that we are not doing things that trigger some of those mitochondrial things. .    That I was talking about. I do not want to turn on the fat switch. I do not want to get my body to use just glucose or make glucose instead of burning fat. The first thing is, obviously, that everybody is going to say this is processed food. Anything that has a bag or a label on it, especially if somebody is promoting it on TV, you should not eat. Stay out of the middle of the grocery store. There’s nothing healthy for you there. That’s all profits for big food. 

You want to shop around the perimeter. You want to eat a lot of vegetables. You want to eat healthy proteins, and you want to eat healthy fats. You want to get your starchy carbohydrates from either healthy legumes, starchy vegetables, or healthy fruits, sticking to those arenas and staying away from things that have been processed—milled, floured, that thing—because that just makes it faster to turn into sugar. But it is also going to pull that uric acid level up; those foods trigger it, and you want to stay away from table sugar, fructose, and high fructose corn syrup. Do not fall for agave. It is all toast. You want to avoid those foods because they are going to raise uric acid very quickly. You’ve got to remember that you are already battling with a little bit of flat switch sliding upwards. We cannot get away with saying, I am having just one Coke a day, or Sweet Tea, I had a conversation yesterday. Why Sweet Tea? I am. Are you buying it? It is sweet. That’s fructose in a bag. Put some stevia or low-hanging fruit in it. We just want you to make your sweet with something that is a non-caloric sweetener that is healthy. Yes.

 

Beverly Yates, ND

We did that all together, so you are not checking your brain because of the Facebook brain thing.

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

100 percent.

 

Beverly Yates, ND

It is nasty.

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

Nasty. Well, it messes with your gut microbiome, and it does dysregulated insulin. But I do have people who are, and I am dying if I do not have them. Okay, one packet of sweets every day looks.

 

Beverly Yates, ND

Bargining.

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

Yes, it is bargaining. Work your way off of those things because you do not want to drink your calories now. Give me another one. Don’t drink your calories, ever. Because our brain does not register food as liquid calories. You to your body, your brain registers it through the pre-op reception in the brain. I would say the other side of it is that I hear from women a lot, especially if they have done a lot of low-carb dieting, because there are a lot of women who are insulin resistant who are still low-carb. Carbs are not the only game, and a lot of times they are eating protein, and then I will hear, Oh, I am eating a lot of protein. I am having a protein bar, I am having a protein shake, and I am eating my protein at my meal. Then I am, what? What vegetable do you have? They are. Well, I had one at dinner, so you’ve got to remember that your liver can make glucose, and your liver can also make insulin as a response to high-protein meals and a big meal. It is an appropriate protein, but we need lots of fiber and lots of veggies. We want to make sure that that is balanced. Those would be my biggies. 

 

Beverly Yates, ND

Great. Thank you so much for that wonderful summary. To take home along the way: how do you make this work in today’s world? Not in a theoretical world, in a lab, or in a lifestyle that very few people enjoy. How can the vast majority of people really benefit? Betty, thank you so much for your advice, your expertise, and your insights today. If people want to get in touch with you, where can they find you? How do they get in touch?

 

Betty Murray, PhD-Candidate, MS, CN, IFMCP

Sure. They can find me at BettyMurray.com. That is B E T T Y M U R R A Y. You can also catch me on my podcast called, Menopause Mastery. It comes out once a week. That is a great place to see me.

 

Beverly Yates, ND

Great. Thank you so much for being such a great guest and giving us all of these pieces of the puzzle, the points of view, and the aspects of something that I think sometimes people just feel really confused by or perhaps do not necessarily have the hope or inspiration that they need. I know today that you helped give people hope, inspiration, and clarity. Friends, thank you for watching this session. Please share this with anyone that you know who cares about their health, anyone who is going through menopause, or anyone who has pre-diabetes. Type 2 diabetes. This affects so many people. There’s a lot of needless struggling and suffering. If you would be so kind as to share this with the people that you care about, that would be fantastic. Betty, thank you so much.

 

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