Hello everyone and welcome back to the Rebel Nutritionist Podcast today. I am actually really, really excited about our episode today because I get so many questions on this. We get questions about a lot of things, but I think this is one of the areas and one of the topics that is the most confusing for women, and we are talking about why does your cholesterol rise in menopause, and it’s not what you think everyone thinks it’s estrogen.
And it’s certainly not a statin deficiency. You can laugh at that, but if you’re a woman over 40 or 45 and your cholesterol is suddenly going up, chances are you’ve heard, oh, it’s just menopause. Your estrogen drop drops and that’s what happens. Or sometimes. They don’t even, nobody says that, right? The doctors don’t even make a correlation that it’s likely your estrogen goes up because you’re in menopause. Or it’s likely that is the reason and they don’t talk about it. They don’t address it. It’s up to us folks to actually bring this to the service, and I truly don’t even think most physicians who are in, who are gynecologists or even in the. Medical space are paying attention to what happens with women’s lipids and a lot of their labs during menopause.
It’s just a fact. I hear this all day long. I can tell you my cholesterol went up. It’s now come down because I’ve addressed some of these things, but it is, I think, more common than not, more likely than not, that as you go through menopause, you’re going to experience that and it’s an incomplete picture because it’s not just, oh, your cholesterol’s going up and take a statin.
Because menopause isn’t just about the ovaries shutting down. It’s your body going through a full metabolic recalibration. That is so true. Your body is recalibrating now during menopause, and so when cholesterol rises during menopause, it is totally not random. It’s not anything that you did, and it’s not just age.
It is basically a signal. And today we’re gonna unpack what that signal represents clinically, metabolically, and syst systemically, because it really is. All about that and there’s a lot of information. This is gonna be little bit science, but it’s certainly going to be chockfull of tons of information.
So buckle up. We’re going in. Okay. We’re gonna talk about things like estrogen and the LDL receptors. We’re gonna talk about visceral, fat redistribution. Insulin resistance, cortisol in the brain, muscle loss, inflammation, the gut liver access, because here’s the thing, cholesterol does not rise in isolation.
It rises in context. So I’m gonna call this the obvious layer because it’s estrogen and lipid metabolism. It’s how does estrogen actually impact? How your body handles lipids. And when you talk about lipids, I’m talking about cholesterol and LDL and HDL and VLDL and all of those particles in between. So if you are only getting a cholesterol panel, meaning.
Total cholesterol. H-D-L-L-D-L, triglycerides, maybe VLDL. You are getting an incomplete picture. You have to get particle sizes because that is so important as is what we call LP little A, so we could talk more about that if you have questions about that. But. Let’s talk about what everybody’s talking about.
How does estrogen play a significant role in lipid metabolism? How your body uses fats essentially, so in the liver estrogen, the hormone upregulates, LDL receptors, it enhances LDL clearance. It supports reverse cholesterol transport. Increases L HDL production and suppresses hepatic lipase activity.
Okay, so what does that mean in English? Okay. Before menopause, estrogen acts like a traffic controller for cholesterol. Essentially your liver. Liver has little grabbers on its surface that basically pull LDL, which is the cholesterol carrying particle. Out of your bloodstream. Think of them like docking stations.
Okay. There’s a docking station for that. Estrogen tells your liver, make more of these grabbers. Take those grabbers and make more of them so that we can take that LDL out of the bloodstream and it can clear efficiently. So when estrogen drops, you make fewer docking stations. So it’s not that LDL is skyrocketing.
Because you’re not making more, it goes up because you’re actually clearing less. Out of the blood. You following me? All right. Now let’s talk about HDL. HDL is like the cleanup crew. It goes around your body picking up excess cholesterol and bringing it back to the liver for recycling. So estrogen helps HDL do its job well.
So after menopause, HDL may decrease or it may become smaller and less effective. So even if your number looks fine, the function of it may not be as strong. There’s also an enzyme in the liver called hepatic lipase, and estrogen keeps this enzyme in check. So when estrogen drops, this enzyme becomes more active.
And that can shift cholesterol particles into smaller, dense patterns. And it’s these smaller, dense particles that are more likely to contribute to plaque formation, right? Hardening of the arteries. So here’s the takeaway before menopause. Estrogen helps clear that LDL deficient efficiently, and it keeps HDL functioning well.
So you have a healthier particle pattern. After menopause, the cleanup system slows down, so that doesn’t mean your body is broken. It means the regulation has changed, and that’s why cholesterol often rises, not randomly, but because the system managing it has shifted. And so when estradiol declines, your estrogen declines.
LDL receptor expression decreases. LDL clearance slows. Particles start to accumulate. Your triglycerides might rise and HDL can shift to smaller, less protective subfractions. And this is well documented in longitudinal studies like swan, the study of women’s health across the nation where LDL cholesterol increases sharply around the final menstrual period.
So yes, estrogen loss does matter, but here’s where we need to zoom out. If estrogen deficiency alone explained everything. Then guess what? Hormone therapy would normalize cardiovascular risk. And we know that it doesn’t normalize it. Hormone therapy may improve some of your lipid markers, but it doesn’t completely eliminate cardiovascular risk in women, and that’s really important to hear.
So this tells us something even more important, while estrogen loss might initiate the change, it doesn’t fully explain that whole cascade of what goes on. So we’re gonna get to, solutions in a moment. But the next part that I wanna talk about is visceral fat redistribution. And this is a real turning point for a lot of women.
What does this mean? It’s, why does men menopause push belly fat or fat into the belly because we accumulate fat in the belly. Most women, have this happen. Maybe not to a great extent. Some have more than others. But one of the biggest misunderstandings about menopause is that women just gain weight.
That’s not actually what’s happening. Again, the more important change isn’t total weight ’cause you could weigh the same and just have it distributed differently. Okay. Before menopause, estrogen actively influences where fat goes. Fat tissue has estrogen receptors, especially subcutaneous fat in the hips and thighs.
Think about it. Childbearing. We need fat more there. So estrogen basically tells your body store energy there and that lower bo the fat in the lower part of the body, in the hips and the buttocks and the legs. Is actually metabolically quieter. It doesn’t signal inflammation molecules, for example.
Okay, so we have less inflammation. We have less in insulin resistance when we store fat there, but when estrogen drops, the signaling changes. Subcutaneous fat loses is its preferential storage signal, meaning there, that’s not the preference. Okay? At the same time. Visceral fat. The fat around the organ loses what we call inhibition, meaning it’s more accessible, okay?
It’s more that’s not putting out these messengers that say, no, don’t store fat. Here it is, becomes more accessible. So here’s where it gets a little biological and a little science, but I want you to know this. If you don’t wanna listen, just skip forward a little bit. But I think it’s important that you understand the mechanism.
We understand what’s going on and not just say, oh, I need to starve myself. I need to do this, and I need to work out harder because I need to lose the fat. It’s a very different mechanism because estrogen normally suppresses, right? It reduces the enzyme called lipoprotein, lipe lipase. Lipoprotein lipase in abdominal fat, and that’s the enzyme that allows fat cells.
To pull triglycerides out of storage, out of circulation, excuse me, and store them. So when estrogen declines, that suppression is lifted. So now your abdominal fat becomes more efficient at pulling in and storing fat. So the storage machinery becomes better at holding the fat. Again, you’re not necessarily eating more, you’re not necessarily moving yet less.
The distribution system has completely changed. So now let’s add another layer. After menopause, the ratio of androgens, a K, a testosterone, for example, to estrogen shifts, what does that mean? Testosterone declines more slowly than estrogen. That relative, let’s call it testosterone dominance, is associated with more central fat accumulation.
And so we see similar patterns. Like this in exam, in conditions like PCOS. Okay? So that’s where just the whole testosterone, estrogen balance gets shifted. Then we look at cortisol, visceral fat has a higher density of what we call glucocorticoid receptors. So what does that mean? It means that.
That visceral fat is more responsive to stress hormones, so estrogen normally buffers some of cortisol effects, but without estrogen buffering, stress has a stronger impact on central fat storage. So midlife stress, caregiving, career pressure, sleep disruption, this becomes metabolically amplified. And then we know muscle mass starts to decline.
This is why lifting weights, heavy weights in menopause really before menopause. This is why lifting weights is so important, so you can preserve your body’s metabolic engine. Because estrogen plays a role in maintaining muscle, and when muscle declines, insulin sensitivity worsens and higher insulin promotes fat storage.
And when there’s low estrogen, that storage is in the belly. So again, you don’t have random belly fat, you have altered receptor signaling. Enzyme changes in fat tissue, your hormone ratio shifts. You have , increased cortisol sensitivity and reduced muscle mediated glucose. Disposal, meaning glucose is not processed the same way it was before.
This all points to fat storage in the abdomen and once visceral fat increases. It changes everything downstream, meaning visceral fat releases more free fatty acids into the bloodstream, and those free fatty acids flood the liver and the liver responds by increasing VLDL, so it’s that fat production triglycerides and small dense LDL .
Particles. Now cholesterol rises, not because cholesterol suddenly became the VI villain, but because the metabolic traffic pattern has changed. So menopause does not randomly add belly fat. It rewrites the instructions for where energy should get stored and where fat is stored determines how cholesterol behaves.
So it is this. Turning point, but it is this back and forth mechanism where things are talking to each other, but the signals are a little different. And so now let’s layer in insulin resistance. Now this is what I’m gonna call the silent amplifier. So we wanna think of menopause like a metabolic stress test.
Estrogen improves insulin sensitivity. Through many things. I don’t need to go through the science of it, but there’s many ways that estrogen improves insulin sensitivity, and so reduced visceral fat is one of them. And mitochondrial health. Okay? So when again, estrogen declines, insulin sensitivity worsens your fasting insulin rises.
This is why we see this on blood tests, and I see this all the time. Hepatic insulin resistance increases. So again, in the liver, your insulin, your liver becomes insulin resistance. And that becomes a problem. So high insulin will stimulate how the liver is making fat from scratch, essentially.
And so when in when insulin is elevated, which happens in menopause, the liver starts converting extra glucose into fat. Packaging it into triglycerides and sending it back out into the bloodstream. So that process directly contributes to higher triglycerides and more atherogenic cholesterol particles, more of those particles that stick to the wall of the arteries.
So again, this is why we cannot look at cholesterol in isolation because if LDL rises. But fasting insulin rises. That’s not a coincidence. This is giving us metabolic context. And so menopause often unmask insulin resistance that was quietly brewing for years. And I have said this over and over, and we talked about, I talked about this a little bit in the podcast about hormones and hormone replacement.
This is why it’s so important to get your metabolic health in order before you even go on hormones, because detecting all of this stuff before you start hormones actually can fix your issues, period, right? Without even having to go on hormones. But we’ve gotta look at these underlying imbalances. If you wanna be healthy, it’s not just about slapping a bandaid of hormones, and again, not against hormone, but it’s never just slapping the bandaid on.
It’s understanding what downstream is out of sync and how do we rebalance it? Because how many women complain about brain fog memory issues? Guess what? The brain. Also gets rewired in menopause and we’ve got cortisol to pay attention to. So this is where it gets super interesting.
Okay. Menopause is not just ovarian, it’s not just what goes on in the ovaries and so forth. It’s hypothalmic, meaning we have the hypothalamus in the brain. Estrogen modulates mean it impacts the hypothalamus. So this is the area. Guess what? Get ready for it. This is the area of the brain that regulates hunger, satiety energy, expenditure, temperature, stress response, all of those things.
So when estrogen declines the hunger signaling, it’s called neuropeptide y, but it’s really the signal that. Is impacting hunger. This hunger signaling shifts, and so it affects energy and body weight. So these neurons are part of your, I’m full stop eating and burn energy system. When these signals are active, your appetite decreases.
Your satiety, your feeling of fullness increases. Energy expenditure goes up and fat burning is supported when these signals weaken as what happens when estrogen starts to decline. Satiety signals weaken appetite, increases energy conservation, meaning stored fat becomes more likely. So in simple terms, these neurons help you feel satisfied and metabolically on when the signaling drops.
Your brain nudges your body towards storing rather than burning. So energy conservation signals say increase fat storage. At the same time. Estrogen also buffers cortisol without estrogen’s, buffer and protection. Cortisol’s metabolic effects intensify. So cortisol preferentially promotes. Visceral fat deposition.
That’s why that stress in midlife, again, the caregiving, the career, the sleep disruption, this compounds this visceral fat storage. When you have higher cortisol exposure, more central fat storage, more liver lipid, right? Fat production. This is not. Cosmetic belly fat. This is what we call neuroendocrine reprogramming.
So it’s really important that we understand there’s such, everything’s all connected. You can’t just have something without the other thing. We are all connected and we are all one system and everything talks to everything else. And understanding that is part of this process, and it’s part of understanding how you help your health along the way.
So let’s talk about muscle loss and metabolic rate because this is a big one and it impacts muscle development or . How muscle is metabolically active. So we know menopause accelerates what we call sarcopenia muscle loss. This is why lifting weights before menopause is so important.
Putting on the muscle before your estrogen declines so important. So estrogen interacts with muscle tissue. Mitochondrial function, that energy and protein synthesis, how your body makes protein, the loss of estrogen contributes to decreased lean mass, lead decreased muscle, which will then cause your me metabolic rate to lower and it reduces how your body handles blood sugar.
So think about muscle like a glucose sink. It literally hoards glucose. So think about this. When your muscle mass declines, where does that glucose go? You guessed it into your bloodstream. And then what happens when glucose is in your bloodstream? Insulin rises. And again, the liver has to make more fat.
And if those LDL receptors are not efficiently pulling in the fat to the liver, guess what? You’re gonna have higher circulating fats, cholesterol. So this is why resistance training is not just aesthetic. As a matter of fact, it’s zero aesthetic in my opinion. Yes, it’s important. It looks nice.
It is literally cardiometabolic therapy, like it should be a prescription. That’s how important. It’s okay. And then there’s another major reason that cholesterol shifts during me menopause, and it has absolutely nothing to do with diet. It’s inflammation. So menopause is associated with what we call low grade chronic inflammation.
Sometimes you’ve heard it as inflammaging, and so estrogen normally has anti-inflammatory effects. Estrogen is a steroid. Steroids have anti-inflammatory effects because it helps regulate immune signaling and keep certain inflammatory molecules in check. So now when we start to lose estrogen, that restraint, that protection starts to diminish.
So when inflammatory markers are elevated, it means the body is under stress and inflammation in and of itself changes how the liver manages cholesterol. It can increase cholesterol production, reduce how efficiently it’s cleared from the bloodstream, and make cholesterol particles more likely to contribute to that plaque buildup.
So when inflammation is high, cholesterol doesn’t just go up. It really becomes more likely to create risk. So that’s why lowering inflammation is often just as important as lowering the cholesterol number itself. And what I want you to also think about is inflammation also impacts how those fats are either protected or destroyed.
And so oftentimes. When we don’t eat a healthful diet, when we’re eat, when we’re exposed to toxins, even from the environment that creates free radicals, and those free radicals can create inflammation in and of themselves, it oxidizes these fats, creates a whole issue. So we’re not gonna get into that, but.
Not having a supported diet will also impact the health of that plaque. Believe it or not, not all of that plaque on your arteries is bad. It’s actually, if it’s not bothered by free radical damage, sometimes it just sits there and it does nothing. It’s not dangerous. It’s when it becomes oxidized that it becomes super dangerous.
Okay, so let’s take a breath. There’s a lot to really unpack here, and this is why cholesterol numbers are never just what they seem. And I really we’re gonna talk about the microbiome, but I really want you to take a moment and think about what testing you’ve had. And if you haven’t had it done, you need to have it done and tell your friends because they need to have it done.
But we need to understand the nuances of how all of this works. All right, so now let’s layer in the microbiome as if your mind isn’t always like right already. So estrogen and gut bacteria interact in both directions. Okay. Certain gut bacteria help regulate estrogen and when estrogen declines, microbial diversity, meaning the different kinds of microbe, often shifts.
So in post menopause, we see reduced microbial diversity, more inflammatory bacterial patterns. Altered B acid metabolism. And so think about it, if you never had gut issues, if you never had gallbladder issues, or even if you had gallbladder issues before, these things start to worsen in menopause. Because again, if the foundation isn’t strong, going into menopause, all of these things are now going to bubble to the surface.
So it’s not that you suddenly have insulin resistance. It’s not that you suddenly have. Gut microbiome, liver, gallbladder issues. It’s that all of these things were there. They were just protected while you had all that estrogen. And here’s the key connection. Cholesterol leaves the body primarily through what we call bile acids.
So the liver converts cholesterol into these bile acids. Those bile acids go into the gut, the bacteria in the gut modify them. And some are reabsorbed and some are excreted. And that excretion is how cholesterol leaves your body, right? That’s how cholesterol is detoxified through your body. So think about this.
If your microbiome, if your gut bacteria is altered, bile acid metabolism becomes less efficient, so then cholesterol clearance will decrease. And now guess what? You have more inflammatory signaling. You have more liver driven cholesterol production, as we’ve mentioned, and you have less efficient cholesterol elimination.
So the gut is a huge driver here as well. And then we think of gut and liver. Menopause isn’t just changing hormones, as I’ve mentioned. It’s altering immune tone, microbial ecology, again, the health of the microbiome and liver metabolism all. Which influence cholesterol behavior. So when lipids rise, it’s not random.
It’s the result of a system that’s recalibrating. And this is what we call systems biology. This is looking at all the systems and how they crosstalk to one another. So before you start thinking this aging thing sucks, and I’m sure you’ve already been thinking that through this whole podcast, okay.
And asking why is all of this happening? I want you to really think about, perhaps this is evolution at its finest. Okay? So think about this. When fertility declines, when you’re out of the childbearing ages, the body may shift from reproduction to survival, right? So we go from, okay, I’m done having babies.
Now it’s all about how do I stay alive in this crazy world? Okay, what happens is again, from an evolution perspective, the stored belly fat actually provides rapid energy access. So if you think about in times of famine, that would’ve served us very well because we would’ve had readily stored energy available.
It also protects the vital organs. It can support immune resilience. And so we think of like cholesterol as stabilizing the cell membranes. It serves as a steroid precursor, so it helps make steroids, it does support repair. So if you think about in ancestral environments, again, in our, ancestors, this shift may have been protective and it likely was, but if we now fast forward in a modern environment.
When there’s chronic stress, ultra processed food, sedentary lifestyle, this evolutionary adaptation becomes maladaptive. It becomes a problem. So what do we actually do? We can’t stop this from happening, but how do we move the needle on this? So if your cholesterol is rising during menopause. First, don’t panic.
Okay? Please don’t panic and don’t rush to just go get a statin. That’s gonna make all of this actually much worse because statins impact blood sugar in a negative way. They impact muscles in a negative way. Whole lot of stuff goes on with that. Okay. And it’s not gonna necessarily protect you from cardiovascular risk because statins don’t always impact those small, dense particles.
So don’t panic, okay? And don’t reduce this to, like I said, just take a statin or just cut out the fat, because as I mentioned, doing either of those, just cutting out fat, you’re eating well, that may help if you’re eating a high fat diet, but it’s certainly not going to fix this whole problem. Okay. And we don’t treat that cholesterol lab number in isolation because cholesterol, as I mentioned during menopause, is not a morality test, okay?
It’s a metabolic signal, and when you understand the signal, you get leverage. So let’s talk about where that leverage lives. Number one, first and foremost, preserve and build your muscle. Yeah, everybody thinks you, especially we, there’s a lot of talk about the GLP ones and you know how important it is to build muscle.
Yes. But it’s also, that’s part of this whole conversation. Again, if you don’t have muscle and you’re on a GLP one and you’re going into menopause, this is like your metabolic time bomb. So if there’s one intervention I want women to take serious in midlife, it is resistance training. Muscle is your metabolic insurance.
It improves insulin sensitivity, it improves glucose disposal, it improves mitochondrial efficiency. If you’re that person who’s always tired, guess what? The more muscle you have, the less tired and fatigue you are, and it improves how your body handles lipids, those fats. When you build and preserve muscle, you are gonna lower your insulin levels and when insulin comes down, the fat in the liver.
Decreases the production of the fat in the liver decreases, and that will directly impact triglycerides. VLDL and small dense LDL. So you see there is this cascade of action. So this is less about aesthetics and more about metabolic infrastructure. How do you create that metabolic foundation? You need two to four.
Resistance sessions per week. I’m gonna tell you it’s at least three to four, right? I would say two on the low side, four to five on the high side, and it meaningly. You will see. It will mean that in and of itself can meaningly meaningfully shift your lipid dynamics. And we wanna think about a number two, addressing insulin early.
If you’re fasting insulin, and this is why not just mes measuring glucose and not just measuring hemoglobin A1C is so important. You need to look at insulin fasting insulin. You need to look at C peptide. We need to look at some of these numbers that show the trend. So if fasting insulin is creeping up, if your triglycerides are going up, if your waist circumference is increasing.
Don’t wait for the 30, 40 pounds to come on your waist. Okay? When it starts to go up, this is your cue because again, insulin, higher insulin is going to drive the liver to make more fat. Period. So the earlier you improve your insulin sensitivity, the less pressure you put on your liver to overproduce triglycerides.
And so that point being, there’s so many more women that I know of that are being diagnosed with what we call non-alcoholic fatty liver disease. So it’s not the alcohol that’s driving liver disease, it’s all of the stuff I just talked about. So you wanna think about that? How do we improve insulin sensitivity?
You wanna do protein forward meals, but you don’t wanna overdo the protein because guess what? When you have protein, typically in an animal product, protein carries fat. There’s always gonna be the fat associated. So you wanna just be careful that you’re not overdoing the protein. People who are recommending a gram.
Per pound of body weight for women, it is much too high. Unless you are in the gym two hours a day, five to six days a week, you do not need that much protein. Okay. Protein is all about structure, creating muscle structure. It’s the glucose, as I mentioned. Glucose is a meta, is a sink, sorry. Muscle is a sink for glucose.
The more glucose you have, the more muscle you have, the more glucose it will absorb. So it’s less about the protein. You wanna think of 0.8 to one gram. A protein per kilogram of body weight. How do we get there? Figure out your kilograms by dividing your weight and pounds by 2.2. Okay? Weight and pounds by 2.2 times 0.8 to one.
That will give you your protein. I guarantee you it’s about half of the other. So think about that. You wanna add more fiber? I’m telling you. More fiber than the protein is going to matter. You wanna walk after your meals. This is a great way proven. To lower your, to increase insulin sensitivity. Okay?
Strength training, as I mentioned, reduce your refined carbohydrate. Everybody is I wanna be on a low carb. Low carb, no. Things like potatoes and root vegetables and even your fruit are super supportive. Get rid of the refined carbohydrates, the baked goods, the packaged goods, the crackers, that garbage, even things like pastas and rice, like your grains.
Do them minimally. Think about your root vegetables as your carbs, okay? And don’t wait for diabetes to show up, okay? Don’t wait for those. Get proactive on where your numbers are. And of course, last but not least, improve your sleep. Sleep, and stress. Okay, go hand in hand here. And we have got to pay attention.
Sleep. I will say everything backs into sleep. When you hear me talk, I always talk about sleep. If your sleep is not spot on or you’re not getting 7, 8, 6 and a half to eight hours of sleep, we gotta talk. Okay? And remember, respond. When you see the first whisper, I always say, your body whispers. Don’t wait for the roar.
Roar. My friend Sherry Coon said that, dunno who said it before, but I love it. And your body is talking to you. You need to pay attention. How do we reduce visceral fat? This is a big one. Everyone wants to know. And how do we do it strategically, it is not about crash dieting and it’s not about eating less because guess what?
Crash dieting raises choles cortisol. So if you’re crash dieting and you’re eating less, guess what? Your cortisol’s going up and this whole thing is gonna backfire on you. The goal is to stabilize blood sugar. Give yourself adequate protein. Again, like I mentioned, adequate recovery and stress. Nervous system regulation is going to be paramount.
Even a small reduction in visceral fat, five to 10% actually can in improve. Inflammatory markers and your lipid profiles. So we’re not chasing thinness. We are targeting metabolically active fat. And as I mentioned, sleep is a lipid intervention in and of itself. Sleep deprivation will increase something called IL six, interleukin six TNF, alpha cortisol and insulin resistance.
It is a metabolic nightmare when you do not sleep. As I mentioned, less than six hours of sleep consist consistently is associated with worse triglycerides and a higher inflammation burden. So again, sleep alone, just improving that can improve lipid metabolism, and that is physiology people, right?
Visceral fat. Let’s talk about stress. Visceral fat is highly responsive to cortisol. As I mentioned, it’s really sensitive to cortisol and midlife and is often for so many women. The highest stress load in a period of a woman’s life. Caregiving career, aging parents, teenagers, hormonal shift. Stress is not just emotional, it is biochemical.
So think about breath, work and boundaries. I talk about boundaries all the time. It is so important. Stop being the people. Pleaser. Okay. Sunlight, exposure. Parasympathetic. Parasympathetic activation. Things like breathing. Being in nature, those things calm down the nervous system and trigger what we call parasympathetic activity.
Those are metabolic interventions, so slowing down, calming down, loosening the res on control is gonna be a metabolic intervention because if cortisol stays elevated, visceral fat is more likely to expand. We wanna think about supporting the liver and the gut. Cholesterol leaves the body through bile acids.
That means bowel regularity matters. You need to be pooping regularly if you’re constipated. This is a problem. Fiber matters. Microbial diversity matters, and hydration matters more than staying hydrated is going to be so important, and oftentimes it’s not just water. So don’t go run out and get those, electrolytes that have all the natural flavors and the colors and too much sodium.
Most of them have too much sodium. You can use a little bit of a natural fruit juice, press your own orange juice. Little bit of OJ in, two ounces of OJ in. 10 ounces of water, so it’s diluted. Use coconut water. Coconut water is one of the best. Electrolyte replacers, little bit of coconut water.
As a matter of fact, I have mine here. This is a little bit of coconut water in here, and then the rest is water. And I drink that multiple times throughout the day, okay? Because if bile acids are not efficiently metabolized then and excreted, your cholesterol clearance is going to decrease. Okay? So think about the gut liver access.
Again, it is not just, on the side here, okay? It is central to lipid metabolism. And then if you have done all of these things and you’re still not feeling the way you want, you’re not seeing any movement, you can. Carefully consider hormone therapy, but it needs to be thoughtfully done in the appropriate candidates.
We can see hormone therapy improve. Improve LDL receptor expression, improve HDL function, reduce central fat, improve insulin sensitivity, but it’s not for everyone. And again, if all the stuff that I just talked about isn’t addressed, hormone therapy will never fix it alone. So when it’s used thoughtfully.
Particularly closer to menopause onset, it can be metabolically protective. So this we think of as individualized medicine. It’s not a blanket prescription, and you want to measure what actually matters. As I mentioned in the blood work, LDL alone doesn’t tell the whole story. You wanna look at your A POB, your triglycerides fasting insulin, HS high S-C-R-P-C reactive protein.
So it’s HS, CRP. Waist circumference. And remember, cholesterol particles matter more than total concentration. Context matters more than fear. Don’t let your medical practitioners scare the shit out of you oh, you’re gonna have a heart attack if you don’t go on a statin. If there’s nothing else you learned from today, it should be that is not the case.
Okay, so if you are looking at higher cholesterol levels after menopause, it is not your body turning against you. This is your metabolism going help, help you are not broken During menopause. Menopause is actually exposing what’s been brewing inside insulin resistance, stress overload, muscle loss, and inflammation.
And guess what? Here’s the truth that no one’s saying out loud. You don’t fix this by fearing cholesterol. You fix this by building metabolic strength, build muscle, stabilize insulin, lower inflammation, support your liver, calm your nervous system, because I want you to know cholesterol isn’t the enemy.
And the other thing that I want you to know is if you drive cholesterol too low, if you aren’t a statin, and your cholesterol is less than one 50. Your metabolism is going through like metabolic shock. You need cholesterol to be able to do a lot of these things we’ve just talked about. If you are driving your cholesterol so low, guess what?
Your cells, the mitochondria, your cells need a layer of that cholesterol around it. Cholesterol helps do so many things in the body. It is not the bad guy. Actually, cholesterol is an antioxidant. It’s a it protects things in the body. So let’s stop villainizing cholesterol and let’s pay attention to the signals in our body, because midlife is not about a decline.
It is your metabolic wake up call, okay? And wake up calls can be super powerful if you decide to answer them. So I hope this information was helpful. Please reach out with any questions. We’ll probably do a live on this because there’s so much information to unpack and I look forward to answering your questions.
Make sure you check out some of our programs. If you wanna get tested. Our comprehensive blueprint is a great way to do that because it’ll give you all these numbers and then some, and you can get answers from me to help support you. Maybe you wanna listen to this again, make down, jot down some notes, share it, subscribe, like it, and enjoy it.
This is your rebel nutritionist signing off, everybody. Make it a great day. Okay?
