Ep. 517 The Hidden Heart Risks No One Talks About – A Masterclass on Women’s Cardiovascular Health
- Cynthia Thurlow
- 21 hours ago
- 27 min read
I’m excited to share a new AMA episode with you today, dedicated to risk factors specific to women.
In this AMA session, I dive into the lifestyle factors that influence lipids, exploring the latest research and discussing Lp(a) and ApoB. Rather than answering your individual questions, I have woven them into the overall outline to create a cohesive and informative conversation.
IN THIS EPISODE, YOU WILL LEARN:
How women’s lifestyle choices directly affect their lipid profiles
How knowing if you’re a hyper absorber or hyper producer of cholesterol will change your treatment strategy
What the Boston Heart Cholesterol Balance test will reveal about your body’s ability to handle cholesterol
The best treatments for hyper absorbers, and the best treatments for hyper producers
How hard plaque differs from soft plaque, and why that matters for women’s heart health
How the new AI-assisted Clearly scan provides a more complete cardiovascular risk picture than a standard calcium score
How chronic stress and elevated cortisol fuel insulin resistance and inflammation, and damage blood vessel linings
The benefits of Mediterranean-style eating for improving lipid balance, vasomotor symptoms, and overall metabolic health
The importance of managing trauma, stress, and emotional health in midlife
How my “n=1” experiment with Zetia and micro-dosed GLP-1s significantly improved my ApoB and inflammation markers
““Chronic stress raises cortisol, blood glucose, and insulin, so managing it proactively is critical.”
– Cynthia Thurlow
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Transcript:
Cynthia Thurlow: Well, I feel like this has been a long time coming. When I interviewed Dr. Tom Dayspring earlier this summer with an Ask Me Anything format, Dr. Dayspring very politely said, “Lifestyle management, lifestyle-related concerns are not really my area of expertise.” And so, because there were so many of you that sent questions in, I wanted to do a dedicated AMA that's going to talk about risk factors specific to women, that is going to talk a bit about the lifestyle piece and how it impacts lipids. We're going to look at research, we're going to talk about Lp(a) and ApoB and hopefully through the synthesis of this information, I'm not going to necessarily be calling out specific people's questions. I've just incorporated them into my outline so this can be a very cohesive conversation.
Again, for those that may or may not know, I spent 16 years in clinical cardiology, both inpatient management and outpatient management. And I know so much more now that I want to be able to make this actionable. I want you to be able to feel comfortable, confident, talking to your healthcare prescribers, practitioners. And we do have a PDF that I created in the aftermath of the amazing podcast, seven published podcasts. I have two additional podcasts that are still forthcoming with Dr. Dayspring that gives you a high-level PDF and so we'll make sure that is included in the show notes so that you will have actionable advice to take away and lab values and ranges and what we need to be looking for.
So, let's talk about risk factors in women because I think this is really important and transparently, I think most healthcare professionals are probably not saying to patients, like, as an example, if you had a really early start to menstruating or really late start, that in and of itself can be a risk factor for atherosclerotic cardiovascular disease. But for the benefit of listeners, I'm not going to say that mouthful every time. I'll just say heart disease and you'll understand what I'm referring to. So, let's talk about female specific risk factors for heart disease. As I mentioned, these can occur throughout the lifespan. So, obviously if you start your menstrual cycle really early, like a lot of young women are now, because women are getting breast buds, they're hitting sexual maturity a whole lot earlier than even my generation, subsequent generations.
I would say how do we define early? We're looking at like 7, 8, 9 years old. That's very early. I don't think I got my first menstrual cycle until I was 14. On the other side of that, we have some women that are not developing in that normal-- When I say normal, the normal distribution of the curve. Looking at the age range, young women that don't start a menstrual cycle to their 16, 17, 18, that does happen, although probably less so now. If you have a history of polycystic ovarian syndrome and as Dr. Heather Hirsch said recently, “This is really a spectrum.” Like obviously I am thin phenotype PCOS. I have never been insulin resistant. I just had these anovulatory cycles. And that was a much more mild form of PCOS. I was thin phenotype.
But there are people that run the spectrum from that all the way up to people that are very insulin resistant, very inflamed, obese, metabolically unhealthy women that are also having abnormal hair distribution. We call it hirsutism. They may be also anovulatory, they may have a lot of acne issues, a lot of high androgen excess symptoms, infertility. I've got two of the three already. Anyone that is struggling with infertility issues that could potentially be a sign of PCOS, those anovulatory cycles, we know that many women that are metabolically unhealthy are in many instances also infertile. This is not my area of expertise. Let me be very clear. But we have a lot of male factor and female factor infertility right now, meaning it is not just a woman-related thing. Sometime it can also be for men.
And as Dr. Tracy Gapin has mentioned more than once on the podcast, one of the number one reasons for infertility and low sperm count is related to insulin resistance, endocrine mimicking chemicals. So that all matters, right? Spontaneous pregnancy loss, miscarriages, multiple miscarriages. If you've never had a child, that can also put you at risk. Adverse pregnancy outcomes like eclampsia, preeclampsia. These are people that sometimes have to deliver early. They have exceedingly high blood pressure during pregnancy. They may have a lot of protein in their urine. These are people that sometimes have premature infants because they're delivering at the very end of their second trimester, very beginning of their third trimester. I have a personal family friend, both of her children who were delivered under the pretense of hypertensive urgency. So, she was very sick during her pregnancies.
Lack of breastfeeding, which I know can be controversial. And I know some people, it wasn't that they didn't want to breastfeed, they were just physically incapable of breastfeeding. But we know that breastfeeding can be very protective. Looking at long-term outcomes and then early menopause, defined as the longer you go without hormones, specifically estrogen, progesterone, testosterone, the more likely you are to suffer the long-term effects. So, if you have premature ovarian insufficiency, you have an autoimmune condition, hopefully reversible. But if you're no longer menstruating and you're in your 30s, that's a poor prognostic outcome. Doesn't mean that with hormone replenishment and it is indeed replenishment, it's not just replacement.
Because if you're 36 years old and you've gone into early menopause, that is very different than a 52-year-old who's been able to have an additional 6 years of hormones prior to going into menopause. So, like early menopause, whether it's before 40, before 45, really, really important that you're having conversations with your prescriber about hormone replenishment. And then anyone that has chronic inflammatory conditions. So, looking at the autoimmune, things like lupus, rheumatoid, all of which can just put us at a higher likelihood of not just endothelial dysfunction. And endothelial dysfunction is the internal lining of the blood vessels, which is exacerbated by a loss of estrogen, loss of nitric oxide signaling. I've done many podcasts on some of these topics, around these topics, including solely dedicated to nitric oxide.
So, crossing my fingers that by the time this is published, we're going to have lots and lots of resources for everyone to be able to better understand some of these concepts. And one thing that I always like women to understand is that we don't present as typically as men. So, men may get the crushing chest pain, they may get short of breath. Women tend to present differently. We have different anatomy. We tend to have small vessel disease. That means the types of vessels that cannot be stented. It may also mean that we have more collateral circulation, meaning that our body has developed a network of blood vessels around the occluded or reduced blood flow of specific arteries but women present differently.
I used to say that I had a patient, gosh, this is like 30-- almost 30 years ago and she was a nun. The only symptom she had when she presented to the ER was that she had pain in her hand. And it was just such an odd symptom that I took it really seriously. I remember I was at triage, brought her back, got an electrocardiogram, which is an EKG, and sure enough, she was tombstoning, which for anyone that's listening, that's in healthcare, they know that's a pretty bad outcome, a bad sign of a pretty significant blockage in a heart valve and heart vessel. And so, she went right to the cath lab, got stented, and did really well.
But most women will present with things like fatigue, or you might just be short of breath, or you may just feel like you have less exercise tolerance. I've even had women, and especially if you're not metabolically healthy, if you're diabetic, you're not going to present with the same symptoms. So, anything that feels like an adjustment in your energy or exercise tolerance or breathing needs to be evaluated. Do not pass, go urgently to have that evaluated if it's an acute issue. But there's also not as much research on women and I think we've talked about this on the podcast, that there was a period of time where women were just considered to be-- They didn't want to do research on us. Whether it was the confounding factors of having a menstrual cycle, having to control for where women were in their cycle.
There has not been enough research done on women. So, the research that has been done is certainly not where it needs to be. And so, I know there's lots of incredible researchers and clinicians at big academic centers that are pushing for this. Women are more likely to have decreased blood flow or ischemia from nonobstructive coronary artery disease, which I talked about. We tend to have more vasospastic symptoms, which means the blood vessel just kind of spasms. So, imagine you've got a cramp in a muscle, but instead of a cramp, it's a vasospasm. It's like a cramp in a muscle, but instead you're getting in a blood vessel. Women are much more likely to have specific types of cardiomyopathies, which is a weakening of the heart muscle. There's something called takotsubo, which is a Japanese term that I think it's octopus.
The shape of an octopus is what the heart can look like on ultrasound and echocardiogram and that can be stress induced. They call it broken heart syndrome, takotsubo cardiomyopathy. Big fancy way of talking about stress-induced muscle weakness. Generally reversible, but obviously for a lot of women, I used to see a lot of women that a loved one died, their spouse died, maybe they lost a child, maybe they just went through a really stressful illness, surgery. Same thing with a loved one. Maybe they lost their job. Just a stress-induced insult to the myocardium, which is the heart muscle. And so again, generally reversible, generally followed very closely by cardiology, usually involves an echocardiogram, which is an ultrasound of the heart, as well as other types of diagnostics.
The biggest thing that I can say is we need more research, and so hopefully that is forthcoming. When we're talking about specific hormones and the heart, I always think a lot about estrogen. Estrogen is really important for many things in our bodies. But we know that our lipid profile starts to shift and we'll talk about that in a minute. There's actually a really good research article that I will make sure is incorporated in this podcast episode notes, so that you have that talk specifically about what does the research say about the menopausal transition and what that looks like for our lipids, but understanding that estrogen has a lot of effects on our lipids. And so, with that loss of estrogen, we start to see things sliding sideways.
And so estradiol is the predominant form of estrogen our bodies make in our ovaries prior to menopause. And then we have fat tissue which also produces a weaker form of estrogen called estrone. And I always say that our body, although frustrating, we start to have shifts in body composition in menopause or that perimenopause to menopause transition, it is really our body's way of finding a solution to your problem. There's less circulating estradiol, so our body's trying to make more in fat tissue. There's not one woman I know who loves the fact that they tend to have shifts in body composition at this time in their lives, but that estrone is a byproduct of adipose tissue and it's our body's way of looking for a solution. And interestingly, I think about why estrogen is so important. It is heart protective.
I've talked about this interrelationship, interplay between nitric oxide production, again, our ability to dilate and ensure that those blood vessels stay flexible. One of the things that happens with age, if you're not on hormone replacement therapy, not metabolically healthy, you tend to get stiffer. It's almost like a stiffer garden hose if you want to think about that way. Like I know when we have our outside garden hose, it is very stiff, right? It's hard to like compress it versus like a silicone straw in your house is easily compressible. And it's the same kind of thing. As our arteries get stiffer with age, we are more likely to experience the sequelae of endothelial dysfunction as well as high blood pressure. In fact, I'm embarrassed to admit this, but I'm going to say it and admit to it. Know better, do better.
I used to tell my patients it was completely normal to develop high blood pressure or hypertension with age. And it has a lot to do with that stiffer arteries, like more pressure that your body has to pump blood out against, the more likely you are to develop high blood pressure. But now understanding it is a byproduct of some of these hormone changes, loss of nitric oxide, loss of metabolic flexibility can all worse than that. So, let's talk about the effects of changes related to lipid panels. I think it's probably a good time to mention this. And I am looking at a Frontiers in Pharmacology 2022 study. The effects of menopause hormone therapy on lipid profile in menopausal female, a systemic review and meta-analysis. So, this is looking at a lot of data, 73 eligible studies were selected. The results showed that--
So, let's back up. The things that happen in menopause, we see increases in total cholesterol, we see increases in LDL, Lp(a). We know that oral menopausal hormone therapy led to significantly higher triglycerides compared with transdermal. That could be for a couple different reasons. But the benefits of low-dose hormones on triglycerides were also concluded when comparing conventional dose estrogen. So, the things that I think about is menopausal hormone therapy can help offset some of these changes which includes like higher total cholesterol, higher LDL, higher Lp(a). If you're losing insulin sensitivity, it would not be surprising to see an alteration in triglycerides. And just remember that if you are not metabolically healthy, very likely your HDL will be lower. We want to see it greater than 55. Our triglycerides will be higher.
And Dr. Dayspring and I are in 100% agreement that your triglycerides should be less than ideally as low as possible. But if you look at conventional numbers, they'll say less than 150. And I would say by the time you're at 150 mg/dL of triglycerides, you're already becoming insulin resistant. So, I actually like to see that number less than 70, ideally less than 50. I think the last time I had my lipids looked at, my triglycerides were fairly low, like in the 40s. And it's not that I'm carbohydrate restricting, it's that I am adding muscle and that's helping with insulin sensitivity. So, this article talks about how hormone replacement plays a positive role in lipid profiles and menopausal women. There's some controversy as I look at the literature about oral estradiol versus transdermal.
I think a lot of that really depends on the individual. Anytime you're taking a hormone orally, you get a first pass effect, which means that your liver gets the first go at breaking down that estrogen metabolites. And so more often than not, transdermal, which is skin absorbed estrogen is more efficacious, generally better tolerated. The other thing is when you're taking oral estradiol, again, that's the bioidentical. We're not talking about conjugated equine estrogen or Premarin as it's probably more popularly known. We're speaking specifically to oral estradiol. For some people, they actually need oral estradiol to get their estrogen levels therapeutic in the blood. And that's a whole separate tangential conversation. But I think this is a very bio-individual choice.
I think, like for myself, I use transdermal estrogen and that gets my estradiol levels high enough, based on the research, to be able to confer bone protection. And that is very important for me because I'm already osteopenic. There's also a history of osteoporosis in my family. I'm a thin Caucasian woman. There's nothing I can change about those two facts other than working diligently to ensure that my bone stay strong. And in fact, both by recent DEXA and REMS, which Dr. Doug Lucas will be talking about, we have a two-part podcast that's coming out in November and we'll be talking about REMS and what that is. So back to what this is showing. Hormonal replacement therapy is beneficial for lipids.
And so it's interesting, this is really looking at multiple studies that have been done again on higher levels of total cholesterol, LDL, triglycerides, Lp(a), also with a decrease in the level of HDL. All of these can put us at greater risk for developing heart disease and so again precipitated by this loss of ovarian function, ovarian senescence. Menopausal hormone therapy has been shown to have a favorable risk benefit ratio for women without abnormal lipids who underwent treatment at age under 60 or within 10 years of menopause onset. That's important. It says a meta-analysis conducted in 2001 concluded that hormones could decrease the levels of total cholesterol, LDL and increase HDL. A review performed in 2017 showed that hormones significantly decreased Lp(a) concentration.
I think I recall from previous conversations with Dr. Dayspring that estrogen acts as a very mild PCSK9 inhibitor. Now, this is a specific type of drug therapy that is generally not covered by insurance criminally and has been shown to be beneficial for those with elevated Lp(a), which is again a genetically mediated aka not lifestyle mediated marker for increased risk of atherosclerotic heart disease. I've talked about how Lp(a) is really important. Everyone that's listening to this podcast needs it done at least once. If you have a borderline Lp(a) prior to menopause, it probably is worth it to do it again. What's interesting is 20% of the general population has elevated Lp(a) doesn't know it. 50% of African Americans. So, if you are African American, you absolutely positively need this drawn. Actually, everyone does.
I personally, as I very transparently have shown, I could not do a better job with lifestyle. This is all genetics. We know that my husband has elevated Lp(a), I do, my younger son does. We need to figure out if my older son does. Again, it's genetics. It's inherited. And that's why it's even more imperative that women are not waiting until menopause to have these labs drawn. Because if you know at 25 or 30 or 20 that you have elevated Lp(a), it means it is critically important for you to ensure that you remain as metabolically healthy throughout your lifetime as possible to decrease the likelihood that you will go on to develop heart disease. Lp(a) is seven to eight times more atherogenic than other lipid abnormalities. And that's important, really, really important. Okay.
To date, long-term effects of hormones or different routes of administration of estrogen on the lipid profile were scarcely reported. In addition, it has been shown that both the dosage and type of progesterone are of great importance for these lipoprotein fractions. And then it goes on to talk about the Women's Health Initiative and conjugated equine estrogens and medroxyprogesterone acetate, which we know is not equivalent, is not bioequivalent to progesterone. So, we scoot that information out. So that again-- this research article will be available for you all in the show notes.
I want to talk a little bit about Lp(a) because so many questions came in on Lp(a) and I think there's still a lot of confusion. So, we've talked before about how Lp(a) is an independent risk factor for heart disease as well as a valvular issue called calcific valvular aortic stenosis. For anyone that is in medicine, critical care medicine, cardiology, pulmonology, you understand that aortic stenosis is a bad thing. So, as that valve gets stenotic and narrows, it can create other heart problems, can create a lot of symptoms. And we know that Lp(a) levels typically do not change after 5 years of age except during times of significant inflammation.
So, if you are going through a recent illness, you have liver or kidney disease, you might not be able to interpret those results as readily. Current guidelines support once in a lifetime measurement. Emerging data appear to show a strong correlation with high-sensitivity CRP levels for predicting cardiovascular disease risk. My high-sensitivity CRP is always low, thank goodness. This is a really good research article that's really going over current research on this. An estimated 20 to 25% of the world's population is believed to have elevated levels. That's consistent with what I said earlier. They're genetically predetermined. Studies have shown that inflammatory conditions, pregnancy, which no one's going to address this in pregnancy, [unintelligible 00:22:56].
Hypothyroidism, so, if your thyroid's not being properly managed, if you're taking growth hormone therapy that can elevate it, or if you have chronic kidney disease, Lp(a) levels are decreased in the settings of severe acute phase conditions. They can go down with hormone replacement therapy. Hence checking levels at steady states is advised. So, if you're going through an illness, that is not the time to check it, and that's pretty much for most lab work.
So, we know it's an independent causal risk factor for heart disease as well as aortic valve stenosis. And I'm not going to get into the biochemistry of this because it's a little bit complicated. We want to see levels less than 50 mg/dL and that's based on American College of Cardiology, American Heart Association guidelines. Less than 30 mg/dL is considered to be normal. 30 to 50 mg/dL is intermediate and greater than 50 is abnormal based on the European Atherosclerotic Society consensus statement. And greater than 50 mg/dL is accepted as a risk enhancing cutoff in the National Lipid Association scientific statement. So, you'll see that there's kind of some overlap.
Interestingly enough there's a couple studies that have not provided sufficient Lp(a) level reduction except for the PCSK9 inhibitors which are very expensive, still not covered by most insurance companies. And when I say expensive, I think even the oldest one, which is Repatha, is like $600 a month. There was a study called the Odyssey. So, it was evaluation of cardiovascular outcomes after an acute coronary syndrome that was a trial with one of the PCSK9 inhibitors indicated an approximate 23% reduction in Lp(a). And then there is another study that was also done. What's interesting is a lot of knee jerk reaction in traditional allopathic medicine is just to prescribe a statin which actually can elevate the Lp(a) even further. Zetia reduces Lp(a) by 7.6% according to the findings of one meta-analysis.
Other drug therapy like bile acid sequestrants, fibrates, and niacin you might see very negligible. I think in this study it talks about niacin decreases Lp(a) by 23% but you actually have to take quite a bit of niacin and niacin tends to be self-limiting. Meaning when I used to prescribe highose niacin therapy, a lot of people get very uncomfortable having-- they call it niacin flushing. I'm on low-dose niacin and I don't tolerate more than what I'm currently on. But it says here niacin decreases Lp(a) by 23%. It's not recommended for use because it lacks mortality, morbidity benefit in patients at risk for heart disease. Bempedoic acid, which we'll talk about in a minute, is relatively new, appears to slightly increase Lp(a) levels by 2.4%. So not something that we would use as well. But this is a really interesting article.
Again, an update on Lp(a). The latest on testing, treatment and guideline recommendations. This is from September of 2023 American College of Cardiology. We will also link this in with the show notes as well. Just as a resource and then there was another paper that was actually a review article from the Journal of Cellular Physiology. This is from 2019 and it mentions in here because there's always people asking like I don't want to take drug therapy. And this is not judgment one way or another, but this is talking about options for natural products. So, in severe several preclinical and clinical studies as well as meta-analysis natural products including L-carnitine, CoQ10 and something I cannot pronounce that I think must be, it is Xuezhikang were known to significantly decrease Lp(a).
Other natural products such as pectin, which would you get like apple pectin, ginkgo biloba, flaxseed, red wine, resveratrol and curcumin can also reduce Lp(a), but to a lesser degree. Aforementioned natural products may represent promising therapeutic agents for Lp(a). So, something that is probably worth considering but having conversations with your healthcare prescriber. I emphasize prescriber because I want to be very clear that if you have lipid abnormalities you want to be working with someone that actually can prescribe medication, not just do lifestyle. I think both are very important. Obviously, you know Lp(a) is this challenging piece because it is genetically mediated and I know a lot of you have shared with me that you have elevated Lp(a). I would say lifestyle has little to no impact. But that doesn't mean the lifestyle is not important.
It just means you're probably not going to get much bang for your buck. But it is still important for the lifestyle piece. Maintaining muscle mass, eating an anti-inflammatory diet, making sure you're sleeping, making sure you manage your stress, consideration of hormone replacement therapy because you don't want to set yourself emotion to developing diabetes or even insulin resistance which will put you at greater risk for the sequelae related to this more atherogenic lipid abnormality. ApoB is one of these things that can be impacted by lifestyle, unlike Lp(a). So, there's things that you can think about if your Lp(a) is high, your LDL is probably high. I think that maintaining metabolic flexibility, making sure you're not insulin resistant.
Everyone should know their fasting insulin level. You want it somewhere between 2 to 5 mg/dL. You can also reduce your carbohydrates which can impact your triglycerides if those are elevated. Understanding that the lower your triglycerides the lower your ApoB burden will because you have to traffic fewer triglycerides with the cholesterol. So, think about it as little boats. I've done two podcasts with Dave Feldman and his analogy about boats and cholesterol. I think it's very helpful. You can also cut saturated fat. Like I personally don't consume a lot of saturated fat. My ApoB is much lower now. I think it's down to 60 mg/dL. Some of that is Zetia, some of that is eating less saturated fat.
So, really a monounsaturated diet, things like olive oil are going to be more efficacious for me than coconut oil or a lot of fatty meat. We know that if we have fewer LDL in circulation, we generally tend to have lower ApoB levels. And if you're on both a low-carb diet, which can be defined different ways, it doesn't necessarily need to be a ketogenic diet, but it could be the average Americans consuming 200, 300 carbohydrates a day generally from processed foods. But even if you get it under a 100 g of carbohydrates, sometimes that can make a big difference. Maybe under 75. If you have lower carbs, lower saturated fat, that should help with your ApoB. So again, like this is an instance where ApoB can be mitigated by lifestyle quite significantly.
I think it's really important for people to know that if your ApoB is elevated, it's really helpful to do that Boston Heart Cholesterol Balance Test and you can determine whether or not you're a hyper absorber, which is what I am, or hyper synthesizer. I think sometimes those things get magnified in the perimenopause to menopause transition. Zetia works really well if you just absorb too much cholesterol like I'm just like a little sponge. And that's why those saturated fats for me are not ideal. It doesn't mean that I never consume saturated fat. I just don't do a lot of it. I tend to do leaner meat, lower fat diet. Lower fat doesn't mean no fat.
And when we're talking about the Boston Heart Cholesterol Balance Test, things to keep in mind, if you are a hyperabsorber, you definitely want to increase your fiber intake, especially pectin products. You can add in Zetia, as I've talked about before, that's also called ezetimibe. And then if you're a hyper producer of cholesterol, you can look into supplements like berberine, bergamot, red yeast rice, or even consider a statin although I know many of you are not interested in taking even a low-dose statin, I think it's really important that whether you're a hyper absorber or you are a hyper synthesizer that you consider things like garlic extract, CoQ10, and even essential fatty acids. Those were the Omega-3s.
I just tend to concentrate more on carbs and protein for me personally. But if you're a hyper-synthesizer, then taking Zetia is not going to beneficial. You might actually do better with either a plant sterol like red yeast rice, which is like a plant-based version of statin, or considering low-dose statin therapy. Now I know many of you have made it very clear you don't ever want to take a statin. But I think that my conversations with Tom Dayspring have really like reaffirmed for me that there are definitely people that do benefit from a very low dose-statin and have little to no side effects. And go back to some of the podcasts I've done with him. There's specific labs that you can look for to see who's at most risk for developing some of the neurocognitive effects of statins if a particular sterol is low in your body.
I'm thinking specifically about Zetia. Zetia is easy tolerate. It prevents you from reabsorbing cholesterol. It acts in the very specific place in the gut and is not a systemic drug. So, for a lot of people, they do really well with that. One thing that I want to make sure that we talk about, other than modifying saturated fat if you're having issues related to high ApoB, is that the bulk of our fats I think should come from monounsaturated fats. And those are the olive oil and nuts and seeds. Like when you really think about a Mediterranean diet, there's a lot of good research on how the Mediterranean diet actually will ameliorate vasomotor symptoms and improve body composition in middle-aged women. I think for a lot of people having fruits and vegetables and lean proteins, lean fish is generally pretty well tolerated.
And I think about just physical activity in general. I think many of us just get more sedentary as we get older. And the importance of not just strength training but also just being active, like tracking your steps. Like how many steps are you getting over the course of every day or over the course of a week? Obviously, I do a lot of business travel. Some days I get all my steps in, some days I don't, I don’t beat myself up about it. But I think that diet, exercise are important stress. I think for a lot of people they understand that chronic stress can impact our sympathetic nervous system, which can lead to higher cortisol, which I've talked a lot about how cortisol it's not a bad hormone, it gets a bad rap.
But chronically elevated cortisol overtime can degrade our immune system, can lead to leaky gut, can raise our blood glucose and correspondingly our insulin levels. It can also have effects on the endothelial lining of our blood vessels. And I think really managing stress is important and this is something we unpack and talk about on the podcast quite a bit. But those lifestyle pieces are still very important. I think for a lot of people they're just like, “Oh, I don't need to worry about stress.” And I'm like, “We are less stress resilient.” So, I think it's really, really important-- I think it's really, really important for us to have these conversations. Let's talk a little bit about evaluation of risk for heart disease.
I used to talk a lot about CACs. CACs are coronary artery calcification scores. It's interesting about 15% of people who have a zero score, it's actually false negatives. That's concerning. So, people walking around saying I have a negative CAC, I have abnormal lipids, my CAC is normal or negative. About 15% of us actually that's-- a false negative is actually concerning. People sometimes then go on and do a CT angio and it has finer slices. So, you can get more information from a CT angio than you can from a CAC. You may also see evidence of soft plaquing, which is the differentiator. Like CACs look at hard plaque, CT angios look at soft plaque. But I'm starting to evolve and I think that there's another test that I think is actually even better if we're really wanting to get cardiovascular risk assessment. It's called Cleerly, C-L-E-E-R-L-Y.
So, that coronary artery calcification score does not provide a complete picture of our actual state of heart disease. A score of zero means there's no calcified plaque. But you can still have other types of plaque like soft plaque and Cleerly and I'm reading this specifically from their website, I went last night to pull it so that I could identify what it is. It's AI-assisted CT angio. So, it takes artificial intelligence and takes a CT angio and it's like AI and CT angio had a baby. And this is Cleerly. It's different from calcium score because it provides a more comprehensive report that shows all types of plaque buildup and the difference between high and low risk plaque.
The analysis is a thorough evaluation of the presence, amount and type of plaque and the heart's arteries based on a heart scan called a coronary CTA. The Cleerly software, it's a set of artificial intelligence-based algorithms and translated into measurements and reports for review by your prescriber. They give a clear understanding of how much plaque are in the arteries. I think that it's important if you have high Lp(a), you have a bad family history, maybe you aren't on HRT, maybe your lifestyle is not dialed in. This might be a helpful diagnostic test. Now, transparently this is not always covered by insurance. I think Cleerly and their manufacturer are working diligently to change that.
But I think for a lot of people, it's helping them understand that if they're really trying to get a better sense of what's going on, this might be a better test. I've talked to my provider about it. He said because I'm not symptomatic, it might not be indicated yet. And so, we're just watchfully waiting. But lastly, I want to just run through some of these drug therapies. I've talked about Zetia, it blocks the hepatocytes and enterocytes of the gut, so the liver cells, gut cells and it prevents reabsorption of cholesterol. And it's generally really well tolerated. Although, I have had patients that have taken Zetia and have gotten the same symptoms that they had from statins, although mechanistically, they work very differently.
There are PCSK9 inhibitors like Repatha, that's probably the best known one, generally not covered by insurance, but has been shown to reduce Lp(a). And then there's a drug called bempedoic acid, which is actually a pro drug, which means it has to go to the liver and get activated. And then in the liver, it's a cholesterol synthesis inhibitor and it inhibits cholesterol synthesis in the liver, whereas statins do so throughout the body. So, it is a drug that acts just on that organ and not systemically. And so, it's a little less potent than a statin and but it's more selective. So, depending on who you're seeing for your lipid abnormalities, it's always and should always be lifestyle first.
Obviously, a lot of the questions that I received, which I literally have sitting in this pile in front of me, I think the big thing is HRT, we know can be helpful. Maybe not as much for Lp(a), which again, is this genetically mediated, but it is a mild PCSK9 inhibitor. I think for a lot of people it is the lifestyle piece that needs to be foundational. So, again, I'll go back like seven to eight hours a night of high-quality sleep, making sure you're physically active, strength training, moving your body daily, tracking your steps. Mediterranean diet seems to be the one that is mentioned most often, but it's really just speaking to a less processed diet. If you are insulin resistant, not metabolically healthy, then it may be beneficial for you to go on a lower carbohydrate diet.
I know for some people that like obliterates their fun foods, but less-processed carbs are going to better. A sweet potato is superior to a piece of bread. Having low glycemic berries are going to be superior to having like a gluten free cracker or gluten free tortilla. And it isn't to suggest that you never consume anything that's processed. It's just finding alternatives to things that you feel like you really need in your diet. When we talk about the microbiome, and certainly I got a lot of questions about the microbiome, the health of your microbiome is critically important for the health of your body. It's not just the gut. It's every microbiome in the body. Oral microbiome, vaginal microbiome, lung microbiome, skin microbiome, they're all interrelated.
They're not existing as a siloed vacuum like traditional allopathic medicine would like for us to think about. But I think for a lot of different people it's understanding that hormone replacement therapy, managing our stress, eating an anti-inflammatory diet, not too much exercise, doing things that bring you joy. Oxytocin is not emphasized enough. And I think for a lot of people, like oxytocin is one of these things that you get from hugging a loved one or hugging your pet or your kids or a good friend, that lowers cortisol, which lowers our stress levels.
And so, really speaking to the fact that it always goes back to these core tenets, the other thing that I would say is if you are not addressing underlying trauma which leads to chronic cortisol activation, chronic sympathetic dominance, etc., that's another piece. Whether it's finding a trauma informed therapist. I feel like for a lot of women when they get into perimenopause and menopause, if they haven't dealt with their stuff, it has a way of making sure you address it. Whether it's the higher rate of divorce. I think the statistic I was looking at the other day, it was of women in perimenopause and menopause, we initiate 70% of the divorces. So, men really don't want to get divorced. And hopefully if you're navigating a tenuous situation with your spouse or significant other. Sometimes couples therapy can be helpful.
Sometimes doing your own therapy separate of your significant other can be helpful. And I just mentioned that because I think it's important to understand that there's a lot can contribute to how we navigate the transition of perimenopause to menopause. Some things we have control over, others we do not. Obviously, we can't control what we grew up in as children, but we can control our relationships with others, our relationship with ourself, managing our stress in a proactive manner. And I jokingly say it's not five minutes of meditation once a day. So, keep your questions coming. I hope this has been helpful. I have two more podcasts coming out with Dr. Dayspring that will be out before the end of the year.
We are stockpiling podcast episodes right now ahead of the book launch, just to ensure that I have a little bit of bandwidth to be able to do quite a bit of travel and other people's podcasts and doing press and things for the book. So, thank you as always for your questions. I tried to incorporate as many questions as I could into the content that I went over. We've covered a lot today. We've talked about risk factors. We spent time reviewing some relevant research. There is a PDF that I created from my conversations with Dr. Dayspring. We talked about how estrogen is really instrumental in upregulating or downregulating our cardiovascular disease. We talked about CACs versus CT angios versus Cleerly. What we need to be looking for, a little bit of drug therapy because I know many of you are adamantly opposed.
And that's why I transparently say, like I am on Zetia. I've been on Zetia that dropped my ApoB precipitously. And now it's like 60 mg/dL. And I think at one point it was easily double that, my Lp(a) we're waiting to see my response to microdosing GLP-1s. And let me be clear. There's been mixed experiences when I've talked to other prescribers about this. Some people have had great results, some people have had no results. There's definitely a reduction in inflammation in my body because it was never the intention to lose weight. But I've lost some body fat, which clearly was inflammatory body fat, and that is a byproduct of taking the GLP-1s. So, the N of 1 experiment continues. Obviously, I will transparently share with you what my repeat Lp(a) looks like.
We'll probably do labs before the end of the year and I'll be happy to share my N of 1 results. I appreciate each and every one of you. It is hard to believe it's almost the end of 2025. It's been a heck of a year, right? Appreciate all of you as always. Keep your questions coming. I love seeing them and my team does too.