We have the second part of our mashup on heart health today, featuring insights from Dr. Stephen Hussey and Dr. Thomas Dayspring on the real drivers of cardiac disease.
In this episode, Dr. Hussey challenges conventional views on heart disease. Dr. Dayspring dives into the key markers for cardiovascular risk and the essential role of lifestyle changes for heart health.
Join us for a fresh perspective on heart health.
[8:52] After experiencing a massive myocardial infarction, Dr. Hussey came to realize that chronic stress, metabolic health, and environmental factors play a far more prominent role in heart disease than is commonly acknowledged. Yet the medical system remains fixated on cholesterol as the primary cause of cardiac issues, ignoring evidence that both acute and prolonged stress can directly trigger cardiac events.
[22:11] Due to liability concerns and lack of approval, Western medicine operates within a rigid system that prioritizes standard treatments over potentially effective alternatives like intravenous magnesium sulfate for clot prevention. That limits physicians in exploring innovative approaches despite promising research.
[29:13] Dr. Hussey explains that metabolic heart attacks can occur without arterial blockages due to oxidative stress forcing the heart into an inefficient glucose-dependent state, leading to tissue death instead of cancerous growth. His insight challenges conventional views on heart disease that tie into the historical shift driven by the flawed research of Ancel Keys that vilified saturated fats while promoting processed vegetable oils.
[53:35] Heart attacks are often triggered by stress rather than just cholesterol buildup. Managing stress, along with metabolic health, inflammation, and nervous system balance, is the key to heart disease prevention, with fasting being beneficial across all three areas.
[00:02:33] APO(b) Levels are essential for assessing cardiovascular risk. Dr. Thomas Dayspring recommends an APO(b) below 80 mg/dL for general health and below 60 mg/dL for optimal longevity. He highlights the benefits of lifestyle interventions before considering pharmacological treatments, especially for those genetically predisposed to high APO(b).
[00:24:00] The loss of estrogen during menopause increases APO(a) protein production, leading to higher LP(a) levels. That can elevate cardiovascular risk, and factors like pregnancy complications, PCOS, and lipid issues can indicate future heart disease risk, making early monitoring and appropriate hormone therapy crucial for women's long-term health.
Bio: Dr. Stephen Hussey
Dr. Stephen Hussey, MS, DC, is a Chiropractor and Functional Medicine practitioner. He attained his Doctorate of Chiropractic and a Master's in Human Nutrition and Functional Medicine from the University of Western States in Portland, OR. He is a health coach, speaker, and the author of two books on health: The Health Evolution: Why Understanding Evolution is the Key to Vibrant Health and Understanding The Heart: Surprising Insights Into The Evolutionary Origins Of Heart Disease - And Why It Matters. Dr. Hussey guides clients from around the world back to health using the latest research and health-attaining strategies. In his downtime, he likes to be outdoors, play sports, read, write, and travel.
Bio: Dr. Thomas Dayspring
Thomas Dayspring MD is a Fellow of the American College of Physicians and the National Lipid Association and is certified in internal medicine and clinical lipidology. After practicing in New Jersey for 37 years, in 2012, he moved to Virginia and served as an educational director for a nonprofit cardiovascular foundation, and until mid-2019, as a Chief Academic Advisor for two major CV laboratories. Since then, he has served as a virtual cardiovascular / lipidology educator. Career-wise he has given over 4000 domestic (in all 50 states) and several international lectures, including over 600 CME programs on atherothrombosis, lipids/lipoproteins (and their treatment), vascular biology, biomarker testing, and women’s cardiovascular issues. He has authored several manuscripts and lipid textbook chapters and performed several podcasts. For several years, he was an Associate Editor of the Journal of Clinical Lipidology. He was the recipient of the 2011 National Lipid Association’s Presidents Award for services to clinical lipidology and the 2023 Foundation of NLA Clinician/Educator Award. He has over 34K followers on his educational Twitter (X) feed (@Drlipid). He has Gold Heart Member status as a professional member of the American Heart Association and serves as a Social Media Ambassador for the European Atherosclerosis Society and the National Lipid Association.
“With APO(b), you do not want to live at the 50th percentile because that's Russian roulette.”
-Dr. Thomas Dayspring
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Transcript:
Cynthia Thurlow: [00:00:02] Welcome to Everyday Wellness Podcast. I'm your host Nurse Practitioner Cynthia Thurlow. This podcast is designed to educate, empower and inspire you to achieve your health and wellness goals. My goal and intent is to provide you with the best content and conversations from leaders in the health and wellness industry each week and impact over a million lives.
[00:00:29] February is Heart Month, and I could not think of a better theme to use, compiling some of my favorite podcasts that I've done with experts with regard to heart health. As many of you know, I spent over 16 years as a nurse practitioner in cardiology, and it is a near and dear subject to me.
We you look at current statistics that run the gamut with regard to cardiovascular disease in women. Heart disease causes 1 in 32 deaths each year, and remains the number one killer of women, approximately accounting for one death every 80 seconds.
[00:01:06] We know that women present differently than men. And by the time women get a diagnosis of cardiovascular disease, they typically have more severe disease than men do. 64% of women versus 50% of men who die suddenly of heart disease have no previous symptoms. And pathophysiologically, the incidence of heart disease in women lags behind men by about 10 years, and the incidence of heart attacks or myocardial infarcts and sudden cardiac death in women lags behind men by 20 years.
[00:01:38] We know that a great deal of the delay in onset of these symptoms is related to the cardioprotective effects of estrogen, which women, as they make that transition from perimenopause and menopause, become much more susceptible to heart disease.
[00:01:57] So, today, I humbly share with you a compilation of podcasts with Dr. Hussey and Dr. Tom Dayspring. Again, this will be divided over two podcasts, because it is quite lengthy, but particularly relevant given its Heart Month and why I want to bring greater awareness to the number one killer of women, heart disease.
[00:02:19] I know you will enjoy this conversation and hopefully to have some actionable steps that you can take that you can discuss with your internist, your primary care provider, to help with risk stratification and to help identify if there are any areas that you need to tighten up on in terms of lifestyle.
[00:02:39] Let's segue into, being a very young adult and the stress of the pandemic and being disconnected from loved ones and not being able to do the things we really took for granted. It's during this time period that you actually had this event. And so, before we dive into statistics, I think your story is really, really powerful. I'm hopeful that listeners will really connect to that, because I think there's this presumption that people that have MI’s or have heart attacks or of a certain age and you're a really great example of the fact that it can happen in younger adults.
Dr. Stephen Hussey: [00:03:16] Yeah. So, this was something that-- If people read the book, they'll get the story. And then, also, a couple weeks ago I did a talk at Roanoke College, where I talked about the updates of what I've discovered since then too. So, people want to check that out, it's on my YouTube about the heart attack. So, you know obviously took me by surprise, I had a massive myocardial infarction, 100% blockage of my left anterior descending artery, which is the biggest artery supplying the heart.
[00:03:42] It's easy for a lot of people to say, “Oh, it's your diet.” But as I'm laying there in the hospital recovering from this, having written, pretty much completed the book that people have now read, I'm sitting here thinking, my whole purpose in writing this book was that heart disease is not just about diet. I almost think that it's a much smaller part than some other things we need to be concerned about. Yes, metabolic health is very, very important, and that's pretty much if your diet's not creating metabolic health and you need a different diet, no matter what diet that is. But heart disease is also about stress. It's also about toxin exposure.
[00:04:19] When I say stress, that's encompassing a lot of different things. We're talking about stress metabolically, we're talking about stress, toxic exposure, we're talking about stress socially, psychologically, lots of different things. But the more and more I looked into it, especially writing this book, I realized that heart disease is, it's so much more than just a lipid panel and a cholesterol medication or something like that. That's extremely narrow minded, and I don't even think necessarily warranted in a lot of cases. It's way overused. But the problem with it is that it allows us that theory and that method of treating heart disease has allowed us to almost ignore everything else that's super important.
[00:04:58] And so, for me, I knew all this stuff, but there were circumstances where I let things get to me. I was in this chronic stress situation, and predisposed as a type 1 diabetic. I'm always going to be more prone to oxidative stress, more prone to insulin resistance. And so, those things, I think-- One of the big things is that I'll have low endothelial progenitor cells, which are cells that go in and heal the lining of the artery. And so, with all that predisposition, and then in the year leading up to the event--
[00:05:30] People need to know that. My CAC score was zero six months before I had a heart attack. Because these are all theories that I talk about in detail and quote the research in the book, but I'm not convinced that a narrowing of an artery is what causes heart attacks. It's not a good thing to have. But a stenosis of an artery doesn't guarantee or doesn't increase the likelihood that you'll have a heart attack in my opinion, just based on the evidence, based on the research. Again, it's an indication that there's things happening that shouldn't be happening, like damage the lining of an artery that the body's trying to repair.
[00:06:01] But heart attacks can happen without any narrowing whatsoever. Lots of times they do. Sometimes they happen in spots where there's no atherosclerosis whatsoever. And that seems to be what happened with me, was that a large enough clot formed. And notice I say clot, not accumulation of cholesterol over time. But a large enough clot formed because of situations I was in, because of being type 1 diabetic and the stress I was under from not just a pandemic. It's easy to say, oh, yeah, the pandemic was stressful, because it was. It was stressful for everybody, so why did I have a heart attack and other people didn't? The answer to me is that there was type 1 diabetes and other things as well.
[00:06:40] But when we look at the evidence, and I talk about this in the talk I gave a few weeks ago that's on YouTube, it's the prolonged chronic stress that predisposes us, that increases a clotting state. The blood's more likely to form clots when we're in that state, and then that all can be perpetuated and then triggered by an acute stress, which is exactly what happened to me. In my life, I was under this chronic stress from being separated from loved ones, some personal relationship issues I was having at the time. And then, I heard some unfortunate news about a very close family member that I was unable to do anything about. And so, I heard that news, and then a day and a half later, I had a cardiac event. And so, to ignore that correlation and to not look into that is incredibly shortsighted in my opinion.
[00:07:27] When I was in the hospital, that's all I heard was, “Oh, it's your cholesterol, it's your cholesterol, it's your cholesterol.” Even though I fit this lean mass, hyper-responder phenotype, where everything else was looked good as far as all the biomarkers and everything, except the cholesterol was a little higher. They just wanted to say that rather than saying, “Well, what else happened to this person, or what's been going on in their life for the last 20 years, like type 1 diabetes?” And then, in the last year, and then you look at the evidence of during the pandemic and cardiac events and cardiac hospitalizations are way up since then because of the stress.
[00:07:59] And so, it's hard for people to wrap their head around. And even people I've told like, “Oh, it was stress induced.” They were like, “But how?” Because this theory of cholesterol slowly building up and blocking an artery causing a heart attack is just so ingrained in us. But when you really break it down and look at it, it really makes no sense. It's almost like this-- I don't know.
[00:08:19] There's this example of this guy named John Hunter way back in the day, and he was convinced that heart attacks and heart disease was caused by stress. Ironically, in a heated debate with a colleague, he had a heart attack and died. He was getting really angry and it happened to him. And so, it's just really, really, I think unfortunate that when I was in the hospital that the answer I got was just, “It was this, don't question us, we know what we're doing,” instead of what could it have been, “This person is really young, looks like they take care of themselves. All their markers are good. How can we blame this one marker that's really not a good understanding of this complex biological ecosystem that is the body?”
[00:09:01] It doesn't make sense that one thing will cause disease. But instead of doing that, there was no open-minded discussion, there was nothing, it was just-- This was the answer, “Go on your way, do what we say.” And so, it's almost like it was like this manifest destiny, like I had all this information about the heart and then I had a heart attack myself. I get that point of view, but later I did find studies that show that magnesium intravenously, magnesium sulfate can be administered, or at least in animals, it has been shown to be just as effective as blood thinners for preventing clots after stents.
[00:09:31] Now, I didn't expect that physician to do that based on if I showed in that study and said, look, because there's no approved treatment to do that in a hospital setting. However, it makes us step back and say, okay, what's going on within Western medicine, this business that is Western medicine, that has prevented a therapy to be perfected or developed with magnesium sulfate, rather than blood thinner that has the risk of bleeding and things like that. So, we have to step back and recognize that.
[00:10:04] You talk about your fellow practitioners and everything and how much you love them and how great a job they're doing. That's exactly the way it should be. We should have love for these people. But I hope that they understand this is the system they work in. They need to recognize this is a system they work in, so that they can make their decisions accordingly when it comes to these types of situations down the road.
[00:10:26] Well, it's just the research that shows that the intravenous magnesium sulfate has been shown to, at least in animals, to be effective at preventing clots forming after a stent placement. If I showed the practitioners that study right there, I wouldn't expect them to say, “Oh, okay, yeah, then we'll just do intravenous magnesium sulfate.” Because that's not an approved treatment for that. But what I want people to understand, is that this is the kind of world that Western medicine, physicians and practitioners are operating in, is that they have to abide by the standard of care. If anything goes wrong, they're liable, and so in a way that prevents them from investigating what could be effective in other ways.
[00:11:06] And so, it's just important for practitioners to understand that that's the system that they work in. Not just ignore it and say, “I'm going to do my job and this,” but also understand that they work in the system that may not be giving them all the facts. And so, I detail this whole series of events that can happen, that can lead to what I call metabolic heart attacks, where we get tissue death when there's no blockage whatsoever. And so, without going into all the details of that, what's in the book-- But when that happens, it can cause tissue death by forcing a shift in metabolism, forcing the heart to burn more carbohydrate more glucose than it wants to. That has to do with our stress response and oxidative stress and things like that.
[00:11:45] But in that case, if it was forced to burn more glucose and go into this fermentable state in a normal tissue in the body, that cell would choose to become cancerous, because that's a short-term fix to this metabolic problem that's happening in the cell. So, it's like, cell says, “Stay alive rather than die,” by rapidly dividing, being undifferentiated, anaerobic, not using oxygen cells. So, in the heart, where division is not possible, rapid division is not possible because it gave up its ability to divide cells, the tissues die. It has no choice. When it's forced to burn more glucose and go into this fermentation state, the tissue dies rather than rapidly divides. That's how we can get tissue death in a certain situation that can cause that. It's also why cancer of the heart is so rare, because instead of become cancerous, the tissue dies.
[00:12:33] And so, it's just this interesting thing that I fleshed out and hopefully you think I found the answer to one reason why the [unintelligible [00:12:40] the heart is so rare. But a lot to do with metabolism and a lot to do with oxidative stress and keeping those mitochondria healthy, which is very, very important, especially for the heart, which is one of the most mitochondrial dense tissues in the body, because it is always contracting. It's using a lot of ATP to do that. S,o that's the story there.
Cynthia Thurlow: [00:12:58] No, I think it's really interesting. Like I said, when I was reading your book, it really encouraged me to think beyond what I was taught as a new nurse practitioner. Obviously, I started as an ER nurse, and the hospital I worked at in Baltimore, we did a high amount-- At that time, I think we had the highest rate of cardiac caths in the whole area. We had a very talented interventional cardiologist. So, we got very attuned to the anatomy of the heart and the widowmakers, what we call when the LAD gets blocked, that left anterior descending artery.
[00:13:30] But let's pivot a little bit and let's talk about Ancel Keys. I've had many, many guests and we have talked a lot about Ancel Keys. And so, his net impact on the trajectory of our health, I say our health as a nation and a community has been very profound. His cherry picking of data has also profoundly impacted our health.
[00:13:53] And so, let's start there and talk about how things have changed in terms of the focus on fearing fat as opposed to sugar, and how that changed the trajectory and the focus of not only the processed food industry, but a lot of the information that clinicians were giving to their patients. My grandparents talked about this, that they went from enjoying butter and steak to all of a sudden being told that you need to have these hydrogenated oils, these bastardized plant oils and really being fearful of any type of animal-based fat.
Dr. Stephen Hussey: [00:14:26] Yeah. I don't know how familiar your listeners are with this whole backstory, but yes, Ansel Keys was a scientist who in the 1950s gave America an answer to this rising epidemic that was heart disease. President Eisenhower had a heart attack so famously when he was in the White House, and people were fearing this disease and it was new, which I think people should note, it was new. So, just thinking about that and thinking about what humans ate for years and years prior to this epidemic of heart disease, what was the difference, what changed? You could say toxin exposure, you could say that there was a shift to more processed foods, vegetable oils came on the scene, things like that, stress, I mean, all the stress of war and things like that happened in the previous few decades, that kind of stuff.
[00:15:11] But anyways, Ancel Keys gave the population, gave the world an answer, which was more saturated fat, more cholesterol, more heart disease. He did this based on very poor-quality cherry-picked research, I'd say, because it's epidemiology, which is the lowest form of research, because it can only show things are associated with each other. It can't show that one thing causes another. It's supposed to do this type of research to develop clinical trials after that. Okay, these things are associated, let's test and see if one's causative.
[00:15:38] Unfortunately, that's very expensive to do and it's not done a lot of the time. And so, they take these associational studies and they make our nutrition guidelines based on these associational studies. That's what happened with Ansel Keys, is he originally published this research that just basically showed in these countries that he took data from the more saturated fat and cholesterol you ate, the more heart disease you had. However, he only picked the six countries that gave him the association he wanted to see. But there was data from 22 countries at the time and so we cherry picked the data that gave him his result for whatever reason, whether he wanted to be famous or whether he had a lot of backing from certain industries, I don't know, but yeah.
[00:16:15] So, by the time this theory was actually tested in clinical trials, which it was over the next 10 years, 15 years or so, Ancel Key is doing some of the studies himself. By the time it was actually tested, and they did all these studies where they replaced saturated fat with unsaturated fat in the form of margarine or vegetable oils and had terrible results with that. People had more heart disease and more all-cause mortality with the more unsaturated fat they ate. Unfortunately, more common around holidays or sporting events where people are betting on everything and they got a lot of money on the line. Or, Mondays, when they're coming back out of the weekend to a stressful day of work. Heart attacks are more common on these days because of the clotting that's initiated during this stress. And so, it really takes the-- To me, it takes the whole prevention of--
[00:16:59] I think atherosclerosis and heart attacks can almost be seen as two totally different things. And one doesn't necessarily cause the other. One is clotting, one is just repair, but it takes the-- Instead of focusing on this idea that cholesterol accumulates in arteries and causes atherosclerosis and narrows artery, restricts blood flow, which is not really proven, and says, “Okay, how do we manage our stress?” That's the big thing that I think we need to be talking about. Stress can cause insulin resistance. It puts you in an insulin resistance state. That's the way forward, I feel like, with heart disease is, is this stress management piece, which is hard to do, because it involves significant changes in lifestyle, and getting rid of things you may not want to get rid of and things like that. But yeah, that's a big message in my book.
Cynthia Thurlow: [00:17:45] No. And it's interesting, something that really stood out for me. Listeners know I have an Oura Ring and I love my Oura Ring, I like data. One thing you mentioned is that heart rate variability, which is something the Oura can track, is the best measure of stress response and declines with age. And so, yes, you don't expect your HRV at 50 to be what it would be at 20. But for me, it really gives me a sense of how well recovered I am. So, I just did back-to-back travel.
[00:18:11] Even though I enjoy traveling, it is super stressful dealing with Ubers and airports and cities. You were saying about the city response. It's absolutely true, because I live in a very quiet part of Virginia. Even the airports and navigating all of those things. My HRV was completely in the tank while I was traveling, even though I was sleeping. And then, it took three days before my HRV bounced back into the 50s when I was at home. And of course, my husband thinks I'm a gigantic nerd, that I'm so focused on this stuff. I said, but it really is a reminder that you may perceive your stress levels are low, when in fact they are not.
[00:18:45] Now, I would be remiss if we didn't at least touch on fasting, because you do talk about this in the book. In terms of evolutionary adaptation and the changes that have occurred in the last 50 to 100 years, what's your take on meal frequency and snacking as it impacts heart health? I know your answer, but I wanted to hear you say it.
Dr. Stephen Hussey: [00:19:07] Yeah. So, in the book, I have these three themes that I keep coming back to, and that's metabolic health, oxidative stress, less inflammation and balance in the autonomic nervous system, which is our stress response dealing with our stress. And so, every time I think about a therapy or a lifestyle or whatever that you could do to improve your risk or I guess decrease your risk for heart disease, is how does it match up with these three imbalances. Does it help with these three imbalances?
[00:19:31] When we talk about fasting, the answer is absolutely, yes. It does all three of these things. It helps you improve metabolic health because there were times evolutionarily that food wasn't around so much, especially during the winter. And so, our bodies evolved for it to almost beneficial to when we had to take breaks from eating as often. It used to clean things out and to write your metabolism and develop mechanisms for using ketones and things like that. And so, yes, metabolic health wise, absolutely.
[00:20:03] It's also interesting that there's studies that I talk about in the book that show that when you fast, long term fast, that your cholesterol goes way up. Dave Feldman would tell you that's because they're delivering energy. You have to deliver more fatty acids and ketones and things like that, or just fatty acids to the cells, so LDL goes up. But the very idea that saturated fat and eating more saturated fat and cholesterol causes heart disease is what causes heart disease. But the fact that you don't eat anything at all and your cholesterol goes up, disproves that theory, in my opinion. Anyways, so there's that.
[00:20:34] And then, as far as inflammation and oxidative stress, when we're fasting, we start relying more on ketones, which are an incredibly efficient fuel source that make very little or less oxidative stress, less waste products, although I don't think there really are any waste products. We talk about the cell making waste products and it brings energy, but I don't think there are really. It's all used for something beneficial. But yeah, so there's less of that going on. This has especially been shown in muscle where if we're using fatty acids and ketones, we're making less oxidative stress. And so, when we fast, we're pushing our body to do that to mobilize fatty acid stores and use those for fuel.
[00:21:08] And then, as far as balance in the autonomic nervous system, definitely research has been shown the fasting will do that to an extent. I think that there is a window of time, because I talk about some studies in the book where fasting in the first three days, if you're doing a long fast-- Intermittent fasting I think is beneficial just generally. But if you're doing longer fast, the first three days, it stimulates parasympathetic. But then, after that there's a window of time where it seems to simulate sympathetic, where your body's almost freaking out a little bit. But then, I think it comes back around after a while. But I don't know that we have the data to show that. I just know what I see in people who do longer term fast, that's what they see. So, yeah, in all three phases of what I think are the main drivers, the main imbalance that create heart disease fasting, if whether it's intermittent or longer term fast seems to beneficial in all three phases.
Cynthia Thurlow: [00:21:58] That's fantastic. Well, I've so enjoyed this conversation, and obviously, I could talk to you for hours. Please let my listeners know how to purchase your book, how to connect with you on social media and on your website.
Dr. Stephen Hussey: [00:22:09] Yeah, my website is resourceyourhealth.com. My books are on there. My blog is on there and I do like little health coaching online consulting. So, that's on there as well. My book is on Amazon. It's also on the publisher's website, and Barnes & Noble and things like that. People don't want to use Amazon, there's people that don't want to, so there's that. And then, on social media, I'm just @drstephenhussey on Instagram and Facebook and Twitter, and people can reach out to me there and happy to interact with them.
Cynthia Thurlow: [00:22:36] Awesome. Thanks so much for your knowledge and for putting your story out there. I think it'll help inspire a lot of people.
Dr. Stephen Hussey: [00:22:42] Thanks for having me on.
Cynthia Thurlow: [00:22:46] And so, getting back to the ApoB, especially for people, if they're listening, men or women, and they want to be their own best advocates, what are the lab values we're looking for someone who is metabolically healthy, no diabetes, no vascular disease. What number are we aiming for versus someone who has known vascular disease or diabetes?
Dr. Tom Dayspring: [00:23:09] Yes, that's crucial criteria there, because whatever ApoB or whatever level I'm going to recommend to you obviously depends on your baseline risk. If you're a total nightmare, if you come walking in with a scar on your chest or you've had three stents, [chuckles] I'm going to want to turn you into an infant again with an ApoB at 30. But if that's not you and you're just in middle age, a woman going through menopausal transition, you don't have coronary artery disease that you know of. At a certain point, we actually start screening for that nowadays too with non-invasive imaging that is available to us. But a poor tool earlier in life because what you see in an older person might not be there in a younger person, so you got to be careful who you're doing imaging on.
[00:23:52] So, somebody comes in and obviously they don't know what a cardiologist is, they've never been admitted to the CCU or the bypass unit, they don't have xanthelasma on their eyelids or sticking out of their elbows, which are cholesterol collections, suggesting a serious genetic cause. For whatever reason, they had a lipid profile. They probably even didn't do ApoB. But if you listen to us today, you know the things in a lipid panel that ought to jump out at you and make you think you need an ApoB is total cholesterol being high. It's LDL cholesterol and ApoB particle that primarily drives total cholesterol.
[00:24:28] If you calculate VLDL cholesterol and that's high, you know you have a triglyceride problem, which always translates to an ApoB problem. So, a triglyceride above 70, as Cynthia said, ought to make you think, I want an ApoB before I say, I don't worry about a trig of 110. And of course, LDL cholesterol, if it's beyond a certain level-- I would tell you that level ought to be 70 milligrams. The guidelines would tell you 100, but I would tell you 70. If your LDL cholesterol is 76, I think you ought to be doing an ApoB level.
[00:25:01] And of course, the HDL cholesterol, if it's low, you absolutely need an ApoB level. But we're actually finding now the old mantra that the higher your HDL cholesterol the better is true in some people and not true in others. Women tend to have higher HDL cholesterol than men for reasons we're probably going to explain. But if a woman comes to me and says, “My doctor did the lipid panel and yes, my LDL C is high and there's some other bad stuff here, but my HDL C was 150, so I don't have to worry about anything.”
[00:25:33] My head starts to explode. [Cynthia laughs] Because we know I introduced to you, there are people who have dysfunctional HDLs. They don't do the good stuff they're supposed to. And in some people, overloaded HDL particles full of cholesterol, devoid of Apo-E, which we are not good HDLs. So, that would be a person that you'd worry about. So, how would you solve it? I do an ApoB. I can't solve the H, but if the ApoB is high, I can take care of that.
[00:26:02] So, there's one other test we didn't talk about it. I know at some point we will. It's an inherited lipoprotein disorder called lipoprotein(a). It's an LDL particle that attached to the ApoB is another usurper protein called apoprotein(a), small case A. It's a nightmare atherosclerotic lipoprotein. One out of five Americans has inherited it. One out of three blacks, one out of three Asian-Americans. So, that has to be part of your initial screening. So, the person I'm going to give you ApoB now is also had an LP(a) test and it's negative, because we would want a lower ApoB if I knew you had high LP(a).
[00:26:42] So, you come in, your lipid numbers maybe are a little out of whack, but they don't cross, they're not red on your lipid panel. It comes back from the lab. But if you've listened to us today, “All right, I went out and got the ApoB. Here's my ApoB. Now, what do I worry about?” So, here's how we look at this. I'll send to Cynthia. I don't know if she does slide notes, but I'll give you a nice chart that shows all this that'll be there for everybody to see. At what point do the ApoB particles have the potential to start crossing your artery wall? We make this judgment if we take regular populations, and theoretically they're healthy, and we're excluding the people with coronary artery disease at what percent-- We look at what we call population percentiles.
[00:27:28] So, you could have the lowest levels in the world, and you'd be down at the fifth percentile. That means only 5% of people would have a better reading than you, 95% would have a worse reading. We could look at the 90th percentile and say, “Oh, my God, you're worse than 90% of the people in the world. Not good.” We can look at the 50th percentile where you would say, “Well, half or worse than me, but half are better.” Trust me, with ApoB, you don't want to live at the 50th percentile, because that's Russian roulette. [chuckles] Some will get bad, some won't--
[00:27:56] So, we normally, with lipid concentrations, like to see the lipid parameter that you're looking at under-- you be in the bottom 20th percentile. If you could stay there, your chances of maybe some ApoB particles will get in over time, but not enough to give you serious atherosclerosis, unless there's other things going on, high blood pressure, you're a smoker, blah, blah, blah. We're talking about healthy people here who don't have those issues.
[00:28:24] If you really wanted to have a phenomenal ApoB, there is a set of people that, for whatever reason, they either catabolize their ApoB particles or they don't make many. They wind up with very low ApoB or LDL cholesterol levels. It's called hypobetalipoproteinemia. If you study them genetically through Mendelian randomization studies or if you even follow some of these people over time, they have extremely low incidence of atherosclerosis. If not, no atherosclerosis. So, that's defined pretty much as an LDL cholesterol under 40 to 50 and ApoB under 40 to 50.
[00:29:02] So, if I could snap my fingers and give everybody in the world an ApoB of 40 or 50, I would. But in most people, you just can't get there without pharmacologic done. I don't want to put the world on statins or any other lipid problem right now to make them hypobetas. I just want to maybe get them to the 20th percentile, and I'll follow them over time. If it stays there and they don't start smoking or their BP doesn't go out of whack and their menopausal transition isn't too nightmarish to screw up the lipids and lipoproteins, you'll be happy with that. You can start looking at other diseases that are going to impair either health span or God forbid, longevity. That's why I say with the women, I like the whole body. I look at it.
[00:29:42] But even in man, and there's a lot of parts in-- Men's brains are sometimes important too, so we look at that. [Cynthia laughs] They have certain things below the belt that you want to keep working also. So, there are many things to figure out. Both genders get cancer, so you have to start screening appropriately for that. So, if I wanted everybody's ApoB to be in the 20th percentile, it's really 80 milligrams per deciliter would be fine. But if I really wanted you at the fifth percentile, which is a little bit above hypobeta, but it's close and that would be a level of 60. I think in most healthy people that's pretty much overkill, unless you're reading some longevity book and they know that these hypobetas just don't. So, you make yourself hypobeta. But that's probably, if you're otherwise leading a healthy life, going to require drugs to drop an ApoB that high.
[00:30:35] So if your ApoB is 80, you're at the 20th percentile, if it's above that, that's the time where you bring in somebody who's schooled in nutrition and in lifestyle and they start going over you with proper exercise programs, proper eating programs, and then you can keep your ApoB 80. If it's 90, just doing those things is probably going to make it 80, where I don't have to take out the prescription pad. Even at a certain point, where you know your lifestyle didn't do it, there might be some, not many, but supplemental recommendations I could make that at least might reduce the absorption of cholesterol into the body, which should help ApoB a little bit. So, you should know about those.
[00:31:19] And ultimately, if your ApoB is not budging because you did the great lifestyle or it's at a really high, you come to me with an ApoB 120 unless you're a total pig out nutritionally, you might need a drug. A lot depends on your age and how much willing you're willing to cooperate with the lifestyle and everything. If your insulin resistance lifestyle works like magic, that's for sure. So, at a certain point, you're going to need a drug. But you don't need a drug day one if you're otherwise healthy and your ApoB is even a little scary.
[00:31:48] Look, even if it was in the 80th percentile, which I'm thinking, ultimately, I'm going to need a drug. I would like to give you the time to show lifestyle. How low can you get it with lifestyle? Maybe I need less drug or I don't need two or three drugs to get you to go. So, I never, never want to downplay lifestyle. I have a gigantic Twitter following. People assault me, “Oh, you're just a drug pusher.” No, you got to realize I'm a lipidologist. I see the nightmares of the world. So, [chuckles] in general, they need drugs. But I think people need appropriate advice with pharmacological care, and they sure as hell need appropriate lifestyle whatever you want to call it, nutritional and exercise, mental health advice review. Perhaps, you're taking other medications for other serious conditions. Some of them can putz with lipids. So, I have to know a lot about you. So, it's a complicated decision. But early on, it's--
[00:32:42] The population we're talking about now, it's not drugs. Yes, if you come in with a crack in your sternum or three stents, if you're not already on drugs, you're even going to an incompetent, so I'll put you on. sometimes they're a little not as aggressive with ApoB as they should be for people with coronary disease. So, I'm probably going to give you further pharmacologic advice, but that's for the nightmare population.
Cynthia Thurlow: [00:33:06] No, I think this is so important, because you're really stressing how important lifestyle is, number one. Number two, you can get a patient to a certain point and then considering pharmacotherapy is completely appropriate. For full disclosure to my listeners, I don't think I've talked about it on the podcast, there's a genetic predisposition I am insulin sensitive. I exercise, I sleep well, I'm on HRT, I do all the right things, and I still required medication, because-- Thankfully you're sitting as I say this. My ApoB was 130. This is absolutely a genetically mediated piece. I just had labs drawn last week, so we're going to see the net impact. I'm on a drug called Zetia. It's inexpensive. We very strongly believe that I'm a hyper absorber, which contributes that. But we'll see where the numbers are, but I've been on that for several months now.
[00:33:53] Now, if someone comes to you, let's say hypothetically, their ApoB is high, you want to screen them, the screening tests that you've been talking about-- I'm sure you're talking about a CAC, so a coronary artery calcification, maybe looking at the specialized carotid artery scans, are you doing stress testing? Is it really dependent on if someone's symptomatic or asymptomatic? What are the next steps? Because I'm sure for you it's looking a little deeper to figure out what else may be at play.
Dr. Tom Dayspring: [00:34:21] Look, it's a complex evaluation. This is not something in 30 seconds I can tell you everything you need to know. [Cynthia laughs] Chances are, we will need additional diagnostic studies, for sure. Talk about stress testing. Look, if you have an asymptomatic person, unless they tell you I'm going to climb Mount Everest next month or something, okay, you want to see what their exercise capacity. Maybe you don't want a VO2 max for a fancy stress test. But just a plain stress test looking for EKG changes. You have to have serious coronary disease for them to show up. Hey, a nuclear stress test will pick up, but it's a lot of radiation with a nuclear stress test. So, I'm not a big advocate of those for asymptomatic people.
[00:35:00] Nowadays, we do have the coronary calcium, which is a cheap test looking for calcium deposits radio opaque in your coronary arteries. Not that expensive. Widely available. But it's not good in the younger years unless you have FH who would expect heart disease when they're 16 years old. You a healthy person coming in at 20, 30, even premenopausal, coronary calcium is-- If you come back with a zero, nice. But that doesn't mean anything. You still could have a lot.
[00:35:28] The carotid imaging is certainly the type of imaging you can use in a younger person. But a big caveat, you need to go to somebody who's well-schooled with carotid intimal thickening analyses. Half of the practices that have them in their office, they don't know what they're doing, so you get idiotic readings out. You're going to make some serious decisions based on these. I think you've got to go someplace that really knows what they're doing with carotid intimal. So, again, you got to do your homework to see where you're going.
[00:35:58] There are vascular test flow mediated dilation in other ways where they put blood pressure cuffs, but not everybody is doing them. Again, you have to go to a trusted practice that is well experienced with them and has a long history of doing them. They can all give you worldly clues that your arterial bed is not what it should be yourself. So, that's it.
[00:36:18] I divide this. Nowadays, I have a nice slide. When you're born, those kids we talked about, their ApoB level is normal. And for most kids throughout infancy and even early adolescence, their ApoB is normal. That's called primordial prevention. Yeah, you'll do the oddball lipid test. They don't need them every year at that age. But you don't see an abnormality, you're not going to do anything, unless the kid is overweight or blah, blah, blah, in which case those tests would probably be abnormal.
[00:36:46] But at a certain point, the ApoB starts to cross those thresholds I talked to. But they haven't had coronary disease yet. You probably wouldn't find it-- If you autopsied the kid, you'd find fatty streaks in the aorta-- We first found that out in the early studies where kids were getting hit by cars or run over by trains. At eight years old they had fatty streaks in their aorta, and we knew atherogenesis occurs very early in some people.
[00:37:10] So, once the ApoB is high, I call that primary prevention. I got to work on you through lifestyle or whatever to get you back to the primordial prevention levels. That's usually pretty amenable to lifestyle, unless you're like Cynthia, you've picked the wrong mom and dad and you got some bad genes at play. Look, lifestyle, we never want to dismiss it. Even in her, you can look at her and see she's doing lifestyle things well, but she's still reporting a terrible ApoB. So, of course, keep doing all the things to your healthy lifestyle, but here's what else you need.
[00:37:44] But once, say, Cynthia, if we did say that coronary calcium on her, or even a fancier test called a CTA, computed tomography angiography, don't have sticking catheters up in your home heart and inject and die into the arteries, that's pre bypass stuff. But we would see not only calcium in her arteries, we would see, oh my God, there are some luminal irregularities or even plaque within the wall of the artery, and that's what I call secondary prevention. She hasn't had a heart--
[00:38:12] In the old days, secondary prevention meant you had a heart attack or stroke. Secondary prevention means we've diagnosed atherosclerosis using invasive or non-invasive immune imaging procedures. So, then we know you're a hell of a lot closer to a rupture that I talked about. Once the rupture occurs or the luminal occlusion occurs, that's tertiary prevention. If you survive that, we still can prevent the next one with super aggressive therapy. But you're probably looking at three drugs in those cases. So, these are some of the diagnostic tests you need to weigh.
[00:38:47] But other than the lipid panel, other than just relying on, geez, my trigs is a little high, I do think you need, at a certain level, other tests of insulin resistance or so. So, whether that's going to be a fasting insulin level. If you do that nuclear magnetic resonance testing, the lipoprofile I mentioned, you will start to see certain lipoprotein signatures of insulin resistance. Your LDLs will be small. Your VLDLs will be big, because they're packed full of trigs. Your HDLs will be small, because they're being rapidly catabolized, because they inherited triglycerides. And actually make, based on about six lipoprotein characteristics, something called an LPIR, lipoprotein insulin resistance score. Zero is you have no insulin resistance. 100 is [chuckles] if you're not a diabetic yet, you will be next week.
[00:39:38] And so, obviously, you want a level well below 50 on there. As you start to approach 50 or going higher, long before even your glucose might go up. We know you have the type of insulin resistance we're very worried about. Super opportune time to get in there and start doing lifestyle apart from lipid drugs. The world is full of all these magical fat disappearing drugs nowadays that people sometimes are jumping on a little too soon before lifestyle, but they're out there now, even fraudulent ones that somebody's making in their basement. So, God forbid, you had to go to a GLP1 receptor that I think a prescription product would be smarter to use. They're in short supply and your third-party coverage may not be so good.
[00:40:22] But there are insulin resistance is a whole other animal that, yeah, you're probably going to need some lipid control, but you're going to need a lot of other stuff, insulin sensitivity control, and you're probably borderline hypertensive there too. So, that's going to have to be addressed. So, you can see how we start with the basic lipid profile where we might just-- We got the ApoB, what we do about it depends upon coexisting things. If you did test for that LP(a), everybody right now needs it once in our life earlier rather than later. If that was out of whack right now, all we can really do is I want to take your lowering of ApoB to the next level. I surely want it under 60 if you have a high LP(a). In the future, we may have drugs that address LP(a) production. They're in development, they have to pass rigorous testing and safety testing. So, we'll see when and if they come to the market. Not now.
Cynthia Thurlow: [00:41:15] Yeah, it's really interesting. As I was preparing for our discussion today, one of the things that stood out about LP(a) that I did not actually know, is that it actually can invade our aortic valve. So, this is one of the valves in the heart. And can contribute to calcific aortic stenosis, which for anyone that's listening and saying, what does that mean? This is quite significant. I saw a lot of patients, especially older patients that had aortic valve disease that ended up going on to need to have their valves replaced and or repaired, but this can be quite significant. And so, this is why the screening tool for the LP(a) is so important. Because if you know at 25 or 30 that you've got an abnormal LP(a), you can be doing things then and not waiting until you're diagnosed with a disease or valvular heart disease or a calcific aortic valve, because that's quite significant.
Dr. Tom Dayspring: [00:42:05] It certainly is. And so, if we discover high LP(a), we're certainly worried about your atherosclerotic future. But especially if you get early in life, somebody better be watching that aortic valve closely. In the old days, I'd put a stethoscope on your chest and I'd hear a systolic [unintelligible [00:42:21] that's almost too late. Nowadays, we have echocardiograms. I think periodically, anybody with high LP(a) needs an echocardiogram here and there. Cynthia knows better than I. There are other dynamics that come with the echocardiogram that can give you a lot of things about how good is your aortic valve working.
[00:42:40] In my day we were told, “Oh, every aortic valve, it's just they were born with a bicuspid valve.” Meaning, they had two leaflets instead of three. And now, we're knowing, yes, that's still a big problem. But LP(a) is rapidly coming up as the number one or number two cause of aortic stenosis. And the big characteristic of it's calcified. Apo(a) has a lot of bad properties, but it's osteogenic. So, it makes white blood cells turn into osteoblasts in your damn aortic valve. It's not good to have cement in your aortic valve or bone, not good. Because the aortic valve, for those listings, the main valve that blood flows through when it goes from the heart into your aorta and elsewhere and you can't have that narrowed because over time the muscle pumping, it gets destroyed. You cannot wait till heart failure because then it almost doesn't matter what you do. And fortunately, we have so many better ways of assessing early heart function nowadays.
[00:43:38] The people who know what they're doing, jumping in much sooner with aortic valve surgery, which can be done through your chest wall. They often don't even have to crack your sternum, which is good. But if you know you have LP(a). Anybody who's got a family history, yeah, there was a lot of aortic valve in my family. Good God, get your LP(a) tested.
[00:43:58] One more point on that. When you go through menopause, and ultimately, we will discuss this loss of estrogen causes an increase in Apo(a) protein production. So, if a woman, whatever her LP(a) was, pre-menopause, it's going to go up a little bit after menopause. And most women, the normal LP(a) is still normal, but it's just a little higher. But if you happen to be a serious LP(a), it's going to go up. It was serious before, it's even a little bit more serious. So, that's the one time it can change, Never test it during an infection. It's an acute phase protein that your liver produces inappropriately, because it probably wants your blood to clot when you're in a disaster. But if you're in stable shape--
[00:44:41] The only time we may have to start repeating it, is if any of these drugs that lower it work, they may show us, if you're a nightmare, here's how much you have to lower it. In those cases, in the future, we will almost surely be repeating LP(a). Right now, I don't know if ultimately, we'll get into some of the lipid drugs we're using. There is one available now that can lower LP(a) a little bit. So, maybe if you're on that drug, following LP(a) would be of interest.
Cynthia Thurlow: [00:45:10] Now, we talked a little bit about women in menopause. But in preparation for our discussion, I had heard you on another podcast talking about risk factors for women, things or clues. So, if you're a woman who's not gone through menopause, clues about your medical history, and this is specific to pregnancy history, PCOS, etc., that can clue you in that you are probably at higher risk for complications, lipid issues, etc.
[00:45:42] This I found really interesting, because this is obviously not my area of expertise, but understanding that your age of pregnancy, any complications with your pregnancy. So, if you think preeclampsia is not something that's a long-term issue, it can be same thing with gestational diabetes. Can you speak to that? Because I'm sure there are listeners that are impacted and may be completely unaware aware of this issue.
Dr. Tom Dayspring: [00:46:04] Sure. So, if I was seeing a new patient who knew they were approaching the menopause or even she's in her early 40s or whatever, even if she's not, I would ask very specific questions to at least me to think I think you are in early menopause even though perhaps you haven't recognized it yet. Obviously, there are certain symptoms that it's a no brainer that something's going on.
[00:46:26] But the first thing, if you see a middle-aged woman, when you start doing your initial comprehensive history, you have to spend a lot of time on the pregnancy. First of all, yes, at what age did your periods even begin when you were a teenager or so? Your menarche early, late, that's important information. Then you would want to know where you ever pregnant? Well, no. Well, did you have any miscarriages? That counts as a pregnancy too. If so, how many? So, you want to know the gravida, para, abortion ratio. Because if you know spontaneous abortions do portend future cardiovascular risk.
[00:47:02] If they were successful pregnancies, you say, “Okay, any prediabetes during the pregnancy? Any hypertension of pregnancy that they had to address? Nobody ever found protein in your urine, did they, when you were pregnant? I know they probably never checked it, but would you happen to know what a triglyceride level was in the second or third trimester?” All clues that will pretend future cardiovascular risk. If I delivered, and the son or daughter was fine, “What was the baby's weight? Was it a premature delivery? Did they have to induce it or what did it go to full term? By the way, once junior or junioress was born, did you lactate or did you not?” Very important as far as both for the child and the mom, as far as future cardiovascular vascular risk.
[00:47:50] Now, if she answered yes to any of those and her others that I haven't even elucidated, there are very available women's guidelines with the checklist of things you have to go down, which if you check them, you know potential future vascular issues here. So, and this is so important even for obstetricians to know this stuff nowadays, because they're the ones delivering these kids. The internist is usually not getting involved at that stage of the game, unless the woman was a diabetic during pregnancy or something. But presuming she wasn't, the obstetrician should know, “Listen, I'm done. I've developed junior. You know what to do now. You’ve got a pediatrician for the kid.” But we did see these little bitty risk factors for you. You were a little preeclamptic. You did have subtle hypertension--”
[00:48:40] Any of those that were present, that woman-- I'm looking at her as, “Uh-oh, future cardiac. Big-time trouble.” And that just means that you don't say to that woman who may have had the kid at age 22, when you hit menopause, go see your internist, because they will work you up. You go see your internist soon, and that internist will do some baseline things in you, that internist will be aware of these things that happen during pregnancy and that internist will follow your cardiometabolic risk factors extremely closely.
[00:49:12] And probably, long before you get to menopause transition, you're going to need further lifestyle or even pharmacologic advice. Waiting to 40 or 50, average age of menopause is like 51, that's way too damn late for any woman, because you've given up decades of possible preventative care in that woman. Look, if you're telling a woman to come in, she can drag her husband along once a year too for a lipid profile or a cardiovascular risk assessment, [Cynthia laughs] because the men are actually, depending how ugly their metabolic panel is, do get heart attacks sooner in life than the women. So, maybe there is something about this estrogen story that we have to get into and why when estrogen goes bye-bye at menopause, other issues may evolve.
[00:49:59] A quickie. One of the regulators of that LDL receptor that clear the ApoB particles out of plasma is estrogen. So, women lose estrogen at menopause. All of a sudden, their LDL receptors are in as many as they used or they don't live as long as they used to. So, her ApoB clearance goes up a little bit and ApoB starts to rise. The man never had damn estrogen to begin with, so his ApoB, his LDL receptors are at a probably an unhealthy level sooner than they would be in a woman. So, that's one way you relate hormones to atherosclerosis.
Cynthia Thurlow: [00:50:33] No, I find it all so fascinating and it's interesting. I think a lot of women worry about breast cancer. What we actually need to be more concerned about is cardiovascular disease, ASCVD. This is from a paper that I just read that it said, “1 in 3.2 deaths in women in years, heart disease is the number one killer accounting for one death every 80 seconds.” And HRT, so hormone replacement therapy is a sex specific primary preventative therapy for heart disease and all-cause mortality. So, if you're not talking to your doctor, your NP or PA about HRT and you're in perimenopause or menopause, you should be, because more women are impacted by heart disease than they are breast cancer.
[00:51:15] I'm not saying breast cancer is not important to be concerned about. I'm just saying from a loving place, from someone who spent 16 years in cardiology, there were far more women who presented late, they present atypically, they put it off, because they're worried about taking care of everyone else, and yet this is what's more than likely going to kill us.
Dr. Tom Dayspring: [00:51:33] I'm so full of jokes. I graduated med school in 1972, my postgraduate training in another three years and then I went into private practice. So, through med school and residency program, don't worry about women. The heart attacks are all the men who get him and stuff. I used to scratch my head, because I loved hanging in the CCU. They were just being invented in my day. It was like this-- If you were smart, that's where you wanted to hang out, because you had a chance to maybe save a few. But there were women in the CCU. What the hell are they telling me women can't get heart attacks? Now, some of them were smokers, yes, but still not all of them were, so women get heart attacks.
[00:52:10] And you see these stats where yes, ASCVD is the biggest killer of women and men. And everybody thinks, yeah, it's our great grandmothers who are dying of these heart attacks. [chuckles] Yeah, some of them, that's true. But if they actually live that long, they're probably going to die someday. You don't want to see the modern stats of even premenopausal women who are getting cardiac ischemic, or obstructive atherosclerotic disease or non-ischemic coronary disease, which is a vasospastic issue that women-- So, you just get that out of your head that women don't get atherosclerosis. They do. And like everything else, guys and gals, the sooner we develop it--
[00:52:50] The estrogen story is so interesting. At the early part of my life, you were a jerk if you didn't start every woman on estrogen, including super high dose estrogen. In my early days, what's a progestin? We didn't even know about that. And so, that started to evolve. We certainly have to give progestins. Maybe at a certain point, we could lower the dose of estrogen, because even with the oral contraceptives in those days, we're seeing strokes in young women, because they drown those young women. The first they’ll see the estrogen doses were ridiculous. So, that all got tempered out and rediscovered over time. If you're a gynecologist, every woman was going to be put on hormone therapy as she approached menopause. No exceptions to the rule, unless there was a blatant contraindication, a lot factor V deficiency, blah, blah, blah. A little bit of breast cancer was started to emerge. Early on, there wasn't even that big a worry.
[00:53:46] All of a sudden, these estrogen studies started to come out. The first was the HERS study, where in John Hopkins, they actually took women with pretty serious coronary disease and they gave them the most popular product used, it was Prempro at the time, conjugated equine estrogens and medroxyprogesterone acetate on the belief that giving these women hormone therapy would erase their coronary artery disease. And of course, it didn't. It's actually a null study. Some women did have some adversity at the end. So, oh my God, you know what's the newspaper said is estrogen is killing women. They don't tell you it was women with pretty serious heart disease, which would now pretty much be a contraindication to most hormonal therapies.
[00:54:32] So, that was the first study that came out. But then ongoing was the Women's Health Initiative, which was a gigantic study. But some women who were perimenopausal, early menopausal, and a lot of them were late menopausal women, which we now know is probably not the woman you're going to start on. [chuckles] But these women either got a placebo or they got HRT. Again, Prempro. If they didn't have a uterus, they got just Premarin without the medroxyprogesterone. And lo and behold, as they started to crunch the numbers, before the paper even got published, it came out that, again, there might be a bad cardiac signal. But remember, you're looking at a diverse population of women including grandmas, early menopausal and not even yet menopausal women, but on their way. So, it's tough to know if you're giving women to this diverse population--
[00:55:23] Was estrogen hurting one group and perhaps helping the other group? That didn't come out early on. But the newspapers, oh my God, it was all over TV. “Stop estrogen. Doctors are killing women.” And the MPA, CEA-- there was maybe a little breast cancer signal there. Nobody was looking at the intensity of that signal or what was the risk, but the headlines were nightmarish. So, HRT prescriptions were pretty high over a few years. Even gynecologists were prescribing a lot less HRT.
[00:56:00] You know why that was not good? Because as we now know, there are some women who can get nice benefit from appropriate types of hormone replacement therapy, and there are some women who should never get it for God's sakes. We're a little smarter, now we always are. As blips come in medicine, we always react and do and ultimately, it filters out, but it took a good 15 years of more post hoc analysis of these trials to see. So, now, the indication is pretty much perimenopausal early menopause, unless there's a reason not to use it, appropriate menopausal hormone therapy, if that's what you want to call it, is probably doing good.
[00:56:42] There always is a dilemma then at what stage should I go on forever, should I stop it? That's not an easy decision to make. But again, if a 75-year-old woman is walking in, I'm probably not starting her. This even applies to not only heart disease, it applies to bone, where you really want to get estrogen in early. Yes, we have other osteoporotic therapies. But in my day, it was the bisphosphonates. We drown women with them, and it took us 5 years, 10 years to find out, “Oh, my God, you're creating brittle bones in some women. You're killing too many damn osteoblasts. You don't want to kill it-- Or osteoclasts. You need osteoclast for proper bone remodeling.” So, that was another lesson we had to learn. And then, of course, the anabolic drugs got developed. We have so many more products nowadays. But that's a complex thing that has to be evaluated in a woman.
[00:57:28] Pelvic things is, I'm not going to put you per se on oral estrogen to help your vaginal wall or your prolapsed bladder or so. That's going to be localized estrogen therapy. So, again, it's another whole-- Even no matter what, you're a woman who needs estrogen therapy, is it unopposed? Is it opposed? If it's opposed, are you going to use progestogens? Is the natural progesterone, plus a ton of synthetic products called progestogen? So, with estrogen, which progestogen do I want to recommend? And if I do recommend it, at what points in the cycle? Or, is it intermittent? It's very complex how to figure out.
[00:58:11] And even now when it gets to the estrogen, there are not only are many different estrogen products. I prefer estradiol, which is what the ovary makes. But do I give it orally? Do I spray it? Do I rub it on her? Do I stick a high dose in her vaginal vault? So, you could see and how many do you believe. I will tell you no internist going to residency is giving any education on the complexities. Gynecologists might be. I would hope so, but they're not given any education on ApoB or how do I worry about the heart in a woman, or what woman would I not give estrogen because of the heart? What about LP(a)? That's very controversial too. Should you give estrogen [unintelligible 00:58:54]
[00:58:55] See, we're right back to what Cynthia and I told you, how does a woman get good care nowadays? How do you find a physician that knows everything like that? So, look, I think you got to go to the national or it's now called the Menopause Society, not the North American-- They would have people who are certified in that. Probably, a good choice. Certainly, if you know you have an ApoB problem or for sure an LP(a) problem, you might want to look out somebody certified.
[00:59:23] By the way, they're not all MDs. There are nurse practitioners, there are physician assistants, there are osteopaths and naturopaths. Osteopaths are really the same as an MD. We all have different types of training and interest. At your stage of the game, you should know what your problems are and you got to find the right person. But you don't have to be an MD, per se.
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Cynthia Thurlow: [00:59:47] If you love this podcast episode, please leave a rating and review. Subscribe, and tell a friend.
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