Ep. 474 How Menopause Impacts Heart Health with Dr. Sanjay Bhojarj

Today, I am delighted to connect with Dr. Sanjay Bhojraj, a board-certified interventional cardiologist turned functional medicine pioneer. After 15 years in conventional medicine, Dr. B realized that true healing goes beyond prescriptions alone and founded Well12, a transformational health program that helps millions rethink what it means to be healthy. 

In today’s conversation, the first in a series of discussions with Dr. B, we dive into the progression of heart disease in perimenopause and menopause, discussing the impact of the Women’s Health Initiative, the physiology of the heart and blood vessels, endothelial dysfunction, high blood pressure, oxidative stress, and inflammation. We also explore the limitations of the standard lipid panel, advanced cardiovascular testing, statins as primary prevention, microvascular dysfunction in women, heart rate variability, wearables, and the autonomic nervous system. 

You won’t want to miss this invaluable discussion with Dr. Sanjay Bhojraj, and I look forward to having him back for a follow-up episode later this summer.

IN THIS EPISODE, YOU WILL LEARN:

• The need for doctors to recognize the risk of heart disease in women, especially during menopause

• How nitric oxide maintains cardiovascular health and regulates blood pressure

• Why atherosclerosis is an inflammatory process and not just plaque buildup

• Addressing inflammation and oxidative stress 

• Benefits of HRT for improving women’s cardiovascular health 

• Advanced lipid testing reveals more about heart disease risk than standard cholesterol panels 

• What cardiologists are looking for when they do stress tests

• The challenges of treating microvascular dysfunction in women with medical interventions

• How heart rate variability can improve cardiovascular health

• How lifestyle changes and mindset interventions can lessen cardiovascular risk

Bio: Dr. Sanjay Bhojraj

Dr. Sanjay Bhojraj is a board-certified Interventional Cardiologist turned Functional Medicine pioneer. After 15 years in conventional practice, he realized that true healing is not found in prescriptions alone—it’s in the power of food, sleep, movement, and breath. He’s the founder of Well12, a transformational health program, and a leading voice online where his viral content is helping millions rethink what it means to be healthy.

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“We talk about normal labs in the conventional world, but in our functional world, we talk about optimal labs.”

-Dr. Sanjay Bhojarj

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Connect with Cynthia Thurlow  

• Follow on Twitter

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• Check out Cynthia’s website

• Submit your questions to support@cynthiathurlow.com

Connect with Dr. Sanjay Bhojraj

• The Laguna Institute for Functional Medicine

• Well12 Health Optimization Program

• On Facebook and Instagram 

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] Today, I had the honor connecting with Dr. Sanjay Bhojraj. He is a board-certified interventional cardiologist turned functional medicine pioneer. And after 15 years in conventional medicine, he realized that true healing wasn't found in prescriptions alone. He is the founder of Well12, a transformational health program and a leading voice online where his viral content is helping millions rethink what it means to be healthy. 

[00:00:55] Today, we discussed stats on heart disease and the progression of heart disease in perimenopause and menopause, the impact of the Women's Health Initiative, the physiology of the heart and blood vessels, as well as endothelial dysfunction, which drives not only cardiovascular disease but also high blood pressure and inflammation, oxidative stress, the menopausal machismo, the impact on longevity, why the standard lipid panel only demonstrates part of the story? And specific labs to further evaluate not only cardiovascular disease risk, but also inflammation the role of CT Angio, CIMT, and CAC, the role of statins as primary prevention and the numbers needed to treat, the impact of microvascular dysfunction in women, and last but not least, heart rate variability, wearables, the autonomic nervous system and the impact of lifestyle. This is a first in a series of podcasts with Dr. B. This is truly an invaluable discussion. And for those of you that know that I have this significant background in cardiology, we really enjoyed having this vigorous discussion and he will be back for a second conversation later this summer. 

[00:02:12] Well, Dr. B so good to have you on the podcast. We have a shared appreciation and love for cardiology and I've been really looking forward to this discussion.

Dr. Sanjay Bhojraj: [00:02:22] Boy, it has been months that our schedules have been misaligned, so I'm so happy to be here and just excited to talk about our topic today of cardiology, who doesn't love cardiology? It's the best. 

Cynthia Thurlow: [00:02:31] I know. Well, especially those of us that specialized in it for a long period of time that never leaves me. And I feel like even when I'm talking about gut health or talking about fasting, it's in the back of my mind I'm always thinking of you know what's the cardiovascular edge that we're thinking about? And I think particularly relevant to this community of women is heart disease is the number one killer of women, full stop, why are we not--

Dr. Sanjay Bhojraj: [00:02:57] Why don't we realize this? 

Cynthia Thurlow: [00:02:58] Yes.

Dr. Sanjay Bhojraj: [00:02:59] It drives me absolutely crazy that women don't realize this. But even scarier is doctors don't realize this. Absolute nonsense. The people you're turning to optimize your health don't understand what's the greatest threat to your health. It's frustrating beyond belief. 

Cynthia Thurlow: [00:03:15] Yeah. And I think one of the things that I probably did not realize enough, so I've been out of clinical cardiology for nine years, probably didn't know enough at the time because I was not yet middle aged, was the realization that transition from perimenopause to menopause increases your risk. according to the Framingham Heart Study, it's 2.6-fold higher risk of heart disease than in younger women. And I feel like very appropriately, we acknowledge that women develop heart disease later than men because of the protective effects of estrogen. But how many of us are actually having that conversation with our patients to help educate them about the changes that are occurring in perimenopause that are increasing our likelihood of developing heart disease if we're not working against them?

Dr. Sanjay Bhojraj: [00:04:03] Yeah. And heart disease doesn't just start in menopause age. It starts when we're young. And as early as the teenage years and over time starts to develop. So, when we look at studies of men, people-- They used to once upon a time in the military do autopsies of every GI that came over. So, we learned that from the Korean conflict soldiers who passed away, came over, that you could see evidence of fatty streaks in the arteries as early as 17, 18, 19. So, this isn't some switch that just turns on, but it's an added effect over time.

[00:04:38] So, in guys, our hormones are relatively simple. We don't have as much estrogen, so our effects add more linearly over time. The older you get, the higher the risk. But I think in women, you still have that same risk over time, but then you lose that protection. Right around the time when cardiovascular disease starts to become manifested, right around 40. So, you've had all that protection, but you've had some buildup, but then all of a sudden, at the same time that you're having the perimenopause-type symptoms and your estrogen drops now, we see that bump so you've had not just that time factor, but that loss of protection.

[00:05:18] And, I venture to guess that if you look at curves of the development of cardiovascular disease, that curve after 40 is accelerated. That slope is probably accelerated for women that aren't getting hormone therapy appropriately, as opposed to men who continue on that spectrum now. And even in the cardiology community, as you mentioned, it's just not something that we think about. 

Cynthia Thurlow: [00:05:35] No. And it's interesting because I finished my Nurse Practitioner Program at the end of 2000. So, I mean, I'm dating myself when I say this. 

Dr. Sanjay Bhojraj: [00:05:45] 2000 does not sound that long ago. 

Cynthia Thurlow: [00:05:45] I know. 

Dr. Sanjay Bhojraj: I still have shirts from the year 2000 that I wear. 

Cynthia Thurlow: [00:05:49] [Laughs] Well, at least I'm in good company. So, it was around 2002 when the Women's Health Initiative came out. And so obviously I was already in cardiology. But my female patients coming in and crying either in the hospital talking to me about the being taken off their hormone replacement therapy, all the aches, the pains, the symptomatology, the night sweats, the hot flashes, and I felt incredibly empathetic to what they were experiencing. Of course, I had no real sense of what they were going through. But that entire generation of women, that is probably our parents’ generation that were taken-

Dr. Sanjay Bhojraj: [00:06:22] Yeah. 

Cynthia Thurlow: [00:06:23] -off of HRT and then watching the sequelae of what has happened, along with a whole generation of clinicians that are still not talking to their patients enough about the value of HRT. 

Dr. Sanjay Bhojraj: [00:06:37] It's crazy, good news travels slowly slow and bad news travels fast. And so, if there was a single mulligan that we could take back of the paper, I think Women's Health Initiative is that one, because it really isolated. I mean we have this-- Unfortunately, endocrinologically speaking, a generation of feral women who had to fight it out for themselves because they were left behind by conventional medicine and so they had to turn to plant-based estrogens and all these different things because they were suffering so much. And, cardiology is great at this, that we look at what we care about, which is cardiovascular outcomes without looking at the rest of the human. I mean it was--

[00:07:20] And to your point, is it just a generation of women that have suffered, but a generation of doctors who still feel that hormone replacement is bad both in men and women, even though the evidence now suggests quite the opposite, but you just can't convince someone's mind to change because they've now anchored on that idea that hormones are bad and it's so frustrating to see. 

[00:07:45] And as a cardiologist, I remember when I started addressing hormones and I was in a multispecialty practice and one of the endocrinologists started getting angry at me because I was checking hormones on one of his patients like a hormone panel, and I said, “Well, this is your patient. Why is the cardiologist doing this? If you're so upset that I'm doing this, you should be doing this.” Not that I can't but we have to start thinking about this a bit more because not only is it an issue of patient comfort, but we're talking about actual cardiovascular outcomes. And in the same way that we treat cholesterol as a cardiology community, we should be looking at hormone, both men and women's hormones to optimize or at least get them to somebody who can. 

Cynthia Thurlow: [00:08:23] Yeah. I think-- Kudos to you for thinking outside that proverbial box. I think one thing in medicine that I find frustrating at times is the degree of cognitive dissonance. I always say, “I do not practice like a nurse practitioner like I did 10 years ago, 20 years ago. I have evolved.” And I think we all-- as human beings, we should all evolve, we should not be so rigid in our convictions that we're not willing to consider that. “Yeah, maybe things have changed. Maybe my opinion. Maybe the research and talking to other clinicians, that we need to be more open minded.”

[00:08:56] And right now, when we know that only 4% to 5% of women are actually on hormone replacement therapy, it's just one little statistic that really stands out in my mind. There's so much work that can be done that can improve not just the quality of our lives, but reduce our risks of ever developing heart disease. So perhaps one of the things that we can briefly touch on is what is happening at a tissue level in terms of what is happening at an endothelial level. So, inside the lining of these blood vessels, what's happening as women are losing estrogen? Because I think when listeners understand this, it helps explain why we are at greater risk of developing heart disease as we get older.

Dr. Sanjay Bhojraj: [00:09:39] Absolutely. So, when we look at the arteries, once upon a time we just thought of them as rigid pipes and that is very much not the case. So, when you look at an artery in cross section, it has three layers, really four, I guess. The outer is called the adventitia, which is the elastic layer, the middle is called the media, and the inside is called the intima. And then inside the intima, which is what we call the lumen of the vessel, we used to think of that as just a very static, passive thing, but now we've learned that there's a layer of cells in there called the endothelium.

[00:10:10] I think of it shag carpeting. Remember shag carpeting in your house that you grew up in the 1980s, [Cynthia laughs] so, it's a very active shag carpeting that has a lot of hormonal actions, it has a lot of receptors. And even now, we're learning, inside or on top of that endothelial lining, there's something called the glycocalyx, which is a layer of sugars. Not sugar, like glucose and fructose, but a layer of carbohydrates that helps mediate a lot of the signal transduction that happens inside cells. So, with that in mind, the endothelium is now a very active organ in regulating blood pressure.

[00:10:45] We used to think of arteries get stiff over time. Yeah, there may be calcium in there, but you're not going from rubber to lead. What's actually happening is our bodies are secreting less of the factors that allow it to be reactive and one in particular called nitric oxide gets very important. So, as we get older, as estrogen starts to decline. And in men too, what happens is that that nitric oxide synthase or the enzyme that creates nitric oxide starts to decline. Estrogen is a great hormone to have lying around because it's very anti-inflammatory, it protects lipids, and it is involved in cell signal transduction. So, with estrogen, particularly in women, what happens is estrogen's floating around, it binds the receptor on the endothelial cell, and then a whole host of intracellular factors are at play. So, increasing nitric oxide, but I think even more so decreasing inflammation. 

[00:11:41] And as a cardiologist, I think one of the biggest misnomers we have is we call it atherosclerosis, which the passive buildup of plaque. But really what we need to be changing our mental kind of mindset about is that this is really atheroscleritis? It's an inflammation of the arterial wall. So now you have a milieu where inflammation is at play. Inflammation causes damage of LDL particles that gets taken in. And now intracellularly, you have a whole host of bad players that happen that they can lead to high blood pressure, because now that nitric oxide, which is normally a vasodilator, isn't working correctly. The gap junction between cells, so the integrity of the lining of the blood vessels gets altered. So now these plaques or these LDL particles are more easily translocated into the artery wall. I think of that as leaky vessel. 

[00:12:34] Your listeners are probably very accustomed to hearing about leaky gut, but leaky vessel is what I call this. And so, we get accelerated plaque now because we've got more shots on goal. With estrogen depletion, we have higher LDL, higher triglycerides. You've got an endothelium now that's disrupted and has a lot more leakiness to it. And then you have intracellular signals, nitric oxide being a main one, that now isn't working correctly that leads to hypertension, which now pushes these plaques like almost physically, I think of it pushing them into the artery wall, so it's a bad player all around. 

Cynthia Thurlow: [00:13:06] Yeah. And I think it's so interesting, and I say this very objectively, that when I interact, my team interacts with women across social media. People send in podcast questions, they're emailing us. I think that there are many people that say, “My perimenopausal transition was pretty benign. I didn't have a lot of symptoms.” I have no symptoms in menopause, therefore, I don't need to even have a discussion about HRT. And what I oftentimes have to remind people is that things are going on beneath the surface even if you are metabolically healthy. And this interplay between estrogen and nitric oxide is huge. It is massive. And the more I understand about nitric oxide, the more humbled I am. And I will give a shoutout to my anatomy and physiology professor from, oh my God, 30 plus years ago. That's around the time that nitric oxide was discovered and people were talking about it. 

Dr. Sanjay Bhojraj: [00:13:58] Guy won the Nobel Prize for it right? 

Cynthia Thurlow: [00:14:01] Yes. I remember she basically saying to us-- Well, first of all, the one thing that she said to everyone in the room is, “If you are a premed of any capacity, if you can't get through my class with an A or B, you have no need to-- You might as well just hang up your coat. You don't deserve to be a clinician,” so that was, number one, Dr. Hart. Her name was Dr. Hart, of all things. 

Dr. Sanjay Bhojraj: [00:14:17] Okay. 

Cynthia Thurlow: [00:14:18] But now I fully appreciate and understand why nitric oxide is so important. So, for people that are asymptomatic, they're not having vasomotor symptoms, they're not having hot flashes, they're not metabolically unhealthy, I think there's this common misconception that they can navigate menopause without the addition or consideration, I should say, to HRT. And I'm here to say, even if you're not having symptoms, there's still inflammatory processes, oxidative stress that is a process of that loss of sex hormone signaling.

Dr. Sanjay Bhojraj: [00:14:52] So, we think about osteoporosis. Brain health like brain parameters change with reduction in estrogen, volumetric sizes of hippocampus and other brain structures. So, I'm not sure why there's this-- It's almost like a menopause machismo. [laughs]

Cynthia Thurlow: [00:15:09] Totally.

Dr. Sanjay Bhojraj: [00:15:10] You don't need hormone replacement, but it doesn't make a lot of sense. And it reminds me of--

[00:15:16] I had a patient one time who was having chest pain at nighttime. He called me. Well, I'll tell you the story. So, he had like the most severe chest discomfort of his life. And this is about 10 o'clock at night. And then he calls me the next morning and says, “Hey, Sanjay, can I come in? I need a to see you. Can I get an EKG?” “Yeah. What happened?” “Oh, I had the worst chest pain ever. And I decided, well, if I go to sleep and I wake up, it probably wasn't my heart. And if I go to sleep and don't wake up, it probably was my heart.” I'm, like “Dude, you're absolutely killing me. This makes no sense. You're a doctor for goodness sakes. Get checked out.” 

[00:15:51] And similarly, I think with women, they may be like well, I see Pam over there or whoever. She's having a hard time, hair's falling out, whatever it might be, I'm blessed that I don't have to deal with that, so maybe they feel guilty about needing to take the resources or whatever. But to your point, when you look a couple layers below, you really need to modulate estrogen in the same way that for men, we really need to start thinking about testosterone therapy because there are benefits above and beyond just the vasomotor symptoms or most guys think of testosterone as a virulency factor or putting on muscle, but it is central to our longevity. And really what are we talking about here is we want to live as well as we can for as long as we can, that's the whole health span idea. And hormones are essential. 

Cynthia Thurlow: [00:16:40] Absolutely. It's interesting. I just spoke at a forum past weekend and I was interviewed after I spoke by an amazing-- I think of her as one of these-- At the forefront was way ahead of her time talking about hormones, and so Dr. Erika Schwartz-

Dr. Sanjay Bhojraj: [00:16:55] Oh, yeah, I have like two of her books here, yeah.

Cynthia Thurlow: [00:16:58] -she's amazing. And she is 75.

Dr. Sanjay Bhojraj: [00:17:01] And she looks so great. 

Cynthia Thurlow: [00:17:02] And she is sharp as a tack. We were laughing about it. I didn't actually realize she was that age. She actually told me after we’re done recording and I said, “You are my hero. You are exactly what I want to be at that stage of life where I'm cognitively astute and sharp and able bodied and not frail.” And so, a lot of what we talk about in the podcast is why muscle mass is so important to maintain as we get older. And I know that we'll touch on lifestyles, but I think for everyone that's listening, I'm going to give you full credit for the menopause machismo, but there is definitely that kind of mindset around like “I don't need it because I don't feel bad.” 

[00:17:43] And I'm here to tell you, if I had not-- I would not have believed you and my internist could corroborate this. We looked at what my lipids looked like before I went into menopause and what my lipids looked like when I had a period of time, about six months, where I was off of HRT because we were trying to figure out what direction to go in. I would not have believed it was the same person. And I know that we're going to talk about lab values and some of the key players in lipids and inflammatory processes and why they're so important to check these, but I always say very humbly, I myself, I would never say it was menopause machismo, but it was like we were trying to shake things out, to figure out what direction to go in. But because I wasn't having symptoms, I was like “Oh, it's okay.” And then we looked at the labs and I’m like the labs don't lie. 

Dr. Sanjay Bhojraj: [00:18:25] Well, and I think there's a greater consideration here is that doctors don't understand that either. And so, if your teacher doesn't teach you something, you have no chance of learning it. My daughters just had their final exams and they're taking pre calc and their teacher put some calculus problem on there, and the whole class got it wrong. And my daughters, I've got triplet daughters, so they're all in the same math class, are crying and freaking out and I'm like, “Well, if the teacher doesn't teach it to you, how can she test you on it?”

[00:18:53] So, if as a healthcare community, we're not priming women, and that's why this-- the work that you do is so essential, really, I think, because it fills the gap of teaching women and people, humans, whatever, kind of where the conventional medicine isn't teaching them. It's a different approach. We talk about normal, “Labs” in the conventional world, but in our functional world, we talk about optimal labs. And I mean, just going back to the math example, yeah, 70 is probably a passing grade, but when my kids come home with a 99, I say, “What happened to that one point?” Because we want them to be optimal. 

Cynthia Thurlow: [00:19:28] [laughs] Right. 

Dr. Sanjay Bhojraj: [00:19:29] And that's generational Indian trauma, I'll tell you right now. But we have to do better by women. And kudos to you for empowering women and giving them agency to realize, “Hey, this is not normal,” and I think that as a cardiologist, I need to go back to my cardiovascular community and really, the drum on this, because I think we have an in to one of the earliest indicators of hormonal change, and that's lipid panels. Looking at lipid panels on annual basis-- if you're seeing a cardiologist for whatever reason, looking at cholesterol, if you're seeing a primary care doctor or an NP or whoever your primary care provider is, that is probably one of the earliest indicators that something is off, looking at that LDL cholesterol. 

[00:20:12] And how many of your listeners out there can probably relate to this as “My cholesterol was great forever, like in my 30s, and then all of a sudden one day, something happened and my LDL jumped.” It happened to my wife. She just had her labs done a few weeks ago, and she goes, “Oh, Sanjay, why is my cholesterol bad?” And we look back at the foundational things, diet, lifestyle, all those things because we went on vacation and this and the other, but I said, “You know what? this is bigger jump than just one week out of town. We need to start thinking about hormones and hormone replacement.” Luckily, we found her someone who did it correctly, which I can't say that I have the all the knowledge to be able to do it correctly, but at least I got her to someone who knows how to do it correctly. But it's one of the easiest things to look at is a lipid panel. Women are getting this on a regular basis, annually probably anyway, it’s like the check engine light for hormones really, because we see the consequences of that drop in estrogen. 

Cynthia Thurlow: [00:21:06] One of my biggest bugaboos and I again speak very openly about this, that traditional lipid panel, that is not in most instances, that is just scratching the surface. And how many people are in-- Like we have a free group on Facebook and they'll say, “And they know I cannot and I will not provide medical advice, but I'll give them things to, you know this would be a question. This is a resource.”

Dr. Sanjay Bhojraj: [00:21:27] Think about it [crosstalk] frameworks. 

Cynthia Thurlow: [00:21:29] And I'm like with the exception of triglycerides and HDL, I'm like, just because your total cholesterol is high or your LDL is high is not yet an indication of something that unless you've got vascular disease or diabetes or some other metabolic issue, it just means we have to look a little deeper. And so, from your perspective as an integrative cardiologist, what are your concerns and limitations related to that traditional lipid panel? So, we're talking about total cholesterol, triglycerides, HDL, LDL, looking at that kind of broadly, why does that not give us a full representation of what's going on? 

Dr. Sanjay Bhojraj: [00:22:07] Right. Well, I tell people it's like we're still going to blockbuster  with a black and white TV. [Cynthia laughs] When we look at this old panel, it was great technology for its time, but we need-- Now that we've got so much better tech, no one's going out to a super bowl party hoping to watch it on black and white Zenith ten-inch TV, right? We want these big screen 8K TVs, why? Because we have that technology available to us. And similarly, when we look at lipids, just as you mentioned, it's better than nothing to have the four horsemen, I guess- 

Cynthia Thurlow: [00:22:40] Yeah. 

Dr. Sanjay Bhojraj: [00:22:41] total HDL, LDL. But now we have the ability to look so much further beyond to see the individual pixels. And so, part of that equation has to be looking at LDL particle size and the distribution when-- Getting back to that leaky vessel thing, in clinic, I always talk with my clients about big and bouncy and small and sticky LDL particles. So, some people will have larger LDL particles and those are less likely to cause plaque. And it doesn't really work out this way, but I tell them it's like trying to throw a beach ball through a chain link fence, no matter how hard you try, it won't get through, that's not to say it can't in the biological world, but it's just less likely. 

[00:23:18] Whereas if you have the small dense LDL or oftentimes the oxidized LDL, that's like a golf ball. You can definitely throw a couple of golf balls through a chain link fence, so that's what really drives a lot of that plaque and atherosclerosis. And by the way, that's all cardiometabolic disease. So, there's cardiovascular disease, which is blockage of the arteries, but then there's cardiometabolic that sets up these lipid abnormalities. And so, we have to look a little bit beyond just that LDL number, more specifically to what types of LDL are we looking at? :Oh, I got a new car.” Oh, really, what's the next question you ask? “What car did you get?” Did you get a pickup truck? Did you get a sports car? There's more detail, right? You wouldn't be talking to a friend and not ask a follow up question, right? So, are we talking about really benign LDL?

[00:24:06] I've had actually a female patient of mine who I had a few years ago. Her LDL was like 180 something and got a little bit nervous about it because we could be talking about familial and these issues. And so, we did an advanced lipid panel and she had the biggest, bounciest LDL, fluffiest LDL particles I've ever seen. So, it added a nuance to our discussion because now, I had a little bit more time to breathe. We did some tests and we can talk about what tests I like, I guess. But that showed that she didn't have a lot of vascular inflammation, she didn't have a lot of soft plaque in her arteries. And so now it was a much more nuanced discussion as opposed to, I think what you normally get at a cardiologist, which is LDL high, rubber stamp, here's your statin prescription. And so were able to engage in shared decision making and she opted to try for a more natural, integrative approach. And I was actually okay with, I mean, medicolegally had to sign waivers and stuff, but felt comfortable as her cardiologist saying, “You know we’re going to be okay.”

[00:25:00] On the flipside is that you can be hiding things in that total cholesterol or that regular LDL C number, which is a calculated LDL number. And like myself, so I have a horrible cardiometabolic family history. Just being Indian, that's just kind of how we roll. I say what God gave us in brains and engineering and medicine, he took away in cardiovascular health. [Cynthia laughs] 

Dr. Sanjay Bhojraj: [crosstalk] So, we got in double dose of one and none of another. But my LDL on statin is not bad. It was 104. I've never had a heart attack or anything like that, so thankfully, knock on wood. So, a reasonable number. So, if I just stopped at a total cholesterol and an LDL, “Hey, Sanjay is going to live forever,” but then we looked at my particle size and I don't know how many of these you've looked at, Cynthia, but my LDL particle size was 197, which is the smallest I think I've ever seen in my career. If this were a gold medal sport, I'd be like the Usain Bolt of bad lipids because I'm so far ahead of the game, like Katie Ledecky when you see her swim. So that really changed the game for me and I realized that I need to focus not just on LDL as a number, but my diet, but my lifestyle. Really working on insulin resistance, really increasing lean muscle mass. For me, really reducing carbohydrate intake, which is hard because ancestrally the Indian diet is carbs because we don't have refrigerators ancestrally. So, proteins and fats are less shelf stable in heat, so what sits around forever? Rice and wheat and flour and all these things that are essential in our diet. So, I really had to do a major overhaul based on my numbers.

[00:26:39] But getting back to the original point is had we not done an advanced lipid profile, I probably would have been high fiving and chest bumping with my primary care doc, because “Hey, my cholesterol is great.” On the flipside, so that's LDL and HDL. What we're learning about HDL, which is the “Good cholesterol,” is that it may not be as helpful as we think because we actually have different types of HDL and some are to quote “Animal form, more equal than others,” so some HDL particles are more protective, some of them are less protective. 

[00:27:08] What folks may realize, and you have an intelligent audience, but what some people who aren't as well versed might not realize is, when you look at these things under a microscope, they don't say HDL or LDL, but what we do is look at certain cell surface proteins, so certain markers on the cell that are expressed to say this is an HDL particle, this is an LDL particle. And that's where ApoB comes from ApoA, that's kind of what we're talking about here. And so, you may have a high population of HDL cells by an ApoA cell surface protein, but they may be kind of small, remnant, useless HDL particles.

[00:27:43] HDL tend to be scavengers, so you want them to kind of pick up these busted up, broken particles, so you can have a high HDL, but if they're all the crappy, junky, nonfunctional HDL, you're not going anywhere. And in fact, there's data that shows that folks with a higher HDL, actually, I think it's over 75 or 85, actually have an increased cardiac risk. There's a U shape to it. So, we're learning about a lot about lipids. And it's funny, I call myself a lipid nerd, but who knew it would be this interesting, but there's so much now nuance behind these advanced lipid tests.

[00:28:22] And I think the other part of this equation is there's so few practitioners who really, really understand how to use them. And so, like I think about going and shopping with my daughters. If I'd never had the occasion to have to go into one of these stores where there's teenager crap all over, I would never go in, because I have no use for it. So similarly, if the doctors don't have a use to understand how to interpret these things, they're just not going to order it. They're not going to go in the store. And who suffers there? The patient right? because we're not truly truly reducing that CV risk that we were aiming for. 

Cynthia Thurlow: [00:28:54] Well, and I can't tell you, this is a huge pet peeve of mine. How many women will say my total cholesterol is 225. So, my provider wrote for a statin and I was like-- And then in my head I'm thinking, “You don't have heart disease, you don't have diabetes. You're telling me the rest of your lipid panel looked fine.” And if anyone's listening, we're not telling anyone to stop anything they're doing. What we're saying is we're giving some high-level concepts. 

[00:29:20] But I think for a lot of individuals, and I say this politely and conscientiously about our medical peers, is that a lot of people are still focused on just that lipid panel and they're not looking at particle size, they're not looking at ApoB, they're not looking at Lp (a), they're not looking at fasting insulin, they're not looking at other inflammatory markers. So, in the milieu of your work, let's talk about ApoB, why it's important to look at. Let's also talk about Lp (a), which we know is genetically mediated. I happen to be one of those people who won the genetic lottery. And without medication or without HRT, my ApoB and my Lp (a) would be quite high. So, some things we have control over, others we do not. As you astutely stated with your ancestry, you have to do a lot of lifestyle to reduce your risks. Let's talk about these other markers. And then there's more than that. I'm curious to see some of the other things that you're using in practice. 

Dr. Sanjay Bhojraj: [00:30:15] Yeah, well, let's go back to the statin discussion, because when we look at our conventional colleagues, what they're looking at is they plug your numbers in to a calculator and based on that risk they decide do you need a statin? So, if you have a 10% or higher risk, it's a no brainer. If you have a 5% or less risk, you can consider it. And that 7.5 that average risk is where you are supposed to start people in the low-dose statin according to these guidelines. And new guidelines just came out, lowering the goals even further which is a perfect example of cardiologists are for Mars and everyone else is from Venus- [Cyntha laughs]

[00:30:53] -because we're talking about CV risk, we're not looking at brain health and hormone health. We know what happens when someone's cholesterol is -6, yeah, they may not die from heart disease, but they can't think and they're forgetting to put pants on when they walk outside because they're so cognitively dysfunctional. 

[00:31:06] But when we look at something called primary prevention of cardiovascular disease, meaning you have not had stroke, you've not had cardiac risk equivalent heart attack, diabetes, whatever it may be that we calculate a number called number needed to treat. So how many people do you need to treat to save one life? And it is a very well-intentioned statistic. And studies are designed in different manners. And so, number needed to treat is the way we try to compare apples to apples and oranges to oranges when we look at different studies.

[00:31:37] And when we look at the primary prevention number needed to treat depending on the study that you're looking at, it's anywhere from 90 to 120 or so. So, let's say 90 people. So that means that you're treating 89 people who will never get a benefit from statin medication. In this discussion, the statin medication to save one person who can. And if you're not clear about this, you can go to the Mayo Clinic Statin Decision Aid, plug in your numbers and it'll show you these numbers. This isn't something I'm making up. This is something that's known, but yet, we are treating people with these medications. And I'm not saying statins are evil. I'm not saying they're great. Some people have problems with them, some people don't, but we just have to be more precise. And so now we have these other tools available. 

[00:32:21] I mentioned Lp (a). We'll start with that one first. So, Lp (a) is a lipoprotein, again, cell surface protein that exists that is more or less a genetic determinant of cardiovascular risk. Now fortunately for me, I have a low Lp (a), which means that lifestyle changes really can make a difference in shifting my cardiovascular risk. I had a patient who every year for Christmas, his gift to me on December 21st, 22nd or 23rd would be to come in with a heart attack and like literally for five years in a row. I would--

[00:32:53] His name, I won't say it, but let's call him Steve, not his name, but I would call him up on December 19th and say, “Hey, Steve, you know joking, if you're going to have a heart attack, I'm here for the next few days and then I'm gone.” And sure enough, I don't think it brought it to earth, but he would come in and have to put a stent in him. And finally then Lp (a) came out as a marker and his was like bonkers high, it was like 250 or 300- 

Cynthia Thurlow: [00:33:15] Oh my gosh. 

Dr. Sanjay Bhojraj: [00:33:16] -or some ridiculous number. And now at least we have therapeutics in investigational trial and I think they were just reported. So, we have something that we can do to change this. 

[00:33:27] Famously, that trainer from The Biggest Loser had a heart attack and he talks about it in the public sphere. So, I forget his name, but he had a high Lp (a). And so this is definitely an adjunctive risk, so, you definitely want to get that checked. Interestingly, some of the conventional therapies that we use do have a modulatory effect. Some of the new injectable cholesterol medications can bring it down modestly. 

Cynthia Thurlow: [00:33:47] Yep. 

Dr. Sanjay Bhojraj: [00:33:48] Hormone replacement can bring it down. So, it's not a stuck in time, but you're still going from super high to slightly less high. So, now there are these therapies. So, Lp (a) is a really important marker to look at that is not in the conventional universe yet, but it's definitely getting more traction to look at this. 

[00:34:07] And I think interestingly, and Cynthia, I don't know if you felt the shade that we get from our conventional colleagues, but this is something that I was checking years ago when it was heresy to check these things. And now that they're thinking therapeutics in line, now everybody's checking it, because we have a drug to treat it. You know kind of we're always at the front of the line. The person at the front of the line gets the most spears in the back or whatever. But I think Lp (a) definitely part of that conversation. 

[00:34:31] ApoB is something that we should be looking at. So, we have in our mind again, because of the conventional lipid panel, LDL, HDL in our mind. So high density lipoprotein, low density lipoprotein, but what we forget is there are whole middle ground of IDLs, intermediate density lipoproteins, VLDL, very low-density proteins, all of these lipoproteins, all of these other cholesterol particles that are atherogenic. So ApoB is-- We talked about those cell surface markers. ApoB is a marker of these atherogenic lipoproteins. And as opposed to things like checking LDL particle size or particle number, all these things, ApoB is an excessively inexpensive test. I mean, it’s like five or ten bucks and it's not something that you need to go to a specialty lab for. So, if people are not getting this checked, I think they absolutely need to advocate, hey, can you just-- For your clinician, it's just checking a radio button. 

[00:35:27] I used to-- This is how old I am. I just used to checkmark on the lab slip- 

Cynthia Thurlow: [00:35:30] Correct 

Dr. Sanjay Bhojraj: [00:35:31] -but now it's another mouse click. So just it's a mouse click to check, but it really does give you a much better idea. And we have a whole robust literature now looking at the cardiovascular outcomes associated with elevated ApoB. So, it's something so easy to check that we need to look at. 

[00:35:47] And then we talk about other advanced markers. So, I like markers of vascular inflammation. So high-sensitivity CRP, something called myeloperoxidase, Lp-PLA2. That last one is different than Lp (a), so I think people get that oftentimes mixed up. But Lp-PLA2 is a marker of vascular inflammation. Myeloperoxidase is just kind of a nonspecific marker of inflammation. And then high-sensitivity CRP in and of itself is a marker of cardiovascular risk. 

[00:36:15] So we need to take the three of these together to really get a more robust look at what's going on. Just like in the Cath lab, we have to look at two projections of the same artery to put things together. Because if a pen looks like this in one view and this in another view, you don't have an idea of what the three-dimensional look is. So, I like to get those as markers of what's going on, because now not only do I have an idea that there are a lot of LDL particles or not a lot of LDL particles around, but the inflammatory markers then give me insight into what's going on in the vascular tree and in the body in general. 

[00:36:49] Homocysteine is another one to add into there. There's a lot of prognostic information about homocysteine. How long is this podcast? Things like small dense LDL is something, oxidized LDL, another glycosylated LDL. All these damaged LDL particles floating around. Because again, getting back to what we talked about of inflammation and atherosclerosis, it's the damaged LDL particles that get associated as having damage associated molecular patterns or DAMPs. And that's what initiates the immune cascade. That's what then, you know I think of Hungry Hungry Hippos, remember that game? 

Cynthia Thurlow: [00:37:21] Yeah.

Dr. Sanjay Bhojraj: [00:37:22] The immune system starts grabbing up like Hungry Hungry Hippos, grabbing up all of these circulating lipid particles floating around and bringing them into the blood vessel to sequester them out of the way, so there's a lot of things that can be done. 

Cynthia Thurlow: [00:37:33] Yeah, it's so interesting because I feel like every time I have a discussion around lipids, there's always some nuance, there's something a little bit new. Maybe there's another new lab test are using any of Boston Heart Cholesterol Balance Testing? The reason why I'm asking is this has been huge in terms of helping patients or clients. Oftentimes I'm asked to consult with someone's internist, you know this is the lipid panel. These are the things, the parameters we're looking at. But for someone that if we're trying to differentiate, are they a hyper absorber, are they a hyper synthesizer? What's the best drug modality given what we're seeing in terms of this pattern? Do you feel the Boston Heart Cholesterol Balance Test in particular is helpful? 

Dr. Sanjay Bhojraj: [00:38:14] I mean, so I don't know that we could names, but yeah, I love that. 

Cynthia Thurlow: [00:38:17] Yeah. It's fine, it's fine. 

Dr. Sanjay Bhojraj: [00:38:19] Yeah, I love that panel actually, because rarely you will find someone who's an over absorber. And so, this is another one of the things that people don't realize is that you have something called the enterohepatic circulation. So, your liver secretes bile. Bile is a cholesterol salt that gets spit out to help you digest fats, but then your body reabsorbs it. And so, you have this constant turnover. And so, for some people who really over are very efficient absorbing their bile is that they are also unfortunately very efficient at the absorption of cholesterol from the gut. 

[00:38:50] So, you can look at-- We think of cholesterol as a particle, but there are these precursors to cholesterol. So that's what they're checking is the precursors of synthesis of cholesterol versus the precursors of absorption. And those are two very different pathways. So, I actually love that test because it really helps inform me as to what's going on. If someone is not on therapy and they're an over producer, well, then we have to look at production. If somebody is an over absorber, then putting them on a statin will help, but it may not be the best therapy for what they need. Or for that matter, if somebody's on therapy like an injectable or an oral for cholesterol and it's not quite as at goal and they have high absorption markers, then I know that adding in a bile acid sequestrant, kicking it old school, or a medicine like Ezetimibe or even some of the plant sterols and things may help get that actual nudge that we need to get their cholesterol at goal, so it's all part of the information. I think the problem is not having the information. It's having a provider that knows how to interpret that information and use that information. 

[00:39:56] In Boston, I think, in particular does a great job with their education to really help providers understand. So, I absolutely love that test. The only time I don't use it is when we go through insurance for patients and they have to go to a different lab that doesn't do that. But I've also found, though, that when I specifically discuss with my patients why I think this is a good test, and luckily, I'm blessed to work in Orange County, Southern California, where we have people who have means, but it's a way that-- They don't mind paying the cash for it. But if you're not in that location, then I think getting an ApoB, even if you don't have access to an advanced lipid profile, is very important. 

[00:40:32] I grew up in the middle of nowhere, Indiana. And so, when I think about my patients back in Hobart, Indiana, if I'd practice there, they might not have had the ability to spend a couple hundred bucks on lab tests, but they can certainly spend 10 bucks for an ApoB. So, but yes, I do love that test in particular. I feel clinically it's very relevant. 

Cynthia Thurlow: [00:40:48] Yeah. And the one thing about that particular test is I think it's under $100. So, if it's a differentiator, if someone's having a conversation, they're anxious about statin therapy, understanding are you a hyper absorber? Are you a hyper synthesizer? In some instances, can give them some peace of mind because we know that there are options that may better for them. 

[00:41:08] Let's talk about coronary artery strands and CIMTs. These are these tests that I think can be very helpful. Most importantly, because you're not exposing yourself to tremendous radiation, which is one of the issues that-- If someone needs a CT angio, and I'm sure we can unpack what that is like explaining that there is some radiation exposure like there are with most diagnostics, but I think these can be very helpful and tend to be inexpensive, occasionally covered by insurance. Although it seems like insurance companies tend to lag way behind technology, which is unfortunate. 

Dr. Sanjay Bhojraj: [00:41:42] Yeah. And that's intentional. They're not getting paid to save your life. They're really a for profit company is paid to not spend the money they're paying them. That's a whole other podcast. I will stand down from the soapbox. [Cynthia laughs] 

[00:41:54] But atherosclerosis is a generalized process. I remember it was at W.C. Fields that said, “I'm not prejudiced, I hate everybody just the same.” So similarly with atherosclerosis, if it's happening in the heart, it's happening everywhere. As an interventionalist, I would basically fix stent and balloon from the neck down to the toes. So, I can vouch for the fact that if you have it in your heart, you've probably got everywhere. 

[00:42:19] In fact, I think there's a 30 or 40% association with carotid artery disease and coronary disease. So, as we start screening for this, there's a lot of different modalities and I'm going to share the dirty secret of cardiology. You may know it, but a lot of listeners might. So, if you're here, don't tell anyone this [Cynthia laughs] because the cardiologist will be upset. Is that when we're doing stress tests, treadmill tests, nuclear tests, echo-based stress tests. Those tests are really geared to find flow limiting blockages. So, 70% or more. Those are the types of blockages that would tend to cause symptoms of what we call angina or angina, depending on where you grew up. That elephant on my chest or that heartburn sensation or the shortness of breath with activity or whatever, but they would tend to cause symptoms.  

[00:43:04] But the plaques that rupture and cause heart attack are generally not the calcified ones because those are mature plaques. It is the 30%, the 40%, the 50% lesions with thin caps really inflamed milieu, I think of it like a jelly and the jelly donut has been replaced by battery acid. So really inflamed subocclusive, that's even a word, but they don't block, but they're there and those are the plaques that rupture. So, a stress test, if you're running on a treadmill is not going to pick that up. That's why, we have these stories of so and so got a stress test on Tuesday and came in on Wednesday with a heart attack. These are stories that happen because the test that we think is testing for what we hope it's testing for is not testing for that at all. 

[00:43:49] I feel like I'm in that Friends episode where, was it Rachel and Joey were like, “I didn't know you know about them dating or whatever,” Monica and Chandler. But the test that we hope is testing for our cardiovascular risk isn't really testing for anything but flow limitation blockages. So, we have to look beyond those tests and look into other things.

[00:44:09] And so, with a CIMT scan or carotid intima-media thickness, what we can see is now an ultrasound-based test. So, we're not giving ionizing radiation. Looking at an easily available-- for most people, easily available arterial bed that gets a lot of flow. There's a flow separation. So anytime you have a fork in the road, so to speak, you have turbulence. So, we see that they're coming off the aortic arch. There's a flow separation there going into the internal and external carotid. There's a fork in the road there as well. So, an area that we can see where there's this turbulence now and get a sense of is the wall thickening. Those Hungry Hungry Hippos, are they at play bringing in those LDL particles into the media? That middle part, that middle layer of the blood vessel or are there calcifications? You can pick up asymptomatic carotid artery calcifications on a test as well. 

[00:44:59] So, carotid intima-media thickness is one that you can check. We talked about our good friend the endothelium earlier. So, you can do brachial reactivity testing to see-- You squeeze the blood vessel and see how quickly it reacts so we can get a sense of how the endothelium is working. Those are relatively noninvasive. That also, by the way, is why you need to wait five minutes between checking your blood pressure if you're going to check it on the same side.

[00:45:25] I have patients that-- And a lot of the blood pressure machines just jam out three concurrent events and three concurrent blood pressures and then take the average. That is not how to do it. You actually have to-- feet on the floor, arms at heart height. There's a whole reason for that, but you can't just jam out of blood pressures because if you have endothelial dysfunction, the second, third one will often be not reliable. 

[00:45:46] And then as we go into more ionizing based therapies, then we have to be aware of I think two in that field, which are coronary calcium scores and CT angiograms that we talked about. So, both of these tests are CT scans or CAT scans. A calcium score is a nice test. It's a lower radiation scan that we do of the heart and we're actually able to look at the arteries and identify islands of calcification that are associated with greater cardiovascular risk. And so, it is one of the most scary tests to get the report back for because you will always get this normogram that says “Based on your arteries, you are 8,000 years old or something.” [Cynthia laughs] And so, we always have to talk to the patients about what this means. But it's nice in the sense that you know for the patient you can actually see your arteries, you can see where the blockage is. 

[00:46:34] As we're talking about motivators for change, I think that's a very intense motivator for change. I know I had a calcium score, it was not zero. And that's part of the reason why now I'm so into diet and lifestyle, because I need to be, I want to be around. And so, it's a useful test. Now, things that can hide in the calcium score, noncalcified plaque, so soft plaque. So, you can have a calcium score of zero. We talked about those 20%, 30%, 40%, 50% lesions that are immature. So, you can have a bunch of those that are not calcified by the way that the original testing was done, you can have a zero-calcium score. Of course, you have a lower risk than someone that has a boatload of calcium, but that doesn't mean that risk is zero.

[00:47:14] So, I remember all the time, my patients would be like, “Oh, I have a calcium risk of zero. I'm going to live forever.” I'm like, “We still have to work on your cholesterol, brother. We still have to get you off smoking.” When I worked in the Midwest. “We still have to work on all these modifiable risk factors because it means that you're at less risk, not no risk.”

[00:47:32] And then newer now in the fold are what are called CT angiograms. So, an angiogram is a test where you directly visualize the blood vessels, and this is what I used to do as an interventionalist, is going through the artery in the wrist or in the artery in the groin, snaking up a catheter invasively, actually putting a little plastic tube or a straw into the blood vessel, and then injecting a substance called IV contrast under an x-ray camera and looking at the blood vessel. 

[00:47:32] Now, the misnomer there is not-- We're not really looking at the blood vessel itself. We're looking at the lumen or the opening of the pipe where the water flows, where the blood flows. And then based on that would say it's a 10%, 20%, 30%, whatever amount of lesions. And then, in the time we've had this conversation, if there was a need, I'd pop a stent in, we'd high five, chest bump and call it a day.

[00:48:14] But now we can do this less invasively. So, with just a simple IV and do a CAT scan version of that or CT coronary angiogram or CCTA as we call it, which gives us not just an idea of the lumen or the opening, but it's actually cracked open a whole new area for us to evaluate, which is the actual blood vessel wall. And there are new AI-assisted technologies that are available to us to quantify soft plaque. So, this is what people don't realize about plaque, is that you have the lumen here. And initially plaque grows outward, so it grows away from the lumen. And I don't know that the biology is actually like this, but this is what I tell patients, is that there's that outer layer that we talked about, the adventitia, it's like a rubber band. So, you stretch that until you can't stretch it anymore, and then that plaque has nowhere to grow but inward, right? So now you've got this lumen that starts to get that push from the plaque, and that's where we get blockages from.

[00:49:08] So, you can have a 10% compromise of the lumen of the artery or the opening of the artery with-- if you look at by surface by cross-sectional area, could be a 40% or 50% soft plaque that's now encroaching into the flow. So, the conventional angiograms that we did, not so helpful. I think these CT angiograms and these AI-assisted technologies clearly are awesome. There's no free lunch, now we have to worry about radiation exposure. So, we have to think of these things and that's a nuanced discussion to have with your doctor. I don't think it's something that everybody needs to get, but I think a lot more people need to get it than we are checking right now, simply because of this uptick in metabolic disease and insulin resistance that we're seeing. And really insulin resistance loads the gun and we need to make sure that we've got less bullets in the chamber. Sorry, I feel like I'm from Texas now talking like this, but not California. But we need to reduce our risk, control the things that we can control so that we don't start seeing an epidemic of heart attack.

[00:50:10] And I'll tell you one thing as an interventionalist, the difference between metabolic and cardiometabolic coronary artery disease and the good old days of smoking is that when people would smoke, I would have to do spot welds. It was just one little area. 90% blockage, pop a stent in, call it a day. Now with cardiometabolic disease and insulin resistance, we're seeing entire segments of vessel, 30, 40, 50 mm of vessel now that are affected. And so, you're having to put in longer and longer stents or more and more stents. The scary thing about that is we are losing targets for heart bypass. And so being someone who lived on the inside of people's blood vessels for the better part of the 15 to 20 years that scares the crap out of me. And that's why, I'm focusing this next chapter of my career on really helping people understand the burden of cardiometabolic disease and that it's completely something that we can modify through diet, lifestyle, and meds when needed.

Cynthia Thurlow: [00:51:02] Yeah. And it's such an important discussion. One thing that we have never discussed on the podcast, but I think is important is that men and women obviously are very different. Women tend to have more small vessel disease. So, when you're talking about as an interventionalist, going in and opening up an artery, women tend to have this small vessel disease, things that aren't easily addressed with an intervention. Let's talk a little bit about why that happens and why that's significant. We know that women tend to present later with heart disease symptoms because we take care of everyone but ourselves. But small vessel disease is something that I understand more now than I did before, but help listeners understand what this is and why we tend to see more of this in women. 

Dr. Sanjay Bhojraj: [00:51:47] Yeah. So, there are the arteries that we see. So, the large vessels and. And, we can resolve in the Cath lab up to like half of a millimeter. So, boy, you think about what a half of a millimeter is- 

Cynthia Thurlow: [00:51:58] I know.

Dr. Sanjay Bhojraj: [00:51:58] -that's a pretty tiny vessel. In our world, the difference between a 3, 2, 5 stent and a 3, 5 stent is a world of difference. We're talking about a quarter of a millimeter here. I mean, the level of precision we have to have is important. But women tend to start out and. And, I don't want to make a generalization, but in general, smaller arteries than men, but then a lot of times, the disease that we see in women isn't the visualizable vessels, but we branch and branch and branch and branch. And so, it's not the highways, but the small neighborhood side streets where you see a lot of the problem. And the concern there is that we don't have stents. You wouldn't want to put a 0.25mm stent in. It would plug up like almost by definition. And so, we have to manage these medically. And fortunately, there are some medicines that work, but I think a lot of that is the hormonal milieu treating the endothelium, all of these things. 

[00:52:51] In the course of my career, I can think easily of four or five female patients that I had who for all the world had significant anginal symptoms. I mean like elephant on my chest when I walk up a flight of stairs. We did the workup, nothing else that would cause it. Took the patients to the Cath lab and their arteries-- I should be so lucky to have arteries like theirs, but in the sense of the large arteries. The small vessels or the microvascular dysfunction is what we see. And in the Cath lab, we look at how quickly The IV dye that we inject clears. It's something called the TIMI Blush score. So you go from the arteries, the myocardium gets a little bit of a blush, we call it, and then the dye works its way into the venous system and out. And what we see oftentimes is that there's a delay in that excretion or drainage or whatever I'm supposed to call it, of the IV contrast and so that indicates microvascular dysfunction. 

[00:53:43] It is difficult to treat. In Cath lab, there are medicines that we can inject to provoke and see if we can cause problems. But you're not going to go in and inject or squirt your coronary arteries with something every time you have this, so, it becomes very difficult to treat. But interestingly a lot of that can be hormonally mediated kind of mindset. These tend to be in high anxiety people and men and women both have this, but that's where kind of the diet and the mindset and looking at that things like heart rate variability and deep breathing and all these kind of soft woo-woo kind of things that I shouldn't as an interventional cardiologist ever think of, but these are these interventions that we need to take because literally our minds and I call these virtual tigers, these threats that we impose like a tiger is going to jump out of us. But living in that constant fear state starts affecting over time arteries and our heart. And so, we need to think of different things. 

[00:54:38] So, to your point, yeah, women do tend to-- I see it more often in women than men, these microvascular issues. Then what we do is not statins and all that stuff. And now we have to look at “What's going on?” And the simplest question that I learned to ask because of my functional medicine training honestly is “Do you feel safe?” I mean, that is not a question that I would have asked 10 years ago. And it is unnerving to me as a girl dad and as a husband, like how many women?-- My eyes will start to tear up when I say this, but how many women don't have that in their lives? And it is scary. 

[00:55:14] And we want to talk about a silent epidemic, it's just not right. And just something as intervention is simple as having that conversation. And by the way, interventional cardiologists, if you don't know, we're supposed to be like cavemen. We like grunts and that's about it, right? [Cynthia laughs]

Dr. Sanjay Bhojraj: [00:55:28] Most of us don't have full -- You worked in cardiology. We just grunt and yell. That's kind of how-- That's our lovely language. But to be able to have a discussion and realize something about your patient, and then for me to connect them with the right resources, I mean that I think is as important as any stent I've ever put in. It starts with such a simple question. 

Cynthia Thurlow: [00:55:47] Well, such an important question, because one thing that we do unpack on the podcast with some frequency is the role of Trauma, trauma, and everything in between. And, kudos to you for initiating those kinds of conversations because more often than not, we as healthcare providers shy away from those kinds of discussions because maybe we feel uncomfortable, but yet it's so critically important that a patient, first of all, have someone acknowledge that perhaps they're in an unsafe environment, perhaps they had significant childhood trauma that is leading to dysregulation of their autonomic nervous system, which can put them at risk for a constellation of health issues, not the least of which this particular microvascular dysfunction that you're talking about in terms of the heart. 

[00:56:33] I would love to invite you back because I feel like there's so many things that we could have gotten to. You just did such a beautiful job of the topics that we did cover. Before we end the conversation today, and hopefully I can persuade you to come back. You touched on heart rate variability. You touched on autonomic dysfunction from your perspective as a cardiologist and as an integrative practitioner. Let's talk a little bit about why this is so significant. Obviously, we do talk about these topics in particular, but not from the perspective of cardiovascular risk and risk reduction and how that influences our heart health.

Dr. Sanjay Bhojraj: [00:57:08] Yeah. So, for those of you who don't know, your heart beats right, at 60, 80 beats per minute, and it's not a metronome. It's not click, click, click. There are microsecond, millisecond variabilities in your heartbeat, and that's normal physiology. As you breathe in or out, we see changes in the heart rate, and so we quantify that with a metric called heart rate variability. So, we aggregate these minute-by-minute differences. And wearable devices are actually really good at this. I'm completely plugged in, like every hand and finger and orifice has some sort of a wearable, so you're right with me. And so, it's a--

[00:57:45] Before it was a research tool, and a million years ago when I was in cardiovascular research, I focused a lot on heart rate variability, predicting arrhythmias and things. And then from there it became a biohacker tool. And now it's actually now in-- Kudos to the biohacker movement for a lot of times introducing these things that become part of the contemporary parlance. And so now like almost any device that you have, fitness tracker that tracks your steps, blah, blah, if you wear it 24 hours a day, it'll have some metric heart rate variability, readiness score, fitness score, recovery index, whatever that particular technology calls it. And it's a window into where we are with our sympathetic nervous system, that fight or flight, I'm under attack system versus the parasympathetic nervous system, which is the cool rest, repair. It's like the McConaughey, [Cynthia laughs] “Dude. Hey, calm down.” So, you've got Robin Williams revving you up and McConaughey revving you down, right? 

[00:58:38] But our bodies are always living in a state of tension. It's like a thermostat of that rev up and cool down. So, heart rate variability gives us a very easy way to sort out where on that spectrum we are. 

[00:58:49] HRV scores like basketball, not like golf. So higher scores are better than lower scores. And now as you start to learn this and track it, I always say you can't hack what you can't track. So, as you start to look at your HRV scores, you will see that some days are better than others. And you will see that on days where you're stressed out or you're not sleeping as well, or you had an extra caffeine drink, or for me like alcohol. Rare occasions that I drink it will drop my HRV significantly. 

[00:59:16] But on the flip side, when I have a great night of sleep, like I actually tried a new sleep supplement yesterday, and my heart rate variability jumped 20 points, which is unheard of for me. I don't know if that was a fluke or what. So, I have to test it out tonight as well. What that means is my body in a much more relaxed, calm state. And if you think about it, your body has to be in a parasympathetically mediated or dominant state to repair, to heal. You cannot heal when you're sympathetically driven. 

[00:59:44] And what does that mean to be sympathetically driven? Well, I'm multitasking I have-- My daughters just got their driver's licenses finally, but I was bouncing around Orange County driving around from here to there, trying to mediate phone calls and take this meeting, I had to apologize to take this meeting from the car. And then, oh my gosh, my wife went out of town, so I was having to prep the meals. And not that whatever-- But we all have like a million things that pull us in a million different directions. And so, we just live in the sympathetic dominant state all the time. So, our heart rate variability is low. 

[01:00:15] When I first started tracking HRV when I was-- as an interventional cardiologist, I would be lucky if I'd see the other side of 15. I mean, my Oura ring actually would poke me and say, “Hey, are you still alive?” [Cynthia laughs] 

Dr. Sanjay Bhojraj: [01:00:27] -which is horrible. And what we see then is as you're more sympathetically driven, there's a higher risk of arrhythmia, hypertension, inflammation, all of these things that are the root cause, the underlying issue behind cardiovascular risk. And oh, by the way, if you're inflamed and all things, your hormones aren't working correctly. Your sex hormone binding globulin is elevated, your brain fog is increased. Your blood-brain barrier becomes permeable, and now all these waste products are getting in and out and all this stuff that shouldn't be there, the bouncers in your brain are letting all this bad stuff in. So, to be sympathetically driven, it's not just an issue of cardiovascular risk, which it definitely is, but everything kind of falls apart. 

[01:01:05] So then as we add in lifestyle things like eating the right foods that don't cause inflammation. Remember, inflammation is biological terror. Your body is afraid of whatever is causing it inflammation. So, it's warfare. So, if we're eating foods that incite inflammation, we're putting our body in sympathetic drive. If we're not sleeping well, if we're getting the wrong sources of light, if we're having a bunch of endocrine disruptors, all of these things that we talk about in functional medicine is foundational for not doing these things, we are putting our body in sympathetic mode. So, it's a lovely thing to be able to track and say, “Hey, you know what? My HRV is horrible. It's really low. I am going to try to sleep better.” And now we have something we can track and something that we can hack and say, “Hey, you know what, when I sleep seven and a half hours a day, my HRV improves. Hey, you know what? I'm going to stop drinking and see what that does, right? I'm not going to have that glass of Prosecco or red wine with dinner anymore. Hey, my HRV is better.” So, these are all death by a thousand paper cut things that as you peel these post its away and you start to improve, you'll start to see a real improvement not just in your health, but also I think your overall wellness. 

[01:02:15] Now about 10% of the time people's HRV is just stuck. And it causes people a lot of anxiety. And I say if you're worried about your HRV, nothing good is going to happen, right?

Cynthia Thurlow: [01:02:25] Right. 

Dr. Sanjay Bhojraj: [01:02:26] It's just going to get lower and lower. But there are some technologies, ultrasound based or ultrasound-based vagal nerve stimulation that can help and I've seen remarkable jumps with those devices as well. So, it's something easy for us to use and something that I think really does have a lot of cardiovascular benefit. 

Cynthia Thurlow: [01:02:42] Well, I've so love this conversation, Dr. B. I hope I can entice you back. Please let listeners know how to connect with you, how to work with you outside of this podcast if they live in your area. 

Dr. Sanjay Bhojraj: [01:02:51] Yeah, so I live in California. So, if you'd like to work with me, I practice is called the Laguna Institute of Functional Medicine. So, you can go to lagunalongevity.com, that's my website and I'm getting the telehealth practice started here in a few weeks so you can work with me there. 

[01:03:06] The other thing that I do is I run a cardiometabolic optimization program. So, it's a health optimization program, a HOP, I guess I would call it-- called Well12 that really focuses on cardio metabolic. So, helping improve insulin resistance, helping improve blood pressure. We're getting people off of blood pressure meds, off of their diabetes meds, reducing their cholesterol. Because a lot of the foundational things that we talk about in functional medicine really drive cardiometabolic disease. So that's an online program called Well12. 

[01:03:35] Yeah, lagunalongevity, you can track me over there. If you want to follow me on socials. I did not use my last name because nobody can spell it. So, it's doctorsanjaymd. So, D-O-C-T-O-R-S-A-N-J-A-Y-M-D on Insta and Facebook. And I don't know, I think I'm on TikTok, but that's really reserved for my daughters and the fun dance moves that we do, but follow me. Reach out. If you have concerns and you happen to live in California, anywhere in Cali, let's work together because what I say is the first 15, 20 years of my career were spent adding to people's med lists and this back half of my career, however long God has for me, I'm going to try and spend getting people off of medicines and changing that paradigm of treating people, which is what we do in conventional medicine to healing people. Is to really get to the root cause, put your body back in balance so you don't need to be on 100 medicines when you're 75 years old. 

Cynthia Thurlow: [01:04:26] I love it. Thank you again for your time. 

Dr. Sanjay Bhojraj: [01:04:28] My pleasure. Take care. 

Cynthia Thurlow: [01:04:31] If you love this podcast episode, please leave a rating and review. Subscribe and tell a friend.

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