I am honored to have Dr. Stephen Hussey joining me today. He is a chiropractic doctor with an interest in and a methodology related to cardiovascular disease.
Dr. Hussey suffered from a large STEMI, a type of myocardial infarction or heart attack, and he has been diabetic since childhood. In this episode, we dive into his background and the open-minded curiosity with which he views the world. We talk about statistics related to cardiovascular disease, mitochondrial dysfunction, the impact of Ancel Keys and his research, how cholesterol and statins work in the body, and the causes of heart attacks. We also discuss ways to navigate cardiovascular health proactively and the impact of fasting.
“Cholesterol is what you make all your sex hormones with- and all your hormones, really. That’s one reason why people who take statins tend to have sexual dysfunction. Maybe they don’t have enough sex hormones.”
– Dr. Stephen Hussey
IN THIS EPISODE YOU WILL LEARN:
- Dr. Hussey shares his background and his journey to figuring out how to manage the various physical conditions he suffered from since childhood.
- Why Dr. Hussey believes heart disease is not just about diet.
- The vast number of Americans currently affected by vascular disorders proves that a different and better treatment approach is required.
- Dr. Hussey discusses the frustration he experienced trying to navigate conversations with traditionally-trained providers.
- What may prevent western physicians and practitioners from investigating other effective treatment options?
- What causes mitochondrial dysfunction?
- Dr. Hussey explains the metabolic theory of cancer.
- Why is cancer of the heart so rare?
- How Ancel Keys profoundly impacted American nutritional guidelines and the health of the American population.
- The benefits of cholesterol and LDL, and the problem with statins.
- What causes heart attacks?
- Dr. Hussey shares his take on meal frequency and snacking and how that relates to heart health.
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.
Connect with Cynthia Thurlow
Check out Cynthia’s website
Connect with Dr. Stephen Hussey
On his website
Cynthia Thurlow: 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.
Today, I was joined by Dr. Stephen Hussey. He’s a chiropractic doctor with an interest and methodology related to cardiovascular disease. He himself suffered from a large STEMI, which is a type of myocardial infarction or heart attack. He’s a long-standing diabetic. Today we dove deep into his background and his open-minded curiosity with which he views the world. We talked about statistics relevant to cardiovascular disease, the role of mitochondrial dysfunction, the impact of Ancel Keys in his research, how cholesterol works in the body, as well as statins, causes of myocardial infarctions or heart attacks, how we can proactively navigate cardiovascular health and the impact of fasting. I hope you will enjoy this podcast as much as I did recording it.
Welcome, Dr. Hussey. I’m so excited to have you here with us today and talking about your book, which I mentioned off of the video and off of the recording that I was really, really enjoying your book. I think it’s incredibly impactful and my hope is that listeners and also clinicians listening will purchase the book and really spend some time diving into the research that you did such an incredibly thorough job on.
Stephen Hussey: Well, thank you. What a great introduction. I’m really glad you enjoyed the book. I’m happy to be here so we can talk about it.
Cynthia Thurlow: Absolutely. Let’s start with your background, which I think there’s a lot to be said about your personal history and choices that you were making into your young adulthood and then the impact of having had a myocardial infarction or a heart attack at such a young age. In fact, I didn’t know that about you until we met this past summer at an event in August. And when you shared that with me, I was completely taken aback because you’re obviously a very young man, but you’ve been a long-term diabetic. How old were you when you were diagnosed?
Stephen Hussey: I was nine years old. Yeah. My brother’s actually type 1 as well, but he wasn’t diagnosed until 22, which is very interesting. Yeah. As a kid, I had a lot of inflammatory conditions. I had asthma and allergies and I used to break out and hives all of my body. The solution that the doctors came to was prednisone eventually. That was the only way they could get these inflammatory things under control and IBS as well. Eventually all that inflammation, I know now, eventually became autoimmune type 1 diabetes. My body attacked the cells that make insulin. So, I no longer make insulin. And it did that for my brother years later when he was 22. So, yeah, I mean, my family and I were kind of thrust into this world of Western medicine to help us manage these conditions and keep it being managed.
There wasn’t much talk about why this stuff was happening, and it wasn’t until college that I started finding out that the way I lived my life had a direct impact on my ability to manage these conditions and ultimately cure most of them. Aside from the type one diabetes, it is collateral damage that was done. Those cells are gone, and then unless there’s some stem cell therapy in the future, they’re probably not coming back. So, yeah, we were kind of relying on Western medicine. Once I figured that out, I did a lot of trial there, and it’s been this ever, never ending journey for me of figuring out what kind of environment I could put my body in, whether that’s food or stress or whatever, that can have an impact on my health. And I found it interesting that no doctor ever told me that, especially about type 1, because I thought about it and from the time I was diagnosed to the time I first ever heard the words low-carb diet was about 12 years. I feel like that should have been one of the first things that was told as an option for type 1, but it wasn’t, and so I had to kind of figure that out on my own.
So, yeah, it’s been this journey for me of trying all different types of things. I mean, I was vegan for a while. I was eventually found, like paleo and lower carb and just all these different things I tried. It’s not just diet, it was environmental stuff. I used exercise because I was very active as a kid and a young adult and still am, so I used that as far as managing type 1. But yes, type 1 heavily predisposed me to heart disease. Then, I learned looking at all the posters in the endocrinology offices that I went to that said, “Oh, small vessel disease, your eyes, your kidneys, all this kind of stuff.” So, my ears always kind of perked up when I heard anything about cardiology or the heart and coming at it from my perspective, especially before I got any medical training whatsoever, I was open to everything. I wanted all the information, and I’ve always kind of been that. I credit my dad for giving me that curiosity.
So yeah, even as a chiropractor, it’s a bit of a different education, it’s more preventative and holistic. Even though all the basic science and everything is the same, it’s still like a diagnosis-based system with chiropractic as well. But again, I had no preconceived notions about what I should think about heart disease, and so I was able to take in all the information and so trying to prevent this disease, sometimes successfully, sometimes unsuccessfully, and we ended up here with me putting a book together and trying to share the information that people seem to find interesting.
Cynthia Thurlow: No, it definitely isn’t. And I think because you’re such a young man, understanding that you developed diabetes as a child after being treated with prednisone, and we know prednisone and adults as an example, can chronic prednisone use, can predispose people to becoming insulin resistant. But understanding that all these pieces start to go together, did you feel like any particular nutritional paradigm was most aligned with making you feel good or allowed your insulin levels and your blood sugar levels to be more optimized? How well did you do on a vegan diet, just out of curiosity?
Stephen Hussey: Well, even before the vegan diet, I was just told, “Eat whatever you want. Just give yourself insulin for it.” I remember getting a book that listed literally every single fast food meal or item that I could eat from all different fast food restaurants and just being told, “Go and eat whatever you want. Just count the carbs and bolus for it.” That’s what I did for a long time. In college, like I said, I started changing diet and mixing things and found out that it helped and I could manage things better. I was like, “Oh, that was interesting.” I think the biggest thing was just going toward the whole foods diet. Less processed grains, less processed sugars, even though those weren’t things I was completely eliminating at the time. But that’s what I noticed in college. Then, yeah, I went on a vegan diet, and I was on it for probably about two years. It was helpful because at that point, I knew whole foods were better, and so it was helpful in some regard.
But then, when I compare it to a more paleo or lower carb like I’m doing now, I’m really low carb now, there’s no comparison. The vegan diet, I found that I got sick a lot, and I found that blood sugars were harder to control for me. I was using more insulin even though I wasn’t really eating foods that spike insulin, like the more processed carbohydrate food, I was eating more whole carbohydrate foods. I felt like I had to use more insulin. Whereas with lower carb, more animal-based eating, it was less insulin and easier to control. But I also had to dose my insulin differently because, the blood sugar spike even though it’s not really a spike, but the elevation would happen later. I had to kind of– which nobody ever told me to account for protein. I had to figure that out on myself when I stopped eating carbohydrate because the carbohydrate always dominated the blood sugar movement.
And so when I started eating low-carb and just protein, I had to figure that out and dose that differently, which a lot of type 1s, don’t recognize. At least, I wasn’t told that. Yeah, aside from getting sick all the time, having harder to control blood sugars, the other thing was that when I was vegan, I didn’t know it at the time, but when I started eating animals again, my brain just ignited. It was like all of a sudden, I could read all these different things and put it all together and formulate ideas, whereas before I was just trying really hard to get it into my brain. That’s kind of how I felt. But yeah, it’s been a lot of different trialing there.
Cynthia Thurlow: That cognitive clarity piece I think is really important. Obviously, I respect the choices that listeners make and people choose to make. And the really great thing is we can change our minds if we find that something no longer serves us or works well for us. There’s absolutely no shame or judgment in shifting gears. I do believe that animal-based protein is superior on a lot of different levels in terms of looking at metabolic health. Now 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. And it’s during this time period that you actually had this event. So, before we dive into statistics, I think your story is really, really powerful, and I’m hopeful that listeners will really connect to that because I think there’s this presumption that people that have MIs or have heart attacks or have a certain age. And you’re a really great example of the fact that it can happen in younger adults.
Stephen Hussey: Yeah, so this is something that if people read the book, they’ll get the story. Then also a couple of weeks ago I did a talk at Ronald College where I talked about updates and what I’ve discovered since then too. People want to check that out some on YouTube about the heart attack. Yeah, so obviously it took me by surprise. I had a massive myocardial infarction, 100% blockage of my left anterior descending artery, which is the biggest arteries supplying the heart. 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. And 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 is 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. When I say stress, it’s very big. That’s encompassing a lot of different things. We’re talking about stress metabolically. We’re talking about stress toxin exposure. We’re talking about stress socially, psychologically. Lots of different things. The more and more I looked into it, especially writing this book, I realized that it was heart disease is so much more than just a lipid panel and a cholesterol medication or something like 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.
And so, for me, I knew all this stuff, but there were circumstances where I let things get to me and 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. 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, in the year leading up to the event, I mean, 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 I 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 the image lying of an artery that the body is trying to repair. But the heart attacks can happen without any narrowing whatsoever and lots of times they do and sometimes they happen in spots where there’s no atherosclerosis whatsoever. That seems to be what happened with me, was that a large enough clot formed and noticed as a 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 the pandemic. I mean, it’s easy to say, “Oh yeah, the pandemic was stressful,” because it was stressful for everybody. Why did I have a heart attack and other people didn’t? The answer to me is that there was type1 diabetes and other things as well.
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 the clotting state. The blood is 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, but 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 a day and a half later, I had a cardiac event. To ignore that correlation and to not look into that, it’s incredibly shortsighted, in my opinion. And 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, hyperresponder type phenotype, where everything else looks 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, you look at the evidence of during the pandemic and cardiac events, and cardiac hospitalizations are way up since then because of the stress. It’s hard for people to wrap their head around that. Even people I’ve told, like, “Oh, it was just stress induced,” they were like, “But how?” Because this theory of cholesterol slowly building up a blocking artery, causing a heart attack is just so ingrained in us. And when you really break it down and look at it really makes no sense and it’s almost like this, I don’t know.
There’s an 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 really getting really animated, getting really angry, and it happened to him. It’s just really, really I think, unfortunate that when I was in the hospital, that the answer I got was just, “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. It doesn’t make sense that one thing will cause disease. Instead of doing that, there was no open-minded discussion. There was nothing. It was just, “This is the answer. Go on your way. Do what we say.”
It’s almost like this manifest destiny. Like, I have all this information about the heart, and then I had a heart attack myself. As bad as it was and as much as I wish it didn’t have happened, it’s kind of given me this bigger avenue to address the issues that I saw in the hospital, the health issues that I had in myself and allowed me touch more people who’ve had similar experiences and help them as well.
Cynthia Thurlow: I think through adversity comes opportunity and the fact that you were completed with this book and then you went on to have a myocardial infarction. For anyone that’s listening, I can tell you that the demands on traditional allopathic providers have just gotten to a point where there’s a degree of cognitive dissonance, meaning it’s hard sometimes if you’ve trained hearing this is the modality that drives cardiovascular disease and vascular disease in general. And then you have someone that has the courage to speak out against the typical narrative and do it in a way that’s both very eloquent, but also encouraging people to kind of lean into the possibility that what were taught may not actually be correct. And I know we’ve got lots of touch points that we’re going to hit on as we drive this discussion.
So, I think as someone that used to treat acute and chronic vascular disease, the amount and the time that clinicians have with patients in the hospital is so constrained that I always welcomed these kinds of discussions. But I know not all my peers felt that way. They wanted to just finish their rounding and get back to the office or get on to the seeing someone in the lab or sending someone to surgery. And so, I can imagine that there was a degree of friction and a degree of pushback when you were asking questions which are completely reasonable given your personal circumstances, your personal history and your own experience.
And I know that we’re going to talk about statins, but this is one drug that it took treating an acclaimed NIH researcher who’s very smart, who explained to me what statins did to the brain and why she refused to take one. And that was the very first time I probably had been practicing for seven or eight years. I really leaned into that and asked her to share the papers and asked her to share the research that I could better understand. And it changed the way I practiced. I was still evidence based, but I was way conservative. Do we really have to put this person on a statin?
The standard medical therapy for diabetics when I was practicing was aspirin, as antiplatelet agent and a statin because we used to say that it would stabilize plaque formation and reduce inflammation. And yet statins are not benign. Aspirin is not even benign. And we sometimes don’t question what we’re taught. I’m not suggesting this as a whole, a criticism of my healthcare practitioners because I think the world of them, but I’m just hopeful that future iterations and those of us that have trained 20 plus years ago. I mean, I started training in 1997 that we do question. I mean, that’s how I was trained, was to question everything. Again, I applaud you for having those difficult conversations and for starting the narrative.
I think it’s important for the listener to have context about how many people are impacted by cardiovascular disease. There’s some statistics in the book that I’m just going to just mention. In 2018, 720,000, first time MIs and 335,000 recurrent MIs. Remember, MIs are myocardial infarcts, which are heart attacks in the United States. By 2035, 130,000,000 people in the US will have had some form of vascular disease. That’s staggering. Lastly, and this is based on data from Circulation, which is one of the preeminent cardiology journals, the annual direct and indirect costs of MI and stroke are $329.7 billion a year. So, if you’re listening and you don’t think it’s a problem, you need to lean into the fact that it is a problem. We need to be doing as much proactively to ensure we are lessening the likelihood that we are impacted by vascular disease in general. I’m not just talking about heart attacks, but also carotid artery disease, strokes, peripheral vascular disease. We used to call people that had all the above vasculopaths but anyone that’s impacted by these vascular disorders.
Stephen Hussey: Yeah, for sure. To me, this suggests, like were talking little bit before we started, that those numbers show that our approach is off. If the numbers keep going up and they’re predicted to keep going up and it’s costing us as much money that the approach that we have is not the correct one, or at least not the whole story. That was one of my points in writing my book, is that I wanted to open up the conversation because clearly we need more or we need better approaches or better treatments and things like that, better understanding. My book is called Understanding the Heart. It’s just trying to get better understanding of what does cause cardiovascular disease so that we can develop better treatments. These statistics show that we’re off on the wrong track and we need to get on the right track. That was the most, I think, disheartening thing about my time in the hospital.
And I’m familiar with Western medicine. I’ve been using Western medicine physicians and practitioners for a long time. And all— I don’t know what the word is, but happily doing that, like going to them and getting their opinion and working together with them and things like that. With the shutdown of conversation in the hospital when I would ask questions, whether it was they didn’t understand it or they didn’t have time like you talk about, that was the most troublesome thing to me because here I am, trying to figure out because at this point I wanted an opinion. I wanted to know what they thought because I just had a heart attack and it completely took be my surprise. I wanted to know what their thoughts were. I wanted to know why they wanted me on this medication, that medication, because based on what they were trying to do, I could think maybe I could do it a different way, or maybe I really do need to take that or not.
I wanted that, but I didn’t get much of that conversation. I was branded as a noncompliant patient in my chart, and every new physician or new practitioner that came in kind of gave me that treatment as this noncompliant patient and that they didn’t have time to deal with because they had other things to do. That is what it is, and that’s just the system that they work in. The whole point of this book was to open this conversation, because it’s not happening within Western medicine’s walls to open conversation and actually find the truth. It’s more about standard of care. You said with the type 1, it’s like beyond a statin, beyond this, that’s just the standard of care. If they don’t follow that, they’re liable. I get that.
One example I did give was about magnesium. When I asked him about magnesium as a blood thinner in the hospital, I was directly told magnesium is not a blood thinner. I don’t know if he meant magnesium is not an agent that thins the blood, or magnesium is not as powerful as a blood-thinning drug. I don’t know what he meant, but I tried to expand on that and was basically told that, “You need to take the blood thinner.” And I get that point of view. Later, I did find studies that show that magnesium intravenously and magnesium sulfate, can be administered, or at least in animals, that has been shown to be just as effective as blood thinners for preventing clots after statins. Now, I didn’t expect that physician to do that based on– if I showed him that study and said, “Look,” because there’s no approved treatment to do that in a hospital setting. However, it make us a step back and say, “Okay, what’s going on within this business that is Western medicine that has prevented a therapy to be perfected or developed with magnesium sulfate rather than what they know that has the risk of bleeding?”, and things like that. So, we have to step back and recognize that.
You talk about your fellow practitioners and everything and how much you love them and how great a job they’re doing, and 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 and you know what, they need to recognize this is the system they work in so that they can make their decisions accordingly when it comes to these types of situations down the road. Well, it’s just the research that shows that the magnesium, intravenous magnesium sulfate has been shown to, at least in animals, to be effective at preventing clots forming after a stent placement. I didn’t expect 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 kind of abide by the standard of care. If anything goes wrong, they’re liable. In a way that kind of prevents them from investigating what could be effective in other ways. It’s just important for practitioners to understand that’s the system that they work in and 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 question, “Well, if it’s just as effective, then why hasn’t a therapy using magnesium sulfate after stint placement been developed,” and eventually get to the end of that and they go, “Oh, because it’s not profitable,” probably.
Cynthia Thurlow: That’s exactly what I was about to say.
Stephen Hussey: You can’t patent that and then make money from it, right.
Cynthia Thurlow: I mean, it’s interesting. In cardiology, we use a lot of magnesium, and a lot of my background was working in electrophysiology. So, working with the cardiologists that put in peacemakers and defibrillators and dealt with arrhythmias. I got very savvy with electrolytes, particularly magnesium. And so, to me, there’s like the traditional modalities. Like if you’re in a hospital, most of the magnesium that’s given is magnesium oxide, which has really poor absorption. It’s like a 11% versus mag sulfate, which is what I gave all the time because most people had subtherapeutic magnesium levels. And so, without getting down a rabbit hole, I 100% agree that we need to be open-minded. Unfortunately, we get in this bucket of evidence-based medicine, and we’re sometimes so constrained by the evidence-based medicine that we don’t want to deviate from that because we live in such a litigious environment where, unfortunately, people get sued even when they’re doing the right things. So, I can understand the hesitation to kind of experiment outside that kind of evidence-based medicine model.
Now, let’s definitely touch on the role of mitochondrial dysfunction. My listeners are definitely savvy. They understand the role of the mitochondria. But you brought up Otto Warburg’s work, and we’ve had Sam Apple on and kind of dove into how cancer cells utilize fuel differently in the absence of oxygen than normal healthy cells. And so, let’s talk a little bit about how this impacts this mitochondrial dysfunction, how this can impact those special heart muscle cells, those myocytes, and how this can contribute to some of the beginning stages of issues related to inflammation, oxidative stress etc.
Stephen Hussey: Yeah. So, I initially started looking into this when someone just posed the question to me why heart cancer is so rare because it is one of the rarest forms of cancer. It doesn’t mean it doesn’t happen, but it’s extremely rare. It’s even more rare for it to be the primary site of a tumor. Most of the time when heart cancer does happen is because it’s metastasized from somewhere else, but it can be the primary tumor. But it’s very, very rare. I think one example I gave in the book is that there’s one guy up in Canada who is the closest thing we have to a cardiac oncologist, and he only gets referred like 12 cases a year. So, it’s just really, really rare. So, I was just like, “Why is that?” And I was familiar with Otto Warburg and the metabolic theory of cancer, and I was also familiar at this point with how the heart metabolism seems to be a bit special in that it prefers fatty acids and ketones more than other tissues in the body and lots of organs do that.
There’s lots of studies showing that in heart muscle cells, that even in the presence of glucose, they choose fatty acids and ketones to burn them more predominantly. It’s always burning some of all the metabolites that it could be burning, like carbs and fats and ketones, but it prefers those even in the presence which in other tissues, like to be in a ketogenic state, we have to restrict the carbohydrate, we have to get rid of it completely to force the body to do that, but that doesn’t seem to be so in the heart. When I looked into why this is, the main theory is that at some point early in development, the heart cells kind of give up their ability to divide and become new cells. They think that’s because they’re so metabolically active, these cells that are always contracting, using up a lot of ATP, so they give up this very metabolically demanding or energy demanding process of dividing and becoming a new cell.
That’s just interesting because that’s why heart attacks are so important, or I guess detrimental, is because you kill those cells, your body can’t make new ones. We have to try and repair the ones that were damaged. And so, when I looked at that and we take this metabolic theory of cancer and we see that in this metabolic theory of cancer, it’s when the cells, the mitochondria, lose the ability to use oxygen because they become so damaged. That’s the organelle in our cells that allow the body to use oxygen to make energy.
If they become so damaged that you lose that ability, we go away from what’s called oxidative phosphorylation, where you use oxygen to make energy, and towards something called fermentation, which is where you can make energy without oxygen. But it’s a really detrimental process. It makes more free radicals, I call them Looney Tunes Tasmanian Devil that runs around and causes damage and things like that, but they cause more damage that way, causing more mitochondria to be damaged. This is why we see that cancer cells don’t use oxygen, they love glucose because that’s what you ferment, or at least a lactate from the glucose is what you ferment.
And so, the thing is that with heart cells being that they prefer fatty acids and ketones, especially ketones are a non-fermentable fuel source. If you have a cell that prefers those and is always going to choose those more, it’s much harder for it to get into that fermentable state where it becomes cancer, because it has this preference for burning those ketones. I detail like 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 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.
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. It’s like cell says, “Stay alive rather than die,” by rapidly dividing, being undifferentiated, anaerobic, not using oxygen cells. 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 becoming cancerous, the tissue dies.
And so, it’s just this interesting thing that I kind of flushed out, and hopefully I think I found the answer to or one reason why the cancer of the heart is so rare, but it has to do with metabolism. It’ll have 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. So, that’s the story there.
Cynthia Thurlow: No, I think it’s really interesting and 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 casts in the whole area, and we had a very talented interventional cardiologist. We got very attuned to the anatomy of the heart and the widow makers, what we call when the LAD gets blocked that left anterior descending artery.
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. And his cherry picking of data has also profoundly impacted our health.
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 kind of 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. This is when my grandparents talked about this. They went from enjoying butter and steak to all of a sudden being told you need to have these hydrogenated oils, these bastardized plant oils, and really being fearful of any type of animal-based fat.
Stephen Hussey: Yeah, I mean, I don’t know how familiar your listeners are with this whole backstory, but yes, Ancel Keys was a scientist who in the 50s, gave America 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. It was new, which I think people should note, ‘it was new.’ Thinking about that and thinking about what humans ate for years and years prior to this epidemic [unintelligible [00:32:51] 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.
Anyway, Ancel Keys gave the population, gave the world an answer, which was more saturated fat, more cholesterol, more heart disease. And 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 there is, because it can only show things are associated with each other. It can’t show that one thing causes another, and 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. Unfortunately, that’s very expensive to do, and it’s not done a lot of the time. So, they take these associational studies and they make our nutrition guidelines based on these associational studies. That’s what happened with Ancel Keys as he originally published this research that just basically showed, in these countries that he took data from, the more saturated fat and cholesterol all 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.
He kind of cherry picked the data to give 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, by the time this theory was actually tested in clinical trials, which it was, over the next 10, 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 margin or vegetable oils and had terrible results with that, people had more heart disease and more all caused mortality the more unsaturated fat they ate. By the time this was all tested and fleshed out, theory had taken off, and there was money behind it. Everybody sees the cover of Time magazine with the frowny bacon face.
Yeah, the other industries wanted to perpetuate this theory because it helps them. The sugar industry, the grain industry, the cereal industry, they were putting a lot of money behind this. And you see it today. You can even see with the funding and a lot of research funding behind a lot of research is these companies wanting this theory to keep going. And the same with the pharmaceutical companies. After I think it was like, 1984 or something like that, when they put together this committee to decide if cholesterol was good or bad for us, and they incorrectly, in my opinion, decided it was bad. After this committee, did this, they put together this other committee to educate doctors about how to assess and treat cholesterol.
The pharmaceutical companies got wind of that. They started sponsoring these committees, and they basically sponsored them and encouraged them to lower the guideline of what cholesterol should be LDL, because the lower it is, the more drugs can be prescribed. The lower the recommendation is, the more drugs can be prescribed. At first, they were like, okay, cholesterol LDL should be 250, and they said 200. Then there’s 150, and there’s 100. Now, it should be lower than 100. So, to me, that tells me we have no idea what cholesterol is supposed to be. It’s just based on the idea that we have a drug to treat it. We want to use that drug, make more money. If all you have is a hammer, everything looks like a nail kind of thing. And that’s the idea, cholesterol being the cause of heart disease, it’s kind of based on. It’s not really based on much science.
Now, there is some associational research that shows that higher cholesterol is associated with heart disease, but there’s lots of different healthy user biases and things like that have problems with these studies. So, yeah, it kind of took us this turn. It’s only recently, I think, that even in the research we’re starting to see, like, there was that one article in 2020, they looked at all the evidence behind saturated fat and heart disease and they said, “Oh, saturated fat, the idea that saturated fat caused heart disease is way overblown.” I think it was what the researchers said in that study. It’s only recently started to come around. It’s been, what, 60, 70 years that it’s taken for that idea to come around, which just shows you how slow the process of changing conventional wisdom is and research.
Cynthia Thurlow: Absolutely. I think there was an article that came out that said typical clinical medicine lags 20 years behind research. So, it really does take time. And again, the cognitive dissonance, and it’s not unique to medicine. It happens in probably most industries, but it’s a particular interest now, I think, because on every single level, I just see patients getting more and more sick. And while we’re talking about cholesterol, let’s talk about the importance of cholesterol, because I think that when people understand that we want our cholesterol to be within a healthy range, because there’s a lot of physiologic benefits to having healthy cholesterol levels and having healthy cell membranes and understanding that hormones are all a byproduct of cholesterol level. So, I think back to a lot of my patients are on statins, and I started decreasing their doses when their total cholesterol was getting close to 100.
We know that there is an uptick in morbidity and mortality if your cholesterol is not high enough. I remember getting quite a bit of pushback from my colleagues about this, but if you really look at the research on cholesterol as a whole, we don’t want it to be too low. That’s not beneficial. If you’re honest at and your cholesterol levels within a healthy range, that’s fine. But if you’re someone that’s looking to learn more, let’s talk a little bit about some of the benefits of cholesterol that maybe, like, the average person doesn’t know.
Stephen Hussey: Well, when we say cholesterol, we’re saying like this general term. Cholesterol is the waxy substance that’s carried in lipoproteins. Lipoproteins are LDL and IDL and VLDL and HDL, all those different acronyms that we hear on a lipid panel. Cholesterol is carried around in those because it can’t be carried around in the blood itself, because it’s the fat, it can’t exist in the water like substance to this blood. So, yeah, like benefits, I mean, there’s so many different things. We talk about LDL versus cholesterol itself, I mean, having cholesterol itself, that’s what you make all your sex hormones with, and all your hormones really. But it’s one reason why we see that people who take statins tend to have sexual dysfunction, maybe don’t have enough sex hormones. When we look at you talked about the integrity of the cell membrane and communication between cells.
Part of what I talk about as far as how important that is, because then a cell starts operating like it’s the only thing around it because it can’t sense that other cells around it and that’s a bad situation. We want the cells to all know that there’s other cells around them. That’s really, really important with cholesterol, fat soluble vitamins, really, really important. People think, “Oh, yeah, I get vitamin D from the sun,” like you do. But you need sulfur and cholesterol and the raw material so that when the sun hits your skin, you actually make vitamin D. It’s really, really important. If you don’t have enough, you’re not going to make that. And so that’s kind of like cholesterol. There’s more of those, but then LDL itself. I mean, if we look at LDL molecules and how their ability to deliver energy so if we’re saturated fat and triply survives, really, if we don’t have enough LDL floating around the blood, we’re not delivering energy. Which is why statins can be caused fatigue and also muscle function, really important cholesterol. That’s why statins can cause muscle pain because if there’s not enough cholesterol around or not enough delivery of it from the LDLs, then we can get muscle pain.
And also, one that I was shocked to find is that LDL molecules can actually help in the face of infection. They can neutralize bacteria and even play a role in the combating of viral infection. They do this by kind of binding and neutralizing the pathogen. That’s why I think that when we see the associational studies, the people with higher LDL have lower rates of infection as they age, or at least illness from infection. So, yeah, just lots and tons of time. There’s even cholesterol molecules because I talk about in the book how a statin inhibits the production of cholesterol very early on in the process of the making of cholesterol, which your body takes fatty acids and puts it through all these steps to make cholesterol. The point of that is not just to get to the end, which is to have cholesterol around. There’s also all these intermediate steps or intermediate molecules that are created, the body uses for things.
One of them is the making of what are called selenoproteins. It uses a certain molecule, I forget which one [chuckles] I have to look at the book, to make selenoproteins, which are the precursors to antioxidants like glutathione, which is really, really important for keeping our mitochondria, like were talking about, healthy, keeping oxidative stress low. There’s also another intermediate molecule that’s used to make a molecule called dolichol. You don’t have to remember that name. You just have to remember that’s really important for insulin signaling. If we don’t have enough of that because we’re telling our body not to make cholesterol by taking the statin drug, then that can create insulin resistance. And that’s what we see in some of the studies that I talk about in the book, is that statins are seen to make insulin resistance more likely.
More people who take statins tend to have insulin resistance than people who don’t. That was one of my things I said in the hospital, kind of jokingly. They were trying to recommend statins and I was like, “I already have diabetes. I don’t want type 2 diabetes,” which is, I guess, possible for me. I could develop insulin resistance and develop type 2 diabetes and have double diabetes. Yeah, I guess the list goes on and on. But this molecule of LDL that carries our cholesterol around, natural cholesterol is really important and does so many different functions and you’re talking about different levels. I’ve found many studies, they’re just associational studies, so they don’t really prove causation, but they show that the levels of total cholesterol and LDL that are associated with the least all-cause mortality and the least heart disease and least stroke and everything like that are total cholesterol of 200 to 250, which is above the recommendation currently. LDL at 100 to 150, which is again, above the recommendation currently. Again, those are just associations, but it’s just they’re interesting to look at and think about. The numbers associated with the highest all-cause mortality and illness are lower than 100, which is what is for LDL, which is what we’re told. I know some cardiologists should say lower than 70. It’s got to be 70 or lower. And that is, again, showing the highest all-cause mortality when it’s that low.
Cynthia Thurlow: It’s really interesting because there’s no cognitive dissonance on my end. But I do remember that we used to push statins to as high a degree as a patient could tolerate. More often, not a lot of these side effects of statins that patients will report sexual side effects, insulin resistance, myalgias, which are a fancy way of saying muscle aches, arthritis, joint pain, were so common that we would find very unique ways of trying to administer statins. Sometimes, it was every other day, twice a week, I used to say some is better than none. And so, I very humbly like– as I’m listening to this, is it any surprise that statins are contributing in many instances to worsening insulin resistance? Or people who have been insulin sensitive who suddenly become insulin resistant? I know one of the studies you mentioned talked about a 30% increased risk of diabetes while taking statins. I do recall when that Lipitor study came out because understandably, patients were upset and concerned and we would just say, we’re going to monitor it. I think it’s really important to get this information out there that there’s no medication without side effects and really thinking about the physiology of the body and the way that these drugs work so that you can make a fully informed decision with your doctor or your NP or whomever you’re having the conversation with.
Now, let’s talk a little bit about causes of myocardial infarct. So, causes of heart attacks, you’ve touched on some of these. But I think it’s particularly important because it’s not just the big things. It’s not just as you mentioned, it’s not just the cholesterol piece. And more often than not that’s taken the focus away from what’s really driving the escalating rates of metabolic disease and cardiovascular disease. So, we touched on metabolic and flexibility and that’s a given. What are some of the other pieces that you put together through your research? I think it’s really interesting, the net impact of stress. I think that we collectively as human beings, think of this as stress of stress. Everyone experiences stress. Well, our body’s perception of the stress can be quite significant and profound.
Stephen Hussey: Yeah, and just because I’ve thought of it now, I don’t want to forget to say it. Our physiology is not creatively evolved, whatever you want to say, to handle what we’re handling these days. For many, many years, we had small communities where we knew everybody in the community, maybe 100 to 150 people. Sometimes, people didn’t even go 10 miles from where they were born in their entire life. Now, in a relatively evolutionarily short amount of time, we have gone from that type of living to knowing what’s going on all over the world by watching the news and seeing everything that’s going on. All the stressful things. We have thousands and thousands of friends. They may be just Facebook friends, but thousands of friends that we’re just scrolling through and comparing our lives to.
There’s all the different– not just psychosocial ones, but all the different stresses. Like the wrong type of light can be very stressful, causing oxidative stress and increasing sympathetic response, which is the stress response all the different toxins were exposed to. Just thinking about the environment of the sounds of a city and how those types of sounds have been shown. Research has shown that the body has a stress response to this. Even if our brain overrides it, like, “Oh, it’s just a taxicab honking its horn,” our body’s having a stress response to it. We just have to think about this idea that stress kills with this context of what stress in modern day life actually is and how different it is from anything. Our physiology, our evolved physiology is still that to respond to stress when stressful things happen. Like the example is like a zebra is grazing on the Africa plain. And then a cheetah comes out to try and eat it and it has a stress response because before that, it was then parasympathetic. It was very calm, it was eating, whatever. It has a stress response that we can get away from that threat. If it successfully gets away, then that stress response shuts down and it goes back to normal again. And that’s normal physiology.
That’s how we handle stresses. That’s the ability to adapt to a stress and come back to normal. Unfortunately, in today’s world we’re in a situation where there’s constant things that are convincing us that we’re in a threatening environment even if we’re not really in a threatening environment. We’re the only species in the world that can think your way into that stress response because we have these big brains that just served us very, very well in so many ways. But also we have to think about how that brain perceives our modern environment and how it’s creating this imbalance in our stress response and then carrying that further. How does that affect specifically our cardiovascular system but our health in general?
And so, when you look at this and this is something that I went into more detail in the talk I did a few weeks ago on YouTube than I did in the book, even though I talk about it in the book as well. But when we think about you just kind of started off saying what are some of the causes of heart attacks? I kind of described one already where it can be a forced shift in metabolism. We should know that there are some things that can predispose us to that like poor metabolic health and high oxidative stress which is kind of inflammation and damage that happens in the body. But the triggering thing that happens when we get those heart attacks with no blockage that forces metabolism shift that caused tissue death is an acute stress in the context of already chronic stress. That sends signaling to the heart that tells it to shift its metabolism toward more glucose usage which causes, lactate and hydrogen ion production which causes edema and causes blood flow issues then we get hypoxic blood and we get tissue death.
That can happen whether there’s atherosclerosis there or not. That’s not what happened to me. I had a clot that formed. That’s the other thing, that’s the other way we could get a heart attack is. Probably the more common way, although I’m not sure the exact numbers, I don’t think anybody is, but is that this clot that forms. And we’ve been taught that there’s this idea that the stenosis of an artery with this narrowing of an artery, this “buildup of cholesterol,” even though that’s not what it is, narrows the artery more and more and narrower. It gets it cuts off blood flow and then boom, we have a heart attack.
But that doesn’t make sense to me because there are examples of people who have like a 90 or 95% blockage of an artery, narrowing of an artery who run marathons and they do so just fine. It’s because the body builds collateral arteries around that stenosis. And I talk about research in the book that those collaterals can form within four days of a gradual stenosis. So, that’s pretty fast. But if we get an acute clot that forms instantaneously and it’s big enough to block either an already stenosed portion of the artery or it’s big enough that it blocks the whole artery right there, or it flows down to a smaller artery and blocks there, then that can be an acute situation where we have acute blood flow restriction to an area, myocardial infarction. And that’s what happened to me. I had an acute clot form.
If we look at what makes up atherosclerosis what makes up the narrowing of the artery it’s not cholesterol. I talked about two studies in the talking game a few weeks ago that took atherosclerosis and analyzed what it was and I think it said like 87 plus or minus 8% of that material was clotting materials. It was fibrotic material, fiber, which is what happens when your body initiates a clot. The same thing it does when you cut your skin. It initiates a clot and the scab forms there. The same kind of thing happens on the lining and artery is we get damage. And if it’s too much damage and the body can’t repair itself because it’s insulin resistant, it’s poor metabolic health, it can’t repair itself, then the body has to do something else that’s going to start bleeding from the artery on the inside. So, it forms a clot and it tries to heal it that way. These clots can form on top of each other. That’s how we get the stenosis narrowing of the artery. They can form over and over again on top of each other. Or it could be a significant clotting mechanism that forms that it blocks the whole artery right then and there depending on the situation.
So, yeah, they did find some like when they analyzed this atherosclerosis, they found some cholesterol molecules because when a clot forms, just kind of sucks in whatever else is around and LP(a) delay, which people talk about a lot. It actually prevents clots from breaking down. If your body is trying to initiate a clot, it wants LP(a) delay there so it can prevent that clot from breaking down. That’s why we see other life of proteins there, because LP(a) is a life of protein. So, yeah, I mean, atherosclerosis is a clotting disease.
So, the natural question is what damages the line of an artery to cause clotting? And that’s not a simple answer. There’s many, many things that can do that. Toxin exposure, different toxins require oxidative stress in general, which we can talk about, things that create free radicals. Heavy metals, endotoxemia all these different things that can cause oxidative stress and different toxin exposures. Microplastics, which people talk a lot about, BPA and things like that, even artificial fragrances, different things, all these different toxins that were exposed to every single day can contribute to our oxidative stress load that is then damaging the artery. The thing that breaks the camel’s back is the insulin resistance because normal wear and tear in an artery is supposed to happen and we have repair mechanisms that are very effective at doing that as long as the system is not overwhelmed. However, those repair mechanisms in the endothelial cells are dependent on proper insulin signaling. If we have insulin resistance, type 2 diabetes, poor metabolic health, whatever you want to call it, then our body can’t repair those things and we get more likely to get clots forming on top of clothes, on top of clots and so other things.
The big one we kind of led in this conversation with was stress. I mean, hands down. If you look at the research and I talk about it in the talk I gave a few weeks ago, they looked at the effects on clotting of acute stress and they had this whole list of, I don’t know, like 12 different clotting factors. All but three of them increased significantly during acute stress. So, your body is in this prothrombotic state and the reason being is because in acute stress we think our body is being threatened, being attacked. So, if we get an injury, this is evolutionary explanation but we get an injury somewhere it wants to be ready to clot and prevent bleeding out from that injury.
However, we’re having these psychological– the modern world is psychologically stressing us out even though there’s no physical harm that’s happening to us. So that’s creating this increase in clotting. That’s why heart attacks are more common on stressful days of the year. We see that in the research, definitely. They’re more, 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. Like heart attacks are more common on these days because of the clotting that’s initiated during this stress. To me, it takes the whole prevention of I think atherosclerosis and heart attacks could almost be seen as two totally different things. One doesn’t necessarily cause the other, one is clotting, one is repair. It takes a set 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. And stress can cause insulin resistance. It puts you in an insulin resistant state. That’s the way forward. I feel like with heart disease is the 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, it’s a big message in my book.
Cynthia Thurlow: No, and it’s interesting, something that really stood out for me, and 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. 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, and 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, and 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. It took three days before my HRV bounced back into the 50s when I was at home. 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. 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.
Stephen Hussey: Yeah. So, in the book, I have kind of these three themes that keep coming back to, and that’s metabolic health, oxidative stress, mass inflammation and balance in the autonomic nervous system, which is our stress response to dealing with the stress. Every time I think about a therapy or a lifestyle or whatever that you can 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? 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 here in the winter. Our bodies evolved almost for it to almost beneficial when we had to take breaks from eating as often. It used to clean things out and to write your metabolism and to become used mechanisms or develop mechanisms for using ketones and things like that.
So, yes, metabolic health wise, absolutely. It’s also interesting that there are studies that I talk about in the book that show that when you fast, like 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 cell. 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. The fact that you don’t eat anything at all and your cholesterol goes up disproves that theory, in my opinion. Anyway so, there’s that. 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 [unintelligible [00:57:41] but I don’t think there are really. It’s all used for something beneficial. Yes, there’s less of that going on. This has especially been shown in muscle where if we’re using fatty acid 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. As far as balancing the autonomic nervous system, definitely research has been shown that 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 it’s beneficial just generally. If you’re doing longer fast, the first three days, it stimulates parasympathetic. After that, there’s a window of time where it seems to stimulate sympathetic, where your body is almost freaking out but then I think it comes back around after a while. 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 kind of what they see. So yeah, I mean in all three phases of what I think are the main drivers, the main imbalance that create heart disease, fasting, whether it’s intermittent or longer term fast, seems to beneficial in all three phases.
Cynthia Thurlow: 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.
Stephen Hussey: Yeah, my website is resourceyourhealth.com. My books are on there, my blog is on there. I do like a little health coaching kind of online consulting. So, that’s on there as well. My book is on Amazon. It’s also on the publisher’s website, Barnes & Noble for people who don’t want to use Amazon, there are people that don’t want to, so there’s that. On social media, I’m just @drstephenhussey, Dr. Stephen Hussey on Instagram and Facebook and Twitter. People can reach out to me there and happy to interact with them.
Cynthia Thurlow: Awesome. Thanks so much for your knowledge and for putting your story out there. I think it will help inspire a lot of people.
Stephen Hussey: Thanks for having me on.
Cynthia Thurlow: If you love this podcast episode, please leave a rating and review, subscribe, and tell a friend.