Heart Rate Variability, Polyvagal Theory, The Flaw In Trying To HACK The Body, And More with Dr. Mel Hopper Koppelman

Content By: Ari Whitten & Dr. Mel Hopper Koppelman

In this episode, I’m excited to welcome Dr. Mel Hopper Koppelman back for the third time! Today, we continue our conversation on the overlooked importance of brain development but go on to explore heart rate variability (and how it can easily be misinterpreted), Polyvagal Theory, and her fascinating, physics-based thoughts on how our heart rate variability connects us to the universe!

Table of Contents

In this podcast, Dr. Mel and I discuss:

  • An easy way to visualize brain development: the brainstem is the root that grows up into the trunk of our brain and branches off into the right and left hemispheres
  • The underlying driver of illness for many people with chronic symptoms and why gut or immune health might continue to suffer if this isn’t addressed
  • A clear, easy-to-understand explanation of heart rate variability and why this often-misinterpreted marker is crucial for vital health
  • The 10-second at-home test Dr. Mel recommends to better understand your heart rate variability findings AND the functioning of your vagus nerve!
  • Her physics-backed belief that our heart rate variability connects us to the “breath” or wave of the universe…and how this connection (or lack of connection!) relates to the vagus nerve, inflammation, nervous system development, and long-term health
  • 2 major predictors of mortality, i.e., how long you will live and the interesting pattern often found in people with autism
  • The extreme importance of working with the body and tracking test results versus cleverly attempting to biohack or manipulate the body with supplements or drugs

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Ari Whitten: The highest compliment I can give somebody is inviting them back for multiple rounds of conversation on this show, so I’m really enjoying this conversation with you and exploring your way of thinking about health. For me, it’s a joy to, let me put it this way, I think there are so many people out there who are sort of just regurgitating the commonly taught stuff that’s out there, and I’m really interested in having conversations with original thinkers and people who are trying to put the pieces together in new ways and solve problems in new ways and take seemingly disparate areas of science and knowledge and combine them to generate new ideas and new solutions, and I see that in you and I really appreciate this conversation, this opportunity to explore your way of thinking more with you, and I hope we can continue probably beyond this conversation as well because there’s so much to talk about, and I hope our listeners, I know that our listeners from the feedback on part one are enjoying it as well and getting a lot of value from it.

With that said, I want to pick up on where we left off in the last conversation on brain development and the idea of two hemispheres and how that, this seemingly, I don’t know what the right word is, sort of obvious thing that’s so obvious and so commonly taught in basic anatomy that it’s sort of overlooked as being unimportant. You’re making the claim that actually it is really important, and this fact is something that we ought to pay attention to and has an impact on adult health and how these hemispheres develop in different ways depending on one’s childhood environment and other factors.

With that said, maybe you can give a very brief recap of this because this will be a week later after people listen to the last episode, so maybe you can recap the meta-level idea of brain hemispheres and how brain development as a child links up with adult health.

Mel Hopper Koppelman: Sure. The high-level overview is that we all develop and grow like a tree from the root up through the trunk and then through branches. Our brain develops from the bottom up, and when we’re born, it’s fairly immature, and then it comes up from the brainstem, and first the right hemisphere preferentially develops in utero and in the first two or so years of life, and then it switches over dominance to the left hemisphere. We start to get more complex sentences. We start to get our will and ego and differences of opinion with our caregivers, and we have this back-and-forth sequencing.

As it’s developing up, it’s getting more and more specialized, so neurons that were general are now doing more and more specific things, and then it wants to come back together to integrate into a functional whole. There are various reasons, both nature and nurture, why we might have a tendency towards one or the other, and that’s not really a pathology. That’s just the full richness of the human spectrum of people, and that can be to do with your gifts and your personality, but if there’s a susceptibility there where there’s just too much of an unevenness, then it can become pathology, both physically in inflammation in your immune system, psychologically in your mental health, and it affects things like longevity and pretty much any area of life.

What I’ve observed is that if someone has a very obvious neurodevelopmental problem, then that gets picked up. Things are really not going well, there are functions that are missing, there’s serious problems there, that gets picked up. The gray areas are less likely to get picked up, although now more and more things are getting assessed and looked at, but what is, I would say, very common is that I see adults who are chronically ill, and they may never have had a neurodevelopmental diagnosis, and they’re exploring all these different things, but what they don’t realize is that their current problems relate back to this unevenness of development, and that you may try lots of different things and you might get some benefit from there, but ultimately if this is going on, which is to say brainstem immaturity, retained primitive reflexes, which are never a normal finding in an adult, then this is going to be a bottleneck because this is your infantile development, and if that has not finished, even if you’re in your 20s or 30s or 40s or 50s or 60s, then that’s the first things first in terms of having a regulated nervous system, which is then leading to a happy immune system and gut and aspect on life.

How brain development during childhood links up with the autonomic nervous system

Ari: You alluded to where I want to go with this discussion right at the end there, which is how this idea of brain development during childhood links up with the autonomic nervous system.

Mel: This has everything to do with the autonomic nervous system. The autonomic nervous system, you can also think of it as the automatic nervous system. It’s helping us have our vital functions, our heartbeat and our breathing and our circulation, all those things that we’re not, fortunately, we don’t have to think about in order for them to happen. Most of those are housed in the bottom of the brainstem, because again, you think of this tree, like what’s the first things first here? We need to have a beating heart and breathing lungs before we do anything else, otherwise we don’t have life. That’s going to be at the bottom, that’s at the foundation.

I see people increasingly interested in things like heart rate, heart rate variability, respiration rate from different angles. I think the first folks who were interested in this were probably athletes who were using this data to optimize their training schedules and to measure recovery and things like that, or they’re using their heart rate targets to see what zone they’re in to see what they’re doing. That’s one group of individuals. Another group of individuals are people who are having autonomic issues. People who, let’s say, have POTS. When they stand up, their heart is beating too quickly, or they have low blood pressure when they stand up, or other dysautonomias, or maybe they’re fainting or coming close to fainting.

Then another group are people who just innocently were like, Apple Watches are cool, or Ring, or whatever, Garmin, whatever device. They look at it and they’re like, oh, huh, it said my HRV is 32, is that good? They just have this data now and they don’t quite know what to do with it. What I’ve found for a variety of reasons is that there’s a lot of problems in how this data is interpreted. This is related to neurological development, but I would say that most people do not understand the significance to accurately interpret heart rate and heart rate variability.

I say this because I had my own data and I had my patients’ data, and what I was finding in terms of explanation was not matching up to the data we had. I took a course on heart rate variability. I just checked, I’ve had hundreds of references on my computer. I’ve contacted many of the authors. They’re not aware, or they weren’t aware of some of the issues in the interpretation of heart rate variability. Actually, it’s interesting, part of the problem is that,

Heart rate variability

I’ll explain what heart rate variability is so that I can bring everyone else into the conversation.

Our heart, we’re used to thinking about our heartbeat and what that rate is, but there’s actually some variation in that rate and that’s actually a good thing. Sometimes we think that we want it to be steady, but if it’s varying a little bit, it’s showing a dynamic flexibility. Actually, really what this health aspect is is that when we breathe in, the heart rate is supposed to increase, it’s supposed to speed up. Then when we exhale, it’s supposed to go down. Having these two systems that are communicating well is a really key sign of health. That actually may be a better marker of health than any other single marker available, which is a big statement.

In any clinical area, it is the strongest predictor of all-cause mortality. It’s also a predictor of positive things like conscientiousness, for example. You were saying when we spoke before that that’s one of the biggest predictors of longevity. There’s a relationship there with heart rate variability and neurological developments.

Ari: Something else positive you mentioned earlier, which is athletic performance.

Mel: 100%. Yes. These are all going to have–

Ari: As you said, there’s pro athletes and high-level athletes and other maybe recreational athletes who are training hard at a high level, I’ve used this for many years, use heart rate variability as an objective tool to gauge, essentially to get a window into their body’s recovery and readiness for hard training that day. If you wake up, you take your HRV score and it’s high, that means, okay, I’m going to train hard today. If it’s low, means, oh, maybe I pushed too hard yesterday, maybe I need a rest day or a light day today. This has been used and very, very well validated for regulating performance and long-term training in high-level athletes and bodybuilders and things of that nature.

Mel: That’s right. There’s a little bit of an issue though, that globally, higher heart rate variability is associated with health, less likely to die, better development, better conscientiousness, better recovery, and performance. There’s a small problem, which is that it’s really one aspect of heart rate variability that is making this association. That aspect is called respiratory sinus arrhythmia, which sounds like a bad thing because it’s called arrhythmia but it’s actually a good thing. It’s what I described a moment ago, which is that when you breathe in, your heart rate goes up. When you breathe out, your heart rate goes down. That is respiratory sinus arrhythmia.

That is what is associated with all the good things but you can have other sources that are not that are making your heart rate more variable. That’s going to increase your heart rate variability, but not because you’re healthier. Now that throws a little bit of a spanner into the works and interpretation, but also starts to explain some of the paradoxes that I was finding in my patients.

For example, I know in terms of athletes, for some reason, for one reason or another, the people in the athletic world that have been tracking heart rate and heart rate variability the longest are the Scandinavians and the Finns in particular. They developed a lot of the gadgets and the software to do it, but even their skiing team stopped using heart rate variability as a sign of recovery after a while because at a certain point when you start to get a little burnt out, your heart rate variability can go up, which is–

Ari: Yes, I’ve seen some reference to this, some discussion about this, but it’s never been clear to me exactly what the causes are when this, from my perception, sort of anomalous rise in heart rate variability that is a sort of deceptive high heart rate variability. When that happens, what are the factors that actually cause that?

Mel: I’ve got, this has like been the question that’s been guiding a lot of my research for the last few years, because at first, when I went to look, there was no acknowledgment that this even existed. What I was finding was that I had patients who when they got stressed, their heart rate variability was going up. Once you decide that what they’re reporting is accurate, then you need to figure out why. What I found was that nobody was acknowledging this as a thing that is a phenomenon that exists. That’s actually when I found that paper from, I think it was the Norwegian Cross-Country Skiing, that said, we no longer use this for this reason.

The polyvagal theory

It actually has to do with polyvagal theory. We mentioned this briefly previously, but polyvagal theory was developed by a doctor named Stephen Porges, who realized he’d been studying heart variability in the vagus nerve for a long time, since the 1960s. He was doing research in a neonatal intensive care unit. What he found was that as the babies there are sick, obviously, that’s why they’re there, as their situation worsened, as they got closer and closer to more danger zone of perhaps dying or anything like that, their heart rate would drop, but their heart rate variability would go up, but this was not a sign that they were improving. This was a sign that they were in more danger of what’s called neurogenic bradycardia, which is that, or they had neurogenic bradycardia, which was more danger that their heart would stop, and so it was a bit of a paradox.

I actually contacted him a year ago saying, what is going on that there’s this, there seems to be a phenomenon where people are getting more stressed and their heart variability is going up. He said, you just rediscovered the vagal paradox that led me to develop polyvagal theory. I think a lot of people are becoming increasingly aware of polyvagal theory, especially because of its immense importance of understanding the autonomic nervous system and how it responds to trauma and trauma responses.

The reason why, to answer your question, why increased heart rate variability is usually associated with being healthier, but sometimes it’s not, is because when we have that more newly evolved, later developed ventral vagal part of the vagus nerve that’s associated with resilience and recovery and good digestion, all of that sort of fitness, that will increase heart rate variability, but that shutdown of life threat will also increase heart rate variability. One of the things that I– [sound cut] little pieces of in the literature–

Ari: Mel, go back one sentence. You cut out there.

Mel: Sure. My instinct and I’m finding some support for this in the literature, but one thing I would love to see happen is, one way to test whether or not your heart rate variability measure is going to be reliable or how to interpret it is to do what’s called an orthostatic tolerance test. When you go from lying down or sitting to standing up, your heart rate should go up, your blood pressure should go up. Now, if your heart rate goes up too much, that’s called POTS, postural orthostatic tachycardia syndrome. That is POTS. The vagus nerve, the break of the vagus nerve should come off gently to gently allow the heart rate to go a little bit faster. If the vagal tone is not that strong, then when you stand up, the break flies off and then your heart starts racing too much.

Conversely, if you stand up and your heart rate doesn’t go up, maybe even it goes down and your blood pressure doesn’t go up, which is a problem because you need the blood pressure to go up to keep the brain perfused. If you stand up and your blood pressure does not go up or it even goes down, that is a sign that the dorsal vagal, that survival shutdown part of the vagus nerve is too active and it’s not releasing that break to allow your body to adapt to the new situation of standing up. If someone is in that camp, then I would question the interpretation of a higher heart rate variability, meaning that they are healthier for that person.

Ari: Very interesting. I know there’s some sort of technical aspect of whether the heart rate variability is taken standing, seated, or lying down, and you can get different numbers depending on that. I wonder if given what you just explained, if one of those options of taking HRV might be particularly more accurate in eliminating the variation in people with POTS.

Mel: Yes, I think there are different opinions on that and there’s a lot of literature on, there’s even like a task force paper on the right and wrong ways of taking HRV. What I can say is that taking a heart rate variability measurement in different positions is a different measurement. It’s a different thing. You don’t want to compare apples to oranges. If you’re using this as a measure as an individual, then you just need to make sure you’re consistent. If you’re going to do it sitting, do it sitting, yes.

Ari: It’s interesting given this, some demographic of people or some instances, some scenarios, contexts in some people where heart rate variability goes up but is sort of deceptive in that way, is not actually indicative of better health. It’s interesting to acknowledge that still despite that, heart rate variability is robustly, as you said, and you even made the case, I would maybe push back on this a little bit but that’s a different discussion. I think I largely agree with you that it’s one of the absolute best markers. It’s interesting that it is so robust in predicting health outcomes and mortality even in spite of the fact that sometimes you can have high heart rate variability in instances where it’s not really painting an accurate picture.

Mel: 100%. To give you an example that actually I just got from my dad when I had a conversation with him recently is that if you look at weight in the population, look at weight in the population, then we’ll get a global trend of as people become more overweight then their health tends to be worse and their longevity tends to be less but it’s a J-shaped curve. People who are at the bottom end will also tend to have health problems as well. If you are not, if you’re zooming out or if your level of zoom isn’t right, or if you’re not asking the right question, then that relationship between weight and longevity is going to hold as a positive relationship even though people at the bottom end are going to have the reverse or they might need to gain weight to be healthier.

Ari: I might add a nuance or an additional distinction there, I would say there’s a lot of things like that where we find a J-shaped curve or U-shaped curve where both being on the high end and the low end are problematic. Even in things like cholesterol levels and LDL levels, you can find that kind of thing. mTOR is another good example, and IGF-1 is another good example. Probably not mTOR, but IGF-1 is almost synonymous with that, right? There’s all this hubbub that’s made of excessive mTOR activation and IGF-1 driving risk for cancer, but the risk of mortality is just as high among people who have excessively low IGF-1 levels. There’s a lot of things like this, testosterone and many other hormones.

Mel: mTOR is actually the key molecule to signal summer metabolism.

Ari: Yes, okay, interesting. Maybe we’ll come back to that. Okay, so one nuance that I wanted to add, this is what I thought your dad was going to say, and I have some personal experience with this because I have at many times in my life been told that based on BMI, I’m overweight, right? Generally, I hover around 9% to 12% body fat, I have abs, right? I’m based on this simple measurement, which is just a function of weight over height, rather than taking actual body fat percentage, it tells people who are athletes and who are muscular that they are more in the overweight category often. That is sort of disrupting that metric to a large degree by lumping in athletes with lots of muscle mass who are highly fit with people who are actually overweight and sedentary.

Mel: Yes, BMI, in my opinion, is a measurement that only makes sense to apply to people who are obese. It doesn’t make sense to apply that measure to anybody else, or I suppose very underweight.

The validity of the polyvagal theory

Ari: Yes. I want to go back to polyvagal theory for a minute, and I’m just curious since you’ve explored it in depth. I know that there is some pushback in certain circles against this theory, and I think there’s one researcher in particular that has really gone after Stephen Porges and written a number of peer-reviewed papers attacking him and attacking this theory and saying that this is a bunch of pseudoscience and it’s all, there’s no such thing as this polyvagal stuff, it’s all a bunch of nonsense. What are your thoughts on that?

Mel: Yes, that’s a great question. When I first came across polyvagal theory, I immediately found it very useful. That’s the thing, with any model, it’s not so much, is it the ultimate truth? It’s is this useful? Is this accurately describing something in a way that makes it helpful to navigate things, to solve problems? When I came across it, I thought, wow, because what it’s replacing is this idea that it’s called arousal theory, that it’s this linear, like you’re more awake or you’re more asleep in terms of your nervous system. I was like, wow, this is really interesting. Then my next question is, well, is this valid? Is it true? Is it a real thing?

Amongst the different people I was studying with, some people said it was BS and it wasn’t a real thing. Other people that I respected said that it was valid and I’m very interested in it. I did a deep dive and I’ve read most of what that author has written and other people have written and there are blogs called Polyvagal Theory is Dead. I’ve looked at their critiques and they were interesting and they were compelling. To his credit, Dr. Porges has written a response to that. I think it might be a chapter in a new book. A lot of times they are arguing against something that he never said. That happens a lot.

The key paper where he first presented Polyvagal Theory was written in 1994 and it’s very easy to find. There’s no like him not being honest because it’s just there. Sometimes it’s that he never says something. Sometimes it’s like they’re arguing with a specific detail that even if there’s validity to that criticism, it doesn’t really detangle the accuracy or usefulness of the theory. I think one example was where he’s talking about the evolutionary development of the system and where you have the dorsal vagal system first. Dorsal just means, think of it like a dorsal fin, it’s just on the backside.

Then you have the sympathetic nervous system and then you have the ventral vagal system and how that evolved. I think one of the critiques is that they can find a really old fish that has a ventral vagal nerve and therefore the whole thing is BS. I don’t want to misrepresent Stephen Porges’ very eloquent rebuttal, but at least in my mind, I’m like, this doesn’t completely debunk the whole theory and the theory is sound. I also did a very deep dive on the neuroanatomy of the vagus nerve, because some of these things are just really easy to refute or to support from a neurophysiological perspective.

Like are there two nuclei, which is like the, I think of hooking up an old school stereo system where you just put things in and out and you have your speakers and the player and stuff, so there are two nuclei, okay. Then there’s all these studies, like what happens when you either chemically block one of them, or if you surgically block one and you can see the differences in response.

Another one of the critiques, which I thought was unfair, was talking about in those types of studies, if you block, I think the ventral vagus aspect, what does the heart do? Really a big point of this theory is context. When you’re under life threat is what he’s saying is that the vagus nerve will cause this bradycardia that’s slowing down in the heart. For me, those studies didn’t really answer that question.

It’s an ongoing question, it’s an ongoing debate. I’ve been following it with interest for quite a few years. I’ve read both sides of it for a long time. I think that Dr. Porges’ responses were very eloquent, and like I said, like with most of these things, they’re making arguments against something that he never said.

HRV connects your cells to the universe

Ari: I want to circle back to HRV and quote you because in one of the presentations that I watched of yours, you started out with a slide that says, “How HRV connects your cells to the universe.” What the hell do you mean by that?

This sounds very, I know you get into the traditional Chinese medicine stuff, but what does it mean that heart rate variability connects our cells to the universe?

Mel: Yes, so if we step way back for a moment, and there’s a number of ways I can explore this, but a lot of branches of physics are looking at this, some of my study with my teacher, Dr. Ed Neal, who’s studied denaturing a lot has been looking at this, is this idea of, what is the universe made of, and how does the universe function? We’re now well away from our double-blind placebo-controlled trials. It’s like, what’s going on here?

Ari: I think just based on what you just said, this is officially the most meta we’ve ever gone on this podcast.

Mel: Yes.

Ari: What is the universe made of?

Mel: What is the universe? Well, it’s a really good starting point for all of these conversations. I don’t know why we don’t always start there.

Ari: All conversations should start with that question. [chuckles]

Mel: All my conversations seem to start there. [chuckles] Another researcher I want to bring in is Dr. Irv Dardik, who developed something called SuperWave theory, but what all these things have in common, and, there’s ongoing discussion for this, but there’s an idea that the universe is made of waves, of resonance patterns, of movement, of oscillating motion. Okay? Of course that may sound esoteric. Maybe those folks were onto something, but also physics talks about this too.

We’re talking about a worldview where we tend to think about the universe as being made of stuff and, my table is solid, but, we will find that it’s mostly made of open space and that’s just it. In the Neijing, which is a 2,500-year-old text on which all of Chinese medicine is based, I study with a very brilliant human named Dr. Ed Neal, who is a medical doctor and he was an emergency room physician and he spent decades translating the Neijing. When he read it, he discovered that it doesn’t really say what most of us were taught in Chinese medicine school than it says.

It says a lot of really important things for all curious people. It doesn’t matter if you’re an acupuncturist or not, or if you’re into Chinese medicine or not. It doesn’t matter if you’re interested in how things work and these patterns of the universe, then if you’re a curious person or even an artist, these are really important ideas. It’s really coming back to this idea that the universe is made of a breath motion, of an inhale and an exhale, and we can see this everywhere we look. If we understand reality from that lens, again, I’m not saying if it’s right or wrong, but let’s say, could it be potentially useful? Then what we are seeing is that we have waves embedded in waves, waves nested in waves, or as Irv Dardik would say, waves waving within waves.

I always say when I talk about this that we should do a drinking game, we take a shot every time I say wave. The way heart rate variability connects ourselves to the universe is that we have these much larger patterns, and some might argue that the existence of the universe is just the single inhale and exhale, like the single expansion and contraction, but then within it we have our mundane lives, but our heart beating is a wave. We tend to think of it as a rate, like that boom, boom, but you see how my motion, I’m going in, out, in, out, that’s a wave.

Heart rate variability is measuring the coherence of that wave, and it’s really the neurological regulation of the heartbeat, but it’s letting us know how well developed our nervous system is, and how resilient our nervous system is, and how well functioning it is, and the way it connects this very big thing with this very small thing is that it connects these larger, I said, cosmological patterns, even just like an annual cycle. Whether it’s summer or winter, it connects that to the very, very fast oscillations in our cells, and the cell danger response is really describing the healing wave when a cell gets injured, so we can use heart rate variability to connect those two things.

Actually, let me make the point a little bit further. The reason why the heart rate variability connects to what the cells are doing is through the vagus nerve. When cells get stressed, or injured, or infected, they go through a three-step healing cycle, and that’s what Bob Naviaux has called the cell danger response. When they’re not doing that, then they’re just cycling between day and night, okay? The vagus nerve is a big part of what connects our cells to our brain, and our heart to our brain.

When we, let’s say, have an infection, and this is what not enough people realize, okay? When we have an infection, our body intentionally, let’s say like the cells, it intentionally removes them from the network. The cells intentionally remove themselves from the network so that they can heal. They’re going to stop really being like one of my cells, and part of this network, and they’re going to just focus on being an individual cell so they can go through this response.

If someone is sick enough to the point where they don’t feel well, and they have to lie down, and they have symptoms, the vagus nerve is actually going to turn itself down in order to reduce the coherence of the system, in order to reduce the complexity of the system so that it can go through this process. This is the connection between the heart rate variability because what we know from these studies is that if you are sick, your heart rate variability is lower.

Why? Because when you are sick, your body, in its infinite wisdom of billions of years of evolution, has decided that what it needs to do in order to go into healing mode is to turn down the vagus nerve, turn down the coherence of how well all of these cells are working together so that these parts can run these older, more primitive programs in order to heal. Therefore, you will have a lower heart rate variability, and when you are healed, then that heart rate variability will go up.

There’s a very, amongst people who are aware of the vagus nerve, there is a very popular trend of just stimulating it however you can, like zap that thing and get it on. Sometimes that results in a helpful outcome, and sometimes it doesn’t work. If we understand that it’s, we get our chicken and egg, coming back again, that the first step is that it is by design that vagal tone goes down when we are stressed or we are sick, and that when we complete the healing cycle, it’ll come back on. That’s part of the reason why we have this strong relationship between heart rate variability and health.

Ari: Are you ever going to answer that chicken and egg question, by the way? Are we going to get the answer from you? I feel like you keep debating the question.

Mel: I know, I know. Maybe I’ll put it in the book, we’ll get there.

Ari: Okay. [chuckles]

Mel: I’ll still spill the beans at some point.

Ari: We’ve got to buy the book to find out the answer.

Mel: Yes.

How HRV is a strong predictor of health and mortality

Ari: Okay, so let’s talk heart rate variability and how this is, you’ve just explained it, but can you sort of concretize how this is connecting to our risk of various diseases and mortality? Why is it such a strong predictor of death and, or vice versa? Why is high heart rate variability, generally speaking, with some exceptions, generally a very good predictor of health and performance?

Mel: From my perspective, it’s telling us two things. One of those things is people are more aware of, and one of those things, I want people to be more aware of. Higher heart rate variability is associated with greater health because it means that the system is more coherent. It means that the big anti-inflammatory reflex of the body is through the vagus nerve. Again, this is another measurement. Heart rate variability is very strongly correlated with inflammation because heart rate variability comes from vagal tone. The healthy version of heart rate variability comes from vagal tone, and vagal tone has the anti-inflammatory response for when we are stressed or infected.

It’s also telling us about the development of higher cognitive functions. Executive function, conscientiousness, compassion, and all this prefrontal cortical activity are also associated with higher heart rate variability. It’s a strong relationship because we’re looking at different windows into the same system. What I’ve found is very few people have made the connection of why, oh, okay, inflammation, chronic inflammation is a problem, and vagal tone seems to be good. Now, if we look through the perspective of cycles, of healing cycles, then it starts to make sense about the connection with those.

Now, the other area that I’m only now really putting together, but now is making more sense, and it’s very important, is that also, heart rate variability is also telling you about how well your nervous system has developed. Polyvagal theory is telling us about our evolutionary story in terms of this ventral vagus nerve, which is that connection and relaxation and compassion and empathy. It’s also, for an individual, how the nervous system develops, that first we develop the dorsal vagal root in utero, then the sympathetic nervous system comes online, and then the ventral vagus nerve comes online in utero, but it gets developed and myelinated throughout.

Myelinated means that it’s getting covered in a way that makes it work faster throughout the first year of life. If you have a stressful start to life, for whatever reason, there were stressful pregnancy, illness at birth, momless stress, the whole nine, whatever it is, or you don’t have a consistent and connected and responsive caregiver or a safe environment, then your ventral vagus nerve is not going to develop and myelinate as well, and that’s going to lead to lower heart rate variability.

I tend to think of the lifespan, well, the lifespan is another one of these breaths, another one of these waves, inhale and exhale. You can look at everything as an inhale and an exhale. It may be that you do well enough, depending on your individual situation, maybe you’re okay in your 30s, but development didn’t proceed optimally, so now you’re starting to decline, whereas it used to be people might not decline in their health until 50s or 60s. That’s part of it too. Heart rate variability is associated with health because of this more direct relationship between inflammation and illness and the systems of your body working together, and it’s also telling a story about how well your development proceeded.

Ari: The way you’re looking at this is very interesting and it’s, to some extent, novel to me. I assumed that there was some layer of genetics and early life that will be a determinant of one’s sort of maximal potential heart rate variability, but coming from the athletic performance world, I’m used to really looking at HRV in a sort of very dynamic, malleable, trainable way where we’re analyzing, okay, from day to day, my heart rate variability is fluctuating a lot and I can gain insight into my body’s recovery status and how well I can train it today based on what I ate yesterday, how well I slept, how late did I go to bed, how deep was my sleep, how hard I trained yesterday, and these kinds of factors.

The longer-term is also understanding that one’s fitness level is a hugely important determinant of their baseline range of where that heart rate variability will land. Somebody who is a highly fit, and there’s lots of data on this online, somebody who’s a highly trained, very fit athlete is going to have way, way higher baseline HRV scores than somebody who’s sedentary. When you’re talking about this decline with age, it’s interesting that you’re looking to the childhood development of the autonomic nervous system, whereas my brain would seek to explain that by saying, well, yes, most people become more sedentary as they get older and lose their fitness, and this is sort of an obvious, low-hanging fruit explanation of why HRV would decline as they get older.

Mel: Yes, I love that, and everything you’re saying makes sense. If we use this principle of waves waving within waves, you can look at heart rate variability, and you can change heart rate variability this minute. If we decided to just go rogue on this podcast and do a breathing exercise and get all zen, we could change our heart rate variability in this minute we’re together, regardless of how well we slept and what we ate. We can also change it, it will change from day to day based on training schedules and how much gluten weight and all these lovely things and that sort of thing. It will also change if we come down with a virus or that as well. What I want to point out is that there’s also more of a lifespan aspect to it. Also bringing it back to the hemispheres of the brain, this vagal regulation of the part of the heart that’s guiding the rhythm, [sound cut] and the right vagus nerve is actually larger–

Ari: Mel, go back one sentence. Sorry.

Mel: Bringing this back to the right and left hemispheres of the brain, this vagal and brain regulation of heart rate is more coming from the right vagus nerve. There’s also a skew that people who are a bit more right-brain dominant will tend to have higher heart rate variability, which may come from both healthy and unhealthy sources. I’ve had patients who are more left-brain dominant who tend to have a low heart rate variability. I have patients who are more right-brain dominant and who are having autonomic dysfunction, blood pressure issues, stress, and anxiety. They have a high heart rate variability. Again, it’s not coming from that zen-like connection between their breathing and their heart rate. It’s coming from, more of an activation from this side.

It’s, interesting and important to layer on the development, especially with athletes, where their athletic talent might be layered in with their development. Maybe they’re more right-brained and they have more of a kinesthetic awareness. Maybe they’re a dumb jock, to say that without any judgment, like maybe that’s how they ended up here. Then they tend to have a higher resting heart rate variability, like there’s a relationship there.

Also when we think about heart rate variability, the measurements tend to be taken from minute to minute. It’s just sort of, you’re sitting there and breathing, and then a software is calculating this for you. One of the things that Irving Dardik, who’s developed SuperWave theory and was looking at heart rate variability, he had a little bit of a different take on it, which I really liked, which is also looking at what happens when you are standing and then you sprint and then you stop.

When you sprint, your heart rate will go up, and then when you stop, it will come down. This is also a completely valid measure of your health when you’re talking about athletic performance and training. The folks who will have the higher heart rate variability, in general, will be the sprinters rather than the marathon runners, where we’re getting this variation between their highest heart rate and their lowest heart rate.

There are studies looking at this as well, which is not just what is your heart rate, and not just what is your heart rate variability the way we normally measure it, but what is the difference between your resting heart rate and your maximal heart rate? How well can you get your heart rate up and how long does it take you to get it back down? These are more dynamic measurements, but these are actually the really key measurements of autonomic health and longevity and fitness.

Heart rate and fitness levels

Ari: There’s an interesting focus on heart rate, not heart rate variability, but just heart rate and pulse in traditional Chinese medicine, and they measure the, you fill in the blanks here, but they measure the frequency of the pulse, but they try to get a feel for the strength of the pulse. Can you talk about what exactly they’re doing there in a more intelligent way than I just described? Because you have a lot more familiarity with traditional Chinese medicine and how that ties into the broader discussion we’re having here.

Mel: Yes, absolutely. I’m not going to put myself forth as any sort of pulse master because that’s just not going to be accurate. Also, there’s different styles, and my communication style, especially here, is really focused more on the concrete and things that we can explain, but I also want to recognize there’s lots of things that are going on that we can’t explain, or at least that I can’t explain and those things are happening too.

I don’t want to make everything super reductious, but in terms of the pulse, there’s a lot that, just like I was saying about the gardener who can look out at the landscape and get a ton of information, very specific, accurate information because they’ve trained their eye. Similarly, if someone is trained in the art of pulse diagnosis, they train their fingers to get a ton of information about the health and the dynamics of the person by listening and feeling what’s going on with the pulse.

Some of the things that they are feeling for, as you say, it’s like the rate and the rhythm. They’re also feeling for how palpable or soft the vessel is itself. That, again, we can understand that really relates to circulating hormones and circulating other factors. That’s vasoconstriction and vasodilation essentially. They’re also feeling for the shape of the waveform. What you get is almost like you’re playing guitar, like you can put your fingers on and listen. Then as you push down, you’re feeling for the relative strength of the pulse between the different depths. People who are excellent at this can get a lot of objectively verifiable information about their patient by doing this.

Ari: Yes, it’s interesting that whole methodology was even created prior to the age of modern humans now, where I would imagine that there are even much larger differences between individuals in those sort of parameters of pulse rate, pulse frequency, pulse strength, and these sorts of things, just by virtue of the fact that in more ancient times, people had a more physically active lifestyle. Not because they went to the gym, but because their life required maybe being out in the fields or doing some kind of manual labor rather than sitting at a desk and being at a computer.

You didn’t have, like among modern humans, we have a much broader range between sedentary humans who really have virtually no physical activity, to high-level athletes who have an extremely trained cardiovascular system where they have physical adaptations at the level of the heart, where the heart muscle, the ventricle muscle thickness is much stronger. There’s a much larger ventricle, much better stroke volume, decreased resting heart rate, also lots of adaptations in the vasculature itself, and capillarization that would, I would imagine, influence all of this as far as what a practitioner would discern by feeling a person’s pulse pretty dramatically, much more so than the range of differences that one would have experienced thousands of years ago in ancient China.

Mel: That’s probably, I think there’s a lot of truth to what you just said. I think that in general, there’s just a greater spread of what humans are up to. What you reminded me of, which I always find to be a very comforting thought, because I think, when you study health from this evolutionary biology perspective, it’s easy to get a little bit down and look back on the better times.

One of the things I always find a little bit amusing and refreshing is in the first chapter of the Neijing, which is this book I mentioned that’s 2,500 years old, it starts off by basically saying, and I am very much paraphrasing here, back in the good old days, people knew how to live well and they lived with the patterns of nature and they didn’t stay up too late. They went to bed on time. They got up in the morning. They didn’t drink too much. They weren’t having way too much sex and they weren’t sitting around all the time and they lived to be like 100 years old, 120 years old.

Nowadays, people don’t have any sense and they’re sat around and they’re sedentary and they’re not eating well and they’re drinking too much and they’re dying at 50 and 60, and I’m like, oh my God. That could have been written now. I love that the more things change, the more things stay the same. My– Yes, go ahead.

Ari: I think it’s an interesting insight. I will point out, however, that even that, if we’re talking 2,000, 2,500 years ago, is post-industrial, not industrialization, post the agricultural revolution, which was about 10,000 years ago, which changed us from hunter-gatherers to a very different society which really was extremely deleterious to our health.

Mel: That’s exactly what I was going to say, that I think that there’s probably a global human story that when we did that, we realized that there were good old days where we were more with the patterns of nature. That’s right.

How data can be skewed to support different naratives

Ari: Yes. Though I’ve done in writing the book that I’m working on right now, one of the things that I’m doing, it’s a bit of a digression, but since we’re on it, maybe we’ll go into this. There is a very large myth that’s been created that our human ancestors lived much shorter lifespans than we live today. We’re all sort of indoctrinated with this idea that we all used to die at age 40 or 50, and hunter-gatherers die at age 40 or 50, and a few hundred years ago in North America, and Europe, everybody died at age 40 or 50.

There’s sort of interesting nuances to this discussion, but one of the first layers that we can look at to see how much– Part of this narrative is like, “Oh, modern medicine, just in the last 7,500 years, 75 or a hundred, I shouldn’t say 7,500, but 75 or a hundred years has made these massive advancements that have extended our lifespan. We’re living much longer than we ever have before.” This is a very common belief that a lot of people have, and it’s simply not true.

One of the layers of evidence that we can look to is for example, the ancient Chinese from thousands of years ago who had no modern medicine and no pharmaceuticals who frequently lived into their 90s or 100s, or, there’s certainly lots of cases of that. If we look at lots of– Like the ancient Greeks that we’ve all read about in philosophy courses, and Aristotle and Plato and Socrates and Hippocrates and Dimokrates, and these kinds of people, if you look at their age of death frequently in the ’80s, ’90s, and many of them lived beyond a hundred.

Again, 2000 years ago, no modern medicine, no drugs. What’s interesting about this is that there was actually– Hunter-gatherers as well, tens of thousands of years ago, also frequently lived to the same ages that us modern humans live. In the United States right now, in 2024, the average lifespan is 73 for men and 79 for women. If you compare that 2000 years ago, Greeks and Chinese people were living to those same ages and beyond. It was not uncommon. We are not living longer than we did thousands of years ago.

I will also point out that there are studies of hunter-gatherers now who exist, who are still alive today, for example, the Tsimané tribe and the Moseten tribe in Bolivia who have been studied just in the last few years, where they’re taking samples of these populations who again, have access to no drugs and no modern medical care where they’re taking people who are in their 80s and 90s. The oldest participant in one of the studies was age 94. Again, we are not living longer than them, but what confuses this is what they do have is very high incidence of childhood mortality, and very high incidents of death by accident and death by infectious diseases.

Those are areas where modern medicine has made major advances where we have way lower incidents of infant mortality, maternal mortality during birth, and death by accidents. In these populations, it’s like close to 50% of kids don’t even make it to age 15. Because violence and accidents, and infant mortality is so high.

Mel: This is the perfect example of saying there’s lies down statistics. You can tell wildly different stories about this depending on how you slice and dice the data.

Ari: Yes. It is a statistical issue because they use a term called life expectancy at birth, which factors in– It’s basically the average age of death. If you’ve got 10% or 20% of the population that’s dying in the first year of life or 15 years of life, it will massively skew that average down to 40 or 50. Then people interpret this as saying, “Oh, humans used to live to age 40 or 50 as their maximal age,” which is incorrect. Anyway, sorry for that digression, but since we were on it, I thought I’d do a little myth debunking.

Mel: No, very interesting.

Resting heart rate and heart rate variability

Ari: Let’s get back to resting heart rate as a determinant of health because, like heart rate variability, it’s interesting to note that resting heart rate itself is also a very strong predictor of mortality. I think we get another example of this scenario that you were describing earlier where there is a segment of the population who might– There’s maybe two different kinds of segments of the low resting heart rate that we could single out. One would be high-level athletes who have trained themselves into a low resting heart rate, but there might also be very ill people who have a low resting heart rate, or maybe people who are stuck in winter metabolism, for example.

You explain how you see this landscape because I found your presentation of it fascinating.

Mel: Okay, cool. Resting heart rate and heart rate variability are related to each other because they’re both products of the same systems. If we have lower ventral vagal tone and a higher sympathetic tone, then we are going to have lower heart rate variability and a higher resting heart rate. These two metrics they’re not perfectly coupled because there’s other things that are affecting them, but there’s similar ingredients going into the blender to make them. With resting heart rate is another one that’s a strong predictor of health and all-cause mortality.

That the higher it is suggests worse health, that you’re more stressed. I should say, because this is resting heart rate, we’re asking how low can you go. How well can you rest? If it’s high, then it means that you’re not able to rest very well. When you are sitting and when there shouldn’t be so much demand, your heart is still working hard and it’s not recovering and you’re not recovering well and your ventral vagal system is not calming that down. Actually, I should say in terms of just adding this developmental component, when we are born, our resting heart rate is quite high. It’s like maybe about 100 beats per minute.

Then as our nervous system develops, it goes down so that in adulthood, the resting heart rate should be perhaps in the sixties. That said, I found some new research, which was quite interesting because we have all these wearables now, researchers can now access these giant data sets of people with this 24-hour data and look at these trends that are not just sort of, “I’ve gone to the doctor and sat down and you’ve taken my resting heart rate.” What we’re finding is that the average resting heart rate it’s actually lower than almost all the studies say.

Which is, I think perhaps partly because if we’re getting a 24-hour reading, that includes nighttime, so the resting heart rate should be lowest at night. We’re getting that true river picture.

Ari: I could think of a few confounding variables there. One would be the lab coat syndrome thing that you see with blood pressure when people go to the doctors. On average, they might have some nervousness and so it would skew higher because of that. The nighttime is probably a big one. That might be the biggest one. The other thing is demographically that the people who are inclined to use these wearables are on average going to be more health conscious, people who are more exercisers compared to the average population.

Mel: User bias. I think there might be definitely some sense to that. However, if you look at BMI, you’ll see that it’s a mix of people. People might also be wearing it because they’re unhealthy. There’s probably both going on. Also if you go to the doctors, did they really make sure that you sat quietly for five minutes before they did it? Because that actually makes a big difference. If the resting heart rate never really comes down properly, and you see this, for example, in autistic kids will have a higher resting heart rate and a lower heart rate variability because that ventral vagal system, that right brain never really quite comes online.

The left hemisphere is dominant, and so their autonomic system, their heart rate, and heart rate variability are telling that story. It should come down, but what we see really when we dial in, and I believe, and I’m very happy to be proven wrong or to find an exception that for any naturally occurring thing in the body that you want to measure, there should pretty much always be a J-shaped curve. That’s kind of a principle. When I see a study with a linear relationship, I’m always asking questions. This isn’t going to be true for environmental toxins.

Obviously, you want those to be zero, but for everything else, I’m like, “Okay, who did they include in this, or how are they measuring this?” You’ll usually find in another data set that was maybe more inclusive, you’ll find the J-shaped curve. That’s something to look for that usually there’s a sweet spot and it’s never the case that higher’s better or lower’s better.

Ari: There’s an interesting distinction I’ve been writing a lot about between traditional biomarkers and what we would call in exercise science performance metrics and performance metrics, the simple ones would include things like muscular strength or VO2 max.

In contrast to biomarkers which are things like, let’s say, cholesterol, or blood pressure, or blood sugar levels, where if you– There’s an optimal range, and to the extent one goes out of that range, high or low, it’s indicative of a problem. With performance metrics, it’s not like that. You’re not going to find an unhealthy person, maybe you would find one in the world or something like that. I don’t want to say in blanket terms, but 99.9999999% of the time, somebody who has a high VO2 max is going to be extremely healthy.

Mel: That’s a helpful distinction there. You’re absolutely right. If you’re looking at a performance marker, there can be a more– better performance is better performance.

Ari: The only demographic that will disrupt that relationship is people– With strength or VO2 max, people who are using performance-enhancing drugs. A lot of bodybuilders die young. They would get very high strength scores, but due to their use of drugs, they end up causing all kinds of side effects that end up killing them at young ages. People who are not chemically enhanced in that way, the relationship holds up extremely well.

Mel: That makes sense.

Ari: Resting heart rate. Tell me more about how this matters in determining our health.

Mel: Resting heart rate at night, and I think the wearable data showed, it was between 3:00 and 5:00 AM, is going to be an indicator of your body’s ability to rest and recover in general. We can clearly understand why that would be a helpful thing for health. Then again, at the outlier end, the reason why maybe that’s not always the case, or maybe why there’s exceptions, we mentioned a little bit about winter metabolism, that if someone just doesn’t have enough gas in their tank to get their heart rate up, or the emergency brake is applied.

Again, this is a smaller percentage of the population, but it’s not just one or two either, it is millions of people. It’s just not the majority. Then you can also get a low resting heart rate that may not necessarily be associated with greater health markers, but in general, it’s really just measuring your body’s ability to regulate, and recover, and to heal itself, and to balance itself out, and do all of those really important things that we do while we sleep. Also, a lot of different things are going into this mix. We can look at our stress levels and then our ability to handle those. It’s reflecting both.

How Dr. Mel uses data to understand a patient’s health

Ari: When you look at resting heart rate and heart rate variability, are you looking at it more as– My context is more exercise science, so I look at these as trainable, malleable entities that we can gain insight from and look to say, “Hey, relative to a highly trained person, where am I landing and how can I train myself more so that I’m more in the good or elite categories of these metrics?”

I think you’re looking at them more as how they tie into pathology, and how these are determined as a result of early development, and how our nervous system is functioning as a window into autonomic nervous system function. Once you measure them or as you track them over time with people you’re working with, what do you do with that information? How are you applying it practically and what are you recommending to people in certain contexts?

Mel: Yes, excellent question. What you reminded me of as well is that you have this spectrum from high-level performance to pathology and that people can fluidly move it. My goal is to move people out of the pathological end back into going– A lot of them were athletes or are athletes and they want to get back to it, and being able to still support them there as well. I have a little bit of a different take on how to use biomarkers, and lab tests, and these types of tests.

In this case, let’s say, we’re looking at resting heart rate. We’re looking at the output of a system and it’s what I call an index marker, which is to say that a lot of different things go into the mix to make your resting heart rate. I’m evolving it and adapting it over time as I learn, but it’s to

Not address it directly. We think that, let’s say, if a lower resting heart rate is better, and I can take this supplement or do whatever to lower it, I will be healthier. I find that the cleverer we get, the better we are at changing those biomarkers, and it almost always causes problems because we’re just not smarter than our own system.

Ari: I want to do a two-hour podcast with you just on that one topic alone because I think it’s so important.

Mel: I’m super happy to. Again, this comes from me having done that a lot to myself mainly, and also my patients from like, “Oh, okay. Well, high homocysteine is bad. Let’s lower your homocysteine. Yay.” Then there’s always something down the line because we’re too zoomed in and we’re not looking at first principles, and we’re not smarter than these individual markers. It really is about monitoring it. One thing that was very eye-opening for me is that I have an Oura Ring, which is a sleep tracker and exercise tracker, and I’ve been wearing it for five or six years now.

When I first started wearing it, I was having health crises. I had a chronic fatigue. I had fibromyalgia. I had autoimmunity to my own collagen. My brain was not working very well. I had no short-term memory. I had all this stuff going on. I recently went back and looked at my data to get this dashboard where you can drag out for different time horizons. I was teaching about low resting heart rate, so I wanted to see where was my resting heart rate then and where is it now. My pain has gone down. I’m mobile. I have a short-term memory. I’m doing a lot better. My energy is a lot better. My sleep is a lot better. In those two periods, let’s say the first two years where I was in a crisis, and now when I’m doing a lot better, it’s the same. The resting heart rate is the same. What’s going into and create that resting heart rate is completely different. My nervous system is more regulated. I have better energy. My sleep is better. My mood is better. My memory is better. My function is better. My physical function is better. Everything is better. My resting heart rate is the same. Fortunately, I was smart enough to not try to change my resting heart rate because that would have been a problem, that would have been a distraction. I don’t know what I would have. It was 57. I don’t know, does it go up? Does it go down? Should I mess with it? If I tried to mess with my resting heart rate, it would not have led me in a good direction. I simply note it and I’m watching. For patients, we’re just watching it as an output of your system to monitor in the background, and we can use it depending on the person to assess progress and to see where things are, but I’m not recommending a specific formula to change your heart rate.

I’m not recommending a specific whatever supplement or whatever to manipulate these numbers because I’ve learned the hard way over many years that that doesn’t lead to good outcomes.

The flaw in trying to hack the body

Ari: I don’t intend this to be in any way antagonistic, I intend it to be more of an addition. What I would say is almost like there’s two issues there that need to be sorted out when we talk about modifying the biomarker. I’ll give a few examples. I can give a whole bunch of examples. Let’s say, I’m interested in altering my blood pressure, I can take a synthetic chemical, a pharmaceutical designed to alter receptors or alter how my kidneys process certain minerals and the amount of minerals that are excreted in such a way where it essentially just, I take the pill, it lowers my blood pressure.

I can lower my blood pressure through lifestyle action, through minimizing stress, improving my diet, improving my body composition. I don’t have a problem with trying to improve the biomarker, but we have to talk about how we’re trying to do it. Are we trying to do it through an allopathic or a biohacking model where we’re trying to hack the body, which I think you agree with me on, where we’re trying to interrupt the systems in a way where we think we’re outsmarting the body?

The body doesn’t know what it’s doing, it’s stupid, so we’re going to do this intervention, or pop this pill and this chemical is going to just lower that marker for us, and then we’re healthy. I think that, as you said, I agree with you completely, is almost always going to not result in much benefit and is very likely in principle to result in side effects. I’d say in the vast majority of cases, the side effects generally in the long term outweigh the benefits.

Which is why, after nearly a century of allopathic medicine, applying that very model of health it’s like, how can we hack the body? By the way a lot of people don’t understand this.

The most advanced form of biohacking, of applying that principle of trying to hack the system, is allopathic medicine. They’ve been doing it for nearly a century, and they’ve developed through trillions of dollars and hundreds of thousands or millions of scientists all over the world working for pharmaceutical companies. They’ve developed literally millions of drug candidates which have been tested, and have been further refined down to 19 or 20,000 FDA-approved chemicals.

Among those we don’t have a single one, not one that we can reliably give to, let’s say a healthy 30 or 40-year-old for decades, where we know that the benefits of that compound will outweigh the harms. We don’t have a single one. It’s hard for me to imagine a more powerful proof that this model of trying to hack the body with chemicals doesn’t actually make us healthier.

Mel: I completely agree. I appreciate your distinction about trying to modify these measurements. I’m going to give you another example though that’s a little bit surprising. Because it’s in between the examples that we gave. Because when we take a measurement and then we decide if it’s good or bad, and then what we’re going to do about it. It’s really based on our understanding of the system. A lot of times this understanding is missing context, or it’s not really understanding why it’s there in the first place.

The example where I saw this hacking through seemingly healthy behavior problematic, is that, increasingly people are wearing continuous glucose monitors, which I think is a wonderful thing. You get this immediate feedback cycle, you can take a lot of the guesswork out of all this like fad healthier diet advice. It’s brilliant.

What I saw is that the advice that often comes, there’s a little bit of training that comes with these continuous glucose monitors in terms of how to lower blood sugar, or how to manage it, or how to hack it, includes vigorous exercise after eating. That if your blood sugar goes up and then you vigorously exercise, you can drop it down. Now you were talking about improving something like blood pressure through healthy habits. That is great.

If we take someone from what they’re doing that might be promoting ill health and then move them in the direction of healthier habits and things improve, that’s great. This is more of a hacky way where we’re going to try to drop blood sugar by stimulating certain mechanisms of insulin sensitivity in the body. Overall, these patients were making their systems more stressed. It wasn’t really good advice in general to exercise vigorously. They were getting on the rebounder after eating in order to drop their blood sugar.

Here we get, and it wasn’t a supplement, it wasn’t a drug, it was exercise. Isn’t exercise good? We still want to understand context, which is that that’s not really the best time for vigorous exercise usually. The reason why we’re doing it is because we’re trying to hack this number and to bring it back. What is not talked about nearly enough is that, yes, diet will play a role in blood sugar, no question. Especially if we’re eating highly refined and glucogenic foods. For a lot of people, it’s their nervous system that’s actually making the bigger contributor to what the resting glucose is, and how well they can handle meals and that sort of thing.

Going on a rebounder after exercise and was actually making that problem worse. That experience also feeds into, you know what, I’m not going to try to wiggle this variable. I’m going to try to use first principles and adjust things that I know are going to be useful. Then just see what happens and then iterate.

Ari: It’s a great point. Even healthy things can be unhealthy if applied in the wrong context or with the wrong guiding philosophy. I would say in response to that, I would say, this is where we need to look at ancient humans. We need to look at our ancestral way of life and hunter and gatherers and go, “Do they do vigorous exercise right after eating, or do they generally rest?” There’s probably some wisdom inherent in that and the other animal species more broadly as well.

Let’s wrap up on this idea of heart rate variability, heart rate, nervous system function. Can you summarize how this information is taken into context, and how you’re using it with the people that you work with to guide how you understand what’s going on and how you approach solving it?

Mel: I think it’s helpful for most people to be measuring this. It’s basically like a background temperature reading of their autonomic nervous system. I think it’s also while keeping it a little bit at arm’s length. A little bit just like how we talked about, that we’re not trying to hack it or manipulate it. I think that if someone is sicker, then these variables are going to be less responsive to the day-to-day. Think about the difference between an athlete who overtrains might just need to rest more, and then it comes back.

Someone with chronic fatigue, they’re resting, and they’re not recovering. They’re in a different category. These little hacks aren’t going to work anyway. Their nervous system has become less adaptive, or on the other side, it’s so reactive. Every little thing is setting it off. Then it’s hard to get good feedback about individual things that are affecting it. I think it’s just nice to have it in the background and just notice what happens over time.

I recently had someone I was working with on the other side of the world, and she’s been monitoring hers for close to a year now. She’s able to see how it’s become healthier, how she’s sleeping better, her blood pressure’s improved, and her heart rate variability has improved

I didn’t give her any specific recommendations of things to do in order to change it. It’s more this background marker of her resilience that she can use as another way of knowing herself. I think this is a sound to not be doing things to try to manipulate it. If you do make a change and you can just notice the difference, maybe you go into a different environment and you notice that your nervous system is more resilient. Maybe you make a change and you notice, but it’s really nice because I tend to work with people long-term. They might come for a year, they might stay on longer, and to have that as an ongoing record of how they are doing. That they learn to know themselves and what’s happening and what’s not. Again, I think that at the moment especially with all the misinterpretations and people jumping to conclusions about the meanings of things, I think we’re safer and wiser to just monitor it, and let us know in the background how things are doing without trying to manipulate it

Ari: What would you attribute her changes in those markers to? I was going to give another example, but I’ll leave that out at the risk of going down a rabbit hole. You did something, you changed something in what you were doing. You were doing some treatments and the explicit intention of that wasn’t, “Hey, we’re going to do this to modify your heart rate or heart rate variability.”

Nevertheless, we are using resting heart rate or heart rate variability as a metric which we are inferring that these changes, these treatments, or these things that we’re doing are having a benefit.

Mel: Exactly. I took her through the process that I take people through in order to reverse complex chronic health issues. There’s nothing I would change based on her heart rate variability. That’s to say I’m taking a very conservative view. I’m saying to not jump in. We talked about using caution when we’re interpreting these things and when we’re working with them. You can use this data to ask intelligent questions.

One thing I noticed when I looked back at my data was I was looking at the relationship between how much exercise I had done and what my rest and heart rate was. When I looked at it for those first two years when I had chronic fatigue, the more I had exercised, the higher my resting heart rate was. Which means that I wasn’t recovering. That I wasn’t adapting well to it. Then as I was healthier in the latter two years, the more I moved, the lower my resting heart rate. Which is what you want to see, and that’s what happens in a healthy person.

Seeing that with my own data, lets me ignore all this advice of what you should do and lets me know this this is the relationship between exercise and my nervous system right now. This is how it’s changed. Do I think that I could have gone back and pinpointed the moment where I could have started exercising? I don’t know. I think people try to do that. Because of the cycles I’ve seen of misinterpretation of lab markers, this is why I’m so cautious. It’s more just interesting for me to note that in retrospect and to use that as a positive sign that it’s healthy for me to exercise, which I can also feel in my own body anyways.

I will answer it by saying that I’m constantly actively working on this question about how to use these numbers well without making the mistakes and the hubris of taking a number that we think we understand and maybe don’t understand as well as we hope and trying to make decisions based on that to manipulate it and causing problems that we didn’t intend to. I’m still on that cautious side, but I’m constantly exploring research and data in my practice and my own body to see, can we find things that work, that are helpful, that are safe, that are good to use as guideposts.

Resolving a chronic complex illness

Ari: Very interesting. Mel, I’m curious if you can give a very quick, I know this is a broad thing that you could obviously talk for many hours on, but can you give a very, very quick overview of what exactly your approach, when you said you took this patient through your approach to resolving complex chronic illness, what is the outline of your approach?

Mel: Yes, that’s a great question. I definitely, I am very fortunate to have worked and continue to work with some really smart teachers. I always love to give them credit. This is an approach that I’d found in various places, but the person I’ve worked with the most is Jeremy Cornish at the Damn Good Doctors Club. He’s a very smart guy. This is an adaptation of an approach that he and others learned from a, in particular, a Chinese medicine doctor that they studied with in Sichuan, China. Basically, this guy was treating like 150 to 200 patients a day and getting excellent results because he had dialed in his algorithm and has dialed in his way of thinking so well.

This approach is essentially to work step-by-step in the body using a sequence of systems. Those systems are the immune system, the digestive system, the neuroendocrine system, the tissue repair system. Then if someone still is lacking in energy at the end of it, then we can consider boosting and supplementing, and tonifying. One of the questions I’ve had over the years is order of operations when working with complex chronic illness. Everyone I worked with had– Well, most people I worked with did not have an order of operations. That was just crazy inducing. You’d have a patient who had digestive issues and mood issues and skin issues, inflammatory issues, and you get all this data, and then you need to figure out where you were going to start, and where you start is important. Then I worked with many people who say, start with the gut. As someone who had lifelong digestive issues, I had worked on my gut quite a lot and still had quite a lot of problems. Then I worked with someone else who said to start with hormones. When I did that, it seemed to be useful 30% of the time, which I was not happy with that.

For me, if it’s a sound order of operations, it should be at least 80% on point. Actually the way I’ve been trained, it’s actually even higher because you’re just asking the question, do we start here? Most of the time the answer is yes. Some of the times the answer is no, which means that it’s even more accurate. We start with that. We have clear signs and symptoms that we’re looking for to resolve before we move on to the next stage. Then we’re moving in that step-by-step order.

Honestly, using that order, I started to see it in other places that this is sort of embedded in human wisdom, that we’re going to move from the outside in and we’re going to remove load from the body first before– Most people come in trying to take B vitamins and adaptogens and hormones and all this stuff to boost. They’ve got so much gunk in their system, a lot of which they’re feeding. Studies showing that your dysbiotic gut bacteria love it when you take iron supplements. For them, that’s like an all-you-can-eat buffet.

Same thing with B vitamins. Working in this order has just been really, really sound and really has explained why certain things that should work well or seem to be valuable haven’t worked for my patients or for myself really in terms of the timing of when we use them. It’s a step-by-step process, which in some ways is a little bit agnostic to the specific tools, although I do have tools I recommend. What’s more important is that we’re really clear on what we’re trying to do, what we’re measuring, going back to these first principles.

Are we warming? Are we cooling? Are we getting rid of moisture? Are we adding moisture? What happens when I do that? I think that you seem warm, so why don’t we do this really safe, low-amplitude thing where we remove some of the warmth? Do you get better or not? Based on how you respond, we can interpret the feedback because we’ve been so intentional with how we’ve worked with the system. When you are at the level of reductionist biochemistry, whether that’s pharmaceuticals or supplements, because you’re not working at that first principles level, you can’t interpret the feedback.

All you can do is repeat the lab in however many months and fingers crossed hope for the best. A lot of times people are feeling worse and they’re told to stick with it. Whereas here, if we know exactly what we’re doing, then whether you get better, you have no change or you get worse, we always know what to do next.

Ari: Yes, or they’re told based on their lab markers that they’re better, even though they may feel worse.

Mel: Exactly. This is its own problem.

Ari: Mel, I’m really enjoying this conversation with you as it unfolds sort of organically as we talk through things, really fascinating stuff as usual. I think we still have more to explore in the traditional Chinese medicine front. You gave me a bunch of ideas and I saw in your presentation related to the Nijing. How do you say it?

Mel: The Nijing, I’m not like a Chinese speaker. I apologize to anyone about my pronunciation.

Ari: We’re both offending people. Wonderful stuff really. Let people know again where they can reach out to you if they’re interested in working with you.

Mel: Sure, so I’m over at SynthesisHealth.co.

Ari: Wonderful, thank you so much. I look forward to the next one.

Mel: Thank you, I appreciate it.

Show Notes

00:00 Intro
06:08 – How brain development during childhood links up with the autonomic nervous system
08:58 – Heart rate variability
13:44 – The Polyvagal theory
22:25 – The validity of the polyvagal theory
27:01 – HRV connects your cells to the universe
34:33 – How HRV is a strong predictor of health and mortality
44:07 – Heart rate and fitness levels
50:02 – How data can be skewed to support different naratives
54:40 – Resting heart rate and heart rate variability
1:0:52 – How Dr. Mel uses data to understand a patient’s health
1:08:06 – The flaw in trying to hack the body
1:20:36 – Resolving a chronic complex illness


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