 Thank you very much. You got to see me on top of salt with a guitar that was actually John's guitar. The work that I'm going to be presenting, I've been involved with a little bit, but really is work that was done in Justin's lab. He has presented information about the anxiety study. He presented it yesterday. This is data that comes from that same study, but it comes not in the form of just looking at anxiety. It comes in the form of also looking at physiological indicators. He talked about the heart rate variability yesterday and he talked about blood pressure. We're going to talk about that, but I'm going to be talking about it in a little bit more depth. Not that Justin wasn't presenting stuff in depth, but we're going to go a little bit deeper into that data. First, I'm going to talk about heart rate variability, because I think it's a term that's used a lot. It's very popular now. You can buy all sorts of apps and wristwatches and other things that basically will measure heart rate variability in one way or another, but let's get into a little bit of the science of heart rate variability so you understand exactly what we're talking about in this study. We're going to talk a little bit about why it's a useful endpoint for float research, how it's measured, how are the measurements quantified, and what relationship does heart rate variability have to anxiety? That's sort of the end point here. When we start talking about what we saw in terms of heart rate variability and anxiety, and then what happens when you use a floatation intervention. What is heart rate variability? Most of us know what our heart rate is, and most of us know that we can even use our pulse and a little watch with a second hand to kind of figure out what our heart rate is in beats per minute. That's usually what heart rate is quoted in. You test your heart rate before and after exercise, you get to 160 beats per minute if you're pretty athletic and you're not my age. What you'll find out is that that heart rate will go up and then it will come down, but what you don't know is that actually it's varying all that time also. The variability has to do with that space in between what you see are those spikes. You're measuring the beat to beat variation in the heart rate. Let's get into a little bit of the physiology of what controls this. It's a physiological phenomena, our cardiovascular system, and there's something called the SA node. Let me see if I can actually use these things. I always have trouble with these. There it is, that little piece right there. That's the SA node. That's a clump of cells and it is key to getting the heart muscle to contract on a regular basis. It's automatic. It's separate from the nervous system. It's a chunk right on the heart. If you were totally disconnected from your sympathetic, your parasympathetic nervous system, your heart would still beat, but it wouldn't vary much, which is not too good. It receives several different inputs. Basically, these inputs are from the sympathetic nervous system and the parasympathetic nervous system. They're key to varying the heart for many different reasons. The beating of the heart varies for many different reasons, but one of the main reasons it varies is because our respiration and our heart rate really are connected together. That is because if we take in a breath, the heart rate goes up. If we exhale, the heart rate goes down. If you're normal breathing, you're probably breathing between 12 to 14 breaths a minute. If you breathe like we were instructed to breathe yesterday, where your intake was in four seconds up and eight seconds out, for the four seconds up, your heart rate's going up. For the eight seconds out, your heart rate's going down. So if you've ever used a heart rate variability app that has to do with relaxation, what you usually get instructed to do is follow a breath pacer. Oftentimes, these breath pagers are around six breaths a minute. Basically, getting your heart rate to go up for five seconds and down for five seconds. If you watch it on a graph, you start to see this nice sinusoidal wave, and they sort of call that, when you're doing that well, they call that coherence, that basically the heart rate and the breathing rate are going together. Jumping back into this, so simply, the parasympathetic nervous system is slowing down the heart rate, and the sympathetic nervous system is generally increasing the heart rate. Now, we normally think of the parasympathetic and the sympathetic nervous system as sort of this balancing act, but oftentimes when we talk about the sympathetic nervous system, we say it's the fight-flight system, which sort of implies it's only really acting when we go into an alarm state, but that's not true, right? And the parasympathetic isn't only going, acting when we go into rest digest. The sympathetic nervous system is always operating, and it's always varying things like the heart rate. It's always also all doing a lot of other things. And the parasympathetic nervous system is always operating, and there's a balance. There's a balance between the two. So when we think in terms of what happens during a period of stress, we tend to think of a sympathetic dominance, a sympathetic dominance in that balance between the sympathetic system and the parasympathetic system. And what that would do to heart rate variability is it would tend to take it lower. So once again, it's under sympathetic and parasympathetic control, but rapid fluctuations in heart rate usually reflect parasympathetic nervous system control only. The respiratory sinus arrhythmia that I was just talking about changes in heart rate over time, especially heart rate variability over time, provide a window into autonomic physiology. And that's why it becomes important for the research that we're doing with flotation tanks. When John was talking about a base lining, so one area of base lining that we believe occurs with floating is a base lining of the sympathetic parasympathetic balance in the physiology of the individual. And we believe that this is similar, but different across individuals. Healthy individuals are probably going to be different than people with impaired cardiac systems and maybe different than people with anxious experiences because we feel that there is probably a connection between the experience of anxiety and the constancy of that experience and a shift in the sympathetic parasympathetic balance of the individual. So analysis of heart rate variability quantifies these changes over time and it becomes a reason for us to start looking at it. Now I just want to show this so you can see what a normal heart waveform looks like. That's on the left side. And again, heart rate variability on the right side is measuring between the spikes which are called R-waves. The top thing is called an R-wave. And in order to do this work to the level that you really can get this stuff published in high quality journals, you not only have to measure this and the only way to measure that wave is with something called an EKG, you also have to have graduate students or research associates that will spend hours looking through and looking at those R-waves and making sure they're normal because sometimes they're not. And in heart rate variability it only counts if you've got normal R-waves, okay? So how do we quantify heart rate variability? There's lots of ways to quantify it. I've only put two up here. Time domain is basically using some mathematics on a period of time on the numbers you have as you've measured the variability across it. So the first one is S-D-N-N which is a standard deviation of all those normal peak-to-peak intervals, okay? The other is R-M-S-S-D which is actually the square root of the mean. Do you have to go on? Okay, between the differences between, okay, okay. This is all done by algorithms. We don't actually do these things by, you know, he has MATLAB and I think MATLAB is what he used to do it. The frequency domain is a completely different thing. We don't normally think of heart rate being a frequency domain, at least sort of the average heart rate person. So we, what we're really doing, there's a mathematical thing called a fast Fourier transform that you can do on this data that gives you different powers and different frequency areas. And the areas that have been identified for heart rate are high frequency, low frequency, very low frequency. There's another one called ultra low frequency, okay. But the high frequency, low frequency, and very low frequency are the ones that are most popular in the literature and have really been explored the most as to what they mean. High frequency band is considered a very good indication of the parasympathetic nervous system influences on heart rate. The low frequency band is a little bit more confusing. It's sort of, we'll show you something about the barrow receptors. These are receptors that we have all in our body that are a key to blood pressure regulation. The sympathetic nervous system and the parasympathetic nervous system influences on the heart rate. So it gets a little fuzzier when you start talking about low frequency band. And then very low frequency band gets even a little fuzzier because you have vasomotor changes, thermoregulatory changes, possible parasympathetic nervous system stuff. So as you can see that high frequency band seems to be the one that would give us the most information about this sympathetic parasympathetic possible balance. It also gives us most information about what's actually happening physiologically if we're looking to see is the parasympathetic nervous system actually changing during the flow. So what relationship might HRV have to anxiety? Now a recent mental analysis found that one, looking at lots of studies, anxiety disorders are associated with significant reductions in HRV. Panic disorder, PTSD, generalized anxiety disorder, and social anxiety disorder displayed significant reductions in both time domain and high frequency HRV. So clearly the high frequency HRV is going to be something that would fit with the data that and the group that Justin was looking at. There was no effect really on low frequency HRV. So again with that group there was no expectation that we're going to see much with low frequency HRV. So that is the tank. I think it was the open room. I shouldn't call it a tank. I'm sorry, I always have to call these things tanks. You saw our first tank. From then on it's a tank, right? That was the open room flotation of environment at Liber that was utilized in this study, correct? I think it was utilized with all the anxious patients. And so you can see how easy it would be for an anxiety-ridden person to sort of feel maybe comfortable in there. And also it probably makes it easier to use the wireless equipment only because there's nothing, there's no walls or anything interfering with where the signals are going. We have a little past clinical research on floating and anxiety. We have past uncontrolled basically clinical trials that have shown improvement on rating scales for people with generalized anxiety. We have a pilot trial in self-diagnosed generalized anxiety that was conducted in Sweden that also gave us a set of subjects that had a number of repeated float sessions, 12 sessions, and found significant reduction in the symptoms of generalized anxiety in the float group. And so these were good indications that we should see something. However, these were not studies that were done with basically people that were clearly diagnosed. Even the original Kula studies, the diagnostics on that were not the same as what Justin was able to do. He was able to get a sample that had actually gone through some extensive testing. And along with that extensive testing and diagnostic work, then he did some very important tests to decide exactly where these people stood in terms of anxiety. In terms of the specific disorders, no studies have been done in PTSD, panic disorder, agoraphobia, social anxiety disorder, or major depressive disorder. And no studies to date have examined the short-term effects in any anxious population. So with blood pressure and heart rate, we had had studies in the old days where we looked at blood pressure and heart rate, but that was always pre-post. So it was either pre-post, a single float, or it was across several floats when we're looking at hypertensive people and may have been looking at their blood pressure even when they weren't floating. We've never, nobody has ever, but prior to this study of Justin's, monitored blood pressure actually while people were floating. So this was a first. And some heart rate has been examined during floating or before and after floating. We did a study that John didn't actually speak about in which we had people attempting to control their heart rate, both with feedback and instruction. And we were monitoring it while they were in the tank, but we couldn't examine HRV. Basically, there were only a few people working in HRV back then. We didn't, we were not even aware of it. So you've seen this, this is the kind of the level of our ability to take measurements at that time. We did, once in a while, do stuff while people were in the tank. You saw that I was taking blood while people were in the tank. So we could do that, but we didn't have any remote sensors that were highly intrusive. Now, that's me many years later. That was my arm coming out of the tank, by the way. So that's me many years later. And this is just sort of proofs that I actually took part in this study at some level. Okay, I was an initial guinea pig. That's the neuroverse on my forehead. That's a biopatch on my chest. That biopatch on my chest will record both EKG and respiration. And then there's a blood pressure monitor on my arm, which will activate while I float. And I actually did float and have all that done. So the conditions, if you remember this, there were 37 anxious subjects and 20 healthy subjects. Condition one was Earth that was seated watching a movie. And remember the seated, because the seated may be an issue. We have to figure that one out. The second condition was pool, and that was people floating. We had all the sensors I just showed you, and here are the subjects. You can see that roughly in both a healthy sample and the anxious group, we had about two-thirds, not quite two-thirds females and about a third male. The age range was pretty similar for both groups. The BMI range was a little higher in the anxious group. Anxiety sensitivity. Now this is a measure of basically how much my perception, let's say, of the physical sensations that would normally go along with anxiety. How strong is that within me? How strong is that within me? So that's anxiety sensitivity. Notice how high it is in the anxious group compared to the healthy reference sample. Then, trait anxiety. Trait anxiety is how likely am I going to become anxious when I'm faced with a stressor that might make me anxious. That's a little different than state anxiety. And state anxiety is what we measure. So trait anxiety tells us how likely is this person to be anxious. State anxiety tells us how anxious are you right this moment. So here's a little bit of data. I think this was shown yesterday. You can see that in post-float for both serenity and relaxation, there were huge significant increases in the film, not really. In muscle tension in state anxiety, you saw very large decreases and not really in the film. And then this is telling, if you look at the state anxiety line up there, notice how that is very red and it goes all the way across. And if you look there, it says minus 4. What that's telling you is that the effect size of that state anxiety across to all these various aspects of what we have is the entire anxious group and then a bunch of subgroups along the way, all the way state anxiety comes down. It's a main huge effect. So let's get into the specific data. So this is something called normalized high frequency HRV, slightly different than high frequency HRV. Normalized means we did more math on it. And the math determines basically that relative to the total amount of HRV, it normalizes the numbers of the high frequency, makes it a little bit more powerful. So you see kind of the major difference between those two lines and you see the significance over there. When the people were in the tank condition, the anxious people in the tank condition, there was a very large difference in their normalized high frequency HRV. Is the physiology of the change in HRV driving the reduction in anxiety or is the reduction in anxiety driving the HRV? And this gives Justin, you know, many years of research to do and lots of funding to get, right? Right? Okay. So if we take a look at both groups, the healthy group and the anxious group, we notice that the change in HRV, high frequency normalized high frequency HRV is the same for both. Whoopee, good. This is good. We're getting a float effect in both groups. If we take a look at very low frequency, this is interesting because we see in the anxious group significant differences in very low frequency HRV. But we don't know what it means. And we need to do some further looking into it to understand completely what this is telling us. And it occurs in both groups. So something is occurring in the float tank both in low frequency HRV and in normalized high frequency HRV and we're not sure of what that low frequency is telling us. So all of you out there who are researchers can be scratching your heads going, well, what is it telling us? Okay. Now if we take a look at heart rate, we don't see anything. No differences, except one thing, right? We see that heart rate for the healthy people is lower than heart rate for the anxious people. So that's something we sort of expected. Gives us an idea that there's maybe a little bit difference in the sympathetic balance there, but we don't see any changes across the float. Breathing rate for the anxious people, a little bit significant, doesn't seem to drop much, but there is a change. Breathing rate changing, is that connected to the high frequency HRV change? Good question. Not much of a change, but it may be. A little bit more of a change for the healthy controls breathing rate. Again, is that connected to their high frequency HRV? We've got some looking at this stuff to really take a look at that. Cystallic blood pressure, he showed some of this yesterday, that was significantly lower in the float condition for the anxious people. Same thing, not quite as much for the non-anxious, healthy people, but it was significant. And then huge change in diastolic blood pressure. Now an interesting thing about systolic and diastolic blood pressure, it's not just driven by the parasympathetic nervous system. It's really driven by the force of the heart and the size of the tubes. And the tubes are blood vessels, arterials. And what's going to happen in a float tank, because you're in 94.5 degree water, is generally you're going to get a very nice vasodilation effect. So some of this could be just physically driven by that vasodilation effect, and some of it could be driven by the parasympathetic nervous system getting a little stronger and putting a break on the sympathetic. And so when we look at the diastolic blood pressure for both groups, we see that. Both groups did well. So limitations. We have single-session data only, one session. And these are in fairly novice floaters, not totally novice. This was their second float, correct? And kind of a bigger limitation that we're both kicking around right now is that we don't have a supine control. People were seated in the film, they were laying down in the tank. And it appears that there may be an effect of just laying down on heart rate variability. So we've got to tease that out. We don't have much of baseline in all of this. So we see no differences in heart rate between float and film conditions, increased normalized high frequency in both groups in float condition. Normalized high frequency increased while floating as compared to film, negatively correlates with reported state anxiety after floating. That's great news. And then we get this very low frequency decreases in both groups in the float condition and systolic and diastolic blood pressure decreases in both groups in the float condition. So increased normalized high frequency HRV indicates increased parasympathetic output during the float affecting cardiac function. We feel pretty strongly about that one. The blood pressure decreases observed also indicate changes in cardiovascular dynamics during floating consistent with a parasympathetic response. And the greater the change in normalized high frequency HRV, the greater the change in reported anxiety when comparing float to film. What really excites me about the data is the physiology is back. Okay? You know, when I'm thinking about the fact that research is being done in the lab at Liber as it's being done today. And when I remember first talking to Oshkan in 2011, I think it was, after a biofeedback meeting here and realizing we had no research going on anywhere, we had no conferences going on anywhere. And then in 2012 was the first conference. And then all of a sudden I hear about this guy Justin Feinstein who's a post grad neuroscience. Yes. Okay. Somebody who could really get this thing going again. And this is like 2013. And here we are in 2000. What year is it? 18? 2018. And we've got an active lab at Liber. We've got a bunch of young researchers who are doing different things at commercial float centers but getting IRBs. Okay. They're going to be able to publish the data. We're really heading in the right direction. And so you go back what John was talking about years ago. Justin, why don't you come up on stage. John, come on Oshkan. This community has brought something back. And you know, it's because of people with energy, but it's a community now and the community is going to have to keep it going. So that's the challenge for you and be proud of what you've done to this point because it's the community that made this happen.