75. Sunlight, Mitochondria & Decentralized Science | Alexis Cowan, PhD

We discuss the work of Dr Jack Kruse and the foundations of decentralised medicine based on mitochondrial DNA, sunlight, circadian/quantum biology and independent scientific enquiry.

Alexis Cowan, PhD is a post-doctoral researcher & decentralized health educator in New Jersey, USA.

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Transcript

Speaker 1: 0:06

Welcome back to the Regenerative Health Podcast. Today I'm joined with Dr Alexis Cowan, phd. Now she is a research scientist and she is someone who is really attacking these concepts of circadian and quantum biology in a very unique way. So, alexis, thank you for joining me.

Speaker 2: 0:27

Thanks for having me. I'm really excited to be on. I really started listening to your podcast last year after Uncle Jack was on, and so it feels very full circle to be on here and speaking with you today.

Speaker 1: 0:37

Amazing. Well, tell us about briefly your academic background and how you came to find these topics of more decentralized health.

Speaker 2: 0:48

Yeah, sure. So I did my PhD at Princeton in Joshua Benowitz's lab, which is one of the top metabolism research labs in the world. In that lab I was primarily studying the effects of disparate dietary inputs on metabolism so ketogenic versus high carbohydrate diet versus fasting and seeing how the body essentially responded to those different inputs. And then I kind of transitioned into some pharmacokinetic work on endogenous metabolites. But shortly after that I graduated, I started my business where I was working and consulting with individuals one on one, athletes and just high performers, one-on-one athletes and just high performers. And then I went back for a postdoc at UPenn in the lab of Christoph Theiss, who is a microbiome researcher but also just broadly interested in how the environment shapes health and disease.

Speaker 2: 1:36

And I finished up my postdoc last year and now I'm just back to working on my business, working on building awareness in this important space and ultimately with the goal of building out my light research lab within the next year, hopefully, ideally at Princeton. We'll see I'm going to be hopefully pitching to some PIs in the fall. So ideally. You know I'm already in the New Jersey central New Jersey area by Princeton and if I could build it out there I think it'd be great. I've got some private funding lined up so I don't think I'll have to worry about the centralized machine as much trying to close me out of that institution, and I think money really does talk in general in that space, so I'm feeling pretty good about it.

Speaker 1: 2:13

Cool. One of the concepts that Dr Jack Cruz talks about and I think we both have a similar journey in terms of our intellectual trajectories being pretty irreversibly altered by our encounters with Dr Cruz and one of the things that he repeatedly says is that for the past maybe 50 years, we've been focusing on the wrong genome, and maybe you can expand on that statement and explain to the listeners what that means to you, and especially in the context of your research background.

Speaker 2: 2:50

Yeah, I would love to. So this is something that I feel is really important. It really resonated with me when he said that. So the primary research focus for the past multiple decades has been the nuclear genome, which is the DNA that you get from mom and dad that recombines to ultimately form you, and that's where the vast majority is the DNA that you get from mom and dad that recombines to ultimately form you, and that's where the vast majority of the genes that are present in our systems that get expressed are located.

Speaker 2: 3:12

But there's this other genome located in the mitochondria, called the mitochondrial DNA or the mitochondrial genome. There's about 13 genes in that genome and all of them are essentially expressing proteins involved in energy production within the mitochondria, so within that electron transport chain. So right off the bat you can imagine that this genome is really important because essentially all of the energy and metabolic water of the cell is coming from the mitochondria. Ultimately, like if we're looking at fractional contribution, the mitochondria are the most important energy-producing organs and water-producing organs. And so we have this mitochondrial DNA that's largely been ignored, even though it's so important to the health of a cell, to a tissue, to an organ, etc.

Speaker 2: 3:55

And so I really liked when he was talking about, when Jack was talking about how mitochondrial heteroplasmy and all of Dr was talking about how mitochondrial heteroplasmy and all of Dr Doug Wallace's work out of CHOP showing that these mutations that can occur within mitochondrial DNA accumulate over the aging process and are associated with disease and like an unhealthy aging process.

Speaker 2: 4:17

And so the more that we can reduce that mutation burden means the better our mitochondria can function, because now those machines, those molecular machines that are helping to make that energy and that water, are working better. Doug Wallace's lab showing that mutation burden within the mitochondria directly impacts the nuclear genome and mutation rates within the nuclear genome as well as epigenetic expression of specific genes within that nuclear genome. So it's not like in the cancer space. We often think about mutations in the nuclear genome causing cancer, not realizing that actually the initial impetus was likely to be from the mitochondria sending, let's say, maladaptive signals to the nuclear genome. That's causing those mutations to happen to begin with. And so I think we're really missing the mark by focusing on that DNA within the nucleus versus focusing on the mitochondria and preventing those mutations from happening to begin with.

Speaker 1: 5:23

And you mentioned Doug Wallace's work, and he is a titan in the field of mitochondrial research and I think his paper I'm not sure exactly when it was published, but it's titled A Mitochondrial Bioenergetic Model of Disease. To me that was such an important paper because it really reframed the problem of disease and away from the siloed, organ-dependent model that I got taught in medical school and that's the focus of clinical medicine into this more holistic model where we're more interested in how your mitochondrial colony operates and how efficiently it operates and therefore how its issues in that process will manifest as organ-specific disease. So tell me more about how you think about this bioenergetic model.

Speaker 2: 6:21

Yeah, sure. So I think depending on which mitochondrial colonies in the body are the weakest, that's likely where disease is going to manifest. And it's worth mentioning here that, like the etiology of mitochondrial Eve being like, if you follow that mitochondrial lineage back you can basically find like the first human woman, essentially because ultimately all of the mitochondrial DNA is coming from the maternal inheritance and that's because when there's an egg and there's a sperm, the sperm fertilizes the egg and the egg contributes all of the mitochondria that it's going to become that neonate. And so depending on the quality of those mitochondria in the egg, you know, you can think about those mitochondria kind of multiplying and then partitioning into specific organs. So depending on the quality of those mitochondria, the level of mutations, certain organs may be dealt a worse hand than others. With regards to the starting point, from a mitochondrial health standpoint, and then, as that child's developing like ex-utero, you know, that's, I think, really underlying a lot of early life disease that we see that really crops up and it's very sad and unfortunate but it is ultimately rooted in mitochondrial failure.

Speaker 2: 7:38

In my opinion, based on my understanding of the literature and how these things manifest and so, but that doesn't mean that it's completely up to fate, because there's things that we can actually do to purify, let's say, our mitochondrial colonies in childhood, in adulthood, if we have awareness around this topic.

Speaker 2: 7:57

And I think that's the real problem is that a lot of people aren't even thinking in this way.

Speaker 2: 8:00

But when it comes to, let's say, purifying these colonies, what we really need to focus on is optimizing mitophagy, which is basically the mitochondrial form of autophagy, which is kind of the cellular debris and kind of the garbage man of the cell can come out and get up anything that's damaged or damaged proteins, oxidized lipids, things like this and can kind of recycle those building blocks into useful endeavors.

Speaker 2: 8:27

And mitophagy is similar in that damaged or suboptimal mitochondria can be selectively depleted from a cellular environment, because there's like a tagging system that goes on and depending on how much mutation burden is in a mitochondria, it may get tagged for degradation. And so if you think about that, it then can make sense like oh, if I'm optimizing mitophagy and mitochondrial biogenesis because we want to both deplete the bad ones and then multiply the good ones, then that's an incredible strategy for improving health in every organ system, because now we're going to be maybe taking the bad hands that were dealt or that we developed over time during our life, and now we're going to selectively deplete those and amplify the ones that are working well and ultimately, that's regenerative health, that's healing.

Speaker 1: 9:18

Yeah, and the way I think about the mitochondria and its effect on disease, it's really in many ways an interface with our environment and really responding to environmental cues. And it was, I believe, these mutations, these beneficial mutations in the mitochondrial genome that actually allowed us to essentially migrate north from this high UV light area of warm temperature of equatorial Africa into Europe. So talk about maybe those mitochondrial adaptions and how they affect health.

Speaker 2: 10:02

Yeah, so there's two broad classes of mitochondria that an individual might have. There's the coupled and the uncoupled. The coupled mitochondria that coupled that word means that the flow of electrons, essentially, which is what powers ATP production, is coupled to ATP, that cellular energy currency production, versus the uncoupled. That, in that context, means that the flow of electrons is uncoupled from ATP production, which is beneficial in the context of a more northern region where a lot of these uncoupled mitochondria hail from. The function of. That is really to uncouple that flow of electrons to energy production in order to liberate heat, and that heat is required to maintain basal body temperature and organ function in the face of cold environments. Versus the coupled mitochondria, which hail from more equatorial regions, are very, very efficient at making energy but way less efficient at liberating heat, because that's not essential in the equatorial environment when temperatures are stable year round. And so we essentially evolved these two separate classes of mitochondria to deal with environmental conditions, and I also think this relates to if we think about environments in general, especially in the modern environment, we're exposed to a lot of electromagnetic frequencies that were not present in the ancestral environment and I think ultimately mitochondria are EMF sensing organelles. It's what they're doing at like a very fundamental level. It's just that in the ancestral environment, the primary EMFs that were sensing were the sun and the Schumann resonance, which is like the magnetic field of the earth. But today we have, you know, our 5G, our 4G, our Wi-Fi, our Bluetooth, all of the you know, from dirty electricity in the home to dimmer switches to, you know, poorly wired houses, like there's a lot of forms of electromagnetic frequencies that we're encountering today that are sending these kind of like unpredictable signals to the mitochondria, as well as foreign signals that's.

Speaker 2: 12:00

I mean, even though the literature on this topic is pretty bad, in my opinion, like it's not conducted great, there's still a signal that shows that mitochondrial calcium flux is changing, that resting membrane potential is decreasing, which means essentially that less energy is being produced, that these mitochondria are functioning as well, and so, even from like the poor quality research that we see on this topic, we're still seeing these harmful effects on mitochondrial colonies, and so I think I mean one of the things that I think really needs to get done is, like high quality research on this area of non-native EMFs and what it's doing to our bodies and how it's interfering with the natural rhythms and processes that our bodies are supposed to engage via the mitochondria.

Speaker 2: 12:40

So it's something I spent a lot of time thinking about and I agree with Jack in that, like the precautionary principle kind of reigns here, is that we shouldn't be playing with fire in this way. And I think it's odd because the burden of proof seems to be on, like, the naysayers in today's society versus like on the people actually making the technology, showing that you know that it's safe. They should have to prove that it's safe, not prove that it's harmful, you know, because it's new, it's novel to our species, our species and our biology, and so I think we really need good quality research in this area and in the meantime, we need to mitigate exposures as much as possible. It's really hard, I would say, especially if you live in more urbanized, densely populated areas, but there are still things that people can do to mitigate exposures and kind of de-risk the situation.

Speaker 1: 13:30

Yeah, look, and there's an abundance of animal data, particularly in rodents, showing adverse effects of various radiofrequency radiation and other forms of EMF, and that's compelling. I guess I agree with you that the human data is lacking. I mean, it would be amazing to get two groups of people and sleep in a controlled setting, one group next to 5G routers, within three, four meters of a 5G emitting router, to mimic a real life situation and actually get some more harder endpoints. And unfortunately, up till now we're actually extrapolating the earlier data on mouse rodents, which I think is applicable to humans. But it's almost like in today's day and age we need to serve this evidence on a silver platter. It's not enough to extrapolate this evidence. So, yeah, I agree it really needs to be done. And I do think it's a major problem Extending the idea of the mitochondria as a environmental sensor, because really in the focus of the mitochondria in lifestyle medicine and clinical medicine it's really at the stage and I don't want to use the word stuck, but it hasn't progressed further than basically ketogenic metabolism.

Speaker 1: 14:48

It's at the point of recognizing that putting different fuels like fats through this mitochondrial metabolism process has benefit in Alzheimer's disease, in psychiatric illness, in metabolic disease, but it hasn't yet gotten further than these other environmental sensing mechanisms. So I mean, you've mentioned non-native EMF, but what are these other ways that the mitochondria are actually sensing the environment?

Speaker 2: 15:17

Yeah. So I mean, obviously nutrients play a role here, because the mitochondria is ultimately well, it's ultimately not really seeing nutrients, it's seeing electrons from nutrients, but depending on whether you're burning glucose or fat or amino acids, there's going to be a different level of energy that's going to be able to be produced from each out of like a per carbon basis, and so ketones and fat are the most efficient fuel sources, meaning they can make the most ATP per carbon, and glucose is the least efficient. And so if we're thinking about nutrient inputs into mitochondria, we can think about efficiency, depending on what metabolic substrate is being chosen. We can also think about, when mitochondrial engines start to fail, that the fats and the ketones start to become less ideal, because now those mitochondria aren't as good at processing them, and so the body becomes overly reliant on sugar, which is also problematic, because I truly do think that mitochondrial failure, let's say at the level of the muscle, liver or maybe even adipose tissue as well, is rooted in type 2 diabetes, and we're also seeing insulin resistance in that setting too. So the real problem in type two diabetes that I think about in my mind is that we're literally starving our tissues because they can't really effectively burn ketones and fat and they also can't really burn glucose either because that insulin signaling pathway is also impaired, and so the tissues are just atrophying and becoming less and less functional over time due to this starvation effect. So nutrients are a big one. Activity, of course, is a big one, because if we're engaging a tissue metabolically, whether it's contracting a muscle or going for a run, you're engaging your heart and your cardiovascular system and your muscle and your brain as well in your cardiovascular system and your muscle and your brain as well. But depending on how we're engaging these tissues metabolically, that's going to increase or decrease flux through mitochondria and also potentially increase or decrease energy production and water production. So that's a huge one. And then of course I mean it kind of goes without saying, but it's worth mentioning obviously is the sun, because the sun is directly stimulating mitochondrial water and energy production. And not only that, but specific wavelengths of light are doing that as well as specific wavelengths of light structuring that water that's produced to create more of that fourth phase exclusion zone water. That is what actually facilitates enzymatic reactions.

Speaker 2: 17:39

So I remember back when I was taking biochemistry in undergrad and there was this concept of ATP creating free energy or facilitating the formation of free energy. And I was always like very unsatisfied with that definition because it didn't make any sense. Like what is free energy? Like it's not. It's like this nebulous concept that's not really tangible and able to be visualized very well.

Speaker 2: 18:02

And now, the more and more I thought about it whenever you see ATP involved in reactions. A lot of times it's in enzymatic reactions that phosphoryl group, that phosphate group, is being transferred onto something and then suddenly the reaction goes. Well, the way I conceptualize that now is that once that phosphate group gets put onto something else, it changes the structure of that thing that it's getting put onto. And now water, specifically that fourth phase exclusion zone, water can enter into new pockets of that enzyme or whatever is being acted upon, and that water is actually what's facilitating the reaction. It's not the ATP itself. Really makes sense to me and resonates with me. So I hope that there's more studies on the front of water and its role in facilitating metabolism in every cell of the body, because once we get there, I think it also will become increasingly important to think about mitochondria as this source, this incredible source of cellular water production. And it's not only any water either, it's this deuterium, depleted metabolic water that's being made within mitochondria, that's then able to equilibrate with the cellular environment, and that water is able to do interesting things within, like the cellular milieu. Sunrise and sunset still over 50% of midday sun is red and infrared, and that red and infrared directly stimulates cytochrome 4 of the mitochondrial electron transport chain to facilitate energy and water production that's independent of any movement or any dietary inputs.

Speaker 2: 19:37

And so when you think about the role of red and infrared light in metabolism and mitochondrial health, it becomes really obvious that the way that we're living our lives as indoor creatures in the modern day is completely dissonant with the way our physiology is supposed to work. Because being indoors around LEDs, fluorescent bulbs, device screens that are all depleted in red and infrared light, because it's seen as inefficient, because that infrared is liberated as heat and heat is seen as an inefficiency within, like the world of engineering, for you know, these kinds of tech. And so we looked at infrared light as this throwaway thing that's creating, you know, higher levels of power utilization and not as this essential nutrient for our bodies. And so, as a result, we're living indoor lifestyles, we're not getting any red and infrared light from our tech, our devices. We're getting severely depleted red and infrared light through windows. So about 40% of the infrared, a part of the spectrum, is depleted through window glass and so just by virtue of being inside, you're going to be highly deficient in red and infrared light unless you're selectively engineering it back into your lifestyle and ideally, ideally just getting outside, because we were really meant to experience light from the sun in the perfect ratios that nature provided. That's what we evolved under.

Speaker 2: 20:53

And when we muck around with that and we don't realize the importance of receiving that spectrum in its totality, then we begin running into some problems.

Speaker 2: 21:02

And that doesn't mean you can't use red and infrared light panels. It's going to help, but nothing is going to be able to replace the sun in the lives of humans and the health of humans, so that's extremely important. We also have the uv light part of the spectrum, which uv light also helps to structure the water and create that exclusion zone water within cells. That facilitates metabolism. And if we're living indoors, we're also completely deficient in uv light, because window glass blocks all of UVB and almost all of UVA, and we also obviously have fear mongering around UV light, and so when people do go outside, they're slathered in sunscreen and sunglasses and clothes and just completely blocking out this part of the solar spectrum. And so I think the more that we can build awareness around the biology of red, infrared and UV light parts of the spectrum, the more we can get people back out into nature, into the sun, without fearing it and actually recognizing the important health benefits of these specific wavelengths of light.

Speaker 1: 21:58

Yeah, it's such a massive problem and I think that in the order of addressing these lifestyle contributions to disease, the blue light and the non-native EMF in my mind should be number one because it is the thing, the environmental input, that's changed the most compared to our ancestral past. And not to get into arguments about diet versus light, I don't think that's necessarily helpful. I think both are important. But if we're looking at the magnitude of change, yes, from a dietary point of view, people are collectively eating a whole bunch more linoleic and plant-derived seed oils, polyunsaturated fatty acids. But in terms of what our light diet is and how that is affecting our biology and our circadian biology, I think it's kind of light and day.

Speaker 1: 22:50

And really addressing the light and non-native EMF first should be the order of operations and its effect on mitochondria. How do you think about circadian biology and how circadian biology plugs into mitochondrial function? Because obviously we've got these clock genes. They're in almost every cell, they are nuclear, they're nuclear genes and they're regulating this 24-hour rhythm. So how do you think about that interaction with mitochondria?

Speaker 2: 23:23

Yeah. So I think I mean first of all I'd love to do more research on this topic because I feel like it's understudied a bit, but the way I'm currently conceptualizing that is that there are certain nutrients that are available at specific times of day, at least ancestrally speaking. So if we think about the more ancestral way of doing things let's say it's the summertime we have more carbohydrate-rich foods available. We're going to be eating those throughout the day in addition to eating animal foods, and according to a more circadian approach, we would probably eat more of our food earlier in the day and eat way less later in the day. And that's important because when we eat less later in the day and then we go to sleep, we get into a better state of fat burning and ketosis, especially as we're reaching into the REM cycles later in the night and that ketosis and fat burning really helps to turn on autophagy. So autophagy it's not like an on-off switch, more like a dimmer switch, and so the longer we get into that fasted state or that fat burning, ketotic state, the more autophagy ramps up, mitophagy ramps up so that we can clear out anything that doesn't really belong there. That's gunking up the system. So from a circadian standpoint, it seems to me like at least during this time of year, that we're really going to be focusing on burning more carbs during the day, so insulin sensitivity is going to be higher during the daylight hours and then, as we approach the evening, insulin sensitivity is probably going to be at its nadir, and then that is going to facilitate getting into a really good fat burning state during the sleeping time, especially into the latter half of the sleeping window, and that's going to facilitate the metabolic processes and the autophagic and mitophagy processes that we need to happen in order to keep our tissues and organs in a state of health.

Speaker 2: 25:06

And I think that's in a lot of contrast to the way that we're currently interfacing with, let's say, food and also light, because Dr Jack talks about this quite a bit, but that red and infrared light facilitate autophagy and mitophagy and that's what we're really supposed to be encountering. You know, sunrise, sunset, and if you think about sunrise, it actually makes a lot of sense that we're waking up in this state of ketosis and that we're going immediately to see sunrise, which is going to further augment that state of autophagy that our cells are going to be experiencing. So it really just augments the effect. But today, you know, most people are waking up and not going outside at all. They're just flipping on some lights in the house which are completely devoid of red and infrared light and highly enriched in the blue light part of the spectrum, and that blue light actually impairs mitochondrial water and energy production and that actually blunts the ability for you to clear carbohydrates from your system. And I don't want to mention only that, but also the fact that we're using these artificial light sources at all times of day not is now sending the signal to the body that it's the middle of the day again and that it needs to be alert, that it needs to suppress melatonin, that it needs to boost cortisol, and that of course begets more issues, because then your sleep quality is impaired, which means you're not getting into autophagy and ketosis at nighttime, which you may not have either anyway, because you might have been having a really carb heavy dinner.

Speaker 2: 26:48

That's going to blunt that effect as it is, but it's further compounded by the artificial light that you're exposing yourself to.

Speaker 2: 26:56

And then we're kind of getting this feed forward mechanism where we get poor sleep quality and recovery. We're accumulating this gunk within cells. It's never getting cleared out, we're accumulating likely mutations within the mitochondrial DNA because we're not supporting those mitochondria with the red and infrared light. They need to function and then over time I mean, when you think about it, actually the body's extremely resilient to not get diabetes way earlier, although we are seeing childhood diabetes now. But you know, let's say in our generation people are getting sick, maybe in their, maybe around now, but their first couple decades of life they're relatively fine, despite having the worst environments imaginable for a human body or for a mammalian system in general. So the resilience of the body is quite striking and I also think that's relevant in the context of the healing process too. Just because you got to a place of illness doesn't mean that you can't get back to a place of health with the right inputs into your system.

Speaker 1: 27:53

Yeah, and I love that framing and it was a great breakdown that you just did. And inputs into a system. I think is a really basic but engineering and first principles way of thinking about it and just toggling those inputs and adjusting those inputs for everyone's N of 1. And then as a strategy of health optimization I think that is one that I follow too and it really makes it easier to conceptualize. I like how you mentioned the sunrise and how important that is.

Speaker 1: 28:27

There was a paper in 2018 that showed mechanistically that the host of fat-burning enzymatic steps that are occurring in the liver relied on correct circadian signaling. Correct circadian signaling and the extrapolation of that paper or the finding, was that if you don't see the sunrise, you're not going to be fat burning efficiently. And I think it's a bridge between the metabolic medicine, the low-carb and carnivore-type approaches and doctors to this circadian-focused, light-focused kind of point of view and it's something that I really encourage everyone is yes, do a low carb, do ketogenic diet, do a carnivore diet if that's indicated for you, but make sure that you see the sunrise to kickstart the process and to make sure that it's happening as efficiently as possible.

Speaker 2: 29:22

Yeah, totally, I actually have some thoughts on that paper. I don't know, have you read the paper?

Speaker 1: 29:28

It's a rodent study and it's using I can't remember the exact name of the protein, but it plugged into the clock machinery to kick off. But yeah happy to hear your thoughts on it.

Speaker 2: 29:41

Yeah, so I mean I read the paper fully on the side of of. I believe like seeing the sunrise is really important, getting light first thing is really important. Um, I think we maybe need, like, some human studies. Would be great, uh in this context.

Speaker 2: 29:55

but in that study the way that I remember reading it was that they were basing that off of like the 12 hour light and dark cycles that they have within the mouse facilities. But when that light turns on it's like fluorescent bulbs. It's not sun, there's no red light there. So I don't understand exactly how the extrapolation to sunrise in particular works, because the red and infrared light wasn't actually present in the lights they were turning on. And as somebody who worked in mouse facilities for years, I can tell you the light is really crappy. But what I will say actually that's really interesting, is that?

Speaker 2: 30:28

So if I'm a researcher and I'm trying to do some circadian studies and I need to go and check on my mice at nighttime, I go to the mouse room and I can't put on the white lights because they know that it's disruptive to mouse circadian biology. So when I go into the room I can only put red lights on. I go in, I check my mice and then I go back to my lab. That's blasting me with these white fluorescent lights and it's just the most hypocritical situation I've ever encountered. But that's just to say that I don't think that there's red and infrared light in the lights in that mouse room, unless they specifically engineered it into there. So my takeaway from that paper was that the light cycles are really important, but not the frequencies of light in the light source, if that makes sense.

Speaker 1: 31:07

Yeah, interesting.

Speaker 2: 31:08

Well, definitely worth investigating that, if it could be replicated in humans, for sure, yeah.

Speaker 1: 31:20

Great points. And there's this so-called non-visual photoreceptor system and that to me seems like a massive way that not only human biology, mammalian biology, but a whole very, very evolutionary conserved pathways going all the way back to very primitive organisms, kind of interacts with the environment. So how do you think about non-visual photoreceptors, both in terms of circadian biology and receptor proteins, but also maybe compounds like, say, cholesterol?

Speaker 2: 31:56

Yeah. So I think this is a really interesting topic and it always blows my mind when people vilify UV light in general, in particular UVA light, which is a primary cause of acute burning and photo aging quote unquote. But meanwhile we have this Neuropsin UVA light detector on our skin and on our eyes. So why would our bodies evolve to have these detectors if UVA light wasn't important for our bodies? So that's something I always bring up when somebody's challenging me on this. It's like this doesn't make any sense. And then we also have the UVB part of the spectrum, which is stimulating vitamin D to a very high level. It's stimulating POMC opiomelanocortin to a very high level, and we know that those pathways are both extremely important from a health standpoint. So I feel like the case against UV light really falls apart when we start actually looking at the biology of how these frequencies of light are interacting with the body. Having said that, all of the research on UV light damage on skin and skin cancer etc. Has all been done with UV light in isolation, when less than 10% of midday sunlight is UV and over 50% is red and infrared, and there's also a corpus of literature showing that red and infrared light mitigate the negative effects of UV light on the body, so it reduces the inflammatory response and DNA damage potential. So the case against UV light is just highly flawed in many ways. But with regards to the photoreception, I think we're going to see so much emerge in this field over the coming years, especially with the advent of finding like melanopsin within subcutaneous fat and within the blood vessels and how these like blue light detectors melanopsin is a blue light detector how it's functioning in these areas. Because I think ultimately we're going to find, like Jack talks about, that it's like a light show inside of us and we're just retaining that light out of efficiency. Because if we can retain that light and use it productively, that's going to be much better for our system versus like emitting the light, like the cephalopods that Andrew Huberman studies in his lab right, that like emit that light and that's like Jack talks about. That's like brain 1.0 or whatever, and our brain is like so evolved that it's able to retain that light and use it productively. Like that makes a lot of sense.

Speaker 2: 34:15

But I think the more and more we probe into our bodies to see you know where these photoreceptors are expressed and start questioning like why they're expressed, here we're probably going to begin to realize that there's a lot of functions of light deep in our bodies. That's not necessarily from light from the outside, though some of it might be, but also from light that we're producing internally. And one of the big things I'm actually working with an engineer friend of mine to hopefully build like a colonoscopy probe with a photomultiplier on it, because I really want to see the light produced by the microbiome. Like Jack challenged us to try to do something to discover this, and I think it's really really low hanging fruit. I think we can do it and I think it's going to be really powerful if we can.

Speaker 2: 34:54

And I think when we can discover that the microbiome is primarily communicating with each other and also with the body via light and not via chemicals, I think this is going to be a huge turning point for the science around the microbiome and also, as that relates to mitochondria as well, because we know that mitochondria are derived from bacteria as well and that mitochondria produce infrared and UV bio photons just by the very nature of them doing what they do best by making energy through that electron transport chain.

Speaker 2: 35:27

When electrons are moving down energy levels, light's emitted, and that light is primarily in the red, infrared and UV part of the spectrum and that it's just a really important window into understanding the absolute essentiality of red, infrared and UV light in mitochondrial biology. It's like so important that if you're not getting it from the outside, your body's going to try to make it internally and at some point, if your mitochondria start failing, then that light production starts failing too and the lights go out inside, and then the lights go out in general, right. So I think that's really like the dying process is like this lack of illumination from inside as well. And so, with regards to photoreceptors to bring it back to your question, I think it's really an interesting topic. I'm excited to see how it develops, but at this point I think it's kind of in its infancy. And yeah, I think those are probably my primary thoughts on the topic.

Speaker 1: 36:22

Yeah, to speak to the UVA issue quickly, as you mentioned, uv light is actually a tiny fraction of the total solar light that hits Earth because it is shorter wavelength and much gets absorbed by the atmosphere. 95% of UV light on Earth is in this UVA range. I see how in centralized dermatology and other narratives, UVA really is thrown on the ground and kicked quite robustly for its role in photoaging, because it actually penetrates down into the dermis and causing DNA damage via oxidative stress. And I want to make that point because those are the two contrasting ways that ultraviolet light can cause DNA damage, and UVB directly through strand breaks and UVA through oxidative stress. But, as you've mentioned very, very eloquently, is that the red and the infrared light is providing the antidote to that oxidative stress because it is stimulating melatonin production in the mitochondria of those same keratinocytes and of all those fibroblasts and all those other cells that go down into the dermis. So not only that, but if we were getting sun in an ancestrally appropriate way, we'd be grounded. And we know that the passage of electrons up and the assimilation of those free electrons from the Earth is also a potent antioxidant. So really, the UVA demonization story to me falls apart, as you've said, completely, when we consider sunlight in its natural full-spectrum context, and even before UVA rise, before UVA even shows up, you've preloaded the skin with red and infrared which is acting, as you've mentioned, to prime the system and upregulate collagen production and essentially acting as a natural sunscreen. So just to make that point about UVA light.

Speaker 1: 38:34

But the other point, and let's talk briefly about melanopsin, because that is a photoreceptor that Dr Cruz talks about a lot and he specifically references disease as melanopsin damage. I've seen him reference coronary artery plaques or a coronary artery like a lesion as related to melanopsin damage. It's interesting because you mentioned that melanopsin is this blue light detector. I think it has a peak absorption in around 480 nanometers. It's found, obviously, in the skin, it's found in the blood vessels of the dermis, it's found in subcutaneous fat and I know that it actually mediates photorelaxation of blood vessels. So there's not only a UVA-mediated pathway to release nitric oxide and dilate the blood vessels to help with or prevent hypertension, but there's also a photorelaxation process that's occurring through OPN4, melanopsin. So what do you think about melanopsin damage as a kind of role in disease?

Speaker 2: 39:43

Yeah, I love this question and I think this really comes back to loss of timing mechanisms.

Speaker 2: 39:49

I think timing is everything as it relates to how our biology functions because, like, if you don't know what time of day it is, how do you know where to be, where you need to be, at what time?

Speaker 2: 39:58

Like you don't know the time, so you're just going to be kind of in this nebulous space of like inactivity, let's say just at like the anthropomorphic level, at the cellular level or even the subcellular level.

Speaker 2: 40:12

If we think about melanopsin, we also know that that's highly enriched within the retina and that it's largely responsible for sending that signal from the eye to the brain via the RHT, to tell the master clock in the brain, the SCN, what time of day it is.

Speaker 2: 40:23

And so if we're breaking down these melanopsin receptors due to, you know, a lot of artificial light and maybe even some other non-native EMFs as well outside of, like, the blue light range, that the more we break these receptors down, the more, like free vitamin A we release that kind of targets these receptors as well for damage, that the less our bodies are able to tell what time of day it is because of this really crucial mechanism mediated by the eye to the master clock, but then also direct effects on tissues such as the subcutaneous fat and the vascular system and the skin, and so that's really the way that I've been conceptualizing the damage and the dysfunction that occurs as we're losing activity in melanopsin is that we lose the natural rhythms in our system that are supposed to be present to facilitate healing and health and function at the tissue level.

Speaker 1: 41:16

Yeah, that makes sense, and I think the presence of melanopsin in these places really speaks to a natural physiological importance of blue light, but natural solar blue light, which is always balanced, as we keep talking about and you can see, I think, how the system is so importantly hijacked by this blue-lit artificial world that we've created because of the amount of energy and effort the body has taken to sensing blue light. And this was a topic that was discussed in the Cruise and Huberman podcasts, and Cruise talked about, essentially, the ancestry of this receptor. So is that something you've delved into in terms of the Xenopus, the frog's evolution of melanopsin, or is that something you've delved into in terms of the Xenopus, the frog's evolution of melanopsin, or is that something you've discussed or researched?

Speaker 2: 42:12

Yeah, not really. I've really been focused on what we can do about it now as humans, but I think the lineage is really interesting and important and I like to think about things in the context of evolutionary biology. There's just so much to learn. I haven't quite gotten there yet, but maybe once I get there we can talk about it. Then I'll let you know. Yeah, yeah fantastic.

Speaker 1: 42:32

Let's talk before I finish. I want to talk about POMC and melanin in depth, but before we jump onto that topic, I want to talk about temperature as it relates to a mitochondrial function and body physiology, because we've talked about these other inputs into mitochondria, we've talked about the nutrients, we've talked about light and I'm investigating more and more about temperature and discovering the fact that a lot of these non-visual photoreceptors also act as temperature sensors. So what are your thoughts about temperature and how it interacts and senses and influences mitochondrial function?

Speaker 2: 43:09

Yeah, I think it's huge, and I mean if we think about it through the evolutionary lens. If you're encountering cold temperatures, you're living in more northern latitudes, which means that your sun quality is poorer for a part of the year, which means that you need to make your own endogenous UV light from your mitochondria, which means those mitochondria need to be accentuated, let's say their effects need to be accentuated. Their metabolism needs to be accentuated as well to produce that heat, because those uncoupled mitochondria are liberating heat as well as, through the electron transport chain, emitting this UV light, the UV light bio photons as well. So, from a temperature standpoint, getting cold, especially for more northern uncoupled haplotypes, is going to be huge from a metabolic health standpoint, because that's what those mitochondria were designed to encounter or they evolved to encounter over the course of the evolution of that type of mitochondria from those more northern regions. So if you're somebody who has a maternal ancestry from Scandinavia or any place that's north that has the ground freezing in the winter, that experiences winter, that's a sign that you're likely going to do really well with cold and it's going to feel like crap still, but you'll be able to adapt to it more quickly and it's something that will likely help you specifically to optimize metabolic health and mitochondrial function, compared to somebody with coupled mitochondria, that really those mitochondria were evolved to receive high quality sunlight year round. And that's not to say that you know people with more equatorial maternal lineages can't get cold adapted. I think they still can by engaging their brown fat and Beijing white fat. And you know their mitochondria may be plastic to a certain extent. I think that kind of remains to be seen. We kind of need to study that a bit more. But to lean into your genetics, let's say, or your mitochondrial genetics, getting more high quality sun year round is going to be the most natural thing that your body is going to expect.

Speaker 2: 45:04

I will say it's really interesting from the uncoupled perspective that it seems like the uncoupled mitochondria are more plastic, like they can do well in more northern regions. But if you put them into more equatorial regions they can adapt to a certain extent and those mitochondrial electron transport chain complexes can move closer together and kind of mimic what a coupled mitochondria looks like, which I think is really interesting together, and kind of mimic what a coupled mitochondria looks like, which I think is really interesting. I think we need to study the equatorial mitochondria a bit more to see how much they can deal with aberrant environmental inputs relative to the ancestral inputs. But I really do believe and this ties into something we were talking about before we started recording that a lot of the disparities in health that we see in black and brown individuals who have these equatorial mitochondrial genetics in the US, it's largely because of the poor quality light for a decent portion of the year, that they had higher quality sun year round, that their mitochondrial DNA was expecting and their mitochondria were expecting that we would see way less of the diabetes, the obesity, the cardiovascular disease, the cancers that we see in these populations and especially more northern parts of the US.

Speaker 2: 46:14

And so I think it's really important from like a healthcare standpoint and from like a health disparities standpoint, to think about these things in a really honest way, because and also, that doesn't necessarily mean that if you're somebody who has darker skin, you can't live more northern regions. It's just maybe you have to work a bit harder to re-engineer a life that's more appropriate for your mitochondria. And at the very basic level, the easiest thing would probably be to move somewhere that there's better quality light. Obviously that's not possible for everybody, but I think ultimately we need the information first. We need to just be honest about it, as challenging as it can be, because then we can really start to make positive changes for people's health and their lives. And I actually forgot what your initial question was, but hopefully I answered it. No, you did, you did.

Speaker 1: 47:01

And on that point of health disparity, it fits into a framework of you did. And on that point of health disparity, it fits into a framework of, I guess, a concept that I've had to think about because I put together a course, solar Callus, which is teaching these concepts of deliberate sun exposure for optimal health, and what I've called it is a skin type latitude mismatch, and that's the degree to which someone's skin type is matching the skin type of the native people of that region. And if you're a native Swedish living in Sweden, then there's no mismatch. And if you're South Indian living in South India, there's no mismatch.

Speaker 1: 47:33

But a lot of people are living outside a region where their ancestors developed, and in Australia that's particularly prominent because a lot of people came on a convict ship from England and now they're living in the UV conditions insanely high relative to their amount of melanin they have, and that's a problem and the way I'm thinking about it is that's a mismatch, but it's a mismatch that's much more easily rectified or mitigated because what we can do is simply use shade and you can satisfy the requirements of ultraviolet light in the early morning and later afternoon and simply be in the shade in the midday during the times of highest UV index, but the problem that we're talking about, which is those with darker skin and more melanin being in an area of lower UV light, I think that's a much more difficult mismatch to handle, because there's simply not enough year-round ultraviolet light to ensure optimal health for those people.

Speaker 1: 48:36

And, as you've said and this is something that I advise people, clients and patients as well is the first thing to do is actually to consider moving, and yes, we understand that there's family and work and all these other things keeping you there, but we'd be remiss if we didn't tell you that that was the first thing that you should do for optimal health. And then the second is, as you mentioned, is potentially going on holidays to a lower latitude, and then, I think, at the bottom of the list is things like, you know, artificial UV, and that's a different topic we won't go into now, but it's a critical role, and I agree with you that it's a major player in why there's this health disparities, and probably the same with Indigenous Australians as well, given how everyone's living these indoor lifestyles so have you heard Uncle Jack talk about like how sunlight is quantized across all the habitable as well, given how everyone's living these indoor lifestyles.

Speaker 2: 49:28

So have you heard Uncle Jack talk about how sunlight is quantized across all the habitable regions of the Earth, meaning that actually, if you look at the total amount of UV light and sunlight that reaches any one particular habitable region of Earth, that it's the same? If you look at the year scale, it's just that at the equator you get 12 hours of dark, 12 hours of light, and in England, let's say, you get like 18 hours of light in the summer and then you get like five hours of light in the winter. So the reason I bring that up is because a feasible other option, if it's possible, is to just live your life outside as much as possible during the daylight hours, because then ultimately, if you're having darker, darker skin in more northern regions, you will in theory be getting access to a decent amount of light. It's not going to be as intense as you would have encountered at the equator, but also just another option for people, which I basically do.

Speaker 2: 50:15

Anyways, I live outside for most days and actually one other thing I wanted to mention on this topic is that I really want to probe Jack's brain and hopefully he's going to come back on the podcast soon. I want to ask him about it. So I want to talk about, like, mixed race people like myself, because my mitochondria are from Scandinavia, but my skin is a bit darker right and I can tan really easily, and so my dad's side of the family is African and my mom's side is all Scandinavian, and so I think it's really interesting to think about like especially as we have a lot of culture mixing and we're going to have more and more mixed race people emerging in the population like what the implications are of jungle fever, essentially it's a really it's an amazing great question.

Speaker 1: 50:57

And I think it's fascinating too, because what you alluded to a bit earlier was that there's this plasticity in these Northern Europeans and I think it speaks to the fact that there's an evolutionary memory of evolving in Africa and they're therefore adapting to lower UV light conditions but still keeping deeply embedded the epigenetic toolkit to deal with higher UV conditions toolkit epigenetic toolkit to deal with higher UV conditions. So the mix of an uncoupled maternal line and mitochondrial DNA with maybe more epidermal melanin from a paternal line of an equatorial area, to me seems like an amazing combination, because you can harness UV light very well, avoid burning, but you can also get cold and benefit from all the benefits of cold therapy.

Speaker 2: 51:51

Yeah, I think so too, and also the story of magnetism how it fits into this, because I've heard Jack talk about the Scandinavian mitochondrial DNA is pretty unique in its ability to harness magnetic flux and I really want to learn more about that. I don't know if you want to expand on that at all. I don't know much about it yet, but I think it's really interesting. And I don't know how it really holds unless, like if you're outside of that region where there's lower magnetic flux.

Speaker 2: 52:16

We don't have volcanoes here in New Jersey, so I'm just thinking about like how that fits into the mitochondrial story as it relates to like Scandinavian mitochondria that moved away from that region.

Speaker 1: 52:26

Yeah, I don't know a lot about it at all and I'm not sure how much published literature there is at all. I think it's definitely in the realm of theoretical quantum biology, of which Dr Cruz is you know so far above and beyond anyone else that it's. We kind of just have to ask him, I guess, personally, and then verify that through other means.

Speaker 1: 52:52

But yeah, I only have heard that in places like Iceland, where there is a massive amount of magnetism, that there's certain benefits. But no, I'm not at all familiar about how that might affect individuals. And I mean, is checking a mitochondrial haplotype something that you do routinely when you see your clients?

Speaker 2: 53:12

So first thing I would just ask is if somebody knows their maternal lineages. We don't really need to necessarily do like a 23andMe or any sort of other sequencing means to look at the exact haplotype. I think getting the gross haplotype is probably good enough for most people, but for people who already have the genetic testing, I think it can be good to look at the haplotype and see where their ancestors hailed from. And then I think that actually brings up another important issue, which is like do we want to adapt you to the environment of your ancestors or to your current environment? Right, because I mean, I would think that if you want to thrive in your current environment, then we should probably make you as adapted as possible to that environment, and not necessarily to the one of your ancestors, but also, considering those inputs that your ancestors would have experienced, to try and see how feasible it is to recreate that in your current environment, to make that process as seamless as possible.

Speaker 1: 54:04

Yeah, yeah, it's very interesting and it's really this brave new world of decentralized science and medicine that's focusing on mitochondria, mitochondrial genetics, mitochondrial biology and yeah, so I'm very excited to learn more about that myself. Let's talk about biophotons. You mentioned them briefly before and this idea that the body is making efficient use of light that's being endogenously generated. And, to reiterate the point you raised earlier and for the listeners who haven't heard the Cruz-Huberman podcast, they're very well worth listening. But essentially, andrew Huberman is studying these essentially octopus's central nervous systems and they emit light, but that light is visible, it's actually able to be seen by it's in the visible spectrum. The point that Cruz has made is that subsequent iterations on the brain which have occurred in mammalia and got up to us as humans is that we're emitting that light, but it's essentially being captured and used by neuromelanin, I believe. So talk to this idea of neuromelanin and maybe this endogenous biophoton release.

Speaker 2: 55:25

Yeah, so I think it's really interesting. I read a paper on the topic a couple months ago showing that essentially, the sicker you are, the more biophotons you release into your environment, which may be counterintuitive. To some people it's like, oh, you're releasing more light, that means you're producing more light, but actually it's like a failure to capture that light and use it productively. That's a defect in disease states, and so I think you know we definitely have evidence at this point that it's happening in humans. A lot of it is these ultra weak photons that we're not necessarily detecting with our eyeballs, but they are there. If you use a photomultiplier you can detect them.

Speaker 2: 56:00

I think the neuromelanin story is certainly an important one.

Speaker 2: 56:03

In the brain and the heart, Most likely the most mitochondrially dense organs were probably producing the most light.

Speaker 2: 56:10

I think Jack talks about and I have to look into the literature on this a bit more but that there's like a sheet of melanin within every cell that is next to the mitochondria and also kind of goes along with the notion that there was a paper published called.

Speaker 2: 56:22

It was called something like mitochondria gives cells a tan, and I think they weren't referring specifically to melanin, but I think that I wouldn't be surprised at all if there is melanin at the level of each cell near the mitochondrial colonies that's collecting that light and I think yeah, I think that light is really being harnessed because we know that, especially in the brain and the eyes, that there's this really important interplay between electrical and photonic activity. Like DHA, for example, which is up to 60% of the retina by weight and up to like 20 to 30% of the brain, this DHA molecule is really working at the quantum biological level and there's a couple papers on this topic that just like absolutely blew my mind, talking about the quantum biology of DHA and how it has this ability to convert photonic energy into electrical energy and how important that is, and that's essentially what's allowing you to render reality moment to moment, which is just incredible.

Speaker 2: 57:18

Michael Crawford his paper, yeah, yeah.

Speaker 1: 57:22

Absolutely mind-blowing.

Speaker 2: 57:24

Yeah, so so good, good and I would definitely recommend people check it out. We can maybe link it in the show notes. They can read it.

Speaker 2: 57:29

But yeah, I think there's this really important story about using melanin, that the neuromelanin in the brain that's buried deep in these parts of the brain, that's what, that's the darkest form of melanin in our bodies that's really absorbing the most light.

Speaker 2: 57:42

Melanin in general absorbs all light, but I think I think neuromelanin takes that to the nth degree and the brain doesn't want to lose any of that light. And we also see in specific disease states, such as like Parkinson's disease, where the substantia nigra starts losing that melanin which is ultimately, if you kind of take a first principles approach, leading to more release of light and less of that captured light, able to do productive things and also potentially breakdown of that melanin to support the dopamine pathway that's being changed and dysfunctional in some way in the pathology of Parkinson's disease. So I think it's really interesting to think about melanin as it relates to dopamine, especially in the brain, because we know that they both share tyrosine as precursors and that melanin can be broken down into L-DOPA and converted into dopamine as needed. I think we really need more research, especially in the context of Parkinson's disease, to show what's actually going on here, because it's likely to be a light story.

Speaker 1: 58:41

We're looking at melanin and somehow the centralized docs haven't put the points together that melanin relates to light very intimately yeah, and I I remember back to my undergraduate neuro neuroanatomy and we got obviously taught about um, the, the substantia nigra, and and, and we also had, uh, small teaching about pro-op, melana Corton, but none of these pieces were pieced together in any coherent way. It was almost just like a tick box or just oh, and this is happening, but don't ask any more questions because we don't know anything more than that. But it made me think about what is the stimulus and to back up. Maybe we'll quickly back up so we don't lose anyone. Talk about how melanin gets produced, because propionamide and cortin is so key and obviously that's how it's getting made. How do you think about POMC and not only neuromelanin but the other forms of melanin, about POMC, and not only neuromelanin but the other forms of melanin.

Speaker 2: 59:51

Yeah, so when UVB light in particular strikes the skin and the eyes and the proximal brain regions, we get the production of this pro-hormone, pomc propion melanocortin.

Speaker 2: 59:54

That's cleaved into 10 distinct hormonal products, three of which are alpha, beta and gamma MSH, or melanocyte stimulating hormone. So it's clear that we need those. We need that MSH to be those MSHs to be expressed in order to tan on our skin to prevent burning. But I also think it's really important to think about, like where else is there melanin in the body and what other melanocytes are being simulated? Right, because we often think about in the context of the skin and that POMC can be produced peripherally in the skin. It can also be produced in immune cells and some other cells as well, as well as in the brain. But I really think that the next frontier is going to be to think about how these MSHs are stimulating melanocytes all over and not just in the skin. Because that will, I think, bring us back to the realm of Parkinson's disease and other pathologies that are associated with a loss of melanin and an increase in biophoton liberation, like release from the body.

Speaker 1: 1:00:48

Yeah, because obviously it's easy to measure the POMC and the alpha-MSH or to see the effect of that cutaneously on the skin. Because essentially, as you've mentioned, uvb predominantly hits these keratinocytes. It upregulates p53. That increases transcription and translation of POMC, and then POMC gets cleaved into alpha-MSH and then the alpha-MSH from the keratinocytes stimulates the first melanocortin receptor 1 on the melanocyte and then the melanocyte starts upregulating synthesis of eumelanin and pheomelanin to essentially protect the nucleus of the keratinocytes. And a byproduct of that is the cleavage of beta-endorphin to kind of give your body a reward for doing the important job of continuing your survival by harnessing the ultraviolet light. The question that I have and you've alluded to it was how are we stimulating this melanin production deeper in the body if UV light from the sun is only penetrating at most in terms of UVB into the epidermis? That is the question that I would like to have more information about.

Speaker 2: 1:02:10

Yeah, I mean same. I really would like to know. It could be either one of two things, right. It could be that UVB light from the environment is being relayed deeper into the system, or it could be that UVB light from the environment is triggering the production of UV light internally. That's then stimulating those effects deeper into the brain. So I think those would be the two apparent pathways by which that could happen. Which dominates, or both are equally important, I think. Remains to be seen in my mind, but I'm excited to see where this field goes and where this topic kind of blossoms into over the coming years. I think it's really interesting.

Speaker 1: 1:02:50

Yeah, I mean anecdotally. I know just family friends two dentists and both of them got Parkinson's disease. And if you look at the environment that a dentist, unfortunately, is subject to their working conditions and say they're a hardworking, industrious dentist, they're in this isolated blue light, without UV, without infrared, for 12 hours plus a day. And to me that seems like the absence of UV light and having an absence of relaying pathways that stimulate that production of neuromelanin inside the substantia nigra inside the brain would therefore accelerate this process of those loss of those neurons and therefore developing a Parkinson's disease.

Speaker 2: 1:03:40

Yeah, I mean, I wouldn't be surprised either. Everybody that I know, including one of my uncles that has Parkinson's disease, lives a non-circadian lifestyle, so he's a quote-unquote night owl. And also well, he was a teacher so he was indoors all day under fluorescent lights for 30 years of his life and wore sunscreen.

Speaker 1: 1:04:00

Wow. I had another anecdote from a patient who was very motivated and would practice some of these circadian practices. He had diagnosed Parkinson's disease and his symptoms markedly improved in that early morning period when he was outside grounded and getting full spectrum sunlight. So I mean there's lots of pathways and I think the causal contributors to the development of Parkinson's disease is evidence that paraquat and other forms of herbicides are having a role and potentially infection, viral infection, these antioxidant and all these other beneficial effects that we should be doing as much as we can to stimulate the endogenous production of it in order to prevent and potentially ameliorate symptoms in Parkinson's disease.

Speaker 2: 1:05:03

Yeah, and we also do know that, at least on our surfaces I don't know about the deeper parts of the brain, but we could think about that that when sunlight strikes the melanin on your skin, that melanin is actually able to split neighboring water molecules into H2 gas O2, which is oxygen that's needed for a respiratory chain. H2 is a very potent antioxidant within cells and for free electrons, which can then directly power mitochondria as well, and so melanin has this really incredible way to actually allow you to eat the sun in a way and that also should make sense, because the people with the most melanin are exposed to the most sunlight and it becomes like highly efficient if you're directly getting electrons from your environment via the sun and also through grounding, through your feet as well that you're ultimately able to eat less food and make energy more efficiently relative to somebody who has a more northern, uncoupled haplotype that requires more food to make heat and to make their metabolism go.

Speaker 1: 1:06:00

I'm so glad you brought this point up because it gets to another function or a physiological effect of these POMC and POMC cleavage products, which is alpha MSH, which is the same alpha-MSH that stimulates melanin production in melanocytes is also able to reduce appetite and is a very potent satiety signal in the hypothalamus to stop eating. And that is why, again, I assist and encourage people to get in the sun if they're needing to correct metabolic disease or lose weight is because you potently induce satiety if you get out into ultraviolet light because of this effect of alpha-MSH. So then, in my mind, the next question was why is a POMC peptide? Why is alpha-MSH telling the organism to stop eating? And the only logical answer in my mind is because ultraviolet light is providing this energy source through the mechanism that you mentioned, so that we don't need to eat as much. I mean, to me that's logical. I don't know what you think about that.

Speaker 2: 1:07:10

Yeah, I completely agree, and I mean just anecdotally myself. I barely have an appetite in the summer. I'm essentially living outside. I, yeah, I completely agree, and I mean just anecdotally myself. I'm barely have an appetite in the summer. I'm essentially living outside. I I eat more fruit, I eat some meat as well, but, like during the winter time, I eat much more like fat and meat and I literally crave it, my body craves it and just like I just have personally noticed, like the caloric requirements that my body is asking of me is just vastly different between the summer and the winter, and from a mechanistic standpoint, it makes so much sense that you know if we're getting electrons elsewhere, we don't need to get them through food, and it's actually funny.

Speaker 2: 1:07:43

So I pitched part of this project to a PI at Penn like a year ago, and the first thing that he said was like oh, alpha MSH, like that's highly correlated with obesity.

Speaker 2: 1:07:52

It's been known for a long time and meanwhile we know that it's one of the products of UVB light exposure and stimulating POMC and all of this.

Speaker 2: 1:08:00

So there's this very interesting and important link between UV light exposure, pomc, energy balance and the fact that you know we see obesity at an all-time high now, when people are also living highly indoors, not getting outside.

Speaker 2: 1:08:16

When they are outside, they're slathering sunscreen or wearing clothes and sunglasses and they're blocking all these beneficial effects, especially into the brain. Because if you're wearing this is kind of another tangent but it's worth mentioning I think that, like with all of the device use and artificial light, we're having myopia at a much higher rate than ever before in our species and with myopia we're wearing glasses and contacts like 24-7. And if you're wearing glasses and contacts, you're not getting that UVB light stimulus into your central nervous system and that's going to prevent you from being able to engage that system and interact with your environment, independent of whether you're going outside or not. If you're going outside and you're wearing them, you're not getting that stimulus. If you're living an indoor lifestyle, you're already not getting it. So it's just like a lose-lose. But there's this really important link between obesity and metabolic syndrome and alpha msh that I think is so interesting and and emerging as this really important player as it relates to, like, the crises we're facing societally yeah, great, great points, points.

Speaker 1: 1:09:15

And if you look at, there's a couple of monogenic obesity syndromes and some of them are mutations in leptin pathway. But I believe one of them is a mutation in one of the melanocortin receptors, or actually it's in POMC. And, incidentally, um I believe it's a lab the labradors have a mutation in, in um, either the the receptor, or in pompsi, and that is meaning they have a deficiency in one of the melanocortins, whether it's alpha or I can't remember which, but showing again the role of of this pathway in in satiety and and whole body energy homeostasis. So I mean painting the picture of most people, 93 of the time indoors under, under artificial light, hermetically sealed chambers um no infrared, and they're essentially uv deficient and that uv deficiency is leading to what we call hyperphagia or increased appetite. To me that is obvious.

Speaker 1: 1:10:17

I think what's not so obvious is that the consequences of this sun avoidance narratives, particularly everywhere in the world, but very, very much so strongly in Australia, is obesity and metabolic disease. I don't think the dermatologists who are advocating this the most strongly are realizing that they are contributing to this tidal wave of metabolic diseases which affect so many facets of health, not just diabetes but all the sequelae of diabetes and heart disease, stroke etc. Sequelae of diabetes and heart disease, stroke, etc. Because they're advocating so strongly the blocking of UV light and therefore the synthesis of alpha-MSH and these other melanocortins.

Speaker 2: 1:11:03

Yeah, and that's the thing that really frustrates me too when I'm going through the literature that there's actually a really strong literature for regular chronic sun exposure being preventative in the context of multiple cancer types breast, colon, prostate, blood cancers, as well as cardiovascular disease, diabetes and obesity. And then the dermatology literature likes to focus on oh well, if you go out into the sun you're going to get skin cancer. Well, we can actually unpack that narrative and show actually frequent regular sun exposure is not, it's like, inversely correlated with melanoma incidence and mortality. So that's not even true for melanoma. But if we look at BCC and SCC, okay, maybe there's increased risk of BCC and SCC in response to sun exposure, but nobody dies from those. Meanwhile, how many people are dying from these other diseases that sun avoidance causes? So it's absolutely disingenuous the narrative that's being pushed.

Speaker 1: 1:11:56

Oh, it is, and I've been delving into that lately. And vitamin D deficiency and this is a reminder that you're only synthesizing vitamin D from 290 to 315 nanometers of UVB light and Vitamin D deficiency is associated with incidence of melanoma. It's associated with Breslau thickness. It's associated with poorer prognosis in metastatic melanoma. So that just goes to show that people who avoid the sun, they're more likely to have those negative outcomes.

Speaker 1: 1:12:32

And then the next question is okay, what about people if they get more sun?

Speaker 1: 1:12:36

And then we know from the melanoma in southern Sweden cohort that those who had skin-diagnosed melanoma had better survival.

Speaker 1: 1:12:43

I believe it was an eight-fold relative increased survival if they had the more sun exposure in the more sun exposure groups We've also got. There was an Italian study that showed survival in malignant melanoma was increased if those people had been on a sunbathing holiday. And it fits with this lab-based research which we know, which is that the active form of vitamin D, which is 125-dihydroxyvitamin D and 25-hydroxyvitamin D, if you culture malignant melanocytes, malignant melanoma cell lines, you stop proliferation of those cancers if you culture them with the active form of vitamin D and storage form of vitamin D. So there's so many lines of evidence. And then, as you mentioned, alexis, there is no epidemiological link between chronic low level sun exposure and malignant melanoma and there is no increased risk of outdoor workers for malignant melanoma compared to indoor workers, and some studies even suggest that indoor workers have a higher risk of developing melanoma. So I think sunscreen use and sunglass use for the prevention of malignant melanoma is nonsensical and is not supported by either the basic science literature, the human data or the epidemiology.

Speaker 2: 1:14:08

Yeah, I agree, and it's a battle that I'm fighting almost every day online with people who are just stuck within the propaganda machine, but I also see, slowly, people coming around and a lot of people reaching out, being very receptive to the information too. I think, especially post-COVID, people are waking up to like the narratives that aren't serving us anymore and are hungry for information that is actually life affirming, information that is actually life-affirming, and so I have been shocked at the outpouring of positive information, as I've been sharing about these topics in the primary literature as well. So I think I'm hopeful. I'm hopeful for the future.

Speaker 1: 1:14:43

Yeah, well, I mean. The other point about that is the dermatology literature will suggest that early life sun exposure is associated with malignant melanoma, and there are two Mendelian randomization trials that suggest that there's a reasonably strong association. I haven't delved into them deeply to critique them. The point that I think needs to be made is that a lot of these findings are from case control studies that are prone to recall bias, meaning that if you developed a malignant melanoma you're more likely to say, oh yeah, I got sunburned more frequently.

Speaker 1: 1:15:20

But if we really unpack, what we've just said is that chronic sun exposure is going to be protective, like building your solar callus. Building a vitamin D is actually going to be protective of developing malignant melanoma. And then on the topic of non-melanoma skin cancer, which you just brought up, because I was much more sympathetic to this idea that these are sun-related cancers because obviously they're occurring in more sun-exposed areas, until I found two studies. One was a South African study showing that 94% of non-melanoma skin cancers were vitamin D deficient, and a Latvian study that showed that both the size and severity of basal cell carcinoma was a vitamin D deficiency, related to vitamin D deficiency. So to me it seems like vitamin D deficiency is linking all forms of malignancy, not just the internal but also the cutaneous skin cancers.

Speaker 2: 1:16:20

Yeah, and I think it's also important to note here that, given the ubiquity of sunscreen use in the past couple few decades, let's say we're not actually correcting for that either. Because what if these people who had, let's say, in the melanoma studies, like the early childhood sun exposure, what if they were slathered in sunscreen the whole time? Like we don't have that information, we don't know if that could actually be resulting in pathology later in life, like remains to be seen.

Speaker 1: 1:16:46

Yeah, there's lots of holes in the whole narratives. And it's yeah, like you, it's a topic that I have been working hard on. I'll make the quick point too, that overdiagnosis seems to be a really important point, and that was a paper by a dermatologist called Adole Adamson that was published in the New England Journal two years ago and essentially there's been a six-fold increase in diagnosis of malignant melanoma in 40 years, and even if you play with the toggle of UV exposure and hypothetically turn that up to the maximum, you'd only expect a two-fold increase in diagnosis. So there's a lot that, and Professor Richard Weller thinks that this is simply an overdiagnosis and I think he's making a solid case for that.

Speaker 2: 1:17:40

Did you see the other study? I don't remember the author on it, but it was basically modern-day dermatopathologists looking at slides and pictures of slides from like 30, 40 years ago and they diagnosed melanoma at an exceedingly higher rate than the initial dermatopathologists that looked at those samples back in like the 80s, which is just wild right.

Speaker 1: 1:18:00

Yeah, I mean, and it's a product, in part, of litigation culture in the US.

Speaker 1: 1:18:04

Doctors don't want to miss anything, they don't want to be medically legally liable and look not to diminish the scariness of malignant melanoma and metastatic melanoma. It's scary Brain metastases and it's very unfortunate. But I think we need to have open conversations about reducing the risk by paradoxically and I put paradoxical in quotation marks because it's not a paradox if you understand what we've just talked about for the past hour and 18 minutes but these people need more sunlight, not less. They need more chronic UVB exposure. But the harm of this overdiagnosis and this fear-mongering is that it is driving more sun avoidance. It's driving all these other harmful avoidance, sun avoidance narratives that therefore impact on systemic disease, like the biggest killers in society, which are ischemic heart disease, stroke and internal cancers.

Speaker 2: 1:19:07

Yeah, you took the words out of my mouth. I was just thinking. You know the mainstream docs may think you know if I'm catching a potential melanoma early, or you know it's not yet, but I suspect it might be like there's no harm to a patient to, you know, just get that removed. Meanwhile, when they do get that removed, they now think one, their doctor, just like, save their life, and then, two, they have to avoid the sun even more. So it's like creating this feed forward loop that's actually increasing their likelihood of developing melanoma or other types of cancers or chronic diseases in the long term.

Speaker 1: 1:19:39

Yeah, it's this like backwards, upside down topsy-turvy world that we find ourselves living in. And I mean, I heard one centralized researcher say you know, we're seeking to end melanoma and other cancers, yet he is the proponent of sun avoidance as part of this prevention primary and secondary prevention of melanoma. He wants everyone to get out of the sun and slip, slop, slap the moment the UV index climbs above three. And I'm thinking in my head. Those goals are diametrically opposed.

Speaker 2: 1:20:12

If you want to prevent melanoma and prevent all other cancers, you need people, need to be doing the exact opposite of what you are telling them yeah, yeah, I mean, I think this it's not even that big of a leap for people at this point, because we see that, like, our health is in a state of crisis more than ever before and we're more detached from nature and like our evolutionary history more than ever before. So the logical route is to try to get back to our roots as a species as much as we can in the modern day, to try to put our bodies in that evolutionary environment that they're known to be able to thrive in yeah, yeah, and I mean that that that is makes intuitive sense.

Speaker 1: 1:20:47

It sounds to me and and both of us are scientists, we both, um, you know, referring to evolutionary biology and uh, again, we shouldn't be the onus of proof or the burden of explanation shouldn't rest on the people who are using, uh, evolutionary biology perspective and lens. It is. It is. I mean, when did humans use sunscreen before? 40 years ago or 30 years ago? Yeah, exactly.

Speaker 2: 1:21:12

it doesn't make any sense and I always laugh because, without fail, in my comment section, somebody will show up and be like well, ancestrally people only live to 30 years old. That's why they never got sun damage. And I'm like so let's just clear that up real quick that if infant mortality is averaged in with the lifespan of, let's say, our ancestor hunter-gatherers, then yes, the lifespan is 30 years old, but if you exclude infant mortality from the equation, the adult lifespan was quite similar to what we're experiencing today, upwards of 70 or greater years old.

Speaker 1: 1:21:42

Yeah, I mean it's the most common midwit comment that gets bandied around, but, yeah, it needs to be continually debunked and corrected. And so I mean this has been an amazing interview and I think we've covered a whole bunch of topics. Maybe let's quickly because I've got you let's talk about centralized science and maybe a way forward. And I went to El Salvador in the beginning of the year and I met Dr Cruz in this conference called the Age of Light and he addressed, or he put out a blueprint in many ways for medical rights and medical freedoms, but also has proposed solutions to this kind of centralized scientific model where the important questions in science and medicine that we've just discussed, they're simply not getting the funding or they're not getting the research that they need in order for us to, as clinicians and doctors, to actually start healing and helping people on a large scale. So what's your diagnosis of the problem and maybe some solutions that you think?

Speaker 2: 1:22:50

Yeah. So I mean it's something I'm thinking a lot about. I think I mentioned earlier in the podcast that I'm going to be building out a light research lab, hopefully within the next year, hopefully at Princeton. We'll see, we'll see how it goes. But I think the biggest hurdle is likely going to be on the funding side of things, and that's coming from my experience in the field, not my experience trying to seek funding on these topics, because I mean there is a corpus of literature in support of what we're talking about here. We're not pulling the stuff out of our asses. So I think and I'll also say at the same time that every time I've brought these topics up to my scientists, friends and colleagues, they've been quite open and curious about it. So I think there is like a hunger and a thirst for this information that it's really resonating with people, even in in the scientific community. So I'm not even totally sure that if I went the traditional funding route that I would get blocked, like I might be able to make some headway there. But my approach at this point is to really just avoid the government funding altogether, to seek philanthropic and private funding to get this done, because I think it's going to muddle the science less. The science is going to be more pure because we're not beholden to funding agencies that want specific objectives and are looking for specific outcomes, because I mean just the way humans work, like if you're looking for an outcome, you're going to find it. And you know, even scientists aren't infallible and all professionals, you know they're humans first, and so the more we can eliminate bias and and any sort of constraints on the information that we're going to be discovering is going to be helpful.

Speaker 2: 1:24:27

Outside of that, I'm honestly really excited to bring this information to a larger populace of scientists and, like my old boss from Princeton too, because I think ultimately they are typically pretty open minded, especially if it's not the specific field of study, like it's not dermatology research specifically, or, you know, necessarily translational research. And that's one really good thing about Princeton it's primarily a basic research institute. There's no medical school there. There's no, you know, graduate schools there. I mean, outside of the PhD programs, there's no like medical school or law school etc. So it's really focused on understanding life, ultimately like a very fundamental basic level, and I think that would actually be a good environment for me to do this work, for me to do this work.

Speaker 2: 1:25:15

And so I think you know number one, we need to, you know, get the funding sorted, because the governmental funding bodies, like I mentioned before, they do have their biases and they're also going to subtly shape the kinds of questions you're asking, because they have their objectives that they want prioritized, and so I think that's a disingenuous way of doing science, and so I think that's a disingenuous way of doing science no-transcript.

Speaker 2: 1:25:48

And so I think it takes a certain type of personality and individual to actually do hard science and like ask hard questions that maybe go against narratives. And I mean I've personally somebody who's been, I would say, more of a dissident my whole life, like I never had respect for any authority figure I ever met. So I think maybe I'm a good fit for it and yeah, so I mean those are some of the big things I really think. Once one or a handful of people start on this path, then it's going to be easy to bring other people online as well. It's just a matter of getting past that point of activation energy. That's like people are just scared to ask the important questions due to fear of, like, how they will be viewed.

Speaker 1: 1:26:29

Essentially, yeah, the private funding model, I think, is key. No-transcript is a complete, absolute waste of time. So all that energy that they could be dedicating to solving these important questions about how to improve our human health is diverted into bureaucracy and just time-wasting. And then, as you mentioned, if they aren't asking a question that's convenient for the funders, then we're just sorry. It's just not going to get funded. So I'm very, very, very bullish on private funding Nicole Shanahan, who is the vice president candidate with Bobby Kennedy, and funded Got my pin on.

Speaker 1: 1:27:41

Oh really Nice. Yeah, I mean this isn't a political podcast, but from what he's talking about from a health and science point of view, he seems to be the most clued into that. But she's funded autism research.

Speaker 2: 1:27:55

I believe there's research in the University of Texas who is looking at red light and autism and I think that is so powerful that rich philanthropists and cruisers calling on rich Bitcoiners to fund this type of research because the, the centralized bodies, the governments, aren't doing it yeah, and I mean worth mentioning is that before the 1950s, or like starting in the 1950s, most research was blue sky research, which was, like the funding bodies believed in specific individuals and just gave them money to do what they do best, not like labor them with grant proposals and, you know, make them exactly, do all this bureaucratic work just to get meager funding to survive for the next year and then have to do it all over again.

Speaker 2: 1:28:41

It's not a productive way to do science and like harness great minds essentially, and so I think you know we're kind of paying the toll in that by having, you know, pis that are not hands-on in their lab. They're kind of distant because they're constantly working on writing and acquiring more funding, and that's the primary focus now of the leader of that lab, instead of them actually shaping the science that's being done.

Speaker 1: 1:29:04

Yeah, and look, you think that the worst case scenario would be that the money is wasted, and I think that is. The vast majority of funding is simply just wasted on asking questions that aren't relevant. But I think over the past four years we've learned that in some situations that funding is actually used in ways that for the research into synthetic pathogens that could even actually have harm, and it's just again. It's emblematic of this topsy-turvy world that we're living in that this kind of stuff can happen, and the quicker it all gets decentralized, I think the better.

Speaker 2: 1:29:43

Yeah yeah. There are definitely a lot of research objectives that just are misguided, and I think it goes hand in hand with the medicine that we're practicing as well the centralized medicine where everything is focused on disease remediation and not understanding the etiology of disease and how to prevent it to begin with. Understanding the deeper mechanisms involved and why these pathologies are arising is just not really looked at. It's looked at in a very shallow way and primarily the initiatives are to develop the next hot blockbuster drug that's going to be able to treat this disease, versus not letting it happen to begin with. So I think that the objectives are just kind of perverse.

Speaker 1: 1:30:23

Yeah, and that's why I respect your work so much, alexis, because you're in a unique position of both doing this type of research and advocating for, obviously, setting up your own lab and answering these fundamental questions, but also educating and discussing these topics on your own podcast and with other leaders. So it's great to see, and I think that there's really just going to be a bifurcation. There's always going to be people that are going to sign up for their. They don't want to do any kind of lifestyle work and want to just take their Zempik but there's also going to be people who are receptive and listening to these type of message. Maybe if you got an hour and 30 into this conversation, then you're one of them and that will make these changes and hopefully, in places maybe like El Salvador, with a leadership group that is closer to the people there's less layers of bureaucracy that places like that might be able to foster change quicker than maybe these calcified and fossilized structures in certain places.

Speaker 2: 1:31:32

Yeah, I totally agree, and I'm visiting El Salvador later this year, so I'm going to scope it out for future residents.

Speaker 1: 1:31:37

So I'm really excited about it.

Speaker 2: 1:31:39

It's going to be great. Kira invited me for the event. I heard you couldn't come because of some family stuff, but hopefully we can meet in person sometime soon.

Speaker 1: 1:31:47

Yeah, no, unfortunately it doesn't quite work out, but I'll no doubt be back to El Salvador at some point. And, yeah, anything that you want to mention that we haven't talked about in closing.

Speaker 2: 1:32:02

I mean we really kind of covered the gamut. One thing I will mention, just because it was a topic that I was very interested in before discovering the light story, is the microbiome and how it's really viewed through this myopic lens in modern science, through, basically, food. And the way that I conceptualize the microbiome now, with my new perspective, is that the reason that food is so important is because we've removed all the other inputs that shape the microbiome and the microbiome's health. So if we think about the diversity of the microbiome and its function, we can think about, you know, our ancestral populations, which were outside, exposed to a lot of biodiversity. So that's one really important factor that's going to shape which microbes, which fungi, bacteria and viruses are present in and on the body, compared to the semi-sterile indoor environments that we're constantly inhabiting today, which restrict that biodiversity. And then we're also eliminating natural light from the environment. So the sun activates, specifically UVB light activates this gut-skin axis that directly can shape microbiome diversity and improve microbiome health at the level of the gut. And so now we're kind of left with just food as this last of the three pillars, and sure you can make some potential adaptations to that microbiome from food.

Speaker 2: 1:33:14

But I think the reason that food has become so important is because we lost the light and we lost the nature in our lifestyles and now we're kind of left with this just like very unidimensional way of shaping that microbiome, and I think the microbiome suffers as a result of that too.

Speaker 2: 1:33:29

So the more we can think about re-engineering and sun into our lives, it's going to improve everything from digestion to hormone health, to cardiovascular health and cancer risk, and literally everything that you can think of is going to be improved by getting back out into natural environments more. An earlier paper that came out, I believe, in January this year showed that red light exposure alone I believe it was 670 nanometer red light for 15 minutes on the upper back reduced the blood sugar response to an oral glucose tolerance test by 30%. Now imagine the effect that that would have if you were outside in the sun, with over 50% of that light being red and infrared light during the middle of the day or even more around sunrise and sunset and you're taking your meals outside. Now imagine if you do that every day, what a big difference that can have on your total blood sugar burden, on your metabolic health.

Speaker 1: 1:34:21

Yeah, I'm really glad you brought that study up. Glenn Jeffrey at the University College London I actually just spoke to him. He's a very, very nice guy, very, very smart and interesting researcher who's doing great work. And it's exactly that To me it seems like, if you're getting these environmental inputs correctly, which is the sunlight and the temperature and specifically cold, if you're in northern latitudes, that has such an amazing ability to essentially pull blood glucose out of your system and to power brown fat and this uncoupling process that you don't get diabetes.

Speaker 1: 1:34:55

And really diabetes is a disease of artificial light and indoor environments. And I think the food does become proportionally more important when we're ignoring the light and the temperature. And that is the state of what Dr Cruz calls the food gurus, which is they're correct in that if you're not getting outside, you're inside these sealed chambers all day. Yes, your food diet becomes important and you can't deviate from a strict carnival diet without falling in a heap. But if you've gotten all those light and outdoor signals correct, then, one, you're never going to develop diabetes in the first place because you're going to have prime glucose regulation. And two, if you do, then it's quickly fixed once you reestablish these ancestral solar habits.

Speaker 2: 1:35:46

Yeah, and I mean just to put a nice bow on it, we kind of touched on it tangentially throughout the episode but that really all modern chronic diseases are rooted at some level of mitochondrial dysfunction in specific one or more tissues essentially. And the more we can do to support our mitochondria at a whole body level or maybe a tissue-specific level in the future we'll see how that goes but the more we can support those mitochondrial colonies, the better off we're going to be from a healthspan perspective.

Speaker 1: 1:36:15

Yeah, that's a very nice bow, taking it all the way back to the beginning of the episode. Well, this was a tremendous discussion. I think people are going to really love it. I think we made a lot of references and really tied a lot of concepts together, and it's really helped me refine my understanding of a lot of what I've been learning and hearing from Dr Cruz and other people in the space. So I really appreciate your time, alexis. I think it was a very valuable discussion. So thanks again, and tell us where can people find you and get in touch with you and learn from you.

Speaker 2: 1:36:46

Yeah, sure, so I'm primarily active on Instagram at DrAlexisJasmine. You can link to it. The spelling is a little unpredictable, so you can link to it in your show notes. That's where I'm mostly active. I post content almost every day, very active in my stories. Uh, I answer almost all my dms at this point, though that's becoming increasingly more difficult. Um the lab you can stay tuned at my instagram for developments on the lab front. Um, other than that, I have courses. I have some one-on-one work. That's becoming more scarce as I just become less flexible in my time, but that's available too in my LinkedIn bio. We have courses. We have some consultation work and some other resources that people can access if they're trying to learn more on these topics. And yeah, thank you so much for having me. This was really fun.

Speaker 1: 1:37:32

Great, all right, I'll conclude all that information. Thanks, alexis, have a great day.

Speaker 2: 1:37:36

You too Bye.