Discover how maintaining mitochondrial health can protect and heal gut-related conditions
INTERVIEW
Christine Schaffner, ND
Welcome to the Reversing Chronic Crohn's and Colitis Summit. I'm your co-host, Dr. Christine Schaffner. Today, I'm delighted to introduce Dr. Hemal Patel. We're going to be talking all about the role of the mitochondria in health and healing, especially about inflammatory gut issues. Welcome, Dr. Patel. It's always an honor to interview you.Hemal Patel, PhD
Christine Schaffner, ND
Hemal Patel, PhD
I did my PhD back in 1999, from 1999 to 2002, at the Medical College of Wisconsin. The broad topic of the lab was protecting the heart from ischemia injury. this is where you deprive an organ of oxygen and nutrients, and it dies. It doesn't respond when you resuscitate it because it's lost that capability. It turns out that one of the key features of creating resiliency in an organ when it's deprived of oxygen and nutrients is preserving mitochondrial function. Typically, organs will go into a hyper-native state when they're deprived of these raw resources. When you flood the system with resources, that's typically when the injury happens. They call this a reperfusion injury. It's driven by this flooding of oxygen into the system. The mitochondria are now dormant. They haven't had to live with that oxygen. Now they get flooded with it, and they make a lot of oxidants. the thesis that I focused on was how opioids of all things create this protective paradigm where they allow the mitochondria to become resilient, where they can take in more oxygen during reperfusion and do more with it to create less injury and more energy. This is where I started as a graduate student. When I started my postdoc at UCSD, it evolved into looking at the membrane as a target for how to regulate cell biology. We made this early discovery that it turns out that the membrane sits near mitochondria. There's this idea that mitochondria are symbiotic organisms, but it turns out there's an even bigger symbiosis that happens with our membrane structures and mitochondria and how they respond to stress adaptation. now you have a conduit for how to get information from outside of you. Things, or organelles and all these things respond to the outer environment. You have drugs, chemicals, and toxins that bind to stuff on the receptor. They now manipulate this microenvironment, and they change the energetic profile. this is what my lab's been focused on for the last 15 years: looking at that micro-relationship of the membrane to mitochondria and ultimately how that regulates whole energetic systems within cells, organs, and then the organism as a whole.
Christine Schaffner, ND
That's fascinating. I know about your work, but as you talk about that, I'm just thinking about people in that chronic illness world, especially if they've had mold illness, which, as we've looked at mold and its relationship to energy and hypoxia, and then usually downregulation probably gets the mitochondria in this hibernation state that you're talking about. One of the tools we use to heal people from toxic mold is phospholipids using cytochrome IV or, orally, or even rectally for some people. Just thinking in my brain, I'm thinking that's doing way more than it's doing. By healing that cell membrane, you're getting rid of toxic ions lodged in that membrane or, oxidative fats that are in that membrane. Getting out of that restores not only the receptors but also allows the mitochondria to communicate better and restores the mitochondria as well. Can you help me understand that?
Hemal Patel, PhD
There's an old evolutionary story around this. The thought is that when organisms left the water and came onto land, one of the biggest pressures that they adapted to was the oxygen environment. The evolution's answer to adapting to living in a high-oxygen environment was putting cholesterol in your plasma membranes. Cholesterol binds oxygen. These membrane domains that we study are called Caveolae. They are enriched in glycol single lipids, and cholesterol. They create this structure in the membrane that's very different from the rest of the membrane. It's a platform for signaling to happen. This creates a sense of how efficient biology is. When we see it, we see instantly that it doesn't take proteins randomly colliding to create this effect. It's an instantaneous thing. by having this molecular machine assemble in a very tight space in the membrane, you now have everything you need when a compound comes in to bind those receptors, all of the effector molecules are there.It turns out that oxygen becomes a ready-made molecule that supports energy and other things. Your mitochondria use oxygen to make energy. If you had an unopposed flow of oxygen into the system, mitochondria wouldn't know what to do with all of that oxygen. The hypothesis we have is that we think that these lipid structures that are created in membranes bind that oxygen, and they deliver it in a very tempered way so that your system becomes hyper-efficient. One of the side effects of the first-generation statins that were out there was that they lower cholesterol in your body and cause cataracts. It turns out that the lens fiber in your eye has the highest density of cholesterol in your body. If you lower that, this is where you have actual direct contact with oxygen. You oxidize everything. You create these cataracts. It suggests that there is this crazy, amazing relationship between cholesterol and oxygen in this environment. The next biggest place where you see these structures is in your body in your lungs. Your lungs have a ton of caveolae that are super-enriched in cholesterol in these microdomains.Because this is how you're exchanging oxygen from the outside environment and putting it into your body. We think that there's this intimate relationship that the membrane creates with the energetic systems in the body. and targeting membranes is probably one of the first things you want to do with chronic diseases. Mitochondria are something that everyone understands that energy use and generation become dysmorphic in a lot of diseases. But the primary culprit in all of this is membrane degradation, which then leads to the demise of mitochondria. Because if you can't keep the outside environment from the inside, you're going to create a lot of disturbances in a cell.
Christine Schaffner, ND
No, I hadn't heard that before in that way, that reiterates because, again, one of the treatments that I find is that when people are fried, their nervous systems are damaged, and they've had a lot of toxic and exposure, congested liver. They're just very sensitive to, like, we give them IV sertraline, which we get from Switzerland. I can't tell you how many people responded. Then there's another product called plasmalogens on the market that are little more precisely fatty acids that can kill membranes, and myelin is what they say. Have you worked with that in the lab?
Hemal Patel, PhD
We haven't. We do like single lipids and cholesterol. But the other way to rebuild this structure is with the protein that was discovered in the early 1990s, around the cancer diagnosis. It was a substrate for sarc, which is a kinase that activates in certain cancers. It's called a Caveolin. it turns out this caveolin protein is a membrane marker protein that creates this invaginated membrane structure where cholesterol accumulates. It turns out that if you just put more of this protein in the membrane, the lipids will come and reorganize into that shape. we're using this as a therapeutic for all kinds of neurodegenerative diseases. We have a product currently hopefully moving into a clinical trial by the end of the year for ALS that's built around this idea of overexpressing this caveolin protein to create this new platform for all of the lipids in the signaling to come back.
Christine Schaffner, ND
Would it be just to reiterate and summarize for the audience, caveolin is when it's high, it's batter high, it's therapeutic and remodeled in the membrane?
Hemal Patel, PhD
That's the crazy part of biology. It's both right.
Christine Schaffner, ND
It depends on the cells.
Hemal Patel, PhD
This is what we were on the cover of a journal called Molecular Pharmacology a couple of years ago, where we wrote this review article on the good and the bad of these caveolin proteins. It's a yin-yang thing in organs where they are susceptible to oxygen deprivation. The brain and the heart upregulate caveolin, which becomes therapeutic. It drives the ability of the cell to survive in or in systems where you already have hyper-survival. It turns out they hijacked the caveolin mechanism to do this. Certain cancers upregulate caveolin, and so in those you want the opposite. In our lab, we've developed tools to not only upregulate Cav but also knock it down as well. so you can cell-specifically target the susceptibility in unique ways. In cancer, we can deliver RNA molecules that will knock caveolin out in brain cells. We can deliver the product that will upregulate the expression. You can do a concerted up-and-down.
Christine Schaffner, ND
Is it clinically true that this marker is available for lab testing, or is it just research-based?
Hemal Patel, PhD
It's not. We've been playing around with this in blood plasma as a surrogate for measuring global levels and things like that, and it hasn't gone very far with it.
Christine Schaffner, ND
Maybe that's your next test. then we'll talk about their tests. Patel has developed. some of our patients are unhurried, like hibernation, or rather, hibernation of mitochondria. They thought immediately. The danger response is that something else that's happening in the state as well.
Hemal Patel, PhD
Possibly. The idea is that when your system goes into stress, it typically shuts down. It doesn't have the resources it needs to do its normal activities. so the cell responds to shut that system down and keep it dormant. It's not creating oxygen pools and other things. Mitochondria do two things very well. The energetically feeble reaction is that they make free radicals, which then cause injury to lipids, proteins, DNA, RNA, and those sorts of things. The less favorable reaction is that they couple tightly, electron transport across the electron transport chain to create this hydrogen gradient, and then the big payoff at the end is making a ton of ATP relative to glycolysis and other processes that go on, so it has to control this uniquely, and it needs oxygen to move and create this efficiency. If oxygen is deprived, these have to go into stasis-like quality. One of the things that I've read a lot of the literature on when I was looking at ways to protect the heart from a schematic injury, is the hibernation world.Some organisms go into a cave, and there's a trigger that causes their physiology to shut down to the point where they seem like they're dead. They live in that dormant state for months, and then they wake up as if nothing happened. and so that we think is one of the dynamic features of figuring this out. If we could figure out how these organisms go into stasis and ultimately how they wake up and their physiology reanimates to the point where it's completely homeostatic, we could answer a lot of questions about how to adapt living organisms that are not hibernating to this process as well. The key to that, again, is two things. One observation that has been made is about bears and other organisms. I don't know who goes in to bleed them right before I go. What they've noticed is that when you look at their blood plasma, it moves from a yellow color, which we typically see if we were to take yours and mine, to this opaque milky white plasma. That would suggest that there are a lot of lipids right before an organism goes into this hibernation induction trigger. This is where these lipids come back. There's this notion that there is something that the lipids do to put this into a stasis phenotype. and then the other aspect is mitochondria. The mitochondria create this energetic pool. They shut down, and then they reanimated. understanding the connection between lipids and mitochondria could be a core feature of this. One of the other unique ways we've started looking at this. We were collaborating with a group on campus. There are a couple of blood-borne cancers that are very responsive to chemotherapeutic agents. These NiB compounds essentially knock out that leukemia and it's gone. Then the idea is, well, then it's gone, so I can stop taking the drug. When people stop taking the drug, it repopulates. We were trying to figure out, well, what is the cause of that repopulation, and why isn't it completely knocked out? It turns out that these compounds work because they antagonize mitochondria in the peripheral cell. However, the stem cell environment where this cancer propagates is protected in this lipid-rich environment. You never get access to this space for that drug to knock it out. As soon as you stop taking the drug, in that lipid-rich environment that is maintained, these progenitor cells essentially repopulate. the target for cancer like that to create a once-and-done therapeutic is to figure out how to create this loss of cells in this lipid-rich environment that then supports that survival. This is why these critical cells, like stem cells, sit in bone marrow: they're surrounded by lipids, which gives them that protection that you don't have in other cell types right there in this rich environment that gives you fuel, resilience, resources, and likely this hyper-native component. I guess we, in a sense, hibernate as well. Certain cells in our bodies sit dormant. These are the stem cells.
Christine Schaffner, ND
That's fascinating. Laying the foundation for this dynamic role of the mitochondria, and that's very complex. Dr. Patel is here to help us honor that and also to make a clinical gateway for you to understand the role of your mitochondria, especially if you're in a state of inflammation or chronic illness. It led to Dr. Patel thinking about, like, chronic inflammation states. states that people have; we're talking about gut health. inflammation in their colon or their whole digestive tract. Usually, there's a trigger, and we're taking the stance that there's something that's not just purely genetic, but there is maybe a genetic propensity. Then there is a trigger, either an environmental, infection-borne, or trauma event. When you think about inflammation, especially about the gut, what have you learned about the mitochondria that you haven't shared?
Hemal Patel, PhD
In my limited understanding of Crohn's, it's mostly Western developed countries that see large elements of Crohn's. Asia and Africa have very few cases of Crohn's. There's something about the European population that then migrates into the West that has this. I suspect that there is some genetic component to this and some tracking with environmental exposure as well. Mitochondria become interested in this tracking. I gave this lecture recently at a biohacking conference where you can track migration patterns of humans based on mitochondrial DNA because you inherit them from your mother. All of your mitochondria come from the egg. The sperm uses all the mitochondria to swim upriver. Then those mitochondria are exhausted because they're overworked, and they tend to create a lot of mutations. Biology's figured out a way to not take those into the new organism. Now that you have the genetic lineage of the mother, you can trace patterns of how people came out of Africa, went to Europe, and diverged into Asia. It would be interesting to look at the mitochondrial etiology in that population. I'm sure someone's done it with Crohn's and inflammatory diseases, and so I bet you there's a tracking pattern along with that, with genetic mutations that exist in the mitochondrial versus the genome component, and so that they become this interesting conduit for identifying disease etiology. In terms of the gut, one of the things we've been thinking about is the interplay between your gut microbiome and your mitochondria. One of the big questions is: how does the gut communicate with the rest of the body? The big idea is that everyone now fixates on the gut as the true mind. This is what's now regulating the gut-to-brain axis, the gut-to-the liver, the gut-to-heart. It interacts with all of your other organs in the body.I have this idea that the way it does this is to communicate with what it knows. Gut bacteria, if they're going to communicate with the known, should communicate with your mitochondria because they're old primordial bacteria that get incorporated into our cells. that's the communication pattern that we need to understand: how does the gut regulate mitochondrial behavior in the cell? Most people think of mitochondria as being just the powerhouse of the cell, which is true. They make a lot of energy, and they keep this balance. The thing that's emerging now is that they do so many other things in a cell and an organ. They're involved in dynamic shifts. They're involved in signaling, they're involved in buffering, and they become a toxin sink as well. The other thing that most people don't think about is how mitochondria work. Cholesterol is synthesized in your body. This is the building block for all the hormones you have as well. The hormonal balance likely comes from mitochondrial pools and stores as well. If you have dysfunctional mitochondria, this could explain why you have all these imbalances in hormonal dynamics as well. All of this then ultimately feeds into this inflammatory phenotype. Where this has been pushed and new hypotheses have been developed long COVID. There's a paper that came out, I believe, from a European group that suggested that all of it has to do with mitochondrial dysfunction. They took muscle biopsies and did some phenotypes. We're working with a couple of groups on campus here, where we suggest that the dysfunction starts in immune cells with their mitochondria. This is what derails the phenotype. It creates chronic fatigue, brain fog, POTS, and all these other things that you see in long-term COVID kinds of things. There is an inflammatory component to all of that; how that all integrates and connects, I don't know, but mitochondria are a central part of all of this.
Christine Schaffner, ND
No, I could agree. I've always known about mitochondria, and I've always treated them indirectly. But when Covid came on the blog, it was very important. I like to use my knowledge and strategies to repair and support people and help and improve mitochondrial function. That's getting methylene blues, and then melatonin. Cocaine became very popular during this time.
Hemal Patel, PhD
For the gut, it's the leakiness aspect as well. mitochondria are drivers in maintaining that barrier functionality as well.
Christine Schaffner, ND
I hadn't thought about that because if there's just biotic flora in the gut and that's affecting regulation on my level, that can affect cellular. That's a great point. I want to circle back to something. You said that mitochondria are toxin sinks. You saw it and said, like, they're absorbing intracellular toxicity. Can you just?
Hemal Patel, PhD
I went to grad school at a time when medical school students and grad school students were together. I met my wife, and we will meet forever. we were in medical school. I was in graduate school. We took the first two years of courses together. The bane of my existence was physiology. I still remember one question I got wrong on physiology: which ion does the cell regulate at the tightest level, it turns out it's calcium. The calcium level outside versus inside the cell is the largest gradient you will see in the system. Mitochondria are sinks for calcium. They suck all that calcium out of the system. they create this buffer. When your mitochondria are dysfunctional, that calcium is now available to the rest of the cell. All the things that calcium activates become hyperactivated and do untoward kinds of things. We've shown studies where you use nanoparticles and things like that as a way to tag and target specific things. All of them tend to start accumulating in the mitochondria, the sticky organelles. They'll suck all these things out of the regular cell environment. They become this hypersink for these toxic kinds of things, which then creates two things. They become this sink that then allows you to survive and live because those toxins get eliminated. But then ultimately, when they accumulate to a level too high, they start impacting mitochondrial function, and then they feed back into the system to create disarray.
Christine Schaffner, ND
I thought that could be the case, but the way that you explained it and then with the calcium, there are some models, like for some modern-day toxicants, flooding, cells with more calcium, there's a model of, like, EMF exposure and why that is so problematic. Just now, we're trying to create many ideas and models for that. Marti Parham popularized the idea of increasing intracellular calcium. that indirectly affects the mitochondria.
Hemal Patel, PhD
We're doing some studies around this with Beatrice Golomb, who is here at UCSD and at the Salk, where she's very interested in EMF toxicity as well as environmental toxin exposures and things like that. You're starting to look at mitochondrial phenotypes in this. We're using our new technologies around mitochondrial testing to do this at scale. Which allows us to do a lot.
Christine Schaffner, ND
That gives me such great hope that I, as a researcher, am starting to look at that because, honestly, that's why people are so sick today this ever-increasing environmental toxic exposure has been happening over the past year. In the backdrop of that, our bodies, like our immune systems, get impacted by mitochondria. We can have more models. Hopefully, that site will change.
Hemal Patel, PhD
Sadly, we have models where we can study this. The place where Beatrice is doing this primary study right now is East Palestine. That chemical spill. We're deploying our Cod technology, and now we can get samples from people at different sites. We're also testing animals that were exposed at those sites as well. Now you can look at humans versus their companions, like dogs and things like that, and their companions and see if there's a relationship between how close you are to an exposure site, time of exposure, and all these other things that play into the epidemiology of all of that.
Christine Schaffner, ND
I'm glad people are studying the impact, of course. That is always a clue. Sometimes some people have sick animals. I find that they're the canary before the person within something that you're studying. A big reason why women want to have you this summer is not only for all the awesome information you just shared, but one of the things that are going to change how we approach mitochondrial dysfunction in the chronic illness community is looking at the mitochondria through this lens that you created, this test called the Mescreen. Why don't you just walk straight through, like where mitochondrial testing was, and then this whole thing you've created?
Hemal Patel, PhD
The gold standard has always been direct muscle biopsy testing. we do a lot of these on campus. You go into the research study, and the subject comes in in the morning. Their leg is numbed with the local anesthetic. You take a gigantic needle, stick it in that leg, pull it out, and we get about 200 mg of muscle tissue that comes out. We can then do lots of phenotyping of that muscle. We have a system called the Oroboros, which allows us to look at a direct mitochondrial function in that tissue. You do have some anesthetic effects, but everyone goes through the same thing. You control all of that. It typically takes us about six hours to analyze mitochondrial function in pretty fine detail. In this lab, we have a pretty well-equipped lab. It takes us about six hours. We can look at three samples a day. There's no way to scale this outside of the research studies that we're doing. We can do a 200-person human clinical trial over three to four years pretty easily. Typically, you'll get a grant for about $4 or $5 million to do that.There's no way to get this to the consumer. In the next iteration of this, we were involved in the NASA twin study, where the twin went up into space for a year and his counterpart stayed on the ground. We had access to blood samples before, during, and after the flight. NASA's challenge was that we could only give you plasma without cells. platelet-free plasma, could you predict time and organ dysfunction during the flight and where things will go south? The thought I came up with is that plasma has your metabolites, your exosomes, your proteins, everything your cells are being bathed in is captured in that microcapture of that blood. We can capture this fairly easily at scale. We were able to do it in space for a year. Essentially, every three months, Elon Musk would send a rocket up and send the samples back down. the idea was to do an adoptive transfer experiment. We capture your environment and your exposure in this sample and transfer that onto a plate that has humans on it. We can buy cells from commercial sources that represent every organ of the body. Those cells are now exposed to that plasma environment. Now we can see how their mitochondrial function changes in real time in the systems that we're assessing. You can look at muscle dysfunction, immune dysfunction, neuro dysfunction, or cardiac dysfunction. We have all these cells that manipulate this.We were able to predict unique time points where you'd see muscle endothelium immune dysfunction. It became a way to see if we could commercialize this to the rest of the world. The fact that you had to do the blood collection still creates a barrier. You'd have to go to Quest, Lab Core, or something. It has to be processed in a certain way. How do we get rid of that to then scale to the next level? We came up with these cards that lots of companies, like every well, and other companies use. Ours is a bilayer system. You drop a couple of drops of blood in this first window. The bilayer wicks the serum into the second window. The card dries. We've shown the stability of this card for two months at room temperature. This gives us the ability to get a sample from anywhere in the world that you can capture fairly easily. Six drops of blood match. once this arrives at our facilities, we punch that serum out. We reanimate the serum in our proprietary buffer, and then we're off to the races.We essentially do the NASA-type assay, but now with the serum that we've archived on this card, anywhere in the world, any person who can poke a finger and give us a blood sample, we can give you an assessment of your mitochondria. Now we do an adoptive transfer experiment to show that serum has metabolites, exosomes, and proteins. We transfer that to a muscle cell. We see how that cell's mitochondria behave in unique ways. We can look at a mitochondrial stress response. We can look at homeostasis. What type of energy systems are you driving, how many mitochondria, and how much glycolysis? We can look at reactive oxygen species generation. Then, importantly, what we talked about as the signaling component is that we can now start looking at the dynamics of your mitochondrial network. We created a cell line where all the mitochondria glow green. We can see how your environment now shapes those network dynamics. we give you, with a few drops of blood, a real assessment of your function structure and dynamics, which then gives you some deep insights into how to move that number to the next level. We've seen some interesting results that have popped out. and we've been able to show people this is where your mitochondrial status is for providers. It gives them a way to track what things they're doing and if they're making a benefit to their mitochondrial functionality, and if they're not, it gives us some ways to tweak that uniquely.We can give you some suggestions on where to start. In terms of my biology and how about it, it's what you started with: you have to fix membranes first for most people, after that, it's time to activate these, mitophagy, and autophagy pathways, to clear out all the death and decay in the cell. Then, finally, you want to go to Antioxidant on board. If you can manage those three elements, most people will do well with their mitochondrial functionality. But there are a thousand ways to achieve that. It works differently for everyone. It's to find that balance of what works for everyone.
Christine Schaffner, ND
That's incredible. It will have all the ways to get this innovative test. It's one of the tests I've been most excited about in the last few years. There's always a specialty lab coming up. While they're helpful, they don't always have a clinical application. This is exciting to me. With all hypotheses, unless you've seen this data, with people in this community with gut inflammation and inflammatory bowel disease, do you have any hypotheses about where their mitochondria will most likely break down?
Hemal Patel, PhD
For those individuals, it tends to be something that starts with their gut microbiome. It's a dysfunction of the gut microbiome that then propagates these bacteria that are opportunistic and create an inflammatory environment. This then feeds into the metabolite pool that's circulating your body, which then allows that phenotype to migrate away from the gut to the rest of the body and creates this global phenotype. In that case, there's an element of understanding that energetic dysfunction that you see, which then gives you some insights into how to manage the gut microbiome. and the best way to couple our test is to look at gut microbiome information as well, and then to look at the metabolite pools that you're creating. Having an integration of those three gives you a unique window into your overall health that ties to the microorganisms that live in our gut and how the microorganisms that live in our cells interact globally.
Christine Schaffner, ND
One of the things that we're attuned to clinically and the treatment of chronic illnesses and, gut dysbiotics in patients, we look at biotoxin, a secretion that happens especially when people are taking an antifungal or acidic antibiotic. A lot of our strategies are to mop up the biotoxins because, usually, people feel better after that treatment. I'm curious if one of the drivers of mitochondrial dysfunction is biotoxins in that metabolite pool.
Hemal Patel, PhD
Possibly one of the things we do see in a lot of individuals that take our test, is the first thing we run is a baseline respiration. It's this muscle cell that's cooking away. We add that environment to this cell. For an ideal individual, nothing should happen. That cell shouldn't be impacted in any way. However, what we see in a lot of individuals is that they have a decrease in baseline respiration or an increase in baseline respiration. What this suggests is that there's something inside their serum that's either shutting mitochondria down or a possible toxin that's creating this non-resiliency pool. Or there's a toxin that's hyperactivating their mitochondria. You see this increase in basal respiration. Typically, in those individuals, you'll find some dysfunction downstream in the other parameters we run in our test as well. The ones that tend to not move have a baseline that stays average. They tend to look pretty good when you look at other parameters. That would suggest that there is some activating or deactivating toxin that's sitting there.
Christine Schaffner, ND
With Clostridium difficile, or Clostridium special species, it's like p-cross; all that is very inflammatory. I'm sure there's something; there's some contribution, probably not the full story, but, I think it's a brilliant idea and model to go after because when you fix the mitochondria, We talk a lot about regulation. In regulatory medicine, we think about the autonomic nervous system and the fascia. But the mitochondria are regulatory organelles at the root of it because they're not only energy, oxygen, all of that but the whole apoptosis, senescent cells, all of that, which is regulation in my mind. It opens you up to keep expanding my ideas and model. thank you. Dr. Patel, anything before we share, like how to get this test, how to connect with your company, or any other rules that you want to share with this population right now?
Hemal Patel, PhD
People ask a lot about who should get tested for this. If you're living and breathing, you should have a minute. You should know what your mitochondrial number is and that our test allows you to get that baseline. if you're well on it every six months to a year, just to make sure you're tracking along. If you're not, knowing where you sit is going to give you deep insights into where to move. and it's all about energy. People want to live well-resilient lives. One of the things that I've seen in this, in the spaces where we've started interacting with wellness, is that most people are trying to hack health and longevity through the nucleus. The nucleus is not where the answer is; this is an organelle that's designed to kill us. Genes are selfish. What they want to do is move to the next generation, and they're designed to get rid of that first generation. You don't take resources away from your children. This happens evolutionarily in every organism. The way to hack health and longevity is something outside of the nucleus. It comes down to your membrane because this is what you have to keep active for the rest of your life outside too, inside separation. Then the energy balance, the thing that ties the energy to all of that. It's membrane mitochondrial health. That's going to give you resilience against chronic diseases and the ability to live a long, healthy lifestyle overall. That's resilient.
Christine Schaffner, ND
Great points. Why don't you share how people can get their mescreen? if they want to get a consultation as well if they don't have a doctor who's doing this test yet.
Hemal Patel, PhD
Ideally, they come to someone like you who is part of our larger network and it's available through providers. We do have a direct-to-consumer model that we're working on right now. mescreen.com is where you can land and find information about the test. The model will be that, if you go through the direct-to-consumer, we'll give you a consultation about how to interpret that test result. The goal is to give people insight into their mitochondria. On the new landing page that we're developing, we'll have an educational arm as well. Not only will you be able to see all your numbers, but you'll also get to learn about mitochondria, why they're so important, all the different tests and features that we have, and what basal respiration means versus your mitochondrial potential versus your rest level. It's to educate that population. The other thing that we want to drive in this is that I assume consumers are going to be interested in this because there's a buzz around mitochondria right now, which is a great thing for people to know what they want. But the way we built this company was by going after the providers. First, we wanted to get a network of providers across the US that were starting to engage to teach them about this. Then when this direct-to-consumer population comes, we can funnel them to people who understand how to look at whole health, which mitochondria are a big part of, but then give them conduits to change health dramatically. there are lots of ways to do these providers or go to mescreen.com.
Christine Schaffner, ND
As I mentioned, this is a test I'm very excited about. I've used it personally as well as clinically. There's just going to be so much more information. I'm always saying in my process that we're trying to get the most elegant path for healing for people who've been suffering for so long. This is going to be a big piece of that puzzle. I want to just thank you so much for your contribution and your work in creating this test and also furthering this knowledge. It's always so lovely to speak with you.
Hemal Patel, PhD
A great talk with you.
Christine Schaffner, ND
Thank you.