Warren discuss mitochondria with Dr. Michael Ruscio, DC from Get Healthy and Get Back to Your Life
To listen click here
Also available here on itunes
Mitochondria are organelles, or “small bodies”, within your cells responsible for producing adenosine triphosphate (ATP), the energy currency of the body. If mitochondria aren’t functioning properly, your cells aren’t fed. Some contributors to mitochondrial damage include environmental toxins like Roundup in food, poor diet that includes refined carbohydrates and added sugars, and even too many nutrients overall. The result could be inflammation, and other conditions like diabetes, cardiovascular disease, infertility, or neural degeneration. To restore optimal function, consider a regimen that avoids packaged, processed foods and incorporates polyphenols and heart health supplements. As well, incorporate light exercise and proper breathing.
Dr. Michael Ruscio, DC: Hi everyone, welcome to Dr. Ruscio Radio. This is Dr. Ruscio. Today I am here with Warren Cargal, and we are going to talk further about mitochondrial health. So, Warren, welcome to the show.
Warren Cargal: Hey, thanks, Michael. Great to be here with you.
DrMR: It’s great to have you here, and this will be the third conversation we’ve had on mitochondria, each one with a slightly different perspective. One with a dentist, Al Danenberg, who was discussing the periodontitis/oral health/mitochondria connection. Also with John Kaiser, who started to see some connections to mitochondrial health in his HIV patients, and how certain drugs and immunosuppression were common problems as a byproduct of mitochondrial dysfunction. I’m hoping you’ll give us another slightly different and nuanced view, being trained as an acupuncturist and herbalist, and in Chinese medicine.
So I think this will be a great addition to what we’ve already covered. With that as a segue, will you tell people a little bit about your background?
WC: Well, I’m an acupuncturist and a Chinese herbalist. We have six practitioners here in the practice, and we’ve been focused on fertility issues for a number of years. That’s actually how I got interested in the mitochondria. One of the things that would typically happen here in the clinic would be that we’d work with a woman to help normalize her cycle, the luteal phase, where the progesterone was peaking everything properly, and she would get pregnant. Then within the first two or three months, there’d be a failure of the pregnancy.
We didn’t have this happen often, but it was something that made you ask, well, what’s going on here? When I started really exploring that, I found out that a female egg has about 100,000 mitochondria in it. Just to put that in perspective, your skin may have 100 mitochondria in a cell. Whereas a heart cell, a cardiocyte, may have anywhere from 5000 to 8000 mitochondria. And they’re all producing energy continuously. ATP is the energy, which is energy currency for the body. So 100,000 is a huge number, but when you really think about it what happens in the first month or three months after conception, there’s a tremendous amount of growth that occurs. This single cell bursts into a million-cell organism, with high specialization occurring in it.
So if the mitochondria, which is producing the energy for this growth, are weak or malfunctioning, then the pregnancy will not be viable. Once we found out that, we made some changes in there and in our protocols that we were using, and that did improve the conception rates that we were getting here in the clinic.
DrMR: Wow, that’s really fascinating. I haven’t heard that connection to fertility. Is there anyone who is researching this? Is there anything published here, or is this something that you’re maybe one of the first people to stumble across?
WC: Well, I don’t know, I haven’t gone into that. I put it down after that first thing. But let me just give you a couple of other two pieces of quick information. In the Chinese classics, it was always said that the woman contributed the majority of the gene—in Chinese medicine, gene is considered essence—to the child. So that phrase was always floating in my mind. What did they mean? Where did they get that information?
So as I was doing this research about the mitochondria, the 100,000 mitochondria in the egg, it turns out that recent research has actually found a Mitochondrial Eve. Because the mitochondria is solely passed through the woman’s line, whether it’s from mother to daughter or mother to son, it’s solely the female mitochondria that’s being passed down. Does that make sense?
DrMR: No, completely, yep.
WC: And I guess for you, in the context of your work on the microbiome, it’s the same thing. When you’re having a vaginal delivery you’re passing down both the mother’s microbiome from the rectum and the vaginal areas. It’s this fascinating link here, that gets linked to the feminine side. It’s really amazing, I think.
DrMR: Yeah, that is fascinating. And as we’re talking here, I’m looking just quickly in PubMed for abstracts and it seems there’s been at least a couple papers published that are touching on this. Of course I can’t really read into the details, but that’s very interesting. And I have heard, of course, that the mother is the one who passes on her mitochondria. I just didn’t hear that there was potentially a connection to infertility, but that’s a very interesting way that you first started to make an insight into the importance of mitochondria.
Mitochondria, and Why They Matter
Can you tell people, just in case they haven’t caught our previous episodes, what the mitochondria are and why they’re important? WC: Well, this is another little fascinating area here for me. The mitochondria were also called organelles, which means small bodies. So there are these small bodies within the cells that produce ATP (adenosine triphosphate), which is the energy currency of the body. Now, this is where it gets interesting. When most people think about energy, they think about the food they’re ingesting, they think that it’s being broken down in the intestines to produce something. After that, that something kind of falls off the map, what it is and how it’s being used. But fundamentally, at the most basic level, all cells require energy. And that energy is derived from the mitochondria producing the ATP. That’s it. And without the mitochondria, we wouldn’t be here.
Where it gets interesting, again, is back to your book and the microbiome. It turns out that the mitochondria are kind of a bacteria in origin. What that means is that sometime in the distant past, there were single-cell organisms covering the whole planet and they were really limited by the size they could grow. There wasn’t specialization, all the nutrients were being absorbed through the membrane. If they got so big then gravity would crush them. At one time, something really special happened, where another single cell was absorbed, there was some sort of agreement struck: “Well, look, buddy, if you don’t eat me I’ll supply your energy, and in turn you just give me the food.” And that particular occurrence is what fundamentally allowed specialization to occur.
Specialization right now, the way we see it, is that we’re this very complex structure. There are internal structures in the cells. There are lysosomes that break components down. There are bones, livers… all of that is specialization. That cannot occur without an energy source, and the energy source is the mitochondria.
DrMR: So on a cellular level, we’re really dependent on the mitochondria for energy. Theoretically, we can tie this to almost any symptom or dysfunction of an organ or tissue. But to help people try to understand what symptoms, diseases, or conditions might be most tightly associated with mitochondrial dysfunction, share with us what you found in terms of the most common symptoms or conditions. You said infertility was one. That’s very interesting. What else?
WC: So the book is about how the mitochondria drive age-related diseases. And as we age, we would typically see neural degeneration, cardiovascular illness, diabetes or metabolic syndrome (which is obesity), cardiovascular issues, arthritis. Those would be the common symptoms that you would see driven by the mitochondria. And cancer. Cancer is the big one.
Let me just throw this in, because we’ll pick it up as we come back to these: one interesting study was done a number of years ago. They looked at the muscle tissue sample of a number of five-year-olds, I believe, and compared it to 90- or 95-year-olds. The only thing that they could see going on was that in the 95-year-old, the mitochondria were deformed. So that’s really what drives the disease process here.
Normally, there’s all this mitophagy which occurs, a process within the cells when mitochondria get damaged. There are these little molecules that will go in there, take pieces of them away, and they’ll get dissolved or they’ll actually break down an entire mitochondria if it gets damaged. But what they see in aging people is that that process is not happening. Instead of seeing vibrant, alive mitochondria, you’re seeing mitochondria that are deformed, not viable, and not producing a lot of energy. Instead what they’re producing is a lot of reactive oxygen species, which drives the inflammatory process.
You can look at reactive oxygen species like toxins or radioactive material. They have the ability to punch holes in the mitochondrial membranes and damage the cell membrane. So you want to minimize the production there.
DrMR: You used a term that I think is important for us to touch on, which is age-associated mitochondrial dysfunction. We should probably clarify that. Feel free to modify this, but there are diagnosable mitochondrial diseases which are quite rare. And then we have more, what you would functionally term, age-associated mitochondrial dysfunction. What we’re discussing here is probably going to pertain to age-associated mitochondrial dysfunction and not to some sort of genetic mitochondrial disease.
WC: That’s right.
DrMR: Okay. Do you know how prevalent age-associated mitochondrial dysfunction is? Any data there?
WC: I don’t, other than it’s all over the place. It’s a big issue here. From your book, the microbiome and the mitochondria go hand in hand. So when we’re talking about aging, we’re also talking about what’s happening at the level of the gut, and how that’s driving inflammatory processes which then affect the mitochondria. The inflammatory processes could be obesity, which is at epidemic proportions now. It could be diabetes, it could be cardiovascular symptoms, neural degeneration which would be Parkinson’s or Alzheimer’s. The inflammatory process is what’s going to drive this age-related disease process for the mitochondria.
DrMR: And in terms of diagnosing this, there are a handful of methods, some direct, some indirect. Do you have any methodology that you find practical for getting a handle on if this is actually present?
WC: Yeah, I don’t. There are some new tests that have recently come out that look at oxidative stress as a measure. Here in the clinic we don’t particularly do that. If people come in, they’ve got conditions that would point to it… like they’ve got diabetes. We’re really automatically working at the level of the gut, and then we’re also working at the level of inflammatory processes to clean those up. I mentioned mitophagy. You would add in specific herbs, polyphenols, to increase that functionality. Because we definitely want to clear the debris that’s occurring in the cell which is driving the disease process.
DrMR: Sure, and I think that’s certainly fair to presume that condition is present when there are enough clinical indicators for a given condition.
Mitochondria in a Clinical Hierarchy
That’s a good transition into, how are you weaving this into the clinical process? You just alluded to the fact that you’re starting, it seems like, with most patients with gut and many with mitochondria.
But I always ask this question to different clinicians, to try to help both the layperson and the clinician organize: where does this go in the clinical hierarchy or one that a patient is building for their own healthcare? Is this foundational? Is this level two? Is this more of an if-this-then-that sort of scenario where a certain constellation of symptoms, if they are present, would indicate this?
I know it’s a broad question and there may be some nuances, but do you have any general rules of thumb you use to know when or when not to integrate into the clinical process?
WC: So I would always integrate it into the clinical process. If someone’s coming in and they’re telling me they’ve had irritable bowel issues for a while, there’s quite a bit of evidence right now that links bowel issues with higher incidence of cancer. So I’m immediately looking at things like fiber. I’m looking at ways to increase the short-chain fatty acids, the butyrate, which are all energy sources for the mitochondria at the level of the colon.
It just depends on what their presentation is. We have a lot of people that are athletes that are training. At that level it’s more dietary concerns, things for energy to help them, their cognitive functions. On the other hand, we get people in here who are dealing with early-stage dementia or Parkinson’s disease. Again, it’s a place where we would start in the gut, but a lot of that is being driven by the inflammatory processes going in the brain specific to the mitochondria.
By that, I mean, when you think about transmission of nerve impulses and things like that, all of that is being driven by mitochondria. It takes energy–
DrMR: Let me just interject with a question here, because I think this may help organize this in the listener’s mind. Would it be fair to say that you’re looking at almost two different facets of mitochondria? You’re looking at gastrointestinal mitochondria, like in the colonocytes?
WC: Mm-hmm.
DrMR: And if it’s got mitochondria, you’re looking for things like fiber and prebiotics to support short-chain fatty acids which essentially feed these cells, and that’s one track. Then on another track, you’re thinking more metabolic and neurological, and that’s going to be a different suite of therapies, perhaps a low-carb diet. Perhaps fasting or certain nutrients. Would that be a fair way to divide some of these therapies?
WC: Yep. To your point about the metabolic diet and things like that, one thing to keep in mind is the mitochondria’s preference is fats, not sugars. For mitochondria energy production, for every unit of sugar you put in, you’re going to get about two units of ATP out of it. But in contrast, for every unit of fat that you put in, you’re going to get about 32 units of ATP. So the energy difference is phenomenal there. Those are really easy explanations to give to people about the need to change up their diets quickly.
How We’re Damaging Our Mitochondria
Sure. And I want to come more to the treatments in a second. But before we go there, one of the things that I’m wondering about your take on is—and I don’t wanna gloss over this—what do you feel the most common insults to mitochondria are? Of course diet, potentially pollution, potentially EMFs. But what do you feel are some of the big knocks to the mitochondria?
WC: Well, the big one is sugar. Sugar and refined carbohydrates.
DrMR: Now, are you delineating between sugar and the amount of carbs? Would you be against someone eating a moderate-to-higher carb diet, let’s say 200 even 300 grams of carbohydrate per day, if those were coming from fruits and healthy starches like potatoes or squashes or what have you?
WC: Yeah, that’s fine. We’re supportive of that. The issue comes down to… you remember the original agreement these two cells made. You supply the nutrients, I’ll supply the energy. One of the big issues is, there are excess nutrients being taken in, and that has a profound effect. They just get backed up in the energy chain within the mitochondria and then that starts a whole process of oxidative stress. So I don’t have a problem with those types of foods that you mentioned, we’re supportive of those, but then there is an issue of excess, or caloric restriction that needs to be implemented.
When I say caloric restriction, I’m talking about, you’re eating 2500 calories a day, maybe you drop it down to 1800 or 2000 calories a day. It’s nothing drastic, but it’s beginning to understand this energy in, energy out equation.
DrMR: And what about EMFs? Have you looked into any of the literature there? WC: Yeah, I have, and truthfully I just haven’t gotten into it. What I’m really into right now is the shikimate pathway with plant enzymes, what RoundUp is doing to the foods we’re ingesting, and how that is affecting the tight junctions of the epithelial cells in the gut. And what that does to the inflammatory process, in turn to the mitochondria, as far as clearing the mitophagy.
DrMR: Okay, do you want to expand upon that? That’s definitely something interesting.
WC: I packed a lot into that one, right? You know what I’m talking about, right? The shikimate pathway plant enzymes.
DrMR: No, I’m not familiar with that specific pathway, so please illuminate me.
WC: So here’s how it plays out. The neurotransmitters require a plant enzyme to be made in the gut, like tryptophan makes serotonin and stuff like that, which is then uplinked to the brain. So there are all these little tendrils in the gut that directly communicate back and forth with the brain.
So the first cut is, we require plant enzymes to make these neurotransmitters. Those plant enzymes come from a specific pathway in the plant called the shikimate pathway. And it turns out that in agribusiness, there are probably six major crops that are worldwide. There are corn and wheat and soy, and those things, but they’re sprayed with RoundUp which has a profound effect on that shikimate pathway. Then we start getting situations where the enzymes that are coming in from these processed foods were not able to make the needed neurotransmitters. So one of the things that you begin to see is more anxiety, more emotional issues, depression, ADD, stuff like that, because the enzymes are deficient to make these needed neurotransmitters.
But the other effect that occurs here is with the epithelium. The epithelium is that single cell, like a sausage skin, that the intestines reside in, and it’s pretty amazing. It’s a single cell and it’s able to open and close. It has things like little Velcro strippings. But this RoundUp affects that pathway and causes it to begin to leak. And that leakage drives an inflammatory process. So at that level we’re back to the mitochondria, where we want to diminish these inflammatory processes as much as we can, because what they do then is create these misfigured, broken, malfunctioning mitochondria.
How to Treat Mitochondrial Damage: Diet & Lifestyle
DrMR: To treat this, I’m assuming avoidance is going to be one of the most foundational pieces, but are there are other synergistic therapies that you’re using along with this?
WC: When you say treat it, do you mean the tight junctions?
DrMR: Well, the shikimate pathway that’s being somewhat retarded by exposure. I’m assuming the first thing you want to do is avoid exposure. But if you’re doing a good job with your diet, you’re not going to be able to completely avoid it, so anything else that you’re doing for that?
WC: Yeah, unfortunately you probably want to avoid all those center aisles in your grocery store because that’s where the packaged, processed foods are, right? So that would be the first cut. Secondly, you’re just adding much, much more fiber to your diet. Like in your book, I noticed that you talked about that a lot, the importance of fiber.
I think an American today is probably at about 50% below the normal requirement for fiber. And then, as you and I’ve talked about, the fiber produces the short-chain fatty acids which is the butyrate. The butyrate is used by the colon cells to produce energy for the mitochondria, and that energy for the mitochondria is what’s driving the tightening and loosening of those tight junctions. Within those tight junctions, that little epithelium wrapper there, are all these mucus cells, mucins. And 80% of the immune system resides around the gut, so all those require the mitochondria to produce all this stuff. If there’s insufficient energy going on, I think it’s easy to begin to understand the relationship of gut issues with the increased incidence of cancer.
DrMR: So I have to ask you a question here, which is, I think, a very clinically-relevant question. It seems the further you go down the continuum of gastrointestinal symptoms, the higher the prevalence of reaction to dietary fiber and prebiotics you will see. How are you confronting that clinically?
WC: Yeah, that’s a problem you’re identifying there. It’s not quite clear, because as you probably already know in your practice, gluten intolerance is off the chart right now. Some of that we can attribute to the RoundUp sensitivity being sprayed on the wheat and then carrying over into the gluten, but it’s a little confusing and it’s not quite clear. Man has been eating grains for 3000 years, but it’s clear that there’s a higher incidence of gluten sensitivity going on. So the question is why? And how do we treat that?
Back to your question, if someone’s really sensitive, how do you reintroduce these fibers back into the diet?
DrMR: Is that something that you’re still trying to figure out, or are you reverting to other strategies with people who might be intolerant to higher fiber and prebiotic intakes?
WC: Yeah, it’s something we’re still trying to sort out yet. We do see it. It’s like the issue that I first alluded to, about the fertility issue with the eggs. We’ll see this occasionally happen, and it’s not quite clear yet. We’re starting to investigate it here in the clinic and how to approach it. And I saw in your book you had some very clear definitions about how you’ve been approaching it.
DrMR: Sure. That’s why I’m curious to get your take, in terms of how you’re grappling with that. In theory, it’s nice to feed the gut microbiota and provide nourishment of the short-chain fatty acids that are going to be produced as a by-product of that. But like I said earlier, the more symptoms you see from the gastroenterological perspective, the higher likelihood someone may flare from doing that.
Let’s continue forward, because I’m really curious to hear what your favorite or go-to treatment strategies are. I know in your book, you mention breathing, diet, exercise, and I believe you also have some choice supplements. Take us down the rabbit hole of what you are liking in terms of treatments here.
WC: Well, we try to really keep it simple. For someone just getting into it, we didn’t want to blow them out with a lot of stuff. So the first thing is, the mitochondria are like little engines and they require oxygen. In that context, right now I’m sitting at my desk. When I’m sitting at my desk, there’s a little tendency to slope, the cave-in right at the sternum. And that drives low oxygen content. Over the course of the day, if I was sitting at my desk all day, I would end up starting to drive hypoxia, which is low oxygen availability.
And low oxygen availability has a profoundly negative effect on the function of the mitochondria. So the first thing is, if you have a job where you’re having to sit around a lot, you’ve got to be moving. Every 15-20 minutes, you’ve got to be able to get up out of your desk, move around, and breathe. Breathing is fundamental. And without that breath going in there, that’s just going to drive more of the reactive oxygen species, which—as I’ve already mentioned—punch holes and damage the mitochondria. That’s the first thing.
The second thing would be mild exercise. Again, this is just for people just starting out. If you have a strenuous exercise program worked out, that’s great. But mild exercise for the mitochondria is important for mitogenesis production, fusion, and fission of new mitochondria. It’s also important for mitophagy, the clearing out of the debris in there. So back to the original statement: you’re supplying the nutrients, I’m supplying the energy. If you’re not moving and you’re supplying a lot of excess nutrients to the mitochondria, they’re just sitting in there and causing damage to the mitochondria. So whether it’s walking or whether you’re biking, whatever it is, that there’s some focus—20 minutes a day, a half hour a day—or that something is being done for mild exercise.
One of the final two things we talk about, I’ve already mentioned, which is stepping back on the amount of food that you’re eating. Nothing big, to where you feel like you’re starving, but just a small reduction in the quantity of food that you’re eating. The final thing would be the preference for the mitochondria to get the higher energy production, the fats as opposed to raw sugars.
DrMR: So are you recommending any kind of fasting protocol? Like intermittent fasting a few days per week or a day-long fasting?
WC: I get that question all the time, and that’s fine. We have a lot of older people who want to use the thing and I don’t want to make it where it’s going to fail for them. I want to keep it really simple, and then as they get into it and start feeling benefits from it, I think intermediate fasting would be fine.
Supplements for Optimizing Mitochondrial Function
DrMR: Gotcha. And are there any supplements that you’re using for optimizing mitochondrial function that you like? WC: I talk about this around the cardiovascular disease. As we age, your CoQ10 production diminishes. CoQ10 is really a fundamental factor for the heart. Recently, with statins and things like that, you’ll see these suggestions where you also take CoQ10 because statins deplete the CoQ10 in the heart. In the energy transport chain—the process that makes this ATP, in that third phase—there’s a high demand for CoQ10. So if you’re having heart issues you want to be taking CoQ10, or if you’re concerned about that, if your blood pressure is high.
The other thing is D-ribose. D-ribose is a five-carbon sugar and it’s quite a lengthy process for the body to make that. So here’s what happens. If someone has a stroke or something and some of their mitochondria die, what happens when they try to do a re-perfusion (when they introduce the blood back into the heart to get the heart moving again), because the heart is depleted of the D-ribose, you have a situation where you actually lose more mitochondria. The oxygen is there, the D-ribose is not there. Right now, what’s happening in cardiovascular work is, when people have heart attacks and they’re trying to do re-perfusion, they’re introducing the D-ribose intravenously to compensate for that. And then, back to the heart, L-Carnitine moves fats into the energy transport chain, into the mitochondria. Finally—and this would be a thing that’s more specific to the heart issues—when a heart muscle contracts, it requires magnesium to relax. It turns out that a lot of people are deficient in magnesium. So those would be our four basic recommendations here. And then, as I discussed a few minutes ago with you, the polyphenols. Polyphenols are used, like curcumin or resveratrol, or those kinds of things. Those are used by the colonocytes and also to support the mitophagy, the clearing up of the debris in the cell and keeping the mitochondria healthy.
DrMR: So you’re typically using a combination of both polyphenols and some of the nutrients like CoQ10, ribose, carnitine, and magnesium?
WC: Yup.
DrMR: Any other thoughts on this topic before we move to a close?
WC: I think that’s everything. That was a quick overview of everything!
Episode Wrap-Up
DrMR: I know you have a book out. Can you tell people a little bit about your book, your website, and anywhere else you want to point them where they can connect with you? WC: Sure. I just released my second book, which is The Reality We Create, an extended version on the mitochondria. I’m really examining how energy is flowing at a quantum level within the body. The first book was Your Mitochondria: Key to Health and Longevity. Both of these books are available at Amazon. Or if you’re not sure if the book is of interest, maybe it’s too technical for you, you can visit my website, which is wcargal.com. There are discussions about a lot of the stuff we’ve talked about today, plus there’s some free downloads for each of the books. So that would be a real simple way to find out if the book would be of interest to you.
DrMR: Cool. Warren, thank you for taking the time here to discuss mitochondria and appreciate the input. I guess I’ll talk to you here soon in the future.
WC: Hey Michael, it was a lot of fun chatting with you and I look forward to talking to you again too.
