Want to know the secret to boundless energy, amazing health, and incredible longevity? It’s optimizing your mitochondria! In recent years, multiple studies have emerged unveiling the immense role mitochondria play in everything from stress resilience, to resistance to disease, to energy levels, to aging itself. It used to be thought for decades that our mitochondria in our cells were just these mindless little energy generators that burn food and pump out energy.
In Biology courses, they’re ofen referred to as the “powerhouse” of the cell, or “batteries” of the call, or “engines” of the cell. In recent years, scientists have been discovering that our mitochondria are so much more than just mindless little energy generators in our cells, but that they are playing key roles in regulating our metabolism, regulating inflammation and the immune system, detoxification processes, resilience to stress, energy production, and even how fast we age. It turns out that our mitochondria are way more important your your biology professors ever could’ve imagined.
So, how do mitochondria work? Is there a direct connection between the health of your mitochondria and fatigue? And what can you do to optimize your mitochondria and live to 100?
This week, I have a very special guest, whom I’ve been wanting to interview for a very long time. His name is Ted Achacoso, MD, who is a world-renowned anti-aging, hormone, and mitochondria expert. We are going to be talking about the function of mitochondria in our bodies and how they influence everything from disease, chronic inflammation, stress resistance, and aging.
This is a very special episode and there is so much to discuss with regards to mitochondrial health that we ended up talking for almost 2 hours. (Side note: Since this interview was recorded, I recently spend a few days with Dr. Achacoso at an event in San Francisco, and he is not only brilliant, but one of the most generous and most open-hearted people I have ever known. Truly a remarkable man on every level. He also never gets tired of me asking him all sorts of geeky science questions, which is extremely fun for me.) 🙂
Also, a little warning: Please be aware that this is a HIGH-LEVEL discussion and Dr. Achacoso does use a fair amount of science jargon that you may not be familiar with. I did my best to pause and try to make things simple and as clear as possible in many of these instances, but there are still some parts which might be a little challenging to the non-science geek. ( I say that lovingly, as I am a science geek myself.) Although you may find some of the interview challenging to understand completely, I promise that it will ultimately be worth it, because Dr. Achacoso is truly a genuis (literally, he is known for having one of the highest IQ scores ever recorded) and he offers some seriously valuable, cutting-edge, and amazing content here. Make sure to stay turned all the way through, because I have him give away his top practical tips for optimizing mitochondria. I am incredibly excited about this episode, and I hope you will appreciate this wonderfully geeky science around optimizing your mitochondria! I know I do!
In this podcast, you’ll learn
- A 10-minute summary of millions of years of evolution, and how mitochondria ended up in human cells
- The main reason why you age and how you can slow down aging
- How mitochondria communicate with your nucleus and literally affect the expression of your genes
- Why mitochondria are essential for vitamin D production
- How environmental changes affect your mitochondria
- How your gut microbiome impacts mitochondrial function
- How overeating cause breakdown of the mitochondria and how fasting improves their health
- One of the most common things people do to be healthy that damages their mitochondria (and how you can avoid it)
- Why avoiding blue light at night keeps your mitochondria healthy
- The 4 major keys to optimizing mitochondrial health and living to 100
- How relationships affect your mitochondria
- The best type of exercise for healthy strong mitochondria
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Listen outside of iTunes
Dr. Achacoso’s Full Bio:
Dr. Achacoso has trained, researched, and worked in many different fields:
1) Interventional neuroradiology and pharmacology in Manila
2) Medical informatics and artificial intelligence in Washington, DC
3) Scientific advisor to local venture and global institutional investment funds in Bethesda, MD.
4) As Founder and Chief Technology Officer of a group communication and collaboration software company in Rosslyn, VA
5) As a quant trader for an incubator hedge fund in Reheboth Beach, DE
6) In Anti-Aging Medicine and Nutritional Medicine in Paris, Brussels, Monte Carlo
His representative body of work includes a book containing the first-ever neural circuitry database for an organism (C. Elegans), journal articles, US patents, software, grants, and recorded interviews, webcasts, and speaking engagements in the areas of
Dr. Ted Achacoso is the pioneer of the clinical practice of Health Optimization Medicine (HOMe), which is the detection and correction of imbalances at the level of the metabolome. He is based in Washington, DC, maintains a tri-continental (Manila-Paris-Washington DC) HOMe practice, and performs HOMe lecturing, mentoring, and international corporate consulting activities involving nutritional supplement formulation and the establishment of metabolomics, mitochondria, and microbiota laboratories.
How To Optimize Your Mitochondria To Beat Fatigue and Live to 100 with Dr. Ted Achacoso – Transcript
Ari Whitten: Everyone, this is Ari Whitten and welcome back to the Energy Blueprint Podcast. Today, I have an episode that I am very, very excited about. A guest I’m very excited about, Dr. Ted Achacoso, who is a Double Board Certified in Nutritional Medicine and Interventional Endocrinology and is a mitochondrial expert. His favorite topic is mitochondria and my favorite topic is mitochondria.
Today, this is actually a little bit of a selfish podcast because I’ve been wanting to talk to Dr. Ted for a long time just for my own benefit for getting to clear up certain questions that I have where the science, there isn’t a consensus among researchers about certain things and there’s kind of arguments back and forth. I wanted to talk to a true expert in this field who is also an expert on the clinical level in the trenches and kind of what actually works in practice.
We’re going to be talking about longevity, disease prevention, decreasing chronic inflammation, stress resistance. We’re going to be talking about aging itself, what’s actually driving that? Let’s get into it. Without any further ado, I’m very excited to introduce you all to Dr. Ted Achacoso. Welcome.
Dr. Ted Achacoso: Thank you.
Ari Whitten: Yeah. I would love for you to talk about … Maybe, first to talk a bit about your background of how you got into this because looking at your bio, it looks like you started more in neurology, and neuroradiology, and in pharmacology, and more of I guess standard conventional medicine types of things.
Dr. Ted Achacoso: Yes, yes.
Ari Whitten: Then at the age of 45, you got into anti-aging medicine, nutritional.
Dr. Ted Achacoso: Yes.
Ari Whitten: So, what prompted that shift for you?
Dr. Ted Achacoso: Actually, I’m trained in interventional neuroradiology, and I think they call that field now minimally invasive neurosurgery, and also in pharmacology and toxicology.
Then, here in Washington, D.C., I trained under the pioneer of medical informatics, and I did artificial intelligence research. At the time, I was asked by another pioneer of socially responsible investing to be the senior science and technology adviser for his investment funds. He asked me, he said, “So Dr. Ted, where is medicine headed?” I was 35 years old at the time and I said, “Well, it’s going into regenerative medicine, into anti-aging medicine, into real-time preventive medicine where you don’t have to think about vaccinations, etc. You can just do minor tweaks in your lifestyle. It should be preventing diseases.” I said, “It’s all going into the direction away from illness and into health.”
10 years later, I decided to put my money where my mouth was. I said, “Well, the technology is here.” We could detect a lot of metabolites that now could indicate information, indicate disturbances in your mitochondria, disturbances inside the cell because what has transpired in medicine in general is that we’re very technology driven. The initial diagnostics that we had we’re all organ-based, so therefore we took a look at organs like liver function tests for example. Then, came the tests for the specialty cells like the insulin that’s being produced by the endocrine pancreas. You could test for fasting insulin now, but still you’re looking at the specialized function of the cell.
Then suddenly about 25 years ago, clinical metabolomics came about and it’s now just reaching the clinics and said, “Well, hey guys, remember that Krebs cycle that you just used to memorize in medical schools? Now, you could measure all of those, and you could measure the cofactors that drive it.” Suddenly, you are moved away from illness of organs and dysfunction of the specific organs into the more general or fundamental cell that is the basis for your entire body.
Illness medicine is not used to looking at the body network. We’re used to looking at it in organ parts or in discrete parts. In fact, one of the first experiences that I had when I was pioneering this whole technique was they thought that I was going to steal their patients. It’s really a change in that you have to do in order to say that all of these cells are actually foundational to your entire body. They are the ones that composed the organs. No one’s taking care of them.
So, I went to Paris. I trained with Thierry Hertoghe who is the pioneer in using hormones for hormone balancing for anti-aging. He also taught nutritional medicine, and after that I just took a leave. Left wherever I was and I said, “This is where I want to be. This is where medicine is headed as I predicted 10 years ago.” I was 45 at the time.
Then, I started this whole practice like really, really putting in mitochondria, microbiota, everything that has been neglected in medical school like epigenetics, chronobiology, evolutionary medicine, all of those stuff that are not taken at medical schools. I said, “This is Medicine 2.0. This is where we should be focusing in now, so we can actually prevent all of these diseases that are coming on,” not in a vaccination sort of way, but in a lifestyle sort of way.
I have many patients who are very young, 30 years old who says, “I don’t want to have Alzheimer’s like my grandfather. What do I do?” We are able to answer these questions a little bit better now. Whereas before, we just say, “Hey, it’s a neurodegenerative disease. You can’t do anything about it,” but now you can. That’s my journey into this. That’s why I started Health Optimization Medicine. It’s a clinical practice. I really zeroed in on bioenergetics because without energy, there’s nothing that moves, so you’re basically dead.
What bioenergetics is and how it relates to mitochondria
Ari Whitten: Yeah. I think that’s a beautiful segue into mitochondria, which is what I want to talk about for pretty much the rest of the time here. So bioenergetics, for people unfamiliar with that term, what does that mean and why are mitochondria is so important in this new paradigm? You kind of alluded to it, but there’s been a shift I think over the last several decades away from focused just on the genes, or just on the organs, or just on the brain. Now, people are looking more and more at the cellular level, and I think more and more specifically at mitochondria. So, why is the shift going on towards a focus on bioenergetics and mitochondria?
Dr. Ted Achacoso: Well, one of our big mistakes was assuming that the genes were going to answer everything for us, because mutations of dominant genes can give you all sorts of dramatic things in terms of the manifestation. Second to the last count, we only have 26,000 genes and the last count that I know, we’ve had 19,500 genes. The answer isn’t really there and looking at the new science of epigenetics that controls the genes from aside. You see, oy vey, suddenly we’re not looking at the genes anymore. There are other factors that would affect that. Then I said, “Well, before anything can move inside the cell, there must be something that powers it up.”
I focused on where does it derive energy from, and looking at it from an evolution of perspective, if you take a look at the last universal common ancestor for example, the cell were all other cells were derived. They actually were encapsulations of membranes, which relied on a passive gradient of hydrogen outside and then less negative inside. So, there’s a passive inflow of hydrogen and then that gradient can be used to create ATP, which is a very ancient molecule. It’s already being used even during the passive gradient period.
Then, what we did simply as animals, we actually simply automated. The passive gradient become an automated gradient. We started pumping out protons outside of the membrane, but it’s more interesting how that happened because initially under anaerobic conditions or conditions without oxygen, you have your alpha proteolytic bacterium which is supposed to be prototypical. The prototypical bacterium that can use glucose for energy without using oxygen.
Then, there was another organism that could actually use oxygen. The sanitized version of that is that they went into a cooperative agreement, but actually before, there was a fluctuating levels of oxygen in evolution. There was a klepto gene inside the mitochondrial bacterium, which gained, actually steal the ATP that’s being produced from the alpha proteolytic bacterium, but then the oxygen levels rose and therefore we have this symbiotic relationship now.
The plants or even ones that they’re behind you, they’re even one step ahead of us. They incorporated cyanobacteria, which are now the basis of chloroplast and they are able to photosynthesize, and therefore they don’t need to move to get their energy. We need to move in order to find energy for ourselves. If you take a look at what a cell really needs to do, it needs to survive, and for that it needs to find an energy source. Then, when conditions are ripe, they will reproduce and it will protect itself from harm by either the primitive fight or flight syndrome, either they attack or they actually run away. These things are still very basic in us, inside us.
For the modern way of looking at it is you think of it as the amount of money that you have in a bank. So, there is the energy that you’re currently using, meaning the amount that you have withdrawn, and there’s the amount in there that’s actually saved, and you should actually keep a balance between those because you cannot be overdrawn. If you’re overdrawn, then you could have conditions like one of the topics that you mentioned, which is the chronic fatigue syndrome or otherwise called myalgic encephalomyelitis, and now it’s called something else. I think it’s something like…
Ari Whitten: Yeah. S-E-I-D, what is it? Systemic Exertion Intolerance Disease.
Dr. Ted Achacoso: Systemic Exertion Intolerance Disease. Yes, that’s it.
Ari Whitten: Yes.
Dr. Ted Achacoso: I kind of like the myalgic encephalomyelitis because it’s actually very descriptive. There’s information of the neurons and there’s information of the muscles, but let’s see what the IOM comes up with next. For bioenergetics, we see that we actually need to have an energy source somewhere in order to do all of these functions. When you see that energy being produced by the anaerobic cell, you see it’s being produced very inefficiently, but there was use for that. That was used for low oxygen environments. You could still see that being used extensively by sprinters.
Sprinters for example, have huge muscle cells which is filled with glycogen. They could run at a really, really, very, very fast speeds for short periods of time because they could use the glucose as fuel because at that particular speed, it’s very hard to pump oxygen and blood into your muscles. That’s the advantage of that. If you’re doing endurance running, etc., then you want to have more efficient mitochondria and fuel adaptive way. As I said, we’re always looking for this in order to do what we want to do, in order to do what the cell wants to do which is first and foremost to survive. After surviving, it wants to thrive. So, it likes to find the right environment where there’s food, and so on, and so forth, and then after that it could reproduce.
One of the other things that you wanted to touch on was the cell danger response. If you take a look, this is like two things. These are like our current parasympathetic and sympathetic nervous systems, and the response is sympathetic. Essentially, you fight or flee. We just have it in an organ system, and we have it in a cellular molecular level at the level of individual cell. So, looking at bioenergetics from this point of view as a fusion between two organism and energy production is done that way, makes you see immediately that there’s a symbiotic relationship. The thing that I don’t want to get lost is that these are bacteria, so I call mitochondria and the symbiotes. We have 100 quadrillion of them in the body that is powering you up for everything that you do.
So, when you take a look at that, I really like to touch on how bacteria actually operate. They don’t do cell division. They do fission. They divide like regular bacteria. Mitochondria have circular DNA, and there is about one to 15 per cell. It’s average of five. Some of the cells in the body have a high number of mitochondria like the liver of one to 2,000 per cell. The average about 500 mitochondria per cell. The red blood cells used to have mitochondria, but no more because mitochondria is actually the origin of the heme in blood cells. You see all of these functions of the mitochondria that are already have been transferred to them aside from being an energy source.
As an aside, and I don’t like this to be forgotten. For the vitamin D freaks out there, the vitamin D is actually activated in the inner membrane of the mitochondria. I don’t like that to be forgotten because it tends to get lost in the equation. When you have mitochondria like this, dividing that weight, you could have mitochondria that actually will have mutated DNA on one side and healthy DNA on the other when they divide, since they divide [inaudible] or randomly. That division, can give you healthy mitochondria or defective mitochondria. Defective mitochondria are automatically … Actually, if your body is working properly, then they’re automatically removed by your garbage collect … Actually, they kill themselves by a process called mitophagy and they go away.
The mitochondrial DNA mutates very rapidly and that can give rise to variations in even how much energy produced. It is like having a microchip and having variance of the microchip depending on how much speed the microchip. They all will operate within a certain range, but certain combinations will provide you a better throughput, and certain combinations will provide you with lesser throughput. That is actually exemplified by what’s called the mitochondrial haplotypes.
In energy production, the mitochondria will have different types of haplotypes as described by Doug Wallace in his studies where he traced the mitochondrial Eve, since mitochondria come only from women. He traces from Africa that has a haplotype of L. Then, as you go move northward, you find that a measure called coupling coefficient of the mitochondria changes. So, coupling coefficient is this. If I eat an equivalent amount of glucose, this is the amount of ATP that I produce. If I were a runner from Kenya, I would probably have a one is to one. I would convert it very, very quickly.
However, if I lived in northern climate which is very, very cold, then suddenly, I will have to use some of my gradient for heat production and that heat production will actually help me survive the winters in these cold climates. So, suddenly you could see the efficiency of energy production because now it’s being used to produce heat. More recently, as recently as two years ago, you probably read this. Mitochondria, actually producing light. So, they postulated that is being used. Much of my work on artificial intelligence was consciousness and we were looking for a way where how is coherence produced in as much faster way is probably from light emitted by mitochondria, but I don’t know. I’m just guessing at this point in time.
If you look at that now, you have many variants of mitochondria that are produced because of the bacteria-like action. Fission, they actually exchange DNA material. So, they actually exchange DNA material with the main nucleus of the cell which is the anaerobic cell. Remember, I said that they were two organisms. So, what has happened then is that it transferred much of the structural protein formation into the nucleus of the cell. This energy circuit is preserved within the mitochondria, but those that created structure, much of it has already been transported to the nuclear DNA. The reason for that is really very simple. Again, it’s an energetic equation. It requires so much energy to produce structural proteins.
So, if you’re going to produce rapidly adapting mitochondria depending on energy conditions, you just replicate the circuit and allow the nuclear DNA to produce the encapsulations for you or the body that the circuit is going to inhabit, so to speak. Then, because they’re bacteria, they move. So, in these types of movements, it’s necessary. For example, your neurons are very long. They have to traverse this entire length in order to get into your synapses for example, to power up the release of those neurotransmitters first.
Then, as I noted to you earlier, they have a way of killing themselves if they’re no longer useful. It’s actually interesting because I always like to remember their trigger, is really nothing more than a loss of that proton gradient, a loss of electrical charge. You could see the loss of electrical charge and when the body sees that it’s too low, then it bounces itself off with the proper molecules to say, “Okay, I’m marked for killing myself.” This is a Pink/Parkin type of things that you probably had been reading about.
So because of this, fission, fusion, they fuse, they form rings around the nucleus to power up all the cell functions. They move in order to power up all parts of the body. Then, they kill themselves. So, these are typical bacteria actions. If there’s anything wrong with any one of them, then you develop diseases. If there is no fusion, you have a very, very small mitochondria that are not able to generate enough energy. If there is no fusion, then you cannot form the large bridges of a mitochondria that are needed to actually power up huge sections of the nucleus and the large parts of the cytosol. If there is no movement, then you can accumulate garbage on one side and nothing on the other, and your cell is going to die at that particular point in time.
Ari Whitten: This is a beautiful tour of millions of years of evolution compacted into 10 minutes.
Dr. Ted Achacoso: Yes.
Ari Whitten: I also know that there’s probably a significant segment of viewers who were only able to understand half of what you just said because it’s just too advanced for them. So, to make this really relevant to people, how does that all translate on a practical level? Why is it … To somebody listening to this who just they’re having symptoms, they have chronic fatigue, they are having various health problems, why is all of that everything that you just explained and what mitochondria are and what they do? How is it relevant to them on a practical level in terms of their health?
Dr. Ted Achacoso: That is relevant on the other side of what the bacteria do, which is their function, what they do for you. They do really, just a few major things. One is the production of energy, which is what it’s known for. As I said, I don’t like looking at the mitochondria as batteries for the cell, I like looking at them as kitchens that cook the food for you. Mitochondria are the only organelles in your body that can actually metabolize your fat. These are the things that it does for energy production, but actually one of the major things that it does inside the cell for you is what’s called … I don’t know whether or not this is too much, is called redox balance.
It’s a reduction oxidation balance. Because it uses oxygen as the final acceptor for the electron when it degenerates energy, any factory that is going to be generating energy is going to produce some garbage, and that garbage is in the form of rust. However, a low rusting level, which is called reactive oxygen species is the name of the rust. A low rusting level, of course nature is quite very penurious in its use of signaling molecules. So, it will use the reactive oxygen species to actually signify to the nucleus, this is how much energy production that we have. It will use other things like ratio of your ATP to ADP, and AMP. Your NADH ratios and so on, but essentially those low levels of reactive oxygen species will signify to your nucleus, this is how much clean output that we’re having.
Then if it’s too high, then it’s like, “Oh, we’re already having dirty output,” and the nucleus can signal biogenesis, meaning let’s generate new kitchens for you because your kitchens are all overworked.
Why you should always view your mitochondria and cell nucleus as two separate organisms
Ari Whitten: This is already I think an important point that I want to emphasize, which is a lot of the way that conventional cell biology was taught for a long time was like the nucleus is the master. That’s the brain. This is the place that’s dictating everything that goes on in the cell because that’s where our genes are stored. What you’re saying is actually, mitochondria are doing things. Mitochondria are sensing things, and then communicating back to the nucleus, which in turn influences things like which genes are being expressed, and so on.
Dr. Ted Achacoso: Yeah. That’s why I said that you should always take a look at them as two separate organisms.
Ari Whitten: Mm-hmm.
Dr. Ted Achacoso: They are communicating. It just so happens that one of them lives inside the cell, it doesn’t mean that it has lost its full autonomy from that cell. A lot of people, researchers describe it as semi-autonomous, but for the most part, those mitochondrial bacteria are pretty dang autonomous except for the fact that they cannot build their own house. They can actually dictate a lot of stuff to the nucleus. It just so happens that our initial focus historically, again because of technology, our initial focus historically has been on the nucleus and the cytoplasm, and because the mitochondrias and organism is very small, we tend to have that point of view.
However, if you erase that and just say, “Well, they’re equal. They’re equal organisms. They are talking to each other.” Then, suddenly you will have a different point of view in looking at these two. They are in a symbiotic relationship but not 100% symbiotic. The anaerobic cell will protect itself when it needs to, and the mitochondria will protect itself when it needs to from the anaerobic cell.
As you can see, this is actually can be generalized as a whole, that directive of the cell, if the cell doesn’t want to cooperate, it transforms into a cancer cell because it wants to survive and be independent of everyone else. So, you could see all of this evolutionary drives that are in there, that we have masked with so many layers of things, but essentially we as organisms are doing exactly what those organisms are doing.
An important point Ari, is this. I failed to mention at the outset that I actually subscribe to the super organism theory of the human being.
Ari Whitten: Can you explain with that?
Dr. Ted Achacoso: That we actually … Yes, comprised of all of these different organisms that got into relationships to each other and here we are forming a cell. I think the fancy name right now is a holobiont theory.
Ari Whitten: Mm-hmm.
Dr. Ted Achacoso: Then that’s why for me, it’s the only tenable way to look at mitochondria, to look at the nucleus, cytosol, and to look at gut microbiota because all of these maybe are talking to each other.
Ari Whitten: Mitochondria are doing a few key roles that are influencing our functions. One is obviously energy production. They’re also influencing metabolism like our body fat stores. They’re involved in that process. Like you said, they’re kind of kitchens in our cells, and they’re also involved in various kind of signaling roles back to the nucleus of the cell that are influencing gene expression.
Dr. Ted Achacoso: Yes.
Ari Whitten: Are there any other-
Dr. Ted Achacoso: I just like to add to that, actually one thing. Mitochondria is also the calcium sink of the cell, so it’s like your bones. If there’s any excess calcium in there, your mitochondria will try to balance it out. Aside from energy production, and rust production, and redox balance maintenance, it does calcium balance inside of cells. You could take a look at your mitochondria, it’s actually taking as a microcosm of the function of your bone in your system and the calcium metabolism for the entire cell, which is very important really for heart diseases for example because when you get a heart attack, the biggest injury would come from the reperfusion or when blood supply comes right back into your heart. It’s deprived of oxygen and suddenly there is oxygen coming in, that can generate a lot of reactive oxygen species and inducing further damage. Mitochondria is very much implicated in that.
One of the things that you could actually do is to give the patient a lot of melatonin. That would actually stabilize the mitochondrial membrane. That’s the clinical part of that.
Why it is important to talk about mitochondria
Ari Whitten: Yeah. For anybody that’s got lost in all these little mechanisms, why is it worth talking about mitochondria? Why is it worth doing a whole podcast talking about mitochondria? Why are they still important to health longevity, diseases? Is there evidence linking mitochondrial problems to various diseases? Can you talk a bit about that, just so people can get a sense of why mitochondria are actually important?
Dr. Ted Achacoso: The reason why it’s worth talking about is just asking where do you derive your energy. For example, in the clinics it’s as simple a question as why do you breathe. When you ask the question of bioenergetics, it’s basically tied to that question why do you breathe? You breathe in order to have that oxygen, and that oxygen is actually delivered by your red blood cells to your mitochondria and because your mitochondria uses it to generate the energy for you. That would be a very simple way to remember how important the mitochondria are.
Ari Whitten: Yeah, that’s a great analogy.
Dr. Ted Achacoso: Mitochondria would be … As I said, they are kitchens. They are energy generating and so on, and so forth. The rest of the things that happen are actually consequences of the fact that they’re bacteria, and they are actually factories that produce these things and they would be producing garbage and other stuff. There will be consequences that happen in terms of … In fact, almost all diseases because you need to power it up.
So let’s take a look at, if you don’t have any power. Say, my favorite example is a city in a blackout. You have absolutely no power. You have no energy in the city, etc., etc. The first thing that you think about is something that stinks. “Well, you know, there’s no garbage collection.” You can think of chronic neurodegenerative diseases like Alzheimer’s for example, where there’s a failure of the removal of the amyloid. Of course, there’s the question of whether or not this is really an amyloid problem.
Anyway, even Aubrey de Grey in his theories of aging for example, would say that part of it is actually the failure of removal of the garbage, not only inside the cell but also pericellularly, or just immediately outside the cell. You could see that. Then of course, there’s no money to pay for your police force, there would be anarchy. Therefore, you can have DNA mutations because that cell cannot repair itself. The DNA cannot repair itself. The mechanisms try to be in protective mode but they can’t because there’s also no power to protect yourself. So, you become susceptible to infections. You have a lower immune tolerance and so on, so you’re more likely to get sick with infectious diseases.
If you have no power, also then since you have no police force, etc., aside from regulating cell growth, there’s also the regulation of the various processes inside the cell. So essentially, your cell would be in a standby mode. Without any power, the simplest way to think about it is when your phone is in low bat mode, like absolutely, and it will turn itself off if you don’t power it enough. That’s what happens to us when we don’t take care of our mitochondria.
How environment affect mitochondrial health
Ari Whitten: Beautiful. I want to transition into aging, and you just alluded to some of it there. There’s been lots of theories of aging, and you mentioned Aubrey de Grey. He’s a very well-known aging researcher today that has his own theories, but there’s been a transition. There used to be Harman’s free radical theory of aging that was popular for many decades, and now that’s kind of mostly dead and aging researchers don’t really look at that so much. Then, there’s the mitochondrial free radical theory of aging which is more focused on reactive oxygen species, free radicals produced within the mitochondria, by the mitochondria. Then, there’s all sorts of other theories of aging and scientists debating about which theory is the most correct.
Some saying it’s about telomeres, and others saying it’s about genes, and others saying it’s about mitochondria. All these different kind of debates going on. What in your opinion are the major drivers of aging, and what is the role of mitochondria in that process?
Dr. Ted Achacoso: First of all, I’d like to say that we don’t have a real definition of aging. At one point in time, aging was going to be classified as a disease rather than as a natural process. Now, people are saying aging could be stopped, but how do we really define aging? If you take a look at it just from the body clocks, the body uses very, very different clocks. The skin uses a different clock from your eyes, so different parts. Different parts of the brain uses different clocks.
In fact, Nobel awards were just given for the discovery of this various different clocks. For example, one of the more used measures of aging would be the life of your telomeres, your telomere’s activity, and do you belong to a certain cohort when it’s longer, and so on. There are various ways by which you want to measure aging, so what are you going to use? What category are you going to lump in? So, if you’re going to take a look at the mitochondrial theory of aging, then that’s one thing. You’re looking at it from an energetic perspective.
So, you have to look at the genesis of the mitochondria inside your body. What kind of haplotype you actually inherited? Whether you’re coupled and uncoupled, whether or not you’ve moved to a different environment, whether or not you change your diet and so on, because those are all going to influence your mitochondrial function.
Ari Whitten: I don’t want to get digressed too much here, but real quick. Can you just talk about what you mean by moved to a different environment in the context of mitochondria? What does that mean for people listening to this?
Dr. Ted Achacoso: Yes. For example, it is now being established that actually if you move to a different environment, you can accumulate mutations very rapidly for that. The mitochondrial DNA mutations for that environment that will adapt you to that environment, even if you don’t have the specific haplotype yet for that environment.
Ari Whitten: On a practical level, if somebody from Kenya moves to London, would that be an example of this?
Dr. Ted Achacoso: That would be an example of that. It’s not as rapid as a change in your gut microbiota. Your gut microbiota can change in 24 hours based on the food that you eat. I’m guilty of that. I’m rarely a single time zone for two weeks. That really totally fucks up my mitochondria. What I mean by that? If you take a look for example, people in colder climate. For example, you’re from Boston. As you get older, they actually don’t like the cold anymore because their DNA has mutated. Many of them fly down south to Florida. If you do a test of the mitochondria when they were in Boston, they had a lower coupling coefficient than they were when they move to Florida.
Ari Whitten: So, their cells were designed to produce more heat?
Dr. Ted Achacoso: Yeah. Why we have to start with those basics because this will explain things more simply.
Ari Whitten: Yeah. So, when somebody is in the wrong environment and they’re accumulating mutations, are those adaptive mutations or they’re bad mutations that are harmful by having this mismatch between the haplotype and the environment you’re in?
Dr. Ted Achacoso: They’re mostly adaptive because the body … As I said, they are bacteria. They would like to have the most optimal environment possible. When you put them in a different environment, the first thing that the bacterium will ask is, what we ask is, “Where’s my energy source?” What do we ask when we go? “Where am I going to eat? Where am I going to stay?” These are fundamental questions that are also answered by your bacteria.
So the mitochondria says, “Well, okay. This is a cold climate. We need to have more of the loosely coupled mitochondria because we have to produce more heat.” We used to think that it occurred very slowly, but now we know that within a few years alone, they can change as exemplified by the snowbirds. The just fly over through the south and they enjoy the warm weather that way.
These are the kinds of changes that we see. When we’re talking about mitochondrial theory of aging, because mitochondria power is at your cell. There’s a significant number of them that needs to be alive, producing enough energy to actually keep your cells alive. This is one by Douglas Wallace in his paper where he said that at around 45 years or so, that’s your tipping point where you accumulate a lot of mutations in your mitochondrial DNA, rendering the energy production inefficient, or you become highly heteroplasmic in other words, that’s the term for that; such that at the tipping point, that after that you cannot recover. Probably that is one when you don’t do any intervention.
Ari Whitten: Just complete that thought for a minute because what happens then? So, you accumulate a lot of mitochondrial damage, mitochondrial mutations in the cell and then what? What is the consequence of that?
Dr. Ted Achacoso: Actually, the consequences of that are many fold, but the primary one which we were talking about earlier, there’s a rise in the production of the reactive species, the reactive oxygen species and reactive nitrogen species. If you have an old factory, it doesn’t know how to deal with its garbage efficiently because it’s rickety. It’s old. Its collection mechanisms are not as good as when it was a new factory, and its checks and balances are already very loose. What happens then is that it cannot produce enough power for the cell.
The cell tries to produce more of this mitochondria, but if there are too much of that heteroplasmic mutation, meaning most of them will produce the same circuit anyway, the same type of kitchen that is inefficient, then you will have less and less of efficient mitochondria. Then, there’s less and less available power for yourself. Now, in the course of that, you produce a lot of this reactive species. There are two types, the active oxygen species and reactive nitrogen species, and this is actually going to signal your nucleus. It says, “Hey, try to produce more mitochondria,” but the mitochondria produces are actually more defective ones. Then, the number of healthy cells die when you get older. There’s brain atrophy. There’s muscle atrophy and all of these things. You lose the cells in your body and that is-
The main driver of aging
Ari Whitten: Do you mind if I just interrupt you for a sec? The link between the loss of cells and the damaged mitochondria is basically, what you’re saying is as cells accumulate more damage or dysfunctional mitochondria, at a certain point the whole cell gets the message, “Hey, we’re not able to produce enough energy to keep up with cellular-“
Dr. Ted Achacoso: Right.
Ari Whitten: The cell commits suicide and then over time, when lots of cells commit suicide, you actually lose cells.
Dr. Ted Achacoso: Yes.
Ari Whitten: As I understand it, the mitochondrial theory of aging is basically suggesting that as mitochondria get damaged, then enough of them get damaged that the cell doesn’t meet these demands, then you lose cells. That loss of cells through cells committing suicide, is a major driver of aging.
Dr. Ted Achacoso: Right. Mainly, your first trigger will be a rise in the loss of garbage collection. Inefficiency of your neutralizing, very high levels of your active species. I think that’s still very much there, but it’s more of a … For me, it’s a secondary action of the fact that you have accumulated too much of variations in your mitochondrial DNA, such that it is producing dirty kitchens for you instead of clean ones.
Ari Whitten: Okay. Let’s dig into that a bit more because the original free radical theory of aging was basically like free radicals are bad. They’re kind of rusting and damaging your cells, and the idea that the logical extension of that was taking antioxidant pills would neutralize all these free radicals and therefore prevent the damage and extend your lifespan. We now know there’s lots of evidence showing that it doesn’t really work that way and lots of antioxidants supplements have shown not to extend lifespan.
Dr. Ted Achacoso: There’s also antioxidant-induced toxicity.
Ari Whitten: Yeah. The other logical extension of this theory is that things which promote free radical production would therefore accelerate aging, and accelerate your demise, and shorten your lifespan. One example of that would be exercise or other forms of hormesis, which stimulates your free radical production and we know that, that was also not true. Exercise actually helps extend longevity.
Dr. Ted Achacoso: Mm-hmm.
Ari Whitten: The free radical theory of aging like I said has been mostly discarded, but what you’re saying in contrast is there’s this kind of other picture which is the mitochondria themselves are producing their own free radicals.
Dr. Ted Achacoso: Yes.
Ari Whitten: That those free radicals are in some way linked with aging.
Dr. Ted Achacoso: Yes, because they actually damage more the mitochondria. They actually damage more of the … If there’s a high hydrogen peroxide for example, that’s traversing into the cell’s nucleus, that itself can actually trigger if it is not … I was going to say dismutated property. If it’s not taken care of properly, then it can actually cause defects in your DNA by attacking the DNA. Then, all of the sequelae of diseases due to aging, more cancers, more immune diseases, etc., etc., you could see it as coming from the mitochondria itself. I think that is the important pathway that you look at.
As I said, you always have to look at it as two organisms. If you’re looking at the effect on the somatic cell for example, or just like looking at the effect on the body, you should look at how this microorganism is actually communicating with your nucleus and communicating with the rest of the cytoplasm. Then, you’ll see there, how it contributes to aging in itself. Aging is either there’s also the accumulation of DNA mutations that cannot be repaired. There’s so many of this, but I said, “We don’t have any clock by which to base it on.” So, the mitochondrial theory of aging is unique because it actually takes into account the energy production. It goes by the dictum, without energy, you’re dead anyway. So, why not look at energy first, right?
Ari Whitten: Yeah.
Dr. Ted Achacoso: We’re so conditioned to chronological or chronobiological types of aging. Now, we’re looking at it from a bioenergetic form of aging and that becomes more analog. It’s not a digital kind of thing where it’s on you’re aging off, you’re not. You need to have particular ratios of healthy mitochondria to one another in order to sustain cell viability. You have a healthy ratio …
How you can slow down aging
Ari Whitten: Yeah. Let’s dig in to that a bit more, and I think this is where I’d like to transition to get practical for everyone listening that’s like, “Okay, enough with the theory. Tell me what I can do to slow down aging and help my mitochondria.” We know that taking antioxidant pills doesn’t really work to neutralize this production of free radicals by the mitochondria.
Dr. Ted Achacoso: Unless you measure the levels first and see what the person needs.
Ari Whitten: Okay.
Dr. Ted Achacoso: Because if there are severe deficiencies or even subtle deficiencies, you can tweak the mitochondrial function by just giving the supplements. The thing that I learned from the clinics is that your patient or your client if they’re athletes and they’re not sick, will never take the diet that you prescribe them. You always say, “Here, take the supplements and go,” but the big improvement that they have now, is now we could measure the mitochondria metabolize. We could measure mitochondrial cofactors. We know what things make it hum, and we know what could enter the mitochondria and what can’t.
Based on that, then we could measure. Then we could do the proper supplementation, and we could at least optimize the function of mitochondria currently, those that are currently alive in your system.
Ari Whitten: Okay. Let’s dig in to some specifics here. What are the specific types of things that would actually trigger more of an oxidizing environment, more free radical production by mitochondria? We destabilized the membrane potential and that’s one question that I’d like to get into first. Then the second part of it is, what are the types of things that we can do to stabilize and protect our mitochondria and decrease their production of reactive oxygen species?
Dr. Ted Achacoso: I think your listeners will hate what I’m going to say. If you eat too much food, if you’re going to put too much food for your kitchen to cook, you’re going to stress out your kitchen. You’re going to make it throw off lots more garbage. You’re going to make it more dirty, especially when you’re taking in lots or refined carbohydrates like glucose, which is processed by the anaerobic part of the cell. Then, it goes into mitochondria’s pyruvate. You need vitamin B1 to get into that, and then you dump in all of this pyruvate in itself and you get what’s called a reverse electric transport, meaning everything will go backwards. It will not generate energy for a year. It will actually reverse the entire process for you.
Ari Whitten: Say that again, what triggers that? Just overeating in general?
Dr. Ted Achacoso: Yes. If you’re putting in excess of the substrate pyruvate, too much acetyl coenzyme A there. It’s like, “Oh my God. You have lots of vitamin B1.” That’s transferring everything in there. The kitchen is saying, “We’re already fucking full. Why do you keep on doing this?”
Ari Whitten: I don’t want to digress too much in the mechanisms here, but does this relate to the concept of pseudohypoxia and the NAD plus and NADH ratio, which is not related to hyperglycemia.
Dr. Ted Achacoso: Yes, yes. It’s related to pseudohypoxia, which is I’d like to touch on that also on the other side where how to keep the mitochondria healthy because oxygen is the final acceptor for the electron that’s used to generate proton gradient for energy. The one thing that you said earlier, which I think your listeners should think about is that we’re not intended to eat continuously. We’re horrible as a species because we have permission to eat from the time that we wake up to the time that we sleep. So, one of the things that is easy to do based on this or taxing your kitchen with food is why don’t you shorten your feeding window and give your mitochondria a time to actually rest.
When you do that, then your mitochondria get rested and your body says, “Okay, let me generate new mitochondria for you,” a process called mitochondrial biogenesis, and let me remove the inefficient kitchens for you and let’s do this. It does during the fasting period.
Ari Whitten: Autophagy and mitophagy specifically relate to that fasting window and having enough break from shoving food into your body that your cells in your mitochondria have this time to go into autophagy and mitophagy. Can you explain mitophagy just a little bit?
Dr. Ted Achacoso: Yes. Mitophagy is a process by which the mitochondria actually kill themselves. It’s used in several processes in the body. The first is during fertilization. That’s how the egg actually kicks out the mitochondria from the sperm. It uses the mitochondria to swim, and the body uses that in mitophagy. A second use is in the formation of your red blood cell. There’s a mitochondria there initially and then, the mitochondria kills itself in order to have the heme for your hemoglobin. Then, there’s mitophagy of course when the proton gradient of the mitochondria that’s generated is very low and insufficient, the body identifies that and marks it immediately for recycling. It means it’s an inefficient kitchen. Let’s take it out. That’s mitophagy.
Autophagy however is a different thing. It’s the suicide of the cell in general. Unfortunately, the trigger for that is also in mitochondria. There is a molecule in the mitochondria directly involved in the production of energy called cytochrome c, and when that is released out of the mitochondria, that’s the death now for the cell. It’s like time to kill yourself, which means it has opened a pore. There’s a pore that it opens up. It has a name. The mitochondrial membrane transport at pore, and when it goes out there, the cells says, “Okay. We’re marked for suicide. Here’s the cyanide.”
This is necessary in normal balancing of anabolic processes or processes that make your body grow, and catabolic processes, the processes that remove or break down things from your body, which is all necessary, which is what we do with food. We actually break down the food in a catabolic process, and anabolic is building our muscles. It’s the same things that cell is doing, that the mitochondria is doing. It’s doing that to itself.
Ari Whitten: Overeating in general, overeating refined carbohydrates-
Dr. Ted Achacoso: Particular.
Ari Whitten: … and eating too frequently in too many hours of the day?
Dr. Ted Achacoso: Yes.
Ari Whitten: All of those factors. What other factors are going to damage our mitochondria?
How overtraining damages mitochondria
Dr. Ted Achacoso: You mentioned earlier something that is not naturally done, which is a chronic exercise. When you over exercise especially if athletes overtrain, you are actually going to induce your mitochondria to produce lots of that rusting molecule called the garbage, the reactive oxygen species higher than what would be required to just do a signaling process. That will actually turn on the information cascade or what’s called molecular inflammation. In fact, molecular inflammation is lovingly called inflammaging, another aging pathway, but that’s more on the origin of chronic diseases type of aging like diabetes and all of these other diseases. That’s called inflammaging, but the major player in there is of course your reactive oxygen, reactive nitrogen species.
I used to have fights with coaches because I would allow their athletes to rest, and I would allow them to only practice or train on two days a week, but the classic training of the coaches, “Yeah, you have to train every day.” No, you don’t because you have to build your mitochondrial reserves. You have to decrease the inflammation. You have to make sure that the proper anabolic processes have occurred. For example, enough for muscle growth that there’s strength for whatever the athlete is supposed to do.
That’s why the whole phenomenon of high intensity interval training came out. The easy way of remembering that is very natural really. If you were hunting for a rabbit, you’re not going to run after the rabbit continuously. You’re into run a little bit high intensity. You got to hide behind the tree, run again, and then hide behind the tree, and then run and run until you can club the rabbit. That’s the way we are intended to be. We’re not intended for example to have continuous supply of food. For the most part, we had parts where in our evolution, we’re there was famine, which is now the fate of the Pima Indians in Arizona. They have genes that they’re actually used to about six months of famine. Now there’s 24/7, diabetes is over 90%.
Ari Whitten: Just real quick for anybody unfamiliar with the Pima Indians. They’re studied in obesity and diabetes research circles because they’re among the most obese and diabetic populations. They’re also unique because there’s part of the tribe is in the United States, and part of them remained in Mexico. I think they’re in Arizona, or Texas, or maybe both, and then part on Mexican side of the border, and then historically there was a period where there was a famine and then they were rescued by government rations, US government rations where they send all these processed food to them, and then obesity and diabetes rates just skyrocketed. Whereas the tribes still in Mexico, same genetics but different diet and have very low obesity rates. Anyway, just wanted to quickly add that for anybody unfamiliar with the Pima Indians.
Dr. Ted Achacoso: Yes. Of course, these would be very easy for your listeners. Things that stress out your mitochondria, anything that stresses you out especially your significant other or your work. That’s because it drives up several things, most prominently your cortisol. Your cortisol levels are essentially responsible for driving up your blood glucose levels because you have to fight or flee. Before, the only purpose of that was to either clobber a tiger or run away from it. Now, someone does this to you on the road, and you would get hot under collar and you’re ready to fight.
That will induce the same sort of stress mechanisms. It’s symbolic, but it will induce the same sort of stress mechanisms as if a tiger were about to pounce at you. Since your body needs to process all that glucose and so on, then it will have to [inaudible] your mitochondria. Again, it goes back to, “Hey, we need to provide an energy source for a perceived threat.” We talked beforehand about the cell danger response, which you said. This is actually a part of that whole thing is that while we’re actually wired to do this, to raise blood glucose, to be able to respond to threat and so on. Then, when the threat is gone, we go back to a dynamic equilibrium.
If there is a continuous assault or continuous stress, even for example photo toxicity, continuous assault of blue light even late at night, these are stressors to your system that actually will stress out your mitochondria because your mitochondria will have to always provide the energy for you, not only for the fact that you’re going to stay up late, you’re also going to be dancing and you’re going to be taking some psychotropic agents.
How blue light at night affect your mitochondrial health
Ari Whitten: Just on that point, you mentioned earlier that melatonin is actually a stabilizer of mitochondrial membranes and that links with what you’re just talking about as far as blue light photo toxicity because if you’re every night suppressing melatonin levels, that’s ultimately going to lead to over time. That means your body has produced less melatonin that can get into those mitochondrial membranes and stabilizes, so it’s making your mitochondria. I think it’s not just damaging them directly but it’s also making them more susceptible to damage from other stressors.
Dr. Ted Achacoso: Yes, because you’re going to be inducing the production … Since you’re always under threat, what will you do if you’re always under threat? You will develop mechanisms to detect the threat earlier, earlier and earlier. Look at what we’re doing with our airports. It’s ridiculous now. There’s one shoe bomber and everyone has to take off his shoes. The mitochondria is the same way. It will change its circuitry such that it’s able to detect all of this earlier and earlier for you because as I said, it’s an organism. It will try to protect itself.
How food dyes and prescription drugs affect mitochondrial health
Ari Whitten: What other factors? Is there a role for things like poor gut health or bad gut microbiota, dysbiosis, toxins, heavy metals?
Dr. Ted Achacoso: Yes.
Ari Whitten: Any worth mentioning here?
Dr. Ted Achacoso: Yes. Actually, the whole gamut of lifestyle. If you take a look at for example, let’s just take for example environmental toxins. If your liver is actually always getting poisoned by the blue dye that is in your cotton candy. Aside from the fact that you’re eating cotton candy, I’m going to kill you for doing that, but your liver also needs to detoxify those. In its detoxification, it will need a lot of energy to do that. You’re actually going to be taxed, not only your liver but your entire body because it has to handle the toxin for you.
Ari Whitten: On that note, I remember seeing maybe a year ago or two years ago. I saw a study that was looking at a food coloring dye, commonly in a lot of processed foods, showing it directly destabilizes mitochondrial membranes.
Dr. Ted Achacoso: Yes.
Ari Whitten: I mean, if you’re asking your liver to metabolize this toxin, but it’s at the same time also acting to directly damage and destabilize mitochondria.
Dr. Ted Achacoso: Yes. Historically, there was a drug that was introduced in the United States, 2,3-Dinitrophenol. It’s being sold in the black market that can cause … It’s called an ionophore, so what it does is it pokes a whole in your mitochondrial membrane directly. It pokes a whole in mitochondrial membrane directly and collapses the proton gradient that was available to produce ATP, so everything is produced as heat. When everything is produced as heat, then that person actually loses a lot of body fat because you’re heating up, but it also causes cataracts very rapidly.
Corollary to that, that’s an extreme example. Very simple drugs like metformin for example, which is a very common anti-diabetes drug, will poison complex one of your mitochondria of the mitochondrial oxidative phosphorylative chain. There are various drugs that can inhibit each and every aspect of the electron transport chain which produces the energy for you. In other words, you are fucking up your oven by taking into these drugs.
For example, if you have a patient on metformin that’s given by another physician, I usually ask them to stop after about six months. Withdraw it a little bit, give the body a chance to rest before actually going to do that all over again. Things like this are just beginning to surface in terms of how you do drug therapy because many of the simple things that we thought were safe are actually poisonous to the mitochondria.
Ari Whitten: What about like statins and CoQ10?
Dr. Ted Achacoso: Of course, the production of CoQ10 is mediated by hydroxymethylglutaryl-coenzyme. Anyway, HMG-CoA. It’s an enzyme that actually helps in the production of cholesterol. What they do, each statins do is that it inhibits this enzyme, and in the process you’re actually inhibiting the production of coenzyme A, which are naturally produce. Just as an aside, coenzyme A by the way comes from vitamin B5 or pantothenic acid.
Just in case you’re wondering what the supplementation equivalent is, if you’re going to inhibit that, then your CoQ10 goes down. It drastically, in fact in some patients in two days, they experience muscle weakness and for most patients they could not identify it. They actually get low back pain on the second day of treatment and they go to an orthopedic surgeon. They say, “Well, I now have low back pain,” but it’s actually just due to statin administration.
Now, you can also measure levels of CoQ10. So, when you’re administering statins, you could measure the levels of CoQ10 and supplementation is actually pretty good. There are now targeted forms of CoQ10 that can go inside the mitochondrial membrane directly.
Ari Whitten: Excellent. Any other factors worth mentioning here as far as through the mitochondrial dysfunction?
Dr. Ted Achacoso: Yes. I could mention seven.
Ari Whitten: I’m sure that we could spend three hours on this topic if we all talk about it, but anyway.
Dr. Ted Achacoso: On the general class, first these are your toxins and your drugs. You know that occur. Then of course, there’s your sleep cycles. For example, if you are going to have a disrupted sleep cycle, that will actually have an impact on your energy production and your mitochondrial performance. If you are going to push your mitochondria to produce energy for you to stay up late at night, what do you think that’s going to happen? It’s going to happen to them. You’d be actually forcing them to go on overtime. They will produce more inflammatory molecules for you. Ever notice that if you lack sleep, the next day you’re slightly puffy? You see that there’s actually a mild inflammation that really occurring in your body.
As we mentioned, there’s continuous stress. This is what’s called evolutionary medicine where the cell danger responses, where there’s unmitigating stress. One of the things you could get is get out of a toxic relationship, get into a divorce. I’m kidding. I’m not. Get a handle on how to deal with your boss who’s toxic to you. These are very practical things. When I started to practice, I wasn’t thinking of this, but it has a huge impact on you, meditation practice, etc., and that has actually an impact on what’s called epigenetics. These are the things that switch on your DNA for certain genetic expressions, for certain proteins etc., and that’s where the food that you eat, the exercise that you do, the meditation that you do and so on, actually come in.
Most physicians do not understand for example, the epigenetic pathway of control. So, the big mistake that we did was just jump into the genes right away without taking a look at all the other enomes or omes that are out there. The proteum, the epigenome, the metabolome, and so on, which are more indicative of what’s happening to the organism. The food that you eat can be very stressful. We mentioned about that. For example, if you eat biotin rich foods and stuff, or broccoli, and these things, they actually affect the expression of the genes themselves. This affects the way the nucleus of the somatic cell, communicates with your mitochondria. It says, “We’re all good up here. We’re well-defended. This is how much energy that we need.”
Remember, the currency is always how much energy do you need for what you need to do, and are you in distress? This is always an exchange like, “What’s your status now? What’s your status now? How much do you need? What’s your status? Do we need to kill you?” This is what’s called the greater good agreement. “We agreed to be together in this, so let’s all work together.” That’s where this whole field of epigenetics for example to come in. Then, there’s of course the gut microbiota. If you’re eating badly, if you have a leaky gut. Last year, there was just a paper that was published showing that the gut microbiota and your mitochondria being both bacteria actually talk to each other.
How the microbiome and mitochondria communicate
Ari Whitten: Mm-hmm. Yeah, I’m glad you brought this up because I was going to ask you about it.
Dr. Ted Achacoso: Yeah. That’s why, we know that your diet can alter your gut microbiota directly, and your gut microbiota can actually talk via short chain fatty acids or bile acids signals to your mitochondria and influence their energy production. For example, they can also tell them, “Can you please ramp up your energy production for defense of the intestinal lining because there is an assault that’s coming in here? There’s an imbalance of microbiota. We need you to generate more energy to be able to generate new cells that are actually more protective to the intestinal lining.” The body is cooperative that way, but these are bacteria that are talking to one another.
Ari Whitten: You alluded to this earlier but there can be changes in the microbiome within a matter of a day or even hours. I mean, literally just eating a couple of meals or bad meals and cause a shift in the microbiome, and that’s going to then those bacteria that are now proliferating are going to communicate in certain ways to the microbiota inside of the cells in your body.
Dr. Ted Achacoso: Right.
Ari Whitten: In many ways.
Dr. Ted Achacoso: For example, if the bacteria are too much in distress, and for example they get toxic, you get a leaky gut syndrome for example which is mediated by microRNA. They cleave your intestinal lining. They allow toxins called glyco polysaccharides to get through. These are called endotoxins. They poison your body in an inflammatory way, again. What it does is when it happens, it’s a signal to the mitochondria, “Hey, we need to ramp up a lot of energy for repair.” If you’re not supplying the right energy for repair, you’re giving more refined carbohydrates for example, then more of those gut microbiota that will feed on your refined carbohydrates will proliferate. It’s like a balance jungle in there.
Ari Whitten: On the other note, I’ve seen quite a bit of data from people who have gone long term keto that have done gut microbiome profiles and have ended up with pretty significant dysbiosis in that way too coming from lack of diversity of fibers in the diet.
Dr. Ted Achacoso: Yes, and that’s because you’re supposed to retake this stuff. As again, you do not do chronic exercise forever and ever. You do not eat sugar forever and ever.
Ari Whitten: You don’t fast forever and ever.
Dr. Ted Achacoso: Forever and ever, yes. Ari, this is significant because I have counseled some very important people on the vegetarian diet. I tell them, “If you want to go vegetarian, why don’t you do it for two weeks every three months because it will induce hormetic stress. It’s a good stress for your body. It’s kind of like for your mitochondria to be in a hypoxic environment.” For example, if you’re training at high altitudes, then what happens there is that you generate a lot of more mitochondria because they are temporarily out of oxygen, “Hey, we need more kitchens to actually snag the oxygen from the air,” and you develop more red blood cells too.
These are hormetic or good stressors just like properly executed and timed exercise. The body is not intended to go keto the whole day. For example, me, I do what’s called the mini-ketogenic diet. I’m complete within a day. I fast with 16 hours. My first meal is a ketogenic meal. It’s absolutely no carbs. My second meal is a high fiber carbohydrate diet but the net carbs are still low, but rich in high fiber, and then I do my protein. I step out of it every day. I step out of nutritional ketosis every day.
Again, that cycles for those who’ll be long, and some will do it in a week. They replenish during the weekends, and so on, and so forth. For me, I am a fan of something that you can do, that your listeners can do. It’s like, “Yeah. Why don’t you just eat everything within eight hours and be done with it, if that’s all that you can do.” Then, you’ll induce mitochondrial biogenesis. You have fresh mitochondria. You’re burning fats for fuel, and the reason why you want to burn fats for fuel for the mitochondria as I said is mitochondria is the only organelle that can burn fats for you.
The reason for the MCT craze is that the 8-carbon chain actually can pass through the mitochondrial cell membrane without needing carnitine as a shuttling mechanism. It could just pass through and go through a process called beta oxidation where it’s shelved to produce energy. That’s the reason why these things are currently out there in the market is to feed your mitochondria directly. It’s doing quite a good job. I’m using MCT powder actually, every day. The whole point is that you do not need to be in that state the whole time. For me, complete within the day is my mantra. I live my life that way. I don’t forget. Wherever I am, whichever time zone I am, here’s and here’s my eight hours. This is where I’m going to eat it.
Ari Whitten: Yeah. That’s a great message. Thank you for mentioning that. I want to be sensitive to time here because I know we’ve gone overtime and I appreciate you doing that. Can you just say a few words on maybe the link, and I know this is a big topic, so trying to condense… This is a tough task, but the link between … talking about the role of inflammation and the aging process, the concept of inflammaging, and maybe the role of mitochondria. How mitochondrial health relates to inflammaging?
Dr. Ted Achacoso: Okay.
Top 3 tips to improve mitochondrial health
Ari Whitten: Then actually, the final thing that I’ll ask you to do is just to give maybe your top three tips to improve mitochondrial health.
Dr. Ted Achacoso: Okay. The inflammaging concept or molecular inflammation concept of aging is actually based on the production of reactive species, reactive oxygen species and reactive nitrogen species. You have basically three main sources of the reactive oxygen species. The first one would be your oxidases. These are enzymes that actually use oxygen. There are two major ones of course. The xanthine oxidase and NAD oxidase. Then, the second one is what is called uncoupled eNOS or the endothelial nitric oxide synthase. That’s another pathway that uses lesser known, but actually difficult to synthesize supplement but already available. It uses tetrahydrobiopterin, BH4.
Some of your listeners may have actually heard about that. It’s actually used to stabilize your nitric oxide synthase which is essential. Your cardiologist knows about this. It’s essential of renewing [inaudible] vessels. Then of course, the third source would be of reactive species would be a mitochondria. In your mitochondria, the main sources of the reactive species would be complex one, complex three, complex four, and pyruvate dehydrogenase. Those are the major sources of it.
Your mitochondria has ways of dealing with this. That’s the role of what’s called the superoxide dismutases. What they do is they convert this highly reactive species that can damage you into water. Ultimately water, but first into hydrogen peroxide, and then by various mechanism using glutathione and using catalase enzyme. The one that’s actually scary is when this combine with iron in a thing called the Fenton reaction. We don’t have a way to actually neutralize hydroxyl radicals, but they occur, they’re in bursts. They occur in very sharp bursts and they’re actually used by the body in order to kill viruses.
There’s a use for it, but at the same time if there’s too much of it, then you’re actually going to destroy some of the circuitry inside the cell. If you now have this and you have an overproduction of the reactive species, then they will actually cause a progressive decline. These are called the instigating agents. They will actually cause a progressive decline in cell function by increasing the production of inflammatory molecules.
Now, that is a normal response of the body. Again, if you look at it from an evolutionary point of view, the body will try to fight the stress with its own acute inflammation especially. It’s a natural response of the body to fight for itself and it will. It will bring up transcription factors like NF-kappaB in all of these wonderful transcription factors that will actually raise the inflammation in your body and so on. However, the body also knows how to balance itself. There is a pathway called Nrf2 which will try to quell that whole information. There’s that balance that occurs.
So what happens if you are in a continuous stress? If there’s a continuous production of reactive species is that the Nrf2 pathways unequal to actually keep up with the whole thing. What’s bad about the inflammatory cascade is that it’s self-feeding. The higher the NF-kappaB, the higher the response, the higher NF-kappaB will be produced. That unmitigated will cause your inflammation. Then, that will start attracting of course your classic inflammation pathway, which is like the swelling, redness, and all of the pain, and all of these other things that you would experience in chronic fatigue syndrome, in diabetes, and all of other disease conditions that are there, and they are usually the seed of many of the chronic diseases. That’s what inflammation is all about.
How to exercise for optimal mitochondrial health
Ari Whitten: Yeah. Just go back to something you mentioned earlier about over exercising and chronically exercising every day, activating that Nrf2 mechanism constantly so you never give it a break. You’re constantly stimulating this inflammation of the body and never giving it a chance to recover and reset.
Dr. Ted Achacoso: Yes. You’re not giving the NF-kappaB any rest. So, you’re not giving Nrf2 a chance to actually go undercover. That’s why, say you’re doing resistance training two times a week, would be probably enough. If you’re not the body builder, two to three times a week, or two times a week separated by two days and the rest will be aerobic days is pretty decent. If you’re following HIIT program, especially the 10-minute programs, actually I recommend that you do it at least twice a day, 10 minutes in the morning, or 10 minutes at noon, or some other variant.
Ari Whitten: Twice every day?
Dr. Ted Achacoso: Yeah, twice. I recommend actually twice a day.
Ari Whitten: Okay. Seven days a week?
Dr. Ted Achacoso: You’ve seen the concept. They’re considering exercise as a drug and there’s a minimum exercise dose, and they’re trying to figure out what that dose is.
Ari Whitten: Right.
Dr. Ted Achacoso: They came up with this thing where an aggregate of two minutes and 30 seconds of all out, which is on 30 seconds this burst every two minutes. Yeah, that maybe true for Caucasians, but what about for Asians, and what about for those with different mitochondrial haplotypes? Then, it’s actually very different. For me, I said, “Well, okay. If this is the recommendation, I tend to double it because I think it would have minutes under the curve over this burst every two minutes is insufficient to actually maintain even just good cardiovascular health. I think one of the major criticisms in high intensity training is that at that time, you’re actually using the glycolytic pathway.
Ari Whitten: Mm-hmm.
Dr. Ted Achacoso: So, when you’re using the glycolytic pathway, you’re depriving the mitochondria of oxygen, and when you’re depriving mitochondria of oxygen, you know that it’s a hermetic stress for them and it will induce mitochondrial biogenesis. However, if you do that all the time, then you’re going to kill your mitochondria by not giving them oxygen.
Ari Whitten: Just to be clear, you’re saying two times a day of high intensity interval training at seven days a week?
Dr. Ted Achacoso: Yeah, just 10 minutes.
Ari Whitten: Okay. Seven days a week or some resting?
Dr. Ted Achacoso: No. For me, I just recommend three times week.
Ari Whitten: Three times a week. Okay.
Dr. Ted Achacoso: Yeah, three times a week. Yes.
Ari Whitten: On those three days, you do it two times per day?
Dr. Ted Achacoso: Yes, yes.
Ari Whitten: Okay, got you.
Dr. Ted Achacoso: It’s just my recommendation. If you can’t, just do it once a day. Something is better than nothing, right?
Ari Whitten: Okay.
Dr. Ted Achacoso: If I see a person walking, then that’s good enough, or a really big person trying to run, I stop the person and actually say, “Hey, you know what? Probably you’re better off just walking rather than destroying your [inaudible].” Anything, any movement is better than no movement at all, right?
Ari Whitten: Yeah.
Dr. Ted Achacoso: Again, we’re not intended to go chronic years. Of course, it’s also practical especially for people that they’re with their families on weekends, Saturdays and Sundays. So much of there, of this goes out the window. It’s more practical for them to have control of their time during the week. That’s why that’s my recommendation.
Ari Whitten: Got you.
Dr. Ted Achacoso: It’s come from experience.
Ari Whitten: Okay. Just real quick on the inflammation and NF-kappaB kind of this inflammatory signaling cascade and Nrf2, the cell defense, antioxidant defense system. Hormesis ties into that because hormesis is strengthening some of those antioxidant defense mechanisms. Is that right? Hormesis ties in to the … In a way it can counteract some of the inflammaging process to some extent?
Dr. Ted Achacoso: Yes, because there’s mitochondrial memory. It’s preserved in the molecules that are in the mitochondria. It’s preserve in the DNA of the mitochondria and so on. So, if you have hermetically induced stress, the equivalent is like this. Since the mitochondria have naked DNA, they have no histones. They have nothing. They’re circular and so on. They have to preserve their epigenome via the molecules that are floating around in them and inside themselves. That’s why they mutate there rapidly.
Each time you induce hermetic stress, then that’s where it’s going to affect it. So, the future mitochondria that are created, will actually have that kind of memory in it. It’s more resilient to stress. Whereas in the big epigenetic picture of your body, it is actually stored in the chromatid material or in the material that’s outside of your DNA. That’s where all the changes are made and that’s also heritable. So, we’re just basically mirroring what’s happening to the somatic cell and the mitochondrial cell.
Ari Whitten: Yeah, beautiful. The high intensity interval training exercise stuff is great. I’m wondering if you have maybe two or three more quick tips that you can give to improve mitochondrial health? Also just as a side note to this, I’m wondering if you have any tips or tricks up your sleeve to help people who are locked in cell danger response mode? Have you found anything to be particularly effective in helping people get unstuck from that?
Dr. Ted Achacoso: You mean other than suramin? No, I’m kidding.
Ari Whitten: Other than suramin, yeah.
How to sleep to optimize your mitochondria
Dr. Ted Achacoso: Ari, it’s really very cheap and very simple. A lot of the things about mitochondria can really be addressed by lifestyle, and it’s the most difficult thing to address. My first advice is get adequate sleep because it’s the time that your body’s actually regenerating itself. It’s producing new mitochondria for you. It’s doing all sorts of repair mechanisms for you. It’s preparing you for the next day. I have what I call a sleep anchoring technique, which I tell my patients. I device this. I tell them that your day begins at the time that you sleep. This is a rule that you never forget that sleep is important to you. It’s the first activity that you should pay attention to.
Ari Whitten: Yeah, that’s beautiful. I love that.
Dr. Ted Achacoso: Yeah. We go to it in terms of lifestyle. You go sleep, when you wake up, hydrate yourself. Your body is begging for water in the morning. It has used up a lot of that water. As an aside, we’re talking earlier, there’s a paper that showed that mitochondria actually produces its own deuterium-depleted water for the entire cell to use in order to prevent cancers. That’s just a very new study that came out. Just hydrating, you don’t need to drink deuterium-depleted water, just nice clean water in order to hydrate yourself because you’re 60 to 80% water anyway. Most of you, you are cell membranes, and therefore most of you is fats.
If you take a look at it that way, then you address it immediately, and then you were all yoked to the sun. That’s what we’re forgetting. We have to sun ourselves. Vitamin D is not enough. UVA has its own merits. You’re going to the sun. We are intended to actually go and follow the sun signals. We are what’s called heliotropic organisms. We followed the sun’s signals.
Then, you make sure that you cut down on refined carbohydrates and have a lot more. The fast disappearing macronutrient from the human diet is fiber. So, we need about 34 grams of fiber daily that not only addresses your mitochondria, it also decreases your need for carbohydrates because your net carbs will be lower for you if you eat a lot more fiber. As we talk about earlier, this gut microbiota actually talk to your mitochondria on a bacteria to bacteria basis. If you’re not able to eat well, then at least time you’re eating such that you’re in a narrow time window enough to give your mitochondria a rest.
One of the worst culprits as I said is ingesting too much sugar. I was just looking at a poster lately of some heart association showing pork [inaudible] as a culprit. It was morphing into a wreath. In response, I put a sugar jelly news instead. What about this? The body is intended to use all these sources of fuel, we must train it to adapt to the source of fuel that it needs in order to meet its goals.
If you’re going to be doing a lot of marathoning and you’re a competitive triathlete and so on, and so forth, there should be a timed way to give your carbohydrates. If you’re going to be sitting on your office the whole day, of course it will be calorie-restricted. People think it’s ad libitum, then we could actually give you your majority of your fuel and fats. So, by the thing that you I’m strict about, if you want to optimize your mitochondria while managing your diet, you have to optimize your micronutrients all the time.
Micronutrients are your vitamins, minerals, and cofactors that make not only the cell [inaudible 01:35:22], but on the mitochondria itself. The cofactors that it needs to do its work. You can measure those now, and if you can afford it, go get yourself a measure and then do the proper supplementation for it.
Ari Whitten: Is there any particular test that you recommend for assessing nutrient deficiencies?
Dr. Ted Achacoso: Yeah. Right now, there’s a urine metabolites from Genova, for example. I use that. It’s not expensive, and you don’t have to draw blood. We can just take a look at urine and so on, but if you want to take a look at amino acid components, etc., then you have to draw blood. The other thing that you can do for yourself is test for your food sensitivities because those can throw off reactive oxygen species or reactive nitrogen species when they cause inflammation. When these cause inflammation, of course you’re increasing the molecular intermediates of inflammation. Your body has to deal with that. Then, if you cannot deal with that, then your aging goes faster.
Ari Whitten: The elimination diet is your preferred …
Dr. Ted Achacoso: Yes, but you know what? What I do? As I said, something that the patient can understand quickly. What I do is just I remove everything that they’re sensitive to for six months. Then, reintroduce it one month at a time, and then introduce it once every week, and then minimum distance of one to four days. It’s so fucking difficult to do elimination diets. I just say, “Eliminate everything for six months,” because your gut microbiota is going to change at that time. That’s what people who do elimination diets in a very strict fashion fail to understand that the food is preprocessed by the gut bacteria and gut bacteria is going to change dynamically every day. So, there is no point in actually controlling, just remove everything. What is easy for your patient? Do you want your patient to do something, or you’re trying to do something or not? Make him do something that he can remember, right?
Ari Whitten: Yeah.
Remove toxic environments and relationships from your life
Dr. Ted Achacoso: Then, of course my final piece of advice. Aside from eating, and exercising properly, and moving well, move properly, is to love well. Meaning, get rid of your toxic relationships. Get rid of toxic bosses or let your toxic bosses get rid of you. Find something where your stress is actually lower, not that low because you need hermetic stress. You need to be pushed every now and then. As I said, we’re not intended to be in full parasympathetic mode all the time, and we’re not intended to be in full sympathetic mode all the time. Unfortunately, this world, this environment that we are created, pushes us into full sympathetic mode all the time like your texts need to be answered right away.
If you develop healthy lifestyles controlling your time, and I’m talking about relationships here because it’s your relationships to your devices. It’s your relationships with your devices. You have to develop healthy relationships with your devices. Not even with the people that are messaging you from there, but how you deal with your devices. When do you pick them up, and when do you actually keep them away from you. These are the kinds of things that will actually make your energy production more even, because then the brain is saying, “Okay. We’re in good shape here,” and the mitochondria will say, “Okay, we’re not being forced to produce more energy and therefore, we’re not going to produce more of those reactive species that might destroy you.”
Ari Whitten: Yeah, beautiful. I love that. It’s such a great way to end. Love well, perfect way to end. Dr. Ted, this has been an absolute pleasure and an honor to do this with you. I’ve been looking forward to this for a really long time, and thank you a million times over for spending all of this extra time. This is like double the length of a normal podcast episode, but there were just so much I wanted to talk to you about. So thank you, thank you, thank you for spending all this extra time with me. I really appreciate it and honored.
Dr. Ted Achacoso: You’re welcome. I really wanted to do this podcast and I know Ari … For those who don’t know this, Ari has been trying to catch me since a long time, and I was in Asia. I really owe him this time. I hope I did justice for you.
Ari Whitten: Oh, definitely. This has been amazing. On a final note, speaking all your travel, you have a tri-continental medical practice.
Dr. Ted Achacoso: Yes.
Ari Whitten: For everyone listening who hopefully is amazed with everything that you just explained on this podcast, who might be interested in working with you and your anti-aging nutritional medicine practice, how can people reach you and get in contact with you?
Dr. Ted Achacoso: I started a nonprofit here in the US called healthoptimizationmedicine.org. You can go look us up. It is just a simple website right now. All of the physicians and health practitioners, nonphysician health practitioners who are interested in practicing the way I do, which is detecting and correcting subtle toxicities and borderline deficiencies in the metabolome. That’s where we all go, so you can reach me from there. You can also reach in Asia. I’m there 30 days every quarter. You can reach me at biobalanceinstitute.com, and that’s based in the Philippines, and very happy to actually announce here that the first comprehensive metabolomics laboratory in Southeast Asia, which I pushed for building four years ago is now going commercial this June.
Ari Whitten: Awesome.
Dr. Ted Achacoso: Yes. Now, more problems for physicians who don’t like to learn their Krebs cycle all over again.
Ari Whitten: Dr. Ted, just like I said, it’s just been an absolute pleasure and an honor to do this with you. Thank you, so, so much for taking all these time to do this. I know my audience is going to love this. Thank you.
Dr. Ted Achacoso: Thank you.
Ari Whitten: Have a wonderful rest of your day.
How To Optimize Your Mitochondria To Beat Fatigue and Live to 100 with Dr. Ted Achacoso – Show Notes
What bioenergetics is and how it relates to mitochondria (6:47)
Why you should always view your mitochondria and cell nucleus as two separate organisms (25:32)
Why it is important to talk about mitochondria (30:25)
How environment affect mitochondrial health (34:18)
The main driver of aging (43:19)
How you can slow down aging (48:18)
How overtraining damages mitochondria (55:51)
How blue light at night affect your mitochondrial health (1:01:36)
How food dyes and prescription drugs affect mitochondrial health (1:02:35)
How the microbiome and mitochondria communicate (1:11:56)
Top 3 tips to improve mitochondrial health (1:18:18)
How to exercise for optimal mitochondrial health (1:23:15)
How to sleep to optimize your mitochondria (1:29:35)
Remove toxic environments and relationships from your life (1:36:22)