The Wound Is the Product

Victimhood is the highest-paying content on the internet. The system rewards it, the reward selects for it, and most of the people participating in the process have no idea it is happening. Including, on plenty of days, me.Somewhere in the last fifteen years, being wronged became a business model. Not simply a feeling or a misfortune, but a reliable way to generate attention, loyalty, and revenue. If you want reach on any platform that matters, one of the most reliable ways to get it is to show an audience that someone has done you harm and that you are bearing it with dignity. That post will travel farther than your best argument, raise more money than your best work, and bind followers to you more tightly than almost anything you could accomplish by simply being right. The wound outperforms the insight.This is not a moral failing in the people it happens to. It is the result of incentives built into the system.I want to take this apart carefully, because the easy version gets it wrong.The easy version says that people who play the victim are frauds working a grift. A few are. Most are not. Most believe every word, and that is the most interesting part of the story.Most people are not sitting around plotting how to become professional victims. They are doing what all of us do. They post something, watch what happens, and learn from the response. The posts that get attention get repeated. The posts that disappear do not. After enough repetitions, the process starts selecting for itself.Nobody has to decide to run the play. The incentives do most of the work.Breaking Through the FloorTo understand why grievance is so powerful, you have to start with a simple reality. The internet does not distribute attention evenly, or anything close to it. A tiny number of accounts receive most of it while everyone else receives almost none. Much of what gets posted, including thoughtful and accurate work, is seen by very few people and disappears without a trace.For anyone trying to be heard online, that is the central fact. The hard problem is not producing good content. The internet is already full of good content. The hard problem is getting noticed at all. Most people who try never manage it.So ask what actually breaks an unknown account through.It is usually not careful analysis. Careful analysis fills the internet already. What breaks through is emotional and moral charge, and one of the most potent forms of that charge is grievance.The people who study how messages spread online have a technical term for this. They call it moral-emotional contagion. Words carrying both moral and emotional weight are shared far more often than ordinary language, with each additional moral-emotional word measurably increasing a post’s reach (Brady et al. 2017).Grievance is built almost entirely from those ingredients. Outrage. Betrayal. Courage. Harm.The important point is not that grievance performs slightly better than a calm post. The important point is that grievance is one of the few things that reliably gives an unknown person a chance to be noticed at all.This explains something that otherwise looks like an indictment of human nature: nearly every successful influencer appears to run on the same fuel.But we only see the people who made it through.Most thoughtful and fair-minded people never break through at all. Their work receives little attention, they eventually stop posting, and they disappear from view. The mistake of studying only the winners while ignoring the much larger number who vanished has a name: survivorship bias.When you look at successful influencers and notice that many rely on grievance, you are not necessarily learning something dark about the people who become influencers. You are observing a selection process. The people who broke through often did so because grievance worked.There is a specific mechanism behind it.To break through, a small account often has to borrow a larger account’s audience. Grievance is one of the most effective tools for doing that. You identify someone bigger than you and argue that they have harmed you, or harmed the people watching. The accused, or the people who rush to defend them, respond. That response carries your name into an audience you could never have reached on your own.In my own social media universe, I have watched this dynamic play out again and again.Over the years, I have been called everything from a mass murderer for my role in early mRNA technology development to a government operative, a pharmaceutical shill, and now, apparently, a DARPA and  CIA propagandist (despite the fact that I have worked for neither organization).Just yesterday, Dr. Jack Kruse launched another attack, built on demonstrably false claims. But the specifics are almost beside the point.If Jill and I sat down and made a list, we could probably name dozens of individuals who have built substantial audiences around the claims that I personally wronged them or their audience, deceived them, betrayed them, or somehow stand at the center of whatever problem they are trying to explain. Some individuals have written hundreds, even thousands, of posts about me across Substack and X. Some are still at it today.The interesting question is not whether they are right. They aren’t.The interesting question is why this pattern keeps repeating.The answer is that grievance works.A public feud is audience acquisition. A villain is a growth strategy. The larger and more visible the target, the greater the opportunity. The truth is that responding is counterproductive because every response expands the reach of the attack.In fact, by mentioning Dr. Kruse here, I am probably helping him gain followers. That is simply how the system operates.He is not unique. He is merely the latest example to cross my path. One in a long line of attackers.Malone News is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber.Conflict becomes the distribution mechanism.This is why challenging powerful people is often such an effective way to grow an audience. It may or may not be morally justified, but it also works as a form of distribution. The larger the target, the larger the audience available through the resulting conflict.The same research I cite below found that signals of victimhood also make audiences more willing to view the accused as fair game. In market terms, that is an additional advantage for the person making the claim.I know this territory because I have stood on both sides of it.At the end of 2021, within days of each other, Twitter and LinkedIn both acted against me. Twitter removed more than half a million followers in an afternoon. LinkedIn made its ban permanent, and LinkedIn was not a vanity platform. It was a primary channel through which I found consulting clients and maintained a professional reputation built on credentials, scientific work, and experience rather than grievance. That door closed for good.Days later, I sat down with Joe Rogan for what became the most-watched conversation of my life.I am not going to claim with certainty that the platforms coordinated their actions, although Congressional evidence suggests that the Biden administration had a hand in what happened. I cannot prove that, and I do not need to. What matters is the result.One professional channel was effectively destroyed. The grievance channel that emerged in its place reached a much larger audience.I had started this Substack a few weeks earlier, so the new path was already there. The bans simply slammed one door shut and threw the other one wide open.At the time, I said publicly that the bans meant I was over the target. I believed that, and there was truth in it. There is another truth as well.The censorship was real. The injury was real.It was also the largest single breakthrough in reach and audience growth I have ever experienced on Substack.The suppression was a real injury and a real act of censorship. It was also the largest breakthrough of my life. The wound became the launch, not the setback.When the Old Controls BackfireThere is a larger point hidden in my own experience, and it took me a while to see it.For most of the last century, the people who could injure you and the people who controlled access to an audience were often the same people, or closely aligned. Suppression worked because once they silenced you, there was nowhere else for the audience to go.That is no longer true.The thing that can injure you and the thing that distributes you are now different systems. In many cases, the distribution system rewards the conflict created by the first.As a result, the old tools of narrative control have not merely weakened. In many cases, they have reversed.A categorical official denial, the flat declaration that “this is false,” was designed for a world in which the institution controlled distribution. Today it often accomplishes the opposite. It signals that the topic is worth discussing, gives the target a fresh grievance to distribute, and exposes the target to the institution’s own audience through the ensuing conflict.The denial no longer closes the question. It often amplifies it.An institution still relying on the historic approach to narrative suppression in 2026 (posting statements like “Total BS”, for example) is not demonstrating control. It is demonstrating that it no longer understands the environment in which it operates.Before anyone on my side of these debates celebrates, however, the same dynamic applies to manufactured grievances. The medium does not distinguish between truth and falsehood. It rewards whatever travels.A real injury and a manufactured one spread through the system in much the same way. Both are amplified by the same mechanisms.How Grievance Becomes PowerOnce you break through, the wound continues to pay in ways that go beyond reach.The first was identified by a team of researchers led by Ekin Ok, who described what they called the virtuous victim signal (Ok et al. 2021). It occurs when a claim of injury is paired with a claim of moral goodness.“I was harmed, and I was harmed because I am one of the good people.”That combination attracts sympathy, money, trust, and deference.The second payoff receives less attention. The wound becomes armor.Criticizing a self-declared victim is costly because it looks like attacking someone who is already down. Most people avoid doing it. Those who do often create a fresh grievance for the next news cycle.The signal becomes self-reinforcing.It attracts attention, generates resources, and shields the sender from many of the normal costs of being wrong.Now follow the money, because all of these benefits eventually become revenue.Reach becomes subscriptions, donations, advertising revenue, speaking fees, and book sales. The audience built around a victim narrative is one of the most durable revenue streams available, more durable than shared beliefs and often more durable than entertainment, because followers no longer see themselves as customers. They see themselves as participants in a struggle.People who think they are helping defend a persecuted truth-teller are remarkably loyal.A subscriber who believes he is helping sustain a persecuted truth-teller is likely to remain subscribed.Grievance is not adjacent to the business model. It is the business model.You can watch it operate in plain sight, where a paragraph about censorship or defamation may sit directly above a button asking readers to become paid subscribers.That juxtaposition is not hypocrisy.It is the design.Nobody has to Plan ItThis is where the ugly version of the story falls apart.When a behavior pays this well, nobody has to plan it. This is operant conditioning, the basic principle that governs the behavior of any animal with a nervous system. You do more of what gets rewarded and less of what does not, and you do not need a theory to explain why.A creator posts twenty things in a month. Five succeed, and fifteen disappear. He has no explanation. He simply notices the response to the five and the silence surrounding the fifteen. Over time, his output drifts toward whatever gets rewarded.He never consciously decided to become a grievance entrepreneur. He simply learned what worked.That is why people can tell you, with complete sincerity, that they would never stoop to playing the victim and still be telling the truth as they understand it.I have said it myself more than once. Be a lion, not a victim.I meant it when I wrote it, and I mean it now.Yet the pattern still appears sometimes in my own feed because the part of us that consciously decides what we believe is not always the same part that responds to rewards. My disavowal is not evidence against the system. It is evidence of how the system works.Victimhood as a MindsetPsychologists have measured a more durable version of this as a personality trait (Gabay et al. 2020). Some people consistently experience the world as a place where they are being wronged. The pattern has recognizable features: a strong desire for their suffering to be acknowledged, a belief that they occupy the moral high ground, a tendency to revisit old injuries long after the fact, and an asymmetry in which their own pain remains vivid, while the pain of others fades into the background.The most revealing finding is that the filter tends to operate in only one direction. Present an ambiguous situation, and these individuals reliably assume the worst interpretation rather than the best.Most influencers are nowhere near the extreme end of that spectrum, and they do not need to be. Modern platforms make it easy to adopt the mindset without fully inhabiting it. The incentives encourage people to interpret events through the lens of grievance because grievance performs.There is also a status component. Researchers who study public moral conflict describe what they call moral grandstanding (Grubbs et al. 2019), the use of moral language primarily to elevate one’s own status rather than to resolve a disagreement.It generally takes two forms.One seeks admiration: the courageous truth-teller who paid a personal price.The other seeks dominance: shaming opponents until they retreat.Much grievance content contains elements of both.Since everyone assumes this is the vice of the other side, it is worth noting that the research found little relationship between political affiliation and the tendency to engage in this behavior. The incentives operate across the political spectrum.When Grievance Becomes PowerFor most influencers, grievance converts into attention and money.For politicians, it converts into attention, money, and power.A loyal grievance-based audience is simultaneously a donor list, a voter base, and protection against potential challengers. The same dynamic is operating. The stakes are simply higher.Look across the political landscape and the ideological differences largely disappear.Marjorie Taylor Greene built a powerful small-dollar fundraising operation and left Congress with a public narrative centered on betrayal and mistreatment.Alexandria Ocasio-Cortez built an almost entirely people-funded operation and produced some of the most prominent personal-victim narratives of the January 6 era.Kari Lake carried a stolen-election narrative through repeated defeats and never abandoned it.These politicians do not share an ideology or a constituency. What they share is a common set of incentives.The most useful example, however, is the politician who had one of the strongest claims to victimhood and largely refused to use it.Thomas Massie endured the most expensive House primary challenge in history while being personally targeted by the President of the United States. Yet his public message remained focused on constitutional questions and fiscal realities rather than on his own grievances.He lost.  Because grievances convert into votes.  Issues and logical debate often do not.But he demonstrated something important.Genuine victimization does not require victim-signaling.The signal is a choice the system rewards. It is not something the situation forces upon you.Our own side is not exempt from any of this, and pretending otherwise would make this essay worthless.Bobby Kennedy was, in demonstrable fact, deplatformed and savaged in print for years, and his grievances have real foundations under them, the same as mine do. That is exactly why the machine works on (and for) him, and on the movement around him. A real wound is the honest raw material the signal is built from - but an entire ecosystem has been built around those grievances. The question is never whether the injury happened. Mostly it did. The question is what gets built on top of it, and how much of what gets built is the system quietly paying us to keep the wound open.That is precisely why the dynamic works.A real injury is often the raw material from which the signal is built.The question is not whether the injury happened. Much of the time it did.The question is what gets built on top of it, and how much of that construction is being quietly rewarded by the system.This article is public. If you found it useful, share it widely. The incentives described here do not belong to the left or the right. They belong to all of us, which is precisely why they are worth discussing.ShareThe Cost of SuccessThis brings me to the part that should make all of us uncomfortable.The problem does not disappear once you build an audience. It gets worse.Moving from ten thousand followers to one hundred thousand, and from one hundred thousand to a million, is often the same challenge repeated at a larger scale. The audience that initial grievance assembled around must continue to receive grievance if it is going to remain engaged.The incentive does not weaken. It strengthens.And underneath it sits the ugliest fact in the entire arrangement.An audience that pays to support a persecuted truth-teller has a vested interest in the persecution continuing.Not because anyone planned it. Not because anyone wants it. But because that is how the relationship was formed.The audience gathered around the wound.The result is a subtle but powerful incentive structure. It rewards the person who discovers a new outrage every week more than the person who solves a problem and reports that it has been solved.You can see this dynamic across the political spectrum. Once an influencer reaches a certain scale, the challenge is no longer attracting an audience. It is maintaining one.Consider what happened after Candace Owens leftThe Daily Wire. Whether her claims about Charlie Kirk, his wife Erika, Brigitte Macron, or anyone else were true is not the point. The point is that the audience's incentive increasingly favored conflict itself. Every new feud generated attention, engagement, discussion, reaction videos, rebuttals, and fresh content for supporters and critics alike. The conflicts became self-sustaining.That is not unique to Candace Owens. It is simply a highly visible example of a broader phenomenon. Once a large audience has been assembled around controversy and opposition, the pressure to find the next controversy never entirely goes away.The audience gathered around the conflict. The conflict becomes part of the product.That incentive quietly rewards the person who finds a new outrage every week over the person who solves a problem and reports that it is solved.Solutions end stories.Grievances extend them.Once you see that dynamic in your own feed, it becomes difficult to ignore.One of the most striking examples emerged during COVID. Entire audiences formed around resistance to lockdowns, mandates, censorship, and official public health messaging. Many of those grievances were legitimate. That is not the point.The point is that once those audiences existed, they became economic assets.Media outlets, publishers, advocacy organizations, conferences, subscription platforms, supplement companies, telemedicine services, and alternative healthcare businesses all emerged to serve them. A large audience of people who believed institutions had failed them became a market. Some organizations sold information. Some sold memberships. Some sold products. Some sold treatments intended to protect against the very threats that had helped build the audience in the first place.None of this required a conspiracy. It is simply what markets do. Audiences attract entrepreneurs. Demand attracts supply.The uncomfortable part is that the incentives do not disappear once the crisis passes. An audience assembled around institutional failure, censorship, corruption, persecution, or the corruption of big pharma must continue to hear about the same issues if it is to remain engaged. So now, the company formed to sell ivermectin against COVID-19 has become the company selling ivermectin asan antiparasitic to restore gut balance and vitality. Hint: As a pathologist, I have examined thousands of human biological samples from Americans under the microscope. Generally speaking, parasites are not a significant problem in the United States, despite the attention they often receive on social media. And yes, when I read such claims from our side, it makes my skin crawl.The institutional side operates according to the same logic. Pharmaceutical advertising influences legacy media. Government agencies defend their budgets and authorities. Public health organizations protect their reputations. The fear product I describe in the book we are currently writing called “The Grift” was monetized by institutions in much the same way grievance is monetized by their critics.Different products.Different customers.Similar incentives.An analysis that recognizes only one side of that equation is not an analysis. It is advocacy.The Way OutThere is an easy way out of this argument, and it is also the wrong one.“The system made me do it.”That is the easy escape, and it is really just another version of the victim’s argument wearing a lab coat: the system made me do it, so go look somewhere else.The system selects for behavior. It does not force it. People can recognize the incentives and choose differently. In fact, one of the simplest ways to tell who is sincere and who is merely working the incentives is to explain the mechanism and watch the reaction.Sincere people usually become uncomfortable. They look at their own feed, their own behavior, and the incentives acting on them. The operators become defensive. For them, the grievance is no longer just a belief or a habit. Grievance has become an asset, and you have just questioned its value and moral integrity.This is also why the burden now falls on the audience.The old information order had external checks. Editors, producers, publishers, and gatekeepers could suppress a claim, whether true or false. They often abused that power, but it existed. Today, most of those checks are gone. There are no guardrails to prevent a grievance from spreading, whether it is legitimate or fabricated.That leaves only one remaining check: your own judgment.So how do you tell when a legitimate grievance has crossed over into something else?First, ask whether the injury was real. Most of the injuries discussed in this essay were real. Mine were. Bobby Kennedy’s were. Many others were as well. But some aren’t. That is the first test.Next, the question to ask is whether the grievance remains tethered to reality, or whether it has become a self-sealing narrative.One of the warning signs is that nothing is allowed to count as evidence against it.If people attack you, that proves you are over the target.If they ignore you, that proves they cannot answer you.If the prediction fails, then they must have changed their plans because you exposed them.Every outcome becomes evidence for the same conclusion.At that point, the grievance is no longer being tested against reality. It is being protected from reality.That is the moment to be careful.A real injury does not require a permanent story built around it. A true claim should remain vulnerable to contradictory evidence. It should be possible to imagine what would change your mind.When you can no longer answer that question, something important has changed. The injury may still be real, but the narrative built on top of it has taken on a life of its own.That is when the incentives begin doing some of the thinking for you.I have caught myself doing exactly that more than once while publicly insisting that I would not. I am not offering that observation as a gesture of humility. I am offering it because it may be the most useful fact in this entire essay.If this pattern can operate in someone who is aware of it, has publicly rejected it and sincerely meant the rejection, it can operate in anyone.Most of us have been wronged in real ways. That is not the question.The question is whether what we build on top of those injuries is true, and whether we would still say it, if saying it cost us the audience.Marshall McLuhan once famously observed that the medium is the message.In the decentralized media environment of 2026, one can observe a similar dynamic.The wound is the product.If essays like this are worth having, they are worth supporting. Malone News is funded by readers, not advertisers, corporations, political parties, or government grants. If you would like to help keep it that way, please consider becoming a paid subscriber.ReferencesBrady, William J., Julian A. Wills, John T. Jost, Joshua A. Tucker, and Jay J. Van Bavel. 2017. “Emotion Shapes the Diffusion of Moralized Content in Social Networks.”Proceedings of the National Academy of Sciences114 (28): 7313–7318.Gabay, Rahav, Boaz Hameiri, Tammy Rubel-Lifschitz, and Arie Nadler. 2020. “The Tendency for Interpersonal Victimhood: The Personality Construct and Its Consequences.”Personality and Individual Differences165: 110134.Grubbs, Joshua B., Brandon Warmke, Justin Tosi, A. Shanti James, and W. Keith Campbell. 2019. “Moral Grandstanding in Public Discourse: Status-Seeking Motives as a Potential Explanatory Mechanism in Predicting Conflict.”PLoS ONE14 (10): e0223749.Ok, Ekin, Yi Qian, Brendan Strejcek, and Karl Aquino. 2021. “Signaling Virtuous Victimhood as Indicators of Dark Triad Personalities.”Journal of Personality and Social Psychology120 (6): 1634–1661.

Summary: The highest paying content on the web is victimhood


Oxygen, Mitochondria, ATP and Origins of Cancer (Riordan Clinic)
YouTube video by Dr. Frank Shallenberger (https://www.youtube.com/watch?v=85EPbiABqJs). Transcript is the auto-caption track — verbatim ASR, not a certified transcript.

There's this uh great truth in life that everything happens for a reason even though at the time that it happens you don't know why it's happening. And what indeed may seem as a misfortune down the road may be one of the best things that could have ever happened to you. And there's been a few occasions in previous symposiums where I thought we were suffering a great misfortune when Dr. Schallenberger through one reason or another could not make it, but at this moment I understand now, my eyes are opened that this is the reason he couldn't make it at the other two symposiums because his timing right now even even this symposium uh there was a difference in the schedule that seemed like a adverse event that now I do understand that because he's speaking at this moment in this symposium which I think has just been outstanding I think this will be the true icing on the cake. I don't want to throw too much glucose in here, but uh but I do really think that Dr. Schallenberger who is the president of the American Academy of Ozone Therapy and who really was the reason why my thinking kind of moved in this direction because it's always been of profound interest to me that uh high dose vitamin C or vitamin C the what I I used to call the bioxidant paradox, it's really not a paradox at all but it's the it's the pro-oxidant effect of vitamin C that's so hard for conventional doctors to understand and and for Frank the the pro-oxidant thing I think is just second nature to him. So it's really nice to have Dr. Dr. Frank Schallenberger here to talk about oxygen, mitochondria, ATP, and the origins of cancer. Will you welcome Good morning. It's a real pleasure to be here. I'm honored. Thank you. It's a fantastic lineup you have and I'm certainly honored to be in the presence of um of you all. Uh I want wanted just to have a little show of hands before I get going here. How many of you all treat patients with cancer? God bless you. Do you realize that uh if uh if if we if we were successful with advanced cancer as the West Africans were with Ebola, it'd be a really good thing. So, I know we all know humility. Yeah. Okay, so that's not unusual, is it? That's too bad cuz uh you know, when I first got into treating patients with cancer, boy, I had to go back to school. It's really something. So, I applaud you all for for being here and uh for your interest in this work and for helping patients and putting yourself in difficult situations that uh be be a lot nicer to be a dermatologist giving out hydrocortisone cream all day, I think. In many ways. Okay, uh uh one one more question. How many of you all in here use ozone therapy? I know some of you. Wow. That's fantastic. Uh uh so, what what I hope to do today is um is to uh enlighten um most of you that don't know much about ozone. So, and then those those of you who do use ozone, uh, hopefully I'll give you some more tidbits of information. I do, um, we do have a American Academy of Ozone Therapy. And the next meeting, uh, is going to be, uh, the weekend after Valentine's Day in Dallas. So, I'll promote that to you. That's a going to be a great way for you to learn a lot more to do with your ozone treatments. Um, also, uh, we, uh, do offer trainings in ozone therapy. So, for anybody that, uh, wants to know this, you've heard this lecture and you think you might want to know this, just keep that in mind. You can contact me about that. Um, I have a dictum that I sort of came up with about oh, maybe 15 years ago, and it was the best treatment for any disease is not to get it. So, as I'm going through this, uh, and I think we can really put cancer in that, uh, in that in that, uh, definition. Uh, as I'm going through these slides, I want you to really think about preventing cancer. Cuz the treatment of it is so darn difficult, and as the last speaker pointed out, it's so darn expensive. And, uh, wouldn't it be nice if you just didn't get it anymore? So, uh, as we talk about the origins of cancer, it's good to think about what we can do with our patients who don't actually have cancer to prevent them from getting it. Okay, with that said, let's see what Okay. Okay, yeah, okay. So, um, some interesting facts about mitochondria. Uh, you know, just about 40% of your cells are made up of mitochondria. Just almost half the mass of your cells, uh, is made is are mitochondria. Do you think they're kind of important? There's a lot of them in there. Um, there about uh million billion mitochondria in an adult uh uh adult human. That's getting pretty close to the national debt. That's a lot. Um, yeah, mitochondria aren't static. They move, they change, they grow, they die, they live, they divide, they multiply. So, if your mitochondria are in in a pitiful state right now, they can be in a really good state in 3 months. Likewise, if your mitochondria are in a really good state right now, they can be in a pitiful state in 3 months. They change, they move. And so, keep that in mind. They Of course, you know, they divide. So, they actually have their own genetics, they have their own DNA. You get your mitochondrial DNA from your mother. If you want to have kind of an idea of what sort of cards you've been dealt, you can look at the maternal side of your family. And somebody down in that on that side lived to be 95 and never got cancer and had their wits about them. Like, I had a patient come in the other day, and I was doing my family history, and I said, "How How about your parents?" She said, "Well, my mother died when she was 105." I said, "What she die of?" She said, "She fell off the roof." So, if you guys are that old, I'd stay Um, oh, this is interesting. And you were mentioning this about thyroid. How important is thyroid? I'll tell you, the the more I get into this field that we call practicing medicine, which means you practice what you think you're doing, um, the more I'm thinking about thyroid. I I measure mitochondrial function in all my patients, every single one of them. I've been doing it for almost 15 years. Uh, I use an oxygen uptake type of assessment to do that. When you do that in a resting state, what do you get? You get basal metabolic rate. What does thyroid do? Controls basal metabolic rate. In the old days, before we had these ridiculous things they called thyroid blood tests, which were absolutely useless, um they used to determine if you needed thyroid based upon your your metabolic uh rate. Cuz your metabolic rate's low, since thyroid controls metabolic rate, something's wrong there, right? Okay. You know how many patients I've seen with normal metabolic rates that have cancer of any kind, even your basic lumpectomy? Zero. None. You know how many patients or how many people, period, over the age of 50 that have normal metabolic rates? Probably maybe 10%. There's almost nobody in this room that doesn't need thyroid. And particularly uh T3, because uh the number of mitochondria you have in your cells is literally controlled by T3 in a Uh there it is. There's a sort of a demonstration of it, and you've got these uh uncoupling proteins in here, and fatty acids going through here, and I'm not going to get into all this. Thank god. Okay. Uh but that's your basic mitochondria. They're the complexes through here, and protons are being pumped out here, and then the protons got to come back in here, and they either come back in here and make ATP, or they come back in through here to release the pressure, and guess what controls UPC3? Thyroid. The whole metabolic way your system works. If you think mitochondria important, think thyroid. Thyroid's really important. I don't think there's a patient you're going to treat with cancer of any kind that doesn't need thyroid replacement, some kind. And iodine. Okay. All right. So, what's the most important nutrient you can take in your body? Is it vitamin C? No, you can be without vitamin C for about 5 minutes, right? So, what's the most important? It's obvious. Okay, but it it this this nutrient called oxygen is no different than any other nutrient. It's not what you take in that's important. You have a normal oxygen level in your blood, who cares? It's what are you doing with it? Because oxygen only has one purpose. It only has one thing it does in body, which I find to be very interesting. See, vitamin C and vitamin B and so forth have a multiplicity of things they do. Oxygen only has one thing it does. For all intents and purposes. And that's it gets converted into energy through the electron transport chain. That's kind of fascinating. So, it only does one thing. So, just because you have a decent level of oxygen in your blood and your O2 sat's fine, does that mean that you're utilizing oxygen properly? Not at all. I'm here to tell you most people aren't utilizing oxygen properly and I'm going to make a point that that is the fundamental cause of cancer. I'm going to show you two very interesting papers that I hope you'll go ahead and read. They're going to tend to back up my point. So, I'm going to use this term called oxygen utilization. Um that would be synonymous with another term called aerobic capacity. But, it's your body's ability to metabolize oxygen. Either you can metabolize it well, you don't metabolize it so well. Significant difference between you now and when you were 20 and you were in when you were 70 is not that your cells don't work. I mean, the cellular function is maintained. Did you know that? You take a senescent animal, the cellular ability for the cells to actually synthesize protein, multiply, divide, do all that kind of stuff cells do, it's pretty much intact in a senescent animal. The thing that's not intact is the electron transport system. So, what we become as we get older is we become like really good flashlights with batteries that are fading. You throw in some new batteries. What do So, the key to the treatment and the prevention of disease, in my opinion, I'm going to make the case and for cancer, by the way, is oxygen utilization. So, think of this, every single one of your patients that come in with cancer or any other disease that's chronic for that matter are suffering from a deficiency of oxygen utilization. They maybe have enough oxygen, maybe they don't, but either way, they can't utilize what they have. What's the likelihood you're going to help that patient if you don't improve that? It's really diminished. And so, we need to think about this. When every single patient who walks in your office, you need to ask yourself the question, are they using oxygen efficiently? Uh because they need a lot of energy to get well. If it takes a certain amount of energy to be well and maintain your health, how much more does it take to Uh here's here's sort of the general concept uh of oxygen utilization. So, here's here's your cell and here's one of the here's one of the uh thousands of mitochondria that are in the cell. And when I was in medical school, they said, "You know what? You got some oxygen, you're cool." We can go to the next slide. Actually, that's a little bit more complex than that. Because in order for that oxygen to get into that mitochondria, you got to have some lungs. You got to have lungs that work pretty well. What what happens to your lungs as you get older, by the way? Your FVC, your functional capacity, does it go up or down? It goes actually down. It's uh decreasing lung capacity is a hallmark of aging. Um you got to have a heart pumping it out. So, as you get older, do you get in great better cardiovascular fitness or worse? And then you have to have a circulation. So, undoubtedly, as you get older, your circulation gets better, right? Your endothelial function improves, and you don't get any atherosclerosis, and there's no fibrinogen activity, and everything's really cool, right? So, these are some problems. These are some problems. Just because your O2 sat looks pretty good, doesn't mean anything's getting in here. Uh okay, so now you got fat on your body. So, you got to mobilize that fat, move it down to the cells for uh metabolism. As people get older, they No, what what what what's happening with that fat? How come they're not burning that fat? What I'm telling you is it's not going from here to here, okay? And finally, get glucose. So, uh you know, as as you get older, do you do your body get more responsive to glucose? Does your insulin reception Does your insulin sensitivity improve? One of the earliest The speaker just last time he he mentioned a little bit about the ketogenic diet, and uh we're going to I'm going to show you some information on that. It's absolutely fascinating how the how insulin resistance is absolutely tied to the genesis of cancer. And why? Because of this axis right in here. You need to get these three players in here. Now, once you get those players in there, through this process that I'm going to call oxygen utilization, it's basically electron transport system, you make energy, and everybody's happy. It uses that energy to put the cells to do what they need to do. Uh part of that energy is used to uh promote apoptosis. Okay? If you don't have enough energy, you can't promote apoptosis. You're going to select out cancer cells, okay? We'll We'll talk about that more. But But this oxygen can It does two things. One, it forms free radicals, which are good, by the way. They're not bad. If you didn't have free radicals in your cells right now, you'd be dead in a couple of minutes. You need them. Uh but here's here's the problem. If you don't if there's something messed up with this, this is where the oxygen goes. And so, you get an excessive amount of the bad guys and not enough of the good guys, and that's not a battle you're going to win. Uh then there's some other things that that are in interest here. Probably won't talk too much about them, but there's there's little buddy T3 right in there. Okay, so that's the sort of the general setup. Uh oxygen utilization, how important is it? Name me something that goes on in You can't. Okay. Uh okay, so just some definitions. The process whereby oxygen metabolizes either fat or glucose into water. You know, we're water makers. Did you know that? You're a water maker. You make water. Uh when you get older, do do your cells get more hydrated or worse hydrated? Is it because you drink less water as you get older? I don't think so. I don't think so at all. It's because you don't make the water as well. You're not as good a water maker. Okay? Uh so, you metabolize the oxygen metabolize the fat or glucose into water and to heat. So, as you get older, do you tend to get warmer So, you can start to as have some clinical assessment for your patient. My patient says, "I'm cold all the time." You can probably think to yourself, maybe their oxygen utilization not that hot. Uh check them out. They're Oh, they're dehydrated. They don't look so good that way. Might be a problem with their uh oxygen utilization. Then you make this stuff called NAD, nicotinamide dinucleotide. So, we will spend uh probably more time than you want to, but I want to tell you it's really good time learning about NAD if you don't know already about NAD. And then you make free radicals. Of course, we need free radicals. And then you make carbon dioxide that can be measured. By the way, the efficiency at which you produce oxygen can be determined really simply. When you process oxygen into energy, a byproduct is CO2. The more efficiently you do it, the less CO2 you make. The more inefficiently you do it, the more CO2 you make. So, by looking at the ratio how much oxygen you going into your body and how much CO2 is coming out of your body, I can tell you how efficiently you're processing oxygen. Simple. And then finally you make ATP. So, that that's what oxygen utilization is. That's the definition, okay? Oxygen itself doesn't really do anything in the body. It's got to get converted into intermediates, right? So, as a single entity it has to get converted through this process called oxygen utilization. So, the main things we we we talk about is NAD and ATP. These are These are the main things it gets converted to. It's these oxygen intermediates. That's what runs everything. That's the bottom line for all cellular function. There you go. I knew you wanted to go through this slide. Cuz it's so easy to see. Actually, pretty really is. This is a mitochondria right here, okay? There's sugar. There's fat. Here's oxygen coming in. So, it's kind of just like the more simple slide I showed you, but I what I want to really do is uh just just look at the little NADs. Okay? Cuz I'm going to point something Fat can't even get into the mitochondria without NAD. Glucose can't even get into the Notice that these reactions, when NAD processes pyruvate and acetyl-CoA enzyme A, it gets converted to NADH. The NADH goes down here into the electron transport chain and gets converted back to the NAD. Bingo, we're in business. Okay? Um Same thing over here. It gets converted to NADH. But what if there's some kind of problem down here? What if this system doesn't work so well and you don't get as much NAD made? So you're building up the NADH relative to the NAD. Well, if that were to happen, notice these reactions are reversible. Okay? So as this ratio of NAD to NADH is that ratio decreases, as you get more NADH relative to NAD, what happens to those reactions? They slow down, right? They slow down. Is that good? Let's go over that again. So let's say something's wrong down here. Let's say you got some heavy metals like mercury. How many people in here have mercury? Anybody You know, all your hands should be up. Okay? You guys have your hands down, you're either have you know, rotator cuff injury or you're sleepy or something's going on there. Maybe you got too much mercury to even raise your hand. I don't know. Okay, but you know, there's lots of trans fatty acids. They're uh They're uncouplers. Hey, you know what? I don't know if I have this slide in this presentation, but do you know what the biggest mitochondrial suppressant that people in this country get is? You have any clue? Anybody want to guess? Medications. Right? I mean, I have a slide that will show you that just about every medication your patient on is a mitochondrial suppressant. FDA black box approved. One of the first duties of medicine is to get your patient off the drugs they're on. Anyhow, I digress. So, um So, yeah. So, things going in here that are tying this up, we're not getting the NAD. This ratio is backing down. Things can't get in. That makes it even worse. It's a vicious cycle. How soon does this start? I'm going to show you evidence it starts in your 30s. It's a vicious cycle. You start getting sick. You start getting cancer in your 30s, at least most people do. That's the time to intervene. Not after they get the disease. But, wouldn't it be really cool if you could just go out and do a blood test and measure those? Sorry, you can't. We're working on it, but you can't do that. But, that'd be really nice, cuz that's as you can sort of see that's what it's all about. And I'm going to bring this up in a little bit, but but when we get in kind of get into the Warburg stuff and cancer is specifically relates to cancer because look what here. As this ratio is going down, say this got a problem down here. And you have less NAD relative to the NADH. The NADH ratio is building up. Everything's starting to slow down. How can you replenish that NA How can you turn the NADH back into NAD other than through here? There's a couple of ways. One of them is just obvious. Look up here. When pyruvate goes to lactate, NADH goes to NAD. Aha! How about that? My NAD NADH ratio is going down, but not to worry. All I have to do is become anaerobic and I'm going to make it back in shape again. Cool. And we know that that's got a little something to do with cancer cells and selecting them out. Um That's probably all I want to touch on this slide here. Just look here, lipoic acid's awfully important. We're going to touch a little bit on the PDH enzyme here in a second. Like um And you know, you can look through here and you can see that there's other players. I mean, you got insulin, you've got cortisol. There's There's your T3. Um you know, you got carnitine. So, there's all kinds of other issues that you guys are aware of. So, it's kind of a nice little slide to give you an idea, but mostly I just wanted to show it to you to give you a sense for what we're going to be talking about a little bit Just couple of clinical signs. Uh you know, I when I In my office, I like to go to actually pick up my patients in the in the waiting room. I go get them. I don't have a nurse go get them. And I open the door and say, "Okay, George, come on in." Cuz I like to see him get out of the chair. And I want to see if he does it the old man way or the young man way. I also want to see when he walks the 30 ft back to my waiting room when we sit down in the chairs to face each other, You know, a lot of the times uh they're doing that and guess what? Their O2 sats perfect and they're not cyanotic. I Okay, so how common is this problem? We took 50 subjects. This was maybe 10 years ago. And uh they were in various places around the world. They were all in their in their 20s to 40s, most of them in their 30s. These people were healthy. They're actually coming in to get their mitochondria checked because they were health conscious. And uh nothing wrong with them, completely asymptomatic. Okay? So, that's the group we had. We measured their mitochondrial function. Uh 54% had normal mitochondrial function. That's not so good for this group. I'm sorry. If they were 65, I'd say, you know, all right, that's probably normal. But, we're talking asymptomatic people in their 30s, okay? 46% had decreased mitochondrial function. 36% had greater than greater than 90% were decreased less than 90% of the predicted 26% greater than less than 80% of the predicted and 12% of them had less than six uh 60% of the predicted mitochondrial function. That's pretty bad. Um so, you can see it starts very very early when you don't know that it's going on. And unless you're measuring it, you don't even have a clue as a physician who's doing what. So, it's hard to intervene. What's the most important thing in Measurement or therapy? Is it more important to have a blood pressure cuff or a blood pressure medication? Mhm? I maintain to you the cuff is more important. Cuz if you don't have the cuff, you don't even know who to treat. And if you are treating them, you don't know if your treatment's working. So, if we want to treat mitochondrial function, it's probably a pretty good idea to have some way to measure mitochondrial function. Then, that way you'd pick up some of these people you could intervene a little bit earlier. Uh but, here's the interesting thing right down in here. Of the 24% of subjects with optimal mitochondrial function, uh had a decrease only 24% had a decrease in the PDH function. But, of the ones that didn't have optimal, every single one of them had suboptimal PDH function, pyruvate dehydrogenase function. That was this stuff right in here, which is lipoic acid dependent, okay? We're going to talk more about that. Every single one of those young people that had poor mitochondrial function, that was bad. So, you can start to catch a little bit of a clue of what what's important here. Here's an amazing observation. I've been doing this for 13 years. Uh and every one of my patients, they all like come they come in once once a year. I have patients that I've been doing this for 13 years with. Um I've never seen one of them get cancer who had optimal scores, ever, once, yet, in 13 years. We're talking The other side of that coin is I've never had a patient come in to my clinic with cancer that has optimum utilization of oxygen, period. Never one, never, nada. And I don't need I'm talking about lumpectomies. I'm talking about essentially, quote, healthy people. Why? Why is that observation true? How could that possibly be? Do you think oxygen utilization might In fact, I'll tell you, you know how many people I see that have optimum oxygen utilization that get sick with anything? I mean, none. It just doesn't happen, you know? They might get run over by a car, but that's about the worst that's going to happen let's go through some points here. Cancer is caused primarily by a decrease in oxygen utilization. That's the premise. This general decrease in oxygen utilization conditions and selects out certain cells. You have certain cells in your body that are predisposed to get cancerous. Those cells get selected out for survival when you place your body into a state of decreased oxygen utilization. Why? Because they're more adaptable without oxygen. In hypoxic conditions, these conditioned Now Now you got these cells so you've gone years with the low oxygen utilization. You've conditioned these cells. They're all ready to roll and all they're waiting for is a hypoxic moment cuz as soon as they get hypoxic moment, all the healthy cells that aren't selected out are going to die or rapidly decrease their function and these guys are going to take over cuz they're just ready to roll now. They don't need oxygen. You've been training them. In hypoxic conditions, these conditioned and selected cells adapt by turning cancerous. In contrast to healthy cells which just die. These guys are ready to roll. These cellular changes lead to the hallmark of cancer, increased mutability. We're going to go through these by the way. Self-sufficient growth. Limitless growth potential. Tissue invasion. Evasion of apoptosis. And sustained angiogenesis. All of that happens as these cellular changes start to happen. Now here's the deal. Oxidation therapies I hope all of you want to start doing these things cuz oxidation therapies improve oxygen utilization. And I'll just give you a clue right now in case you didn't figure it out already. How do they do that? They oxidize NADH back to NAD. Simple. They correct the ratio. They correct the problem in the first place. Uh so they antagonize and reverse the cancer growth. Okay. So, they're applicable in virtually every single patient you see with chronic disease. Obviously, cancer's right in the middle of that. Okay, decreased oxygen utilization exerts its negative effects by causing a decrease in the ratio. It's basically the same thing. When I say decreased OU, I'm talking about decreased NAD and NADH ratio. So, what do you suppose a good healthy ratio would be in your cells? What do you think? A good healthy ratio of NAD to NADH. Do you think that it would be about 700 to 1? Think your body likes NAD? Think it doesn't like NADH too much? 700 times more NAD than NADH is typically what we see. That would be a healthy ratio. If it's down at 300 to 1, things aren't so good. And everything starts to slow down. You start to become anaerobic. You start to select out those cells and train those cells. So, then when a hypoxic moment comes, bingo, they're ready to roll and Um so, we're going to go through just a few slides here. Uh uh just to tell you that NAD is more than what I just said. So, I was talking about just the metabolic implications of NAD, which are huge in themselves. And if that's all it was about, I think you'd be pretty impressed. But, that's not all it's about. NAD impacts on virtually everything you guys have ever read about. So, here's a study. It's called nicotinamide dinucleotide as a metabolic coregulator of a few things that we think are important, like transcription. That's sort of important. Longevity and disease. See, the authors say that NAD is a muse has emerged as a putative metabolic regulator of transcription, longevity, and several age-associated diseases, including the one we almost never see in our culture anymore called diabetes, and we hardly ever see cancer, and neurodegenerative diseases, they're on their way down, too. Um guess how calorie restriction works. What's the only accepted thing amongst everybody? Nobody argues about this. The animal studies are are not controversial at all that extends life. Calorie restriction, right? How's it work? You know how it works? It improves the NAD NADH ratio. Okay. And so the authors just said here, studies in yeast suggest that calorie restriction it functions by increasing the NAD level or the ratio. Okay, but that's not all. There's more. More knives. NAD is rate-limiting for ADP ribosylation. ADP ribosylation reactions are involved in cell signaling. That's important. And the control of many cell processes in the cell nucleus, including DNA repair, apoptosis, and telomere maintenance. These have a lot to do with why people get cancer, and why they can't get over cancer, and why it relapses. Somebody's got cancer. We know it's a metabolic issue. We know it's not a lump issue. We know Right? We know it's a metabolic issue. The surgeon takes out the cancer, you're cured. No, you're not. The metabolic problem that caused the lump in the first place is still going on. So you ought not to be really shocked when it comes back again. Cuz you didn't actually fix anything. So we want to think about fixing things. And certainly if you get a patient in and they had a lump, and the lump was removed, and they're quote cured, this is a really good time to intervene and to get their oxygen utilization up to maximum. Another function of NAD in cell signaling is as a precursor of the cyclic ADP ribose, which regulates intracellular calcium channels. Now, I'm in no way any kind of an expert on calcium channels physiology, but I got to tell you it's all over the place. And maybe some of you guys know about this stuff more than I do. Uh but just just remember uh that anytime you read anything about calcium channel physiology, intracellular physiology, NAD is right at the center of it. Okay, sirtuins. You've heard about sirtuins. Sir stands for silent information regulator gene. Sir 2 is short for silent mating type information regulator 2. So, they call them sirtuins. Pretty cool, okay? Uh sirtuins have been shown to protect from genomic instability upon genotoxic and oxidative stress, protecting the genome from mutations that can drive into tumorigenesis. That's pretty cool. We want sirtuins. Guess what? Okay. So, we'll review. Oxygen does not directly catalyze cellular reactions. It indirectly catalyzes them using NAD to solve the things, but primarily we're just going to focus on that. When NAD catalyzes a reaction, it's converted to NADH. Oxygen utilization, that process, then recycles the NADH back to NAD. Everybody's happy. The problem when that doesn't work is that it results in decreased levels of NAD combined with increased levels of NADH. As that ratio decreases, all cellular activity slows down. Less NADH is produced in the Krebs cycle. The decrease in the NADH further depresses the oxygen utilization cuz now there's no NADH from the Krebs cycle. The decreasing NAD to NADH ratio insidiously spirals downward and slow but constant vicious cycle starts in your 20s, 30s. We call this process aging. NAD NADH ratios are reversed in order to normalize the ratio. So, what do you have to do to reverse them? So, your body's now compensating. So, you're screwing it up because of your lifestyle or your genetics or whatever is going on with you. I don't know what you're doing, but but somehow you're doing something that's screwing up your NAD NADH ratio. So, the body's trying to compensate for that. So, it's going to upregulate mechanisms that convert NADH back to NAD, right? So, we already saw one of them was. One of them this So, the cost of reversing that ratio. Here's what it's got to do to do do this, okay? You get increased anaerobic glycolysis leading to increased mesenchymal acidosis and some other issues we're going to touch on. I don't know if you guys are aware of the plasma membrane oxidoreductase system of the PM OR system. This is an enzyme system that takes the NADH out to the inner aspect of the cell membrane and then puts um an electron out into the interstitial space. It gets transfers into the interstitial space thereby generating from the NAD back to NAD NADH back to NAD. This So, this system is upregulated when that ratio decreases. And what's it doing? It's creating free radical injuries in the interstitial space. Okay? Uh increased mesenchymal acidosis and this free to radical activity in the med and medical space. So, that's what we got now. And the mesenchyme is becoming more oxidant stressed and more acidotic, okay? It leads to metas- metastasis, local tissue invasion, and it infects all the cells that are around it. I'm going to show this in a second. I'll show you some slides. Increased oxygen utilization um in Greek increase glucose utilization 19 times. So, as you're beginning to shift into anaerobic metabolism of glucose, how much energy do you have to how much glucose do you have to burn to um make the same amount of energy? 19 times more glucose to get the same amount of energy, okay? So, you turn now turn into a glucose machine. You are a glucose machine. You don't get your glucose, you got a problem. Any of you guys have patients like that? You know, I need my carbs, doc. Are you crazy? I don't need my carbs. You You got to be nuts. I don't need my carbs. I don't feel so good. You're a glucose machine. Um okay, so when you're a glucose machine, what do you got to have a lot of? Got to have a lot of insulin, right? Got to have a lot of cortisol, right? Got to have a lot of IGF-1. All these things are uh issues that we have to deal with with our patients that have cancer and any kind of chronic disease. And the increased intracellular free radical stress leads to the mutability of the changes in the genomic structure of the cells. These changes select out the cells with precancerous potential, and you all have them. You all have cells with precancerous potential. Anybody here over the age of 60? You have cancer. Okay? I'm I'm not even kidding. It's proven. You all have thyroid cancer. 100% of people over the age of 60, autopsy studies show have thyroid cancer. Interesting. Well, there's probably other cancers you have too that you don't know about. So, so that's just part and parcel of being alive. Doesn't mean you have to die of cancer. It just means you've got cells in there that have precancerous potential. Can actually turn into something, and your body has systems that's been designed with systems to control it. Uh uh and unless we screw those systems up, they Okay, so let's talk about let's go into this a little bit more depth. Cells are different. They're not all the same. Some people some cells have the potential to do better in a low oxygen environment than others. It's just the way it is. Now some of us are born with more of those cells than others and that's sort of a lot of what the genetics of cancer is. But all of us have cells like this, cells that do better in low oxygen environment than other cells. Decreased oxygen utilization conditions those cells to develop their potential to the point that they're capable of surviving really low oxygen environments when other cells aren't. So then you an incident of hypoxia like smoking comes along or some other incidents of hypoxia and we're going to talk about that sec. And so basically it's the survival of the fittest deal. The phenotype of these fully developed cells when they actually reach their full fruition is in fact cancer. Decreased oxygen utilization is the prime cause. Remember, if you don't have that you don't get cancer, at least not in my world, not in Carson City. You do not get cancer if you don't have that. Hypoxia is the trigger. So it kind of looks a little bit like this. I think this is a halfway decent thing. So you got decreased oxygen utilization. That by the way could be for a like a lot of reasons. Stress is right in there. Bad diet's right in there. Lack of fitness is in there. Atherosclerosis is in there. Ischemia, poor endothelial function, heavy metal toxicity, you know, nutrient deficiencies, all there's all these issues that everybody knows about and we and we we focus on. Those are kinds of the reasons that that happens. But as that happens, what do you get? You can get increased free radical formation. You get decreased free radical buffering cuz the enzymes that are supposed to buffer these guys, they're all NAD dependent. So, you get less of the less of the good guys, more of the bad guys. What does that do to the mitochondria? Screws them up even more. This is a vicious cycle going around around around. And uh normal cells, when this happens to them, they just die. But not our little friendly pre-cancer cells. They don't die. They sort of like that. We're helping them out a little bit. All the all the all their neighbors are going. That means more space for them to grow, more food for them to get. And you were just feeding that fire. So, you all heard about Otto Warburg. I'm going to spend a lot of time on him. Um Uh let's see, what can I say here? Yes, I just skip down the bottom. He gave a talk at 1966 in Germany. Uh Warburg, he presented evidence proving that the primary cause of cancer is decreased mitochondrial function. Now, here's the interesting thing. We used to think that cancers don't have functioning mitochondria. They actually do. Mitochondria in cancer cells does function. What they do is they just don't use them. Basically, a cancer cell says to itself, "You know what? I could use mitochondria. I could use my mitochondria, but I do better when I don't. I actually function better when I don't. For me, the kind of cell I am, I don't really do all that well if I use my mitochondria. I could get apoptotic and die. So, I'm not going to do that. I'm just going to like turn it down. I'm going to find ways to turn it down. Uh this is a pretty good little paper that was published back in '05. It's called mitochondria cancer. Warburg addressed cancer cells have decreased mitochondrial function. This decrease in mitochondrial function occurs first when the cell is healthy. I'm telling you, the decrease in mitochondrial function causes increased free radicals to form switch mutate the nuclear pro-oncogenes. That's the initiation. Then they drive the nuclear replication. That's promotion. And this is called cancer. The authors say that cancer cells exhibit multiple alterations in mitochondrial content, structure, function, and activity. And that the researchers So what they did is they overexpress the protein of frataxin in several colon cancer cell lines. When you do that, it causes it it has the effect of improving mitochondrial function. So when you overexpress that protein, you're basically upregulating mitochondrial function in the colon cancer cells, okay? What do you think happened to them? Were they happy about that? They were not happy. You made them unhappy. Consistent with Warburg's hypothesis, these cells bang decreased growth rates increased doubling times bang inhibited colony formation capacity a reduced capacity for tumor formation when injected into nude mice. They didn't like it. And the authors say these results support the view that an increase in oxidative metabolism may inhibit cancer growth in animals. I'm telling you. If you measure your mitochondrial function like I do and give a patient an ozone treatment and they come back an hour or two later and measure the mitochondrial function, what do you think happens to it? You bumped it up. The cancer cells don't like that. I'll bet you a nickel if you did it with vitamin C, same thing would happen. I just got a feeling. Cancer cells just don't like that kind of stuff. Okay, so here's one that came out called the alteration of bioenergetic phenotype of mitochondria is a hallmark of breast, gastric, lung, and esophageal cancer. You guys probably most you probably already know this stuff. So, I'm going to kind of run through this uh you know, fairly fast. But, uh mitochondria function is depressed in all cancer studies so far including breast cancer. Hello? It's important now. Talking to every single person, okay? The findings reported in the present paper in addition to the previous findings in liver, kidney, and colon carcinoma strongly suggest that altered bioenergetic function of mitochondria is a hallmark of carcinogenesis as was hypothesized by Warburg almost 8 years ago. Uh okay, so this is the paper This is one of the papers I want you to get. If you haven't seen this paper, it's pretty amazing. Uh you can get it for free. There's no excuse. So, you can get the PDF for free. Just uh go online. So, get and being Gillies 2004. The title is why do cancer cells have high aerobic glycolysis? And uh what they point out is some stuff we're going to talk about here. Survival of the most adaptable, basically what I've been telling you. Precancerous latent cancer cells have a survival advantage in hypoxic environments because they have already been trained by living in a condition decreased oxygen utilization. Hypoxia is the trigger according to these guys. It selects out these trained cells cuz they adapt best to hypoxia and hence have a proliferative advantage. Now, what this paper points out is get kind of gives you a rationale so you can actually understand how the actual process of getting a tumor gets involved because a lot of people have low oxygen utilization and don't actually get tumors, don't they? I'm I'm my Uncle Jack is like the essence of the most unhealthy human being you could possibly imagine. He's got lung disease. He's got heart disease. He's got peripheral vascular disease. He's on 19 different drugs. He's in and out of the hospital all the time. Guess what Uncle Uncle Jack smoked four packs of Lucky Strikes every day of his life and drank a um uh a a case of beer every day in his life. He drank a gallon of milk, got some protein, every day in his life, never had a vegetable. We sit down for dinner, Uncle Jack would say, "I don't want that dang salad. Get that out of here." He ate steak and pasta. That's my man, okay? Uncle Jack never got cancer. Think of that. Isn't that crazy? How could Uncle Jack not get cancer? I never measured his oxygen utilization cuz what's the point? There's absolutely no point in that. But he never got cancer. I think that's just amazing. So, obviously, there other factors involved. Uh and and there's genetics involved. And so, and that's I think where this paper touches upon is there's other factors involved. But underneath it all, if you have those other factors and your oxygen utilization is good, you don't get cancer. But if your oxygen utilization is no good and you don't have those other factors, you might just not get cancer. So, that's kind of how it works out a little bit. That's what they point out. They point out the carcinogenesis begins in a hypoxic environment. Let me just go go right to the slide here and show you. So, this is a uh uh light stage uh ductal carcinoma in situ. Uh here's the carcinoma right in here. Uh these are stromal cells, so they're the healthy cells that surround the tumor. This is a tumor. T is tumor. Um and notice there's a basement cell membrane here. These blue things are all blood vessels. Notice how many blood vessels are inside the basement cell membrane. Like none. Okay? So, if we go over here, here's another area. Now, this is actual cancer here. These are not These are what you would call a pre-cancer area. We have a basement cell membrane and there's no blood vessels inside there, okay? The blood has to transport across the basement cell mem- the oxygen has to get across the basement cell membrane. And of course, as that it slows it down, okay? So, these cells that are further away, like the guys right in here, they're not going to have access to oxygen like these cells right out in here. Cuz the basement cell membrane's getting in the way. And so, what you have here is you got a tumor that's developed for the reasons we just mentioned. Inside here are cells that have been preconditioned by decreased oxygen utilization. And now there's a hypoxic as the basement cell membrane develops and maybe becomes thicker, they're getting they're now getting hypoxic in here and this is generating the cancer. Inside here's This is all necrotic material inside the cancer cell. That's because it it it can't even get enough uh nutrients in there. It can't get enough glucose to live, so it's actually becoming necrotic in here. But this is what uh Gattenby uh uh postulate is is this hypoxia resulting from these basement cell membranes in these uh areas of ductal uh of carcinoma in situ, which we all have, I'm assuming, or at least most of us do. That's the triggering event in the person that's already been preconditioned. Okay, how are we doing with time here? Okay. Uh so, mechanisms of uh okay, let's see. Yeah, this is the other paper I want you to get. You You may may know already of this paper by uh Seyfried, Cancer as a Metabolic Disease. Pretty interesting paper. Very fascinating He points out that cardiolipin uh decreases with aging. Cardiolipin is the um is the uh substance that the mitochondrial membrane's made out of. It decreases with aging, decreases with hypoxia, decreases with decreased oxygen utilization, decreases from inflammation, decreases from reactive And cancer cells have decreased cardiolipin. It's not accidental. Tissue invasion, decreased oxygen utilization increases uh MMP through the reactive oxygen activity of the PMOR system. So, as the PMOR system is dropping electrons out into the interstitial space, it's upregulating matrix metalloproteinase, which is of course a hallmark of cancer cells and their ability to metastasize. Decreased oxygen utilization increases the mesenchymal acidosis because of increased glycolysis. It lives off sugar. This This potentiates metastasis and local spread. Both of these effects induce apoptosis in healthy cells. So, all the healthy cells are dying off, but they're just great for the cancer cells. Uh angiogenesis, decreased oxygen utilization induces hypoxia inducing factor alpha. Uh so, when you have lower oxygen utilization or you hold your breath or you can't breathe or whatever, your body's going to compensate by making this HIF alpha uh factor. Uh HIF alpha's activity is elevated in virtually every cancer cell there is. HIF alpha increases VEGF and uh basic fibroblast growth factor. So, HIF alpha increases all these growth factors, it's elevated in almost all cancers, it's also a potent angiogenic promoter. And finally, it inhibits PDH kinase. So, it induces PDH kinase. So, I'm going to explain that to you in a second cuz this is pretty critical. We I just mentioned PDH P- PDH function a a moment ago and you know you can remember how critical it was. HIF-alpha screws it up. Published studies ozone decreases HIF-alpha production in So, just just remember the the PDH kinase thing here, okay? Just remember that cuz we're going to come back to that. Okay, so here's this title of this study is declining NAD that induces a pseudo-hypoxic state. That's what I'm talking about. Disrupting nuclear-mitochondrial communication during aging. So, he now he's looking at an entirely different concept. This nucleus and mitochondria have to talk to each other. They self-regulate each other. They got to talk to each other. When that NAD falls down, they stop talking. They They go on their separate ways. Um the author says mitochondria dysfunction is a hallmark of aging, but its causes are debated. We show that during aging there's a specific loss of mitochondrial but not nuclear-encoded OXPHOS units. We trace the cause to an alternate independent pathway of nuclear-mitochondrial communication that it is induced by a decline in NAD and the accumulation of HIF-alpha under normoxic conditions. Decreased oxygen utilization. O2 sat's just fine. Deleting Let's see. Just skip down the last bullet. Thus, a pseudo-hypoxic state that can disrupt that independent pathway contributes to the decline of mitochondrial function with age, a process that is apparently reversible. That's That's the kind of the key part here. It is reversible. We can reverse it. So, when you find out that your 20-year-old has decreased oxygen utilization, you can intervene. You can say, "You can reverse this." And by reversing this, you will not get the diabetes that you're headed for. You will not get the cancer that you're headed for. You will not get the heart disease that you're headed for, and so forth. Okay, this explains this a little bit. So, here's your PDH, okay? And here's your pyruvate. It's going to acetyl coenzyme A. It needs PDH to do that. Here's our little friend. Uh and uh but here's the thing. PDH kinase converts this to an inactive form of PDH. So, this enzyme, PDH kinase, renders this So, things that upregulate PDH kinase, not good. Got it? Okay. HIF-1 alpha does exactly that. Ozone reverses it. Ozone reverses this whole process. Ozone upregulates this enzyme, which returns it to the active form, and downregulates Oh, all you DCA fans, that's how DCA works, by the way. Okay, survivin is an anti-apoptotic inhibitory factor. It inhibits apoptosis, so it's called survivin, okay? Survivin's only found in cancer cells and embryonic cells. And stem cells. Overexpression of survivin results in an accelerated S phase and resistance to G1 arrest, which is the reason the chemo won't work. Cuz of the survivin. Increased PDH kinase induces survivin. So, once again, you can start to think about NAD. You can start to think about all the carbohydrates that people are eating. You can start to think about the inactivity. You can start to think about the various things that combine to cause this cancer in this person that's sitting in front of you. How successful you're going to be able to treat it any disease if you don't treat the cause? You're not going to be very successful. You can help them out, but you're not going to be very successful. So, it's it's important for us as we're talking about treating any disease to start thinking about, "Okay, what caused this in the first place?" I better be dealing with that. It's an emotional issue, fine. It's a toxic issue, fine. It's heavy metals, whatever it is. If it's all the above, but in order to get for me get the best results, I got to start thinking about what's causing it. And so, you start thinking in terms of oxygen utilization and surviving and diet and PDH kinase and stuff like that. Okay, here you go. Uh pyruvate So, this is a study just uh not too long ago. This is pretty recent. I have actually have the date there, but it's pretty recent. Uh it's recent advances in mechanisms of regulating glucose oxidation at the level of pyruvate dehydrogenase complex by PDKs. by PDKs. By PDH kinases. And basically, the the the the bullet point that's at the top there is pyruvate dehydrogenase stimulated by NADH. Hello. Uh this one. Okay, so this is a 1998 publication. Insulin downregulates pyruvate dehydrogenase kinase. Potential mechanism contributing to increased lipid oxidation in insulin resistant subjects. Basically, what he points out there is oxidative metabolism of glucose is regulated by PDH. And that can be inhibited by PDH kinase. Okay, you got that. PDH kinase 2 and 4 uh messenger RNAs were positively associated or correlated with the but fasting plasma insulin. The higher the insulin levels were, the the higher those uh expressions were. A 2-hour plasma insulin concentration in response to an oral glucose and a percentage of body fat. Hello. I mean, we're talking about America. This is America. Okay? Our data indicate the insufficient down-regulation of PDH kinase because of insulin resistance could be a cause of increased PDH kinase expression and leading to impaired glucose oxidation leading to decreased oxygen utilization. So, yes, diet is gigantic. Lose the carbs. Uh Cocoa Puffs. Cocoa Puffs. Anybody get their Cocoa Puffs this morning? They had Cocoa Puffs at the hotel I'm staying. I'm not staying at this hotel. They had Cocoa Puffs. I passed on them. Uh Yeah, carbohydrates are for kids. Kids are growing. They they need carbohydrates. Okay? So, don't put your kids on a ketogenic diet, please. Okay? We don't need them. You know how many essential carbohydrates there are? Count them all. Zero. Zero essential carbohydrates. And they're they're they're for kids. Give them to your kids. Okay? But for you, leave them alone. You want to have them every now and then, want to have a piece of bread on your birthday, I'm good with that. Uh mutability. Okay? So, we're just going right down the list. I'm trying to correlate all this, okay? Decreased oxygen utilization decreases methylation. Methylation occurs in the mitochondria. There's a one-to-one relationship with methylation and mitochondria and oxidative phosphorylation. The very first phase of methylation is induced by ATP. You don't have enough ATP, you don't even make your S- S- Sammy. It don't even happen. The whole process shuts down. So, there's a direct one-to-one uh correlation there. Decreased methylation results in decreased gene repair and increased mutability, okay? Decreased methylation decreases P53 activity. That's the gene that's supposed to be a suppressor gene, okay? Decreased methylation happens as a direct result of oxygen decreased oxygen utilization. Hold your breath and you're not making as many methyl groups, period. Okay, now unbridled proliferation. So, we're talking about we just talked about all kinds of factors that induce cancer. Now that you've got the cancer, it's going to proliferate. Uh O- O U decreased oxygen utilization decreases the P53 activity. That causes proliferation. Also decreases some called retinoblastoma protein activity, which is another tumor suppressor protein. Uh in all my patients I do this test from RGCC, which gives me all these genomic markers. And you know, I have to say it's a it's a a very intimidating alphabet soup of things that you know, I have to like look up all the time, but uh it's pretty cool because all these things we're talking about are typically on there. Like HIF1 alpha and and uh retinoblastoma protein activity, all those markers are on the little test I get. And they're all high. All the cancer cells always have these markers. Um uh so, retino- uh blastoma protein acts to prevent excessive cell growth by inhibiting cell cycle progression until the cell is ready to divide. And uh and then finally uh decreased O U activates telomerase. So, most cells don't have a really active telomerase, but cancer cells do. A lot of cancer cells upregulate their telomerase. Finally, apoptosis is induced through normal mitochondrial function, but cancer cells choose not to do that. So, decrease oxygen utilization selects out cells for survival advantages that can down regulate regulate mitochondrial function in favor of glycolysis even in the face of normal oxygen tension. And that's the definition of cancer according to Warburg 80 years ago. You got a cancer cell, you give it oxygen, it won't use it. It chooses not to use it. It's fascinating. It gets it then it doesn't have to die then. What causes decrease oxygen utilization? That should be a good question on your mind. I don't want that cell, so what causes it? I won't spend a lot of time here, but but but these are the the factors, you know, you can't break down your fat, you've got insulin resistance, uh you've got ischemia. This is exceedingly common in the older age group. You've got hypoxia maybe, uh inflammation obviously is a is plays a role in all this. Toxicity, um heavy metals most notably specially mercury, uh infections huge, stress huge, all kinds of nutritional deficiencies, um hormonal deficiencies this is big, decrease methylation, so the factors have to do with methylation MTHFR so forth, and decrease fitness. So, these are all the kinds of reasons that that would put you into a state where you're at risk. Um so, the take-home message here at this point is the most effective way to maximize the effects of oxidation therapy is to combine combine it. So, I'm not here to tell you to just, you know, throw out all your therapies and just start giving your patients ozone that'd be ridiculous. But what we want to do is I want you to understand that every patient in my clinic I use a lot of low-dose uh insulin potentiated chemo. That's my go-to. That and vitamin C is my go-to. I'm always tag teaming it with ozone. One right after the other. Always, all the time. And And my patients get ozone not only in the form of ozone treatments of the blood, they also go into the ozone sauna, they get ozone up the rear. If they got cancer in the bladder, they get ozone in the bladder. They get cancer in the vagina, they get ozone in the vagina. They get cancer in the stomach, they get ozone in the stomach. They drinking ozonated water, they taking ozonated oil. They get a lot of ozone. Okay, the most effective way to maximize the effects of oxidation is to combine it with other therapies aimed at eliminating the decreased oxygen utilization. Um so just a just a quick little note, the keep one and the NRF2 are absolutely important for anti-cancer behavior. Oh, this published study is ozone upregulates these two. Okay? Okay, that's it. How am I doing

Summary: There's this uh great truth in life that everything happens for a reason even though at the time that it happens you don't know why it's happening. And what indeed may seem as a misfortune down the road may be one of the best things that could have ever happened to you. And there's been a few occasions in previous symposiums where I thought we were suffering a great misfortune when Dr. Schallenberger through one reason or another could not make it, but at…