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The Metabolic Classroom with Dr. Ben Bikman
Ivermectin Explained: The Science Behind the Controversy
00:28:44
More Knowledge, Better Health
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- [00:00]
Sean Linda
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- [01:53]
Ben Bickman
Welcome to the Metabolic Classroom Podcast. I'm Ben Bickman. Thanks for letting me be your guest professor for the next few minutes. Don't worry about any pop quizzes. I'm here to simply make the science of metabolism clear, practical and engaging. Welcome back to the Metabolic Classroom. I'm Ben Bickman, metabolic scientist and professor of Cell biology. Today's mini lecture steps into one of the most politically charged and I would say, scientifically misrepresented drugs of the past several years, Ivermectin. Now, I'm not here to wade into politics. We are here to do what we always do on the Metabolic Classroom, which is follow the peer reviewed science. When you set aside the noise and look at what research actually says, you find a molecule with a profound and underappreciated metabolic story, particularly when it comes to mitochondria, cancer, metabolism, inflammation and signaling pathways that we talk about regularly here on the Metabolic Classroom. So today we're going to cover where ivermectin came from, how it works classically, where it does, where it does its job, and what it does to the mitochondria in particular and in cancer cells specifically. And then we'll broaden out to explore the wider metabolic effects. I'll also address the so called horse dewormer narrative directly because that framing deserves a science based response. Let's get into it. The story of Ivermectin starts in a patch of soil in Japan in 1975 where a bacterium called Streptomyces avermitilis was isolated and cultured. What made this bacterium remarkable is that it produced a compound eventually named avermectin with extraordinarily effective antiparasitic properties. Avermectin was subsequently modified chemically into a more potent derivative, which we now call ivermectin. The discovery of this compound was so significant that it earned the 2015 Nobel Prize in Physiology or Medicine, the Nobel committee's first award for treatments of infectious diseases in over six decades. The Nobel assembly explicitly recognized ivermectin for its ability to radically lower the incidence of devastating parasitic diseases, including things like river blindness and one called lymphatic filariasis. Look it up. That's a crazy one. We need to appreciate that this is a Nobel Prize winning drug and the prize wasn't for its use in horses or livestock at all. It was for its transformative impact on human health. In fact, in a single year 2014, the World Health Organization, the WHO, reported that 139 million people were reached with Ivermectin through its elimination program for lymphatic filariasis alone. It is on the WHO's list of essential medicines and is FDA approved for human use. It's worth noting that access to human grade ivermectin has been expanding at the state level here within the United States as of in fact, Just recently, late 2025, at least five states, namely Tennessee, Arkansas, Idaho, Louisiana and Texas, have passed legislation allowing Ivermectin to be sold over the counter at pharmacies without a prescription. More states have legislation pending, actually. So it could in fact become even broader in its access. This means that for many Americans, obtaining this pharmaceutical grade ivermectin is becoming as straightforward as picking up some ibuprofen so when Ivermectin gets dismissed as just a horse dewormer, what we're really seeing, I think, is a rhetorical sleight of hand that strips away the drug's entire humanitarian history and Nobel Prize winning science to make it sound fringe and even dangerous. Yes, Ivermectin is also used in veterinary medicine, but so is metformin, which is used in horses and dogs. So is aspirin. The use of a drug in animals doesn't make it inappropriate or inherently toxic for use in humans. What matters is the pharmacology and the evidence. And on both counts, Ivermectin has a stellar track record. Of course, this is the metabolic classroom and we'll get to the metabolism. But before we do that, including the metabolism as it's relevant to its anti cancer role, let's briefly establish how I Ivermectin works as an anti parasitic. This context is important for understanding why it's relatively selective in how it affects different organisms. Ivermectin's classical mechanism of action involves binding to glutamate gated chloride channels found in invertebrate parasites. All right, now that's a lot. So when Ivermectin binds to these channels, it causes them to open up, it forces them open and to stay open. And in turn that will flood the parasite cells with chloride ions, which then paralyzes the parasite's nervous system and its muscular systems, which will lead it to die. The key reason this is relatively safe in mammals is that these specific glutamate gated chloride channels are essentially absent in our nervous system, which, and we have different receptor types. So it's not going to work on us. And that realm on top of that, mammals have a blood brain barrier which under normal conditions is going to prevent Ivermectin from accumulating in the brain anyway. The drug therefore has a favorable therapeutic window, meaning it can be effective against parasites at doses that don't significantly harm the human. Now that said, Ivermectin doesn't only interact with these parasite channels. As research has expanded over the past two decades, we've discovered that Ivermectin also interacts with several mammalian targets. And that's where the metabolic story opens up. All right, now let's talk about the mitochondria. What I want to do now is transition into that, that sort of section or chapter of this mini lecture looking at mitochondrial function and how it relates to disease. Cancer cells often rely on altered mitochondrial function for biosynthesis and Rapid proliferation. So in other words, helping it grow really quickly and, and proliferate or multiply. And so if you disrupt that already changed mitochondrial function, it can be lethal to the cancer cell. This is where ivermectin enters the picture in a very interesting way that needs some attention. Multiple peer reviewed studies have demonstrated that ivermectin can inhibit mitochondrial complex 1, which is the first and largest enzyme complex in what we call the electron transport system. Complex 1 is the entry point for electrons coming from what we call reducing equivalence, A molecule called adh. In fact, for a little more information on adh, look back at my previous metabolic classroom on nad. But complex one takes in the NADH and introduces it into this respiratory chain or the electron transport system. And we need this to happen for the mitochondria to produce nutrients, ATP, that main molecule that the cell will use to purchase some kind of work. A neuron fires because of ATP. A muscle can contract and relax because of ATP and every other effect in the body. So given the important location and role of complex I, when complex I is inhibited, the electron transport chain stalls research. In glioblastoma cancer cells, one of the most aggressive and treatment resistant brain cancers, it's shown that ivermectin produces a dose dependent reduction in both basal oxygen consumption and maximal capacity. These are standard measures of mitochondrial respiration. In fact, indeed standard measures that we use in my own lab. These same studies have documented decreased mitochondrial membrane potential that refers to the electrochemical gradient across that inner mitochondrial membrane. So we have to have this, this not a chaos, but a tension that, that creates the, what we call the membrane potential. We must have that in order to create ATP. And in turn, in addition to disrupting that membrane potential, it increase, we also have an increase in reactive oxygen species and, and mitochondrial superoxide, that's that main oxidative stress mole. This combination represents a state of profound dysfunction of the mitochondria. Again, that's helpful because we're trying to kill these cancer cells. And cancer cells, because of their very high metabolic demand, are disproportionately sensitive to this kind of mitochondrial disruption compared to a normal slow growing cell. Studies comparing leukemia cells to normal bone marrow cells compared to, and that matters because these leukocytes that are affected in leukemia come from the bone marrow. And also looking at renal or kidney cancer cells to normal kidney cells, they found that cancerous cells were substantially more sensitive to ivermectin's effects. This selectivity is exactly what you want in a potential anti cancer agent. When complex one is inhibited, ATP levels fall and the cells experience an energy crisis. This in turn activates ampk, AMP activated protein kinase. Again AMPK is the acronym and AMPK functions as a sort of cellular energy sensor. When the amp, which is a metabolite, when you break down ATP, because you've used it for some kind of work, when you break down ATP, you get amp as the product. So you can look at the ratio of amp, the sign of ATP breakdown to, and compare that to ATP. When that ratio rises, meaning you're breaking down more ATP than you're rebuilding, AMPK is activated. And then when AMPK is activated, it in turn suppresses mtor, another one we've talked about previously on the Metabolic Classroom. That is MTOR is a very important driver of cancer cell growth and multiplication or proliferation. So in ivermectin hits the mitochondria, it sets off a cascade and it looks a little something like this complex one slows down, ATP drops, AMPK is activated and then MTOR is suppressed and the cancer cells are pushed toward growth arrest where they stop growing and eventually they'll die. That is the, I would say very coherent and even a well described molecular story. There's one more dimension worth understanding here when it comes to cancer. When the mitochondrial membrane potential collapses, which happens following complex 1 inhibition, it triggers intrinsic apoptosis, meaning programmed cell death initiated from within the cell. So this is when a cell dies, but not because there's some external stimulus telling it to die, but within its own substance, the cell gets the signal. It's time for me to die. In cervical cancer, esophageal carcinoma, leukemia, glioblastoma and glioblastoma models, studies have documented this exact sequence. The collapse of the membrane potential, an increase in reactive oxygen species and then a shift into the pro apoptotic signaling. So the cell is ultimately now getting more death signal in these cancer cells then survival signal. This mitochondria initiated apoptosis has now been documented across multiple cancer types in multiple peer reviewed publications. Now as compelling as the mitochondria story is, and as loathe as I am to step away from the mitochondria, it is in fact just one thread in a larger tapestry. Here two additional mechanisms are worth mentioning. First, ivermectin inhibits a kinase or an enzyme called Pacific1PAK1, which is overactivated in the vast majority of human cancers. Ivermectin promotes the degradation of Pack 1, essentially tagging it for destruction by the cell's own protein recycling machinery, if you will.
- [15:00]
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- [15:30]
Sean Linda
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- [16:00]
Ben Bickman
Studies in breast cancer, ovarian cancer, glioblastoma, melanoma, nasopharyngeal carcinoma, so in the oral cavity have all documented this exact effect. In fact, in one well designed study, ivermectin had no significant effect on PAC1 levels in non tumorogenic breast cells, only in cancer cells. Once again, there is this selectivity that's very important. The same selectivity I noted for the parasites. We're starting to see a different version of it with these cancer cells. Second, there is a standout preclinical example in pancreatic cancer. One paper that was published in Frontiers in Pharmacology found that the combination of ivermectin and another one called gemcitabine produced significantly greater apoptosis of pancreatic cancer cells than just the normal than the gemcitabine alone. The combination increased cell death through oxidative stress from the mitochondrial dysfunction, and it in turn suppressed the tumor growth in vivo. So in the living models, pancreatic cancer is notoriously treatment resistant. So this kind of synergy with an existing chemotherapy, the gemcitabine, is genuinely noteworthy and the kind of preclinical data that should be prompting serious clinical investigation. Now let's shift to something with even broader metabolic relevance, which is inflammation. Regular listeners, those of you who tune in often to the metabolic classroom, you know by now that chronic low grade inflammation is one of the primary drivers of cardiometabolic disease, and specifically a primary driver of insulin resistance. So anything that meaningfully Modulates inflammation is worth understanding from a metabolic standpoint. Ivermectin has been shown in multiple studies to suppress the activation of NF kappa bacteria. You've heard me describe that before. NF kappa B is a master transcription factor of inflammation. When NF kappa B is activated, it in turn drives the production of myriad pro inflammatory cytokines, thereby promoting inflammation throughout the body. Well, ivermectin blocks NF kappa B's ability to do that. It prevents it from getting into the nucleus, which in turn is reducing the downstream cytokine production and response. Research in animal models showed that ivermectin reduced inflammatory markers and significantly increased survival after administration of a lethal dose of lipopolysaccharide lps. That's a bacterial component. It's a molecule on bacteria that triggers a massive inflammatory cascade similar to in humans what we see with sepsis, which is this life threatening version of inflammation. In animal models of allergic asthma, ivermectin at therapeutic doses significantly reduced immune cell recruitment into the airway. It also lowered cytokine levels in general circulation and it suppressed the production of immunoglobulin E, which is a very important mediator of that asthma response. So all of these markers of allergic inflammation were turned down with ivermectin. And there is once again a metabolic component here worth holding onto. Ampk, that energy sensor that I mentioned in the cancer kind of chapter of my mini lecture here, is also a potent anti inflammatory molecule. When AMPK is activated, it suppresses NF kappa B. So when ivermectin activates AMPK through its effects on complex one, it may be contributing to its anti inflammatory effects through this same pathway. The mitochondrial effect, the anticancer effect and the anti inflammatory effect may be more unified than you would think at first glance. One more area of emerging clinical interest deserves attention. Ivermectin's potential influence on insulin resistance and glucose metabolism. This is perhaps the most surprising chapter in ivermectin's ever expanding story of effects. This specifically this metabolic focus. Ivermectin activates something called fxr that stands for far faroid X receptor, Farnesoid X receptor FXR and it has a high selectivity for that receptor. FXR sometimes is sometimes called the bile acid receptor. In fact, I've discussed it previously in that context. It's a nuclear hormone receptor and it's expressed in a lot of tissues like the liver, the intestine, the kidneys and adrenal glands. It's previously, it's already been Established as a meaningful regulator, regulator of glucose homeostasis and insulin sensitivity. But it's previously just been thought to have this effect through its role in bile acid signaling. You'll recall, not that long ago, in a metabolic classroom, I discussed how bile acid molecules act as signaling, as signals to help improve metabolic function. And again, FXR is the mechanism. Well, ivermectin binds it and this binding is what's at least in part driving some of ivermectin's metabolic effects in a. In a preclinical model of diet, induced obesity, high fat, high carb diet. These animals were treated with ivermectin and in so doing, compared to the control group, they had a reduction in their fasting glucose and their fasting insulin, both signs of improved glucose tolerance and improved insulin sensitivity. Subsequent rodent work extends these findings into models more directly relevant to metabolic syndrome. Going from the mice into a rat study and rats are, if you will, one step closer to understanding the human response. Once again, using a high fat, high carb diet, or the chow, as we call it when we give it to the animals, Ivermectin therapy prevented the rise in fasting blood glucose. It improved glucose tolerance as measured by glucose tolerance tests, and it even reduced blood pressure. And it improved the overall health of the of the liver as evidenced with liver enzymes. You know, when you create this diet induced obesity and metabolic syndrome, it's very common to see an increase in the liver enzymes in the blood indicative of liver damage, while ivermectin lowered that, suggesting improved liver health. In this study, the authors actually concluded that ivermectin could be a promising candidate for combating metabolic syndrome. There is also an adipocyte biology angle here. You, of course know by now of my affection for studying the fat cells. I like to call myself a fat scientist in cultured fat cells, meaning when we grow the fat cells in a petri dish. Ivermectin has been shown to inhibit the differentiation of pre adipocytes into mature fat cells and to reduce the triglyceride accumulating in those fat cells. They found that this effect was mediated through PPAR gamma.
- [23:30]
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- [24:23]
Capital One Bank Guy
With no fees or minimums on checking accounts, it's no wonder the Capital One bank guy is so passionate about banking with Capital One. If he were here, he wouldn't just tell you about no fees or minimums. He'd also talk about how most Capital One cafes are open seven days a week to assist with your banking needs. Yep, even on weekends it's pretty much all he talks about in a good way. What's in your wallet terms apply see capital1.com bank capital1NA member FDIC.
- [24:56]
Ben Bickman
But that has some implications, right? If you're setting a metabolic milieu where you are accelerating improving insulin sensitivity while you are limiting fat growth, maybe there's some weight management or weight loss potential here too. And with that sort of in mind and related to this, even here, like we saw with the inflammation section, AMPK can connect some of the dots. AMPK activation improves insulin signaling and it improves it directly stimulates actually glucose uptake. Further, the suppression of NF kappa B in the reduction of the downstream inflammation. Of course, well known drivers of insulin resistance adds once again another layer. We're connecting another dot. The metabolic effects of ivermectin, if they hold up in humans, are unlikely to be reducible to any single pathway. In other words, there's probably not one single reason or mechanism whereby ivermectin is having these benefits. It's appears to be multifactorial. In fact, given with all of this kind of meandering winding story, hopefully you're following. Though as meandering as it may seem, I cannot help but compare ivermectin and its effects on Complex 1, its activation of AMPK, to a very well known, in fact the most famous, most well prescribed insulin sensitizing medication on the planet, metformin. A lot of what I've described here with regards to ivermectin, I could almost have been replacing the word ivermectin with metformin, the inhibition of ampk, sorry, the inhibition of NF kappa B, the activation of ampk, the improvement on insulin signaling and glucose uptake, Metformin does all of those things. Ivermectin appears to as well. Now, of course I have to note that the evidence in humans with ivermectin, unlike with metformin, is very preliminary. But I'm optimistic because a report was just published last year that described four type 2 diabetics whose HbA1C levels improved with daily Ivermectin administration over a few months. In fact, even proceeding out to a couple years, establishing once again the safety with the drug. But there's been no large scale clinical trials conducted yet to look at Ivermectin's effects on these metabolic markers like insulin resistance or glycemic control. But the mechanistic coherence across FXR activation, AMPK signaling, anti inflammatory action and even the anti adipogenic signals in these preclinical models, the cell culture work and the animal work, and then that human pilot study, I think it definitely makes this a question genuinely worth asking in larger, abundant, multiple controlled human studies. Now let's quickly address safety and where the science stands, because credibility does matter here, of course, at standard human therapeutic doses, doses that have been administered to hundreds of millions of people, Ivermectin has an excellent safety profile. The WHO had long listed Ivermectin as an essential medicine precisely because its benefit to risk ratio is highly favorable. The, the, the narrative that it's dangerous largely conflates potential misuse of veterinary formulations with properly dosed pharmaceutical grade human medicine. Like any pharmacological agent, it should be used with some medical supervision. But of course the safety of it is being evident in the fact that it's being more widely used over the counter. That it is as safe, I think we could reasonably say, or the FDA would say, these states at least are passing legislation to indicate that it is as safe as any other medication you would buy at any pharmacy. The majority of the cancer and metabolic data that I've described in this mini lecture is preclinical with a little bit of human evidence, but there is a lot of human evidence coming. I'm aware of direct efforts to increase funding on the use of Ivermectin across various states. So if not from the federal level, we are seeing it across the United States at a state level, which I appreciate. And the more we're seeing, the more we're learning that the findings are rigorous. It appears to be that we're getting reproducible results across multiple research groups. And with this cancer, the anecdotal reports I'm emphasizing, the word anecdote is remarkable across multiple cancers, multiple clinics and individuals. We just need the peer reviewed evidence to start catching up. But nevertheless, the data as they are now provide a very compelling mechanistic rationale for much greater clinical investigation. You would have a hard time finding a drug that I think is more justified to be taken seriously than ivermectin. What I do find troubling is that the political controversy surrounding ivermectin May be creating barriers to the very clinical work that would resolve the uncertainty. When a compound has this much mechanistic rationale and history, the appropriate scientific response is to study it more rigorously in humans, not to dismiss it. The history of medicine contains many examples of drug repurposing. Aspirin, metformin and rapamycin all began life serving one purpose, and then they were found to have a much broader utility. There's no reason ivermectin shouldn't be given the same consideration that previous drugs have. Let's wrap this up. Ivermectin is a nobel prize winning drug with over three decades of safe use in hundreds of millions of people worldwide. Peer reviewed research has documented that ivermectin inhibits mitochondrial complex 1, disrupting the electron transport system function in cancer cells and thereby collapsing the mitochondrial membrane potential and triggering an oxidative stress response that can help reduce cancer cell growth and proliferation. These effects have been documented across a wide range of cancers. Beyond cancer, Ivermectin suppresses nf kappa b, that key inflammatory pathway, and reduces systemic inflammation. Subsequently, it also activates ampk in a way that links its mitochondrial and anti cancer and anti inflammatory effects into a single, I think, very coherent metabolic story. None of this means ivermectin is a cure for cancer or anything else necessarily. But it might be. What it means is that this is a molecule with a rich and I would say, very underexplored biology, A very strong safety record, and a body of preclinical evidence that should be driving serious clinical investigation. Not something that is dismissed because of political alignment. As always, my goal here is not to tell you what to do clinically. Remember, I'm not your clinician. I'm just your friendly neighborhood scientist. And in that role, I just want to help you understand the science at a level that empowers you to have a better conversation with your healthcare provider. And to think critically about what you read and what you hear. The science of Ivermectin deserves far more credit than it's been given, and I hope you feel like now you know why. Thanks for joining me in the metabolic classroom. I'll see you next time. Until then, remember, more knowledge, better health.
- [33:03]
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- [33:34]
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- [34:27]
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