Capital One Bank Guy (14:59)

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 capitalone.com bank capital1na member FDIC

Sean Linda (15:30)

hi friends Sean and Linda from two black guys with good credit here. Whether you're running a non profit, a school or a small business, Walmart Business is here to support your mission. They make it easy to order what you need, from tech and cleaning supplies to everyday essentials, all at low prices and with helpful tools like spend tracking and tax exempt purchasing for eligible organizations. Because when your operations are smooth, your impact can be bigger. Visit business.walmart.com to get started.

Ben Bickman (15:59)

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.

Paige Desorbo (23:29)

Hey, this is Paige Desorbo from Giggly Squad, and today I want to talk to you about Boost Mobile. Quick question. Why are we letting our phone bills bully us? Here's a money tip. So stop paying a carrier tax when you bring your own phone and switch to boost Mobile's $25 Unlimited Forever plan. You can unlock up to $600 in savings. That's real life Money, not money trapped in a pricey phone bill. $600 is a trip, a shopping spree, or paying something off. Your money belongs in your life. You get unlimited data, talk and text for $25 a month with no contracts and no minimum line requirements. Your phone, your rules. Head to boost mobile.com to switch today and unlock the savings you actually deserve. After 30 gigabytes, customers may experience lower speed. Customers pay $25 per month while active on Boost Mobile Unlimited Plan savings claim based on a January 2026 Boost Mobile survey comparing average annual payments of major carrier customers to 12 months on the Boost Mobile Unlimited plan. Visit boostmobile.com for details.

Capital One Bank Guy (24:23)

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.

Ben Bickman (24:56)

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.

Boost Mobile Advertiser (33:03)

Unlock the savings at Boost Mobile and save up to $600 a year I've been scouting these big carriers for a minute now and I've seen them pull the same play a thousand times. They promise you the world, then hit you with a price hike right when the game gets tight. But boost mobile, their $25 a month unlimited wireless plan is the most consistent player on the floor. No contracts, no price hikes. Unlock the Savings today@boostmobile.com Unlock based on average annual single line payment of AT&T Verizon and T Mobile customers compared to 12 months of the Boost Mobile Unlimited Wireless plan as of January 2026. For full offer details, visit boostmobile.com hey,

Paige Desorbo (33:33)

this is Paige Desorbo from Giggly Squad and today I want to talk to you about Boost Mobile. Quick question. Why are we letting our phone bills bully us? Here's a money tip. Stop paying a carrier tax when you bring your own phone and Switch to boost mobile's $25 unlimited forever plan. You can unlock up to $600 in savings. That's real life money, not money trapped in a pricey phone bill. $600 is a trip, a shopping spree, or paying something off. Your money belongs in your life. You get unlimited data, talk and text for $25 a month or with no contracts and no minimum line requirement. Your phone, your rules. Head to boost mobile.com to switch today and unlock the savings you actually deserve. After 30 gigabytes, customers may experience lower speed. Customers pay $25 per month while active on Boost Mobile Unlimited Plan Savings claim based on a January 2026 Boost Mobile survey comparing average annual payments of major carrier customers to 12 months on the Boost Mobile Unlimited plan. Visit boost mobile.com for details.

Hannah Burner (34:27)

Hi, this is Hannah Burner from Giggly Squad. Have you ever put on a bra that makes you feel like a goddess? Prepare to with the Dream Angels Wicked Bra from Victoria's Secret, the iconic brand behind the world's most comfortable bras. And I only wear the most comfortable bras. The bestseller features an innovative sling for perfect lift without padding and the fit is chef's kiss. Awaken your inner goddess with new colors and super femme lace embroidery. Find out why this bra has thousands of five star reviews and counting. Shop it in stores and online@victoria's secret.com.