Cancer Supplements, Chemo Side Effects & Immunotherapy: Live Q&A with a Cancer Drug Designer

In this live Q&A, Dr. Jay Chaplin breaks down supplements, chemo side effects, NK cells, apigenin & explains clinical trials.

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Episode Description:

Most cancer patients are researching supplements at 2 a.m.

The drive to do something is completely valid.

But here's what's often missing:

• Not all supplements support the same part of the immune system
• Cold stress and heat stress do very different things for NK cells
• Apigenin at the wrong dose can backfire for breast cancer patients
• Glutamine and magnesium timing matters more than most people realize
• Adding everything at once is one of the fastest ways to cause serious side effects

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info@elevatingcancertreatment.com

https://elevatingcancertreatment.com

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Disclaimer:
The information provided in this podcast is for educational and informational purposes only, and does not constitute medical advice. It is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have heard or read in this podcast or on this channel.
Reliance on any information provided by Dr. Jay Chaplin or Elevating Cancer Treatment is solely at your own risk. Dr. Jay Chaplin is a scientist and drug developer, not a medical doctor providing patient care. The content presented here reflects general scientific understanding and research, and may not be applicable to your individual health circumstances. Individual medical conditions and treatments vary, and no two situations are exactly alike.
Always consult with your personal healthcare provider before making any decisions about your health or treatment plan.

Transcript

SPEAKER_00 0:03

Hello everyone. I'm starting just a moment early to wave and say hello. All right. Welcome to yet another live. And this one is office hours, general questions. We've already got uh one and three-quarters questions in here. Um I do want to deal with a little bit of housekeeping information right at the very beginning. So uh again, for those of you who haven't heard this before, I am a PhD, not an MD. Everything that we're talking about today is medical education. It's not medical advice. Please talk to your particular healthcare team about that. Um, my lovely wife and our admin person, IT person, Pauline, is going to be moderating and putting things in the chat. If I mention a particular episode, something like that, she will post links in the chat. Um, you have to be a subscriber in order to be able to comment. So if you're trying to comment and it won't let you, it's probably because you're not a subscriber. Go subscribe. Uh there's a pinned comment at the top about the Git guidance link, and that's to be able to set up a free 30-minute consultation call with me. And there's also a pinned comment for the free uh overview document. 10 things to elevate your chemotherapy. Um, all right, and definitely let us know if you have topics that you want to see covered for future lives. I'm happy to do open office hours like this one, and it's also good to have topics occasionally, so let us know that. And I'll repeat this at the end. But our upcoming lives will we will have another one on May 18th, same time, 7 p.m. to 8 p.m. Eastern, and every two weeks after that. So we'll have one on June 1st and another one on June 15th. All right. Um okay. Um sorry, I am making some notes. And so the questions that I'm seeing so far, and and I'm sure there will be more, are number one, um, and this is from 22 Lance 09. Will cold shock proteins enhance NK cells? Got a definitive answer for you there. Uh, there's another one from Seamus about antigen expression technologies, and I I want to to drill into that and get more specific about it because I've worked extensively with antigen expression technologies in multiple formats. That is a huge arena. Um and then from Judith Costa, um, top five supplements and doses for cancer care. And that is a complex one. It depends a lot on the kind of cancer. So let me start with the first one uh for you, Lance. Will cold shock proteins enhance NK cells? And and the answer is a definitive no, but cold shock will. And and what do I mean by that? So the cold shock proteins themselves don't actually change the susceptibility of a cancer cell to being killed by NK cells. That that's just not really how NK cells work. NK cells have a very different way of recognizing cancer cells than killer T cells do. And so many of the things that cold shock proteins do, uh, which changes antigen expression, it changes the way those are displayed, it changes the way that your immune system can see something going wrong inside of a cell. Cold shock works that way for T cells, but it doesn't work that way for NK cells. But I said that cold shock does enhance NK cells, and and why is that? That's because when you stress mammalian cells, when when you stress a human being's cells, it will react to that and upregulate proteins on its surface that show that it is stressed out. Um, two of the major ones are called MiC A, MICA, and MiCB. Those are key stress proteins, and again, they show your immune system that that cell is stressed out. Now, whether it's cold shock or heat shock, both of those going outside of the normal temperatures will upregulate those proteins, MIC A and MIC B, on cells, and it will do that through cells throughout your entire body. But since cancer cells are already dysregulated, they're a little more finicky, they're a little less able to adapt to extremes of temperature, when you do that, they upregulate those signals more. And NK cells look for either an absence of the proteins that T cells require. So if a cancer or a virally infected cell is trying to hide from the T cells by eliminating those proteins, then an NK cell will find it and kill it. Or if it is very stressed out, an NK cell will find it and kill it. And so the cold stress upregulates the MiC A and MiC B proteins, the NK cells kill it. That definitely does work. Therapeutically, and I know this wasn't part of the question. Therapeutically, if you're going to use something like this, it is generally more beneficial to go in the opposite direction and do heat stress rather than cold stress. And here's why. And I realize I'm going a bit off the rails here. Um, cold stress upregulates those MiCA and MiCB stress proteins. And it will, for a very short period of time, make NK cells work better. And that is about all that it does. It doesn't really encourage misfolding of proteins, it doesn't load anything more onto the membrane, it doesn't give T cells more to react to. And excess cold actually suppresses most parts of your immune system. It doesn't suppress NK cells, but it does suppress T cells and B cells, antibody-producing cells. Heat does the opposite. Heat unfolds a lot of proteins that causes a lot more proteins to be chopped up, placed on the membrane, makes it easier for T cells to see them. It also upregulates those stress proteins, and it also generically activates your immune system. You can fake a fever. And Pauline, this is the fake a fever, excuse me, fake a fever episode would go well here. That um you can end up stimulating your immune system across the board with that. And so you're getting a three for one hit with a high temperature stress and a one hit with a low temperature stress. That one hit with low temperature is just NK cells. The three for the high temperature includes NK cells and T cells, so broader. Um so, Judith, in terms of uh the top five supplements for for cancer, it depends very, very, very heavily. Again, and I I've said this um a couple of times, it depends very heavily on whether it makes sense to try and stimulate your immune system to contain and eliminate the cancer, or whether you're going to go after the cancer itself, because many of those pathways interfere with the immune system. You for a lot of them have to pick one or the other. And so for cancers that are very amenable to being attacked by the immune system, your melanomas, your uh uh colorectal cancer, uh anything GI system, those are really good. Lung cancer in some cases, then it makes sense to go with more of an immune system boosting approach. Uh, you've got your baby aspirin, you've got your apigenin, which is another question. I saw that. Uh, you've got certain mushrooms, certain mushrooms work very, very, very well for stimulating different parts of the immune system. Again, please, please be aware the immune system is not one thing. It's a big collection of things, all with very different functions. So if you're trying to stimulate killer T cells, turkey tail mushrooms actually work very well. There's good data on that. Uh, chaga mushrooms work very well for that. If you're trying to stimulate dendritic cells, uh, the mitake mushrooms are good for that. And you can't take all of these at the same time, your immune system will go haywire, you'll get nowhere, and you'll just make yourself feel sick. So it's a matter of knowing which one you want to go for and structuring it appropriately. If you want natural killer cells, none of those work particularly well. You actually want to use a very highly purified extract of shiitake mushrooms called AHCC, active hexose correlated compound. So, so it again, if you're going for immune system boosting, those are some of my favorites, the the baby aspirin, the apigenin, um, and those mushroom extracts, the turkey tail, shaga, mitake, and AHCC. If you're going in the opposite direction, if you're trying to shut down the cancer, and particularly if it's a more inflammatory type of cancer, and not all cancers are inflammatory. Um, I know that's circulating on the internet. That is clearly not true. And and this is part of the reason that you have this interplay. Your immune system runs on inflammation. Anything that shuts down inflammation fairly thoroughly is going to shut down your immune function. So, curcumin in very large doses is actually a very good anti-inflammatory and very good at slowing or stopping the growth of many different kinds of cancer. It doesn't get rid of anything, it doesn't kill it, but it can stop growth for a period. That's very, very good. However, again, in doses large enough to have that effect, it will also suppress your immune system. Resveratrol actually works fairly similarly, very high doses of genistine, though many of these flavonoids that are sort of in the same family are not bioavailable. I I know many of you have heard a lot about quercetin, about uh there's a whole other number of them, physetine, etc. Most of those don't exit the intestines into your bloodstream. So, unless you are actually dissolving it in alcohol and injecting it, those guys don't do you any good. But um, just in general, if you're going for not immune function, but direct cancer suppression, um, curcumin, resveratrol, genistine, there are a few others there. And again, the very, very high dose vitamin K2 does not interfere with immune function, and it's good for anti-cancer. So that's sort of a foundational one that I would recommend. I hope that answers your question. It sounds like it's more nuanced than you were working for. Um be a dream. Okay. Um so moving down a bit, um, the comment about beetroot for red cell support, um, hemoglobin support during chemo, it there's nothing, there's nothing wrong with beetroot. It's not a particularly potent approach for that. Um you can use it. In terms of supporting red blood cells, often it's a matter of taking away things that interfere or structuring your chemotherapy well. Again, for most chemotherapies, and and I know this sounds counterintuitive, for many of your chemotherapies, your best and easiest bet to deal with them is to not, how do I put this, not let them cause the damage and then try and heal from it with something like beetroot, but to directly counter the damage with something like glutamine. Glutamine is very good for most of the traditional chemotherapies, whether it's doxorubicin that causes heart damage, whether it's oxaliplatin or taxol that cause GI issues, problems like that. Glutamine is very good for dealing with that, and it doesn't undercut the function of the chemo. So that's a really great way to go. Beetroots, good low doses of B12 and low doses of iron in a fairly consistent fashion and a very high protein diet tend to help with red blood cell and also platelets. Um, platelet counts are helped more by the folate and the deep green, leafy greens, the kind that you need to cook before eating. Um those are good. The one thing to know about pretty much anything having to do with red blood cell effects or platelet effects is that all of that is lagging indicators because your bone marrow has to make a precursor cell, that has to mature, then it turns into these things. And the the impact that you make today by changing something is going to play out in like a week and a half, two weeks. So you really have to be consistent with what you're doing, and you have to be patient and follow it all the way through. Does that make sense? Okay. Uh bah ba. I know I'm skipping a bit. I I was gonna write this these things down and get back to them in order. I I'm curious, um Rich, you're saying that apigenin has a major warning with ketruda for counteracting the specific immune activation required for ketruda to be successful. I'm very curious where you saw that, because apigenin is actually apigenin stimulates killer T cell function. It apigenin works well in combination with ketruda. It makes ketruda work better, not less well. So, so what you're saying is is very strange to me. It it's the exact opposite of everything that I've I've seen. I I'm not I'm not questioning you, I'm just questioning where you saw that from. Um it's very strange. Um and Ketruda and Linvatanib, Ketruda actually works really well with linvatinib. Um, in most cases, Ketruda is synergistic with linvatinib. That combination works better than either drug alone. So that warning with linvatinib doesn't make much sense to me. And they've been studied in combination. The combination has merely, how do I put this? If you take ketruda and linvatnib together, they have additive side effects. It's it's the same as taking the two separately and just adding them together, but the efficacy that you get is more efficacy than additive, which is really good. Um and levithyroxin, levithyroxin has absolutely nothing to do with Keetruda. That I have to say that I find that all very strange. Um if you find that, or if you can point me toward that reference, I'd be really curious to read that because again, that's exactly the opposite. Um exactly the opposite of what I'm honestly everything I've seen. Um all right. Um B vitamins for cancer with glioma, the B1, B3, niacinamide, and aspirin. I am not familiar with that. I'm happy to look into it. My understanding, I'd be really surprised if if that combination had any significant effect. Gliomas are already incredibly metabolically active and very metabolically diverse. Um, gliomas tend to make and export pretty much every uh metabolic substrate and and vitamin. They recycle vitamins and export them to their surrounding cells. Um, really, the only thing that they are deficient in in any way, shape, or form is sugar. They are sugar hogs. Um, but I will look into that. The the thing that I would be concerned about if you try and go down those roads is that you stick to those particular B vitamins because XSB12, which comes along for the ride in most multi-B supplements, XSB12 is especially bad for gliomas. So if you go this route, uh definitely look at those individually rather than as a complex, and I will look into that and get back to you. All right. Um that's not there. Okay. Uh dose and function for apigenin. So that was a little higher up there. Um yes. Uh dosage for apigenin depends a little bit on who you are. So for the vast majority of cancers, um, pretty pretty much all of the cancers that you would use apigenin for, and and I'll come back to this in a moment. The dosage is 200 milligrams per day. And it helps to take that with a meal with a little bit of fat in it, whether it's fat from a steak or fat from olive oil, something like that, it's all good. It's just to have something to carry it along into your system. Specifically for breast cancer, because there's a bit of a paradoxical phytoestrogen effect. If you take a little bit, it may trigger an estrogen-like sensing pathway and increase growth. If you take a higher level, that does not happen. For breast cancer, it makes a lot more sense to pulse it to take, say, a week of higher dose, say 600 milligrams every day, and then take a week off. So you're going above the threshold for a while and then below the threshold and staying away from that. Now, now, apigenin, again, the places where it is useful, there are really two. So, one of the places that it's useful, it, and again, this is this is where I come back to to your comment, Rich. The place where apigenin has been useful is in activating and potentiating killer T cells, CD8 positive T cells, because it blocks the thromboxane A2 receptor, and thromboxane A2 tells T cells to not work as much. It tells them to put the brakes on. By blocking that, you actually get more activity out of the killer T cell system. This has been shown repeatedly. It's the same system, but a different part that baby aspirin works on. So if you are looking at stimulating immune function, particularly killer T cells, that's a place where apigenin can be really useful. Now, there are some cancers that don't fit that very well. Most breast cancers don't respond. Terribly well to immunotherapy. There are exceptions, but in general, they don't. Prostate cancers, pancreatic cancers, there are a number that don't respond well to immune system control. And for those, in general, apigenin doesn't make a lot of sense. But the other place where apigenin also makes sense, completely separate of immune system boosting, is the space of mitigating side effects from certain kinds of chemo. So apigenin is very good at increasing the efficacy of phi fluoruracil, its prodrug, cape cytabine, uh eriniticin, any and all of those. And so that will increase the efficacy of those chemotherapy drugs at the same time that it protects from the nausea and diarrhea and GI distress that those typically cause. That's been shown in multiple clinical trials. Similarly, um apigenin is very, very good at offsetting some of the effects of oxaliplatin and carboplatin, the whole platin class of drugs. So again, being able to, and and also um doxorubicin again with the heart damage, being able to offset those side effects is a great place to use apigenin. Again, 200 milligrams a day consistently for just about anything other than breast cancer, where you want to go very much higher above that and pulse it. Good. All right. Um as you can see, there's a lot of details to a lot of this stuff. If you look at most YouTube content, most social media content out there, it is just blanket. Do X, it's great for you. This one thing works for all cancers or it works for all cases. Again, this is this is one of the things that I work with people on is individualizing all of these. Because again, if you got the message that apigenin is great, and you got the message that it's 200 milligrams per day, but you have breast cancer, you might not get that caveat about needing to go to a higher level to make sure that you're not stimulating the breast cancer. That's an important thing to know. You might hear about apigenin for its immune boosting function, but you might not hear about it for mitigating side effects. All of these things, all these details are really important. And again, that's something that I enjoy and do well. That's something we do with clients. Um, moving on. Uh triple F355. When a drug in development that is eligible for FTD to skip phase two to three and able to use ORR as an endpoint approval, is it significant? Ah, the BICE specific for Claude in 18.2. So skipping phase two is always a bit dicey, and it's important to understand what the different phases are. Um, how how many of you, and I know I probably won't get to this till later, this is more for my education about where you're all at than answering the question. Um, do you know what the different phases of clinical trials are for and and what they support? So in in cancer trials, very often it's done differently. Phase one and two are smooshed together. That is very common, but to skip phase two entirely is a bit dicey. So phase one is your safety trials, making sure that you know, just because it the drug worked in mice and dogs and monkeys doesn't necessarily mean that it will be safe for human beings. There have been many, many drugs that work very well in lab animals, and as soon as you go to human beings, they become lethal. So phase one is safety testing. You have to do that no matter what. Phase two is finding the right dose, because again, dose is critical. If you give too little of a drug, it may be a fantastic drug, but if you give too little, it's not going to be able to do anything for you. If you give too much, you run and run into an issue with side effects. You overdose, you don't get any more benefit, but you cause massive side effect problems. So phase two is finding that dose, finding that sweet spot where you get as much efficacy as you possibly can and you don't cross over the line and start causing more problems with side effects. Skipping phase two means jumping blind into efficacy testing, phase three. Now, for bi specifics, we do have a pretty good idea how we should dose those. You could make a pretty good educated guess and get within a factor of four, but a factor of four could easily mean you're not getting as much efficacy as you should, or you're getting significantly more side effects than you need to. So it is a bit dicey. Um, the nice thing about clotin-18-2 as a cancer antigen, it's a bit of a weird one. Clotinate 18-2 is all throughout your body, it's everywhere. But what clotin 18-2 does is it's a tight junction protein. It's it's part of the molecular glue that holds cells together. And so it's not on the top sticking out, it's only in between the cells where antibodies can't get to it and they can't do anything, except that cancer cells overproduce it and dysregulate it, and now it's sticking up all over the place, and it's able to be seen and tagged with the antibody and bring in killer T cells in order to function as a bispecific T cell engager. And now that brings T cells in and forces them to recognize the cancer, even if they normally wouldn't. That is actually a great way to go. Um, I I just I wish they wouldn't have done that, because again, it's it means that people they're gonna move to phase three without having optimized the dose, and they're not gonna know if they're doing excess harm or providing insufficient benefit, and they're just gonna run right into phase three, and as soon as phase three is done, if they get enough data to get it licensed, that will be the dose that will be fixed for everyone everywhere, unless they go back and redo it. To have done a phase two ascending dose trial, if if they did it properly and if they compressed it as much as possible, they should have been able to do that with only adding another month or two to their phase one. So it's it's a very strange approach. Um, and can a phase three be done with under 400 patients? It can. That's pretty thin. Um for a first in class kind of drug, normally you want to see 600, 700 patients per group. Um you can potentially get away with 700 total if you do a crossover study where where you have half of the people start with standard of care and half of the people start with the experimental drug, and then you flip-flop those. Um, so everybody ends up getting the drug. That's that's an easy way to go, and it limits your size because everyone is both in the control group and everyone is both in the treatment group. Um yeah. I could talk about this for hours. Um Lance, can the people who increase their terpene concentration also hands? Lance, we we should talk about that offline. There there is a lot of territory there, and it depends a ton on the details. Um that jumped too far. Tanya just passed a second round of carbotaxol. I'm assuming that's carboplatin and taxol. Uh, is there anything specific I can do for the side effects to those drugs? Okay. Um we'll come back to the BRACA one. So again, for carboplatin, carboplatin, a good way to mitigate a lot of those side effects. Carboplatin causes an upregulation in calcium, and calcium precipitation in the nerves is a significant component of neuropathy. Before you go in for your infusions, try and limit calcium, limit your dairy, limit antacids containing calcium, throttle back on your calcium and dramatically increase your magnesium for the couple of days going into your platin class drug infusion. Again, you can also take glutamine. We did a whole episode, Pauline. This is a great place. We did a whole episode about glutamine and we did a whole episode about neuropathy, both of those. Um, so glutamine is really helpful for preventing neuropathy there. In terms of the taxol component, the glutamine doesn't help so much with the taxol neuropathy component, but high-dose vitamin E does. Um, so that's useful. And in terms of GI issues, again, glutamine is your best friend there. Um and definitely if if you want to talk more, uh set up a free consultation call, talk to me, we can go through your specific situations. With the BRCA1, it depends a bit if the BRCA1 is hereditary. If it's hereditary, if you've inherited it through your family line, then it's in every cell throughout your entire body. That is a very different case. That will predispose you to cancer, but it doesn't open up treatment possibility. If the BRCA1 mutation is just in your cancer, then it opens up treatment with a whole class of drugs called PARP inhibitors, P-A-R-P, parp inhibitors like oleparib or rucoparib. Those are very good. They're commonly used, pretty much only used for breast cancer and just now beginning to be used in prostate cancer, where there are also quite often BRCA1 mutations. But if you have a BRCA1 mutation and you can convince your oncologist to write you a script for off-label drugs andor get your insurance company to cover it, if you have a BRCA1 or BRCA2 mutation in your cancer specifically, those drugs, the PARP inhibitors, are a really good, really good way to go. Um is there a cancer treatment in early clinic, pre-clinic that you're particularly excited about? I there are actually many drugs that are coming up fairly soon that I'm very excited about. But honestly, one of the ones that we got a data report out on fairly recently, the Diraxon RASIB, everyone's been talking about it for pancreatic cancer, but the the value there is so much bigger than just pancreatic cancer. Again, it's a strong drug, it's a harsh drug, but it allows targeting of the entire RAS family signaling pathway. Um, KRAS, HRAS, NRAS doesn't even have to be mutated, covers pretty much all of the mutants anyway. That is absolutely enormous. That drug will be out this year. That's going to change things for a tremendous number of people. I'm very excited about that. Oh, triple F355. Oh. You just had to poke the bear, didn't you? You had to poke the bear. Uh, the PD1 veg F development trend. It has been, it's been about three and a half months since I have looked into that at all. Um, I got very tired of hearing about it. I it was the only thing I heard about for a long long period of time. Uh, so so what this is, for those of you who don't know, Merck's blockbuster drug, Keytruda, is going off patent fairly soon. There has been a big rush to find the next big thing in immunotherapy. And there is there's very little good thought going into this. Um so somebody in the business sphere of biotech, not a researcher, not a scientist, uh, came up with the great idea that we have key truda and it's going off patent, and we want to capture that that market. And we've got another great drug, a vastin, that blocks angiogenesis. It blocks the formation of blood vessels to a cancer, so it cuts off resources to the cancer. They're both big blockbuster drugs that are either off patent or going off patent. Let's just smoosh the two of them together and make one combination molecule. It it sounds great if you don't understand anything about the biology. The trouble is that these two drugs work in completely different spaces. One of them works on the surface of the immune system cell, the other one works in the space around a tumor. They work on different things. One of them, again, binds to the immune cell and protects it from go kill yourself signals that the tumor sends to try and protect itself from the immune system. The other one is supposed to float around in huge amounts. You need huge amounts of it, of astin, you need tons of it, to bind to the hormones that the cancer secretes to try and recruit new blood vessels to it. The amounts of these drugs that you need are vastly different. You need eight times as much vastin to have a good effect as you do anti-PD1, ketruda. Eight times as much. And they work in different spots, they work on different cells, they work in different ways. Putting those two together, putting those two together, you're gonna get added benefit over either drug, and that's what people are showing. This combination is better than quetruda. Yeah, it's better. It's it's a little better. It's like five, ten percent better. Is it better than a full regular normal dose of quietruda and a full regular normal dose separately administered of a vastin? No, it's not as good as the separate independent drugs. This is just a business development way of developing one drug that captures the market, but it it's not it's not an improved drug. It's not a better drug. It is a cash grab, and we don't have to think about it too much kind of drug. Um I'm I'm I'm about as excited about that as I am a new flavor of pickle, and I hate pickles. Um Deb, I I see your comment, and we should talk about that. I am very curious about that. Apigenin apigenin can be a problem with ketruda, but not because it blocks the function. It can overactivate the immune system and cause more side effects, which is why when you add it in, you have to add it in very carefully. But it it doesn't it doesn't block ketruda that that's odd. Um Judith, okay, um can't take mushrooms because of gut distress, uh, various mushrooms. What's the next best alternative for mushrooms for immune system stimulation? Then you start moving over to cytokines, uh like IL-2 and IL-15, and things like Anctiva, though that's incredibly expensive and not particularly durable. Um, there are some things that you can take that convince your body that you're having an infection, um, particularly toll-like receptor agonists, but those are very, very, very difficult to dose. And if you if you get it right, they can be good, but you're running a very, very high risk of causing a lot of inflammation, a lot of distress for not a lot of value. Um yeah, we we should talk more about that. There are some approaches, honestly, probably again for for immune function, probably again, the baby aspirin, the apigen, so the the baby aspirin effect does wane as you get older. As you get above 70 years old, the baby aspirin has less effect. But baby aspirin, apigenin, uh, faking a fever by raising your core body temperature, all of those are good and don't involve the beta-glucans from mushrooms. Um, dietary steric acid versus oleic acid in dealing with metastases. Um I would be cautious, John, about overinterpreting the data there because the the data showing that steric acid increases metastatic activity is primarily cell line data. It's showing upregulation of signaling pathways that promote metastasis, but that's not that's not really the same as human clinical data. Those cells that we have in culture have been lab adapted for sometimes decades, almost always decades, in some cases up to 70 years. They're not like human cells anymore, they have very different biology. Uh again, Pauline, this is a a good place for the um cell line problem episode. Um so so there's that, and even if those cell lines are then implanted into small animal models, the behavior is still not that of an actual cancer cell. And when we when we look at these things, nobody consumes just steric acid. There are there are a number of other components. And so, you know, how how do we balance these things when you quit talking about a particular compound? Steric acid, in and of itself in a purified form, may or may not promote metastasis. But steric acid in animal products, well, those animal products also contain transvicenic acid, and transvisinic acid is an immune stimulant and contributes to cancer control. And so you're consuming a mixture of these things. You're consuming something that might promote metastasis, and you're consuming something that might significantly improve immune function and suppress the cancer. What do we see from actual food items versus artificially purified single molecules that are given in a way that really doesn't mimic how we eat? We can come back to that, but but right now I really don't think there's enough data to say with any any real compelling argument either for or against any of those. I I'm still not convinced by the transvasinic acid piece. I'm still not really convinced by the steric acid piece or propionic acid. Um we jumped ahead. So Deb AI and the drug interaction website. Okay. Yes. Was it AI or was it the official drug interaction website that I told you about? So the drug interaction website is just going to post interactions of any type whatsoever. And and for all of you who are looking online and using AI, there's absolutely nothing wrong with using AI. I just want to point out from my own personal experience that when I test AIs and I do it on a fairly regular basis, I have a handful of questions that I use where that there are technical questions that have binary answers. They are either yes or no. So I regularly ask those questions of multiple different AI platforms. And so far, pretty much all of them have about a 40% rate of confidently saying the exact wrong thing. So AI is a great place to start, just like Wikipedia is a great place to start. Google's a great place to start, not a great place to finish. You really want to take that and you want to fact-check it extensively. I can definitely see apigenon being flagged as an interaction with Keetruda on the drug interaction website because it increases ketruda efficacy, not because it decreases. So that can that can lead you into significantly worse side effects unless you're careful. And so that's why you want to add one thing at a time. You don't want to add turkey tail and AHCC and chaga and baby aspirin and apigenin all at once. That is a great way to have your immunotherapy go gangbusters and give you massive, massive GI distress, rashes, attack your thyroid, attack your adrenals. You don't want that. You want to make sure that you're not having any interactions with your therapy right now, and then add a thing at a time, add one at a time. Start with something that is fairly focused, like the turkey tail. Take that through an infusion, see how your side effects are. If they're still good, then you add in the chaga. Take that through around, see if it's still good. If that's the case, then you add in baby aspirin and apigenin. See if that's still good. If that's still good, then you add in the next thing. But do it in a sequenced approach rather than throwing everything in, because that really does have a higher risk of causing bad side effects. All right. Ummunity Bio is trying to expand on its bladder cancer any. And again, the FDA hates that. Um, I really do think Anctiva, if it was used appropriately, could be good, but the way that they're using it and the way that they're testing it, I wouldn't bet on it. There, there's plenty of companies that if we had if we had spare money sitting around that I would invest in because there's great things happening in the cancer treatment space right now. Um, Anctiva and Immunity Bio, I just don't see them getting their act together. Um Dan, I was told by my doctor that while being treated for P16 tonsil tumor, the apigenin would conflict with something else in my protocol. Um it's it's highly unlikely that apigenin would have conflicted with anything. However, if you have a P16 positive cancer, that means that the cancer is being caused by or heavily influenced by an HPV, human papillomavirus infection. So if that's the case, something to know about HPV infections, they cause a downregulation of that protein that I mentioned earlier, the um major histocompatibility complex or human leukocyte antigen complex. Immunologists are awful. They gave the two completely different names to the exact same thing. HLA is the human version, MHC is the version in every other animal. They are the same darn thing. Um, so those proteins are shut down by HPV. It's a way to hide the HPV infection from the immune system so that they're not killed off. That means that apigenin, which primarily works on T cells, isn't going to actually help you with that particular kind of cancer. Because there's no HLA class one or MHC class one, T cells will not help you, and apigenin revs up T cells, not going to help you. What you want there is not the turkey tail or chaga or apigenin or aspirin. You want the AHCC, active hexos correlated compound. It's an alpha glucan. There's good clinical trial data on that. I would look that up. Specifically, HPV and AHCC. Good stuff. Yep. Uh, question on vitamin K2. Bought a bottle, but unsure about it. Uh Hodgkin's lymphoma. Left a message for another person saying it was questionable for some. So, so K2 does seem to be a good approach for most kinds of cancer, and especially for all of your uh blood cancers, immunological cancers, Hodgkin's lymphoma, non-Hodgkins, uh multiple myeloma, ALL, all of those. Um the yeah, um the place where it doesn't work, the K2 approach does not work for calangiocarcinoma. It doesn't really work very well for breast cancer. You need a huge whopping dose. The dose is already huge, but for breast cancer, it's even higher. And it does not work at all, at all for gliomas and astrocytomas. But for Hodgkin's lymphoma, it should work just fine. Um, the one thing that I'm sort of kicking myself about with that episode, Pauline, that's that's the K2 episode, is when I recorded that, I was not very clear. I talked about taking it for three days and then taking a long break. And the long break definitely has to happen, but the three days is the minimum. You really have to take it for at least three days because it has to build up in the cells, it has to build up in the mitochondria in order to have that function. Um, so so with that, three days is the minimum, but I never said the maximum, and that left most people with the idea that you take it for three days and that's all that you can do. You can actually take it for up to about two weeks. But after that two weeks of taking it, you really have to take a break for another two weeks and let it calm down and let the rest of your body recover. And so that that actually puts it on essentially the exact same schedule as the doxycycline approach that I talked about in in different episodes. That's the doxycycline episode, Pauline. Um you can do those two together, and because they're both mitochondrial focused, you get more efficacy out of doing those two together on the same schedule than you would if you did them separately. So that works well. Umctiva is gonna be safe. Um, the the only real issues with Anctiva in terms of safety or tolerability is when you start injecting it. When it goes sub Q or when it goes systemic, you can have massive immune system flares. It doesn't tend to cause a cytokine release syndrome the way that many T cell-focused drugs do. But the safety isn't that big of a deal. It's it's just the efficacy that's going to be the question with Anctiva. Uh, head and neck HPV, they said it was easy to treat now two years later, and after chemo radiation and immunotherapy is spread to the liver, throat, and lymph nodes. Hey, Elka set set up a call with me. They uh they should have been able to do better than that. HPV uh requires some modifications to treatment. If they just did standard of care treatment uh for him, then uh then it's likely that they were not as intense as they needed to be. And that's unfortunate. Um but that uh that doesn't mean that there isn't more to do. Um gotcha, Tanya, okay. Um the piece, how bad is it that is spread to the liver? It it is bad, it's harder to dose a lot of things to liver mets because the the liver is the primary source of metabolism and elimination of very foreign chemicals. So something gets introduced into your body if it really doesn't belong there, and we don't have normal metabolism systems for it to get rid of it, it gets processed by the liver, it gets made more water soluble and inactivated, and you pee it out. That that's that's what happens. And all the enzymes to do that are located in the liver. And so this creates a problem, not so much for immunotherapy, but for most chemotherapies and most kinase inhibitor drugs, that kind of thing. They don't tend to work as well for the liver because it's kind of like imagine you you've got a sink and you've got water running and it's continually going down the spout. That's your exit hole. Now try and plug that spout with cotton candy. As soon as you stuff it in, it's going to get dissolved, it's going to get flushed down the drain. That's kind of what you're trying to do with a lot of these small molecule treatments. Again, not the immunotherapies, but chemotherapies and targeted therapies. If you're trying to target something in the liver and the liver is the organ that's getting rid of those drugs and flushing them out, then it's really hard to do that. You do tend to have to have either multiple drugs that work through multiple pathways or give a higher dose to compensate for that, or use very specific drugs that are not metabolized by the liver. Again, give me a call. Let's talk about the particular specifics. All right, uh, I'd mentioned to take artemisinin the day before and the day of ADC. Should apigenin be added in as well? I would not. Um, so so again, apigenin is good for stimulating immune function and it's good for blocking side effects from many different kinds of chemo drugs. But ADCs or antibody drug conjugates deliver the vast majority of their cargo directly to the cancer. And so apigenin isn't really going to help you with preventing those side effects, and it's not stimulating the immune system during a time when it could potentially take up this ADC and hurt itself in the process is not a great thing either. You really want to keep your immune system quiet around infusions, including ADC, something like that. I believe we also talked about taking high dose vitamin D3 the day before and the day of. The the artemizanin actually works well with the particular ADC that we're talking about. I sorry folks, this is a client. Um the particular ADC that we're talking about, because that ADC antibody drug conjugate has a payload that works on DNA and the coiling of DNA and ends up damaging DNA. And artemisinin also damages DNA through a different pathway. And so two different things attacking the DNA and maintenance and repair processes together at the same time, they have much more potency together than they do separately. And that's why we're specifically talking about artemisinin. I would not add in apigenin. At best, it does nothing and it might slightly increase immune system damage from the ADC. Um chemo brain. Yeah, and gym cytobean will do that. Um Diane, that that is a very good topic, and it's not one that I can cover in the next couple of minutes. Do keep reminding me about that though, and I should put together something in the next week or so in terms of episodes. I I our next episode is pretty much in the can. I wanted to talk about how to talk to your oncologist and how to have better and more fruitful conversations with your oncologist. That's next, but uh chemo brain is actually something that's been coming up for a lot of folks lately, and I should definitely dive into that. Thank you for bringing that to the top. Um MNCs are now going overseas for assets licensing. Uh we actually we did an episode about that one too. Um early research, uh anything up to clinical trials in the US has pretty much stalled and tanked um since about March last year. Um it was bad before, but it's getting worse. Um development inside the US, early development is is stalled, it's all late stage. Um 50,000 IU vitamin D. Vitamin D is not cytotoxic. I I know that there is there's a lot that is said about that. Um, you cannot take an amount of vitamin D that directly uh hurts your cancer. You can use it to slow growth somewhat, you can use it to inhibit immune function or support immune function, depending on the dose that you're taking. But in terms of actually killing cancer cells, the the only data for that is in cell culture systems again, and those cells are are not remotely reflective of actual cancer in the body, and you can't get that amount of vitamin D into your system. Those amounts are absolutely insane. Um yeah. Uh moving down. My lovely wife saying he really does hate pickles. It's true. I let me back up. I will end on this, and and I see you there. Very happy one. Um I grew up next to a pickle factory. Apparently, when I was a very small child, pickles were one of my favorite foods. My family moved when I was three and a half. They moved to the LA suburbs. We moved two blocks away in downwind of a self-sustaining pickle factory that made its own vinegar. So giant grain silos full of rotting grain with water sludge in them and bubbling air from the bottom. So it wouldn't go to alcohol, it would go all the way through and make vinegar, which made this absolutely horrible, horrible smell. And my little three and a half-year-old brain put together the image of the pickles on the side of the building and on the side of the trucks going in and out with that horrible smell. And pickles went from being my favorite food to something that I couldn't stand, and it was all psychosomatic. If I didn't know that I ate a pickle, I was totally fine. A little bit of relish mixed in. If I didn't get it, fine. If I realized that I'd eaten a pickle, projectile vomit like something out of the exorcist. Literally in a Bob's big boy when I was a teenager, vomited over, out of my booth, over the next booth, over the next booth, into the third booth. Yeah. Um, I can't eat pickles now, still don't like them. Not my favorite, but it's all psychosomatic. I can eat pickled onions, I can eat pickled asparagus, I can eat Indian pickle, which has nothing to do with pickles. Um, but pickled cucumbers, no, just don't like them. Probably never will. That brings us past eight. This has been awesome. For those of you who didn't get your questions answered, still keep them coming. I will take a look at those and and try and answer them in upcoming episodes or wedge them into lives. And again, please do add anything that you want us to cover as the topic for the next live. It would be really good, at least for every other live, to have a focal point and try and stay on track. Thank you all so much for coming. Really appreciate you all. Um again, May eighteenth, June first, June 15th, seven to eight. Awesome. Take care.