80: Why Biologics Fail (Humira, Remicade, Stelara, Skyrizi, Entyvio, etc.)

Biologics are not as reliable as your doctor makes them sound. In fact, 30% of patients who get one have no response, and 1 in 6 will have it fail within the first year. 

Worse than that, once you do get your biologics - it's almost guaranteed to fail at some point in the near future anyways. So why is this happening and what can you do to reduce the risk of your biologics from failing?

TOPICS DISCUSSED:

• How biologics work (Humira, Remicade, Stelara, Skyrizi, Entyvio, etc.)
• Important stats on biologics you need to know
• Why biologics fail
• Why some biologics work better than others
• How to get the most from you biologic drug(s) and how to reduce the risk of failure

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Transcript

0:01

Biologics are common drugs that are used in Crohn's and colitis, but do you know why they'll work one day and then someday they just stop working? It's like, oh, I was getting really good benefit out of the biologic for X amount of time, suddenly I'm not. What's going on? Well, in this episode, you're going to learn why this keeps happening, why some biologics work better than others, and what you can do to get the most out of the biologics you're taking right now to make sure that you feel as healthy as possible for as long as possible. Contrary to what your doctors told you, Crohn's and colitis are reversible. Now, I've helped hundreds of people reverse their bowel disease and I'm here to help you do it too, because inflammation always has a root cause. We just have to find it. This is the Reversing Crohn's and Colitis Naturally podcast. Now, I do these live trainings in my Facebook group every single week and put the audios here for you to listen to. If you want to watch the video versions of these episodes, just click the link in the show notes to get access to our Facebook group and YouTube channel. And for weekly updates, information, tips, and tricks, you can sign up for our email list by clicking the link in the show notes below. Now, I will preface this. If you don't know me already, my name is Josh Dech. I'm an IBD specialist, physician's consultant, and researcher for Crohn's and Colitis root causes, and I'm here to help you learn how to heal yourself naturally. At the end, we are going to take some questions. As a preface, even though I'm in the functional medicine side and I look for root causes, it doesn't mean I'm anti-medication. I'm not at all. The problem I have with biologics and medications as a whole is how they are used, which is we take these chronic inflammatory conditions. We take acute treatments like Humira and Tibio, etc. We take this chronic inflammatory condition and use acute treatments chronically. It's not the way to actually get better. It's a way to manage pain. I describe it simply as this. If you've got a nail stuck in your foot, that hurts. If you take numbing cream and put it on every single day and the pain keeps coming back, you're medication dependent. It's not the way to remove the nail or heal the foot. The same thing in bowel disease. Using biologics gives you great relief. It's sometimes very necessary. So, we're talking about that in that context today. Not that they're the be-all end-all and not that I believe they're the only solution. I know for fact there are root causes. We've seen it. We're getting research published on it as we speak. So, all that being said, we're talking about the use case of biologics in the sense of still working towards root causes, which we'll also get to. Here are some stats we do need to know. When it comes down to a few different things surrounding biologics, we obviously want to avoid surgery. We're dealing with surgeries. It's very common in Crohn's colitis. In fact, 75% of Crohn's patients and up to 30% of colitis patients will need surgery at some point in their lives. That's major abdominal surgery, resections, colostomy bags, whatever it may be. We also know that 25% of patients who are taking drugs like infliximab will still end up with surgery within five years. So, we know that 75% of Crohn's and 30% of UC and 25% on those, the particular study was infliximab. I'm not saying it's not the best drug, just saying that's what the study was on, are going to need surgery. These odds are not very good. So, there's a couple of things we can do to hedge against these odds. Number one, we'll get to that later, obviously looking for root causes. What are the drivers of your bowel disease? The big one, number two, is pairing yourself with the right biologic sooner. There is a way to do that right now. Doctors are kind of shooting in the dark, but there are ways we can start looking at to get better at it. I'm getting some research out on that, hopefully sooner than later here, and working on some systems for you guys. So, if you're looking for biologics to help you find one easier. So, these are the stats on surgery. Here's what you also got to look at. Biologics themselves have their own set of data. We know surgery is in the cards. We don't control the inflammation. Inflammation erodes the tissues. You need surgery because it's going to perforate. You can die. It's life-saving in the event it gets there. Here's the thing. We know that 30% of biologics or patients who go on biologics will get no response from the first one. You go to the doctor, they say, yep, try that out. Didn't work. Oh, well, let's try the next one, which can take months to get you through, sometimes a year or more, to find one that actually suits you. We also know that once you do find that drug, 17% of patients within the first year, it'll stop being effective. This is about 1 in 6. So, 1 in 3 get no response from the first, so you're guessing, guessing, guessing. It takes you 6 to 12 months to find a drug. You finally find a drug, get your 30 bowel movements a day under control, there's a 1 in 6 chance it's going to stop working within a year. You got to rinse and repeat the cycle. That sucks. We also know that once a biologic sticks, so you went through, you're the 1 in 3 you got unlucky, you're the 1 in 6 you got unlucky, so you finally got one that sticks, you tried it. Only 50% of those people actually get enough relief to call it remission, to call it clinically, you're good, you're in remission, you're down from 15 bowel movements a day to 5 or 6, they're calling that remission. Only once all this pans out and everybody finds the drugs that they want, roughly 20 to 25% of people actually get what's called histological remission, which means now they have no inflammation, the scopes and colonoscopies can't find any inflammation, like on paper, per scopes you look good, you're still drug dependent, but you look good. But drug dependency is the key here. You need these to keep you in remission. That's the problem I have with them. On top of that, I'm going to throw some more numbers at you. If you are finding a biologic that finally sticks, so 1 in 3 doesn't work at all, you finally get one, you're the 1 in 6 and it fails, then you finally get one, you're one of the half who's going to get some relief but not enough. We also now know that 64%, a little over two-thirds of people are going to need steroids in a year as well, or within that year. The stat is specifically steroids at least once a year, is what the data said. So even though your inflammation is being pushed down, two-thirds of people need steroids at least once a year for breakthroughs and flares. And then you finally go through all this, and then 50% of biologics fail within five years. So you've gone through all of this, 1 in 3 you get no response, you finally find it, then you're the 1 in 6 who's unlucky enough and it just failed in the first year. It takes another one or two years, you finally find a drug. So here you are three years in looking for drugs with nasty side effects, minimal to no relief, they're putting you on drug after drug after drug, you finally get one that sticks. 50% of you, if that, are going to have enough relief to say yes, I'm in remission. Most of you are going to get some relief, maybe from 50 bowel movements down to 20. That's still a rough way to live. Then a few or even fewer get true histological remission and that's going to fail half the time anyway within a few years. So no matter what you do, this is effectively a no-win situation with health that's up and down and up and down and you're guessing and hoping and praying. That sucks. So what we need to know is a couple of things. Number one, it's how do you find the best one that suits you? Number two, it's how do we understand or what can we do rather to get the most out of your biologics? How can you make them more effective? And that's what we're going to be talking about. Now in order to understand that, I want to talk about why some biologics work better than others. When your immune system is overactive and inflamed, picture your immune system kind of like an octopus. That's a lovely little octopus. All right. He's very happy. Your octopus will be sad because now he's inflamed. Okay. So picture your immune system like an octopus. There are all these different arms, right? We name these different things. In bowel disease, we see different arms. We call them Th1, Th2. We can see Th9. We can see Th17, Th22. Treg is a common one. These are called T helpers. There's different paths of your immune system we can see. Now, when we're looking at your immune system being active, not all things activate all paths of your immune system. So all these arms aren't busy all the time. These are just things that we tend to see in bowel disease. So what we're looking at with you now, we want to figure out which immune pathways are active. Because here's the thing. Let's say one, two, and nine are really active for you. They're over inflamed. You're dealing with a symptom specific to each pathway, but that's another conversation. Then you get on a drug. Well, that drug might only help suppress number two. So two thirds of your active immune pathways are still active. That's why the drug only works a little bit. If you get a drug and your pathways one, two, and nine are overactive, and that drug happens to call them one, two, and nine, you might be one of the few people who get into full histological remission. So your drug is actually suppressing enough, and now you're symptom free, and there's no inflammation. You look good. But it's kind of like shooting darts at a board in the dark. We don't really know which one's going to work for you or why. So different drugs do different things. You have anti-TNF drugs like Remicade and Humira. They're very broad spectrum. They do a decent job of hitting a lot of things, but not all the things. You get breakthroughs. You have your anti-integrin. So you've got your, that's an antivio. It's very gut selective, but that blocks the white blood cells like neutrophils. These white blood cells are part of that immune inflammatory response that create the inflammation and pain. So it blocks them from getting to your gut. It's very gut selective, which is good in theory, unless it's not your immune pathway that's elevating. Right? If you look at Stelara, it's what we call an IL-12 and 23. It's unrelated. It means, anyway, different pathway. But point being, you have this drug that's targeting specific signaling proteins. It's like, hey, we're calling for help, and it dampens the signal to call for help. So they don't really get to where they need to go. So what we effectively end up with here is different drugs targeting different immune pathways. We end up with what we call a lock in key, where you have the wrong key for the wrong lock. Your immune pathway is the lock. There's a certain something, a combination of things you need, and a certain fit to get your immune system suppressed enough. What we don't have is the correct key to fit that perfectly. It might get in there. It might fit. You might get a little twist. I'm sure you've tried a key in a lock before. You're like, hmm, that's not quite getting in there. It doesn't even fit into the lock. Got it. Next one, oh, I got it in, but it didn't twist. Got it. You try the next key. Like, shit, that one worked. That's the house key. I figured out which one it is. Yay. Because the lock in key doesn't always fit, and that's the issue. So we end up having the wrong tool for your specific pathway of inflammation. So that's why biologics don't always work. What we can get now is what we're gonna call the flicker, okay? So now we've got this lock in key. I'm gonna write that up here. You got this lock in key. So you're looking for the correct fit to your specific inflammatory type. Now we end up with what's called that flicker. And this is when those stats come in, right? We know that 50% of biologics fail within five years. We know that one in six fail in the first year. It's like, oh, they worked, but then they didn't. So it's on, then it's off. We're gonna call that the flicker effect, something we just named right now because and that's the way, that's the law according to the rules. So the flicker, why does this happen? The problem is we have a couple of different things going on with your immune system at the same time. The first one, think of it like a Trojan horse, right? Your immune system, it's designed to find foreign proteins. That's its job, okay? Biologics are large proteins. So what happens is your immune system's on the alert for these proteins, specific types of proteins. Biologics are like proteins, they're just a little bit bigger. So it's unexpected. We don't expect it to be a problem, but it kind of is. And what happens, you create these anti-drug antibodies. So if you have a protein that looks like a protein your body's already got a reaction to and that drug, that biologic is that same or similar looking protein, your body goes, oh, we know you, bounce. And now your immune system reacts. That's number one. Number two, we also have clearance. Now, clearance is a problem where your body clears out, burns up, or uses up that drug faster than it typically could or should in a better circumstance. So your body gets rid of the medicine too fast and so you end up with these low trough levels. And the amount of drug left in your blood, it drops low enough, you have a breakthrough flare. Think of it. If I'm trying to push through, I'm trapped inside of a box and I need 30 pounds of pressure to punch through the top of that box, that drug is keeping me weak. All I can do is apply 20 pounds. I don't have enough to get that box broken. But let's say that drug wears out of my system. Now, suddenly, I can push 32 pounds. I can suddenly break through the lid. It's not a lot, but it's a little bit. Maybe I'm capable of pushing 40 pounds through the lid of that box, but the drug's got me capped down at 20. I'm not breaking through. Suddenly, that drug wears out of my system very quickly. Boom, I punch through the top of the box. I'm trapped in. I can escape. Not the best analogy. Didn't think that one through. But you get the idea is that your immune system, when it's not suppressed enough, it breaks through because the level, the trough levels of drug in your blood have come down enough. It's not suppressing your immune system. It's not strong enough to keep it at bay or not reactive. And so it breaks through. And now you have a reaction. That's what happens when you burn through. The other is now we have going to call this one your escape. There's always an escape pathway. Your body is highly intelligent. And this is the biggest contention I have with using these drugs chronically or acute drugs chronically on a chronic condition. There's always an escape hatch. Inflammation is simply your body reacting to something in an attempt to heal you from something for a reason. It's trying to protect you, defend you, to heal you. Inflammation is a good thing. Imagine this. You fall down. You scrape your knee. You get a bacterial infection. If you never got inflamed, that bacteria would colonize in your body, wear down your joints or something, and you would die. Inflammation is your body's rushing its cytokines and inflammatory things and prostaglandins and white blood cells and all things to the area saying, hey, we see a problem. We found the problem. Let's go kill the problem and clean it out so your body can heal. And it signals all these healing responses. That's what inflammation is. So your body, when you are inflamed in the bowel, has identified a problem which says we need to get rid of this thing or these things. Or it's pushed your immune system out of whack so it thinks it needs to get rid of more things than there actually are. But it's called an immune-mediated response, where your immune system is too active and it's burning holes through your intestines, effectively. So now you shut that inflammatory pathway off, that immune response. You say, no, body, don't worry about it. You silence it. You take the drugs. You shut down your immune system's responses. Got it. Here's the thing. Your body still believes there's something there, and there probably is if you're living in a moldy environment or whatever it is. There's inflammatory things within your body still. So your body, very intelligent, you shut down pathway one, two, and nine. It says, hold on, buddy. I still have to clear that thing. So it reroutes to 17 or 22 or something else. And now you have this escape pathway, this breakthrough inflammatory response. Because your body is still trying to fix the thing that it started responding to in the first place. Because you didn't randomly. It's not genetic. You had that from birth. It's not autoimmune. There's no antibodies attacking your own tissue. It doesn't just randomly happen. There is a root cause and several drivers. They created the inflammatory response. Your body's been responding ever since. But what you've done is taken drugs to shut that response down. And it rewrote it and said, we never got the job finished. Let's find another way around, because we still have to clean up that thing. That's when we get these breakthroughs. And so we're talking about getting the most out of your biologic. There's two big things that we want to look at. Number one, of course, if you're sticking to the biologic route, you're like, Josh is a quack. That's fine. That's cool. Stick to the biologics. It's your call. It's your life. You do what you want. You're an adult probably. But here's the thing. You can also do what we're going to call therapeutic, what they call therapeutic drug monitoring. So you don't wait for the flare to come up. You don't wait for that breakthrough. Oh, oops, I got to get more drug. You can go in and get drug levels tested in your blood to see, hey, are my trough levels high enough? You can go and get blood done to see if you're developing antibodies to that drug. You don't have to wait to flare. Get proactive on it. Test early. If you're like, hmm, something doesn't feel right, get tested. It's that simple. It's early intervention and being proactive. That's one way. The other way, my preferred method, is going to be to consider other inflammatory drivers. What other things are you currently doing? Doctors will say, eat whatever you want. Food doesn't matter. That is the stupidest nonsense I've ever heard. If your doctor says food doesn't matter, honestly, I'd say find a new doctor because you're missing the fundamentals of basic biology. Especially if I've got a sick 300-pound doctor telling me nutrition doesn't matter. I'm like, buddy, that would be the best thing you could do for yourself right now. Food matters. Food alters your microbiome. It causes inflammatory. It's too simple to even bother talking about right now. Food matters. Simple as that. But here's the thing. If there are other inflammatory drivers besides diet, you have herbs, you've got sleep hygiene issues, if you've got a toxic environment, you're living in mold, if you've got other root causes and drivers that you're not dealing with, there are so many things that are actively driving your inflammation. So make sure you reduce those things that can drive your inflammation. In addition to your biologics, other things you can use, there are lots of other anti-inflammatory compounds which may or may not be a good fit for you. Whether it's high doses of curcumin, omegas, chingai, there's dozens. Vitamin D is chronically low in those with IBD. Maybe you're taking oral iron pills which are actively irritating your gut. You can switch to a heme iron or a fermented iron. There's dozens of things we can do in addition to simply looking for the root driver and understanding how you got the disease. But that's the combination therapy. So if you want to get the most out of your biologics, yes. Make sure you test, see how you're performing, understand what immune pathways are active and match accordingly. Test proactively to see if your drugs are leaving your system too early. See if you're getting breakthrough flares and then work on combinations in addition to finding the root causes. Now you can find all this information, of course, more and more about it in my podcast called Reversing Crohn's and Colitis Naturally where I walk you through how to actually find those root causes and drivers. There's 77 episodes, almost 80 episodes published by now, so make sure to check those out. But here's the big one. I want you to take this away today. Being in remission isn't just about feeling good. It is a confirmed mucosal healing and doctors want to see that, but that's drug induced. The problem is if it's a drug induced remission, you're always drug dependent. Unless you identify the root cause, you will always be drug dependent. Once you get the root cause, you remove it. Your body can heal. You don't need the drugs to keep you in remission. And that's how that works. So am I being rushed off here? Oh, my camera's getting hot. Hold on, let me just open the door. I should just let it vent a little bit. Camera's getting spicy hot. All right. Easy enough. I thought she was just bored of hearing me talk, but that's fine. She's like, dude, shut up. All right. Here's what we're going to do. We're going to turn over to questions right now. And while we're waiting for those to come in, I'm going to tell you exactly how you can get some help. If you're on YouTube or listening on the podcast, all you got to do is click the links down below, send us an email directly, book a call directly, send an email to my team and ask some questions. We've got lists for resources. It's all there. Now we're going to turn over to the questions. What do we got? I'm going to get a little closer so we can hear the questions. Yes. I don't know if this person is 11 years old or has had UC for 11 years. Main symptom has always been blood in the stool, was on a Remicade for a year, and it didn't completely stop it. What's causing this? Got it. So whether you're 11 years old or have had it for 11 years, you've been on Remicade and you're having some symptom relief, but not full relief. This is the octopus. So let's go back to the octopus drawing. My octopus is so adorable. He's got one really fat hand though. You should see a doctor about that. He has a head now and that's a penis. So our octopus is very necessary. All men are still boys. So let's say the drug you're taking, you said you were on Remicade. Remicade is an anti-TNF, so tumor necrosis factor. So it's a different inflammatory pathway. Oh, it's for your child who's 11. Got it. So here's what we're seeing. This drug is covering this immune pathway. Now this immune pathway, this hand still has fingers, right? Looks like Edward Scissorhands. So this hand still has fingers. So this anti-TNF, this pathway, there's other inflammatory cytokines and markers that can get suppressed from this drug. But not all things on that arm fit inside this drug. So your drug is suppressing some of the pathways related to your inflammation, but not all of the pathways. So you get these breakthroughs. That's if the drug only worked a little bit. On the other hand, if the antibodies you developed, it can be your immune system shifting. If that inflammatory thing, the origin was in there, eventually it can get worse in spite of immune suppression. So think of it, again, back to the nail. Got a nail stuck in my foot. I show you my hand because my feet are gross, so I'm going to keep my hand up here. So you got a nail stuck in your foot. You put numbing cream on it over and over and over. Eventually the nail is going to start to rust, which now causes an infection or a blood infection or something else. So that same root driver in the body for long enough can create other inflammatory drivers. Let's say, for example, you are in a moldy environment and your 11-year-old is responding to the mold. So he might have some dominance in his Th2 immune pathways and Th17. These are very common in mold. So Th2 is allergies and histamines. And Th17, this is mucosal, so sinuses, gut, oral, etc. So if you have inflammation, those histamine drivers, mold can drive that and it can drive this mucosal inflammation. You get that right away. Like, hmm, something's up. He's bleeding. We get him in the doctor. That pathway is active. So you can go to the doctor, they give him the drugs. It helps for a little bit. The problem with mold is it suppresses another immune pathway called Th1. That's your ability to fight viruses and parasites, etc. Mold also damages your microbiome, your gut bacteria, and your gut lining. So the longer you're in mold, the more dysbiosis you have. So maybe now you have fungus overactive in your immune system or inside of your body. You have dysbiosis, you have parasites. Well, they recruit some of the same but also different immune pathways. So now he's having breakthrough infections that were in there and driving up because the drug was suppressing the symptoms, not the root driver. The root driver, like a rusty nail in the foot, was left to fester. And it got worse and worse and worse. That's probably what had happened. That immune system begins to shift its focus. Another question. I'm going to sneak in with the microphones. How do you know which biologic is best for you? What tests or data do you need to determine the best meds for your case? And then we have just another question along the lines of meds about L-glutamine. So the first one is how do you know which drug is best for you? Let's stick to the octopus for a moment. I'm working on a system right now to try to develop something for you guys that you can just access and your doctors can have. It's going to be a while to FDA approval, truth being told. But the idea is that if you can identify, well, here's what immune pathways are inflamed. There's a great lab report right now from Cyrex Labs. You got to pay for it. It's expensive. It's about $400. It's called Cyrex. C-Y-R-E-X. They have something called the lymphocyte map. That lymphocyte map, and you can message me. You might be able to order it on your own. You might need a clinician. My team and I order them for our people all the time. So this lymphocyte map, this takes all your blood cells, CD4 and 8 and 16 and 56 and all these different things, Treg cells and NK cells, these different cells of your immune system. And it says, here's where you're skewed. You're TH2 dominant. You're TH17 dominant. You're this. You're that. So it gives you an idea. Symptomatically, we can also oftentimes match up your symptoms with an immune pathway, but it's not perfect. There's many markers we need to look at in a very well-rounded way. So if you had the ability to understand what your immune system is doing, you could hedge against what drug is likely the best. You say, okay, well, I know these pathways are active. This drug suppresses those pathways. So this is probably my better bet. And that's where we'd have to do it right now. It's a manual job, but I'm trying to build a system that you guys can just log into and jump online and find out your drugs. So a question about L-glutamine. L-glutamine, what's the question? Does it work? Oh, sure. So L-glutamine's the next question. Does L-glutamine work? Yes and no. L-glutamine, it is a repair tool. It's like my house is broken down. There was an earthquake. L-glutamine are bricks. It's a great part of the puzzle if that's what you need at that time. Some people respond poorly. Even non-inflamed or non-diseased guys, general IBS or non, can have some negative reactions, bloating, constipation, depending on the dose of L-glutamine. Generally speaking, yes, L-glutamine is great. It's a wonderful amino acid. Consume it if it feels good. What we often get stuck in is, well, I heard it was good. Therefore, it must be good for me. So we take it even though we're feeling bad. We attribute it to something else and think, well, this good thing couldn't be bad for me because it's good for everybody else. But it can still be bad for you. Even Qing Dai, I've seen negative reactions. So consider L-glutamine can be beneficial, but it can also have some immune modulating properties, though low. But if you're one of those people who are sensitive to that particular push, it might make you feel worse. So I hate to say a little bit of everything, but the truth is it's good and or bad. A lot of questions. All right. Well, let's throw them. I got to go soon, guys. So I'll take a couple more questions. Believe it or not, Josh needs a haircut and that's what I'm going to get done tonight. I have an appointment. So there's a question here about how you determine root cause. Yes. But we also have questions here about... How many questions we got? Three and then one on Facebook. It's banging, but let's do it. We'll make it quick, guys. I promise you. If I can't answer them, just DM me. So this question, what would you say to a 17-year-old? So first symptoms were erythema and nardosum. Yep, erythema and nardosum. It's a skin condition. Strep titers, blood work indicated IBD, which led to a diagnosis of Crohn's, started steroids when tapering developed. Got it. So something drove the skin issue. That could be microbiome. It could be other. Sorry, what's the question there? Is it how we ID the root cause? They followed up. That was a different person. They followed up. They said it was a fistula. So doctor recommending Remicade. Would you start that or recommend something else? Good question. So fistulas are TH17 typically issues. Other things that can drive that, that's mucosal damage. So a fistula is when your gut starts eroding the tissue or your immune responses start eroding the tissue and it creates a tunnel. It's kind of like a pimple comes outward, a fistula goes inward, and then infection burrows. It can actually, worst case, connect your small to large intestine. I've seen that before. I've seen what's called a rectovaginal fistula, which is exactly what it sounds like. So there's different tunnels that can burrow and it's highly inflammatory and you can go septic and die. So what we have to look at is even though that particular immune pathway is active, we can't guarantee that that specific drug would be the best fit. So what I would say is if you want to send me a message directly, it's something I can certainly run through. I'm building a software right now to try to do this, and I can try to connect that for you and get some info on specifically what drug might be best, but it's not medical advice, of course. Okay. So we just have a question here about how we find the root cause. Okay. So how to find the root cause. It's a matter of a couple of things. One, we have to look at your environments. We had a fellow come through our program. We said, I believe mold created your, or your root cause, when even food or I forget the exact data, but long and short, we said, mold is currently making you worse. He said, well, mold didn't create my disease. So I'm not going to worry about it. I'm not going to clean my house. Well, he went through the program and got better, but not perfect because to him, mold didn't create the problem. So therefore, mold can't be the problem, but it can be part of the problem. It's like, well, I stepped on a nail. That's why my foot hurts. Now I got rocks in my shoe. Like just pull the nail. I'm like, yeah, but we've got to get the rocks out too. You're like, yeah, but the rocks didn't hurt me first. So it doesn't matter. It's like, no, it all matters. So your history tells us everything. Quick example for you, and I do got to wrap up. We'll get one more question in is we had a client came in. It's one of my favorite stories. It's so apparent what drove it. I said, how'd you get colitis? She said, I got COVID. I was like, no, you didn't like, I'm sure you got COVID, but how many billions of people got COVID and didn't get colitis? So I said, why did you get it? So we started peeling back her history. She said, well, I was born and raised in Columbia in 1984. And I grew up in a very long house, poor family. Everybody lived together. Her room was in the back of the house. She remembers mold up and down the walls on her bed. It was in her body as well. So she had boils on her skin and tonsil infections and ear infections and all kinds of nasty business. And so she was on antibiotics after antibiotics. So mold damages microbiome, antibiotics damage microbiome, mold pushes your immune system, et cetera. Before she was 20, she had almost 40 doses of antibiotics. So here she is, her immune system has been disrupted. She's had ongoing gut issues and constipation, et cetera, all these different things. So by the time she got COVID, it was a straw that broke the camel's back. Not to mention Columbia in 1984 was a literal war zone. So there was stress and trauma, et cetera. That was the story we built to say, okay, COVID tipped it over the edge. And so your history tells us everything. Last questions over on Facebook? Yeah, I shall. All right. Or Melissa? Melissa, yes. All right, Melissa. Antivio failed within a year. Now I'm on Humira. My last two test results showed elevated neutrophils. Those are a type of white blood cell. Gotcha. I've seen elevated eosinophils, another type of white blood cell on a blood test before, and I was diagnosed eventually put on biologics. I've never seen elevated neutrophils until recently. Well, here's what we can say. Neutrophils we know are the primary driver of inflammation and bowel disease. Most of the time, they're the ones that produce your calprotectin. Eosinophils are typically linked to parasites and allergens. The bigger things that create those same responses are parasites and mold. So if I see eosinophils, my first two looks are going to be mold and parasites. Even if it's EOE or eosinophilic esophagitis, elevated eosinophils, I'm looking at mold and parasites immediately. But oftentimes, mold suppresses that path of the immune system, number one, which lets parasites come in, driving up eosinophils. So I'd be looking there first before anything else. On that note, guys, you know how to reach me. I know it's a lot to take in. It's a whole lot of everything. So comment the word solution and send me a DM. Or if you're on podcast, YouTube and podcast, you guys know how to reach me. There's links down below. Send us an email, book a call directly. We're here to help whatever you need. Resources are free as always. Reach out anytime. Thanks for coming. See you next. One of my favorite things to hear as an IBD specialist is something along the lines of, I learned more from you in 15 minutes than from my doctor in 15 years. And if this for the first time is really starting to click and it's starting to make sense, you're going, wait a minute, this might be reversible. I think there's more that I can do. This condition came out of nowhere. It happened to me out of the blue. I was healthy for 10, 20, 30, 40 years, and suddenly I wasn't. And you're telling me there's no cause. If you're understanding finally that there is a cause, that something is driving this, I want to invite you to check the link in the show notes below. Send me an email, ask a question, see if a program is a right fit for you. Because I promise you, this doesn't have to be a lifelong sentence. You're not doomed to this, and IBD can be reversed.