Andrew: I’ve gotta say, I have always been, historically, a big fan of colostrum. And I’ve used it with such great effect, and with very, very rare side effects, but I have seen it in a couple of people with, like, really weird IgG sensitivities and things like that. But I was so excited when ImmunoLin came onto the market, and I’ve just, I’ve dropped colostrum. I just use ImmunoLin now. But let’s talk about this. Can you explain for our audience what ImmunoLin actually is, and how it differs from colostrum?

Chris: Yeah, absolutely, Andrew. So, ImmunoLin is just a serum-derived bovine immunoglobulin protein isolate. And that is, it’s a lot of words together, but I can break them down. They all make sense. So, serum-derived just means it’s from plasma. It’s from blood, right? Bovine is obviously cow. Immunoglobulin, these are the antibodies that we all have, that cows have, in their blood, to be able to protect them from infection, right? And a protein isolate just means that it is a highly purified protein mixture. So, greater than 90% of the powder is actually protein. And so, that’s it. That’s what ImmunoLin is. It’s a proprietary product, that ProLiant Health and Biologicals has developed, and I’ve been working with it for about 12 years now.

Andrew: And so, when we’re talking about colostrum, we talk about secretory IgA, which is the immunoglobulin A, two of those, joined by a J chain. But we’ve also got things like lactoperoxidase, lactoferrin, blah, blah, blah. Tell us what’s in ImmunoLin, that differs or acts the same, indeed.

Chris: So, it’s very similar to colostrum, in that it’s a complex protein mixture, right? So, you talked about a peroxidase, right? So, colostrum is IgA, IgG, a lot of other proteins, casein. And non-proteins as well, such as lactose and fats. ImmunoLin, when it comes to what it is molecularly, is also very similar, in that it’s a complex mixture of the proteins you would find in your plasma. And so, we’ve actually done a lot of proteomics work on ImmunoLin, to assess what are the other proteins that are there. Albumin is one of the other major proteins, non-IgG, but ImmunoLin itself is over 50% IgG. And that’s kind of one of its defining features, especially when compared to colostrum, you know. So, coming from blood, blood is a very stable, consistent raw material, and that begets being able to process it in a way that lends itself to a stable, consistent final product. And so, for us, we manufacture it to be a really high concentration of IgGs. And so it’s greater than 50% IgG on a powder basis, 90% protein, so there’s still a lot of other proteins in there. So, I mentioned albumin. Albumin is the dominant protein in blood. It helps regulate the blood pressure of animals. It helps transport nutrients, like fatty acids, and other small molecules. Also within ImmunoLin is some transferrin, which is a protein that’s responsible for iron binding, and iron binding transport, and actually does have some ability to break down bacterial cell walls, and bind some toxic components.

But there’s a lot of other proteins in there as well. All in all, it’s approximately 180 proteins, most of which are very, very small abundance. But in our kind of analysis of it, what we’ve determined is, think there’s effectively no significant difference, lot to lot, of the concentration or identity of those other proteins. So, again, think it goes back to consistency, for ImmunoLin, and what it is molecularly. And I think, you know, you compare that to colostrum. Colostrum is a great product. Just, you look at that raw material, and it’s the kind of first milking from a cow that’s given birth, the second milking from a cow that’s given birth, the third, maybe the fourth. And over the course of those milkings, the IgG concentration starts very high, and then it steadily decreases, right? And the reason it starts high is obviously to confer immunity from the mom to the baby that doesn’t have any. But what that means is, for the people manufacturing colostrum, they are dealing with a raw material that’s more variable up front. So, that more-variable raw material means it’s harder for your process to be able to control. And all in all, that just leads to a much more variable product in colostrum, but when you can… Colostrum, you know, we’ve done lots of analysis of ImmunoLin versus some of our colostrum competitors, because when we initially launched ImmunoLin, it was as a colostrum replacer. And I think what you see is just a bunch of variance in that market. You have some colostrum products that are really, really good, 40% IgG, and then a bunch of others that are 20%. And now, nowadays, with the shortage of colostrum, you get people that, you know, end users that can’t even put an IgG percent on their label, because the colostrum, they can’t source it consistently at 20% or 40%, anything like that, versus, again, for us, ImmunoLin, which, it’s always manufactured to greater than 50%, which lends itself to being on the label as 50% IgG, and lends itself to consistent dosing. You know, it’s very hard to have consistently good efficacy and results from a product that you’re taking if the product that you’re taking is never the same, even though the bottle looks it.

Andrew: That’s indeed why I swapped. That is the factor, why I swapped to ImmunoLin. Because I remember, like, in past days, I used to use colostrum with great effect. And I’ve just seen over the years this degradation of percentages. And also, whether it’s a labeling requirement in Australia, I’m not sure. But I now see, with colostrums, I just don’t see lactoperoxidase, lactoferrin, I don’t see it being mentioned. Now, I don’t know about that. Maybe somebody who’s out there can let us know in the comments. I’d love to know. I’d love to learn about this. So, can we go further, then, into the usages? Usages? Into the uses of ImmunoLin. Andrew will learn English one day. And how is it clinically relevant from colostrum, when you’re choosing between the two in practice?

Chris: Yeah. So, I think, in practice, really, what we’re talking about goes back to that consistency, right? Consistency in dosing, and consistency in better tolerability, right? And I think that better tolerability is driven from couple of different things. One is that colostrum, being a dairy-based product, there’s a lot of lactose in that. And there are a significant number of people that are lactose intolerant, so… I wasn’t sure what that rate was in Australia. I did look it up. It was somewhere between 15% and 30% is what I was seeing. But we have some partners all over Asia Pacific, and elsewhere in Asia Pacific, the incident rate of lactose intolerance is up at 70%. And so, really, really, a high number of people are unable to take colostrum because, what does the lactose do? It leads to bloating. It leads to diarrhea. And if these are the kind of GI effects that you are looking to reduce, or you’re looking to promote GI health, obviously you can’t be taking the lactose in.

Additionally, I think something that spawns out of the inconsistency of that raw material, and just how dispersed the collection is, is, when you’re processing colostrum, a lot of those final products end up with some endotoxin in the final powder. And so that’s something, we’ve done two different colostrum comparison studies over the last seven years, let’s say. And every time we’ve tested a colostrum product, what we’ve seen is detectable amounts of endotoxin in that powder, versus our ImmunoLin, which doesn’t have it. But the endotoxin is an insult to the GI system, which will cause inflammation, gut barrier damage, all of these negative things that you’re looking to prevent. What you’re looking to do is stop that inflammation, and endotoxin is very much the cause of it, and it’s coming along in some of these colostrum products. And so those are really the two big differences that I see for it, in terms of clinical relevance.

Andrew: So, you’ve just tweaked something in my mind here, because I used to think about ImmunoLin for gut, and stops at the gut barrier sort of thing. Now you’re getting me thinking, though, in helping patients with what we used to call NAFLD, non-alcoholic fatty liver disease, and now we’re calling it MASLD, which is metabolic dysfunction-associated liver disease. So, is ImmunoLin now indicated in helping to decrease that LPS assault on the liver?

Chris: For liver, I wouldn’t be able to say. It is absolutely indicated for reducing inflammation associated with lipopolysaccharide…

Andrew: Yeah.

Chris: …LPS, or endotoxin. In fact, that is, LPS is one of the major drivers of inflammation, right? It’s a breakdown product of bacterial cell walls, that commensal bacteria, pathogenic bacteria that are in your gut, and it, you know, presents at the epithelial layer of the lumen, right? But is also able to translocate that, especially in people that have leaky gut, and then cause inflammation, right? And so, ImmunoLin, what is really cool about it in the world of GI health, is that ImmunoLin acts as kind of a binder and a neutralizer, right? The LPS molecule can be flowing through your upper/lower GI tract, and ImmunoLin, that antibody, will just come along and bind it, right? And so, it will become so large they can’t get through the holes of the leaky gut.

One of my co-workers likes to talk about this like a volleyball net, right? What is the epithelial layer? This is basically skin cells in your gut, right? But it’s kind of like a, if it’s healthy, it’s like a ping pong ball net. Really, really fine holes. You get a little bit of translocation across that barrier, into the immune reactive layer. But if you don’t have a healthy gut, if there’s a lot of insults, then it’s more like a volleyball net. And so you get these LPS molecules that can kind of translocate across that layer, but ImmunoLin will come in and bind it, and make it so large that it can’t pass through that hole anymore, right? And that’s one of the reasons, one of the ways it’s able to prevent inflammation in the immune reactive layer. And actually, what that does is it prevents an entire immune cascade, this negative feedback cycle, where you have lipopolysaccharide presenting to the gut, translocating through the holes in the epithelial layer, into the lamina propria, being bound by a dendritic cell, being presented to a lymphocyte, causing a pro-inflammatory response, like a tumor necrosis factor alpha, which then goes back and damages the epithelial layer, and just, it’s like a self-reinforcing cycle of damage. And so, well, I can’t say on the liver end, because we haven’t done those studies. We’ve done the studies to back up the binding neutralization on the, just general gut health, and for specifically for studies around HIV enteropathy, for IBD, IBSD, ulcerative colitis, and Crohn’s.

Andrew: Chris, thanks so much for explaining that. Can I just catch myself in something that you said there? I made this quantum leap from leaky gut, which you were correctly talking about, to me erroneously talking about the end condition, which may result from that, and that is MASLD. So, can I just correct myself and bring it back to what was going through my mind, was leaky gut?

Chris: Absolutely.

Andrew: So, thanks for that. So, can we lead on from there?

Chris: Yeah. So, I think this is really the interesting thing about ImmunoLin, and is…it actually helps to prevent the kind of inflammation cascade, negative feedback cycle that is the leaky gut, right? And so, talked a little bit about how LPS can translocate, the epithelial barrier, cause inflammation, inflammation then creates more damage to leaky barrier, and it creates that cycle, right? I often liken it to, like, a house that has water damage in it, right? And think about this in terms of, you know, that roof is very much the epithelial layer, right? And the rest of your house is very much the rest of the structure, of the mucosal layer. And, you know, oftentimes, you know, our symptoms of this are bloating, diarrhea, abdominal discomfort, and it all results from this leaky gut. And, effectively, you know, our standard treatments today, or historically, have been, well, you go in and you try and treat the symptoms, and you try and treat the symptoms by fixing the flooring before you’ve removed the water, the standing water, fixing the roof while it’s raining out. And really, what you need to do here is you need to…the problem is not the fact that you’ve got a leaky roof. The problem is that you’ve just got water, water coming in. That’s first and foremost. Those are the antigens. It’s the LPS. You can’t fix the leaky roof if you don’t have a sunny day. And that’s what ImmunoLin is, is, right? It’s the sunny day. It comes in, and it’s like these little hands that go up there and catch the water droplets, so you actually have time to repair the leaky roof, get rid of the standing water, and just let the whole mucosal layer have a breath. And during that breath, it’s actually has some time to repair itself, right? Produce anti-inflammatory cytokines, produce more tight-junction proteins, reduce the leakiness of the gut, so that you have an intact roof, and actually break that cycle of inflammation and damage that is so hard to repair.

Andrew: So, this is why I use it, not just in infectious conditions, which was my original sort of attraction, if you like, to the old colostrum, and indeed, ImmunoLin. But now, I use it in things like IBS, and other conditions where there’s inflammatory modulation that needs to happen in the gut. Can I ask a question, though, with regards to identification of things to bind to, right? Or to settle down. And I think I know the answer to this, but I’d love your confirmation. So, when we’re talking about, let’s say SIBO, when we’ve got an overgrowth of otherwise helpful bacteria, but now I guess you’ve spoken about settling down that terrain, which of course is everything. So, is that the answer? Is that why ImmunoLin is indeed indicated in conditions like SIBO, where the good guys are overgrowing?

Chris: That’s absolutely correct. And so, I think the microbiome is a really interesting part of this. So, you refer to SIBO, the small intestinal bacterial overgrowth. Lately, we’ve also been interested in small intestinal fungal overgrowth, yeast overgrowth. And ImmunoLin’s perfect for that, because even good bacteria can become bad when they break down, right? And the breakdown products cause inflammation. And that’s why ImmunoLin is so great in those, is because it doesn’t really matter if it’s good, if it’s bad. It’s a breakdown product that causes inflammation. ImmunoLin effectively binds to it, right? We’ve got, I don’t know, somewhere over 40 different antigens, and we’ve demonstrated binding of our IgGs, too. You know, the cows themselves, that produce this, are exposed to lots of different bacteria, lots of different viruses, and very, very similar ones to us. And because of that, they produce these polyclonal IgGs, that can bind to so many different types. So, the disease indication, SIBO is a good one, IBD, IBS, all of these really hard-to-treat disease conditions is where ImmunoLin has been so great because, for patients that have been on…there’s an example case study that we have, where there’s an 18-year-old with Crohn’s, that was basically refractory, and was not responding to infliximab anymore. And put them on ImmunoLin, and suddenly, his dysbiosis went away, the presenting symptoms of diarrhea went away, and he’s just a really hard-to-treat patient. And we’ve seen that over and over with ImmunoLin.

In fact, we have a couple of different case studies for IBD, on hard-to-treat patients, where I think we had roughly 45 patients or so in a 12-week study, and saw that almost threefold, the patients on ImmunoLin were almost threefold more likely to report improvement in their clinical symptoms. Another study for IBSD, similar number of patients, I believe, pilot study, where I think it was 100% of the patients saw at least a 50% improvement in their symptoms, and then 75%, or was it 50% of the patients reported 75% to 100%. So, these are the hardest-to-treat patients, right, the ones that have the SIBO, the IBD, and ImmunoLin is really just what works when nothing else does for them. And so, to this idea of who can take it, it is, we started off on the hardest-to-treat patients, and the idea really was, at that point, if we’re able to have success with these patients, what else is out there for us? What can we do in somebody who doesn’t have the extreme inflammation of somebody with Crohn’s or UC?
Andrew: Can I ask about dosing with this? Did you have to do a step-up dosing, like, starting off with these really fragile patients, or did you just go in with a standard dose?

Chris: So, we did a step-up… So, actually, it’s not a step-up dose. Really, what we did is we went in, and we went in with kind of a get-you-back-on-track dose, right? So, for the patients in the studies that we’re talking about, they were taking the medical food version of this product, which is, you know, a 5-gram dose. And for them, we came in, and it would be 10 grams would be typical, right? Kind of trying to right the ship, get them back on course, reduce that inflammation, reduce the leakiness, and then step it down to a maintenance dose, where, you know, they can just kind of slowly heal themselves. But the idea was really let’s get them back on track, and let’s get them back on track quickly. From a safety standpoint, there’s really, there was no concern. This is effectively just a protein product, right? And so, we’re able to go in, and because we have this generally recognized as safe designation, when we went into the IRBs, institutional research boards, and ran these case studies or clinical trials, there’s very low concern on safety, so we’re kind of able to go in, treat the hard ones, give them a higher dose, and then walk it back down.

Andrew: Oh, right. So, this is your ethics committees and things like that, yes?

Chris: That’s correct.

Andrew: Gotcha. Gotcha. Okay. So, the next thing is, I’m just talking about these super-sensitive people, patients who maybe can’t tolerate even, you know, fibers. Certainly, some antimicrobials, and certainly in the natural world, the antimicrobials tend to be a bit lacking on taste, let’s say. Bit of a taste challenge. These people that are super sensitive, I don’t… Where am I going? Things like, let’s say histamine intolerance, MCAS, patients like that, these really recalcitrant patients, that are hard to treat. How does ImmunoLin fit with them?

Chris: So, I think, for these patients, ImmunoLin is a really great place to start. Frequently, these highly sensitive patients have kind of an overactive immune system anyway, right? And I think this is one of the cool things, another cool thing about ImmunoLin, is that, you know, when you think about stimulating the immune system, to make it more effective, you know, how is that done? It’s typically increasing white blood cells, macrophages, neutrophils, antibodies. And you think of increasing as a good thing. But this inflammation cascade that we referred to earlier, more inflammation, more immune response, is not always a good thing. So, these patients have an overactive immune system, right? It’s like Goldilocks and the Three Bears, right? You don’t want porridge that’s too cold or too hot. You want it to be just right. And if you’re sensitive, you’re already like a car engine that’s overheating, right? And so, you stimulate that immune system more, it can cause fluid breakdown, right? The metal expansion, eventually you lose a head gasket. And so, the cool thing about ImmunoLin is it can come in, and it doesn’t stimulate the immune system like we would think of traditionally, right? What it does is it allows a cooling-off period. It can come in, bind up these pro-inflammatory molecules like LPS, that are causing the insults, crossing into the immune reactive layer, and leading to pro-inflammatory cytokines. And it just, again, it allows a cool-down period for these highly sensitive patients, to just allow their immune system to get to a state of homeostasis, right?

Andrew: Can we go in further about…can we talk a little bit further about dosing? So, when you’re talking about these rather sick patients, with Crohn’s, and you actually did a higher dose, almost like a rescue dose, and then brought them down to a maintenance dose once they were stable, can you take us through appropriate dosing, the range that you’d use in various conditions? Like, for instance, in post-infectious, well, not post-infectious, infectious diarrhea, to inflammatory conditions, to, let’s say, even go into autoimmune conditions.

Chris: Yeah. So, again, I think our standard dose for these harder patients is kind of 5 grams a day. We had, the two studies that are top of mind for me here are an IBSD study that we did, where we gave patients either 5 to 10 grams per day, over the course of a month and a half, and looked for reduction in the number of days that they would have kind of these global symptoms of IBSD. So, think, again, loose stools, urgency, abdominal discomfort, bloating. And what we saw with the 10-gram dosing was, and I’d have to look back at the 5, but definitely with the 10-gram dosing, was a reduction of, a 33% reduction, in terms of the mean number of days with symptoms, right? So, over the course of a year, what we’re talking about is four months. Four months where these patients, on 10 grams per day, did not have abdominal discomfort or urgency. So, they were able to get some form of their life back.

Another study that we have, that I think is relevant here, is patients with HIV-associated enteropathy. And so, we’ve done a few different randomized clinical trials in this space, and range from anywhere from 2.5 to 20 gram, per day, for various time periods, 4 weeks up to 20 weeks. And I think what we’ve seen in a lot of these patients is this kind of 5-gram-per-day dose has made real significant improvements, of, both lowering systemic inflammation, so, think reduction in IL-6 that these patients would have in their blood, and improve their gut barrier function, as measured by decreasing markers of inflammation of the gut, like intestinal fatty acid-binding protein, or zonulin, which would, you know, decrease in zonulin being indicative tightening of the gut barrier. And so, really good 5-gram-per-day data.

And then just kind of thinking, maybe one step down, for healthy patients, we had a study with the University of North Texas, because we were really interested in what happens when you get down to something that’s really more of a supplemental dose. Our entire dosing strategy was based around the amount of immunoglobulins that are made per day in the typical human gut, which is 5 grams. And so, that’s kind of where 5 grams came, 10. And so, for a supplemental dose, is defined, it’s in the United States, would be 20% of that. So, 1-gram-per-day dosing. So, we looked at, we have a study with the University of North Texas, where we recruited a bunch of college students, and gave them a high-fat diet, in a single setting, right? And they actually got to choose what that was, and they chose a large cheese pizza. So, these students sat down, ate their whole large cheese pizza, and then five hours later, we did a blood draw and we tested them for circulating LPS in their blood. And what you saw was, you know, roughly, like, a doubling in the amount of LPS that was in their blood. And then we gave them ImmunoLin for, you know, 1 gram per day, 2 grams per day, for 45 days. And then at the end of that 45-day period, gave them pizza again, and said, go ahead, eat it. They ate the pizza, and then we again did a blood draw. And in that blood draw, for the patients that were on ImmunoLin, that had initially this increase in LPS upon eating, what we saw was just no increase in LPS, after 45 days of treatment at these lower 1-gram, 2-gram-per-day dosages.

And so, I think, getting back to this question, you know, for these really severe, hard-to-treat cases, this 10 gram per day, which is that kind of rescue dose, does a really good job over six weeks. You know, these longer patients, these patients that have longer-term treatments, like the 20 weeks at 2.5, 5 grams, that did really well for those patients with HIV and associated enteropathy. But then, your standard college kid, that just is worried about leaky gut, that’s attached to just standard living habits, right? The food you eat, how you live, the type of exercise you do, really, these lower maintenance doses were able to establish a positive effect for them.

Andrew: But, you know, I’m thinking now about the gut-brain super highway. You were mentioning college kids. I’m thinking about brain fog, studying, anxiety, as part of the therapy, maybe not the sole therapy, but I’m thinking this is such an important part of the therapy, where you can really heal the gut, along with probiotics, along with fibers, along with whatever else you’re doing, but you can make a marked difference in reducing that LPS, and reducing the effects in distal areas. So, you know, chronic rhinosinuvitis, allergies, brain fog, we mentioned mood stabilization, blah, blah. The uses just go on and on.

Chris: Yeah. I think this is one of the areas I’m most interested in, when it comes to ImmunoLin, is the fact that you get these non-GI effects, right? And so, the… So, I come from a chemical engineering background. I did my postdoc at a metabolism and aging institute, at Scripps. And one of the really interesting things that I came across in my time there was this microbiome effect. And so, one of my coworkers was studying the impact of bacteria on the longevity of fruit flies. We had another professor that was really interested in ghrelin, an appetite hormone. And ghrelin, if you’re not familiar with it, is produced in the gut. And then it crosses into, across the gut-brain axis, into the brain, where it stimulates a dopamine response to make you hungry, right? And specifically, it stimulates dopamine type 2 receptors, D2s. And those are also associated with exactly what you’re talking about, mental health, anxiety, depression, things like that. And I think this ability to mine the gut-brain axis is just absolutely fascinating, when it comes to some of the efficacies that we’ve seen with plasma proteins.

Andrew: Chris, and just leading on from that, something I said before, about sort of using instead of probiotics. And I need to sort of say a little spit story. Like, I’ve, when I’ve had an infectious episode, I’ve previously used ImmunoLin to catch it early. Whereas probiotics would take, you know, when you look at the literature, days to have an effect. One of the fastest ones would be Saccharomyces boulardii, where, if you take truckloads of it, and I have, that you can catch it quite quick. But ImmunoLin is like, as long as you’re not vomiting, as long as you can keep it down, it works so fast. But, I wanna just make it the point that I’m not saying that it takes the place of probiotics. It indeed helps them. Am I correct in saying that?

Chris: Absolutely. I think this is one of the areas of research that I’m particularly interested in with ImmunoLin, is how it interacts with probiotics and prebiotics, things that modulate the microbiome. And so, in studying ImmunoLin, the effects on binding and neutralization of antigens became pretty clear pretty early on. However, there is a lot of these non-GI effects that were not clear. Plasma proteins have been shown to reduce effects of respiratory viruses, improve cognition, reduce cholesterol, and not all of those are immuno, right? But they’re all related. ImmunoLin is a plasma-derived protein. In fact, we, because of some of these non-GI effects, we looked at a COVID trial, and saw efficacy there. But what’s interesting about it is those are not binding and exclusion effects, but those are something else. And so, one of our sister companies makes a spray-dried plasma product that they use, and they feed it to weaning pigs, right? Because they have leaky guts, and traditionally, they’ll use antibiotics. And instead, a lot of these farmers used this spray-dried plasma. And this sister company of ours looked at modulation of the microbiome, and saw some modulation, and changes to phyla and families. And so we then looked to kind of repeat that work with ImmunoLin. And what we saw were very similar things. We compared ourselves to the prebiotic, ImmunoLin, and we saw changes to phyla. We saw changes to family-level bacteria, and then, from that, increases in short-chain fatty acid production, which led to increased intestinal epithelial layer integrity. And I can keep going on that. I think it’s really interesting. Led to decreased TNF-alpha pro-inflammatory cytokines, and increases in these beneficial microbial metabolites, like these tryptophan catabolites, that can do multiple things: repair gut homeostasis, increase tight junction expression, some of which can cross the gut-brain barrier, getting back to the gut-brain axis. But I think what’s really cool about this is we did that, and we compared it to inulin, right? And I know I’ve seen another study where it’s a comparison of… Anyway. When we compared our results to inulin, what we saw was a clear difference in the type of bacteria that were being overexpressed by ImmunoLin versus inulin. And in follow-up studies with N-acetyl-glucosamine, the same thing happened. ImmunoLin stimulates one population, NAG stimulates another. But you put them together, and what you see is a complementary effect, in terms of increasing the diversity, increasing short-chain fatty acids. It’s really where a lot of, why a lot of people are interested in the microbiome, right, and that diversity. It’s increasing acetate and butyrate, because they help heal the colonic cells, help repair tight junctions. And I think this is what’s really cool, is that you can have this new alternate mechanism for ImmunoLin, that plays hand-in-hand with prebiotics and probiotics, and doesn’t negate their effects. It really just helps amplify them, make them broader.

Andrew: You’re opening up my mind here to many more uses for ImmunoLin than I considered. So, you were just talking about the tryptophan metabolites then. And I remember some research done by Dr. Megan Rossi, when she was looking at probiotics or prebiotics use in chronic kidney disease, and its effect on dampening cardiovascular disease outcomes from these toxic metabolites, from the indoles.

Chris: Really?

Andrew: I mean, this is indoxyl sulfate, I’ve got in my brain. So, one, I’m thinking about chronic kidney disease maintenance, or part of therapy. I don’t know where this is going. I can’t say results. I’m just sort of exploring possibilities. But the other one, that is a duh, to me, is vaginal health. I mean, you’ve just spoken previously about SIFO, about the fungal overgrowth. Man, this is a huge area. I should say, “Woman, this is a huge area.”

Chris: Yeah, and this is something I think we’ve had a, certainly, our business development team comes to me all the time, and they’ve asked a lot about vaginal health in this. It’s an area I’m not particularly familiar with. You know, microbiome modulation, absolutely. All I know is that I think any time you’ve got a microbiome, right, and you’re able to take something like ImmunoLin, which you can take orally, digest, partially digest, partially absorb, it still will reach, you know, these common mucosal systems, and be able to have an effect on the microbiome. I’d be really curious to see what somebody would do with ImmunoLin in those type of applications.

Andrew: Yeah. Absolutely, quite amazing. You know, such a needed area. There are so many frustrated women, who are frustrated with current medications. And it’s not so much the lack of response, but just the recurrence. And so much of that has to do with landscape, with terrain, you know? So, it’s just, it’s opening my mind to possibilities for this agent.

Chris: And you say that, and I brought back to conversations, and Candida, albicans, is, if I’m remembering correctly, is a big one for overgrowth right? I believe. Anyway. Candida was one that we were really interested in more around small intestinal overgrowth, but, you know, it is a fungal, and it’s one where we’ve been able to demonstrate binding to, I think both a lysate and a protein that’s expressed on the surface of that, by the IgGs in ImmunoLin.

Andrew: So, just as a last question, let’s give a call out, I mean, to clinicians that might have been hesitant, that maybe they’ve used colostrum in the past, and run into sensitivities or issues. I mean I’ve certainly seen a degradation in the quality of colostrums available to us in Australia, whereas I used to be pleased, I’m not now, and I just don’t use it, don’t bother. What’s your call-out for those people that might be hesitant about their experience with colostrum, what they think ImmunoLin is, and what it actually isn’t, and maybe just to help them overcome any concerns they may have with allergenicity, or sensitivity with gut, that sort of thing.

Chris: Yeah. I think what I would tell them is that all the inconsistencies that you have from colostrum, ImmunoLin is developed to prevent that, right. So, here, what we have is a standardized non-dairy source of greater than 50% IgG. And you’re able to deliver predictable immune binding, with improved tolerability. This is a product that still has that efficacy that you want from colostrum, but it can deliver on the dosing, and it doesn’t create the sensitivity problems that other patients have.

Andrew: Chris, thank you so much, and I really mean this, so much, for taking us through the many, many more benefits of ImmunoLin than I ever imagined today. Like, it’s just, it’s really opened up another aspect of care for me, and I hope to others who are listening, because it’s such a versatile product, that works on that base immunity, and it’s not just upregulating or downregulating, it’s modulating. It’s a fantastic, fantastic innovation.

Chris: Yeah. I think it’s fantastic in terms of what it can do for our patients that take it. I love hearing the stories of people who’ve gotten some form of their life back because of taking it. And, you know, being the scientist that I am, I just find it immensely interesting in terms of how it works, and these amazing biological systems that are our bodies.

Andrew: Yeah. And indeed, more than, you know, testimonies and thank-yous and things like that, but it’s formalized research in people that really need care, particularly when, you know, the gold standard of medical care just is not holding their inflammatory conditions, and I think that’s a real call-out for practitioners to start using this stuff. I mean, it’s just, it’s blowing my mind. I’m really thinking about where else I can use it. So, I’ve gotta thank you for joining us today, and thanks for explaining the many uses of ImmunoLin.

Chris: Thank you for having me, Andrew. I really appreciated the conversation and enjoyed it.

Andrew: And thank you, everyone, for joining us today. I really hope you got a lot out of this. And we’re gonna put so much information, as much as we can, on ImmunoLin up on the website for you. So, you can look at the other podcasts on your favorite app, and of course, you can look at the show notes on the Designs for Health website. Thanks so much for joining us. I’m Andrew Whitfield-Cook. This is “Wellness by Designs.”