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Galectin-3: A New Target For Inflammation with Dr Isaac Eliaz

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Galectin-3: A New Target For Inflammation with Dr Issac Eliaz

What is Galectin-3 and how is it connected to disease?

Galectin-3 (Gal-3) is a protein that modulates an array of biochemical processes in the body and is becoming increasingly implicated in the development of a multitude of diseases, including cancer, fibrosis, and metabolic diseases. But what if there was a way to lower levels of Galectin-3 with a natural compound?

Today we welcome clinician and researcher, Dr Isaac Eliaz who shares with us his research on modified citrus pectin (MCP) and how, through influencing Gal-3, it has the potential to be applied to a broad range of inflammatory diseases. Dr Eliaz also discusses his passion for the profound effects of mind-body medicine practices, including how meditation can influence Gal-3 and improve wellbeing.        

Covered in this episode

[00:52] Welcoming Dr Isaac Eliaz
[02:03] The origins of modified citrus pectin (MCP)
[06:54] Galectin-3 and its role in the body
[12:29] Treating Galectin-3 as a target for disease treatment
[13:33] Galectin-3 and acute kidney injury
[16:17] Galectin-3 and preventing fibrosis
[20:22] Potential effects of blocking Galectin-3 for the healthcare system
[23:21] Attributes of modified citrus pectin and how it affects the metabolic system
[27:07] The possibilities of MCP in autoimmune disease
[30:17] MCP, Galectin-3 and gut health 
[33:45] MCP and liver diseases
[35:15] MCP and sepsis
[37:30] MCP and cancer therapies
[41:36] Galectin-3, MCP and inflammation driven disease
[45:49] Normal function of Galectin-3
[50:24] Emotional stress and Galectin-3

   


Andrew: This is FX Medicine. I'm Andrew Whitfield-Cook. Joining us on the line today is Dr Isaac Eliaz, who's an integrative medical doctor, licensed acupuncturist, researcher, product formulator, and frequent guest lecturer. He's been a pioneer in holistic medicine since the early 1980s and has published numerous peer-reviewed research papers on several of his key integrative health formulas. He's the founder and medical director of Amitabha Medical Clinic in Santa Rosa, California, an integrative health centre specialising in cancer and chronic conditions. Dr Eliaz is also widely regarded as the leading expert in the field of modified citrus pectin research. And we warmly welcome Dr Isaac Eliaz to FX Medicine today. How are you, Isaac?

Isaac: I'm wonderful, Andrew, and thank you for the opportunity to participate in this important service that you're providing. I'm really excited. And I'm excited to talk to people in Australia because I love Australia, I've been there a few times. I have family in Australia and I just need a good reason to come back.

Andrew: We will hopefully give you that reason.

Isaac, well, look, I guess, firstly, we have to go back to modified citrus pectin. Now, this is something that I've used clinically for years and years with great effect in especially cancer patients. We're going to be delving into a few other areas. But I'd really like to go back to where this all started with modifying a pectin, a citrus pectin. Where did the research start? Where does the idea start?



Omega-3s for Pain and Inflammation by Claire Georgiou


 

Isaac: You know, it's really, it's a remarkable story that is, it is multifaceted. The person that originally came with the idea of modifying pectin to a low molecular weight, more for in-vitro testing and for animal testing was Dr Avraham Raz from Wayne University, who's Israeli in his origin and has been around for many, many years. He's one of the people who discovered lectins and galectins in the late '80s. And I just published actually, a landmark paper with him on the function of modified citrus pectin in high impact a peer-reviewed journal. So we collaborate, actually. 

But from a practical point of view, I'm a native of Israel. So in 1971, I was 12 years old, you can calculate, I just turned 60. I was taking a walk in our neighbourhood. Our neighbours, Ruth and Leo Cohen, both were PhDs in organic chemistry, and were pioneers of the citrus industry in Israel, which Israel was famous for its citrus industry. People may not be aware, of most of Israel used to be citrus plants, you know, and trees was the main thing. 

Andrew: Yeah.

Isaac: And there was a key organic chemist who developed the industry. And out of the blue, he turned to me, you know, I was 12 years old, he told me, "Isaac, one day they will find the treatment for cancer from the peel of the citrus fruit."

So in 1995, the first paper comes out, and somehow it stuck in my mind. You know, 24 years later, I pick up the phone, I call Ruth, I tell her, "Ruth, it's Isaac. We're very happy to talk, you know, I don't expect you to remember but you told me this thing when I was 12 years old. I need your help." And she put me together with the main pectin scientist in the world, and we developed this very unique modified citrus pectin called PectaSol, and it's important to emphasise because all the published papers on a commercially available product are just on PectaSol. 

Andrew: Yeah.

Isaac: And, of course, is always downward science with people who try to copy you, and they use the generic name because modified citrus pectin is a misleading name. Every pectin is to be modified to be taken out of the peel, right? You have to extract it.

Andrew: Yeah.

Isaac: But it's really PectaSol which is the one that has the low molecular weight, this specific structure we have proven, the only pectin to ever be shown, where we developed an antibody, we have shown absorption through the gut in human subjects.

So we know, we have proven it gets absorbed, and because of its unique structure which we can reproduce, it has this really remarkable benefits. And, Andrew, as you mentioned, we all started by using it with cancer. But over the years, we realised that its role in blocking Galectin-3 is so much bigger than cancer, that it's literally mind-blowing, literally mind-blowing.

Andrew: Yeah. I do want to just put in a point for our listeners, and that is that FX Medicine tries to be non-branded wherever possible. But in the interests of both skill set and safety for our practitioners around the world, I think it's important to make this distinction that this is the researched product. There is sometimes when you cannot escape the naming of a certain product. So I just wanted to clarify that point.

Isaac: I really appreciate your comments. I always...actually I avoid mentioning it, but, you know, we adjusted 3, 4 landmark papers, and there are over 20 papers showing, without question, the benefit in inflammatory fibrotic diseases of lung, liver, heart, kidney, etc. And there was one paper published that challenger didn't work, and sure enough, it wasn't our product.

Andrew: Right.

Isaac: So it takes one drop of lemon to spoil a bucket of milk, you know. And people need to know this. And this is why I decided once this happened, and I did respond to the journal and they published my response, and the original author has acknowledged the issue. But then I said, "You know what? The world needs to know. I can't be the best kept secret in town." So that's why I'm mentioning it now.

Andrew: I want to go into why that's important, but I think we need to backtrack first and talk a little bit about Galectin-3. And that's this receptor that's involved in more than what I originally thought was. And that was certainly like prostate cancer and maybe a few other cancers, like breast cancer. So can we talk a little bit about Galectin-3. 

Isaac: Absolutely.

Andrew: What is this receptor?

Isaac: Yeah, we can talk. It's more than a little bit. So it's very fascinating, and if I can take two minutes to explain it. It's interesting for me on a personal level, because you discovered...you described the different areas that I have expertise in, you know, regular medicine, licensed acupuncture, classical homeopathy, serious researcher, you know, from double-blind clinical trials with Harvard, to Tufts, to Columbia, to Johns Hopkins and kind of going down the east coast, to the USDA, to MD Anderson, really dozens of institutes. But I'm also a healer. I'm mainly a healer, I'm mainly a hands-on practitioner. And for me, I was fortunate to get trained by some of the most legendary Tibetan Buddhist masters in Tibet. So I teach meditation and healing on a volunteer basis, and it's all about how to transform difficulties, negative emotions, survival responses into love and compassion. Why am I telling this story? Because this is where I come from meditation into health.

What I found out and is so fascinating how life brings you to what you need, Galectin-3 is our master survival protein, Andrew. It's really important for the doctors to understand this. And our survival response is at the root of every chronic disease. Because, what is cancer? Cancer is one cell that decides to survive.

Andrew: Yeah.

Isaac: What is autoimmune disease? That a certain organ fights with the rest of the body. So this survival mechanism has effect, especially inside the cell, it helps to develop the cell normally, because we want to survive, right? We have 50 trillion cells that are surviving together. We are a miracle, each of us. So inside the cell, Galectin-3 is important for embryogenesis, for normal cell development. But that's not our issue. Our issue is on the cell membrane, as you said, as a receptor, and in the circulation. And there, it allows different cells, different tissue, different bacteria, or parasites to survive by creating a microenvironment.

So actually Galectin-3 is defined as an alarming. It's a protein that sounds the alarm. So if, 20 years ago we thought that Galectin-3 is a chronic protein that is in charge of... Actually 20 years ago, we thought more about the cancer. But let's say 15 years ago, or 10 years ago, we thought it's...we realised it's in charge of injury repair, and it does it by creating inflammation and fibrosis, which is pretty bad. But now we know that Galectin-3 in acute conditions like myocardial infarction, like sepsis, it goes up, Andrew, in minutes, in minutes.

Andrew: Right.

Isaac: And it starts the whole cascade of inflammation. How does it do it? If one looks at the structure of Galectin-3, it is a carbohydrate recognition domain. So it binds to different carbohydrate. So oligosaccharides, proteoglycans, glycolipids, it binds to VGF. It binds to CEA. It binds to a sticky molecules like integrin. It binds to fibronectin. It binds the CD45. And based on what it binds, based on the carbohydrate sugar signature, it will create different responses.

So it's the master protein that creates the microenvironment that allows the atherosclerotic plaque to thrive, that allows an aggressive invader to create an impenetrable biofilm. It allows a cancer cell to create a microenvironment with apoxia, etc.

And Galectin-3 goes up with age. It goes up with any trauma or stress or injury, physical, emotional, mental, psychological, we know we have studied about it. And as a result, it degrades our body.

So blocking Galectin-3, and this is not something I would say even five years ago, but blocking Galectin-3 is, in my opinion, the most important thing for longevity. Because it affects literally, if I showed you the charts, every single chronic disease. We're right now doing research myself on multiple cancers. We're starting a research on scleroderma. We did an osteoarthritis and we're starting rheumatoid arthritis. We're doing, you know, on idiopathic pulmonary fibrosis…

Andrew: Wow.

Isaac: …we’re doing research on CKD, on AKI, on congestive heart failure, on hypertension, all of these with the same compound. How is it possible? Because we are addressing our basic unhealthy survival instinct, which really causes havoc. It's like the body goes to war, when it can survive with peace.

Andrew: Okay. So it's not just a marker but a target. For instance, you say that it goes up in minutes. Now, normally we see things like, you know, CRP, say, C-reactive protein or ESR going up with, as an acute-phase protein to a stressor. But we don't target that. We just measure it and we say, "That's how we measure what's happening. We target other tissues." 

Isaac: Correct.

Andrew: However, this turns out to be a target, not just a measure.

Isaac: Absolutely. And we know that it's a target because when we block it, the condition reverses itself. 

Andrew: Right.

Isaac: It not only stops, but in certain conditions, you look at animal studies with atherosclerosis, with osteosclerosis, with fibrosis of the heart, with kidney damage, with liver damage, and you actually not only stop it, in many studies, we actually reverse it. Because there is still energy in the tissue.

Andrew: Yeah, right. Okay. So this is something I picked up. When you said AKI, that's acute kidney injury. And if you don't nip that in the bud really quick you can possibly lead to devastating disorders like sepsis.

Isaac: Exactly.

Andrew: So if we can recover this early enough, if we can be maybe measuring Galectin-3 in the serum and address acute kidney injury in its early stages, we could be preventing the progression of sepsis.

Isaac: Of course. This is, you know, it's so interesting that you're jumping, it's kind of amazing. Because we had four papers of this lately, I just came back from China when I lectured in a, for me, I'm like a holistic outpatient doctor, I actually lectured in an International Critical Care Conference, okay?

Andrew: Right.

Issac: ICU conference because of the Galectin-3, because now there are studies that's showing, listen to this, a really good study, high impact journal, that and a combination of human study and animal study. So in the human studies, it showed the patients who survived sepsis in the ICU, 1100 patients, their damage to the kidney was proportional to the level of Galectin-3 at the time of discharge. But more important, patients who are going to have coronary artery bypass, okay?

Andrew: Yeah.

Isaac: Their level of pre-surgery Galectin-3 directly correlated to the kidney damage and the heart damage from the surgery. Unreal.

Andrew: Wow.

Isaac: And then what they found out, when they took animal, when they did an acute kidney injury by shutting down the circulation to the animal..

Andrew: Yep.

Isaac: …if they gave them the modified citrus pectin, they actually eliminated the damage to the heart, not only to the kidney, to the heart.

So why is AKI so important? You can have an AKI and you have no long-term kidney damage. But guess what?

Andrew: You can damage the heart.

Isaac: Alarming has been set on, in the bone marrow, and the alarming is going to go to the target organs like the heart, is going to cause remodelling of the heart, and you know, and the atherotic dysfunction and stiffening fiberoptic heart and early death. And it all started with the kidney injury and the mediator exclusively for this or the main one is, Galectin-3. And when you block it, or you doing it in the animal that don't have Galectin-3, you don't get this damage. Unreal, right?

Andrew: Absolutely.

Isaac: Multiple studies on this.

Andrew: Now, also you mentioned, you know, fibrosis, endothelial fibrosis, and I'm picturing here, things like fibrotic plaques, so fibrotic caps. Can we manipulate, modulate an atheroma by the use of modified citrus pectin?

Isaac: Absolutely. Absolutely. And we know research, it's shown it. Even years ago they've already shown that from old fibres pectins are most effective for plaques in general. But of course, and we know why. If you look at the fibroblast and myofibroblast, if you look at TGF-β.

Andrew: Yup.

Isaac: TGF-β is the driver of the fibrotic process. TGF-β is excreted from macrophage in response to Galectin-3…

Andrew: Ahh.

Isaac: …for inflammatory and IL-1 B, IL-10, IL-8, IL-4, TNF-alpha. All are excreted from inflammatory macrophage in response to Galectin-3. Extracellular matrix modulation increasing in extracellular mesenchymal stem cells which causes fibrosis, excreted, stimulated, by Galectin-3. In the same time, the Galectin-3 will go to our normal T cells and will shut down the normal immune response. If you take T cells, and you put Galectin-3, no cytokines, zip. Anergy, complete anergy. Why? That how the cancer survives. The cancer is smart. It also uses the Galectin-3. It wants to survive. We talked about it. And then you put it a Galectin-3 blocker…

Andrew: Yeah.

Isaac: Guess what? You get your cytokines back, you get an immune response with less inflammation. And that's why it's a winning combination. Less inflammation, and better immune response.

Andrew: Yeah. I think you may have actually answered a question that's dogged me for years, and that is with regards to the macrophage, something initiates the macrophage to turn into a foam cell. And I've always wondered, does the macrophage turn into a foam cell upon engulfing oxidised LDL in the blood? Or after it migrates into the tunica intima of the artery? i.e., does the inflammatory or atheromic process start after that foam cell has migrated, or does it initiate before? And I think what you're telling me is that it's initiated within the blood?

Isaac: Yeah, but it's interesting. It's a great question, great observation! I just spoke about it. So, the body communicates. So, for example, when you do an AKI, okay? You do an AKI on an animal, on let's say on a mice that's a knock out mice, no Galectin-3, you don't get the response, okay? Then you transfer that into the bone marrow, okay, into the bone marrow…

Andrew: Yeah.

Isaac: …you advise the bone marrow that is normal bone marrow, okay? From the AKI, the macrophage in the bone marrow gets stimulated, they excrete Galectin-3 that goes into the heart, and there, the local macrophage also spike in response to the bone marrow. So you have a systemic response…

Andrew: Yep.

Isaac: …and you have an extracellular response.

But if you cut the systemic response, you will affect the extracellular response. We see it. When we give modified citrus pectin with down-regulation of expression of Galectin-3 intracellularly, the cell knows that it's safer now, it doesn't have to excrete so much Galectin-3. So it's intricate relationship, but you're right, it starts far away sometimes from the target tissue totally.

Andrew: If you think about health care dollars spent on heart disease, and hospitalisations, indeed re-hospitalisations, chronic care, and all of that sort of thing, this could save the healthcare dollar of countries, millions. This is a huge preventative...

Isaac: Billions. Billions. Billions, actually billions, not millions.

Andrew: Yeah.

Isaac: Because you know, CKD; chronic kidney disease...

Andrew: Yep.

Isaac: is the biggest, even with overcharging in the field of cancer, CKD is the biggest expenditure of the medical system in the United States.

Andrew: Right.

Isaac: And a lot of these can be prevented. The sepsis patients, 600,000 die in the United States. All the bypass patients that get the complications afterwards and you can prevent it literally, either by taking modified citrus pectin, or mainly, you know, just by taking more modified citrus pectin and developing some more dramatic medical devices for the ICU where we're going to filter out the Galectin-3, but that's many years out. 

Andrew: Ah.

Isaac: But we have shown now that just by giving modified citrus pectin, we're actually modulating the effect, we're showing that...and we're going to publish this soon, that in kidney damaged models, if we just feed the animal, my modified citrus pectin a week before and then we do the regular injury, okay? We are dramatically changing the outcome. Which is similar to the study about the levels of Galectin-3 preoperatively will determine what will happen afterwards, and Andrew, it's based on what you said, it's the cell in the blood is sending a signal to the target tissue. So we are cutting the signal.

Andrew: I just want to make this clear in my mind. So if you have a Galectin-3 knockout mouse...

Isaac: Right.

Andrew: ...and you induce, forgive me, but this is how science is done. I hate this, how this happens to animals, but it's the way.

So if there is an injury initiated in that mouse that has no Galectin-3, then that acute kidney injury let's say, does not progress because it can't drive it further. Is that true? Is that the same?

Isaac: Right. Right. Yeah in this specific study it did not create damage to the heart.

Andrew: Wow.

Isaac: They were interesting in the kidney to... Exactly.

Andrew: Right.

Isaac: In the knockout animal and in the regular animal when you gave MCP. But when they took the knockout animal and they just created a bone marrow that had Galectin-3...

Andrew: Right, yep.

Isaac: ...they were able to still create the damage because that's why it's such an elegant study that got so much attention.

Andrew: Yeah.

Isaac: The signal to this specifically they identified the inflammatory macrophage, just like you were talking about, and they are the ones who created the effect. And again, when you gave our modified citrus pectin, when they used PectaSol, it cancelled the negative effect.

Andrew: Right. Now, I just want to talk a little bit about modified citrus pectin and the attributes that it must have. It's got to be of a certain size, and it's got to have a low esterification, correct?

Isaac: Right. Correct.

Andrew: Can we discuss why that's important? What causes the problem if there is high esterification, for instance?

Isaac: It's a very protein structure is almost a little bit of mystery. The idea is if it has low esterification it has much greater affinity for binding to positively charged material like heavy metals. You know, we have a number of very impressive papers on our ability to bind to lead, to mercury. We just published a paper on uranium, binding an increased excretion in the gut in a peer-reviewed journal. But it's also you have to preserve the side branches of the pectin. So, for example, very unique feature we have in PectaSol that it has 10% of rhamnogalacturonan I and II. And rhamnogalacturonan I and II is the, for example, the active immune-enhancing compound in mistletoe is rhamnogalacturonan I and II.

Andrew: Right.

Isaac: So we weren't so aware of it until we did a study on volunteers, and we tested different medicinal mushrooms, because I love medicinal mushrooms, to see the immune effect, and then we tested our MCP, and we never published on the mushrooms because our MCP was so much more effective. And at this time, and this is almost, this is almost 15 years ago, we really didn't completely understand even why. And now we know because it allows the immune system to respond. So, the specific modified citrus... And the other thing that we have found, talking about modified citrus pectin which actually it's a mistake I've made, we see the effects of modified citrus pectin at a partial dose. So if the full dose is 15 grams a day, taken two or three times a day and based, you know, 15 minutes before food is enough and maybe an hour after food, then because of the response, I used to recommend for maintenance 5 grams a day. But what I've found, especially in the last year, is that if you have any health issues, if you really take the full dose, you will see different effects. And one of the effects you see is a metabolic effect. And why is this? Because the insulin receptors, you know, when you have metabolic syndrome, you often have extracellular inflammation, you have inflammatory macrophage. But often the inflammatory macrophage are excreting Galetin-3 that blocks the insulin receptors. As a result, AMPK gets blocked, and then mTOR-1 and HIF, hypoxia inducing factors get turned on.

Andrew: Yeah.

Isaac: PDK gets turned on, PDH gets blocked, you know, the mitochondria shuts down and you get abnormal metabolism. You see this it in diabetes, you see this it in metabolic diseases, you see it in infections…

Andrew: Yep.

Isaac: …and, of course, you see it in cancer because the microenvironment. So there is something about people taking your full dose. I know from my own personal experience that I finally...I had haemoglobin A1C no matter what 5.8, 5.7, 5.8. Now, I just increased my MCP dose to full dose and sure enough, you know, it's down to 5.4. I haven't been to 5.4 for 15 years.

Andrew: So we could use this not just as an initial treatment to, you know, purportedly block the initial insult, but we can actually use this to track response. That's what I'm wondering here. We could use this let's say that, you know, the normal waxing and waning of autoimmune disease, for instance. We could use increasing and decreasing a dose along with the inflammation that accompanies...

Isaac: Yes.

Andrew: ...rheumatoid arthritis or other autoimmune diseases.

Isaac: You're really picking, very interesting. So autoimmune diseases, for example, Rheumatoid arthritis, all of them will have very high levels of Galectin-3. 

Andrew: Yep.

Isaac: But it's important to talk about testing for Galectin-3 because it's a double-edged sword. Why? Because, we have a relationship between Galectin-3 being in the bloodstream as monomers and being as pentamers which means five Galectin-3 attached together. But the antibodies that detect Galectin-3 attaches to the N-terminal, not to the carbohydrate recognition domain, and it can read a pentamer as one Galactin-3.

Andrew: Right.

Isaac: So you cannot decide on treatment based on the Galectin-3 level. When people ask me, "Who needs to take modified citrus pectin?" I tell them anyone that is breathing because of its very basic, basic, basic structure. However, if you have a healthy patient that is really doing great, now, this is somebody in their mid-30s, they're really doing well, you know, no health problems. They're doing great.

Andrew: Yeah.

Isaac: And you happen to check their Galectin-3, and it's now, it is the high teens 17, 18, 20, they are a ticking time bomb. It's much higher than you expect. Then these people need to go on a full dose modified citrus pectin and you need to look for fibrotic places in the body that can produce Galectin-3, and one area is scars. Scars on the surface, scars from surgeries, scars after infection, emotional scars, you know, things that are producing ongoing inflammation and repair. And addressing them is very important because Galectin-3 increases in level as we age. And very interesting, if we compare levels of Galectin-3 in centenarians, compared to people between 70 and 80, it's a really nice study...

Andrew: Yeah.

Isaac: ...and we have to do it, we have to remember that the ones who are 70 and 80 include a few which are going to become centenarians, the centenarian's average levels of Galectin-3, are very significantly lower than those between the '70s and '80s. But you can see in the '70s and '80s, I can send you the study, it's really neat, you see the cluster of the low Galectin-3, and these are probably the ones that are going to make it to be centenarian.

Andrew: Right. There's a point that you made earlier also about the structure of the modified citrus pectin. And you mentioned the rhamnose molecular.

Isaac: Yeah, the rhamnogalacturonan I and II, right.

Andrew: Got you. So what I'm wondering about here is interaction at the gut level, interaction with the glycocalyx or the mucus of the gut lining. And I'm wondering about T cell, you were mentioning energy before. So T cell activation or modulation, so that we can get T zero, rather than T1, T2, T17, etc.

Isaac: Yes.

Andrew: So how effective is modified citrus pectin, on treating at the gut level? And how...like, have you looked at absorption studies and all that sort of stuff as well?

Isaac: Yeah, we know there's good absorption and we know the T half life, we haven't published yet, but it's between eight and 10 hours but it's interesting. We have between 4 and 6 different papers specifically on our modified citrus pectin showing as a benefit in enhancing, for example, antibiotic therapy, and improvement in reducing resistance to aggressive bacteria, and in any... So we definitely have a number of papers showing the importance of modified citrus pectin in balancing the microbiome and the biofilm. Because the Galectin-3 is a key structure of the biofilm a lot of the molecule that we try to target, people say they are heavy metals, they're oxidised lipids they're all sitting on the Galectin-3. There are many, many papers on Galectin-3 in relationship to the gut mucus and into the biofilm. Aggressive bacteria, you know, if it's staphylococcus or salmonella, they use Galectin-3 to anchor into the gut lining and create issues that will increase permeability in the gut, etc. So from this sense, one thing that I see, for example, in Lyme patients that usually are sensitive to almost everything, they will tell you when they take modified citrus pectin, "Wow, it really feels good. I really feel my gut healing."

Andrew: So is this acting on, you know, lipopolysaccharide activation of mucosal infiltration, if you like, or activation at the gut lining level of an inflammatory process?

Isaac: This is a great comment. Lipopolysaccharide binds to Galectin-3. So now you start to get the other piece of the, like in sepsis. So you got Galectin-3, okay, it's going to the nasty places in the body, right?

Andrew: Yeah.

Isaac: And it's delivering your lipopolysaccharide where the saccharide is bound to the Galectin-3. So you take modified citrus pectin and you competitively get rid of the lipopolysaccharide and you cut down the inflammatory process.

Andrew: Right.

Isaac: People from sepsis don't die from the infection. They die from the abnormal inflammatory response.

Andrew: Yes, that's right.

Isaac: Absolutely. We know that LPS is directly related, is carried by Galectin-3. Definitely. What you said is extremely accurate.

Andrew: Okay. So that would then tie in to what you were speaking earlier about with regards to liver fibrosis. Do you see Gal-3 in the actual Kupffer cells of the liver? Do you see increased Gal-3 in there? And I'm wondering here about the use of modified citrus pectin in things like non-alcoholic fatty liver disease in, as you said, liver fibrosis, in alcoholic liver disease, in Hep C?

Isaac: Andrew, I feel like you're reading my mind. I just came from Asia where I specifically was looking at this. There's solid evidence on the role of Galectin-3 in NASH...

Andrew: Yeah.

Isaac: ...non-alcoholic steatohepatitis that's what you mentioned.

Andrew: Yeah.

Isaac: Which, you know, honestly, many doctors and don't realise what a huge problem it is. Millions of people, and even there are some drugs in development specifically for NASH. There are papers on our modified citrus pectin showing reversal of liver damage when you give them modified citrus pectin. So, absolutely. NASH is driven by Galectin-3. It's Galectin-3 that will determine, are you going to go into fibrosis or not? So modified citrus pectin is very important for NASH patients. But again, you kind of expect it based on what we've been talking about. It drives inflammatory in the fibrotic point.

Andrew: Yeah. Okay.

Isaac: Absolutely. NASH is a big target.

Andrew: Two things I'm wondering about with combinations here. First one is with regard to sepsis, you know, it's diagnosed late, and it's misdiagnosed often. And, you know, drug treatments that were previously tried, like one called Xigris was found not to work. And so there's doctors now crying out for help, and indeed, doctors who are normally totally dismissive of, you know, complementary approaches are now initiating intravenous vitamin C to help reduce sepsis.

Isaac: Oh, absolutely amazing study, because if these study that you're referring to was a drug, every ICU now I would be using vitamin C IV, right?

Andrew: Yeah, you'd think, you would hope.

Isaac: So it's a great combination, and why is it a great combination? Because vitamin C modulates the extracellular matrix. And in this sense, PectaSol will be very helpful. You know, we have a very reputable physician from Southern California who got sepsis...who got an infection in his hand and did not respond to it, it turned to sepsis, did not respond to antibiotics. This happened like three, four months ago. 

Andrew: Yeah.

Isaac: And he was just scheduled for amputation of the hand literally within hours. Okay? And he knows me. So he went on a full dose of modified citrus pectin plus our mushroom combination which is very similar, you know, oligosaccharides. And sure enough, you know, he started responding and it went away. And the ideal for this patient, he would have also done a high dose level of vitamin C. So yes, it's a very good combination. And as you said, I mean, people don't realise there is very little interest in developing drugs for sepsis. Surprisingly, you know. I got an NIH grant from the NIH to study removal of Galectin-3 in sepsis because there is very little as an alternative guide. There is very little interest in Big Pharma because it's hard to prove and nothing is working, you know, and hundreds of thousands die every year.

Andrew: Yeah.

Isaac: Hundreds of thousands in the United States, 600,000.

Andrew: And what about with regards to, we'll talk about your research in one second, but I guess firstly, I want to talk about the concurrent use of modified citrus pectin with chemotherapeutics, in cancer chemotherapeutics we're talking about here. Are there any caveats that you have to be aware of like, for instance, you know, the biologics that are now out on the market, the monoclonal antibodies? Do we have to be cautious with any of these?

Isaac: Another excellent question. So we have now multiple studies in vitro, in vivo, subhuman data showing that MCP is synergistic practically with every chemotherapy, and we specifically have data showing is that MCP is synergistic with PDL-1 inhibitors.

Andrew: Right. Okay.

Isaac: In fact, we know the mechanism. So all these biological, you know, Keytruda...no, nivolumab differently in one inhibitor. 

Andrew: Yep.

Isaac: And we specifically understand why, because when you modify the intracellular metabolism, when you block NPK because of the receptors outside, you are increasing PDL-1 expression. So actually it's important. We, in fact, we were approved, we have IRB approval for two different PDL-1 inhibitors, studies in bladder and kidney cancer with PDL-1 inhibitor and our modified citrus pectin, just our investigator move to another hospital so we have to move the approval. But we actually got approved already for a formal clinical trial because of pilot study data. So yes, modified citrus pectin is one of the key supplements I give during chemotherapy and during immunotherapy. But, it's the last supplement at a elevated dose, okay? Twenty grams a day...

Andrew: Right.

Isaac: ...that your patients should take before a biopsy or surgery with a high probability of cancer to prevent the spread, and it's an essential supplement with radiation therapy. We've published showing how cells that cannot, resistant cells to radiation were not getting killed by radiation therapy. When we add the modified citrus pectin to the same dose of radiation, we get a kill of the cell.

Andrew: Okay.

Isaac: We have to publish this paper.

Andrew: Right.

Isaac: And all of this, because we are changing the microenvironment and we are exposing the cancer cell to the treatment.

Andrew: So what about things like side effects from cancer therapies? For instance, radiation therapy, let's say breast cancer, you've got the radiation dermatitis, you've got CIPN, the chemotherapy-induced peripheral neuropathy. It's almost like a necessary poison, the side effect. You need that poison to kill cancer but the poison has side effects on healthy tissues. Can modified citrus pectin have any effect on abrogating these bad effects.?

Isaac: Yes, definitely. And again, you know, your audience are integrated physicians. They understand you don't use only one time...one thing. But yes, especially the radiation side effects, because the radiation enhances a fibrotic process, and modified citrus pectin, which is Galectin-3 driven. And modified citrus pectin, Andrew, will cut the process. But, definitely. And interesting enough, for neuroinflammation which is tricky, for neuroinflammation, we have a number of studies showing that when you take in animal studies when you induce LPS-driven neuroinflammation, the neuroinflammation is cut significantly and sometimes completely eliminated when you introduce our modified citrus pectin, you see a decrease in TNF-alpha, in TGF-beta, in certain interleukins, inflammatory interleukins back to normal level. Yeah, we actually have published papers on this.

Andrew: It seems like the Gal-3 should be measured in all sorts of inflammatory driven diseases no matter what the aetiology.

Isaac: You know, it's a very good comment. And you and I know it takes, now with the internet, it goes faster, it's not 50 years, it just 20 to 30 years. But Galectin-3 is an approved test in the United States, paid by every insurance.

Andrew: Ah. Yeah.

Isaac: But again, I mean, I don't know the situation in Australia. But I can tell you the United States if you have insurance, the insurance will pay the lab $30 for the Galectin-3 test, and if you want to pay in cash, they will charge you $300 to $500.

Andrew: Yeah, yeah.

Isaac: So this is the politics of medicine. But there is more and more interest in it. It's hard to know how to read it. Why? Because doctors, and I really want to encourage anybody who is listening, doctors love protocols. 

Andrew: Yeah.

Isaac: And one of my favourite sayings is the only protocol I have is that I don't have a protocol.

Andrew: Thank you.

Isaac: So for a patient with congestive... Very important. So for patients with congestive heart failure, having Galectin-3 under 17.8, one out of eight will die in one year. Okay? One out of eight, 12.5%. I do a study on 582 people. If you're Galectin-3 is over 25.6, not such a big difference, 37% will die in one year. 

Andrew: Oye.

Isaac: So if you have a congestive heart failure, you definitely want to check your patient, okay, because it's life and death. But, in the normal population, if you're Galectin-3 is 17.5 and the lab comes under 17.8 normal, you are not normal. The average is 10. You have elevated Galectin-3. You have a lot of risks. So you have to read the test dynamically. It should not determine if you're going to use modified citrus pectin or not. I want to emphasise this point, as somebody who has done thousands and thousands and thousands of Galectin-3 test. But, for certain patients, like metastatic patients or patients with autoimmune diseases or, you know, fibrotic diseases where their specific Galectin-3 chemistry is demonstrating that as they get worse the Galectin-3 go up, as they get better as the Galectin-3 goes down. For this patient, Galectin-3 becomes a great marker. Now, you have to remember, you can have the same amount of Galectin-3 in the blood. 

Andrew: Yeah.

Isaac: But if it's blocked by motivated citrus pectin its not...we call it blocked, inactivated Galectin-3, it's no longer causing damage.

Andrew: Right.

Isaac: But over time as your inflammation gets reduced, your Galectin-3 gets better. I know I used to volunteer and go up to to to Tibet to treat the different Buddhist masters, and one time, you know, there was really high, 14,000, 15,000 feet, and I really, I had no oxygen, I was surprised and I probably had some heart damage, and I came back, my Galectin-3 was 17. Then I took modified citrus pectin at the full dose, my Galectin-3 now is 11, right, and my arrhythmia went away. Why it's 11? Because I've less inflammation.

Andrew: Right.

Isaac: But it took a long time of blocking. So you don't want...you want to give modified citrus pectin understanding how fundamental is Galectin-3. You know, some of my colleagues, my friends say, "Isaac, how come the word didn't go out for such a breakthrough?" You know, we have over 60 published papers in modified citrus pectin and we get an average twice a month papers from major universities. It's much bigger than me and my work. 

Andrew: Yep.

Isaac: Because I was so focused on research and research, I didn't have time to go around and tell the whole world about it. But now I really feel with what I'm seeing, it's an essential supplement for every single patient. You can see why. You can see how many diseases we covered, you know, in this podcast.

Andrew: Okay. Now, you've mentioned levels of, you know, like 17 is quite high, and you mentioned that you got your level down to 11. Now, what's a safe level of Gal-3? What's a normal level? If Gal-3 exists in the body, it exists for a reason. What it's normal function?

Isaac: Of course. So intracellularly it functions for normal cell development. For example, "American Journal of Nephrology" had a great article about a year ago showing Galectin-3 helping nephrogenesis and making Galectin-3 a target for fighting CKD outside of the cell. So inside the cell, remember we started this conversation by talking about survival.

Andrew: Yep.

Isaac: And I said, inside the cell survival mean embryogenesis. Outside the cell, survival is a fight. Because one cell is a part of a community. 

Andrew: Yeah.

Isaac: If a cell wants to survive, doesn't want to die, it no longer becomes a part of community. It's really, you can see it in the geopolitical environment, right? It's nationalism is creating boundaries. What happens? You create a microenvironment that the body cannot control, classically what happens in cancer. So in this sense, Galectin-3 is needed for acute injury repair. But what's the beauty? The beauty is that even if you give people modified citrus pectin, if you need it at a certain place, it will still get expressed where it's needed. That's why it's not a double-edged sword.

Andrew: Right.

Isaac: But you got to block it all the time in the circulation. Because, Andrew, if you look at numbers, if normal Galectin-3 is 10 and then it's telling you that 20 is a real issue, we just doubled Galectin-3. 

Andrew: Yeah.

Isaac: If you look at CRP, you can have CRP of under 0.5, and when someone is really inflamed, you'll get 100. It goes up 200-fold. 

Andrew: Yeah, yeah.

Isaac: Same with cytokines. Why? Because these are downstream instigators. It's a little bit of change of Galectin-3 turns on the alarm and then everybody else goes crazy.

Andrew: Right.

Isaac: So we are really dealing with a master protein when we address it.

Andrew: But modified citrus pectin doesn't infiltrate the cell and disrupts say embryogenesis and things like that.

Isaac: Exactly.

Andrew: Right. Okay.

Isaac: It's the other way around. 

Andrew: Right.

Isaac: Because, when the cell is... Remember when the cell receptors are working better and now AMPK is working better...

Andrew: Yep.

Isaac: ...and mTOR-1 is shut down, we get 36 molecules of ATP from every glucose, we don't get lactic acidosis, we don't get,you know, reactive oxygen species, we're in great shape. But when we go into survival mode, we go to glycolysis. We produce energy 10,000 times faster, inefficient and we change the same metabolism. We get more hypoxic, it gets worse. That's why it's so important to address Galectin-3. You know, it's part of the, you know, intracellular, people are using Metformin, our, a compound that I use a lot onocuole is even better, benefits. This is intracellularly. Galectin-3 starts the process through the cell membrane, because the cell membrane is really the boundary of the cell. And every cell, we can look at every cell as, I look at it as a living organism with boundaries, with neighbours, with a community. If it's willing to be a part of a community, like a bee and a beehive, I like to say, then what the bee cares is for the beehive is to survive. But if a bee goes crazy and starts attacking the other bees, beehive is not going to work. So Galectin-3 throws us off. It gets us to the survival. And the survival response starts with the sympathetic nervous system in the immediate second response, but then it can quiet down. But the metabolic signal is Galectin-3, and that's why it's so fundamental, it is such effect. We don't have time to talk. You can see in people post-MI who meditate, Galectin-3 goes down and their heart damage goes down dramatically. Beautiful studies on this human clinical trial.

Andrew: Wow.

Isaac: Double blind.

Andrew: There is so much more to cover here, but just on one last point. So you're talking about stressors in the human body, and normally we default to a physical stressor. So, do emotional stressors increase Galectin-3? What importance do we have to place there for, on our emotional health?

Isaac: I can't thank you enough for making this your last point, because my passion, my third act, I just turned 60, is really teaching meditation and healing because I have a very unique... Because I treated these legendary Tibetan Buddhist masters in Tibet I was fortunate to get very unique meditation training. 

Andrew: Yeah.

Isaac: And I translated it into healing. And it's amazing what emotional, psycho-spiritual mental thing can do. And the reason is, we are built to take stressors and turn them into love and compassion. And that's why I told you the beginning when I told my story, that's what I meant. And thank you, I don't know how you do this, but you kind of closed the whole thing. Because, if you think about the heart, the heart gives clean blood with no discrimination. The aorta cannot contract or expand like a small arteriole. It keeps blood everywhere, open heart. And it also feeds itself. By the first artery the aorta gives the blood is the coronary artery, which means self-love is very important. In order for the heart to give clean blood, what does it need? It needs to get dirty blood. It needs to get stuff that the cells feel they don't want. So we use these stressors, we use traumas and the heart knows how to transform them into clean blood. How does it do it? By connecting with the universe, to our breath. We are all a part of one big picture. So when I go back to survival, the cell is part of a tissue, the tissue is part of an organ, the organ is part of the body, and we are part of a community, we are part of the planet and the planet is part of the solar system, it's all the same. So eventually, survival goes all the way to the universe. And as long as we see the bigger picture, and we let go of our own drama, you know, if we don't contract into our drama, we live a healthier, happier life. I think in my retreats, I see cancer markers, I see neurological diseases, improving in a few days, you know. Now I'm doing some trials on this in more focused things. But it's the same thing. It's a Galectin-3 story. And I'm writing a book about it that hopefully will be out in a few months and the title is "The survival paradox." Because survival is a paradox. So your question is so right. We know from the study I told you about MIs. They took patients straight for MI, and 10 patients just didn't do anything and 10 patients meditated, just simple meditation. Then, the improved in profusion was so dramatic that even on 10 compared to 10, P-value was under 0.001...

Andrew: Wow.

Isaac: ...and Galectin-3 was lower. But when they took them six weeks later, and they did another session, and they checked Galectin-3 between, before the session and after the 20-minute session, okay? A drop of 15% in the level of Galectin-3...

Andrew: Yeah, that's huge.

Isaac: ...during the meditation session after six weeks. So the beauty now, there are so many studies, there are over 9,000 papers in Galectin-3, that we have publications, all these insights like that you just said now, you know? It's nice that there's research to support like the insight that you just said.

Andrew: Well, I would love to get you back on to FX Medicine at some stage and we can perhaps delve into certain parts of the research that you've been involved in, and maybe, you know, also discuss some of the other research that's moving ahead with Galectin-3 and how to treat it. Dr Isaac Eliaz, I can't thank you enough. One of the reasons I love FX Medicine is because of meeting people like you, not just an expert, but...not just involved in medical science, but is driven by love and compassion. A true doctor. Thank you so much for joining us on FX Medicine today.

Isaac: Thank you so much. It was truly my honour. I mean, your interview I must tell you was the most sophisticated interview I've ever had, and I'm not saying it lightly. I'd hundreds of them. You really know the topic and I would really be glad if we can have another one. Yeah, it was really fun. Thank you to everybody in Australia. Take care.

Andrew: This is FX Medicine. I'm Andrew Whitfield Cook.



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FX Medicine Podcast
FX Medicine is at the forefront of ensuring functional and integrative medicine gains the recognition it deserves and ultimately establishes itself as an integral part of standard medical practice. Hosted by Andrew Whitfield-Cook, our podcasts are designed to promote research and evidence-based therapeutic practises, acting as a progressive force for change and improvement in patient health and wellbeing.