FX Medicine

Home of integrative and complementary medicine

Understanding the Cytokine Storm with Dr Isaac Eliaz

Isaac_Eliaz's picture

Understanding the Cytokine Storm with Dr Isaac Eliaz

In this episode, taken from our live interactive podcast, we're joined by Dr Isaac Eliaz to explore something that has been the subject of a lot of robust discussion; the cytokine storm.    

Join Andrew and Dr Eliaz as they explore the mechanisms that underlie the alarm response our immune system initiates in response to infection or attack. 

Covered in this episode:

[00:40] Welcoming back Dr Isaac Eliaz
[01:13] Cytokines: friend or foe?
[04:30] Can we influence resilience?
[10:35] Galectin-3 origins
[12:40] Can cytokine storm be rescued?
[15:09] Natural influencers of Gal-3
[27:47] Understanding modified citrus pectin (MCP)
[29:33] Listener question: COVID and Gal-3
[32:13] Listener question: inflammasomes 
[33:11] Combining science with mind-body medicine
[39:22] Listener question: can Gal-3 be used as a predictor of illness onset?
[41:54] Dr Eliaz's Honokiol research
[45:27] N-acetyl-cysteine (NAC)
[47:29] Dr Eliaz future research visions
[48:40] Thanking Isaac and final thoughts



Andrew: This is FX Medicine. I'm Andrew Whitfield-Cook. Joining me today, again, is Dr Isaac Eliaz, and we're going to be talking today about the cytokine storm, what it is, what it isn't, when it happens, and what it causes. Welcome, Dr Isaac Eliaz, to FX Medicine again. How are you?

Isaac: Very well, and I'm very happy to join you again, Andrew and I'm really excited about it. Our conversations are always like the highlight for me, so...

Andrew: I guess the warning to all of our viewers is “heaven help you” because Isaac and I could talk for hours and hours and hours. 

But I guess to start off with, our first discussion, our first podcast that we did was in very, very different times. And we're going to be talking, obviously, regarding viral infections here. Australia's coming into our winter flu season, America has come out, and now you've got your summer happening, as I can see by your window behind you, Isaac. So I guess, where do we start with the cytokine storm versus just cytokine initiation and inflammation?

Isaac: You know, it's a very important topic. Let me just take...give me a second because, I apologise, somehow I lost...oh, here I am. Good. 

You know, if you remember, Andrew, our previous podcast was so relevant to what's happening now. In many ways, we were really discussing things that are happening now, we just were discussing them ahead of time. 

So cytokine, in general, is a very necessary response for us. That's how the immune system responds. And as I discussed with you briefly last time, and now I'm in the final stages of spending two years on writing a book called "The Survival Paradox." And the survival paradox is how our survival response in the nervous system, through the autonomic nervous system, in the metabolic system, through an alarm system, through galectin-3, is actually: what protects us is what gets us sick.

Andrew: Right.

Isaac: Because we don't know how to turn it off. And in the book, I go into greater detail...into great detail into the whole, how it affects us emotionally, psychologically, physically. It's kind of mind-blowing. It's a paradigm shift.

Because we now...everybody knows this concept about cytokine storm, inflammatory storms, but as we know, inflammation is not a bad thing. We wouldn't be alive if we didn't have the inflammatory response. 

When it goes out of control, when it doesn't become regulated anymore... And so the question is: so, as we get to appreciate this whole issue, this whole complexity of multiple cytokines, is it interleukin-6, is it interleukin-10, is it interleukin-1 beta, is it TNF alpha, is it NF-kappa beta? How does hydroviscosity come into it? How does the inflammation on the cellular level, on the membrane level, on the blood level...? But we want to step back and try to understand the process. 

And when we understand the process, we can see how we can regulate it and control it. And in this specific case, what we are interested in is viral infections. We are now focused on the COVID-19, but you know, influenza and the H1N1, there are a lot of studies that galectins really played a central role in the inflammatory process in the previous epidemic. 

So when we understand it, we can say, “Okay, what can we do about it right now, and what can we do about it on a daily basis?” Because they really react... they interact with each other.

Andrew: Okay, so when we're talking about this, why do some people react and not others, this is constitution. So, how important is one's constitution? And I guess we can go into genetic profiling here and stuff like that, but how important is one's constitution, one's resoluteness...what's the word...Carrie Jones will be talking about this in this in the symposium… Ah, the word's gone out of my head, but that ability to resist.

Isaac: Right.

Andrew: How important is that? And can it be changed, can it be modified? What's the link with galectin-3 then?

Isaac: Yes, yes...yes. You know, in Chinese medicine there is a beautiful discussion about it, a very poetic, metaphoric...like in Chinese medicine, again, it's not the Chinese medicine studied in schools, but the more esoteric Chinese medicine looks at the immune system from a behavioural point of view. 
What will make a lymphocyte say “I don't care if something is going wrong?” Or what will make a lymphocyte say “Oh, my God, this is terrible,” when something is miles and miles away and we don't have to respond? So, certain people hyper-respond. So when they hyper-respond, they can often fight the infection, they can fight different invaders, but they can really set everything on fire in the same process. So there has to be a... 

So, the body has regulatory systems. And really, it's a shift from...I call it from survival. From surviving to thriving. And it's really based on the regulatory system, on the recognition that we are no longer in danger. 

So if you look at it from a behavioural point of view, which is constitutional, it's epigenetic...it's deeply epigenetic. Deeply, you know. As a Jewish person, a big part of my family died in the Holocaust, I know how behavioural patterns move forward in generations. And I know how, by me changing my own patterns, my mother changed her own patterns when she's not aware of it. 

So this all relates to the cytokine storm, and this survival of how our grandmothers save the family, that somebody fights. But there is a cost to it. You put things on fire.

Andrew: Right.

Isaac: So, the autonomic nervous system is built to do it with the fear of fight/flight, right? It's the reflex...it's the same thing. It's very immediate, but we can more easily turn it off. If we are on and stressed all the time, we'll have a long-term effect. So, that's the autonomic storm that we're not talking about so much. 

So for your perspective, it's very obvious. If we are more relaxed, if we move to a parasympathetic dominant system, we get better clarity. We know where we need to respond, where we don't need to respond. Our immune system will function better. And there is tons of research on it. 

Then you have, too, the metabolic. The metabolic system, the alarm is a protein called galectin-3. And we really...see, it's much deeper than what we knew, you know, when I started my journey 25 years ago, with focusing on cancer. 

And now, that's why this survival paradox, so that… So, galectin-3 tells the body that something is wrong. How quickly...how quickly, Andrew, does it tell the body? In minutes. Immediately.

Andrew: Right.

Isaac: We...I can't share the exact data because we are publishing it in a major journal, but we just finished a study that is very relevant to COVID-19. It's called a CLP model, we did a rat study, big group, 18 rats in a group. That's a large study for rats. 

You take the cecum of the rat, you tie it and you make a hole, and you get sepsis. After seven days, 60% of the animals died from acute kidney injury, and from sepsis. 

Now interesting, we know now that COVID-19 patients get acute kidney injury, they get myocarditis, they get inflammation everywhere. Why would somebody get inflammation at a certain organ? Because of their constitution, because of their predisposed weaknesses. 

So we as practitioners, if we want to prevent a patient and make them more resilient, don't look at the immune system as one big umbrella. Yeah, we've got to address galectin-3, everything's out there. Everything. It's mind-blowing. 

But we have to address the different stations where a person has weakness. So if we look at these rats, going back into these rats, so indeed, after seven days, eleven out of eighteen rats died. But the most important death is in the first three days because if somebody has sepsis, you treat them.

Andrew: Yeah.

Isaac: Whoever doesn't die in the few...you know, in humans it's a much longer period of time, they recover. Rats, you don't treat them. After three days, ten out of eighteen rats died. In the group that got to one week before the procedure - not afterward, it was a preventative - they got MCP at the high dose, only two out of eighteen rats died in three days. 

Andrew: Wow.

Isaac: Ten out of eighteen, compared to two. There was no kidney damage, and interleukin-6 spiking got cut in a statistically significant way. So what we showed is that galectin-3 goes up in twenty minutes, spikes in two hours, and goes down. It sends a signal. 

Interleukin-6 starts going up and up and up and up in a much greater range, but much later. It peaks at eight hours, it goes on after twenty-four hours. When you stop the galectin-3, you stop the cytokine storm. So this is a way...what happened? We turned off the alarm. 

So now we want to look, what in our body causes alarms? galectin-3 is on one level, emotionally, physically, toxins, it all affects us.

Andrew: So, I've got to go back there. So when you're saying that galectin-3 is released, if you like, in minutes, on what cells… or where does it come from? Like, is it...I thought it was present in certain tissues, not in immune cells.

Isaac: Right. So no, galectin-3 is secreted by macrophage...by inflammatory macrophage. But also, when macrophage get a sense that something is going wrong, they will also stimulate galectin-3, so it's a symbiotic relationship. 

But what we know now, I don't want to start going into studies after studies because it would take a lot of our time, but if we look at the data, we know now that there is a very unique interdependence between the tissue that is mitigated through the blood. So for example, the kidneys are specifically important. 

Andrew: Right.

Isaac: So if you take animals that you cause kidney damage, the kidney will release galectin-3 that will travel to the heart, and cause heart damage, heart remodelling, very much like we are seeing in COVID-19, right? In the other direction. The damage is in the lungs, then it goes to different organs and causes damage. 

If you take the animals, you give them MCP or you block...you take out the ability...knock out the animal's that cannot produce galectin-3, you don't get it. But you just let the bone marrow produce it, the signal from the kidneys go to the bone marrow, the bone marrow excretes galectin-3 that travels to the heart, and there stimulates the inflammatory macrophage to create damage in the heart. So there is an interdependence, but in a moving system, it can happen in seconds, you know? It can be so quick.

Andrew: Right...that's incredible. Okay, so one thing I picked up about the rat study was that you were talking about pretreatment. What about treatment after the fact, how quickly can you rescue a cytokine storm, or indeed, the progression of sepsis?

Isaac: So, we expect that after the effect to be very, very important if you start right away. And it depends how dramatic you are. So for example, when we take any oral agent, if it's a drug or if it's something as safe as modified citrus pectin, we expect to have a certain rate of response, where you know, it will have some benefit, it will get to some cells. Cells that are very inflamed, the circulation is not good, it will not get there. 

But so, it's very important, for example, for me during this time, full-dose modified citrus pectin is the most important supplement because I know I'm preventing the cytokine storm. The infection is, for me, secondary. 

Now, because we are developing also a much more sophisticated therapy by creating galectin-3 apheresis, where we actually, similar to plasmapheresis, similar to dialysis, we separate the plasma from the cells and we filter it. 

In these kind of therapies, you get… We have seen the large animal studies we've done with Harvard, MGH, Mass General Hospital in pigs, that we produced an aggressive inflammatory response on the skin that affects the blood. We can see the response being completely cut during the treatment. 

Andrew: Right.

Isaac: And when it happened five years ago, wow, we really couldn't understand it. It was more than we expected. Now, the cytokine storm phenomena helps us understand it, because galectin-3 stimulates interleukin-1B, interleukin-6, TNF alpha, all of these things that can create such an aggressive response, each of them in a little bit of a different way. 

So in many ways, if you look at it, you can say that there is a big waterfall, falling, and then you try to catch the water in different angles, or you can just shut down the water at the top.

Andrew: Yeah, yeah.

Isaac: So when you block galectin-3, you shut the water at the top. And that's really the idea. And into it, of course, you add a lot of other therapies. It's not a standalone. But I think the importance of galectin-3 is coming to the forefront with what's happening now.

Andrew: Yeah, when you're talking about other therapies, one therapy that interests me is the...what is it, hydrocortisone, thiamine, vitamin B therapy, called HAT therapy. 

So, I should say that correctly, hydrocortisone, ascorbic acid and thiamine, which is HAT therapy, by Paul Merrick. So intravenous vitamin C, I think it was 1.5 grams every six hours, 50 milligrams of thymine, and 200 milligrams of hydrocortisone. 

What's interesting is the research that's going around the world now. There's research going on at I think it's Emory and Johns Hopkins, there's a big trial there called VICTAS, and there was one trial, controversial trial because it got the “no” result, and that was the VITAMINS trial at Monash University

But what's interesting to me is how often people are giving the vitamins. So, I guess the scheduling of the regimen. And although it was very similar, the one thing that was different to me was the thiamine, strangely, not the vitamin C. 

I guess for my question, would you espouse, would you advocate the use of MCP with this sort of therapy? Now, realising that this is in sepsis and advanced sepsis, but would you espouse that sort of use for inflammatory runaway conditions?

Isaac: Now first, if you look at the trial, it's really neat because in one approach, they're trying to just suppress inflammation with hydrocortisone. 

Andrew: Yes.

Isaac: The point is the vitamin C for the extracellular connective tissue regulation, and the other thing, the thiamine to open the mitochondria. To open the mitochondria, you've got to stay away from the HIF, from the N21, from the hypoxia-induced inflammation.

Andrew: Right.

Isaac: So, it's a neat study from a biochemical point of view, definitely, because we have a lot of work, for example, in the combination of MCP with honokiol, which is very similar, the MCP has an extracellular effect. 

So if we show a synergistic anti-inflammatory, antioxidant effect for exactly the same reason, the MCP will affect the galectin-3, which will affect positively all the intracellular pathways, while it will work well with something like vitamin C. 

And at the same time, the honokiol will suppress N21, will suppress HIF, will open the mitochondria, and will allow a normal mitochondrial function while reducing NF-k beta and TNF alpha, etc. 

So in this sense, yes, one of the things that we see in studies is again and again, no matter if it's for what condition, that MCP has such a synergistic effect, now we really understand why. It's a very important standalone, but it's really something that can be combined with other treatments. 

So you know, as I'm talking to the people who are really good at energetic testing, some of my top colleagues in the United States that I really respect, they're telling me, “Isaac, wow. MCP is testing so good no matter what we are using it with.” If they need, you know… so you have some people who have a viral infection, or have caught a bacterial infection, and the secondary infection we can forget it. So if we use, you know, antibiotics, if we use antivirals, if we use...whatever we're using, we are finding a synergistic effect because of these mechanisms.

Andrew: Just a point on galectin-3, and this is something I constantly confuse myself over, I'm reading papers, and more and more now that you've woken me up to the uses of MCP. 

But I read about galectin-3, and that sometimes it's a double-edged sword, it can have both good and bad effects. But I keep getting caught in galectin-3, rather than MCP binding to galectin-3 and stopping it's effect.

Isaac: Right.

Andrew: So the question is, I guess, how can you help us wade through when is galectin-3 important, when is MCP important, and when do you have to be very careful with that double-edged sword?

Isaac: So, it's a great question. So, modified citrus pectin, galectin-3 is mainly...galectin-3, remember, it's a survival protein. 

Andrew: Right.

Isaac: So in the uterus when a cell develops, as part of its survival, it needs to have good development. So galectin-3 intracellularly, and especially in uterus, the kidneys are a great example, it helps nephrogenesis in the kidneys in uterus. The effect stops when we are born, which is...

Andrew: Right.

Isaac: Now, so the survival inside the cell wants to keep the cell in good shape. The survival on the cell membrane, where it interacts with the world, where the cell now has its own boundaries, it wants to survive. But it's part of a community. 

If a cell forgets that it's a part of its community and it creates an isolation or a tissue, it creates an isolation around it, this isolation is created by galectin-3. This is the famous lattice formation, right? The different galectin-3s come together with the different ligands, and then you get a microenvironment that can be lower in oxygen, it can be acidic, and then the whole trouble starts. 

So what MCP does is it dislodges the ST ligands. So you think about the galectin-3...let's say it's a bacterial infection, okay? It's delivering the lipopolysaccharide all the way to the tissue. Lipopolysaccharide attaches to the tissue and creates inflammation.

Andrew: Right. Yeah.

Isaac: Now we disrupt the process, the galectin-3 falls apart, the process doesn't happen. What's amazing about the sepsis study is the baseline levels of galectin-3 were the same in the control group as in the MCP group, in two different dosages of MCP group. 

We did not lower the amount of galectin-3, but we lowered all the unwanted ligands that were ready to start. So when we had the sepsis stimulus after two hours, the galectin-3 really spiked in the non-MCP group, and the spike was completely prevented in the active group. And as a result, it prevented later on the kidney damage, the sepsis, the mortality, the interleukin-6 spikes. 

So it's really about disrupting the extracellular and the membrane. Now going back to your question, if a tissue really needs galectin-3, it will still excrete it.

Andrew: Right.

Isaac: Because that's the beauty, so there is no double-edged sword here compared, for example, with blocking TNF alpha. 

Andrew: Yeah.

Isaac: When you block TNF alpha, you don't get inflammation, right, like many of the drugs, right, for autoimmune disease. But you also don't get an immune response, you get more leukaemias, more lymphomas, be careful if you have an infection, you can die from them, that's a double-edged sword strategy. 

With galectin-3 you are blocking the excessive galectin-3, but on the local tissue, because it expresses itself so quickly, it can always express itself. 

Andrew: Okay.

Isaac: But the only thing you need is a short signal, and then stop it. 

Andrew: Right.

Isaac: The body fails to stop the signal, that's all.

Andrew: So has this got to do with a runaway inflammatory picture causing a different formation of the galectin-3? I understand there's, like, four conformations, is that right?

Isaac: Of course...of course. It moves from a blocked, inactive galectin-3 to an active galectin-3.

Andrew: Right.

Isaac: The moment an ST ligand comes, then it makes galectin-3 attach to each other. Or if there is a crisis in tissue, galectin-3 expresses on the surface and binds to ligand, or certain receptors bind to galectin-3. 

For example, insulin receptors will bind to galectin-3. So an inflammatory macrophage, if there's inflammation, will cause more excretion of galectin-3. Galectin-3 will bind to insulin receptors. You'll get resistance to absorption of glucose. You'll get diabetes. 

Very similar mechanisms cause so many… We're looking now at diseases... I mean, I'll give you an example. The one thing that COVID-19 is very important for us, but please, for anyone which is listening, watching, don't lock yourself to one condition, okay? 

If you look at CABG, Coronary Artery Bypass, okay? Coronary artery bypass, it's a very urgent situation, but most patients are not sick yet. They went to the doctor, they did an angio, and “Oh, my God, everything is blocked, we can't put a stent, we've got to rush you into surgery.” 

You look at these patients, study 1,100 people...you look at these patients that you exclude anybody with pre-existing kidney or heart disease, and you do the CABG. The level of galectin-3 before the surgery...before the surgery will determine who will get AKI after the surgery, which means 10-times the mortality. Ten-times, okay? 

Out of the 2% that die from CABG, over half of them die from AKI, which less than 10% have. And who will have long-term kidney and heart damage? Determined by galectin-3. Why? The same survival response from the crisis, from the interruption in the circulation from the heart/lung machine. It's very similar to the mechanism in COVID, in sepsis, in CKD, in NASH, in cancer when it gets aggressive. Very universal processes.

Andrew: I just want to point out to our viewers that those who may not be au fait with it, CABG...we're not talking about the vegetable, that's Coronary Artery Bypass Graft, CABG. And AKI is Acute Kidney Injury. 

That's incredibly important, though, when we consider the... You know, most people come out of a bypass graft pretty well, but then you've got comorbidities, particularly those who are overweight, who are already pre-diabetic or something like that. 

You talk about acute kidney injury or even chronic kidney injury, if you think about taking something as simple as a modified fibre to prevent these sort of inflammatory cascades from happening, this is...this has the potential of saving millions of dollars in healthcare spending.

Isaac: Well, and potential to save, worldwide, tens of thousands of lives. Yeah.

Andrew: Lives...well, yes, there is that.

Isaac: And actually it's not millions, it's many billions of dollars. But it's interesting, you know, because now, because of my level of invention, now I deal also with Big Pharma. And you can't get them to wrap around a supplement, you know?

Andrew: No.

Isaac: If you look at some of the PD-L1 inhibitors, they want to...I don't want to mention companies, the big and most common immunotherapies, they now know...and it's a problem they have to disclose to their investors. 

These are drugs that, you know...$20 billion a year, okay? They know now when the patient's galectin-3 is elevated, immunotherapy is not working. They've got a supplement that works. No, they will develop a drug that will cost them 100-times more, will have more side-effects, will be ready in 10 years. 

But it's interesting, the reason why I mentioned the CABG, it's a great approach, for example, for the therapeutic aphaeresis because the patient already has a catheter ready for the procedure. You clean up the galectin-3, and you see what happens. 

So often, our door to show the world that simple things like a sophisticated fibre are so important has to come through a very sophisticated therapy, you know? And then okay, now that you see this sophisticated therapy, you can combine it, also use something really, really simple, you know? But it's...

Andrew: I do want to touch on that. I know that we've touched on it in our podcast, but I think it's really important that people understand about modified citrus pectin. So a normal pectin is over 60,000 daltons, and it's got a high level of esterification.

Isaac: Right.

Andrew: The one that you've looked at and devised is a far smaller...is it less than 5,000 kilodaltons?

Isaac: No, they're...usually, pectin is 150 to 300 kilodalton, and highly esterified.

Andrew: And yours is less than 60...

Isaac: Ours is between 3 and 13 kilodaltons, has a very specific structure, and is produced...you can reproduce it. And so if you look at the literature, practically all the papers except one study done in Australia on a cardiovascular condition, which didn't work because they didn't use our MCP... And actually, I wrote a letter to the editor, and they acknowledged the difference

Yeah, so you know, we talk about the generic thing, but it's not exactly generic because it's a natural compound, it's not like a chemical that is always the same. So the modified citrus pectin I am talking about, that I have worked on for 25 years, is a very specific structure. And it's critical. If it's another structure, it will not have this effect.

Andrew: Okay. Now, there is a couple of questions, so I'm going to go to the questions, where I should be... All right, so from...I'm going to go Deanne. So De-...no, that's not a question. 

This is from Sarah Riley, "Ninety per cent of the deaths from COVID-19 in the U.S.A. had at least one comorbidity being one of the top five inflammatory diseases. Is this because G-3 is already elevated in those chronic inflammatory diseases, which took off into a cytokine storm uncontrolled, with galectin-3 propelled?"

Isaac: This is a great question. For many patients it is, and you will see a higher level in the bloodstream. And for some of these patients, it is more on a local level, in a certain tissue. 

And the ratio between the levels in the blood and the galectin-3 response is not linear, we talked about it last time, because of MMP-9, metalloproteinases, and the ratio between pentamers and monomers, that when you detect, you detect only as one. 

But in general, it's completely true. This is completely... And remember, how do we know that galectin-3 isn't upstream alarming? Because Andrew, it doesn't go up. 

You know, look at C-reactive protein. Normally it's under one, in severe inflammation, it's up to one hundred. If I tell you interleukin-6 can go up thousands of times, galectin-3 will go up 50%, two times, sometimes three times. It doesn't need a lot because it... You know, if you think about an angle opening, in the beginning, it's a tiny difference, and as you go, go, go it becomes huge, right? So the small message from galectin-3 will go a long way in the end results. 

And we see it, actually, in our prostate cancer patients, which are not really related in our long-term study. We just finished our trial on 60 patients with MCP, we see patients who are benefitting for three, four, five years. And at the same time, their chronic inflammatory issues are going away. 

So the answer in general is yes, this is the reason. Because what was the problem, hypertension, about 20 papers specifically on our compound in hypertension, different studies. Diabetes that we know is a mechanism, all of this...yeah. So the answer is definitely yes. Definitely.

Andrew: Okay, so let's talk about inflammasomes. This is another question by Sarah, and she was talking about the NLRP3 inflammasome and the induction of interleukin-1B, leading into the fibrotic implication of COVID-19 and ARDS, so Acute Respiratory Distress Syndrome. "Why is galectin-3 not considered as an opportunity for interception, given that it's the predecessor of the NLRP3?"

Isaac: So first of all, there are studies on this, that when you block galectin-3 look at any publication on MCP, it will lower and block this pathway, and will lower interleukin-1B. That's a great question, and Sarah is extremely knowledgeable to actually get into this kind of level. It's really something you see in people who hold to integrative medicine, or who are not just focused on protocols. So, you know... 

And it's a famous answer, you know? First they ridicule you, then they fight you, and then they say it's self-evident. So, we are moving to the self-evident now, we just need a few more studies. 

And the COVID-19 is going to help us, you know, because the world realised, “Wow, all these people who are telling us about diet and lifestyle and inflammation, maybe there is something to it,” you know? Definitely.

Andrew: And you know, I come back to what you said at the beginning... And by the way, the word that I was searching for right at the beginning was "resilience."

Isaac: Oh, yeah, yeah. Right. Yeah.

Andrew: But I come right back to the beginning of our talk, and you're talking about danger signals. We know that sleep, restful sleep affects our microbiota, and that we have high levels of cortisone because of our autonomic response, our flight or fight response. So, these are the danger signals. Talking about your mum, who saved your family, but there was that real initial danger...

Isaac: Right.

Andrew: How do we then recover, both I guess on an environmental, a bodily, and a micro-...a biochemical level from ingrained chronic stress?

Isaac: Wow.

Andrew: In one sentence.

Isaac: Yeah, that's really my life work. That's why I...that's really what I'm doing. You know, part of my training is as a research clinician, and part of my unusual training is that I'm highly trained in Tibetan Buddhism and I was a doctor of the greatest Tibetan meditation masters in Tibet, which taught me one-on-one. 

So, it's by moving...it's by changing our reactivity. And that's...I mean, it's a great...I mean, there is no better topic to start wrapping this discussion with. {}Because remember we talked about the sympathetic response, the survival response, the fear or flight response that creates all of these cytokines? And we talked about that from a nervous system, from a metabolic system. And if you look at our body, each organ in the body is on its own.

Andrew: Yes.

Isaac: It gets clean blood, it takes what it needs, it detoxifies what it doesn't want into the system, and the blood circulation moves. Each cell is the same. 

There is one organ in the body which is different. It takes what the other organs throw away without discrimination, it connects with the universe through the lungs and through the air, and it gives blood in an unconditional nourishment to the body, and that's the heart. 

So when we connect to our heart on a physical level, on an emotional level, on a psycho-spiritual level, that's why open heart medicine....I have a book that I'm writing in Hebrew, which will be translated, almost done, it's called...and it's based on this meditation and healing, it's called "Open Heart Medicine: The Infinite Healing Power of Love and Compassion." So, this thing is not esoteric. I mean, you know me by now. You know, I'm tied to research, I'm a practical guy, you know?

Andrew: Yeah. Yeah.

Isaac: This is how a cell responds. When a cell loses its interdependence with its environment, its commitment, its support, its empathy to its environment, that's what causes cancer. The cell thinks that it cannot die, it has to survive, and it changes its environment. 

So the behavioural levels are so profound, but we combine them with the level of breathing or bringing oxygen, and the level of physiology, you know, the supplements and diets. And you know, I see, for example when I do meditation and healing retreats, I see cancer markers changing in a few days because of this kind of work. 

And if you look at how the heart, the heart...you know, the aorta is a rigid artery. It doesn't decide where the blood goes, it gives it everywhere. But who does the heart feed first? The heart feeds first...

Andrew: It feeds itself.

Isaac: ...it feeds itself. It feeds the coronary arteries. So part of, you know, self-love is part of loving others. We are really in one boat. 

Now, why is the COVID-19 so amazing? Because for a short time, everybody was in the same boat. For a very short time. I remember, I was giving… I was supposed to travel to Israel to give a big retreat, so I gave a Zoom retreat. And it was, like, in the middle of the COVID, and I was telling people that the people who are aware of this are just going to be more aware, and the ones which are not aware, unfortunately, they're not going to change. And you see it again, habits are very strong, you know?

Andrew: Yeah.

Isaac: So now you see the divisiveness, you see the separation, you see the politics. It's sad, you know? But at the same time, you know, when it's really dark, every bit of light really has a big effect. 

So galectin-3 for me, from a physiological level, it's what isolates us. It physically isolates...it creates a lattice formation, that's a scientific phenomenon. It creates a micro-environment. But when we are not connected with our hearts, we are also separated. So, there is a way to change it. And the way to change it, when a stimulus comes your way, instead of reacting with a survival approach, you understand and you react with an open heart. 

When we bring it to the cellular level, we are not going to die from COVID-19 because we will not have an inflammatory response in the lungs, we will not have kidney damage, and we definitely will not have heart damage because our heart is opened. 

And that's the beauty of looking at the big picture, and at the same time looking at all the small details. If the big picture is not supported by the small details, then it's just philosophy. It's not real, you know? It doesn't hold water.

Andrew: What is it, before you can fly like an eagle, you've got to walk like a tortoise? Is that what...is that the saying?

Isaac: Yeah.

Andrew: I've got another question, again by Sarah, and it ties in with my next sort of ponderings, and that is something I learnt from Datis Kharrazian. He's going to be speaking at the 2020 Symposium, BioCeuticals Symposium. 

And what he's worked out is that he can predict when patients with autoimmune disease are going to have a flare or a remittance, beforehand. Now you know, controlling it, well, that's another...that's another game all in itself. But he can predict when something's going to happen. 

Do you think galectin-3, or I should say, MCP has propensity here, particularly when we're talking about Th17, what happens in the gut, the gut milieu, all of that sort of arena?

Isaac: How does he predict it? I'm so curious.

Andrew: I know. Well, so he was looking at interleukin-1B, TNF alpha...

Isaac: So he's predicting it not, like, from pulse diagnosis, but more...

Andrew: No, no...no, from labs.

Isaac: Yeah. Yeah, so the answer is definitely. Galectin-3 is... You see, survival is not only ours, survival also belongs to our microbiome. When we have a synergistic, harmonious relationship with the microbiome, it's amazing. 

But when we put the microbiome in a defensive position, like antibiotic therapy, or Lyme disease is a great example, okay? The microbiome will react. And we know that aggressive bacteria and viruses and parasites anchor to the gut lining with galectin-3. 

We know that MCP is a prebiotic, we know that it enhances different antibiotic therapies, it has a big effect on the microbiome. So the answer is absolutely, it regulates this effect. And that's why if you look at galectin-3, galectin-3 is universally high in autoimmune diseases, which was part of it, universally. And the gut-brain, the gut system relationship is so deep, it's so important. And this is part of our regulatory system, the gut is a regulatory system, the brain is a regulatory system. The heart is an offering system.

Andrew: I was very interested a little bit further back, when you were mentioning your work with honokiol. You know, traditionally that's been used as a relaxant formula, if you like. 

Isaac: Right.

Andrew: And some of the initial data, I think it was rats, forgive me, was showing that it allowed the body, by way of relieving stress, to therefore allow the body...and I stress that reason, to reduce its manufacture of cortisol.

Isaac: Right.

Andrew: So it didn't stop the manufacture of cortisol itself, it allowed the body to. But are you finding different biochemical effects? You're finding other things.

Isaac: With honokiol?

Andrew: Yeah.

Isaac: Yeah, honokiol is huge in cancer. In fact, the first paper on honokiol IV...actually, I was giving it intravenously, now I can say it because I'm not allowed to do it, so I'm not afraid to say it. But it just got accepted, and it should be published any day in Integrative Cancer Therapy. I have a number of case reports that I'm presenting there. 

So yeah, honokiol has this remarkable...in the Magnolia bark, you know, honokiol has this remarkable way of adjusting its function based on the status of the cell, very much based on the p53 expression. 

Andrew: Okay.

Isaac: If p53 is well expressed, the oncogenic pathways are suppressed, AMPK is well...is active, we have a normal functioning cell, honokiol becomes an antioxidant. If a cell has abnormal effects, it becomes a pro-oxidant. It's really fascinating, and that's why I combine it with MCP. It has this built-in wisdom. 

And of course, in many levels, the fact that it relaxes the nervous system is very much through moving glutamate into GABA, it creates more of an inhibitory effect, that's very much a regulation of the survival response from the nervous system, right? We're not as reactive, we're not as excitatory. 

And so yeah, it's fascinating. It's a remarkably… It's one of the most underused compounds. I mean, I've been a leader in moving it forward, I published probably four or five papers that have a lot of discoveries on honokiol. But it's a remarkable compound. But it's very synergistic with modified citrus pectin, and it's really powerful, especially for inflammatory cancers.

Andrew: And oral use as opposed to intravenous?

Isaac: Yeah, yeah, oral. Yeah. We have studies on it, and a lot in bladder cancer, in prostate cancer, in kidney cancer, and we are planning some clinical trial on the MCP/honokiol combination in glioblastomas. Because the honokiol penetrates very well into the brain, and galectin-3 is the driving force in glioblastomas, as it is in neurodegenerative inflammatory diseases, which is logical, right? If you look at the Alzheimer plaque, the galectin-3 is 10, 20-times higher.

Andrew: Wow. Now, there's an area of research for you.

Isaac: Yeah, well...we are actually trying to catch all of it. I mean, I'm a pretty good delegator.

Andrew: We are running out of time, but there's a couple of things I wanted to ask about. And I guess, you know, you're talking about using with other therapies, what about the facility of NAC, with regards to viral pneumonias? You know, traditionally with cystic fibrosis, it was used as a mucolytic.

Isaac: Right.

Andrew: Now, of course, naturopaths mainly use it for its antioxidant...they always do that, antioxidant capacities. I hate that word. I think we've got a…

Tony actually just posted thing about oxidative buffer, and I think we need to learn a different vernacular about these compounds that we term "antioxidants." Because as you say, honokiol works both ways.

Isaac: Exactly. Yeah, it's a problem when you try to explain, like in my book I'm writing now, the survival...and you have to write something about...and you know, it's really...whatever you write is not going to be accurate because it's dynamic and people can't really rest. 

I love NAC. For me, NAC is very beautiful because it relates to relation between the liver and the lungs, right? It's a mucolytic. It takes mucus from the bottom of the lung, it also removes mercury, which is a very heavy metal. 

Andrew: Right.

Isaac: So when we have heavy stuff in our body, heavy...not only physical stuff, heavy emotional stuff that we cannot release through the lungs and we hold it at the bottom of our lungs, I use N-acetylcysteine. And so if you look at some of my formulas, I use it. 

So I have a little bit of a unique way of using these substances because I don't just rely on the biochemistry, I connect the imaging of where they are, and the organs and what they express, and why certain things are in certain ways. 

So, yeah...and I mean, when you use NAC and the lungs have less mucous, they are less sticky, you're going to be in better shape. I mean, it's really an underused...it's kind of almost criminal how underused is this stuff. Even for liver toxicity, for Tylenol, you know, it's so crazy how it's not used, you know?

Andrew: Oh, to be in your mind, sir. You and I could talk for hours. Unfortunately, we have to end it. But my one...I can't get away with it, my one last little question: where to now? 

What's the next phase of research, or the next phase for you? You're finishing your book, you've finished a study. Is there any more studies, any area of research...?

Isaac: Yeah, I'm finishing my book in English, "The Survival Paradox," that comes into this idea of breaking the boundaries between us from a scientific point of view. 

And then I'm working on "Open Heart Medicine" from a spiritual...from an open heart point of view. And now we just finished our study on 60 patients with cancer, and we're going to start some more studies. 

But the most exciting thing for us is we hope to now use our apheresis work. We have some people that really want to support us, and really, really create a therapy that, if it works well, and we think for AKI, for sepsis, and for CKD, for NASH, it can really save millions of people a year. And they have no idea...

Andrew: Dr Isaac, I love speaking with you. Your mind is incredible, but your heart is even more beautiful. Thank you so much for joining us on FX Medicine today. 

And everybody, I hope you got some useful things out of this to help you in your practise, and to...you know, I guess specifically for the use of MCP, but also in the use of other things that can help your people through cytokine induction. And God help us if it was a cytokine storm which needs to be handled in a hospital situation. 

But Dr Isaac Eliaz, thank you so much for joining us once again on FX Medicine.

Isaac: Thank you. Thank you for everything. Thank you, everyone. Have a good day. Bye.

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

Other podcasts with Isaac include


The information provided on FX Medicine is for educational and informational purposes only. The information provided on this site is not, nor is it intended to be, a substitute for professional advice or care. Please seek the advice of a qualified health care professional in the event something you have read here raises questions or concerns regarding your health.


Share this post: 
Isaac_Eliaz's picture
Dr Isaac Eliaz

Dr. Isaac Eliaz is an integrative medical doctor, licensed acupuncturist, researcher, product formulator, and frequent guest lecturer. He has 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 is the founder and medical director of Amitabha Medical Clinic in Santa Rosa, California, an integrative health center specializing in cancer and chronic conditions.

An expert in using highly strategic, synergistic protocols to address numerous areas of health including metastatic cancer, immunity, digestion, detoxification, diabetes, cardiovascular health and more, Dr Eliaz is also widely regarded as the leading expert in the field of Modified Citrus Pectin research.