Jun 19 2024
Dr. Joel Rosen:
I would like to welcome Bayou Ck. I believe this is our third interview with Bob. Yeah, he is a traditional naturopath specializing in the field of genetics-specific nutrition. Bob is also an educator. He lectures nationally and internationally at seminars to educate health practitioners about genetic variants and nutritional supplementation for obtaining optimal health. Bob is also a researcher. He’s expanding his genetic research efforts. He founded and personally funded the NutriGenetic Research Institute to study the relationship between genetic variants and presenting symptoms. He’s also a nutritional supplement formulator and a genetic analysis software creator.
Bob here is going to help us learn about cracking the code. So, Bob, welcome once again to another edition of helping people get their health back.
Dr. Bob Miller:
Oh, it was a pleasure to be with you. It’s um, I always enjoy these interviews because we’ve, we always have a good time, we kind of geek out a little bit on some of the deep dives on biochemistry, and it was a lot of fun. So yeah, do the same thing today.
Dr. Joel Rosen:
Excellent. So okay, so Bob, go ahead and share your screen and give our listeners what’s the latest and greatest, in what you’re researching.
Dr. Bob Miller:
Already? Well, our subject today is going to be superoxide. Now, you know, the traditional naturopathic philosophy has always been that most problems we see come from inflammation, from excess free radicals. We’ve been on that path for all of our time working: what is creating extra free radicals, and then what is causing us to not be able to break those free radicals down.
Now, on the other hand, free radicals are bad if they’re in excess, but they can be our friend. One of my favorite sayings has been, you know, they can be your friend unless they’re not. So we need free radicals to kill viruses and bacteria. And even if we have bad cells inside the body, we need inflammation to kill them. But on the other hand, if it goes to the extreme, that’s when we have a problem. So we tend to villainize free radicals, and rightfully so. But on the other hand, we have to be careful that we don’t eradicate all free radicals, that they do play a role for us.
Our subject again is superoxide. And again, we always mention that we’re not treating any disease here. This is for educational purposes only and informational. So our learning objectives today are what superoxides, and random superoxide, and then we’re going to delve into how excess superoxide impacts. We’re going to look at pathways of how we make superoxide and pathways of how we reduce it. And then we’re going to dig into something called ferroptosis, where superoxide causes iron to do some really bad things.
So, you’ll see here it’s all about balance. Superoxide plays a role in the body at times, but in excess, it can cause all kinds of problems for us. Now, this little chart here that you see. You’ll see on the left there it says oxygen o2 and unfortunately, that too got knocked off. But as you know, oxygen is o2. So what you’re seeing and by the way, do you see my little love? Okay, good. So the oxygen is two oxygen atoms, and you see these two little dots there. That’s electrons. So we all remember even from high school that, you know, you’ve got the neutron-proton and the electron, and they need to be paired. So here’s two together, here’s two together, here’s two together, they’re all paired up. This superoxide occurs when an extra electron comes on here that shouldn’t be there, and that makes it very unstable. And I’m going to show you in a little bit why this can be the root cause of a lot of our problems.
Now, the body is pretty amazing. There are multiple ways here, but I’m going to show you one of the main ways. There’s an enzyme called superoxide dismutase. Number two, so this is superoxide. Dismutase means to break it down. And it takes the mineral manganese, not magnesium, manganese. And I’ll show you a better chart later, but it turns it into oxygen. But it also turns it into hydrogen peroxide.
And hydrogen peroxide again, is not all bad. Sometimes we use hydrogen peroxide to kill pathogens. But if we have too much of it and we have dysregulated iron, we’ll make what are called hydroxyl radicals that damage the DNA and just wreak havoc throughout the body. However, we do have other mechanisms. If we have enough catalase, that’ll turn that hydrogen peroxide into water and oxygen.
And there’s something called glutathione that we’ll dig into a little bit later. And there’s an enzyme called glutathione peroxidase that takes that glutathione and turns it into two water molecules. So there’s a lot that can go wrong here; we can overproduce superoxide. We’re going to show you how you can have less than optimal production, less than optimal catalase glutathione, where you can have iron dysregulation. So this is a rather complex, sometimes we call it Joel, the 3d chess game played underwater, multiple factors going together. And I believe in the past, we’ve done live on podcasts on iron, haven’t we?
Dr. Joel Rosen:
Yeah, what I’ll do, Bob is I’ll put a link to those two other podcasts that we’ve done so the listeners can go deep dive deep into there, but yes, we’ve talked about that as well. And I
Dr. Bob Miller:
believe we did we do a podcast on Lyme disease? No,
Dr. Joel Rosen:
I don’t think we did. We talked about it at some level, I think we did G six PD. Right. And I think we also did just NADPH
Dr. Bob Miller:
Right. Right. Okay, so this is the crux of what we’re going to be talking about today.
Now, I’d like to introduce you to a biochemist named Erwin Friedovitch. He went to Duke University as a student and then returned as a biochemist. He was there for a total of 60 years. If anyone you know, a researcher, goes on PubMed, this name will come up quite often because he published more than 500 academic papers that have been cited more than 51,000 times.
When you look at a lot of research papers today, they refer to who did the work, and you’ll see this name come up. One of his papers was published in the Journal of Biological Chemistry all the way back in 1969 and has been cited 9,300 times.
Now, here’s this gentleman at the age of 85, back in 2014, still lecturing. By the way, Joel, I’d like to still be able to lecture at 85. We’ll see if I can do that. He identified the two forms of superoxide dismutase. That’s what breaks down superoxide. There’s one that’s based on copper and zinc and another one on manganese.
Our topic today is going to be the manganese one. He proposed the superoxide theory, that superoxide is the origin—the beginning of most reactive oxygen species, which is inflammation. It undergoes a chain reaction in a cell, playing a central role in that inflammation. That damages the cells and can lead to all kinds of things—Alzheimer’s, Parkinson’s, ALS, all kinds of things.
I’m going to show a couple of slides of things related to excess superoxide. He said superoxide is the major factor in oxygen toxicity. Inside your mitochondria, as you all know, you’re made up of 60 to 100 trillion cells—amazing. There are mitochondria in there that make energy, and manganese superoxide dismutase is what degrades superoxide. Manganese is a mineral, not magnesium, manganese. It’s your essential defense against superoxide.
So, how many people do you see that are just dead tired, and no matter what they do, no matter what kind of things they take for energy, they just can’t get on top of it? How many people do you see that are dead tired and can barely function, and no matter what you try, it doesn’t seem to work? How common is that in your practice?
Dr. Joel Rosen:
Yeah, I mean, I think everyone that we see comes in with a chief complaint of being exhausted and tired. They are the toughest of the tough, like you. They’ve been to so many other practitioners, and now they’re just throwing their hands up in the air. I think that what you’ve mentioned in the past is that one day we’ll look back at all of the environmental triggers we put in place and say, “Oops,” because we’ve created this perfect storm. But yes, I think probably everyone that we work with, to one extent or another, has had very little success and is completely exhausted and burnt out.
Dr. Bob Miller:
Absolutely. Now, I’m not going to say this is the case in every one of those who are, that would be a little too optimistic, but this is probably a factor in many of the people who are experiencing exhaustion.
Now, let’s look at what this mitochondrial superoxide does—a key player in Alzheimer’s disease. So, this is a peer-reviewed study. For people who are not familiar, this is on PubMed, not somebody blathering on the internet. Our findings have reinforced the idea that mitochondrial superoxide plays a critical role in Alzheimer’s disease. That’s one of the things that people are so scared of. We were able to show that increasing the expression of the mitochondrial antioxidant, SOD2, prevents memory deficits and amyloid plaque deposition associated. Wow, that’s pretty astonishing there because that’s one of the things that seems to be on the rise. You know, people know that they’re going to leave this earth someday and they’re pretty much okay with that. What really scares them is if they don’t know who they are and there’s a burden to their family. That’s a real, that’s a real realistic fear.
Right here is diabetic complications. Oxidative stress plays a pivotal role in the development of diabetes complications, both microvascular and cardiovascular. The metabolic abnormalities of diabetes cause mitochondrial superoxide overproduction in endothelial cells, both large and small vessels. And of course, diabetes is becoming a serious problem. The increased superoxide production causes the activation of five major pathways involved in the complications. So we didn’t have time today to go through all those when somebody really wants to dig into them, just Google oxidative stress and diabetic complications, and the whole paper will pull up, and they can read it. I found this fascinating: orally administered superoxide dismutase can exhibit a glucose-lowering effect. Isn’t that fascinating? So even if someone is diabetic, making sure you have SOD may be able to help you lower the glucose levels.
So, we were talking about manganese working with the enzyme superoxide. This was fascinating: overexpression inhibits the growth of androgen-independent prostate cancer cells. I found that fascinating because, the subject for another day, but if we have cancer, we have to be careful with the antioxidants. Because your body is using free radicals to kill the tumor. That’s why people get chemotherapy. So if you do too many antioxidants while being treated for cancer, you can actually protect the cancer cell. But I found this one to be an exception. It affects cell proliferation. Our results are consistent with manganese SOD being a tumor suppressor gene in human prostate cancer. I found that particularly interesting.
Alright, arteriosclerosis, I mean, this is atherosclerosis. A serious issue that might be number one or number two on our concerns. As we all know, it’s a chronic inflammatory disease of the vascular system, the leading cause of cardiovascular diseases worldwide. Here we go. Excessive generation of reactive oxygen species leads to a state of oxidative stress, which is a major risk factor for the progression of this disease. Now, we’re going to talk later about nitric oxide. And there’s an enzyme called eNOS (endothelial nitric oxide synthase), and that is what makes the nitric oxide that dilates your blood vessels. If you Google nitric oxide Nobel Prize, you’ll see three scientists won an award in 1998 for their research on cardiovascular and nitric oxide. So when it says it becomes uncoupled, in other words, rather than making nitric oxide, we make superoxide. So what they’re saying is your oxidized LDL stimulates an enzyme called NADPH oxidase, and that increases your superoxide production. Then superoxide reacts with nitric oxide to form peroxynitrite. And we’re going to show you that in a little bit, which oxidizes that essential eNOS cofactor tetrahydrobiopterin BH4 and we have this whole graph out. You’ll see that in a little bit. So then eNOS becomes uncoupled and generates superoxide. So that’s a lot of biochemistry there. But bottom line is when we create more superoxide that is a contributing factor to it. Heart disease.
So, cataracts, a huge problem among those of us as we get older. It was concluded that oxidative stress plays an important role in the onset and progression of cataracts. The Pro-oxidant serum MDA levels were increased in the cataract patients. The blood levels of the enzymatic antioxidant SOD and GPX (glutathione peroxidase), an enzyme that uses glutathione to neutralize free radicals, was decreased.
Macular degeneration, the study showed that low glutathione peroxidase activity and total antioxidant status are associated with age-related macular degeneration. SOD modulates the association of glutathione peroxidase and advanced macular degeneration. The antioxidant enzymes’ activity and serum total antioxidant status could be promising markers for the prediction of macular degeneration.
Bone fragility, of course, particularly for women, osteopenia, osteoporosis, a serious condition. These results imply that intracellular redox imbalance caused by SOD deficiency plays a pivotal role in the development and progression of bone fragility. We present a valuable model for investigating the effects of oxidative stress on bone fragility. And again, if someone really wants to read this one, just type those words into Google, and that whole paper will come up. I just took like one sentence that summarized it.
Alright, skin aging. As you know, you can see some people that are 65 and they look like 55 and some people are 65 and they look like. Oxidative stress is a consequence of the imbalance of pro-oxidants and antioxidants. With increased inflammation concentrations, it has been demonstrated in aged skin, suggesting the important role of the antioxidant balance.
Heart failure, a mechanism responsible for impaired endothelial function and heart failure, is enhanced biodegradation of nitric oxide by the superoxide anion. Now, that sounds pretty complex, but again, I’ll show you a chart later, that superoxide takes that nitric oxide, remember that won a Nobel Prize, and actually turns it into something bad. Both nitric oxide and superoxide, when exposed to one another, undergo a limited radical reaction to form something called peroxynitrite. Again, I have charts I’m going to show this because just I’m sure hearing these words gets confusing. So hang in there, don’t give up on us. We’ll show you the charts on this.
Now, as you know, we are seeing such a dramatic rise in autism. I mean, this is a catastrophe. There’s decrease in the expression of SOD2 and SOD3 from autism patients compared to healthy control participants. I’m going to be speaking in the middle of May 2024 at a medical conference, and I’m going to be presenting this concept for all of these mental health issues, autism, ATD, ADHD, multiple reasons, but one of them being extra superoxide. Not enough superoxide dismutase. So the study also found differences in who the found peroxidase and GPX3 was downregulated. Here’s another one on
Dr. Joel Rosen:
Yeah, you know, it’s interesting, Bob, I don’t have the same referral network as you do with practitioners. But ultimately, when the parents come and see me And we help them then it gets more into well, oh, my son has autism, or my son or my daughter has is on the spectrum. And you did so well with me. Ultimately, can you help them? It’s more of that. But, yeah,
Dr. Bob Miller:
yeah, it’s frightening how serious this is getting. Now, even among adults ATD ADHD, you know, I’m sure you’re seeing in our clinic, we are here that, you know, people are having a harder time understanding their mom or are frustrated. The nitric oxide levels in patients were significantly higher than those of controls, and the SSD activity was significantly lower. So high levels of oxidative nitric oxide, low s OD, oxidative imbalance in that attention deficit disorder.
This is the first study evaluating the oxidative metabolism in ADHD. So, Crohn’s disease and autoimmune oxidative stress can be a major contributing factor to the tissue industry in injury in Crohn’s disease. When we get to two arthritis superoxide is over produced in joint inflammation, rheumatoid arthritis, osteoarthritis, increased superoxide production leads to tissue damage articular, degeneration and pain. The in these conditions, the defense superoxide dismutase is decreased. So we keep seeing the same thing over and over again, as people do studies.
All right, now we’re going to look at, well, if this is bad, how do we make it so we’re going to talk about what’s called the electron transport chain. Nos uncoupling. The Knox enzyme, over activation of what’s called the NMDA receptor will explain that glutathione your master and ox are not being recycled. Interestingly, poly aromatic hydrocarbons, that’s when we get from our air pollution that can even create superoxide and a new one here, Joel called the Aryl hydrocarbon receptor. So there’s so many ways now that we can make superoxide. So we’re not gonna get too deep in the woods here. But inside your cells, you know what’s called the mitochondria.
And inside there, we have what’s called the electron transport chain. And this appears to be the largest source of superoxide. So what happens, nutrients come in, including co q 10. And they go through these steps, and the end result is ATP. That’s your adenosine triphosphate. That’s your energy. We spoke earlier about people being tired. Well, what can happen is that there can be problems in here. And we don’t have time to dig into this today. But it’ll create superoxide.
And then, as we showed you earlier than the sod two enzyme makes hydrogen peroxide, we need glutathione peroxidase. One, we need hydrogen peroxide. If we don’t, it’ll combine with iron to make hydroxyl radicals. These little green boxes are supplement formulas that we formulated. So if somebody’s got peroxynitrite, we have formulas that calm that down, there’s formulas to clear hydrogen peroxide. We’re not going to get into Thrive toxin today, but that’s another way to clear it. And we have glutathione peroxidase. So there are ways if this is occurring, we can slow this down.
And I’ll tell you what, Joel, I’m beginning to believe that this may be the major source of inflammation that we’re creating more superoxide. And then we do not have the mechanisms to to break it down. So there’s the first one electron transport chain. Now, this is the other one that want to spend a little more time on this. As we said earlier, nitric oxide is really important. It’s a gas and it dilates your blood vessels. This is not nitrous oxide that the dentist’s gives you.
This is nitric oxide. Again, as I said, Nobel Prize 1998. Now people think they may have never heard of it, but they probably have. If you know of anyone who carries nitroglycerin with them. They get chest pain. They put the nitroglycerin under their tongue. They dilate their blood vessels. And if you haven’t heard of that, everyone’s heard of Viagra and Cialis. You know, men need good blood flow for the penis for erectile function. And those drugs help with the nitric oxide or blood flow.
So what happens is we make something called BH for tetrahydrobiopterin. We make BH four. And then there’s you can have genetic or environmental issues that you don’t make enough of this. Then that combines with something called NADPH and arginine to make nitric oxide. So I’m sure people have anyone who’s in unnatural health I’ve seen formulas for nitric oxide that have arginine. And sometimes that works. And sometimes it backfires. Because if you don’t have enough BH four, and you take arginine, what you can actually do is rather than making nitric oxide, you can make superoxide.
So that’s what we said earlier. Remember, we talked about the nozzle, uncoupling the nozzle, uncoupling, is when we make superoxide, free radicals are over to the left here and over here, so we can make superoxide rather than nitric oxide, then that superoxide combines with nitric oxide, and makes her oxynitride. The peroxynitrite Then further inhibits the BH four.
And I’ll tell you what, Joel, you’re on a not-very-fun merry-go-round. Now, unfortunately, is one of your opening statements was about environmental factors. One of my favorite jokes is I was born in 1954 when Earth was a completely different planet. We didn’t have many of these other things. And I believe that’s one of the major reasons why we’re seeing so many difficulties today. So look at what will stimulate that no, two, oh, I should explain. Nas three is what makes the nitric oxide that dilates your blood vessels. Nos two makes a lot of nitric oxide to kill pathogens because not nitric oxide.
Although it can be a dilator. It can also be oxidative. And nos two is designed if you have a bacteria or a parasite, totally speculation, but I have to wonder if there was a time in man’s history when there were a lot of parasites, and having nos to being upregulated was to your to your benefit. But now if nos two is upregulated, it will suppress nos three. One of the telltale signs of that occurring is cold hands and feet.
And in the extreme something called Raynaud’s or rhinitis, people say in different ways. That’s where the hands turn white or purple because they’re not getting good circulation because nos two is suppressing the NOS three. So look at the who’s who here, aluminum. So what are we doing? Many people are smearing aluminum into their armpits. We’re going to look back on this someday and say, What were we thinking?
And there are other sources of aluminum that we’re getting. Mercury, uranium, BPA from plastics, ethanol, electromagnetic fields, high fructose corn syrup, which came about in the late 1970s, horrible gluten, fluorine, fluoride, Roundup, glyphosate, high homocysteine, high iron, iron overload, all of these will stimulate that no to enzyme to suppress the e nos enzyme, burn out your BH four, start making superoxide I believe this is a very common thing that’s, that’s going on.
And even your BH for, again, mercury, lead, aluminum, iron, high protein diet, hydrogen peroxide, high ammonia peroxynitrite Sun on ultraviolet. And we’re not going to get into this today. But BH four is needed to make serotonin. So depression, oh, my goodness, this is going through the roof. multiple factors. I’m not saying this is the only cause. But if you don’t have enough pH four, you’re gonna have a hard time making serotonin depression seem to be on the rise.
So we have done some really bad things with our environmental factors. And if you’ve got a genetic weakness on top of it, it just compounds. So we could do a whole lecture here today just on this whole process. But I just want to get the major point. That one environmental factor combined with those who have genetic weakness, because there are two ends to Rs numbers as part of your genetics that will cause this to be overactive. And there’s genetics that will cause this to be underactive. Well, if this guy’s inherently overactive, this guy is underactive, you’re exposed to all these environmental factors. And you can’t clear them, or you have genetic issues that you don’t make enough BH for. We’ve created the perfect storm to be a superoxide factor to make sense from
Dr. Joel Rosen:
Yeah. Can I ask questions? Last observation? As far as all of the different ways you’re demonstrating that we can make this superoxide or add that extra electron to oxygen? You’re showing this pathway here. But would it be safe to say that all of these factors would also upregulate the production of superoxide in the electron transport chain pathway as well-meaning everything that you see here that is creating more superoxide It would be the same factors that would spill off superoxide in our, in our demand to make energy? To keep up with all of this,
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Dr. Bob Miller:
I mean, I haven’t seen any papers on that. But I mean, it just makes total sense. I mean, that’s a that’s great observation don’t really be right. Now let’s move on to the next to the next one. And this again is one of my favorite subjects NADPH oxidase. So, NOx NADPH oxidase I often say this is our friend unless it isn’t. If you take an animal and knock out their NOx enzyme, in about a week you’ll be dead from infection. Because this is the guy who says, Oh, bad guy here, we need to take you out. So very important. The problem becomes, and you’ve probably already guessed it if it’s overactive. That’s the problem. So what happens is, there’s an enzyme called TNF a and NF kappa b.
Again, our friends unless they’re not, you know, if we didn’t have these again, we die of infection. So but when we’re exposed to mycotoxins, virus level, polysaccharides, Clostridium glyphosate, Lyme disease, beryllium, we stimulate TNF A, then NF kappa b, then the KNOX enzyme, then there’s an enzyme called interleukin six, a cytokine, a whole subject of its own.
And by the way, if anyone’s really interested in il six, I have done an excellent interview with Dr. Joe Carnahan, just go on YouTube, Joe Carnahan, il six, we spend an hour and 45 minutes just on this subject right here. So there’s multiple things here, that will cause it, and there’s actually even genetic mutations, these two right here, that will cause tumor necrosis factor to be overactive. Now, interestingly, there’s an enzyme called cert one that holds back the inflammation. And there’s a whole enzyme process called heme oxygenase that makes biliverdin bilirubin that holds this back.
This is controlled by Nerf Two and heme oxygenase. We need to make him again if you find this fascinating. Go on YouTube, Joe Carnahan, heme, we geek out for an hour and a half, just on this subject right here. But here’s again, our glyphosate, possibly messing with this sessional COA from the Krebs cycle. So if our Krebs cycle or energy production is less than optimal, this process isn’t going to work. We’re not going to have the heme we need to support the heme oxygenase to make the believer in bilirubin, and we’re not going to hold this back.
And in case you’re already looking ahead liquinox makes superoxide combined with nitric oxide to make peroxynitrite. Here’s our sod two and manganese, to try to bleed some of that off and turn it into oxygen. This was one of the subjects we spoke about, I believe it was 20 sets 16 or 17. We were in Hershey, Pennsylvania where we presented now was Denver, Denver, Colorado, where we presented what I call the NADPH steel. Were NADPH is critical for so many functions, if you remember we needed to make nitric oxide is overused by the NOx enzyme. And I call that the NADPH steel so you’re using it here.
So you don’t have it for the many other functions. So if somebody lives in a moldy house, okay, mycotoxins, and it does appear as though mold is getting stronger. You’re going to stimulate these enzymes. If you have a gain of function on here, that’s amplified. So one of the things we often see in people who are really struggling. They’ve got genetic mutations that are gain of function. They’ve got they’re living in a moldy house. They may be the sort of One maybe not doing his job. Sadly, high fructose corn syrup inhibits this. So if you’re consuming high fructose corn syrup if you’re being exposed to a lot of glyphosate, and then also if you have a gain of function, interleukin six, and then weakness inside to perfect storm. And I believe that’s what we’re seeing in so many individuals.
Dr. Joel Rosen:
A quick question sorry, sorry to interrupt. So just for the listener because they may not understand what gain of function is. So when you look at these genes, and you see that they’ve inherited, an alteration in that gene, ultimately, they think that that gene might be slower.
And it’s, it’s a loss of function, and it’s not working at the level that it should. Whereas there is research that shows that when they inherit a gene that is not functioning at full capacity from mom, or from God, or from both, again, a function can mean it is creating more of that enzyme than it’s designed to do. You made an observation earlier, that you think that potentially the gain of function was protective in the past. And now because of so many environmental factors, these these gains of functions are actually detrimental. Is that what you’re noticing Bob with?
Dr. Bob Miller:
Absolutely, Dr. Julia, thank you for pointing that out. That’s one point that I forgot to make it so there is that gain of function. So hypothetically, if there was a culture somewhere where there was a lot of bacteria or virus, and this tumor necrosis factor was overactive, that actually was protective to them. You know, the one that’s very well known is the hemochromatosis gene, extremely high in the English and the Irish. Now, if anybody knows the Irish history, the reason many of them migrated to America was the potato famine.
So people were starving to death. However, if you had a genetic mutation, where you actually absorbed more iron, these were the ones who survived. So it was protective. And now, you know, here in today’s culture, we don’t have we don’t have a problem. Many of our foods are fortified with iron. So that genetic mutation is now at your disadvantage. Dr. Joel? So in the same way with G six PD, we did the webinar on how G six PD is what helps make NADPH very common in Africa, and South America. Well, what’s interesting is the UN I don’t know the mechanism, but that G six PD deficiency protected you from malaria.
So again, in a time of malaria, having that G six PD was to your advantage. But back then they didn’t have all these other problems. Now that G six PD mutation is to our disadvantage. And just as a side note, clinical observation is only when people seem to have the iron mutation, that they absorb more iron and G six PD, these are the people that have a lot of inflammation. So thank you, Dr. Doe, for pointing that out. Thank you for explaining it. Yes, no gain of gain of function. All right, calcium. We all know that calcium is critical. We need it for our bones, we need it for our teeth, we need it for our muscles, we need it for all kinds of things. But we need calcium in the right place. And the wrong place is inside too much of it inside the mitochondria. And there’s something called the NMDA receptor that we’re going to talk about in a little bit, that will bring calcium into the cell.
And this is an area we have really been researching because electromagnetic fields will stimulate this NMDA receptor to bring too much calcium at the wrong place. And we get higher what’s called intracellular calcium that stimulates what are called mast cells. And again, we could do a whole program on mast cells.
But the cliff notes are, it’s a white blood cell that protects you, but it harms you if it’s overactive. It can create the production of arachidonic acid. And then we’re gonna get into how environmental factors stimulate something called the Aryl hydrocarbon receptor. So bottom line is, again, we have multiple environmental factors that we weren’t exposed to before. Remember, I said I was born on a different planet in 1954.
We didn’t have EMF, one of my favorite jokes is back then if we wanted to make a phone call and we weren’t home, we had to find this funny thing called a phone booth. But now we’re all exposed to electromagnetic fields, no matter where we go. I mean, unless you’re in a cave, probably 20 feet under, you’re being exposed to high levels of electromagnetic field. And we really don’t know what the long-term effect of that of that is. Now, here is the chart that we made that I actually presented my art to some conferences. There is no evidence that there are higher levels of intracellular calcium in the autistic child. But what does it do through the KNOX enzyme, it makes superoxide. But let’s look at what doesn’t. glyphosate or Roundup stimulates the NMDA receptor. There’s an enzyme called Pon one, that helps clear it.
And there’s the RS number, if somebody’s got a mutation there, there’s the potential that they don’t clear glyphosate white as well. homocysteine stimulates it, arsenic, and we’re finding now more arsenic in rice and chicken, high fructose corn syrup can’t emphasize enough how bad this is. Then also the electromagnetic fields will stimulate, here the NMDA receptor bringing excess calcium in, and making superoxide. Now, one other environmental factor that is finally getting attention, you know, those of us in the functional world, we talked about microplastics years ago, and everybody was like, oh, yeah, whatever that is.
But if anybody’s paying attention you’re seeing even the mainstream media is now starting to talk about microplastics. And that is what breaks off from all of our plastic bottles. January, I mean, if somebody just Googles microplastics in plastic bottles, a University did a study, and they found there are 10 to 100 times more microplastics in bottled water than anticipated. And it’s not just bottled water, things are wrapped in it. The oceans, or you know, we’re dumping huge amounts of plastics. I understand there’s plastic, the size of Texas floating around and some of the big oceans, and the fish are eating that. So these microplastics are getting in the fish. And it’s creating all kinds of problems.
There’s even just recently some concern that these microplastics are part of the plaquing of the arteries. And it’s estimated that each of us consumes a credit card a week in plastic. That’s scary. Dr. Doe. Now, the term is 30 late. That’s what we get from these microplastics. These are more insidious than you ever thought. I mean, if somebody said, how can we really hurt people? I don’t think we could have been this creative as what these things are.
As we make something called NAD, which is critical. If anybody’s studying longevity, they’re looking at NAD. NAD is what you need at the electron transport chain to make the energy we spoke about fatigue earlier. It’s part of recycling you’re going to find recycling your or making your nitric oxide. It also calms down mast cells that are a product of this. As we come down what’s called the Kira Nene pathway, we make something called when Olynyk acid the QPR T enzyme needs to turn that quinolinic into an ad. Look what the latest do. So here’s what they do. Dr. Joel, they inhibit the QPR T enzyme. Ouch. Now, the quinolinic acid also stimulates the NMDA receptor. Oh my goodness.
So we’re stimulating NMDA we’re making superoxide and mast cells in our defense against it is impaired. This is a big deal, Dr. Doe, then zinc is really important for the body because one of the things that zinc does, it calm down the NMDA receptor for zinc to be carried around we need Pika linic acid. This enzyme right here, this AC MSD is what takes this molecule that I’m not even going to try to pronounce and turns it into Pika clinic acid. So you can have genetic mutations, right, this one right here. There’s the RS number. If you’ve got a mutation on there, this gene doesn’t do its job as well. But if you’re exposed to 30 leads, that also impacts it. So if you’ve got a genetic mutation, you’re drinking out of plastic bottles you’re microwaving and plastic.
And also, sadly, personal care products that have fragrance are a feeling. So that’s why some people are sensitive to so many personal care products because these elites are impacting them. Show the quick clinical story. And a lady an elderly lady who was just barely functioning and we determined that she was going to get coffee every morning in a huge plastic cup. And as soon as she stopped doing that, I mean, she’s still not 100% But dramatic improvement when she wasn’t putting hot coffee in a plastic cup. Yeah,
Dr. Joel Rosen:
and even the cups that make you know, the little cups that make the I don’t know the name brands but they now sell them everywhere where they have just a cup and you put it in the machine and it’s in the package that ready. Absolutely
Dr. Bob Miller:
Knoxville. Yeah, it’s a big promo recommend they don’t do that. Just as a side note for me, for my children and son-in-law for Christmas, I got their soap, shampoo, and conditioner. That was the lead-free. Right? Yeah, they they kind of shook their head Oh Dad, but you know, someday they’ll appreciate that. So I think we have to be aware of our affiliates. So if somebody’s struggling, make sure you’re not microwaving in plastic. Make sure you’re not putting hot food in plastic.
And then also look at your personal care products. If it’s got fragrance, that can be a problem. So even some people they have those little dryer sheets they put in and or they have those little things they plug in on the wall, you know, to smell good, and you’re getting the leads. So anyway, this is a this is a big deal. We could do a whole hour on this subject right here. So I’m not going to dig into this too much. But here they’re just saying how pickle linic acid helps the human brain neuro-protective pickle linic acid.
Pickle linic acid increases the turnover of zinc in addition to enhancing the absorption and excretion and it’s helpful with zinc deficiency. Here they’re talking about homocysteine activating and I’m not going to read this whole thing but it’s you know, it’s important that you have good homocysteine levels. Fructose modifies the NMDA receptor and can make seizures worse. So, fructose will increase activation of the NMDA receptor function. And how many people are getting a lot of fructose, the latest comes from ingestion and inhalation, and dermal absorption, it can leak into the food.
Even now some of our dairy products, fish, seafood, and oils have high levels of elites, personal care products, people who live near the lead manufacturing industries are more likely to have the leads in their bodies through dermal absorption. One of the best ways to get the leads out is a sauna. research suggested because of the late structural similarity to tryptophan metabolites. And I should have mentioned that it’s tryptophan that comes down that pathway. Several elites are capable of inhibiting those enzymes, therefore decreasing the clearance of quinolinic acid. And they are associated with neurotoxicity.
So here’s a little chart that again, shows this is the thing elites are going to inhibit your body from making peak Olynyk acid. And it’s going to inhibit your body’s ability to make that critical NAD. When you think about this, Dr. Joel is like the perfect storm. You can’t imagine the damage that this is that this is doing to us. And then the net result is superoxide. Now we saw this part before Dr. Joel but now what we’re going to do is going to show how this stimulates glutamate. Now glutamate makes you intelligent, highly motivated, go-getter. It appears his own Northern Europeans seem to have a more predisposition to glutamate.
There are genetic mutations on the DAO enzyme that can make more, we can have genetic mutations that we don’t turn glutamate into GABA, which is relaxing. And we can if we have trouble with our biotin or some of these other enzymes, we don’t make something called oxaloacetate. That turns glutamate into energy. So glutamate makes you intelligent, highly motivated, go-getter, but can make you extremely anxious. And it will also keep you from sleeping. Make people sensitive to bright loud lights and loud noise. mind races, they can’t focus.
They’re brilliant, but yet they can’t focus. Now, here’s one other insidious little thing it does. Glutathione, which most people have probably heard of Dr. Joel is an important antioxidant. And it does all kinds of good things for us. But the body needs to assemble it. And it’s made out of cysteine glycine and glutamate. The CES team has to use his enzyme called X c t, to come inside the cell to make glutathione. And look what happens. Glutamate inhibits that enzyme. Ouch. So I don’t know if you’ve heard this, Dr. Joe, but you know, people are learning about acetylcysteine. And they think oh, it makes glutathione that’s going to be good for me.
And they feel horrible. Because the cysteine is not coming into the cell and actually turning into a soul fight and being inflammatory. So is that irritating? When you think you’re going to take something that’s going to help you and it hurts you? Same way with glutathione. I heard this dozens of times. I went to a doctor and he said I’m going to give you intravenous glutathione you’re going to feel one Wonderful.
They were sick for weeks. Because this glutamate was inhibiting this and was actually making them worse. So you have to make sure your glutamate is down. Before you start, start taking glutathione. And unfortunately, some of these people are just horrible. You must be imagining things that can’t be happening.
Well, it can. So now they’re sick and somebody tries to make them feel guilty. Like, there’s something wrong with you. You’re imagining this, you’re a hypochondriac. And they just get so discouraged because somebody yells at them that who found the mark the perfect antioxidant, we need it. Absolutely true. But if you have this going on, it can backfire on you. So I can’t tell you how many people were relieved when I told them that. Nope, you’re not crazy. There’s nothing wrong with you. It’s glutamate. Get the glutamate knocked down. Then all of a sudden, glutathione is good for you. And that amazing Dr. Joe? It
Dr. Joel Rosen:
is are you finding too, Bob that a lot of people happen to have that x CT challenges as well genetically on top of the glutamate being?
Dr. Bob Miller:
Actually I’m not finding very many FCT mutations, maybe we haven’t found them all. Now, there might be some, but I’m not seeing a lot of mutations on Fct. But when you think about the glyphosate, the arsenic, the high fructose corn syrup that they lead, the electromagnetic fields, all of those stimulating glutamate. You know, there’s an I think that’s why we’re seeing so much difficulty. I mean, when I talked to elementary school teachers who’ve taught just more than five years, you know, how are the kids today versus five years ago, and systole. They can’t focus, they’re agitated. And we’re seeing that in the world with people being more, more agitated, more angry. Because the glutamate is going up because of all these environmental factors
Dr. Joel Rosen:
to mention the food supply, right with all the artificial stimulants that are in the food that produce glutamate.
Dr. Bob Miller:
Sure, oh, and by the way, these people cannot handle MSG, right? So they’re exposed to MSG, and boom, they’re over the they’re over the top. So this high glutamate is a real, real problem. But we’re going to talk about a little bit of ferroptosis ferroptosis is where the iron starts damaging your lipids. And we’ll have a chart on that. We desperately need our glutathione to handle that. And if we can’t bring our glutathione in runaway inflammation in the mind in the cell membranes. So speaking of glutathione Dr. Dole here is how we make glutathione. This is somewhat of an oxymoron, you think reduced means less, but in biochemistry, reduced means it has a spare electron on it to neutralize free radicals. So what the body does, is it takes glycine.
Actually that glutamate if it’s used properly, turns into glutathione, and cysteine, cystine, glutamate, and glycine, all go together to make glutathione then glutathione, through glutathione, ‘s transferases. And Glenavon. peroxidase does all kinds of good things. But in doing so it gives away its electron and it becomes oxidized. Now what happens is again, one a miracle the body is there’s an enzyme called GSR that takes if ad from riboflavin NADPH controlled by something called Nerf two, which is a subject all on its own. And it recycles it. What a beautiful thing Dr. Dole. It uses it recycles it.
But if the GSR enzyme is mutated, if we don’t have enough riboflavin, and there are multiple mutations in these enzymes and compare riboflavin transport, if we don’t have enough NADPH because of mutations or because NOx enzymes are upregulated or because of nerf to problems. We don’t recycle our glutathione and look what happens superoxide nitric oxide combines with peroxynitrite In all these greens are nutrients that can intervene. So we’re finding where it is level now that we can actually find out where there’s weakness and compensate. So these are the people that if you if this has mutated, this has mutated, you don’t have NADPH. You don’t have FTD. You take glutathione it feels good for a day or two and then you crash because we don’t recycle. All right, poly aromatic hydrocarbons. They’re chemicals consisting of numerous carbon atoms joined together to form multiple rings.
There are 10,000 different pH compounds. Oh my goodness, from the incomplete combustion plan. Under animal matter, carbon fuels, coal or petroleum, and there’s smoke or ash and all of these can have an impact on us. So, this is one of my most interesting subjects here, Dr. Tool. It’s called the Aryl hydrocarbon receptor. Outside of Academia, most people don’t know about this, but we really need to learn about this in the functional world. Now, most enzymes, take one substance, combine it with something else and make something new. And they either do that slowly, they do it at the right pace, or as we discussed earlier, they can be overactive. Well, the Aryl hydrocarbon receptor is a different animal. It all depends on what goes in it.
What it does. Smoke Kleinereneene mold and mold are becoming such a serious problem. High homocysteine, high iron, and arachidonic acid that we’ll talk about a little bit, and here are those aromatic hydrocarbons that will stimulate this guy to make massive inflammation. Drive the intracellular calcium that drives the superoxide that drives the ferroptosis is one bundle of inflammation. Reduce these and start putting in Rosemary resveratrol is which in quercetin, milk thistle indole, and three carbinol, we turn on what’s called Nerf two, and n q o one that’s anti-inflammatory. So there’s a lot to learn about this, and then the Aryl hydrocarbon receptor through CYP one, b1, makes superoxide. And then il six and NOx stimulates new stimulates the superoxide. So you can see here we’ve just got so many ways that we can make more superoxide. And even here, as we drive the intracellular calcium, we make more superoxide. Now there’s an enzyme called N q o one nerf two controls.
And it’s also dependent upon riboflavin. It maintains your mitochondrial membrane potential and restricts oxygen protection. So you know, you’re going to be as healthy as your cell membranes are. And using NADPH as a cofactor, and reduces what are called Quinones. I’ll show a picture of this in a minute.
It also helps recycle your co Q 10 and vitamin eat, which are important, very important inside the body. And balance keeps the balance of NADH and NAD plus it’s been found to reduce superoxide and use NADPH as the reducing agent. It has been suggested that relatively significant quantities would be needed. So it’s not as powerful as other things, but it does calm down that superoxide, and guess what, I’m sure he figured it out already, Dr. Joel, you can have genetic mutations on in Cuba, one that lowers its function. So here’s one of the ways that there are many ways that in Cuba one helps us. But when there’s Aryl hydrocarbon receptor is stimulated from these polyaromatic hydrocarbons, the cytochrome P 450s. create what’s called a coin own, then it turns into loops and it turns into a semi coin own, then it turns oxygen into superoxide.
However, if MQL, one is doing its job, and we have adequate NADPH and we have adequate hydrogen, we turn it into oxygen. So here again, another source of superoxide ferroptosis When iron goes bad, you know iron is critical for life. I mean, we didn’t have iron, we wouldn’t carry oxygen around. If we’re too low in iron, we’re in trouble. But there’s a two-edged sword iron. Iron can be used to actually cause oxidative damage that can lead to cell death. It’s driven by loss of activity of the glutathione peroxidase and it creates what is called lipid-based reactive oxygen species, particularly something called lipid hydroperoxides.
It’s iron-dependent, and it’s distinct from other ways of killing the cells. It’s involved with autism, acute lung injury, kidney injury, rheumatoid arthritis, epilepsy, sepsis, neuralgia, neurodegenerative diseases, it’s even related to autism. There’s a correlation between ferroptosis and Autism Spectrum Disorder. Now here’s how ferroptosis works. Dr. Joel, when we’re exposed to mycotoxins, lipo, polysaccharides, Borrelia, and glyphosate clostridia, we stimulate tufa.
And remember we said earlier, you can have genetic issues where this guy overreacts Knox enzyme oxygen into superoxide superoxide dismutase then makes hydrogen peroxide, your thumbs iron. The iron then combines with hydrogen peroxide and makes a hydroxyl radical damaging your lipid membranes. Here’s that MCT that we spoke about. Here’s where cysteine comes in. And I really should have included glutamate on here that glutamate inhibits this driven by Nerf two, and glutathione peroxidase. Fourth is what does the repair BH for that we talked about does the repair.
And so it is CO q 10. So, if we have excess over here, deficiency over here, cell damage to the membranes. So here’s what happens. Iron, hydrogen peroxide, lipid peroxides ferroptosis, cell membrane damage. And this, I believe, is behind a lot of conditions that people are having. We need glutathione peroxidase to cut this off in the past. But if we’re having trouble making a recycling glutathione, we don’t have that. So again, another mechanism can cause damage to the cell membrane. All right, now we spoke about all the ways that we can make superoxide. Now, how do we take care of how do we take that electron off? Manganese, not magnesium, manganese, the enzyme sought to superoxide. Here’s the keyword dismutase. That’s what breaks it down. People get confused and say well that way, you’re saying superoxide is bad. But this superoxide is good. superoxide dismutase, using manganese to reduce the superoxide. And that’s one of the ways that we do it. Another one is actually B 12. Fascinating. And an enzyme called Pon one.
So here’s how manganese does its magic. This is the symbol for superoxide. It’s oxygen with an extra electron. The sod to enzyme says Mr. Manganese, I need you to help me out here. Why don’t you just grab that electron? So we can turn superoxide and oxygen. Now the manganese then has that spare electron, then what it does, is it takes two hydrogens and superoxide and makes hydrogen peroxide. Now that’s okay. But hydrogen peroxide can be damaging as well. So we need catalase glutathione and something called Thrive toxin, declare that because I’ve noticed over the years, that sometimes he gives people sad. And they feel phenomenal, and some people feel worse.
So, Dr. Doe, we got to make sure what I’ve been doing is I’ve been observing that many times before we give S O D, we got to make sure we’re clearing hydrogen peroxide. Because even the manganese so D is good as it is. If it starts making hydrogen peroxide, and you can’t clear it, you’re going to be worse. So you’ve really got to do things in the right order. Now talk about environmental factors, glyphosate, and Roundup, will interfere with the uptake and read treelines and translocation of calcium, magnesium, iron, and manganese by binding and mobilizing. So that’s the way glyphosate works as an herbicide, it ki latest those minerals. So I don’t know if I put this slide in here, I don’t if I did it, I think I might have. Studies have shown that when cows eat glyphosate feed, their manganese is inadequate.
Now there’s a delicate balance of manganese. So you shouldn’t go out and just take boatloads of manganese. Because if you get too little, we have a problem. But you can get manganese toxicity. So I want to caution people just because we’re talking about this today. Don’t go out and buy manganese and start taking boatloads of it thinking you’re doing yourself a lot of good work with a qualified practitioner on this because too little is a problem. Too much is a problem. So there’s a delicate balance one of my favorite jokes is all you need to do is follow Goldilocks and the Three Bears. Not too hot, not too cold. So warning, don’t go out and you know, go on the internet and find manganese and start digging boatloads of it.
You can hurt yourself badly. I mean serious problems if you have excess manganese, but to fish shunt is a problem as well. Now, Dr. Dole, this is one of the things that I’ve been most intrigued by over the years, I don’t think I’ve seen anything quite so fascinating. Here’s your manganese’s OD. And it does all these wonderful things. We spoke earlier about how you can be lighter, I mean one second we get a drink here. Now when nitric oxide uncouples, we make peroxynitrite peroxynitrite, nitrates tyrosine, which is a big part of your manganese so D working and hold on your head here Dr. Joel peroxynitrite can inhibit manganese SVOD up to 97%. Oh, my goodness. So this very critical to our well being SLD can be basically shut down by peroxynitrite. Yikes.
Then there I’m going to show you later. There’s an amino acid called lysine and Altair, I have a map that’ll show you that later. But if we have lots of lack of activity on cert three, we mess with the lysine as well. So if we reduce the peroxynitrite and we boost up cert two and three that again, I’ll show later, the manganese so D can do his job. So here’s a little chart we made Dr. Dole. And it shows here’s manganese s od right in the middle.
And here’s manganese taking superoxide in the oxygen, then it takes and then it takes a superoxide and two hydrogens to make hydrogen peroxide. Now there’s a lot that can go wrong here. We can have genetic mutations in the enzymes that transport manganese. And we can also have too much glyphosate which will happen if we get mutations on pond one that we don’t get the manganese over here. Then here we said this tyrosine can be nitrated by peroxynitrite. So if we have peroxynitrite, it can nitrate the tyrosine.
So that that shuts us down. CERT one that we spoke about earlier also supports sod two, you can have genetic mutations on cert one clinical observation only. When both parents are given a mutation on a certain one these people are usually struggling greatly. High fructose corn syrup, I should have put that on here. High fructose corn syrup shuts this down. We recently found another mutation called f 12.
That shuts down sod too. And then lysine, again another amino acid has a positive charge to it. So it takes that negative electron and says Hey, Mr. Electron, come on in the weather’s fine. I want to introduce you to Mr. Manganese. However, there’s a process called acetylation that takes that positive charge off and the body is so amazing here ductile because there’s an enzyme called cert three, that deacetylates lysing. So, therefore, it says to the electron come on in the weather’s fine. We want to take care of you here.
But if we have mutations on cert three, and here you can see snip in this one, this is the one that impairs the ability of DSC to lead micing. Okay, now, cert three and cert one are also dependent upon NAD. And remember, we just spoke about 30 late, reducing your NAD. So that’s why some people need to supplement with NAD. But you have to be careful because if Knox enzyme is overactive, it’ll make more superoxide. So you got to calm down NOx before you give NAD once again, people are learning about NAD and it’s like it’s the anti-aging, it’s the miracle. Yep, it is. Unless Knox upregulates, then it becomes a problem. So here we map out how tryptophan comes down in NAD.
And I don’t have that in here. But if you remember the theory leads can just cut this off in the past. So if you got three late and you don’t have enough NAD and there’s genetic markers that will have genetic mutations that will impact your body’s ability to make NAD then if you got mutations on cert three, your lysine is not going to be able to do its job. So you can see there’s a heck of a lot that can happen here. Dr. Joel, it shuts this down. 3d chess game played underwater. And finally, you can have fun attic mutations in aisle 13. That results in a gain of function, thus inhibiting Sed. A lot that can go wrong here. We’ll just have some literature on that F 12 mutation, and how it will impact mitochondria, you can see in this example here from our genetic software, that homozygous from both parents causes a shutdown of about shutdown, but a reduction in his od activity. And then I’m not going to read this, this family really wants to geek out.
There’s way too much to cover today. But we have mutations in il 13 that make them more active, which can shut down the sod know what happens is that manganese as 32 is an antioxidant. But if we have deficient manganese, we might have excessive iron. Interestingly, I’m sure people know the periodic table of elements, Dr. Joel, manganese and iron sit right next to each other. So they’re somewhat similar in their makeup. For whatever reason, iron can go into that side rather than manganese. Oh, oh. So mitochondria incorporated with iron is a pro-oxidant peroxidase. So the cells and animals accumulate this, when manganese iron levels are low iron, this hoody in cells leads to oxidative stress and mitochondrial dysfunction, you’re going to be in pain, and you’re going to be tired. So here’s that same chart. But we’re showing iron being there rather than manganese. So this doesn’t work. So your superoxide is going to stimulate ferroptosis and wreak havoc inside the body.
So guess who’s really struggling? Those who have genes that absorb more iron, they’ve got an F towel. Or they’ve got no uncoupling. Or they’re sort of threes now working or they’re il 13 is overactive. Now, you’ll see down here it says glutathione inhalation. We don’t have this down yet. We’re in a, we’re in a research phase on this. But this is another serious way that we’ll shut this down.
Can’t speak about it yet. If you want to know we’ll come back someday to speak about that. But this is another serious way that the Sistine gets impacted. Now, again, we don’t know yet. You know, maybe that’s affecting the way you make glutathione. I don’t know. For those who are practitioners, we do a webinar every other Thursday evening. And at the end of May, June, probably July, we’re going to be talking about this. So we’re in a research phase, but you can see Dr. Dollar has so many things that can go wrong here that it can really mess things up.
All right, B 12. You know, we tend to think of B 12. As you know, it gives you energy and all it does. But there are three kinds of Eatwell eyedrops all methyl adenosine, there’s an enzyme called TC n one and TC N two that helps get it into the stomach. And then from the blood into the tissue, particularly this one right here, there’s the RS number. When you’ve got mutations here, you can have all this B12. In the blood, it’s not to the tissue. And when that happens, somebody measures their B12. And so you’re taking too much B 12. You got to cut back. And sometimes they’ll say but I’m not taking B 12. Well, you must be taking the 12 to heart. Well, the problem is it’s not getting into the tissue, and they actually need those high levels to at least push them in. So one of the I mean be 12 does a lot but for illustrated purposes here.
The Cabal lemon, which is cobalt, by the way, we’ll turn that superoxide into hydrogen peroxide. Now once again, you’ve got to have adequate catalase. thyroid oxygen and glutathione peroxidase from glutathione to do that, if not this won’t work. And I believe that’s why some people don’t do well on v 12. Because they’re not clearing this hydrogen peroxide. But B12 is so much neater I don’t have it on here but you know the adenosylcobalamin is what helps make energy inside the mitochondria. Now Pon once again this is a little too deep.
If somebody wants to read it just get get the study or just pause here. But one works in a collaboration against oxidative stress, especially superoxide radical scavenging. We know for sure that Pon one helps with oxidized LDL and helps reduce those that stimulate superoxide. We believe there’s a way that it breaks down superoxide. But we don’t have it down yet. But there are genetic mutations on pond one that are pathological, that don’t allow you to clear glyphosate.
So here’s the oxidized low-density lipoproteins increased superoxide production by the endothelial nitric oxide synthesis. So these results indicate that a decrease in the activity of the endothelial cells is associated with the D phosphorylation of e nos, this association of the NA signaling complex, and the enhanced production of superoxide. So you can see all roads coming back to this. So peroxidase inhibits the oxidized LDL, and I think everybody knows that’s the bad cholesterol. So here’s the study, it says the main conclusive judgment is the presence of Pon one in the plasma, isolated or CO ligated to other proteins, and HDL favors the activity of e nos, that’s the good one. And then that supports the production of nitric oxide, which are vasodilators and platelet anti-aggregate.
So as you know, we’re seeing such a dramatic increase in blood clots, and strokes. So that’s it, if anyone wants to contact our clinic, there’s Tree of Life Health, there’s our phone number 717733 2003, tell, health.com. Practitioners, please only, we have software that that does all this analysis. And there’s the information on our executive director who can help you get an account. And of course, Dr. Joel, you have been studying this for a long time. And you’re quite capable, of doing this, this work as well. So you know, people can reach out to you to do the genetic test, and do the analysis and try to figure this all out. Oh, that’s
Dr. Joel Rosen:
awesome stuff. Bob, thank you so much for sharing your May your years of coming to where we are right now, in this information, I always do these interviews selfishly, because I like to get the front seat of the accelerated what you’ve learned recently, and I appreciate your time, a couple of things I wanted to discuss is, you mentioned that we’re getting to a level where the where we can understand the clinical picture with the software, and then be able to support patients.
And I think it’s really important to stress that like you mentioned the Goldilocks, not too much, not too little, don’t run out and just buy massive amounts of manganese and expect that to be the trick. And same thing for superoxide dismutase. Because if you’re producing too much hydrogen peroxide, and you take a superoxide dismutase supporting nutrient, and you make more hydrogen peroxide and you have challenges with clearing that then you need to get rid of that hydrogen peroxide first.
And that’s where having the printout and, and the graphs and the sort of the understanding the lay of the lie or the land of the lay of the land, and having a sort of a genetic blueprint as to what the potentials for this patient may be so that you can understand when to implement the strategies first.
And I think that takes a lot of practice from the practitioner to understand that. And what has your software done to help the practitioner I know they’re smart software, there’s also Hey, if you have this gene and that gene, you may want to consider this and that. So maybe give the the listener who’s still here listening to this. And that’s going to be the sophisticated person or the practitioner themselves. How has your software made it easier for practitioners to accelerate their learning curve?
Dr. Bob Miller:
Sure. Well, one of the things we’ve done, you know, a lot of genetic reports just lists the RS numbers and where they’re mutated. And you can look at that. And as they I have no idea what that means. So we have created maps, where you can actually see on the screen like these maps that I showed you, though, that wasn’t from the software, but the software actually creates the map.
And you can look at it and then color-coded. But one of the things that we’re working on now is recording this in early May 2024. We’re working on what we call Executive Reports, where the practitioner only takes the data and says we’ve got this mutation and this mutation here. So consider this. Now it’s also important to mention that when you’re conceived when that sperm goes into the egg, that’s when your genetic pattern is made, and it doesn’t change, right? When you leave this earth, it’ll be the same as conception.
So it’s the blueprint. So it’s never a diagnosis. It’s a predisposition. So then what the practitioner has to do is do the appropriate testing or look at the symptoms. So if you think muscle uncoupling is going on, and the person says, yeah if it’s 60 degrees outside, my hands are turning white and purple. Well, there’s a good chance you’ve got loss, and uncoupling going on. But you have to compare labs and or symptoms, with the genes, you can never make a decision based on that. Because it’s kind of like your blueprint. And just because you have genetic mutations doesn’t mean it’s a problem. You know, I’ve seen people with Pon one mutation and their glyphosate is just fine.
You see people that have mutations that can lead to oxalates, and they don’t have oxalates, or they do. So genetics is never a diagnosis. It’s the predisposition, but I think it’s so valuable because it tells you where to look Ray never thought I was looking before. So if you see upregulation of nos and downregulation of e nos, what do you have cold hands and feet? How’s your blood pressure? How’s your inflammation? Then you can try. Like there’s a level there’s a protocol design OS that comes down on us not supporting that booziness They’re pure nutrients are not going to hurt anybody. So you can try them. How are you feeling? It’s like, my hands are warm. I feel better. Okay, cool. So another analogy I heard that I really like, is looking at your functional genomics is like walking through the house, and seeing if there are any cracks in the wall.
And if there is maybe patch them up a little bit. And it’s also important to know that you can’t fix your genetics every once in a while somebody says, so I’ll do the test later. And I’ll see if they’re better. It’s like, nope. Yeah, got what you got. So one of my favorite expressions is we have good news and bad news. The good news is we can compensate. The bad news is we can compensate. Right. So if somebody has a hard time genetically breaking down fats, they may need nutrients that help them digest fats, and they’ll feel better. But if they stopped taking it, they’ll go right back where they were. So interestingly, some people are fine with that concept of it’s like, hey, if I can find the weakness, then I can compensate. Cool.
And for some reason, some people like, I don’t want to do that. I shouldn’t have to do that. Well, okay. So, but it’s interesting, the psychology of how some people embrace it, and others just rebel against it. Well, I’m not doing that like, Well, okay. You know, I don’t, I don’t argue with anybody. But genetics gives us a predisposition of where there might be some weakness. And I’m often like to say, it’s easier to keep you out of a ditch than to pull you out of one. And some people like to be kept out of a ditch and other people don’t want to do anything until they’re in one. So it’s like, okay, I’m sure you’ve seen that as well. So,
Dr. Joel Rosen:
yeah, well, I will say that the software has gotten so much more helpful for the doctor as well, in terms of understanding as you saw the maps. And as you do the research to understand your presentation today, you also didn’t really explain but you could have, how you came up with the green stuff on those maps that support that function, because those are the research base nutrients that have been shown to help those processes. So that can really help the practitioner for sure.
And I think also, maybe you can correct me if I’m wrong on this, but even if you have the patient that feels that they shouldn’t have to do that, I would imagine that the people by the time they’ve come to you or by the time that the doctor who’s working with them doesn’t have any more answers and comes to you that they look at this as a understanding of what their challenges are, and know when a symptom arises.
And they know in the past, this thing made them worse, why that was or this thing made them better why that was when to initiate the protocol. So it’s not just to pound the gavel. Okay, Mrs. Jones, take this every single day of your life for the next, you know, to the end of time, but it’s more okay. When I feel this, I get stressed this way. I can’t turn my mind off. I can’t go to sleep, whatever it may be I have brain fog. I have cold hands, whatever it is, they know this thing must be expressed and they are the more sophisticated person because they want to understand whether Is true or not.
Dr. Bob Miller:
I mean, 99% of the folks are referred by physicians to us. And they’re like, We need another set of eyes at this to see what’s going on. And one of the cool things about doing this is the relief you see on people’s faces You know, when you tell them that the reason you might not have a very good mood is because you don’t have enough pH. And they’re like, oh, so one of my absolute favorite things to do is to tell people, I have four important words for you, you’re ready for this, you know, it’s not your fault. People are starting to cry. So one of the things is, you know, there’s a substance called BH four that we spoke about that we need to turn tryptophan into serotonin.
And if your BH four is being taken up by the ions, or it’s desperately trying to fight ferroptosis, or you don’t make enough, then your body doesn’t make enough serotonin. Now, one of the things that is rather irritating is that sometimes when people are depressed, I call them well, meaning people tell them well, you have nothing to be depressed about. Everything’s okay. Just Buck up. And then, in the end, by the way, I’m firmly in favor of prayer and all that good, but that’s fine. But then sometimes people say, Well, you’re just not praying hard enough. Oh, there must be sin in your life. Okay. Then the New Age crowd? Well, if you just say the right affirmations, I am happy today.
And it doesn’t work. Okay. And then when you tell them that, well, you know what, if you have a car, and there’s no gas in it, you can think positive thoughts, you can do all kinds of things. It’s not starting, let’s get your BH four levels up, and you’ll be okay. And that people are like, Thank you, because they’re made to feel guilty, you know, or the same way with anxiety, oh, just calm down, you have nothing to be anxious about? Well, if your glutamate is through the roof, you can’t calm down. And then when you show people that you are not converting glutamate to GABA, you’re not turning glutamate into energy. No wonder you’re anxious. The relief on their face is just unbelievable.
And the thankfulness because, by the way, if you’re one of those, well, meaning people who tell folks to just Buck up, you may want to reconsider that. Because it’s really not to the person who’s struggling, you know, if somebody has diabetes or something else, it’s like, oh, you poor thing. They’re depressed or anxious, and they’re trying to make sure that it’s their fault. And now, some people get themselves into the problems. And they are, you know, it is it is related to their life. But sometimes it’s not. And to make those people feel guilty is just so sad. It really is.
Dr. Joel Rosen:
Yeah, it definitely is very empowering. And I would probably ask another follow-up question is, whether it’s the will the doctors that are referring you, they’re their most difficult types of presentations, that they are also getting, you’re you’re getting feedback. No one’s ever said this to me before. I’ve never heard that before.
But yet, they’re the people that have started with, I’ve done everything there is to do, there’s nothing else I can do. And once you explain to them things that they’ve never been told, but you’re explaining it to a tee and then you’re asking them questions, will do you feel this? Or you did feel that? Yes. How would you? How did you know that? I think that that also helps with finally having someone who’s validating what they’re feeling, but be things that they haven’t been told before that already start them on the healing path.
And then, as you said, you’ll get a difference of some people want a full court press it and other people just want to sort of do a trial and see, but ultimately, you’re seeing the needle move for the first time. Is that Is that correct?
Dr. Bob Miller:
Absolutely. And the thankfulness that we sometimes hear from people is incredible, you know, finally somebody’s explaining to me what’s happened, there’s a lot of relief and just knowing what’s the reason, you know, there’s an old adage of Know Your Enemy. And when you say that, excess glutamates for energy, it says histamine is your enemy. And we’re going to knock that down. So if somebody has high histamine that might be, you know, stopping some of the high histamine foods. Right.
And, and unfortunately, you know, there’s some people that think everyone should be eating all these high histamine foods to rebuild the duct. That can happen. But if you already produce too much histamine, and you don’t break it down, you’re throwing fuel on the fire when you throw these high histamine foods in. Same way with bone broth, you know, bone broth is a fine food, but it’s high in glutamine and histamine.
So if you have high glutamate and high histamine, and you start guzzling down bone broth every day and throwing fuel on the fire. So, one of my favorite sayings is when somebody says everyone should I get very worried because we’re all unique. And one person’s medicine is another person’s poison. So it’s and that’s why we have to have individualized care. One size does not fit all FMLA, it
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The post [EP.17]Mastering Your Genetic Code for Optimal Health: Dr. Bob Miller’s Latest Insights appeared first on Dr. Joel Rosen.