In Episode #23, PART 2: Dr. Jill interviews Bob Miller of Tree of Life Health on Why NAD+ and NADPH are Critical for Your Long Term Health

Related Products

Tru Niagen PRO 500 https://www.drjillhealth.com/product/tru-niagen-pro-500-30-count/
H2 tabs – https://www.drjillhealth.com/product/h2-absorb/
Vital Reaction H2 machine (Mention Dr Jill referral for 10% off) https://www.vital-reaction.com

Dr. Jill is your Functional Medicine Expert specializing based out of Louisville, CO. She has countless free resources on mold, autoimmune health, detoxification, brain health, and more.
Dr. Jill's Miracle Mold Detox Box: https://www.molddetoxbox.com/

Dr. Jill

Dr. Jill Carnahan is Your Functional Medicine Expert® dually board certified in Family Medicine for ten years and in Integrative Holistic Medicine since 2015. She is the Medical Director of Flatiron Functional Medicine, a widely sought-after practice with a broad range of clinical services including functional medical protocols, nutritional consultations, chiropractic therapy, naturopathic medicine, acupuncture, and massage therapy. As a survivor of breast cancer, Crohn’s disease, and toxic mold illness she brings a unique perspective to treating patients in the midst of complex and chronic illness. Her clinic specializes in searching for the underlying triggers that contribute to illness through cutting-edge lab testing and tailoring the intervention to specific needs. 

A popular inspirational speaker and prolific writer, she shares her knowledge of hope, health, and healing live on stage and through newsletters, articles, books, and social media posts! People relate to Dr. Jill’s science-backed opinions delivered with authenticity, love and humor. She is known for inspiring her audience to thrive even in the midst of difficulties.

Featured in Shape Magazine, Parade, Forbes, MindBodyGreen, First for Women, Townsend Newsletter, and The Huffington Post as well as seen on NBC News and Health segments with Joan Lunden, Dr. Jill is a media must-have. Her YouTube channel and podcast features live interviews with the healthcare world’s most respected names. 

The Podcast

The Video

The Transcript

#23: Dr. Jill Interviews Bob Miller on NAD+ Pathways and Functional Genomics

Dr. Jill 0:12 

Hi, Bob Miller. It is so good to have you back. You get the honor of being my first [repeat] guest. [This is] number two [for you], and we're going to do number three next month too because the last one had the most views of any of the live episodes so far. So, any of you who are watching, first of all, welcome. I'll introduce Bob Miller, if you don't know him already, in just a minute. But his first episode, you can find on my Facebook page or on my YouTube channel. My YouTube channel now has over 20 episodes, and they are great. But Bob's [episode] is one of the best. I know you're going to enjoy it. So please be sure to go back there and watch our first episode. Today we're going to talk about NAD and dive into what that is, what it means for your health, and why it might be the most important thing that you hear this year in regard to your health and overcoming chronic disease. 

Dr. Jill 1:05

Just a little background: You can get free blogs and free information on my website, jillcarnahan.com. Later, we're going to be talking about an upcoming conference that Bob is putting on. And his events are just fantastic, so we will talk about that. You'll definitely want to save the date. This will be recorded here, so you can watch it. You can share it with your friends or colleagues. And of course, it will be on my YouTube channel. 

Dr. Jill 1:28

So welcome, Bob Miller. I'm going to give a little introduction in case anyone didn't hear the first one. You've got such a wonderful bio. Bob Miller is a traditional naturopath specializing in the field of genetic-specific nutrition. And what you'll find about Bob is that he goes deep. He has the mind of an engineer or electrician, as we talked about. And I love that because I do too. It's pathways and processes—these things all come together and give us really great information on how to help our patients and clients. He earned his traditional naturopathic degree at the Trinity School of Natural Health and is board certified through the ANMA. In '93, he opened the Tree of Life practice, where he served as a traditional naturopath for 27 years.

Dr. Jill 2:11

For the past several years, he's been engaged exclusively in functional nutrition genetic variants and related research. And some of the pathways he puts together and some of the conclusions about what causes what and what intervenes nutritionally at this pathway level have been so helpful to practitioners like me because we get these complex patients. And the medicine we're taught, at least in my allopathic background, is one-size-fits-all. As we know more than ever, it doesn't work that way. Every patient that we see in front of us is different genetically, spiritually, emotionally, and physically. So this really takes into account the genetic and individual variations of our patients. And I find, Bob, that a lot of the stuff you teach and that we learn with these pathways helps us make little tweaks and breakthroughs that make all the difference in their care. You can find his full bio on his website. What's your website, Bob? 

Bob Miller 3:05

Tolhealth.com. 

Dr. Jill 3:06

Perfect, tolhealth.com. There's information there. But we will, without further ado, jump into everything about NAD. And if you wanted to share your slides, we can do that now as well. 

Bob Miller 3:18

Okay, we're going to do a screen share. Again, what a pleasure to be back here. We had so much fun the last time. It was absolutely incredible, and I'm so honored that so many people watched it. So we're going to dig right in. As you said, we're going to geek out here a little bit. We're going to be talking about why supporting your NAD+ and NADPH levels may be your key to longevity and health. 

Bob Miller 3:45

Now, we're going to talk about these molecules. But first, I want to say they're critical for many things, first for detoxification. As you know, Jill, we're living in a world that's more toxic than it's ever been. We need to have energy production. We're going to talk a little bit about mTOR and autophagy, the growth of cells, the cleaning of cells, supporting sirtuins—which perhaps a lot of people haven't heard about—and recharging our antioxidants. 

Bob Miller 4:14

Now, let's just get into a little bit of the theory behind it. In metabolism, NAD+, or nicotinamide adenine dinucleotide, is involved in redox reactions and transferring electrons. When you really get down to it, we really are an electrical beam. Einstein told us a long time ago that E equals MC squared—energy and mass are interchangeable. It's a little hard to grasp, but that's what we are. Now, NAD+ is an oxidizing agent, and it accepts electrons from other molecules and becomes reduced. And this forms NADH, which can be used as a reducing agent to donate electrons. And of course, we all know that in the Krebs cycle, at the top of the electron transport chain, that's how we make our ATP. So they have a critical role in maintaining homeostasis. And then we're going to be talking about NADPH, which is actually synthesized from NAD and has similar functions. 

Bob Miller 5:19

Now let's talk a little bit about these. They're fundamental  common mediators of various biological processes: As we said, energy metabolism, or mitochondria, is where we make our energy. Calcium homeostasis. To me, this is the key one right here—antioxidants. It actually takes your antioxidants after they do their job—they become oxidized, and we'll talk about this more later—and recycles them. But it wears two hats. You will actually generate oxidative stress. And I'm going to just get into that a little bit today, but that's going to be the primary thing we're going to be talking about in our August interview: How NADPH is actually used to make free radicals and why I believe that this is getting out of balance because of genetic and epigenetic factors and all the things that we've done. We're going to look back someday on some of the things we've done to our environment and say: “Oops. What were we thinking?” 

Dr. Jill 6:17

Yes, and Bob, I just want to comment here because, in my mind, I always think about: Glutathione—we've known about oxidized-reduced—it goes in this cycle. Would you say that we're looking at—it's totally different, but it's a parallel cycle—if we need oxidized reduced states. And if either one of these states gets imbalanced, we lose our ability to basically recycle those enzymes. Is that correct? 

Bob Miller 6:37

Absolutely. Let's take a peek here as well while we're on that subject. So here is glutathione, the master antioxidant. We have to have it. It's part of glutathione conjugation. I'll be talking about that a little bit. After it does its job, it becomes oxidized. So if it sits here and doesn't recycle, it will combine with oxygen to make superoxide. Then it'll combine with nitric oxide to make peroxynitrite, a very strong oxidizing agent. So for this to happen properly, what we have to have here is adequate amounts of NADPH because that ADPH takes your oxidized back to your reduced. So if that doesn't happen, boom, [it goes] down here into an oxidizing agent. So that's why many times people are so confused. They've got inflammation. Some well-meaning practitioner says: “Oh, I'm going to fix you up. I'm going to give you some glutathione.” They feel better for a couple of days, and then they start tanking. Sometimes people are told, “Well, that can't be happening because this is a master antioxidant.” If you don't have enough of this guy, you're going to go down this pathway. So that's why I'm so excited about NADPH. So I'm glad you brought that up because that's a critical, critical piece. 

Dr. Jill 8:02

And Bob, I just want to mention [something] because, again, you hit the nail on the head for probably so many people watching today. I'm one of those people. We've talked about this before. I had this massive mold exposure in 2015 and got so sick. And of course, glutathione, what do you do? Well, I did not tolerate it at all. And back then, five years ago, I didn't understand why. All I knew was that I got way, way worse when I took glutathione. And I know some of you listening are having that experience, and it doesn't make sense. This is part of understanding why that happens and why you need to really make sure. It's like carts and horses, and you have to have things in order. If you just push the end product, you may not get where you want to get, and you may actually cause more harm or damage. Now, I have a question real quick here. What I found from my personal journey was that precursors of glutathione were fairly safe and tolerated, like glycine, vitamin C, selenium, NAC, and even alpha lipoic acid in small amounts. If someone is trying to replenish their NAD, would that be a safer way to go than giving loads of glutathione? 

Bob Miller 9:05

Well, let's first talk about your selenium. Your selenium is part of recycling your glutathione as well. So selenium will help the glutathione peroxidase recycle. 

Dr. Jill 9:16

So if people are low on selenium, could they also have trouble with the recycling? 

Bob Miller 9:20

Oh, sure. I don't have it on a chart right here, but the selenium is part of recycling what's called glutathione peroxidase, which clears hydrogen peroxide. Now, you talked about some of the precursors, [like] glycine, right here. So glutathione is made from glutamate, cysteine, and glycine. Now, one of the interesting things is that sometimes people have a genetic mutation on this gene right here, GCLM and GCLC. If they do, that cysteine does not come down here, and in some instances, this can combine with iron to make hydroxyl radicals. So then cysteine doesn't work. And then also, glycine sometimes stimulates the NMDA receptors. It can make the person more anxious. And then, finally, here's the GSS enzyme. If this enzyme is not working properly, you're not going to make glutathione from it. And then, to make it just a little bit more complex, something called Nrf2 and Keap1 control all of these. So if you've got a weakness in Keap1 and Nrf2, they're not turning these enzymes on. 

Bob Miller 10:34

And let me just mention what a miracle we are. I give the analogy that Nrf2 and Keap1 are kind of like a sprinkler system. In a rough sense, think of Keap1 as the sprinkler, and Nrf2 kind of like what turns on the water. So when oxidative stress comes along, Keap1 says: “Hey, we've got a fire here, folks. Let's turn on these enzymes to make more glutathione.” I mean, what a miracle we are, the way the body actually responds and reacts. Mutations here can impact that. And that's why I call it the 3D chess game played underwater. [There are] so many factors that intertwine. And there just aren't easy answers; they're really hard. 

Dr. Jill 11:15

And I want to comment. If you're a practitioner listening or a patient, what's so easy to do is want a one size fits all [approach]. You want the hook book; what's the formula, Dr. Jill? And I just want to reiterate what Bob's saying here: There is no formula; it really has to be individualized. And I always get nervous when people have a one-size-fits-all trick. None of those things work for everyone. And this is why: Some of the variants that we have genetically, the processing of different nutrients, our depletions, and our toxic exposures all play into this. 

Bob Miller 11:45

Absolutely. A 3D chess game played underwater, as we said. Now, let's talk about NADPH—the other things it does. I'm sure people have heard of nitric oxide—Nobel  prize winning back in the 1980s. Not only is it vasodilative, but it's also anti-inflammatory and has many other processes inside the body. If we don't have enough NADPH, we don't make nitric oxide. And this is where people have cold hands and feet, or Raynaud's [disease], high blood pressure,  erectile dysfunction, or cardiovascular disease. Many people have never heard of thioredoxin, but it's a very important antioxidant. Again, it takes the oxidized back to the reduced. Not enough NADPH? That doesn't happen. Now, we just talked about glutathione. However, many people don't know about this: NADPH is needed to take heme and turn it into ferritin. So heme is where the body takes iron by the FECH enzyme and makes the heme. And when the heme is aged, what's called the HMOX enzyme takes heme and puts it into ferritin. Well, if we don't have enough NADPH, that doesn't happen. So the iron gets dumped, becomes a free radical, and the ferritin is low. 

Bob Miller 13:05

And then, if you think, “Oh, my ferritin is low, let me take more iron,” and if that's what's happening, you can make more inflammation. Then heme also makes something called biliverdin, which is a very powerful antioxidant that actually calms down mast cells. And so many individuals now—everyone is talking about mast cell activation. Well, this could certainly be because of environmental factors. That'll primarily be what we'll be talking about in August: All of the environmental factors that stimulate the mast cells. But we need biliverdin to calm that down. And then we also turn heme into carbon monoxide, which interestingly stimulates the Nrf2. So now you can see why I am so excited about NADPH when you look at all the functions that it performs. 

Bob Miller 13:56

Now, this is fascinating. You know, 12 to 15 years ago, we started learning about MTHFR, C677, and A1298. And everything you've heard about that is correct. It's what puts a methyl group on the folate. And we all know that we need folate for so many things, [including] making our SAMe, our methylation. It's needed by pregnant women. I won't go into all the details of this; somebody can read this slide later. But what's interesting is that if we don't have enough NADPH, taking folate actually shifts the balance toward oxidation. 

Bob Miller 14:36

So once again, somebody says: “Oh, I have MTHFR. I need to take methyl folate.” They feel great for two or three weeks, and then they start feeling anxious, angry, and inflamed, and they don't know why. And to this day, I still see people [who say], “Oh, I saw somebody who says I have MTHFR, so I need to take methyl folate.” My answer is maybe, because if you don't have things lined up properly, folate will actually stimulate what's called mTOR—the mammalian target of rapamycin—which, of course, is needed for the growth of new cells. So that's why pregnant women need it. But interestingly, a lot of people don't know this, but the COVID virus hijacks mTOR for replication. So if our mTOR is running too high, there's the potential here that we could give COVID an opportunity to replicate too fast. So that's why before I give people folate, it's like, “Let's make sure we've got enough NADPH.” And I'm sure you've probably seen lots of people who were told they needed methyl folate; they took it, and they felt worse. 

Dr. Jill 15:45

Yes, Bob. And I just want to comment. When I was 25, a long time ago, I had breast cancer. 

Bob Miller 15:51

Oh, that was three years ago, right? 

Dr. Jill 15:52

Yes, just three years ago. [laughter] I love you! So anyway, all that to say, I found out I had methylation issues. I had one copy of the C677. I was low in B12 and methyl folate. And of course, what do we do? And this was years ago; I didn't have all the understanding that we do today. I took methyl folate. This was after the cancer. But as we talked about through mTOR—without appropriate levels of NAD, of which I'm sure I've been depleted all my life until recently—I actually created more cells and had more breast lumps that they thought were potential issues. That was all because I had really pushed some high doses of methyl folate. So you can really get into trouble with even cancer, pre-cancerous [tumors], fibromas, or cystic things with this process as well. And you want to work with a practitioner who understands and does not just push methyl folate without the other precursors. 

Dr. Jill 16:45

The other thing you said that I think is very relevant is that mTOR is hijacked by COVID. Now, we've seen some evidence that perhaps patients who are really into bodybuilding are pushing mTOR with amino acids, some of the peptides, and rapamycin. So there are all these things that a lot of the anti-aging groups are doing to push mTOR. Could it be that some of those people are at a little higher risk for complications of COVID? We don't know for sure, but some of the evidence points to the fact that that might be true, and this is why. 

Bob Miller 17:13

Yes, absolutely. Now is not the time to be pushing mTOR in my opinion. If it doesn't make any difference, well, it doesn't matter. But if it does, I'd rather be safe than sorry. 

Dr. Jill 17:26

Sorry to interrupt you again, Bob. I just want to mention, for practical terms: The opposite of mTOR is autophagy. When your cells are actually eating up the bad guys that are doing the wrong signaling and going to go down a wrong pathway, your body says: “Hey, you need to kill yourself,” and that's autophagy. So autophagy and mTOR are always balanced, and we want that balanced. And Bob, I'd love to know if there are other things that you know of, but one of the things that helps autophagy is fasting. So that's one reason why intermittent fasting can be helpful to balance that mTOR autophagy pathway. 

Bob Miller 17:54

Sure. Well, let's take a quick peek at that while we're on that subject. Let me just pull in the maps and charts here. So let's take a look at that. 

Dr. Jill 18:03

You are so good at finding the details—I love it—right on the spot. But I think it's important and practical for those listening. So I love that you brought that up. There we go, the beautiful mTOR chart. 

Bob Miller 18:14

Yes. So let's look at the mTOR chart. This is actually what I did—one of my studies in 2018 on Lyme disease. So one of the things that I really believe is happening: As you said, mTOR is [responsible for] the growth of new cells. So we have mTOR growing new cells, and we have autophagy cleaning the cells. And interestingly, autophagy, we believe, takes out the virus as well. Now, what have we done to our environment? We have all these plastics that are creating xenoestrogens. What do they do? They stimulate mTOR. So, as you said, [they're found in] some of these protein drinks and things. I think we're going to look back someday and say, “What were we thinking giving our animals growth hormones?” “Well, they'll get fatter faster, and we can make more money.” Yes, but that gets passed on to more mTOR and higher levels of glucose and insulin. Iron will stimulate it, [as will] methionine, SAMe, glutamate, and, of course, folate. And that's why, of course, women who are pregnant need folate because if they don't have fast reproduction, they're not going to make the new baby. So either you'll not get pregnant, have a miscarriage, or [a child with a] deformity. So during pregnancy, you want to push that mTOR. But if you're not pregnant and you're concerned about inflammation, pushing mTOR too much can be a problem. 

Bob Miller 19:36

So you talked about intermittent fasting. Well, of course, when you stop the amino acids, the carbohydrates, the iron, the glutamate, the folate… I give the analogy: Think of mTOR as the construction crew, and it is building. When you take away the materials, it says: “Well, I can't do any building. Okay, janitors, come out and do your job.” And that's what they do. The janitors, so to speak, come out and start cleaning. And I found in my one study on Lyme disease that those who were chronically ill with Lyme had epigenetic and genetic factors that threw them into mTOR dominance. And I think you said intermittent fasting—right there—a ketogenic diet. But also, resveratrol and turmeric will slow down mTOR, while lithium, vitamin D, and berberine support the AMPK enzyme that supports autophagy. And I believe we have just done so much in our environment. And even cytokines—you know, we're getting more cytokines now because of inflammation. They're all stimulating the mTOR to our detriment. Again, that's why I believe we're seeing such great results with intermittent fasting and the ketogenic diet. 

Dr. Jill 20:52

Thanks for going over that. I think it's so important for people to understand the balance. 

Bob Miller 20:55

Absolutely, yes. So I'm glad to go down that little bunny trail there. It's a good one. This is how we make NADPH. So tryptophan, which most people know about, is what we get in our turkey. Most people know that goes into serotonin, but it will also go down this direction by TDO, IDO1, and IDO2. Well, if we've got genetic mutations here, this pathway may not be as robust. And there's a scientist doing some research. I'd love to do an interview with him. But he believes that when there are mutations here, this is where you get the excess serotonin, and you don't get it moving down through here. And this is the de novo pathway—more enzymes, more mutations there. And then, quinolinic acid. Now, this induces NMDA receptor-mediated lipid peroxidation and anxiety. So when people have mutations in QPRT, these are the people that are getting hit in two ways: Their quinolinic acid is too high, and then they're not getting the NAD that they need. 

Bob Miller 22:04

Now, a lot of people are learning about nicotinamide riboside, nicotinamide mononucleotide, and even niacin. This is what comes down through NMNAT. And as we age, this is what weakens for us, and therefore, we don't get as much NAD. Now, interestingly, NAD+ can go up to NADH or it can come down to NADPH. One of the mutations that we find very clinically significant is NQO1 because this is the NADH to NAD+. When these are out of balance, this is when people are in a hyper state—tremors, migraines—because they're not getting down through here.

Bob Miller 22:53

Now, I'm going to talk about this more, but NAD+ also supports PARP, which is DNA repair. So as our DNA gets damaged, PARP jumps in and says, “[inaudible], do some repair.” So the bottom line here is that there's a lot that can go wrong here in making your NAD+. And again, the same thing; we are learning about all the benefits of NAD, and I'm going to talk about more of them. So we tend to think, “Gee, the more nicotinamide riboside or nicotinamide mononucleotide I take, the better off I am”—sometimes. The same as methyl folate. 

Bob Miller 23:34

So let's dig just a little bit deeper. And this is a complex chart. We really don't need to get into a lot of the details. But NAD+ stimulates what are called sirtuins, which are involved in longevity. And part of it is because they make SOD and catalase. And I'll be showing a chart on that in a little bit. These are major antioxidants that neutralize free radicals. And if you've got way too many free radicals going on, you're going to age prematurely. And as we spoke about, here's the NADH and energy production, and then my favorite, NADPH. And I want to get into this again later: Recycle your antioxidants or free radical production. To me, that is what is so fascinating. This guy will either help you make antioxidants or make you make more free radicals. To me, that's fascinating. And the whole premise of our research is that I believe epigenetic factors are tilting that balance: That this NOX enzyme is being unnecessarily upregulated, pulling away from all those good things, and making excess free radicals. Now, a lot of people tend to think, “Well, free radicals are bad.” No, they're not. They kill the pathogens; they're signaling. Without them, we die of infection. But if they're in excess, that's when we have a problem. 

Dr. Jill 25:03

And Bob, I just want to ask you a question real quick. So in that SOD you mentioned with catalase, which is really critical for decreasing free radicals, I noticed there's a SOD mutation. I happen to have that. Is that related to a downregulation of the production of SOD and catalase? 

Bob Miller 25:19

Absolutely. Well, just SOD. There are CAT genes that make catalase, and then there are SOD genes that make SOD. And what we find is that when people have a lot of mutations in SOD, they're really struggling. If you remember, when we talked about peroxynitrite a month ago, we showed many times that superoxide combines with nitric oxide to make peroxynitrite. And if we don't have enough superoxide dismutase, that feeds upon itself. And peroxynitrite is a very oxidizing agent. 

Dr. Jill 25:57

Again, I'm just always wondering, and based on some of my personal and clinical experience, I definitely have a lot of SOD mutations. And I've noticed that, like hyperbaric chambers and ozone, anything that creates some oxidative stress [is something] I don't tend to tolerate well. Do you think that's correlated with the SOD types of mutations? 

Bob Miller 26:14

Oh, absolutely. Yes. I'll be showing a map a little later on here that shows how we need the SOD to turn some of those things into hydrogen peroxide. Well, why don't we just jump there now? 

Dr. Jill 26:28

Oh, I love this. You go on rabbit trails with me. Now, one other question. H2 inhaled—I know we both like that. And I use it almost every day after work for about 30 minutes. I love it. But I'm assuming that is a pretty safe bet for someone like me with SOD mutations. Is there any way that that pathway could be overdone with hydrogen?

Bob Miller 26:45

No, I don't think so. No, I don't think so. Hydrogen is very safe. So here is your free radical, superoxide. We need SOD to turn that into hydrogen peroxide. Then we need the glutathione peroxidase that we spoke about, [we need] thioredoxin to turn this into water, and then we also need NADPH to keep recycling these guys. So if we don't turn this into water—and here is catalase that turns it into water and oxygen—it'll combine with iron to make your hydroxyl radicals. And that's where the hydrogen water or from breathing the hydrogen will neutralize these hydroxyl radicals. Because look what this guy will do: Combine with nitric oxide to make ONOO, peroxynitrite. And the same way here, if we don't have enough SOD, we make our ONOO, peroxynitrite, which suppresses the immune system and leads to osteoporosis, inflammatory bowel disease, and on and on, and depletes our glutathione. So yes, that's why I'm a big fan of hydrogen water and breathing hydrogen. In preparation for the show, I always try to have my brain as clear as possible. So I did about 20 minutes of hydrogen about an hour and a half ago, just to feel on top of my game.

Dr. Jill 28:03

I love it! And like I said, I do too. And I know people are always asking, so I'm going to get practical really quick. I know you have hydrogen tabs for sale in your line of products. So do I at my store. So make sure to check out Dr. Bob's on those. They're super easy. They're not expensive. You can put a couple of tabs in water, and while it's fizzing within about 90 seconds, you just drink it down. And I find that for people who do that, this is a much more simple and cheap way to do it than [with the] inhaled [method]. The inhaled [method] is probably more powerful, for sure. But the machines cost thousands of dollars. I got mine from High Tech Health. I'm curious as to where you got your machine, Bob. 

Bob Miller 28:37

The same place. Yes.

Dr. Jill 28:38

Okay. The same place. So you can go to High Tech Health if you're interested. They might run upwards of $5,000 for the machines. You can get the tabs for a lot less. 

Bob Miller 28:47

Absolutely. So these NAD levels decrease with age, and that's why the aging process takes a toll on us. One of our researchers found it absolutely fascinating. They found that perhaps the best time to take NAD is around 3:00 to 4:00 p.m. from an oscillation standpoint. 

Bob Miller 29:08

Now, probably a lot of people have never heard of sirtuins. And we're not going to get into a lot here, but there's a process called acetylation and deacetylation. In a normal cell, these are balanced. In an abnormal cell, the acetylation is weakened and the deacetylation is strengthened. And [for] all of these, this is dependent upon adequate amounts of NAD. Now, we spoke about PARP, and that is DNA repair. So when peroxynitrite or other free radicals damage our DNA—again, what a miracle we are, Dr. Jill—we have the ability for the repair team to come out and start to fix us. And PARP does that. But look what it needs. It needs NAD+ to repair the DNA. So if we don't have enough NAD+, when the cells get damaged, we don't have the ability to do the repair. So that's why NQO1 is so important, because if you're stuck in the energy production and not down in the NAD+, you don't have the ability to do that.

Bob Miller 30:18

So now would probably be a good time for me to swing in another chart here. And it shows all the things that the NAD+ does. So let me bring this guy over here. So here's your NAD+, which we spoke about earlier. But now in this chart, we show the downstream effect. Here are your PARP enzymes—DNA repair. And in our talk on peroxynitrite, we talked about how the peroxynitrite creates the carbonate radical CO3, which oxidizes the guanine. And then here are the sirtuins. SIRT3. And look what this guy does: Turns glutamate into alpha-ketoglutarate, which is energy, helps the urea cycle clear ammonia, and stimulates the FOXOs that makes your SOD and catalase. So are mutations in SOD important? Sure, they are. But if the SIRT3 is not working or it doesn't have enough NADPH, you could have perfect SOD here, and you're still going to be low in superoxide dismutase. So that's why we have to look at this globally, not just SOD mutations. That's important, but it starts all the way back here. NAD+ feeds SIRT, feeds FOXOs, feeds SOD. So that's why I believe this NAD+ is so important. 

Bob Miller 31:51

But hang on to your hat. Look what happens here: SIRT3 supports autophagy. SIRT1 inhibits mTOR. We talked about this imbalance of mTOR and autophagy. An inadequate NAD could actually be one of the contributing factors to this imbalance between mTOR and autophagy. And as you said, mTOR replicates cells. It's like a copy machine. It doesn't care whether it's a healthy cell, a cancer cell, or a virus; it replicates it. And these two have to be balanced. There are many factors that go into this. Like, over here are those enzymes we spoke about, and AMPK. There's a lot that gets involved in here. Nrf2 regulates them all. But for now, we're just pointing out how a lack of NAD could lead to an imbalance of mTOR and autophagy. 

Dr. Jill 32:49

Quick question, Bob, for clinicians like myself. I'm assuming insulin-like growth factor in the blood would be a way to measure, like, an offshoot of mTOR. Is there anything else—if we were measuring in the blood, serum, or urine—that would tell us the status of mTOR versus autophagy in a real-life patient in real time? 

Bob Miller 33:08

That's the only one I'm aware of. But I'm hoping that we're going to learn more as time goes on. Now, again, the 3D chess game. The sirtuins that we talked about do all these protective things. PARP is needed to repair your cells. So the more you damage your cells with peroxynitrite or other agents, the more your NAD gets tied up in PARP and is not available to SIRT. So not only do we have to make sure we have enough NAD, we also want to make sure that we're doing all we can to minimize damage to the cells. And again, I'd encourage people to go back and listen to that other interview that we did a month ago where we talk about the myriad of ways, even including EMF, that can cause damage from peroxynitrite. And here's just showing how peroxynitrite stimulates PARP activation. So when the body makes that peroxynitrite, it says, “Uh-oh, damage is occurring”—PARP comes in. Again, what a miracle we are! God put us together with the miracle of being able to repair. But if we overwhelm that with too much peroxynitrite, we just can't keep up. And that's when people break down quickly. 

Bob Miller 34:24

You know, I'm sure we've all seen people that are, say, 50 years old. And somebody looks like they're 35, and another one looks like they're 70. The difference is the oxidative stress on the cells and the ability to repair. So again, that's why I'm a big fan of NAD. Now, we already spoke about the production of it. I just thought I'd show that one more time. These are the steps. And these are the genes, TDO, IDO1 and IDO2, tryptophan, kynurenine to quinolinic acid, QPRT, a big one. Grape seed extract, interestingly, [may provide] skin support. So it's amazing how people can reduce their anxiety and make more NAD just by [taking] grape seed extract if they've got mutations in QPRT. These are your final steps. And I already spoke about NQO1. And interestingly, there's an old herb from South America, Pau d'Arco. It's a source of beta-lapachone, which supports that conversion. I've seen many people who have tremors and other things improve dramatically when they start taking Pau d'Arco. 

Dr. Jill 35:36

Bob, I love that. I just want to comment again. [From a] clinical perspective, quinolinic acid is a bad one. I always hate to see that, especially with neurological and neurodegenerative diseases. We can actually measure in the urine kynurenate, quinolinic acid, and 5-HTP metabolites and see what's happening here. But just like you were mentioning there, I find it hard in clinical practice to say, “What can we do to stop that fire?” It's a fire on the brain, a fire on the nervous system. You mentioned grape seed. That's a powerful one. I've heard that magnesium and NAC may have some… Is there anything else that we could do with quinolinic acid from a nutritional perspective? 

Bob Miller 36:12

That's all I'm aware of. Now, here's why it's so important that we understand this: If you just start taking nicotinamide mononucleotide or nicotinamide riboside and you're stuck up here, you can actually make things worse. Just a quick clinical study; I had a gentleman with tremors. Nothing medically worked. I mean, they were ready to put probes in his brain, which he wasn't too excited about. We put him on Pau d'Arco [and saw] about an 80% improvement. Then I said, “Okay, let's put a little bit of nicotinamide mononucleotide in,” and as soon as we did, the tremors came back. So, we actually had to back off here and just keep going with Pau d'Arco. So, that's why it's so important to know if you've got NQ01 mutations, because you can think you're doing well by throwing this in because we all know the benefits of it. But if we're stuck here, we can make things worse. I hate when that happens.

Dr. Jill 37:09

Yes. I love putting these clinical things in because, again, I'm a wealth of guinea pig experience. When I first got NAD, I was like, “Wow, this stuff is amazing!” And I felt so good. And just like you're talking about, you need folic acid, NAD, and all of these different pathways. Well, again, as we already know from the comment I mentioned before, I tend to be lower on my methylated B vitamins, or historically have been. And after about a month or so, I started feeling more tired, more depressed, and more [like I had] a lack of stamina and energy. And of course, as you know where I'm going, I was depleting my methyl donors. And so patients who are more, I would say, fragile—although I don't like that word—like myself, kind of walk this fine line. I find it's really important to make sure they have TMG, methyl folate, methyl B12, a few of the methyl donors, along with… Especially nowadays, we're pushing really high doses of this. So you've got to make sure you have… Any comment on that? Is that an experience you've seen happen as well? 

Bob Miller 38:05

Oh, absolutely. People who are low in methyl groups—I mean, this really is a form of niacin—so you do need the methyl groups. And again, that's for the people who are undermethylators. For people who are overmethylators, it probably helps them by depleting some of those methyl groups. Again, one size does not fit all. Everyone is unique. 

Dr. Jill 38:25

So besides the MTHFR gene, are there any other things you look at with undermethylators versus overmethylators? Are there a few of the top genes you would look for with that? 

Bob Miller 38:34

Well, yes. I mean, COMT uses… Let's just take a quick peek here. So COMT, catechol-O-methyltransferase, needs SAMe. So if you've got a lot of mutations here, you may not be using the SAMe, possibly putting your methyl groups up. Now, I don't have a chart on this, but SAMe also turns into creatine, which is needed for your muscle strength. So if you've got mutations in the genes that make the creatine, you can also have excess methyl groups. And then, conversely, if you've got difficulty with your MTHFR, MTR, or MTRR, you may not take this homocysteine back up through, and then you'll be low in SAMe. 

Bob Miller 39:23

Now, everyone looks at MTHFR, but you've got to look a little bit deeper. You've got your folate receptor sites, your DHFR, your MTHFD1. Is MTHFR important? Sure. But I've seen people with MTHFR mutations, and they're doing just fine. I've seen people without them, and they're not because the problem is way over here. Or, you might be chewing up all your methyl groups because you're desperately trying to have histamine and methyl transferase get out all this histamine. So if we don't have enough COMT activity, this is where your dopamine comes in. Now, look what weakens COMT: Quercetin—so for some people, if their COMT is low, quercetin can make them worse—estrogen. And of course, we're living in a sea of estrogen and tyramine foods like cheese. Interesting. 

Dr. Jill 40:22

Yes, I've got another quick example for that. So I love my quercetin when I have allergies. I remember when I used to take that, and all of a sudden, in my cycle, I'd get breast tenderness, Bob. And guess what? I was inhibiting COMT and creating less detoxification for my estrogen. So I realized that for me, again, there was a very fine line between too much quercitin and not enough if you have a COMT mutation. 

Bob Miller 40:44

Absolutely. And then your testosterone supports COMT. So what's happening in the world today? We're living in a sea of plastics, we're swimming in estrogen. And when I talk to physicians who specialize in hormones, they tell me that, particularly in young men, testosterone is dropping. And that's possibly why. When you talk to college professors, you say, “Tell me about the freshman coming in.” “You know, they're sensitive. They get upset quickly. They anger quickly.” Well, if you're not clearing your dopamine, that could be happening. There are many factors. Before we started the show here, we talked about how people are getting so angry. Speculative here, but perhaps if this is being weakened, we're not clearing our dopamine, and people are just getting angrier. I mean, it's clearly multi-factorial, but that could be a factor in what's happening. 

Dr. Jill 41:34

And stress will affect COMT because you're going to produce more of those hormones too, so that's probably a factor we're seeing right now in this environment as well. 

Bob Miller 41:42

Sure. Absolutely. Spot on. G6PD is extremely common in people with Italian backgrounds, particularly Southern Italians, Native Americans, and Africans. It is very, very common for G6PD mutations, which make your NADPH. And interestingly, just a clinical observation: When people have northern European descent and they make a lot of free radicals from iron, and they also have southern Italian [descent so] that they don't have enough G6PD, these are the people that are often very inflamed that nobody can seem to figure out. A pattern that we see all the time: Excess hydroxyl radicals, G6PD mutations. Interestingly, I'm in Lancaster County, Pennsylvania, where I work with the Mennonite and the Amish. And there is one group called the Martins that… Well, let's back up. The Mennonites are primarily Swiss German. However, there were three brothers whose names were Martino from Sicily who converted to the Anabaptist Mennonites, and their ancestors had these G6PD mutations. So when I talk to people in the region, I'll say, “Is there a Martin in the background?” And they're like, “Okay, how did you know that?” 

Dr. Jll 43:06

Wow, now, Bob, this goes really close to home because I grew up in Central Illinois. Apostolic Christianity was the background of my family, but they were close, close Swiss-German Mennonite relatives. So it's very, very similar to my background. I know that group; I know those people very well. And I know that these mutations do exist, and we have a lot of Martins that were neighbors. So it was very fascinating to hear that today. 

Bob Miller 43:28

Yes, Martino. You'll notice— 

Dr. Jill 43:32

I'm sorry. Go ahead. 

Bob Miller 43:33

No, go ahead. 

Dr. Jill 43:34

Well, I wondered too… So with the G6PD, we talked about southern Italy, and in my studies, it seems that there is a correlation with the complications and infectiousness of COVID in relation to this gene. Do you have any insights into that? 

Bob Miller 43:49

Well, sure. Let's think about what that does. That recycles your glutathione. Well, not the G6PD, but the NADPH. So it's a purely speculative hypothesis that the more G6PD variants you have, the less you're going to be able to recycle your glutathione, and the more likely you might be for that cytokine storm. Again, this is potentially a hypothesis: Maybe this is why African Americans have more trouble because the G6PD mutations are significantly higher in African Americans. 

Dr. Jill 44:22

Yes, again, it's really speculative. But that was my thought with Italy, and the real difficulty they had in the beginning—I bet there's this genetic variant that's playing into that as well. 

Bob Miller 44:31

Yes. Well, keep in mind that Southern Italy, particularly, was closely tied to Northern Africa as people migrated over. ME1 is also involved. IDH is also involved. So mutations in any of these could impact your NADPH. And again, I just summarized them here—the genetics involved in that production. So how can we support it? Niacin, nicotinamide riboside, nicotinamide mononucleotide, grape seed extract for that quinolinic acid to NMN, and/or Pau d'Arco for the NADH to NAD+. 

Bob Miller 45:06

Now, phase one detox—maybe people have not heard of this, but there's something called the cytochrome P450s. They're the very first step in detoxification. What they do is take toxins and make them into something fat-soluble, and then phase two comes along and puts them into water-soluble. Look who we have here: NADPH is needed for that cytochrome P450 to work properly. So everywhere you turn around, you see NADPH. So if you don't have enough of that, even your phase one detox may not be as robust. We spoke a little bit about glutathione conjugation. And the GST is the glutathione S-transferase. This is what takes the byproducts of CYP450 and turns them into something water-soluble. So if you have any mutations in GSTs, that's not going to work very well. 

Bob Miller 46:05

So here you can see what's happening here. Here are your CYPs, making your xenobiotics. And then your GSTs, through phase two glutathione conjugation, put these toxins into stool or urine. But what do they need? They need glutathione, the proper function of GLRX, and you need the master control, Nrf2, and Keap1, telling everybody to do their job properly. Now, once again, after it does that, it's oxidized. We'll go on and make peroxynitrite if we don't. And here's our NADPH once again [coming] to the rescue to bring this guy back. So if we don't have enough NADPH, even this phase two glutathione conjugation won't be working. And this is one of the pathways through which we take out many toxins, particularly mold. And I know that's something of tremendous interest to you, Dr. Jill. 

Dr. Jill 47:00

Yes, fascinating. It's so important. 

Bob Miller 47:05

Oh, and these are just some of the genes related to glutathione production. Now, I jumped ahead, but I'll just take a peek at this again. Many people, particularly English, Irish, and Norwegians, have genetic mutations where they overabsorb iron. Interestingly, this was by natural selection during times of famine. The people who overabsorbed the iron were healthy enough to have babies. So in times of famine, overabsorption of iron was helpful. Today we don't have famine. We put a lot of iron in foods. So if you have that genetic predisposition to overabsorb the iron and then you don't clear the hydrogen peroxide, [it can lead to] hydroxyl radicals. 

Bob Miller 47:50

Now, this is what we're going to talk about in a month, but I just wanted to give a preview of what's coming up. There's a fascinating enzyme called NADPH oxidase, or NOX. Interestingly, it's got one job: To make the oxidizing agents superoxide and hydrogen peroxide. Now why would we want to do that? When we're hit with a bacteria, a parasite, or some other pathogen, again, God put in us the ability to put on a fight to kill. So that's why all free radicals are not all bad. If we didn't have NOX, we would die of inflammation. It's helpful. However, overexpression or overactivation plays a major role in oxidative stress and premature aging. So we have to, again, have everything in balance. Too much of anything can be harmful to us. So if we have increased cardiovascular disease, neurodegeneration, organ failure, cancer, and even autism… Here is a study that said that targeting these reactive oxygen species sources with natural compounds may be an important tool. Now, here you can see—this is what we're going to get into in a lot of detail in our next talk. 

Dr. Jill 49:11

I was going to mention that I'll put this on as well, Bob. If you're listening, stay tuned: August 28th. It's about four weeks away. The same time, 3 p.m. Mountain, 4 p.m. Central. We'll be back, and this is what we'll be talking about on August 28th. 

Bob Miller 49:25

Yes, and the reason I wanted to point it out now is that I don't want someone to listen to this lecture and say: “Boy, I see all the importance of this. I'm just going to start taking some NAD+.” Because what can happen, as we said, is that NADPH does all those good things that we talked about; however, when we're hit with a pathogen, the NOX enzyme says: “Hey, we've got an invader here. Iron, give me some oxygen. NADPH, give me an electron. Let's make some superoxide, hydrogen peroxide, stimulate the mast cells, stimulate some cytokines, some interleukins, and histamine, and we're going to kick up a fuss here and we're going to kill this pathogen.” Is that needed? Absolutely. Without it, we die of infection. So what we're going to talk about in August are all of the epigenetic factors. We'll look at the studies on them that can artificially upregulate this, kind of like the military that starts shooting the citizens rather than the enemy. 

Bob Miller 50:29

And look who is here: Nitric oxide and oxytocin. They actually calm it down. Now, this is our latest research, and we've just started to talk about this, so your people are some of the first to hear this. There's a substance called renin that is produced in the body to stimulate something called angiotensin-1. And then the ACE enzyme makes angiotensin-2. And that's why sometimes—I'm sure as a physician—you give people ACE inhibitors for their blood pressure. Then it makes something called aldosterone. And aldosterone causes you to hold on to sodium, excrete potassium, and hold on to water. But it stimulates NADPH oxidase, which then stimulates superoxide, stimulates hydrogen peroxide, stimulates mast cells, and stimulates histamine. And again, when we've got a pathogen to go after, that's a good thing. But if this is running rampant, this is where we create a problem. 

Bob Miller 51:36

By the way, I've put down here that COVID comes in using ACE2. And ACE2 takes angiotensin-1, an angiotensin-2, and turns it into angiotensin-1-7, which is anti-inflammatory. Now, hold on to your hat. High glucose, peroxynitrite, histamine, dopamine, and mast cells all stimulate renin. And if you have genetic mutations in renin, it overreacts. If you've got a genetic weakness in ACE2, it runs faster down this pathway. And I believe this research that we've done here is very clinically significant. 

Bob Miller 52:22

Let me first say that I call this the ‘NADPH steal.' I've given it this name because when the NOX enzyme is overstimulated, the NADPH, in a sense, is stolen away from all of its other good functions. So what do you think happens if NOX is upregulated and somebody also has a genetic weakness where they don't make enough NADPH? They're inflamed, and they can't detox. I'll be presenting this at some other medical conferences, but I think this is very clinically significant. I found literature on this; we just didn't come up with this on our own. There's peer-reviewed literature that shows that peroxynitrite stimulates renin, mast cells stimulate renin, and histamine stimulates renin. So what do we have here? A vicious cycle of inflammation. 

Bob Miller 53:17

And I've just come up with the name, the ‘Holmes cycle.' This is somebody who was a relative of mine and was influential. So I'm going to call this the ‘Holmes cycle' of these three guys coming down, stimulating renin. So what does this do? This just feeds on itself. So the more peroxynitrite we make, the more aldosterone [we make]. The more mast cells, the more aldosterone. The more histamine, the more aldosterone. This thing just feeds on itself. And of course, I know you're a big fan of making sure we have enough mycotoxins. Well, the mycotoxins stimulate the mast cells. Lyme stimulates the mast cells. So all of these things can kick this off. And that's why I believe some people are told that their Lyme disease might be gone, but they still feel horrible—purely a hypothesis. But I have to wonder if this thing is just not feeding on itself. 

Dr. Jill 54:10

Bob, that makes so much sense. I love this, and I'm so excited that we get to hear your brilliance here today as some of the first listeners on the topic because I know this is going to be big. Now, one thought is that we can measure aldosterone in the blood, and I've done that. And you and I have talked about different patients and said, “You know what? We should probably measure.” Do you know if we can measure renin? 

Bob Miller 54:30

Yes. And I don't know what they are, but apparently, there are proper ratios that should be in place. So again, mutations in renin will cause it to be overactive. Mutations in ACE2 will cause this to be underactive, and then we're stimulating NOX, and off we go. 

Dr. Jill 54:49

And then there's the IL-6 in there too, which is a big player with COVID, which is a big player with many of my inflammatory patients, and also is a genetic issue too, for people. 

Bob Miller 54:58

Oh yes. You can have genetic mutations in IL-6 that are up-regulation. And I was just going to point out—it's a little hard to see here—that angiotensin-2 stimulates IL-6. IL-6 stimulates NOX, and then NOX stimulates IL-6. Feedback loops all over the place. And I don't have it on here, but vitamin D helps calm down IL-6. And then HMOX, or heme oxygenase, also calms down angiotensin-2. So mutations on here can be a problem. And heme oxygenase also calms down mast cells, as well as luteolin. So I think we may have come across something very significant here as to how these patterns occur. 

Bob Miller 55:42

Now, purely [as] a hypothesis, [it's] speculative: When a child gets strep throat and perhaps starts this up, could that be a factor in why they go into PANS/PANDAS? I have no idea, but I'm just throwing that out as a hypothesis. Does something like that kick this off? And do many of the people who are inflamed and can't seem to get out of it, possibly going into that cell danger response, have this going on? So again in August, we're going to dig into histamine, oxalates, iron, and glutamate and how all of them stimulate NOX. And then we might talk a little bit about interleukin-13 because when interleukin-13 is stimulated, if it's mutated, it actually comes back and makes more mast cells. And then, if we have difficulty breaking down histamine, we can't break down that histamine. So again, the 3D chess game played underwater—so many moving parts. 

Bob Miller 56:39

So one of the things we're doing is experimenting with things that support ACE2, superoxide dismutase, things that calm down the mast cells, and things that calm down the histamine, preliminarily [with] very, very good results. So stay tuned. This is not a hypothesis. There are peer-reviewed papers on all of this. But the hypothesis is: Is this something that's common that feeds upon itself? And we've got to continue to research that, but my hunch is that it is. 

Dr. Jill 57:13

Gosh, Bob, I love this. This is so practical. And again, as a clinician, you treat some of the toughest cases in the United States. This is the kind of stuff that we, as clinicians and patients, need because it is a game changer. And if I were to kind of summarize—a big picture thing—I remember 10–20 years ago when I started, I would get a patient coming in with hypothyroidism, Hashimoto's, menopause symptoms, or a sore throat. Simple  and straightforward; we'd do an intervention, and within two or three months they were better. I never see those anymore. And part of it is the complexity. But part of it is what you just laid out here at the core, [which] is the infectious burden and toxic load in our environment. 

Dr. Jill 57:52

How I see it, the toxic load, whether it's EMFs, chemicals, estrogen disruptors—endocrine-disrupting chemicals—all of these things are getting more and more in our environment. The stress is [getting] more and more [severe], and our food supply is [getting] more and more adulterated. And then we have these old underlying infections. Number one, tick-borne infections are getting more prevalent because the encroachment of the types of vectors that carry ticks are coming into the city areas, and the city areas are coming out into that area. So most of the swaths of places where you can get them now are widening. 

Dr. Jill 58:26

But all that to say, this toxic load is weakening our system, allowing old infections or new infections to become a bigger issue. And no greater example exists than right now with the pandemic. Part of the reason it's such a big deal is that our systems are weaker than they used to be 100 years ago. So all that just to put it into place—that toxic load, infectious burden. But I don't want to leave you hopeless. Great researchers like Bob are finding us answers clinically. And there are ways to decrease inflammation and change these pathways. So thank you so much for bringing this [information]. And yes, I wanted to mention the conference. Tell us about the conference coming up. 

Bob Miller 59:04

Yes, September 18 to 20. We were going to hold it live, but of course, now we can't because of COVID. We're so thankful you're going to be one of the speakers. But Stephanie Seneff, who is brilliant, is going to be talking about a fascinating subject, and that is deuterium and how to get deuterium depletion and how that's related to some of these inflammatory pathways. She's doing new research that she's going to present for the first time. Neil Nathan—you know Neil from his [research on] mold. Sandeep Gupta, from Australia, [will be] speaking on mold remediation. Two of the people at NutriGenetic Research have actually done literature reviews on the pathways that clear the mycotoxins—in other words, various mycotoxins—and which pathways might need to be supported. Of course, this histamine wears out the adrenals. Joel Rosen is going to speak about that. Mackay Rippey—again, part of the research team—is going to be talking about IL-13. Bill Shaw from Great Plains—mycotoxins 101. A new good friend of mine, Andrew Campbell, is going to be talking about mycotoxins and illness, and some of his testing. Beth O'Hara [will be speaking] on [the topic of] mycotoxins and mast cells. Emily [will be speaking] on [the topic of] oxalates—the relationship there. And then I'll be talking about the cytokine storm. So, since it's across the United States, we're starting at 8:00 a.m. Pacific, 11:00 Eastern. So, the people on the west coast don't have to get up too early. Three days and $385, which we think is very reasonable. 

Dr. Jill 1:00:34

Very good. Bob, I can't wait! I'm excited to be part of it. I'm writing my book, which will be out in about a year. So I've been very selective about who I've said yes to, and you are among the top because I love what you do. I love your platform. I love the information you're bringing. And you always bring together really, really quality information. So thanks for what you do. 

Bob Miller 1:00:55

Absolutely. A final thought here: If someone wants to talk to our clinic, here's our phone number. If a doctor is watching this and says, “You know, I'd like to do this genetic work,” there's the website for online certification. Here's our technical support and the supplements that we've made. Again, health professionals only; they're not available to the general public. So if somebody wants to learn this, I have a lengthy online certification course that teaches functional genomics. What a blast this has been, Dr. Jill, like always!

Dr. Jill 1:01:29

As always! It's so much fun. Thanks for going down the rabbit trails with me to get some practical information for people listening. I was looking at questions and also trying to monitor that as we went. Thank you, as always. I hope you guys will join us next month. And, Bob, have a great afternoon and evening. 

Bob Miller 1:01:44

Okay, my pleasure. And I'm looking forward to the next one.