Habits and Hustle - Episode 129: Charles Brenner – Discovered Nicotinamide as NAD Precursor, Dept. Chair at City of Hope

Episode Date: August 17, 2021

Charles Brenner discovered Nicotinamide Riboside as a NAD Precursor and is the Alfred E Mann Family Foundation Chair in Diabetes and Cancer Metabolism at City of Hope National Medical Center. A “scientists’ scientist” Charles isn’t afraid to ruffle feathers in the defense of scientific truths. If it doesn’t have scientific backing in a legitimate peer-reviewed essay with double-blind studies and placebos Charles doesn’t want to hear about it. He explains his own scientific breakthroughs, the possible future for his work, and a bit of the new studies that have recently come out on the subject, while also answering Jen’s questions about the latest fads that may or may not have any scientific backing. Intermittent fasting, “calories in; calories out,” longevity, and more. Charles is the real deal. You won’t find him caving to the pressures of what’s “in” at the moment or who might be paying off who. He’s here for the science and science alone, and I hope you’re ready, cuz that’s exactly what this episode’s about. Youtube Link to This Episode Charles Brenner’s Twitter – https://twitter.com/charlesmbrenner Charles Brenner’s Instagram – https://www.instagram.com/charlesmbrenner/ ⭐⭐⭐⭐⭐ Did you learn something from tuning in today? Please pay it forward and write us a 5-star review on Apple Podcasts. 📧If you have feedback for the show, please email [e-mail]  📙Get yourself a copy of Jennifer Cohen’s newest book from Habit Nest, Badass Body Goals Journal. ℹ️Habits & Hustle Website 📚Habit Nest Website 📱Follow Jennifer – Instagram – Facebook – Twitter – Jennifer’s Website Learn more about your ad choices. Visit megaphone.fm/adchoices

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San Antonio, Texas. I got his Tony Robbins you're listening to Habits and Hustle, fresh it. On Habits and Hustle today we have Dr. Charles Brenner. Dr. Brenner is one of the world's foremost authorities in the emerging area of NAD. NAD is a molecule that is critical to the healthy function of the trillions of cells in our bodies. He serves as the Alfred E. Mann family foundation chair in the newly created department of diabetes and cancer metabolism at the city of Hope. He is also the chief scientific advisor to Chromodex,

a global bioscience company behind the popular NAD boosting supplement called Tru Nijin, which, of course, I'm a huge fan of and talk about all the time. Among his most significant discoveries in 2004, he identified Nicotinamide riboside, otherwise known as NR, as a precursor or a booster of NAD levels. His pioneering research has paved the way for NAD research around the world. So without further ado, here is Dr. Charles Brenner. So let's just go from the beginning. So what is, I mean, I've been a huge fan of NAD. I've been

taking true nitrogen for two years at least. And people always ask me what it is, and I describe it, and still there's some confusion. So in the laymins of laymins terms, can you explain what NAD is and what the purpose of it is? Yep, yep. So NAD refers to four things inside of cells that are called coenzymes. They're the central catalysts of metabolism.

So metabolism is the set of processes that allows us to convert everything that we eat into everything that we are. Not only produce the ATP biological energy that runs our bodies, but our cells have to make their own DNA, RNA, and protein. Our cells have to make their own DNA, RNA, and protein. Our cells have to prepare themselves. We don't eat bone in order to make bone, right? We don't, right? We can choose to eat liver or not,

but we generate our own hepatocytes no matter what we eat. Right, right. So all of those processes are metabolism. And metabolism is the key to life. It's what the difference is between living things and non-living things. And what we found over the years is that NAD comes under attack in conditions of metabolic stress.

And so that's the use case for taking what are called the vitamin precursors of NAD. And probably I can ask you and I in 2004 discovered the vitamin activity of NR. That NR is an additional unanticipated vitamin that can allow ourselves to rebuild NAD and basically help, you know, basically help everything run in the body. Okay, so let me just, like, kind of interject a little bit, right? So because NAD is something that we all have in our body, right? Yes. And so when I describe it to people, I always say something, because this is how I believe it to be,

is that as you age, the levels of your NAD levels decrease, which makes it's basically connected to your mitochondrial function, correct, and then that decreases, which is why having a high supply of NAD in your body is really important. What am I missing? Well, it's close-ish. Yes. Right. So, yes. So, yeah, there's a lot of reports of NAD declining in aging.

I would say that we don't fully understand that story of in which tissues NAD is declining by how much and how that occurs. The way we see it in our laboratory, and when we look at the quality of the data, we really see NAD coming under attack at the NAD system being constantly barraged by conditions of stress. Right. So, for example, we live in the air and we go outside in the sunlight. Those are two things that attack the NAD system. Like oxidative damage, reactive oxygen species from oxygen, churns something called NADPH, which is one of the NAD coenzymes.

Sunlight breaks our DNA, NAD plus comes under attack. The net result of all of those things probably is that NAD is declining and in all our tissues is a function of age. So that's probably not wrong. And probably not wrong. Probably not wrong. I'm cautious. I'm cautious, I try not to get ahead of my skis.

Yes. Because I don't think that aging is one thing. I think that NAD isn't even one thing. It's four things. And so I don't like to make outlandish claims that we can't prove what we see in the laboratory is we see very powerful effects of NR in animal models, right, in mouse and rat models. So we see protection against heart failure, we see protection against neurodegeneration, we see protection against alcoholic conditions in animals, we see better exercise functions, so forth and so on.

And then that is what's called hypothesis generating. So then we can go into human beings. And in human beings, we've seen anti-inflammatory effects of NR, we've seen NR in a combination of supplements, accelerate time to recovery from COVID. Right, right. I mean, I have all these things. I mean, that's the thing that I find.

So, because I lot of people, like a lot of times, and I know because you got, you especially are very, very anti, like making, you know, the claims of like it being a magic pill or you don't like when someone says it's anti-aging or aging in reverse because it's not exactly scientific. It's not evidence-based. I mean, the thing is that's how it's being sold, right?

Like that's how people understand it. So that's like the simplest way to understand it. Yeah, maybe. I would say that legitimately, protection of NR, in different tissues protects cellular and tissue function, enhances resiliency, repair. NR is a, you know, we went through a process where there were patents and, you know, Chromedex, as you know, as I think you introduced me, decided to, you know, develop NR as a nutritional supplement as an ingredient. And then when, um, is NR the main? So I know that you, because you also are the first to create NR as a supplement,

like you just said, um, what is an, and what is a precursor? So what does that mean to me? Yeah. So basically, so NAD are these four things inside cells that are co-ensives. And like most many, many molecules and cells have what are called phosphates in them. And the phosphates are put on inside of cells. So there is no vitamin that has the phosphates

already on, right? And NR is the biggest piece of NAD that can get into cells, right? So it's the biggest piece of NAD that cells can use to make NAD, right? Nobody can produce it on its own. Well, so yeah, because it's what's called, I mean, it's the key part, right? So, you know, our bodies will make an AD just the same way a cow's liver makes an AD and livers a great source of an AD, by the way. It is?

In part, because it has so many mitochondria, right? It is. It is. It is. It is. It is. It is. It is. It is. It is. It isrosmilk, we showed that a number of years ago. Foods really living things, whole foods with a small W and a small F, contain NAD coenzymes in them. So minimally processed foods when you're eating them really have big supplies of NAD in them. The NAD breaks down in our digestion, the NAD breaks down into the vitamin precursors

that are then used in order to rebuild the NAD supply. Oh, okay, yeah. Now, with age and metabolic challenges, and you don't have to be really old like you could be a 22-year-old football player and feel like, you know, NR supplementation gives you an edge and allows you to repair after all of this contact and so forth and protects against, you know, the effects of the sport. When you are eating food, your food is being broken down into these NAD precursors. You're using those precursors to rebuild the NAD supply, supplementing with the vitamin precursors,

basically enhances that process. But it's true that there's NR in milk, but really the source It's true that there's NR in milk, but really the source of NAD precursors in food is really NAD. So it's a cycle of life. Living things have NAD in it. They also have macronutrients, protein fat and carbohydrate, they have micronutrients. Everything gets broken down, everything gets rebuilt. The rebuilding process

is metabolism. NAD is critical for metabolism, right? And NAD gets challenged by metabolic stress. So the use case for NAD precursor vitamins is that it allows you to keep your NAD stores full, resistant to these challenges, which even include things like coronavirus infection. We've shown in the laboratory that that attacks the NAD system. But like also with the longevity thing, I'm just gonna go back to those things.

Because yes, you can't make a longevity claim, however, it helps with your resilience, it helps with recovery, it helps with your cellular health, it helps with being tired, with our energy, all those things decline as you get older, right? Absolutely, the old declines are repaired to climb as you get older and all those things decline. So my hypothesis would be,

So your hypothesis is that it's engaging, but I'm not gonna say that because I can't test that. I know you can. And actually no one else can really either, right? So the actual trials are done in conditions of metabolic stress. So like you can enroll people, right? And you can have an anti-inflammatory thing as an endpoint. You could see whether NR lowers those inflammatory markers.

You can get a definitive answer to that in the course, actually in three weeks. There was a study in Birmingham, UK, that showed that in three weeks older men, placebo-controlled trial, had lower inflammatory markers if they were on NR. It even persisted after they switched over and were on the placebo, the fact that they had had been on NR, their inflammatory markers were still low. See? Right, so that was impressive, right? But you score that result as a win, right?

Yes. You don't go back, you can't, you don't have the money to test them for their survival in five, 10, 20 years, right? So that's why effective longevity trials, you know, are not practical, they're not really being done. There's something called the Metformin team trial.

I was gonna ask you about Metformin also. Yeah, I'm not a fan. I mean, so the thing is the data show. Explain what Metformin is for people who don ask you about Metformin also. Yeah, I'm not a fan. I mean, so I the thing is the data show explain what Metformin is for people who don't know what Metformin is. It's basically a diabetes drug. Right. A lot of people take it for longevity and anti-aging. So that's not, in my view, what? Why? Why? Because it's actually inhibits mitochondrial function. It literally, you just, you said that you were understanding, okay, as a fitness person, is that NR and NAD is good for mitochondria.

Right. So I could show you data that metformin depresses mitochondrial functions. How do you feel about it now? Okay, well, this is why I wanted to have you on so badly because there's such conflict, like, one person says, one thing, and I'm not the scientist. I had, I had, you know, I had Davis Tinc there's such conflict, like one person says one thing and I'm not the scientist. I had, I had, you know, I had David Sinclair

on the other a while ago. And he was talking all about NAD as being, you know, a longevity drug. He takes it every day, also met for him and we talked about as well. And, you know, people build their platform and business around using words like anti-aging or longevity because A, I think, is easy and palatable for people to understand.

But you're like the antithesis. You're like a scientist, scientist, unless you have clear, exact, I'm going to guess what every, that's how I'm going to say it. I don't want to say it, right? You're both zero. I mean, the thing is that I actually think that high parts. And the metformin and repamysin thing

may be out, maybe a great example of that. So you're taking drugs that are indicated for people that have conditions. So metformin is used as a diabetes drug. It helps people that have diabetes control their blood glucose. Blood glucose levels. Right. That's important, right? And, you know, Rapunmyson was, you know, developed as an immune modulator

that will allow people to do, you know, that avoid graph versus hose and other things. I really don't wanna take something that is gonna depress my immune system, right? Then some of the, you know, the rapamycin fans come out and say, well, you know, it's immune modulating, it's upregulating this and then it's downregulating that.

To me, it's not, you know, it's something that's sure it's being tested in dogs. It there's a lot of data on mice, but I don't think that I think it's easily demonstrable that prescription drug use is associated with shorter life spans. It's easily demonstrable that for thousands of years, the claims that people have made about fountains of youth and anti-aging have been wrong and not evidence-based. So I'm just, generally my starting position is gonna be, I'm gonna take the other side of that bed.

Okay, well I like, okay, so good. So I'm gonna go through a few of them. So you said already, so met Foreman, because people, I think it's more of like a biohack, right? People are using it more for bioh, they think if they're regulating their blood sugar, that will help them with long-term- What if they-

How? The why are they taking, what is their, what is the other sides? Some of those people are also keto and exactly and then usually they are or are intermittent fasting. Do you like intermittent fasting? Well, you know, it's extremely powerful in in mice, but of course, course, you know, a mouse has a much more rapid metabolism and you know, hour per hour comparisons of fast are much more severe in a mouse than they are at a human, right? And so, you know, some of that stuff doesn't actually translate. So for example, Ethan Weiss, who's a very accomplished cardiology professor at UCSF, actually practiced intermittent fasting for seven years. He believed in intermittent

fasting. He set up a very wise, well-controlled clinical trial of intermittent fasting versus non-intermittent fasting, and basically could not demonstrate a benefit. So I think that the intermittent fasting idea is, you know, science-y, and I think that it's very evidence-based in mice, the idea that, and personally, for sure, over nutrition, over eating is bad and associated with obesity and type 2 diabetes and, you know, orthopedic problems, sleep apnea, you name it, right? And a lot of bad outcomes and a lot of shorter health spans, life spans. But that doesn't mean that fasting

is necessarily going to be a life span extending thing. For me, I think that I'm a breakfast person. Okay, so I get up, I have black coffee, I have breakfast, and then I can work, I can exercise, I can function fine. I don't eat too late at night. I think it is important to have the hunger cycle in there, but absolutely am I on the clock about feeding, fasting, no.

No, that's not a practice of mine. What about the how about, that's why I like love having you on. It's like you're the opposite of what so many scientists, doctors have said on the show. What about a pathology? Wouldn't mean a pathology.

Okay, so a pathology, fascinating molecular mechanism, right? So the idea in a topogy is that, you know, there are cells that have too much stuff and some damaged proteins and stuff like that. And so with some, you know, sort of nutritional deprivation, they turn over some of their molecules and then they kind of get refreshed and stuff like that. Absolutely, we know that that's a mechanism in the lab. When people say, oh yeah, I'm fasting and my levels of this and that are set and such.

And so I'm kicking out my autophagy. I think it's kind of babble. You know, there's no measurement of their autophagy. And strangely, strangely enough, some of the same people that take, you know, rapamycin, right, are also taking like lucine and luc and losing related amino acids, that whose biochemical effect

is to stimulate the tour pathway, in order to make more muscle. Yeah, make more, yeah. And they're literally taking losing, which is gonna like stimulate tour, and then they're taking rap but my son, which is gonna inhibit tour. It's sort of like too many drugs, too many supplements and it makes no sense. It's like basically doing too many different

diets at the same time. It gets it's all basically counteracting each other. Yeah, it makes no sense. That's basically it. Okay, so then how about, okay, metaphor when we got res vera trough. Res veras wrong. Reservoirs wrong. Yeah. So, Reservoir is a perfectly nice antioxidant, right? It's found in grapes, right? It's also found in peanuts. And you know, people have, it has a lot of, you know, proteins in human cells that it, you know, associates with. There's a lot of proposed mechanisms for beneficial effects of it. There's a lot of things that it does in cell culture. There's a few things it does in mice. I'm pretty doubtful of anything

demonstrated that it does in people. One of the proposed mechanisms of Resvertral is that it binds to a human protein called CERTI-1, it doesn't. And then... It doesn't? No, no, no. So where did this all come from? Because that was, do you remember, that was like the biggest craze, the biggest... Yeah.

Like, think it's always cycle, right? Like, now, I mean, that was... Yeah, it came from a series of, you know, peer think it's always cycle, right? Like now, I mean, yeah, came from a it came from a series of You know pure reviewed studies whose conclusions are not reproducible, right? So it was found initially it was found in supposedly a yeast assay in which it made yeast to live longer, right? right so in which it made yeast to live longer, right? Right. So, and I've used that assay before, and that assay depends upon a yeast gene called Sir 2, and Sir 2 is a perfectly nice yeast gene. The problem is that increasing the lifespan of a yeast is not the same as increasing the lifespan of a worm fly or

mouse or human and all of the subsequent stuff that was said about the sir-to-related genes in in worms turned out not to be true in flies turned out not to be true It couldn't be demonstrated in in mice Resvertral was said to bind to the or not not to be true, it couldn't be demonstrated in mice. Resvertral was said to bind to the yeast, sir to protein, and then to the human, sir, one protein that doesn't do those things. Now there's a paper a few years ago that said,

oh, here's the way it really does bind to human, sir, to one, But if you look at the structure and how it supposedly binds to CERTI-1, if that's true, then it couldn't have been discovered. The way it was discovered by binding to yeast CERTI-2 because they don't have the same amino acid sequences like the protein structure. So the whole thing is a mess, it's a mess. And the people that were convinced to take Resveratrol were really sold a bit, bit of goods. And anybody that is still defending it

is not being evidence-based. Wow, that is unbelievable. Because that was like the big thing that everyone was told to take. Yeah. So basically, all of these are just more, more just like myths, you know, metformin was very... Well, no, no, no, you know, metformin, metformin to medicine. It's a metnobum saying for the uses of longevity for the use of...

Oh, that's not a myth. That's a way... I lost. Also weight loss. People would take it because they thought it would, as your blood sugar is becoming more balanced, you obviously made me lose more weight because you're not having those spikes of cortisol, you know, insulin. No, so, no, so well, the carbohydrate insulin hypothesis has also been pretty much debunked.

And you know, so ited. And so Kevin Hall, tremendous researcher at NIH, has very carefully compared isocoloric diets, total number of calories, that are low fat versus high fat essentially. And according to the carbohydrate insulin model, carbohydrate insulin hypothesis, those diets should not behave the same way because according to the carbohydrate

insulin hypothesis, it's all about carbs driving your insulin to sequester, you know, fat in the adipose blah, blah, blah, and you'll never lose weight with a high percent carb diet. That's just not true. There's thousands of years of history in the Far East in which people had a high percent rice, high percent carbohydrate in their diet, high glycemic index. And they were not overweight and they were not obese. And the obesity epidemic in the Far East is total calorie driven. And in fact, it's an increase in the amount of fat

that is in the Asian diet as more animal products, more meat, more animal fat. It's accompanied by a lower percent carbohydrate, Kevin Hall study, where you look at diets that have very different compositions. It kind of comes down to calories and calories out. Basically, if you're in an energy deficit, meaning you're expanding more energies than you're putting into your body, then you're going to lose weight, so it's about sustainability. It's about then you're going to lose weight, right? So it's about sustainability. It's about if you're going to do a lifestyle intervention, that

is going to, you know, result in weight loss. It's got to be something you can keep live with. Yeah. So if that turns out to be high fat, if that turns out to be keto, and it's a sustainable thing for somebody. Consistency. Then basically, and they are losing weight, they're losing weight because they're in a calorie deficit and because they can sustain their diet. That doesn't invalidate anybody else's experience that is on a low fat diet that can also lose weight. The key is can they sustain that?

You know how many cheat days they have? Yeah, absolutely. Couple of you said the whole thing, because that's like a bad word, right? Like, it's people get very, very mad if you say calories in versus calories out. They think that's too simplistic, right? So if I was just going to eat M&M's and chocolate bars, but keep it at like my calorie count. There's actually data showing that there's a person that ate nothing but baked potatoes for a month or something like that. I can't cite the study. But potato actually has a pretty high satiety number. It does.

It's all about the resistance starch in it. Yeah. And you know, but it is a pretty high glycemic index food. But no fat. It has no fat, right? So it's essentially an almost an all carb. It's full carb, yeah. And, and, and, and, you know, that's for me would not be very pleasant.

I like baked potatoes. I would like to actually put some, you know, sour cream and onion. And why I do olive oil because I'm lactose intolerant, so, but, you know, all the good stuff that you can put on it, it makes it much more enjoyable, right? But, so, calories on plate. Yeah, it is not a mechanism.

Calories in and out is a basically physical constraint on the way the body works, right? Right, right, right. And, but there's a big thing about what people are like, what calories you're putting in, your body reacts different, body composition, all the other things that happen if you have them. So a lot of that stuff is not evidence-based, and it's really not evidence- It's like anecdotal, it's basically anecdotal, as you say. Well, everybody wants to wait their own anecdotes, right? So people that swear by keto

are the people that can sustain that diet. People that swear by low fat are the people that can sustain that diet. And now, basically, I think that 2021 in terms of weight management is gonna go down as the year in which, you know, semiglutide at 2.4 milligram per week was. So semiglutide. So there's something called, um, in crew, they're called, there's a bunch of

different names in Creetans is one name. The others think they're called GLP1 analogs or GLP1 receptor agonists, GLP1 RA. Okay. Okay. Everyone should have their Google opiumatists to this podcast or have like a historic. So I think there might be a trade name and I don't have anything to do with the company. Okay. But the I think the trade name is maybe would go V, but like scientists call it semiglutide. And it's related to something called GLP1. Okay, GLP1 actually helps your body make more insulin. Okay, so the idea that something that helps your body make more insulin could help you lose weight

is already a head scratcher for somebody that thinks that insulin is the enemy. Okay, insulin helps drive body into your adipose and your skeletal muscle. Insulin and all the other hormones, they're all functioning in physiology as something that are your friend until we have a problem and then things can get messed up.

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So remember what I said to you? Let's keep it very lame in terms for these people. To the end for me, those people being me. So the bottom line is. What's the 2021 thing? Semaglutai, basically the way it works is by allowing people to follow through on their intentions to eat less. Basically, at Axen the Brain, at the satiety center. So it acts in a bunch of places.

But I'm a big believer in that. But basically it gets people to feel full, right? To the point that you want it, it's amazing. Actually what the side effect is, right? So the side effect is it can make people feel nauseous. Well, you know that feeling that you feel like late and thanksgiving dinner. Yes.

When someone brings out of the kitchen, the third pie, like the pecan or whatever, but you already had the apple and the pumpkin, right? Yeah, absolutely. And you would have loved that pecan like two pies ago. Yes. But there's a point where it's like, no, you know. Right.

Yes, yes. So it turns out that people don't have, you know, the problem with overweight and obesity, it's not a failure of willpower. It's actually the brain gets programmed to defend a level of fat. And basically, this new class of drugs, and I know this is a lifestyle thing where you not pushing drugs, and I'm not really pushing anything, but they allow people to feel the satiety as their body gets full. And so it's actually amazing. And I think that-

I heard, is that the needle? It's like a one to week injection. There's gonna be an oral version of it. I told you, first of all, and of course, I've got no dog in the game for this. I heard about that. Does that actually work though? It really works.

Like 15% weight loss in six or 12 months, and what compared to the same guidelines. So they basically, they'll randomize people and they say try to eat less, move more, right? Which we know sort of doesn't generally work, right? But enrollment in a trial gives you some responders, okay? You get some people that will lose weight on the placebo, right? You see, it's called a waterfall plot. You see a few people that will gain weight. There's a lot of people in the middle that had no effect because it was on placebo. And then you see some responders and those are the people that are like really coachable

or whatever and they didn't get any Some agglutide and yet they lost some weight over this trial, right? Right then you compare that group. Yeah, so remember I cautioned you against anecdotal data because your friends are not the same as everybody right? Right exactly. So then you but you enrolled people that had the same only they had an intention for weight loss They're overweight, right? And then you see the whole curve shifted where there's much greater weight loss, much greater compliance basically. There's no magic. They all had different

whatever they eat in their all of their different homes and their own different homes. But the people that were losing weight basically were able to sustain an energy deficit and so they lost weight. So, okay, so what's that thing called though? The shot, it's a shot, isn't it? Yeah, wagovia, I think is the trade name. It's a...

Can anybody, I mean, do you have to be a certain, you have to be obese, you have to be a You have to be a certain BMI like what is the way? Insurance is gonna be the problem in the US, right and so so but I mean there They're ought to become more available, you know, especially for people that you know over overweight is you know And and obesity you know are our conditions that challenge know, and obesity, you know, are our conditions to challenge people's health and well-being, their ability to work. No, I saw whole article on this.

Yeah, big deal. And it's a huge deal, but then don't you have to be taking it your whole life thing, because once you stop, what happens? I don't know. Or does it, or is it neuroplasticity you get used to it? You know, it may be that, you know, It may be that after substantial weight loss, then you have a different set point and you might be able to go off it.

But I would say given the safety of it, I would say it's way safer than a lot of other things that people do, including crazy dieting, right? Not sustainable dieting. I have a girlfriend who try who's unfortunately very very overweight and You know she tries everything every program Yeah, and then what happens it like to your point like you're doing so many different things Everything's counteracting and she's more overweight than she was even before she started this whole yeah

Yeah, that's this whole spiral. Yeah, we don't want to create sort of orthorexia or, you know, mischigasse about how you want food, right? You don't, I mean, people, you want people to restore balance, you know, eat when they're hungry. And, you know, to my mind, if there's some medication in the last people do that, I think it's a great thing. It's time to get back to the beach with America's favorite vacation company, Apple Vacations. Book your summer getaway with confidence and enjoy a one-stop vacation shop filled with

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Don't wait. Go to applevacation.com slash habits dash hustle to get the steal of a deal to your favorite Ibero star hotel resorts today. Let's get back. I'm curious about this the aging and then the longevity stuff. So if you won't say because you it's that's not your thing to say, NAD, I'm just going back, I'm just kind of circling back, that it's good for longevity or anti-aging. What is good for longevity and anti-aging? Is there anything? Yeah, of course. We know that public sanitation, we know that clean food and clean water and vaccination and

probably not having a gun in the home and being protected from infection. I think it's I'm not sure if the data are the same in men and women, but like for a man to be married is actually good for his, I don't know, but. Oh, for a long time. They've been hurt serious, I don't know. I don't know, but. That's gonna say, I don't know, and one would say that. But if you cite a lot, then it's not good for your longevity.

Probably not, probably not. But, I don't know if there are really good data, but I would tend to think that a positive outlook on life is good. But you're just saying a lot of like, medicine. Yeah, you're just saying a lot of like, like, medicine uses, prescribing medicine use is probably associated with, see the thing is

you could call anything a longevity drug. Like a type one diabetic needs insulin, right? So if you deprived a type one diabetic of insulin, they could go into shock and die, right? But endocrinologists don't call insulin a longevity drug, right? It's just a sloppy term. So, okay. Okay, however, can I interrupt something? Why is it that I feel like in the last probably five years,

maybe the last four years, you've been hearing a lot of hype around NAD and NR, but before that you really weren't. Like you're hearing much more about, I can never pronounce it, it was Rosemary Troll, and that was more the mainstream one. But NAD still not mainstream by any means, but it's still being, I feel like it's getting

much more well-known than what number one. Well, NAD is the key to life. It's key to life. It wasn't something that if you go right now to like 10 people, I would guess 8 out of 10 of those people won't know it, NAD. Yes, yeah, yeah. Okay. That's what I was gonna say. Yeah.

And the second thing is, then if it's not really proven for longevity and to Asian, why would someone take it and who should be taking it? Yeah, so I would say the conditions of metabolic stress that attack the NAD system are essentially inevitable. Back when in the day when I used to give these big presentations and crowded rooms, you and I are both vaccinated and sitting in your kitchen with air circulation. But we're doing okay. But, you know, I say okay, show of hands. How many people would, you know,

if we had a giveaway, would hop on a jet, many time zones fly to Ibiza, you know, sit out in the sun, listening to loud music, drinking wine, and eating lots of food and laid into the night. Everybody would just like every aspect of that. Sounds amazing, right? Right.

So sunlight, you know, disrupts your DNA, air, and probably, you know, some of the air travel, there's like a radiation exposure. The loud music we know in animal studies, sufficient noise to induce hearing loss, so that's probably greater than the music. But maybe right up against the speakers, that attacks the NAD system, right? How is it because it's not entirely clear how and why? Not entirely clear. But many conditions of metabolic stress, attack the NAD system.

Alcohol, we know how that works. So that leads to a direct effect in the liver. We know that's operational in human beings. We've actually looked at what's called the NAD metabolomes in the liver of people that have alcoholic liver disease. We publish that. Over nutrition, meaning eating too much, we know from animal studies that the NAD system is disturbed. Again, in the liver, in animals that are overfed, we know that NR is corrective, protects against fatty liver development in overfeeding.

So, and now, I barely drink now, and I'm not overfed, but we are in conditions, we are exposed to inevitable conditions in metabolic stress. And when the immune system gets activated, it's actually burning some NAD. So we think that there's a use case of NR,

potentially in prevention of infectious diseases, which are a huge cause of mortality and morbidity. So if someone ever did an N.R. longevity trial, you know, it may be fewer deaths from, you know, from infection, you know, that, but I would personally, I would rather do an infection trial because I can complete an infection trial, you know, distinct amount of time. But what, with your example that you just gave, going to a visa, drinking, and loud music. That would mean if NAD is being disrupted

or decreased by the stress of your body, I would say then why wouldn't teenagers take it or young adults? So why are people who are usually over the age of, you tell me, 35, 40 years old, the ones who are really... Well, I mean, I know that... I know they're gravitating. afflites, you know,

that have, right, there's a lot of athletes, right? Yeah, tons of athletes, there's athletes, there's athletes in, you know, in college, university programs and pro, and they're, you know, they're much younger. So I mean, they're, they're, they're involved in conditions of metabolic stress. You know, teenagers, they drink a lot, they go out late, they do all those things. Why are they not the ones who are...

I don't know, there's potentially a use case there. Right? Maybe we should do a... Maybe that should be your next lab study of some kind. Why? There was something proposed... When I was at the University of Iowa, there were things that were proposed that related to some kinds of behaviors,

like binge drinking or I didn't really want to do those types of interventions, but they could be done. They for sure. I mean, so because all those things are stressing your body, it shouldn't be a drug for people who are aging then. It should be a drug for really anybody. Well, all aging. I mean, as I say, that's what I'm saying. Like, you know, 16 year old or, because, you know, me being 29, I'm joking. Or my friend or whatever. I'm 59, so just full disclosure.

You're 59. I mean, people are taking it who are on the aging path quicker than a 16 year old, let's say. So then let's talk about NR. So NR is what you are also the Godfather of or the Pya Nerov creating that into the supplement. So as a precursor, that helps your body create NAD on its own by itself. Yeah, basically, yeah.

So NR was kind of a known compound when I started working on it, but it was really known to be like a growth factor for this weird bacterium that nobody, like 12 people in the world, wanted to grow that bacterium. So, I essentially, I discovered by Chromodex. So the idea is that you take it early and then it supports your body, keeping NAD levels in multiple tissues. Okay, so when I had David seeing Clare on, he was talking about something called NMN, right? What, okay, so, and then I saw later on

that you guys had a little bit of like a Twitter conversation. So conversation. Yeah, conversation. That's a euphemism for battle, perhaps, over how it gets into your body better. Is it the NR system? Is it the NNN? And it looks like you won the battle a little bit, but I mean, yeah, so well, it's, I mean, it's not even a little bit.

It's decided science. You won the battle a little bit, but I mean. Yeah, so well, it's, I mean, it's not even a little bit. Decided science. I think you won the battle. It was decided science in the sense that, you know, if you take the body, yeah, so you could take, I just said to you that, you know, we could, we could eat on processed foods and they have NAD in it, right? So NAD is is gonna break down. NED gets splinted to two pieces, it's NMN. NMN gets further, you know, digested basically, it's NR.

NR could be further digested, it's gonna be nicotinamide. And even one step further, it's gonna be nicotinic acid. The last three things that I mentioned, NR, nicotinamide and nicotinic acid are the vitamins. Okay. NMN. The smaller part of the whole.

Yeah, they're small part and they can get into cells. And, you know, I'm pretty sure that David knows that NMN doesn't get into cells intact. So there's been some obfuscation on that. But, um, NMN has to have the phosphate removed before it can get into cells. NMN is, it is, it basically is going to act as NR, you know, after it gets, you know, into your, your body, the phosphate is going to be removed. NR is going to get into a cell. And then the phosphate has to be put on again.

It makes no sense to me. Okay, you lost me. Okay, so I'm like, okay, honestly. Okay, so basically NMN, okay, so if someone is, what is, if I took NMN versus taking NR? Well, the first problem with that is like who's making that NMN and why do you think there's NMN in it? That's the first problem. So is there an actual supplement, NMN supplement?

Yeah, there are NMN supplements, but their safety dossiers are basically unknown to me. I mean, there might be one that is claiming by themselves to be generally regarded as safe, but I don't believe that there are any NMN supplements that have anything near the safety dossier of the NR that was commercialized by by Chromatics. So the first question is, do you know what you're getting? Is there NMN in there? And are there other contaminants in there? You know that that you'd be exposing yourself to?

So to me, it doesn't seem like a super safe activity. The second is, let's say there is NMN there. Okay. So you would need for you know, 300, I guess you said you were thinking 500 milligrams of for 300, I guess you said you were taking 500 milligrams of Nige in which is NRR chloride. You'd have to have 5, 50 or 600 milligrams of NMN to have the same effective amount of NAD precursor, because why? Because NMN is bigger has its phosphate on. Then the only thing that's gonna happen is,

your body's gonna take the phosphate off, the NR is gonna get into your cell. So at best, NMN should be acting as NR. So it's hard to understand the use case of NMN other than some folks went out there and advocated for it. There are animal studies that show NMN essentially does the things that NR does. But the data indicate that the phosphate comes off and that NMN is acting as NR.

So why not just take NR basically? Yeah, if you're gonna take a, if the idea is to take a vitamin to replenish your NAD, the choices are nicotinic acid, which causes flushing, right? Okay, what do you mean flushing? Flushing means you think you're hot now. If you take nicotinic acid at like 250 milligrams,

your face will turn red and your extremities will be hot. Oh, wow. Okay. And then nicotinamide, not a lot of people have advocated for really high dose nicotinamide in like mice, it's one of the ways to induce type 1 diabetes. So it's sort of like not considered to be the world's best thing

in high amounts. In low amounts is great. In niacinamide, vitamin B3, as niacinamide is in small amounts in multivitamins, nothing wrong with that, but no one has really made a very few people have made a strong argument for really high amounts of nicotinamide.

But the other advantage of nicotinamide riboside in R is it doesn't, okay, so it doesn't cost flushing. It's not associated with the negative effects that have been seen in the container. My end, when NAD comes under attack, the NR pathway, the gene pathway that basically my group discovered, that pathway gets ramped up. So basically the stressed cell and tissue is telling us that it's looking for NR in order to fill up its NAD stores. And nicotine might and are don't work identically in some of those models.

So like there's a heart failure model where the NAD is coming under attack. The mouse heart is losing its NAD, right? And it's losing its expression, it's, sorry, it's gene expression for turning nicotinamide into NAD. While it's turning up the NR pathway. So we give those animals side by side, nicotinamide doesn't really restore their NAD, we give them NR, restores their NAD,

and their cardiac function. That's amazing. Then how about other stuff, NR and Alzheimer's, NR and Parkinson's? All being tested, yet all being tested. And so far do you have any type of data that you can get? So there's something that just came out on Alzheimer's that was a placebo controlled study

of NR in what's called the nutritional cocktail or something like that. It's the four, something it contains, some lucine, carnitine, and anacetal cysteine in addition to anar. And they're reporting a benefit of this nutritional cocktail in Alzheimer's patients. Haven't carefully looked at the study,

that's being reviewed. There's something I'm involved in that is being reviewed that I won't talk about yet, but I think- You guys a little hint? Well, you know, there's more and more studies of NR in neuroprotection and for sure that there are studies in Parkinson's,

in mild cognitive impairment, which is kind of a people they're progressing into Alzheimer's. And I'm excited by the trials. The mechanism is that NAD is coming under attack and that NR is supporting their blood flow, their cognition, and so forth. So what's the minimum amount

that someone should be taking? What's the maximum? I know it's all over the board. Yeah, I don't talk about my own dose because I don't feel like I'm not your doctor and stuff. So the basic product was introduced at 300 milligrams per day as a typical consumer dose. There's something called true nige and pro that, you know, doctors offices can get, practitioners can get that, so 500 milligrams of a higher dose.

And then most of the... That's what I take. And most of these therapeutic trials are kind of one gram a day, or even one to two grams a day, we know it's safe. And then do you cycle it? Like I thought like, did you body acclimate to anything, like any supplement?

I don't know. So does it better to like do do a month on a week off, cycle things like a good? I don't have a, like a do my allergy medication. I don't have a base for doing that. We think it's sustainable. Excuse me, there's always longer term trials

that are being done. But we think it's safe to take. And most people take it in the morning. I know some people will take it in the evening. And I think that the one gram, the two gram people probably split it one in one. But that's kind of done in like disease trials and stuff. Wow.

How about just in general, how did you even get into doing this research? What were you doing before? Like give me some of your background or you didn't just one day be like, you know what, I want to really kind of figure out this whole NAD problem. Yeah, I was basically... Maybe you did. No, I was mining my own business, you know,

2003, 2004, working on an enzyme, which is, you know, what was busy. Maybe you did. No, I was mining my own business, you know, 2003, for working on an enzyme, which is, you know, what biochemists love to do, right? Pretty nerdy stuff. And, and, you know, I, I like, you know, I like this particular enzyme. And, you know, we have a phrase in science that did not escape my notice that this enzyme's product, the thing

that enzyme is there for, is to make NAD, right? I know that NAD is a central catalyst for metabolism, right? So I think, gee, I wonder what else is known about NAD and whether other people might be interested in NAD. And then I started questioning what I call the received wisdom of how NAD is made, which is like, there's an arrow coming from trip to fan. It takes eight different enzymes to make NAD from trip to fan. There's an arrow coming from nicotinic acid that takes like three enzymes to make NAD

that way in a yeast cell. And then there's an arrow coming from nicotinamide and people thought that they knew all of the ways to make NAD that way in a yeast cell. Yeah. And then there's an arrow coming from Nicotinamide and people thought that they knew all of the ways to make NAD. And I thought, you know what? I can, it's like a side project of how I'm figuring out this enzyme. Right. I want to see if the received wisdom on making NAD is correct.

Maybe something's wrong. You know, I don't believe everything that I'm told. Right? That's for sure. So, I want to see if it's wrong. You know I don't believe everything that I'm told, right? So I want to see if it's correct and I want to see if the parts, even if they are correct, are complete. I didn't actually find anything that was wrong other than it was incomplete and that there was this NR pathway. And then we could see from the genes and the sequences of the genes that this pathway exists from yeast all the way to human beings. And that NR would not only have vitamin activity in yeast,

but that it would have vitamin activity in humans. And then subsequently, and others have been able to see that the NR genes, the NR kinase genes, get ramped up just when your body needs NAD. So that's kind of the unique aspect of NR. Okay. Because it's not only not flushing, doesn't have the, you know, the side effects of high nicotine oride, but it's the precursor that stress cells want.

So we think that it has a higher value to the body. Wow. Now, what's the next, like what's next though? Are you, are you, are you, these sides finishing or doing more research on, of course, Alzheimer's and Parkinson's, or anything else that you're working on, even at the city of Hope?

Yeah, so I'm not doing that. I mean, I, I collaborate with groups that are doing the NeuroProtection. I do a lot of what are called NAD Metabolome. So I analyze what happened to the NAD system. My group is blinded. So I think the samples come in with a number on them and we analyze them.

And then the stuff gets unblinded. We look at the data. But we're interested in a data. But we're interested in, one thing that we're interested in is, I know you're a mom. So you've undergone the amazing process that is postpartum. And I'm not referring to depression.

I'm just referring to the fact that you had kids. Yes. So at the moment that you had a kid, your body went from this amazing transformation of producing this child. This child. Yes. Twice.

Twice. Twice. Now your body transforms again, suddenly, right? Not so sudden, but okay. No, but the prolactin program gets turned on immediately. Oh, wow. The hormones change immediately.

And immediately, your body is trying to mobilize your protein fat and lipid to your memory to produce this amazing stuff to this milk that was evolved to produce all of the nutrition for the baby. Whether mom chooses to do that or not, that's the program, right? And so we discovered using rodent models that postpartum is an example of metabolic stress to the NAD system.

Yeah. And that for a liver gets supported by oral nicotine or my drive aside. She can accelerate and increase her weight loss. She can produce more milk. The milk has a higher quality. And even the offspring development is better if the mom is supplemented. So there are people at UC. Yes, really cool.

So there are people at UC Davis that are going to do clinical trials on this, you know, to improve our mom's lactation and in the context of preemies and non-premise as well. I think there's two trials. Oh, why? And then I want to see the quality of the milk and then I want to understand the mechanisms of all that. Like, what's doing for the mom and how's it doing that and stuff like that? So again, like, when did you start with the city of Hope or when did you get just August, August of 2020? Yeah, I was going backwards. I was headed by chemistry at University of Iowa 2009 to 2020. Okay. Six years the six years prior so 2003 to 2009. I was at Dartmouth Right frozen north of New Hampshire. Right. I saw that. Yeah, and then the seven years prior to that

I was in Philly at Thomas Jefferson University and Then the three years prior to that. I was a postdoc at Brandeis, and then the three years prior to that, I was a postdoc at Brandeis in Boston. And a Stanford also. And then the four and a half years prior to that, I was a graduate student at Stanford. Oh my gosh. And then I did biotech actually in the San Francisco Bay Area

as well for five and a half years. I graduated from college in 1983. My gosh. So have you always just been, even as a kid, like, what, do you have any hobbies besides this kind of, besides NAD and what do you like to do? I like building things with my hands. I like trying to fix things.

I don't always succeed. I like gardening. I like, like, build raised bed gardens. I grow things. Do you hang around all other scientists? No, no, no, no, build raised bed gardens, they grow things. I hang around all other scientists. I go to an academic, an academic. Yeah, I love hiking. My new gym is a climbing gym.

So I'm trying to learn the wall, the boring thing. Yep. I like being a novice novice. Yeah. I like the rate of growth. So, so there I am on the wall doing V zero V one whatever the easiest Roots are up and was your family all scientists to no no no no no no doctoral degrees before mine No scientists like what it like what made you feel like this is what you wanted to do

We as I as like a young okay, so I went to Wesley and went to Wesleyan, I was gonna be a bio major to do ecology. Okay. Then they said, we're not that great at ecology, you should learn molecular biology here, right? So I learned molecular biology, I was in a fly lab, Drosophila, melanogaster, and then I had to turn. The world, I mean, yeah, so that's a fly. That's a fruit fly.

Okay, thank you. Okay, thank you. Can you just dumb it down please? I'm sorry, it so that's a fly. That's a fruit fly. Okay, thank you. Okay, thank you. Can you just dumb it down please? I'm sorry, it's just like too many. Please. Too many syllables, right? Wait, too many. So that kind of a statement.

So it's still can't do that. As a mom, you're gonna like this. Okay. So I had the quaint idea that you go to college not to be a burden on your parents to get a job, right? And to support yourself. Oh, my God.

My son actually agrees. My son did the same thing. My son, what is your son do now? He works at a credit union in Iowa City. Got his degree from University of Iowa. Okay. Interview for one job. Got the job.

Salary and benefits. Day one. It was amazing. And he's happy and fine. Yeah, he's happy. He's fine. Yeah, he's happy. He's great. Okay.

And shout out to Freeman Brenner. So I wanted to support myself. Right. What do you do? The biology degree gradually in 1983, biotech, not even called biotech at the time. Right. It was called the genetic engineering industry. And it started in Route 128

Strip in Boston, which is basically where I'm from. The San Francisco Bay Area, which is where I ended up. Yeah. Yeah. So I basically, yeah, so basically I wanted to use what I learned in college, and then I was in two different environments. Basically, one is chiron corporation, and then was, I was at DNX, research institute, DNX, which was owned by Shearing Cloud at the time already, but both of them had a really research component to them, even though they had profit motive. They also taught me how to function as a team, because you have fully formed PhD scientists at both of those organizations that could put their brains together with teams and get a project done, which is kind of rare in academia, where it's like a little fiefdom.

So, I learned something really valuable about doing science and organization of science when I, in my biotech era, but I also realized I'm going to hit a glass ceiling there without PhD. So, I stayed in the Bay Area, but I went to Stanford. It got my PhD there. Wow. And so basically then, you're doing all this stuff with a team of people then all this. Oh, you can't do it by myself. You can't. So how big is your team?

Not big enough now. We're rebuilding, having moved. But, you know, we have a very talented lab manager, technician, Jeff Hagelin, actually, he's from my alma mater, Wesleyan University. I have a research assistant professor, Abdullah Elkall, who was like spent a decade at Harvard, you know, doing NAD related things. It's very complimentary to my own. I have a postdoc, Dr. Udo, we call her, and she's phenomenal. She came from kind of a DNA repair background, and I have a new graduate student. His name is a little hard to pronounce also, but he goes by high fam, so high fam. And he's working on NAD, Mattel.

So we're kind of like split between cancer, which we want to kill by understanding something about NAD and then metabolic diseases that we want to prevent and treat. And that's kind of a unique thing about our unit at SIDIFO. So then can I ask you a question? Then because one thing we didn't talk about, I mean, talked about all timers and everything else,

can there, can NAD or something help with cancer? Because you just meant that's one thing. Is there any kind of research being done on that? Yeah, so that's like two or three part question. So one is that we've had data for a long time and publish it, that NR is active in a mouse model of diabetic neuropathy and then in a rat model of chemotherapy.

So dose limiting side effect of a lot of cancer chemotherapy drugs is neuropathy. So dose limiting side effect of a lot of cancer chemotherapy drugs is neuropathy. And you know Donna Hammond, my former colleague at University of Iowa, is really interested in that. And so we showed NRS protective in rats. And then she's gone on to show, doesn't increase tumor incidents and looks like, you know, from the animal data, it ought to be safe. And then she's testing it in women that are undergoing cancer chemotherapy to see whether it prevents against neuropathy, which is great.

So there's some animal studies that show that by improving, you know, DNA repair, it could be protective. There's huge study in Australia showing that daily B3 nicotinamide was protective against skin cancer, which is very high incidence in Australia. So we think that NR would be safe in the context of cancer. But my collaborator, Dr. Renjie Bindra at Yale University, and I discovered that there's certain tumors that have dysregulated NAD where you could target NAD. You want to knock NAD down, basically to kill tumors. Not in every person's cancer,

like it's not gonna be a breast cancer drug, but it'll be a drug for tumors that have a dysregulated NAD system. So it could work for some fraction, maybe 20% of breast cancer, maybe 20% of a glioma population, maybe 20% of this, and so it'll be combined with a companion diagnostic.

So, so Ranjit and I are co-founders with Kevin Rakin of a new company that is getting off the ground in order to target NAD and cancer. Wow, so how do people find more information? They want to know more about your research, what your findings are. Good, good, good. Where can they find you?

Okay, so BrennerLab.net. So they can go to HTTP BrennerLab.net. They can follow me on Twitter. It's Charles M. Brenner. And you actually answer questions about NAD almost every day. Do you? Yeah, on Twitter. And so you get you get your response people.

Yeah, I do. Yeah, I'm pretty accessible. And yeah, they can look at our lab website. And yeah, it's always a pleasure. Yeah, they can also go to chroma-dex or trunidejan.com there's a lot of information there if you want. But you've been a pleasure. Thank you. Although I didn't, I got to go to ChromaDex or trunyogen.com is a lot of information there if you want, but You've been in pleasure. Thank you. Although I didn't I got to go back and listen to it three more times I didn't really understand everything and try to listen very intently. I

Literally said to you before we start please keep it like it laments her I know you I think but you know given some of the other interviews I think this was actually an improvement because you- Okay, I've been worse in the past. Why don't you be worse? Maybe the host has been smarter. I don't know, it'll bring better, but I think, you know, I think that I kind of followed.

I hopefully people follow the majority. Right. But I said to everyone, please have Google open and please have either a Thosaurus or someone who's in the science world The side you so you can stop and pause and kind of continue, but thank you so much for coming on pleasure and all right. Bye This episode is brought to you by the YAP Media Podcast Network. I'm Halataha, CEO of the award-winning Digital Media Empire, YAP Media, and host of YAP Young & Profiting Podcast, a number one entrepreneurship and self-improvement podcast where you can listen, learn, and profit. On Young & Profiting Podcast, I interview the

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