[EP.2]How to Crack the Code: Ways To Boost NAD & Reduce Cellular Aging

Crack the Code to Cellular Aging_YT

Dr. Joel Rosen

Our guest here is Dr. Nicola Conlon. She’s a molecular biologist specializing in the study of cellular aging. After a career in drug development, Dr. Nicola founded the Nuchido laboratories to deliver disruptive innovation in the fields of aging, rejuvenation, and health spending. 

She has a passion for sharing her latest science and accomplished speaker, and has a skill in translating event science to help educate the support the wider population encouraging people to age well and achieve their optimal life experiences. Perfect for our podcast today. Thank you so much, Nicola, for being here today.

Dr. Nichola Conlon

Thank you so much for inviting me. I’m excited to have it and have a great chat today. Yes, excellent.

Dr. Joel Rosen:

And so what I like to do is I usually go back and figure out why you get into the area that you did. But I want to fast-track that in terms of how you go from drug development to more of a, I would imagine a more holistic or alternative route. Maybe tell us about how that came about.

Dr. Nichola Conlon:

Yeah, that’s a great question, because it’s quite unusual, I guess. And so as you mentioned, my background was in drug development. And I originally worked in cancer therapy. And then one day, I got moved on to looking at aging, and which at the time, you know, we’re talking about a decade ago now, and was quite a new thing. 

And even I was like, okay, drugs like aging, like, how does this all fit together? However, what we know is that there was a huge change in the science surrounding agents. And there was a lot of evidence coming out that we could reverse aging at the cellular level. 

And we know that aging is our biggest risk factor for every disease, you know, every major disease that drug companies are trained, to treat or to cure. So the idea was, if we can slow aging at the cellular level, even just a little bit, will it reduce our risk or our onset of age-related disease? So I was fortunate enough to be able to, you know, basically traveled all over the world, meeting all of the people who were experts in the longevity field, or the conferences and learning what this science was all about, and how we could incorporate it into drug development. 

So that was exciting. But two things annoyed me in the world of drug development. The first was that it takes a very, very long time to get anything from the research lab. abs, you know, really initial drug development, early stage out into actually being a medicine that somebody can take and benefit from, you know, you’re looking at about 10 to 15 years, hundreds of millions of pounds to do this. 

So, you know, I was looking at all this cool science and thinking, Okay, this is great. But it’s going to take a long time before it gets to benefit anyone. The second annoying thing was that part of my role was to, you know, we’d send a load of molecules to the lab to be tested, and we then get a spreadsheet back, which was like, okay, these things work well at the top. 

And these things don’t work at all at the bottom. Quite often, some of the things that were potent and had high efficacy were not drug molecules, they were natural molecules, things that were already very well known things that were already approved as supplements, that worked brilliantly, but unfortunately, drugs, companies aren’t interested in them, because they can’t patent them. 

And if a company can’t patent it, it can’t own it and, therefore, wouldn’t put all the money into development. So often, we would go through the list and go to something that worked half as well. And that would be the thing that got put into drug development. So I was like, Okay, this commercially makes sense, but ethically is just not right. 

And there are this shows us that there are things that are out there already that if they had the right research and testing, we could have some pretty good, you know, things and molecules that could help people right now. So in 2017, I left that world and founded my own company, Nichido Laboratories. 

And the whole mission behind what we do is to do the same science that we did in drug development, the same testing, and not to the degree that they do in drug development. But get that science out there and test the molecules that weren’t drugs, the things that we know, we can get into consumer products, and out to people so that they can benefit from them now. 

So that’s kind of a decade, sometimes. But I think, you know, the real, the real mission behind you know, a lot of people said to me, Oh, my goodness, you are leaving your very credible job in drug development to start a supplement company. And supplements have a terrible reputation, like, what are you doing? 

And I always had to keep reminding people that actually, your body has no idea what is a drug. Or what is a supplement? What is a nutrient? It’s, you know, regulatory authorities that put them on lists. But actually, a lot of the other molecules that are on drugs have just as equally powerful physiological effects on the body. And unfortunately, we’ve been trained not to think that and to think that only a drug can help. And that is not the case.

Dr. Joel Rosen

Yeah, no, it’s an excellent preview of a review of what you’ve done. And I love that you brought the same approach in terms of validating it and setting up studies. And I know you’ve created a study, which I want to get into shortly. 

But as far as you mentioned, you noticed that there was it was possible to reverse your biological age, maybe discuss what that means to the layperson in terms of the biomarkers that are correlated with age and what that means, as far as reversing and what those are.

Dr. Nichola Conlon

Yeah, absolutely. So what we know now as scientists is that there are key things that go wrong in ourselves with age. Now, famously, within the scientific community, these are referred to as the hallmarks of aging. And there are now known to be 12 hallmarks of aging. So essentially, these are 12 critical processes that seem to start to become dysfunctional as we get older. And anything you can do to kind of fix those processes seems to reverse the aging process. Now, a really interesting way of measuring this is to look at your biological age. So you have your chronological age, which is the age that you have existed on this planet.

And you know, it’s to do with when you were born and your birth certificate, and that’s your chronological age, there’s nothing you can do about that. It is what it is. The biological age, on the other hand, is the age at which your cells are functioning on the inside. So this can be measured. You can Take a sample of your cells, different types of cells. And you can look at what the biological rate of aging is in the cells.

And what is known is that actually, your biological age is a much better predictor of your future health than your chronological age. Because what we found is that quite often people’s chronological age and biological age don’t always match up. And what I mean by this is, for example, somebody may have a chronological age, they may be 50. But if you look at the biological age of their cells, they may look more like 60. This is bad because it shows that aging at a faster rate than they should be. Alternatively, you can go the other way, and you know, someone that’s age 50 could have a biological age of 40. And that’s good because they’ve got a lower rate of cellular aging in their cells. So this has been a really interesting development.

And it’s allowed us as scientists to be able to look at how different interventions, different molecules, different drugs, things like that actually can reverse the aging process by having this way of measuring aging, because obviously, when you’re looking at aging, and trials and things like that, you can’t, you know, wait for a person to age and see, you know, and measure how long it takes them to become old and frail. That’s just, you know, something that’s not possible. So this is a really good biomarker way of being able to measure the aging process.

Dr. Joel Rosen

Right. And I think that what, I guess, brought the research together, maybe you can agree on this or not, is the fact that it’s tied into outcomes, right? I mean, as far as it’s one thing to say, what your chronological age and biological age is, but does it relate to all causes of mortality and so forth? So maybe speak about that briefly, if you will, of what, what risk factors are what how they are tying in, or what they’re benchmarking the biological age to the outcomes are? 

Dr. Nichola Conlon

Yes, I think so this whole area is new. So there are still a lot of ongoing studies looking at, you know, how your biological age links into more of the clinical factors and things like that, there are multiple different ways to be able to measure biological age as well.

And what a lot of the scientists behind this research are doing is looking at more longitudinal studies of measuring people’s biological age, and then looking at their health outcomes. A really interesting one that was done with one type of biological age test which looks at something called glycan age, was looking at studies in twins. So these are people that are biologically, you know, genetically identical.

So any difference in biological age is therefore down to their lifestyle, and looking at how lifestyle and in different diseases and you know, is impacting twins biological age. So I think this is still a huge area of research. I think there’s, you know, there’s still a lot of argument over, you know, how much is the biological age correlating to health span and disease and things like that. But every day now, there’s more and more evidence coming out that your biological age is a very good predictor of your future health.

Dr. Joel Rosen:

Right? No, I appreciate that. And I think it’s a paradigm shift in the way health is headed towards being preventative and understanding better markers, because so many people that are exhausted, Nicola are being told that they’re, their blood chemistry is looking normal and that they don’t feel normal, and they’re not getting the true answer.

And it’s sort of like they have to wait before they get sicker before some of these less sensitive or specific tests come up with identifiable risk factors. When I always use the analogy, it’s like a grade school teacher telling their student, you’re not getting low enough grades on your report card yet before us. Before we can implement any strategies, we have to wait before you’re getting an F or a D minus before we can do anything. So I guess the transition and the question would be NAD and NAD plus, and where does that all fit into that age-related changes and maybe give us some insight on that?

Dr. Nichola Conlon

Yeah, I think what you’ve just said, you know, is something that I’m very passionate about as well. And a lot of healthcare is sick care. And you know, it isn’t healthcare. It’s not preventative, and I think that’s something that does have to change. When it comes to aging. As I’ve mentioned, age is our biggest risk factor for every major disease. You know, Getting older is the worst thing you can do for your health, it’s worse than a lot of the other things that we are told are bad for us.

And but people, unfortunately, you know, don’t register it like that. So what we know is that everything to do with aging starts at the cellular level. So even though traditionally a lot of people think of aging on the surface and treat it at a surface level, and ultimately it starts at the cellular level, therefore, anything that you can do to improve your cellular health is only going to have a beneficial outcome when it comes to aging.

And this is where something like NAD comes in. Because we know that NAD is naturally found in every single cell in our body. It’s very important for cellular health because it’s involved in hundreds of different reactions to begin with. But it’s probably most famous for two critical cellular functions.

And that is cellular energy production. So helps to convert all the food we eat into the energy that our cells can use to have a healthy cellular function. And the second thing it’s important for is for switching on a lot of cellular maintenance and repair processes. So NAD seems to act as a signal to keep our cellular maintenance and repair pathways turned on. So we know that NAD seems to be linked to aging because it declines with age.

And so when you’re young, you seem to have higher levels of NAD, then as you get older, these levels decline. And when NAD goes down, you get less energy reduction, you get less repair and maintenance within the cells, and also a whole host of hundreds of other processes that rely on NAD that start to get turned down. And this can accumulate as cellular damage. And this is you know, ultimately results in a lot of the signs and symptoms that we experience as aging. So sign aside, okay, if we’ve got this molecule that seems to be important.

And when it declines, and it causes all these problems, then why don’t we just not let it decline? Why don’t we top it back up to useful levels or not let it decline in the first place? And, you know, to cut a very long story short, what hundreds of peer-reviewed papers have now demonstrated is that if you boost NAD levels within the cells, you switch on a whole host of beneficial pathways that protect cellular health. So NAD is one of the only things that can impact every single hallmark of aging. So because of that, there’s a lot of excitement around the potential for NAD to restore cellular health, and how that can protect us from some of the negative consequences of the aging process.

Dr. Joel Rosen:

Well, that’s a great answer. I’d be interested to know how your research design went because I know it’s just not as straightforward as it depletes on its own. There are reasons for it to be depleted. And I would imagine it’s not just take it set it and forget it type mechanism. So maybe give us some insight into your research design and what you found and share that with our audience. Yeah,

Dr. Nichola Conlon

well, first of all, just to mention, whenever I do a presentation talking about NAD decline, I always show a graph. And the graph I showed doesn’t just go straight down. It’s bumpy. And it’s lots of peaks and troughs. And it’s a bit all over the place. And the reason for this is because everyone’s slightly different. So we know, in general, that NAD declines, but in some people, it declines a lot faster, and in some people, it declines slower.

And some tissues, it’s faster and some tissues, it’s slower. In disease states, it can accelerate NAD decline. So it’s not a straight down, everyone is slightly different. And that’s obviously because we’re all individuals, we all have different genetic makeup and snips and different enzymes that can affect it. But as it is a general rule, it does decline.

And so a lot of research is focused on okay, what is causing the root cause of NAD decline? Because if it’s so important, then you know, why is it declining in the body? What’s been found is that they’re not there’s not a single cause of NAD decline, but a couple of things within our NAD network within the cell that seems to become dysfunctional. The main issue is that our natural pathway for NAD production in the cell, which is called the salvage pathway, seems to decline with age. The reason that this happens is that a key enzyme within this pathway called na MP Tea declines. And again, this has been well studied and well documented.

The issue with the decline in this enzyme is it’s the enzyme that our cells rely on for not only making NAD but also recycling it. So what many people don’t realize is that the vast majority of our NAD that is produced when we are young, is actually by recycling. So every time our NAD is used in the cells, and when it’s used by DNA repair enzymes, for example, or by longevity proteins, such as the sirtuins, it gets split apart and broken down into its building blocks.

And one of the main things that gets broken down is a compound called nicotine amide. Now, in young cells, what happens is this, this salvage pathway with this key enzyme, literally will scoop up this nicotine made and recycle it straight back into fresh NAD again.

And when you think about it, it’s kind of like the perfect design. Because really, we don’t want ourselves to run out of NAD. This design means that as the consumption of NAD goes up, recycling also goes up to restore what is being used. So it’s not great in ourselves, as we become older that this enzyme seems to become turned down for various reasons. The other thing that’s been found to reduce NAD levels is that more NAD is used in our cells as we get older.

And this is largely due to chronic low-grade inflammation, which we know is a major issue as we get older. We know that inflammation causes increased expression of a protein called CD 38, which is on our cell membranes and degrades NAD. So if you put those two things together, it’s kind of like the perfect storm. Not only are our cells using more NAD, but they’ve lost the ability to recycle the breakdown products and restore them. So you know, you’ve got this perfect situation for a huge NAD decline as you get older.

So what we were looking at was, okay, how can we restore NAD? But how can we do that by actually fixing these issues? Unfortunately, a lot of the sort of ways that people are trying to restore their meds and things like precursors, IV drips, or anything like that are ignoring the reason why it’s declined. And what we wanted to do was design something that would fix the root causes that are causing the NAD decline in the first place.

Dr. Joel Rosen

So what was it that you did, you’re leaving, leaving me on a cliffhanger here?

Dr. Nichola Conlon:

Sorry. Yeah, so we just designed a dietary supplement. And in the supplement, not only do we have a precursor in there, which is the building blocks that the body uses to make NAD but it has ingredients in there, which restore levels of that key enzyme. So they restore that salvage pathway recycling, There are also ingredients in there that will inhibit CD 38 to reduce the wastage of NAD.

We’ve also got ingredients in there, that prevent the methylation and excretion of some of the NAD precursors, which I haven’t discussed, but is an issue. As we get older, we see a reduction in methyl groups because the cell is using them and wasting them trying to get rid of the buildup of some of these precursors. After all, it can’t recycle them. So again, we have ingredients in there that are designed to inhibit that process. So everything about it is basically how we look at the problem as a whole and fix the issues that are causing NAD decline? And as we mentioned, my background is in drug development.

And when I started the company, I said, you know, a key sort of mission of ours is to bring more credibility to the supplement industry through testing. So we did a double-blinded, placebo-controlled crossover study, which as far as clinical trials go, is a gold standard to test did our supplements work.

And we measured a lot of different biomarkers within this study. The key thing to measure was NAD does it boost NAD levels we found that it does so after 28 days of supplementation we saw a significant increase in NAD and actually after seven days the increase was significant. So we know that x pretty quickly. We also measured levels of this key salvage pathway enzyme in the participants and demonstrated it again after 20 days, we switched back on and boosted levels of this key enzyme. That’s the first human study to demonstrate that a supplement can be used to switch back on and fix one of the root causes of NAD decline. And so yeah, we measured a lot of other things as well as if you want me to go into all of them, or if you have any questions, hi,

Dr. Joel Rosen:  

hope you’re enjoying our interview so far. Today’s show is brought to you by Nuchido time. This is the NAD product that we are talking about, make sure you check out our show notes and click on the link, and if you use Dr. Joel 20. That’s all capital D R. Jo E. l 20. You will get 20% off your first order.

Dr. Joel Rosen

That’s excellent. I am curious to know, you mentioned earlier and now we talked about a couple of tests we talking about potentially measuring the CD 38 levels as a marker of whether is that decreasing or increasing. Or where is it in the beginning? In the end? The intracellular end ADM? Sure. looking at potentially that particular enzyme that helps to recycle that NAD. And then you mentioned the glycan test, I’m not sure. Is that the same thing as a DNA methylation test? Or is it what can you tell me a little bit about that? 

Dr. Nichola Conlon:

Yes, slightly different. So this was something we included in our trial to measure biological age. And so the way the glycan age test works is it looks at IgG cells, so our immune cells, and it measures the levels of glycans, which are small sugar molecules that are found to be attached to the surface of the cells.

And what is found is that as we get older, the pattern of these glycans changes. So if you were to look at young person cells, they’ll have a particular pattern. And if you look at a much older person’s cells, they’ll have a very different pattern. And you can see across all these sorts of years or decades that there’s a very predictable shift in the pattern of these sugar molecules. And that can be used to look at the biological age of the cells. So that is how that test works. We did it in our trial.

And what we found was that in 28 days, throughout that time, and the entire set of participants, we on average, reduced biological age by 1.26 years, and that was in 28 days. So we were pretty pleased with that. And I think it’s, it’s, you know, it’s demonstrating the power of NAD at the cellular level, excuse me, and how it can be used to help address some of the issues of aging at the cellular level. 

Dr. Joel Rosen:

Sorry, that’s fine. So alright, that’s sort of like the glycation process and the browning and understanding. Okay, gotcha. So curious to know, then, before I ask you a little more of a technical question. What was the dosing of the actual precursors? Or what I mean, it was your product. Yeah,

Dr. Nichola Conlon:

yeah. So the supplement, so it was the actual finished supplement that was used, which is you’ve got to be careful, as well. And supplement companies say they’ve done clinical testing, because often what it’ll be is it’ll be clinical testing of one very small component of that right supplement, often not at the same dose that is used in the supplement. So what we did was we gave all the participants they were given the actual final finish, you know, as you buy it off the shelf supplement.

The supplement is six capsules per day, which again, seems like quite a lot but that is from our pilot study the amounts that we know work, and there are no fillers or anything like that in there it is all active ingredients and because that’s the concentrations that work and the participants took the capsules daily.

And as far as their blood sampling and things like that, they have baseline bloodstones they had a blood sample done at the very same time, the same time every week to ensure continuity because what a lot of people again don’t realize is that NAD fluctuates throughout the day. And a lot of trials that have been done on sampling NAD don’t take this into account. And you know, you can measure your NAD at two different times of the day and it will be very different. So it’s very important when doing any trials that you have continuity with testing times.

Dr. Joel Rosen:

Right, gotcha. So with your company See, it’s the product that you’re promoting that you used in the clinical trial. What are you also doing? And I saw it somewhere and I didn’t see it before I got on. So I apologize. Are you also doing the intercellular? NAD or the glycan testing, as a retail product or more for research stuff?

Dr. Nichola Conlon:  

No. So we do it for research. So you know, NAD itself is a bit of a tricky thing to measure. We don’t provide that as a service, all of our NAD testing was done in academic labs, and it is very unstable. So it’s got to be processed very quickly, to be able to measure it accurately. And so this means it’s, you know, it’s not available to many consumers to measure. So what we wanted to do was put a test within our clinical trial that was accessible to consumers, so that they could do some sort of tests at home to, you know, see that there that their supplement is having an effect.

And because a lot of people say, Well, how do I know it’s doing anything? And so we actually, we don’t sell kits or anything, but we promote a lot of our customers to go and do a test and say, you know, in our clinical trial, we use this kit. It was used in our trial, but this is commercially available for you to go and independently by yourself. And if you want to know it’s working, you know, we’re so confident in our product, go and test it. And so yeah, we don’t sell them or do it as a service, but we promote customers to test it themselves.

Dr. Joel Rosen:  

Yeah, I find that more and more sophisticated. Users want to know because they have been that person who went to the doctor and was told that something wasn’t working, and they want to become their study one. So the question I have now is a little more complicated. But we talked about sirtuins, and how that supports NAD in the relationship and CD 38. Then you also talked about how it has to be recycled.

And the recycling enzymes tend to get weaker as we get older, by the way, the gene site that I’ve shown you tests for those enzymes as well. So if someone has sort of an inherent weakened ability, I always tell them, there’s no bad news, it just means that it’s not working at full capacity, and we know where some of the hiccups are, or the weak links in the chain are to be able to support that’d be interesting to see with any of your research people that may not have had the same outcomes, or may have been a little bit of the outliers if they did have those weaknesses.

But anyway, with that being said, what I find to be very difficult is we talk about the balancing of mTOR and autophagy. Right, and maybe you can talk to the listener about what that is and how that relates to cellular aging and NAD. But what I find difficult is how you drive with your foot on the gas and the accelerator and the brake at the same time. Meaning? Is there a research method?

Or is there a way to figure out that might be different from person to person, when they should be focused more on rebuilding, repairing, generating growth, like factors that are there every day all day, but I think environmentally, even just with iron EMFs, insulin, glyphosate, its histamines all of those things are very mTOR stimulating that I feel like we never get a break from it.

And we are important to be able to turn on our sirtuins on our toffee G factors so that we get a break. I guess the long-winded question is, have you seen any research? Or is there a specific way to implement strategies that are designed for repair processing or a toughie G and clearing out versus full-on growth-like factors? Have you seen anything done with what you’re doing? Or do your recommendations consider that or I guess I would love to hear your insight on that.

Dr. Nichola Conlon:  

Yeah. So I think what’s important to note is that when it comes to aging, it’s probably one of the most complicated things that we know in terms of biology. You know, if you were to look at, obviously, I’ve simplified it quite a lot and said, there are 12, Hallmark hallmarks of aging, there are 12 things that go wrong in ourselves. But, if you were then to look at each of those 12 things and look at everything that’s influencing them, then everything that’s influencing them, you would end up with a huge, huge network that has 1000s of different genes and proteins and pathways in it that are all interlinked and they’re all influencing each other. So when it comes to the hallmarks of aging, everything is in a length there is nothing that is standalone.

And although You know, we focus today a lot on NAD just because you know, that’s a topic that we’re interested in, you know it’s some, you can’t just, you know, boost your NAD and think that’s going to be the be all and end all of it as you say, you’ve got to factor in a lot of the other areas like mTOR, NPK, and all of the other things that are going on senescence, that all having an impact, not one single thing will fix the aging process, that is never going to happen.

And so when you know, when you mentioned things like balancing between building and repairing and protecting the sort of the mTOR pathway, things like that, the best way that I find to explain to people about this is, is to kind of get people to think about why we age in the first place. Because a lot of people don’t understand that they don’t understand that. You know, they think aging is just this natural thing.

And you know, it’s like it’s programmed. And there’s nothing we can do about it. But actually, aging is quite a new thing in terms of the human race. And it’s quite a new phenomenon. And this is because we never used to live long enough for aging to ever become a problem. And the reason for this is because we are as a species essentially designed to, you know, be born and have a life purpose of reproducing, passing on our DNA to the offspring. And then as far as our biology is concerned, that is our job done.

And this is called the disposable. So my theory of aging, which is basically that our body is a shell, protects our DNA to make sure that we pass it on to the next generation, which seems incredibly crude. But as far as evolution is concerned, that is what we’re designed for. So evolution has done a very, very good job at optimizing our bodies at being very good at being young.

And this is because up until about two 300 years ago, our average life expectancy was around age 40. We never lived till age 80. So everything in terms of our biology is designed to be very good and living up to around this age, which by no coincidence is just past childbearing age.

And then that’s it, because why would evolution do a good job of optimizing our biology to be good at being old when we never reached old, therefore, none of the traits that would make us good at being older, whatever selected for? What this means is that we have a lot of pathways in our bodies that are very good at keeping us up being young. But think about what our lifestyles were like when evolution designed us in this way.

We were hunter-gatherers, we were going for long periods without food, we weren’t eating three meals a day with a snack in between, like were promoted to, we weren’t sitting at computers, we were a lot more active. So what our biology is designed for is this way of life. So what you see is that a lot of the beneficial pathways that are involved in things like repair autophagy recycling and cellular health only get activated in times of cellular stress.

So in times when there’s a you know, we’re deprived of nutrients, or we are exercising hard. This is when things like autophagy, the sirtuins, NAD, all of these things suddenly sprang into action. When we sit at a desk all day not doing anything, and eating, none of these pathways get activated. Right.

And that’s because as modern humans, we’re now living a completely different lifestyle to what our genes and our biology were designed to do. So for me, the best way to act start activating some of those cellular pathways that are involved in repair, and autophagy.

And things that are known to be associated with good cellular health is to go back to how we’re designed to be, which is introducing periods of fasting to switch on these pathways because what I always say is that our bodies are very, very good at looking after their cells, it just gets switched off.

And you just need to switch it back on these pathways are not lost, they’re just switched off. So fasting is a great exercise and you know, high-intensity exercise as well as endurance exercise are all very good ways to activate a lot of pathways. And guess what a lot of these processes these lifestyle processes work by actually increasing NAD.

Dr. Joel Rosen:

Yeah, you know, I love the answer, I give that a lot to the people that I work with as well when I do these genomic interpretations, especially like you said, like, think about how we were designed over the millennia, and how much we’ve deviated from that.

And I even find now Nicola, maybe you could agree or not, that some of these more favorable genes that got turned on or turned off, or were passed down, are now less favorable, obviously, because of our environment, what we’ve introduced into the environment. Now I see that the lot of people that we work with, have major issues with recycling their iron, and NADPH is a major coenzyme that’s needed for that process.

And just like NAD, the environmental triggers with glyphosate and fortification and synthetic nature’s EMFs. I mean, I hate to say that the sky is falling, but a lot of these environmental triggers, turn on those genes that were evolutionarily favorable in the past. And now they’re not. I mean, have you seen that as well? Or?

Dr. Nichola Conlon:  

Yeah, so a very classic example of this is senescence. So we know senescence for people that haven’t heard of it before is a process whereby if we accumulate so much damage and ourselves to the point where it can’t be repaired, our cells trigger like an alarm bell that says, Oh, my goodness, we have to stop this cell from replicating and shut it down.

And rather than recycling and getting rid of the cell, what happens is the body just puts it to sleep. So often, these are referred to as zombie cells, because they’re not dead. They’re just sort of sleeping in, like in a trance, but they remain in the body. And when we’re young, you know, this was a very good way that evolution designed to stop us from getting cancer, essentially, it meant that if too much DNA damage accumulated in the cell, which could then become cancerous and replicate uncontrolled.

And you know, this was a way of very quickly, nipping it in the bud and getting rid of that cell while putting it to sleep. But now that we are living long, you know, what happens is these cells accumulate in our bodies, which, you know, hundreds of years ago would never happen, because we never live long enough for these cells to accumulate, but now we are. So this is something called antagonistic player trophy, where it’s something that our evolution has designed, which is beneficial when we’re young, but then becomes an issue as we get older.

Because yeah, again, you know, it was never selected to help us live longer, it was selected to help us get to childbearing age, and then that was our job done. But now these senescence cells are sitting in our bodies secreting inflammation, they’re taking up space. So it’s estimated that around 30% of our tissues and organs, as we get older, are comprised of senescent cells, which is why you see in older people, they get heart failure and, you know, organ failure, the skin loses its elasticity because all of these cells are sitting there taking it room, but not performing the function that they should be.

Dr. Joel Rosen

Yeah, you see that with the brown spots or what they call the liver spots? Yeah, no, that’s excellent. I love the way that it’s headed now, it’s not just here’s the product and take it but we’re doing research-based clinical trials to determine exactly what the outcomes that we’re looking for validating it having these variables that you’re manipulating and proving that it’s there.

But more so of what we just said in terms of well, it’s not a magic bean and you have Jack at the end of the beanstalk with a pot of gold, you have to fast and move and get outside with nature and do the things that are free in life that you don’t need to have a PhD to understand. So awesome. So the product name is Time Plus, and you know, you’ve been fortunate Are you kind enough to do a discount I’ve put it as Dr. Joel 20. Where did where did they go to check out the product?

Dr. Nichola Conlon

Yeah, if you want to learn more about the product, you go to our website, which is nichido.com, which is spelled out as uchido.com. And I’m sure you’ll pop that in the notes. But yeah, and we’ve got all the information about our clinical trial results on there all the different ingredients in the product and what the target and how they work. And yeah, we’re I’m a huge advocate of education. I think it’s very important for people to learn about all this science. So you’ll also find it a huge resource of has lots of different blog articles, all about aging. Well, I guess So,

Dr. Joel Rosen

yeah, that’s awesome. So I have two questions. Two more questions, and I’ll let you go, I appreciate your time. And the first one, I’m putting you on the spot, because I told you beforehand that I wanted to get your DNA and be able to run it.

And maybe we can do a part two and get your insight with my insight as to how this fits into your research and what I teach people about these factors that ultimately are the perfect storm that could either preserve your NAD or look at it as a demand and supply these are the things that demand its production. These are the things that supply its production. And we find that you know, you have a surplus or deficit and these are the things you could work on. So the first question is, what’s next in the research for new Chico? Are any any interesting things coming down the pike?

Dr. Nichola Conlon:

Yes, so you know, I am still an active scientist, I have a lab that I manage, and I have Ph.D. students who are chained. We do a lot of active research. We’re currently very focused on senescence, which is exactly what I’ve just been talking about. Senescence and NAD go hand in hand, it’s thought that a lot of the inflammation that degrades NAD comes from senescent cells. An equally low NAD can then cause senescence because lack of repair causes senescence cells. So it’s like a vicious cycle. So yeah, senescence is a key area that we’re working on at the moment. And that’s probably an indicator of what may be on the horizon.

Dr. Joel Rosen:

Awesome. Okay. And then lastly, which I mentioned earlier, is that knowing what you know, now Nikola, in terms of health and longevity, and things that you can do proactively, I guess the question is, what would you have told the younger self that may not have been privy to that information that might have helped you along and any journeys challenges or? Yeah, that you may have had along the way,

Dr. Nichola Conlon

I just think it’s just incredibly important to understand your biology. And I think I tell this to everyone now because I guess when I started in this field, it wasn’t available to consumers. So you know, like some of the tests we’ve been talking about, like genetic tests, biological age tests, the blood testing, I think it’s just so important to get a good snapshot of your biology when you feel good. So that when things start to slip, and you think, Okay, I’m not feeling great, you know, what all of your biology is, and your biomarkers and your numbers are when you are good. Because otherwise, you end up in a situation where you go to the doctor and go, I don’t feel good.

And the doctor goes, oh, we’ll take your Bloods, oh, well, they’re within average, as he as you were talking about earlier, and then, you know, you’re like, Well, I don’t feel good. So something must be wrong. And unfortunately, we’re not average, we’re not, you know, we are all individuals. And I believe in the future that when you know, every child is born, they’ll have the genetics done.

And they’ll know exactly what they are going to respond to in terms of lifestyle in terms of drugs, in terms of, you know, a lot of different things, what their risk factors are things they need to be careful with, you know, the future will be personalized, but we’re not yet. We’re not there yet. But consumers do have access to things that can start them off on that journey now.

Dr. Joel Rosen:

You know, awesome. And I find obviously, with AI how accelerated the learning curve is. It’s quite amazing. But yeah, you shared amazing information today. I appreciate your time. There’s a lot more I could ask you, but I wanted to keep it brief. And I think we gave a great overview of it. I appreciate everything that you do. And I look forward to potentially doing a part two with every view of what you send me and I wish you nothing but future success in everything that you do.

Dr. Nichola Conlon:

Thank you so much. And likewise, thank you so much for having me on. And I look forward to digging into my DNA and yeah, having a bit of a geek out about that.

🔥My favorite NAD Supplement https://nuchido.co.uk/DRJOEL use discount link DRJOEL20 


Instant Energy Surge Cheat Sheet

Claim your 5 Hidden Energy Triggers