132: I Tested a Fasting Supplement for a Year — Here's What It Did to My Biological Age | Chris Rhodes, CEO of Mimio Health

Extra: Dr. Chris Rhodes PhD is a leading expert in nutrition, biomimetics, and healthy aging. Eight years of rigorous clinical fasting research at uc. Davis led him to discover unique molecules. Nico Sperm Aine, PEA and OE. A upregulate in the body during a fast working to reduce inflammation, fight oxidative stress, and support heart and metabolic health.

This led him to create mimeo, the world's first fasting mimetic supplement. Designed from human biology award-winning mimeo delivers the same beneficial molecules the body produces during a 36 hour fast, providing measurable, cellular, metabolic, and longevity benefits without requiring any change in diet or lifestyle.

MK: Before you fast forward. I know, I know nobody likes ad breaks, but hear me out. What if I told you our sponsor this week is literally a device designed to make you less stressed? Seems like the least annoying ad you'll hear all day. And here is my take. I've been experimenting with wearing Apollo all day, not just at night, and the difference is hard to ignore.

Apollo is a wearable that uses gentle sound wave vibrations to signal safety to your nervous system. And smart vibes is the AI that learns your patterns and delivers the right support automatically throughout the day. On days I do it, I feel more at peace, less reactive. I get more done without it. Low grade background stress that usually follows me around and I'm not doing anything differently.

I'm just wearing it and letting smart vibes run. That's the thing about Apollo that most people miss. Even when you're doing everything right, eating well, sleeping well, training modern life still generates background noise. Your nervous system has to process. Apollo helps take some of that load off.

Smart Vibes learns when your body actually needs support and delivers the right vibration at the right time. You don't manage it, it adapts to you. The longer you use it, the better it works. It becomes one of those things where I notice it most when I forget to wear it. So check it out at Apollo neuro.com/michael Kummer and use code primer shift for $60 off.

Alright, Chris, so happy to have you on the show, um, for numerous reasons. One of 'em, you're, I know that you're a very smart cookie and know a lot about fasting and you know what's happening inside of your body when you're fast and the downstream benefits and consequences of doing that and some of the molecules that you know, you can, I guess, supplement with to mimic fasting.

Right. I know that you launched a product that does specifically that. The most interesting aspect of all of this. We conducted an experiment and it's been going on for a very long time. Not intentionally, but because of some mishaps. Uh, we basically did a, um, a true age test to figure out, uh, what is my true age and what are some of the.

Um, epigenetic markers before we began sub or before I began supplementing with, uh, with Miu, which is the supplement that you created. And then we actually did one in between and then at the end as well. That in between was supposed to be the, the last one, the end of the experiment. But, um, you know, we've, uh, I made some mistakes not fasting on the day of, of taking the second test.

Um, even though it later turned out that what might not have been necessary anyway. So we took a couple of tests in between that experiment and so I got the reports with me. Um, and I wanna dive into those with you and kind of help me, or you help me understand what are we looking at, what does it really mean?

How much in trouble am I, do I need to do anything differently? Um, can I do anything differently? Um, but before we get to that, maybe, you know, just give a little bit of background. What, what do you do? Um, what is your research expertise and how did you come up with developing a supplement to mimic fasting?

Chris: Yeah, absolutely. So I got my PhD in nutritional biochemistry from, uh, uc Davis. While I was there, I was really, really interested in fasting, mainly because it's one of the only ways that we know of. Right now to reliably extend lifespan in animal models. So if you put animals on, let's say an alternate day fasting regimen, so eating normally one day, fasting the next day, eating normally one day, fasting the next day, rinse and repeat for an organism's entire life.

They can live anywhere between you. 30 to 80% longer. And that's often in the absence of caloric restrictions. So literally, just by changing around the timing of eating and doing this alternate day fasting, you can significantly extend lifespan. And then even beyond that, when you dive into all the resource that's been done on fasting, it also really helps to.

Uh, extend health span as well, so helping to treat preventive delay most major diseases. And what I found really fascinating about fasting. Was that it does all of that without actually adding anything into the system, right? So it's not like this superfood or this wonder drug that's triggering all these amazing benefits that happen, but somehow your body is essentially activating this innate Longevity Bio program is what I like to call it, the kind of restructures cellular functionality towards repair, maintenance, and survival.

And. When that kind of clicked for me, I actually got mad about it because I was like, great, my body knows how to live to be 120 years old in perfect health, but it's just not doing it right. So that kind of catapulted me into the fasting research zone of, you know, what is happening in the human body during these longer fasts, and is there a way that we can recreate those benefits without having to do something like, you know, alternate day fasting for the rest of our lives.

MK: Right. I mean, one thing that you said was super interesting and I think that's, that's one nuance to fasting that is underappreciated. You said without caloric restrictions. So if, if I hear that, what that means for me is if I fast today and eat tomorrow, I just eat twice as much tomorrow and then. Not, you know, on, on the next day.

So I'm really eating the same amount. I, I don't have to because caloric restriction only works for so long, right? I mean, if, if, if you've been trying a, you know, eat less kind of diet, at some point you say, screw it, I'm hungry. I need to eat. And you'll probably then make everything up again. Um. Of course, if you eat a little bit or if you restrict every single day, if you have a caloric deficit every single day, you're never fasting.

You just feel grumpy all day. 

Chris: Yeah. The anger. Yeah. 

MK: Right, right. Exactly. But if you, if you suck it up for one day and then just eat, you know, twice as much the next day. That's really an amazing kind of thing, because I assume, I mean, yes, the, the experiment has been done on an alternate day fasting, but I assume there is some sort of flexibility where you might get fewer or more benefits depending on the fasting window, right?

Extra: Yeah, absolutely. 

MK: So you could even say, okay, I'm gonna, you know, not eat, instead of not eating for 24 hours, I'm gonna do it only for 20 hours, or I'm gonna, you know. And you probably get a little bit less, maybe, I don't know if those experiments have been conducted to see where is the sweet spot? How, how long do I really have to fast at a minimum.

Chris: Yeah, there have definitely been many experiments looking at the different lengths of fasting and what the general benefits of each of them are, generally speaking. You are probably not getting the amount of fasting benefits that you think you're getting, especially for the more typical style of 16 eight fasting.

So biologically speaking, your body actually has to get to. A depletion of its glycogen stores or its stored carbohydrates in order to actually get that metabolic switch from, you know, glucose metabolism over to fat metabolism, ketosis, fasting pathways getting activated, that usually takes around 20 to 24 hours.

So, gotcha. We're doing 16, eight fasting. People often think, oh, I'm getting like these autophagy benefits, I'm getting these anti-inflammatory benefits, I'm getting, you know, stem cell regeneration, things like that. And those things don't show up until at least 24 hours of fasting. And then oftentimes they don't peak until, you know, the 72 hour mark.

MK: Mm-hmm. 

Chris: In order to get these benefits of fasting that we really think we're getting, especially on the longevity side mm-hmm. You really need to do these longer terms. Fasts like a 36 hour fast, and that is one of the reasons why we made Mimeo was to help people really get the most out of the fast that they are doing, or to get the benefits of that 36 hour fast, but without actually having to do the fast.

MK: Right. Gotcha. Now I'm super excited to look at the reports, but maybe one thing before, because. I know, I remember a time a few years ago where intermittent fasting was the thing. 

Chris: Yeah. 

MK: And then as so often the case, you know, a couple of years later, it's like, oh, fasting is the worst thing you can do. It's gonna ruin your hormones.

You know, especially if you're a woman. Don't ever think about not eating, because what's the deal? I mean, are are there. Downsides to fasting? Is it, you know, are there, you know, sex specific things to consider? Maybe cycle specific. Not only whether or not you're a woman, but you know, are you menstruating?

If so, what's, you know, part of your cycle you're in? Um, is there such a thing as, um. If you're fast and you're already super stressed, you add more stress to your body that you might not be able to handle. What is the nuance to all of that? Um, 

Chris: yeah, there's a lot of differences in not only, yes, gender specifics for fasting, but also individual responses to fasting as well.

So one of the main, you know, consequences, downside of prolonged fasting is of course if you are doing fasting and stacking caloric restriction on top of that, which tends to happen because people find it very difficult to, you know, condense the whole amount of calories that they're supposed to be eating.

In a day, let's say, down to like one meal, right? If you're doing a one meal a day fasting schedule, or if you're doing alternate day fasting, people have a hard time putting in double the calories the next day. That's one of the reasons why fasting became so popular in the first place, is because it's kind of like, oh, it's effortless weight loss as long as you mm-hmm.

The program. Um, and it really helps get your glucose levels back in. Check your hunger signaling back in, check your circadian rhythms back in check. But when you do that for a long period of time, especially with women, you do disrupt the hormonal cycle. You do disrupt the menstrual cycle because you are essentially telling your body at a metabolic level, this is not a good environment for bearing children.

Right, right. We can, we don't even have the resources to be able to. Feed ourselves. This is not the time to try and procreate and bring a child into this, that we're not gonna be alive. Right? So like that's actually one of the reasons why fasting is very good for longevity, um, because both men and women get that signal.

Like this is not a good childbearing environment. So the body focuses on we're gonna try and keep. This generation alive and functional as long as possible. Mm. Go out and find a new environment that's rich in resources and we can actually, you know, support the next generation of progeny. 

MK: Uh, I mean, you know, it's makes a whole lot of sense.

Um, and, and it's not necessarily surprising, but it's, I think something that. I dunno if most people probably don't think about, you know, extending there is probably such a thing as a, as as an optimal lifespan. Mm-hmm. For a human, right? 

Chris: Yeah. 

MK: Yeah. And there are ways I suppose to extend that. But it's not without a cost.

Chris: Yeah. The the saying that I love about it is that in order to live longer, oftentimes you have to live less, right? Yes. So a lot of the things that we love about living, right. Alcohol consumption, right. You know, like eating like every day or every mm-hmm. Hours, right? Never being hungry. Things like that, those tend to actually accelerate the aging process going out and, you know, sunbathing, right?

Same thing. Uh, so oftentimes the things that are pleasurable and you know, we like to do are often bad for us. And the things that are good for us are often just kind of like boring and bland. And that's just another fun facet of longevity. A lot of it just comes down to. You know, we, we talk about longevity all the time as like anti-aging, right?

Like, oh, I always want my cells to be renewing. I always want my cells to be turning over so they remain like youthful and fresh. But that's not actually the way that you achieve longevity. That's actually accelerating aging because your cells can only divide so many times. Mm-hmm. Before they reach the ha flick limit where they can't divide anymore and they just start dying.

You. Start building up a bunch of mutations. Your telomeres get short. Your DNA starts getting damaged. Your cells just can't function as well. So what we actually want to do for longevity is not super duper speed up the cellular growth and renewal cycle, but actually slow it down as much as possible so that we're not doing a bunch of replication and we're actually focusing on cleaning, maintaining and repairing the cells that we already have.

Mm-hmm. That leads to maximum survival. 

MK: All right. Uh, you know, from a, I guess from an athletic perspective, the, you know, uh, something comparable would be, well, if, if you wanna be the best in something, you know, being the strongest guy, the fastest guy, what have you, you're not necessarily, that's not necessarily good for longevity, for the longevity of your joints, of your muscle tissue, of, you know, none of that because you, you, you pay the price for being strong, right?

For being, you know, being able to lift 500 pounds or what have you. You know, so there is, the question is, okay, shouldn't there be a, and I, I hate the word kind of balance because it very much or very often implies a lot of good and a lot of bad. And somewhere in the middle is, is okay. Um, I, I, I'm, I'm not a balance kind of right in the middle type of guy, but nonetheless, I think there is got to be a.

A balance where you live your life to the fullest, but also achieve decent longevity and health span. Right. I think for me, the health span is arguably more important than, than lifespan. I don't care that I live for a hundred, you know, 120 years, but in a wheelchair for the last 20. Um, but I also don't want to have a health span of, you know, of.

Of 60 years and then drop that as a perfectly healthy, you know, human being. So there's gotta be, I guess somewhere in between where you also have to, I guess there is, I guess no way around of, of, of, uh, having a decline. You know? I mean, we're not gonna get any, none of us are getting any younger, right? The question is, where do you wanna keep that balance?

Do you wanna look like Hulk until you drop debt or are you okay with being just more of an average person? Maybe with more mobility, maybe with, you know, just being able to walk without pain. Whereas the guy who lived all of his life might have troubled walking pain free, you know, 50 years into his lifting career.

Chris: Yeah. 

MK: You know, and, uh. 

Chris: Yeah. And I think that that's a really good distinction. Like especially when you look at the longevity of, say Olympic athletes like elite athletes mm-hmm. High performers, they do not typically have exceptional longevity. And that kind of comes back to exactly what you were saying, that you are doing so much high intensity, uh, work on the early end of your life.

Like that kind of exercise at a high level for a very long time really over activates the immune system. So you're kind of accelerating inflammaging, right? You're putting a lot of stress on the joints, you're putting a lot of stress on just the musculature itself. You're kind of always in this growth.

High metabolic rate, high energy consumption, high energy production, um, state of the body. And that often leads to a lot of. Oxidative damage, a lot of inflammation. Mm-hmm. A lot of cellular dysfunction that can happen that's kind of accelerating these pathways that are associated with aging. And what's interesting is almost all pathways that are associated with aging are also associated with meta metabolism and specifically metabolic growth.

So things, mm-hmm. mTOR and IGF one and insulin glucose levels. Those things are really gonna be the thing that's gonna be driving a lot of cellular growth, proliferation and ultimately, you know, accelerated aging. While these other sides of the coin, these anti-aging pathways are also metabolic things like a MPK, NRF two, PAR Alpha, like NAD cert pathways.

All of that is highly related to metabolism as well. But those are the things that are, um, anti-aging and those are the things mm-hmm. Activated by fasting. So if we have a longevity program that's already inside of us right now, it is absolutely activated by fasting. And fasting then kind of becomes this.

For, all right. What are the pathways that are being activated? What are the things that are activating those pathways? And then how can we recreate that so that we can, like what do what we do at Mimeo, which is put fasting in a pill. 

MK: Right, right, right. Okay. It makes a whole lot of sense. Um, maybe not before we, we start, um, looking at, at my reports, talk a little bit more about Mimeo, what's in there.

How does it mimic fasting? I mean, how can I take a capsule and, and tell my body, Hey, I'm actually fasting even though I'm, I'm might be, you know, downing, you know, five pounds of brisket at the moment. Um, how, how does that 

Chris: add up? So, uh, what Mimeo is and what it's doing is based on all of the research that I was doing for my PhD at uc Davis.

So what we did is we had people come in. For a 36 hour fast and looked at their before and after. And what we saw was that when people fast for 36 hours, they became really functionally enhanced at the cellular level. So they had, you know, less oxidative stress. Better antioxidant cap capacity, uh, better anti-inflammatory ability, better cardioprotective ability, better metabolic function, and metabolic flexibility.

And that was really interesting to us because what we were looking at was young, healthy people. So mm-hmm. The three, six hours of fasting was able to turn these already young, healthy people, essentially into super people just through a single day of fasting essentially. So we wanted to know, okay, what is happening that could be driving these changes in functionality?

So we did what's called comprehensive metabolomics, basically looking at all of the small molecule components of the plasma. And what we found was that when people fast for 36 hours, there's this unique set of molecules that are produced by the body that are really only elevated during a fast. Mm-hmm.

And those were the ones. Responsible for activating a lot of these cellular health and longevity benefits. So we screened through those molecules. And we're able to eventually find this synergistic combination of four that when we put them together, could recreate these cellular benefit that we were seeing.

So those same anti-inflammatory effects, those same antioxidant effects, those same protective and metabolic effects. When we took this formulation and did a lifespan extension study in animal models, we were able to extend their lifespan by 96% just through supplementation. So what Mimeo is doing is essentially taking what your body would naturally produce during a fast, and then just giving it back to you as a supplement so you can recreate fasting at the molecular level, activate those same pathways, get those same benefits.

Without actually having to fast. 

MK: Mm-hmm.

And how did you guys find out that those molecules are actually doing in the body? 

Chris: Yeah, so in the initial study we were just looking at their, uh, functionality on human cells. So we had taken cells from the participants in the study, added in the bioactive fasting metabolites, and just we're tracking what happens to cellular functionality when this happens.

After that, we've then done three different clinical studies with the formulation to make sure that it's safe, that the molecules are bioavailable when you take them, you know, they appear in the body, they're actually doing things, and that they have, you know, functional benefits at the end of the day. So the first one that we did was basically looking at.

What happens when you give someone Mimeo while they are eating? Mm-hmm. So we had people come in, ate a standardized breakfast, alongside a placebo control, and then looked at their cellular functionalities in the postprandial state, the post eating state. And just track that through. Then we had them come back after a washout period, eat that same breakfast, but then with supplementation, with Mimeo and track those same functions.

And what we saw was that when people ate the standardized meal on its own with the placebo control. There was this big loss of cellular functionality, so they became, uh, prooxidant, they became more inflammatory, they became less cardioprotective. But when they eat that same meal, but with supplementation, with mimeo, not only were we able to prevent all of that loss of function, but then we were also able to add gains of function on top of that.

That mimicked what we saw during a fast, so they became anti-inflammatory and antioxidant and cardioprotective and metabolically flexible. So that was really our first one. Then, uh, we've done another one in conjunction with Mount Sinai, basically a a, a. An eight week study looking at what happens to the metabolic side of things, what happens on the biological age side of things.

What we saw there was that we have really great impacts on both glucose and cholesterol control, so improved glucose levels improved. HV A1C levels improved. Total cholesterol, higher HDL, lower LDL, so that was great. We saw a 50% increase in free testosterone in that, uh, eight week. Time period, which is amazing.

And then we also saw a two and a half year reduction in biological age. And then the third one after that was our latest randomized double-blind placebo controlled study. This was just published in Nature Scientific Reports, and what we found there was, uh, we took a equal population of both men and women on either a placebo or on mimeo just for eight weeks.

And no change in diet or lifestyle at all. And what we saw there was a really powerful impact on appetite suppression and hunger control. So people reported much less, uh, hunger over time. They reported improved satiety, so getting fuller faster, staying fuller longer. They also reported decreased food noise, decreased distractions from cravings, and just less hunger overall.

Mm-hmm. Uh, there were digestive benefits, so less bloating, less abdominal pain. Um, we also saw those same metabolic effects again, so improved glucose levels, improved cholesterol levels. We saw lower oxidative stress levels throughout the body. So, you know, all of these things together, kind of like this is actually activating these fasting like pathways, right?

These fasting like benefits even when people are eating and without having 

MK: mm-hmm. 

Chris: Test at all. 

MK: All right. Well, that's, I guess, a good segue now into, into our experiment, which was not a double, uh, blind, um, control to anything, and it was more like an n equal one. But nonetheless, I only care about myself, not even broader population.

You and Brian Johnson. 

Chris: Good company. 

MK: Thank you. All right, so let me share my screen. All right, so I'm 44 years old, well, 44.09. Apparently at the time of the test. Which was in February. Mark took forever. Get this back. 

Chris: It did. 

MK: Um, all right, so apparently I'm 44 years old. Great. We already knew that. But I think the nuance to that is, um, I think here it shows actually.

Some of the history. 

Chris: Yeah, a little up and then a little bit back down. 

MK: Yeah. So I'm not sure exactly what I did in there, but um, I was at one point, almost four years older. 

Chris: I actually think that this was the one where you had gone in and you were not in a fasted state when 

MK: Yes. 

Chris: You were in before. So that could be, you know, one of the things.

Correct. That was driving a bit of the markers up there. 

MK: Correct. Yeah, that's a good point. All right. And now we have this, this looks different every single time I take it. 

Mm-hmm. 

MK: Um, so maybe tell us a little bit about what is this? What does it say about my organs? 

Chris: Yeah. Well, I actually can't give you too, like in depth of an analysis since this isn't, um, you know, I don't, I don't know all the backend of the true age systems and what they're actually testing here, but I believe what they're going for is they're taking DNA methylation patterns from.

All of these different, uh, gene sites that are associated with things that are important on a functional basis and blood markers, right? So they're testing specifically the methylation patterns that are all around these genes on things that control production of CRP or IL six or, you know, fasting glucose levels, things like that.

So, and then, you know, aggregating them together to say you are. X, Y, and Z age older or younger than your actual chronological age. So these should hypothetically be giving you a measure of biological aging versus chronological aging. 

MK: Okay. All right. Yeah, the, the one thing that has always been much younger is my lungs.

I don't know exactly why that is. I mean, I've never been a smoker, but beyond that, um, 

Chris: some 

MK: of the, 

Chris: I mean, you're a, your fit guy, right? You know, you, I'm sure you do a lot of cardio. I'm sure you do a lot of weightlifting, so I would assume that your lung health would be very good. 

MK: Yeah. More weightlifting, I guess, than anything else.

Um, but well, and some high intensity stuff, but. Okay. Then the next thing I think that's also somewhat important is the rate of aging. 

Chris: Mm-hmm. Yep. Exactly. 

MK: And so the good news is I'm, I appear to be aging slower than, uh. Then I should, 

Chris: right. Exactly. And this was also the metric that improved over time. And this, you know, very, I think importantly is also the metric that's kind of considered to be the gold standard of biological age tests right now that's been very well validated and very highly used.

This is actually the score that. We use for the, uh, rejuvenation Olympics. Right? So the global tracking on who is aging, the slowest is done with the dunin pace at, uh, 

MK: okay. All right. I think that was it on this, and then we have the, the advanced report. Let me bring that up. 

Chris: Mm-hmm. 

MK: To see what that says. So here it looks like we have two different ages.

Chris: Yep. One of them being the, yeah, the symphony age versus the OICM, and I think that the symphony age is what we were seeing before where it's all based around the biological ages that they're scoring your organ systems at. 

MK: Gotcha. Okay. Same pace of aging, I guess. Not much has changed here. Fasting glucose high.

Um, that's one, one thing that's, well, there are two things that I always find interesting. My, typically, my fasting glucose when actually done a blood test is never high. Um, the one thing that is consistently high is my hba one c, even though my insulin. Is somewhere between 1.8 and 2.5, which I think is at least below two, is very much on the lower end, I would argue.

Yeah, 

Chris: definitely. 

MK: Uh, and. And so tho those never appear to match. I appear to be very sensitive to insulin, but I have high average, and the one, the only explanation I found is that apparently my red blood cells might be living a little bit longer. 

Chris: Mm, yeah, absolutely. 

MK: And so it skews the, the calculation.

But what I've not, what I've yet to figure out is, is that a good or a bad thing that my, the longevity of my red blood cells is. 

Chris: Longer. 

MK: Yeah, 

Chris: it's actually very interesting. So there, something that happens during fasting is you typically see a high level of bilirubin, um, in the bloodstream, and that's because a lot of the red blood cells are turning over in terms of.

Their functionality. So your body during a fasted state kind of looks at the older red blood cells and say, eh, you're not functioning as well. We can't keep you alive quite as much as these young healthy cells that are really doing their job. Let's start lysing them and like moving them toward the end of their life cycle.

So we can just have young mm-hmm. Healthy blood cells. So you get a high level of bilirubin because you're doing that red blood cell lysing and it. Is basically that exactly what we were talking about, that cellular refresh that's happening. So higher longevity on your red blood cells I'm sure can actually be a good thing, right?

Because it just means that they're sticking around longer. However, at the same time, it could also mean that you have more on the higher end of the spectrum where they're not quite as functional, so, 

MK: mm-hmm. 

Chris: I can tell you, I'm just hypothesizing, but it's an interesting balance. 

MK: All right. Creatinine has also always been high.

I guess that's, you know, just due to the fact, I assume muscle breakdown or muscle turnover because of workout and those kind of things. 

Chris: Yep, absolutely. Same kind of situation we were talking about with the red blood cells. 

MK: Um, those things I'm actually not familiar with. 

Chris: Yeah. Uridine kind of has to do with like the methyl pool.

So basically looking at how much like mRNA to a certain degree you have floating around your system, as well as how your methyl donor system is, um, is behaving. So a low uridine level can mean that you're. Your methyl pool is low, which can hamper some, um, some metabolic functions and hamper some like critical like methylation patterns and methylation functions as well.

So this could also be kind of like a little hint for us on seeing some weird things within your, uh, your biological age or your methylation patterns. If there's a, if there's low uridine that will affect the methyl pool. And the epigenetics. 

MK: Okay, same with that. Gluconate cut, added sugar. I don't need edit, sugar 

Chris: and 

MK: process.

Chris: Always a good decision. Yeah. So I mean, you know what they're, what they're basically telling you here is to consider LALA consider Bering consider, you know, dihydro, berberine, right? These are all things that activate AMP kinase. Which will shift cellular metabolism over to fat oxidation rather than glucose metabolism.

Mm-hmm. Right. Okay. So, um, that's gonna be something that Mimeo also does. So we have like OEA and PEA that are in there, that are A MPK activators and can help shift that cellular metabolism over 

MK: Okay, gotcha. Symphony H. All right. We talked about that.

I think that's pretty much the same thing that we saw before. No, that one, I mean, we talked offline before, but the one thing that always, uh, amazes me is my immune marker. You know, I'm the one who never gets sick when people around me get sick. I, I would argue that I have a very robust immune system from a practical perspective, but this.

Says something different. 

Chris: Yeah. Which is really interesting. Right. So I think a good thing to to consider here, which we were talking about offline before, is that in biology, in biochemistry and cellular metabolism, all of this stuff, we have what's known as the transcription translation gap, which is essentially.

That there are different stages of how something goes from, you know, being inside of your genetic code to then getting, uh, transcripted, which basically means becoming mRNA, which is like the little messenger molecule that then goes on to go through translation and turned into. Let's say like a protein, right?

Or some other substrate or some other molecule or some other chemical. So there's a bunch of different steps within the transcription translation cycle, and oftentimes we think, okay, if you know we have a bunch of mRNA that's being created from the DNA. That should lead into a higher amount of this protein or this marker being produced.

But oftentimes that's not actually the case because there are a lot of inhibitory factors. There's a lot of different like null fires that can come in and either act as counterbalances to the mRNA or disrupt their signaling or like gobble them up. So it's not the, that's not always gonna translate over into, okay, I have high mRNA for IL six or an inflammatory cytokine, or something like that, which actually ends up.

Meaning I have high produced levels of IL six, which are actually more clinically meaningful thing, and so we are actually even one step further back from this. Right now we're at the DNA methylation level. So even before we create the mRNA, and even before we translate that into the marker. We're over here on the DNA side.

So that's, those are the changes that we are tracking right now. So sometimes, you know, what's happening at the DNA level is not gonna show up in the transcription level, and then that's not gonna show up in the translational level. So even though you're seeing these markers change around, right, they necessarily have to do with your actual blood values of these 

MK: things.

Right? So, I mean, practically speaking, just to pick out, you know, one marker that I know from the top of my serum, you know, high, high. High sensitivity CRP C-reactive protein, you know, that I've been tracking for years and years and years. Always been below 0.3, so fairly low levels of inflammation, and over the years I've tracked some other inflammatory markers along the way as well.

Also very, very low, so evidently inflammatory wise, and that I guess is somewhat related to the immune system as well. There does not appear to be a problem, not a, and and I have always said, well, that's because of my lifestyle, right? But seeing this what I'm not, what, what I'd like to know is, okay, based on what I'm doing, should I be doing something to address it on the epigenetic side already?

Even though all those things appear to be mitigated, then. Along that pathway and I'm not really affected with by it. I is there, is there a benefit to trying to address the epigenetic side? Is there a way to address the epigenetic side that is not, that is different to how I address the practical implications and my actual blood work?

Chris: That's a great question. And from what I know right now, not entirely. So there are certain. Interventions that we know of that do alter epigenetic patterns. Fasting is definitely one of them. So fasting and caloric restriction in general also, uh, run through this pathway. NAD cert. Right. And what sirtuins do is essentially they are, uh, histone.

Deacetylase is, so they. Um, in order for your DNA, which is wrapped around these little histone molecules to unravel so that they can actually be transcripted and then translated into whatever specific protein or marker or molecule your cell wants to create, they have to be like unraveled and they have to be stuck out from the histones with these little.

Acetyl group markers that allow them to get enough space from the, um, from the histones to actually be trans transcribed. What sirtuins do is they remove those acetyl groups, which then tightens the DNA back around the histones. They can't be trans, uh, transcribed. So it ultimately. Reduces the amount of proteins that are being created.

It reduces the amount of mRNA that are being created, and that ends up reducing DNA damage, reducing, um, mutation rates, and then also conserving cellular energy. So those are kind of the things that epigene modifications can, and how fasting and tion actually affect. Do we know anything right now that can give you a one-to-one of, if I do this thing, my epigenes will change and that epigene change will, uh, absolutely go on and impact my health from like a, you know, A to B2C mm-hmm.

Of situation. No, we don't really have that right now. Okay. Very early on in our understanding of epigenetics, it's kind of like the new microbiome, right? 

MK: Right. Okay. Fair enough. So then, you know, ba, based on what I've heard, you shouldn't be doing anything differently until we 

Chris: got better. I mean, I, I, I, I would say that health often comes down to the, what we call the phenotype, right?

Mm-hmm. So you have the genotype, which is, this is what the genes say, and you know, based on what the genes say. You know, this should give us an idea of how the end organism is actually gonna end up looking. But in reality, that's not true. The phenotype is actually what the end organism ends up looking like from a health mm-hmm.

Perspective or from a, you know, physical manifestation perspective. So if you are not having problems with your phenotype, I wouldn't worry too much about the genotype. Right. 

MK: Gotcha. Okay. Alright. Makes a whole lot of sense now. Maybe, you know, to zoom out a little bit, because I'm, I'm just looking, I think in March, 2025, that was the test before, right?

Yeah. That was the before test. This 

Chris: one was the baseline. Yeah. And then 

MK: right. The middle one was the one where I was not fasted, 

Chris: correct. 

MK: And then the last one was the post, uh, experiment. Yep. Now, if we zoom out, um, what are some of the things that you notice where I'm like, okay, this, this has changed.

Obviously the one thing that's I think my, my pace of aging, um, even though, funny enough, when I was not fasted, it was even lower. So. I'm not sure how to interpret that. Um, but definitely from March, 2025 to almost a year, holy mo, we, that was a long experiment to February of 2026. Um, I. I slowed down, my aging slowed down.

Chris: Yeah, exactly. And that's really what we can take from this is that although your chronological age didn't change within that one year time period, right? Your pace of aging did slow down, so that would totally track through, right? We're basically testing you one year later from your baseline, and you are still at that same chronological age.

So if, if that's the case, what your pace of aging is telling you is essentially for every year that you get older, you're actually only getting, I think your score was 0.85, so you're actually mm-hmm. Getting 0.8, five years older. 

MK: Yeah. It looks like, uh, I made up 0.2 or 0.1 years. 

Chris: Okay. Yeah. There you go.

MK: That is, I guess if you look at the pace of aging, I mean that is what is zero point 85 of 12, so that's maybe what, what is it, three years or so? Eh, three months. 

Chris: Yep. Exactly. 

MK: Of a year. 

Chris: I keep stacking that up over time. Right. That gives you some major gains. 

MK: Yeah. All right. Um, is there anything else that you saw in there?

I'm like, okay, this is something that we, you know, we, we, we should talk about. I know there's a whole lot of stuff back there that means nothing to me. 

Chris: Yeah. These are, these are all, you know, interesting, interesting markers to look at from a. Like oftentimes we look at these at blood markers. Again, we're looking these at a DNA methylation level rather than a what is circulating around in your system level.

So it's always hard to tell how those results are gonna translate to each other. Mm-hmm. But I think, you know, kind of going back to what we were saying before. Um, your IL six data was the thing that really stood out to me, um, because that was the one that had a big increase, um, at the final level, which is probably the thing that's driving up your inflammatory age and your, um, and your immune age and that I would be really curious about looking.

At your blood markers to see if you actually mm-hmm. Have elevated IL six. From everything that you've told me, it seems like, no, you probably don't. IL six is typically, it's both an exercise induced, uh, cytokine as well as a food in cytokine. So it's possible that, you know, if you. Had just done like a high intensity workout or something before you got this test done.

Maybe there were some methylation changes that happened on the backend, but just to kind of see how much these results actually translate into the phenotype rather than the genotype. Doing a blood test and looking at actual IL six levels would be really interesting. 

MK: All right. And I assume, because you said it's an exercise induced, I've had the case so many times where actually one time I went CrossFit and then the lab was across from my box, and then I just hopped over and, and got my blood work done and my CRP was through the roof.

Yep. Even some of the liver enzymes are completely off charts. Yep. And I'm like, okay, maybe there was not a good idea because my workouts, you know. 30 minutes before very likely impacted all of those markers. 

Chris: Mm-hmm. 

MK: So same with IL six. I guess I should, what would you recommend for someone? Because I've, I've, I've been asked that question now.

I personally try to not work out, uh, two days leading out nothing major. At least I don't wanna do like a MUR or anything, you know, two days before getting my blood work done because I know that my markers are gonna be off. 

Chris: Right. 

MK: So same with the IL six, as opposed give it at least a day or maybe even two.

Chris: Yeah, absolutely. For, for IL six, IL six and cytokines themselves are fairly, uh, transient molecules, so they pop up and they go down. Is if you're a normal, healthy person. Mm-hmm. If you have chronic inflammation, that's where you kind of see this steady creep up of these in pro-inflammatory molecules, these pro-inflammatory cytokines that end up damaging the system over time.

But often, especially if it's exercise induced, it's gonna be a. Pretty quick peak and then it's gonna return back down to baseline. I don't even know if you know you need a full two days. I would say if you, you know, do a regular workout the night before your blood draw, you wake up fasted, you're not working out after having slept, that's probably gonna be a good baseline reading.

MK: Alright, 

Chris: is a lot like fasting in that it's what we call a hormetic stress. Mm-hmm. So what that means is a small amount of stress that you're doing to the body that ultimately ends up resulting in a higher defensive stress, resistance, protective response from the body. So it's a little bit of stress that makes you way more resilient and healthy.

Um, over time, and so that is probably what could be happening here as well, where the IL six, you know, goes up during the exercise because it's an acute stress, but then goes back down and then you get a larger he response after that. 

MK: Gotcha. Now, because I have this page open up post-Inflammatory Marker, CRP and the IL six, I appear to be on opposite sides of the lines.

Chris: Yeah, I think, 

MK: does that make sense? 

Chris: That's a really interesting thing as well. Generally speaking, that doesn't make a ton of sense just because they're both pro-inflammatory molecules that are often. Uh, you often see them together, especially during a pro-inflammatory response or a post-exercise response, something like that.

Generally speaking, CRP is a better marker for long-term inflammatory status because it sticks around in the system longer, has a, a longer half-life, a lower turnover rate than IL six does, which is more about these acute in, uh, inflammatory processes. So it's definitely possible that. Again, you could be having really good long-term inflammatory status, which is what your CRP will be telling you, but you could have a short-term inflammatory bump that causes the IL six itself.

MK: Mm-hmm. Beyond exercise and I mean as suppose it's there, you know, sauna bathing, cold plunging, any hormetic stressor could, could cost that a spike because I've paid attention, obviously during my testing, specifically with exercise. There are other things like, I mean, I'm just, you know, to give you a very silly example, but you know, a few days ago I got 2,500 pounds of feet delivered and I had to unload those from pallets, you know, with a five gallon bucket into feed drums.

And I was doing, you know, it was like, you know, scooping. Turning Pourings and that for like, you know, an hour or so. At the end of the day, it's a workout, but if, if I have a blood work or whatever, I would not necessarily even think about that. This could potentially cause a change in my blood chemistry, or I dunno, sauna bathing or.

I dunno. Running, you know, after a hawk trying to kill one of our chick, you know, those kind of things. I mean, what other things could potentially cause a, a temporary spike in, in IL six? Mm-hmm. 

Chris: In IL six specifically something like heat shock. Could do that. Something that's gonna lead more towards a pro-inflammatory response rather than an anti-inflammatory response.

So on the spectrum of hormetic stresses, you have on one side, kind of like exercise and sauna, which have more to do with energy production. They run very. Uh, very much through mitochondrial processes, right? Mm-hmm. Cellular energy or heat production through the electron transport chain, all that fun stuff.

So those would basically be the two major stresses, or, you know, potentially even like a thermogenic, right? If you're taking that and in some way or another, those are the things that could, you know, cause pro-inflammatory stress on the body. On the other side of the coin, you have things like chloric restriction, fasting and cold exposure, which are more about activating these energy conservation paths.

Mm-hmm. So they're not going to trigger inflammation, and oftentimes they're gonna be very anti-inflammatory because that lack of energy is essentially telling your cells, we don't have enough resources for you to just be making cytokines and creating inflammatory responses willy-nilly. We actually have to like dial that back and only.

Activate the immune system if there is an actual legitimate threat. So that is one of the reasons why chloric restriction, fasting cold exposure, those things are really good for autoimmune diseases. Mm-hmm. They really help to tamp down any inflammation that's happening in the system already and help to reorient the immune system more towards.

Only respond to things that they are real. Mm-hmm. And not just, you know, making stuff up in your head. 

MK: Right, right, right. Uh, what about stress? Like an acute stressor? Or, or, 

Chris: yeah. Mm-hmm. Yeah, so you can, you like, typically stress is gonna be a bit more related to cortisol and that system. Mm-hmm. Which can increase inflammation, but it's a little bit more.

Um, it's a little bit more nuanced. Cortisol can increase or decrease inflammation depending on the context. 

Extra: Mm-hmm. 

Chris: But any, I would say that anything that's causing any kind of actual damage to the body, which of course, like exercise and to a certain degree, science Right. Can that, that's really gonna be the thing that's driving any kind of pro-inflammatory response.

MK: And food you said, right? 

Chris: That's Oh yeah, definitely. Definitely food. That's a great, that's a great point as well. So there's this thing that we call postprandial inflammation. So when that essentially means post eating inflammation. Mm-hmm. And people often think of inflammatory foods as like, oh, like, you know, pizza and trans fats and you know, these like big snack foods.

But in fact every food that you eat has some kind of inflammatory response that it happens in your body. And that is because anything that you. Take into your body is a foreign molecule and your immune system is designed to react to foreign molecules. Mm-hmm. So there's always gonna be a transient inflammatory response that happens when you eat food.

That is what we saw in our clinical study of Mimeo. The first pass through when we looked at, okay, these people ate a meal and their cellular functions went down, they were pro-inflammatory, they were prooxidant, right? That's a very common thing that we see in the postprandial state all the time, and that's why it's so interesting that Mimeo was able to prevent that oxidative stress.

It was able to prevent that inflammatory response. Um, in response to the food itself. And I think that's also why we ended up seeing improvement in digestive symptoms in the double blind study was because mm-hmm. We have this kind of, you know, broad spectrum anti-inflammatory intestinal, um. Intestinal beneficial that are happening.

MK: Mm-hmm. Now, I mean, you know, define food, would, would coffee count as black coffee count as food? Does it mean calories trigger? An inflammatory response or trust. Anything that's foreign because you know, whatever is in coffee, caffeine, and other molecules, they're foreign to the body too. 

Chris: Yes, very good point.

And by and large, you can definitely get an inflammatory response from things that don't have, you know, any kind of nutrition behind them. Right. If you're taking in a bunch of like, yeah. Coffee, tea. Whatever else it might be that's non-native to the body, your body can have a immune response to it. From the perspective of will those things actually end up breaking your fast or will you have as much of a inflammatory response to them?

Mm-hmm. Versus something like, you know, two slices of pizza or just, you know, eating a whole pizza. Right. 

MK: Right. 

Chris: It'll probably be to a lesser extent, unless you are specifically allergic to those things, right? Mm-hmm. So one of the reasons why. Food in and of itself, like a whole pizza would be more disruptive to the system and more pro-inflammatory is because in that postprandial state, your body completely shifts its priorities around going from.

Okay, let's be in maintenance mode. Let's be in repair mode. We're just in homeostasis, right? Mm-hmm. Just paining in the body to then into another kind of survival response where it's like we've got all of these nutrients that are coming into the system, these fats, this cholesterol, these carbohydrates, this glucose, right?

And we need to prioritize all of our energy towards digestion, absorption, and metabolism, so that, mm-hmm. These things that are coming into the system where they need to go so they don't actually kill us, right? If we get too high of a glucose response, we'll die. If we get high of a cholesterol response or too high of like a lipid clog, then we'll die.

So your body literally has to reorient its entire function to digestion, absorption, and metabolism. And so it can't really focus on healing, growth and protection. 

MK: Which is then probably also why late meals are not super good for getting quality sleep or restorative sleep, right? Because the body has no resources to it.

Do any of that. 

Chris: Exactly, yeah. You go basically into a little tiny, you know, biochemical fight or flight mode where it's like we have to, we have to take all our resources, we have to get these things out of the system and stored where they need to be and utilized the way they need to be utilized, or else we'll die.

So yeah, it's, it's not always the best for sleep. 

MK: So, I mean, we are getting way off topic here, but you know, because it's interesting and I think a lot of little nuggets for people to take away. But you know, I would argue then there is a case to be made for just resting. 

Chris: Mm-hmm. 

MK: After eating instead of, I don't know, even I would, I mean, I know that, you know, going for a walk, you know, can help with, you know, your glucose response and all of those things, but at the end of the day, anything you do in addition to nothing.

It takes away resources that your body needs to digest, absorb, and metabolize. Right. 

Chris: That is, that is correct. And, and to a certain degree, that is what you want. So, you know, taking a walk after a meal helps to stabilize glucose levels so they don't get so high because your body is taking in energy while utilizing energy.

MK: Mm-hmm. 

Chris: So you get kind of like a net neutral. Impact to a certain degree. So there can be, you know, totally great benefits to, you know, working out after a meal. Especially if people are doing like a pro, like a pre-workout protein shake that has, um, you know, the right amino acid blend to actually mm-hmm.

Power a workout rather than detracting from it. And as long as it's not something like I just ate a whole, you know, Thanksgiving, Turkey, and then decided to go to the gym. 

MK: All right. Makes a whole lot of sense. Okay, cool. Well, I think there was a, a lot of, lot of good information, a lot of details. Um, where can people find you?

Where can people find mimeo if they want to give it a try? I mean, I've taken it now it looks like for almost a year. Um, and my aging has slowed down, so what can I say? I mean, that's a good thing. Yeah. You've. Studies to back up that it was not only me, you know, it's, it, it works for others too. And, uh, so where can people find Mimeo?

Chris: Yeah, you can find mimeo@mimeohealth.com and all of our socials are at Mimeo Health. And if you wanna find me, learn more about me, I do have a TikTok channel at. That nutrition Dr. That nutrition doctor. 

MK: So you, so what are you doing? Like dances and stuff on that? 

Chris: Actually, like if you wanna see me scream about nutrition into my bathroom mirror, please head over to my table.

MK: Alright. All right. Fair enough. All right. Well thanks so much Chris. Appreciate it. Uh, again, a lot of good information. Um, I'm gonna link everything, um, in the show notes where people can find you. I think we also, you set up a discount code for us, right? 

Chris: Yep, absolutely. 

MK: Uh, so I'm gonna have that in the show notes as well, so if people wanna try it, MiiR, um.

It's great. It works as far as I'm concerned. And um, you know, that's, let's combine some and maybe one last thing. Combining actual fasting with mimeo even better, 

Chris: uh, 

MK: even better 

Chris: than the 

MK: individual. 

Chris: Yeah, for sure. Uh, because like we were talking about before, right? Mimeo work has, was designed from a 36 hour fast.

So all of these molecules both not only evolved to work inside of a human body on their own. But also evolved to work together to achieve these fasting benefits, this fasting bio signaling. And they're gonna work best in the environment of fasting. So in all of our clinical studies, we have shown that Mimeo works to achieve fasting like benefits.

Even when you're eating, you don't have to change diet or lifestyle at all, but. If you do something like a 16 eight fast mimeo can be a great fasting enhancer to that. Mm-hmm. Because it's gonna help supercharge your benefits, like actually give you some autophagy benefits rather than not getting any at all with those shorter, fast.

And then it's also gonna help make fasting easier. Because we have these appetite suppression and energy and cognition impacts as well. 

MK: Yeah. I noticed, I remember from almost a year ago where I said, you know, taking the full serving, I wasn't hungry. I was undereating, and because I, I just didn't feel like eating.

Chris: Yeah. 

MK: So I've, I've not, I've noticed that. 

Chris: Yeah, yeah, exactly. That was, that was one of the big things that we saw from the clinical study. 91% of people had, you know, better hunger control, appetite suppression, better satiety. So that is one of our primary effects. 

MK: All right, cool. Again, thanks so much and um, with that we're gonna wrap it up.

Chris: Yeah, this was great. Thanks for having me on, Michael 

MK: Elizabeth. Absolutely. Cheers.