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

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.

Nicotinamide, spermadine, PEA, and OEA

up-regulate in the body during a fast,

working to reduce inflammation, fight oxidative stress,

and support heart and metabolic health.

This led him to create Mimio,

the world's first fasting-mimetic supplement.

Designed from human biology,

award-winning Mimio 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.

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All right, Chris, so happy to have you on the show.

For numerous reasons, one of them,

I know that you are very smart cookie

and know a lot about fasting

and what's happening inside of your body when you fast

and the downstream benefits and consequences of doing that.

And some of the molecules that you can,

I guess, supplement with to mimic fasting, right?

I know that you launch the product

that does specifically that.

And the most interesting aspect of all of this

we conducted an experiment that it's been going on

for a very long time, not intentionally.

But because of some mishaps,

we basically did a true age test to figure out

what is my true age and what are some of the

epigenetic markers before we began,

or before I began supplementing with memure,

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 last one,

the end of the experiment.

But I made some mistakes,

not fasting on the day of taking the second test,

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

and we 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?

Can I do anything differently?

But before we get to that, maybe just give a little bit

of background, what do you do?

What is your research expertise

and how do you come up with developing

a supplement to mimic fasting?

Yeah, absolutely.

So I got my PhD in nutritional biochemistry

from 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 30 to 80% longer.

And that's often in the absence of chloric restriction.

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 research

that's been done on fasting,

it also really helps to extend health span as well.

So helping the treat preventive delay

the 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 super food

or this wonder drug that's triggering

all these amazing benefits that happen.

But somehow your body is essentially activating this innate

longevity bioprogram 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 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?

Right.

I mean, one thing that you said was super interesting

and I think that's one nuance to fasting

that is underappreciated.

You said without caloric restriction.

So 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 eat not, you know, on the next day.

So I'm really eating the same amount.

I don't have to because caloric restriction

only works for so long, right?

I mean, if you've been trying to eat less kind of diet,

at some point you just screw it, I'm hungry,

I need to eat and you'll probably

then make everything up again.

But 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.

The anger, yeah.

Right, exactly.

But if you suck it up for one day

and then just eat twice as much the next day,

that's really an amazing kind of thing

because I assume, I mean, yes,

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?

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 long do I really have to fast at a minimum?

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 16-8 fasting.

So, biologically speaking, your body actually has to get

to a depletion of its glygogen 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, you're doing 16-8 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.

In order to get these benefits of fasting

that we really think we're getting,

especially on the longevity side,

you really need to do these longer term 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 faster.

Right, gotcha.

Now, I'm super excited to look at the reports,

but maybe one thing before, because, you know,

I know I remember a time, if years ago,

where intermittent fasting was nothing.

Yeah, and then as to 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 your woman don't ever think about not eating

because what's the deal?

I mean, 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 urine?

Is there such a thing as, 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 new install of that?

Yeah, there's a lot of differences in,

not only gender-specific 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're 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 is casual, 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 the program.

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?

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 going to be alive.

So like that's actually one of the reasons

why fasting is very good for longevity

because both men and women get that signal,

like this is not a good child bearing environment.

So the bottom thing is that we're going to try

and keep this generation alive and functional

as long as possible and go out and find a new environment

that's rich in resources

and we can actually support the next generation of problems.

I mean, it makes a whole lot of sense

and it's not necessarily surprising,

but it's I think something that,

I don't know if most people probably don't think about,

extending, there is probably such a thing

as an optimal lifespan for a human, right?

For a human, right?

Yeah.

And there are ways I suppose to extend that,

but it's not without a cost.

Yeah, the same love about it is that

in order to live longer,

oftentimes you have to live less, right?

So a lot of the things that we love about living, right?

Alcohol consumption, right?

You know, like eating like every day

or every hours, right?

Never being hungry, things like that.

Those tend to actually accelerate the aging process going out

and sunbathing, right?

Same thing.

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 talk about longevity all the time

as like anti-aging, right?

Like, oh, I always want myself to be renewing.

I always want myself 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

before they reach the hayflick 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

that leaves to maximum survival.

All right, you know, from, I guess from an athletic perspective,

the, you know, something comparable would be,

well, if you want to be the best in something,

you know, being the strongest guy,

the fastest guy would have you,

you're not necessarily, that's not necessarily good

for longevity, for the longevity of your joints,

of your muscle tissue, you know, none of that

because you, you, you pay the price for being strong

for being, you know, being able to lift 500 pounds

or what have you, you know, so there is the question

and it's okay, shouldn't there be a,

and 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.

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 probably arguably

more important than, than life span.

I don't care that I live for a hundred, you know,

120 years, but in a wheelchair for the last 20,

but I also don't want to have a health span

of, you know, of 60 years and then drop that

as a perfectly healthy, you know, human being.

So that's got to be, I guess, somewhere in between

where you also have to, I guess there is,

I guess, no way around of having a decline, you know,

I mean, we're not going to get any,

none of us are getting any younger, right?

The question is, where do you want to keep that balance?

Do you want to look like Hulk until you drop that

or are you okay with being just more of an average person

but maybe with more mobility, maybe with, you know,

just being able to walk without pain,

whereas the guy who lifted all of his life

might have trouble walking pain-free, you know,

50 years into his lifting career, you know?

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,

high performers, they do not typically have

exceptional longevity and that kind of comes back

to you exactly what you were saying,

that you are doing so much high intensity work

on the early end of your life,

you're like that kind of exercise at a high level

for a very long time, really overactivates the immune system

so you're kind of accelerating, inflomaging, 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,

state of the body, and that often leads to

a lot of oxidative damage, a lot of inflammation,

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 metabolism and specifically metabolic growth.

So things like MTOR and IGF1 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 accelerated aging

while these other sides of the coin,

these anti-aging pathways are also metabolic,

things like AMPK, NRF2, P-PAR, alpha,

like NAD, CERT pathways, all of that

is highly related to metabolism as well,

but those are the things that are anti-aging

and those are the 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 road map 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 do what we do at MIMIO,

which is put fasting in a pill?

Right, right, right.

Okay, I make the whole lot of sense.

Maybe now before we start looking at my reports,

talk a little bit more about MIMIO, what's in there?

How does it mimic fasting?

I mean, how can I take a capsule and tell my body,

hey, I'm actually fasting even though I might be,

you know, downing, you know, five pounds of brisket

at the moment, how does that end up?

What MIMIO 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 there 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 less oxidative stress,

better antioxidant capacity, better anti-inflammatory ability,

better cardio protective ability,

better metabolic function and metabolic flexibility.

And that was really interesting to us

because what we were looking at was a young healthy people.

So the 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.

And those were the ones responsible

for activating a lot of these cellular health

and longevity benefits.

So we screened through those molecules

and were able to eventually find

this synergistic combination of four

that when we put them together,

could recreate these cellular benefits that we were seeing.

So those same anti-inflammatory effects,

those same antioxidant effects,

those same active and metabolic effects.

And when we took this formulation

and did a lifespan extension study and animal models,

we were able to extend their lifespan by 96%

just through supplementation.

So what Mimio 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.

And how did you guys find out

that those molecules are actually doing in the body?

Yeah, so in the initial study,

we were just looking at their functionality on human cells.

So we had taken cells from the participants in the study,

added in the bioactive fasting metabolites

and just were 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, they appear in the body,

they're actually doing things

and that they have 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 Mimio while they are eating.

So we had people come in, ate a standardized breakfast

alongside a placebo control

and then looked at their cellular functionalities

in the post-parandial state, the post-eating state

and just tracked that through.

Then we had them come back after a washout period,

eat that same breakfast,

but then with supplementation with Mimio,

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 pro-oxidant,

they became more inflammatory,

they became less cardio-protective.

But when they eat that same meal,

but with supplementation with Mimio,

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 cardio-protective and metabolic reflexive.

So that was really our first one.

Then we've done another one in conjunction with Mount Sinai,

basically 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 HVAC levels,

improved total cholesterol, higher HDL, lower LDL.

So that was great.

We saw a 50% increase in free testosterone

in that 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 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 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.

They were digestive benefits, so less bloating,

less abdominal pain.

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 all of these things together, this

is actually activating these fasting pathways,

where these fasting benefits, even when people are eating

and without having any effects at all.

All right.

Well, that's a good segue now into our experiment,

which was not a double-blind controlled anything.

And it was more like an n equals one.

But nonetheless, I only care about myself.

Not if I'm brought up on the line.

Good job, then.

Good job.

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.

It did.

All right, so apparently I'm 44 years old.

Great, we already knew that.

But I think the nuance to that is,

I think here it shows, actually, some of the history.

Yeah, a little bit back down.

Yeah, so not exactly what I did in there,

but I was at one point almost four years older.

I actually think that this was the one where you had gone in

and you were not in a fasted state when you were in a state

before.

So that could be one of the things

was driving a bit of the markers up there.

Correct, yeah, that's a good point.

All right, and now we have this.

This looks different every single time I take it.

So maybe tell us a little bit about what does it say

about my organs?

Yeah, well, I actually can't give you

to the in depth of an analysis.

And this isn't, you know, I don't know all the back end

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 gene

sites that are associated with things

that are important on a functional basis and blood markers.

So they're testing specifically the methylation patterns

that are all around these genes on things

that control production of CRP or IL-6

or fasting glucose levels, things like that.

So and then 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.

OK, all right.

Yeah, there's 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,

some of the, you know, I'm sure you do a lot of cardio

or you do a lot of weightlifting.

So I would assume that your lung health would be very good.

Yeah, more weightlifting, I guess, than anything else.

But well, and some high intensity stuff.

But OK, then the next thing I think that's also somewhat

important is the rate of aging.

Yeah, exactly.

And so the good news is I'm a peer to be aging slower

than I should.

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 rejuvenation Olympics, right?

So the global tracking on who is aging the slowest

is done with the Dunedin pace at OK.

All right, I think that was it on this.

And then we have the the advanced report.

Let me bring that up to see what that says.

So here it looks like we have two different ages.

Yeah, one of them being the 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.

Gotcha.

OK, same pace of aging.

I guess not much has changed here.

Fasting glucose high.

That's one one thing that's well, there are two things

that always find interesting.

My typically my fasting glucose when actually

done a blood test is never high.

The one thing that is consistently high is my HBA1C.

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, definitely.

And and so those never appeared 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.

Yeah, absolutely.

And so it skews 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 delumptivity

of my red blood cells is longer.

It's actually very interesting.

So there's something that happens during fasting

is you typically see a high level of billy rubin in the blood

stream, 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,

and 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

to the end of their life cycle.

So we can just have young blood cells.

So you get a high level of billy rubin

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 it 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 I'll tell you, I'm just hypothesizing.

But it's an interesting balance.

All right, creatinine has also always been high.

I guess that's just due to the fact

I assume muscle breakdown or muscle turnover

because of workout and those kind of things.

Yep, absolutely.

Same kind of situation we were talking about

with the red blood cells.

Those things I'm actually not familiar with.

Yeah, your edin kind of has to do with the methyl pool.

So basically looking at how much mRNA to a certain degree

you have floating around your system,

as well as how your methyl donor system is behaving.

So a low edin level can mean that your methyl pool is low,

which can hamper some metabolic functions

and hamper some critical 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 biological age,

your methylation patterns.

If there's a low edin, that will affect the methyl pool.

And only the epigenetics.

OK.

Same with that.

True conate, cut and a trigger, and a trigger.

All process.

Always a good decision.

Yeah.

I mean, what they're basically telling you here

is to consider ALA, consider berbering,

consider dihydroberbering.

These are all things that activate amythinase,

which will shift cellular metabolism

over to fat oxidation rather than glucose metabolism, right?

So that's going to be something that Mimeo also does.

So we have OEA and PEA that are in there

that are AMPK activators and can help shift that cellular metabolism

over.

OK.

Gotcha.

Symphony H. All right.

We talked about that.

I think that's the pretty much the same thing

that we saw before.

No, that one, I mean, we talked offline before,

but the one thing that always amazes me

is my immune marker.

You know, I'm the one who never gets sick

when people around me get sick.

I would argue that I have a very robust immune system

from a practically prospective, but this says something different.

Yeah, which is really interesting, right?

So I think a good thing to consider here,

which we were talking about offline before,

is that in biology and 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 being inside of your genetic code

to then getting 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 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 is a lot of different nullifiers that can come in

and either act as counterbalances to the mRNA

or disrupt their signaling or gobble them up.

So it's not always gonna translate over into,

okay, I have high mRNA for IL-6

or an inflammatory cytokine or something like that,

which actually ends up meaning I have high produced levels

of IL-6, 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 those are the changes that we are tracking right now.

So sometimes 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,

they necessarily have to do

with your actual blood values of these things.

So I'm practically speaking just to pick out one marker

that I know from the top of my high sensitivity CRP,

CR reactive protein, that I've been tracking

for years and years and years.

Always been below 0.3.

So fairly low levels of inflammation.

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.

And I have always said, well, that's because of my lifestyle,

right?

But seeing this,

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

along the, along that pathway.

And I'm not really affected by it.

Is there a benefit to trying to address the epigenetic side?

Is there a way to address the epigenetic side

that is different to how I address the practical implications

and my actual blood work?

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 chloric restriction in general,

also run through this pathway, NAD, CERC, right?

And what CER2ans do is essentially,

they are histone deacetylases.

So they, 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 unravelled

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 histones to actually be transcribed.

What CER2ans do is they remove those acetyl groups,

which then tightens the DNA back around the histones.

They can't be 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 mutation rates,

and then also conserving cellular energy.

So those are kind of the things

that epigenetic modifications can do

and how fasting and chloric restriction actually affect them.

In terms of, do we know anything right now

that can give you a one to one of,

if I do this thing, my epigenics will change

and that epigenic change will absolutely go on

and impact my health from like a A to B to C

of situation.

No, we don't really have that right now.

Very early on in our understanding of epigenetics,

it's kind of like the new microbiome, right?

Right.

Okay, very enough.

So that, you know, based on what I've heard,

it shouldn't be doing anything differently.

I'll tell you more about it.

I would say that health often comes down

to the what we call the phenotype, right?

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 going to 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 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?

Gotcha, okay.

All right, makes a whole lot of sense.

Now, maybe, you know, to zoom out a little bit

because I'm just looking, I think in March 2025,

that was the test before, right?

That was the, before test.

This one was the baseline, yeah.

And then, right, the middle one was the one

where I was not fasted.

Correct.

And then the last one was the post experiment.

Now, if we zoom out, what are some of the things

that you notice when I'm like, okay, this, this has changed.

Obviously, the one thing that's,

I think my pace of aging, even though funny enough

when it was not fasted, it was even lower.

So I'm not sure how to interpret that,

but definitely from March 2025 to almost a year,

holy moly, that was a long experiment.

To February of 2026, I slowed down, my aging slowed down.

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 were still at

that same chronological age.

So 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 getting 0.85 years older.

Yeah, it looks like I made up 0.2, or 0.1 years.

Okay, yeah, there you go.

Ah, yeah.

So I, and that is, I guess if you look at the pace of aging,

I mean, that is what is 0.85 of 12.

So that's maybe what, what is it, three years or so?

Yeah, three months.

Yep, exactly.

You keep stacking that up over time.

I think that gives you some major gains.

Yeah.

All right.

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 was a whole lot of stuff back there

that means nothing to me.

Yeah, these are, these are all, you know,

interesting, interesting markers to look at from a,

like oftentimes we look at these blood markers again.

We're looking 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 in a

translate to each other.

But I think, you know, kind of going back to what we were

saying before, your IL-6 data was the thing that really stood

out to me because that was the one that had a big increase

at the final level, which is probably the thing that's

driving up your inflammatory age and your,

and your immune age.

And that I would be really curious about looking at your

blood markers to see if you actually have elevated IL-6.

From everything that you've told me, it seems like no,

you probably don't.

IL-6 is typically, it's both an exercise-induced cytokine

as well as a food in the kind.

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 back end.

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-6 levels

would be really interesting.

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 a cross

from my box and then I just hopped over and got my blood

work done and my CRP was through the roof.

Even some of the liver enzymes are completely off charts.

And I'm like, okay, maybe there was not a good idea

because my workout, you know, 30 minutes before,

very likely impacted all of those markers.

So same with IL-6, I guess I should,

what would you recommend for someone?

Because I've been asked that question.

Now I personally try to not work out two days leading out,

nothing major at least.

I don't want to do like a mer for anything, you know,

two days before getting my blood work done

because I know that my markers are gonna be off.

Right.

So same with it, IL-6 as opposed to give it at least a day

or maybe even two.

Yeah, absolutely.

For IL-6, IL-6 and cytokines themselves

are fairly transient molecules.

So they pop up and they go down

as if you're a normal healthy person.

If you have chronic inflammation,

that's where you kind of see this steady creep up

of these 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 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.

Okay.

All right.

It's a lot like fasting in that it's what we call

a whoremedic stress.

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 over time.

And so that is probably what could be happening here

as well where the IL-6, you know, goes up during the exercise

because it's an acute stress,

but then goes back down and then you get

a larger healthy response after that.

Gotcha.

Because I have to pay to open the post-inflammatory

markers, CRP and IL-6,

I appear to be an opposite size of the lines.

Yeah.

Does that make sense?

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, 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 a long-term inflammatory status

because it sticks around in the system longer

has a longer half-life, a lower turnover rate

than IL-6 does, which is more about

these acute 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-6 itself.

Beyond exercise, and I suppose there are sauna bathing,

cold plunging, any hermetic stressor could cost that a spike

because I've paid attention, obviously,

during my testing specifically with exercise,

but there are other things like,

I mean, I'm just to give you a very silly example,

but a few days ago, I got 2,500 pounds of feet delivered

and I had to unload those from pellets

with a five-gallon bucket into feet drums,

and I was doing, it was like scooping, turning, pourings,

and that for an hour or so.

At the end of the day, it's a workout,

but 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 don't know, sauna bathing,

or I don't know, running after a hawk trying to kill one

of our chicken, those kind of things.

I mean, what other things could potentially cause

a temporary spike in IL-6?

In IL-6 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 hermetic stresses,

you have on one side kind of like exercise

and sauna, which have more to do with energy, production,

they run very much through mitochondrial processes,

right, cellular energy, or heat production

through the electron transport chain, all that fun stuff.

So those would basically be the two major stresses,

or potentially even like a thermogenic, right,

if you're taking that in some way or another,

those are the things that could 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 path.

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 yourselves,

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 because it 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

and not just making stuff up in your head.

Right, right, right.

What about stress?

Like an acute stressor or a...

Yeah, so typically stress is gonna be a bit more related

to cortisol and that system, which can increase inflammation,

but it's a little bit more, it's a little bit more nuanced.

Cortisol can increase or decrease inflammation

depending on the context, but 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 salt can,

that's really gonna be the thing that's driving

any kind of pro-inflammatory response.

And food you said, right?

Oh, yeah, definitely food.

That's a great thing as well.

So there's this thing that we call post-parandial inflammation.

So when that essentially means post-eating inflammation

and people often think of inflammatory food

as like, oh, like pizza and trans fats

and these 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 in to your body

is a foreign molecule.

And your immune system is designed to react to foreign molecules.

Oh, 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 pro-oxidant, right?

That's a very common thing that we see

in the post-parandial 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

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 we have this kind of broad spectrum

anti-inflammatory intestinal,

intestinal benefits that are happening.

Now, I mean, you know, define food.

Would coffee count as black coffee count as food?

Does it mean calories trigger an inflammatory response

or just anything that's foreign because, you know,

whatever is in coffee, caffeine and other molecules,

they're foreign to the body too.

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 an inflammatory response to them for something like,

you know, two slices of pizza,

or just, you know, eating a whole pizza, right?

It'll probably be to a lesser extent

unless you are specifically allergic to those things, right?

So the one of the reasons why food in and of itself,

like a whole pizza, would be more disruptive to the system

and more prone inflammatory is because in that post-parandial 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?

Just gaining in the body.

To then into another kind of survival response

where it's like we've got all 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 they'll get 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 it, I have a cholesterol response,

or too high of like a lipid clog, then we'll die.

So your body literally has to reorient its entire

from the digestion, absorption, and the metabolism.

And so it can't really focus on healing, growth, and protection.

Which is probably why late meals are not super good

for getting quality sleep or restorative sleep, right?

Because the body has no resources to do any of that.

Exactly, yeah, you go basically into a little tiny,

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 utilize the way they need to be

utilized or else we'll die.

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

So I mean, we are getting away of 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

that there is a case to be made for trust resting

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, takes away resources

that your body needs to digest, absorb, and metabolize,

right?

That is correct.

And into a certain degree, that is what you want.

So, you know, taking a walk after a meal helps

to stabilize glucose level so they don't get so high

because your body is taking in energy

while utilizing energy.

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 pre-workout protein shake

that has, you know, the right amino acid blend

to actually work out 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 blend.

All right.

All right, makes a whole lot of sense.

Okay, cool.

Well, I think there was a lot of good information,

a lot of details.

Where can people find you?

Where can people find me, if they want to give it a try?

I mean, I've taken it now.

It looks like for almost a year, and my aging is slow down.

So what can I say?

I mean, that's a good thing.

Yeah.

Studies to pack up, but it was not only me, you know,

it's, it works for others too.

And so where can people find Mimeo?

Yeah, you can find Mimeo at mimeohealth.com

and all of our socials are at Mimeo Health.

And if you want to find me, learn more about me,

I do have a TikTok channel at that nutrition DR,

that nutrition doctor.

So what are you doing, like, dances and stuff on it?

Actually, like, if you want to see me scream about nutrition

into my bathroom mirror, please head over to my table.

All right, fair enough.

All right, well, thanks so much, Chris.

Appreciate it.

Again, a lot of good information.

I'm going to link everything in the show notes

where people can find you.

I think we also, you set up a discount code for us, right?

Yep, absolutely.

So I'm going to have to end the show notes as well.

So if people want to try at Mimeo, it's great.

It works.

As far as I'm concerned, and you know, let's combine some

and maybe one less thing, combining extra fasting

with Mimeo, even better and individual.

Yeah, for sure.

Because like we were talking about before, right?

Mimeo 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 biosignalling.

And they are going to 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 16-8 fast,

Mimeo can be a great fasting enhancer to the,

is it's going to 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 going to help make fasting easier

because we have these appetite suppression

and energy and cognition impacts as well.

Yeah, I noticed I remember from almost a year ago

where I said, you know, taking default serving,

I was not hungry, I was under eating

and because I just didn't feel like eating.

Yeah, I've noticed that.

Yeah, exactly, that was one of the big things

that we saw from the clinical study.

91% of people had better hunger control,

appetite suppression, better satiety.

And so that is one of our primary effects.

All right, cool.

Again, thanks so much.

And with that, we're going to wrap it up.

Yeah, this was great.

Thanks for having me on my list.

Absolutely.

Cheers.