Hello and welcome to the VP Life podcast, brought to you by

vitalityPRO . My name's Rob and I'll be your host on today's episode.

Today we're sitting down with Dr.

Jin-Xiong She Dr.

She is a renowned scientist and entrepreneur who's made it his career's

objective to further our understanding of genomics and human cellular metabolism.

During today's discussion with Dr.

She, we will discuss what his views on nutrition and longevity are, why

he prefers NMN as an NAD booster, and why niacin may actually be harming us.

Today's episode covers a lot, so if you lose track, be sure to

check out the show notes linked in the video description below.

Hi Dr.

She thank you for joining us today.

Um, so yeah, if you could just quickly introduce yourself and what

it is that you are all about and Jinfiniti and we'll go from there.

All right.

Very nice to be with you, Rob.

It's my pleasure to, uh, have the opportunity to talk to you.

So, uh, I am Jinxiong Xi.

I have been an academic scientist for over four decades, and I

Published over 400 papers, and I, I'm tired of writing papers.

So I decided to quit my academic job a little over two years ago.

And I've been focusing on my company, Jinfiniti Precision Medicine, for the

last, I guess, 20, about 28 months.

And it has been a wonderful journey.

And what I'm most excited about is the ability to impact people's

life right now on the spot.

Okay, that's awesome.

And a bit more about Jinfiniti.

It's very much a company sort of built around testing specific

biomarkers, especially ones that are, uh, aimed at longevity.

Is that correct?

That that's generally the idea.

Yeah, it's, uh, in general, correct, but.

I, I would say Jinfiniti is about teaching people new philosophy.

And I'm, I'm getting, uh, older chronologically, so I, uh, I become

more a philosopher than ever before.

So the philosophy that I try to teach or preach is called, is based on the

ancient Chinese philosophy known as Taoism, or T A O, and Taoism . actually

applies very well here when we're talking about wellness and longevity.

How it's about staying in harmony, staying in balance, and how do you find

the balance between our genes and our lifestyle, and that's the essential

elements to achieve health and longevity.

So very specifically, we preach a program that's called TAO, T A O.

TAO stands for Test, Act, and Optimize.

So, I, I, I want as many people as possible to understand that this is

a philosophy or program that will allow everyone to achieve better

health and longer health span.

And I and the Jinfiniti are all about, uh, extending health span or closing the

gap between life span and the health span.

So in most industrialized countries, the life expectancy

or life span is about 80 years.

All right.

Yeah.

And COVID has reduced it by about two

years in the US

now, well, at about 78.

Uh, if you look at the health span, or the number of healthy years, it's about only

55 and maybe 60, somewhere in that range.

We have two decades of gap, at least, between health span and life span.

I believe the most important goal for society, and at least

for me, is how we close the gap between health span and lifespan.

If I can help, you know, even just one person who, uh, extended their

health span to, let's say, 80 years.

I mean, we want longer, obviously, but even if we just close that gap of 20 years

between health span and lifespan, and we can achieve a nod on the individual level

and as well as on the societal level.

So that's my first goal.

How do we increase health span?

The TAO program is really paying use of the currently available technologies and

it does not cost a huge amount of money.

Everyone can do it and we want everyone to do it.

Okay.

That's awesome.

So.

Essentially, that's your, your take on, on longevity, uh, is it

sort of a supplemental program?

Does it include sort of lifestyle factors as well?

Um, could you give us an overview of, of the program?

Yes, sure.

So the first step is test.

We want to use as many biomarkers as possible and affordable to identify the

top, what I call the sub health issues.

for suboptimal health issues.

These are inflammation, oxidative stress, senescence, metabolic

dysfunction, micronutrients, and so on.

We use tests to identify which of these major issues are the

problem for a given individual.

And with the health data in hand, we can come up with a very precise

and personalized action plan.

So that's the second part.

We want to act precisely in a personalized way, and we also

want to act in a proactive way.

And we also have to act.

You know, very persistently.

So, so once the, um, the actions are taken, we retest to evaluate the

effectiveness or network efficacy.

with the actions that, uh, uh, were recommended.

So that's where the fine tuning or the optimization part comes in.

So if you repeat this, uh, test, act, optimize steps, uh, you

can continue to make a progress.

You can continue to address the most important issues first,

and then you go down the list.

If we take the first risk factor away, we can extend the health span

by 5 to 10 years, and maybe longer.

If we take the second one away, we gain another 5 to 10 years.

We take the third one away, we gain another 5 to 10 years.

If we just take the Top three risk factors away, you can likely gain

15 to 30 years of health span.

And that's how, that's why I think the Test Act Optimized

approach is so essential.

You want to know which risk factors are the most important

ones for each specific person and do it in a very personalized way.

Okay.

Uh, your company Jinfiniti are you guiding individuals through this process?

Do you have a sort of a program in place?

Is that, uh,

We do, we do provide.

So, uh, so after tests, the actions include both, uh, lifestyle, uh,

changes, you know, people needed to be more active, uh, more engaged in,

uh, exercise, they need to have a balanced nutrition, you know, avoiding

certain food that are not good.

And you also want to have a diet that's rich in and balanced in a lot of the

nutrients, not only macronutrients that everyone knows about, but there

are many micronutrients that we, uh, needed to, uh, pay attention to.

Unfortunately, in the modern diet, many of the micronutrients we need to

stay healthy are deficient and they are depleted by modern, uh, agriculture.

So that's where, you know, supplements come in, and if you cannot get

enough from food, you have to take it from the supplements.

So, so I'm using both lifestyle and supplementation and from time to time,

you know, we may have to, uh, use very specific, uh, uh, medical procedures.

You know, for example, I'm a big fan of, uh, therapeutic plasma exchange, or TPE.

And we've, while doing a clinical trial, we find it very

effective at removing toxins.

So it's a great detoxification procedure.

Unfortunately, it's a little too expensive for everyone to afford it.

But, but if toxins are a major issue for individual, that may be a

very appropriate procedure to take.

Yeah.

So That's why you, you need to, you need to test to figure out, you know,

what, what each person needs the most.

Yeah, you have to identify which variables are at play and sort

of upsetting someone's homeostasis.

TPE, that's something I've looked into and, uh, well, maybe not as deeply as you

have, but essentially that's almost like a whole body, uh, PRP in a sense, is it not?

You are separating the plasma out from a large quantity of blood and then

re perfusing it back into the body.

Is that generally the idea?

Roughly, but not, not exactly.

So with the TPE, you take the plasma out, uh, from one arm.

You replacing with, uh, saline solution and albumin and plus other

nutrients depending on the protocol.

So if it's done correctly using the right protocol, it's both a detoxification

protocol and the regeneration protocol.

It's a detoxification because you are removing everything that's in,

in the plasma except the blood cells.

We put a blood cells back.

Right, we don't put the plasma back, we put the, uh, we put the blood

cells, we put albumin, we put the saline solution, and then we put, uh,

other nutrients back in the other arm.

So, it's, uh, removal of all the plasma, and replace, uh, with healthy

and rich in nutrient, uh, solution that's comparable to the plasma.

50 percent of the protein in the plasma is albumin.

That's why we replace it with albumin.

So essentially it's almost like an updated version of the quote unquote

young blood transfusions, where you would sort of take blood from a, from a

younger mammal and insert it back into an older mammal of the same species.

It is.

So the only difference is, uh, in the young, young plasma exchange

protocol, you put someone else, um, probably someone younger.

Yeah.

The plasma back into, uh, into yourself.

I'm not, uh, a huge fan of young plasma exchange.

Personally, I wouldn't do it because someone's young.

That doesn't mean that the person is more healthy than I am.

No, definitely.

I mean, uh, everyone's going to have their own sort of pathological microbial makeup.

And unless you're sort of filtering it and really sort of checking it for

something that's, uh, that you, yeah, you could sort of, I suppose, sort of

transfer an infection across as well.

So, and I'm sure it's something Brian Johnson actually was

experimenting with at one point.

I don't think he did it for very long.

Not surprisingly.

It's a, it's a kind of a three way experiment that he did.

So he got the plasma from his son and he give his plasma to his father.

So Brian did not get any benefits from his son's plasma

based on the test that he did.

But his father did get some benefit from Brian's plasma.

I can totally understand because, you know, Brian is pretty optimized.

I work with Brian and he uses our test and our supplement.

I mean, Brian is pretty optimized.

Less to tweak there, that's for sure.

It's very hard for him to get additional benefits, right?

Yeah, definitely.

On the other hand, his father was less healthy, so he,

uh, he can potentially get the benefits from Brian who is optimized.

So I don't, I don't think it's only an issue of age.

You cannot just define it by age.

Young plasma doesn't necessarily mean it's better plasma.

Yeah.

It's, it's relative to the health of the individual in question to a large extent.

Yeah.

Yeah.

Right, that's why I have some concerns because you don't, you don't

know who is healthier and you don't, you cannot control the quality and the sources

of so called young plasma or healthy, I would prefer to call it healthy plasma.

I think that would be a better term than young plasma.

Yeah, I think that, uh, and this is going a little bit of a

tangent, but the same issue is present with fecal matter transplants.

They're obviously an amazing modality, especially when it

comes to infections like C.

diff.

Um, but controlling the, uh, the donor and getting a consistent viable

product transplant has always been the major issue with the technology.

So, yeah, that's interesting.

Um, getting back to your program.

So typically with TAO, what are the, The main things you see with

an individual, I assume you, it's, it's a lot of the same things.

Uh, so you're seeing sort of dysregulated blood trigger, high

levels of systemic inflammation, high levels of oxidative stress.

Do you, uh, do you work with specific sorts of diets, sort of

like a ketogenic approach, a low carb approach, a high carb approach?

Or do you generally sort of personalize those sorts of protocols and

interventions to the person in question?

So we, so we do the test and then based on the test results, we, uh,

we can recommend, uh, specific actions.

I'm not a nutritionist and I don't have a team of nutritionists on our program.

So we, um, from the nutritional point of view, we, uh, we

recommend, uh, balance the diet.

I mean, obviously, you know, you, you want to consume more

vegetables and more, more foods.

One is a fine.

And the one thing that we really focus on is to reduce the carbohydrate intake.

You know, I, as we were talking before you started recording, I came off of rice

about three months ago and lost 15 pounds.

And carbohydrates, especially, you know, rice seem to be Major health, uh, risk.

Then even red meat.

So we, from the data net, we see the top three, maybe four issues are inflammation,

oxidative stress, micronutrient deficiencies, and uh, uh, senescence.

These are these and, and, and sugar and, and lipids.

I mean, these are the.

Information everyone talks about in both medical professionals

and, uh, you know, the general public, uh, do pay attention to it.

But what we found, uh, is that oxidative stress or reactive, uh, oxygen species.

Uh, a much bigger problem in the United States, uh, than actually inflammation.

About 80 percent of Americans have high oxidative stress.

And inflammation is only detected in about 10 percent or so.

Okay.

Do you think that oxidative stress is sort of Obviously, obviously

it's environmental, but do you think it's, it's, is have you picked up

any sort of specific cause, specific toxins, uh, or was it more sort of a

pathology that somebody has picked up?

So if I was to clarify that, or is it something like dirty air that's

causing it specifically, do you think, uh, is it, or is it more sort of the

end result of a poor diet and having maybe, uh, high AGEs in the diet?

Um, what

Yeah, I, I, I, I'm pretty sure it's the food.

In America, we eat a lot of the ultra processed food.

Yeah.

If you look, if you look at, uh, European Caucasians and white

Americans, Europeans are doing great.

They don't have very high levels of oxidative stress.

We tested people from Europe as well.

And that's true for other ethnic groups.

People who live in the U.

S.

have higher oxidative stress, irrespective of their genetic background.

Do you think that's down to food quality to any level?

Literally the, the quality of the, I mean, obviously your, your sort of more

Southern European countries, uh, such as France, they eat, they eat a lot of

carbohydrates yet they seem to, at least in some part anyway, remain, maintain

a high level, a level of metabolic health, sort of generally speaking.

Do you think food quality comes into it or is it just A case of overconsumption.

Uh,

I think, I think it's both.

I think it's the additives that, uh, we added to, uh, to

the, uh, process of the food.

I mean, I cannot pinpoint it to very specific, you know, compounds or

anything, but in general, you know, I lived in France for five years.

I mean, we, we didn't eat any of the box of food or anything.

We, on the weekend would bike to the supermarket, uh, the open

market and to buy fresh produce.

In American.

You know, we, we consume a lot of the processed food, even, uh, even for

vegetables is frozen and the additives in, and it certainly has something to do with

how the food, uh, processed and stored and under the quantity, uh, as well.

In America, we tended to eat a lot more than in other parts of the world.

So, you know, oxidative stress is a huge issue for many, many people.

diseases because it has a major, it's mostly produced in the mitochondria and

the mitochondria defect or dysfunction is probably one of the most important

risk factors for various diseases.

Yeah.

This is an issue that very few people talk about and Um,

medical professionals don't know about it, they don't talk about

it, no one really talks about it.

So how are you measuring sort of oxidative stress at

the level of mitochondria?

Are you looking at cell membrane health, cardiolipin, those sorts of markers?

We have a marker which is a kind of a metabolite of

oxidation, it's called hydroperoxide.

It's a metabolite of the reactive oxygen species.

Uh, different radicals.

So, so the hydroperoxide can combine it to macromolecules, combine

it to cell membrane and damage, you know, DNA, RNA proteins and

cell membranes and everything.

That's, I believe, a major risk factor for many health issues we see.

Yeah, no, definitely.

And I mean, obviously, aside from sort of improving diet, how are you sort

of then reversing that sort of damage?

Are you utilizing compounds like phosphatidylcholine to improve the

cell membrane or, or the cell itself?

How do you sort of generally suggest people fix those sorts of issues?

Well, the, the approach is increase, uh, the

anti oxidant the capacity.

And there are many potential ways you can increase, let's say, you know,

vitamin C, vitamin E, and CoQ10.

Another one is glutathione or glutathione precursors, NAC.

We tried many of these compounds, and unfortunately, we have not found one

that's very, that's highly effective.

And about two weeks ago, now we think we are on the right track.

Coming up with a formulation that can reduce oxidative stress.

Super antioxidant, as it were.

That was, uh, sort of all the, for want of a better word, sort of the rage in the

early 2000s, well, in the late 90s and early 2000s, was looking at antioxidants

as a cure all for pretty much all disease.

Was that not the case?

Yeah, with the antioxidants, you, you actually need, uh, in

most of the studies, they only evaluate one a time, and that's not

a, that's not a good, good enough.

You really have to look at the multiple compounds, multiple antioxidants, you need

to, you know, reduce them all the way to, uh, uh, CO2 and water, and, uh, otherwise

it's not, it's not going to work.

So, and the second issue is, you know, how, how much that one needs

to take, and they absorb, because most of these are fat soluble.

And also.

It's um, the, the test for oxidative stress has been, uh, very difficult.

You know, what we should test and how we should test it, and also issue.

And most of the supplement companies, unfortunately, don't really conduct,

uh, well designed studies to figure out, uh, whether their products work or not.

So at Jinfiniti we, we, we tried to change that and we don't put any, any

product out until we absolutely know that's going to help a lot of people.

No product is going to help everyone, but we, we wanted it needs to help

the vast majority of customers who, uh, who may take the product.

Yeah.

You're chasing clinical outcomes, not just mechanism, essentially.

Right, right.

You want the clinical outcomes and you, you know, you, you, you want to

have biomarkers that can be assessed relatively easily and quickly.

To predict what's going to be longterm outcome.

Okay.

That sounds like an amazing program.

I think it's probably a good time to sort of maybe move on to

NAD, which I suppose is, is maybe what Jinfiniti is best known for.

And we certainly get a lot of questions about sort of NMN and

NR, your, your main NAD precursors, not including Niacin, et cetera.

What are your thoughts on.

NR and NMN specifically.

And I know that you're more of a fan of NMN, if I'm correct.

And uh, yeah, why?

Let's probably back up one step.

Um, so you can call them probably about five different NAD precursors.

Right.

So the closest one to NAD is NMN, nicotinamide mononucleotide.

It's a one step precursor because you only need one enzyme to make NAD from NMN.

So it takes one step and then the next one is NR, nicotinamide riboside.

Right.

Mm-Hmm.

NR needs to go to NMN and that's called, that's through the, uh, NRK or NR kinase.

And then you will, will be made into NAD.

So two step precursor for NR.

Then a little further, you have nicotinamide, nicotinamide.

It can be made into NAD through a pathway that we call a salvage pathway.

Mm-Hmm.

. Right.

So that, that takes, so that, that, that's another, uh, NAD precursor.

The fourth, fourth precursor is, uh, niacin and niacin, uh, goes

through a very different pathway to be made into a, uh, NAD and then

the fifth one is trytophan, right?

An urine pathway.

Yes.

There we go.

Yeah.

Yeah.

Trytophan can be converted into NAD as well.

So what we know now is NMN and NR are both.

Highly effective, uh, precursors for ourselves to make NAD.

We, we actually have compared NMN and NR in a number of individuals.

In most people, the efficacy is comparable.

So from that point of view, uh, NMN and NR both work quite well.

So there is a small percentage of individuals who can be deficient in NRK,

so they cannot make NR to NMN effective.

What I don't know is what a percent, what a percentage of people are relatively

deficient or suboptimal for NRK.

And certainly you are going to find some individuals, right?

But I know the percentage is not very high because if it's very high,

we would have enough data to know.

So from that point of view, NR and NMN are comparable I like NMN better

than NR, uh, because number one, everyone who can benefit from NR

can potentially benefit from NMN.

And the argument against NMN by the NR camp was that there was no transporter

of NMN there, was a transporter for NR . This was changed about, uh, two years ago.

So an NMN transport was, was found and we know, uh, NMN can elevate

NAD very effective in people.

So whether there's a transporter or not really doesn't matter.

You know, it works, we know it works.

So, but both NR and NMN also have their own biological functions.

And it's not, their function are not just through serving as an NAD precursor.

I mean, these are compounds, they have functions.

Yeah, they've got other signaling processes as

Well.

They've got other signaling processes and, you know, how they work

exactly are not fully understood.

But for example, NMN, we know it's pretty, you know, anti inflammatory.

So, with our data, we know that NMN, uh, seems to provide more health benefit

than, uh, and that's, that's debatable and we can, we can debate on that.

The next, uh, piece of data that, uh, we have and it's not published,

I think it's very important, is that People who take high doses of niacin

for, to reduce cholesterol level, have extremely high levels or can

have extremely high levels of NAD.

They also can have extremely high levels of insulin, can they not?

Niacin, high dose niacin therapy has shown to actually be

positive of insulin resistance.

Is that not the case to some extent?

I actually don't know what niacin causes insulin resistance,

I'm not, I'm not aware of, of that.

So what, what we, what we do know is niacin can reduce LDL, but it does

not reduce cardiovascular events.

It does not reduce death from cardiovascular.

Uh, uh, diseases and you actually can increase, uh, CVD death slightly

or may not be significant, but it, that have a potential to increase it.

So using niacin to, uh, to reduce LDL and uh, and CVD is really not, uh,

well, you can reduce the LDL, but it does not reduce, does not provide.

benefits for the CVD if you want.

That's kind of the current knowledge that I know.

And a lot of people are trying to use niacin to increase their NAD levels.

And I get this question all the time.

Yeah.

Why do I just use the cheap Niacin to increase my why I should use, you know,

NMN and NR that are more expensive.

Well now we know You mentioned that a recent paper came out in Nature

Medicine and actually about two weeks ago So what this Nature Medicine paper

found was that In a cohort with high risk for CVD, and many of them are

probably taking niacin, and probably high dose of niacin to reduce LDL.

They produce a higher level of 2 NAD or actually nicotinamide

metabolites called 2 PY and 4 PY.

Which are now named.

We're not going to try

to try those ones again.

2 nicotinamide, they call it NAD metabolites.

Actually, it shouldn't be called NAD metabolites.

It should be called nicotinamide metabolites.

Okay.

Determine metabolites of NAD.

And they are actually broken down from nicotinamide, so 2 PY and 4 PY.

What they found is individuals in this cohort in the fourth quartile, the 25%

of individuals who have the highest level of 2 PY or 4 PY, uh, have increased,

uh, uh, risk for cardiovascular event.

Now, that's a very important finding.

What it means is people who are taking niacin and have higher

nicotinamide metabolites may have higher risk for, for CVD.

And, and that's not, not, not good.

Definitely not.

Did they, I haven't, I've only read the abstract of the paper, wasn't open access.

Did they happen to go into the potential mechanism behind why?

Yeah,

the potential mechanism is these two metabolites may increase the vascular

inflammation, they can specifically.

So I think the problem is For a lot of, uh, so-called experts are interpreting

the data as that it's not a good idea to increase, uh, to take NMN or NR

or what's the appropriate doses of NMN and NR to increase the NAD level.

And I don't blame them because they don't, they don't have the data that we have.

The data we have is, if you take a niacin, high dose of niacin, your

NAD level can go to, you know, 100 to sometimes 180 micromolar.

Okay.

Very, very high levels.

So that's why they have very high levels of nicotinamide metabolites,

and potentially they have higher risk of cardiovascular events.

So, in our program, what we recommend is to take enough doses for NMN

or NR, So your energy level stays within 40 and 100 micromolar.

We, if it's over 100 micromolar, there's potential, uh, harm.

I mean, we have been recommending that for four years.

At the end, endothelial level.

Exactly.

Right.

So with this additional evidence, you know, actually re emphasize our

recommendation that you don't want to get your NAD levels way too high.

More is definitely not better.

Yes, more is not necessarily better.

And we know it's definitely bad here in terms of NAD, but I didn't,

I suspected it, but I did not have enough evidence to specify the up

limit of the optimum range for NAD.

Now with the data we have from Niacin.

And also the recent Nature Medicine paper, we know that you should not get your

NAD level higher than 100 micromolar.

And ideally, probably we're going to reduce it to 80 micromolar to be safe.

90, about 70, 80 percent of customers following our recommendations get

their NAD between 40 and 80 micromolar.

Okay.

About 5 percent of individuals taking various NAD

products and getting their NAD.

Uh, to over a hundred micromolar.

So with all the evidence that we see now, what's very clear is

you don't want to just take a NMN or NR product without testing.

Yeah, no, you want a baseline.

Um, just out of interest, what are the, what are the, what base levels

do you see, uh, with people who come to you initially, maybe people who

are unwell, uh, how they're presenting to you in terms of their NAD levels?

Yeah.

So, so it is age dependent and it's a country, maybe ethnic, uh, uh,

group dependent for, for Americans and for Caucasians, naturally

in their forties and beyond, uh, usually in the mid twenties.

Yeah, no, and occasionally we'll have someone in the, uh, uh,

in the high 30s or middle 30s.

So most people are somewhere between, you know, 25 and maybe 32 or so.

And if the age is above 40, uh, 40 years, the old, the older the person is, the more

likely their NAD level is lower, and it's not a perfect correlation if you want.

We also find the deficiencies in, even in very young, young children.

About 25 percent of teenagers are deficient in NAD.

Do

you think that's a nutritional issue?

I do not really know.

I am certain it's probably nutrition dependent.

Partly it's genetic.

We do, we do some, do see some, uh, clustering of NAD levels in families.

If, if, uh, if it's low in, uh, in, in someone, um, there's higher chance

to be, uh, low in other, uh, family members, um, blood related members.

So that, I'm pretty sure that's a genetic component, but

it's not a very well studied.

And we also see a major difference between ethnic groups.

Caucasians tend to have higher NAD levels.

And Asians, especially, uh, Vietnamese.

Koreans and Indians tend to have lower levels of NAD.

Chinese tend to be low as well, but they seem to be a slightly higher than, than

the Vietnamese and Koreans and Indians.

Do

you have any working theories for that?

Uh, obviously there's a, uh,

It's a genetic and the whole lifestyle, right?

I think both, both are involved.

I don't know exactly what percentage is contributed by genetics versus lifestyle.

The good news is, even if someone is very deficient at the baseline, we

can get their NAD levels Optimized how people respond to the energy

supplementation does not really depend on the baseline level and that's kind of

a misconception, you know, many people asking me, well, should I take in this

amount of, uh, based on my baseline.

I said, No, we don't see a correlation between how people

respond and their baseline level.

The baseline test is important because you know how deficient you are.

And you can see the progress after supplementation.

Yeah, it's, it's, it's relative again.

It's just.

Yeah, but even if they don't have this, even if they don't want to spend

the money at the baseline, I'm fine.

What I'm not fine is that they don't take a test after supplementation.

And then you're taking, The much bigger risk here.

Yeah, getting to the level.

Now, one is you don't know whether your NAD strategy

is working for you or not.

That's the first question.

And now, and that's also equally important.

We do have a small percentage of individuals who get their NAD levels too

high.

Yeah, definitely.

And they may.

They may have, uh, increased cardiovascular, uh, risk or, or

vascular, uh, in inflammation.

It's not a very high percentage, but there is a small percentage if

they take, uh, uh, recommend NMN and, and NR dosage not the big risk

is I think the vast majority of

people taking NMN and NR supplements

on the market don't get their NAD

optimized.

Because they're not taking,

uh, taking enough or not, not, or not taking a high quality product.

Yeah.

Something that's actually going to work.

That leads me to two questions.

Uh, next I would actually like to quite

chat about Accuri, but before

that, how are you testing Well, I know how you're testing NAD levels.

Uh, I've seen your test product, but up until recently, it was always sort

of debated that in order to actually test NAD, you literally had to take

it out of somebody's arm, put it in cold storage, then put it into,

uh, Yeah, and then put into HPLC.

I think if I'm correct, uh, I know you're, you're now doing

a, a dried blood spot test.

How do you ensure that that test, uh, actually reaches your lab and that it's

the NAD levels in it that's stable?

Could you walk me through that?

Yeah, sure.

So we, you know, NAD is degraded by, by enzymes.

So we have, we came up with a NAD stabilizing buffer and that's why,

uh, the NAD is, um, it's stable for a period of, uh, about a month.

We, we don't, we don't process samples that are beyond the Beyond one month old,

and so we, we get a reliable data within a month, um, because of the stabilization,

uh, buffer we, uh, we develop.

Okay, so that sort of removes the issue of oxidation as well, it's then

Yeah.

Yeah.

Okay.

So, so that, and I think that's the key.

And then, you know, there are many different ways that you can measure

energy level and mass spectrometry can be used, but mass spectrometry is

very expensive, not very reproducible.

And we, we use mass spectrometry, uh, as well when we're

developing the, uh, the method.

And we use a chemical enzymatic, uh, uh, approach and that's highly

specific, highly reproducible and it's automating, um, at least semi automating

that allows us to, uh, you know, get it done quickly and reproducibly.

Let's

chat about Accuri for a bit.

I know it's your, your flagship product and I know

it's more than just the NMN.

I think before the, uh, we started recording, we started talking about

molecular reductionism and how sometimes just targeting a specific

pathway within one molecule isn't always the best approach because

just throwing pure precursors at the problem doesn't always increase

levels.

I know Accuri also contains,

in addition to NMN, D ribose and creatine.

Uh, would you be happy just to sort of walk us through the process there

and why you chose those specific, uh,

Yeah, I mean, I can I can answer your questions in in two, uh, two, uh,

two different at a two different levels.

One is Overall picture of what I would like to do.

So we have the test.

We have the major categories of risk factors.

We are formulating supplements targeting each of the main

categories of risk factors.

So we'll have a oxidative stress formulation, we'll have

inflammation formulation, and so on.

So all these products are actually coming online in the next, uh, a few months,

and they're actually in production now.

Specifically for, for the NAD product, We have four ingredients.

We're testing, you know, hundreds were given the combinations in terms of

ingredients and also

proportions.

And we came to this particular formulation with four ingredients.

So we have

NMN base.

NMN is the main.

Uh, NAD precursor.

We have D-Ribose , we

have,

uh, creatine, uh, monohydrate and we have nicotinamide.

So why

this product?

We know this product works, uh, works better

than pure NMN or pure.

NR uh, you know,

I'm, I'm not here to, to sell my, my product or

anything, but as an example to

discuss how, how we should move forward, uh, in terms of science.

What do you think about utilizing cofactors and other molecules that

help to recycle NAD specifically in a product or things to actually help

increase sort of enzymatic production, NAMPT and those sorts of things?

Oh,

yeah.

So.

So those

are important.

I'll come back to that question.

Let me finish

the four ingredients

. Dr She: So we, we, we did not understand how it works at the beginning, frankly.

I mean, it took us quite a few months and even over a year, and I'm still learning

now as to why this works so much better.

It does work.

It does increase NAD better, but that's not the main benefits.

It actually provides much more health benefits than pure NMN or NR as well.

You know, we're getting incredible data from from customers And that's

because each of each of the ingredients provide the biological functions

and they work synergistically and We

have creatine you know creatine increase

the muscle mass increase muscle efficacy and

also creatine is uh The

neurotransmitter.

I mean, that's recent finding.

And D ribose, uh, D ribose is a, uh, activity in AMPK.

I was learning, you know, last night.

Oh,

I did not know that.

That's awesome.

Yeah, I didn't know until last night when someone

sent me a paper, you know.

So much to to

know.

And D - ribose has

all kind of, uh, uh, functions in addition to be

the backbone of, uh, the NAD

molecule.

Niacinamide is,

you know, it's

a part of NR, NMN and NAD,

so we, and it has its own function.

So for some magic reason, when we put it together in the proportions we

have, it just provides, um, you know,

better energy levels and better.

more importantly, you know, better health benefit.

That's what I care, care the most.

Okay.

Do you notice sort of improved parameters in terms of lowering blood

sugar and those components as well?

Uh, we, we do, we do not have, uh, we do not have data on,

um, blood sugar levels, but we do know it reduces insulin resistance.

It reduces triglyceride.

It can reduce LDL in some individuals.

and also reduces inflammation.

But, you know, more importantly, it improves cognitive function.

It, uh, reduces arthritis.

I mean, my allergies are gone.

I have many people coming back and why my allergies are gone with the product.

Asthma is gone.

Um, so

So

it's, it's,

it's almost stabilizing mast cells as well then?

Yeah, yeah.

No, almost every day we're finding, we're finding new, uh, new, new function

from, uh, from, from the product.

Sort of

miracle little electron accept and it's sort of changing human biology.

That's awesome.

Okay, cool.

Should we quickly just get back to the question that we

mentioned slightly earlier?

Um, Not that I can remember what it was.

I think I

need some Accuri...

How are

you dealing with senescence?

I know that you've got a marker that helps to actually track it.

It's a senescence associated beta galactosidase.

I think that's quite a new marker, quite a novel biomarker and it's

It's something we've not been able to track before as a community.

How exactly does that work?

And what are the clinical implications of that?

So senescent cells produce a bunch of molecules that are called

SASP or SASP, senescent associated phenotype, um, secreted phenotype.

Um, most

of the.

SASP molecules

are proteins, informatory, uh, cytokines, and

one of the SAPS molecule

is, uh,

beta galactosidase, or I

call

it Beta Gal.

And there

there are different, different

isoform of beta Gal,

and what's specific to senescent cells?

Is the isoform of beta Gal that

functions in the lysosome and the

pH of 6 or in acidic environment.

So, um, this is a relatively specific enzyme to senescent cells.

You know,

nothing is you know,

very specific when it

comes to SASP or anything

related to, uh,

Biology

or to, uh, to senescence, you know, don't, don't expect to find, uh, a

magic molecule that's going to be, uh, you know, very specific to senescent cells.

It's just not going to happen.

But if you

look at the all the all

the potential biomarkers,

uh, beta Gal, or SA beta Gal.

is, uh,

uh, the best one and it's one that can be measured easily

and can be measured in single.

So it's the, it's currently the best proxy that we have at the moment.

Is that correct?

Yeah, it's the best proxy that we, we can have

that, that, that is very useful.

We, we analyze it in, uh, in, you know, tens of thousands

of people who is healthy and

with various, uh, conditions.

And for example, we know, we published a paper about four years ago.

We showed that it can predict outcome of chemotherapy in cervical cancer patients.

And now we, we also know, uh, the changes,

uh, after senolytic treatment.

So, so we have a pretty good evidence that this is a

useful, uh, useful biomarker, both to assess the health status of an

individual, and also to evaluate

what the senolytic uh, uh, products

are doing anything.

If you do have a test that, well, an individual who tests high for this

marker, what are your preferred, I'm sure you've got a product coming out for it

soon as well, but what's your preferred senolytic products out there to actually

combat the buildup of senescent cells?

Yeah, so, so the first recommendation I normally give is a

combination of Quercetin and Vitamin C, and these two have synergistic

effect to reduce senescence.

And we can also add,

add some Fisetin into

the, into the formulation.

And it seems to work, uh, pretty well.

Another very popular protocol is called the D plus Q protocol.

It's, uh, Dasatinib plus Quercetin.

Dasatinib is, uh,

anti cancer drug, um, developed for CML.

And I'm, I studied this drug for actually a number of years, uh,

while I was working on cancer.

It's basically, it blocks the cells.

I mean, basically, that's basically what it is.

Okay.

And you're utilizing the vitamin C in that protocol purely as an

antioxidant, is that correct?

Or does it have effects beyond just that for

senescence?

Well, Quercetin,

Quercetin Is a widely

known, uh, senolytic compound.

I meant, sorry, the Vitamin C.

Vitamin C.

Yeah, Vitamin C.

No one knows exactly why Vitamin C, uh, synergizes with Quercetin.

At least I don't know.

I have not found any, any published data.

And I I cannot come up with a potential mechanism.

And,

Fair enough.

That's what it is.

But it works.

I mean, I, I didn't dive very deep into it as to why they couldn't synergize.

Uh, I guess now after your question, I needed to, uh, uh, study a little more.

No, that's all right.

Uh, I sometimes think that people, especially science, uh, scientists

sort of get too wrapped up in mechanism and not, and don't get concerned

enough about the clinical outcome.

So I think, yeah, if it, if it's doing people good.

And that's solving the problem.

Maybe at this point in time, that's all we need to know.

Yeah.

My reaction normally is I I'm going to leave the mechanism

questions to, uh, my academic peers, uh, that I used to be part of.

And now I, I want to deliver outcome.

Yeah, no, definitely.

That's, uh, I mean, that, that's what you want at the end of the day

from, uh, academic researchers to be able to provide people with an

actual answer that improves lives.

Shall we move on to age tests?

I know we discussed that, uh, beforehand as well.

What are your thoughts on epigenetic age tests?

I'll quickly sort of throw my opinion into the ring just to lay it out there and

then you can tell me if you agree or not.

I think they're an

interesting marker.

But I don't

think they have any specific clinical outcome just yet.

They seem to sort of broadly indicate that there is a high level of

inflammation, but they don't sort of indicate, A, what sort of inflammation,

and B, very seldom, seldomly do they actually seem to provide you with any

sort of, way to actually

improve that age score.

What are your thoughts?

Do you have a preferred one, whether

it's the Dunedin age clock or like glycans?

Uh, what

are your thoughts on those as a whole?

So in general, I, I agree with your assessment.

So I, I think the biological age is, is a very interesting measurement,

and it's easy to understand for non scientists, and you know, everyone

understands what's the age, right?

And if you tell someone you're younger or older than your age, You don't need to

explain anything else, so it's very good.

I think it's a, it's a good psychological indicator and it can also be a useful

tool to assess intervention outcomes and so, so you give, you give, uh, you

give someone easy to understand the number that they can be associated with.

So it, I'm, I'm not against biological age.

I think it does serve a purpose.

The problem that I have with Biological Age is it's overhyped.

Yeah, definitely.

It has its position, you know, everything that can

be measured has its utility.

And it all depends on how you use the information and for what purposes.

So what you said was very, uh, very good is I don't find

biological age tests actionable.

And what it means is you cannot derive very specific, uh, personalized

action plan for after the test.

If your age is, if your biological age is worse than your chronological

age, you know, you needed to, uh, do something, you probably don't

need to test your biological age to know that you need to do something.

And so it's kind of, uh, redundant, uh, not very useful information to me.

I know I needed to constantly improve.

So, um, I personally prefer tests that will tell me exactly what I

needed to do, how I'm going to do it.

And then after the specific actions, We can measure what the progress is made.

So, um, I unfortunately, biological came to the same for anti-aging and longevity.

And a lot of people are pushing the idea and lot of companies

are coming up with, uh, the test, including you, you, you sell test.

I have a test as well, even though I, frankly, I, I'm not a big

proponent of biologic age test.

If not, if they have to make a choice of what to test.

If they have, are willing to spend the money on testing everything,

sure, you know, get a biologic test.

I got a test on myself and I actually got tested a couple of times.

I'm fine with the, uh, information and then it's, it really does

not tell me what to, what to do or not want, what not to do,

but you can ,if you have money, then they

are much better more important tests to, uh, to do

than just a biological aging test.

And biological aging test is, uh, includes a variety of different tests.

Some people are using the expensive

tests for methylation or glycans.

Other people are using proteins or the routine biomarkers to calculate age.

Instead of calculating age, that I refuse to do, we calculate a W

index or wellness index.

I think a wellness index

is more appropriate in many situations than calculating the age,

even though ages easier to understand.

So I'm, I, you know, I'm, I'm going to continue to push, uh, what I believe

is the right thing is to assess your health status using various markers

and, uh, and come up with specific information and, and, and assess

what any actions are working or

not.

Dr.

She, this has

been amazing.

Thank you.

Can you tell us where people can find you and, uh, a bit Yeah,

well, they can find, find us

online.

Go to jinfiniti.com.

That's

J-I-N-F-I-N-I-T-I.

Jinfiniti

Well, they can just search my name and,

yeah.

And you've got a very impressive Google Scholar profile too.

Yeah.

Looking, find me on, uh, on Google Scholar and LinkedIn.

YouTube, um,

Instagram.

All social media.

Thank you so much.

Why?

It's my pleasure to talk to you.