Welcome to the VP Life Podcast, the show

where we bring you actionable health

advice from eating minds.

I'm your host, Rob.

And my guest today is Gillian Crowther, a

functional nutritional

therapist and medical researcher.

Gillian has a passion for all things

mitochondria and heads up research at the

Academy of Nutritional Medicine, UK's

leading provider of advanced

mitochondrial and cellular tests.

Expect to learn how

mitochondria actually function?

What the cell danger response actually is

and whether or not Prignell alone steel

is based in science or is

a functional medicine myth.

Now onto the

conversation with Gillian Crowther.

Morning Gillian, it's great to have you

on the podcast today.

So this is something that's come up a lot

of my conversations recently, the cell

danger response, I mean, which is

something I know will be just, which is

something I know we'll be discussing

during our conversation today.

Before we get into the nitty gritty of

that though, would you mind introducing

yourself to the audience and how you

ended up in this sort of world of

functional nutrition,

one might say, naturopathy?

I'll get that word

right one of these days.

But yeah, just your intro to

all of this would be amazing.

Thank you so much.

Well, thank you for having me here today.

And I'm delighted to talk about one of

the topics closest to my heart.

I suppose, you know, it began with

studying herbalism when I

was very young, about 20,

straight out of the university.

And then I spent a lot

of my life in Germany.

My husband as a doctor was working in a

very sort of holistic field there.

And so I came into contact with many,

many wonderful doctors and began studying

the mitochondria with a group of

naturopaths and doctors there in great

detail, probably about 21 years ago.

And the Cell Symbiosis Academy, with

which I was working, was very active.

It's no longer really in existence.

Unfortunately, some of the key doctors

running it have sort of retired now.

But when I came back to England, I

continued my studies and certified as a

nutritional therapist and naturopath and

found myself working together with the

Academy of Nutritional Medicine, where I

still am, about 15 years ago.

I'm now the director of research and we

run a lot of fascinating niche tests,

tests that nobody else is running really,

like very specific ways to detect stealth

infections and mitochondrial tests, which

are really unique worldwide, actually,

and tests of autoimmune encephalopathy.

Quite a few different kinds.

I won't go through them all.

We also organize events and webinars and

do a lot of sort of cross pollination.

We link up a lot of different

organizations as best we can and hope

that they'll speak to each other and

exchange information.

And that's sort of our mission, really.

That's quite the story.

And I suppose having a husband who's

already in the sort of the alternative

world, for the want of a better word,

probably opened your eyes up to a lot of

maybe where conventional medicine maybe

doesn't work, perhaps.

You said you started off in herbalism

straight out of uni and

then you went into nutrition.

Were you at university initially for

anything medical or

what was your story there?

No, I attended Oxford University,

Bresnose College and

actually studied German and history.

So no, it's a slightly different area,

but I found I moved into sort of

health-renated topics

quite quickly after that.

Okay, fair enough.

Sorry, I hope you don't mind me asking.

I'm just sort of fascinated by people's

backstories and how they

sort of end up where they are.

Yeah, no, it's the AONM is something I've

been sort of looking at on and off for a

while, especially your mitochondrial

tests, as you say, they are

very unique and intriguing.

However, I'm not going to go down that

road at all because I've sworn to myself

to try and keep on today's topic of

conversation trying

in the operative word.

So yeah.

So the cell danger response, as I

mentioned earlier, this is something I'm

fascinated by because, well, for me

anyway, it's really arguably the lowest

common denominator when you comes to talk

about disease in general.

Obviously, I know that's a bit of a

blanket statement and it does skew

towards more diseases that have the sort

of cellular metabolic

dysfunction and origin.

But I do think it opens a lot of doors to

view disease that we've made the sleep

that had been previously shut off,

the idea that we can sort of look at

disease broadly

speaking through this CDR lens.

Before we jump into CDR specifically,

though, I'd like to backtrack just a

little bit and maybe discuss

mitochondria for a little while.

I know most folks are likely familiar

with these little organelles, these sort

of cellular components, in that they are

that they really help produce energy in

the form of ATP within the

cell and within the body.

However, they do a lot more than that.

And while we won't have a whole

discussion about mitochondria, I'd love

to talk about maybe how they're involved

in the endocrine system or later on in

the conversation as well.

But at a baseline level, can you describe

what mitochondria are and

what they do in the body?

Yeah, maybe asides from

just creating cellular energy.

Yes, well, they originated from bacteria.

And then there was an endosymbiosis event

where this sort of cyanobacteria and

archaea joined up and were able to

produce a lot more energy.

That way, it's a bit of a complex story,

but absolutely fascinating.

And they're responsible for, as you say,

a lot more than just our energy, though

they are considered to be the sort of

power plants of the cell.

They're responsible for nutrient sensing

and energy metabolism.

That's really the sort

of bioenergetics sphere.

And then also for biosynthesis, they

synthesize a lot of molecules.

For example, heme is synthesized largely

in the mitochondria.

And if they're down, then you'll have a

lot of issues with heme production.

Cholesterol is cleaved in the inner

mitochondrial membrane.

And so without proper operation of the

mitochondria, you'll find that you don't

get the steroid hormones downstream that

you need in the proper order.

It's also responsible for signaling.

And the ROS, the reactive oxygen species,

very much have their

role to play as well.

Oxidative shielding is what Dr.

Navio from the CDR field that we'll be

talking about soon actually calls it,

rather than oxidative damage.

That it's shielding that these reactive

oxygen species are

providing as well as signaling.

A lot of cell to cell communication takes

place via the mitochondria, too.

And they're also able to form chains.

And it's fission as well as fusion.

They're not just sausage shapes.

They can actually transfer

electrons from one to another.

They migrate to different organs,

different parts of the body where more

energy is needed and

multiply as required.

So they're very, very

intelligent little beings.

I call them sort of our biochips.

Yeah, I mean, all sorts of jokes aside, I

mean, if you'd said that a couple of

years ago, you probably would have gone

into trouble talking about chips in your

cells and all of that.

But, yeah, I think what I'd love to jump

down with the rabbit hole there that I'd

maybe like to explore a bit further is

maybe the hormonal connection.

So we had Dr.

Eric Belkowicz from the States on a few

months back to talk about thyroid.

And he's very focused on treating the

thyroid and the endotransystem in general

and dysfunction there from a

pharmatic control standpoint.

And, yeah, that sort of got me down the

thyroid mitochondrial rabbit hole, which

maybe we can touch on later as well.

But it does raise the question of of what

you really pointed to earlier, this idea

that mitochondria take and

let me see if I got this right.

They take cholesterol and they help turn

it into pregnenolone.

That's right.

And that whole sort of

steroid cascade there.

Would you mind breaking this process down

a little more for us?

Because I do think it's quite fundamental

to not only our discussion, but also to a

sort of a broader discussion on why

people maybe don't necessarily react as

well to hormonal replacement therapy as

they think they would if they've got sort

of a mitochondrial issue.

Yes, absolutely.

It's the cholesterol side cleavage enzyme

called the P450CC that converts

cholesterol into pregnenolone and that

takes place in the inner

mitochondrial membrane.

And if your mitochondria are

dysfunctional, then obviously that will

not be happening as well as it should.

Obviously, it's not going to

break down all over the body.

But depending on where the dysfunction is

taking place, you'll find that you don't

make your steroid

hormones as well as you should.

And obviously, that's

that's a large number.

So I totally agree with you that if

you're using bioidentical or even non

bioidentical hormone therapy, that might

well be a reason why it's just not

getting into that cascade and simply not

functioning if you've got the

mitochondrial dysfunction underlying it.

Yeah, it's it's it's definitely something

that I think a lot of individuals and

practitioners like miss that that

hormonal function is always sort of at

least from a mitochondrial

standpoint in the way I view it.

And feel free to correct

me if you if you see fit.

It's always sort of the last piece of the

puzzle to really come into play.

And I think lots of people will

oftentimes jump into HRT and then sort of

still be sort of upset, surprised, sort

of unhappy about the fact that they still

got a lot of the symptoms that they they

currently have because they've been told

that their issues are just hormonal.

When in fact, it's it's a mitochondrial

issue that has

manifested as a hormonal issue.

And yeah, I just one more

question there while we're at it.

What do you think about this idea of

pregnant alone, pregnant, no, no, no, no.

Excuse me, I'll get that word right.

One of these days, I know it's it's often

taught in sort of the

functional integrative space.

It's something I don't agree with this

idea that you only have a

certain amount of pregnant alone.

And if you use and if you take pregnant

alone, it's going to be maybe buffered

towards one or another type of hormone.

When in reality, the way I view it is

that each cell, each cell is obviously

going to contain mitochondria and that's

going to be specific to each

organ system or gland system.

So the way I view it is that pregnant

alone actually can't be stolen because

it's always been made.

It's been made locally within the the

group of tissues that it's been utilized

in by those mitochondria.

Would you agree with that?

Or do you think that this concept of

pregnant alone still is real?

No, I do completely agree with you.

And it's fascinating actually to see

sometimes how high cholesterol in the

serum, which is the only place it's ever

measured, is often actually due to the

mitochondrial dysfunction that we're

talking about and the fact that the

pregnant alone isn't being converted.

And therefore, you're getting this

buildup of cholesterol outside the cells

in the serum and that's being measured.

And you're getting alarm signals and

actually the

ramifications go far, far deeper.

Yeah, no, it's something it's it's yeah.

Like I said, I think a lot of people have

a lot of opinions about

it and I'm just a chemist.

So it's always great to hear this from

someone who's in clinical practice and

who sees this in the real world apart

from me just trying to piece these parts

of the puzzle together and wondering if

I'm missing something or not.

OK, I'd love to sort of start to maybe

steer the conversation towards CDR and

where mitochondrial function CDR and

maybe why we have

dysfunctional mitochondria.

But before we get into that, maybe maybe

if we could explore why mitochondrial

become dysfunctional to begin with.

Now, I know there's a lot to unpack there

again and that mitochondria can be made

dysfunctional or become dysfunctional for

a number of reasons.

Infections, high levels of the toxic

exposure, et cetera.

And with regards to the latter, if anyone

really is interested in toxic exposure, I

invite them to listen to the podcast,

excuse me, that we did with Dr.

Jenny Goodman a few months back.

It was really was a good listen,

a good conversation, should I say.

But from your perspective and clinically

speaking, I suppose, which is really what

counts at the end of the day, what are

you finding to be the biggest triggers

with regards to why mitochondria are

becoming dysfunctional to begin with?

Well, I mean, it falls into several

categories, biological, as you've just

mentioned, in the bacteria, the viruses,

parasites, fungi and then chemical,

particularly electrophilic chemicals due

to the energy systems in the cell.

You know, lyndane and all the different

sort of chemical additives and metals as

well, heavy metals, lead and cadmium and

things like glyphosate

fall into that category.

Absolutely as well.

Yes.

OK.

And then, of course,

psychological slash emotional, which

converts into physiological stress, too.

So it stresses all these different kinds.

And then, of course, metabolic stress, if

any pathways are not working properly due

to lack of cofactors.

And that's a very important stress, too.

So the stresses along those, I would say,

four different pathways, biological,

chemical, metabolic and

physiological slash emotional.

Yeah.

And can I just add one more?

Which, of course, we've suddenly

encountered these last five years, which

is SARS-CoV-2 virus and the spike protein

is able to fragment the mitochondria.

And that's very, very serious.

And it also prevents apoptosis in a much

more intense way than other viruses that

we've seen previously.

And so apoptosis being pre-programmed

cell death, is that correct?

Exactly.

And so the lysosome and phagosome are

unable to link up as they should and sort

of get rid of the

dysfunctional cells and mitochondria.

And that's really very, very serious

indeed, making it very

difficult for people to recover.

It's being called long covid, whatever

the condition actually is.

Yeah, we interviewed Dr.

Tina Peirce and she's got a she

definitely looks at the whole long covid

thing from a mast cell standpoint

specifically, which I

do think is interesting.

I'm not sure it's the entire picture, but

for a lot of people, I think, yeah, long

covid definitely seems to drive sort of

an exacerbated histamine response.

And I've actually got a

question on that on that later.

But I do find it interesting that you

raised the whole

psychological side of things well.

I think what, again, most people miss is

that stress is stress and everybody's

always looking for some sort of broadly

speaking external trigger, I think.

Somebody's looking for an infection as to

why they have the ailments they have or

they are looking at some sort of

underlying toxic exposure.

And I think what most people miss,

unfortunately, is that ultimately the

body is going to take all that stress at

some level and it is going to be that

sympathetic or that final flat response

in the body, which is then going to drive

all those transcription factors and

pro-inflammatory pathways, which then is

going to drive that mitochondrial

dysfunction at the level of CDI, as we

will discuss shortly.

Absolutely.

I work quite closely with Dr.

Dietrich Klinghart, who

works on five levels of healing.

And we've seen incredible change in

patients as a result of even looking at

sort of ancestral trauma that they may be

carrying down with them.

This is something that he learned through

working with someone called Bernd

Hellinger, who lived with the Zulus for

many, many years, working as their priest

and found how very, very important the

extended family is and how that sort of

morphogenetic approach.

If you begin to sort of look into that

can also be a missing

piece of the puzzle.

Sorry, did you say

the Zulus as in the S.U.

Zulus?

Yes, they sort of have incredible

practices that do take into account

missing members of the family, whether

it's because it was a miscarriage or an

early death or a murder or whatever, but

all of that has an impact

on the larger family, too.

Yeah, I just mentioned it because I grew

up in Kuzu-Lunatal in South Africa.

Did you?

Yes.

So originally from the UK, then spent my

entire sort of, well, most

of my life in South Africa.

How fascinating.

Yeah.

So it's a lovely country.

It really is.

It's going through a sort of, should we

say, a bit of a struggle at the moment.

And if you like electricity and I suggest

you don't live there.

But beyond that, it

really is a beautiful country.

I'm sure I'd love to get in.

Yeah, no, it's yeah, maybe not somewhere

to live at the moment.

But from a just from a cultural

standpoint, from a geographic sort of

standpoint, it really

is an amazing country.

Anyway, so I'd like to get back on track,

as I was saying earlier,

Dr.

Balcovic, who I interviewed at the

beginning of the year,

looks at this through the lens of it

being adaptive physiology.

And in his from his vantage point, from

his viewpoint, he sees all of this

dysfunction as the body not necessarily

entering into a state of dysfunction, but

rather downregulating its physiology sort

of based on the fact that it's under this

sort of high elastatic load.

And that we shouldn't view this

physiology as broken, per se, but as the

result of being in the state where it's

sort of, yeah, it's downregulating these

vital bodily processes.

Well, that does sound a little bit

similar to the CDR in that that's the

mitochondria sort of ability to detect

potential harm and damage

to the cells, organs, body.

And therefore, they downregulate and

change a lot of their functions to,

you know, it's an evolutionary sort of

conserved protective mechanism.

Absolutely.

Yeah.

And the different steps of it are

obviously quite complex, but have been

very, very well mapped out by Dr.

Navio and his teams.

Yes, one day I'll get him on to a call.

I think I sent him an email.

Oh, that would be fantastic.

I sent him an email, an

email at least once a month.

I get to have a reply,

but I'll keep on pushing.

Let's keep trying.

Yeah.

Keep on pushing my luck.

I'm a bit like a dog with

a bone when it comes to it.

Honestly, I think that's a perfect time

to sort of segue into CDR and maybe we

can discuss that in a

fair amount of detail.

I think the way I see it, there's these

three sort of stages of the cell danger

response and we sort of

we get stuck in there.

However, this is definitely your realm of

expertise and something I just look at

with the sort of the from a passionist,

passionate hobbyist sort of viewpoint.

So, yeah, I'd love it if you could start

to how to break down this, to break down

CDR and help us to understand what

exactly is going on there.

Yes.

Well, according to Dr.

Navio and his teams, as I say, you know,

they've even done very large studies

using NIH grants of millions on this.

So it's not just sort of a couple of

articles that he wrote back in 2014.

It's really been taken up really

worldwide, though it's not fully

integrated into, obviously, conventional

medicine thinking yet.

It's not reached the

medical textbooks, I don't think.

But there's CDR1, which is the sort of

innate immune response to these various

different factors

that I mentioned earlier.

And if the mitochondria detect a threat

along any of those lines that I

mentioned, and I think I forgot to

emphasize physical as well, I mean,

obviously, a major car accident or even

breaking your arm or

whatever, that's all included.

Then they will decrease their oxygen

consumption initially in order to allow

the oxygen to instead

suffuse the cytosol.

And that changes the pH, it changes the

way that enzymes act.

And it also,

it's both oxidant and increases the

oxygen for antioxidants.

So, you know, having more oxygen in the

cytosol has a dual function.

It's both able to, for example, kill or

attempt to kill the pathogens that have,

for example, been found there, but it can

also power the superoxide dismutase,

glutathione peroxidase,

catalase, thioidoptase.

All these antioxidants need a little

oxygen to actually power them.

And if you see higher levels of oxygen

being used outside the mitochondria in

the cell, then that's a very good sign

for this kind of battle that's going on.

It's often called the power plants

turning into the battleships, as it were.

So they're down-regulating in order to

allow this sort of battle

to take place in the cytosol.

And another thing that happens is that

the cell membranes are stiffened in order

to prevent egress of, again, you know,

any pathogens that may be detected.

For example, spike

protein to prevent in and out.

So the composition of

the cell membranes changes.

And they also release antimicrobial and

antibacterial, well, antiviral chemicals.

Interestingly, they're able to do that.

Yeah.

And they increase

autophagy to the extent they can.

Obviously, if you've had a major blow

like the spike protein, as I mentioned,

preventing that, then they'll do their

very best to via mitochondrial fission

and mitophagy, which is the breakdown and

recycling of the mitochondria themselves.

And they'll attempt to sort of

operationalize that.

And at this point, would cardiolapine be

damaged within the

mitochondria within the cell?

I don't think it

would be damaged as such.

It would just be not allowing fats into

the mitochondria to the

extent that it normally does.

That's its key role.

But I mean, if you're not going to fire

up the mitochondria like you would

normally, then you're neither going to

take in the fats to the extent that you

would normally know the carbohydrates.

And it also releases ATP,

as a sort of, it's called E-ATP,

extracellular ATP, that acts as a warning

signal and actually communicates to other

cells, a bit like the pheromones of sort

of trees that one hears about in plants,

sending up warning signals to each other.

And it also alters post-behavior in that

the person themselves loses energy,

becomes a lot less active, you know, may

just feel they have to

spend some time in bed.

But that's all part of

this healing response.

The energy simply isn't there any longer

for those kinds of activities.

So that would be CDR1.

And hopefully, if that resolves the

individual's issue, then soon enough, the

mitochondria will take up the normal

activities again and the cell danger

response will discontinue.

But it is possible for it

to get what's called stuck.

And for, or maybe there's a need for it,

if it's been very, very major

inflammation that's taken place, then the

cell does need to spend a lot of time

building the new macromolecules that you

need for new cells to replace those that

have gone under through inflammation.

So it's building new lipids and new

carbohydrates and new proteins.

And so all of that will

require the glycolysis.

And increasingly, if you move to aerobic

glycolysis of CDR2, which is where there

is oxygen present, but it's being again

used for this sort of

rebuilding of cells outside the cell.

This is called a sort

of proliferative phase.

And obviously, you don't want this to go

on for too long because proliferation,

obviously, signals at the

end of the chain cancer,

which is just one stage along a

particular trajectory.

You know, we shouldn't be frightened of

that word like we are, but nevertheless,

this proliferative stage CDR2 of aerobic

glycolysis will hopefully

not continue indefinitely.

But move on to what's called CDR3, which

is the third stage that Dr.

Navio and his teams have identified,

which is where the oxidative

phosphorylation is

beginning to start up again.

But you've still got the cells in many

parts of the body working and the

mitochondria as well working

independently rather than in a sort of

very coordinated way.

I have a slide here that includes all the

different conditions

under CDR1, 2 and 3 disorders.

And it's absolutely incredible the number

of disorders that are even listed under

CDR3 like autism and chronic fatigue, of

course, which can persist

for years and even decades.

And it's a kind of hibernation of the

mitochondria that has really

to a certain extent got stuck.

What we have is the vagus nerve,

which is, of course,

extremely extensive and that has both a

ventral and a dorsal kind of

chain to it component exactly.

And Porges and others have written really

comprehensive literature on this.

It would appear that the ventral stage,

which is the sort of healing component of

the vagus nerve, is in

these cases downregulated.

And instead, you have an upregulation of

the dorsal, which corresponds to the CDR.

And that can,

in some cases, simply become it's a bit

like cellular memory.

It can become the sort of

new normal for the patient.

It's like a set point

that has been changed.

And so a lot of work has been done by

Porges and others, including,

interestingly, even Dr.

Gerald, the Professor Gerald Pollock, you

know, his work feeds into this massively

as well to kind of try and regain the

normal cell functions, including the

dorsal signaling of the, I'm sorry, not

the dorsal, the ventral

signaling of the vagus nerve.

That's fascinating.

I wasn't aware Dr.

Pollock was doing any

specific research into.

Well, not directly, but it all links up

because the EZ water, the exclusion zone

water, which you'll know about and have

probably done other sort of podcasts on,

is so central to getting

that signaling back again.

And in fact, the electrons, the neutral

charge, it's a bit like a battery

functioning in the cell and getting that

battery sort of conduction, the

electrical conduction working again

properly does appear to a lot be

connected to this fourth phase of water

that Professor Pollock talks about.

So he doesn't directly mention the CDR,

but it is clearly part of it, as is even,

you know, deuterium depletion.

You know, we're beginning to see very,

very big pictures now, I think, coming

together, you know, the dots are sort of

being joined very quickly now.

Yeah, no, deuterium depletion is

something I've, it's on my list of things

to sort of dive into.

But yeah, I think that's fascinating,

especially from a sort of an oncological

standpoint and the research that's been

done into, yeah, reversing various

metabolic, again, diseases, again, by

from a deuterium depletion standpoint.

Let me just mention, sorry to make that

connection so that it's a

bit easier to understand.

It's because the mitochondria are

continually producing metabolic water.

This is the extraordinary thing.

It's actually water that's been produced

at cytochrome C oxidase as part of the

part of the oxidative phosphorylation.

And this metabolic water, it can be a

huge amount, it's like

sort of, I think, 17.

We'd have to talk to Professor Borish

about that, but certainly thousands of

liters a day if it's being

produced and recycled properly.

And that's how camels work.

Exactly.

Absolutely correct.

Yes.

And it's their fat and it's the fats that

we're eating, actually, that are making

it possible for us to produce that a lot

more efficiently than, you know, again,

if the mitochondria are working.

So it's gradually encouraging that

metabolic water in our system to begin

working again, because without it, the

mitochondria can't work either.

And it would appear to be low deuterium

or deuterium depletion that both the

Krebs cycle and the electron transport

chain are creating in our mitochondria.

And I'm quite sure that Dr.

Navier, when you speak to him, will agree

that part of the recovery process will be

encouraging this metabolic water to be

created in a much more efficient way.

That's fascinating.

I mean, I've taken from that more so than

anything, is if camels get

fried, they're probably stuffed.

Sorry, maybe just a bit more of a

technical question, if you don't mind.

Do you think that that that that that

that EATP that you mentioned earlier, and

then other metabolites there are so

things like Saxonate, Adenosine, etc.

Do you think that they could play a role

in amplifying also sustaining that that

CDR response across tissues and cells if

they're if they're elevated?

Oh, absolutely, yes.

But I mean, hopefully they're working in

an intelligent manner in order to simply

get the message across.

Look, there's danger, Ahoy.

We've got to alter pathways in these

different manners, but not in a

completely dysfunctional way.

But I suppose eventually, I mean, I know

that it's possible to measure DNA that's

sort of floating around in the

bloodstream that

shouldn't be there as well.

And to do that.

Exactly.

Mitochondrial DNA.

And that's a bad sign if you see it.

But again, I very much go with Dr.

Navier's thinking, which is that we

shouldn't be considering these things as

a, you know, from a negative standpoint,

but just trying to understand what the

signal is that they're trying to get.

And I think, yeah.

Again, just that sort of viewpoint of the

physiology being

adapted, not necessarily broken.

Exactly.

Yeah.

What about epigenetic changes?

And I think maybe the best example is,

okay, hypothetically speaking, of course,

say we were exposed to a sort of a

massive viral pandemic.

I mean, imagine that.

And then we were then treated with a

quickly developed vaccine that may or may

not have undergone

any sufficient testing.

Would it be sort of plausible in your

view that maybe a vaccine like this could

sort of create epigenetic changes by sort

of altering histones and other DNA and

RNA components that could then drive up

immune system activation and that and

that purigenic signaling.

And then to the extent that the body

might end up stuck in CDR1, obviously

through that epigenetic lens, do you

think that's at all feasible?

Most definitely.

I'm very, very unhappy about what we've

seen over the last four years or so.

I know it's not a good idea to talk about

this too much on podcasts that are going

to go out on YouTube and so on.

But yes, I mean, the body has such

incredible intelligence and these tiniest

little pathways and organelles and so on

are all working at a rate of knots in

such a sophisticated way that introducing

something of the kind that you've just

mentioned that could

potentially disrupt that processing is

I think misplaced on

many, many different levels.

Yeah, and it's not for me,

obviously, really to decide.

But I think that some of the difficulties

that therapists and doctors are finding

worldwide in

assisting patients to recover,

finding it much, much harder than they

used to at the moment, could partly be

linked to the whole pandemic and set of

issues related to that we've experienced.

I think for me, and this is a very slight

tangent, is that maybe the silver lining

of the pandemic and long COVID is that

it's brought to light this idea of these

chronic fatigue-like syndromes, myalgic

encephalomyelitis, broadly speaking,

these issues, which I suppose originally

sort of started off as golf wall

syndromes, PTSD and these other issues.

And for me anyway,

having struggling with

it myself, to an extent,

I think it definitely has, yeah, it's

brought an awareness to the issue at

large, which obviously, as you know,

dealing with people on a regular basis,

I'm sure, is a very sort of

proliferative issue in society.

So, yeah, I mean, obviously, we never

would have wanted it to occur, that

silver lining and all of that.

I think it's, yeah, it's just brought a

greater awareness to these mitochondrial

disorders if you view long COVID

essentially as a mitochondrial disorder,

which I think we'd probably agree that it

fundamentally is when you

sort of remove all the triggers.

Gillian, I think this would be a great

time to sort of maybe segue into how you

start to deal with, well, not deal,

excuse me, how you start to work with

clients when helping them

to overcome these issues.

Actually, you know, first, maybe we could

discuss mitochondrial tests.

Sorry, I'm a bit all over the place.

I know through the AONM, I'll probably

get that right at one point, there are

several, you have several options with

regards to mitochondrial testing, and

they're all amazing.

And I'm definitely going to have to

somehow convince you to

send me some sample reports.

Delighted to, yes, we do an ATP profile,

which shows the total ATP, which is, of

course, composed of the site of the ATP

being produced along glycolysis as well

as within the mitochondria.

So one must never forget, you know, some

ATP is obviously being produced outside

the mitochondria too.

And then the capacity of the mitochondria

to produce ATP and of

the glycolytic pathway.

And then the alternative sort of reserve,

as it's called, ATP production as well.

So that's the mitochondria at rest.

And then there's a second one, which is

called the mitochondrial health index

that shows the

mitochondria under pressure too.

And that would indicate the, first of

all, the degree to which oxygen is not

being used in the mitochondria, as it

should, you know, a maximum of, you know,

10% should be used outside for the

processes that we've just talked about,

but not more than that.

And if there is more than that, then you

can usually, you know, what would

determine exactly what

processes might be causing that issue.

It is a sign of a cell danger response.

And there are markers, it's an 11-page

report, so it contains a lot of markers

like the proton leak, you know, exactly

whether, you know, the mitochondrial

membrane is not quite as sort of patent

as, you know, integral as it should be.

The coupling efficiency, in other words,

how well the electrons are sort of

popping from one complex to another.

And the degree of post-exertional

fatigue, you can also work out from

what's called the reserve.

When the mitochondria are put under

pressure, they should be able to expand

by about 400% in terms of the energy that

they produce, and often

it's a lot less than that.

So there's a number of different markers

that you can sort of put together.

And there's an algorithm that calculates

the what's called mitochondrial health

index, which is useful to compare if you

want to sort of repeat it

after six months or whatever.

And then there are tests to calculate the

mitochondrial DNA

compared to the nuclear DNA.

Obviously, you have one nucleus but many

mitochondria, so you can work out from

that how many

mitochondria there are in the cell.

And if you have too few, mitobiogenesis,

which is the generation of new

mitochondria, would be useful.

Whereas if you have too many, then that's

a sign of the cell having detected a lack

of energy and attempting to compensate

for it by producing more mitochondria.

But there is also a marker for how

functional they are.

And if a lot of them are dysfunctional,

even if you have many, what's called

mitophagy, which we discussed earlier,

would be the approach rather than

generating lots of new ones.

And you can work out the degree to which

the mitochondria is suffering from

reactive oxygen species actually

beginning to impact the DNA of the

mitochondria, which is serious.

So it's good to pick that up early.

And the lactate pyruvate index actually

shows you the fuels that are getting into

the mitochondria, which is very useful.

Yes,

you can work out whether the mitochondria are able to process fats or whether

they're at a stage where they're more

readily able to process carbohydrates, or

perhaps that the carbohydrates aren't

even getting in and they're being

backpedaled into lactate, which the body

can use, but it's a messier process.

And so if you've got a high lactate

level, then that's a sign that the

mitochondria really have shut down to a

large extent and they're not even

allowing the carbohydrates in.

But they're not allowing the carbohydrates in. So you can tell quite a lot about the

mitochondrial fuels from that.

And there are various others as well.

I'm either going to rob someone, break

the piggy bank or put in for a job

because those all

sound absolutely amazing.

I love the fact that you brought up those

various metabolic shuttles and I think a

poor man's version of that would be to

measure glucose, ketones, and then

lactate, which obviously you can do

independently and use those as proxies as

well, which I think would be interesting

to cross reference those values directly

with some of those tests to identify how

you are, how effective you're utilizing

fatty acids for fuel sources.

I was actually going to ask this later,

and actually I will.

I was going to ask a question about

ketogenic diets later

and we'll get there.

Well, we could just throw in now that

that does show quite effectively that in

some cases attempting to utilize a high

fat diet for a patient is simply not

going to be the right thing for them at

that particular time.

You can of course attempt to encourage

ketones by giving beta hydroxybutyrate

precursors and so on.

That's a kind of way of leaping over the

normal pathways into the mitochondria and

hopefully as in the books about how

useful ketones can be for Alzheimer's and

so on, the Newton book and so on.

There's good evidence that you can

encourage that pathway, but actually

utilizing a high fat diet, which is

obviously often part of a ketogenic diet,

is not always the right thing for the patient and they'll probably be able to

give you a feedback as well.

Yes, I'm sure they will very quickly.

I think it's fascinating and again, I

know people like Dr.

Mai who are great proponents of the

ketogenic diet, but as you've just

alluded to you now, I do think that they

can be problematic, which can be

problematic in my view when you start

dealing with people with these sort of

apophimating gut tissues as well when

there are some reactive carbohydrates.

I think that starts to provide a

challenge, but I suppose that's where you

start to look at things like maybe a low

FODMAP diet to remove potentially those

triggering FODMAPs to help maybe allow a

certain amount of carbohydrate ingestion

while still not creating that

fermentation that drives

those dysbiotic conditions.

Yeah,

no, it's definitely a rabbit hole.

Just maybe one more

question if you don't mind.

Just regarding the ketones, clinically,

do you find there's any difference

between the salts and the esters when

providing somebody with a ketone

supplement or do you not

find it makes that question?

Well, the esters are very much more

expensive and so there's often a bit of

reluctance among patients to use those, but salts have been very effective as well.

I've had very good reports from patients

and from doctors who are

working with them as well.

One doctor I know who managed to, or at

least his patient managed to overcome

this diabetes type 2 by using ketone

salts along with obviously there's so

many other things that a patient is using

that you can't always

identify that it's the one thing.

But I do need to mention that I am and

I'd love you to interview Morley Robbins

at some point as well.

He is actually coming over to England on

the 21st and 22nd of May.

He'll be holding two events here.

I've sort of helped to liaise that and I

have been following his approach with the

Root Cause Protocol for about three years

now quite intensively.

I must say that despite all my, you know,

a couple of decades of studying the

mitochondria, I had not realised how

very, very important bioavailable copper

is for not just complex 4, you know, the

cytochrome C oxidase, but also complex 5

and the PrEP cycle and, you know, the

production of heme and so on.

It's absolutely central and also retinal.

And so the pathway that's been worked out

over many, many years by the Root Cause

Protocol group, I first heard him in

Seattle when I was over

there actually with Dr.

Klinghart, who was speaking

sort of from the same platform.

And I made a mental note for myself,

gosh, this is somebody who I've got to

follow as well and

finally got round to it.

And I'm very happy to be here. I've got round to it.

And I must say this has

extraordinary knowledge there.

He's just done a very

brilliant podcast with Dr.

Malek that would be worth listening to

for anybody who wants to sort of, you

know, understand where he's coming from.

But it's centrally involved in the

mitochondria and that's because you were

asking me what I suggest to patients.

Very, very often I find that sort of

sorting that mineral pathway, the

electrolytes, making sure that they're

getting sufficient retinol, which is

problematic if it's a vegetarian or vegan

patient because you can't really obtain

retinol from non-meat sources or dairy.

And then introducing the bioavailable

copper that can really be miraculous and

really, really help the mitochondria to

get sort of back interaction again.

So that is one of the very

first pathways that I think about.

And I sort of think back to cases I've

had in the past like fatty liver, where I

now understand the vital importance of

those pathways in that as well.

And sort of think, gosh, you know, I

probably would have gone to that

immediately in the past

too if I'd known of it.

So I think that's extremely useful.

If you can't make it

down to London in May,

well, we're already in May, aren't we?

For the events, then I'll send you the

recording if we manage to make one.

Oh, that'd be lovely.

And if you could ask Morley Torrance my

emails, that'd be better.

Oh, I will do.

Absolutely.

I'm sure he gets thousands.

So I'm not too...

He publicly displays his

email address everywhere.

MorleyRobbins at gmail.com.

So I'm sure he gets five and a half

million emails on daily.

But yeah, I've been trying to...

As soon as he's over

here, I'll mention that.

Maybe he can even find time while he's

over here, which is about seven days to

have an interview with you.

That would be super important.

Yeah, no, we can make something happen.

That would be amazing.

Yeah, I've not dived that deeply into the

root cause protocol.

I think as you know, you sort of, you

have your list of things to get through

and then inevitably

something falls by the wayside.

I know, it took me a long, long time to

get to it, but I'm so glad that I did.

And I did want to start to mention that

because you asked me what

the different initiatives are.

Another great

inspiration I find is actually Dr.

Jack Cruz.

I don't know if you know of him,

the neurosurgeon, but he emphasizes the

importance of light for the mitochondria.

Yes, but I mean, if he's different, he

just doesn't work to...

Yes, if you were to ask me what sort of

the key influence for

the mitochondria is.

I mean, something that we all find so

difficult these days

because of the kinds of jobs and

residences and where we live.

It's so hard, but actually getting out

into the sun and into nature and

grounding more and so on.

It all sounds so simple, but

it's very, very hard to do.

How much of our day

do we spend doing that?

And that's what our mitochondria are

craving, actually, a lot of the time.

Yeah, definitely.

They're photoelectric, photodynamic

organelles, and they require this input.

I don't mean this with any disrespect,

but I think people sort of, they don't

realize it was sun beings and it's become

culturally appropriate to analysis in the

dark room all day, whereas technically we

photosynthesize to a large extent.

So by removing that aspect of our

biology, we are essentially, yeah,

becoming completely dysfunctional.

Yeah, Dr.

Cruz is someone I would also like to talk

to, although I'll be honest, he scares

the living day lights out of me.

And when he goes down the physics rabbit

hole, I get a bit bamboozled.

I must admit, I think I did, the last

time I did physics was maybe second year

uni, and then that was it.

Yeah, it's always a long listen, but it's

just brilliant in there as well.

No, definitely.

He is a wealth of

knowledge, that is for sure.

So I suppose ultimately dealing with

these chronic diseases and comes down to

sort of ultimately

identifying what causes the trigger.

And what I'm trying to do is maybe create

a framework for people who are on

physicians or

practitioners to sort of follow.

And it fundamentally, and feel free to

interject wherever you see fit.

But the way I see it is you first got to

find the root cause, your trigger, which

is driving this dysfunction to begin

with, whether it be mold and infection

like a lime or what have you, and then to

concurrently lower the toxic load on your

body as much as possible.

Then again, and that I think is where

most people are going to struggle the

most and where it is behoove, the correct

word, then to work with a

practitioner such as yourself.

And then to start to start working

through the other components of this

dysfunction, sort of dealing with

emotional issues, dealing with adverse

childhood events, etc.

And then to slowly reintroduce the

nutrient-set support mitochondrial

function, and to then

hopefully get to the point where they

have proper hormonal

signaling and less despotic guts, etc.

With that, it sort of has a hierarchy,

sort of be a functional

way to sort of approach.

Yes.

And what's very interesting is there that

you mentioned supporting the mitochondria

a little bit later in that process.

And often one sort of gut reaction, one's

knee jerk reaction is to start giving

large numbers of mitochondrial nutrients

very quickly like CoQ10,

300 milligrams or whatever.

And actually, if the mitochondria have

down regulated intelligently and

intentionally and unable to process those

kinds of nutrients at

the present time, it's just

an inappropriate thing to do.

I mean, you've always got to be

supporting the mitochondria in a basic

way, of course, but giving lots and lots

of very specific nutrients at the

beginning of that process when you're

still in CDR1 or 2 is

probably less efficient.

Yeah.

With the exception of something like

methylene blue, which I'll ask you about

in a bit, but otherwise, I see it.

If you're bombarding a system that is

electrical with too many electron donors,

you're potentially just going to create a

high reactive oxygen, just a high level

of RRS between complex 4 and 5.

So ultimately, you're going to end up

doing more harm potentially than good.

Yes.

And a lot of it will be escaping through

the UCPs, the uncoupling proteins, and

it's creating heat rather than creating

energy if it's getting into the

mitochondria at all.

So I work not only directly, but I have a

lot to do with a lot of bodybuilders, and

a lot of them use these various

uncoupling agents to utilize

from a fat loss perspective.

And interestingly enough, there have been

a few who have sort of shown some sort of

signs of clinical remission

by utilizing these compounds.

Not that I would suggest, or I'm sure you

would, that using something

like DMP is in any way safe,

these thermogenic compounds, if you

overdo them even slightly,

they can actually kill you.

But yeah, it is interesting that by sort

of uncoupling mitochondria deliberately,

you can actually see an improvement in

energy, which I suppose makes sense.

But yeah, it comes with a lot of

potential drawbacks.

Anyway, that is rabbit hole in a tangent.

Gillian, you've been a star.

I think I'd like to close off with a few

rapid fire questions, if that's okay.

We can answer them.

They're never rapid fire.

But we can, yeah, just a few sort of

off-the-cuff questions.

Okay, so starting off, if you could fast

forward mitochondrial medicine, say 10

years, what

breakthrough would you hope to see?

Would you like to see?

Oh goodness.

I'd like to see a lot more simplicity.

It's the simplicity

beyond the complexity.

And so I do hope that together with

others, we can work towards that to make

it a lot easier to overcome the cell

danger response and restore patient's

health, not have people

stuck in ME for 20 and 30 years.

I love that.

I mean, someone like Ron Davis, Professor

Davis in the States, the Open Medicine

Foundation, his son is in a...

That's what gives him his motivation,

unable to even take in

sensations from around him.

He sometimes can't even speak to him.

This is so clearly a

mitochondrial issue, and to be able to

find simpler solutions would be

absolutely tremendous.

And affordable solutions as well.

Yes, there we go.

Unfortunately,

medicine, I think, is still in that place

where health is bought.

And these problems aren't complex.

I mean, they are complex to solve, but I

feel there are so many

solutions that are readily available.

They just aren't accessible to 99.9% of

the population at the moment.

And that's a bit of a tragedy, and it's

definitely what is a

stumbling block for most,

because it really, when you sort of

understand the basics of it, like I do,

and I'm nothing special, you do realize

how simple these issues, broadly

speaking, are to solve, at least

initially.

Obviously, if you're dealing with

something more complicated, like a long

code, where there's potentially a spike

protein involvement, then

it gets more complicated.

But there are definitely solutions.

They've just got to be accessible.

Your answer is definitely,

yeah, it's great.

I was going to be obnoxious and say

something like mitochondrial

transplants, which I think...

No, no, no.

The body is too intelligent to need that

kind of intervention.

Yeah.

I'm just excited.

Aubrey de Grey and his

attempts over the years.

Thank you.

Thanks very much.

What can I say?

It's a biochemist in me.

I just want to see what happens when

someone prods

something or something else.

Okay, next one.

Red light therapy is thought to improve

mitochondrial function.

And I suppose it does,

at least peripherally.

Do you think it's effective at helping to

improve CDR or is it not that...

Yes, absolutely.

I think that photobio-modulation is

massively important.

And that, along with the light, as I

mentioned earlier, sometimes patients

can't take a lot of supplements and they

can't even take a lot of...

Obviously, transdermal nutrients,

electrolytes, and so on can help.

But sometimes you really do have to start

with these more sort of

extracorporeal types of therapy.

And I think the red light, perhaps just

an umbrella above the person's head,

perhaps just for three minutes.

Once every couple of days, I've seen that

make a huge difference as well.

It's got to be the right frequency.

And there are specialists like Dr.

Damien Downing, who I know you're

interviewing very soon, who have spent

many, many years looking into that and

have a whole range of

products related to that.

It would be very, very important really

not to waste your money on the wrong

frequency, but there are specialists

available who can give one

that kind of information.

Yeah, there definitely are.

Vegas mode stimulators.

There are a few out there.

Are you a fan of these?

Do you think they're effective?

I haven't used them myself.

Items like the Sensate, again, through

working closely with Dr.

Damien, because I am a member of the BSCM

as well on the committee.

So I attend every event of theirs, and

he's seen benefits from that.

And I do have colleagues who also have

done, but I haven't

recommended them myself.

Not yet.

Fair enough.

And the last one, and maybe

this one is a bit obscure.

So if needs be, we can cut it down.

But what do you think about

mitochondrial support peptides?

Things like MoTSI or SS31?

I don't know if you've come across these

or if you've got any thoughts on them.

Do you think they're effective?

Have you utilized them in practice?

Dr.

Holtz-Dolfen states, for example, as a

great specialist in those.

I haven't used them, and they're

difficult to access here.

And I think he would really need to, A,

B, and M, D, I would

say really to use them.

I think even in the states, they've, the

FDA has removed a lot of them from the

market now, perhaps

without any justification.

But it's a bit of a hot potato.

I would much prefer to start with

something simpler, like I was just

explaining previously, the right balance

of minerals, checking the

patient's sodium status.

COTS is so often just a matter of getting

the potassium and the

sodium ratios right.

Starting with the basics, and often I do

find people have been

through the most incredible

odysseys, perhaps even using apheresis,

which is filtering of the blood, the

entire blood, attempting to remove the

antibodies and aspects such as I've just

mentioned, have not

been touched on at all.

So diet, of course, is

so important as well.

So using the, as I say, simpler, sort of

more accessible

techniques would be my preference.

But I'd be very prepared to sort of take

part in seminars and

learn more about the peptides.

I just haven't done that yet.

Yeah, they're definitely interesting.

And things like MODC, sort of which

enhance insulin sensitivity and promote

the sort of mitochondrial biogenesis, it

acts on the folate AMPK pathway.

And it's also thought to

be an exercise mimetic.

And I think Downstreamer that promotes

some PGC1R for activation.

And then you have things like SS31, which

more instead of that sort of the

biogenesis aspect, it, let's see if I can

get this right, it binds to cardiolipine

and I think it improves the membrane

health and the structure thereof, thereby

sort of reducing ROS

and improving ATP output.

So they definitely are interesting and

there's definitely some

therapeutic potential there.

But I think, as you alluded to, it's,

I think the FDA has, I hate this term,

clamped down on a lot of them because of

the gray market aspect.

And I think people have just

had too much access to them.

And yeah, I don't think they're inherent

inherently a problem.

But I think when you start looking at

things like where they're sourced, they

can become an issue.

A lot of them come from, they're not even

compounded, they just come from the Far

East or whatever where they're just

manufactured and you don't

know what you get alongside them.

The endotoxin load,

obviously, yeah, the endotoxin load, the

lipopolysaccharide

load, heavy metals, etc.

But they are, when they use correctly,

they definitely are incredible.

Okay, last one.

What are your thoughts on methylene blue?

I don't use it myself.

I do have some concerns when I listen to

what it does to the MAO pathway

or enzyme.

MAO, A, I think.

And B, yeah.

Is it B?

Yes.

An enough dosage to be fair.

Yes, I sort of, again, I'm a little bit

perhaps cautious that way.

And I would prefer to see it used by

doctors and not too widely accessible

just because of the risks that appear to

be in the dosage and so on.

But I'm very happy to

work in teams where people,

which I do prefer to do, actually, I

always prefer to work in

multidisciplinary teams and there might

be a doctor included.

I know that Dr.

Klinghardt, for example, does use it and

other doctors who I know as well.

So they're willing to be guided by them,

but I don't recommend it myself.

Yeah, again, it's a

very interesting molecule.

And obviously, being an electron donor

and being able to bypass some of those

block complexes, I think for the right

person, it's definitely a good option.

And somebody who's already got healthy

liver mitochondrial function, it's

definitely not warranted.

And it can actually, again, cause

electron leakage with excessive use.

I think one of the things it's able to do

is to switch from ferrous ion to the

ferric ion, i.e. from the 3 to the 2 plus

stage and the methanolabemia, which is a

problem as well, and for which it was

originally used and still is.

It just makes me wonder whether there are

other ways of encouraging better ion

transport and releasing the trapped ion

and creating the right form of ion for

the body to utilize rather than

necessarily using that.

But I'm open to learning more about it.

Yeah, no, it is an interesting molecule.

And there's a large amount of data there

around its use and sort of regulating

things like ferroptosis, which is another

rabbit hole for another day.

But yeah, I think for a lot of people in

this who are struggling with CDR, the

point you touched on with regards to it

being an MAOI, yeah, an monoamine oxidase

inhibitor, is very on point because,

yeah, I mean, if you're going to inhibit

MAO, you're going to sort of increase

histamine levels potentially, which is

going to cause all sorts of

people all sorts of issues.

So I think a little

knowledge can be a dangerous thing.

And it's ultimately up to the individual

to educate themselves thoroughly if they

do choose to use these

sorts of compounds, but

causing the serotonin

syndrome as well, which patients

generally do disclose everything to one,

but not always

absolutely every last thing.

Sometimes they forget.

And if they are an SSRI,

it can potentially be fatal.

Yeah, I think it's ultimately a bit of a

done in Kruger at the

end of the days, isn't it?

You sort of, little

knowledges can be a dangerous thing.

Jolynn, you've been a star and this

conversation has been

delightful and informative.

Thank you so much.

And I'll thank you.

It's been up and delighted to be here.

Thank you.

If people want to work with you, if they

want to find out more about the AONM, I

think I got there, where

would you like to point them?

Where can they find you?

Well, the Academy of Nutritional Medicine

AONM is readily

accessible at the url aonm.org.

And all our tests and

our events are there.

I hold a bit like you, you know, a

podcast about a

webinar about once a week.

And I'm always there and have an email,

Jolynn, with 1L, interestingly, at

aonm.org, where I can

always be reached as well.

So thank you so, so much.

It's absolutely stunning for different

speakers you have available.

And I'm going to go back now over all of

your recordings and listen to them

because it sounds as though you have

amazing topics that you've covered and

are planning to cover.

Thank you.

That's very kind of you.

Thank you.

We'll chat soon.

Thank you.

Bye bye.