Good morning, Dr.

Seyfried.

It's a true pleasure to

have you on the podcast today.

Obviously, we'll be discussing all things

cancer in short order.

But before we get into it, would you mind

introducing yourself to the audience for

those who aren't familiar

with you and your body of work?

Yeah, well, well, thank you, Rob.

It's nice to be here.

I'm a professor of

biology at Boston College.

I have been here for,

well, since 1985, 40 years now.

And before that, I was at Yale University

in New Haven, Connecticut.

Here at Boston College, I've taught a

broad range of classes over the years,

neurobiology,

neurochemistry, neurogenetics.

Now I teach general biology to the

non-majors, as well as an advanced class

in cancer metabolism.

Cancer is a metabolic disease.

So our background for

biochemistry was lipid biochemistry.

I did a lot of work

on lipid biochemistry.

And as far as diseases are concerned,

lipid storage diseases, as well as

genetic diseases, epilepsy in particular.

And now our main focus over the last

quarter of a century has been

predominantly cancer.

But we are moving into also

other chronic diseases as well.

So I have a kind of a

broad-based experience.

I have a degree in genetics and

biochemistry, a

master's degree in genetics.

So those are the background educational

experience that I've had.

That's incredible.

And a reason, I

suppose, I could only dream of.

I think one of the big issues in the

health podcast space is creating content

that is sort of based on actual science

and to have someone with your background

and credibility, I feel just, well, at

least hopefully sort of highlight that

we're not here just to obviously discuss

pseudoscience today, that this is all

sort of based in empirical data.

Dr.

Seafree, I know we're here to really talk

about the metabolic theory of cancer, but

I think it would be prudent to maybe

start off with having a quick

conversation about

what cancer actually is.

And I know it's likely a dull question,

but I do feel it's that very few people

actually know what the disease is.

It's just something that

they aim to just not get.

I've got a few questions there, but yeah,

maybe we could just start off with that.

Cancer Biology 101, as it were, if you

would just mind running

through what cancer is.

Well, it's actually a very, it's a

complicated problem, but it's a very

simple definition of what cancer is.

It's cell division out of control,

dysregulated cell growth.

So people say, well, what's cancer?

It's just a bunch of cells that are no

longer regulated in their growth.

Of course, the origin of

that phenomenon is broad.

But what is it that makes a population of

cells in a particular organ of someone's

body to start growing in a dysregulated

way as opposed to normal cell division,

which is regulated?

In parts of our body,

there's wear and tear.

Cells naturally die and are replaced.

But the replacement of dead cells is a

very organized process.

They grow, they divide, and they, however

many divisions is necessary to replace

those that are missing, is a

well-regulated process.

And we know now that's all

controlled by the mitochondria.

But an example of cell

division under control,

one of the, is in the gut, you have the

crypt cells that seem to always replace

other cells in a very regulated way.

And in the liver, you

have liver regeneration.

Liver is an interesting organ because if

you remove a lobe of the liver, the liver

will regenerate the

missing part of the lobe.

And the speed of liver regenerating cells

is just as fast as that

of the fastest cancer.

The only difference is that the liver

regeneration is regulated growth, whereas

the hepatoma of the liver, which is liver

cancer, is dysregulated growth.

And the biochemistry of those two

populations is strikingly different.

So when you ask what is cancer, it's

dysregulated growth in a population of

cells in someone's organ, which differs

from regulated growth

of cells in that organ.

So sort of after control mitosis, you

might say, in a nutshell.

Yeah.

And the question that has perplexed the

field for decades is what regulates, what

is responsible for

regulated growth in the first place?

Why would one cell know when to stop

growing and another cell

not know when to stop growing?

And that all comes back to the role of

the mitochondria and the cytoplasm.

The mitochondrion controls calcium

signaling within the cell.

Nobel prizes have been awarded for people

to learn the cyclins and

going through the cell cycle.

And that cell cycle is all controlled by

calcium signaling from the mitochondria.

So when mitochondria of the cell become

dysfunctional in the sense of producing

energy and that calcium gradients, they

fall back on a fermentation metabolism,

which is an ancient form

of energy without oxygen.

And the mitochondrion loses control of

the differentiated state.

That being anaerobic respiration.

Yeah, anaerobic.

You can grow cancer cells in the absence

of oxygen or in the presence

of cyanide and they survive.

So which would

normally kill normal cells.

And that's because their energy

metabolism is of an ancient type.

It's the type of energy that existed on

the planet before oxygen came into the

atmosphere two and a

half billion years ago.

It was a fermentation metabolism,

generating energy without oxygen.

And the default state of

cells is proliferation.

The default energy state

of cells is fermentation.

So when what cancer cells are doing is

they're simply falling back on their

default proliferative state and their

default energy state behaving, behaving

much as they were of all cells that

existed before oxygen, which was

unbridled proliferation.

And they would die as soon as the fuels

that drove the flow drove the

fermentation metabolism would dissipate

in the micro environment

and the cells would die.

So it was purely an energy

driven process without regulation.

During the origin of life on the planet,

archaeobacteria fused with other other

cells to develop the mitochondria.

And it was the mitochondria that allowed

the division of energetic labor in the

cells, allowing metazones to form and the

most complex multicellular organisms that

we have today all all due to the energy

capacity of the mitochondria.

And the nucleus, which everybody seems to

have focused on, is because you could see

it sometimes even with the naked eye,

whereas the mitochondria for centuries

could not be seen clearly until you had

the electron microscope and more

sophisticated ways of

looking at this organelle.

But in a nutshell, it's the mitochondria

that controls the

regulation of genes in the nucleus.

So all the epigenetic stuff you hear

about is mostly mitochondrial controlled

mitochondria controlled.

So the nucleus is kind of an obedient

slave of whatever the mitochondria does

because of that

organelle becomes corrupted.

The cell falls back as a and one of these

dysregulated growths.

So everything comes back to the origin of

cancer as a corruption of mitochondrial

function only in cells that can switch to

the ancient fermentation pathways, which

can explain why certain cells

in our body never become tumor.

Red blood cells can't become a tumor

because they have no mitochondria or

nucleus in the first place.

Neurons of our brain

cannot sustain fermentation.

So you rarely, if ever,

get cancers from neurons.

They get from real cells.

What about cardiac tissue?

Cardiac tissue rarely, if ever, gets

cancer because they cannot replace

oxidative phosphorylation with substrate

level phosphorylation.

So you rarely, if ever, get cancer of

muscle, a striate or cardiac tissue

because they die and you can't get a

cancer cell from a dead cell.

So we're able to go through the body and

look at the kinds of tissues that form

cancer because they have the capacity to

transition from oxidative phosphorylation

to substrate level phosphorylation, which

is a protracted event that

doesn't happen overnight.

You really have to abuse the hell out of

your mitochondria in a

chronic way to get cancer.

Cancer is very hard to get.

I know it's exploding as an epidemic, but

we abuse the crap out of our bodies and

that's why we're getting so much cancer.

But it's really hard to get cancer.

So when you say, well, how come so many

people because they because their bodies

have been chronically abused by a variety

of insults, many of which

they're not even aware of.

But that's that's how you get cancer.

It's a chronic disruption of oxidative

phosphorylation coupled to a compensatory

substrate level phosphorylation.

And Warburg knew this a long time ago

from the 1920s, but he only knew that it

was a glucose driven transition from.

But we now discovered and have I had the

concept but not the evidence.

But now we published the big paper

recently that the cancer cell can ferment

an amino acid called glutamine.

So you get sugar and amino acid

fermentation are driving the dysregulated

growth of the tumor cell.

And the field all thought it was

glutamine respiration oxidative but it's

not its glutamine fermentation within the

mitochondria itself.

So the very organelle that's supposed to

get energy through oxidative

phosphorylation is also producing energy

through substrate level phosphorylation,

which is a fermentation mechanism.

This is what's blowing

the doors off the field.

You know, they never realized that the

very organelle could also ferment.

And that goes back to its organ its its

origin as a bacteria itself.

So, you know, once once you understand

evolutionary biology, all the pieces of

cancer fall into place

quite, quite reasonably.

Now, it really does.

And I just love the fact you do brought

up the mitochondria as being more than

just this sort of this

energy factory or the body.

It's just involved in so many genetic

processes beyond just

helping to create ATP.

And yeah, thanks for that.

It really does sort of provide some

context to what is going for

the rest of the conversation.

I reckon the natural follow up then

again, this is quite a

loose question, I suppose.

I suppose.

And you've really answered this too,

to an degree.

But I'd sort of and beyond the sort of

the metabolic side of it, I'd love to

sort of get your your thoughts on the

different theories that

are sort of driving cancer.

Obviously, it's a complex,

this complex aetiology there.

And it's it would be and it shouldn't be

viewed from this sort of reductionist

viewpoint that there is just one

mechanism that causes cancer.

I know in my brief experience in academia

that people studying these conditions can

often get wrapped up in their own

mechanisms and

occasionally be blinded by research.

Obviously, you have a

fairly well-rounded view.

So would you mind talking us through the

various sort of and I hope sort of

phrases correctly proposed triggers,

maybe or underlying mechanisms that sort

of lead to the development of this

condition, sort of the genetic causes,

the environmental risk factors, the

immunological side of things?

I don't know if I phrased that correctly,

or if that makes sense.

Yeah, well, it does.

I mean, when you look at the history of

of the disorder that has intrigued

scientists, you know, for centuries,

you know, we knew about cancer a long

time ago, VirCal, and the 1800s people

were studying these things.

You know, and how does it start?

You know, you have the emergence of

different ideas, concepts of

what cancer, what cancer is.

The current view taken by all major

research centers and academic centers is

that it's a genetic disease.

I know the UK thinks that the United

States government, National Cancer

Institute, believe that.

I think most of the cancer institutes

around the world, the French, the

Germans, the English, all Western major,

and even in China and Japan and Korea,

you know, South America,

they're all of the view

that cancer is a genetic.

It seems to be some sort of a paralytic

mindset throughout the world.

It's an indoctrination of brainwashing,

if you will, of what this

disease is supposed to be.

But it wasn't always that way.

You know, there was the viral cancer was

a virus caused by viruses.

Cancer was a metabolic disease.

You know, cancer is a genetic disease.

So you have to put all the views over

time into what it is.

And, you know, Warburg started the idea

that it was a

mitochondrial metabolic disease.

But he couldn't explain certain things

which we now can't explain.

He didn't know about the glutamine issue,

nor did he realize that a lot of the

oxygen that cancer cells consume is not

used for ATP but produces reactive oxygen

species, ROS, which are radicals.

And they cause, in large part, the

mutations in the nucleus.

So, you know, certain viruses, okay,

well, we knew certain like papilloma

viruses and hepatitis

viruses and the Rous sarcoma virus.

Peyton Rous was a Nobel Prize receiver

for his virus particle.

We now put all that together.

We know all these viruses damage

oxidative phosphorylation, chronically

causing this transition to

substrate-level phosphorylation.

But it was the Watson and Crick DNA

structural analysis that kind of sent the

whole field off into the abyss,

chasing stuff that we are still chasing.

Because it became exciting to bring a

very complicated mishi-marshi disease

back into a molecular configuration.

And I think that was,

I call it physics envy.

Biology had always been a poor stepchild

to the pure, rational thought of the

human mind, which was physics.

And when the DNA structure was defined,

and you could explain the arrangement of

amino acids and RNAs all linked back to

the structure of the DNA, biology was

brought from an observational

observational kind of a disorder or a

field into a more quantitative way.

And then, of course, as soon as you

started looking at cancer cells, you

start to see chromosomal abnormalities.

That goes back to Theodore Bovary, who

knew nothing about cancer.

And he said, "I think cancer might be

something to do with chromosomes."

Purely speculative.

He even said, "I'm probably wrong about

everything," and he was.

But the field grabbed ahold of him as the

father of the genetic theory of cancer.

And then, of course, you started to see

gene mutations

associated with certain cancers.

And then we spent billions of dollars on

the cancer genome projects, looking at

every kind of a mutation.

And then therapies, precision in medicine

and all this developed around the genomic

view of cancer, where we're going to have

precision medicines,

targeted therapies, and all this kind of

stuff, which is where we are today.

And all the governments and academic

institutions are giving away millions of

dollars in grants to people trying to

hunt down genes that could be responsible

for the dysregulated cell growth.

So it comes back.

We know cancer is a

dysregulated cell growth.

What's causing that?

Well, according to the somatic mutation

theory, which is the dominant theory

today, it's mutations

that are causing that.

But I've clearly shown that those

mutations are largely irrelevant.

With our research, they can't attack it

because the evidence is too strong.

So when you have evidence that's

overwhelmingly strong and it's not

consistent with your general

theory, then you ignore it.

But you're only going

to ignore it for so long.

So when you develop a theory,

theories are supported by a massive

amounts of evidence.

The somatic mutation theory was very,

very strong because you found almost all

cancers with somatic mutations.

And these somatic mutations, some of them

were linked to the cell cycle, which you

could then link a mutation in the genome

to something that would lead to

dysregulation or

dysfunction of the cell cycle.

And that made a lot of sense.

So people grabbed onto that.

And because it was so molecular and so

quantitative and approachable by really

sophisticated technologies which have

developed around cancer, like all these

sequencing, unbelievable AI now,

artificial intelligence helping analysis

of sequencing, and all of the different

kinds and types of mutations that were

found in cancer cells.

I mean, it was an explosion of molecular

biology associated with cancer.

So that was very

attractive to a lot of people.

But then having done work in Meyerle lab

and seeing research that was far more

consistent with what Otto Wirberg said

than with the somatic mutation theory, I

began to look at this.

But getting back to theories, I like to

compare what's happening today with the

mitochondrial metabolic theory replacing

the somatic mutation theory because it really takes a lot of

evidence to replace a theory.

Einstein's theory of relativity could

still be replaced, but has not yet been.

And there are physicists that are

constantly trying to show where Einstein

was wrong, and they believe

they might, but they haven't.

Darwin's theory of evolution has been

challenged many times, but it has not

been overthrown because the data that

support it are stronger than the data that don't support it.

And then you have the geocentric

heliocentric theory of the solar system,

where for 1800 years, people thought that

the Earth was the

center of the solar system.

And we developed equants, deference, and

epicycles to try to predict

the positions of the planets.

And Copernicus just

replaced the Earth with the sun.

And all of a sudden, a lot of stuff was

far less complicated and more understandable.

So the heliocentric theory replaced the

geocentric theory, opened up a scientific

revolution during the Middle Ages,

the Renaissance period.

What we're having today is that

mitochondrial metabolic theory is

overturning the somatic mutation theory.

And the consequences are going to be

every bit as phenomenal as what happened

during the Copernican revolution.

So we look at

evidence to support a theory.

If cancer is a disease of somatic

mutations, which is the current dogma,

irrefutable truth, the silent assumption,

cancer is a genetic disease.

Well, now with deep sequencing and deeper

analysis, we find some cancer cells that

don't have any mutations, yet they're

growing out of control.

So when I looked at those, there's not many papers that I've looked at.

So when I looked at those, there's not

many papers, but there are

some very clear findings.

And then when I say, what do the

investigators who believe that cancer is

a genetic disease say about cancer cells

that don't have mutations or

they can't find any mutations?

And they don't say anything.

So when I went back and looked at their

explanation, they

didn't even, they ignored it.

They didn't even talk about the cancer

cells that had no mutations.

They just seemed to focus on all the

cancer cells that had mutations.

And I said, you got a glaring

inconsistency in your theory, staring you

in the face and you did not address it.

What the hell is going on with that?

Then, of course, they realized that

there's so many hundreds of thousands of

mutations in some of these tumor cells.

They all can't be drivers

of dysregulated cell growth.

So then the field decided to reclassify

some of the mutations as

passenger genes and driver genes.

So we then moved into the driver gene

mentality, which lasted several decades.

Where only some of these many mutations

are truly responsible for dysregulated

cell growth and we

redefined them as called drivers.

And that got, that generated a lot of

excitement since the 19, early 1980s, I

guess, middle eighties, driver genes,

driver, oh, the driver genes.

So now with deep sequencing and more

sophisticated technologies, we're finding

all kinds of mutations in

driver genes in our normal tissues.

Like you and me.

I mean, we got all kinds of mutations in

P53 and MIC and RAS and all these kinds

of genes that are in our normal tissues

and are not dysregulated in growth.

How do you explain that?

That's inconsistent with

your somatic mutation theory.

Are there any real sort of polygenic risk

goals maybe that sort of have been

identified in respect to this?

Well, the nuclear mitochondrial transfer

experiments throw, that's the real nail

in the coffin for the whole thing.

Because what was done on a variety of

different types of cancers is that the

nucleus of the tumor cell is now placed

in the cytoplasm of a

non-neoplastic cell.

And invariably you get regulated growth,

despite the continued presence of

whatever kind of genetic abnormality

might have been in that nucleus.

Whether it was polygenic, whether it was

chromosomal, whether it was point

mutations, frame shift mutation, didn't

make any difference.

When that cancer nucleus was placed into

the cytoplasm of a non-cancerous cell,

that new cell no longer

had dysregulated cell growth.

That's quite interesting.

And that's been done repeatedly.

And in vivo and in vitro.

So in all kinds of experimental systems,

meaning that normal cytoplasm

suppresses neoplastic growth.

On the other hand, if the nucleus of a

normal cell is now placed in the

cytoplasm of a tumor cell, you've got

dysregulated growth,

which is completely the opposite of what

you would have expected on

the somatic mutation theory.

So when you have the opportunity to sit

down and carefully evaluate all of the

evidence from the nuclear mitochondrial

transfer experiments, also, if you have a

raging tumor cell and you replace the

mitochondria with normal mitochondria,

just put normal mitochondria, you get

complete downregulation of this

dysregulated growth.

You can convert a raging tumor cell into

an indolent tumor cell by putting normal

mitochondria back in the cytoplasm,

mitochondrial medicine type.

I was about to say, I'm getting ahead of

my curve and I'm going to shoot myself in

the foot by asking this question now, but

just with regards to that, then, is there

any thought to the idea that

mitochondrial transplants could be a

potential therapy in that regard?

Absolutely.

But that's the future.

It's not here yet, because we have to

make sure that the mitochondria that are

transplanted are normal in numbers,

structure, and function.

And during the very process of

manipulating these

mitochondria, you can also damage them.

And you have to know how to do that.

So mitochondrial medicine

is going to be the future.

But where the technology

to do that is not here yet.

So our approach to managing cancer is

killing the tumor cells while not harming

the rest of the body and then allowing

people to live far longer with a higher

quality of life, while mitochondrial

medicine is under development.

That's the thing.

It's very interesting, because when you

have dysregulated cell growth in cancer,

they're fermenting like crazy.

And the oncogenes, which have generated

tremendous interest, we have shown, and

others, HIF1, alpha, MIC, and these

things, they are there.

And they are facilitators of opening the

floodgates for fermentation

fuels to get into the cell.

And when you put new mitochondria into

the cell, the oncogenes turn off.

You don't need them anymore.

Why are you going to

ferment when I can respire?

So the oncogenes are no longer needed.

And normal mitochondrial respiration turn

off oncogene expression.

So you shut down the glycolysis and the

glutaminolysis pathways, because you

don't need glucose and glutamine.

You can respire.

Everything makes perfect sense.

And the data show that.

So where did all the mutations come from?

They came from the biology of inefficient

oxidative phosphorylation, throwing out

reactive oxygen species, which is the

superoxide and the anion, the OH radical,

which are carcinogenic and mutagenic.

And they come out of the dysfunctional

mitochondria, creating an escalating

situation of biological chaos.

So what we're seeing, or what the field

is mostly focusing on, is downstream

epiphenomena of the damage to

mitochondria and all the

sequelae that follow that.

It's really amazing to me.

I just can't figure out how the field

doesn't understand this.

I try to, I don't know, maybe

I have to write it in crayon.

Sometimes you just have to do that.

You have to take the back of a neck and

smash the guy's face into

the evidence to let him see it.

But the interesting thing is that you see

all these clear evidence that you can

manage this disease quite effectively by

just depriving the cell of the two

fermentable fuels that it needs and then

transitioning the whole body over the

fuels that the tumor cells can't use.

So intrinsically,

people say, oh, cancer cells are so tough

and hardy, and they're so versatile.

That's total crap.

How do you explain a cell with a nucleus

blown to hell with all these mutations?

And you're going to

have that cell behave more

transitional and more flexible than the

cells in our body that evolved over

millions of years to adjust their

metabolism to the situation.

And the cancer cell can do this with a

nucleus that's blown to hell.

Makes no sense in evolutionary biology.

People don't

understand evolutionary biology.

The way you understand cancer and many

other diseases, you must understand

evolutionary biology.

And if you don't do that,

you're going to be in the dark.

You're going to be in the dark.

And that explains a lot of the stuff that

we have in medicine today, because people

don't understand evolutionary biology.

They remain in the dark.

And as long as you remain in the dark,

you ain't moving forward.

So here's what they say.

Oh, cancer cells are tough to kill

because we're throwing everything at

radiation and chemo and immunotherapies.

And those damn cancer cells can survive.

They're protecting themselves with the

waste products of

fermentation metabolism.

Everybody knows.

They say, oh, the cancer environment is

so acidified, it protects them from the

therapies that we have.

Where does the acidification come from?

The waste products of glucose and

glutamine fermentation.

If you take away glucose and glutamine,

you remove the acidification of the micro

environment, making the tumor cells

extremely vulnerable to small doses of

radiation, chemo, and

these other procedures.

How is that not understood by guys that

are supposed to be smart?

Don't you understand why the damn tumor

cells are not dying from

what you're throwing at them?

Because they're fermenting.

If they ferment, you take

away the fermentable fuels.

Oh, that can't be right.

It's too simple.

Yeah.

And it works.

And it is right.

Get over it.

You want to live longer, you take away

the fermentable fuels, and then you give

them fatty acids and ketones, and the

cancer cell can't because

you need a good mitochondria.

Fatty acids and ketone bodies cannot be

used as a fuel by cancer cells because

the mitochondria are inefficient.

Fatty acids and ketone bodies can be used

by most of our normal cells because we

have good

mitochondria, healthy mitochondria.

So we lower the blood sugar, elevate the

ketones, and then come in and target the

glutamine pathways strategically in an

approach that we developed, the press

pulse therapeutic strategy.

Glucose is a non-essential metabolite.

Glucose is a non-essential metabolite.

We can live with very, very minimal

levels of glucose just to keep our

erythrocytes moving oxygen

and CO2 through the body.

It takes tiny amounts of glucose.

But the majority of muscles and brain can

all transition over to ketone bodies.

Tumor cells cannot.

We tested them.

We interrogated these cells.

Tumor cells collect huge droplets of

fatty acids in the cytoplasm because they

cannot use the fatty acids.

If you force the tumor cell to use the

fatty acids, it develops reactive oxygen

species and explodes and dies.

So that's why they store the fatty acids

in the cytoplasm because if they try to

use them, they're going to kill them.

So this is simply a protective mechanism.

I can't tell you how many people are

writing papers saying tumor cells love

fatty acids because they store them in

the cytoplasm because

they need them for fuel.

Yeah, well, try to goose the cell to use

the fatty acids and all

of a sudden the cell dies.

Try to grow your cells, your cancer cells

in the absence of glucose and glutamine

in the presence of fatty

acids in ketone bodies.

With no glucose, no

fermentable fuels, they die.

So it becomes very

clear how to manage cancer.

So we're aware of this.

Unfortunately, the field still has to

come to grips with this

and I think they slowly are,

but it takes time, unfortunately.

Yeah, I know.

I think we could

probably stop the podcast there.

That was incredible.

Thank you.

I'm definitely going to have

to re-listen to a bunch of that.

Well, not only listen, not only re-listen

to it, read the damn

papers that we published.

I go into great biochemical details.

I have the evidence put out in those

papers that we published

and they're open access.

So everybody can read them.

Anybody with a few functional brain cells

can sit down and read these papers and

make their own decision as to what they

think in light of that.

I do a compare and contrast the theories.

I do the evidence supporting the

different theories and you tell me what

you think is happening.

And I learned there's very few people

that actually understand or not

understand that who read

actually read the literature.

They all wait and they only do what other

people are doing and they ask other

people what they think.

And if the person

says, "Oh, no, it can't be.

Okay, then I believe it can't be."

Why don't you use your own brain cells

and analyze the data for yourself?

That's one of the great things about

humans is we have a rational mind.

That's what we were gifted with.

But I'll tell you, dogmatic views,

political, religion, all that takes away

from rational thinking.

And when you lose your ability to sit and

rationalize, then you

lose a part of your humanity.

And what we're seeing here, the reason

why there's a delay in the movement from

the somatic mutation theory to the

mitochondrial metabolic theory, which

will prevent and manage

diseases dramatically.

We're going to drop cancer death rates

like there's no tomorrow.

We're going to keep people alive because

we understand the science

supporting what we're saying.

And then once people start looking at it

and seeing that we are essentially

correct, not on all the minutia, we can

always work out minutia later on.

But the bottom line is how long can I

keep somebody with a

stage four tumor alive?

Oh, he's got three months to live.

Are you kidding me?

We've got people that were given those

days, they're still alive five and six

years later because they've transitioned

their body over to nutritional ketosis

and came in with certain low dose

medications to kill off the tumor cells.

So I know it's going to work because I've

seen enough preclinical studies and human

studies, small trials, to know this will

work and keeps people alive.

Unfortunately, you go to the top

hospitals and they tell you,

oh, no, you got to have this.

Did you ever hear the

cancer is a med about?

No, I never heard of it.

Eat sugar, eat all the

high carbohydrate diets.

Why?

Oh, because you're losing weight.

Why am I losing weight?

Well, you have cancer and

we just try to poison you.

Anybody who's poisoned loses weight.

So you get nausea and

vomiting, diarrhea, fatigue.

Why are you doing that?

Well, we use the toxic poison on you.

Why are you doing that?

Well, we're trying to

kill your tumor cells.

I went bald.

Why?

Why you go bald?

I lost all my hair.

Oh, did you have tumor cells growing in

your hair follicles?

No, they just happened to die.

You're trying to kill tumor cells, not

kill your hair or blow out your gut.

That tells you that those are the

procedures of people who lack knowledge.

What we're seeing is the result of

massive lack of knowledge on the

biochemistry and biology of the very

disease that people are working with.

And we're using medieval therapies that

are torturing people.

I think people during the Spanish

Inquisition would be very impressed with

how we're torturing cancer

patients in these hospitals.

They could say, "Well, we can learn

something from you guys.

Where do I get Red Devil Doxorubicin?

We could give that to a heretic."

It's terrible for me

to say stuff like this.

But when you see 1700 people a day in the

United States dying from cancer, 70

people an hour, and you see cancer

getting worse and worse around the world,

I mean, grab somebody by the throat and

say, "What the hell are we doing?

Why are we allowing this to happen?"

Because of a failed theory.

That's what it is, a theory that's no

longer supported by the evidence.

And you guys keep treating people based

on an incorrect theory,

and the outcome is abysmal.

Yeah.

What did Einstein say?

Insanity is doing the same thing over and

over again and expecting a different

result, something to that extent.

Yes.

Well, why are they doing?

Don't they know what Einstein said?

Did they not hear what Einstein said?

And there's another issue of morality,

which is even a worse issue.

You don't like to be referred to as an

immoral person, but when you're taking

drugs that are not based on the correct

theory and treating people with them and

knowing that they won't work,

and that's immoral.

And the other part of this is that many

of those drugs are very, very expensive.

And what happens, they not only cause

physical toxicity, they

cause financial toxicity.

Many people, their marriage is dissolved,

they commit suicide, the cost is passed

on to the surviving relatives.

And for folks that are not well off, a

$20,000 bill, even though they covered

80% of the 100,000,

20,000 can cripple a family.

With limited means.

This is immoral.

The whole cancer

industry is an immoral industry.

They're allowing people to suffer and die

based on an incorrect theory.

And they're allowing

physical and financial toxicity.

These are immoral acts.

And we have a strategy that can

absolutely reduce the deaths of cancer,

keep people alive with a higher quality

of life, and it's not being

done anywhere on the planet.

Now you tell me what's wrong with that.

Yeah, I'm not even going to try and sort

of answer that

question just at this point.

Dr.

Seifried, again, that

was an amazing answer.

Thank you.

I'd just like to take a step back quickly

and discuss, have a quick discussion

about your thoughts on testing.

Now, the way I see testing, testing is

generally done quite acutely when

somebody presents with

a disease in this case.

You'll obviously get a physical exam

done, some sort of imaging, probably some

sort of biopsy as well, some blood tests

looking at various biomarkers, et cetera.

But in no way is this

sort of testing preventative.

It generally is only treated and dealt

with when the issues arise.

Now, obviously, there are various

technologies that are starting to sort of

come up to things like liquid biopsies.

Maybe you could elucidate on that

slightly and these full-body MRIs, which

are obviously somewhat controversial in

the sense that they may or

may not pick up incident lomas.

The idea of finding an issue that may not

be an issue that then requires further

investigation that then may or may not

actually turn into an issue.

What's your stance on

early detection as a whole?

Do you think it's something we should be

exploring more beyond just the basic get

your colonoscopy done

when you hit 40 plus?

Or does the whole thing again about

incident lomas and treating cancer from

that perspective and, excuse me, treating

and scanning for cancer from that

perspective generally make

it a bit of a mute point?

Yeah, well, you have a couple

of things here to break down.

The diagnostics, I'm in favor of

non-invasive diagnostic approaches.

If we have a liquid biopsy that's 95%

accurate in determining whether or not

you have a neoplastic growth somewhere in

your body, I'm all for that.

And then non-invasive imaging, whether

it's a PET scan, MRI, CAT scan, or one of

these kinds of things, I'm not in favor

of biopsy because I have seen so many

papers published in the scientific

literature showing that when you stab a

cancer, you run the risk of causing

metastasis, metastasis where the spread

of the tumor, the cells can spread around

your body making what was formerly a

localized problem, a systemic problem.

So I'm in favor of four diagnostics,

colonoscopies and and breast

things and stuff like this.

Those are, you know, I

don't know what to say

about that.

I know there's a lot of

controversy about that.

And most people who develop cancer have

certain physical signs in

their body that something is wrong.

Like you said, a lump,

a wound that doesn't heal blood that

continues to come from some location.

You know, those can be then liquid biopsy

to see if there's a real linkage to some

neoplasia, a scanning of the body or

something along these lines.

And then once you would make a diagnosis

without a biopsy, you see a lump.

Okay, let's launch into metabolic therapy

and see if we can shrink the lump

naturally with diet drug combinations,

non-toxic drugs and diets that we've

developed here at BC.

And if you shrink the lump and it goes

away, and the imaging analysis and the

liquid biopsy data, what happened?

Where did it go?

I don't see any of the

markers that were there previously.

That's great.

And if it doesn't go away completely,

you might have shrunken it down and make

it much smaller, in which case a surgical

procedure or a dose of radiation at a

very defined spot could

be potentially curative.

So there's a lot of ways to diagnose and

treat cancer in the early stages

different than what we're doing today.

You know, we're doing too

radical on this whole thing.

You know, you see a lump in the rip the

person's breasts off

or something like this.

You know, I don't know what to say about

colonoscopies or breast exam exams.

Breast cancer rises every

year in females in this country.

Colorectal cancer is on the rise.

So I don't know what's going on.

All the major cancers seem to be, many of

the major cancers seem to be on the rise.

It's happening in

younger and younger people.

Yeah, if you're to speculate, do you

think that is an environmental issue,

just sort of maybe excess sort of

zenoestrogens in the environment that are

particularly just from a breast cancer

perspective, maybe

triggering these issues?

Or is that a bit productionist again?

I think most of it is environmental.

I mean, there are some people who have

genetic predispositions to

insults from the environment.

You have to realize

that cancer is a disease.

In fact, not only cancer, most of the

chronic diseases that we are dealing

with, which is dementia, type 2 diabetes,

obesity, hypertension, high blood

pressure, a lot of neuropsychiatric

problems, are all the result of

mitochondrial dysfunction in one way or

another, caused by the diet lifestyle

that we're all under.

And we know this pretty much because

Paleolithic men would not have had any of

these kinds of conditions.

They died predominantly

from infections and injuries.

They did not have orthopedic surgeons to

repair a broken knee from

some guy gored by a buffalo.

And how do we know that?

Because people say, "Well, you weren't

there during Paleolithic

period 500,000 years ago."

But we have people on the planet who

still live, according

to traditional ways.

And these folks also didn't have cancer

or a lot of the chronic

diseases that we have today.

How do we know that?

Because Albert Schweitzer and a number of

other physicians and humanitarians were

investigating these primitive tribes.

And they said, "Wow, they're remarkably

different from those that live in the

United States and England."

So they were not obese.

They didn't have any chronic diseases.

They had bacterial infections, parasites,

and things like this.

So what's the difference between the

Western diet lifestyle and the

Paleolithic diet and lifestyle?

And predominantly, it's the availability

of highly processed

carbohydrates in our diets.

A Paleolithic man never had highly

processed carbohydrates in his diet.

We did not evolve to evolve in an

environment with highly processed carbs.

But highly processed carbohydrates, are

you talking, obviously,

and my evolution biology is definitely

not my strong point, but I assume you

mean very high GI carbohydrates, things

like your processed sugars, honeys, etc.,

opposed to things like root vegetables,

things that are potentially

lower on the glycemic scale.

That maybe wouldn't...

Yes, predominantly.

Things that can

remain edible in a package.

Like I have a Twinkie here.

This Twinkie is 10 years

old, and it looks edible.

And a mouse, it's 10 years old, and a

mouse ate it, broke in and ate one of

these two years ago.

And he didn't complain.

And there are people that are hungry that

would eat 10 year old Twinkie.

This is a synthetic thing made from all

chemicals and sugars.

This kind of stuff will kill you.

Yet we eat large amounts of it.

Not only that, we deep fry it and put

powdered sugar and

chocolate syrup on it, damn thing.

You should go to Scotland.

That's the Shon's Act breakfast.

Yeah, right.

So then we wonder why we got cancer and

high blood pressure and hypertension and

neuropsychiatric problems.

And the lack of exercise is unbelievable.

Paleo, you know how hard it is to track

down and kill a big animal?

It's not easy.

You have to have well runners.

You have to have strong guys to track

down and kill these buffalo.

And you have to kill a mammoth, a woolly

mammoth, and these kinds of big animals

that lived in paleolithic times.

And that was a lot of energy to kill, not

only to kill the big thing,

but to chop it up and eat it.

You know, they'd go for the bone marrow

as a fuel source that

was very rich in nutrients.

We're sitting in traffic today.

We're sitting in front of computers.

We don't nearly have the amount of energy

that was expended

during paleolithic times.

We're eating highly

processed carbs, bad food.

We have bad sleep.

We have emotional stress.

We have all of these things that impact

negatively the number structure and

function of mitochondria in our cells.

It is not surprising that we have all of

the chronic diseases in cancer that we

are currently suffering with

in modern Western societies.

It's absolutely understandable in terms

of our evolutionary biology.

We are still paleolithic man

biologically, but living in a modern,

industrialized society where all of the

desires that we would have had in

paleolithic time are now at our

fingertips in any supermarket.

We don't have to go out

and hunt down animals.

Everything is prepared, packaged, and

ready for us to eat right away.

We don't have to expend a lot of energy

to cook it up, kill it,

and cook it every night.

It's preserved, well preserved, so we can

store it for a long

period of time and eat it.

Eventually, it beats the hell out of your

mitochondria in your body.

Some people, you get obesity, type 2

diabetes, hypertension, high blood

pressure, macular

degeneration, dementia, cancer.

Every one of those diseases, disorders,

is the result of mitochondrial

dysfunction in one way or another.

Some cells up and die become

dysfunctional, not becoming cancer.

Some cells that have the capacity to

switch from oxfoss to substrate-level

phosphorylation become cancerous.

We can link all of the major chronic

diseases, including cancer, back to

mitochondrial dysfunction, which then

begs the question, well,

how do you prevent cancer?

And you keep your mitochondria healthy.

It's extremely difficult to get cancer if

you're mitochondria healthy.

Well, how do I keep my

mitochondrial healthy?

Do a lot of exercise, stress management,

avoid highly processed carbohydrate

foods, try to get good sleep.

Do all the things that keep mitochondria

healthy, and you don't get dementia, you

don't get cardiovascular

disease, you don't become obese,

you don't get cancer.

You significantly reduce the risk for

cancer and all these chronic diseases by

keeping your mitochondria healthy.

It's very interesting.

In the United States,

the NCI National Cancer Institute says,

"We reduce cancer by 33% over the last

several decades, mainly because we had

the anti-smoking campaign of the 1990s.

And if we all continue to smoke like

crazy, like we were in the 1990s, we

would have 33% more dead cancer patients

today than we actually have."

So clearly, the major drop in cancer

deaths came from the

elimination of a provocative

behavioral situation, which was smoking.

So why?

Because our mitochondria are healthier

when you don't smoke.

And everything comes back to the health

and vitality of the mitochondria.

Do we want to go back and become, again,

live in a cave like Paleolithic Man?

No.

No,

but finding that happy middle ground.

Yes.

But now we have an awareness.

And not only that, we develop the glucose

ketone index calculator.

My next question was

going to be exactly that.

Which is now going to be the tool to

allow every person that can measure their

blood, glucose, and ketones with a meter,

either by pricking their finger to get a

drop of blood or using a continuous

glucose ketone monitor on your cell

phone, you will be able to know when you

apply the GKI index, you will know

exactly what zone of

health you are in or not in.

So you can know that you will be in a

high risk red zone if you have a GKI

that's over 50, up to 100.

You are going to be in a zone of

mitochondrial ill health.

Can we backtrack quickly, Dr.

Seifried?

Sorry about that.

Just briefly discuss what the glucose

ketone index is, just for those in the

audience who maybe

aren't familiar with it.

Obviously, it's a biomarker that I know

you have been intimately

involved in developing.

But what exactly is this

index and then how does it work?

Obviously, we are monitoring two

different biomarkers here, ketones,

things like butyl

hydroxybutyrate, acetate, etc.

And then obviously glucose.

But how does looking at those two markers

from a metabolic health standpoint help

us to, well, a, determine metabolic

health and maybe just a

bit more nuance there.

I know there's

generally a range there as well.

I think you want to aim for about a three

when looking to try and deal

with things therapeutically.

I may be wrong there.

But yeah, if you could just fill us in

sort of very fiduciary on

what that index is all about.

So again, go back to

evolutionary biology.

Paleolithic man was always in a state of

nutritional ketosis, mainly because they

did not have access to highly processed

carbohydrates in their diet.

So they had a lot of exercise and they

had a diet that was largely carnivorous

with some vegetables, some

tubers and this kind of thing.

But they were complex carbs.

They weren't these highly processed, like

you mentioned already, highly glycemic

index kinds of things.

And food was limited.

So when you put that body and you look at

the, if they could look at their glucose

and ketones at that stage, they would

find themselves in a state of nutritional

ketosis, which is an elevation of ketone

bodies and a very low glucose level, or I

should say very normal, like 65 to 85

milligram per deciliter, maybe

a 3.2 to 4 millimolar glucose.

These are normal body levels of glucose

produced by the combination of

gluconeogenesis as well as carbohydrates

that we would get from the diet.

So we would always be in this beautiful

insulin, super insulin sensitive zone, no

insulin resistance at all, because

diabetes would be unheard of, type two,

of course, not type one.

Type one would have been afflicting us

from the beginning of

time in one way or another.

But our bodies would have been in

metabolic homeostasis as long as we

weren't starving, of course.

But we could go long periods of time

without eating and still maintain

metabolic homeostasis because we would be

burning ketone bodies that would be

mobilized from stored fat.

So we developed the glucose ketone index

as a marker, biomarker, to allow us to

know what level of metabolic

homeostasis we would be in.

So if you have a glucose ketone index of

20 or 10, I mean, you're in some level of

metabolic homeostasis.

If you want to go into a deeper level of

what we call therapeutic ketosis, then

you'd go down to a level of two, which is

the ratio of blood sugar divided by the

ratio of beta hydroxybutyrate, which is

the main ketone body.

And then you would say,

oh, how do we know this?

Because I have friends, Dom DiAgostino,

Anthony Chapp in these guys, they're

always in these states

of nutritional ketosis.

What do they do?

They do a lot of exercise

and they eat a lot of meat.

And they stay in these

paleolithic kinds of zones.

And these are the zones that keep your

mitochondria super healthy.

So what we do is we take people from the

population and look at guys that have

type 2 diabetes,

obesity, and all these things.

And you find these GKI values over 50,

100, sometimes above 100.

Are you kidding me?

I mean, it should be down in

the 5 to 10 zone or 20 zone.

And you've got 200?

Oh, I'm obese.

I got systemic inflammation.

I got to, of course, you're not in

metabolic homeostasis.

So the glucose ketone index tells us I

built it for the cancer patients, because

we knew that if we lowered blood sugar

down far enough, the tumor cells need the

sugar to grow, and they

can't switch to ketones.

So you put them in a

very compromised condition.

Now, what we do is we see cancer

shrinking down tremendously when you get

the GKI 2.0 or below,

but you still have the glutamine issue.

So then we develop the pulse therapy to

come in and target with low dose of

glutamine inhibitors while the person is

in a state of nutritional ketosis.

And glutamine being the fermentable amino

acid that is then utilized as an

alternative fuel source by various

cancers in the absence

of glucose is accurate.

Yeah.

And people always ask me, what can you do

to lower, what diet can

I use to lower glutamine?

And if I eat meat,

won't that raise glutamine?

The glutamine in our body is already

super saturated because we use it for so

many things, the gut

and our immune system.

We already have more than enough

glutamine circulating in the body to

provide a tumor cell with more than

enough fuel in that regard.

So there's no diet that will lower

glucose, correction glutamine.

And the glutamine will always be there.

So you can't, even if you do exercise,

yes, you can lower glutamine, but it's

not to the level where you're going to

kill the tumor cell.

So that's why we need drugs.

But the drugs have to be strategic.

While you're in nutritional ketosis,

blood sugar is down,

ketones are elevated.

So you got a choke hold

on the glucose pathway.

But you got the

glutamine pathway still opened.

And then we come in with specific drugs

that will block glutamine's availability.

But we have to do this very strategically

because the same fuel is

needed by our immune cells.

Our immune cells and our gut use the same

fuel the tumor cells are using.

So that's why we

developed the press pulse.

So we pulse glutamine.

We do pulsing of glutamine targeting,

killing tumor cells over a short period

of time, removing the pulse, and allowing

the immune system to come in and kill, to

pick up the dead corpses.

So you have to have the undertakers

coming in and get rid of the dead bodies

in the microenvironment.

And that's your immune system.

And they need glutamine as well.

So this is why you need to understand

evolutionary biology and biochemistry to

effectively manage cancer.

If you don't understand biology and

biochemistry and evolutionary biology,

you are still in the stone age when it

comes to this kind of stuff.

You're just peddling drugs and hoping for

the best case scenario.

Yes.

You don't know why things

are working or how they work.

We know exactly how things

are working and why they work.

And we try to perfect the system to keep

these tumor cells under

restricted fuel conditions.

And the body itself, when increased in

its health, will turn on the tumor cell,

on the tumor cells,

and use them for fuel.

It's called autolytic cannibalism.

So the body itself, when put under energy

restriction, every cell in the body must

earn its existence in that body.

There can be no weak, lame, inefficient

cells because the body will turn on them

and use them for fuel.

The tumor itself becomes a fuel source

for the rest of the body when you're put

into these states of nutritional ketosis.

So part of the solution to the problem is

when the normal cells recognize a

population of cells that are inefficient

in utilization of energy.

And they turn on them and dissolve them

and use them for fuel.

And people say, "I don't know what

happened to my tumor.

It just kind of disappeared when I was in

nutritional ketosis."

Well, you're damn body-ated.

Because it was inefficient.

They were using energy inefficiently.

And the body recognizes that.

And this is the term

autolytic cannibalism.

I published that.

But we also can strategically target

glutamine to work together.

It's a whole systems approach to

eliminating a bunch of cells that are

growing out of control, using energy very

inefficiently, being dependent

predominantly on glucose and glutamine,

and not being able to

burn fatty acids or ketones.

It's an elegant system.

It's so beautiful.

It works for the majority of people.

And nobody's doing this.

There's no clinical

trial anywhere on the planet.

Don't make much money out of it, can you?

Well, the money issue

now becomes another issue.

It's revenue first,

patient outcome second.

And I think people need to know that.

They should know that their disease is

supporting a giant industry.

Many people are grateful

for those who have cancer.

Because the cancer patient supports a

very lucrative process that would be

potentially disturbed if we were to find

a method or a way to prevent

or manage cancer effectively.

But man has made adjustments and

adaptations to disruptive technologies.

And they will do the same with this

cancer and chronic disease situation.

It's just a matter of time.

Because we cannot continue on this path

of this abysmal path that we've been on

for the last 75, 100 years.

So we will begin to change.

But there will be new industries and new

strategies for exploring

and keeping people healthy.

And others, so we're trying to get a

revenue transition of revenue generation

from one failed system to a system that

really works but has not yet been mature

to replace the revenue

lost from one system.

But I think that's all

part of the future as well.

But right now, my job is just to keep

people alive with a higher quality of

life, using the knowledge of the biology

and biochemistry of the

disease that we understand.

Yeah.

Now that's fascinating.

And I definitely would love to come back

to that in a minute.

I'd just like to quickly chat about the

ketogenic diet a bit more.

And I'm going to ask my question first

and then Ramblom from a group of mine.

I have a few concerns about sort of long

term utilization of the ketogenic diet,

not for everybody, but just I have found

that there are various people who do

follow a ketogenic diet, obviously are

going to run into certain problems, some

of them endocrine in nature, etc.

Now, I think of course, most people who

are going to explore this meta,

who are going to explore cancer treatment

from a metabolic standpoint, are going to

utilize a ketogenic diet as their first

step and why should they not?

Now, as I mentioned, I've

got a few sort of concerns.

For example, I believe there's rodent

data out there to show that ketogenic

diets long term may impair, I think it's

hepatic FGF21 signaling due to receptor

downregulation and that there are other

drivers issues there as well.

For example, peripheral insulin

resistance, which I'm sure you're

familiar with for the audience listening,

that being the idea that in some people

long term ketogenic diet,

adherence can essentially cause an

insulin resistant like state at the level

of the muscle because the body is sort of

not able or not readily utilizing the

glucose at its disposal effectively.

Now, I'm just some second here, but I

would be at least mechanistically

concerned that those high levels of

glucose might then also be a contributing

factor if you're sort of becoming more

and more insulin resistant.

So, the way I see it, just from the GKI

score side of things, and again, this is

just me piecing a few things together, so

tell me where I'm wrong, but are there

other ways that you can sort of look at

increasing your GKI score

maybe without necessarily

utilizing long term ketosis?

And I suppose that's

a question in itself.

Should we always be in a state of ketosis

or should we sort of keep it for a period

of time, such as when, hopefully not, you

have a disease like

this where it's needed?

But beyond that, what about strategies

where you are either intermittently

fasting and obviously including a certain

amount of carbohydrates

in that eating window?

Would that fasting period, obviously

again, the lower glycemic things, not

talking about swallowing large quantities

of honey and processed sugar,

and then, yeah, other fuel sources maybe

that can sort of increase ketone

production, your ketone

esters, your NCT oils,

yeah, again, I hope that makes sense.

I am rambling a bit and as you've no

doubt already figured out, I'm definitely

outside more with your house here.

But are there, do you have any concerns

again for the average person following a

ketogenic for a longer period of time,

perhaps in light of those

mechanisms that I mentioned?

And then beyond that, are those other

strategies aimed at sort of improving a

GKI index maybe without being in a

constant state of ketosis, are they worth

exploring or is it just not enough to

actually deal with the matter at hand?

Yeah, well, you got a lot of stuff that

you just threw at me right there.

Yeah, sorry about that.

But we can break it down.

But you're 100% correct.

There's a lot of people who use ketogenic

diets inappropriately that are not

balanced with micro and macro nutrients,

which then can lead to some of the

conditions that you mentioned in your

rambling.

Yeah, in your ramblings.

But I have seen the same thing.

I mean, when we fed

ketogenic diets to the mice,

or humans, in an unrestricted way, diets

that were not completely balanced in

micro and macro nutrients,

we got all of many of the health issues

that you mentioned were seen.

The tumors actually grew faster.

There was a complete

metabolic in homeostasis.

You found conditions that would be

reflective of some of

what you have mentioned.

That's why we try to get

away from the term diet.

And we talk about nutritional ketosis as

a state of metabolic homeostasis, where

your levels of ketones are not

exorbitantly high, and your levels of

glucose are not exorbitantly low.

But you are balanced in micro and macro

nutrients with a GKI of five or 10.

And exactly as you said, in our new paper

that we're working on right now, which

will revolutionize the treatment of

cancer and all these chronic diseases,

we have built a color-coded chart to

allow people to know what zones they're

in at any given time, and whether or not

they can move effectively

from one zone to the next.

Like, yes, intermittent fasting.

Or the enjoyment, if you have been in a

state of nutritional ketosis and you go

out and party, and your body then shows a

much higher GKI,

which would be unhealthy,

you would then know what you would need

to do to bring it back into a normal

range with the types of foods and

exercise is extremely important.

You can move these zones up and down.

So you don't have to feel compelled to be

locked into a particular state.

But having the knowledge of what are the

healthy states and what aren't the

healthy states, knowing, like for

example, the Greek patients that did

really well on the keto diet, it was a

calorie-restricted Mediterranean diet.

Sardines, salmon, avocados, olive oil,

and this kind of thing that most people

can do without too much difficulty.

They had good GKI.

They were very balanced in

micro and macro nutrients.

But you could switch

from that to a carnivore.

There's a lot of flexibility in what a

person can do to move in and out of these

health zones without

causing metabolic in-homeostasis.

So we're working on that.

We've published a big paper for the brain

cancer patients to tell them exactly and

address the questions that you raised.

What are the choices?

What are the variations that you can use

to maintain constant pressure on tumor

cells while constantly keeping the

homeostasis of your normal cells at the

highest level and metabolic homeostasis?

So we're working on that.

And to address your questions, most of

the health problems associated with

long-term ketogenic diets result from

micro and macro nutrient imbalances that

lead to pathologies, some of which you

have already elucidated.

So once the base of knowledge becomes

available for people,

they can then build diets.

And we call it nutritional ketosis,

because you can achieve that with a

carnivore diet, a

Mediterranean diet, a pescatarian diet.

Vegan diets are a little harder.

A veganism, you have to supplement with

micronutrients and some macronutrients in

order to maintain metabolic home.

It's not a natural situation.

Humans did not evolve as vegans.

If we were vegans, we would have been

extinct a long time ago.

But we are omnivores.

Our bodies were evolved to eat anything,

walks, crawls, flies,

or swims on this planet.

And you can build nutritional ketosis

from combinations of the natural foods

that we evolved to eat.

You just have to adjust the amounts that

you're eating and the

types that you're eating.

So in our new study that will come out

for managing cancer and chronic diseases,

deals exactly with what you have

mentioned, to allow people to always

remain in a state of maximal metabolic

homeostasis, but allowing the individual

to know what zone of health they're in to

allow mitochondria to be as healthy as

possible, and not too restrictive in

rigidity in what you're doing.

Because part of enjoyment of life is the enjoyment of what we

like to eat and drink.

And we don't like to be pigeonholed into

a particular way of doing something that

eventually turns someone

from being happy into miserable.

But now with our new system that will

come out on the apps, you will know at

any given time what you can eat, for how

long, and how healthy it can be.

So everybody will, and

everybody's unique individual.

We also have to recognize that we have

sex differences, we have age differences,

we have cultural differences, and we have

religious differences.

So people are in these cultural,

religion, different ages and things.

They have to build their diet and

lifestyle around a GKI that meets their

needs and keeps them

in a comfortable zone.

And they'll know the quantification of

that by looking at their glucose ketone

index and matching it to a

particular zone of health.

So we will eliminate adverse effects,

allowing people to be flexible so they

can prevent these kinds of situations.

And I think what we're running into now

is people say, "Oh, I'm doing a keto, I'm

eating lard every day, and I'm getting

unhealthy and I'm getting unhealthy."

Yeah, who wouldn't get unhealthy?

The question is, we want to eliminate

those kinds of ambiguities in what people

can and cannot eat and give them the

level of flexibility that will make it

comfortable for their existence while at

the same time

maintaining mitochondrial health.

And I think knowledge is power and every

individual will adjust their own GKI and

build their own diets and know how much

exercise they need to do and to keep

their body in a state of

nutritional and physical health.

So this is the future.

But we're aware of everything you said.

And when you start something off in the

beginning, people sometimes overdo it,

they do it the wrong way.

And then they end up with these

pathologies that become apparent for,

like you mentioned, with all these...

Our registry, sex, home industries.

Yeah, I mean, that

should not have to happen.

Paleolithic man never had

to deal with these things.

His main problem was starvation.

When you don't have any

food, you starve to death.

Well, you can only get ketones if you

have hormonal insulin levels.

Your ketones can never get ketoacidotic.

That's type 1 diabetes predominantly

where you have very high glucose and very

high ketones together in your body.

That's pathological.

Natural therapeutic ketosis is low

glucose elevated ketones, but not

elevated to the level of ketoacid because

you piss out excess ketones.

But when you don't have insulin, you keep

all that in your body.

Your body seems like a starving.

You can't get rid of the...

You're making ketones and too high of a

level, keeping too much in your body.

So again, and we also know that there are

some people that have carnitine

deficiencies that

can't metabolize ketones.

There are people that get severe rashes

from trying to get into these conditions.

And there's certain people take

medications that interfere with the

ability to metabolize ketone bodies.

So we have to be aware of the

interference of nutritional ketosis.

But at least when you're aware, you can

alert people to these hazards, metabolic

hazards, and they can

make adjustments themselves.

So all of this, we have

thought about all of this.

Why?

Because we don't do anything else in our

life except think about

these kinds of things.

We're laser focused.

We don't think about anything else except

what you just talked about.

Not just occasionally, 24 seven.

That's what we do.

Dr.

Seifried, thank you so much for that.

That was incredible.

To be honest, I think I've got through

what, 20% of the questions that I'd hoped

to be able to talk to you about today.

So I'm going to have to twist your arm

somehow, God willing, and to get me back

from at some point in the future.

What was your main

question that I did not answer?

Oh, no.

I wanted to go down the rabbit hole

regarding various fatty acids and

specifically talk about saturated fats

versus unsaturated fats and the issues