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.
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
regarding some people running into
insulin resistance, having sort of high
amounts of saturated
fats in the ceramides.
I don't know if you've
seen that to be an issue.
We published a big paper looking at all
that stuff in mice,
unrestricted and unrestricted.
It's hard to get into ketosis on
polyunsaturated fatty acids,
but they're, the omega three fatty acids
are very healthy for people.
Some of the omega sixes are not.
So we published a big paper on all this.
So almost everything I have looked at in
one way or the other, I just don't have
time to talk about it at all, but our
open access papers on restricted and
unrestricted diets, high carb keto and
fish oil diets and
all this kind of stuff.
So we have looked at that and the body is
a machine that
metabolizes the fuels effectively.
Ketones will be
produced from saturated fat.
MCT oil, little MCT oil, is really great
in producing ketone bodies endogenously.
D beta hydroxybutyrate rather than L's.
There's a way to do all that.
We've looked at almost
every damn thing we can look at.
So I have papers on that, but yes, we
have looked at that.
We try to do everything, always remember,
everything is metabolized majority in the
mitochondria, the cytoplasm.
So once you understand these metabolic
pathways, you know how to keep your
mitochondria as healthy as possible,
which will make you, because ultimately
you're interested in
avoiding chronic disease.
That's it.
You don't want chronic disease.
You don't want cancer.
You don't want chronic disease.
How do you prevent that?
Keep your mitochondria healthy.
How do you keep your
mitochondria healthy?
Keep glucose down and
elevate ketones, the mitochondria.
And I don't have time to talk, but in our
new paper, we talk about the
bioenergetics of burning fatty acids,
ketone bodies, and pyruvate.
The bioenergetic related to the delta G
prime ATP hydrolysis.
And how we can get
more bang for your buck.
Every breath of air can give you more ATP
when you're burning ketone body than when
you're burning pyruvate or fatty acids.
So we know the bioenergetics.
We published that.
And our big paper is going
to be coming out on that.
And we got all that from the late Richard
Veach, one of the great, and he was Hans
Krebs' last graduate student.
So he and I would talk for hours and
hours and hours about all the
bioenergetics of mitochondria and what
you need to keep it
healthy and functional.
So there's a strong bioenergetic
explanation for a lot of what I'm saying.
And that's in our papers.
We'll definitely be sure to
link them in all the show.
Yeah.
Make sure, yeah.
Tell folks that all of
our papers are open access.
So anybody with a
computer can get the information.
Now people are going to be overwhelmed
and say, oh my God,
Seifree published so many papers.
Yeah.
Well, a lot of it's on
what I'm talking about.
A lot of it's on other things.
But you can go through and
ferret out what we're doing.
And people need to know that all of our
research is supported by philanthropy and
private foundations.
So when we keep people
alive who are stage four cancer,
they so-called terminal.
And all of a sudden you're living a lot
longer with a higher quality of life.
Some people feel very compelled to donate
to our research because they
want to.
And one thing I want to make sure, never
say we have a cure for cancer.
Because I have no clue whether what we do
will cure cancer or not.
The only thing that we have seen over and
over again is we have a longer
progression-free survival without
symptoms and a very increased overall
survival of cancer patients.
Whether they're cured
or not, we don't know.
But I consider success in keeping people
given terminal diagnosis alive far, far
longer than what the establishment
predicted their lifespan to be.
So I never like to use the term terminal
because I have a lot of people that I
know who are still alive.
I don't know.
Sometime in the future they may be
terminal, but they're not dead yet and
they're pretty healthy.
So what the hell does that mean?
And they were told they only had nine
months to live and
they're around six years.
Who made the mistake there?
Why was someone told they have six months
or a year to live and they're living five
and six years or even longer?
How did anybody make
that level of mistake?
They made the mistake because they don't
understand metabolic therapy and how long
you can possibly live with
a higher quality of life.
But whether you get a
cure or not, I have no clue.
All we know is we have a new strategy for
managing cancer and chronic disease that
is far more powerful and successful than
anything out there right now.
The problem is people just don't know
about it and don't know
how to implement it yet.
And that's going to take
that will be the future.
That will be down to people like us,
aiming to educate the greater public.
Dr.
Seifried, thank you
so much for your time.
For people who are interested in your
work and to learn more about your various
metabolic therapies,
where can we point them to?
Well again, I have my metabolic papers
already published, open access.
And donations go to Travis
Christofferson's Foundation
for Cancer Metabolic Therapy.
It's a legitimate foundation.
And the university, Boston College
itself, the biology department for sure.
So that keeps us going and we've got a
couple of blockbuster things coming out
that are really going to transform the
healthcare industry dramatically.
And they'll be out within the year.
And then you're going to see
organizations set up around these
approaches for metabolic health.
And we're going to bring a lot of people
back into what we call normalcy,
metabolic homeostasis, if they want to.
I'm not twisting anybody's arm here.
It's only if people who want to, if they
want to live in a toxic
state, that's their choice.
But we have a tool now to allow them to
come out of those toxic states and live a
healthy, productive life with a clear
quantitative assessment to do that.
And that is coming down and you'll see
that within the next
year or two, for sure.
So we're very hopeful for
managing chronic diseases.
And I think most people are going to be
very appreciative as they begin to
benefit from what we're doing.
No, I'm sure they're well.
I mean, ultimately, I think most disease,
the way I'm starting to view it, it
ultimately comes down to sort of removing
the environmental burden or whatever
environmental trigger there is as driving
the disease, improving the metabolic
health and subsequent treatment,
mitochondrial health, and then dealing
with the stress component, which is also
obviously overlooked.
And I think when you get those three sort
of components sort of dialed in, you sort
of solve 90% of the equation, at least
when it comes to chronic disease.
Which is mostly
crippling Western societies.
Yes.
So it's the single most biggest problem.
Cancer and chronic diseases are dementia,
type 2 diabetes, obesity,
cardiovascular disease, cancer.
You can go right down the list.
It's just like everything.
So what do we do with all these healthy
people if they will...
We're keeping a lot of people alive,
working for a longer period of time with
a high quality of life.
I mean, you're going to have to have a
readjustment of society.
Yeah.
Well, let's aim to get there and then we
can do what that problem arises.
Yes, absolutely.
All right.
Well, listen, thank you very much.
Thank you, Dr.
Seifried.
It's been an absolute honor and I
appreciate your time.
Yeah.
Well, thank you. I'll