Shownotes
Thomas N. Seyfried is Professor of Biology at Boston College and received his Ph.D. in
Genetics and Biochemistry from the University of Illinois in 1976. He did his
undergraduate work at the University of New England where he received a
distinguished Alumni Achievement Award. He also holds a master’s degree in Genetics
from Illinois State University, Normal, IL. Thomas Seyfried served with distinction in the
United States Army’s First Cavalry Division during the Vietnam War and received
numerous medals and commendations. He was a Postdoctoral Fellow in the
Department of Neurology at the Yale University School of Medicine and then served on
the faculty as an Assistant Professor in Neurology. Other awards and honors have
come from such diverse organizations as the American Oil Chemists Society, the
National Institutes of Health, The American Society for Neurochemistry, and the
Ketogenic Diet Special Interest Group of the American Epilepsy Society. Professor
Seyfried previously served as Chair of the Scientific Advisory Committee for the
National Tay-Sachs and Allied Diseases Association. He has received the Lifetime
Achievement Awards from the Academy of Complimentary and Integrative Medicine,
the International Dose Response Society, and the Uncompromising Science Award
from the American College of Nutrition for his work on cancer. He is a member of the
Sigma Xi honor society and presently serves on several editorial boards, including those
for Nutrition & Metabolism, Neurochemical Research, the Journal of Lipid Research,
and ASN Neuro, where he is a Senior Editor. Professor Seyfried is also author of the
book, Cancer as a Metabolic Disease: On the Origin, Management, and Prevention of
Cancer (Wiley Press), which has been translated into Chinese and Korean. He has
described his research on many podcasts and radio shows and his work is central to the
documentary film, The Cancer Revolution. Professor Seyfried has over 200 peer-
reviewed publications and a current h-Index of 77.
> During our discussion, you’ll discover:
(00:02:08) What is cancer
(00:11:53) The different theories of cancer
(00:25:23) Are mitochondrial transplants a decent therapy for cancer
(00:38:49) Early detection cancer testing
(00:43:27) Is the rise in cancers an environmental issue
(00:52:22) What is the glucose ketone index
(01:03:03) Are there issues with doing the ketogenic diet long term
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- Dr Seyfried Publications
- Home - Thomas Seyfried
- Cancer as a Metabolic Disease: On the Origin, Management, and Prevention of Cancer | Amazon.co.uk
- Dr Seyfried Pubmed
- Thomas N. Seyfried - Biology Department - Morrissey College of Arts and Sciences - Boston College
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Transcripts
Good morning, Dr.
Speaker:Seyfried.
Speaker:It's a true pleasure to
Speaker:have you on the podcast today.
Speaker:Obviously, we'll be discussing all things
Speaker:cancer in short order.
Speaker:But before we get into it, would you mind
Speaker:introducing yourself to the audience for
Speaker:those who aren't familiar
Speaker:with you and your body of work?
Speaker:Yeah, well, well, thank you, Rob.
Speaker:It's nice to be here.
Speaker:I'm a professor of
Speaker:biology at Boston College.
Speaker:I have been here for,
Speaker:well, since 1985, 40 years now.
Speaker:And before that, I was at Yale University
Speaker:in New Haven, Connecticut.
Speaker:Here at Boston College, I've taught a
Speaker:broad range of classes over the years,
Speaker:neurobiology,
Speaker:neurochemistry, neurogenetics.
Speaker:Now I teach general biology to the
Speaker:non-majors, as well as an advanced class
Speaker:in cancer metabolism.
Speaker:Cancer is a metabolic disease.
Speaker:So our background for
Speaker:biochemistry was lipid biochemistry.
Speaker:I did a lot of work
Speaker:on lipid biochemistry.
Speaker:And as far as diseases are concerned,
Speaker:lipid storage diseases, as well as
Speaker:genetic diseases, epilepsy in particular.
Speaker:And now our main focus over the last
Speaker:quarter of a century has been
Speaker:predominantly cancer.
Speaker:But we are moving into also
Speaker:other chronic diseases as well.
Speaker:So I have a kind of a
Speaker:broad-based experience.
Speaker:I have a degree in genetics and
Speaker:biochemistry, a
Speaker:master's degree in genetics.
Speaker:So those are the background educational
Speaker:experience that I've had.
Speaker:That's incredible.
Speaker:And a reason, I
Speaker:suppose, I could only dream of.
Speaker:I think one of the big issues in the
Speaker:health podcast space is creating content
Speaker:that is sort of based on actual science
Speaker:and to have someone with your background
Speaker:and credibility, I feel just, well, at
Speaker:least hopefully sort of highlight that
Speaker:we're not here just to obviously discuss
Speaker:pseudoscience today, that this is all
Speaker:sort of based in empirical data.
Speaker:Dr.
Speaker:Seafree, I know we're here to really talk
Speaker:about the metabolic theory of cancer, but
Speaker:I think it would be prudent to maybe
Speaker:start off with having a quick
Speaker:conversation about
Speaker:what cancer actually is.
Speaker:And I know it's likely a dull question,
Speaker:but I do feel it's that very few people
Speaker:actually know what the disease is.
Speaker:It's just something that
Speaker:they aim to just not get.
Speaker:I've got a few questions there, but yeah,
Speaker:maybe we could just start off with that.
Speaker:Cancer Biology 101, as it were, if you
Speaker:would just mind running
Speaker:through what cancer is.
Speaker:Well, it's actually a very, it's a
Speaker:complicated problem, but it's a very
Speaker:simple definition of what cancer is.
Speaker:It's cell division out of control,
Speaker:dysregulated cell growth.
Speaker:So people say, well, what's cancer?
Speaker:It's just a bunch of cells that are no
Speaker:longer regulated in their growth.
Speaker:Of course, the origin of
Speaker:that phenomenon is broad.
Speaker:But what is it that makes a population of
Speaker:cells in a particular organ of someone's
Speaker:body to start growing in a dysregulated
Speaker:way as opposed to normal cell division,
Speaker:which is regulated?
Speaker:In parts of our body,
Speaker:there's wear and tear.
Speaker:Cells naturally die and are replaced.
Speaker:But the replacement of dead cells is a
Speaker:very organized process.
Speaker:They grow, they divide, and they, however
Speaker:many divisions is necessary to replace
Speaker:those that are missing, is a
Speaker:well-regulated process.
Speaker:And we know now that's all
Speaker:controlled by the mitochondria.
Speaker:But an example of cell
Speaker:division under control,
Speaker:one of the, is in the gut, you have the
Speaker:crypt cells that seem to always replace
Speaker:other cells in a very regulated way.
Speaker:And in the liver, you
Speaker:have liver regeneration.
Speaker:Liver is an interesting organ because if
Speaker:you remove a lobe of the liver, the liver
Speaker:will regenerate the
Speaker:missing part of the lobe.
Speaker:And the speed of liver regenerating cells
Speaker:is just as fast as that
Speaker:of the fastest cancer.
Speaker:The only difference is that the liver
Speaker:regeneration is regulated growth, whereas
Speaker:the hepatoma of the liver, which is liver
Speaker:cancer, is dysregulated growth.
Speaker:And the biochemistry of those two
Speaker:populations is strikingly different.
Speaker:So when you ask what is cancer, it's
Speaker:dysregulated growth in a population of
Speaker:cells in someone's organ, which differs
Speaker:from regulated growth
Speaker:of cells in that organ.
Speaker:So sort of after control mitosis, you
Speaker:might say, in a nutshell.
Speaker:Yeah.
Speaker:And the question that has perplexed the
Speaker:field for decades is what regulates, what
Speaker:is responsible for
Speaker:regulated growth in the first place?
Speaker:Why would one cell know when to stop
Speaker:growing and another cell
Speaker:not know when to stop growing?
Speaker:And that all comes back to the role of
Speaker:the mitochondria and the cytoplasm.
Speaker:The mitochondrion controls calcium
Speaker:signaling within the cell.
Speaker:Nobel prizes have been awarded for people
Speaker:to learn the cyclins and
Speaker:going through the cell cycle.
Speaker:And that cell cycle is all controlled by
Speaker:calcium signaling from the mitochondria.
Speaker:So when mitochondria of the cell become
Speaker:dysfunctional in the sense of producing
Speaker:energy and that calcium gradients, they
Speaker:fall back on a fermentation metabolism,
Speaker:which is an ancient form
Speaker:of energy without oxygen.
Speaker:And the mitochondrion loses control of
Speaker:the differentiated state.
Speaker:That being anaerobic respiration.
Speaker:Yeah, anaerobic.
Speaker:You can grow cancer cells in the absence
Speaker:of oxygen or in the presence
Speaker:of cyanide and they survive.
Speaker:So which would
Speaker:normally kill normal cells.
Speaker:And that's because their energy
Speaker:metabolism is of an ancient type.
Speaker:It's the type of energy that existed on
Speaker:the planet before oxygen came into the
Speaker:atmosphere two and a
Speaker:half billion years ago.
Speaker:It was a fermentation metabolism,
Speaker:generating energy without oxygen.
Speaker:And the default state of
Speaker:cells is proliferation.
Speaker:The default energy state
Speaker:of cells is fermentation.
Speaker:So when what cancer cells are doing is
Speaker:they're simply falling back on their
Speaker:default proliferative state and their
Speaker:default energy state behaving, behaving
Speaker:much as they were of all cells that
Speaker:existed before oxygen, which was
Speaker:unbridled proliferation.
Speaker:And they would die as soon as the fuels
Speaker:that drove the flow drove the
Speaker:fermentation metabolism would dissipate
Speaker:in the micro environment
Speaker:and the cells would die.
Speaker:So it was purely an energy
Speaker:driven process without regulation.
Speaker:During the origin of life on the planet,
Speaker:archaeobacteria fused with other other
Speaker:cells to develop the mitochondria.
Speaker:And it was the mitochondria that allowed
Speaker:the division of energetic labor in the
Speaker:cells, allowing metazones to form and the
Speaker:most complex multicellular organisms that
Speaker:we have today all all due to the energy
Speaker:capacity of the mitochondria.
Speaker:And the nucleus, which everybody seems to
Speaker:have focused on, is because you could see
Speaker:it sometimes even with the naked eye,
Speaker:whereas the mitochondria for centuries
Speaker:could not be seen clearly until you had
Speaker:the electron microscope and more
Speaker:sophisticated ways of
Speaker:looking at this organelle.
Speaker:But in a nutshell, it's the mitochondria
Speaker:that controls the
Speaker:regulation of genes in the nucleus.
Speaker:So all the epigenetic stuff you hear
Speaker:about is mostly mitochondrial controlled
Speaker:mitochondria controlled.
Speaker:So the nucleus is kind of an obedient
Speaker:slave of whatever the mitochondria does
Speaker:because of that
Speaker:organelle becomes corrupted.
Speaker:The cell falls back as a and one of these
Speaker:dysregulated growths.
Speaker:So everything comes back to the origin of
Speaker:cancer as a corruption of mitochondrial
Speaker:function only in cells that can switch to
Speaker:the ancient fermentation pathways, which
Speaker:can explain why certain cells
Speaker:in our body never become tumor.
Speaker:Red blood cells can't become a tumor
Speaker:because they have no mitochondria or
Speaker:nucleus in the first place.
Speaker:Neurons of our brain
Speaker:cannot sustain fermentation.
Speaker:So you rarely, if ever,
Speaker:get cancers from neurons.
Speaker:They get from real cells.
Speaker:What about cardiac tissue?
Speaker:Cardiac tissue rarely, if ever, gets
Speaker:cancer because they cannot replace
Speaker:oxidative phosphorylation with substrate
Speaker:level phosphorylation.
Speaker:So you rarely, if ever, get cancer of
Speaker:muscle, a striate or cardiac tissue
Speaker:because they die and you can't get a
Speaker:cancer cell from a dead cell.
Speaker:So we're able to go through the body and
Speaker:look at the kinds of tissues that form
Speaker:cancer because they have the capacity to
Speaker:transition from oxidative phosphorylation
Speaker:to substrate level phosphorylation, which
Speaker:is a protracted event that
Speaker:doesn't happen overnight.
Speaker:You really have to abuse the hell out of
Speaker:your mitochondria in a
Speaker:chronic way to get cancer.
Speaker:Cancer is very hard to get.
Speaker:I know it's exploding as an epidemic, but
Speaker:we abuse the crap out of our bodies and
Speaker:that's why we're getting so much cancer.
Speaker:But it's really hard to get cancer.
Speaker:So when you say, well, how come so many
Speaker:people because they because their bodies
Speaker:have been chronically abused by a variety
Speaker:of insults, many of which
Speaker:they're not even aware of.
Speaker:But that's that's how you get cancer.
Speaker:It's a chronic disruption of oxidative
Speaker:phosphorylation coupled to a compensatory
Speaker:substrate level phosphorylation.
Speaker:And Warburg knew this a long time ago
Speaker:from the 1920s, but he only knew that it
Speaker:was a glucose driven transition from.
Speaker:But we now discovered and have I had the
Speaker:concept but not the evidence.
Speaker:But now we published the big paper
Speaker:recently that the cancer cell can ferment
Speaker:an amino acid called glutamine.
Speaker:So you get sugar and amino acid
Speaker:fermentation are driving the dysregulated
Speaker:growth of the tumor cell.
Speaker:And the field all thought it was
Speaker:glutamine respiration oxidative but it's
Speaker:not its glutamine fermentation within the
Speaker:mitochondria itself.
Speaker:So the very organelle that's supposed to
Speaker:get energy through oxidative
Speaker:phosphorylation is also producing energy
Speaker:through substrate level phosphorylation,
Speaker:which is a fermentation mechanism.
Speaker:This is what's blowing
Speaker:the doors off the field.
Speaker:You know, they never realized that the
Speaker:very organelle could also ferment.
Speaker:And that goes back to its organ its its
Speaker:origin as a bacteria itself.
Speaker:So, you know, once once you understand
Speaker:evolutionary biology, all the pieces of
Speaker:cancer fall into place
Speaker:quite, quite reasonably.
Speaker:Now, it really does.
Speaker:And I just love the fact you do brought
Speaker:up the mitochondria as being more than
Speaker:just this sort of this
Speaker:energy factory or the body.
Speaker:It's just involved in so many genetic
Speaker:processes beyond just
Speaker:helping to create ATP.
Speaker:And yeah, thanks for that.
Speaker:It really does sort of provide some
Speaker:context to what is going for
Speaker:the rest of the conversation.
Speaker:I reckon the natural follow up then
Speaker:again, this is quite a
Speaker:loose question, I suppose.
Speaker:I suppose.
Speaker:And you've really answered this too,
Speaker:to an degree.
Speaker:But I'd sort of and beyond the sort of
Speaker:the metabolic side of it, I'd love to
Speaker:sort of get your your thoughts on the
Speaker:different theories that
Speaker:are sort of driving cancer.
Speaker:Obviously, it's a complex,
Speaker:this complex aetiology there.
Speaker:And it's it would be and it shouldn't be
Speaker:viewed from this sort of reductionist
Speaker:viewpoint that there is just one
Speaker:mechanism that causes cancer.
Speaker:I know in my brief experience in academia
Speaker:that people studying these conditions can
Speaker:often get wrapped up in their own
Speaker:mechanisms and
Speaker:occasionally be blinded by research.
Speaker:Obviously, you have a
Speaker:fairly well-rounded view.
Speaker:So would you mind talking us through the
Speaker:various sort of and I hope sort of
Speaker:phrases correctly proposed triggers,
Speaker:maybe or underlying mechanisms that sort
Speaker:of lead to the development of this
Speaker:condition, sort of the genetic causes,
Speaker:the environmental risk factors, the
Speaker:immunological side of things?
Speaker:I don't know if I phrased that correctly,
Speaker:or if that makes sense.
Speaker:Yeah, well, it does.
Speaker:I mean, when you look at the history of
Speaker:of the disorder that has intrigued
Speaker:scientists, you know, for centuries,
Speaker:you know, we knew about cancer a long
Speaker:time ago, VirCal, and the 1800s people
Speaker:were studying these things.
Speaker:You know, and how does it start?
Speaker:You know, you have the emergence of
Speaker:different ideas, concepts of
Speaker:what cancer, what cancer is.
Speaker:The current view taken by all major
Speaker:research centers and academic centers is
Speaker:that it's a genetic disease.
Speaker:I know the UK thinks that the United
Speaker:States government, National Cancer
Speaker:Institute, believe that.
Speaker:I think most of the cancer institutes
Speaker:around the world, the French, the
Speaker:Germans, the English, all Western major,
Speaker:and even in China and Japan and Korea,
Speaker:you know, South America,
Speaker:they're all of the view
Speaker:that cancer is a genetic.
Speaker:It seems to be some sort of a paralytic
Speaker:mindset throughout the world.
Speaker:It's an indoctrination of brainwashing,
Speaker:if you will, of what this
Speaker:disease is supposed to be.
Speaker:But it wasn't always that way.
Speaker:You know, there was the viral cancer was
Speaker:a virus caused by viruses.
Speaker:Cancer was a metabolic disease.
Speaker:You know, cancer is a genetic disease.
Speaker:So you have to put all the views over
Speaker:time into what it is.
Speaker:And, you know, Warburg started the idea
Speaker:that it was a
Speaker:mitochondrial metabolic disease.
Speaker:But he couldn't explain certain things
Speaker:which we now can't explain.
Speaker:He didn't know about the glutamine issue,
Speaker:nor did he realize that a lot of the
Speaker:oxygen that cancer cells consume is not
Speaker:used for ATP but produces reactive oxygen
Speaker:species, ROS, which are radicals.
Speaker:And they cause, in large part, the
Speaker:mutations in the nucleus.
Speaker:So, you know, certain viruses, okay,
Speaker:well, we knew certain like papilloma
Speaker:viruses and hepatitis
Speaker:viruses and the Rous sarcoma virus.
Speaker:Peyton Rous was a Nobel Prize receiver
Speaker:for his virus particle.
Speaker:We now put all that together.
Speaker:We know all these viruses damage
Speaker:oxidative phosphorylation, chronically
Speaker:causing this transition to
Speaker:substrate-level phosphorylation.
Speaker:But it was the Watson and Crick DNA
Speaker:structural analysis that kind of sent the
Speaker:whole field off into the abyss,
Speaker:chasing stuff that we are still chasing.
Speaker:Because it became exciting to bring a
Speaker:very complicated mishi-marshi disease
Speaker:back into a molecular configuration.
Speaker:And I think that was,
Speaker:I call it physics envy.
Speaker:Biology had always been a poor stepchild
Speaker:to the pure, rational thought of the
Speaker:human mind, which was physics.
Speaker:And when the DNA structure was defined,
Speaker:and you could explain the arrangement of
Speaker:amino acids and RNAs all linked back to
Speaker:the structure of the DNA, biology was
Speaker:brought from an observational
Speaker:observational kind of a disorder or a
Speaker:field into a more quantitative way.
Speaker:And then, of course, as soon as you
Speaker:started looking at cancer cells, you
Speaker:start to see chromosomal abnormalities.
Speaker:That goes back to Theodore Bovary, who
Speaker:knew nothing about cancer.
Speaker:And he said, "I think cancer might be
Speaker:something to do with chromosomes."
Speaker:Purely speculative.
Speaker:He even said, "I'm probably wrong about
Speaker:everything," and he was.
Speaker:But the field grabbed ahold of him as the
Speaker:father of the genetic theory of cancer.
Speaker:And then, of course, you started to see
Speaker:gene mutations
Speaker:associated with certain cancers.
Speaker:And then we spent billions of dollars on
Speaker:the cancer genome projects, looking at
Speaker:every kind of a mutation.
Speaker:And then therapies, precision in medicine
Speaker:and all this developed around the genomic
Speaker:view of cancer, where we're going to have
Speaker:precision medicines,
Speaker:targeted therapies, and all this kind of
Speaker:stuff, which is where we are today.
Speaker:And all the governments and academic
Speaker:institutions are giving away millions of
Speaker:dollars in grants to people trying to
Speaker:hunt down genes that could be responsible
Speaker:for the dysregulated cell growth.
Speaker:So it comes back.
Speaker:We know cancer is a
Speaker:dysregulated cell growth.
Speaker:What's causing that?
Speaker:Well, according to the somatic mutation
Speaker:theory, which is the dominant theory
Speaker:today, it's mutations
Speaker:that are causing that.
Speaker:But I've clearly shown that those
Speaker:mutations are largely irrelevant.
Speaker:With our research, they can't attack it
Speaker:because the evidence is too strong.
Speaker:So when you have evidence that's
Speaker:overwhelmingly strong and it's not
Speaker:consistent with your general
Speaker:theory, then you ignore it.
Speaker:But you're only going
Speaker:to ignore it for so long.
Speaker:So when you develop a theory,
Speaker:theories are supported by a massive
Speaker:amounts of evidence.
Speaker:The somatic mutation theory was very,
Speaker:very strong because you found almost all
Speaker:cancers with somatic mutations.
Speaker:And these somatic mutations, some of them
Speaker:were linked to the cell cycle, which you
Speaker:could then link a mutation in the genome
Speaker:to something that would lead to
Speaker:dysregulation or
Speaker:dysfunction of the cell cycle.
Speaker:And that made a lot of sense.
Speaker:So people grabbed onto that.
Speaker:And because it was so molecular and so
Speaker:quantitative and approachable by really
Speaker:sophisticated technologies which have
Speaker:developed around cancer, like all these
Speaker:sequencing, unbelievable AI now,
Speaker:artificial intelligence helping analysis
Speaker:of sequencing, and all of the different
Speaker:kinds and types of mutations that were
Speaker:found in cancer cells.
Speaker:I mean, it was an explosion of molecular
Speaker:biology associated with cancer.
Speaker:So that was very
Speaker:attractive to a lot of people.
Speaker:But then having done work in Meyerle lab
Speaker:and seeing research that was far more
Speaker:consistent with what Otto Wirberg said
Speaker:than with the somatic mutation theory, I
Speaker:began to look at this.
Speaker:But getting back to theories, I like to
Speaker:compare what's happening today with the
Speaker:mitochondrial metabolic theory replacing
Speaker:the somatic mutation theory because it really takes a lot of
Speaker:evidence to replace a theory.
Speaker:Einstein's theory of relativity could
Speaker:still be replaced, but has not yet been.
Speaker:And there are physicists that are
Speaker:constantly trying to show where Einstein
Speaker:was wrong, and they believe
Speaker:they might, but they haven't.
Speaker:Darwin's theory of evolution has been
Speaker:challenged many times, but it has not
Speaker:been overthrown because the data that
Speaker:support it are stronger than the data that don't support it.
Speaker:And then you have the geocentric
Speaker:heliocentric theory of the solar system,
Speaker:where for 1800 years, people thought that
Speaker:the Earth was the
Speaker:center of the solar system.
Speaker:And we developed equants, deference, and
Speaker:epicycles to try to predict
Speaker:the positions of the planets.
Speaker:And Copernicus just
Speaker:replaced the Earth with the sun.
Speaker:And all of a sudden, a lot of stuff was
Speaker:far less complicated and more understandable.
Speaker:So the heliocentric theory replaced the
Speaker:geocentric theory, opened up a scientific
Speaker:revolution during the Middle Ages,
Speaker:the Renaissance period.
Speaker:What we're having today is that
Speaker:mitochondrial metabolic theory is
Speaker:overturning the somatic mutation theory.
Speaker:And the consequences are going to be
Speaker:every bit as phenomenal as what happened
Speaker:during the Copernican revolution.
Speaker:So we look at
Speaker:evidence to support a theory.
Speaker:If cancer is a disease of somatic
Speaker:mutations, which is the current dogma,
Speaker:irrefutable truth, the silent assumption,
Speaker:cancer is a genetic disease.
Speaker:Well, now with deep sequencing and deeper
Speaker:analysis, we find some cancer cells that
Speaker:don't have any mutations, yet they're
Speaker:growing out of control.
Speaker:So when I looked at those, there's not many papers that I've looked at.
Speaker:So when I looked at those, there's not
Speaker:many papers, but there are
Speaker:some very clear findings.
Speaker:And then when I say, what do the
Speaker:investigators who believe that cancer is
Speaker:a genetic disease say about cancer cells
Speaker:that don't have mutations or
Speaker:they can't find any mutations?
Speaker:And they don't say anything.
Speaker:So when I went back and looked at their
Speaker:explanation, they
Speaker:didn't even, they ignored it.
Speaker:They didn't even talk about the cancer
Speaker:cells that had no mutations.
Speaker:They just seemed to focus on all the
Speaker:cancer cells that had mutations.
Speaker:And I said, you got a glaring
Speaker:inconsistency in your theory, staring you
Speaker:in the face and you did not address it.
Speaker:What the hell is going on with that?
Speaker:Then, of course, they realized that
Speaker:there's so many hundreds of thousands of
Speaker:mutations in some of these tumor cells.
Speaker:They all can't be drivers
Speaker:of dysregulated cell growth.
Speaker:So then the field decided to reclassify
Speaker:some of the mutations as
Speaker:passenger genes and driver genes.
Speaker:So we then moved into the driver gene
Speaker:mentality, which lasted several decades.
Speaker:Where only some of these many mutations
Speaker:are truly responsible for dysregulated
Speaker:cell growth and we
Speaker:redefined them as called drivers.
Speaker:And that got, that generated a lot of
Speaker:excitement since the 19, early 1980s, I
Speaker:guess, middle eighties, driver genes,
Speaker:driver, oh, the driver genes.
Speaker:So now with deep sequencing and more
Speaker:sophisticated technologies, we're finding
Speaker:all kinds of mutations in
Speaker:driver genes in our normal tissues.
Speaker:Like you and me.
Speaker:I mean, we got all kinds of mutations in
Speaker:P53 and MIC and RAS and all these kinds
Speaker:of genes that are in our normal tissues
Speaker:and are not dysregulated in growth.
Speaker:How do you explain that?
Speaker:That's inconsistent with
Speaker:your somatic mutation theory.
Speaker:Are there any real sort of polygenic risk
Speaker:goals maybe that sort of have been
Speaker:identified in respect to this?
Speaker:Well, the nuclear mitochondrial transfer
Speaker:experiments throw, that's the real nail
Speaker:in the coffin for the whole thing.
Speaker:Because what was done on a variety of
Speaker:different types of cancers is that the
Speaker:nucleus of the tumor cell is now placed
Speaker:in the cytoplasm of a
Speaker:non-neoplastic cell.
Speaker:And invariably you get regulated growth,
Speaker:despite the continued presence of
Speaker:whatever kind of genetic abnormality
Speaker:might have been in that nucleus.
Speaker:Whether it was polygenic, whether it was
Speaker:chromosomal, whether it was point
Speaker:mutations, frame shift mutation, didn't
Speaker:make any difference.
Speaker:When that cancer nucleus was placed into
Speaker:the cytoplasm of a non-cancerous cell,
Speaker:that new cell no longer
Speaker:had dysregulated cell growth.
Speaker:That's quite interesting.
Speaker:And that's been done repeatedly.
Speaker:And in vivo and in vitro.
Speaker:So in all kinds of experimental systems,
Speaker:meaning that normal cytoplasm
Speaker:suppresses neoplastic growth.
Speaker:On the other hand, if the nucleus of a
Speaker:normal cell is now placed in the
Speaker:cytoplasm of a tumor cell, you've got
Speaker:dysregulated growth,
Speaker:which is completely the opposite of what
Speaker:you would have expected on
Speaker:the somatic mutation theory.
Speaker:So when you have the opportunity to sit
Speaker:down and carefully evaluate all of the
Speaker:evidence from the nuclear mitochondrial
Speaker:transfer experiments, also, if you have a
Speaker:raging tumor cell and you replace the
Speaker:mitochondria with normal mitochondria,
Speaker:just put normal mitochondria, you get
Speaker:complete downregulation of this
Speaker:dysregulated growth.
Speaker:You can convert a raging tumor cell into
Speaker:an indolent tumor cell by putting normal
Speaker:mitochondria back in the cytoplasm,
Speaker:mitochondrial medicine type.
Speaker:I was about to say, I'm getting ahead of
Speaker:my curve and I'm going to shoot myself in
Speaker:the foot by asking this question now, but
Speaker:just with regards to that, then, is there
Speaker:any thought to the idea that
Speaker:mitochondrial transplants could be a
Speaker:potential therapy in that regard?
Speaker:Absolutely.
Speaker:But that's the future.
Speaker:It's not here yet, because we have to
Speaker:make sure that the mitochondria that are
Speaker:transplanted are normal in numbers,
Speaker:structure, and function.
Speaker:And during the very process of
Speaker:manipulating these
Speaker:mitochondria, you can also damage them.
Speaker:And you have to know how to do that.
Speaker:So mitochondrial medicine
Speaker:is going to be the future.
Speaker:But where the technology
Speaker:to do that is not here yet.
Speaker:So our approach to managing cancer is
Speaker:killing the tumor cells while not harming
Speaker:the rest of the body and then allowing
Speaker:people to live far longer with a higher
Speaker:quality of life, while mitochondrial
Speaker:medicine is under development.
Speaker:That's the thing.
Speaker:It's very interesting, because when you
Speaker:have dysregulated cell growth in cancer,
Speaker:they're fermenting like crazy.
Speaker:And the oncogenes, which have generated
Speaker:tremendous interest, we have shown, and
Speaker:others, HIF1, alpha, MIC, and these
Speaker:things, they are there.
Speaker:And they are facilitators of opening the
Speaker:floodgates for fermentation
Speaker:fuels to get into the cell.
Speaker:And when you put new mitochondria into
Speaker:the cell, the oncogenes turn off.
Speaker:You don't need them anymore.
Speaker:Why are you going to
Speaker:ferment when I can respire?
Speaker:So the oncogenes are no longer needed.
Speaker:And normal mitochondrial respiration turn
Speaker:off oncogene expression.
Speaker:So you shut down the glycolysis and the
Speaker:glutaminolysis pathways, because you
Speaker:don't need glucose and glutamine.
Speaker:You can respire.
Speaker:Everything makes perfect sense.
Speaker:And the data show that.
Speaker:So where did all the mutations come from?
Speaker:They came from the biology of inefficient
Speaker:oxidative phosphorylation, throwing out
Speaker:reactive oxygen species, which is the
Speaker:superoxide and the anion, the OH radical,
Speaker:which are carcinogenic and mutagenic.
Speaker:And they come out of the dysfunctional
Speaker:mitochondria, creating an escalating
Speaker:situation of biological chaos.
Speaker:So what we're seeing, or what the field
Speaker:is mostly focusing on, is downstream
Speaker:epiphenomena of the damage to
Speaker:mitochondria and all the
Speaker:sequelae that follow that.
Speaker:It's really amazing to me.
Speaker:I just can't figure out how the field
Speaker:doesn't understand this.
Speaker:I try to, I don't know, maybe
Speaker:I have to write it in crayon.
Speaker:Sometimes you just have to do that.
Speaker:You have to take the back of a neck and
Speaker:smash the guy's face into
Speaker:the evidence to let him see it.
Speaker:But the interesting thing is that you see
Speaker:all these clear evidence that you can
Speaker:manage this disease quite effectively by
Speaker:just depriving the cell of the two
Speaker:fermentable fuels that it needs and then
Speaker:transitioning the whole body over the
Speaker:fuels that the tumor cells can't use.
Speaker:So intrinsically,
Speaker:people say, oh, cancer cells are so tough
Speaker:and hardy, and they're so versatile.
Speaker:That's total crap.
Speaker:How do you explain a cell with a nucleus
Speaker:blown to hell with all these mutations?
Speaker:And you're going to
Speaker:have that cell behave more
Speaker:transitional and more flexible than the
Speaker:cells in our body that evolved over
Speaker:millions of years to adjust their
Speaker:metabolism to the situation.
Speaker:And the cancer cell can do this with a
Speaker:nucleus that's blown to hell.
Speaker:Makes no sense in evolutionary biology.
Speaker:People don't
Speaker:understand evolutionary biology.
Speaker:The way you understand cancer and many
Speaker:other diseases, you must understand
Speaker:evolutionary biology.
Speaker:And if you don't do that,
Speaker:you're going to be in the dark.
Speaker:You're going to be in the dark.
Speaker:And that explains a lot of the stuff that
Speaker:we have in medicine today, because people
Speaker:don't understand evolutionary biology.
Speaker:They remain in the dark.
Speaker:And as long as you remain in the dark,
Speaker:you ain't moving forward.
Speaker:So here's what they say.
Speaker:Oh, cancer cells are tough to kill
Speaker:because we're throwing everything at
Speaker:radiation and chemo and immunotherapies.
Speaker:And those damn cancer cells can survive.
Speaker:They're protecting themselves with the
Speaker:waste products of
Speaker:fermentation metabolism.
Speaker:Everybody knows.
Speaker:They say, oh, the cancer environment is
Speaker:so acidified, it protects them from the
Speaker:therapies that we have.
Speaker:Where does the acidification come from?
Speaker:The waste products of glucose and
Speaker:glutamine fermentation.
Speaker:If you take away glucose and glutamine,
Speaker:you remove the acidification of the micro
Speaker:environment, making the tumor cells
Speaker:extremely vulnerable to small doses of
Speaker:radiation, chemo, and
Speaker:these other procedures.
Speaker:How is that not understood by guys that
Speaker:are supposed to be smart?
Speaker:Don't you understand why the damn tumor
Speaker:cells are not dying from
Speaker:what you're throwing at them?
Speaker:Because they're fermenting.
Speaker:If they ferment, you take
Speaker:away the fermentable fuels.
Speaker:Oh, that can't be right.
Speaker:It's too simple.
Speaker:Yeah.
Speaker:And it works.
Speaker:And it is right.
Speaker:Get over it.
Speaker:You want to live longer, you take away
Speaker:the fermentable fuels, and then you give
Speaker:them fatty acids and ketones, and the
Speaker:cancer cell can't because
Speaker:you need a good mitochondria.
Speaker:Fatty acids and ketone bodies cannot be
Speaker:used as a fuel by cancer cells because
Speaker:the mitochondria are inefficient.
Speaker:Fatty acids and ketone bodies can be used
Speaker:by most of our normal cells because we
Speaker:have good
Speaker:mitochondria, healthy mitochondria.
Speaker:So we lower the blood sugar, elevate the
Speaker:ketones, and then come in and target the
Speaker:glutamine pathways strategically in an
Speaker:approach that we developed, the press
Speaker:pulse therapeutic strategy.
Speaker:Glucose is a non-essential metabolite.
Speaker:Glucose is a non-essential metabolite.
Speaker:We can live with very, very minimal
Speaker:levels of glucose just to keep our
Speaker:erythrocytes moving oxygen
Speaker:and CO2 through the body.
Speaker:It takes tiny amounts of glucose.
Speaker:But the majority of muscles and brain can
Speaker:all transition over to ketone bodies.
Speaker:Tumor cells cannot.
Speaker:We tested them.
Speaker:We interrogated these cells.
Speaker:Tumor cells collect huge droplets of
Speaker:fatty acids in the cytoplasm because they
Speaker:cannot use the fatty acids.
Speaker:If you force the tumor cell to use the
Speaker:fatty acids, it develops reactive oxygen
Speaker:species and explodes and dies.
Speaker:So that's why they store the fatty acids
Speaker:in the cytoplasm because if they try to
Speaker:use them, they're going to kill them.
Speaker:So this is simply a protective mechanism.
Speaker:I can't tell you how many people are
Speaker:writing papers saying tumor cells love
Speaker:fatty acids because they store them in
Speaker:the cytoplasm because
Speaker:they need them for fuel.
Speaker:Yeah, well, try to goose the cell to use
Speaker:the fatty acids and all
Speaker:of a sudden the cell dies.
Speaker:Try to grow your cells, your cancer cells
Speaker:in the absence of glucose and glutamine
Speaker:in the presence of fatty
Speaker:acids in ketone bodies.
Speaker:With no glucose, no
Speaker:fermentable fuels, they die.
Speaker:So it becomes very
Speaker:clear how to manage cancer.
Speaker:So we're aware of this.
Speaker:Unfortunately, the field still has to
Speaker:come to grips with this
Speaker:and I think they slowly are,
Speaker:but it takes time, unfortunately.
Speaker:Yeah, I know.
Speaker:I think we could
Speaker:probably stop the podcast there.
Speaker:That was incredible.
Speaker:Thank you.
Speaker:I'm definitely going to have
Speaker:to re-listen to a bunch of that.
Speaker:Well, not only listen, not only re-listen
Speaker:to it, read the damn
Speaker:papers that we published.
Speaker:I go into great biochemical details.
Speaker:I have the evidence put out in those
Speaker:papers that we published
Speaker:and they're open access.
Speaker:So everybody can read them.
Speaker:Anybody with a few functional brain cells
Speaker:can sit down and read these papers and
Speaker:make their own decision as to what they
Speaker:think in light of that.
Speaker:I do a compare and contrast the theories.
Speaker:I do the evidence supporting the
Speaker:different theories and you tell me what
Speaker:you think is happening.
Speaker:And I learned there's very few people
Speaker:that actually understand or not
Speaker:understand that who read
Speaker:actually read the literature.
Speaker:They all wait and they only do what other
Speaker:people are doing and they ask other
Speaker:people what they think.
Speaker:And if the person
Speaker:says, "Oh, no, it can't be.
Speaker:Okay, then I believe it can't be."
Speaker:Why don't you use your own brain cells
Speaker:and analyze the data for yourself?
Speaker:That's one of the great things about
Speaker:humans is we have a rational mind.
Speaker:That's what we were gifted with.
Speaker:But I'll tell you, dogmatic views,
Speaker:political, religion, all that takes away
Speaker:from rational thinking.
Speaker:And when you lose your ability to sit and
Speaker:rationalize, then you
Speaker:lose a part of your humanity.
Speaker:And what we're seeing here, the reason
Speaker:why there's a delay in the movement from
Speaker:the somatic mutation theory to the
Speaker:mitochondrial metabolic theory, which
Speaker:will prevent and manage
Speaker:diseases dramatically.
Speaker:We're going to drop cancer death rates
Speaker:like there's no tomorrow.
Speaker:We're going to keep people alive because
Speaker:we understand the science
Speaker:supporting what we're saying.
Speaker:And then once people start looking at it
Speaker:and seeing that we are essentially
Speaker:correct, not on all the minutia, we can
Speaker:always work out minutia later on.
Speaker:But the bottom line is how long can I
Speaker:keep somebody with a
Speaker:stage four tumor alive?
Speaker:Oh, he's got three months to live.
Speaker:Are you kidding me?
Speaker:We've got people that were given those
Speaker:days, they're still alive five and six
Speaker:years later because they've transitioned
Speaker:their body over to nutritional ketosis
Speaker:and came in with certain low dose
Speaker:medications to kill off the tumor cells.
Speaker:So I know it's going to work because I've
Speaker:seen enough preclinical studies and human
Speaker:studies, small trials, to know this will
Speaker:work and keeps people alive.
Speaker:Unfortunately, you go to the top
Speaker:hospitals and they tell you,
Speaker:oh, no, you got to have this.
Speaker:Did you ever hear the
Speaker:cancer is a med about?
Speaker:No, I never heard of it.
Speaker:Eat sugar, eat all the
Speaker:high carbohydrate diets.
Speaker:Why?
Speaker:Oh, because you're losing weight.
Speaker:Why am I losing weight?
Speaker:Well, you have cancer and
Speaker:we just try to poison you.
Speaker:Anybody who's poisoned loses weight.
Speaker:So you get nausea and
Speaker:vomiting, diarrhea, fatigue.
Speaker:Why are you doing that?
Speaker:Well, we use the toxic poison on you.
Speaker:Why are you doing that?
Speaker:Well, we're trying to
Speaker:kill your tumor cells.
Speaker:I went bald.
Speaker:Why?
Speaker:Why you go bald?
Speaker:I lost all my hair.
Speaker:Oh, did you have tumor cells growing in
Speaker:your hair follicles?
Speaker:No, they just happened to die.
Speaker:You're trying to kill tumor cells, not
Speaker:kill your hair or blow out your gut.
Speaker:That tells you that those are the
Speaker:procedures of people who lack knowledge.
Speaker:What we're seeing is the result of
Speaker:massive lack of knowledge on the
Speaker:biochemistry and biology of the very
Speaker:disease that people are working with.
Speaker:And we're using medieval therapies that
Speaker:are torturing people.
Speaker:I think people during the Spanish
Speaker:Inquisition would be very impressed with
Speaker:how we're torturing cancer
Speaker:patients in these hospitals.
Speaker:They could say, "Well, we can learn
Speaker:something from you guys.
Speaker:Where do I get Red Devil Doxorubicin?
Speaker:We could give that to a heretic."
Speaker:It's terrible for me
Speaker:to say stuff like this.
Speaker:But when you see 1700 people a day in the
Speaker:United States dying from cancer, 70
Speaker:people an hour, and you see cancer
Speaker:getting worse and worse around the world,
Speaker:I mean, grab somebody by the throat and
Speaker:say, "What the hell are we doing?
Speaker:Why are we allowing this to happen?"
Speaker:Because of a failed theory.
Speaker:That's what it is, a theory that's no
Speaker:longer supported by the evidence.
Speaker:And you guys keep treating people based
Speaker:on an incorrect theory,
Speaker:and the outcome is abysmal.
Speaker:Yeah.
Speaker:What did Einstein say?
Speaker:Insanity is doing the same thing over and
Speaker:over again and expecting a different
Speaker:result, something to that extent.
Speaker:Yes.
Speaker:Well, why are they doing?
Speaker:Don't they know what Einstein said?
Speaker:Did they not hear what Einstein said?
Speaker:And there's another issue of morality,
Speaker:which is even a worse issue.
Speaker:You don't like to be referred to as an
Speaker:immoral person, but when you're taking
Speaker:drugs that are not based on the correct
Speaker:theory and treating people with them and
Speaker:knowing that they won't work,
Speaker:and that's immoral.
Speaker:And the other part of this is that many
Speaker:of those drugs are very, very expensive.
Speaker:And what happens, they not only cause
Speaker:physical toxicity, they
Speaker:cause financial toxicity.
Speaker:Many people, their marriage is dissolved,
Speaker:they commit suicide, the cost is passed
Speaker:on to the surviving relatives.
Speaker:And for folks that are not well off, a
Speaker:$20,000 bill, even though they covered
Speaker:80% of the 100,000,
Speaker:20,000 can cripple a family.
Speaker:With limited means.
Speaker:This is immoral.
Speaker:The whole cancer
Speaker:industry is an immoral industry.
Speaker:They're allowing people to suffer and die
Speaker:based on an incorrect theory.
Speaker:And they're allowing
Speaker:physical and financial toxicity.
Speaker:These are immoral acts.
Speaker:And we have a strategy that can
Speaker:absolutely reduce the deaths of cancer,
Speaker:keep people alive with a higher quality
Speaker:of life, and it's not being
Speaker:done anywhere on the planet.
Speaker:Now you tell me what's wrong with that.
Speaker:Yeah, I'm not even going to try and sort
Speaker:of answer that
Speaker:question just at this point.
Speaker:Dr.
Speaker:Seifried, again, that
Speaker:was an amazing answer.
Speaker:Thank you.
Speaker:I'd just like to take a step back quickly
Speaker:and discuss, have a quick discussion
Speaker:about your thoughts on testing.
Speaker:Now, the way I see testing, testing is
Speaker:generally done quite acutely when
Speaker:somebody presents with
Speaker:a disease in this case.
Speaker:You'll obviously get a physical exam
Speaker:done, some sort of imaging, probably some
Speaker:sort of biopsy as well, some blood tests
Speaker:looking at various biomarkers, et cetera.
Speaker:But in no way is this
Speaker:sort of testing preventative.
Speaker:It generally is only treated and dealt
Speaker:with when the issues arise.
Speaker:Now, obviously, there are various
Speaker:technologies that are starting to sort of
Speaker:come up to things like liquid biopsies.
Speaker:Maybe you could elucidate on that
Speaker:slightly and these full-body MRIs, which
Speaker:are obviously somewhat controversial in
Speaker:the sense that they may or
Speaker:may not pick up incident lomas.
Speaker:The idea of finding an issue that may not
Speaker:be an issue that then requires further
Speaker:investigation that then may or may not
Speaker:actually turn into an issue.
Speaker:What's your stance on
Speaker:early detection as a whole?
Speaker:Do you think it's something we should be
Speaker:exploring more beyond just the basic get
Speaker:your colonoscopy done
Speaker:when you hit 40 plus?
Speaker:Or does the whole thing again about
Speaker:incident lomas and treating cancer from
Speaker:that perspective and, excuse me, treating
Speaker:and scanning for cancer from that
Speaker:perspective generally make
Speaker:it a bit of a mute point?
Speaker:Yeah, well, you have a couple
Speaker:of things here to break down.
Speaker:The diagnostics, I'm in favor of
Speaker:non-invasive diagnostic approaches.
Speaker:If we have a liquid biopsy that's 95%
Speaker:accurate in determining whether or not
Speaker:you have a neoplastic growth somewhere in
Speaker:your body, I'm all for that.
Speaker:And then non-invasive imaging, whether
Speaker:it's a PET scan, MRI, CAT scan, or one of
Speaker:these kinds of things, I'm not in favor
Speaker:of biopsy because I have seen so many
Speaker:papers published in the scientific
Speaker:literature showing that when you stab a
Speaker:cancer, you run the risk of causing
Speaker:metastasis, metastasis where the spread
Speaker:of the tumor, the cells can spread around
Speaker:your body making what was formerly a
Speaker:localized problem, a systemic problem.
Speaker:So I'm in favor of four diagnostics,
Speaker:colonoscopies and and breast
Speaker:things and stuff like this.
Speaker:Those are, you know, I
Speaker:don't know what to say
Speaker:about that.
Speaker:I know there's a lot of
Speaker:controversy about that.
Speaker:And most people who develop cancer have
Speaker:certain physical signs in
Speaker:their body that something is wrong.
Speaker:Like you said, a lump,
Speaker:a wound that doesn't heal blood that
Speaker:continues to come from some location.
Speaker:You know, those can be then liquid biopsy
Speaker:to see if there's a real linkage to some
Speaker:neoplasia, a scanning of the body or
Speaker:something along these lines.
Speaker:And then once you would make a diagnosis
Speaker:without a biopsy, you see a lump.
Speaker:Okay, let's launch into metabolic therapy
Speaker:and see if we can shrink the lump
Speaker:naturally with diet drug combinations,
Speaker:non-toxic drugs and diets that we've
Speaker:developed here at BC.
Speaker:And if you shrink the lump and it goes
Speaker:away, and the imaging analysis and the
Speaker:liquid biopsy data, what happened?
Speaker:Where did it go?
Speaker:I don't see any of the
Speaker:markers that were there previously.
Speaker:That's great.
Speaker:And if it doesn't go away completely,
Speaker:you might have shrunken it down and make
Speaker:it much smaller, in which case a surgical
Speaker:procedure or a dose of radiation at a
Speaker:very defined spot could
Speaker:be potentially curative.
Speaker:So there's a lot of ways to diagnose and
Speaker:treat cancer in the early stages
Speaker:different than what we're doing today.
Speaker:You know, we're doing too
Speaker:radical on this whole thing.
Speaker:You know, you see a lump in the rip the
Speaker:person's breasts off
Speaker:or something like this.
Speaker:You know, I don't know what to say about
Speaker:colonoscopies or breast exam exams.
Speaker:Breast cancer rises every
Speaker:year in females in this country.
Speaker:Colorectal cancer is on the rise.
Speaker:So I don't know what's going on.
Speaker:All the major cancers seem to be, many of
Speaker:the major cancers seem to be on the rise.
Speaker:It's happening in
Speaker:younger and younger people.
Speaker:Yeah, if you're to speculate, do you
Speaker:think that is an environmental issue,
Speaker:just sort of maybe excess sort of
Speaker:zenoestrogens in the environment that are
Speaker:particularly just from a breast cancer
Speaker:perspective, maybe
Speaker:triggering these issues?
Speaker:Or is that a bit productionist again?
Speaker:I think most of it is environmental.
Speaker:I mean, there are some people who have
Speaker:genetic predispositions to
Speaker:insults from the environment.
Speaker:You have to realize
Speaker:that cancer is a disease.
Speaker:In fact, not only cancer, most of the
Speaker:chronic diseases that we are dealing
Speaker:with, which is dementia, type 2 diabetes,
Speaker:obesity, hypertension, high blood
Speaker:pressure, a lot of neuropsychiatric
Speaker:problems, are all the result of
Speaker:mitochondrial dysfunction in one way or
Speaker:another, caused by the diet lifestyle
Speaker:that we're all under.
Speaker:And we know this pretty much because
Speaker:Paleolithic men would not have had any of
Speaker:these kinds of conditions.
Speaker:They died predominantly
Speaker:from infections and injuries.
Speaker:They did not have orthopedic surgeons to
Speaker:repair a broken knee from
Speaker:some guy gored by a buffalo.
Speaker:And how do we know that?
Speaker:Because people say, "Well, you weren't
Speaker:there during Paleolithic
Speaker:period 500,000 years ago."
Speaker:But we have people on the planet who
Speaker:still live, according
Speaker:to traditional ways.
Speaker:And these folks also didn't have cancer
Speaker:or a lot of the chronic
Speaker:diseases that we have today.
Speaker:How do we know that?
Speaker:Because Albert Schweitzer and a number of
Speaker:other physicians and humanitarians were
Speaker:investigating these primitive tribes.
Speaker:And they said, "Wow, they're remarkably
Speaker:different from those that live in the
Speaker:United States and England."
Speaker:So they were not obese.
Speaker:They didn't have any chronic diseases.
Speaker:They had bacterial infections, parasites,
Speaker:and things like this.
Speaker:So what's the difference between the
Speaker:Western diet lifestyle and the
Speaker:Paleolithic diet and lifestyle?
Speaker:And predominantly, it's the availability
Speaker:of highly processed
Speaker:carbohydrates in our diets.
Speaker:A Paleolithic man never had highly
Speaker:processed carbohydrates in his diet.
Speaker:We did not evolve to evolve in an
Speaker:environment with highly processed carbs.
Speaker:But highly processed carbohydrates, are
Speaker:you talking, obviously,
Speaker:and my evolution biology is definitely
Speaker:not my strong point, but I assume you
Speaker:mean very high GI carbohydrates, things
Speaker:like your processed sugars, honeys, etc.,
Speaker:opposed to things like root vegetables,
Speaker:things that are potentially
Speaker:lower on the glycemic scale.
Speaker:That maybe wouldn't...
Speaker:Yes, predominantly.
Speaker:Things that can
Speaker:remain edible in a package.
Speaker:Like I have a Twinkie here.
Speaker:This Twinkie is 10 years
Speaker:old, and it looks edible.
Speaker:And a mouse, it's 10 years old, and a
Speaker:mouse ate it, broke in and ate one of
Speaker:these two years ago.
Speaker:And he didn't complain.
Speaker:And there are people that are hungry that
Speaker:would eat 10 year old Twinkie.
Speaker:This is a synthetic thing made from all
Speaker:chemicals and sugars.
Speaker:This kind of stuff will kill you.
Speaker:Yet we eat large amounts of it.
Speaker:Not only that, we deep fry it and put
Speaker:powdered sugar and
Speaker:chocolate syrup on it, damn thing.
Speaker:You should go to Scotland.
Speaker:That's the Shon's Act breakfast.
Speaker:Yeah, right.
Speaker:So then we wonder why we got cancer and
Speaker:high blood pressure and hypertension and
Speaker:neuropsychiatric problems.
Speaker:And the lack of exercise is unbelievable.
Speaker:Paleo, you know how hard it is to track
Speaker:down and kill a big animal?
Speaker:It's not easy.
Speaker:You have to have well runners.
Speaker:You have to have strong guys to track
Speaker:down and kill these buffalo.
Speaker:And you have to kill a mammoth, a woolly
Speaker:mammoth, and these kinds of big animals
Speaker:that lived in paleolithic times.
Speaker:And that was a lot of energy to kill, not
Speaker:only to kill the big thing,
Speaker:but to chop it up and eat it.
Speaker:You know, they'd go for the bone marrow
Speaker:as a fuel source that
Speaker:was very rich in nutrients.
Speaker:We're sitting in traffic today.
Speaker:We're sitting in front of computers.
Speaker:We don't nearly have the amount of energy
Speaker:that was expended
Speaker:during paleolithic times.
Speaker:We're eating highly
Speaker:processed carbs, bad food.
Speaker:We have bad sleep.
Speaker:We have emotional stress.
Speaker:We have all of these things that impact
Speaker:negatively the number structure and
Speaker:function of mitochondria in our cells.
Speaker:It is not surprising that we have all of
Speaker:the chronic diseases in cancer that we
Speaker:are currently suffering with
Speaker:in modern Western societies.
Speaker:It's absolutely understandable in terms
Speaker:of our evolutionary biology.
Speaker:We are still paleolithic man
Speaker:biologically, but living in a modern,
Speaker:industrialized society where all of the
Speaker:desires that we would have had in
Speaker:paleolithic time are now at our
Speaker:fingertips in any supermarket.
Speaker:We don't have to go out
Speaker:and hunt down animals.
Speaker:Everything is prepared, packaged, and
Speaker:ready for us to eat right away.
Speaker:We don't have to expend a lot of energy
Speaker:to cook it up, kill it,
Speaker:and cook it every night.
Speaker:It's preserved, well preserved, so we can
Speaker:store it for a long
Speaker:period of time and eat it.
Speaker:Eventually, it beats the hell out of your
Speaker:mitochondria in your body.
Speaker:Some people, you get obesity, type 2
Speaker:diabetes, hypertension, high blood
Speaker:pressure, macular
Speaker:degeneration, dementia, cancer.
Speaker:Every one of those diseases, disorders,
Speaker:is the result of mitochondrial
Speaker:dysfunction in one way or another.
Speaker:Some cells up and die become
Speaker:dysfunctional, not becoming cancer.
Speaker:Some cells that have the capacity to
Speaker:switch from oxfoss to substrate-level
Speaker:phosphorylation become cancerous.
Speaker:We can link all of the major chronic
Speaker:diseases, including cancer, back to
Speaker:mitochondrial dysfunction, which then
Speaker:begs the question, well,
Speaker:how do you prevent cancer?
Speaker:And you keep your mitochondria healthy.
Speaker:It's extremely difficult to get cancer if
Speaker:you're mitochondria healthy.
Speaker:Well, how do I keep my
Speaker:mitochondrial healthy?
Speaker:Do a lot of exercise, stress management,
Speaker:avoid highly processed carbohydrate
Speaker:foods, try to get good sleep.
Speaker:Do all the things that keep mitochondria
Speaker:healthy, and you don't get dementia, you
Speaker:don't get cardiovascular
Speaker:disease, you don't become obese,
Speaker:you don't get cancer.
Speaker:You significantly reduce the risk for
Speaker:cancer and all these chronic diseases by
Speaker:keeping your mitochondria healthy.
Speaker:It's very interesting.
Speaker:In the United States,
Speaker:the NCI National Cancer Institute says,
Speaker:"We reduce cancer by 33% over the last
Speaker:several decades, mainly because we had
Speaker:the anti-smoking campaign of the 1990s.
Speaker:And if we all continue to smoke like
Speaker:crazy, like we were in the 1990s, we
Speaker:would have 33% more dead cancer patients
Speaker:today than we actually have."
Speaker:So clearly, the major drop in cancer
Speaker:deaths came from the
Speaker:elimination of a provocative
Speaker:behavioral situation, which was smoking.
Speaker:So why?
Speaker:Because our mitochondria are healthier
Speaker:when you don't smoke.
Speaker:And everything comes back to the health
Speaker:and vitality of the mitochondria.
Speaker:Do we want to go back and become, again,
Speaker:live in a cave like Paleolithic Man?
Speaker:No.
Speaker:No,
Speaker:but finding that happy middle ground.
Speaker:Yes.
Speaker:But now we have an awareness.
Speaker:And not only that, we develop the glucose
Speaker:ketone index calculator.
Speaker:My next question was
Speaker:going to be exactly that.
Speaker:Which is now going to be the tool to
Speaker:allow every person that can measure their
Speaker:blood, glucose, and ketones with a meter,
Speaker:either by pricking their finger to get a
Speaker:drop of blood or using a continuous
Speaker:glucose ketone monitor on your cell
Speaker:phone, you will be able to know when you
Speaker:apply the GKI index, you will know
Speaker:exactly what zone of
Speaker:health you are in or not in.
Speaker:So you can know that you will be in a
Speaker:high risk red zone if you have a GKI
Speaker:that's over 50, up to 100.
Speaker:You are going to be in a zone of
Speaker:mitochondrial ill health.
Speaker:Can we backtrack quickly, Dr.
Speaker:Seifried?
Speaker:Sorry about that.
Speaker:Just briefly discuss what the glucose
Speaker:ketone index is, just for those in the
Speaker:audience who maybe
Speaker:aren't familiar with it.
Speaker:Obviously, it's a biomarker that I know
Speaker:you have been intimately
Speaker:involved in developing.
Speaker:But what exactly is this
Speaker:index and then how does it work?
Speaker:Obviously, we are monitoring two
Speaker:different biomarkers here, ketones,
Speaker:things like butyl
Speaker:hydroxybutyrate, acetate, etc.
Speaker:And then obviously glucose.
Speaker:But how does looking at those two markers
Speaker:from a metabolic health standpoint help
Speaker:us to, well, a, determine metabolic
Speaker:health and maybe just a
Speaker:bit more nuance there.
Speaker:I know there's
Speaker:generally a range there as well.
Speaker:I think you want to aim for about a three
Speaker:when looking to try and deal
Speaker:with things therapeutically.
Speaker:I may be wrong there.
Speaker:But yeah, if you could just fill us in
Speaker:sort of very fiduciary on
Speaker:what that index is all about.
Speaker:So again, go back to
Speaker:evolutionary biology.
Speaker:Paleolithic man was always in a state of
Speaker:nutritional ketosis, mainly because they
Speaker:did not have access to highly processed
Speaker:carbohydrates in their diet.
Speaker:So they had a lot of exercise and they
Speaker:had a diet that was largely carnivorous
Speaker:with some vegetables, some
Speaker:tubers and this kind of thing.
Speaker:But they were complex carbs.
Speaker:They weren't these highly processed, like
Speaker:you mentioned already, highly glycemic
Speaker:index kinds of things.
Speaker:And food was limited.
Speaker:So when you put that body and you look at
Speaker:the, if they could look at their glucose
Speaker:and ketones at that stage, they would
Speaker:find themselves in a state of nutritional
Speaker:ketosis, which is an elevation of ketone
Speaker:bodies and a very low glucose level, or I
Speaker:should say very normal, like 65 to 85
Speaker:milligram per deciliter, maybe
Speaker:a 3.2 to 4 millimolar glucose.
Speaker:These are normal body levels of glucose
Speaker:produced by the combination of
Speaker:gluconeogenesis as well as carbohydrates
Speaker:that we would get from the diet.
Speaker:So we would always be in this beautiful
Speaker:insulin, super insulin sensitive zone, no
Speaker:insulin resistance at all, because
Speaker:diabetes would be unheard of, type two,
Speaker:of course, not type one.
Speaker:Type one would have been afflicting us
Speaker:from the beginning of
Speaker:time in one way or another.
Speaker:But our bodies would have been in
Speaker:metabolic homeostasis as long as we
Speaker:weren't starving, of course.
Speaker:But we could go long periods of time
Speaker:without eating and still maintain
Speaker:metabolic homeostasis because we would be
Speaker:burning ketone bodies that would be
Speaker:mobilized from stored fat.
Speaker:So we developed the glucose ketone index
Speaker:as a marker, biomarker, to allow us to
Speaker:know what level of metabolic
Speaker:homeostasis we would be in.
Speaker:So if you have a glucose ketone index of
Speaker:20 or 10, I mean, you're in some level of
Speaker:metabolic homeostasis.
Speaker:If you want to go into a deeper level of
Speaker:what we call therapeutic ketosis, then
Speaker:you'd go down to a level of two, which is
Speaker:the ratio of blood sugar divided by the
Speaker:ratio of beta hydroxybutyrate, which is
Speaker:the main ketone body.
Speaker:And then you would say,
Speaker:oh, how do we know this?
Speaker:Because I have friends, Dom DiAgostino,
Speaker:Anthony Chapp in these guys, they're
Speaker:always in these states
Speaker:of nutritional ketosis.
Speaker:What do they do?
Speaker:They do a lot of exercise
Speaker:and they eat a lot of meat.
Speaker:And they stay in these
Speaker:paleolithic kinds of zones.
Speaker:And these are the zones that keep your
Speaker:mitochondria super healthy.
Speaker:So what we do is we take people from the
Speaker:population and look at guys that have
Speaker:type 2 diabetes,
Speaker:obesity, and all these things.
Speaker:And you find these GKI values over 50,
Speaker:100, sometimes above 100.
Speaker:Are you kidding me?
Speaker:I mean, it should be down in
Speaker:the 5 to 10 zone or 20 zone.
Speaker:And you've got 200?
Speaker:Oh, I'm obese.
Speaker:I got systemic inflammation.
Speaker:I got to, of course, you're not in
Speaker:metabolic homeostasis.
Speaker:So the glucose ketone index tells us I
Speaker:built it for the cancer patients, because
Speaker:we knew that if we lowered blood sugar
Speaker:down far enough, the tumor cells need the
Speaker:sugar to grow, and they
Speaker:can't switch to ketones.
Speaker:So you put them in a
Speaker:very compromised condition.
Speaker:Now, what we do is we see cancer
Speaker:shrinking down tremendously when you get
Speaker:the GKI 2.0 or below,
Speaker:but you still have the glutamine issue.
Speaker:So then we develop the pulse therapy to
Speaker:come in and target with low dose of
Speaker:glutamine inhibitors while the person is
Speaker:in a state of nutritional ketosis.
Speaker:And glutamine being the fermentable amino
Speaker:acid that is then utilized as an
Speaker:alternative fuel source by various
Speaker:cancers in the absence
Speaker:of glucose is accurate.
Speaker:Yeah.
Speaker:And people always ask me, what can you do
Speaker:to lower, what diet can
Speaker:I use to lower glutamine?
Speaker:And if I eat meat,
Speaker:won't that raise glutamine?
Speaker:The glutamine in our body is already
Speaker:super saturated because we use it for so
Speaker:many things, the gut
Speaker:and our immune system.
Speaker:We already have more than enough
Speaker:glutamine circulating in the body to
Speaker:provide a tumor cell with more than
Speaker:enough fuel in that regard.
Speaker:So there's no diet that will lower
Speaker:glucose, correction glutamine.
Speaker:And the glutamine will always be there.
Speaker:So you can't, even if you do exercise,
Speaker:yes, you can lower glutamine, but it's
Speaker:not to the level where you're going to
Speaker:kill the tumor cell.
Speaker:So that's why we need drugs.
Speaker:But the drugs have to be strategic.
Speaker:While you're in nutritional ketosis,
Speaker:blood sugar is down,
Speaker:ketones are elevated.
Speaker:So you got a choke hold
Speaker:on the glucose pathway.
Speaker:But you got the
Speaker:glutamine pathway still opened.
Speaker:And then we come in with specific drugs
Speaker:that will block glutamine's availability.
Speaker:But we have to do this very strategically
Speaker:because the same fuel is
Speaker:needed by our immune cells.
Speaker:Our immune cells and our gut use the same
Speaker:fuel the tumor cells are using.
Speaker:So that's why we
Speaker:developed the press pulse.
Speaker:So we pulse glutamine.
Speaker:We do pulsing of glutamine targeting,
Speaker:killing tumor cells over a short period
Speaker:of time, removing the pulse, and allowing
Speaker:the immune system to come in and kill, to
Speaker:pick up the dead corpses.
Speaker:So you have to have the undertakers
Speaker:coming in and get rid of the dead bodies
Speaker:in the microenvironment.
Speaker:And that's your immune system.
Speaker:And they need glutamine as well.
Speaker:So this is why you need to understand
Speaker:evolutionary biology and biochemistry to
Speaker:effectively manage cancer.
Speaker:If you don't understand biology and
Speaker:biochemistry and evolutionary biology,
Speaker:you are still in the stone age when it
Speaker:comes to this kind of stuff.
Speaker:You're just peddling drugs and hoping for
Speaker:the best case scenario.
Speaker:Yes.
Speaker:You don't know why things
Speaker:are working or how they work.
Speaker:We know exactly how things
Speaker:are working and why they work.
Speaker:And we try to perfect the system to keep
Speaker:these tumor cells under
Speaker:restricted fuel conditions.
Speaker:And the body itself, when increased in
Speaker:its health, will turn on the tumor cell,
Speaker:on the tumor cells,
Speaker:and use them for fuel.
Speaker:It's called autolytic cannibalism.
Speaker:So the body itself, when put under energy
Speaker:restriction, every cell in the body must
Speaker:earn its existence in that body.
Speaker:There can be no weak, lame, inefficient
Speaker:cells because the body will turn on them
Speaker:and use them for fuel.
Speaker:The tumor itself becomes a fuel source
Speaker:for the rest of the body when you're put
Speaker:into these states of nutritional ketosis.
Speaker:So part of the solution to the problem is
Speaker:when the normal cells recognize a
Speaker:population of cells that are inefficient
Speaker:in utilization of energy.
Speaker:And they turn on them and dissolve them
Speaker:and use them for fuel.
Speaker:And people say, "I don't know what
Speaker:happened to my tumor.
Speaker:It just kind of disappeared when I was in
Speaker:nutritional ketosis."
Speaker:Well, you're damn body-ated.
Speaker:Because it was inefficient.
Speaker:They were using energy inefficiently.
Speaker:And the body recognizes that.
Speaker:And this is the term
Speaker:autolytic cannibalism.
Speaker:I published that.
Speaker:But we also can strategically target
Speaker:glutamine to work together.
Speaker:It's a whole systems approach to
Speaker:eliminating a bunch of cells that are
Speaker:growing out of control, using energy very
Speaker:inefficiently, being dependent
Speaker:predominantly on glucose and glutamine,
Speaker:and not being able to
Speaker:burn fatty acids or ketones.
Speaker:It's an elegant system.
Speaker:It's so beautiful.
Speaker:It works for the majority of people.
Speaker:And nobody's doing this.
Speaker:There's no clinical
Speaker:trial anywhere on the planet.
Speaker:Don't make much money out of it, can you?
Speaker:Well, the money issue
Speaker:now becomes another issue.
Speaker:It's revenue first,
Speaker:patient outcome second.
Speaker:And I think people need to know that.
Speaker:They should know that their disease is
Speaker:supporting a giant industry.
Speaker:Many people are grateful
Speaker:for those who have cancer.
Speaker:Because the cancer patient supports a
Speaker:very lucrative process that would be
Speaker:potentially disturbed if we were to find
Speaker:a method or a way to prevent
Speaker:or manage cancer effectively.
Speaker:But man has made adjustments and
Speaker:adaptations to disruptive technologies.
Speaker:And they will do the same with this
Speaker:cancer and chronic disease situation.
Speaker:It's just a matter of time.
Speaker:Because we cannot continue on this path
Speaker:of this abysmal path that we've been on
Speaker:for the last 75, 100 years.
Speaker:So we will begin to change.
Speaker:But there will be new industries and new
Speaker:strategies for exploring
Speaker:and keeping people healthy.
Speaker:And others, so we're trying to get a
Speaker:revenue transition of revenue generation
Speaker:from one failed system to a system that
Speaker:really works but has not yet been mature
Speaker:to replace the revenue
Speaker:lost from one system.
Speaker:But I think that's all
Speaker:part of the future as well.
Speaker:But right now, my job is just to keep
Speaker:people alive with a higher quality of
Speaker:life, using the knowledge of the biology
Speaker:and biochemistry of the
Speaker:disease that we understand.
Speaker:Yeah.
Speaker:Now that's fascinating.
Speaker:And I definitely would love to come back
Speaker:to that in a minute.
Speaker:I'd just like to quickly chat about the
Speaker:ketogenic diet a bit more.
Speaker:And I'm going to ask my question first
Speaker:and then Ramblom from a group of mine.
Speaker:I have a few concerns about sort of long
Speaker:term utilization of the ketogenic diet,
Speaker:not for everybody, but just I have found
Speaker:that there are various people who do
Speaker:follow a ketogenic diet, obviously are
Speaker:going to run into certain problems, some
Speaker:of them endocrine in nature, etc.
Speaker:Now, I think of course, most people who
Speaker:are going to explore this meta,
Speaker:who are going to explore cancer treatment
Speaker:from a metabolic standpoint, are going to
Speaker:utilize a ketogenic diet as their first
Speaker:step and why should they not?
Speaker:Now, as I mentioned, I've
Speaker:got a few sort of concerns.
Speaker:For example, I believe there's rodent
Speaker:data out there to show that ketogenic
Speaker:diets long term may impair, I think it's
Speaker:hepatic FGF21 signaling due to receptor
Speaker:downregulation and that there are other
Speaker:drivers issues there as well.
Speaker:For example, peripheral insulin
Speaker:resistance, which I'm sure you're
Speaker:familiar with for the audience listening,
Speaker:that being the idea that in some people
Speaker:long term ketogenic diet,
Speaker:adherence can essentially cause an
Speaker:insulin resistant like state at the level
Speaker:of the muscle because the body is sort of
Speaker:not able or not readily utilizing the
Speaker:glucose at its disposal effectively.
Speaker:Now, I'm just some second here, but I
Speaker:would be at least mechanistically
Speaker:concerned that those high levels of
Speaker:glucose might then also be a contributing
Speaker:factor if you're sort of becoming more
Speaker:and more insulin resistant.
Speaker:So, the way I see it, just from the GKI
Speaker:score side of things, and again, this is
Speaker:just me piecing a few things together, so
Speaker:tell me where I'm wrong, but are there
Speaker:other ways that you can sort of look at
Speaker:increasing your GKI score
Speaker:maybe without necessarily
Speaker:utilizing long term ketosis?
Speaker:And I suppose that's
Speaker:a question in itself.
Speaker:Should we always be in a state of ketosis
Speaker:or should we sort of keep it for a period
Speaker:of time, such as when, hopefully not, you
Speaker:have a disease like
Speaker:this where it's needed?
Speaker:But beyond that, what about strategies
Speaker:where you are either intermittently
Speaker:fasting and obviously including a certain
Speaker:amount of carbohydrates
Speaker:in that eating window?
Speaker:Would that fasting period, obviously
Speaker:again, the lower glycemic things, not
Speaker:talking about swallowing large quantities
Speaker:of honey and processed sugar,
Speaker:and then, yeah, other fuel sources maybe
Speaker:that can sort of increase ketone
Speaker:production, your ketone
Speaker:esters, your NCT oils,
Speaker:yeah, again, I hope that makes sense.
Speaker:I am rambling a bit and as you've no
Speaker:doubt already figured out, I'm definitely
Speaker:outside more with your house here.
Speaker:But are there, do you have any concerns
Speaker:again for the average person following a
Speaker:ketogenic for a longer period of time,
Speaker:perhaps in light of those
Speaker:mechanisms that I mentioned?
Speaker:And then beyond that, are those other
Speaker:strategies aimed at sort of improving a
Speaker:GKI index maybe without being in a
Speaker:constant state of ketosis, are they worth
Speaker:exploring or is it just not enough to
Speaker:actually deal with the matter at hand?
Speaker:Yeah, well, you got a lot of stuff that
Speaker:you just threw at me right there.
Speaker:Yeah, sorry about that.
Speaker:But we can break it down.
Speaker:But you're 100% correct.
Speaker:There's a lot of people who use ketogenic
Speaker:diets inappropriately that are not
Speaker:balanced with micro and macro nutrients,
Speaker:which then can lead to some of the
Speaker:conditions that you mentioned in your
Speaker:rambling.
Speaker:Yeah, in your ramblings.
Speaker:But I have seen the same thing.
Speaker:I mean, when we fed
Speaker:ketogenic diets to the mice,
Speaker:or humans, in an unrestricted way, diets
Speaker:that were not completely balanced in
Speaker:micro and macro nutrients,
Speaker:we got all of many of the health issues
Speaker:that you mentioned were seen.
Speaker:The tumors actually grew faster.
Speaker:There was a complete
Speaker:metabolic in homeostasis.
Speaker:You found conditions that would be
Speaker:reflective of some of
Speaker:what you have mentioned.
Speaker:That's why we try to get
Speaker:away from the term diet.
Speaker:And we talk about nutritional ketosis as
Speaker:a state of metabolic homeostasis, where
Speaker:your levels of ketones are not
Speaker:exorbitantly high, and your levels of
Speaker:glucose are not exorbitantly low.
Speaker:But you are balanced in micro and macro
Speaker:nutrients with a GKI of five or 10.
Speaker:And exactly as you said, in our new paper
Speaker:that we're working on right now, which
Speaker:will revolutionize the treatment of
Speaker:cancer and all these chronic diseases,
Speaker:we have built a color-coded chart to
Speaker:allow people to know what zones they're
Speaker:in at any given time, and whether or not
Speaker:they can move effectively
Speaker:from one zone to the next.
Speaker:Like, yes, intermittent fasting.
Speaker:Or the enjoyment, if you have been in a
Speaker:state of nutritional ketosis and you go
Speaker:out and party, and your body then shows a
Speaker:much higher GKI,
Speaker:which would be unhealthy,
Speaker:you would then know what you would need
Speaker:to do to bring it back into a normal
Speaker:range with the types of foods and
Speaker:exercise is extremely important.
Speaker:You can move these zones up and down.
Speaker:So you don't have to feel compelled to be
Speaker:locked into a particular state.
Speaker:But having the knowledge of what are the
Speaker:healthy states and what aren't the
Speaker:healthy states, knowing, like for
Speaker:example, the Greek patients that did
Speaker:really well on the keto diet, it was a
Speaker:calorie-restricted Mediterranean diet.
Speaker:Sardines, salmon, avocados, olive oil,
Speaker:and this kind of thing that most people
Speaker:can do without too much difficulty.
Speaker:They had good GKI.
Speaker:They were very balanced in
Speaker:micro and macro nutrients.
Speaker:But you could switch
Speaker:from that to a carnivore.
Speaker:There's a lot of flexibility in what a
Speaker:person can do to move in and out of these
Speaker:health zones without
Speaker:causing metabolic in-homeostasis.
Speaker:So we're working on that.
Speaker:We've published a big paper for the brain
Speaker:cancer patients to tell them exactly and
Speaker:address the questions that you raised.
Speaker:What are the choices?
Speaker:What are the variations that you can use
Speaker:to maintain constant pressure on tumor
Speaker:cells while constantly keeping the
Speaker:homeostasis of your normal cells at the
Speaker:highest level and metabolic homeostasis?
Speaker:So we're working on that.
Speaker:And to address your questions, most of
Speaker:the health problems associated with
Speaker:long-term ketogenic diets result from
Speaker:micro and macro nutrient imbalances that
Speaker:lead to pathologies, some of which you
Speaker:have already elucidated.
Speaker:So once the base of knowledge becomes
Speaker:available for people,
Speaker:they can then build diets.
Speaker:And we call it nutritional ketosis,
Speaker:because you can achieve that with a
Speaker:carnivore diet, a
Speaker:Mediterranean diet, a pescatarian diet.
Speaker:Vegan diets are a little harder.
Speaker:A veganism, you have to supplement with
Speaker:micronutrients and some macronutrients in
Speaker:order to maintain metabolic home.
Speaker:It's not a natural situation.
Speaker:Humans did not evolve as vegans.
Speaker:If we were vegans, we would have been
Speaker:extinct a long time ago.
Speaker:But we are omnivores.
Speaker:Our bodies were evolved to eat anything,
Speaker:walks, crawls, flies,
Speaker:or swims on this planet.
Speaker:And you can build nutritional ketosis
Speaker:from combinations of the natural foods
Speaker:that we evolved to eat.
Speaker:You just have to adjust the amounts that
Speaker:you're eating and the
Speaker:types that you're eating.
Speaker:So in our new study that will come out
Speaker:for managing cancer and chronic diseases,
Speaker:deals exactly with what you have
Speaker:mentioned, to allow people to always
Speaker:remain in a state of maximal metabolic
Speaker:homeostasis, but allowing the individual
Speaker:to know what zone of health they're in to
Speaker:allow mitochondria to be as healthy as
Speaker:possible, and not too restrictive in
Speaker:rigidity in what you're doing.
Speaker:Because part of enjoyment of life is the enjoyment of what we
Speaker:like to eat and drink.
Speaker:And we don't like to be pigeonholed into
Speaker:a particular way of doing something that
Speaker:eventually turns someone
Speaker:from being happy into miserable.
Speaker:But now with our new system that will
Speaker:come out on the apps, you will know at
Speaker:any given time what you can eat, for how
Speaker:long, and how healthy it can be.
Speaker:So everybody will, and
Speaker:everybody's unique individual.
Speaker:We also have to recognize that we have
Speaker:sex differences, we have age differences,
Speaker:we have cultural differences, and we have
Speaker:religious differences.
Speaker:So people are in these cultural,
Speaker:religion, different ages and things.
Speaker:They have to build their diet and
Speaker:lifestyle around a GKI that meets their
Speaker:needs and keeps them
Speaker:in a comfortable zone.
Speaker:And they'll know the quantification of
Speaker:that by looking at their glucose ketone
Speaker:index and matching it to a
Speaker:particular zone of health.
Speaker:So we will eliminate adverse effects,
Speaker:allowing people to be flexible so they
Speaker:can prevent these kinds of situations.
Speaker:And I think what we're running into now
Speaker:is people say, "Oh, I'm doing a keto, I'm
Speaker:eating lard every day, and I'm getting
Speaker:unhealthy and I'm getting unhealthy."
Speaker:Yeah, who wouldn't get unhealthy?
Speaker:The question is, we want to eliminate
Speaker:those kinds of ambiguities in what people
Speaker:can and cannot eat and give them the
Speaker:level of flexibility that will make it
Speaker:comfortable for their existence while at
Speaker:the same time
Speaker:maintaining mitochondrial health.
Speaker:And I think knowledge is power and every
Speaker:individual will adjust their own GKI and
Speaker:build their own diets and know how much
Speaker:exercise they need to do and to keep
Speaker:their body in a state of
Speaker:nutritional and physical health.
Speaker:So this is the future.
Speaker:But we're aware of everything you said.
Speaker:And when you start something off in the
Speaker:beginning, people sometimes overdo it,
Speaker:they do it the wrong way.
Speaker:And then they end up with these
Speaker:pathologies that become apparent for,
Speaker:like you mentioned, with all these...
Speaker:Our registry, sex, home industries.
Speaker:Yeah, I mean, that
Speaker:should not have to happen.
Speaker:Paleolithic man never had
Speaker:to deal with these things.
Speaker:His main problem was starvation.
Speaker:When you don't have any
Speaker:food, you starve to death.
Speaker:Well, you can only get ketones if you
Speaker:have hormonal insulin levels.
Speaker:Your ketones can never get ketoacidotic.
Speaker:That's type 1 diabetes predominantly
Speaker:where you have very high glucose and very
Speaker:high ketones together in your body.
Speaker:That's pathological.
Speaker:Natural therapeutic ketosis is low
Speaker:glucose elevated ketones, but not
Speaker:elevated to the level of ketoacid because
Speaker:you piss out excess ketones.
Speaker:But when you don't have insulin, you keep
Speaker:all that in your body.
Speaker:Your body seems like a starving.
Speaker:You can't get rid of the...
Speaker:You're making ketones and too high of a
Speaker:level, keeping too much in your body.
Speaker:So again, and we also know that there are
Speaker:some people that have carnitine
Speaker:deficiencies that
Speaker:can't metabolize ketones.
Speaker:There are people that get severe rashes
Speaker:from trying to get into these conditions.
Speaker:And there's certain people take
Speaker:medications that interfere with the
Speaker:ability to metabolize ketone bodies.
Speaker:So we have to be aware of the
Speaker:interference of nutritional ketosis.
Speaker:But at least when you're aware, you can
Speaker:alert people to these hazards, metabolic
Speaker:hazards, and they can
Speaker:make adjustments themselves.
Speaker:So all of this, we have
Speaker:thought about all of this.
Speaker:Why?
Speaker:Because we don't do anything else in our
Speaker:life except think about
Speaker:these kinds of things.
Speaker:We're laser focused.
Speaker:We don't think about anything else except
Speaker:what you just talked about.
Speaker:Not just occasionally, 24 seven.
Speaker:That's what we do.
Speaker:Dr.
Speaker:Seifried, thank you so much for that.
Speaker:That was incredible.
Speaker:To be honest, I think I've got through
Speaker:what, 20% of the questions that I'd hoped
Speaker:to be able to talk to you about today.
Speaker:So I'm going to have to twist your arm
Speaker:somehow, God willing, and to get me back
Speaker:from at some point in the future.
Speaker:What was your main
Speaker:question that I did not answer?
Speaker:Oh, no.
Speaker:I wanted to go down the rabbit hole
Speaker:regarding various fatty acids and
Speaker:specifically talk about saturated fats
Speaker:versus unsaturated fats and the issues
Speaker:regarding some people running into
Speaker:insulin resistance, having sort of high
Speaker:amounts of saturated
Speaker:fats in the ceramides.
Speaker:I don't know if you've
Speaker:seen that to be an issue.
Speaker:We published a big paper looking at all
Speaker:that stuff in mice,
Speaker:unrestricted and unrestricted.
Speaker:It's hard to get into ketosis on
Speaker:polyunsaturated fatty acids,
Speaker:but they're, the omega three fatty acids
Speaker:are very healthy for people.
Speaker:Some of the omega sixes are not.
Speaker:So we published a big paper on all this.
Speaker:So almost everything I have looked at in
Speaker:one way or the other, I just don't have
Speaker:time to talk about it at all, but our
Speaker:open access papers on restricted and
Speaker:unrestricted diets, high carb keto and
Speaker:fish oil diets and
Speaker:all this kind of stuff.
Speaker:So we have looked at that and the body is
Speaker:a machine that
Speaker:metabolizes the fuels effectively.
Speaker:Ketones will be
Speaker:produced from saturated fat.
Speaker:MCT oil, little MCT oil, is really great
Speaker:in producing ketone bodies endogenously.
Speaker:D beta hydroxybutyrate rather than L's.
Speaker:There's a way to do all that.
Speaker:We've looked at almost
Speaker:every damn thing we can look at.
Speaker:So I have papers on that, but yes, we
Speaker:have looked at that.
Speaker:We try to do everything, always remember,
Speaker:everything is metabolized majority in the
Speaker:mitochondria, the cytoplasm.
Speaker:So once you understand these metabolic
Speaker:pathways, you know how to keep your
Speaker:mitochondria as healthy as possible,
Speaker:which will make you, because ultimately
Speaker:you're interested in
Speaker:avoiding chronic disease.
Speaker:That's it.
Speaker:You don't want chronic disease.
Speaker:You don't want cancer.
Speaker:You don't want chronic disease.
Speaker:How do you prevent that?
Speaker:Keep your mitochondria healthy.
Speaker:How do you keep your
Speaker:mitochondria healthy?
Speaker:Keep glucose down and
Speaker:elevate ketones, the mitochondria.
Speaker:And I don't have time to talk, but in our
Speaker:new paper, we talk about the
Speaker:bioenergetics of burning fatty acids,
Speaker:ketone bodies, and pyruvate.
Speaker:The bioenergetic related to the delta G
Speaker:prime ATP hydrolysis.
Speaker:And how we can get
Speaker:more bang for your buck.
Speaker:Every breath of air can give you more ATP
Speaker:when you're burning ketone body than when
Speaker:you're burning pyruvate or fatty acids.
Speaker:So we know the bioenergetics.
Speaker:We published that.
Speaker:And our big paper is going
Speaker:to be coming out on that.
Speaker:And we got all that from the late Richard
Speaker:Veach, one of the great, and he was Hans
Speaker:Krebs' last graduate student.
Speaker:So he and I would talk for hours and
Speaker:hours and hours about all the
Speaker:bioenergetics of mitochondria and what
Speaker:you need to keep it
Speaker:healthy and functional.
Speaker:So there's a strong bioenergetic
Speaker:explanation for a lot of what I'm saying.
Speaker:And that's in our papers.
Speaker:We'll definitely be sure to
Speaker:link them in all the show.
Speaker:Yeah.
Speaker:Make sure, yeah.
Speaker:Tell folks that all of
Speaker:our papers are open access.
Speaker:So anybody with a
Speaker:computer can get the information.
Speaker:Now people are going to be overwhelmed
Speaker:and say, oh my God,
Speaker:Seifree published so many papers.
Speaker:Yeah.
Speaker:Well, a lot of it's on
Speaker:what I'm talking about.
Speaker:A lot of it's on other things.
Speaker:But you can go through and
Speaker:ferret out what we're doing.
Speaker:And people need to know that all of our
Speaker:research is supported by philanthropy and
Speaker:private foundations.
Speaker:So when we keep people
Speaker:alive who are stage four cancer,
Speaker:they so-called terminal.
Speaker:And all of a sudden you're living a lot
Speaker:longer with a higher quality of life.
Speaker:Some people feel very compelled to donate
Speaker:to our research because they
Speaker:want to.
Speaker:And one thing I want to make sure, never
Speaker:say we have a cure for cancer.
Speaker:Because I have no clue whether what we do
Speaker:will cure cancer or not.
Speaker:The only thing that we have seen over and
Speaker:over again is we have a longer
Speaker:progression-free survival without
Speaker:symptoms and a very increased overall
Speaker:survival of cancer patients.
Speaker:Whether they're cured
Speaker:or not, we don't know.
Speaker:But I consider success in keeping people
Speaker:given terminal diagnosis alive far, far
Speaker:longer than what the establishment
Speaker:predicted their lifespan to be.
Speaker:So I never like to use the term terminal
Speaker:because I have a lot of people that I
Speaker:know who are still alive.
Speaker:I don't know.
Speaker:Sometime in the future they may be
Speaker:terminal, but they're not dead yet and
Speaker:they're pretty healthy.
Speaker:So what the hell does that mean?
Speaker:And they were told they only had nine
Speaker:months to live and
Speaker:they're around six years.
Speaker:Who made the mistake there?
Speaker:Why was someone told they have six months
Speaker:or a year to live and they're living five
Speaker:and six years or even longer?
Speaker:How did anybody make
Speaker:that level of mistake?
Speaker:They made the mistake because they don't
Speaker:understand metabolic therapy and how long
Speaker:you can possibly live with
Speaker:a higher quality of life.
Speaker:But whether you get a
Speaker:cure or not, I have no clue.
Speaker:All we know is we have a new strategy for
Speaker:managing cancer and chronic disease that
Speaker:is far more powerful and successful than
Speaker:anything out there right now.
Speaker:The problem is people just don't know
Speaker:about it and don't know
Speaker:how to implement it yet.
Speaker:And that's going to take
Speaker:that will be the future.
Speaker:That will be down to people like us,
Speaker:aiming to educate the greater public.
Speaker:Dr.
Speaker:Seifried, thank you
Speaker:so much for your time.
Speaker:For people who are interested in your
Speaker:work and to learn more about your various
Speaker:metabolic therapies,
Speaker:where can we point them to?
Speaker:Well again, I have my metabolic papers
Speaker:already published, open access.
Speaker:And donations go to Travis
Speaker:Christofferson's Foundation
Speaker:for Cancer Metabolic Therapy.
Speaker:It's a legitimate foundation.
Speaker:And the university, Boston College
Speaker:itself, the biology department for sure.
Speaker:So that keeps us going and we've got a
Speaker:couple of blockbuster things coming out
Speaker:that are really going to transform the
Speaker:healthcare industry dramatically.
Speaker:And they'll be out within the year.
Speaker:And then you're going to see
Speaker:organizations set up around these
Speaker:approaches for metabolic health.
Speaker:And we're going to bring a lot of people
Speaker:back into what we call normalcy,
Speaker:metabolic homeostasis, if they want to.
Speaker:I'm not twisting anybody's arm here.
Speaker:It's only if people who want to, if they
Speaker:want to live in a toxic
Speaker:state, that's their choice.
Speaker:But we have a tool now to allow them to
Speaker:come out of those toxic states and live a
Speaker:healthy, productive life with a clear
Speaker:quantitative assessment to do that.
Speaker:And that is coming down and you'll see
Speaker:that within the next
Speaker:year or two, for sure.
Speaker:So we're very hopeful for
Speaker:managing chronic diseases.
Speaker:And I think most people are going to be
Speaker:very appreciative as they begin to
Speaker:benefit from what we're doing.
Speaker:No, I'm sure they're well.
Speaker:I mean, ultimately, I think most disease,
Speaker:the way I'm starting to view it, it
Speaker:ultimately comes down to sort of removing
Speaker:the environmental burden or whatever
Speaker:environmental trigger there is as driving
Speaker:the disease, improving the metabolic
Speaker:health and subsequent treatment,
Speaker:mitochondrial health, and then dealing
Speaker:with the stress component, which is also
Speaker:obviously overlooked.
Speaker:And I think when you get those three sort
Speaker:of components sort of dialed in, you sort
Speaker:of solve 90% of the equation, at least
Speaker:when it comes to chronic disease.
Speaker:Which is mostly
Speaker:crippling Western societies.
Speaker:Yes.
Speaker:So it's the single most biggest problem.
Speaker:Cancer and chronic diseases are dementia,
Speaker:type 2 diabetes, obesity,
Speaker:cardiovascular disease, cancer.
Speaker:You can go right down the list.
Speaker:It's just like everything.
Speaker:So what do we do with all these healthy
Speaker:people if they will...
Speaker:We're keeping a lot of people alive,
Speaker:working for a longer period of time with
Speaker:a high quality of life.
Speaker:I mean, you're going to have to have a
Speaker:readjustment of society.
Speaker:Yeah.
Speaker:Well, let's aim to get there and then we
Speaker:can do what that problem arises.
Speaker:Yes, absolutely.
Speaker:All right.
Speaker:Well, listen, thank you very much.
Speaker:Thank you, Dr.
Speaker:Seifried.
Speaker:It's been an absolute honor and I
Speaker:appreciate your time.
Speaker:Yeah.
Speaker:Well, thank you. I'll
