48. Dr Laszlo Boros: Critical link between dietary Deuterium, Visceral Fat and Metabolic Diseases

Episode Transcript
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Dr Max Gulhane (00:53):
Today I am speaking with Dr Laszlo Boros.
He is a former professor ofpediatrics at UCLA, a research
scientist and world expert ondeuteronomics.
Deuteronomics refers to thestudy of deuterium, the heavy
isotope of hydrogen, and how itinteracts with biological
systems.
This is an almost two-hourtechnical interview in which we

(01:13):
delve deeply into the role ofdeuterium in causing metabolic
disease and the deposition ofvisceral fat.
Dr Boros takes us down to thelevel of the mitochondrion and
explains exactly how foodsenriched in deuterium, such as
processed carbs and seed oils,contribute to metabolic
dysfunction by wrecking theATPase nanomotors in the inner

(01:34):
mitochondrial membrane.
While we talk a lot aboutmechanisms, we also discuss some
practical steps, so you willalso find out why fully
grass-fed beef fat is theoptimal human energy source.
This is a topic that I continueto learn more about, but, based
on the information that DrBoros and previous guests, dr
Jakruz and Sarah Pugh havepresented, it makes a very

(01:57):
strong case that metabolicdisease is a problem of excess
deuterium.
Carnivore, low carb andseasonal ancestral diet are
effective in reversing obesity,insulin resistance, diabetes and
all these metabolic diseases,precisely because they are low
deuterium diets.
So let me know what you thinkabout this and hope you enjoyed
the show.

(02:19):
Dr Lazlo Boros.
Thank you for coming on thepodcast.
Thank you very much forinviting.
So I am a family medicine doctorand I am interested, amongst
other things, in how we canprevent metabolic diseases like
obesity, like type 2 diabetes,fatty liver, all these kind of
things.
And your research and yourperspectives using deuterium are

(02:43):
fascinating because I think itcan offer us a lot in terms of
insight into these problems.
But, maybe because this is sucha niche topic and it is
sometimes quite technical, Ithink it's worth starting from
the very beginning and in termsof explaining people what
deuterium is, before we even godown the rabbit hole of clinical

(03:05):
implications.

Dr Laszlo Boros (03:06):
Sure, thank you again.
So deuterium is practically theSUV in your driveway or in your
garage where you can fit yourpassenger car any longer.
So it's a hydrogen.
And that's the beginning ofthis whole story.
Carbon and oxygen make up theliving organisms as the most

(03:28):
common atoms or elements.
Hydrogen is the smallest of alland it helps to transfer energy
and also provide chemical bondsbetween oxygen and hydrogen and
nitrogen and sulfur and so on.
But the most common ones arecarbon, oxygen and hydrogen, and
hydrogen is the ping-pong barthat oxygen and carbon is

(03:50):
playing a ping-pong game.
In the meantime, obviously,photosynthesis and biological
oxidation are connected tohydrogen itself and practically
deuterium is the heavy or thelarge medicine bar in the
baseball game, in the sense thatso practically it's a heavy

(04:15):
hydrogen, hydrogen.
The nucleus of hydrogen is aproton, is made up by a proton
and there's an electron spinningaround it, and the deuterons or
deuterium, is a proton and aneutron and an electron, meaning
that the nucleus of thedeuteron is twice as heavy and

(04:37):
twice as large as the proton andchemically behaves different,
meaning that in chemical bondsit requires 8 to 15 times more
energy to remove that wherehydrogen would be placed.
If it's replaced by deuterium,then the chemical behavior of
the molecule is dramaticallydifferent, involving metabolism

(05:00):
and so on.
More importantly, deuterium canget into mitochondria and ATP
synthase nanomotors, where theyactually behave like a boy in a
china store or elephant in achina store.
Practically they break thesevery delicate moving proteins

(05:20):
and nanomotors and, for thatmatter, there are going to be a
lack of T-C cycle orKrebs-Sendier-D-Cycle metabolism
, meaning that there's going tobe a molecular or metabolic
crowding and, because the lackof proper mitochondrial function

(05:44):
to burn fuel completely, thereis going to be a buildup of
various organic molecules,including fatty acids, glucose
and so on, and metabolicdiseases develop and, based on
the specific tissue presentation, human diseases develop

(06:05):
depending on what kind ofmetabolic and how severe the
metabolic defect is or howdamaged the mitochondria are and
their nanomotors because ofdeuterium effect, which is again
twice as heavy and twice aslarge.
When we look at its nucleus,then hydrogen is, and hydrogen

(06:26):
is the most common element inour system, in our body, and it
works and it performs most ofthe work as far as energy
transfers and structuralchemical bonds.
And replacing hydrogen withdeuterium has major effects on
protein structure, proteinmovements and so on and the
activity of metabolic enzymesand the result of all of these,

(06:51):
we develop various diseases,disease processes that you have
to handle in your familypractice.

Yeah, thanks for that explanation and just to
zoom out and really keep a bigpicture before we delve into the
weeds the mitochondria forthose who are listening are
these little organelles insidealmost all your cells that are
the sites of energy productionin the cell.
And what Dr Lazer was talkingabout is that these mitochondria

(07:22):
take energy inputs in the formof food and they also receive
the cytochromes, or can alsoreceive a light frequencies, and
they tunnel electrons from thefood and use it to pump these
hydrogens against a gradient.
So imagine pumping water uphilland then at that fifth, the

(07:43):
fifth cytochrome of thatelectron transport chain.
They're supposed to flow downthis gradient like the water,
supposed to flow down a hill andrun through this nanomotor and
then allow us to make ATP fromADP.
But what Dr Borosz justexplained to you is that if we
use this heavy isotope ofhydrogen instead of H+, if we

(08:04):
use a deuterium, then thatbasically wrecks the ability of
that nanomotor to spinefficiently.
And I talked to Dr StephanieSenef andI like to.
Someone used the analogy of afat kid going down a slippery
slide at a water park and kindof getting stuck in the middle.
But it's really more than thatbecause, as you've talked about

(08:27):
it, it's not only blocking thenanomotor from spinning and
therefore preventing us fromoperating efficiently, but it's
actually destroying the ATPase.
Is that correct?

That's right.
And it's not only a destructionbut it's also a permanent
chemical bond of these protonspinning amino acids.
That means it's irreparable asfar as the damage is delivered.
And once these nanomotors stopfunctioning, we cannot transfer

(08:59):
protons from carbons to oxygen.
And if that occurs, then ourcellular level energy production
system is diminishedpractically and those cells
become a target of apoptosis, orinformation for that matter,
and those cells, because ofcytochrome C, which is part of

(09:21):
the electron transport chain,signal for self destruction.
Simply, that's what the organdisease or organ damage and
chronic disease would actuallyline up.
There's practically dying cellsreplaced by fibrotic tissue or
inflammatory tissues and so on.

(09:41):
And because of the lack oforgan function or the lack of
your cellular functions thathave these organs to perform
certain functions that could betransport of certain metabolites
, it could be storage of certainorganic materials, fatty acids,
glucose, glycogen and so on,these cells are missing their

(10:05):
functions, these cells arereplaced by fibrotic or
inflammatory tissues and thenorgan damage sets in and chronic
diseases develop practically.

Yes, and I really like that framing because
it gives us a framework ofunderstanding how things going
wrong at the basically submolecular level can end up
manifesting as a disease in theentire organism.
And I think it's a great placeto make a quick mention of Dr
Doug Wallace and he's basicallytheory of the mitochondrial

(10:36):
bio-energetic etiology ofdisease, which is exactly what
you're talking about.
And Dr Doug Wallace has madethe point that the mitochondrial
dysfunction, when that happens,when the mitochondria start
failing, the energy output ofthe cell obviously fails the
cell's ability to do its job,whether that's contract as a
cardiomyocyte, whether that's tomake insulin as a pancreatic

(10:59):
beta cell, whether that's totransmit a signal as a neuron in
the brain.
That fails when themitochondria inside the cell
start failing.
So it's interesting becausewhen that mitochondrial
efficiency drops, then thingslike DNA repair, the
mitochondrial DNA repair, allthese processes start impeding
and then you get this kind offeedback or this process, this

(11:23):
cycle that leads to that leadsto apoptosis and basically
failure of the cell.
Are you familiar with DrWallace's work?
Are you up to speed with that?

I did hear about many of these efforts.
The new way of looking atenergy production in
mitochondria is not only ATPsynthesis.
The deuteronomics or the studyof deuterium in mitochondria is
changing every day, simplybecause there's so much data and
information coming in.

(11:54):
And right now what we areworking on is extending the
energy production scenarios inmitochondria, not only looking
at ATP, but the actual formationof metabolic water, which is
how oxygen and hydrogen cometogether after these nanomotors

(12:14):
are power.
Now protons are necessary forwater formation from food and
the result of this is 280 kJ permole energy in the form of heat
when metabolic water is formingthe mitochondria.
In the meantime, there is anadditional 20 to 30 kJ per mole

(12:37):
energy producing the form ofATP-ATP synthesis.
But practically the majority ofheat energy that is produced in
mitochondria is because of theelectron transport chain
activating oxygen and the protonthat falls into the
mitochondrial matrix afterpowering these nanomotors, and

(12:57):
this is what we call theexplosive gas when oxygen and
hydrogen joins together.
But it's very controlled andvery precisely controlled in the
mitochondrial matrix to theelectron transport chain and
those proteins or cytochromeenzymes.
Practically it's a verydelicate, controlled, highly

(13:22):
energy yielding process byproducing metabolic water and
also by producing ATP in theprocess.
And they all depend on thesesmooth work of these nanomotors,
because those are the ones thatare able to transfer from the
inter membrane space of themitochondria, the protons, into
the mitochondrial matrix.

(13:42):
The metabolic water is formedand in the meantime that the
Crap San Diode cycle isabsorbing or recycling this
metabolic water to fumaratehydrates and citrate synthesis
and so on.
So it's practically physicsconnected with biochemistry
tunneling, which means that oneof the nuclear atomic events

(14:07):
linked with biochemicalreactions.
So it practically covers allthat is related to what we know
quantum physics andelectromagnetic radiation and
biochemistry.
And this is why so many peoplework together on these scenarios
, simply because these includeand involve all major parts of

(14:31):
physics and biology, as you know.

Yeah, and for the listeners who have followed
my work up till now, we exploredthese concepts in the first
instance with my series with DrJack Cruz and essentially how he
described what is going on inthe mitochondria are oxidative
phosphorylation is the oppositeof photosynthesis and this idea
that you know it's like a spideron a mirror doing push-ups it's

(14:57):
this process, that what'shappening in the mitochondria is
just a reversal of thephotosynthetic process, and the
output of what we've describedis obviously ATP, but it's more
than that.
It's carbon dioxide and it'sthis metabolic water, and the
unique idea of the metabolicwater is that it's deuterium,
depleted.
I think that is the key pointand summarizing what we've

(15:18):
talked about in the first set.

It's important matter.

Deuterium free.
Yeah, it's got no deuterium init.

What we desire is that the outside is 155 ppm
and the most inner part of yourcells are deuterium free and the
gradient goes in and betweenthrough various filtering
biochemical mechanisms.
And this is what practicallybiology or medicine should be,
as far as understanding verybasic principles and concepts in

(15:47):
energy production for thatmatter.
But we prefer the least amountof deuterium in mitochondria to
prevent diseases, diseaseprocesses.

Yeah, and it's interesting because I guess we
previewed in the first 10minutes.
The biology has evolved very,very specifically to preclude
deuterium from the whole processof energy generation.
I think that's the point thatyou've made so far.
If people can understand thatconcept is that for the cell to

(16:19):
operate optimally, we don't wantthis heavy hydrogen in the
whole process.
And whether we use the analogyof the SUV trying to fit into a
small garage, whether we use theanalogy of the eight ball I
heard you use that analogy therethe Q ball, the big eight ball
that doesn't fit down the hole,whatever analogy you want to use

(16:40):
, and I think the key takeawaypoint for the first part of this
interview is that biologydoesn't like deuterium.
And even though deuterium ispresent naturally in 155 parts
per million in the ocean and inthe environment, there's been
specific reasons why we haveevolved to not have deuterium
inside the, in a mitochondrialmatrix.

That's right and we need to consider
deuterium as a structuralelement.
So some structural proteinslike collagen, proline
deuterated prolines are veryimportant for animals that live
in harsh conditions, under harshconditions in environments.
So in structural proteins andthis is why we now talk about

(17:24):
the regulation of deuteriumDeuterium has no place in moving
proteins, energy production orenzyme reactions and so on,
especially when tunneling comesinto the picture.
Now, in structural proteins, invery small amounts, in certain
amino acids, deuterium is a veryimportant stabilizing element

(17:47):
and, for that matter, it can behigh, as high as as a 315 parts
per million in cell collagen,simply because those animals
have to dive and come up at veryhigh speed and they have to
escape from predators and so on.

(18:08):
So their structural element,their skeletal elements and
their collagen have to bemodified chemically to these
demands.
So now we actually use energyproduction, covering
mitochondrial and proxysomalmetabolism and how they

(18:28):
interrelate to one another.
That's a new aspect of deuteriumresearch and we may cover this
in this conversation, based onhow deep you want to dig in to
this process.
And for the structural elementsof our body, we need to

(18:48):
regulate deuterium according tothe need of how stable and how
structurally durable thoseelements need to be.
So we are looking at inbiological samples from zero
parts per million deuterium,which is the mitochondrial
matrix, up to 315 parts permillion, which is the collagen

(19:10):
proline of under challengingliving conditions and
environment.
So in between there's thishuman deuteronomics project
where we actually use thesevarious wide range deuterium

(19:31):
distributions to explainphenotype and to explain disease
processes, because what webelieve is human disease is a
tissue specific presentation ofa deuterium overload or a
deuterium dysregulation process.

Yeah, and if we think about the two major causes
of human chronic diseases, it'sneurodegeneration, like
dementia and Parkinson's disease, and cardiovascular disease.
So heart failure,atherosclerotic cardiovascular
disease, and I don't think it'sno surprise or it makes sense,
because these two tissues aresome of the most mitochondrial

(20:10):
rich tissues in the organs inthe body and the heart, having
between three and five thousandmitochondria in every
cardiomyosite.
It makes sense that if we'regetting failure of mitochondria
in those organs then that in along enough time frame is going

(20:30):
to manifest as disease.
I want you to just talk acouple more instances of the
physiological role of deuteriumin the body.
So we've already establishedthat it can't be in moving parts
in energy generation inside themitochondria, but it might be
useful and it is useful instructural components like
collagen.
Is there an in between herewhere the body is also using

(20:52):
deuterium physiologically?

Well, it depends on the species and the
challenging conditions.
And this is actually a paperfrom the Collinska Institute by
Dr Roman Zubarev, who measureddeuterium in seal and pellet
green falcons and swan collagenand he found a huge variation

(21:17):
based on how challenging theseanimals live their everyday
lives.
The swan, which just kind ofswims around the lakes and eats
some plants they have 155 ppm intheir collagen.
Obviously their life is notvery demanding or challenging

(21:41):
compared to seals and pelletgreen falcons.
The pellet green falcons, theycome down at 300-400 km per hour
and they have to slow downusing their wings in the last
40-50 meters of their of theirdiet, so that actually puts
their wings under extremefriction forces and so on.

(22:03):
So they have to develop acollagen, a protein that
actually helps their bonestructure to do to deal with
this very demanding frictionalforce.
To be able to do that it takesdeuterium up to the range of 300
parts per million.
In the meantime these animals,because they fly so fast and

(22:27):
they have to climb so fast to dobefore these dives, their
muscles have to be deuteriumfree, for that matter, than
animal rules, meaning that theirglycolysis is controlling
food-based deuterium to get intometabolic or cytoplasmic water
through isomerase reactionsthese are actually glycolysis

(22:50):
related enzyme reactions whereactually deuterium
discrimination effect and thisdiscriminated deuterium can be
loaded in some other parts ofthe body or biochemical
reactions, for example proteinsynthesis and hydroxy protein
synthesis, which will make thesecollagen proteins and it's

(23:12):
unique to this proteinstructural protein, and cancer
cells like to use this hydrodeuterium protein as well.
So this is why the cancer, themalignant tissue's trauma is
when you touch it.
You probably in medical schoolyou had to rotate in surgery
oncological, surgical, surgicalsurgical units and you can

(23:33):
actually tell by touching tumorsthat they are almost like bone
or cartilage type tissues andthat's because they accumulate
deuterium in their stroma and intheir structural proteins.
So it seems that knowingdeuterium or being aware of how

(23:54):
deuterium is distributed amongspecies and also in tissues, you
can actually describe a verycritical biological behavior
type of situations and you canargue based on deuterium content
, what to expect from thatparticular tissue, how to
operate in our body.

That's a fascinating point.
I want to just make two quickpoints.
One is that the body is if youlook at the TCA cycle and for
anyone who's taken chemistry,whether that was in school or in
university, there's a long listof enzymatic steps that are
involved in the whole process,and it seems to me, and what

(24:41):
you've talked about in yourlectures, is that the reason for
those steps is because the bodyis selecting for proteam over
deuterium in terms of thoseenzymatic reactions.
So is that the chief reason whythere are so many enzymatic
steps?
Is it solely to select againstdeuterium in the mitochondria?

That's correct.
I actually gave talks aboutthis at UCL back in 2017 and
2018, talking about glycolysisbeing a deuterium scavenging
mechanism, a deuterium sortingmechanism through water exchange
reactions and proton exchangereactions from cytoplasmic water

(25:23):
, which should be diluted bymatrix water to be low in
deuterium so you can actuallyexchange deuterium between
compartments of your cells.
And that's right.
Glucose, for example, has 12hydrogens and glycolysis have 10
reactions and one of thosereactions in a lace takes a

(25:46):
whole water molecule out ofglucose.
So practically what glycolysisdoes?
It checks every hydrogen in aglucose molecule and replaces it
with cytoplasmic waters protonsto make sure that there is no
deuterium can actually enter themitochondria as using glucose
as a trojan horse.

(26:07):
So practically it's adisassembly of the trojan horse
to see what's inside and thenreassembling it to take it to
the mitochondria.
And the mitochondria ishydrating the precursors, which
is pyruvate and acetylcoenzyme A, and it adds metabolic water

(26:28):
through citrate synthase,through aconitase and through
fumarate hydratase as the waterconsuming reactions.
But in reality every 99.9% ofevery enzyme reaction in our

(26:48):
body uses water as the chemicalsolvent or water protons to
perform that particular reaction.
So every reaction in glycolysisand every reaction, nine
reactions of thecrepseniodicycle or the TCA
cycle, use water for that matter.

(27:09):
So water deuterium content andwater deplete it.
Deuterium deplete a water inchemical reactions is a key for
those reactions to operate.
So even though the moleculeitself does not have or not
necessarily deuterated, if thewater of our system is

(27:31):
deteriorated then thosereactions also again slow down.
So deuterium goes far fartherthan we would expect.
Just simply looking at exchangereactions, it is actually kind
of the medium or the chemicalsolvent water, and that's why

(27:53):
our body is made up of so muchwater, because we have to
provide a solvent base for allthese chemical reactions,
biochemical reactions.
And if those are not in adeuterium or low deuterium
environment depleted or lowdeuterium environment or
deuterium free environment, ifwe talk about the matrix those

(28:14):
can cause chronic diseases andthey can actually, if it's food
based, the deuterium overload,then it can actually cause
epidemics of chronic diseases inpopulations that consume the
kind of the bad food or diet.

Yes and I use this analogy with Dr Senef is
the fascinating way that thebody has evolved this checking
process which you've justdescribed.
It's almost like you're burninga furnace with timber, but
you've evolved this intricateinspection process of the logs
and unless the log is perfect,the body is going to discard

(28:54):
that and it's not going to allowthat log to go down and get
burnt in the furnace becauseit's that important to the
function of the factory which isthe mitochondria.
That mitochondrion is thatthose logs are just the right
thing.
If it's got a branch stickingout the wrong way which is an
analogy for deuterium then it'slike no, sorry, we don't want
that.
It's a great point, sorry, goon.

And this is very important from the
tunneling point of view, becausein our system everything
happens by tunnel, meaning thatthose very tight enzymatic
reaction compartments, they onlycan achieve chemical reaction
to occur at especially suchspeed if actually those protons
are pushed around physically byother protons and if there's a

(29:39):
deuterium in between, if there'sa log that stands out in
different, like as is supposedto, it can actually stop the
whole process.

Yeah, and that's a great place to talk about
fats, because glycolysis is aprocess of checking these
carbohydrates for deuterons.
But what is unique about thefatty acid molecules that make
them problematic for thisprocess?

Fatty acids are produced from citric acid,
which are formed in mitochondria, so they are low in duty.
That's why fatty acids don'thave to go through glycolysis,
because our cells expect fattyacids to be low in deuterium, so
for oxidation they areappropriate, meaning that they

(30:24):
can be taken into themitochondria, into the cell, and
into the mitochondria to thiscarnitane transport proteins
without checking every proton orhydrogen in those molecules, if
those are deuterium or not, oryou don't have to replace them
with your metabolic waters.
Low deuterium protons, sopractically fatty acids.

(30:46):
Because nature or the creator,I like to use both to kind of
help everybody to imagine howthis system work practically.
They it's designed, or thesereactions are designed to kind
of work with a very efficient,very effective deuterium

(31:08):
depleting mechanism when it'snecessary.
Yet if there's a perfect fuel,for that matter it's animal
based, grass-fed, carnivorestyle, animal saturated long
chain fatty acid which is verylow in deuterium, in the range
of 110 ppm compared to 155 ofglucose.

(31:31):
That's safe to use for bothproxysomes and mitochondria and
for that matter, your body hasvery quick access to those
because those don't have to bechecked.
They are actually in the 100meter sprint run, they just run.
There are no blockages orthere's no gaze that they have
to hump over, and this is whythose are very efficient fuels.

(31:57):
Saturated animal fat, grass-fedanimal fat, is so efficient fuel
for our cells and for ourmitochondria because those are
low in deuterium and your cellsare able to scavenge that
smaller amount of deuteriumusing the ureocycle, using

(32:17):
various water exchange reactionsin the mitochondrial, in the
TCSAC and so on.
So our biochemistry is designedbased on deuterium intake and
deuterium scavenging and alsoefficiency based on oxygen
availability and oxygentransport.
So practically it's astoichiometric method simply

(32:39):
just to deal with the right,appropriate balance of these
systems and mechanisms thatinclude food, water or nutrients
that we take in oxygenavailability and mitochondrial
processes to actually burn andmake these exchange reactions,

(33:01):
atomic reactions, efficientwithout the participation of
deuterium itself.
So it's practically the key tohealth to understand these
processes and it's the key tomanage chronic disease epidemics
and so on and to treat patientsindividually using natural

(33:23):
patek or natural approaches thatactually limit the deuterium
intake through the appropriatefood incorporation.

Yeah, and I'm glad you brought up the
grass-fed meat and fat and we'llactually talk about that a bit
later.
I'll just make a quick flag andseed oils which are
polyunsaturated fatty acids richin fatty acids, like linoleic
acid.
Are they deuterium enriched?

At unsaturated bonds.
They are very low in deuteriumbased on where they are from.
If they are actually natural orindustrial source, they could
have very different variationsor very different levels of
deuterium.
If those are plant-based andseed oil and those are not

(34:14):
industrial, gmo or fertilizer orglyphosate treated plants,
naturally those could be forcertain species.
Those could be not for humans,but for certain species those
could be useful substrates.
Their microbiome have to beadopted to the food that they

(34:37):
consume.
It can be even fruit-based incertain birds.
That's when they have a veryhigh turnover of microbiome, for
that matter.
But let's say this way theypoop a lot.
But practically as far ashumans are concerned, we are

(34:59):
designed to eat animal fat,saturated long chain fatty acids
, preferentially coming frombone marrow.
This is what we believe.
The prehistoric menanthropologically started
consuming brain and bone marrowof animals, carcasses that were

(35:22):
left behind by predators,because they had tools to break
through the bony skeletalstructures.
Our species or our societies,going back to caveman's time,
prehistoric time, were alldependent on this saturated

(35:43):
loaded-tium animal-based,grass-fed fat source.
This is how mitochondriaadopted to the food and
environment.
But prehistoric men lived inand the cavemen lived in.
It's only since the industrialagricultural processes set in is

(36:08):
when chronic diseases occurredas we know, now More food items
are replaced on the shelf byprocessed industrial food items,
more severe chronic diseaseepidemics are.

Yeah, great, we'll come back to that because
I want to delve into that a bitdeeper Before we finish.
On this idea of physiologicaland partitioning of deuterium in
the body, you've mentioned thatin your slides.
That deuterium is present inthe serum at around 12
millimoles, which is higher thanthe other ions in the body.

(36:49):
Is the body specificallykeeping deuterium there, or
explain to us the role ofdeuterium specifically in the
blood?

Actually it's a lot higher because if you look
at potassium, eukacium or otherinorganic elements, those are
actually one tenth or one fifthof the concentration of
deuterium.
Deuterium is very common andvery abundant in circulation

(37:21):
simply because there are so manywater and hydrogen based
molecules circulating andpractically this is how the body
gets rid of deuterium throughcirculation and kidney function
urine, saliva, sweat and poopand so on.

(37:43):
So practically our plasma iswhere the first significant
deuterium exchange occurs, inred blood cells which use
glycolysis to produce lacticacid and in the meantime they
keep these NADP moleculesreduced because they have to

(38:04):
overcome the effect of oxygen,so they have to have reducing
equivalence.
So this glycolysis that takesplace in red blood cells, very
high flux, provides lactic acidwith high deuterium.
That gets into the liver andthrough the core cycle it's
returned as glucose.

(38:24):
But in athletes there's avermicillin bacteria that starts
using this high deuteriumlactic acid to produce propionic
acid, which is a ketone body.
It's a low deuterium containingketone body which can actually
replace the core cycle todeplete the deuterium very
efficiently and because of thehigh water content of the plasma

(38:49):
, which is 99.
Above percent, deuterium matchespractically your body's ability
to deplete deuterium by gettingrid of through circulation of
deuterium, mostly by dissolvedurea and uric acid.

(39:11):
So simply, these are all partof a very complex biochemical
process, but very simplebiochemical process.
If we just talk about deuteriumdepletion and overcoming
deuterium, overloaded tissuesand it's definitely the most
abundant inorganic element inour blood and it should be

(39:31):
measured just like everythingelse or anything else in the
plasma.
If you go to a lab study or aclinical or diagnostic panel of
blood work, then those inorganicelements are part of your
history and that's how deuteriumshould be approached to measure

(39:56):
it in blood and in other fluidor liquids, for example you say
at breath, which gives you abetter idea of how much
deuterium is returned from yourtissues into the circulation.
And by those ratios you cantell how efficient your body is

(40:16):
able to separate deuterium fromprotons or proteome and how to
actually keep your tissues ortissue level operations in the
loaded tube range.

That's interesting and the usual reason
in medicine why an assay isn'tperformed or a test isn't
performed is because themainstream clinician doesn't
know what to do with it, withthe result, and the rule of one
of the rules in medicine isdon't order a test that you
can't interpret.
A classic example of this is afasting insulin level, which is

(40:52):
a very easy way to give aninsight into someone's metabolic
health, and a higher fastinginsulin level can give insight
into the development of insulinresistance well before the blood
glucose level starts arranging.
But I imagine that no oneorders a serum deuterium because
the implication of a high levelis that we need to be going

(41:14):
through a lifestyle change thatyou've previewed for us, which
is specifically consuming foodsthat are low in deuterium.
I'm guessing I've never orderedthis and I'd be interested in
the interpretation of it but I'mguessing that if someone has a
high serum deuterium, then thatis just representing is it
correlating well to whole totalbody deuterium level, and that

(41:36):
implies that they need to bedoing these lifestyle measures.
Yeah.

I'd say in between, it's what you consume
as far as food is concerned, howhard your microbiome is or what
kind of microbiome componentsor composition you have, and
also your age, your sleepingpatterns, your ketosis versus
glucosis, your daily activitiesand also your underlying disease

(42:06):
processes.
They all impact on blooddeuterium levels.
So for just to dig out exactlyhow those relate to diseases,
you also want to do a what wecall the organic acid test from
urine where you can actuallycheck on the TCA cycle
intermediates to see how yourmitochondrial branch out, the

(42:31):
TCA, the senioric rapps, cyclehigh branches out of organic
acids.
Meaning that you can interpretyour data based on mitochondrial
functions as far as deuteriumlevels are concerned.
And then you would ask thepatient what kind of food,
what's the source, what they eat, where they get their food, how

(42:52):
much water they drink and fromthese components.
If you do this with somebiochemical knowledge then you
can kind of pinpoint to variousproblems in lifestyle
consumption of certain fooditems, the sources and age

(43:15):
related, sleep related andlifestyle related issues.
So eventually you can and youwould be able to interpret the
data very efficiently and withspecifics of how and what kind
of diseases to expect and how toovercome those and usually when

(43:38):
I get questions about what doyou know levels they should or a
patient should reach, I usuallystart by just simply asking
them of what their nutritionaland what their source is,
because usually that's the firstobstacle that you have to

(44:00):
overcome of how to deal withcertain lifestyle and food
related issues to preventchronic diseases and to treat
efficiently chronic diseases andeventually to provide a better
life expectancy and also abetter life quality for those

(44:21):
patients, especially obesity,diabetes and cancer.

Yeah, great.
And let's pivot now and talkabout this idea of metabolic
disease, because essentially, asfar as I'm conceiving it, so
many of the preventableconditions that are putting
people in nursing homes stemfrom metabolic dysfunction,
insulin resistance, and they'reall tissue specific

(44:46):
manifestations, whether that'scardiovascular disease, whether
it is dementia, or whether allthese problems come down on a
hormonal level to insulinresistance.
But on a mitochondrial level,it's dysfunctional mitochondria.
I like to look at things likethe presence of ectopic fat or

(45:08):
visceral fat that is evenpredating or anti-seeding the
development of a raised fastinginsulin.
I want to ask you about acritical thing that's been on my
mind, which is is the presenceof ectopic fat, which I guess
they're spilling over of energyoutside physiological white

(45:28):
adipose depose?
Is that a fundamentally aproblem of excess deuterium?

Yes, and it becomes more clear if you think
about this process, what we callmetabolite or molecular
overcrowding, because anyparticular accumulation process
amyloidosis, glucose, fat theyall indicate a problem with

(46:01):
complete sub-shape oxidation,where the products are carbon
dioxide, water and energy.
This is what your Formula Onerace car engine does.
It burns fuel very efficientlyat high rpm, delivering
incredible force.
For that you have to tweak itand very precisely you have to

(46:22):
kind of adjust all the intake ofthe exhaust parts and very
efficiently you have to bring itinto a highly precisely
calculated manner that your bodycan actually do if everything
works fine, meaning that ifthere's ignition and there's
sufficient exhaustion, you canactually load or you can

(46:46):
actually perform in thosemitochondria more efficiently,
much more efficiently if yourdetune is low, if your
nanomotors are spinning at highrotation, your metabolic water
formation efficient, your TCcycle is able to produce carbon
dioxide, which is the optimalgas form of any burning or

(47:09):
biological oxidation process.
If this set of reactions isblocked anywhere, that could be
mitochondria, that could bemitochondrial nanomotors, that
could be oxygen delivery, thatcould be the electron transport
chain.
Not enough light, not enoughnatural light, not enough

(47:33):
exposure to red light, for thatmatter.
You actually diminish thesemitochondrial functions.
So there is no complete subshade oxidation which results in
carbon dioxide and you can justkind of exhaust like in a
exhaust pipe through your breath.

(47:55):
Practically you can exhale.
If these steps or if thesereactions are diminished, then
metabolic crowding or metaboliccrowding steps in and you have
to store those molecules untilthey break down and a certain
body compartment it could bevisceral fat, it could be

(48:16):
compsive fat, it could be fattissue itself, it could be
excessive glycogen, it could beexcessive protein of any sort
based on tissue specifics.
But it's practically a part ofa inefficient complete
biological oxidation systemwhere you have to store

(48:40):
molecules instead of burningthem completely.
And once that's set in, thenyou start at tissue levels, you
start building up fat.
That compromises tissuefunctions, oxygen delivery,
blood flow, circulation, so on.
The simple swissiosis ispractically just stepping in in

(49:01):
apicronic disease where you dealwith this metabolic crowding
and the truth is we don't needglucose, we don't need
carbohydrates.
Our body is designed our liveris designed to produce
carbohydrates from glycerol orfat, meaning that it's a
gluconeogenic precursor.

(49:22):
So, provided that you eatenough fat and a little fat,
which is not the same as fattyacids fat is composed of a
glycerol, where all theseglycerol is a three-carb
molecule and each of those canhave fatty acids attached to
them.
These are what we calltriglycerides or phospholipids,

(49:45):
if there's one phosphate and twofatty acids, and this is how
your liver exchanges fatty acidswith adipose tissue and heart
muscle, for example.
The most efficient way ofdelivering energies in this form
of this fat, because it's verysaturated with hydrogen.
A fat, a hard hydrocarbon isvery different from a glucose

(50:14):
molecule, which is a six-carbonsmixed with six water molecules.
So hydrocarbons are carbons inhydrogen, a carbohydrate are
carbons in water.
So practically, if you look ata hydrocarbon, it has twice as
many almost hydrogens comparedto the same amount of carbons

(50:36):
that they carry and for thatmatter they are much more
efficient and much more suitedfuel source for metabolic water
formation, which is oxygen andhydrogen, and also for ATP
synthesis, which needs theseprotons to come into the
mitochondrial matrix.
And those are the mostefficient low-duty soft rays to

(50:57):
deliver this hydrogen protonsand not neutrons to the
mitochondria.
So hydrocarbons andcarbohydrates are very different
how they behave in our systems.
Hydrocarbons and carbohydrateshave very different dutium
contents simply because the waythey are made in nature.

(51:20):
Again, photosynthesis andbiological oxidation are the
reverse or opposite processes ina sense that, but they all will
fare the same biological roleis practically to capture the
energy of sunlight and deliverit to species that are

(51:44):
chemotrophic or heterotrophic,and I gave these talks based on
basic biochemical orbiochemistry teaching at UCLA
and Jack Rusch took some of thatin his arguments.
But practically it's abiochemical scenario when we

(52:04):
look at these reactions andthere are actually rows of
electromagnetic radiations inthe form of lights and so on
which actually interact withthese electron transferred chain
proteins.
And also what's very importantis that there's a mitochondrial

(52:24):
process, what we call thesenanoconfinement and proton,
these table stabilizationprocesses, which also produce
energy against the zero pointenergy scales.
We actually beaming up theseenergy producing scenarios just
to understand human energyproduction, or you carry out

(52:47):
cell energy production ingeneral.
Now we are actually linkingthis with the obligatory fatty
acid oxidizing or fatty acidmodifying cell organ and what we
call peroxazones, and theresult is hydrogen peroxide,
which can be, by catalase turnedinto a metabolic water.

(53:12):
And sleep is very importantbecause during sleep you slow
down oxygen delivery and that'swhen molecular oxygen, or two,
steps in and this is how yousupply your peroxazone with
oxygen and the breathing, or theslow breathing, during sleep

(53:33):
serves this process of deutymdepletion from fat and the
result is hydrogen peroxide,which produces metabolic water
in mitochondria with the use ofcatalase.
But practically, sleep is justto go into a ketosis, a fat

(53:53):
burning state, without eatinganything.
The problem is during daytime,if you get hungry, you go to the
freezer, you open the door andyou start eating all kind of
stuff.
If you sleep, you actuallyallow your, with low oxygen
tension, simply because yourbreathing slows down, these

(54:13):
peroxazones to kick in, eventhough they don't produce much
energy.
They produce low detunehydrogen peroxide which can be
taken to mitochondria to producelow detune metabolic water from
there.
And this process is so criticaland so important that, for
example, if you want to climb tothe top of the Mount Everest,

(54:38):
if you want to climb to the topof the Himalaya without
supplementary oxygen, you haveto be nutritional or grass fat
ketosis.
Otherwise you're not going tomake it so practically, as it
comes to not only chronicdisease but also human
performance or extremechallenges.

(54:59):
In that matter, these systems,the peroxazome or mitochondria,
or the proton destabilization,the light effects, the heat
production, these are allinterconnected in a very simple
way and that's practically.
Carbohydrates and hydrocarbonsbehave differently as far as

(55:20):
their energy and detune load, sopractically you want to operate
under nutritional and metabolicketosis on low detune saturated
animal fat and from then on youcan actually, metabolically and
energetically, you canchallenge your system and you

(55:43):
will be able to perform and youwill be able to reverse certain
disease processes, mostlychronic metabolic diseases,
simply because now yourmitochondria is able to
completely exhaust those storedfatty acids, proteins,

(56:05):
carbohydrates, whatever thoseare, because of you actually
treated metabolic crowding atthe cellular level with
appropriate low detune, highenergy substrate delivery in the
form of saturated grass fat,animal fat, and that's key to
health.

I'm blown away, lazlo.
This is absolutely amazing.
I think you're really helpingme put together a whole bunch of
pieces in my head around thepathogenesis of metabolic
dysfunction.
Let me go through a couple ofthose things that you said in
turn, because there was so muchgold in what you've just said.
Essentially, when the state ofthe art in terms of most of the

(56:49):
metabolic clinicians, that andkind of thought leaders on this
topic is that metabolicdysfunction starts in
dysfunction of the adipocyte andthen the adipocyte reaches a
personal fat threshold, it canno longer store substrates in
there.
So these spill out into, youknow, ectopic fat deposits,
whether that's hepatocyatosis,fat in the liver, whether that's

(57:10):
, you know, white adipose, butin in in an ectopic depot such
as the viscera in the abdomen oreven within the muscle, another
form of ectopic fat deposit.
But I was never satisfied bythat explanation and it didn't
help me understand pieces ofevidence like circadian
disruption, which is this ideathat and there was a recent

(57:32):
there was a study done wherethey had two groups of mice.
They fed them the exact samediet but one had a circadian
disrupted shift work, a lightenvironment, and that group of
mice developed a fibrotic andinflammatory adipose tissues,
expansion of of of theirvisceral and subcutaneous
adipose depots and theydeveloped insulin resistance.

(57:53):
So there's obviously morefactors at play than what we're
eating in terms of developing orexceeding this personal fat
threshold, and then we'redeveloping ectopic fat deposits
and then, on the way, insulinresistance and then type 2
diabetes and the rest.
But what you've just describedis that it's a backup of
substrate.
It's incomplete oxidation orincomplete combustion of these

(58:15):
substrates, that is, that istherefore being altered or built
up in different organs, and youknow any other metabolic doctor
that you talk to that they'llmake the note that certain
patients can, will manifestmetabolic disease in different
ways and some get, some will get, will only have the tiniest bit
of visceral fat, but they'll befloridly type 2 diabetic.

(58:36):
Others will have massiveexpansion of their subcutaneous
fat and be metabolically fine.
Others will get hypertensionand get kidney specific
manifestations.
So it's all a massive spectrum.
But what you're helping meunderstand is that this is a
fundamental mitochondrialproblem and a backup of
substrate and and there'smultiple different steps that

(58:59):
things can go wrong.
But you know it's all kind ofcoming back to the mitochondrial
function in terms of of howthings are and why things are
going wrong yeah.

So you need to think of, like how you come to
this plant.
When you're a baby, when you'rea newborn, you have a 2.9
millimore per liter glucose andand one millimore per liter beta
hydroxy butyrate.
That means you you're born inketosis, you're born in a

(59:30):
metabolic ketosis, which is whatyou reach in the morning after
asleep as well.
So you're, you come to thisplanet in ketosis, you wake up
in ketosis in your teamdepleting ketosis, and the key
to this is practically regulateoxygen intake and switch from
mitochondria to proxazone.

(59:51):
Proxazone to mitochondria,another.
It's more like a hybrid engine.
The proxazone can only use andonly modify fatty acids and long
chain saturated fatty acids.
Mostly they produceacetylcoinsame and they produce
using O2.

(01:00:12):
So it's it's not the red bloodcells and hemoglobin that
provides that O2, but it'sdissolved oxygen in your blood
which is available.
It doesn't matter how slow yousleep, actually sleeping in deep
and this is Wemhoff and someother methods that then you can

(01:00:34):
actually improve increaseproxazomal beta oxidation and,
for that matter, you can depleteduteum and produce the tumor,
depleted metabolic water orhydrogen peroxide for for
mitochondria.
Once you wake up and you starteating, you eat a mixed diet.
That means carbohydrates mix inif you don't keep ketosis,

(01:00:58):
meaning that you have to startdealing with duteum.
Some other ways and this islike by glycosis is inserted,
embedded in the system.
Practically during daytime youcan get rid of certain amount of
duteum, but if your duteumintake is overloading these

(01:01:22):
systems the trash holds areoverloaded then you're gonna
start breaking mitochondria down.
And once you start breakingmitochondria down, you're not
able to completely oxidize fattyacids, neither fatty acids, nor
carbohydrates or or or aminoacids, and the result of that is
gonna be a fat storage or or ora metabolic, metabolic crowd,

(01:01:48):
and they all go down to themitochondrial mechanisms and
processes.
It doesn't matter how and wherethe fat shows up or how
extensive it is.
Practically they are all tissuespecific presentations of a
duteum overload and broke up,broken mitochondria.
And those can you.
You can improve with food,nutrition, light, sleeping

(01:02:11):
patterns and so on.
There's no supplements, there'sno drug, there's.
There's nothing.
You can actually fix this verycomplex system.
You as a physician, use adoctor who actually talked to
the whole system.
As far as patients presenttheir diseases, you have to look
at them from the bottom up,meaning that you have to kind of

(01:02:33):
deal with the mitochondriafirst and think over how you can
improve the complete biologicaloxidation and exhaustion of
carbons from the whole system,because that's practically the
form of carbon dioxide, that'sthe and when metabolic water
production.
That's the whole idea.
Be behind a responsivemetabolism to challenges and

(01:03:00):
physical exercise and so on,meaning that you are more kind
of ready to take physicalchallenges, you are less prone
to develop chronic diseases, youare healthier in general, you
can perform some other foxfunctions more efficiently,
focusing on certain things,performing specific tasks.

(01:03:26):
And what is really veryimportant, which we observed
over time, is how much water youdrink, because water intake is
also a source of duteum and thisis the sneakiest part of the
team because there is no carbonsinvolved.
So they actually get absorbingyour tissues and get diluted and

(01:03:46):
get mixed with its cytoplasmicwater and first through the
circulation and the interstitialtissue compartments and then
your cellular water.
And in the meantime your brainwill swell because the osmotic

(01:04:06):
lack of osmotic, osmoticpressure and, for that matter,
you develop these kind oflow-grade.
If you drink too much waterwith no salt, excessively,
without thirst, you can developa diabetes insipidus which is
again compromising your ureacycle.

(01:04:27):
It compromising youranti-diarrheal vasopressin,
anti-diarrheal hormone output,because the pituitary gland
produces sexual hormones for thecostimulating hormone, growth
hormone and thyroid stimulatinghormone then you can actually
kind of disrupt all metabolicregulators and all metabolism

(01:04:51):
that are linked so so well andso tightly together.
You can disrupt these, thiswhole process and and for that
matter you can you will start up, you will start building up
visceral fat.
Then, when visceral fat storagespaces are not really sufficient

(01:05:13):
to store that fat, then you,you're gonna build up
subcontinuous fat and once thatstarts, you, you, you carrying
deposit, depositing fat in invarious other tissues,
especially when inflammatorycells kick in, because they
sense that there's cells thatsignal to apoptosis or or

(01:05:34):
degenerative processes set in.
Inflammation is always part ofit, because a dying cell is also
signaling for, for phagocytidesor or cells that will clear up
the remnants of those of thosenon-functioning mitochondria

(01:05:55):
bathing cells.
And this whole process startswith is characterized with
metabolic syndrome, variousinternal medical challenges like
high blood pressure, highglucose, high circulating fat is
practically because you cannotexhaust all those, you cannot

(01:06:15):
actually get rid of the carbonskeleton, the carbon sources,
and the only way they canactually be stored is in the
form of their most compact, letlargest, I would say, chain
length fatty acids and that'show BCD, diabetes and type one

(01:06:36):
type to develop after all,because you lose metabolic
sensitivity to oxygen andprotons and mitochondrial
processes.
So after all, you just end upwith a big stuffed oxidative
system that is not able tooxidize completely the subchase

(01:06:56):
that are provided.
I can't hear you right now.

Dr Max Gulhane (01:07:06):
Sorry, On a basic level it's just the use,
the analogy of an engine.
It's like the Formula 1 enginethat needs the precise inputs
and the precise tuning.
The metabolic syndrome andmetabolic dysfunction is just a
complete mismatch of the fuelsources and an inefficient
engine that is simply notworking properly.

Dr Laszlo Boros (01:07:28):
Imagine a Formula 1 race engine that has a
very tight intake of air oxygen.
Oxygen is the only element theyneed burning practically
hydrocarbons, which is ahigh-octane fuel.
Octane is the 8th carbonphalliacid, phalliacidineal fuel
, and higher that number is moreefficiently those fuels burn.

(01:07:52):
And if you actually overloadyour cylinders with either
oxygen or with fuel, thisburning process will be
insufficient and immediately youdrop performance, Immediately
you drop energy production andwhat we call is the choking of

(01:08:14):
the engine.
We know how that works.
We know oxygen limitedenvironment.
You have to adjust.
I'm not sure if you have flownairplanes, but if you are flying
a Cessna and you reach acertain flying altitude, then
you have to close your oxygenintake or you have to close your
fuel intake because your oxygenis less pressurized in higher

(01:08:38):
altitude.
So you have to adopt, you haveto adjust your hydrocarbon
intake based on the oxygenavailability.
If you keep overstuffing yourfuel, if you keep overstuffing
the system with excess fuel andthere is not enough oxygen and

(01:08:58):
not enough mitochondrialprocesses to make these two to
meet the hydrogen from food andoxygen from air, because you
overstuff this, then practicallyyou break the engine and the
first you see a decrease inperformance, and then you break
the engines because thoseengines will stop after all.
So these have to be verytightly regulated and we have

(01:09:21):
all the biochemical processes toregulate these very tightly,
very efficiently for ourmitochondria.
But once these proportions areand the due content of the fuel
breaks the engine, or the otherway around, if there's too much
fuel coming in or there's lessoxygen and these are not

(01:09:43):
balanced, then there's going tobe a major impact in your fuel
ruining system.

I love that.
Thank you, lazlo.
And I will make a quick pointabout how the light fits in,
because the near infrared lightis helping the mitochondria
produce melatonin and melatoninis one of the most ancient and
efficient antioxidant hormones.
So we talked about themitochondrial dysfunction
because they're building upexcessive reactive oxygen

(01:10:12):
species.
Well, if you're not getting, ifyou're circadian rhythms
disrupt, if you're not gettinginfrared during the day to help
make that melatonin, then theengine is again, you're not
going to have enough oil andthen it's also going to break.
And if you're not getting redlight, which we know helps
potentiate the efficiency of thefourth cytochrome, then again

(01:10:32):
that's going to contribute tomitochondrial dysfunction.
And then red light is alsobeing absorbed by mitochondrial
water inside.
So it's fascinating and eleganthow all these parts interact and
when you don't get the lightright or you don't get the food
right, you need to get bothright, and I talked to patients
about getting their light dietright and their food diet right

(01:10:54):
and that's plenty of grass-fedanimal fat and plenty of
regulated circadian rhythm.
But you basically need to doboth of those.
So I really like that the point.
I just want to go back to thisidea of ectopic fat as a
deuterium depot, because I gotin a Twitter argument with
someone about this and theyinsisted that it is.

(01:11:17):
The ectopic fat is the actualdepot for excess deuterium and a
sign of deuterium accumulation,and a good friend and colleague
, dr Sean O'Mara, is doing greatwork in terms of recommending
people identify visceral fat,especially through MRI, which is
showing them the problem.
But biochemically, the actualmechanism is what we're talking

(01:11:39):
about and this idea thatdeuterium is building up and
isn't being excreted properly Isthat correct?

Yeah, that's right.
When you have deuteriumimbalanced and you overload your
system with deuterium, it willfind a storage form for itself,
meaning that it's going to endup in glycosis and water
exchange products, simplybecause if you label glucose

(01:12:07):
with deuterium it's going to endup inside a plasma quarter.
That side of plasma quartersupplies all the biochemical
reactions, including fatty acidsin days, which is an extra
mitochondrial process.
But the substrate, not only acoenzyme A, comes from citric
acid.
But if the fatty acid synthesisprocess, which is a huge

(01:12:30):
complex in your cytoplasma, ifit has water or NADPH or
reducing the equivalent, whichis loaded with deuterium, then
your fat may become deuteriumloaded and those are again
stored because of the lack ofbiological oxidation in the

(01:12:52):
actopic fat tissues and fataccumulation.
If you look at MRI images, onMRI images those fat pads may
look darker because of theaccess to deuterium, because
deuterium does not allow protonsto move as freely and as
quickly during MRI.
So if it's a proton MRI, thenyou're going to see a lack of

(01:13:17):
signal and by comparing thosesignals you can actually
determine the deuterium contentof your fat tissue, which you
can actually do using theseimage processing softwares.

I'm so glad you brought that up because that was
my exact next question, whichis using MRI to basically
identify deuterium.
As far as I was aware and I'mnot a radiologist and even the
radiologists that I've talked todon't seem to have any
understanding of this but thereis deuterium specific
spectroscopy modes on MRI thatinvolve, and certain protocols,

(01:13:55):
especially in your oncology,involve, ingesting deuterium
rich traces.
But explain to us how we canidentify deuterium rich tissues,
maybe on standard MRI modes?

Yeah, so MRI is practically a magnetic field
where actually you delocalizeprotons using a radio frequency
and that means when they spinbecause protons they spin they
use absorbed electromagneticenergy to change their location

(01:14:28):
we call it nuclear protondelocalization and as they
return they emit the energy theyabsorbed during this changing
of their positions.
And that's what you detect inMRI Spectrically a proton moving
or a proton movement measuringdevice, proton MRI or magnetic

(01:14:52):
resonance images.
Now, if there is deuterium inyour tissues, one single
deuterium, for example in icewater, can actually stop a
thousand protons around it toresonate appropriately, meaning
that those protons are tight intheir structures, meaning that

(01:15:13):
they're unable to delocalize andthey're unable to return and
emit this energy.
So in certain scan modesthere's two kinds of scans.
One is the lattice and spinrelaxation and the other one is
the spin-spin relaxation.
Those are both affected bydeuterium, because deuterium

(01:15:34):
does not allow protons to moveas freely as just simply just in
proton environment.
So you can see a darker or adiminished image.
Now the problem with what yourefer to is called deuterium.
Metabolic imaging is when theyactually use a glucose molecule

(01:15:55):
that has deuterium on it and asit breaks down, certain products
can be measured using magneticresonance imaging or
spectroscopy.
The problem with labelingglucose is that 90% of the label
of deuterium ends up incytoplasmic water through
glycolysis.
So again, how much is lost ishard to determine based on just

(01:16:21):
gassing.
So we believe that kind ofgetting a deutonomous type of
approach to MRI or using MRI asa methodology.
Then you can actually comparethese images based on signal
strength and from there, for fattissue you can determine based

(01:16:42):
on the lack of proton movementor the lack of signal how much
deuterium those tissues maycontain.
And in the meantime you canactually do water discrimination
, fat discrimination scans andyou can get closer to these
answers.
But practically anywhere.

(01:17:02):
When proton movements areinvolved in any kind of
biological diagnostic processesindirectly, those are all
deuterium measuring devicesbecause deuterium compromises
proton movements.

Okay, so we should be able to get an idea
just using a standard MRI.
We don't need to use specificimaging mode or most MRIs we're
going to be able to use.
We're going to be able tovisualize deuterium by using
this approach.

Indirectly, indirectly again and you have to
kind of again work with somesoftware aid to be able to
analyze those images moreefficiently and you have to kind
of consider the deuterium thatis embedded in connective
tissues, collagen, fiber tissuesand so on, which are also part

(01:17:52):
of fat tissue, and you can usedeutonomics or deuterium
metabolic imaging only if youwant to look at flux, but you
have to calculate for the lossof the tracer into metabolic
water, which is it does not makethis process easier to use.
It's practically a differentangle or different window to

(01:18:14):
look at the same kind of problemof how much deuterium there is
in tissues.
We don't recommend loadinganything with deuterium simply
because they break downnanomotors and based on their
amount or their level ofconsumption, those can harm
especially mitochondrialstructures.

(01:18:37):
And for us it's easier to workwith some alternative approaches
, for example red light, whichmakes interstitial water in
mitochondria more viscous, so itimproves mitochondrial
functions, besides improvingcomplex five, complex four and

(01:18:57):
complex five, and it actuallymakes these proton bonds
resonate more efficiently,especially in the 670 nanomater
range.
It's really interesting that myhigh school buddy, dr Kraus,
france Kraus, won the NobelPrize in Physics since in 2023.

(01:19:18):
He was born in May 1662.
I was born in June 12 in 62, sowe are just a few weeks apart.
In high school we were actuallycompeting in physics very
efficiently.
So actually my classmate inhigh school beat France Kraus,
the Nobel Prize winningphysicist, for the Atos second

(01:19:40):
laser in a high school physicscompetition, national or
international physicscompetition, which is kind of
the final part of the story, butanyhow.
So now we are designing aproject where we actually use
this at the second laser toexcite biological samples with

(01:20:02):
this very short laser impulseand measure the red light output
of the system, just to see howmuch proton and how much
deuterium is involved in thechemical makeup of the sample.
So it seems that combiningresonance, which is magnetic, or
light, it almost orelectromagnetic frequency it

(01:20:28):
does not necessarily matter, inthe sense that as long as you
can sensitively measure this orapply this electromagnetic range
which is in the red light andinfrared light range, you can
actually mobilize protons andmobilize metabolic water,
interfacial water, moreefficiently.

(01:20:49):
So you can improve a lot ofbiological processes.
Yet in the meantime, based onred light emission, if there's a
lack of red light emission,then protons are not moving very
efficiently indirectly.
This is a deuterium measuringapproach or a deuterium
measuring device, and this iswhere we are kind of tweeting,

(01:21:12):
just kind of establishing in ametabolic research arena.
But there are many, many newinteresting things are coming
along.

Yeah, very interesting.
And look the reason I wasasking.
I wasn't proposingadministering deuterated tracer
in terms of routineinvestigation and management of
metabolic disease.
It was more an academicinterest.
But I think the point is givingpeople an insight into their
visceral fat is a very powerfulmotivator to implement the
lifestyle changes that we'vediscussed earlier.

(01:21:43):
And if we could relativelyeasily, with no additional time
on the MRI table, give people aninsight into the deuterium
content of that visceral fat orof their organs, then that would
be even more stimulus, in mymind, to help them adopt a low
deuterium lifestyle, becauseit's just another way of giving

(01:22:06):
them more impetus to make thosechanges.

Yeah, I actually approach this
practically.
I look at how fast my neas aregrowing, how long I need to
sleep at night to get intoketosis, measure my ketone body
levels and measure my glucoselevels occasionally and eat once
a day at night or my dinomiasare the main courses, and those

(01:22:40):
are animal, grass-fed animal,and I like this kind of fasting,
little bit thirsty, kind ofexhaust all kind of organic
molecules to mitochondrialcomplete sub-shade oxidation,
simply because you don't have toload fully your system always

(01:23:08):
because of kind ofindustrial-based recommendations
.
You need to operate in theoptimal mode.
Simply, you don't fuel in allkind of gasoline or diesel oil
when your engine is not designedfor that.
You don't put diesel fuel intoa formula of a race car simply

(01:23:34):
because it's not designed forthat.
It's a very different idea.
It's a very different concept.
It's a very different set ofprinciples how these engines
operate and simply it's theeasiest way to describe this is
that for optimal biochemicaloperations you have to use the
optimal fuel source and you haveto use the optimal regulatory

(01:23:56):
processes and those aredependent on how you understand
this system.
It's practically a doctor, Iwould say, is a good mechanic
that can actually adjust thecarburetor, the injector intake
and the oxygen intake and theexhaust pipe how clean, and the

(01:24:19):
catalysator and so on.
This we have to bring it downto the mitochondrial level and
as long as you understand howthese hybrid proxysol more of
mitochondrial beta oxidation andsubstrate oxidation systems
work hand in hand and how theystep in in different stages of
your lifestyle or theircircadian rhythm, then you can

(01:24:42):
actually tell them or design afood and the lifestyle pattern
that can actually help orreverse chronic disease
processes.
And it is just my general kindof experience that this seemed
to work in every case where wehave an opportunity and have a
compliance with these.

Yeah, and look, I have delved down very you know
, the evolutionary rabbit holesof what is a species appropriate
diet, and there is debate aboutthe role of DHA in terms of
encephalization or thedevelopment of advanced human
intelligence, and I think thatdefinitely played a role in

(01:25:24):
terms of scavenging bioavailableand very readily available
sources of DHA from the shores.
But I mean, there's no doubtthat we were carnivorous during
periods of our evolution andthere is stable carbon isotope
data showing that during periodsof in the late I believe it's
the late middle or latePleistocene in the Paleo getting

(01:25:47):
my, my, my periods confused butthere was a period where Homo
erectus was essentially a hypercarnivore so we were hunting
other carnivorous animals.
Just going to show that we'vegot deeply programmed genetic
machinery and metabolicmachinery to deal with with
animal factors.

Listen, if you go to the cave, art you never
seen, you only saw hunting.
You know cavemen.
You never saw one eatingcarrots or you know kind of
gardening.
It's practically allarchaeological or historic and
all art data points to thiscarnivore lobster.

(01:26:31):
And more fatty it is, moredetuned, depleted, it is more
beneficial for our braindevelopment.
And I was actually very stunnedand very interested in
exploring a 4.2 million yearsold exploration in North

(01:26:54):
Northern Ethiopia where actuallythey found four and a half
million years old carnivorebehavior from prehistoric men.
They even found those tools,the stone tools that were used
to break in through the schoolsof these herbivores or large
plant eating animals, and thatmust have been a prehistoric man

(01:27:18):
who learned how to use thesetools, the other kind of species
that lived in those faunas orlived on those biological
conglomerates or communities.
They were actually eating themeat, the proteins, the

(01:27:40):
interiors, the visceral fat andso on, but the best stuff was
left for this little prehistoricman, which is the bone marrow
with the highest fat content,and they didn't have to compete
with other predators becauseother predators were not
interested in those carcassanimals.
So safely, with plenty of food,they could evolve, with less

(01:28:04):
deuterium to develop.
They didn't have to repairnanomotors, because how do you
hide deuterium foods?
They actually could use thebrain and their fine finger
joint movements to actuallyperform some more complicated,
more complex tasks memory,society and providing or

(01:28:28):
building life kind ofsurroundings that are more safe.
They started cooking thesesoups these bone soups or these
because they moved them aroundand then, about 400,000 years
ago, close to Tel Aviv, theyfound cavemen's habitats where

(01:28:52):
they actually used these bonesand they saw back the skin
around the bone and the bonemarrow to conserve these bone
marrow like canned food or thecaveman that was actually good
for eight weeks to consume.
So it was a huge part of humanadaptation and human evolution,

(01:29:16):
if you call it that way.
But this is how the creatordesigned our system biochemical
systems, biological systems tobe able to use these very
valuable, incredible, beneficiallow deuterium fat sources or
hydrocarbon sources.

(01:29:36):
To design to supply these fourmobile race car nanomotors which
we have as part of ourmitochondrial complex five with
the best fuel whatsoever,because some of those they spin
about 100,000 rotations perminute and those are the ciliae
of some bacteria.
They use the same nanomotors.

(01:29:58):
If you look at any livingspecies, as long as they use
nanomotors, they use the samedesign and, for that matter,
they are all efficiently able touse either carbohydrates or fat
.
And, based on what they use,this is what their phenotype
behaviors and performance andtheir abilities as species or

(01:30:24):
individual hunters and so on,are able to find the best
sources food sources and, forthat matter, this is how and why
, and that's why the lions areso powerful and the cheetahs are
so powerful, because they don'tmess with anything else other
than just saturated animal fat.

And I want to make the comment, and I agree
because I think in empirical,clinical practice, when you put
a patient on a high animal fat,grass-fed beef diet, all their
problems go away, to use a verysimplistic term.
And I also think why thereplacement of saturated animal

(01:31:08):
fat in the human diet which wastallow, which was fatty steak,
which was butter, thereplacement of that with these
refined polyunsaturated seedoils like canola, soy, corn,
vegetable sunflower, has beenpossibly the most important food
issue, even more so than sugar,even more so than carbohydrate.

(01:31:30):
I think that is a criticalproblem in our society is
because not only was it theintroduction of these fat fats
as the main fatty acid source inour diet collectively, but it's
also the absence of thosesaturated animal fats and the
fat soluble vitamins that we gotremoved.
So I talked to Tucker Goodrichabout this and he has

(01:31:53):
extensively looked into thepathology of why these oils are
so harmful, and it's his opinionthat it's the breakdown
products of linoleic acidspecifically that are
interfering with the function ofthe mitochondria.
And he's talked about theincorporation of linoleic acid

(01:32:13):
into mitochondrial cardiolipin,which is problematic.
And then I talked to Jack Cruzand he makes the point that it
is actually the presence ofdeuterium in the seed oils that
are making them so toxic and soharmful.
So can you square that this forme, or help us, as the

(01:32:35):
listeners, understand themechanism of harm of highly
refined industrial seed oils?
Is it mostly the deuterium?
Is it mostly this linoleic acidbreakdown products?
Is it both?
How do you think about it?

Now we wrote a paper about this in a oncology
called what to Eat, what Not toEat that is the question, and
you're right.
Are these plant-based oilnutritional items either
hydrogenated or treated withsaturated?

(01:33:09):
They actually use their oily,fatty nature by using industrial
saturation, using hydrogen gas,and some of those have 250 ppm
deuterium concentrations.
So once you start processing,using organic solvents and

(01:33:31):
extracting certain oil types,especially unsaturated fat, and
you want to saturate it so theyactually hold longer and hold
better on the shelf, when youput them in the cellar, you know
this yellow big bucket offrying, whatever those are, I
just I don't even walk throughthose eyes, I just kind of just

(01:33:56):
stay out of them, simply becausethose are probably the worst
stuff you can encounter when asfar as nutrition is concerned
and because those are notnatural.
Even the plant-based oils arenot natural simply because they

(01:34:17):
use organic extraction processes.
They use various saturationprocesses to actually make them
look in a certain way, make thembe consistent in a certain way
and, for that matter, those areunsuited for human consumption,
high in deuterium, because ofthe saturation of organic

(01:34:38):
extraction processes.
And actually we wrote a paperabout this in New York College.
You can go and check them outand when you post this
conversation we can all linkthose, we can attach those
publications, because this hasbeen a big problem for a long
time.
There's a French team, drRobbins with Dr Gabor Chomier.

(01:35:03):
They did work together onmeasuring deuterium content of
plant-based and deuteriumcontent of animal-based oils and
fat products.
Practically those are verydifferent because plants they
cannot eat fat, meaning thatthey have only access to

(01:35:24):
inorganic elements in the formof water, carbon dioxide and
sunlight.
They cannot deplete deuterium.
They cannot.
Their deuterium depletionprocess is based on light
resonance, practically.
So they are not able to controldeuterium in their oil or in
their hydrocarbon products aseasy as animals can, because

(01:35:48):
animals eat grass.
They use citrate mitochondrialproduct to produce their own fat
, so they all have to bedeuterium depleted.
That's why saturated animal fatis the safest to eat, because
they have the most efficientdeuterium depleting process
during fatty acid synthesis.
And that's their mitochondria,that's their citrate synthase

(01:36:09):
enzyme reaction which usesmatrix water to produce that
citric acid which is thenthrough the citrate shuttle,
it's shuttle to the cytoplasm.
Non-manonar coenzyme oraceticity coenzyme if it's
cholesterol synthesis isproduced.
And they all come frommitochondria Plants.

(01:36:29):
They cannot do this plants.
They have their own metabolicpriorities, simply because they
depend on photosynthesis.
That's why they have to stay inone place, soak up as much
water as they can, and then theydepend on animals to spread
their seeds and they wrap theminto these sweet, addictive

(01:36:54):
deuterium bombs called fruits.
The wild boar comes, they eatthe apples, they walk two
kilometers and sorry, excuse mylanguage, but they have a diary
and they shit everywhere.
So that's how trees propagatethemselves, because they can
produce a high deuteriumaddictive sugar, load fruits and

(01:37:20):
kind of embed the seeds inthere and the animals that eat
them.
They go into sugar calm andthey start running around like
lunatics and they spread theseeds everywhere.
That's the purpose of sugar.
That's the purpose ofcarbohydrates.
It has no role in humannutrition.

(01:37:41):
The only safest food that wecan consume is grass-fed animal
saturated fat.

Yes, it's interesting and I want to.
I'll definitely include thatpaper in the show notes.
Did you have specific deuteriumconcentrations for canola oil,
for sunflower oil?
Can you tell me now, are they250, are they 200, what is the
deuterium level in these oils orhow can we test it?

I can be anywhere from 150 to 250, based
on what kind of saturationprocess, what kind of organic
expression process.
They need to read our paper in.
What to eat.
What to eat?
That's the question.
Because that's that paper wasaccepted in 24 hours by the
chief editor.
Because he said finally finally,the only thing he asked me is

(01:38:33):
just to reduce the length of thepaper from like 1200 words to
750 words.
But practically it was like alight opening to like a li-bob
kind of situation, to aoncological or cancer-related
project where they actuallyfigured that actually the

(01:38:55):
ketogenic diet is not working inthose animal models.
So we looked at the the supplyof those animal diets and sure
enough it was loaded with plantbased oils, the organic
extraction and organic solventextraction.
It's describing that paper.
So my best guess is what?

(01:39:17):
250 ppm or somewhere around.
I just you know, if you look atDr Robbins papers, if you get
capsaicin from Paprika, which isfrom home growers, it has 110
ppm.
Once you go and buy capsaicinfrom any chemical company, they

(01:39:42):
produce capsaicin that has a ppmof 160.
So the natural processes areall very different from the
industrial processes and itdoesn't matter what the oil
comes from.
When the industry steps in youcan forget about the routine
regulation of what nature istrying to accomplish.

Yeah, and that really makes me think that, yeah
, how important the deuterium isin the terms of the seed oil
toxicity story.
And yeah, it's the omega-6,yeah, it's the oxalams, but
they're essentially deuterium,as you, as Cruz talked about the
deuterium bombs, it's deuteriumand deuterium enriched, not

(01:40:24):
only because of the industrialprocessing but also because, as
you've mentioned, photosynthesisis inherently the process of
plant metabolism, is inherentlyunable to engage in deuterium
depletion.

So because they cannot oxidize, they cannot eat
fat.
Practically they only useinorganic elements to assemble
an organic molecule.
They don't have the luxury likea cow can do practically
producing their own fat usingmitochondria.

And that really gets us to the next point, which
is why grass-fed fat is so muchmore favorable than other forms
of food.
And have you recorded andapologies if this has already
been talked about in your paperhave you noticed a significant
increase in deuterium contentbetween grain-finished beef or
grain-finished tallow, comparedto fully grass-fed beef fat?

Yeah, I'll give you an example.
We did run IRMS isotope ratio,mass-pectronology studies on
food sources, mere components,mere products from grass-fed and
from industry-based grain-fedanimals, but there is about a 20
to 30 degree CPM difference,which is huge.

(01:41:43):
So it's big, it's really huge,it's big.

And Lesley.

I mean I, it's big.

Yeah, part of my podcast is actually promoting
the uptake of local regenerativefarming which is fully
grass-fed, because if I'madvocating to my patients to eat
a carnivore, high meat diet, Iwant them to do so in an ethical
, ethical way.
But what you're telling me andwhat you're suggesting is that
this is another reason why weneed to be eating a fully

(01:42:10):
grass-fed animal is because thefat, the tissue, the adipose
tissue, the fat tissue in thatanimal is going to be much more
deuterium depleted compared tothe grain-finished animal.
The next question is if I'meating a wagyu steak which I
don't do but historically I havein the past if that has

(01:42:33):
intramuscular marbling, which ismyosteatosis or ectopic fat
deposition in the cow's muscle,is that fat intramuscular
marbling going to be deuteriumenriched compared to
subcutaneous fat cap, say, on aporterhouse steak?

No, those are going to be deuterium depleted.
It doesn't matter how fat isdistributed in a grass-fed
animal.
You are in the range of below120.
Now there may be variationsbased on where you recover that
fat.
It's from muscle or from fatpads, or from hind steak, from

(01:43:11):
lint steaks, from sirloin, fromfilaminone, from T-bone.
They may have a slightvariation but they are all going
to be below 120, 115 ppm.
That's what matters.
If you eat a steak that comesfrom an industry kind of based.

(01:43:38):
It's called total nutritionalprotocol for cows.
They use soybeans, they usedried jellyfish powder for
protein supplements.
They have no access to grace orpasture-based plants.
Those actually overload theirfat because they don't have the

(01:44:03):
ability to deplete sufficientlydeuterium from their fat that
they build up in their musclesimply because they are
overloaded with grains.
I mean, look at corn, look atthose are actually deuterium
bombs.
Practically those cows die infive years.
They are not healthy either.
Don't think those are actuallygood food sources.

(01:44:29):
You actually eat disease animalmeat with very high-duty content
and the animals are sick.
You're going to get sick.
They have animal metabolicdiseases.
You become, after all, what youeat, unfortunately, and what

(01:44:49):
you don't know.
Practically this is the trickto understand this whole process
is that you cannot really eatdiseased animals, simply who are
not fed in their naturalhabitat, simply because they are
going to be carrying the samediseases, like you would eat

(01:45:11):
grains and you would eatcarbohydrates.
That your system is just not.
Your mitochondria are just notdesigned to burn those.
Eventually, these diseases gofrom species to species once
they are lifted or taken out oftheir natural environment.

Yes, I'm so glad to hear that from you because
it's exactly what I have beenadvocating for, along with
friend Jake Wolke, who'sregenerative farmer, and Tristan
, who interviewed you recently.
You know all in a grudge that afully grass-fed animal, in
eating its natural diet whetherthat's venison, whether that's
beef, whether that's bison,whether that's even seafood the

(01:45:52):
best is going to be awild-caught animal or a fully
grass-fed animal, which is, interms of beef, cattle
agriculture is going to be fullyrotationally grazed.
That's going to enrich that fatwith the highest quality
nutrients.
Another way of conceiving whywe should be avoiding grain-fed
or feed-lottered beef why shouldwe be avoiding confined-fed

(01:46:15):
pork?
Monogastric animals, pork andchicken, which have been
consuming the industrialproducts of monocropping
agriculture, which are going tobe those grains, are
contaminated with industrialherbicides because, in the US
particularly, they're allsprayed with glyphosate or other
kinds of herbicides, especiallyif they're round-up ready,

(01:46:35):
which is most of the corn andsoy in the US.
So, as you said, you argue whatyou eat, but you're actually
what you eat to eat.
So we need to be very specificthen in terms of food selection.
We've got so much to talk aboutstill that I think we maybe
just have to record anotherepisode, but I want to ask you a

(01:46:56):
couple final things.
And, in terms of testing usingI believe it's mass spectroscopy
that you use to determine thedeuterium level, is that an easy
process?
Because I really feel like weneed to redo the food pyramid
based on the deuterium contentof food and we need to be
advising our patients to eat themost deuterium-depleted foods,

(01:47:19):
which, as we've talked about, isgoing to include animal fat
predominantly at the top.

Yeah, so the most standard method of
measuring deuterium in water isthrough spectrophotometry, but
it is only able to measure waterdeuterium content and you can
turn each and every organicmolecule into water if you

(01:47:47):
oxidize and just like my friendCandia does.
So the spectrophotometry is thestandard method.
The isotope ratio massspectrometry is the organic
molecules can be directlymeasured, but those are more
expensive.
Now there are certain testingsites for deuterium from Brett,

(01:48:13):
from saliva and from urine.
Those are available in Europeand in the United States.
You can search around.
I can put some links up therewhere you can kind of give them
some really good connectingpoints to measure these.
But I agree with you after all,deuterium content has to be

(01:48:37):
shown, just like kilocaloriesand sugar content and so on.
I think those don't need to beshown on the label of any food
item and then they don't evenhave to provide kind of any
other detail.
I really just want to see thedeuterium content.
I don't care what else there isin there.

(01:49:00):
I think that's the mostimportant when you see a patient
.
I think, after all, the mostimportant lab result is your
deuterium content in serum, inBrett, in saliva, urine.
Whatever is accessible, itshould be part of the workup
protocols and the laboratoryprotocols and, after all, you

(01:49:21):
have to teach your patients tokind of monitor their nail
growth, monitor their hairgrowth, monitor their sleeping
patterns, just so.
Are they really sleeping a fewhours and getting up like in
good rested state, meaning thattheir deuterium is probably low?
Or they sleep a lot and theyare not able to kind of rest

(01:49:46):
enough, or they don't sleep welland they are not rested as part
of their problem.
So there are many ways of kindof living with this deuterium
conscious kind of lifestyle andthese can be part of either your

(01:50:07):
consultation.
I can consult on these.
It's very simple.
My website analyzed this.
I'm very happy to talk aboutthese on any individual.
I'm not a medical, like I don'thave a medical doctor but I
don't practice.
I just kind of give some ideasof how deuterium or living with

(01:50:29):
deuterium is very practical andwhat's the scientific and how do
.
Scientific scenarios are linedup behind these kind of examples
of lifestyle.
There are papers out there nowthat actually report on

(01:50:51):
deuterium content of certainfoods.
Gavosomja he just published one.
It's in the cancer controlwhere he actually measured the
deuterium content of certainfood items and you can actually
get original data from there.
We are planning to publishresults based on grain fed and

(01:51:15):
grass fed animals.
Those papers are in the processof writing.
The variety of university inAmsterdam we have a course due
to Novics course where you canget into kind of details of
these biochemical processes andthese gardening and cultivating
processes that are due tofriendly and sure enough.

(01:51:38):
Whatever you need.
We are very happy to kind oflist with this podcast, with
this conversation, and we cancome back and talk a little bit
more.
If you have more questions, I'mhappy to do that in time.

Yeah Well, thank you so much, lazo.
And yes, I think that everyoneshould be aware of the deuterium
content of their food, andparticularly their fats.
And if you're eating seed oils,then you're eating a lot of
deuterium and if you've gotmetabolic dysfunction, then
you're going to be wanting tohave a deuterium depleted diet.
So we can definitely pick thisconversation up again, because

(01:52:11):
we haven't talked about cancer,we haven't talked about a whole
bunch of other interestingthings.

Yeah, let's do another one specific disease
related processes.
Now we covered the basics andthe nutrients and nutrition
elements and some lifestyle, butif there are particular disease
processes that you would liketo discuss, I'm very happy to do
so at the time.

Amazing.
Well, thank you so much foryour time and I'm very excited
to push this one out.
So, yeah, we'll talk again soonand thank you again.
Thank you so much.

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48. Dr Laszlo Boros: Critical link between dietary Deuterium, Visceral Fat and Metabolic Diseases

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