93. Dr Brian Grimm: Field Theory and the Quantum Biology of Clinical Medicine

Episode Transcript
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Speaker 1 (00:00):
Okay, back on the Regenerative Health Podcast and
I am speaking with Dr BrianGrimm Now.
He is a practicing high-acuitymedicine physician and he is
someone who's emerged on myradar quite recently with some
very, very insightful writingsand posts on the topics of light

(00:20):
and health and a new field he'scoining as field biology.
So, brian, thanks for joiningme.

Speaker 2 (00:29):
Thank you, it's a pleasure to be here.
Thanks, matt.

Speaker 1 (00:31):
So tell us about this idea of field biology and how
is it relevant to what you'redoing with patient care and
thinking about medical care thatyou're administering.

Speaker 2 (00:43):
Yeah, I think you know I don't think it's the
go-to answer for everything, butwhen it comes to what I think
about field biology, it's moreof a kind of a coherence sort of
thing.
We talk about light, water,magnetism and how they affect
the body, but then what happenswith those once they kind of
interact with a molecule, andit's these feedback loops, it's

(01:04):
these circuits that we don't inemergency medicine and primary
care, that sometimes we don'ttake a look at those and we
don't consider those withtreatment plans and things like
that.
So I think zooming out andtaking a look at the field and
how that field is being createdand how it's reverberating with
those molecules, and makingthose little lock and key

(01:27):
mechanisms work, I think isimportant.
I don't use it really as theanswer, but I use it as kind of
a flag in a field ofbattleground of health versus
disease, and I just it'ssupposed to.
What I use it for is to remindme to take a look at these
things that are kind of betweenthe CBCs.

(01:48):
Right, that isn't thehemoglobin, it's not the
hematocrit, but it may be ratiosbased on that, and I think
that's why I like the term.
I'm not trying, there's a tonof overlap.
It's quantum biology, fieldbiology, and I'm not trying to
to own some phrase, I'm justtrying to remind myself to say
hey, sometimes it's not aboutthis one thing, it's about all

(02:11):
of these things together and wehave to take in all those things
at one time, which, as doctors,we don't love to do.
We love one answer to be theanswer for everything, but
unfortunately it's not usuallythe case.

Speaker 1 (02:24):
I think the fact that you're even thinking about a
framework to better informclinical decision-making in a
mechanistic way makes you unique, and I don't mean that in a way
to denigrate our colleagues.
But it's too easy, I think,once progressing through medical
school and residency, for usprofessionally as doctors to

(02:45):
simply follow clinicalguidelines, follow mechanistic
flow paths of patient care andnot actually think deeper about
the root causes of our patients'illnesses.
So I want to congratulate youoff the bat for actually making
that attempt at a betterunderstanding what is actually

(03:05):
going on.

Speaker 2 (03:07):
It's definitely an attempt.
I mean, these labs that we use.
They measure levels, but Ithink the fields measure life a
little bit and I think thatyou've got to get a different
lens.
And I always try to talk aboutbifocalness, and even when I'm
talking to patients, Iunderstand that you know

(03:27):
patients.
Translating this information topatients is the most important
thing.
It's not you and I talking, max, because you know all this
stuff already and it's prettyredundant, probably in a lot of
ways.
But if you can translate, ifyou can figure out a way to
simplify it and translate it topatients, it's just that's how
you effectively change behavior,that's how effectively you cure

(03:48):
or fix disease processes.

Speaker 1 (03:50):
In my opinion, yeah, and let's drill into it, let's
explain these concepts, whatyou're thinking about, so that
perhaps colleagues who arelistening can adopt at least
some of these ideas.
And you mentioned the lock andkey.
And, for anyone who's listenedto my series with the Guy
Foundation researchers, theirforays into quantum biology

(04:12):
research were prompted by thisidea that the lock and key
biochemistry mechanisms areinadequate to describe what is
actually going on in the body.

Speaker 2 (04:24):
Yeah, I mean the locking.
I think the locking key isobviously necessary.
I think you look at the, lookat smell, right, I think was it
Turin or something they weretalking about.
The locking key is there.
But what if it's a differentisotope of hydrogen?
It changes the signal once thatlocking key have actually kind
of connected, right.
So so I mean, when we have, youknow, uh, when we have, a

(04:44):
photon that hits the skin, whatdoes that photon do?
It actually stimulates amolecule whatever molecule is
actually absorbing thatparticular wavelength and then
it creates a field kind ofgeneration, through either
mitochondria, upes, or throughdecoupling of into mitochondria.
So it's about these fields thatare created, whether they're

(05:06):
magnetic, whether they're light,all of these fields together
that are communicating what thestate of the organism is and
what the state of the cell is.

Speaker 1 (05:16):
And I think that's kind of what I think of it as
and to clarify that acronym thatyou just used UP for the
listeners, is an ultra-weakphoton emission, and maybe
unpack this, because, again,we've been delving into this for
a while, but for mostclinicians they will have

(05:37):
absolutely no idea what you'retalking about.

Speaker 2 (05:40):
Well, the idea is that our system, our organism as
a mammal, really absorbs andreleases certain frequencies
right, certain frequencies oflight and some of these stronger
frequencies, especially a UV,blue light, sort of um and
violet, those sorts of things.
We've got somewhat of a Faradaycage right that we protect the

(06:01):
system interiorly to probablyhave that differential gradient
right.
When we talk about life andwhen we talk about energy, it's
kind of about these gradients.
It's about high temperature,low temperature, it's about high
potential, low potential.
It's about high voltage orhyperpolarization and
depolarization.
So the body is actually creatingkind of a safe spot in the

(06:23):
middle, but these higher energyphotons are coming in and then
it's up to the molecule or theelement to absorb that and then
it sends a different signal back, oftentimes in a UPE sort of
way, to subtly, subtly release afield locally, which then has
reverberating effects andsometimes abscopal effects right

(06:44):
, locally, which then hasreverberating effects and
sometimes abscopal effects.
Right, if you shine anear-infrared light on the back,
you get a low decrease inglucose as well as you get
visual improvement.
So it's just about.
It's really about using theenergy on the outside and to
stimulate more fields on theinside, and those fields are
oftentimes stimulated by or inthe form of UPEs, which are

(07:07):
generated typically from what weknow right now, we think
they're generated frommitochondria, right from the
reactive oxygen species,reactive nitrogen species, but
we're also starting to see thedecoupling of the mitochondria
producing a field too, and allthose sorts of things are
signaling mechanisms not only tothe local cells around but also
to the nucleus in the nuclearDNA.

(07:28):
So it's this exterior signalingthat's then being changed to an
interior controlled kind ofenvironment, so that you can get
the right information at theright places, a la Picard and
Merugin's resistance principles,right.

Speaker 1 (07:44):
Yeah, it's fascinating stuff and I'd refer
people, if this has been toomuch too quickly, to listen to
my earlier podcast withparticularly the first podcast
with Dr Jack Cruz, where hetalks about the story of human
health and contrasting orpresenting this idea of light
being reliant on or using bothexternal light, ie solar photons

(08:07):
, and then using light, butinternally generated light,
which are these ultra-weakbiophotons internally to, I
guess, coordinate whatever'sgoing on inside the cell.
So I guess the question that Ithink is relevant is how do
these ideas help inform yourthoughts about disease and when

(08:32):
the cell is working compared towhen the cell is potentially not
working?

Speaker 2 (08:36):
It depends on the disease process, right.
And so if you're talking about,say, a diabetic, for instance,
with high glucose, right,diabetics typically have
elevated glucose in theirbloodstream.
The idea currently is that youknow our insulin isn't working
appropriately or you're not onthe right medications.
But if you take a look from aquantum biology standpoint or a

(08:58):
field biology standpoint, whatyou're looking at is the
signaling on the inside,especially from near infrared,
which they're starting to lookat.
Is the near infrared arestimulating that mitochondrial
functioning, or the ATPase, tospin fast enough that it pulls
more glucose from thebloodstream to actually decrease
on these patients' glucoselevels.

(09:19):
And so in a case like that,that's great.
Now, if you have a case likecancer, this is, you know, I
don't want to be provocative,but in a case like cancer it's a
different sort of story.
It's a different mechanism ofhow the electron transport chain
moves electrons.
Is it going reverse, is itgoing forward?
Is it a Warburg, is it not?

(09:41):
And I think, if you talk about afield within there, there was
an interesting article I don'tknow if you read it very
recently and they talked abouthow the mitochondria, which is
our energy producers, right,amongst other things, that when
you have a cancerous cell, thatwhen that cell detects that the
mitochondria automatically goaround the nucleus.

(10:03):
I don't know, did you see thatarticle which is very
interesting?
And the point of the articlethey suggested was is because
the cell needs to replicate sofrequently that the mitochondria
that were there to actuallygive it ATP because of the
energy requirement.
But what I was wondering aboutis I'm thinking more it's almost

(10:24):
like a field buffering systemwhere you're getting that energy
that's being broken down by theDNA strands that are being
broken at the hydrogen bondingand that's releasing energy and
the mitochondria functioning isto absorb that and then to kind
of resist where it needs to beresist and then transmutate it
to cells locally or toorganelles within the cell.

(10:45):
Does that kind of make sense?

Speaker 1 (10:48):
That's fascinating and I think it invites a bit of

(11:08):
discussion about how theresearch in the science exists
that mitochondrial dysfunctionor you can call it mitochondrial
maladaption potentially ifyou're being really pedantic is
at the root of why thesehealthcare systems yours in the
US, ours in Australia areessentially headed towards
bankruptcy, becausemitochondrial dysfunction

(11:31):
manifesting in a different organ, depending on people's genetic
factors and these exactlifestyle behaviors, is crashing
these organ systems and leadingto all these hospitalizations.
So talk about mitochondria abit more.

Speaker 2 (11:47):
Well, as I think all of your viewers know,
mitochondria.
We didn't used to havemitochondria within our system,
but they become our slaves.
I think it was Stephanie Seneff, her theory of where we pulled
in mitochondria to kind of doour work.
And I think what's happened?
Uh, in my opinion, when itcomes to mitochondria, uh, the

(12:09):
talk has always been thepowerhouse of the cell.
But honestly, every single monththat I practice medicine I read
a new article that says youknow, the mitochondria may not
just be the powerhouses, guesswhat?
They're also the signalers,they're also the controllers,
they're also the resistantorganelles, they're also the
transmutation organelles and now, even more, they're the

(12:31):
protection of the cell.
And I think that's what isreally interesting and how this
is evolving so much.
I think I had a talk with oneof my colleagues about eight,
nine years ago and he was likeyou think everything is
mitochondria.
I'm like, because it is.
They may not know it yet, butwe're going to get to the

(12:53):
conclusion in medicine that, yes, it's probably a mitochondrial
dysfunction.
And if you look at Doug Walls'work right, most disease
processes, the assumption andit's probably a very valid
assumption ismitochondrial-based.

Speaker 1 (13:02):
Besides the nuclear genetic diseases, the true
nuclear genetic disease, yeah, Ithink it was a lynn margulis,
carl sagan's uh partner yes, yes, yes sorry, came up with a
theory of endosymbiosis but, uh,yeah, the the, this idea that
our health as an individual orhuman is reliant on this colony

(13:22):
of ancient bacteria what theywere originally cyanobacteria
that have become everyone'sroommates in our cells.
I mean it's incredible, but Ithink useful.
It's useful to think, andthat's how I think, about health
and longevity and disease iswhat's going to be good for us
long-term, has to be good forour mitochondrial function and

(13:44):
everything that we should bedoing needs to essentially tend
those mitochondria.
The interesting point youraised about biophotons and
mitochondria again I wasspeaking with Professor Jeffrey
Guy at the Guy Foundation and hewas really speaking about the
mitochondria, photon emissionsas being essentially the

(14:04):
controller and how themitochondria are actually
directing these.
It's not just random splashes oflight here, there and
everywhere, it's really directedin a very intentional way.
And that got me thinking thatthis bio-photon story is not
only one of inter-cellcommunication but also

(14:25):
intra-cell communication.
So the photons are helpingcoordinate what's going on
between the nucleus, themitochondria inside the cell,
but then beyond that, at thescale above that, that cell is
then using that light to helpcoordinate with its cells in the
local field and say, coordinatemitosis, which was Gerwich's
work back in the 1920s.

Speaker 2 (14:47):
Yeah, no, I completely agree.
And I mean we haven't eventalked about, you know, phonetic
kind of the sound waves thatsome of these create and some of
the reverberations, thephysical kind of reverberations
that the mitochondria, that thefield that comes off the
mitochondria are actuallyproducing.
And I think, yeah, I mean, andthen we oftentimes I feel like

(15:09):
we overlook just the decouplingmechanism of the mitochondria,
the NIR that comes off of that,the infrared that comes off of
that.
That's a signal in of itself,especially definitely locally.
And so I think, yeah, you hitthe nail on the head about that
and I think the science is sonew on that.
But you know, glenn Jeffery'swork is fantastic and the Guy

(15:31):
Foundation is amazing.
So, yeah, I completely agree.

Speaker 1 (15:36):
Let's talk.
I don't know if you have anythoughts about different
ancestral origins, perhapsdifferent mitochondrial
haplogroups, and how thataffects disease susceptibility.
And the reason why I think it'srelevant for you in the US and
even here in Australia, even inthe UK, is that we have
essentially and I don't meanthis in any form of racist way,

(15:59):
but we've got ethnic explants,we've got people who have a lot
of melanin, whose ancestorsevolved at the equator, who are
living at high latitude, and inAustralia we have lots of people
who are adapted their ancestorsadapted to high latitude and
now living in high UV areas.
And we've also, on anepidemiological level, have a
health disparity between thosepeople of darker Fitzpatrick

(16:22):
skin types more melanin comparedto the people of lighter colors
, and it's been my hypothesisthat I think a large degree of
this health gap or healthdisparity can be explained by
these people's solar light needsnot being met and the fact that
they have such larger light andenvironmental signaling needs.
So do you have any thoughts onthat topic?

Speaker 2 (16:45):
light and environmental signaling needs.
So do you have any thoughts onthat topic?
Sure, I mean, I think you knowyou look at things like MS, you
look at all these diseaseprocesses that are
latitude-based right, and Ithink we all have these genes in
us that whether can we awakenthese genes?
And I think that's wherehormesis kind of comes in,
that's where these differentialsas far as temperature, as far

(17:07):
as energy, cold thermogenesis isreally good about awakening
these genetic kind of thingsthat we've had that have been
asleep for so long.
Me being Norwegian and German,I've got them in my system, but
I can tell you, the first 40years of my life I really didn't
utilize them at all.
So now you know, with theability that we have to awaken

(17:27):
these, if we use the photonicenergy appropriately, then I
think it's really earthshattering what we can do, what
I've seen in practice,especially from, say, patients
of darker complexion or ofAfrican descent.
We've seen such an increase in,say, autoimmune disease, such
an increase in prostate cancer.

(17:49):
And yes, I think the pigmentplays a role.
If I get enough solar exposurein a safe way, with the right
ratio of UV to NIR, then whathappens is I will increase my
pigmentation through palm C andthrough, you know, melanin
regeneration.
But if you already have apatient that has so much melanin

(18:12):
on the surface of the skin andthat you're asking that patient
to actually, when they spend 93%of their time indoors, to
actually utilize the energy, thelimited energy that they get
outside, with all the resistancethat melanin is doing on the
outside, it doesn't allow forthe proper signaling on the
inside and I think it's almostlike it's almost a function of

(18:35):
so much armor to the point whereyou just can't get the signal.
And I think we have to realizethat it's a challenge, because
I've seen, you know, multiple.
You know some of my firstpatients with the pandemic that
passed away were of darkercomplexion and it's unfortunate

(18:55):
that we have that and we haven't.
In medicine we try to treat allthese patients the same and we
have to start, we have to take astep back and say they're not,
their field is different, theirbiology is different, their
melanin is different and thatdictates what the internal
disease process does anddictates what the internal
health is.
And so, yes, I agree, there'ssuch a disparity.

(19:18):
We have a higher population ofpatients of Mexican descent or
Spanish descent, so those alsohave an increased pigmentation.
So we're seeing those patientshave higher diabetes, higher
obesity, and that's all comingfrom the way that our skin, the

(19:40):
way that our eyes and the waythat our brain is actually
getting these signals on theoutside, transmutating them to
the inside and informing all thecells to kind of do what
they're supposed to do.

Speaker 1 (19:50):
Yeah, I'd like to riff on this because metabolic
disease is so prevalent andreally the way it's talked about
in some circles, I think, isincomplete.
I think it is simply, it is aflavor of mitochondrial
dysfunction and, yes, we canframe it in the way of metabolic
syndrome.
Insulin resistance sure,absolutely.

(20:12):
But I think if we're drillingall the way down and being as
accurate as possible, then it isdisruption of this coherence
that you're describing, Brian,and it is mitochondrial
dysfunction.
And in what you just said, I'mreminded of the subcontinent.
I mean the subcontinent.
However, 1.3 billion people.

(20:33):
They have enormous amounts ofmetabolic disease and they also
have habits and social normsthat involve essentially wearing
long-sleeve clothing.
A lot of them work in tech and,yes, they're eating a very
nutrient-poor diet.
But let's talk a little bitmore about how these people

(20:55):
particularly seem to be at mostsusceptible, or even more
susceptible, to metabolicdisease and its complications.

Speaker 2 (21:03):
Yeah, well, you said subcontinent.

Speaker 1 (21:08):
India, pakistan, bangladesh, yeah.

Speaker 2 (21:11):
Well, we don't have as many I don't see as many
patients out here in the WestCoast of the US with that but it
is kind of interesting that ifyou look at the amount of
diabetes that's kind of poppingup in the world, one of the
highest percentages is in theMiddle East.
And you can make, you can havetheories and hypotheses.
As far as it does have to dowith EMF, which probably plays a

(21:33):
role, we just can't really, youknow, we can't really tie those
things together.
I think the fact is that a lotof these patients, from a
genetic standpoint, their systemis based on a certain one thing
is they're based on a certainlighting structure, but they're
also based on a certaintemperature structure.
So now you've moved them to adifferent location and now that

(21:55):
their system it's aboutmitochondrial adaption, it's
about epigenetics, right, andit's not a function that our
mitochondria won't be able toadapt if we move from the Middle
East to the USS or Middle Eastto Australia.
It's a function that we're notgoing to be alive long enough to
make that adaptation.
And in the current technologyenvironment, because it's moving

(22:20):
so fast, which is anotherreason probably why in the
Middle East we're getting a lotmore of these skinny diabetics.
I think the technology ismoving so fast that it just
doesn't give our system time toadapt.
And unfortunately, when it comesto our medicine that we
subscribe and prescribe is, wehave the innate ability to treat

(22:41):
these acute kind of diseaseprocesses right.
We've heard this a milliontimes, you've talked about it as
well.
But the challenge that we haveis we look at this patient and
we look at the disease processthey have.
We treat them acutely to try tofix that acute problem, but we
don't take a look at the fieldenvironment that they're in,
take them out of that or adjustthat field environment to

(23:01):
ultimately make them better.
You know, we just destroy cellsthrough whatever chemotherapy
or whatever and we just hopethat their current environment
that actually got them sick inthe first place then figures out
in a quick enough fashion sothat they don't get that disease
process again.
And for me that's what'sconfusing, especially when we

(23:24):
talk about patients that havetransferred from Africa, that
have moved from whatever othercountry and have a different
genetic profile.
I think we have to take thatinto account.
But it's difficult, I think usas doctors, I think we're just.
The system is set up in a waywhere the more patients you see,

(23:44):
the better off you are.
And I think if we're notallotted the kind of long-form
discussions which we need tohave, then all we're going to be
able to do is prescribe, andbecause it's turning into a
prescription subscriptions kindof society and is reading
headlines and that's it, I thinkit's up to us as doctors to

(24:08):
kind of stop and to hold thesepatients and just say, hey, this
is the cause, this is thedisease process.
We've got to adjust theenvironment based on your
genetics and based on yourability to deal with the current
environment.
We've got to do that first andthen we can prescribe things and

(24:28):
then, hopefully, thesemedications, these prescriptions
that we've got are bridgetherapies from unhealthy to
healthy.
Because if we can do thatbridge these patients but also
change their environment better,lighting better, you know, more
hormetic kind of stress thenthat's where these disease
process can improve, especiallyfrom patients that have

(24:48):
transferred from one location inthe world to another.

Speaker 1 (24:52):
Yeah, absolutely.
And I'm going to offer somethoughts on diabetes because I
think my perspective on it haschanged a lot since when I first
started this podcast two yearsago.
And in terms of inappropriateprescribing or failing to see
the root cause, I think insulinfor a type 2 diabetic or a
gestational diabetic has to beup there with the most myopic of

(25:17):
mechanistic treatment goals andthis idea that someone who is
so resistant to insulin andtherefore hypoglycemic should be
just treated with higher dosesof insulin.
Again, they're not insulindeficient, they're insulin
resistant.
But the points you make and Ireally like that you brought up

(25:39):
the Middle East, because that'ssomething that Glenn and Glenn
Jeffrey and Bob Fosbury havebeen talking a lot about which
is this idea that you have agroup of people, a race, that
were used to or adapted to veryhigh UV environments in the Gulf
of Arabia and suddenly they'reindoors in these hermetically
sealed chambers with this IRblocking glass and they're

(26:02):
guzzling down sugar sweetenedbeverages with high fructose
corn syrup and I mean they aregetting extremely diabetic.
But this idea that simply beingoutside is like a tonic
anti-diabogenetic stimulus, Ithink that's game-changing,
because then when you realizethat when you're simply being

(26:23):
outside, you're spinning thatATPase and sucking glucose out
of the system.
It really doesn't become aproblem of too much processed
food.
It becomes an absence ofdaylight, which the processed
food is simply exacerbating.

Speaker 2 (26:38):
Yeah, I completely, completely agree.
I think the challenge that wehave in medicine is sometimes
things are so easy that theydon't seem like that they could
be accurate.
You know, and if you bring upthat with patients, they tend to
pause and they say, dr Graham,no, I would rather a

(26:58):
prescription that doesn't.
I've never heard that beforeand I think, yeah, I think, if
we can start doing that moreespecially from a timing
circadian perspective, startdoing that more especially from
a timing circadian perspective,right, and I think, like out
here in California, when I bringup this topic about getting
outside more, and I try to talka little bit about ratios, about

(27:18):
the NIR versus UV ratio, whichplays a big role, their first
thought is okay, sun means goout at 1pm in the afternoon, lay
out on a chair and get fried,and I tell them, no, no, no,
it's about getting out in themorning time, getting under
shade.
You'll get some of the best NIRlight there underneath the

(27:39):
shade and you'll also get, youknow, nonlinear photo effects of
the UV that pops out early, aswell as the blue that you really
need on a daily basis.
So, yeah, I think it's almosttoo for my patients, it's almost
too easy.
But you have to find theiron-ramp right and I think that's
why you have to put it in somany different ways and I think,

(28:02):
in time and pretty soon.
I'm thinking especially withsome of these transdermal sort
of testers where now we can seethese patients that have
increasing glucose just by beingunder a fluorescent light.
I have one of my colleagueswho's got one of those and we
can see the glucose just risebased on being in a different
light environment, and then if Iswitch them and I put them

(28:24):
under, say, a Neuralight orsomething like that, then it
kind of stabilizes.
So it's really kind ofinteresting.
It's interesting and it'samazing and it is important to
really start to get these peopleout more, because all we're
doing now is we're spending moreand more time inside and less
and less time outside, and theeffects that it has on the

(28:45):
system is amazing.
Even if it's just retinaleffects right, the retinal
effects will stimulate asystemic effect just downstream.

Speaker 1 (28:54):
Yeah, it's so interesting and it's so timely.
And you see, colleagues who arein the system of an indoor work
environment probably circadiandisrupted home environment, with
tech, with tech use and bluelight, and you can just see that
and you know they're nevergoing to lose any weight.
They're overweight, they'reobese, it doesn't matter how how

(29:17):
many um.
You know calories, they count.
You know, even if they go onthese glp-1 agonist injectable
medications, you know that ifthey don't change their daily
habit of sitting in ice in awindowless room under
fluorescent bulbs, that thatweight's just going to pile
right back on.

Speaker 2 (29:35):
Yeah, I mean, I think it's a definite field problem
internally, right, where thesepatients their sugars.
All of a sudden it's 115 on anOzempic.
But how do they feel inside?
Typically they feel awful.
The patients I'm seeing onmedications like that typically
have nausea, vomiting, abdominalpain a lot of times bowel

(29:56):
obstructions, ileus, things likethat.
So, yeah, I mean, I think we'retrying to figure this out from
a pharmaceutical lens but we'renot focusing on the most
important thing and what kind ofeffects internally and how you
feel.
And I think we should flip thescript a little bit, right?
So, max and I see patients, andwe see patients and they come

(30:19):
and they say, doc, I don't feelwell.
And you do all these labs, youdo all these x-rays and these
CTs and whatever, andeverything's fine.
And I go back to them I'msaying, well, from what we can
see, everything looks great.
And they say, doc, why don't Ifeel well?
That not feeling well, that'sthe field differential inside.
That's why patients don't feelwell, because the field has been

(30:40):
changed.
If you give insulin to a typetwo diabetic, what are you doing
?
You're changing the field.
You're changing the field to astorage field, to a storage
signal environment.
How are they ever going to getbetter?
They're ultimately not, I think, and I think some of us docs.
We just keep our fingerscrossed and hopefully they you
know, eat less and exercise moreand hopefully they'll magically

(31:01):
get better.
One of the one of the mostamazing things that I talked to
my colleagues about, I think,when you talk about you know,
blue light and signaling andwhat's the proper sort of
functioning or what's the properphotonic field we should be in,
is one of the things I don'thear too many people talk about,
and you may know this, max, iswhat's the most focal point in

(31:23):
the eye as far as your visualfield, what is it?
You remember what this?

Speaker 1 (31:28):
is the fovea, right.

Speaker 2 (31:35):
But what's even more focal and more concentrated than
the fovea Dermacula, thefoveola right, okay, the foveola
.
And so what cells, whatphotoreceptors are in the
foveola?
So we have, typically conesright.
So you have a high amount ofcones.
You have S cones, m cones and Lcones right.
So which ones are those cones?

(31:56):
And if you separate those foryour listeners, s cones are
typically shorter, wave coneslike blue light, violet light, m
cones are the middle ones,green things like that.
L cones are the longer ones.
M cones are the middle ones,green things like that.
L cones are the longer ones.
So the ones that we're missingin the foveola are these short
cones.
So what does that tell you?
It tells you that the foveola,the highest point of focus

(32:19):
within a retinal field, is notsupposed to have as the main
actor a blue light source.
And if you look in theenvironment, if you look at
evolutionary, wise, look at theworld, do we ever see anything
that's blue, just blue, thatsignals that foveola?
No, but now we're justbombarding these photoreceptors,

(32:40):
especially within the foveola,with these blue images, and our
body and our mitochondria aretrying to kind of compensate,
and that's the reason why wehave so much visual issues.
That's the reason why we haveso much retinal detachments,
macular degeneration, because wejust can't keep up with the
amount of regeneration that'srequired because of the

(33:00):
activation of a wavelength thatwe're not supposed to have.
We're supposed to see a blueocean with colors inside.
We're supposed to see a bluesky with colors inside.
We're supposed to see a bluesky, but we're supposed to use
that as the backdrop and it'snot the main actor.
It's supposed to always be thebackdrop.

Speaker 1 (33:16):
That's fascinating and I'm immediately reminded of
the curve of spectralsensitivity which human vision
is optimized over, and it peaksat green light, and Alexander
Wunsch, who's one of the world'sleading photobiologists, made

(33:38):
the point that this is likely tocoincide with an arboreal
evolutionary niche where we werein treetops, within the canopy
and everything is green.
So what you just said withrespect to blue sensitivity and
central vision kind of makessense in that light.
That's fascinating.
I had no idea.

Speaker 2 (33:59):
Yeah, and look at green too.
I think what they're looking atgreen now, even though it's
kind of a mono wavelength,they're looking at green to kind
of calm the system down, right.
They're using it sometimes withmigraines now and there's some
really interesting new articlesabout that.
I know I think Thomas Seegeractually is making a green light
for that.
But even just wearing greenglasses can improve migraines on

(34:23):
patients in certain studies,which is interesting.
And so, yeah, if you look atlike inside the body, look at,
look at, look at bilirubin.
We know about bilirubin, right,we know what what light absorbs,
or what bilirubin, what lightabsorbs bilirubin.
But we also know, but what'sthe precursor to bilirubin?
Biliverdin, right, andbiliverdin is green, right, and

(34:49):
actually you can.
There was a there's anotherarticle that I'm going to
release here shortly where theprecursor to bilirubin, which is
a breakdown product ofhemoglobin, right, the precursor
is biliverdin.
If you can increase the amountof biliverdin, then that
actually absorbs a specialfrequency of light, near
infrared, and it releases greento stimulate a reduction in
glucose.
They got a 60% reduction byjust improving or increasing the

(35:12):
biliverdin content.
So these sort of little goldnuggets, I like to call them, or
these little Easter egg huntsthat we go on, these sort of
things are really telling you.
It's about the lightenvironment and it's about what
that light environment and thatmagnetic environment within the
system, what kind of fields thatcreates and signals the local
cells and the systemic kind ofeffects well, I mean, it's so,

(35:36):
it's so interesting in it and itwe are just discovering these
little easter eggs, as you say.

Speaker 1 (35:40):
But they, yeah, they all make sense in the in the
lens of evolution, of biologyand and this evolved metabolic
envelope that we were occupyingfor the kind of duration of our
time on on, uh, on planet earth,the, the, the interesting, also
interesting thing that, uh, uh,I wanted you to potentially
shed some light on some more uhwas with respect to, um, with

(36:06):
respect to those, that that thevisual phenomenon that you just
described so expand a little bitmore on, with respect to those,
the blue vision, and how peopleare specifically managing to
shortcut this process becauseobviously, comparatively,
there's no, nowhere near as muchblue ancestrally as we are now.

(36:29):
How are people presenting thatblue to themselves every day?

Speaker 2 (36:34):
Well, how are they presenting it without
understanding the downside?

Speaker 1 (36:37):
Implications yeah.

Speaker 2 (36:38):
Yeah, certainly.
I mean they're doing what youand I talk to patients about all
the time.
They're on these screens.
They're on the screens and thenon a daily basis and
unfortunately, even when they gooutside they're on their screen
and now you're getting apolarization of of a particular
light that really signals thosephotoreceptors.
So they're doing what, what wetell people not to do and what

(37:01):
we're currently kind of on,unfortunately, but it's it.
The challenge is is that if we,if we bastardize, say, blue,
then we're missing out on thepositive things of blue.
And I think what our retinasare doing right now and the
reason why our retinas and theorbit or the eyeball itself is

(37:24):
getting longer, it's trying toadjust, it's trying to
compensate.
Nature knows what to do and ourbody's trying to adjust.
It's trying to compensate.
Nature knows what to do and ourbody knows what to do.
But these compensatorymechanisms unfortunately create
disease processes such asretinal detachment, such as
macular degeneration.
So what these people are doingalmost are doing the wrong thing

(37:48):
and I think that if they wereto just utilize light a little
bit better, get outside,especially in the morning Glenn
Jeffries' work is reallyinteresting in that respect and
they talk about red lighteffects.
Right, they talk about nearinfrared light effects, and one
of the things they always seemto talk about is they say the
morning time has a certainstimulus, but it doesn't have

(38:10):
the same effect in the afternoon, and so it's almost like the
priming and the stimulation ofthe ATPase to spin is what we
need in the morning, and then weneed, from a circadian
standpoint, a movement of energyuse and energy production to
change, and that's based on theactivation of UV, because it's a

(38:32):
stronger signal.
So it's all about it is allabout timing.
Just like you know, circadianketosis is about timing.
It's not about the foods asmuch as it is about timing.
So, yeah, I think we've got toeducate the patients better and
I think the current environmentthat they're in, we've got to
make adjustments.
You've got a red lightcurrently on, which is fantastic
, but, you know, is it multiplewavelengths or is it, you know,

(38:57):
one or two?
I think it's great wherepatients are kind of focusing on
that, but I do think we have tokind of, you know, get outside,
get external.
I think it would be verybeneficial.

Speaker 1 (39:18):
Yeah, A couple of points that you just raised
there.
It's fascinating to me that theambient solar conditions for
the day kind of symmetricallyreverse themselves from morning
to afternoon depending on, youknow, atmospheric conditions or
potential atmosphericcontaminations that can change
the scatter of light.
But this idea that the body isgoing to respond differently to
those light wavelengths becauseof the sequence in which they've

(39:40):
been received by the body Imean, that's exactly what Glenn
Jeffries' work showed, and ifyou hear him describe or talk
about his discovery, it was awhole bunch of researchers
getting together in a roominvestigating this red light
effects on cells and findingdiscrepant results.

(40:03):
And then finally someone whowas thinking out of the box
asked put to the group okay,what time are you guys doing
your experiments?
yeah and they realized that thepeople who were doing the
morning experiments were findinga great result and the ones
that were doing the afternoonwere getting peanuts.
So, uh, again, extremelyelegant and how time dependent

(40:25):
and um that that this wholewhole process is.

Speaker 2 (40:30):
Yeah, yeah, it's just another.
It's just another layer that wehave to go through as far as
doctors go and, and we have tostop looking at these
superficial layers.
As far as treatment protocols,we're going to have to look at
what is the feedback loop ofthis and at what time.
Like they have studies thatdate, you know, a decade ago,
and they looked at bloodpressure control.
Like they have studies thatdate, you know, a decade ago and
they looked at blood pressurecontrol and they looked at

(40:52):
typical blood pressuremedications I think it were ACE
inhibitors and the patients didso much better I think this
study was in Spain they did somuch better from a blood
pressure standpoint, from acardiovascular standpoint, if
they took the medications atnight versus took them in the
morning.
And there's tons of studies asfar as chemotherapy timing and
things like that.
So I mean it's we all know thatthere's clock genes within

(41:16):
every cell.
We all know that.
So, but it's there's so muchresistance to taking that as
part of.
You know, could youtheoretically, in a differential
on patients, could you putcircadian disruption on almost
every patient?
You could, you really could getan ICD code and put circadian
disruption.
So I think, and that wouldprobably be the answer to

(41:39):
everything circadian disruptionand maybe mitochondrial
dysfunction.
And there you go, you've gotdisease processes in America,
processes in America.
But yeah, timing it's soimportant and that's why you
know, you, what you tellpatients, what I tell patients
getting out in the morning,clear that mitochondrial process

(42:00):
.
Let's spin the ATPase, let'sclear out the ROS and the RNS
and to have them signal at theright time.
That's the time that theysignal in the morning and they
send out a certain at the righttime.
That's the time that theysignal in the morning and they
send out a certain pulsed,rhythmic signal at that time
than they do at, say, 1 or 2 pm.
And that's based on the amountof energy that's being allowed
to come in.
And when you get in theafternoon you're talking the

(42:21):
melanin that absorbs the UV,that breaks down the water that
surrounds the melanin thatabsorbs the UV and the melanin
gets broken down, water isreleased and energy is released
from there to signal the localcells.
But it's a different energyprocess depending on the time.
It's like a boat moving in onedirection.

(42:42):
Right, you can't turn it all atone time, but if the boat is
expected to make turns at acertain time of day, then it's
much easier to control themovement and that's the energy
movement and the metabolismsystem within a human.

Speaker 1 (42:56):
I want you to talk or give me your thoughts on meal
timing, because you justdiscussed what is called
chronopharmacology, I think, orwhatever that field is called,
or chromochemotherapy, which isthe timing of medications with
respect to the skating rhythm.
But there's also the field ofchrononutrition and this idea

(43:18):
that timing of meals affectsmaterially metabolic health.
So shoot on that topic, becauseI feel like even the section of
medicine and doctors who areeffectively using dietary
therapies to help reversemetabolic disease are themselves
not even aware of thesebenefits of aligning meal timing
to the circadian clock.

Speaker 2 (43:39):
Yeah, I mean, they're so stuck on the macros, right,
and they're so stuck on thelabel of this diet or that diet.
I think I've been through thegamut.
I feel like you know, I didAtkins, which is basically, you
know, ketosis back in the 90s.
I had, you know, when I wasgrowing up, I had issues with
reactive hypoglycemia, where youeat these foods and your sugar

(44:00):
goes up so fast and your body,because it's not under the right
environment, actually pulls thesugar down too quickly and you
actually become low sugar, youfeel kind of dizzy, you start
sweating, and so I was alwayskind of looking for the causes
of that.
And certainly the types offoods that you eat play a role,
but it's the timing that playseven a bigger role.

(44:21):
And so right now you knowthey're talking about ketosis,
they're talking about carnivorethings like that, yes, it will
have a benefit.
But if you can just do acircadian ketotic sort of diet,
which basically means thatyou're eating almost whatever
food you want to, hopefullylocal, hopefully organic,

(44:41):
ideally regenerative if you dothat, but if you stop at a
certain time and allow your bodyto because it runs on a clock
to allow your body to movethings in the proper direction
to have proper field signaling,then you'll get proper storage.
I mean, look at fatty liverright, fatty liver is a prime
example.
I was reading an articleyesterday I think it was and it

(45:03):
was, I think it was a 2014article, and they were looking
at the timing of eating andtriglyceride storage within the
liver.
And they were looking at thetiming of eating and
triglyceride storage within theliver and they were looking at
mice.
So things were flipped right.
They're having where mice couldeat whatever they want,
whenever they wanted, or theycould eat just at night, which
for us is daytime, right andthey found out that there was I

(45:26):
believe it was a 60% decrease intriglyceride storage within the
liver on the mice that ate atthe proper time.
So that's just by doing it.
And this was what 10, 11 yearsago.
And what's the current treatmentfor fatty liver?
Eat right, exercise more anddown the pipe, there's some
pharmaceutical treatment that'scoming in, but that's not going

(45:47):
to treat it.
I mean, I've had patients wherewe've just talked about this,
we've talked about okay, youjust have to go out early in the
morning, you have to just eat,or go out early in the morning,
eat whatever food that you'recomfortable eating, hopefully in
a healthy way, and then stopeating 5, 6 pm and those
patients actually got so muchbetter.
Their fatty liver went away onthe next ultrasound and that was

(46:09):
without medications.
Obviously, we're not treatingpatients on this podcast.
I'm just saying these arethings that we have to take into
account because they have sucha dramatic effect and I think us
in the medical profession wejust have to stop resisting this
and we have to accept that someof these things we weren't
taught in medical school.

(46:30):
And it's OK.
I'm the first one to say I'mnot the smartest person in the
room, I'm not trying to be.
I'm open to say Max, you got anidea.
You tell me the idea.
That sounds great, let's applyit.
Even in an end of one situation, let's try it out.
And I think us, with ourdoctors, I think we've got to
slowly kind of move them in thisdirection and that's why I
think Roger is doing a great jobin there where he's actually

(46:53):
showing you know what, if wemove these ICU patients and get
a little light at the propertime, then they're actually
getting better, they're feelingbetter.
One patient that comes to mindthat I had, and it brings a kind
of a tear to my eye and Iremember it's this older guy he
was probably in his 80s or 90sin a wheelchair and I think his
daughter brought him in and wewere talking about this,

(47:16):
specifically this.
The guy's white as a ghost.
He had some underlyingautoimmune issues as well and we
talked about getting outsideand he looked up at his daughter
and he said I just want to gooutside.
Why can't I go outside?
And it makes me remember thearticle about these nursing home
patients right where they spendon average 15 minutes outside

(47:39):
every month.
And I think we're just we'rekind of disconnected from this
and I think we've got toreconnect.
And once again, I keep givingyou applause You're doing a
great job.
And I think we've got toreconnect.
And once again, I keep givingyou applause You're doing a
great job and I think we need tocontinue doing this and
pointing out these things topatients, but also, providers?

Speaker 1 (47:57):
Yeah, absolutely, and thank you.
Thank you, brian.
I mean it's just so simple.
It's just so incredibly simplethat eating your meal outside
after seeing the sunrise I mean,how simple is that advice?
Yet you know, 99% of peoplearen't doing it and the ability
to clear out that fatty liver,clear out the hepatosteatosis,

(48:18):
without even changing the foodcomposition.
And that is exactly what thestudy that I'm thinking of with
this coronal nutrition studywith type 2 diabetics.
They didn't change the control,they didn't change the content
of the diet in the interventiongroup, they just changed the
timing of the food and that wasenough to see benefits in type 2
diabetes.

Speaker 2 (48:39):
Well, I think one thing it does and we don't talk
about enough is getting to thatfasted state right.
So, even with the carnivore,even with carnivore and I'm not
against that, I'm happy to kindof treat patients like that too.
I've gotten patients betterwith vegan diets.
I've gotten better withplant-based diets, I've gotten
better with ketosis diets all ofthem.

(49:03):
It depends on timing.
But the interesting thing, whenI talk to patients about that,
we talk about the timing,especially of high-protein or
high-fat meals.
At what point, if you eat thosemeals, say 4, 5, 6 pm at night,
at what point are you going toget into the fasted state?
It's dictated by how fast the GIsystem works right and how fast
the microbiome within that GIsystem breaks that stuff down.

(49:26):
And so sometimes eating, say, ahigher protein even though if
you're a carnivore, eating ahigher protein at 6 pm may not
be a great idea, because you'renot getting into a fasted state
until maybe 4 or 5 am in themorning.
And then what's that signaling?
The signaling mechanism that wehave on our skin, on our eyes
and our brain.
Also, the microbiome has asignaling timing too, and those

(49:49):
things like to sleep as well,and they're the ones that are
actually shooting that film onthe wall of the intestinal
lining and telling thatintestinal lining through the
neuropods and theenteroendocrine cells.
What signal?
When do I stimulate the vagus,when do I not?
When do I stimulate this cell,when do I not?
So they're the ones in controlthere and I think we have to

(50:11):
give them time as well yeah,it's, uh, again it's.

Speaker 1 (50:16):
It's this idea of timing and how critical the, the
timing of the body's processes,um, how that, how important
that is to to health.
And again it's like thismissing dimension of health and
wellness.
I mean, how many books havebeen written about diet, about
exercise and aboutsupplementation?
You know the list is on and on.

(50:38):
But the number of practitionerswho are advising on circadian
appropriate activity, foodconsumption, light exposure,
it's just so diminishingly small.
Yet if you look back throughhistory and religious traditions
, they nailed that I mean thetraditional Chinese medicine,

(50:59):
hinduism, they all had this downpat because they'd, I guess
through a process of culturalevolution, arrived at that as
most compatible with health ofcultural evolution arrived at
that is most compatible withhealth.

Speaker 2 (51:10):
Yeah, definitely, we just have to get back there and
I think we have to, you know,put the prescription pad to the
side a bit and take a little bitmore time to explain the
nuances of this and thesimplicity of this and really
kind of connect with thepatients.
The way I think we have lost,and I think, medicine, I feel

(51:34):
like forgot about light, and Ithink that's why the toolbox is
so dim when you open that upright and I think if we bring
that back to them, like we usedto do before pharmaceuticals, I
think that it doesn't mean weget rid of pharmaceuticals.
Pharmaceuticals have donefantastic jobs in keeping some

(51:55):
of my patients alive and keepingthem maybe not healthy, but
still going, surviving,surviving, surviving, and I
think we just have to.
You know, we've got torecalculate and reset, and I
think that's what I try to do ona daily basis and I, you know,

(52:20):
and the way you do that islearning right, and the patients
have to learn too, and I think,and that's about time, and one
thing that you know, I think DrJack Cruz talks a lot about, is
about how valuable time is, andyou and I know that, but I don't
think sometimes we realize whenwe're talking to patients that

(52:42):
they don't know that right, andI think to give them back some
time and that requires us givingthem our time, I think, is so
valuable and so necessary as wemove forward.

Speaker 1 (52:54):
Absolutely Well.
Maybe, brian, you could sharewith us some of your I guess
interpretations using this fieldbiology, using this lens that
you've cultivated, what are somebiomarkers that you look at
when you're assessing patients'health?
How would you interpret themand how do you tie that into the
lifestyle advice that you give?

Speaker 2 (53:13):
Well, a lot of times what we'll do is we'll look at
ratios, like we talk about,right?
We look at albumin, we look atMCV.
Albumin is an interesting onebecause, you know, every protein
in the system has a hydrationshell right, and that hydration
shell is ultimately dictated byoftentimes near infrared or
stimulation of that hydrationcell to see how thick or how

(53:35):
thin it is.
It doesn't just play a role inthe folding of proteins, it also
plays a role in how thoseproteins move through the system
, you know.
So I like to look at albumin tocreatinine ratios.
I like to look at MCV scores.
You know we look at MCV, whichis a part of what we call a CBC
panel, a hemoglobin, hematocrit,mcv and you and I will look at

(53:57):
MCVs, or my colleagues will lookat MCVs and say this is a B12
or folate deficiency or analcohol.
But what I see with anincreased size in MCV, which is
basically saying that the redblood cell is increasing in size
, it's because of the structuredwater within the inside is
collapsing.
The easy water is collapsing.
It's not able to control theenergy from there, so it's

(54:21):
actually getting larger, almostkind of like, I think, what Jack
Cruz talked about maybe adecade ago.
You know what gets larger.
He may have even quizzed you onthat.
When the heart goes bad, doesit get larger or does it get
smaller?
When an ankle gets injured,does it get larger or get
smaller?
So I think I like to use thingslike that.
I won't get into too muchspecifics, but I like to use
things like that because it'ssomething that we don't pay

(54:43):
attention to.
But there's a lot of goldennuggets in those laboratories
that you have already gottenright From a patient perspective
.
You have pages and pages ofCBCs, chemistries, troponins,
urine tests, tshs, without goingto the functional labs that
cost so much.
But you can really parse out alot of disease processes just by

(55:04):
looking at ratios of thesedifferent categories, and that's
what I like to do.
I look at that.
I like to look at the EKG.
I like to look at the EKG.
I like to look at the amplitudeon the EKG, because remember
that if you look at, you knowthat's a function of all these
mitochondrial Christie's allgetting aligned in super
complexes and signaling, havinga field signal when they get

(55:25):
together.
And now we know that themitochondrials, they actually
fuse, don't they?
When they actually fuse, andthey actually can produce a
stronger field signal, dependingon what organ system you're
talking about, whether it'sheart, brain, whatever.
So that's what I like to do.
I like to look at, becausethat's what I come across.
I come across EKGs and labs.
That's what I see most often.

(55:47):
So there's a lot of interestingthings in those and I think we
just have to focus on those alittle bit.

Speaker 1 (55:53):
Yeah, fascinating.
I mean there's so many ways.
The interpretation iseverything.
Anyone can order a test, butthe way it's interpreted and the
advice given from that isabsolutely everything.
And I think the strategy or oneof the core tenets of this
decentralized medicine movementis really helping people to

(56:15):
identify through, again, notnecessarily ridiculously
expensive and obscure oresoteric markers how they're
going wrong and what couldpotentially be fixed.
A question about cardiovasculardisease.
How do you think aboutcardiovascular disease?
Obviously it is up there withstill the leading cause of death

(56:38):
in our society.
How do you think about thatwith respect to this, with your
framework and, potentially,prevention of cardiovascular
disease?

Speaker 2 (56:47):
Well, I think it depends on which cardiovascular
disease you're talking about.
Are you talking about?

Speaker 1 (56:52):
CHF, atherosclerotic CHF or Atherosclerotic
cardiovascular disease.

Speaker 2 (56:56):
So, basically, the go-to question is what do you
think about cholesterol?
What do you think about highcholesterol medications?
So cholesterol is a moleculethat absorbs light, right?
And I think the cholesterol hasso many different functions
besides just the membraneswithin cells, besides

(57:17):
pre-hormones, cholesterol playssuch an important role that I
think that we're looking atcholesterol a little bit wrong
and I think when we see thesehigh cholesterols, it may not be
a signal to say, hey, we'reeating too much fat, too much
cholesterol.
It may be a signal to say, hey,we're eating too much fat, too
much cholesterol.
It may be a signal of the bodysaying they're trying to
compensate.
They're saying we need morecholesterol because we need to

(57:39):
produce more hormones, we needto produce more healthy
membranes so that we can haveproper membrane protection and
proper membrane voltage.
And I think to me, it almostkind of pulls me into the whole
neurodegeneration discussion.
Right, we talk about theseplaques that are forming and

(58:00):
they had these great ideas hey,if we get rid of these plaques,
alzheimer's will go away.
If we get rid of these plaques,parkinson's will go away.
But what they found was it wasthe plaques that were trying to
help the situation, not hurt thesituation.
It doesn't mean thatcholesterol-lowering medications
are wrong.

(58:20):
It just means that we have tolook from a field perspective
and saying what is the feedbackloop that we're and what is the
circuit?
What is the circuit that we'vegot within the system?
If we see elevated cholesterol,we have to look at the other
parts of the system to say isour system creating enough of
the right hormones?
Is our system creating enoughof the membranes?

(58:41):
Is our system producing enoughof the things that our body
needs?
Or is that a signal for ourbody to say, hey, we need more
of that?
You know, like vitamin D is abig example, right?
So elevated cholesterol,vitamin D is low.
This is not a surprise.
The body is trying to say, okay, I need a little bit more UV

(59:02):
stimulation.
Let's make more cholesterolavailable so that we can
potentially do that.
To me, that makes sense.

Speaker 1 (59:10):
Yeah, yeah, no, it's.
The more, I think, we go along,the more perspectives there are
on this problem ofcardiovascular disease
prevention.
And you have perspectives inconventional medicine, which
seems to be ever more obsessedwith lipid lowering in every way

(59:31):
, shape and form, andpharmaceutically induced.
Then you have plant-baseddietary approaches of using
different foods to lower totalcholesterol.
Then you have the ketogenic ormetabolic and low-carb side of
things and having thisphenomenon of lean mass

(59:53):
hyper-response, where we'regetting pretty significantly
high total cholesterol and ApoB.
And then you've got, I think,more of this quantum, biological
and circadian perspective,which is we've got charge, these
blood components are charged.
We've got this exclusion zone,water.

(01:00:13):
And if we're subtracting outthe main energy source of our
life, which is sunlight, ofwhich is, uh, you know, the
majority is in the red andinfrared, then what is that
doing to the way that theseblood components are essentially
interacting?

Speaker 2 (01:00:27):
Yeah, no, I uh definitely agree.
I mean, there was anotherarticle that I just read the
other day talking about nearinfrared and they were talking
about cancer cells and the waythat near infrared actually can
in a cancer cell, can stimulateit to become senescent and so it
decreases the cancerousproperty of that particular cell

(01:00:47):
.
Just that should bemind-blowing and that should be
on every headline in the world.
So if that's the case, butwe've taken that out of all of
our lighting structure and we'veblocked it from all of our
windows, then I'm not surprisedthat cancer is one of the things
that are on the increase,diabetes as well.
So yeah, I completely agree.

(01:01:10):
I actually showed that article.
I don't know if you saw thatarticle.
I showed that article to one ofmy Hemonc colleagues and they
just said, hmm, and that was it,and that told me that I think
sometimes we're so set in ourdogmas and our silos that it's
hard to even get us as doctorsto kind of shift from that

(01:01:33):
because it's uncomfortable.
And if we would, I think inlife in general for patients,
for providers, I think there'ssome room and some necessity to
become uncomfortable, whetherit's cold, thermogenesis or
whether it's fasting.
It's that uncomfortableness.
That actually kind of gives oursystem a stress test right, and

(01:01:54):
I think we need more of that inthe system.

Speaker 1 (01:01:57):
Yeah, I did read that paper by Rhys Mould and, yeah,
selective induction ofsenescence in cancer cells.
I mean the implications are thatif you put yourself outside,
ideally next to a bush or a treeor some other greenery which is
reflecting the infrared light,and you allow that light to pass
through your body, then you'redoing your utmost to help the

(01:02:19):
prevention of the development ofcancer.
But again, we're so far removedfrom that in medicine and in
life in general that I thinkeven just small conversations
like these will hopefully kindof change the piece.
The point I'll make about myinteractions with specialists
and obviously lots of them areexperts in their field.

(01:02:42):
They do great work, yes, but Iwould say that sometimes the
more subspecialized someonebecomes, the more calcified they
are in their structure orframework of reality and the
more convinced they are thatthey're correct.
And the unfortunate aspect ofthis, I don't know, maybe

(01:03:02):
because they think that they'vealready suffered so much study
that they can't possibly bewrong.
It's like a sunk cost fallacy.
But the disadvantage is thatyou have a whole group of
medical specialists who are notin touch with a whole bunch of
topics like the ones that we'rediscussing, which makes someone
like you, brian, who's gonethrough this process and still
managed to keep such an openmind.
A pretty rare, rare breed ofcreature.

Speaker 2 (01:03:24):
Well, I try to be, because I know there's a ton of
stuff that I don't know.
That, max, you could probablyeducate me on so many things.
But uh, I think the design ofthe way medicine is, um
organized currently is what'sstopping some of these
subspecialists from openingtheir minds, because that's

(01:03:44):
where they get paid.
They get paid on.
I mean, think about from a GIperspective.
I love gastroenterology, butthey're paid based on procedures
and if you think going to agastroenterologist to get
dietary advice probably not agreat idea, you know it's
probably not hugely beneficial.
They tend to look at the GItract once it's been cleared

(01:04:06):
with the laxative.
So I think, with thesesubspecialists, I think whether
it's by design or whether it'sby happenstance, I do think that
we have to give them ribbingwith my hemlock specialist and
GI specialist and cardiologistand just to kind of get a sense

(01:04:36):
of what they understand aboutthis sort of information.
And it's not on their radar yet, but I can feel like they're
interested and I think if we canmaybe adjust the payment
strategy in medicine like youwere talking about earlier, I
think that might kind of openthe door to say you know what,
maybe I should do something alittle bit different.

(01:04:56):
Maybe it's not all aboutprocedures, stress tests,
colonoscopies, egds.
Maybe it's about maybe teachingthese patients.
Maybe that's the way to go, andI'm excited.
I'm really excited because I'mseeing a step forward and I
think we've got a long ways togo, but I'm just happy to be a
part of the conversationhonestly, because I love it.

(01:05:19):
I think it's fantastic.

Speaker 1 (01:05:21):
Yeah, it is.
I am optimistic, I guess.
Yeah, when someone's got fourprivate school fees to pay for
each of their children, they'regoing to do the scope.
They're not going to ask toomany questions.
They they're going to do thescope.
They're not going to ask toomany questions, they're just
going to do the colonoscopy,exactly.
Maybe is there anything thatyou wanted to discuss or bring

(01:05:43):
up that you've been reallythinking about before we wrap up
?
If not, I've got maybe one morequestion for you.
If not.

Speaker 2 (01:05:51):
I've got maybe one more question for you.
I'm happy to hear your question.
I feel like you know we've kindof went around most of the
stuff that I think is veryimportant.
I think sometimes, you know, Ithink it can be too much
information.
I think we've touched on theappropriate amount.

Speaker 1 (01:06:06):
Maybe you can again, because you're seeing acutely
unwell patients you can offersome thoughts on.
You can offer some thoughts onrespiratory viral illnesses and
we've come off the back of fiveyears of a very trying time and
I'm going to use that adjective,and maybe not anymore People
can read between the lines, butto me this light story has

(01:06:27):
massive potential for improvingthe preventing, but also
improving the outcome ofpatients with acute respiratory
illnesses.
So yeah, maybe you can shoot onthat.

Speaker 2 (01:06:38):
Yeah, I think, certainly.
I think there's some more andmore studies coming out as far
as how UV can kill virus.
If we're talking about virusesspecifically, uv can cut down on
viruses.
They're using UVC right.
They're using at the beginningof 2020, there was some work in
the ERs where they're actuallyusing UVC a light that would

(01:07:02):
actually turn slowly andactually would destroy the
viruses 99.9% of the viruseswithin an emergency room and I
think so.
If you look at that and if youzoom out, then why don't we use
UV more often in regular life?
So I completely agree.
I think, from a respiratoryvirus perspective, especially

(01:07:22):
viral component, you got to getthese patients outside because
that will help their system cope.
Yes, uv by nature calms theimmune system down, but it just
helps regulate the adaptive andthe active kind of immune
response.
So I think UV is a great thingthat we can implement into
patients, and that's what Rogeris doing by taking patients

(01:07:44):
outside.
What this reminds me of, too,is this whole autoimmune stuff
that we're seeing and as far ashow uv regulates the immune
response at the beginning of2020, what I started noticing is
and this is prior to all theliterature coming out as I

(01:08:05):
noticed, these patients areactually getting better on this
particular viral infection withsteroids Steroids, something
that calms the immune systemdown.
And it was interesting to mebecause I looked back even 10
years prior that I was seeingmore and more autoimmune issues
popping up and at first it was,say, two patients in a day that

(01:08:27):
would potentially get better ifyou gave them steroids, which is
kind of an autoimmune treatment, and then it would go to five
and then it would go to half.
There's been days where I'veseen patients where literally
75% of them, if we gave them asteroid, they would actually get
better.
So what that tells us is ittells us that our system is so
hyper responsive and probably tothe fact that we don't come

(01:08:50):
across something that kind ofhelps regulate the immune
response, which is glaringlywhat you and I know.
It's the UV signaling and we'velost that.
And I think if we do get outside, it will not only benefit viral
upper respiratory infection butalso benefit autoimmune
conditions and we're seeing moreand more of those, whether it's
rheumatoid, whether it'sdiabetes, whether it's lupus

(01:09:12):
Sjogren's all these diseasesthat could be controlled or at
least calmed down by UVsignaling.
I had a patient that had just atypical if you see the lupus
flare where they get thebutterfly rash right and they
went through.
I think they saw their primary,they saw the emergency room.
They went to see a specialistwho prescribed some medications

(01:09:35):
and I talked to her.
I'm like, just go outside, gooutside in the morning, hit that
time where near infrared thenturns to UVA, and she did that
for a week.
Rash went away and she feltbetter.
So that was just one patientwho went through the gamut of
the US medical system of primaryER specialist prescription
subscription and then we talkedand then she's better.

(01:09:58):
So that's my two cents on upperrespiratory symptoms and
autoimmune that can be improvedby UV signaling.

Speaker 1 (01:10:07):
Amazing.
I mean to think about themagnitude of time wasted, of
value left on the table betweenthe one conversation you had and
her previous two months ofinteraction with the whole
healthcare system.
When there becomes so muchresistance or so much difficulty

(01:10:34):
in solving a problem, then whathappens is that there's
inevitability about a solutionthat will arise, especially if
it can make a 10x improvementover the status quo, and what
you did for that lady was 10ximprovement on what advice she'd
been given before then, I don'tdoubt at all.
So, yeah, it's great toactually hear stories like that,

(01:10:57):
because it shows how relevantand important and efficacious
this advice really is for people.

Speaker 2 (01:11:05):
Yeah, and it's applicable for so many potential
disorders.
Right, disease process, I thinkI had a couple of years.
I had a, I think a couple ofyears ago I had an SVT patient,
that which is where the heartbeats really, really fast and
you can see it on the monitorgoing very, very fast.
And one of the first things Idid was I went in and I shut the
light off because there's afluorescent above the head, and

(01:11:25):
I just calmly talked to thepatient and you could see,
within five minutes the rateactually comes down.
What we oftentimes use is thingslike vagal manures, where we'll
rub the carotid or we'll havepatients blow into a straw, or
we'll use adenosine right, whatis adenosine?
Adenosine is the sleep signal,right?

(01:11:46):
So I always talk to mycolleagues about, okay, what is
the chemical that puts you tosleep?
And they're all like melatonin.
I'm like no, it's adenosine,just like it does for SVT.
It calms down the system, butanyway.
So all I did was shut off thelight and the patient's rate
normalized within five minutes,and so it's little things like
that, but they don't come up onthe radar and patients, and

(01:12:09):
certainly providers, oftentimesdon't know that.
Hey, that's best part of thetoolbox too.
You know that you can use,which is it's no risk, right?
There's not a downside toturning off a light, or there's
not a downside from gettingsomeone out at 6.30 in the
morning.
What's the downside?
There's not one So-.

Speaker 1 (01:12:27):
That they lose the prescriptions to their 100 units
of insulin and their SGLT2inhibitor.

Speaker 2 (01:12:33):
Yeah, I mean.
But it is interesting I don'tknow if you noticed this, max is
.
I think it's interestingsometimes too that the potential
of losing an identity to adisease.
You know some patients areidentified by their disease.
It's almost scary for them, itmakes them uncomfortable.
They're like, well, what if I'mnot?
You know, what if I'm not arheumatoid arthritis patient

(01:12:54):
anymore?
What if I'm not, you know, amajor depressant?
What if I don't have that?
That's not.
You know I've lost who I am,and I think that's where I kind
of have to tiptoe around,because you can tell some of
these patients are so identifiedby their disease process that
you just want to slowly kind ofget them into the right kind of
movement from unhealthy tohealthy.

Speaker 1 (01:13:16):
Yeah, absolutely, and you can definitely put people
offside if you try to tell themor make it out that they should
do something.
And really I just presentoptions.
That's how I frame it.
These are the suite of options.
I feel it's my obligation andduty to inform you of something
that I know has a highprobability of working, but it's

(01:13:36):
, at the end of the day, it'scompletely up to them whether
they want to make any action onthat at all.
But I think, yeah, we'vecovered a lot, Brian, and thank
you so much for coming on.
I think you know as I.
To summarize in my point ofview, you know so much of this
chronic health problem andepidemic that we have is just
various shades of sunlightdeficiency, mitochondrial

(01:13:59):
dysfunction caused by sunlightdeficiency, and making some of
these really simple acts, likegoing outside first thing
instead of you looking at yourphone, can be the beginning of a
real healing journey for ourpatients.

Speaker 2 (01:14:13):
Yeah, I completely agree.
I did have one question for youthat I was kind of interested
in what your response would be.
I don't know how many podcastsyou've done, which podcasts
stick out the most to you whichcould actually create change
that you've done throughoutwhatever four or five, six years
that you've been doing thischange that you've done
throughout whatever four or five, six years that you've been

(01:14:36):
doing this.

Speaker 1 (01:14:36):
Well, I mean, that's a.
That's a difficult question.
I think change and and and Imean probably the most the most
uh podcast that's had the mosttraction, probably be my my
first jack cruz podcast, um,that continues to get a whole
bunch of of uh interest andalthough and for people who've
listened to it it's it'scharacteristically in depth and

(01:14:58):
um dense information.
Dense it's, I think, thepresentation and the way that
one flowed.
It still seems to be prettyuniversally applicable, even to
people who don't don't havetraining but um, but um, yeah, I
mean, I think each one speaksto a different type of person
and that's the value of gettingdifferent guests on, because
every, every, every guest,everyone, um, is going to speak

(01:15:19):
to a different person in theaudience who can identify with
that message and understand themessage in a way that resonates
the most with them at that pointin their life.

Speaker 2 (01:15:30):
Yeah, yeah, I think it is about those on-ramps.
It's about giving the patientsthe on-ramp and giving them as
many possible on-ramps aspossible, and I think if you do
that, then they'll be in controlof their disease process and
their healing journey.
And I think all we can do, youand I is probably shine that

(01:15:53):
near-infrared light on theperineum of the medical society
and see if we can get a change.

Speaker 1 (01:15:59):
And I think we'll see how that goes.
Yeah, I 100% agree.
Thank you, brian, again foryour time, for your wisdom and
for sharing all these insights.
I think people are going tolove this one.
So where can people find you ifthey want to get in touch or
read your work?

Speaker 2 (01:16:17):
You know I'm really again.
You and I talked about this.
I'm pretty new to this game,although I feel like I've got a
lot to say.
I do a lot of my stuff onSubstack and Twitter.
That's kind of where I baseeverything from.
I've just got into someInstagram, but it's Dr GrimMD.

(01:16:37):
That's my handle typically and,yeah, I'm interested, I'm open,
I'm happy to try to help, nottreat, but I'm happy to listen
to anything that you have to say.
So come on over and log into mysub stack and subscribe and
we'll see how it goes.
I think this is something that'sreally good.

(01:16:59):
I think we have the ability nowto use long form and carve out.
Some actually make time toimprove the disease treatment
kind of process, and I thinkthat's where this is really
coming in handy and the podcastsare great.
But the ability to really kindof write down on computer now

(01:17:19):
and to dissect this into littlebits I think the opportunity is
there, the information is there.
We just have to take a littletime and take a look at it, and
that goes to my colleagues andit goes to my patients.
Yeah.

Speaker 1 (01:17:32):
And look, I think that's the end of the it, and
that goes to my colleagues andit goes to my patients.
Yeah, and look, I think that'sthe end of the day.
All that we can hope for isthat the people who are ready
will receive the message.
And I'm not interested inchanging everyone's mind at all,
and I think you'd probablyagree with me.
It's about providing andoffering people who are ready
for the message.
And yeah, that's, I guess, whatwe're here for.
And thank you for what you'redoing.

(01:17:52):
And and yeah, I would reallyencourage everyone listening to,
to subscribe to Dr Grimm'sSubstack and start reading what
he's got to say about the fieldbiology, cause it's, it's great
stuff.
Cool, I appreciate it, thanksso much, max.

Speaker 2 (01:18:06):
Have a great evening.
All right, you too.
Thank you so much.

Speaker 1 (01:18:10):
Cool.

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