BYRON HINTERLAND RETREAT - Circadian Living by Regenerative Health Retreats

Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:00):
And now we're realizing, and certainly a lot
of research is now showing, thatindeed varying the magnetic
field alters metabolism andgenerates reactive oxygen
species, which of course gives areally neat insight into what
may happen to astronauts as theygo beyond the moon.

Speaker 2 (00:15):
In this episode of the Regenerative Health Podcast,
I speak again with ProfessorJeffrey Guy of the Guy
Foundation.
I'm also joined with hiscolleague, professor Alastair
Nunn, who is one of theworld-leading researchers in the
field of quantum biology.
Now, if you haven't yet seen myfirst episode with Professor

(00:36):
Guy, check that out, as well asmy previous episode discussing
the Guy Foundation Space HealthReport.
Now onto the episode.
We'd love to dive into a coupleof topics in this episode.
Probably the main one is therecent Space Health Report that
was issued by the foundation.

(00:57):
I guess the implications thatthat report has for health
optimization, for chronicdisease prevention and for
essentially life life on earth.
So so, so, maybe, um, maybe,let's start with how we start,
how you guys started to thinkabout health through a space

(01:18):
lens I'll start off with that.

Speaker 3 (01:21):
Then Max, the Foundation runs twice a year
five symposia series where wecover certain topics and a
couple of years ago we werelooking quite closely at spin,
subtopic spin, and whereasgravity provides weight to mass,

(01:43):
magnetic fields determine thespin of subtonic particles.
And we were beginning to thinkabout the molecular interactions
if you alter spin and that mayhave effects on the outcomes of
molecular interactions and itseemed particularly pertinent to
components of the electrontransport chain in the

(02:04):
mitochondria.
Now we don't have anyepidemiological evidence of
illnesses induced by change inmagnetic fields or spin.
There was some work looking atmobile phones and that sort of
thing, but not in lower levelsof magnetic fields, in
hypomagnetic fields.
So medicine hasn't reallyfocused on that because there

(02:27):
really weren't the patients andthe pathologies coming forwards.
But it suddenly struck us thatthere was an area that humans
were going to be exploring wherethere were no magnetic fields
and that is beyond themagnetosphere of the Earth.
So travel to Mars, travel to theMoon, there's no magnetic
fields next to no magneticfields on the moon, almost none

(02:48):
on Mars as well and none on theway.
And it suddenly struck us thatsome of the pathologies that we
were seeing in returningastronauts may well be
attributed to these changes inmetabolic circumstances and in
mitochondrial function, and notonly to the more conventional

(03:10):
views of microgravity andradiation.
And that's what spurred us tothink about putting a half-day
symposium together, which Ithink we did about a couple of
years ago, didn't we?
Alastair.
It was a half-day symposiumwhere we had some space
scientists and started toexplore this, and it seemed that

(03:30):
it had been overlooked entirelyin terms of space health.
So we then decided we wouldproduce a report and recruited
about 30 top experts around theworld as part of the working
group, and it took us nearly twoyears to put the report
together, and that's the reportthat was issued in October, and
Alistair was the principalauthor, along with other

(03:52):
colleagues.

Speaker 1 (03:54):
Well, what we found was very interesting and this is
something we've found as wedelved into the space health
thing.
Of course there's actually quitea lot out there that was
already out there but wasn'treally being talked about.
And indeed when I starteddigging into the literature, we
found there were actually peopleand these were space scientists
saying 10 to 12 years ago, whatabout hypermagnetic fields?

(04:15):
And of course nobody had reallykind of followed up on this
because certainly as far as NASAand certainly Roskomost and the
other major space agencies,they're all looking at mainly
gravity, the lack of gravity ofcourse, and radiation, but these
other things weren't reallybeing appreciated.
So that's kind of, and werealise now this is very

(04:36):
important and the link here ofcourse in certainly quantum
biology is of course one of thebig areas which kicked off.
Quantum biology was the searchfor the mechanism behind how
birds navigate and this linkedinto the magnetic fields and
this idea of quantum spin.
And now we're realizing, andcertainly a lot of research is

(04:57):
now showing, that indeed varyingthe magnetic field alters
metabolism and generatesreactive oxygen species, so
which of course gives a reallyneat insight into what may
happen to astronauts as they gobeyond the moon there you go.

(05:17):
You've gone quiet.

Speaker 2 (05:20):
Sorry, that's absolutely fascinating and
something that us in mainstreammedicine we're not even close to
thinking about the effect ofmagnetic fields on mitochondrial
physiology and reactive oxygenspecies.
So I want to highlight, I think,the first part of the Space
Health Report that you reallyillustrate a point and it

(05:45):
becomes relevant for the rest ofthe report which is um the
premise, which is that spaceflight is inducing what is what
you you call an acceleratedaging phenotype.
Um, which I think that thelayman can conceive is you go
into space, beyond this, thisgoldilocks zone of, and you
simply just age quicker and yourmitochondria stop functioning

(06:06):
as well.
But you use a definition ofoptimal health that I'd like to
read out, and it is optimalhealth is a phenotype that
maximizes health span andfitness while demonstrating
morbidity compression inrelation to its species, maximum
lifespan, and my translation ofthat for people was you know
the organism or you are healthyfor most of your life, remaining

(06:30):
fit, functional and robust,with little evidence of disease
until very close to you knowyour maximum lifespan and time
of death.
So maybe let's talk a littlebit about that definition and
how you guys came about it.

Speaker 1 (06:45):
Shall I go with that one.
Yeah, this falls out of ourthinking with Professor Jimmy
Bell at Westminster, but reallyan interest we've always had,
which is why?
Is it that?
It seems that a modernlifestyle seems to accelerate
the ageing process, andcertainly this is seen with the

(07:07):
increasing rates of obesity.
There's this thing calledmetabolic syndrome, which you
may or may not have heard of,but it's associated with
increased visceral fat, insulinresistance, diabetes and a whole
number of other things.
Certainly, medicine has beenwandering around this definition
for ages, but what we do knowis that the metabolic syndrome
certainly seems to be associatedwith an increase at a younger

(07:28):
age of all sorts of diseases,and this is not just diabetes
but cancer, alzheimer's and allsorts of things.
And certainly this seems tosuggest that, for whatever
reason, people are beginning toage faster.
And this led us to startthinking about what actually is
health.
And certainly, when we start tolook into the data, what we
actually see is that there's anaverage health life expectancy

(07:52):
which we see from the wholeplanet.
You know this is what averageit all out, and that's between
80 to 85 expect life expectancy.
But what we also see ispotentially that you start
getting ill around 65, 70.
But what we also see, and thishas been known for a long time
if we live a healthy lifestyleso this is the Mediterranean
lifestyle.
We do lots of exercise, youknow we don't be careful in the

(08:14):
sun and everything.
Perhaps some sun people cangenerally live a lot longer and
the key thing is they live a lotlonger and healthier and it all
goes wrong at the end, as yousay, you get this thing called
morbidity compression.
Is who?
They live a lot longer andhealthier and it all goes wrong.
At the end, as you say, you getthis thing called morbidity
compression.
But we also know, if you go theother way, you have a really
bad last us or drink a lot,smoke a lot and get really fat.
You've actually your lifeexpectancy is far less and what

(08:36):
we've seen, certainly within theliterature and certainly within
the research, is this actuallyis.
Is has as an area which has beenquite well investigated in
terms of calorie restriction.
I think you've probably heardof the idea of calorie
restriction and certainly someof the pathways involved in this
are very much involved in theageing.
So there seems to be somethinggoing on about how we control
the ageing process using theenvironment.

(08:57):
This is something we've gotreally interested in, and it
seems to be that with time as weget older, our ability to adapt
we get less and less robust.
Seems to be that with time aswe get older, our ability to
adapt we get less and lessrobust.
But fascinatingly, we now knowthat exercise, for instance,
greatly reduces the rate that weage, and this seems to be an

(09:17):
adaptation to stress.
And so when we have our modernlifestyle, which is, we've got
this potential not to move atall, we've got lots and lots of
spare food.
We don't need to go and get it.
It seems that our systems justcan't deal with it, and one of
the key findings is that we A weget more inflamed, but B our
mitochondrial function goesdownhill and degenerates much
faster.
So of course, this tends tosuggest that there is this kind

(09:37):
of ageing.
And of course, the problem withthis is actually we still don't
fully understand what ageing isand there's still no consensus
exactly on what it is.
And there are groups ofscientists who think, well,
actually with the rightenvironment we can live forever,
but, uh, the suggestion is verymuch that we can't.
We actually do have seem tohave a kind of programmed, uh,
lifespan, but we can modify itusing the environment and these

(10:01):
alistair, when we've hadmeetings on aging.

Speaker 3 (10:04):
Um, we tend to focus not on people extending their
lifespan, but actually remaininghealthier longer, and that
that's probably probably farmore important.
There's an enormous burden onall health care systems
throughout the world now, withpeople spending the last decade
of life in extreme, extremely,extremely poor health.
Maybe useful also as to justthink about and, max, to think

(10:26):
about how we can describe aging,and in the report we talk
really about the differencebetween biological age and
chronological age, and thiscomes out of the work of people
like Steve Horvath, who's lookedat the epigenetic clock.
But there's also proteomic waysin which one can age a subject

(10:47):
or an organism biologically, asopposed to just their
chronological age, and so onefactor of aging is is your
biological age much greater thanyour chronological age?
And it would be very welluseful to know that.
About people going to space, youknow how do they start off?
Are they already starting offwhere their metabolic function

(11:08):
seems to be older than they seemto appear?
One from their outward physiqueas you know, astronauts are
going to be fit as a fiddle andfrom their chronological age.
This is something I think quiteessential for us to begin to
focus on.
Not only does your biologicalage differ from your
chronological age, but thebiological age of different

(11:28):
organs in your body differentfrom one another, and I and this
was the work I think steveorvath mapped out something like
234 or so animals to be able tosort this work out yeah, the
interesting implication fromthis is actually the age you go
into space, for instance, andhow fit you are when you start

(11:50):
could actually have quite animplication how well you do.

Speaker 1 (11:54):
I think most of us we always see the films and we
know that well.
We certainly know allastronauts tend to be extremely
fit, usually younger and highlyintelligent.
Then they come back and say,yeah, we're fine, but actually
you know what is actually goingon and it says the data seems to
point otherwise.

Speaker 3 (12:11):
So there is I'm very much back to here if we went
back so about 16 years or so, wepublished a paper to do with um
, metabolic syndrome in the gulf.
And you know, in the ArabianGulf diabetes has increased
enormously from 1% or 2% 40, 50years ago to nearly 30% within

(12:33):
the population.
It was very important for us tofocus on what might be going on
there and we came to theconclusion that metabolic
syndrome was really acceleratedaging, so diabetes was
accelerated aging.
Then we fast forward to theCOVID era where again we wrote

(12:53):
about the mitochondrialimplication of some of the COVID
symptoms and the sequelae fromCOVID.
Again, those people thatsuccumbed that seemed to be
otherwise fit.
It was determined in a numberof cases that they had
mitochondrial dysfunction.
So really what we need to do isunderstand what's going on at a

(13:14):
mitochondrial level beforesomeone is exposed to these
stresses and in space there area lot of them as they're exposed
and what happens when they comeback.

Speaker 2 (13:26):
And I think that's the main thrust of the report
and we can talk about what wethink those stresses are and the
ones that have probably beenoverlooked essentially and,
alistair, I think you couldprobably address those- yeah,
absolutely, and we will gothrough the different stresses
that are present in exposure to,to space and with regard to

(13:52):
aging and and you brought up themetabolic syndrome, and yes,
I'm, I'm very familiar with thatand I I think it is.
What you've described is a veryelegant way of um posing the
problem, which is how do we, asmuch as possible, optimize this
idea of healthspan and stoppeople ending up in a nursing
home from the age of 65 untiltheir eventual death at 80.

(14:16):
The two concepts I want to bringup and I think they're really
relevant one of them ismitochondrial heteroplasmy,
which I know professor dougwallace has talked about in your
uh, your various series and,and to me that seems to make the
most sense as to explain orunderlie um, the, the
accumulation of.

(14:38):
Well, it literally it refers tothe accumulation of
mitochondrial dna mutations thattherefore affect the
accumulation of mitochondrialDNA mutations that therefore
affect the mitochondrialfunction and accumulate it over
time.
And then you essentially get abrownout, which I describe it as
a power brownout, where thelights are dimming so that the
energy output of the cell goesdown and therefore its ability
to operate, whether that's aheart cell or a neuron or a cell

(15:03):
in the kidney, that's, a heartcell or neuron or a cell in the
kidney, so leading to eventualorgan failure perhaps, and then
aging and death.
And the other concept that isrelevant, especially with regard
to space flight, is hormesisand the fact that a little bit
of a stressor is useful.
But perhaps if we're exposed 24seven to a stressor that is

(15:23):
unable to be have a hormeticbenefit because it's simply
unending or constant, yeah, Imean, which one do you want to
start with?

Speaker 1 (15:34):
I mean the second one .
The hormesis is actually reallyinteresting because in terms of
radiation, this is somethingwhich is turning out to be very,
very badly understood, and thatis that most of the
radiobiology we've done has beenacute in terms of treating for
cancer and things.
But actually when you get intospace you've got a low dose, but

(15:57):
for a very long time, but it'stwo or three hundred fold higher
than we normally experience onEarth.
I mean, on the standardexposure you and I get on Earth
is between what is somethinglike two to three milliservents
a day, but the average astronautsorry, two minute yeah, is
getting something like 10 ormore or 20 or 30 or more, and so

(16:18):
the cumulative dose sorry, it'stwo or three milliservants a
year.
I get that wrong, but astronautsare getting that per day.
So it's two to three hundredtimes more than they would be
exposed to on Earth.
But of course, the interestingthing here is that we haven't
been able until quite recentlyto study a particular what they
call gcr galactic cosmicradiation, and this is high

(16:41):
energy, uh, let uh in the energytransfer particles.
And this seems to be actuallythe main problem they're now
suffering is that, how do we,how do we control for this?
How can we shield against it?
And and what happens in biologywhen you're just exposed to
that level for that long?
And the answer is I don't thinkanybody really knows, although
there are some preliminarystudies indicating that if you

(17:02):
give the same dose of radiationover a short period versus a
long period, you can get quitedifferent effects.
So that's a very good questionand certainly it does fall out
of this.
You know, does a cell have theability to adapt for a couple of
days, but when you do it for 10months, it just runs out of
steam.
You can't do it.

Speaker 2 (17:19):
Alistair, can you break down for us the difference
between the high-let and thelow-let?

Speaker 1 (17:24):
radiation I mean low-let radiation is low-energy
ionizing radiation.
This potentially is things likegamma rays.
Ionizing radiation thispotentially is things like gamma
rays.
But high energy is and this ismore to do with actual nuclei,
heavy nuclei things like carbonand iron, which come from

(17:46):
exploding nebulae and things,and they carry thousands of
times more energy than a gammaray and they tend to scatter in
a very different way than theway gamma rays do, and so they
can impart a lot more energy tothe system.
And I think one of the keythings they're now realising, of
course as I think certainly theoriginal research on radiation

(18:07):
was all about DNA damage and dowe get mutation and cancer.
But they're now realising, ofcourse, certainly with this GCR,
this high energy radiation, itdamages everything in the cell,
including your mitochondria, andthe problem with that is and
this is something we'vesuggested in the report is that
of course this goes on top ofreducing ability of
mitochondrial, reducingmitochondrial function.

(18:29):
And mitochondria and it's noteverybody realizes are essential
to how you maintain your genome, your DNA, because they provide
a lot of the antioxidants andthe molecules which keep the DNA
intact.
So if they're getting damaged,everything then goes downhill
quite quickly and you can'trepair your DNA, so the chances
of something going wrongincrease dramatically.

Speaker 3 (18:50):
And also as mitochondrial function fails.
Then you have the link withmelatonin production and loss of
circadian rhythm All of it.

Speaker 1 (19:02):
That's a whole other area to discuss.

Speaker 3 (19:04):
Of course, and in terms of mitochondrial DNA
mutations, we've spent some timewith the cancer researchers
here in the UK and now they'reable to identify, for a whole
range of cancers now,mitochondrial DNA mutations.

(19:29):
So this heteroplasmia is notonly leading towards poor
function, but perhaps some earlyand acute abnormal function.

Speaker 1 (19:39):
Yeah, I mean, the cancer link is a really
interesting one because it'spredominantly thought as being,
you know, nuclear DNA.
But they're now realisingthere's a lot more to do with
mitochondrial dysfunction orchanging function, which
actually is a very old idea,goes back to the Warburg
hypothesis 30 or 40 years ago.
But actually people thought, ohwell, that's just secondary.
But what we actually think ishappening now, these

(19:59):
mitochondria changing functionand this is an evolutionary
adaptation to accelerate helpthe cancer grow, and so the
whole field is changingdirection now and we have to
start thinking the entire cellhas been completely integrated.
So trying to silo out or just aDNA change in the nucleus, or
just a DNA change themitochondria, isn't good enough
anymore.
And especially if you start todamage other components of the

(20:21):
cell, like the cytoskeleton,which of course something
doesn't everybody thinks about.
But we know GCR can damage anyother component, big molecules
you think about the size ofproteins in cells and
particularly your cytoskeleton.
Damage to that you know itdoesn't do, you know, know,
doesn't really help at all.

(20:41):
And in terms of the rat, interms of the heteroplasmy, yes,
this is, I think, still aslightly misunderstood area, but
certainly I think the person tospeak to is doug bollis on that
, because he's an absoluteexpert on it.
But you're right.
But not all heteroplasmy is bad.
Some is good, but what?
What is not understood is whysometimes it leads to a
malfunction.
And again this could be due tojust natural selection, in the
end, that a particularmitochondria does better but it

(21:04):
doesn't do it much good for therest of the cell, and so you
know so there's a whole area.

Speaker 3 (21:10):
We have to distinguish between malfunction
and dysfunction, because quiteoften when we talk about
mitochondrial dysfunction,actually the mitochondria
functioning perfectly well, it'sjust the net outcome of that is
just not very healthy for thecell yeah, I mean, I think this
is where the origins of lifeidea that we, we, we often refer
back to the origins of life.

Speaker 1 (21:29):
And of course, if you look at the some of some of the
theories on the origins of life, in particular those around
thermal vents, the argument isthat actually life started by a
flow of hydrogen going intoacidic seawater and that
explains what we see in themitochondria as the proton
gradient.
But in modern mitochondria wealways see it as electrons
driving the proton gradient.
But in early life and then thethermal vent, it was the other

(21:51):
way around.
And certainly the biochemistrymitochondria.
They have this merry-go-roundof the thing called the krebs
cycle.
They can operate in manydifferent directions and people
now realize of course oh, thisdoesn't make, it's not quite as
simple.
So mitochondria can go intowhat they call biosynthetic mode
and just operate in acompletely different direction.
They're not dysfunctional atall, they're just doing what the
cell wants.

(22:11):
So and so that's back to thepoint jeff making.

Speaker 3 (22:14):
And if that happens, Having made your point on
hormesis and radiation, I thinkthere was some studies and some
notions that in the increasingcircumference around the two
atomic bombs in Japan, when theygot to a certain distance

(22:35):
further out, there was someevidence that in fact there was
improved health and lifespan inin the population, suggesting
that very small stimuli ofradiation can prompt improved
cellular and improved organ.
That is a function.

Speaker 1 (22:54):
This this is, as I'm sure you're aware, max, is a
very loaded area because aroundthis time there was a lot of
interest.
This go back to the 30s and 40s.
They were trying to understandhow mutation happened and one of
the theories was that it wasjust down to radiation
background radiation and I don'twant to go into too much detail

(23:15):
, but there's a professor, edCalabrese, talks about this a
great deal.
I'm sure you may have heard ofhim this idea that everybody
thought for a while anyradiation was bad, but actually
it became true that actuallythat is not the case at all and
indeed people are now usingradiation very low doses of
radiation, for instance, tosuppress inflammation in COVID
and other diseases.
Radiation, for instance, tosuppress inflammation in COVID

(23:36):
and other diseases.
So and actually looking at themolecular mechanisms of this,
this makes perfect sense becausethey have similarities to other
stressors like, for instance,polyphenols, or even exercise,
and things activate some of thesame pathways in the cell.
So it's a real thing.
But I think the interestingthing here is, of course, what
we're exposed to on Earth, asyou said, is a very low level of
radiation, because it's two,three, two or three, four

(23:58):
hundred fold increased in space.
And back to your earlier pointabout the dose and the timing.
Can that you know?
Do we understand what's goingto happen in biology?
My suspicion is that biology'snever been here before, so it
doesn't know how to handle it,and the natural consequence of
that is it starts going wrong.

Speaker 2 (24:15):
Yeah, and I've heard similar things about the
radiology profession, which issome data suggests that
radiologists, potentiallynuclear medicine physicians, are
actually having a hormeticbenefit from their low-level
exposures, occupationalexposures.
So I mean, that makes sense tome.
And I guess getting to theheart of hormesis is this

(24:38):
low-dose stressor isupregulating antioxidant
pathways and other pathways thatare, yeah, the compensatory
mechanism is having a netbenefit effect.
You mentioned sun at thebeginning, really in passing,
but I think that's a really goodexample of a hormetic stressor,
which is solar and UV light andthe fact that when we are

(25:02):
exposed to UVA and UVB light onplanet Earth, yes, uvb can cause
DNA strand breaks and these CPDproducts and, yes, uva can
cause DNA damage throughoxidative stress.
But it also is the fact thatUVB produces these vitamin D

(25:23):
secosteroid compounds thatupregulate basic scission repair
to essentially correct thedamage that was done.
And it's your countryman,professor Richard Weller, who's
done the epidemiology on onsunlight exposure and all-course
mortality, and there's no datathat that shows that more uv
light exposure actually leads toreduced mortality.

(25:44):
In fact, the opposite so, andthat that's another aspect to
this, this, uh, radiation story.

Speaker 1 (25:50):
Well, that's this this shows how, for instance, we
focus on one thing, we can missthe miss the big picture, and
certainly everybody.
For instance, we focus on onething, we can miss the big
picture, and certainly everybody.
For instance, there's a study,very famous study, done in
Scandinavia, where they lookedat mortality and light exposure
and what they indeed found wasthat people outside more tended
to live quite a longer and morehealth.
Yes, they had more melanoma,but they were healthier.

(26:11):
Exactly to your point that wegot so focused on one thing, we
missed the other obvious thingis that UV light can be actually
doing something beneficial.
This goes back to the studywhen I was working at Harwell.
We were using UV light to imagemitochondria.
Now they can do this becausethey contain this compound
called NADH.
This absorbs a photon of UVlight and then produces a longer

(26:33):
wavelength which we can see asfluorescence, autofluorescence.
But it also can inject anelectron.
But what you see is a veryclear biphasic effect.
So very low dose.
The cell gets slightly stressedand goes oh we've got more
reactive oxygen than we need, solet's upregulate and defend
against it, and off we go.
But of course, most ofexperiments are done with very
high levels of UV, which justblow the cell to pieces.

(26:56):
But of course we haven't lookedat those low levels, so of
course this is hormesis 101.
What's it?

Speaker 2 (27:04):
The fact that this NADH compound is essentially
absorbing light in the UV rangeand UV is short wavelength, so
solar UV isn't actuallypenetrating the body very far at
all.
So, I'm guessing that thecorollary here is that the UV
chromophore capability of thiscompound is adapted to receiving

(27:27):
endogenously generated UV lightfrom what I'm presuming are bio
photons.

Speaker 1 (27:33):
Yeah, well, yeah, absolutely.
But we actually made asuggestion in one of our papers
and I haven't really been pickedup that you could have made the
argument that actually, at theright dose and level, nadh is
actually a sunscreen because itabsorbs the energy and
redistributes it.
So people always think of it asjust being because it's one of
the key electron carryingmolecules in the body and

(27:55):
airborne proton carriers, but itis often doing it under UV
light.
But it also acts as a sunblock.

Speaker 3 (28:06):
As do many of the components of the cell, which
probably protect you.
The early life started wherethere was extreme UV in the
atmosphere coming down on usbecause there wasn't much in the
way of atmosphere, and Isuspect these molecules were
acting to block the effects ofUV on DNA, because DNA is also

(28:29):
sacrificial in terms ofprotecting itself against UV.

Speaker 1 (28:33):
Oh yeah, I mean DNA is a good sunblock.
I mean bacteria do it.
They release these nets of DNAand this, of course, this goes
back to another slightly offsidequestion.
But of course one of the areaswhich is really interesting is
what cell death is.
Now I'm sure you come acrossthis process of apoptosis.
I used to work on this when Iwas a young postdoc, but of

(28:57):
course it came as a bit of arevelation at the time, because
even this process was going on,this idea of cell suicide,
because nobody could explain,for instance, how the immune
system worked.
They then discovered, of course, trillions of cells were
killing themselves, but theywere doing it in such a way that
they were then removed verytidily with no evidence of it.
But it surprises a lot ofpeople to know that bacteria and

(29:17):
archaea, the prokaryotes, alsoundergo apoptosis.
They have a form of cell death.
So death is very, very, veryold indeed.
But one of the mechanisms is,for instance, as Jeffrey says,
in biofilms if they're exposedto a lot of light, a lot of the
cells will die, but they releasethe DNA and that DNA actually
blocks the sun.
So there's more than one thinggoing on here which is really

(29:39):
quite fascinating.

Speaker 3 (29:41):
Going back to your point about penetration, I know
you had Bob Fosbury on one ofyour podcasts a very successful
one, of course, and we workclosely with Bob.
The UV light and the blue lightare subject to first-order
scatter and really get not veryfar into the tissues at all,
whereas the higher order, thered light, infrared, will pass

(30:03):
well through the tissues anddeeply into the body.

Speaker 1 (30:09):
Well, there's actually I mean, you may not be
aware of this, but there's justbeen a paper published where
they think they they found a newmechanism of how blue light
induces reactive oxygen, and itseems that what's and there's
again it probably needs to bereduced.
But what they've shown is thatlight at around 450 nanometers
which is blue, which is a veryimportant wavelength seems to be

(30:30):
absorbed by a like a supermolecule mixture of oxygen and a
tryptophan, which is an aminoacid inside proteins, and they
call it confined oxygen.
This seems to generate ROS,because if this is true, it
means all a lot of proteinswhere this could be happening,
especially in high oxygen levels, could start generating and get

(30:51):
damaged.
And so, if this is true andagain it needs to be repeated
but it suggests that allproteins under UV light, or blue
light in particular, couldpotentially be damaged, and this
is an absolutely fascinatingfinding.
But of course, it changes theway we view reactive oxygen,
because I'm sure you're awarethat reactive oxygen isn't just
a byproduct.

(31:11):
It's an incredibly importantcellular signal.
Cells rely on what they callredox, which is a contraction of
redox, reduction and oxidation.
And if this is true, it alsomeans that we may not be able to
see what's going on inside someof these proteins and, of
course, the mechanisms we lookat the moment in biology to
study a reactive oxygenproduction very, very primitive,

(31:31):
very blunt.
We can't really see what's goingon.
This is one of the big problems.
We have a lot of this research.
At the moment we simply don'thave methods for looking exactly
where the reactive oxygen is ina cell.
But if you've got thismechanism, it suggests there's a
far more sensitive mechanism inthe cell for detecting this and
indeed you could start to arguethat low doses this would

(31:52):
prevent the proteins, forinstance, from folding, which is
a lot of proteins in the bodywhen they're made don't fold
properly and they have to getremoved and they're disposed of
very quickly.
But there's a very, very goodmechanism for recognising and
removing them and if thisprocess is upregulated it clears
out the cell and at the rightlevel it's quite beneficial.

(32:12):
So there's a whole area here wedon't you know.
We've only just been able toopen the box on and have a look
at.

Speaker 2 (32:19):
A couple of points there and I quickly want to
revisit this idea of cellularsunscreens.
I think semantics matters and Ithink the use of the term
non-visual photoreceptor couldalso be applied in this
situation.
And then, because I meantraditionally the idea of
non-visual photoreceptor couldalso be applied in this
situation.
And, and then so because I meantraditionally the idea of
non-visual photoreceptors, arethese um chromophore proteins

(32:41):
that are like melanopsin,encephalopsin, neuropson, that
are essentially absorbing lightand therefore, and then
triggering a enzymatic cascadelike that involves um
entrainment of perhaps localcircadian rhythms in the cell or
or more globally.
But but the other point is thatyou know cholesterol,
cholesterol is absorbing uvblight and that is triggering

(33:04):
that.
This, this uh um vitamin dcascade and but.
But what you're talking aboutas well is that dna is, is a
chromophore for uv light.
Dna is absorbing ultraet lightand now NADH.
I mean, that is another way ofthinking.
Perhaps this is also anon-visual photoreceptor and it
is some enzymatic cascade thatis extremely important for the

(33:24):
cell.

Speaker 1 (33:24):
Well, this takes us back to the origins of life
again, because when you look atthese, you talk about these
bigger molecules that absorblight receptors, but they're all
based around a fundamentalchromophore and this is often
FAD or NAD and others very smalland iron sulfides.
These are very small and thesemolecules would have existed
right at the beginning of life.

(33:45):
What you see as a modernprotein is a huge molecule which
has evolved and got more andmore complicated, but it
surrounds or is involved with amuch more fundamental piece of
chemistry or photochemistry typemolecule, an FAD.
This is kind of one of themolecules in the electron
transport.
Again, it's fundamental to alot of these reactions.
So when you start going backthrough time you can see how

(34:08):
these things are built up.
You know, at the moment we seemassive complexity, massive
complexity, but if you drilldown and go back in time you see
a much greater simplicity,which in particular, is around
controlling electron and protontransport.

Speaker 2 (34:23):
And look at the you mentioned cytochrome, cytochrome
4, cytochrome C oxidase.
I mean, I believe that's builton some copper centres.
Yes, that's right yeah, thephotochromes.

Speaker 1 (34:35):
I mean that's one of the theories about um, how red
light's working, because it doesabsorb in the red red region
near infrared region.
But of course every site, every, every component of the
electron transport chain, uhabsorbs at a different
wavelength.
And this, interestingly, itgoes from the top.
Say, complex one is near a 450,through a way down to 340,
actually with an nf.
But as you go up, go up to theother end of the complex, down

(34:57):
towards cytochrome C, it's at amuch longer wavelength and I
find that fascinating because itsuggests a cascade of energy.

Speaker 3 (35:05):
It's actually an electron transport chain could
be considered as a photontransport chain.
Yeah, it's a photon, yeah,Absorbing at one wavelength,
emitting at another, which isthen absorbed all the way down.

Speaker 2 (35:17):
Yeah, the next.
The key point I think to beemphasised in this light and
biology story is thisdistinction between these solar
photons, photons of solar origin, and photons endogenously
generated photons.
Because to me and I raised thiswhen we talked, jeffrey, in our

(35:38):
first podcast, and it was a bigtheme of my first podcast with
Dr Jack Cruz, which is this is astory.
Life and light story is one ofsolar light and solar photons
interacting with our biology andthen our biology generating
light, but also re-emittinglight that we're absorbing

(35:59):
externally.
That's how I think about it atthe moment.
Would you think that's corrector what are your thoughts?

Speaker 3 (36:07):
uh um well, we need to think about uh bio photons as
well, not yeah, well, I mean,there's, there's, I mean I think
that there is again.

Speaker 1 (36:17):
There's a very interesting thing which would,
which touches on something wementioned in the report, and
this comes back to again theorigins of life, but it also a
definition of life and what lifeactually is.
Now you I guess you're are youaware of the, the idea that life
is basically a far fromequilibrium, a self-organizing,
dissipating structure.

(36:37):
But if you think about it fromthat perspective, it starts to
become very, very interesting,because you start to see all
these cascades.
And you mentioned cholesterol.
But of course, what happenswhen you shine light on
cholesterol?
You go through a wholephotochemistry which dissipates
the energy and you end up withvitamin D.
Was that process right at thebeginning, simply a
cholesterol-like molecule beinga sunblock?

(36:57):
But as the chemistry progressed, with the increasing the energy
, of course that became part ofthe biological signaling
mechanism.
And so you can see how all ofthese pathways and the same as
the calocrinin pathway in thebrain, or what you see as the,
the inflammatory pathway thatagain follows, and same with
melatonin, they, they're allchemistry, it's basic chemistry
going down through like energylevels and following the energy

(37:21):
energy gradient, and they're all.
They're basically dissipatingthe energy.
So when you come back to theidea there's been this idea for
a long time that life exists todissipate the solar potential,
so you get high energy photonscoming in from the sun, but life
has then evolved to dissipatethat down to low energy, so
therefore fulfilling entropy andthermodynamics.
But of course, that's not theonly source of light I've got

(37:45):
too much time to go in this butthere's certainly other sources
of light, like in thermal vents.
They glow in the infrared, sothere's energy in other places
other than just the sun, whichis another fascinating topic in
and of itself.
Indeed, some of these ideassuggest that's how
photosynthesis actually started.
It didn't start with solarlight, it started with thermal
vent light.
Wow, we don't know.

(38:09):
We don't know, but there'sinteresting chemistry in there.
You know, life begets its ownorigins and I and I think this,
this is certainly somethingwhich you know is we're
fascinated with.
I'm certainly trying to lookinto at the moment how this, you
know, fits in with all this butyou're right, it's all about
space travel max yeah, I want to.

Speaker 2 (38:29):
I want to bring it back to the second point that
you made about blue light, andit is relevant for space travel,
because the lighting situationin the International Space
Station although I believe thatthey're trying to make some
steps to correct it has beenhistorically predominated by a
visible only LED lightingsituation, situation such as we

(38:51):
find ourselves thanks to uh veryill, ill-informed governmental
policies, um, we find ourselvescollectively sitting under uh
here on earth.
So, if what, what?
What you?
What you mentioned earlier withregard to the talks, the, the
implications of blue light umbeing absorbed by this
tryptophan protein complex andgenerating massive reaction

(39:13):
oxygen species.
That, to me, could potentiallyexplain part of the reason why
existing in a blue only visiblesituation for 18 hours a day or
longer is contributing to humandisease and perhaps the
metabolic syndrome and thedeleterious metabolic outcomes

(39:34):
that you get in that life.

Speaker 3 (39:39):
You have to think about the balance of the blue
and the red.
Yes, if these mechanisms createtoo much blue of itself may
have detrimental effect, butthere would normally be
balancing mechanisms withinwithin the cell.
In the presence of red light,and throughout the day, the blue
red levels are are changing andover half of the photons that

(40:02):
that, that with which we'reirradiated from the sun we can't
see.
Uh, yeah, so this is half thelight going into the eye doesn't
come to go through the pupil.
It, uh, it just goes straightthrough the sclera and it's in
the 900 to what?
Two thousand nanometer range.

Speaker 1 (40:20):
Yeah, yeah, I mean this is a balance.
That's because you youinterviewed bob fosby, didn't
you?
And he interested with bobfosby about this and scotsman
too yeah yeah, and so if 70% ofthe light coming from the sun is
actually red or in thread whenwe go indoors and exactly the
point you make it's suddenly allblue light.
And this is, I think, that youknow this idea.

(40:40):
If you go into a hospital, forinstance, it's the worst place
to be because it's completelythe wrong light spectrum well.

Speaker 3 (40:45):
Plus, they have double glazing to insulate the
to the heat in, but that stopsall the red light coming in, so
you become red-starved and toomuch blue.
And I think in the spacestation I think Max they changed
the lighting in 2012, possiblyfrom some more incandescent form

(41:06):
to the LEDs.

Speaker 2 (41:08):
They did the same on British submarines as well, and
I think we're reporting the samesort of pattern of of quite you
know well submariners, uh, whenthey resurface after 70 or 80
days underwater so so the wayI'm thinking about um this, as
it relates to mitochondrialhealth and, and you know you,
you we've observed that theseastronauts are coming back

(41:30):
pre-diabetic or insulinresistant and and that is a that
must be a that's a pretty bigdeal, considering these are the
fittest athletes that you knowthe world is, is is sending up,
and they're coming back pre-diet, pre-diabetic.
So, um, I would urge caution.

Speaker 1 (41:46):
It's not always, they're not always that bad,
it's more subtle.
I think, and I think this isbeing part of the problem is
that many I mean I'd beinterested to see how this
couple are stuck up on the spacestation moment come back.
They don't look very well atall.
But, um, I think the I thinkvery fit people will probably be
able to manage this and Isuspect they may have metabolic
changes, indeed as, as you know,they quite clearly have

(42:08):
mitochondrial changes whichwould suggest they're going down
that path.
But I think the real issue hereis what happens with older
people who are less fit whenthey go up.

Speaker 3 (42:19):
And if they come back with accelerated aging.
So they're not pre-diabetic inthemselves because they're still
very, very fit.
But if these changes remain fora number of years and some of
them have been seen to lastabout seven years or so then
they last for a number of yearsas these people get older and
less fit and then they getintervening or attending

(42:42):
pathologies when they call upontheir mitochondria to provide
better homeostasis.
They've lost mitochondrialflexibility, so the problem is
delayed.
It's like long COVID.
I suggest that we haven't seenlong COVID yet.
We'll see that in 10 to 20years' time when 60-year-olds
have the mitochondria of an80-year-old.

(43:02):
And so I think it's why it'sreally important that we have to
get a measure of biological agein terms of metabolic terms, so
we can look at the epigeneticclock, we can look at proteomics
to, because otherwise somebodycould come back with their
metabolic age really accelerated.
But they're effectively goingfrom the age of 30 to the age of

(43:24):
50.
You won't notice any differenceuntil another 20 years down the
line.
I think that's something weneed to think about.
But also that's from returningfrom the International Space
Station low Earth orbit thatactually sits in the Earth's
magnetosphere.
What we don't have anyexperience of?
Is humans spending any lengthof time, any reasonable length

(43:45):
of time, outside, say on themoon's surface for months at the
end, or the eight months ittakes to get to Mars, or when
you get to Mars, and thatextended hypomagnetic
environment, from our view andfrom the research we've
commenced already, may causeextremely severe illness amongst

(44:09):
these astronauts, severeillness amongst these astronauts
.

Speaker 1 (44:12):
I mean because you know the last Artemis 1 mission
which went around the moon andthey measured radiation going
around there and what wasinteresting, they showed that as
the capsule left Earth's orbitit went through the two belts,
which was predominantly a protonbelt and an electron belt, and
that increased the amount ofradiation that it would drop off

(44:34):
.
But as it went around the moonthey were exposed to a much
greater level of GCR and indeed,just orbiting the moon, by far
the greatest radiation dose camefrom the GCR and interestingly
they had problem shieldingagainst that, whereas the others
the protons and the electronfields they could shield against
, but not so much the GCR.
And of course this raises areally interesting question

(44:55):
because, as Geoffrey says, wehaven't done a simple experiment
yet which is to put, say, acolony of mice in orbit around
the moon for two years to seewhat happens to them.
We just don't have thatlongevity data.
You know, what we've got is theonly moon mission is actually,
didn't they go to solar minimum?
And it was when the moon wasactually in the Earth's magnetic
field.

Speaker 3 (45:13):
Briefly, that's why they chose the timing very, very
carefully.
Yeah.

Speaker 1 (45:18):
So we've got no data, we just don't have it.
There's some modeling going onthere, but we just don't have
the real data, and I find thisquite extraordinary.

Speaker 3 (45:28):
Are we to expect, possibly, as people explore way
past low Earth orbit so that'spast 1,500 miles or so and spend
one, two, three months in openspace or on the surface of the
moon or Mars, if they get there,are we to expect to see
something like an ultra-severe,long COVID phenotype where,

(45:53):
effectively, mitochondrialfunction is literally down to
basic survival level and ATP-ROSratios will be off the scale
and all the other sequelae ofthat, both in terms of loss of
homeostasis, loss of adaptation?
What we have to worry about moreis not the chronic effects of

(46:14):
what we see of exposure at lowEarth orbit, but what might be
the acute, so the immediate,early and delayed effects of
going beyond the magnetosphere.
I think nobody knows that We'vestarted experiments at
Westminster and Harwell withhypomagnetic chambers putting
mitochondria and other uhorganelles and cells in, and

(46:36):
we're, you know, beginning tosee what you know the, the
profiles of, of what we mightexpect, and some of that data
will get published in, certainlyin june course the because,
sorry, going on no I'm justgoing to say I mean one of the
things that we were kind ofmaking a point of and just that
we are hopefully getting a paper.

Speaker 1 (46:57):
We submitted a paper talking about this, but actually
it's about one of the ways tolook at a lack of gravity, of
course, is you lose the stimulusfor mitochondrial function and
of course you're then sendingpeople off for seven or eight
months with a degradingmitochondrial function simply
because they're not beingstimulated.
And I think one of the keythings here is and we're not
alone in thinking this it'squite possible that you will

(47:20):
never be able to do enoughexercise in zero gravity to
offset the lack of gravity, andour systems require that 1G and
exercise to function properly.
Take away the 1G and we'regoing to find all sorts of
problems, which of course raisesthe question about will we get
enough gravity on the moon orwill there be enough gravity on
Mars to offset some of theseproblems?

Speaker 3 (47:42):
Well, the moon is only 1 sixth G and there isn't
enough.

Speaker 1 (47:48):
This comes back to the hormesis idea that we would
be evolved at 1g.
We require because gravity is avery powerful hormone what they
call a hormetic, and certainlyhave done experiments with
hypergravity, where you spinpeople around, you know slightly
more and they certainly getbenefits, and there's been, it's
been, investigated as whetheror not you could use that as a
preconditioning mechanism beforeyou send people into space.
You know, you, you spin themaround at 2g for three weeks and

(48:12):
they can survive a bit longerwithout having to do that in
gravity.
But I think you know there arethings here we don't understand.

Speaker 3 (48:21):
At a cytoskeleton point of view.
Alistair and we were talking inour report about super radiance
and microtubules.
Then it might be worth talking,max, about tensegrity, so
gravity and inertia, and howthat might affect the
cytoskeleton and might affectquantum function within
mitochondria.

Speaker 1 (48:44):
Well, I mean to the point.
I think, if you've heard, oneof the key points we made was
that you know, when you look atthe lack of gravity, you know
everything's evolved under 1G.
And you know when you look atthe lack of gravity, you know
everything's evolved under one G.
And of course, in every cell,and including in prokaryotes,
which have a very, veryprimitive, some of the very
primitive cytoskeletons, andcertainly in complex organisms
like us, you know what you carryout, to where we have
mitochondria, mitochondrialfunction is completely

(49:06):
integrated with the cytoskeletonand so as soon as you unload it
, the system is stressed,because it's not used to that,
but on an everyday process, ofcourse, this is important how
cells detect, for instance, themovement of other cells or
stress, or even when you jump upand down.
And the same thing happens withplants, although they have some
quite interesting stressdetection systems and, as it

(49:27):
turns out, because they allthink about mechanotransduction
as the mechanism for gravity,sensing how plants and animals
sense gravitation.
But actually it seems to bemore sensitive than people
realise.
And if this is the case, forinstance, there's arguments that
the organisms can attack lunarcycles through gravitational

(49:48):
changes.
And if this is true, what isthe mechanism?
This goes back to the circadianidea you were talking about,
but in terms of the lack ofgravity, yeah, you unstress a
cell and suddenly, as Geoffrey,there's this concept called
tension-induced integrity, andany architect will explain to
you.
It's like the keystone and thearch.
You require the gravity to pushthe whole thing down, to give
it structure, and we're just thesame and we can survive without

(50:12):
it.
But the whole system suddenlyunstressed, and inside your
cells, the whole of the sky'sskeletons is changing and that
gives a very powerful andgenerally is associated with a
generation of reactive oxygenspecies.

Speaker 3 (50:25):
And so, as there seems, steve thorne's group say,
the gravitational field inwhich we have evolved and we
live is oscillating all the timebecause of the relative
movements of the Earth, the Sunand the Moon.

Speaker 1 (50:42):
We circle because we've got the Moon, but the
Earth actually circles aroundwhat they call a barrio center,
which is the Earth, lunarcentral gravity, which means
there is a wobble, and certainlythere's.
Steve Thorne, who we know wasworking for the Copernican
project, is suggesting well,could this be important Because,
of course, within your nucleusyou have a very heavy?

(51:03):
Well, your nucleus of an atomis very heavy, but the electrons
around the outside are verylight, and so does that mean
that they want the entire atomwobbles a bit more than the
outside are very light, and sodoes that mean that they want
the entire of the atom wobbles abit more than the outside?
And if it does that, of coursethat changes all the
electrostatic interactions andpotentially alters it how it
reacts to a magnetic field.
The answer we don't know, butof course there is other ways of
explaining this.

(51:24):
But certainly this idea thatorganisms can detect
gravitational shifts verysensitive, million times less
than they normally would, doessuggest something really quite
interesting.
So of course, as soon as youremove that or change the
circadian rhythm, you arealtering this entrainment with
the circadian clock again, whichcould be a problem for somebody
circulating around the Earth 16times a day, which is why this

(51:45):
is rather complex.

Speaker 3 (51:49):
People said why don't you just strap a magnet to the
outside of a spaceship?
But it's far more complex thanthat, that the gravitational
fields are oscillating, themagnetic fields have to be right
and as you proceed out in space, we suspect there's going to be
an extremely complex algorithmto try and reproduce, if
possible, the Goldilocks zone inwhich we have evolved for the

(52:10):
last billion years or so.
And unless we can reproducethat zone appropriately and
understand what the physicalstresses are, as opposed to the
biochemical or the physiologicalstresses are, unless we
understand what those stressesare and how they impinge on
mitochondrial function or on allother cellular function, it's
going to be difficult to providean environment where humans can

(52:33):
maintain their adaptability.
As they move out Now, thehumans will have difficulty.
The other issue to think aboutis that the single-cell
organisms, prokaryotes and smalleukaryotes, may adapt far more
quickly because of their youknow their cycle and uh, that
would then have a an impact onthe host, host, um, microbiome

(52:57):
interaction.
And as we also know that, uh, alittle while ago nasa announced
they had found 18 mutations ofbacteria on the space station
which don't exist on earth.
So the on the space stationwhich don't exist on earth.
So the, the microbiome whichforms the majority of the cells
that you're looking at it'sabout 53 percent of us will

(53:19):
probably adapt far more quicklythan a complex organism like
like like humans.
Then if you've got a mismatchbetween the microbiome trying to
adapt and the Hume's to adapt,there'll be all sorts of
downstream issues to consider interms of human health and the
way in which we interact withand rely very heavily on our

(53:40):
microbiome.

Speaker 2 (53:42):
Yes, the implications are incredible and if you will
let me I'll summarize quickly.
It seems like spaceflight isassociated with this accelerated
aging phenotype and that isequivalent, so to speak, to
mitochondrial dysfunction orimpairments in mitochondrial
function.
And the exposures that we'relooking at here are zero gravity

(54:06):
or a loss of gravity and thetensegrity that is helping keep
structure in the cell and themitochondria.
We're talking about radiationexposures that we don't get on
planet Earth, which include thishigh LET, which are these
helium nuclei and other kind ofsolar essentially nuclei and

(54:27):
high-energy particles, and thenthe low-LET, which is the gamma
rays and X-rays, and we haven'teven mentioned things like radio
frequency and, potentially,radiation that man-made emitted,
and that's a discussion foranother podcast.
But it seems like that form ofnon-native EMF is having severe,
well consequential biologicaleffects.
And then we've got the loss ofnear-native emf, is is having
severe consequential biologicaleffects.
And then we've got the loss ofnear-infrared radiation which,

(54:50):
as you mentioned alistair, ismaking up um more than half of
the solar photons that weirradiated on on planet earth.
And and what the consequencesthat are having for
mitochondrial physiology theatpa spinning if we're suddenly
in a near-infrared dark area,the loss of circadian
environmental cues from visibleonly lighting, from this absence

(55:13):
of perhaps true darkness andthe other kind of space station
light exposures, and thenfinally, the loss of the
magnetic field, which you'veeloquently informed us that it's
likely that we're sensitive tothe orbiting of the moon around
the planet Earth.
So to me this seems like anabsolutely quixotic endeavor to

(55:37):
really allow humans to go beyondthis environment that we've
lived in for the past threebillion years, iteratively
growing from single cellularorganisms.
There's no way in my mind thatwe are going to recreate these
conditions to allow people tosurvive or thrive at all in this
environment.
And in my mind it seems likeany astronaut that signs up to

(56:01):
go to Mars or the moon has tosign a piece of paper
acknowledging that they'reprepared to get cancer at the
age of 50, to get diabetes atthe age of 40 and perhaps um,
because of the mitochondrialstresses that are going to be
involved I, I mean I, I thinkthat's interesting, I mean
that's that's, that's true.

Speaker 1 (56:22):
but I think I I was talking to somebody who's um is
a scientist and then he's beenspecializing in building
centrifuges.
Uh, last week, and the evidenceis that if you could and you've
seen all the science fictionfilms, you know the martian they
all have they will haverotating space stations and the
truth is that probably is thesolution, certainly for a large

(56:43):
chunk of at least getting thegravity back, and this has lots
more effects than simplyenhancing a mitochondrial
function.
But he was making the pointthat actually is it really that
expensive to do?
Certainly they put experimentson the space station now where
they've actually had small minicentrifuges and they put things
like fruit flies and cells inthere and they've shown quite

(57:04):
clearly that having the minicentrifuge greatly improves the
health of those cells or fruitflies, and I'm sure there are I
know there are other experimentsthey're looking at at the
moment.
So the question is we canprobably go some of the way to
offsetting that?
We can certainly.
For instance, if we could builda centrifuge in space, we could
certainly, for instance, getthe light right.
That's certainly something wecould sort out fairly easily.

(57:25):
Um, the other factor which, ofcourse and this only came out
quite recently and it's probablywell known, but I didn't
realise that on the spacestation they run at a lower
oxygen level, but they alsoapparently run at a slightly
higher carbon dioxide level.
Now, of course, any biochemistwill tell you straight away that
that can start to trigger offhypoxic mechanisms in cells.

(57:45):
There's this thing called ahypoxia inducer factor, hif1.
But this is very sensitive toROS and if this is the case,
you're automatically pushingmetabolism in a certain
direction, towards glycolysis,which is fine for a little bit.
But what's going to happen forthree years?
And again, this is anotherwhammy on the mitochondria,

(58:06):
because you're asking it to dosomething else, but the body
wants it to do something else,which is not necessarily that.

Speaker 2 (58:11):
And so is this another factor which I mean.

Speaker 1 (58:14):
again, I don't know the actual figures and I'm
afraid I'll have to find out,but if this is indeed the case,
this is a very subtle, yet othershift that we need to sort out.
But again, it's probably notimpossible.
But the reason they reduceoxygen, obviously, is for safety
reasons, as we discovered inthe Gemini mission, the early
Apollo series well, the GeminiApollo.
But the case about this, ofcourse, it is yet something else

(58:34):
which has changed.

Speaker 3 (58:37):
What I think we have to be very careful, though, max,
is when we've looked at thisover the last couple of years,
we've become more and moreconcerned not only about the
long-term health but also theshort-term survivability in
these circumstances, of whichvery little is understood.

(58:57):
And there are some potentialmitigations.
But before we can think aboutmitigations, what we really need
to do is do a couple of things.
One is establish whether thisthinking represents a real
phenotype, a real phenomenon.
If it does, how can wecharacterize it, what is the

(59:18):
impact of it and whatmitigations might be made.
And to what extent will thosemitigations be acceptable in due
course?
And that will then askquestions of whether, whether
man is in fact actually trappedtrapped on Earth.
But there are some mitigations,for example, in the space,

(59:39):
associated neuroocular syndrome.
There's a couple of papersrecently on using near infrared
or infrared light to try andreduce those.
So we could see a combinationof reintroducing some
gravitational effect with it,with it, with it with a
centrifuge, balancing blue andred light appropriate times

(01:00:01):
during the day and make surethere's plenty of uh, uh of
infrared light and uh and, andproviding some sort of magnetic
um environment.
And now that might not be inthe whole spaceship?
It might be, you know, peoplewearing suits which irradiate
them with a little bit red lightand provide us a local magnetic

(01:00:21):
field or whatever.
But the complexity of sortingout this, this uh gold lock zone
, is going to take significantcomputing power, to the extent
that if you had so muchcomputing power you might wonder
whether it might be easy justto send a robot.
And one of the earlier thingsthat we asked the, the quantum
physicists, is that um was thedirection of a magnetic field

(01:00:45):
important in terms ofdetermining spin?
And their view was that thedirection of the field wasn't so
important.
And I was thinking at the timewhen the Earth's magnetic fields
had flipped.
And you do get a complete flipor wobble and, as you know,
recently the North Pole hasstarted moving at 23 kilometers
a year as opposed to nine.

(01:01:07):
And there was a very interestingpaper from your uh part of the
world, from new zealand, lookingat the um sort of the geomatic
magnetic history of the earth,and what it pointed out was that
uh around about the times ofthe magnetic switches, where the
poles switched um and thedirection may not be important
for spin.

(01:01:28):
What happened is the Earth'smagnetic fields dropped
dramatically down to about 5microteslas that's their
estimate from the 45 to 50 or 45to 60 that we exist in, and the
suggestion was that these dropswere coincided with mass
extinction events.
These drops were coincided withmass extinction events.

(01:01:52):
So we're somewhat concernedabout about about the impact of
hypomagnetic fields on on humanhealth, not only here on earth
but, of course, acutely.
We'll be able to study thisacutely in space.
So we can study this acutely inspace.
We can look at metabolicsyndrome in space.
We can can look at aging andyou've got an accelerated
laboratory environment in whichwe can bring the learnings back

(01:02:13):
to hopefully deal with all ofthese issues that are occurring
according to lifestyle changeson Earth has been said that
space is a very good model foraccelerated aging.

Speaker 1 (01:02:28):
I mean, yeah, you know, which is perhaps not what
people want to hear, but we mayI mean back to the fundamental
question of aging, which wedon't still fully understand.
This could be a good model forit, um, which, of course, is not
what everybody wants to hear,but maybe we've got to solve
this one first, and the point wemake, and we certainly
certainly made in ourpresentations on this, is that,
you know, we haven't haven'tsolved the ageing problem and
health on Earth yet.
How can we honestly expect tosolve it in a much more complex

(01:02:50):
environment like space?
You know, when the beast iscosting $2 trillion to $4
trillion a year, we're spendingless than $100 billion on space
health.
You know, you do the maths.

Speaker 3 (01:03:02):
So I think Max, whereas we do have some really
clear concerns.
We don't want to alarm peopletoo much, but if our thinking at
the moment is borne out infurther experimentation some of
which has already been done andone paper came out of our work
looking at prostate cancer cellsand in the hypermagnetic

(01:03:27):
chamber they grew more quicklybut if we really need to get to
grips with this phenomenon and Ithink if we can carry out the
research in the UK and the USand elsewhere, we'll have these
answers within about 12 to 18months of whether this is a
concern and to what extent it'sa concern.

(01:03:49):
I think it'll then take anothercouple of years to characterize
fully, and probably the next twodecades to work out how to
mitigate on the immediate andthe long term and with a
significant amount ofexpenditure.
So in that case, what we see isthat space engineering is

(01:04:13):
probably two decades ahead ofspace biology, with perhaps
exception of the Chinese, whohave been thinking about this
for a few years.
They've got some rather wefound some in some obscure
papers.
We found their references tothe impact of hypomagnetic
fields on hippocampal cellgrowth, that sort of thing, and
with one single line in theirpaper saying and this might have

(01:04:35):
an impact on space travel.
So we do think that some peoplehave been thinking about this
for a while, whereas others havecompletely.
It's not been in the mainstreamof of of their scientific
endeavors.

Speaker 2 (01:04:48):
no, and and that's why I want to congratulate you
both, and I think this report isis an absolute masterpiece
because it's saying theinconvenient part for people
like elon musk you know very,very much out loud, and it's
really bringing some adultdiscourse to what sometimes can
be as I use the word, quixotic,I mean grandiose, that you can

(01:05:11):
pick an adjective.
But, as you mentioned, thespending on space biology is a
single digit or less as aproportion of space expenditure
and it's so far removed from thereality, the biological
realities which, albeittheoretical, you both have
really laid out in this spacereport, and I'd really encourage

(01:05:31):
people who are listening to goand back, read the space report
yourself or check out myprevious video it's on YouTube
and my podcast feed where Iprovided some analysis on that
report, on that report.
But it's just my opinion that Ithink the look towards space by

(01:05:52):
people like Musk it's admirablefrom an engineering point of
view, but it really takes theemphasis away from planet Earth
and the fact that there's somany important unsolved problems
on planet Earth that chasingknow, chasing after, um, you
know, living on other planets,in my opinion, and is a
misdirection of our amazingresources and and and um, you

(01:06:16):
know intelligence and andtalking about things like the
interaction of light and life.
You know I've been talking tophotobiomodulation engineers and
the amount of clinical researchwe could do looking at the
various use of white wavelengthsin cancer in name a medical
condition is yet to be done.

(01:06:36):
I think these are some of themost exciting things that
potentially could be done.
But, yeah, I really want tothank both for for putting this
report out, because it's itsvalue for space, but also for
its implication for quantumbiology and human health are are
enormous well, thank you verymuch indeed.

Speaker 1 (01:06:55):
Thank you, if we, if we can identify the issues and
correct them in terms of findingmitigations, if we can find the
mitigations in the compressedtime scale of the accelerations
in space, then all of thoselearnings should help us, uh,
work out how to treat, um, howto, how to treat the lifestyle
induced illnesses that we'reseeing on earth at the present

(01:07:18):
so thanks I mean there is quitean interesting parallel here,
because we certainly got intothis, because we were looking at
natural products and phenoliccompounds and certainly the
point this was exactly the pointwe're making and we know,
certainly for nasa, they'relooking at, you know, cocktails
of different natural products tosee if they can offset
oxidation and I think there'ssome evidence that it might work

(01:07:39):
, but I don't think it's goingto be anything like enough.
You know, it's like living amediterranean style on steroids
in space, but it probably stillwon't be enough to offset the
problems.
But it'll probably help, but wedon't understand how they're
working.
And this is this again, it'sanother big question.

Speaker 3 (01:07:53):
Yes, it's a great point and we'd leave you with
the thought that the medicinesfrom nature that that are
actually introducing into us andnot only medicines, things like
blueberries for the polyphenolsand and strawberries the
anthocyanins are all helpingmitochondrial function.
Why?
Because they help mitochondrialfunction in the plants yeah,

(01:08:13):
and the plants, and this is whybecause plants have mitochondria
, and probably more as aninformation transmission than
than energy, energy generation.
So we have suggested in thereport that one solution might
be to grow the plants in spaceand feed the extracts of the
plants to the astronauts,because the plants will work out
exactly what adaptive responsesit needs in terms of to

(01:08:36):
maintain their mitochondrialfunction, which will then
maintain the human'smitochondrial function.
Just an interesting thoughtthat we might leave you with.

Speaker 1 (01:08:43):
Well, it's an old idea, it's called xenohormesis
thought that we might leave youwith.
Well, it's an old idea, it'scalled xenohormesis and it was
an idea which was, I think,lambing a long time ago.
Suggested that one of thereasons that plants help us,
certainly in the autumn, is thatwe eat the plants when they're
getting cold and they've beenstressed, but that stress signal
is passed on to us.
That helps us live, be a bitstronger than we were before so

(01:09:04):
so these are old ideas, that'sprobably another podcast for Max
.
I know it's not complete, yeahwell, I would definitely.

Speaker 2 (01:09:14):
I think we need to continue this conversation about
the myriad of topics andquestions this discussion and
ours previously Geoffrey, hasopened up.
So very much interested intalking to you both again,
because I believe this is thecutting edge of of health and
medicine and, uh, it's, yeah,it's a pleasure to to have such
stimulating and interestingdiscussions with with you

(01:09:36):
excellent, thank you.

Speaker 3 (01:09:37):
You can read about it in the book yes, yeah and uh,
that's it.

Speaker 2 (01:09:41):
That's a great time to mention, and the blurred that
, quantum biology.
Yeah, it's all blurred.

Speaker 3 (01:09:44):
Yeah, it's a great time to mention the it's a bit
blurred that quantum biology.
It's all blurred, yeah.

Speaker 2 (01:09:48):
It's a little bit blurry, hang on, that's my Zoom
settings.
But Quantum Biology A Glimpseinto the Future of Medicine by
Dr Jeffrey W Guy.
I highly recommend it and it'sa great overview of the state of
what the foundation is doing atthe moment and I've thoroughly
enjoyed it.
So would recommend everyonegrab a copy.

(01:10:09):
It's on Amazon now, I believeIs it for sale on.

Speaker 3 (01:10:12):
Amazon, yeah, absolutely Worldwide.
So thank you, max.
Thank you very much indeed.
We'd be happy to talk to youagain.
Fantastic, yes, certainly woulddo have a nice day, alistair.
Thanks a lot.
Thanks, man.

All Episodes

89. Magnetic Fields, Mitochondria & Quantum Biology | Professors Geoffrey Guy & Alastair Nunn

BYRON HINTERLAND RETREAT - Circadian Living by Regenerative Health Retreats

Episode Transcript

Popular Podcasts

24/7 News: The Latest

Therapy Gecko

The Joe Rogan Experience

.css-15opob5{left:0;position:absolute;top:0.8rem;} All Episodes

.css-14f5ked{margin:0;word-break:break-word;display:-webkit-box;-webkit-box-orient:vertical;box-orient:vertical;-webkit-line-clamp:2;overflow:hidden;}89. Magnetic Fields, Mitochondria & Quantum Biology | Professors Geoffrey Guy & Alastair Nunn

BYRON HINTERLAND RETREAT - Circadian Living by Regenerative Health Retreats

Episode Transcript

Popular Podcasts

.css-r6mb8g{margin:0;word-break:break-word;display:-webkit-box;-webkit-box-orient:vertical;box-orient:vertical;-webkit-line-clamp:1;overflow:hidden;}24/7 News: The Latest

Therapy Gecko

The Joe Rogan Experience

All Episodes

89. Magnetic Fields, Mitochondria & Quantum Biology | Professors Geoffrey Guy & Alastair Nunn

24/7 News: The Latest