June 3, 2025 • 64 mins
In this presentation, I disucss the evidence for sunlight, Vitamin D system and circadian rhythms in regulating cancer defense and immune function in the body. I also discusses nuances surrounding skin cancer and how to safely obtain sunlight in a skin-type appropriate manner.
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Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 2 (00:24):
The topic of today's talk.
I've intentionally titled itSunlight and Cancer Beyond Skin
Deep, and the purpose of that isbecause I believe that there is
sufficient evidence to supporta profound role of natural
sunlight in supporting healthand in supporting cancer and,
given Australia, particularlyour narrative and our
(00:47):
discussions and experiences withskin cancer and attitudes to
sun, that I think this is goingto be an important exploration
of the whole story, or part ofthe whole story.
So cancer is a growing problemand sometimes I like to look at
economic data because it cantell a very, very interesting
(01:09):
story in and of itself.
But these companies these arethe most profitable
pharmaceutical companies in theworld, and this business website
made the comment that theglobal oncology drugs market was
valued at $201 billion in 2023,and this is forecast to grow to
(01:31):
$518 billion by 2030.
What did they attribute thismarket growth down?
To Well, factors such as therising prevalence of different
types of cancers, increasing newdrug launches and product
approvals, and growing researchactivities by pharma.
Well, factors such as therising prevalence of different
types of cancers, increasing newdrug launches and product
approvals, and growing researchactivities by pharma companies
in the field.
So what is cancer?
(01:53):
I mean a definition of cancer,any various malignant neoplasms
characterized by theproliferation of anaplastic or
de-differentiated cells thattend to invade surrounding
tissues and metastasize to newbody sites.
That's interesting.
But what causes cancer?
That's not going to be thetopic of today's talk.
(02:14):
But I'll give you a couple ofinsights into perhaps the latest
of what we think about could becausing cancer.
These are perspectives fromsome of the top researchers in
the world.
Professor Thomas Seagree talksabout a metabolic disorder,
mitochondrial metabolic disorder.
Professor Michael Levin istalking about the loss of
(02:38):
cellular coherence from abioelectric point of view and
potential regression of thatcell into a more embryonic state
.
And also Dr Jack Cruz hastalked about the altering of
Warburg metabolism, but reallyone being reliant on a change in
light signals.
But, as I mentioned, that's notgoing to be the topic of
(02:58):
today's talk.
What I want to talk about issunlight and cancer particularly
, and the link between sunlightand cancer.
How can we frame that withrespect to what we've been told
about skin cancer and how can weadd nuance to this topic?
And finally, I'll be touchingon how we can use the sun to
(03:19):
help reduce death from cancer.
So this story it starts it'sactually quite an old story and
this is an ecological paper by aUS MD back in 1940.
His name was Frank Appley, andwhat he noticed, and he drew a
conclusion, was that when heobserved the mortality rates
(03:40):
from cancer in the United Statesand Canada, that there was
essentially an inverserelationship or an association,
and he made the comment that thetotal cancer mortalities of the
various American states andCanadian provinces are shown to
fall with increasing solarradiation and the number of
people exposed.
(04:00):
So this generated aninteresting hypothesis that
basically wasn't touched for awhole about 40 years until two
brothers, cedric and FrankGarland, who are epidemiologists
in California, san Diego, andthey in 1980, posited or asked
the question does sunlight andvitamin D reduce the likelihood
(04:25):
of colon cancer?
So they're interested incolorectal cancer and they
proposed that vitamin D was aprotective factor against colon
cancer.
What they did is they did and Iguess drawing on the work of
people like Frank Appley,because they noted that if they
were looking at the geographicaldistribution of cancer and
(04:45):
cancer deaths, that themortality and colon cancer
prognosis, which is another keyaspect of this was that it was
lowest in places with highersolar exposure and it was
highest in places where thepopulations were exposed to the
least amounts of natural light,namely major cities and rural
(05:07):
areas at high latitudes.
So what they did is a study,and this was eight years later.
They did an eight-yearprospective cohort study and
what they found?
And they essentially comparedthe risks of developing colon
cancer and they were stratifiedthat by the level of vitamin D,
(05:28):
and we're going to talk aboutvitamin D and its role in this
story.
But essentially what theynoticed was the lower that your
vitamin D level was, the morelikely you were to develop
colorectal cancer.
And what they said in thispaper back in the 1980s was that
(05:49):
the results are consistent witha protective effect of serum 25
, hydroxyvitamin D on coloncancer.
So to frame this talk, we needto understand a little bit about
physiology and about how thesun affects our skin and affects
our biological system.
So what we have is sunlight anduniquely UVB sunlight, and
(06:13):
that's a narrow range of lightthat actually hits planet Earth
and it's only present for themajority of time when a
sufficient solar angle allowsfor these high energy photons to
penetrate the atmosphere.
What it does is it hits theskin and it converts cholesterol
7D hydrocholesterol intovitamin D-like structure.
(06:47):
So that process is reliant on awhole bunch of different things
, but the key things that willaffect that is the presence and
absence of enough UVB-containingsunlight, as well as how much
melanin exists in the skin, andwe're going to talk about
melanin and skin pigmentationand how relevant that is,
(07:09):
particularly with regard to skincancer.
So what happens and this is aschematic of the physiology of
vitamin D is that vitamin D isformed and then it binds in
circulation to a binding proteinbefore being taken to the liver
and then the kidney andundergoes a range of
hydroxylation and, essentially,activation steps before it is
(07:32):
able to be used.
As you can see here, you canalso obtain vitamin D from the
diet and it's essentiallypreformed because you've
consumed animals that themselveshave made this fat-soluble
hormone.
But really, the vitamin D levelis primarily going to be
determined by solar exposure,because the sun is the main way
(07:53):
that we, as humans, generate andmaintain our vitamin D level.
So what's the role of vitamin D?
Well, most of you would knowabout the bone effects and the
research or the benefits ofsunlight and UV-containing light
predated the actual discoveryof this compound, and in the
late 1800s, in the ghettos ofEurope during the Industrial
(08:16):
Revolution, there was smog thatwas preventing ultraviolet light
from penetrating into theseareas and kids were getting
severe vitamin D deficiency, andthat was manifesting as rickets
and the bow leg look of youngchildren is the unfortunate
consequence of inadequate bonedevelopment and ossification as
(08:37):
a result of vitamin D deficiency.
But what we've learned, andparticularly over the last 15,
20 years, is that vitamin D andthe vitamin D system is not only
important for bone health, andit's actually far from it.
It's a critical part of immunesystem function and, by
extension, the cancer story,because it turns out that cancer
(08:59):
in and of itself is extremelyreliant on or dependent on the
state of your immune systemfunction.
So things like theproliferation or growth of cells
, inflammation and new bloodvessel growth, which is all
again a key part of the cancerstory this is regulated by
vitamin D.
(09:19):
So where else does this vitaminD sunshine hormone, how, what
else does it touch?
Well, I'm not going to speakabout it in this lecture, but it
it is, covering a such a widerange of of really critical
aspects of optimal health andmetabolic health, particularly
insulin resistance, obesity,diabetes, metabolic syndrome, as
(09:42):
well as I mentioned tumorformation, cancer formation and
immunity, and I'm going toexplain now, but I'll explain
later is that vitamin D isactually also and one way of
thinking about this is this is aproxy for your total sunlight
exposure.
So that's going to be somethingI'll emphasize more.
(10:02):
What else does the data suggestabout cancer and vitamin D?
Well, this study essentially isplotting breast cancer risk and
it plotted it against the serumvitamin D level.
So what you can see is a prettyprofound relationship where, as
the vitamin D concentrationincreases and we've got both
(10:23):
nanograms per mil, which is theUS metric, and nanomoles per
liter, which is us in Australiaso, of the women who had in this
whole cohort of 5,000, thosewho had a vitamin D level in the
upper ranges, their risk ofdeveloping breast cancer was
significantly lower.
(10:44):
What about for those who'vealready developed cancer?
And that's another part of thisstory?
Well, it turns out that notonly incidence but also
prognosis of cancer isprofoundly related to associated
with serum vitamin Dconcentration, and this study
suggested that the higher yourvitamin D level, the lower your
(11:05):
fatality rate in people who'vealready developed breast cancer.
And again, patients with thehighest concentration of
25-hydroxy-D had approximatelyhalf the fatality rate compared
to those with the lowest.
This systematic review covered,and it summarized, the state of
the research and it basically itsays that the evidence that
(11:27):
chronic, non-intermittent sunexposure decreases the risk of
colorectal breast prostatecancer, non-hodgkin's lymphoma
is accumulating and graduallygetting stronger.
This is nothing that we gettaught in medical school and
this is not something that you,as members of the public, get
communicated, especially withpublic health messaging around
(11:49):
sun exposure in Australia.
But this isn't locked in amusty case next to the JFK files
.
This is not private information.
You can go into PubMed and youcan search this evidence and it
exists.
So what this is pointing to isthat we've got a strong evidence
(12:10):
that the higher someone'ssunlight exposure, as we
measured via the vitamin Dsystem, the lower the risk of
the cancers that really killpeople, and that's a key point.
And I'll contrast that withskin cancers because, as a cause
of death in society, these arethe cancers that are killing the
most number of people.
(12:33):
This is one of my favoritestudies it was actually
published last year, finally byProfessor Richard Weller.
Now, richard Weller is therarest of dermatologists who's
actually looked into the dataand found that sunlight exposure
has a holistic benefit onhealth, and in this study he
(12:54):
essentially examined a databaseof over 400,000 people in the UK
called the UK Biobank overabout 12 years.
And what he did is hestratified these people.
He classified them based ontheir ultraviolet light exposure
.
So he used UV sorry, he usedtheir latitude, which was a
proxy for their UV exposure, aswell as their sunbed tanning
(13:18):
habits, and he correlated thatto vitamin D levels.
So what did he find?
He found that participants withmore active sun-seeking
behavior and those living atlower latitudes had lower crude
mortality of cancers of thedigestive system.
So I already told you that wealready had strong evidence that
it was linked to lower rates ofcolorectal cancer, but also
(13:40):
breast cancer.
Participants with activesun-seeking behavior had lower
crude mortality from skin cancerBig pause there.
Cancers of respiratory andintrathoracic organs, cancers of
lymphoid, hemopoietic andrelated tissues, which are the
leukemias, and cancers of themale genital organs.
And they also summarize whatI've just told you, which is an
(14:03):
inverse relationship betweensolar exposure and cancer
mortality in multiple sitesorgans.
And they also summarize whatI've just told you, which is an
inverse relationship betweensolar exposure and cancer
mortality in multiple sites,including the bladder, the colon
, hodgkin, lymphoma, prostate,stomach and breast.
So this is really elegantbecause we've got multiple lines
of epidemiological data, oneusing vitamin D, serum vitamin D
, which is an indirect marker ofsunlight exposure, and one more
(14:24):
direct, looking at all-causemortality and basically finding
the same thing.
So if sunlight lowers thecancer mortality, what are the
mechanisms?
So we have to talk a little bitabout the solar spectrum.
We have to talk a little bitabout light and how that affects
the body.
So what you have here is youhave the spectral irradiance, so
(14:48):
this is the solar energy thatwe get hit with on planet earth
just standing outside, and wehave the wavelength of light
here On this tiny corner here.
This is the ultraviolet lightthat is a UVA, and the UVB light
UVB is only 5% of this is thatis a uva and the uvb light uvb
is only five percent of of this.
The rest is uva.
(15:09):
So you're only making vitamin dout of a small amount of of uv
light, and that is also going tochange depending on your
latitude, it's going to dependon your season and it's also
going to depend on time of day.
What you can see with your eyesis the visible spectrum, and
the largest area here by photoncount is in the infrared and
(15:29):
that's non-visible.
So ultraviolet is essentiallybelow the visible spectrum we
can't see in ultraviolet andinfrared is beyond visible.
The key point that I'd like youto understand about this diagram
is that each one of thesewavelengths of natural sunlight
have a profoundly importanteffect on human physiology and
(15:53):
human biology.
The reason for that is becausethese are the conditions of
evolution for three billionyears, and we evolved under this
light, not under this light.
As I said, vitamin d is onlyable to be made with with uvb
light.
So so what are the effects ofuvb?
And and I'll be really specificbecause it's not only a vitamin
(16:16):
d story it stimulates thisincredibly ancient and
incredibly uh unique, uh poly uhpeptide pro-hormone called POMC
or pro-opio-melanocortin.
Pro-opio-melanocortin, as Imentioned, is incredibly
evolutionarily conserved.
It's found in ancestralnathosomes, which were relics
from prehistoric time.
(16:38):
It regulates things like immunefunction, appetite and
metabolism centrally in thehypothalamus, as well as blood
pressure and, obviously, skinpigmentation.
What it also regulates, and thedownstream product of POMC, is
the skin tanning system.
I think the most interestingpart of one of the most
(17:01):
interesting parts of POMC andits effect is that it contains
an endorphin-like chemical.
So when you get in the sun, thesame peptide hormone that is
assisting in tanning your skinis releasing a beta-endorphin,
an opioid-like chemical, toreward you for that tan.
(17:23):
So again, think about this ideaof tanning your skin cells in
trauma, which is a half-truth.
But if the sunlight is inducingtanning, but it's also
rewarding you from being inthere, and that's a
600-million-year-old programbuilt into your biology.
Who's in the wrong here?
(17:43):
What else does it do?
As I mentioned, it can causeDNA damage and particularly
creates these photo products andsunburn.
What I'll explain about as wego through is that Mother Nature
built in an extremely elegantprogram to help you repair those
DNA damage caused byultraviolet B light.
(18:04):
So UVB is a double-edged sword,but it's absolutely essential
for optimal human health.
So what did Garland and MichaelHolick, who is the world leader
on vitamin D, what did they sayabout the effects of vitamin D
in cancer prevention?
Because they were trying toexplain this finding that there
was lower colorectal, breastprostate and lower lymphoma
(18:27):
findings with vitamin D exposureand sunlight.
What they found is that thevitamin D compounds reduce the
formation of new blood vesselsin tumors.
It reduces the malignant andexcessive proliferation of cells
.
It increases or upregulatescontrolled cell death of cells.
It increases or upregulatescontrolled cell death, or known
(18:47):
as apoptosis, and it increasescell-to-cell adherence.
And I mentioned briefly aboutthis bioelectric model or theory
of explaining cancer and thisidea that the cell potentially
loses its understanding thatit's part of a structure in a
whole and therefore inducesthese anaplastic type phenomena
(19:09):
in the cells.
But luckily vitamin D ishelping those cells adhere to
each other.
Now this is a complicated slide, but the purpose is really
simple, and that is to explainto you that when you get in
natural sunlight, it's not onlythe chemical that you take in a
(19:33):
pill from the chemist, becauseit turns out that the body makes
a whole enormous pharmacy ofrelated compounds that were
initially thought to bebiologically inert but have
since been discovered to haveprofoundly beneficial effects,
and again, anti-cancer effects,effects of promoting DNA repair
(19:55):
in the skin cell scales andreally systemically.
So what else?
How else can we account forthis?
Lower rates of cancer in peoplewith greater sun and vitamin D
exposure?
Well, it turns out that yourcircadian rhythm is critical in
regulating the essentiallyoncogenic process.
And what is a circadian rhythm?
(20:17):
Many of you might already know,but it's an endogenous 24-hour,
almost 24-hour cycle that runsin the brain.
The master clock exists in thehypothalamus, behind the eye,
and it sets a rhythm that needsto be synchronized across all
tissues and that rhythm programsthe most critical functions of
(20:40):
the body, from hormonalsecretion, sleep-wake cycles,
activity, metabolism, immunefunction, stem cells you name.
It is regulated on a 24-hourcycle.
What you can do is that you canprogram your circadian rhythm
by the behaviors and thelifestyle that you lead.
So if you get bright lightduring the day, if you sleep at
(21:00):
nighttime and you consume yourfood during the day in a
circadian appropriate manner,then you're going to get perfect
synchrony between the clock inyour eye and the peripheral
clocks in your body, and that'sgoing to lead to optimal health
and optimal function of the body.
If you do the opposite, then youare going to disrupt your
(21:20):
circadian rhythm and that's aproblem.
And that's a problem becauseyour immune system, which is
supposed to be killing theseprecancerous cells that were
spontaneously being generated,they're not going to be able to
do that effectively.
So circadian rhythm and cancer.
Like I mentioned, not only doyou have clocks in all these
(21:41):
different bodies that regulatethese critical bodily processes,
but the cancer killingmechanisms, so key cancer genes
they're all under circadiancontrol.
So cell cycle regulation, dnarepair, cell proliferation and
controlled cell death If you areup all night till 2am looking
at, looking at a blue lit screen.
(22:02):
If you're giving your bodythose profoundly uh disrupting
circadian signals, it willderail your endogenous cancer
fighting and cancer killingmechanisms.
So I think that is a big partof of of potentially these
findings is is that those whohad a higher vitamin D were more
(22:23):
likely to have a more regulatedcircadian rhythm and therefore
this circadian system was likelyworking more effectively.
What's another way to accountfor these findings?
Well, this is extremely newresearch, and Scott Zimmerman
and Russell Ryder are experts inmitochondrial medicine and
physiology.
What they discovered is thatthe melatonin, which is the
(22:48):
body's most potent antioxidantsystem, was not only being
produced sorry, not onlyantioxidant but it's also a
signal for darkness and itinduces sleep.
It's not only being produced inthe pineal gland in the
circulatory system on theabsence of blue light, but it
was actually being produced onsite in your cells, in the
(23:09):
mitochondria, during the daywith exposure to near infrared
light.
So so why is that important?
Because it turns out that whenthe body is making this
melatonin extremely importantantioxidant, this free radical
scavenger and antioxidant is, itis protecting the mitochondrial
(23:31):
DNA and the mitochondrial DNA.
Mutations in mitochondrial DNAunderlie all this march towards
chronic disease, includingunderlying the physiology of
cancer and canceroustransformation.
So, simply being outside andbeing in greenery, next to the
(23:51):
green areas, you are absorbingmassive amounts of near infrared
light that are penetratingthrough your clothing and
through your body up to at least8 to 10 centimeters and helping
your body to synthesizemelatonin, which it's using to
essentially protect the cellularand subcellular machinery that
(24:13):
is allowing your cells to workproperly.
How else is this working?
Well, if we drill down into themitochondria, we can see that
this is the process by whichenergy is actually generated,
and it's a passage of electrons.
It's taking food electrons,it's taking light information
(24:34):
and it's allowing thiselectrochemical gradient to make
energy in the form of ATP andalso in the form of metabolic
water, and metabolic water isthis deuterium, depleted water
that gets produced at the fourthcomplex cytochrome C oxidase.
That process is optimized bynatural sunlight in the form of
(24:55):
all types of red light.
These are chromophores, meaningthey absorb light wavelengths
and they're modulated by lightwavelengths.
So when the body is hummingalong and when this
mitochondrial engine is hummingalong and you put the
appropriate fuel in in the formof a low-carb seasonal diet
(25:18):
that's rich in animal foods anddeuterium-de depleted animal
fats, then this process is aided.
But it's never going to beoptimally aided unless you're in
natural sunlight which, as Itold you, is extremely rich in
red light, because the red lightis helping your mitochondria
produce this metabolic waterthat is essentially hydrating
(25:41):
all the proteins and enablingthem to work properly, as well
as spinning this fifth complex,which is producing ATP.
So mitochondrial dysfunction isa prerequisite for cancerous
transformation.
It is one of the key problemsthat goes wrong when a cell
becomes cancerous, and naturalsunlight not uv but essentially
(26:04):
red and infrared is helpingsmooth this process.
So the question I think isinteresting is do we have a
marker?
Do we have a marker of how muchsunlight we have of have had?
Do we have a fuel gauge?
Because that would be reallyhelpful in seeing where people
are at with respect to thesunlight exposure.
And we do, and that'sessentially what the
25-hydroxyvitamin D test thatyou can get from your doctor
(26:27):
will tell you.
It's a storage form, but it isa rough proxy and a good
indicator of your total sunlightexposure.
And that's not only the UVB andvitamin D system, and that is
why I believe it's one of themost important tests to get and
we can explain about what wewant, and from an optimal level.
(26:49):
So it can give us an indirectidea, because if someone's got a
robust vitamin D level, then itwill imply that they've had
full spectrum sunlight exposure,including ample, near infrared,
which was the ancestral normfor our species.
But if they've got a low,insufficient or deficient level,
then you can imply it impliesthat not only have they got the
(27:12):
daytime sunlight exposure wrong,but they're probably exposed to
some artificial light at nightand they're therefore having
some degree of circadian rhythmdisruption.
Okay, so what about skin cancer?
And now?
This is the critical point.
That, as I mentioned, is thenuance we need to give to
understand this system and thisprocess.
(27:33):
So melanoma Melanoma is themost concerning and dangerous of
skin cancers and the reason forthat is because it has
relatively, compared to thenon-melanoma skin cancers, a
much higher proportion formetastasis, spread and therefore
mortality.
This is compared to thenon-melanoma or keratinocyte
(27:58):
cancers known as squamous celland basal cell carcinoma.
These non-melanoma skin cancersare not the cause of death in
people.
They're easily identified andthey're easily treated.
So the critical and mostimportant issue here is the
identification and prevention ofmelanoma, and no one's in
(28:22):
argument or disagreement aboutthat as a strategy.
So how does skin cancer fit intothis model about vitamin D?
Because I just told you thatall these really important
cancers are associated with lowvitamin D and therefore can be
thought of as a product ofsunlight deficiency.
I don't know if anyone likesStar Wars, but this is one of my
(28:44):
favorite memes and Padme isasking skin cancer patients
should have a high vitamin Dlevel from excess sunlight, and
that again is the corollary ofthe advice to avoid the sun
above a UV index of threebecause of the development of
skin cancer.
So if you extend that train ofthought, those people who are
(29:07):
developing skin cancer shouldhave a pretty robust vitamin D
level, because I told you thatthe only way you're generating
meaningful amount of vitamin Dis through UVB exposure.
So that stands to reason ifwe're following this logical
train of thought.
So this is a study from SouthAfrica.
It was a bunch ofdermatologists did this research
, so they looked at the vitaminD status of patients in Cape
(29:32):
Town so a very high UV indexenvironment with non-melanoma
skin cancer.
So what did they find?
They found that 49% of thosewith non-melanoma skin cancers
were vitamin D deficient and 31were insufficient, and they used
a cutoff of 15 nanomoles perliter.
So, interesting, even in thetumors and the cancers that are
(29:55):
canonically said to be relatedto cumulative UV exposure, we're
still seeing a significantassociation with vitamin D
deficiency.
What about this one Malignantmelanoma vitamin D status as a
risk and prognostic factor?
Now, this is a meta-analysisthat was published in January of
2025.
(30:16):
So this one is hot off thepress and it is a synthesis of
the research for the past, wellup to date with respect to the
relationship of melanoma andvitamin D.
So what did these researchersfind?
This is the conclusion.
We observed significantlyincreased risks for thicker
tumors, mitotic tumors, so thosewith higher cell replication,
(30:41):
higher tumor stages, so cancersthat are more down the track of
spread in vitamin D deficientpatients.
The conclusion was this studydemonstrates an association
between low vitamin D status andboth increased melanoma risk
and worsened prognosis, andthat's further contributing to
(31:02):
the growing body of evidencesupporting the tumor-effective
role of vitamin D.
So Vince thinks that's prettyastounding.
That's pretty against whatwe're being told.
We've been told to avoid the sunto prevent melanoma and prevent
UVB exposure above a UV indexof three with broad-spectrum
sunscreens, but that's flying inthe face.
(31:25):
So what else?
What about in patients thatalready have malignant melanoma?
And this is a British study,and it looked at 123 patients
and they had malignant melanoma,and it obviously excluded
patients taking supplementalvitamin D.
What did it find?
It found that 84% of thesepatients were vitamin D
deficient and of these, 31 wereseverely deficient.
(31:48):
How did that break down?
So, as you can see, the moremild your malignant melanoma,
the less likely you were to havevitamin D deficiency.
And all the way at the bottom,the stage four, distant
metastasis, very poor prognosis.
(32:09):
It's improved since theinvention of immunotherapies,
which has been a great invention, but it stands to reason that
this is a massive finding.
89% were vitamin D deficient.
Again, these are in patientswith metastatic melanoma.
So the question then and I thinkI've already answered it, but
I'm going to continue to promptyou to think about is how do you
(32:31):
become vitamin D deficient?
The reason you become vitamin Ddeficient is because you're
avoiding UV light and you'reusing UV blocking broad-spectrum
sunscreens, which necessitateor necessarily block the block
UV light.
The dermatologists know thisand they are trying to
(32:55):
understand this to the effect ofsupplementation unsuccessfully,
but they haven't understoodthat the critical reason why
this is happening is orassociation is because the
patients are lacking in keyanti-cancer compounds made by
full-spectrum UV-containingsunlight.
So this is just a pause and adigestion of what I've just said
(33:19):
.
So how, again, can UV light beso intimately associated with
both optimal health but also thesevere cancer outcomes?
This is a really interestingstudy and again it was done to
investigate health outcomes inwomen and they took 20,000,
(33:39):
25,000 Swedish women and theyfollowed them for 20 years,
inquiring at baseline about sunexposure habits.
Do they tan in winter, do youtan in summer, do you use
tanning beds and do you traveloverseas to tan?
And the hypothesis of theseresearchers was that those who
tanned the most, who had themost sun-seeking behavior, would
get the most melanoma and thenwould die more frequently.
(34:03):
And really that was theirhypothesis and that's why they
called it the melanoma insouthern Sweden study.
So they were right about thefirst thing the women with the
most sun exposure did get themost melanoma.
But they were completely wrongabout the second part, because
it turned out that the womenwith the most active sun-seeking
behavior had the lowestmortality, and that was a
(34:26):
dose-dependent effect, with theones who avoided the sun having
the greatest mortality.
The conclusions of the paperwas that sun avoidance was a
risk factor on par with smokingfor all-cause mortality.
And the way they worked thatout is that they found that the
women who smoked but gotsunlight and sought the sun and
went tanning they had the samemortality as the women who
(34:49):
avoided the sun and didn't smoke.
So that's a magnitudeequivalence of risk factor for
all-cause death.
What they put it down to wasthe women who were tanning were
dying less of cardiovasculardisease, stroke, but it turns
out that they were also dyingless of skin cancer.
So this graph was a plot ofthose without skin cancer, those
(35:10):
with non-melanoma skin cancerand those with malignant
melanoma, and it was the odds ofdeath, odds of all-cause
mortality, and, as you can seein the groups, the women who
avoided the sun in eachsituation they diligently wore
their sunscreen they had thehighest odds of all-cause
mortality.
And the tanning the onesgetting up there in their
(35:33):
bikinis from the morning to theevening in Sweden had the lowest
mortality.
And that was consistent finding.
What did Peli Linkwes say?
He's the chief investigator andhe's one of the world leaders
in investigating the systemiceffect and benefit of sunlight
on health.
He said there is a relationshipbetween high sun exposure and
(35:55):
malignant melanoma incidence,but an inverse relationship to
prognosis.
But an inverse relationship toprognosis.
Thus, high UV exposureincreases the incidence as in
more people are going to bediagnosed with melanoma, while
low sun exposure habits onvitamin D levels have been
linked to thicker, moreaggressive melanoma with shorter
(36:16):
survival times.
So a very, very profound studywhich is explaining that there's
this trade-off, a veryimportant trade-off.
I'll quickly revisit this datafrom Professor Weller, because
what did they find?
They replicated the findings ofthe melanoma in Southern Sweden
study.
They showed that those withgreater sun exposure had lower
(36:39):
mortality.
Those with greater sun exposurehad lower mortality.
So what's the mechanism here?
How can we explain this?
Well, I told you about thesechemical cousins of vitamin D.
Well, it turns out that theyhave an immense and very
fascinating and profoundanti-cancer benefit.
So this vitamin D herepre-vitamin D3, becomes vitamin
(37:01):
D.
If you stay in the sun and youcontinue to irradiate your skin
with ultraviolet B, this becomeslamisterol, tachysterol and a
whole bunch of other compounds.
What do these do, theseupregulate DNA repair enzymes in
the skin.
The UVB is damaging it and thebasic cision repair and all
(37:22):
kinds of other DNA repairmechanisms are promoted by these
vitamin D metabolites.
So I think that is going to beone of the profound reasons why
we're seeing lower mortality inpeople with greater sun exposure
.
Now, what are the causes of skincancer?
And look, I'm going to explainmy current thinking about this
(37:43):
and this isn't by any meanscomplete, but it's how I'm
thinking about it at the moment.
And there's always going to bean interaction of genetic
predisposition withenvironmental factors.
So I always tell my patientsthat genetics loads the gun and
your environment, your choices,your lifestyle it pulls the
trigger.
Okay, what are the geneticpredispositions?
(38:03):
Those with pale skin types,those with less melanin in their
skin, and it's very rare verycertain genetic syndromes and
there's one there calledxeroderma pigmentosum.
It's characterized by mutationsthat prevent those basic
excision repair enzymes, thoseDNA repair enzymes, from working
.
So how do you marry this withlifestyle?
(38:25):
Well, it turns out, if you havea disrupted circadian rhythm by
looking at blue light all nightand not enough full spectrum
sunlight during the day, you'regoing to impair DNA repair and
the cancer defense mechanisms.
If you have a low vitamin Dlevel and you're near infrared
light deficient, you're notgoing to be making that
(38:46):
antioxidant melatonin hormone Ifyou're immunosuppressed.
People on transplant recipientshave extreme high risk of
developing non-melanoma skincancer.
And that explains becausethey're hamstringing their
body's natural repair and immunesurveillance mechanisms.
(39:06):
What else?
And I haven't talked a lotabout food, but it's an
extremely common and recurrentanecdote that once people go
carnivore, well, they cut outpolyunsaturated vegetable oils,
seed oils, refined oils thatthey find that they're prevented
from burning.
They're essentially resistantto the effects of UVB light.
(39:27):
They're less photosensitive.
We know and it's not a talk fortoday, but we know that omega-3
and the DHA, the EPA fattyacids they confer
photoprotective benefits in theskin.
And as a society we'vecollectively deviated from an
(39:48):
ancestrally normal andappropriate omega-3 to 6 ratio
because everyone is under-eatingmarine seafoods and everyone's
over-eating refined seed oils.
So I think that that is a keyeffect modifier for the
development of skin cancer.
What else?
Melanoma is unique and we dosee melanoma commonly in more
(40:12):
younger people.
Again, they're typically anindoor worker, they have low
vitamin D, but it turns out thatthere's a photoreceptor system,
the melanopsin non-visualphotoreceptor system.
This regulates melanocytefunction.
So if we're sitting in front ofa blue-lit screen all day and
we're sitting under blue light,then this light is highly
(40:35):
stimulatory to melanocytes.
So I believe that the indoorenvironment is a key part of
particularly melanoma diagnosisin younger people.
So how can we think aboutdeliberate sun exposure really
on a broad level?
Because we have to be weighingup the benefits and the risks of
(40:56):
sunlight exposure and sunlightavoidance.
Well, I think that data andevidence suggests that we're
trading up a reduced all-causedeath, reduced cancer death,
reduced skin cancer death and alower cardiovascular death up
against potentially a greaternumber of skin cancers, both
melanoma and non-melanoma skincancers, and they're
(41:19):
particularly going to be inthose fair-skinned prototypes.
Reduction in cardiovasculardeath is a massive part of the
benefit of natural sunlight, andthat was a talk I did last year
, which is a critical part ofthis story.
So quickly, let me discuss howwe're going to use the sun to
help reduce our mortality fromcancer.
(41:41):
So there's a couple of reallygeneral steps here, but what we
want to do is we want tounderstand our ancestry.
We want to understand ourancestry, we want to understand
our risk factors, we need tounderstand our ambient UV
conditions and we're going totitrate our sun exposure based
on those things.
We want to target a vitamin Dlevel.
Again, this is going to be amarker of our sun exposure to a
(42:02):
certain amount in approximatelyaround 125.
And obviously we're going tocheck for any suspicious lesions
that might be forming as aresult of an increased sun
exposure habits.
For a quick explanation, this isthe Fitzpatrick photo scale,
and from one to five and on oneyou have the most pale northern
(42:25):
European, the Ranga, and at sixyou've got the darkest Sudanese,
west African, somalian, perhapsAustralian Aboriginal phototype
and what you have here is agradient of melanin in the skin
(42:47):
and that's a gradient of pigmentin the epidermis.
The number of melanocytesaren't changed, but the amount
of melanin that they've secretedinto the skin has.
And the question is whataccounts for this difference?
The answer is the ambient UVlight.
In Scandinavia the UV indexdoesn't climb above six most of
(43:07):
the year and for one week ithits about six In the places
where people have the highestpigmentation.
They're being bombarded yearround at the equator with
massive amounts of UV light.
So it's a response to theambient UV conditions.
The other key point and I put itin small letters, but it's
important to note is that theless melanin you have, the
(43:34):
easier it is to make vitamin D.
That means because the melaninis itself is absorbing and
dissipating this UV light asheat.
So if you amongst a range ofother effects, but the benefit
of being pale in a high UV areais that you need a very little
amount.
And really, when we're thinkingabout light, we're thinking
about essentially a drug-likereplacement.
So we need to consider thatthis is a dosing that we're
(43:55):
giving ourselves and we can doseourselves, but we have to be
smart about the dose.
Another way of thinking aboutthis is what I'm calling a skin
type latitude mismatch.
So you have to ask yourself doyou live in a similar solar
environment to your ancestors?
If yes, then you're matched andyour skin type's appropriate
for the conditions that you livein.
Sun exposure habits are mucheasier then because you don't
(44:17):
have to mitigate as much,because you're in the
environment that your ancestorswere evolved and you've had the
appropriate amount of melanin inyour skin.
But us in Australia, mostpeople are mismatched and you
can actually be mismatched intwo directions.
You can be a fairer skinnedperson in a higher UV index area
, which is most of Australia'sNorthern European migrants
(44:43):
historically or you can be adarker person in a lower UV
environment.
As you can imagine, it's muchmore difficult to be dark in an
area with low UV light than itis to be a light skin pigment in
a high UV area.
The reason is because if you'reshame-worn, you can go in the
(45:04):
shade.
That a key point.
You can titrate your solarexposure by using shade.
Unfortunately, uh for stormzyhere there is not enough uv
light in the uk year round togive him his sunlight needs and
that and that that actually isassociated with a whole bunch of
of uh you know interestingphenomenon, um related, related
(45:28):
to sunlight deficiency and howthat's affecting health
disparities and this disparityin health outcomes, particularly
in the US but also in the UK,between African-American,
african-british and the nativepopulation greater rates of
obesity, diabetes, cancer,stroke and heart attack.
I believe it's related to thesolar exposure and the
(45:49):
inadequate amount of solarexposure that you're going to
get as a dark person in a low UVenvironment.
What are some key risk factors?
So, if you've got a personalhistory of melanoma, if you've
got a family history of melanomaagain, if you're taking
medications that are going tosuppress the body's response or
(46:10):
repair mechanisms to UV light,and if you've got many atypical
nevi or funny moles, none ofthese are necessarily absolute
contraindications to UV exposure, but it has to be taken on a
case-to-case basis.
You have to understand thesolar conditions.
The UV index is a measure ofUVB intensity and if you go into
(46:33):
any weather website you'll beable to see what that UV light
is doing during the day.
So, again, as I mentioned,seasonally this will change.
But here in Australia wetypically we can get in summer
many days, you know, 11 andabove, and that's a very high UV
dose.
Compared to Tassie, brisbane,townsville, everyone is
(46:55):
extremely different.
So it pays to understand howmuch UV light you're dealing
with.
It also is relevant to knowthat you can't make vitamin D
and you therefore can't getburnt at all parts of the solar
day.
Again, the sun angle isprimarily determinant of how
much UV light comes in and whenthat is reaching above 45
(47:18):
degrees you're going to begetting UVB light.
So the morning and the eveningyou can safely get your full
body out and it's encouraged todo so prior to UV light exposure
.
But just be aware that you'renot going to be making vitamin D
in that time but you're gettingother benefits for circadian
rhythms and other physiologicalfunctions.
So regulating your circadianrhythm it's easier said than
(47:42):
done Bright light during the dayand darkness or moonlight at
night, and we can disrupt thecircadian rhythm either by
getting insufficient naturalsunlight during the day or
excess light at night.
So, minimizing light at night,mitigating with things like blue
light, blocking glasses withred and light, or candle light
(48:03):
close to the ground these areall relatively straightforward
but give you very high valueways of helping preserve your
circadian rhythm and thereforepreserve your immune cell
function, preserve the cancermachinery's ability to kill
cancer cells at the right time.
And what do you do then?
(48:24):
You can titrate your sun dose,and this is an app that was
developed by Professor MichaelHolick, his team, to help dose
sunlight, based on yourphototype, based on the ambient
UV conditions.
It makes it really easy.
Circadian is another app tohelp you understand what time of
day is sunlight present in myenvironment.
Finally, you want to build yoursolar callus, and really you
(48:45):
want to expose your solar calyx,and really you want to expose
your whole body.
What was the norm before clotheswere invented?
Well, from sunset to sunrise,sunrise to sunset full body
irradiation on our skin.
That is what our biology needs,and a lot of people haven't had
sunlight on private parts indecades, and that is a problem
(49:07):
if we're trying to preventcancer, when we understand the
potential and powerful role ofthese vitamin D and these other
secosteroids, as well asnear-infrared light.
So what's an appropriatevitamin D level?
Well, this work by Hollick etal.
They looked at where does thevitaminD level land in
(49:28):
free-ranging humans, innon-human primates, it gets to
anywhere between 125 to 200.
In the Maasai and Hadzabe inTanzania it sits at about 115.
These guys look like aprototype, five or six.
They have a massive amount ofmelanin, but they're still
maintaining a serum vitamin Dlevel that is double the average
(49:53):
Canadian and I would say doublethe average Australian, because
they're simply outside all day.
I mean, how else can we look atthis?
Outdoor workers they'llnaturally have levels of 163.
Puerto Rican farmers 135, 122.
So the average Canadian is 68.
(50:14):
I would tell you from anecdotalclinical experience measuring my
patient's vitamin D, it'sprobably a little bit higher
than that, maybe 78 or 80, butit's nowhere near.
Most people are not gettingclose to those levels, and
Australian dermatologists thisis an interesting one because
(50:37):
it's proof that they're eatingtheir own cooking.
But 35 nanomoles is deficient,and it's deficient no matter
what metric you use, and this isa graph that explains the
different units for both UK andUS.
But under 50 is classified asmild deficiency in Australia.
(50:58):
Above 75 is where we stopseeing bone complications like
subtle subclinical osteomalacia.
If you can get your vitamin Dabove 75, and that's a good
threshold for supplementation toget above.
But really the sweet spot forcancer prevention long-term is
(51:21):
going to be above 100.
And that is putting yourselfinto the lowest risk groups of
those epidemiological studiesthat I presented to you earlier
on.
Obviously, if you havesuspicious lesions, they need to
be identified and we're reallyparticularly worried about
pigmented lesions.
So identify concerning factorsthat include asymmetry in any
(51:48):
lesions, multiple differentpigments, rapid change
anything's concerning.
Luckily we have some of thebest skin doctors in Australia.
These can be readily identifiedand excised, which is great.
The slide I didn't include is astory about melanoma over
(52:10):
diagnosis and it's a little bitof an interesting and
controversial topic.
But the data is clear thatthere's some degree of that
happening, not only in the USbut here in Australia too, and
it's driven by diagnostic creepin terms of what previously
would have been known as calleda pre-malignant lesion or is now
(52:32):
being called a melanoma in situ, and that's been driven by a
whole range of factors,particularly in the US.
It's related to profit and thestructure of their system that
rewards melanoma diagnosis, butthat's not really relevant to
you as individuals, because ifyou have anything that's
concerning, it needs to belooked at.
So let's end on a meme, becauseI love memes, I love the matrix,
(52:52):
and what Neo is saying here isyou're saying that those people
with cancer cancer patientsshould, including with melanoma
should sunbathe to reduce therisk of dying.
Keyword being dying and Morpheussays yes, that is exactly what
I'm saying.
So if you're interested in anymore of this, then join my
(53:14):
private community group.
I've actually put together amuch, very detailed course about
safe and appropriate, sensiblesunlight exposure that includes
the nuances I've touched on,called solar callus, with a
whole bunch of lessons, andinclude on things like
photosensitizing medications,the role of circadian rhythms
(53:37):
and how to optimize everything.
So check that out if you wantto dive into a bit more depth,
and I've got a whole bunch offree podcasts on my channel that
go into this in further depth,including with Professor Richard
Weller and Dr Jack Cruz, whohave done a lot on this topic.
My talk last year is aimed atthe cardiovascular benefit and
(54:02):
if you want to learn from me andyou want to experience how I do
the solar exposure and how Irecommend you do it, then join
me on a couple of retreats inJuly.
That's always a fun time.
So thank you very much forlistening.
Speaker 3 (54:26):
Max Goldhain, everybody Give it up, applause.
Speaker 2 (54:33):
A beacon of wisdom and knowledge.
We've got a couple questions.
Yeah, okay, we've got Cindyover here.
Look at those hands.
Shoot up, gary.
Speaker 3 (54:47):
Everybody goes out into the sunshine and they put
their sunglasses on.
Will you address that please?
Speaker 2 (54:52):
Yes, so photoreception is not only a
cutaneous process and thatbasically means that your eyes
are detecting light wavelengthsand there's a feedback loop that
exists between the eye, thebrain and the skin that
regulates pigmentation.
That means, for that process tooccur properly, you need a
(55:13):
coherence between the signalthat the eye is receiving with
regard to its ultravioletenvironment and the skin.
If you wear sunglasses thatblock ultraviolet A and B they
broke up to 400 nanometer lightyou are going to deactivate or
create a discrepancy in thosesignals.
That is going to impair thetanning process and and that
(55:36):
evidence is very old and it'sbeen done in fish and lower,
lower order animals that, likefrogs, that um show the
pigmentation is is occurringbecause of what is the light
information that's beingreceived through the eye.
Does that include seeing glasses?
So, to a lesser degree,depending on the lens.
(55:57):
It's a different thing type,but if they're UV blocking, then
to some degree they're going toimpair that process.
Yeah, so any car windscreens?
Yes, absolutely, because theyagain are just changing the
(56:20):
proportion of light that you'rereceiving, because they
preferentially block UVB, theypermit a little bit of UVA and
they permit more blue thaninfrared, so they're changing
the proportion or the form bywhich the light is being
delivered to the eyes and skin,and that's different to the
three billion years that yourbody's evolved with.
Speaker 1 (56:38):
Max, thank you for continuing my confusion with
vitamin D and UVB light, becauseI think there's a double
paradox there which keepsarticulating it very well.
I'd like to come to the defenceof UVA and ask you a couple of
questions about that.
Uva light, which we've got alot more here the further south
(56:59):
you go stimulates nitric oxideproduction.
Nitric oxide is the criticalchemical which actually is
involved in our t killer cellresponse to cancer.
So uva light is very beneficialfor cancer mop-up rather than
cancer prevention.
Uric acid, byproduct of fructose, inhibits nitric oxide
production.
(57:20):
That's in some of my talks.
But I want to defend UVAbecause not everyone can get out
just for the right number ofminutes in the middle of the day
.
The other one is linoleic acid,which you alluded to.
There is well associated nowwith 10 years of literature that
there are.
People with melanoma have muchlower, higher levels in the fat
(57:41):
cells of that, because melanomais increasing and predominantly
found now in the non-sun exposedareas.
So how can we worry about UVBthat?
The worrying thing aboutlinoleic acid is it just comes
from the seed oils as ahalf-lifer it's probably about
(58:01):
four years.
So if you want to get rid of itout of your diet, you can
improve your metabolic healthstraight away, but it's going to
probably take a few years.
So can you defend UVA?
Speaker 2 (58:13):
Yeah, so UVA is a critical part of this whole
sunlight story and I didn'tparticularly include its
mechanisms as it relates tocancer.
But with respect to optimalhealth, uva is key and for the
reasons that you mentioned, notonly, as you've said, it
liberates nitric oxide from thevessels, the blood vessels, and
it helps to dilate it.
So you know if we're thinkingabout a patient with essential
(58:35):
hypertension, with metabolicsyndrome, who's got hypertension
yes, it is an insulin resistantcomponent to that and the
effect of insulin on you know,renal sodium absorption.
But I think that patient issunlight deficient and they're
UVA deficient, amongst a bunchof other things.
The other point about UVA isthat Weller's group noted that
UVB actually can lower bloodpressure too.
(58:57):
So it's not only an isolatedUVA effect but it's essentially
a lot of the short wavelength,including blue, can cause
photorelaxation and dilation ofblood vessels.
So I'm a massive fan of uva.
As I mentioned, the vitamin dhere is the biomarker of total
sunlight exposure.
So I think the benefit forcancer too, absolutely could be
(59:18):
uva related, but um and nearinfrared related, so it's the
whole package.
It it's difficult no, exactly,we don't have a biomarker as
like we do, that I'm aware of tomeasure someone's UVA exposure
in isolation.
On the point of linoleic acidand melanoma, yeah, I definitely
(59:38):
agree.
I think to be really nuanced.
It seems like you know thecancer in non-sun exposed areas.
That seems to be super becausethere's multiple types of
melanoma which we didn't go into.
Superficial spreading melanomain younger patients on
non-exposed areas, like on thefinger, typically in a very pale
, you know, 25-year-old officeworker, absolutely.
(01:00:00):
And that's why I alluded to theartificial light, alluded to
the fatty acid components Inolder patients who have lentigo
maligna, some of these morechronic sun-exposed areas do get
melanoma but they're nowherenear the metastatic risk of
(01:00:21):
those other melanoma types.
So, yeah, I guess I agree withyou, Gary.
I think this story is so muchmore nuanced than what we're
being presented with.
And the strategy of slatheringeveryone in sunscreen and
sunlight avoidance isessentially preventing anyone
from building any resistance orbuilding the natural
physiological response tosunlight.
(01:00:42):
So they're even more weakenedwhen they do go into sunlight,
which might be a couple of timesa year, get fried to a crisp
and you know the epidemiologysuggests that's the predominant
risk factor for developingmelanoma.
From an epidemiological pointof view.
Speaker 3 (01:00:59):
Great talk, max.
Thanks so much.
My understanding of melanomasis that it's skin sun damage in
children, infants, childrenrather than adults, and I just
wonder how that would affectsome of the figures you found,
because you're looking at adultswho may have then stopped their
sun exposure and so they mayhave been burned as a child and
say I'm going to protect myself.
(01:01:19):
So I'm worried also that peoplemay be watching this and then
go away and say, oh, I'm goingto protect myself, so I'm
worried also that people may bewatching this and then go away
and say, oh, I'm going to get mykids out there, but are they
still at risk?
Speaker 2 (01:01:29):
Yeah, so the emphasis needs to be made that there's
no evidence that low-levelamount of non-burning sun
exposure is linked to anyadverse health effect.
The issue, as you've identified, is signal for intermittent
severe sunburn sun exposure islinked to any adverse health
effect.
The issue, as you've identified, is signal for intermittent
severe sunburn in childhood.
(01:01:49):
I, I think, and and maybe I'llexplain it a little bit more the
average age, the median age ofmelanoma diagnosis, is 68.
It's in the late, late 60s.
So so what I believe isactually happening here is
people with a pale phototype.
One or two Australians mostAustralians are getting
potentially had a number ofsevere burn episodes early in
(01:02:10):
life.
They then ate their high CEDOLdiet the whole time.
They went inside and worked ina bank or office for 50 years
and then, age 60, becausethey're so vitamin D deficient
and their sunlight sunlightavoided and they're circadian
rhythm disruption, they developa malignant melanoma that
metastasizes and kills them.
So potentially that early inlife sunburn was impactful for
(01:02:34):
them.
But is that a reason todissuade people from
appropriately getting gradual,safer amount of UVB containing
light?
I don't think that's the case.
But, as I said, I'm notadvocating for burning by any
means.
And the paler you are, theearlier in the day you can
safely get UV light before goingin, because the UV index is
(01:02:55):
lower and that's probably themost conservative way to advise
UV exposure.
If your ancestry is from Sweden,where it doesn't get above a UV
index of six, then know the UVconditions of your environment.
And the moment the UV indexclimbs to 10, because you've got
your Swedish ancestry go inside, you've still generated
sufficient more than enoughvitamin D and beneficial
(01:03:16):
sunlight in that time.
But it's culture in Australiafor us to go out in the big day
but we've got our sunscreen on,you know, and really spend a lot
of time in an area that wouldrequire us to be as dark as
those Sudanese people.
But not many people are reallygetting that.
Sorry, guys, that's all we'vegot time for.
If you've got any morequestions, ask Max in the break.
(01:03:39):
Dr Max Gahlhain.
Thank you.
The topic of today's talk.
I've intentionally titled itSunlight and Cancer Beyond Skin
Deep, and the purpose of that isbecause I believe that there is
sufficient evidence to supporta profound role of natural
sunlight in supporting healthand in supporting cancer and,
given Australia, particularlyour narrative and our
(00:47):
discussions and experiences withskin cancer and attitudes to
sun, that I think this is goingto be an important exploration
of the whole story, or part ofthe whole story.
So cancer is a growing problemand sometimes I like to look at
economic data because it cantell a very, very interesting
(01:09):
story in and of itself.
But these companies these arethe most profitable
pharmaceutical companies in theworld, and this business website
made the comment that theglobal oncology drugs market was
valued at $201 billion in 2023,and this is forecast to grow to
(01:31):
$518 billion by 2030.
What did they attribute thismarket growth down?
To Well, factors such as therising prevalence of different
types of cancers, increasing newdrug launches and product
approvals, and growing researchactivities by pharma.
Well, factors such as therising prevalence of different
types of cancers, increasing newdrug launches and product
approvals, and growing researchactivities by pharma companies
in the field.
So what is cancer?
(01:53):
I mean a definition of cancer,any various malignant neoplasms
characterized by theproliferation of anaplastic or
de-differentiated cells thattend to invade surrounding
tissues and metastasize to newbody sites.
That's interesting.
But what causes cancer?
That's not going to be thetopic of today's talk.
(02:14):
But I'll give you a couple ofinsights into perhaps the latest
of what we think about could becausing cancer.
These are perspectives fromsome of the top researchers in
the world.
Professor Thomas Seagree talksabout a metabolic disorder,
mitochondrial metabolic disorder.
Professor Michael Levin istalking about the loss of
(02:38):
cellular coherence from abioelectric point of view and
potential regression of thatcell into a more embryonic state
.
And also Dr Jack Cruz hastalked about the altering of
Warburg metabolism, but reallyone being reliant on a change in
light signals.
But, as I mentioned, that's notgoing to be the topic of
(02:58):
today's talk.
What I want to talk about issunlight and cancer particularly
, and the link between sunlightand cancer.
How can we frame that withrespect to what we've been told
about skin cancer and how can weadd nuance to this topic?
And finally, I'll be touchingon how we can use the sun to
(03:19):
help reduce death from cancer.
So this story it starts it'sactually quite an old story and
this is an ecological paper by aUS MD back in 1940.
His name was Frank Appley, andwhat he noticed, and he drew a
conclusion, was that when heobserved the mortality rates
(03:40):
from cancer in the United Statesand Canada, that there was
essentially an inverserelationship or an association,
and he made the comment that thetotal cancer mortalities of the
various American states andCanadian provinces are shown to
fall with increasing solarradiation and the number of
people exposed.
(04:00):
So this generated aninteresting hypothesis that
basically wasn't touched for awhole about 40 years until two
brothers, cedric and FrankGarland, who are epidemiologists
in California, san Diego, andthey in 1980, posited or asked
the question does sunlight andvitamin D reduce the likelihood
(04:25):
of colon cancer?
So they're interested incolorectal cancer and they
proposed that vitamin D was aprotective factor against colon
cancer.
What they did is they did and Iguess drawing on the work of
people like Frank Appley,because they noted that if they
were looking at the geographicaldistribution of cancer and
(04:45):
cancer deaths, that themortality and colon cancer
prognosis, which is another keyaspect of this was that it was
lowest in places with highersolar exposure and it was
highest in places where thepopulations were exposed to the
least amounts of natural light,namely major cities and rural
(05:07):
areas at high latitudes.
So what they did is a study,and this was eight years later.
They did an eight-yearprospective cohort study and
what they found?
And they essentially comparedthe risks of developing colon
cancer and they were stratifiedthat by the level of vitamin D,
(05:28):
and we're going to talk aboutvitamin D and its role in this
story.
But essentially what theynoticed was the lower that your
vitamin D level was, the morelikely you were to develop
colorectal cancer.
And what they said in thispaper back in the 1980s was that
(05:49):
the results are consistent witha protective effect of serum 25
, hydroxyvitamin D on coloncancer.
So to frame this talk, we needto understand a little bit about
physiology and about how thesun affects our skin and affects
our biological system.
So what we have is sunlight anduniquely UVB sunlight, and
(06:13):
that's a narrow range of lightthat actually hits planet Earth
and it's only present for themajority of time when a
sufficient solar angle allowsfor these high energy photons to
penetrate the atmosphere.
What it does is it hits theskin and it converts cholesterol
7D hydrocholesterol intovitamin D-like structure.
(06:47):
So that process is reliant on awhole bunch of different things
, but the key things that willaffect that is the presence and
absence of enough UVB-containingsunlight, as well as how much
melanin exists in the skin, andwe're going to talk about
melanin and skin pigmentationand how relevant that is,
(07:09):
particularly with regard to skincancer.
So what happens and this is aschematic of the physiology of
vitamin D is that vitamin D isformed and then it binds in
circulation to a binding proteinbefore being taken to the liver
and then the kidney andundergoes a range of
hydroxylation and, essentially,activation steps before it is
(07:32):
able to be used.
As you can see here, you canalso obtain vitamin D from the
diet and it's essentiallypreformed because you've
consumed animals that themselveshave made this fat-soluble
hormone.
But really, the vitamin D levelis primarily going to be
determined by solar exposure,because the sun is the main way
(07:53):
that we, as humans, generate andmaintain our vitamin D level.
So what's the role of vitamin D?
Well, most of you would knowabout the bone effects and the
research or the benefits ofsunlight and UV-containing light
predated the actual discoveryof this compound, and in the
late 1800s, in the ghettos ofEurope during the Industrial
(08:16):
Revolution, there was smog thatwas preventing ultraviolet light
from penetrating into theseareas and kids were getting
severe vitamin D deficiency, andthat was manifesting as rickets
and the bow leg look of youngchildren is the unfortunate
consequence of inadequate bonedevelopment and ossification as
(08:37):
a result of vitamin D deficiency.
But what we've learned, andparticularly over the last 15,
20 years, is that vitamin D andthe vitamin D system is not only
important for bone health, andit's actually far from it.
It's a critical part of immunesystem function and, by
extension, the cancer story,because it turns out that cancer
(08:59):
in and of itself is extremelyreliant on or dependent on the
state of your immune systemfunction.
So things like theproliferation or growth of cells
, inflammation and new bloodvessel growth, which is all
again a key part of the cancerstory this is regulated by
vitamin D.
(09:19):
So where else does this vitaminD sunshine hormone, how, what
else does it touch?
Well, I'm not going to speakabout it in this lecture, but it
it is, covering a such a widerange of of really critical
aspects of optimal health andmetabolic health, particularly
insulin resistance, obesity,diabetes, metabolic syndrome, as
(09:42):
well as I mentioned tumorformation, cancer formation and
immunity, and I'm going toexplain now, but I'll explain
later is that vitamin D isactually also and one way of
thinking about this is this is aproxy for your total sunlight
exposure.
So that's going to be somethingI'll emphasize more.
(10:02):
What else does the data suggestabout cancer and vitamin D?
Well, this study essentially isplotting breast cancer risk and
it plotted it against the serumvitamin D level.
So what you can see is a prettyprofound relationship where, as
the vitamin D concentrationincreases and we've got both
(10:23):
nanograms per mil, which is theUS metric, and nanomoles per
liter, which is us in Australiaso, of the women who had in this
whole cohort of 5,000, thosewho had a vitamin D level in the
upper ranges, their risk ofdeveloping breast cancer was
significantly lower.
(10:44):
What about for those who'vealready developed cancer?
And that's another part of thisstory?
Well, it turns out that notonly incidence but also
prognosis of cancer isprofoundly related to associated
with serum vitamin Dconcentration, and this study
suggested that the higher yourvitamin D level, the lower your
(11:05):
fatality rate in people who'vealready developed breast cancer.
And again, patients with thehighest concentration of
25-hydroxy-D had approximatelyhalf the fatality rate compared
to those with the lowest.
This systematic review covered,and it summarized, the state of
the research and it basically itsays that the evidence that
(11:27):
chronic, non-intermittent sunexposure decreases the risk of
colorectal breast prostatecancer, non-hodgkin's lymphoma
is accumulating and graduallygetting stronger.
This is nothing that we gettaught in medical school and
this is not something that you,as members of the public, get
communicated, especially withpublic health messaging around
(11:49):
sun exposure in Australia.
But this isn't locked in amusty case next to the JFK files
.
This is not private information.
You can go into PubMed and youcan search this evidence and it
exists.
So what this is pointing to isthat we've got a strong evidence
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that the higher someone'ssunlight exposure, as we
measured via the vitamin Dsystem, the lower the risk of
the cancers that really killpeople, and that's a key point.
And I'll contrast that withskin cancers because, as a cause
of death in society, these arethe cancers that are killing the
most number of people.
(12:33):
This is one of my favoritestudies it was actually
published last year, finally byProfessor Richard Weller.
Now, richard Weller is therarest of dermatologists who's
actually looked into the dataand found that sunlight exposure
has a holistic benefit onhealth, and in this study he
(12:54):
essentially examined a databaseof over 400,000 people in the UK
called the UK Biobank overabout 12 years.
And what he did is hestratified these people.
He classified them based ontheir ultraviolet light exposure
.
So he used UV sorry, he usedtheir latitude, which was a
proxy for their UV exposure, aswell as their sunbed tanning
(13:18):
habits, and he correlated thatto vitamin D levels.
So what did he find?
He found that participants withmore active sun-seeking
behavior and those living atlower latitudes had lower crude
mortality of cancers of thedigestive system.
So I already told you that wealready had strong evidence that
it was linked to lower rates ofcolorectal cancer, but also
(13:40):
breast cancer.
Participants with activesun-seeking behavior had lower
crude mortality from skin cancerBig pause there.
Cancers of respiratory andintrathoracic organs, cancers of
lymphoid, hemopoietic andrelated tissues, which are the
leukemias, and cancers of themale genital organs.
And they also summarize whatI've just told you, which is an
(14:03):
inverse relationship betweensolar exposure and cancer
mortality in multiple sitesorgans.
And they also summarize whatI've just told you, which is an
inverse relationship betweensolar exposure and cancer
mortality in multiple sites,including the bladder, the colon
, hodgkin, lymphoma, prostate,stomach and breast.
So this is really elegantbecause we've got multiple lines
of epidemiological data, oneusing vitamin D, serum vitamin D
, which is an indirect marker ofsunlight exposure, and one more
(14:24):
direct, looking at all-causemortality and basically finding
the same thing.
So if sunlight lowers thecancer mortality, what are the
mechanisms?
So we have to talk a little bitabout the solar spectrum.
We have to talk a little bitabout light and how that affects
the body.
So what you have here is youhave the spectral irradiance, so
(14:48):
this is the solar energy thatwe get hit with on planet earth
just standing outside, and wehave the wavelength of light
here On this tiny corner here.
This is the ultraviolet lightthat is a UVA, and the UVB light
UVB is only 5% of this is thatis a uva and the uvb light uvb
is only five percent of of this.
The rest is uva.
(15:09):
So you're only making vitamin dout of a small amount of of uv
light, and that is also going tochange depending on your
latitude, it's going to dependon your season and it's also
going to depend on time of day.
What you can see with your eyesis the visible spectrum, and
the largest area here by photoncount is in the infrared and
(15:29):
that's non-visible.
So ultraviolet is essentiallybelow the visible spectrum we
can't see in ultraviolet andinfrared is beyond visible.
The key point that I'd like youto understand about this diagram
is that each one of thesewavelengths of natural sunlight
have a profoundly importanteffect on human physiology and
(15:53):
human biology.
The reason for that is becausethese are the conditions of
evolution for three billionyears, and we evolved under this
light, not under this light.
As I said, vitamin d is onlyable to be made with with uvb
light.
So so what are the effects ofuvb?
And and I'll be really specificbecause it's not only a vitamin
(16:16):
d story it stimulates thisincredibly ancient and
incredibly uh unique, uh poly uhpeptide pro-hormone called POMC
or pro-opio-melanocortin.
Pro-opio-melanocortin, as Imentioned, is incredibly
evolutionarily conserved.
It's found in ancestralnathosomes, which were relics
from prehistoric time.
(16:38):
It regulates things like immunefunction, appetite and
metabolism centrally in thehypothalamus, as well as blood
pressure and, obviously, skinpigmentation.
What it also regulates, and thedownstream product of POMC, is
the skin tanning system.
I think the most interestingpart of one of the most
(17:01):
interesting parts of POMC andits effect is that it contains
an endorphin-like chemical.
So when you get in the sun, thesame peptide hormone that is
assisting in tanning your skinis releasing a beta-endorphin,
an opioid-like chemical, toreward you for that tan.
(17:23):
So again, think about this ideaof tanning your skin cells in
trauma, which is a half-truth.
But if the sunlight is inducingtanning, but it's also
rewarding you from being inthere, and that's a
600-million-year-old programbuilt into your biology.
Who's in the wrong here?
(17:43):
What else does it do?
As I mentioned, it can causeDNA damage and particularly
creates these photo products andsunburn.
What I'll explain about as wego through is that Mother Nature
built in an extremely elegantprogram to help you repair those
DNA damage caused byultraviolet B light.
(18:04):
So UVB is a double-edged sword,but it's absolutely essential
for optimal human health.
So what did Garland and MichaelHolick, who is the world leader
on vitamin D, what did they sayabout the effects of vitamin D
in cancer prevention?
Because they were trying toexplain this finding that there
was lower colorectal, breastprostate and lower lymphoma
(18:27):
findings with vitamin D exposureand sunlight.
What they found is that thevitamin D compounds reduce the
formation of new blood vesselsin tumors.
It reduces the malignant andexcessive proliferation of cells
.
It increases or upregulatescontrolled cell death of cells.
It increases or upregulatescontrolled cell death, or known
(18:47):
as apoptosis, and it increasescell-to-cell adherence.
And I mentioned briefly aboutthis bioelectric model or theory
of explaining cancer and thisidea that the cell potentially
loses its understanding thatit's part of a structure in a
whole and therefore inducesthese anaplastic type phenomena
(19:09):
in the cells.
But luckily vitamin D ishelping those cells adhere to
each other.
Now this is a complicated slide, but the purpose is really
simple, and that is to explainto you that when you get in
natural sunlight, it's not onlythe chemical that you take in a
(19:33):
pill from the chemist, becauseit turns out that the body makes
a whole enormous pharmacy ofrelated compounds that were
initially thought to bebiologically inert but have
since been discovered to haveprofoundly beneficial effects,
and again, anti-cancer effects,effects of promoting DNA repair
(19:55):
in the skin cell scales andreally systemically.
So what else?
How else can we account forthis?
Lower rates of cancer in peoplewith greater sun and vitamin D
exposure?
Well, it turns out that yourcircadian rhythm is critical in
regulating the essentiallyoncogenic process.
And what is a circadian rhythm?
(20:17):
Many of you might already know,but it's an endogenous 24-hour,
almost 24-hour cycle that runsin the brain.
The master clock exists in thehypothalamus, behind the eye,
and it sets a rhythm that needsto be synchronized across all
tissues and that rhythm programsthe most critical functions of
(20:40):
the body, from hormonalsecretion, sleep-wake cycles,
activity, metabolism, immunefunction, stem cells you name.
It is regulated on a 24-hourcycle.
What you can do is that you canprogram your circadian rhythm
by the behaviors and thelifestyle that you lead.
So if you get bright lightduring the day, if you sleep at
(21:00):
nighttime and you consume yourfood during the day in a
circadian appropriate manner,then you're going to get perfect
synchrony between the clock inyour eye and the peripheral
clocks in your body, and that'sgoing to lead to optimal health
and optimal function of the body.
If you do the opposite, then youare going to disrupt your
(21:20):
circadian rhythm and that's aproblem.
And that's a problem becauseyour immune system, which is
supposed to be killing theseprecancerous cells that were
spontaneously being generated,they're not going to be able to
do that effectively.
So circadian rhythm and cancer.
Like I mentioned, not only doyou have clocks in all these
(21:41):
different bodies that regulatethese critical bodily processes,
but the cancer killingmechanisms, so key cancer genes
they're all under circadiancontrol.
So cell cycle regulation, dnarepair, cell proliferation and
controlled cell death If you areup all night till 2am looking
at, looking at a blue lit screen.
(22:02):
If you're giving your bodythose profoundly uh disrupting
circadian signals, it willderail your endogenous cancer
fighting and cancer killingmechanisms.
So I think that is a big partof of of potentially these
findings is is that those whohad a higher vitamin D were more
(22:23):
likely to have a more regulatedcircadian rhythm and therefore
this circadian system was likelyworking more effectively.
What's another way to accountfor these findings?
Well, this is extremely newresearch, and Scott Zimmerman
and Russell Ryder are experts inmitochondrial medicine and
physiology.
What they discovered is thatthe melatonin, which is the
(22:48):
body's most potent antioxidantsystem, was not only being
produced sorry, not onlyantioxidant but it's also a
signal for darkness and itinduces sleep.
It's not only being produced inthe pineal gland in the
circulatory system on theabsence of blue light, but it
was actually being produced onsite in your cells, in the
(23:09):
mitochondria, during the daywith exposure to near infrared
light.
So so why is that important?
Because it turns out that whenthe body is making this
melatonin extremely importantantioxidant, this free radical
scavenger and antioxidant is, itis protecting the mitochondrial
(23:31):
DNA and the mitochondrial DNA.
Mutations in mitochondrial DNAunderlie all this march towards
chronic disease, includingunderlying the physiology of
cancer and canceroustransformation.
So, simply being outside andbeing in greenery, next to the
(23:51):
green areas, you are absorbingmassive amounts of near infrared
light that are penetratingthrough your clothing and
through your body up to at least8 to 10 centimeters and helping
your body to synthesizemelatonin, which it's using to
essentially protect the cellularand subcellular machinery that
(24:13):
is allowing your cells to workproperly.
How else is this working?
Well, if we drill down into themitochondria, we can see that
this is the process by whichenergy is actually generated,
and it's a passage of electrons.
It's taking food electrons,it's taking light information
(24:34):
and it's allowing thiselectrochemical gradient to make
energy in the form of ATP andalso in the form of metabolic
water, and metabolic water isthis deuterium, depleted water
that gets produced at the fourthcomplex cytochrome C oxidase.
That process is optimized bynatural sunlight in the form of
(24:55):
all types of red light.
These are chromophores, meaningthey absorb light wavelengths
and they're modulated by lightwavelengths.
So when the body is hummingalong and when this
mitochondrial engine is hummingalong and you put the
appropriate fuel in in the formof a low-carb seasonal diet
(25:18):
that's rich in animal foods anddeuterium-de depleted animal
fats, then this process is aided.
But it's never going to beoptimally aided unless you're in
natural sunlight which, as Itold you, is extremely rich in
red light, because the red lightis helping your mitochondria
produce this metabolic waterthat is essentially hydrating
(25:41):
all the proteins and enablingthem to work properly, as well
as spinning this fifth complex,which is producing ATP.
So mitochondrial dysfunction isa prerequisite for cancerous
transformation.
It is one of the key problemsthat goes wrong when a cell
becomes cancerous, and naturalsunlight not uv but essentially
(26:04):
red and infrared is helpingsmooth this process.
So the question I think isinteresting is do we have a
marker?
Do we have a marker of how muchsunlight we have of have had?
Do we have a fuel gauge?
Because that would be reallyhelpful in seeing where people
are at with respect to thesunlight exposure.
And we do, and that'sessentially what the
25-hydroxyvitamin D test thatyou can get from your doctor
(26:27):
will tell you.
It's a storage form, but it isa rough proxy and a good
indicator of your total sunlightexposure.
And that's not only the UVB andvitamin D system, and that is
why I believe it's one of themost important tests to get and
we can explain about what wewant, and from an optimal level.
(26:49):
So it can give us an indirectidea, because if someone's got a
robust vitamin D level, then itwill imply that they've had
full spectrum sunlight exposure,including ample, near infrared,
which was the ancestral normfor our species.
But if they've got a low,insufficient or deficient level,
then you can imply it impliesthat not only have they got the
(27:12):
daytime sunlight exposure wrong,but they're probably exposed to
some artificial light at nightand they're therefore having
some degree of circadian rhythmdisruption.
Okay, so what about skin cancer?
And now?
This is the critical point.
That, as I mentioned, is thenuance we need to give to
understand this system and thisprocess.
(27:33):
So melanoma Melanoma is themost concerning and dangerous of
skin cancers and the reason forthat is because it has
relatively, compared to thenon-melanoma skin cancers, a
much higher proportion formetastasis, spread and therefore
mortality.
This is compared to thenon-melanoma or keratinocyte
(27:58):
cancers known as squamous celland basal cell carcinoma.
These non-melanoma skin cancersare not the cause of death in
people.
They're easily identified andthey're easily treated.
So the critical and mostimportant issue here is the
identification and prevention ofmelanoma, and no one's in
(28:22):
argument or disagreement aboutthat as a strategy.
So how does skin cancer fit intothis model about vitamin D?
Because I just told you thatall these really important
cancers are associated with lowvitamin D and therefore can be
thought of as a product ofsunlight deficiency.
I don't know if anyone likesStar Wars, but this is one of my
(28:44):
favorite memes and Padme isasking skin cancer patients
should have a high vitamin Dlevel from excess sunlight, and
that again is the corollary ofthe advice to avoid the sun
above a UV index of threebecause of the development of
skin cancer.
So if you extend that train ofthought, those people who are
(29:07):
developing skin cancer shouldhave a pretty robust vitamin D
level, because I told you thatthe only way you're generating
meaningful amount of vitamin Dis through UVB exposure.
So that stands to reason ifwe're following this logical
train of thought.
So this is a study from SouthAfrica.
It was a bunch ofdermatologists did this research
, so they looked at the vitaminD status of patients in Cape
(29:32):
Town so a very high UV indexenvironment with non-melanoma
skin cancer.
So what did they find?
They found that 49% of thosewith non-melanoma skin cancers
were vitamin D deficient and 31were insufficient, and they used
a cutoff of 15 nanomoles perliter.
So, interesting, even in thetumors and the cancers that are
(29:55):
canonically said to be relatedto cumulative UV exposure, we're
still seeing a significantassociation with vitamin D
deficiency.
What about this one Malignantmelanoma vitamin D status as a
risk and prognostic factor?
Now, this is a meta-analysisthat was published in January of
2025.
(30:16):
So this one is hot off thepress and it is a synthesis of
the research for the past, wellup to date with respect to the
relationship of melanoma andvitamin D.
So what did these researchersfind?
This is the conclusion.
We observed significantlyincreased risks for thicker
tumors, mitotic tumors, so thosewith higher cell replication,
(30:41):
higher tumor stages, so cancersthat are more down the track of
spread in vitamin D deficientpatients.
The conclusion was this studydemonstrates an association
between low vitamin D status andboth increased melanoma risk
and worsened prognosis, andthat's further contributing to
(31:02):
the growing body of evidencesupporting the tumor-effective
role of vitamin D.
So Vince thinks that's prettyastounding.
That's pretty against whatwe're being told.
We've been told to avoid the sunto prevent melanoma and prevent
UVB exposure above a UV indexof three with broad-spectrum
sunscreens, but that's flying inthe face.
(31:25):
So what else?
What about in patients thatalready have malignant melanoma?
And this is a British study,and it looked at 123 patients
and they had malignant melanoma,and it obviously excluded
patients taking supplementalvitamin D.
What did it find?
It found that 84% of thesepatients were vitamin D
deficient and of these, 31 wereseverely deficient.
(31:48):
How did that break down?
So, as you can see, the moremild your malignant melanoma,
the less likely you were to havevitamin D deficiency.
And all the way at the bottom,the stage four, distant
metastasis, very poor prognosis.
(32:09):
It's improved since theinvention of immunotherapies,
which has been a great invention, but it stands to reason that
this is a massive finding.
89% were vitamin D deficient.
Again, these are in patientswith metastatic melanoma.
So the question then and I thinkI've already answered it, but
I'm going to continue to promptyou to think about is how do you
(32:31):
become vitamin D deficient?
The reason you become vitamin Ddeficient is because you're
avoiding UV light and you'reusing UV blocking broad-spectrum
sunscreens, which necessitateor necessarily block the block
UV light.
The dermatologists know thisand they are trying to
(32:55):
understand this to the effect ofsupplementation unsuccessfully,
but they haven't understoodthat the critical reason why
this is happening is orassociation is because the
patients are lacking in keyanti-cancer compounds made by
full-spectrum UV-containingsunlight.
So this is just a pause and adigestion of what I've just said
(33:19):
.
So how, again, can UV light beso intimately associated with
both optimal health but also thesevere cancer outcomes?
This is a really interestingstudy and again it was done to
investigate health outcomes inwomen and they took 20,000,
(33:39):
25,000 Swedish women and theyfollowed them for 20 years,
inquiring at baseline about sunexposure habits.
Do they tan in winter, do youtan in summer, do you use
tanning beds and do you traveloverseas to tan?
And the hypothesis of theseresearchers was that those who
tanned the most, who had themost sun-seeking behavior, would
get the most melanoma and thenwould die more frequently.
(34:03):
And really that was theirhypothesis and that's why they
called it the melanoma insouthern Sweden study.
So they were right about thefirst thing the women with the
most sun exposure did get themost melanoma.
But they were completely wrongabout the second part, because
it turned out that the womenwith the most active sun-seeking
behavior had the lowestmortality, and that was a
(34:26):
dose-dependent effect, with theones who avoided the sun having
the greatest mortality.
The conclusions of the paperwas that sun avoidance was a
risk factor on par with smokingfor all-cause mortality.
And the way they worked thatout is that they found that the
women who smoked but gotsunlight and sought the sun and
went tanning they had the samemortality as the women who
(34:49):
avoided the sun and didn't smoke.
So that's a magnitudeequivalence of risk factor for
all-cause death.
What they put it down to wasthe women who were tanning were
dying less of cardiovasculardisease, stroke, but it turns
out that they were also dyingless of skin cancer.
So this graph was a plot ofthose without skin cancer, those
(35:10):
with non-melanoma skin cancerand those with malignant
melanoma, and it was the odds ofdeath, odds of all-cause
mortality, and, as you can seein the groups, the women who
avoided the sun in eachsituation they diligently wore
their sunscreen they had thehighest odds of all-cause
mortality.
And the tanning the onesgetting up there in their
(35:33):
bikinis from the morning to theevening in Sweden had the lowest
mortality.
And that was consistent finding.
What did Peli Linkwes say?
He's the chief investigator andhe's one of the world leaders
in investigating the systemiceffect and benefit of sunlight
on health.
He said there is a relationshipbetween high sun exposure and
(35:55):
malignant melanoma incidence,but an inverse relationship to
prognosis.
But an inverse relationship toprognosis.
Thus, high UV exposureincreases the incidence as in
more people are going to bediagnosed with melanoma, while
low sun exposure habits onvitamin D levels have been
linked to thicker, moreaggressive melanoma with shorter
(36:16):
survival times.
So a very, very profound studywhich is explaining that there's
this trade-off, a veryimportant trade-off.
I'll quickly revisit this datafrom Professor Weller, because
what did they find?
They replicated the findings ofthe melanoma in Southern Sweden
study.
They showed that those withgreater sun exposure had lower
(36:39):
mortality.
Those with greater sun exposurehad lower mortality.
So what's the mechanism here?
How can we explain this?
Well, I told you about thesechemical cousins of vitamin D.
Well, it turns out that theyhave an immense and very
fascinating and profoundanti-cancer benefit.
So this vitamin D herepre-vitamin D3, becomes vitamin
(37:01):
D.
If you stay in the sun and youcontinue to irradiate your skin
with ultraviolet B, this becomeslamisterol, tachysterol and a
whole bunch of other compounds.
What do these do, theseupregulate DNA repair enzymes in
the skin.
The UVB is damaging it and thebasic cision repair and all
(37:22):
kinds of other DNA repairmechanisms are promoted by these
vitamin D metabolites.
So I think that is going to beone of the profound reasons why
we're seeing lower mortality inpeople with greater sun exposure
.
Now, what are the causes of skincancer?
And look, I'm going to explainmy current thinking about this
(37:43):
and this isn't by any meanscomplete, but it's how I'm
thinking about it at the moment.
And there's always going to bean interaction of genetic
predisposition withenvironmental factors.
So I always tell my patientsthat genetics loads the gun and
your environment, your choices,your lifestyle it pulls the
trigger.
Okay, what are the geneticpredispositions?
(38:03):
Those with pale skin types,those with less melanin in their
skin, and it's very rare verycertain genetic syndromes and
there's one there calledxeroderma pigmentosum.
It's characterized by mutationsthat prevent those basic
excision repair enzymes, thoseDNA repair enzymes, from working
.
So how do you marry this withlifestyle?
(38:25):
Well, it turns out, if you havea disrupted circadian rhythm by
looking at blue light all nightand not enough full spectrum
sunlight during the day, you'regoing to impair DNA repair and
the cancer defense mechanisms.
If you have a low vitamin Dlevel and you're near infrared
light deficient, you're notgoing to be making that
(38:46):
antioxidant melatonin hormone Ifyou're immunosuppressed.
People on transplant recipientshave extreme high risk of
developing non-melanoma skincancer.
And that explains becausethey're hamstringing their
body's natural repair and immunesurveillance mechanisms.
(39:06):
What else?
And I haven't talked a lotabout food, but it's an
extremely common and recurrentanecdote that once people go
carnivore, well, they cut outpolyunsaturated vegetable oils,
seed oils, refined oils thatthey find that they're prevented
from burning.
They're essentially resistantto the effects of UVB light.
(39:27):
They're less photosensitive.
We know and it's not a talk fortoday, but we know that omega-3
and the DHA, the EPA fattyacids they confer
photoprotective benefits in theskin.
And as a society we'vecollectively deviated from an
(39:48):
ancestrally normal andappropriate omega-3 to 6 ratio
because everyone is under-eatingmarine seafoods and everyone's
over-eating refined seed oils.
So I think that that is a keyeffect modifier for the
development of skin cancer.
What else?
Melanoma is unique and we dosee melanoma commonly in more
(40:12):
younger people.
Again, they're typically anindoor worker, they have low
vitamin D, but it turns out thatthere's a photoreceptor system,
the melanopsin non-visualphotoreceptor system.
This regulates melanocytefunction.
So if we're sitting in front ofa blue-lit screen all day and
we're sitting under blue light,then this light is highly
(40:35):
stimulatory to melanocytes.
So I believe that the indoorenvironment is a key part of
particularly melanoma diagnosisin younger people.
So how can we think aboutdeliberate sun exposure really
on a broad level?
Because we have to be weighingup the benefits and the risks of
(40:56):
sunlight exposure and sunlightavoidance.
Well, I think that data andevidence suggests that we're
trading up a reduced all-causedeath, reduced cancer death,
reduced skin cancer death and alower cardiovascular death up
against potentially a greaternumber of skin cancers, both
melanoma and non-melanoma skincancers, and they're
(41:19):
particularly going to be inthose fair-skinned prototypes.
Reduction in cardiovasculardeath is a massive part of the
benefit of natural sunlight, andthat was a talk I did last year
, which is a critical part ofthis story.
So quickly, let me discuss howwe're going to use the sun to
help reduce our mortality fromcancer.
(41:41):
So there's a couple of reallygeneral steps here, but what we
want to do is we want tounderstand our ancestry.
We want to understand ourancestry, we want to understand
our risk factors, we need tounderstand our ambient UV
conditions and we're going totitrate our sun exposure based
on those things.
We want to target a vitamin Dlevel.
Again, this is going to be amarker of our sun exposure to a
(42:02):
certain amount in approximatelyaround 125.
And obviously we're going tocheck for any suspicious lesions
that might be forming as aresult of an increased sun
exposure habits.
For a quick explanation, this isthe Fitzpatrick photo scale,
and from one to five and on oneyou have the most pale northern
(42:25):
European, the Ranga, and at sixyou've got the darkest Sudanese,
west African, somalian, perhapsAustralian Aboriginal phototype
and what you have here is agradient of melanin in the skin
(42:47):
and that's a gradient of pigmentin the epidermis.
The number of melanocytesaren't changed, but the amount
of melanin that they've secretedinto the skin has.
And the question is whataccounts for this difference?
The answer is the ambient UVlight.
In Scandinavia the UV indexdoesn't climb above six most of
(43:07):
the year and for one week ithits about six In the places
where people have the highestpigmentation.
They're being bombarded yearround at the equator with
massive amounts of UV light.
So it's a response to theambient UV conditions.
The other key point and I put itin small letters, but it's
important to note is that theless melanin you have, the
(43:34):
easier it is to make vitamin D.
That means because the melaninis itself is absorbing and
dissipating this UV light asheat.
So if you amongst a range ofother effects, but the benefit
of being pale in a high UV areais that you need a very little
amount.
And really, when we're thinkingabout light, we're thinking
about essentially a drug-likereplacement.
So we need to consider thatthis is a dosing that we're
(43:55):
giving ourselves and we can doseourselves, but we have to be
smart about the dose.
Another way of thinking aboutthis is what I'm calling a skin
type latitude mismatch.
So you have to ask yourself doyou live in a similar solar
environment to your ancestors?
If yes, then you're matched andyour skin type's appropriate
for the conditions that you livein.
Sun exposure habits are mucheasier then because you don't
(44:17):
have to mitigate as much,because you're in the
environment that your ancestorswere evolved and you've had the
appropriate amount of melanin inyour skin.
But us in Australia, mostpeople are mismatched and you
can actually be mismatched intwo directions.
You can be a fairer skinnedperson in a higher UV index area
, which is most of Australia'sNorthern European migrants
(44:43):
historically or you can be adarker person in a lower UV
environment.
As you can imagine, it's muchmore difficult to be dark in an
area with low UV light than itis to be a light skin pigment in
a high UV area.
The reason is because if you'reshame-worn, you can go in the
(45:04):
shade.
That a key point.
You can titrate your solarexposure by using shade.
Unfortunately, uh for stormzyhere there is not enough uv
light in the uk year round togive him his sunlight needs and
that and that that actually isassociated with a whole bunch of
of uh you know interestingphenomenon, um related, related
(45:28):
to sunlight deficiency and howthat's affecting health
disparities and this disparityin health outcomes, particularly
in the US but also in the UK,between African-American,
african-british and the nativepopulation greater rates of
obesity, diabetes, cancer,stroke and heart attack.
I believe it's related to thesolar exposure and the
(45:49):
inadequate amount of solarexposure that you're going to
get as a dark person in a low UVenvironment.
What are some key risk factors?
So, if you've got a personalhistory of melanoma, if you've
got a family history of melanomaagain, if you're taking
medications that are going tosuppress the body's response or
(46:10):
repair mechanisms to UV light,and if you've got many atypical
nevi or funny moles, none ofthese are necessarily absolute
contraindications to UV exposure, but it has to be taken on a
case-to-case basis.
You have to understand thesolar conditions.
The UV index is a measure ofUVB intensity and if you go into
(46:33):
any weather website you'll beable to see what that UV light
is doing during the day.
So, again, as I mentioned,seasonally this will change.
But here in Australia wetypically we can get in summer
many days, you know, 11 andabove, and that's a very high UV
dose.
Compared to Tassie, brisbane,townsville, everyone is
(46:55):
extremely different.
So it pays to understand howmuch UV light you're dealing
with.
It also is relevant to knowthat you can't make vitamin D
and you therefore can't getburnt at all parts of the solar
day.
Again, the sun angle isprimarily determinant of how
much UV light comes in and whenthat is reaching above 45
(47:18):
degrees you're going to begetting UVB light.
So the morning and the eveningyou can safely get your full
body out and it's encouraged todo so prior to UV light exposure
.
But just be aware that you'renot going to be making vitamin D
in that time but you're gettingother benefits for circadian
rhythms and other physiologicalfunctions.
So regulating your circadianrhythm it's easier said than
(47:42):
done Bright light during the dayand darkness or moonlight at
night, and we can disrupt thecircadian rhythm either by
getting insufficient naturalsunlight during the day or
excess light at night.
So, minimizing light at night,mitigating with things like blue
light, blocking glasses withred and light, or candle light
(48:03):
close to the ground these areall relatively straightforward
but give you very high valueways of helping preserve your
circadian rhythm and thereforepreserve your immune cell
function, preserve the cancermachinery's ability to kill
cancer cells at the right time.
And what do you do then?
(48:24):
You can titrate your sun dose,and this is an app that was
developed by Professor MichaelHolick, his team, to help dose
sunlight, based on yourphototype, based on the ambient
UV conditions.
It makes it really easy.
Circadian is another app tohelp you understand what time of
day is sunlight present in myenvironment.
Finally, you want to build yoursolar callus, and really you
(48:45):
want to expose your solar calyx,and really you want to expose
your whole body.
What was the norm before clotheswere invented?
Well, from sunset to sunrise,sunrise to sunset full body
irradiation on our skin.
That is what our biology needs,and a lot of people haven't had
sunlight on private parts indecades, and that is a problem
(49:07):
if we're trying to preventcancer, when we understand the
potential and powerful role ofthese vitamin D and these other
secosteroids, as well asnear-infrared light.
So what's an appropriatevitamin D level?
Well, this work by Hollick etal.
They looked at where does thevitaminD level land in
(49:28):
free-ranging humans, innon-human primates, it gets to
anywhere between 125 to 200.
In the Maasai and Hadzabe inTanzania it sits at about 115.
These guys look like aprototype, five or six.
They have a massive amount ofmelanin, but they're still
maintaining a serum vitamin Dlevel that is double the average
(49:53):
Canadian and I would say doublethe average Australian, because
they're simply outside all day.
I mean, how else can we look atthis?
Outdoor workers they'llnaturally have levels of 163.
Puerto Rican farmers 135, 122.
So the average Canadian is 68.
(50:14):
I would tell you from anecdotalclinical experience measuring my
patient's vitamin D, it'sprobably a little bit higher
than that, maybe 78 or 80, butit's nowhere near.
Most people are not gettingclose to those levels, and
Australian dermatologists thisis an interesting one because
(50:37):
it's proof that they're eatingtheir own cooking.
But 35 nanomoles is deficient,and it's deficient no matter
what metric you use, and this isa graph that explains the
different units for both UK andUS.
But under 50 is classified asmild deficiency in Australia.
(50:58):
Above 75 is where we stopseeing bone complications like
subtle subclinical osteomalacia.
If you can get your vitamin Dabove 75, and that's a good
threshold for supplementation toget above.
But really the sweet spot forcancer prevention long-term is
(51:21):
going to be above 100.
And that is putting yourselfinto the lowest risk groups of
those epidemiological studiesthat I presented to you earlier
on.
Obviously, if you havesuspicious lesions, they need to
be identified and we're reallyparticularly worried about
pigmented lesions.
So identify concerning factorsthat include asymmetry in any
(51:48):
lesions, multiple differentpigments, rapid change
anything's concerning.
Luckily we have some of thebest skin doctors in Australia.
These can be readily identifiedand excised, which is great.
The slide I didn't include is astory about melanoma over
(52:10):
diagnosis and it's a little bitof an interesting and
controversial topic.
But the data is clear thatthere's some degree of that
happening, not only in the USbut here in Australia too, and
it's driven by diagnostic creepin terms of what previously
would have been known as calleda pre-malignant lesion or is now
(52:32):
being called a melanoma in situ, and that's been driven by a
whole range of factors,particularly in the US.
It's related to profit and thestructure of their system that
rewards melanoma diagnosis, butthat's not really relevant to
you as individuals, because ifyou have anything that's
concerning, it needs to belooked at.
So let's end on a meme, becauseI love memes, I love the matrix,
(52:52):
and what Neo is saying here isyou're saying that those people
with cancer cancer patientsshould, including with melanoma
should sunbathe to reduce therisk of dying.
Keyword being dying and Morpheussays yes, that is exactly what
I'm saying.
So if you're interested in anymore of this, then join my
(53:14):
private community group.
I've actually put together amuch, very detailed course about
safe and appropriate, sensiblesunlight exposure that includes
the nuances I've touched on,called solar callus, with a
whole bunch of lessons, andinclude on things like
photosensitizing medications,the role of circadian rhythms
(53:37):
and how to optimize everything.
So check that out if you wantto dive into a bit more depth,
and I've got a whole bunch offree podcasts on my channel that
go into this in further depth,including with Professor Richard
Weller and Dr Jack Cruz, whohave done a lot on this topic.
My talk last year is aimed atthe cardiovascular benefit and
(54:02):
if you want to learn from me andyou want to experience how I do
the solar exposure and how Irecommend you do it, then join
me on a couple of retreats inJuly.
That's always a fun time.
So thank you very much forlistening.
Speaker 3 (54:26):
Max Goldhain, everybody Give it up, applause.
Speaker 2 (54:33):
A beacon of wisdom and knowledge.
We've got a couple questions.
Yeah, okay, we've got Cindyover here.
Look at those hands.
Shoot up, gary.
Speaker 3 (54:47):
Everybody goes out into the sunshine and they put
their sunglasses on.
Will you address that please?
Speaker 2 (54:52):
Yes, so photoreception is not only a
cutaneous process and thatbasically means that your eyes
are detecting light wavelengthsand there's a feedback loop that
exists between the eye, thebrain and the skin that
regulates pigmentation.
That means, for that process tooccur properly, you need a
(55:13):
coherence between the signalthat the eye is receiving with
regard to its ultravioletenvironment and the skin.
If you wear sunglasses thatblock ultraviolet A and B they
broke up to 400 nanometer lightyou are going to deactivate or
create a discrepancy in thosesignals.
That is going to impair thetanning process and and that
(55:36):
evidence is very old and it'sbeen done in fish and lower,
lower order animals that, likefrogs, that um show the
pigmentation is is occurringbecause of what is the light
information that's beingreceived through the eye.
Does that include seeing glasses?
So, to a lesser degree,depending on the lens.
(55:57):
It's a different thing type,but if they're UV blocking, then
to some degree they're going toimpair that process.
Yeah, so any car windscreens?
Yes, absolutely, because theyagain are just changing the
(56:20):
proportion of light that you'rereceiving, because they
preferentially block UVB, theypermit a little bit of UVA and
they permit more blue thaninfrared, so they're changing
the proportion or the form bywhich the light is being
delivered to the eyes and skin,and that's different to the
three billion years that yourbody's evolved with.
Speaker 1 (56:38):
Max, thank you for continuing my confusion with
vitamin D and UVB light, becauseI think there's a double
paradox there which keepsarticulating it very well.
I'd like to come to the defenceof UVA and ask you a couple of
questions about that.
Uva light, which we've got alot more here the further south
(56:59):
you go stimulates nitric oxideproduction.
Nitric oxide is the criticalchemical which actually is
involved in our t killer cellresponse to cancer.
So uva light is very beneficialfor cancer mop-up rather than
cancer prevention.
Uric acid, byproduct of fructose, inhibits nitric oxide
production.
(57:20):
That's in some of my talks.
But I want to defend UVAbecause not everyone can get out
just for the right number ofminutes in the middle of the day
.
The other one is linoleic acid,which you alluded to.
There is well associated nowwith 10 years of literature that
there are.
People with melanoma have muchlower, higher levels in the fat
(57:41):
cells of that, because melanomais increasing and predominantly
found now in the non-sun exposedareas.
So how can we worry about UVBthat?
The worrying thing aboutlinoleic acid is it just comes
from the seed oils as ahalf-lifer it's probably about
(58:01):
four years.
So if you want to get rid of itout of your diet, you can
improve your metabolic healthstraight away, but it's going to
probably take a few years.
So can you defend UVA?
Speaker 2 (58:13):
Yeah, so UVA is a critical part of this whole
sunlight story and I didn'tparticularly include its
mechanisms as it relates tocancer.
But with respect to optimalhealth, uva is key and for the
reasons that you mentioned, notonly, as you've said, it
liberates nitric oxide from thevessels, the blood vessels, and
it helps to dilate it.
So you know if we're thinkingabout a patient with essential
(58:35):
hypertension, with metabolicsyndrome, who's got hypertension
yes, it is an insulin resistantcomponent to that and the
effect of insulin on you know,renal sodium absorption.
But I think that patient issunlight deficient and they're
UVA deficient, amongst a bunchof other things.
The other point about UVA isthat Weller's group noted that
UVB actually can lower bloodpressure too.
(58:57):
So it's not only an isolatedUVA effect but it's essentially
a lot of the short wavelength,including blue, can cause
photorelaxation and dilation ofblood vessels.
So I'm a massive fan of uva.
As I mentioned, the vitamin dhere is the biomarker of total
sunlight exposure.
So I think the benefit forcancer too, absolutely could be
(59:18):
uva related, but um and nearinfrared related, so it's the
whole package.
It it's difficult no, exactly,we don't have a biomarker as
like we do, that I'm aware of tomeasure someone's UVA exposure
in isolation.
On the point of linoleic acidand melanoma, yeah, I definitely
(59:38):
agree.
I think to be really nuanced.
It seems like you know thecancer in non-sun exposed areas.
That seems to be super becausethere's multiple types of
melanoma which we didn't go into.
Superficial spreading melanomain younger patients on
non-exposed areas, like on thefinger, typically in a very pale
, you know, 25-year-old officeworker, absolutely.
(01:00:00):
And that's why I alluded to theartificial light, alluded to
the fatty acid components Inolder patients who have lentigo
maligna, some of these morechronic sun-exposed areas do get
melanoma but they're nowherenear the metastatic risk of
(01:00:21):
those other melanoma types.
So, yeah, I guess I agree withyou, Gary.
I think this story is so muchmore nuanced than what we're
being presented with.
And the strategy of slatheringeveryone in sunscreen and
sunlight avoidance isessentially preventing anyone
from building any resistance orbuilding the natural
physiological response tosunlight.
(01:00:42):
So they're even more weakenedwhen they do go into sunlight,
which might be a couple of timesa year, get fried to a crisp
and you know the epidemiologysuggests that's the predominant
risk factor for developingmelanoma.
From an epidemiological pointof view.
Speaker 3 (01:00:59):
Great talk, max.
Thanks so much.
My understanding of melanomasis that it's skin sun damage in
children, infants, childrenrather than adults, and I just
wonder how that would affectsome of the figures you found,
because you're looking at adultswho may have then stopped their
sun exposure and so they mayhave been burned as a child and
say I'm going to protect myself.
(01:01:19):
So I'm worried also that peoplemay be watching this and then
go away and say, oh, I'm goingto protect myself, so I'm
worried also that people may bewatching this and then go away
and say, oh, I'm going to get mykids out there, but are they
still at risk?
Speaker 2 (01:01:29):
Yeah, so the emphasis needs to be made that there's
no evidence that low-levelamount of non-burning sun
exposure is linked to anyadverse health effect.
The issue, as you've identified, is signal for intermittent
severe sunburn sun exposure islinked to any adverse health
effect.
The issue, as you've identified, is signal for intermittent
severe sunburn in childhood.
(01:01:49):
I, I think, and and maybe I'llexplain it a little bit more the
average age, the median age ofmelanoma diagnosis, is 68.
It's in the late, late 60s.
So so what I believe isactually happening here is
people with a pale phototype.
One or two Australians mostAustralians are getting
potentially had a number ofsevere burn episodes early in
(01:02:10):
life.
They then ate their high CEDOLdiet the whole time.
They went inside and worked ina bank or office for 50 years
and then, age 60, becausethey're so vitamin D deficient
and their sunlight sunlightavoided and they're circadian
rhythm disruption, they developa malignant melanoma that
metastasizes and kills them.
So potentially that early inlife sunburn was impactful for
(01:02:34):
them.
But is that a reason todissuade people from
appropriately getting gradual,safer amount of UVB containing
light?
I don't think that's the case.
But, as I said, I'm notadvocating for burning by any
means.
And the paler you are, theearlier in the day you can
safely get UV light before goingin, because the UV index is
(01:02:55):
lower and that's probably themost conservative way to advise
UV exposure.
If your ancestry is from Sweden,where it doesn't get above a UV
index of six, then know the UVconditions of your environment.
And the moment the UV indexclimbs to 10, because you've got
your Swedish ancestry go inside, you've still generated
sufficient more than enoughvitamin D and beneficial
(01:03:16):
sunlight in that time.
But it's culture in Australiafor us to go out in the big day
but we've got our sunscreen on,you know, and really spend a lot
of time in an area that wouldrequire us to be as dark as
those Sudanese people.
But not many people are reallygetting that.
Sorry, guys, that's all we'vegot time for.
If you've got any morequestions, ask Max in the break.
(01:03:39):
Dr Max Gahlhain.
Thank you.
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