3:34

In one of the most important episodes of the Regenerative

3:37

Health podcast , I'm speaking with dermatologist

3:40

and researcher Professor Richard

3:42

Weller from the UK . Now

3:45

we discuss sunlight , skin

3:47

cancer and the profound but clear

3:49

and repeated findings from large

3:51

population-based studies that increased

3:54

ultraviolet light and sunlight is

3:56

associated with less death , less

3:58

cardiovascular death and less cancer

4:01

death . I personally believe that

4:03

sun avoidance narratives have

4:05

been some of the most harmful of the public

4:07

health messaging , given the critical

4:10

role that all the wavelengths of

4:12

natural sunlight have for optimal

4:14

human health . Professor

4:17

Weller is doing fantastic work in educating

4:19

and researching these effects and

4:22

adding nuance and balance

4:24

to these narratives . If you want

4:26

to learn how to harness the sun to

4:29

reduce your risk of getting cardiovascular

4:31

disease , cancer , autoimmune

4:33

disease and your risk of dying

4:36

, then check out my recently released

4:38

Solar Calus Course . This

4:41

is the most comprehensive course

4:43

to date that puts together the

4:45

theory , the preparation

4:47

, the execution of

4:49

getting sunlight in a

4:51

way that is respecting

4:54

your evolutionary biology

4:56

. Now onto the podcast

4:58

. Okay

5:05

, I'm sitting down again with world-renowned

5:09

dermatologist , professor

5:11

Richard Weller . Now

5:13

, professor Weller , you have

5:15

released some very , very interesting

5:18

research that we're going to get

5:20

to , no doubt , in this podcast

5:22

. But first I think it

5:24

would very much benefit the listeners

5:26

who don't have necessarily a

5:29

background in medicine or dermatology

5:31

to even understand some

5:33

basic physiology of the skin , and

5:36

that will really set us up for discussions

5:38

about cancers of those

5:40

different skin layers and

5:42

how they're relevant to disease .

5:44

The skin is great . It's

5:46

where we meet the outside world . It's

5:49

got , I suppose , a major

5:52

role which is to keep the outside out

5:54

and the inside in . It maintains

5:56

moisture within the

5:58

body . It keeps the environment

6:01

and foreign organisms outside . It's

6:04

that kind of envelope that wraps us up . So

6:06

it's got quite a complex role . It

6:08

also has to do things like sensation . It

6:10

has to help us touch and feel

6:13

. It has to do things like

6:15

temperature control . So

6:17

it's got a whole series of functions

6:19

and it has to be self-healing . So

6:22

it comes in layers and if the outermost layer

6:24

strata and corneum

6:27

is actually shed , we're continually

6:29

shedding the skin from the outer

6:31

surface of the skin . Below that you

6:33

have the epidermis layer

6:35

, the triple-layered structure

6:38

of the epidermis . These skin

6:40

cells , which we call keratinocytes

6:42

, gradually move up and

6:44

over the period of about three

6:47

or four weeks , keratinocytes , which has

6:49

started off on the bottom of the epidermis

6:51

, move up the surface where

6:53

they're shed , these corneocytes

6:56

. Below that you have the dermis

6:58

, which is the kind of permanent supporting

7:00

structure of the skin , and that's where

7:02

the blood vessels and sweat glands

7:05

are embedded , and

7:07

then sunlight . So that's the kind

7:09

of layers of the skin and

7:12

it varies in thickness depending on body site

7:14

. Palms and soles are very thick . The

7:16

face is much thinner . Skin Sunlight

7:21

, uv , penetrates at

7:23

different levels through the skin

7:25

. So long long

7:28

wavelength ultraviolet light , ultraviolet

7:31

A , will actually penetrate through

7:33

the epidermis down to the dermis

7:35

Is the UVB

7:37

raised . Shorter wavelength UV

7:39

that makes vitamin D and causes burning

7:41

doesn't penetrate as far , just goes

7:44

into the epidermis . So

7:46

yeah , and then so I suppose

7:48

the other thing to add as well as the keratinocytes

7:50

, the main skin cells , you've got other

7:52

cells like melanocytes that produce

7:55

melanin , causes skin pigmentation

7:57

. You've got cells of the

7:59

immune system that pick up

8:01

infectious organisms or cancers coming

8:03

in . You've got sensory

8:05

cells . There's a number of other cell types , but

8:07

the main type of cells are these keratinocytes

8:10

, the skin cells .

8:10

Great , and you

8:12

mentioned that the UV light interacts and penetrates

8:15

to different levels depending

8:17

on its wavelength . What

8:19

are the mechanisms

8:22

that the skin has evolved to

8:24

protect itself from what

8:27

we're both acknowledging is the mutagenic

8:29

effects of ultraviolet light ?

8:31

Yeah , so very interesting . The

8:33

UVB hits us again , and particularly the UVB wavelengths

8:35

will lead to DNA damage and

8:37

mutations and actually the skin

8:39

is continually facing that and

8:42

the skin is continually having DNA

8:44

mutations that might lead to

8:46

cancer . So it's actually evolved

8:48

lots of ways of handling

8:51

that , because it's a constant thing . And

8:54

I suppose the point to make about the skin meeting

8:56

the environment , the skin meeting the outside

8:58

world , is inevitably

9:00

if you're meeting the outside world you're going to meet

9:02

stuff that the body doesn't like and

9:06

UV can cause mutations . So

9:09

it's well set up to handle that . So

9:11

there's a couple of things when DNA mutations

9:13

occur which are caused by UV

9:15

, there's a whole series

9:17

of DNA repair

9:20

enzymes . So the skin is continually

9:22

detecting

9:25

and correcting DNA

9:27

mutations caused by UV . So that's the

9:29

first thing . The second

9:31

thing , of course , is actually where , continually it's a bit

9:33

of a moving staircase . You form your keratinocytes

9:36

at the bottom of the epidermis . They

9:38

move up over a few weeks and are shared

9:40

. That's actually a pretty useful process

9:43

because any keratinocyte

9:45

that might be heading down the route

9:47

to a cancer is probably going to get shared

9:49

. So you have this kind of shedding

9:53

of the stuff that might

9:55

cause problems . You

9:58

then also have the technique called

10:00

apoptosis , whereby

10:02

keratinocytes that look

10:04

like they're heading towards a cancer . If

10:07

you haven't managed to repair that DNA

10:09

, they will undergo a process

10:11

called apoptosis . The body spots that

10:14

and says ooh , and it kind of knocks off

10:16

that skin cell so it can

10:18

be harmlessly removed . So

10:21

there's a lot of continual processes going on

10:23

. I have to say what is really interesting is if you

10:25

look at the

10:28

number of DNA mutations in

10:30

somebody with a keratinocyte skin

10:32

cancer , a squamous cell skin cancer

10:34

, and if you look at the number of DNA

10:36

mutations with someone who's just got sunspots

10:38

, you know active keratosis , something

10:40

that every proper Australian has on their head

10:42

beyond the age of 40 , actually

10:45

the mutation burden is about the same

10:47

. So it

10:50

is interesting that it's

10:52

not the number of mutations that

10:54

lead to skin cancer , it's

10:57

mutations that escape surveillance

10:59

and being removed at least a skin cancer

11:01

. So yeah , yeah .

11:05

And I want to make the point that the ingenious

11:07

function of that

11:09

continual shedding of those keratinocytes

11:12

is in itself a form of protection

11:14

against ultraviolet light , just

11:16

like bark on a tree helps protect

11:19

the living part of the tree .

11:22

Yeah , indeed , and of course , the other thing is pigmentation

11:25

. Melanin really counts , so melanocytes

11:28

accrete melanin and melanin absorbs

11:30

UV . It's a natural sunscreen

11:32

and what's very interesting is you could have a cross

11:35

section of the skin . What you see

11:37

is you see a little cap of melanin

11:39

, a little hat of melanin which

11:42

sits over the nuclei in

11:44

the lower part of the epidermis , giving

11:47

protection against UV

11:49

damage . And , of course , the real

11:51

original Australians , aboriginal

11:54

Australians , have dark skin to handle

11:56

the high UV load . The

11:59

problems we see are when white Europeans

12:01

arrive on their convict

12:03

ships 100 years ago and

12:07

without that natural protection and that's

12:09

where you see the UV and use

12:11

skin cancer on the skin aging In

12:14

people who . Basically

12:17

, if you walk to Australia

12:19

from Africa over 20,000

12:21

years , that gives you time for

12:24

your skin to adapt to that changing UV

12:26

environment . If you spend eight

12:29

weeks on a ship from

12:32

a British prison to an Australian

12:34

to Australia , you

12:36

don't get time to make those changes .

12:40

I think that gets to the heart of the issue

12:42

, which is the , the

12:45

, the deviation or the problem

12:47

with skin physiology that leads to cancer , and

12:49

I think the key issue here is that

12:51

underlying what's going on is

12:53

a mismatch between skin pigmentation

12:56

, genetic predisposition

12:58

to having a certain skin pigmentation and

13:00

latitude , and when

13:03

that is mismatched , then we are more

13:05

likely to get

13:07

these types of malignancies . I

13:09

want to make a point about melanin , because you

13:11

mentioned that it absorbs ultraviolet light and

13:14

, for those who have listened to my previous

13:16

podcast that I've discussed melanin and

13:18

it is essentially a black hole pigment . It's not

13:20

only absorbing ultraviolet , but

13:22

it's also absorbing visible light

13:24

and basically everything on the electromagnetic

13:27

spectrum . Dr

13:30

Jaqruz , particularly , has talked about the

13:33

role of melanin in actually splitting

13:35

, using , having an ability to essentially derive

13:37

energy from the , from

13:40

the use of melanin . So I mean melanin

13:42

is so key and the other

13:44

fact , the fact is that it include

13:48

heavy metal chelation , they

13:50

include antioxidant ability . So

13:52

, and I think

13:54

what maybe isn't being emphasized

13:57

as much is how multi-purpose and

13:59

how useful melanin

14:01

actually is in the skin .

14:04

Yeah , I'm unaware of those other . I

14:07

know nothing about these other post-laterals

14:09

melanin , I mean it's a , you know it's , it's

14:11

important in handling

14:14

UV , which I know best . And of course there's two

14:16

main types of melanin . There's U melanin and

14:18

the black melanin and then there's FIO

14:20

melanin , the red melanin I might

14:22

say very usefully in Australia

14:24

. Just last week in the Australian

14:26

and New Zealand Journal of Public Health a superposition

14:30

paper was published by a bunch of

14:32

excellent in a distinguished

14:35

Australian research

14:37

is led by Rachel Neal at

14:39

the Berghoffer in Queensland and

14:41

they have looked at UV advice

14:44

risk-benefit ratios in Australia

14:46

and they've and they formally

14:49

lay out how skin

14:51

colour determines the

14:54

risk-benefit ratio to UV and

14:56

so you have to consider a constrictive

14:59

skin colour or background skin colour when

15:01

giving correct UV

15:04

exposure advice .

15:05

And that's particularly relevant in

15:07

your country when you have , and in all

15:09

the latitudes , when you have people from the equator

15:12

who are migrated north , and to

15:14

give them the same advice as someone with a Fitzpatrick

15:16

one pale skin makes

15:18

, you know , absolutely no sense at

15:21

all . So I'm glad that that kind of nuances

15:23

is being added into

15:26

the narrative .

15:27

Yes , absolutely right . Of course , the other interesting

15:29

comparison to our two countries . So , first

15:31

of all , absolutely right , somebody

15:35

from a high UV environment coming to Low

15:37

UV Scotland utterly different

15:39

from a red-headed Scott

15:41

in Australia . The

15:44

other thing , of course , is how you get the UV . So

15:46

in Australia you have high UV all

15:48

the time , whereas

15:51

here in the UK our UV exposure

15:53

tends to come in short-shot burst in the

15:55

two weeks in the med in summer . So

15:58

it's not just the amount of UV but

16:00

the pattern of UV which varies

16:02

between the two countries and that

16:05

it's interesting . At the moment in the UK

16:07

we are also just

16:09

reconsidering our advice

16:12

to UV . So the research arm of the NHS

16:14

, the National Institute of Health Research

16:16

, is currently going through a big

16:19

analysis of all the published data

16:21

on UV benefits

16:23

as well as hazards , and that's the important

16:25

matter and they're going to be drawing up their

16:27

conclusions , I think in

16:29

around May of this year and I'm

16:32

interested to see the

16:35

decisions they make . I think I strongly

16:37

suspect they'll be acknowledging the benefits as

16:39

well as the risks . Their advice

16:42

for what we should do , I hope , will take

16:44

into account the

16:46

nature of UV exposure in the UK

16:48

no sunlight at all except for two weeks in

16:50

your summer holidays .

16:52

Yes , and this is a point that you

16:54

made the last time we spoke , which is that melanoma

16:57

, and we're going to explain the different

17:00

types of skin cancers , but melanoma is a disease

17:02

of sun burning , not

17:04

of sunlight exposure . And

17:07

again , people who have listened to my previous podcast , I've

17:09

talked about this concept of a solar

17:11

callus and what I

17:14

have meant by that is the

17:16

idea that gradual , small

17:18

amounts of ultraviolet light that essentially

17:21

cultivates melanin production

17:23

such that we're not in a position

17:25

to get a raging burn

17:28

, and that is essentially

17:30

what people who are doing , who are unprepared

17:33

for sunlight and UV maybe

17:35

they fly from Luton

17:37

Airport down to Ibiza and

17:40

with their friends and they'll absolutely roast

17:42

to a crisp . The

17:44

point here that I think the nuance

17:47

that isn't in this narrative , in this dialogue

17:49

, is that these people have

17:51

essentially a trophic skin

17:53

with regard to the UV

17:56

yield that they're putting themselves in and the

17:58

environment that they're exposing themselves to , and

18:00

perhaps if they had acclimatized

18:02

that area through a process of gradual

18:05

but deliberate but gradual UVB

18:07

and UVA exposure , then they wouldn't have

18:09

been in the position of getting

18:12

a sunburn , but they'd also have built up

18:14

sufficient vitamin D levels , and

18:16

we know that vitamin D deficiency

18:18

is a very , very common finding in

18:20

melanoma and non-melanoma skin cancers .

18:23

Yeah , suddenly , and particularly people

18:26

with low measured vitamin D levels

18:28

have a worse prognosis for their melanoma

18:30

. People who have high

18:32

vitamin D levels when diagnosed

18:35

have better outcomes . So

18:37

the epidemiology of melanoma , as you

18:39

say , is interesting

18:42

and complex . So when I'm teaching my medical students

18:44

I say right , is melanoma common

18:46

in white Australians or white Scots ? And

18:48

they all say white Australians . The next question

18:50

is in Australia , is melanoma common

18:53

in outdoor workers or indoor workers

18:55

? And actually the answer is indoor workers

18:57

. And is melanoma

18:59

common in the untanned or the tanned ? And

19:02

it's common in the untanned . So

19:04

, and then you know why is this ? Now

19:06

that's different from squamous

19:09

cell skin cancers , one of the other . So

19:11

melanoma is a tumor of melanocytes . Squamous

19:15

cell skin cancer is a tumor

19:17

of the keratinocytes . Now

19:19

it's much commoner than melanoma

19:22

but it's got a lower mortality . And

19:25

squamous cell skin cancer is a disease

19:27

of chronic sun exposure , commoner in white

19:29

Australians than white Scots , common

19:31

in outdoor workers than indoor

19:34

workers , common in the tanned and the untanned . So

19:36

squamous cell skin cancers are going to proper old fashioned

19:39

cancer . That's read the books . The

19:41

more of you know smoking , the more you smoke

19:43

, the more likely you are to drop dead of lung cancer . Dose

19:46

dependently , you know , the more cancers

19:48

you have , and it's the same with squamous cell

19:51

skin cancer . The more UV you have , the

19:53

greater your risk of dying , of

19:55

developing and dying a bit . But

19:58

melanoma is not

20:00

just , is actually a family

20:03

of diseases and

20:05

they're all slightly different

20:07

. So

20:09

the ones that are most diagnosed

20:12

now , the superficial spreading melanomas

20:14

and the nodular melanomas , are

20:17

the risk factor there appears to be intermittent

20:19

sun exposure and sunburn , particularly

20:21

in childhood . There's then what are

20:23

called the acral melanomas , which

20:25

occur on the palms of the souls . Those

20:28

are the melanomas that occur in black people

20:30

. They're rare in black people . They're rare

20:32

in white people , probably about equally rare . They

20:35

are unrelated to UV

20:37

. So there is ultraviolet

20:39

. It pays no part in their development . They've

20:42

got a completely different pattern

20:44

of DNA mutations than

20:47

the UV induced one . So that's a non

20:49

somewhat pays no part at all . And

20:52

the final and least common

20:54

probably least , maybe , you know

20:56

or a very uncommon type of melanoma is

20:59

what's called an antagonomalignant

21:01

melanoma . Now , that's

21:03

actually a melanoma of chronic

21:05

sun exposure and it occurs on the

21:07

face , which is chronically sun exposed

21:10

. And it occurs in old people

21:12

I don't think I've ever seen anyone less than 80

21:14

with one and so it occurs

21:16

on the face of really old people and

21:19

that is due to chronic

21:21

sun exposure . But here

21:24

in the UK it occurs in really

21:26

old people who've had decades

21:28

and decades and decades of sun

21:31

exposure and interestingly it's

21:33

often quite thin and

21:35

often it's got pretty good prognosis

21:37

because it's so thin . But

21:40

yes , broadly the melanomas

21:43

that we see , most of the super spreading and

21:45

the nodular , are diseases of

21:47

sunburn , not sunlight

21:49

.

21:50

It's a fascinating implication , and

21:55

the reality or the questions that

21:57

it raises in my mind are exactly

22:00

what is going on here , and to what

22:02

degree is it environmental

22:05

changes that we are experiencing

22:08

that are perhaps unrelated to ultraviolet

22:11

light ? And I

22:13

want to highlight a couple of more

22:15

pieces of this puzzle before we

22:17

necessarily dive deeper into

22:19

the exact

22:22

what we think might be going on . You

22:25

highlighted , too , that outcome in melanoma

22:29

is also poorer with

22:31

vitamin D deficiency , so

22:34

there's a lot of papers that I've

22:36

managed to find that have simply

22:38

been retrospective cohort studies

22:40

that are looking at people who've had melanoma and

22:43

, as you say , and those

22:45

with a lower vitamin

22:47

D level have a higher tumor

22:50

mitotic rate . They have deeper

22:52

thickness . All these outcomes

22:54

that really predict a worse

22:56

and more likely to die are

22:59

lower in people who have a

23:01

higher and people have lower vitamin D , and

23:03

it really makes me think that we

23:05

need to be cultivating the vitamin D

23:07

level in people who have melanoma

23:10

diagnosis , which , paradoxically

23:12

, would involve more

23:14

UVB light , not less .

23:17

Yeah , so we have . We've got a paper on review at

23:19

the moment . We did a big study in

23:22

the . I presented this at

23:24

a couple of meetings so I can talk about

23:26

it because we will meet abstracts but

23:28

the paper review . So we look to the UK bar

23:30

bank . 400,000 people in the UK

23:32

followed . I'm in

23:34

, recruited back in about 2000 . I

23:36

was one of the subjects and then they're

23:39

being followed from then on and a

23:41

mass of data

23:43

collected and all those of us who were subjects

23:45

in terms of behavioral factors

23:47

, lifestyle factors

23:50

, health and baseline , masses

23:52

of measurements taken on people . We're then being

23:54

followed up . And of course in the UK

23:56

we have universal health records in the

23:58

National Health Service and we've got universal

24:01

death records , universal cancer records , so

24:03

you can link each of those people

24:05

and you know what their behaviors are at the start

24:08

with what happens to them with

24:10

time . And we've been

24:12

looking at

24:15

sunlight exposure and how

24:18

does sunlight exposure correlate

24:21

with death

24:24

from any cause ? And we use two main

24:27

measures of sunlight exposure the

24:31

date you have to use the data that was

24:33

collected . We found

24:35

the best measures of sunlight

24:37

exposure were to . First of all , we looked actually at sunbed

24:40

users , not so much because of

24:42

sunbed use , as because of the fact

24:45

that we know that some bed users

24:47

are what we call some seekers , we know

24:49

that if sunbathes more , they actually go out in

24:51

the sun . There's very good data

24:54

showing that , behaviorally , people

24:57

that use sunbeds are different from those that don't . Now

25:00

we had to correct for

25:02

the fact that sunbed users are different in other ways

25:04

they're younger , they're more female , they're

25:07

less educated , they're more likely to smoke , they're more

25:09

likely to come from Manchester , etc . Etc . So

25:11

you correct for all of those factors and

25:15

so you throw in the corrections for that . We're

25:19

then able to measure their vitamin D levels , and

25:21

measured vitamin D is a great

25:24

biomarker for sunlight exposure

25:26

. Vitamin D has a few narrow benefits

25:29

it prevents rickets , it may prevent progression of

25:31

some cancers . It could be relevant to this story

25:33

mechanistically , but most

25:35

of all , from my point of view , measured

25:38

vitamin D is an excellent

25:40

biomarker for sunlight exposure and

25:42

we found that the sun seekers people who use sunbeds

25:44

do indeed have higher

25:47

measured vitamin D levels . And you correct

25:49

the vitamin D for obesity

25:51

. You put in lots of corrections to make sure it's an

25:53

accurate measure and it's not ultimately

25:56

confoundless , and what we found

25:58

were that the sun seekers had

26:00

a lower all cause mortality

26:03

than non-sun seekers

26:05

. They lived but

26:07

they particularly they had about

26:10

a 13% reduction

26:12

in cardiovascular mortality . They

26:14

had around a I

26:17

think it was about a 10% reduction

26:19

in cancer mortality , including

26:22

skin cancer . So

26:24

people that got more sun were less likely

26:26

to have any cause , less likely to

26:28

have heart disease , less likely to have cancer

26:30

, less likely to die of skin

26:32

cancer , and it's interesting

26:35

that that actually kind of matches up to this

26:37

data . We know that people with who

26:39

have higher measured levels of

26:42

vitamin D when they're diagnosed , are

26:44

great by a market for some of that exposure , have

26:47

a better prognosis for their vitamin D . Now

26:49

that doesn't tell you the mechanism . I

26:54

mean , if you want to find a mechanism , if it's vitamin

26:56

D , you do clinical trials

26:58

and you give people vitamin D and

27:00

you have a control group . You know half get vitamin

27:02

D , half don't , and those clinical

27:04

trials have been done and vitamin D

27:06

doesn't do very much . It stops people

27:09

getting rickets . It may prevent

27:11

progression of some cancers

27:14

, but the effect is probably

27:16

pretty small . It's nothing like

27:19

as big as the observational

27:21

size of effect If you

27:23

look at someone who's got

27:25

twice as high . A measured vitamin

27:27

D level has a great reduced risk

27:29

of cancer

27:32

death , for instance . But when you give

27:34

people vitamin D levels double the

27:36

vitamin D level you don't see the same size

27:38

of effect . So it suggests

27:40

you know the

27:43

point is . I

27:46

think the data is very robust . For sunlight

27:48

, I should say the other measure of sunlight

27:50

we use for the first one was sun seekers . Our

27:53

second measure of sunlight exposure

27:55

was how far south people live

27:57

. Now in the UK , unlike Australia

28:00

, the further south you live , the closer

28:02

you are to the equator and the more sun you get

28:04

. And we found , dose-dependently

28:07

, the further south you lived , the higher

28:09

your vitamin D level . The straight line relationship

28:11

, thus straight line increase

28:13

sunlight exposure and

28:15

the further south you lived , the reduced

28:18

all-course mortality , reduced cardiovascular

28:20

mortality , reduced cancer mortality

28:22

. Just the same pattern that

28:25

we saw with the sun seekers

28:27

, the sun bit users . And again , we

28:29

correct for confounders the

28:32

further south you live , the better

28:34

educated you are , the less likely to smoke

28:36

, the younger , the more female you know , etc

28:38

. So we correct for all of those factors . But

28:41

the story is consistent and

28:43

it's the same story that Pelle Lingqvist in

28:46

Sweden showed . Can't

28:48

remember if we discussed this in our previous conversation

28:50

, but Pelle Lingqvist did another similar

28:53

study in Sweden

28:55

where he looked at , recruited

28:57

30,000 Swedish women back in 1990

29:00

, how much sunlight you get , you know

29:02

, our sorts of factors are corrective for all . The confounders

29:04

thought of them 25 years and

29:07

he , just as did we in the UK

29:09

, showed that dose-dependently

29:12

, the more sunlight people get , the

29:15

reduced all-course mortality

29:17

, reduced cardiovascular mortality , just

29:20

the same as us . So what we have

29:22

repeatedly is

29:24

, when we look at North European cohorts

29:27

, separate cohorts , separate

29:29

countries , separate studies , the

29:32

same answer coming

29:34

out , which is that the

29:36

more sunlight people have , dose-dependently

29:38

, the longer they live .

29:40

It's a remarkable finding and

29:42

it is truly I mean groundbreaking

29:45

, and the fact that you've repeated

29:47

a finding that Lingqvist et al found

29:50

in 2016 makes the strength

29:52

of that association even

29:54

more important , and that is the Bradford Hill criteria

29:56

. Is our observed finding

29:58

repeatable ? Yes , it is . I

30:01

want to make a point about the vitamin D and

30:03

, to me , the fact that you

30:05

mentioned that you can't get the same effect

30:07

on cardiovascular mortality

30:10

, on cancer outcome

30:12

, by supplementing vitamin D . This

30:15

makes so much sense to me because the difference

30:17

is between refined and

30:19

supplement and full spectrum sunlight

30:22

. Is there no way equivalent

30:24

? And the fact that the

30:26

vitamin D generated by full

30:30

UV in the presence of full

30:32

spectrum sunlight , is sulfated , it

30:35

creates other vitamin D metabolites . So

30:38

there's chalk and cheese . So

30:40

that makes a lot of sense to me . Maybe

30:43

you can talk about how you controlled

30:46

for and these confounders

30:48

in your study , because epidemiology

30:51

is a topic , especially in the nutrition

30:53

world , that is fraught with confounders

30:56

things like recall bias

30:58

, things like food

31:00

frequency questionnaires . There's

31:02

a lot of confounding in there and a lot of association

31:05

that isn't able to basically

31:08

give us the strength of conclusion

31:10

that you have managed to find . So maybe talk

31:12

about how you were able to

31:15

ensure more robust validity

31:17

of your findings .

31:19

So all observational studies , rather

31:21

than interventional studies , are prone to

31:23

confounding . So confounder

31:25

is something associated with the exposure

31:28

sunlight exposure in this case and the

31:30

outcome death . So

31:34

maybe , if you'll so

31:36

do , people that spend , people that spend more

31:38

time outside , do more exercise . Exercise

31:40

reduces your risk of death . So

31:43

you have to then correct for exercise . If

31:46

you're outside , you're probably exercising exercise

31:48

separately from sunlight , so that's a

31:50

confounder . It's independently

31:52

associated with exposure and outcome

31:55

. So you need to correct for

31:57

that . There is no to correct

31:59

for confounders . You have

32:01

to think what that confounder might be

32:04

. You can't say to the data set

32:06

tell me what the confounders are . It

32:08

doesn't work like that . And actually

32:10

it means you as a scientist and

32:12

doctor need to spend time going out and

32:14

looking at how the world works . Spending

32:16

your whole life in the library will not

32:18

do it . So you know I have been down

32:20

to tanning parlours when

32:23

I'm doing some previous research and just looked

32:25

at who goes in , because you need to

32:27

think to yourself what do I think might

32:30

be different ? You've got to go out and live

32:32

life and think what that is confounders

32:34

would be . So we

32:37

do that and then , of course , in the data

32:39

you then need to see . So

32:41

, for instance , tanning

32:44

bed users are younger and more

32:46

female . You

32:48

need to , and being female is

32:50

very good for you and being young

32:52

is very good for you , so

32:54

both of those are very healthy things to

32:56

have . You need

32:59

to have that data collected in

33:01

your database . So the UK Biobank

33:03

collects gender , it collects

33:05

age , it collects activity levels

33:08

, it collects diet , it collects smoking

33:10

habits . So the date you can only

33:12

correct for confounders if you measured

33:15

it in the first place . So when you're drawing

33:17

up a study and this

33:19

is one of the big things about doing these big prospective

33:21

studies if you did a

33:23

questionnaire with five gazillion

33:26

questions that covered every single aspect

33:28

in somebody's life , yes , you're undoubtedly

33:30

going to be collecting stuff that may be a confounder

33:32

, but nobody will ever complete study

33:34

. So when you're drawing up one

33:36

of these studies , there are lots of judgment

33:39

calls . You need to ask

33:41

enough questions to have robust

33:44

data for later researchers to come along

33:46

and be able to answer their questions

33:48

. But you mustn't make the study so

33:50

onerous that nobody goes

33:52

into it . So actually drawing

33:55

up these studies is harder than you would

33:57

think . Every question needs

33:59

to be considered . So

34:01

that's the first thing how to handle

34:04

those confounders . Well , there's two ways you

34:06

can do it . You can either stratify it . So

34:08

what that means is , say , gender

34:11

, male or female you would look

34:13

at all of the women that are in some beds

34:15

and don't have some beds and see

34:18

, you know , do the some bed user more

34:20

or less death ? And all of the men , and

34:22

you'd see if the men some bed users and non-some

34:24

. So you would handle them separately and

34:27

see if the answer was the same in both cases

34:29

. Now the fact that women tend to live longer

34:31

than men doesn't matter

34:33

, because you've looked at the women separately

34:35

from the men , but you've

34:38

looked for the some bed factors . So

34:40

stratification is one way of

34:42

dealing with it . The other means

34:45

of dealing with it is you give a kind of mathematical

34:48

waiting factor . You say that being

34:50

female reduces your . You find

34:52

, from doing you know complex statistics

34:54

, you find that being female reduces

34:57

your risk of dying by 5%

35:00

or something . So you give a 5%

35:03

correction factor to the men to

35:05

make up for fact . They're not women . And

35:07

that means , rather than just

35:09

looking at men and just looking at women

35:11

, just looking at smokers , just

35:14

you know , if you stratify you've got to look at everything

35:16

individually and go through it one at a

35:18

stage . If you give a waiting factor

35:20

to those separate confounders , you

35:23

can do what's called multivariate analysis

35:25

and you can sort of combine

35:27

the whole lot and see

35:29

what the overall effect is . So there's

35:32

, I mean this is well established . I

35:34

mean I'm not an epidemiologist . I

35:36

work with epidemiologists . This

35:38

is their bread and butter , so

35:40

that's how you do with it . Look , the other thing I would throw

35:42

in with our study and it's important

35:45

is we had our two measures

35:47

of sunlight exposure . We'd

35:51

looked at other stuff that was in the bar bank . So

35:54

people were asked in the UK bar bank

35:56

, how much time do you think you spend outside ? And the

35:58

problem is everybody in summer said two hours . Everybody

36:01

in 80% of people in summer said two hours

36:03

in summer , one hour in winter

36:06

. And

36:08

that's because people think , oh , I go to work

36:10

on the bus , you know , I walk whatever and I

36:12

walk back . When we looked at their measured

36:14

vitamin D levels , this

36:16

great biomarker for sunlight exposure

36:19

, it actually showed that that kind of self

36:21

estimate of what you think you might do

36:24

wasn't very accurate , whereas some bed

36:26

users and latitude were markers

36:28

no-transcript . Back to my

36:30

point . The way the confounders

36:33

moved with our sunbed

36:35

users was different from how

36:37

far south you lived

36:39

. So , for instance , the further south

36:41

you lived , the better educated , and the

36:44

more sun you got because you live further south , the

36:46

better educated , the less likely

36:48

to smoke you were . The more sun

36:50

you got from sunbed use , the

36:52

less educated the more likely

36:55

to be a smoker

36:57

you were . All things moved together

36:59

so some bed users and people

37:01

who lived further south tended to be younger , tended

37:04

to be more female , but other confounders

37:06

moved in different directions . The

37:08

point was these two measures . It

37:11

wasn't as if all the confounders

37:13

moved the same way . The more sun

37:15

you got from living further south , the

37:18

more sun from being inside . All the confounders moved

37:20

in the same direction . Because

37:22

then our concern is maybe there's a confounder

37:25

we missed , maybe it turns out

37:27

that , I don't know , having

37:29

brown eyes makes

37:32

you live longer and people with brown , you know

37:34

, we never considered brown eye colour

37:36

and lifespan and it turns out

37:38

that brown eye people like that , you

37:40

know , and it makes

37:42

it less likely . There was an unmeasured

37:44

confounder , something we didn't think about

37:46

, because the confounders

37:48

moved in different ways and it

37:50

would be unusual for an unmeasured

37:53

confounder to be moving in the same

37:55

way .

37:56

Yeah , thanks for that explanation . In

37:58

when I was preparing for this interview , I also

38:01

did a bit more research into the biobank

38:03

and I found another study that

38:05

I think really again

38:08

gives us another piece of evidence or

38:11

weight to back up the

38:13

idea that yours is a very , very valid finding

38:15

, and the title of the paper is Vitamin

38:17

D status and risk of all cause and

38:19

cause specific mortality . Results from

38:21

the UK biobank . Higher 25 hydroxy

38:24

vitamin D concentrations are non linearly

38:26

associated with lower risk of all

38:28

cause , cardiovascular disease

38:31

and cancer mortality . So

38:33

what that is telling me is that this

38:35

is just a simply another way of looking at

38:37

the data , which backs

38:40

up that the more sunlight people get , and

38:42

therefore the higher their vitamin D level , the

38:44

lower their risk of the same all

38:47

cause hard endpoint mortality

38:50

measurements , as you found , richard

38:52

, in your study .

38:54

Yeah , and then the other important thing to throw

38:56

into so that we got this great observational vitamin

38:58

D , which I think is a bar mark of a sun like this many

39:00

importance is . We then have the interventional

39:03

studies . So the classic , the biggest

39:06

one here . So you've done one

39:08

in , well , new Zealand . So New Zealand

39:10

is a different from Australians , I have to remember . So

39:13

they've done a big study called the VITAD

39:15

study in New Zealand and

39:17

an even bigger study done in America

39:19

called the vital study , and

39:22

these were randomized , placebo

39:24

controlled intervention studies . So the vital

39:27

study in America 25,000

39:30

Americans , half were given

39:32

vitamin D supplements for five years and

39:34

they were middle aged , so middle

39:37

aged people , you like , because they're more likely to start

39:39

getting diseases and showing things up . So

39:43

25,000 Americans have got vitamin D supplements

39:45

, half got placebo and basically did nothing

39:47

. They did it for five years and the results

39:49

are all coming out Absolutely

39:52

no cardiovascular effects , no

39:54

stroke effect . There's a whole list of negative

39:57

findings and the New England Journal

39:59

of Medicine , in July

40:01

2022 , published

40:04

an editorial attached

40:06

to the latest negative study

40:09

from the vital study and it said look

40:11

a stop taking vitamin D supplements . It's

40:13

not doing anything , it stops rickets . You've

40:16

known that for a hundred years and it may prevent progression

40:18

of some cancers . The rest of it is

40:20

pretty negative

40:23

, particularly bearing in mind the huge

40:26

size of the observational differences

40:28

. When you look at the effects on observational

40:30

studies , that is a really powerful

40:33

relationship . It's not some piddly

40:35

little thing that you might just submit out

40:37

in a trial . It is a big relationship

40:39

on the observational studies .

40:41

Yes , and not only in cardiovascular

40:43

disease and cancer , but also in

40:45

autoimmune disease , also in infectious

40:48

susceptibility to respiratory viruses

40:50

, whether that was influenza or

40:52

the SARS-CoV virus

40:55

. I want to make the point that unless

40:57

clinicians realize and researchers

40:59

realize that there is a difference between endogiously

41:02

generated vitamin D from UVB

41:04

sunlight and realize that there's

41:07

a potential of improving health and vitamin

41:10

D is simply the biomarker , as you've said , for

41:13

how much sun someone has got .

41:15

Yes , look , I think for me

41:17

, I think we need to be stepping back to where we were a hundred

41:19

years ago . I think the

41:22

epidemiology powerfully is that sunlight

41:24

has , I'm sure , systemic health benefits

41:26

. Vitamin

41:29

D , as proven by supplementation studies

41:31

, accounts for some of those benefits , the

41:33

rickets specifically . All

41:36

we can say about the rest it is

41:38

a sunlight-driven , I think , non-vitamin

41:40

D effect Sometimes , but I don't

41:42

know . It's sunlight-driven . I think

41:44

the really interesting thing , and what I'm working on

41:46

now , is what are

41:48

those sunlight-driven non-vitamin

41:52

D mechanisms ? It's

41:55

really exciting because there

41:57

are all of these

41:59

health outcomes

42:02

which are worse in winter .

42:04

Yes , let's talk about that . Two points

42:06

I want to make before we jump into that topic . One

42:09

is can you give a quick

42:11

overview of what Pelley Lindquist found in Sweden

42:13

, because I think the

42:16

finding to do with smokers

42:19

is incredibly accessible

42:21

and hard-hitting for our listeners . The

42:23

second point is to what degree can we

42:25

generalize your findings and Pelley's findings

42:27

to Northern Europeans

42:29

, say , living in Australia ?

42:31

Yes , good questions . Pelley

42:33

started it off . Pelley's great . He's

42:35

actually

42:37

an obstetrician in Sweden

42:40

. I've been

42:42

from inside the Dumptology fold saying the

42:44

Emperor has no clothes . Pelley came along first

42:47

as an outsider . I suppose it's easier

42:49

for an outsider to say that the Emperor has no clothes . Pelley

42:53

was looking

42:55

at data on this study called the Melanoma

42:57

in Southern Sweden study . The title

42:59

tells you what they were thinking about

43:01

. They were interested in how much UV do

43:04

you need to cause melanoma ? They were expecting

43:06

to find more UV , more melanoma

43:08

, more death overall . That was the expectation

43:11

when they set the study up . The study

43:13

was set up in 1990

43:15

. They recruited 30,000

43:19

Swedish women in Southern Sweden

43:21

. Melanoma is Southern Sweden study , which is

43:23

sorry . Middle-aged Swedish women

43:26

. Let's go for middle-aged people because they're closer

43:28

to death . Death is a great endpoint

43:30

. That

43:32

was actually about a quarter of the population

43:35

of middle-aged Swedish women in Southern Sweden

43:37

. They were sent

43:39

questionnaires and they were asked broadly four

43:41

questions to assess sunlight

43:43

exposure Do you sunbathe

43:46

in summer ? Do

43:48

you sunbathe in winter ? Odd people

43:50

of Swedes , some of them do . Do you go on

43:52

foreign holidays and

43:54

do you sunbathe

43:56

? There's obviously lots

43:59

of confounders attached to that . If you go on foreign

44:01

holidays you're better educated so you're probably

44:03

less likely to smoke . But

44:06

they corrected all of that . They corrected

44:08

for social factors

44:11

. They corrected for occupation

44:13

income

44:17

. In Sweden , everybody's tax return is published

44:20

openly on the same day every

44:22

year . If you want to find out what

44:24

your boss earns , or your neighbor or the prime

44:26

minister or your cleaner , you can look

44:28

it up . America , I believe , is

44:30

not the same . They

44:33

looked at income , employment

44:35

. They then looked at social factors

44:37

like education level , things

44:41

like that . Health factors , obesity

44:44

, bmi , exercise all

44:46

of these factors were looked for . They

44:49

then followed them up for 25 years

44:51

and went back to find well

44:53

, actually , how many have got melanoma and how

44:55

many have died ? Their expectation

44:58

was the more UV

45:00

you got , the more melanoma and

45:02

the more death was the expectation

45:05

. The first half of that they satisfied . They

45:07

found the more UV people had , the more melanoma

45:10

was diagnosed . But

45:12

they found that the more

45:14

UV people had , the less

45:17

likely they were to be dead . There

45:19

was a straight line relationship

45:21

With your UV exposure habits

45:23

0-4, . Those

45:26

people that had the highest UV exposure

45:28

were half as likely

45:30

to be dead at 25

45:32

years as those goody two-shoes

45:34

who followed the dump , told them to advice and

45:37

lived in a cave . Maybe vitamin

45:39

D supplements ? Who knows this

45:42

huge , great effect ? The

45:44

other interesting thing and to put , pelle

45:46

went back and did a second analysis

45:48

but to try and put this into perspective

45:51

, how big the effect size was

45:54

he found the worst thing

45:56

you can do for your health until now has

45:59

been smoking . Smoking

46:01

is staggeringly bad for you . Pelle

46:03

showed that people that got the most

46:06

sun exposure and who smoked

46:08

had the same

46:11

risk of death at 25

46:13

years as non-smokers

46:15

who avoided the sun altogether

46:18

. Basically , the badness

46:21

on your health of smoking

46:23

is equally outweighed

46:26

by the goodness of

46:28

sunlight exposure . That is

46:31

a powerful effect .

46:35

The way society perceives people standing

46:37

out outside a pub

46:39

or a cafe chain

46:41

smoking cigarettes and the way society

46:44

looks down on that person . Then

46:46

to think , the narratives around

46:48

sun avoidance slip

46:50

, slop , slap down . Here

46:53

in Australia , as you said , live in a cave , take

46:55

vitamin D supplements and God forbid

46:57

you ever get a square centimeter exposed to natural

46:59

sunlight . It's incredible to

47:01

see that disconnect in public narratives

47:04

. Yet the fact is those

47:06

two behaviors , as Pelle discovered , are

47:09

in a Swedish cohort . They're

47:11

equally harmful sun avoidance and

47:14

smoking .

47:15

Now , of course , this was in Sweden Now

47:17

I don't know what happens

47:20

in Australia . Now . Where we have

47:22

a problem here in Scotland is

47:24

our sunlight advice is copied

47:27

directly from your

47:29

advice in Australia . These

47:33

are very , very different UV

47:35

environments . In Townsville , days of

47:37

the year when the UV index exceeds

47:40

6 , high is 365

47:43

out of 365 , 366

47:46

this year . Anyway , the point is , every

47:49

day is a high UV day in Australia . Today

47:52

we're February , the 22nd

47:54

. Today , for the

47:56

first time for four months

47:59

, the UV index here

48:01

in Edinburgh tipped above

48:03

zero . It hit one at midday

48:05

today for the first time

48:07

in four months . Completely

48:12

, completely different UV

48:15

environment . I think

48:17

that what really matters

48:19

and your Australian

48:21

guidance takes this into account is

48:23

skin color and

48:26

where you live . I

48:29

are advice here

48:31

in Scotland where we have lifted

48:34

the advice from Australia . Literally

48:37

Scottish government

48:39

advice is if you're outside between 11

48:41

and 3 at midday , you should

48:43

slip , slap , slap . What

48:47

Absolute madness . I

48:49

live in Cairns and

48:51

, believe me , cairns is different

48:53

from Edinburgh . Perth , australia

48:55

is different from Perth , scotland . It's

48:59

not just the beer they drink either . We

49:03

have very different environments

49:05

. I

49:09

don't think we have all the answers . What

49:11

I'm saying is we need to be reconsidering

49:14

the question and that when looking

49:16

at sunlight , it's not just sunlight

49:18

bad , it's sunlight has health benefits

49:21

. What is my skin color ? Where

49:24

do I live ? There is a

49:26

much more interesting I say complex

49:28

, but actually it's interesting . It's a much more

49:31

interesting question that we need to be considering

49:33

. The other thing I might quickly add

49:35

in here , talking about this skin color , is

49:37

going back to Pelle's work

49:40

. Pelle then went back

49:42

and he looked at his Swedish

49:45

cohorts and their sunlight exposure

49:47

. His cohort

49:50

was scrutinized in 1990 before really

49:52

immigration of any size happened

49:54

to Sweden

49:57

. It was a pretty much solidly white skin

49:59

cohort . He was able to look

50:01

at the red heads , pheomelonin

50:04

and the non-red heads

50:06

. Of course , red heads are the palest

50:08

of the pale

50:10

. He went and looked at sunlight and

50:12

all caused mortality in white

50:15

, red heads compared to white , non-red heads

50:18

. What he found was that

50:20

when he looked at Swedes

50:23

who avoided the sun those

50:25

people that got nought or one on their

50:28

sunlight exposure scores red

50:30

heads lived longer than non-red

50:33

heads In a low

50:35

light Swedes who avoid the

50:37

sunlight . These are people who live in the gloom

50:40

all their lives . Being

50:42

the palest of the pale gives you

50:44

a reduction in all cause mortality . It gives you

50:46

a significant survival advantage . When

50:50

, however , he looked at Swedes that go

50:52

out and get more sunlight , those that get three

50:54

and four that sunbathe and seek

50:56

the sun , red heads

50:58

lost their survival advantage

51:01

. What this tells

51:03

us is that the palest of

51:05

the pale have

51:07

a survival advantage , an evolutionary

51:10

fitness advantage , in a really

51:12

low light environment . So

51:14

again , it confirms that skin

51:16

colour is really

51:18

important , for what amount

51:21

of sunlight is optimal for us

51:23

personally ?

51:25

Yeah , I mean , that makes a lot of

51:27

sense to me . I

51:29

think that this is a prelude to our next

51:31

part of the discussion , which is what

51:33

is mediating these non-vitamin D health

51:35

benefits of sun exposure . And it's

51:38

really pitting , essentially

51:41

the , or putting things in perspective

51:43

, because , as we talked about previously

51:46

, as physicians , as

51:48

medical doctors , it's our job to synthesize

51:51

a clinical situation , understand

51:54

risks and benefits of every intervention

51:56

that we offer to patients and be

51:58

able to present that in a coherent way so

52:00

people can make an informed decision . And

52:03

what I think we

52:05

can think about sunlight is that is a medicine

52:07

, because it has these

52:10

different wavelengths of ultraviolet

52:12

visible infrared and each of them are having

52:14

a biological , biologically relevant

52:16

effect . So the reason

52:19

behind the Sun avoidance narrative in

52:21

Australia and in your country too

52:23

, richard , is that everyone

52:25

is scared or has been scared

52:28

and completely

52:30

scared about metastatic melanoma

52:32

, and I'm not diminishing the fact

52:34

that that is a very , very scary illness . But

52:36

if we're pitting metastatic

52:39

melanoma mortality against

52:41

all cause mortality , cancer

52:44

mortality , cardiovascular

52:46

mortality it's a shrew and an elephant . And

52:50

we're still . We're scared of the shrew or the little

52:52

mouse , which is again what Peli Lindquist

52:54

found in Sweden , yet we're ignoring

52:57

the massive elephant which is all cause and cardiovascular

52:59

mortality , so maybe share

53:01

some thoughts on that topic .

53:03

Yeah , I mean it is interesting . I mean , what

53:07

we do as physicians , I would say almost our

53:09

core skill is risk benefit analysis . You

53:11

know , whenever we do an intervention , when

53:13

we prescribe a medicine to a patient , we

53:16

don't even consciously

53:18

do it . We subconsciously think benefits

53:21

. You know why am I prescribing this medicine ? Unit

53:23

, you've got pneumonia . I'll give you an antibiotic

53:25

because the benefits are it will

53:27

cure your pneumonia and you won't die . The

53:30

risks well , you might get a drug rash , you might

53:32

have an advert , you might have an allergic reaction

53:34

. You know , and we consider that risk benefit

53:36

ratio and it's I

53:38

would almost say it's our core skill . Handling

53:40

is often quite complex equations

53:43

in our head , in discussion with our patients . It's

53:46

the core of what we do and

53:49

for some reason , dermatologists have completely

53:52

forgotten that when it comes to sunlight , they

53:54

only consider risk

53:57

, completely , forget the other , equally

53:59

important side of the equation . And that

54:01

is how , by concentrating on the true

54:03

, we have missed the elephant . And

54:06

you know you're about 100 times more

54:08

likely to die of cardiovascular disease

54:10

than melanoma In Britain

54:12

. In Australia , you have half as much cardiovascular

54:14

disease as us . So the equation is different

54:17

. I wonder if it's with your sunlight . You

54:19

know so . So

54:22

we , you know , we actually have to keep things in

54:25

proportion , as you say , and

54:27

unfortunately dermatologists

54:30

have dominated the debate on

54:33

UV . It's

54:36

interesting I'm now invited . I spoke at the European

54:38

hypertension , the big European hypertension

54:40

meeting last year talking about sunlight and hypertension

54:43

, and it's very nice to

54:45

be there with hypertension

54:48

doctors and cardiologists who

54:50

are a little bit surprised to hear from a dermatologist

54:53

because you know why would a dermatologist

54:55

be talking to them ? And we have very we've

54:57

had this rather compartmentalized

55:00

approach Sunlight is

55:02

for dermatologists who deal

55:04

with skin cancer , blood

55:06

pressure is for primary care

55:08

doctors , clinical pharmacologists , cardiologists

55:11

, multiple sclerosis is for

55:13

neurologists , whereas actually

55:16

it turns out that UV affects all of

55:18

these things and we need

55:20

to be considering all of it together . I mean

55:22

, I would say one of the benefits of my training

55:24

are that I started off doing internal

55:26

medicine . I would say another big benefit

55:29

is I also practiced in Australia for a year

55:31

and that was that

55:33

was hugely influential on me , just in

55:36

the back of my mind . You know just

55:38

I think

55:40

I said this previously that you know Australians , you

55:42

Australians live three years longer than us here

55:45

in Scotland , twice the risk of

55:47

skin cancer , three years longer life expectancy

55:49

and always the story you've

55:51

told us was it's because you're athletic

55:53

gods . You spend your whole life

55:55

running , surfing , doing things . And

55:58

I discovered you're a bunch of bone

56:00

idol , heavy drinking , hard

56:02

living , smoking blooders

56:04

, just the same as us in Britain

56:06

, and you're not these godlike

56:09

figures you pretend to be . So

56:11

I can I can view your

56:13

immensely good health

56:16

with a degree

56:18

of , I says , interest . Now how is it

56:20

that these idle bloods are

56:22

so healthy ?

56:23

Yeah , and that's why I respect your work and what you're

56:26

doing so much , richard , because you're

56:28

really the curiosity

56:30

and the ability to see beyond the

56:33

blinkers of your own specialty

56:35

is what is enabled you to

56:37

essentially make such important scientific

56:40

discoveries that I think will

56:42

rediscover these , because I think the health benefits

56:44

of some of our ancient and

56:46

big that essentially

56:48

and bring this to some

56:51

sanity , to a very , very one sided

56:53

argument I think the point about the

56:55

reduced cardiovascular mortality of Australians

56:57

versus people of similar skin

56:59

color in Scotland

57:02

points to the fact that this UV

57:04

light story is holding in

57:07

in Australia and although

57:09

we don't have the data , I would assume what

57:12

you found , what peri-linkus found , is

57:14

still going to be applicable

57:16

and externally valid to an

57:19

Australian cohort and therefore

57:22

everywhere around the world .

57:24

Yeah , I'm not gonna say I would , I really would strongly

57:26

. Rachel Lill , this super . What

57:29

is interesting to me actually is that

57:31

probably the leading country

57:33

in reconsideration of sunlight

57:35

health benefits , not just

57:37

harms has been Australia . So

57:40

people like Robin Lucas , rachel

57:42

Neal fantastic

57:45

Prouheart , you

57:48

know , shelley Gorman actually a lot of my

57:50

closest collaborators and

57:52

intellectual sparring

57:55

partners , supporters have come from

57:57

Australia and it's fascinating to

57:59

me that you , from a country

58:01

with lots of UV and a largely

58:04

pale skinned population

58:06

, are the ones reconsidering this . And

58:10

I think everyone should go off and

58:12

read this paper by Rachel Neal published

58:14

this week in the Australian New Zealand Journal

58:16

of Public Health , where you actually

58:19

formally sit down and are really

58:21

open to these discussions . So

58:24

you know , advance

58:26

Australia Fair , you're doing some great

58:29

stuff there .

58:31

Great . Well , I'll definitely include that in the show notes

58:33

. Let's talk about these changes

58:35

in and maybe one more point

58:37

, because I don't want to let this go

58:39

, because we have talked about melanoma again . What

58:42

I believe and maybe you can give me your thoughts

58:44

on this , richard what I believe is driving

58:46

the rise

58:49

in incidents of superficial spreading spreading

58:51

melanoma in young people I think predominantly

58:54

, in my opinion is the

58:56

advent of artificial light , the fact that

58:58

people are spending their time mostly

59:01

under isolated blue , narrow

59:03

wavelength , narrow band blue light

59:05

without red , without infrared , and

59:08

they've got disrupted circadian rhythms and

59:10

they've got an ancestry inappropriate omega three to

59:12

six ratio in their bodies , particularly

59:15

in their skin . So that's a

59:17

lot there and we don't necessarily need to go into each

59:19

one of those points , but I just want to put

59:21

that in this . Studies I can

59:23

quote and I've talked about in previous podcasts , but

59:25

I just wanted to put that there as

59:27

a the thing .

59:29

the thing I would , I would really

59:31

like to turn here is over diagnosis

59:33

. Now there's a difference in melanoma diagnosis

59:36

and melanoma death . Melanoma death is

59:38

a very robust end point . You've had a serious

59:40

melanoma , you know they . Now

59:43

there's some data

59:45

from America . Here is tremendous , fantastic

59:47

paper by Adawali Adamson , an

59:50

American dermatologist down in Texas

59:52

, and he had a paper actually in the New England

59:54

Journal about two years ago where

59:56

he looked at Melanoma

59:59

diagnosis in America

1:00:02

over the last 40 years . So

1:00:04

the number of melanomas predominantly

1:00:06

superficial spending melanomas diagnosed

1:00:09

in America now are

1:00:11

six times as many as

1:00:13

the were 40 years ago , so

1:00:16

a six fold rise . Now he points

1:00:18

out in this paper that you know

1:00:20

UV UV

1:00:22

at most doubles your risk

1:00:24

of developing melanoma . So say 40

1:00:26

years ago they all lived in

1:00:28

caves . Say now everybody

1:00:31

got sunburned , maximum UV , you would expect

1:00:33

a doubling of melanoma at most

1:00:35

. And if that has been a six fold

1:00:37

rise . And he

1:00:40

then shows that

1:00:42

what determines your risk

1:00:44

of being diagnosed with melanoma

1:00:46

is not where you live in America

1:00:50

. If it's driven by UV

1:00:52

you'd expect Florida to have lots

1:00:54

more than Alaska . He finds there is

1:00:56

no correlation whatsoever

1:00:59

between how much sunlight there

1:01:01

is where you live and your

1:01:03

risk of melanoma . But he finds there

1:01:05

is an absolutely

1:01:07

tight straight line relationship

1:01:10

between access to a dermatologist

1:01:12

, how many dermatologists there

1:01:14

are , how many biopsies are done

1:01:17

Basically it's

1:01:19

over diagnosis . And

1:01:22

he then shows that

1:01:24

they took microscopes

1:01:27

, slides from 40 years ago which

1:01:29

had been some diagnosis melanoma

1:01:32

, some diagnosed as funny mole , dysplastic

1:01:34

nebis , not melanoma . Put

1:01:37

them in front of pathologists today

1:01:39

and a significant

1:01:41

number of those biopsies

1:01:43

that were diagnosed as not a melanoma

1:01:46

40 years ago are were

1:01:48

diagnosed as melanoma when

1:01:50

being looked at pathologists by now . Now

1:01:53

the problem is the only only way of knowing if something's

1:01:55

going to kill you is to take half

1:01:58

of it out , sit there

1:02:00

and see what happens . And you just can't get the volunteers

1:02:02

, nor can you get the ethics committee

1:02:04

, nor would you write to do it . But the

1:02:06

problem with diagnosis

1:02:08

of melanoma is its dermatologist looks

1:02:10

at it , saying , yeah , it looks like a melanoma

1:02:12

. That's it , pathologist . You

1:02:15

do a biopsy , put it on the slide

1:02:17

. Pathologist looks at it and goes , yeah

1:02:19

, looks like a melanoma . So the whole thing is

1:02:21

based on an impression . Now

1:02:23

, if you're diagnosing a

1:02:26

stroke , if you're diagnosing a heart attack , you

1:02:28

do a blood test , you do the troponin levels

1:02:31

. There is an unambiguous

1:02:34

blood test which gives you

1:02:36

a troponin level , which is a sensitive

1:02:39

and highly specific indicator

1:02:42

of a myocardial infarction . Melanoma

1:02:44

diagnosis is always an impression

1:02:46

and the other thing about melanoma

1:02:48

diagnosis there are no prizes

1:02:51

for missing one . If

1:02:53

you say it looks like a funny

1:02:55

mole and it turns out to be a melanoma and it kills

1:02:57

them , that is the end of your career or

1:03:00

it's a very expensive mistake . If you

1:03:02

say and it harmless

1:03:04

mole , oh , it's a melanoma , and you cut it

1:03:06

out Not only , not

1:03:09

only you then have an incredibly

1:03:11

grateful patient . My God , I had a

1:03:13

melanoma , my life has been saved , even

1:03:16

if the reality of the matter is

1:03:18

they never had a melanoma , it was just a mole

1:03:20

. It was never going to do anything . So

1:03:22

the whole diagnostic

1:03:25

shift it's not malicious

1:03:27

, but it's moving one way . Where

1:03:29

it is wrong is in

1:03:31

America . There's been a big

1:03:34

commercial change in melanoma

1:03:37

practice in the last 40 years . So

1:03:40

in the US venture capitalists

1:03:42

have bought up dermatology

1:03:44

practices and they have bought up

1:03:46

pathologists and they've said

1:03:48

revenue maximization . Now the

1:03:51

more biopsies . I want dermatologists

1:03:54

to do more biopsies a chargeable

1:03:56

event . To feed biopsies

1:03:58

to pathologists a chargeable event

1:04:01

. Who can feed diet . So there's been

1:04:03

this financial pressure

1:04:05

for dermatologists to

1:04:08

do more , see

1:04:10

more , do more biopsies and

1:04:13

to halt this huge , great commercial drive

1:04:15

. So they've

1:04:17

repeated this study

1:04:19

. They've looked again in Australia . It looks

1:04:21

like there is a degree of overdiagnosis

1:04:24

in Australia and I'm going to have to go and revise

1:04:26

these papers . I'm at the moment

1:04:28

trying to get the date of the last 40

1:04:30

years in Scotland and see if

1:04:32

the same thing has happened here , because here

1:04:34

and in Australia , just like

1:04:37

in America , we've had a big

1:04:39

rise in the number of melanomas diagnosed

1:04:41

. Meaning dermatologist says yeah

1:04:44

, I think it is . Pathologist says yeah , I think it

1:04:46

is . That's the level I'm afraid

1:04:48

to say , that's how it's diagnosed

1:04:50

. There has been no change in deaths

1:04:52

and I

1:04:55

am suspicious of

1:04:57

the dermatologist view that this is

1:04:59

thank God we're there saving lives

1:05:01

. If we haven't done it , I don't think dermatologists

1:05:04

are chasing an epidemic . I

1:05:06

think there is a strong chance here that

1:05:09

dermatologists are creating

1:05:11

an epidemic and I

1:05:13

actually think that is . I

1:05:16

think overdiagnosis to

1:05:18

me strikes me as a much

1:05:20

more likely than factors that we haven't

1:05:23

considered leading to more melanoma . I

1:05:25

don't think we've necessarily

1:05:27

got more melanoma . That's

1:05:29

my point , thank you .

1:05:31

That's a very interesting perspective and one

1:05:33

that I hadn't considered at all , but

1:05:35

the same thing has happened in Australia

1:05:38

with regard to the incentive system behind billing

1:05:41

and skin biopsy , and they eventually had to

1:05:43

tighten up some rules and you basically

1:05:45

had to . You only got paid

1:05:47

if what you biopsied , from

1:05:49

a GP point of view , was actually here A suspicion

1:05:51

Billing the government for it .

1:05:55

I mean , this kind of thing actually has huge implications At

1:05:58

the moment in Britain we are in . The

1:06:01

NHS is just falling over

1:06:04

. So I have

1:06:06

been a dermatologist for 30 years now . So

1:06:08

when I trained there were 300

1:06:11

dermatologists in Britain . There's now

1:06:13

700 dermatologists

1:06:15

in Britain and are waiting this

1:06:17

higher than when I trained 30

1:06:20

years ago . You know the pressure

1:06:22

we're under is huge and yet we've got twice as many

1:06:24

dermatologists and

1:06:27

the terms of practice . We've got amazing new drugs . You

1:06:29

treatex for fantastic new drugs . We no longer have

1:06:32

hospital beds because we don't need them . It's

1:06:34

got great new drugs . I think we're doing things

1:06:37

wrong . I

1:06:39

think we have created a problem . I

1:06:44

think we are cycling faster and faster

1:06:46

to go nowhere , because the more biopsies we do , the

1:06:49

more skin checks we do , the more fake

1:06:51

non-fake's word , the more artificial epidemic we're

1:06:53

creating and I think we absolutely seriously need to look

1:06:56

at this Again . You guys in Australia , yeah , I think we're doing

1:06:58

things wrong . We're creating an epidemic

1:07:00

and I think we absolutely seriously need to look at this Again

1:07:08

. You guys in Australia . I love Australian dermatology

1:07:10

research on UV In Australia over in the Burkaw in Queensland . That's

1:07:12

a former care in Spoy , I'm very proud to

1:07:18

say at Queensland Group , you're looking at this in fantastic detail and I'm

1:07:20

keen that we should be doing it here .

1:07:23

So let's talk about these non-vitamin

1:07:25

D related illnesses or impacts , because to me

1:07:27

, what I'm thinking that

1:07:29

these are is all these

1:07:31

are water immune disease , these cancer , this cardiovascular disease

1:07:33

. This is a sunlight deficiency , this

1:07:36

is a UV light deficiency

1:07:38

. That's how I'm thinking about it .

1:07:41

These are . We independently showed

1:07:43

the first major non-vitamin D mechanism

1:07:45

by which sunlight improves health . So

1:07:49

we showed that . Or I showed that the

1:07:51

skin contains large stores , storage forms or something

1:07:54

called nitric oxide . No Big

1:07:57

storage forms this in the skin . And

1:07:59

we then showed Varsum , funky photochemistry

1:08:01

, how sunlight hits the skin and

1:08:04

it releases NO nitric

1:08:06

oxide from these stores into the circulation . So

1:08:09

nitric oxide Nobel Prize for medicine back

1:08:11

in 1998 , when the three

1:08:13

Americans who discovered NO

1:08:15

, actually a brick was

1:08:17

there , but the Americans got the Nobel

1:08:19

Prize Anyway . So

1:08:23

and nitric

1:08:25

oxide dilates blood vessels , lowest

1:08:27

blood pressure and

1:08:29

huge importance of stuff . And we

1:08:31

show that stores fit in the skin . Sunlight

1:08:33

releases it from the skin into the circulation where

1:08:36

it loads the blood pressure . And I did studies

1:08:38

, I had a number of studies . The

1:08:41

most important studies were all done in man I

1:08:43

speak about in my TED talk . And

1:08:45

we show how sunlight lowers blood

1:08:47

pressure by releasing nitric oxide

1:08:49

from the skin into circulation . That

1:08:51

, in terms of benefits

1:08:54

from sunlight . Cardiovascular

1:08:56

disease is the biggest killer in the world

1:08:58

today . Not many people

1:09:01

have rickets in the world today vitamin C , but

1:09:03

cardiovascular disease is the biggie and

1:09:05

that's my nitric oxide pathway

1:09:07

and Kristoff's nitric oxide pathway . So

1:09:10

that's the big one and that's really important

1:09:12

. But I'm now I'm

1:09:15

keen to get a second new route up , you see

1:09:17

. So there's then a whole

1:09:19

lot of gene regulatory stuff . So super

1:09:21

paper by a chap called Doppicoe , who

1:09:25

actually then studied in Edinburgh , was working

1:09:27

, was doing his PhD in Cambridge and

1:09:29

he did one of these great experiments where you do

1:09:31

no active research yourself , you

1:09:34

use other people's data , and

1:09:36

he looked at studies where they'd measured whole

1:09:38

blood transcriptome , so all the genes

1:09:40

turned on and off in the blood . But

1:09:42

he looked at it in

1:09:44

a number of healthy volunteers done

1:09:46

in about half a different studies where they were

1:09:49

measuring gene transcription in the blood , half

1:09:51

different studies done around the world

1:09:53

, some in Australia , some in Europe , some in

1:09:55

the Gambia . But he analysed

1:09:58

the gene expression pattern in

1:10:01

all of these healthy volunteers by the month

1:10:03

of the year in which the blood

1:10:06

was taken and he

1:10:08

showed that about 30%

1:10:10

of all the genes in your blood

1:10:12

show seasonal variation 30%

1:10:15

. A third of your

1:10:17

in-char transcriptome has

1:10:19

seasonal variation . Now we know about circadian

1:10:21

rhythm , your 24-hour sleep-weight

1:10:23

cycle really important , a

1:10:26

key human , you

1:10:28

know characteristic

1:10:30

. There is then a seasonal variation

1:10:33

and , broadly speaking , he

1:10:36

showed that anti-inflammatory

1:10:39

genes are up-regulated

1:10:41

are turned on in summer and pro-inflammatory

1:10:45

inflammation-driving genes turned on in

1:10:47

winter . So that was this first . Really

1:10:49

. I mean I think it sounded like 500 citations really

1:10:51

important study . What

1:10:53

I am doing now is I do my experiments

1:10:56

in winter , is we are you

1:10:58

can now do a technique called single

1:11:00

cell sequencing . Rather than looking at the

1:11:03

blood , you know all the cells

1:11:05

in the blood and there's masses of different types

1:11:07

of cells in the blood . There's red cells and

1:11:10

white cells and platers , but then within the white cells

1:11:12

there's hundreds of different subtypes

1:11:14

, each of those cells

1:11:16

doing different things . You can

1:11:18

now do a technique where you look at every

1:11:21

individual cell type and

1:11:24

you can measure in every individual

1:11:26

cell , every single gene

1:11:28

, which the 30,000 genes humans

1:11:30

have got , which are turned on , which

1:11:32

are turned off , which are expressed and

1:11:35

how they're expressed . So

1:11:37

staggering amounts of detail

1:11:40

and we're taking healthy

1:11:42

volunteers midwinter or in

1:11:44

winter . Now we're just coming to

1:11:46

the end of the experimental season because I've got

1:11:48

a UV index of one a midday

1:11:50

to day . So we're moving

1:11:52

out of no UV worth speaking

1:11:54

of and we take blood from

1:11:56

these subjects and we do single cells so we look

1:11:58

at all of their gene expression and all of

1:12:00

their white cells . We then give them two

1:12:03

weeks of solar simulator

1:12:05

lamps . These are actually old fashioned

1:12:07

tanning lamps which have the same spectrum

1:12:09

as the midsummer

1:12:11

sun in Melbourne actually . So

1:12:14

that's what we match it up to . So we

1:12:16

give them the equivalent of two weeks

1:12:18

sunshine in Melbourne and

1:12:20

we then repeat the bloods to see

1:12:23

which genes are turned on

1:12:25

and off .

1:12:26

Is that UV and visible , or

1:12:29

is that infrared as well ?

1:12:30

Yeah , so , yeah , so it's UVA

1:12:32

and B , because that's

1:12:35

one of the Now , I think , visible . It's

1:12:37

interesting . So we

1:12:40

know from the Most

1:12:43

of our measurements of lamp

1:12:45

output is based on

1:12:48

the spectrum of

1:12:50

sunlight which leads to skin

1:12:52

cancer . So when we

1:12:54

use lamps for experiments

1:12:56

, when we use lamps to treat patients with therapy

1:12:59

, we look

1:13:01

at the sunburn-inducing

1:13:03

abilities of a lamp , because we know that the wavelengths

1:13:06

that are most likely to cause sunburn

1:13:09

are most likely to cause DNA

1:13:11

damage and most likely to cause skin cancer

1:13:13

. So when we measure

1:13:15

the output of a lamp

1:13:18

for use in experiments , we

1:13:20

weight it for how many

1:13:22

, how

1:13:24

many short wavelength , how much 300

1:13:27

nanometers is 3 , 5 , 3 , 6 , weighted

1:13:30

for how much light is called DNA dimension of the place . And

1:13:33

when you do that , basically visible

1:13:35

light and IR does causes

1:13:38

no DNA damage , no

1:13:41

, doesn't make you go red , doesn't cause

1:13:43

skin cancer . So

1:13:46

now of course , I don't

1:13:48

know whether different wavelengths will have different biological

1:13:50

effects . It may well be that visible light

1:13:53

is having beneficial biological

1:13:55

effects and that's

1:13:57

you know . That's the next chapter . The

1:14:00

point is this is the whole

1:14:02

field is unexplored because we've

1:14:04

just said sunlight bad , take

1:14:06

vitamin D tablets . So for 100 years

1:14:08

we've done nothing except avoid

1:14:10

the sunlight and take vitamin D tablets , and

1:14:13

absolutely right . So look that it visible

1:14:15

kind of rolls , blue kind of rolls , I

1:14:17

arc kind of rolls . I'm concentrating on UV

1:14:19

because I know that UV has a lot

1:14:22

of biological effects and

1:14:24

when I'm spending a lot of my own experiments I'm

1:14:28

I reckon I'm most likely to get results when

1:14:30

I've got a big biological

1:14:32

stimulus .

1:14:33

Yeah , and my criticism

1:14:35

of the use of narrow

1:14:38

band UV , which is essentially

1:14:40

what I understand . Most of

1:14:42

the harm you know , uv light

1:14:44

demarization and therefore extrapolated

1:14:46

to the sun harm narrative

1:14:48

is based on is narrow band UV

1:14:51

which is emitted for a lamp . But

1:14:53

the point is when we're in nature and

1:14:55

UV is always balanced by red , it's always balanced

1:14:57

by infrared and we

1:14:59

have Dr Roger Schwelt , who's a

1:15:02

US intensivist but

1:15:04

is now branching into the light as medicine , and it shows

1:15:06

that red specifically

1:15:09

regenerates . It has a positive effect

1:15:11

on mitochondria . That's known

1:15:13

finding and essentially is preparing the skin

1:15:15

for the later UV arrival

1:15:18

.

1:15:18

Yeah , I have said I'm always cautious

1:15:20

about , you know , effects on mitochondria and skin . You

1:15:24

know I just those things

1:15:26

suggest mechanisms but you've got that

1:15:28

then you can't use

1:15:30

them until you've shown it in man and on my

1:15:33

experience I've done my , I've done cell culture

1:15:35

work . I've done my work . I do

1:15:37

human work now because if it doesn't

1:15:39

happen in man , you know what matters in man matters

1:15:41

far more . The other thing I'd

1:15:43

say about narrow band is that actually it's

1:15:45

narrow band is remarkably safe . So

1:15:48

the three 11 nanometers , the

1:15:50

shorter the wavelengths when you're down

1:15:52

at you know the

1:15:55

shorter wavelengths , you know shorter end UVB

1:15:57

. That's where you're tending to get the burning . What

1:16:00

we know from experiments in man

1:16:02

the best experimental model of

1:16:04

all , classic

1:16:06

experiments back in 1986

1:16:08

by Parrish at the Wellman

1:16:11

Photobiology Institute at Harvard , the risk

1:16:13

benefit ratio for so they

1:16:15

were looking at different wavelengths of

1:16:17

UV to treat cirrhosis and

1:16:20

they showed the magic sweet

1:16:22

spot where you get the most

1:16:24

reduction in cirrhosis for

1:16:27

the least chance of causing

1:16:29

sunburn , dna damage , skin

1:16:31

cancer is about 313

1:16:34

nanometers . So actually that particular

1:16:36

wavelength you get the biggest

1:16:38

benefit for risk . So

1:16:41

from that they have developed

1:16:43

three 11 nanometer lamps . My

1:16:46

three 11 nanometer narrow band UVB lamps

1:16:48

have been around now since the 1980s

1:16:51

. We've got 30 or 40 years activity

1:16:53

with them . Everybody getting narrow band

1:16:55

UVB in Scotland is

1:16:58

followed as the big database . There

1:17:01

is no increased risk

1:17:03

of skin cancer shown

1:17:05

in 30 years of narrow band

1:17:07

UVB . I think

1:17:10

that narrow band UVB

1:17:12

lamps should be available

1:17:14

without seeing a doctor , without

1:17:17

any medical intervention , without seeing

1:17:19

a nurse . I think they should be available Open

1:17:22

access . Tanning salons

1:17:24

should stop them , I think , because

1:17:27

there is no downside to

1:17:29

them and at the moment when we treat eczema

1:17:31

or we treat cirrhosis , we have

1:17:33

a treatment , ascending treatment

1:17:36

that does Dioprecipitants

1:17:38

, emollients and topical steroids

1:17:41

. If that fails , move on to narrow band

1:17:43

phototherapy . If that fails , you

1:17:45

move on to systemic agents , ethyl trachocytes

1:17:47

like X-4 , and if that fails you

1:17:49

move on to expensive biologics . That

1:17:52

is our ideal treatment

1:17:55

regimen . The problem is it

1:17:58

doesn't work because if

1:18:00

your topical steroids topical

1:18:02

dovernex , you know cathetrile fails

1:18:04

for your cirrhosis or eczema , you are referred

1:18:07

for a dermatologist . Well , in Britain

1:18:09

that is a six month wait . I

1:18:11

then refer you to my photodermatology

1:18:14

department . Photobelgium says there is

1:18:16

another six month wait . So

1:18:18

you have got mild to modrotexma

1:18:21

. It is not getting better with some topical steroids

1:18:23

. You need the next step up . Well

1:18:25

, it is a year before

1:18:28

you get your phototherapy and

1:18:32

so it doesn't work . So either you have

1:18:34

dreadful eczema dreadful , or

1:18:36

you know , not dreadful , not the worst , but just

1:18:38

bloody , miserable eczema , cirrhosis

1:18:41

going on for a year untreated

1:18:43

, or by the time you get to see me

1:18:45

, it has got worse and we have to move

1:18:48

on to heavier weight drugs

1:18:50

methotrexate we use these

1:18:52

things really carefully , we really experience , we

1:18:54

are brilliant at it . Nonetheless , these

1:18:56

are heavy weight drugs , need lots of monitoring Before

1:18:59

we move on to biologics hugely

1:19:02

expensive , because we

1:19:04

have utterly restricted

1:19:07

and over-regulated this

1:19:09

incredibly safe and effective

1:19:11

narrow band UVB phototherapy and

1:19:14

I think we should just remove medics

1:19:16

altogether from this . Like

1:19:18

paracetamol , when you get a headache If

1:19:20

you wake up with a headache you don't get a referral

1:19:23

to a neurologist six month weight

1:19:25

referral pharmacist . Six or eight here

1:19:27

have 500 milligrams of paracetamol . Of course

1:19:30

we can hardly date .

1:19:31

My criticism of narrow band is in

1:19:34

the research setting , when that is ultraviolet

1:19:36

and then that is used to justify or

1:19:39

demonize natural sun

1:19:41

exposure . In terms of narrow band

1:19:43

phototherapy whether it's in the photobiomodulation

1:19:45

red light , infrared and UV that

1:19:48

makes complete sense to me . That again is

1:19:50

being used like a medicine , has risk-based benefits

1:19:52

and what you're describing for

1:19:54

eczema sounds very , very justified

1:19:56

To me . It would be cheaper and quicker

1:19:58

if that patient took a flight again

1:20:01

down to a more southern latitude

1:20:03

, normalize their circadian rhythm and

1:20:06

I believe their psoriasis

1:20:09

and eczema probably improve much

1:20:11

, much quicker than waiting for 12

1:20:13

months . I wanted to make a point about

1:20:17

the cardiovascular

1:20:19

benefits of sun , and you obviously

1:20:22

you're the pioneer of elucidating

1:20:24

this nitric oxide dependent pathway . I

1:20:27

think that the sunlight touches

1:20:29

cardiovascular disease in so

1:20:31

many ways that we're just appreciating

1:20:34

now , and ones that I've

1:20:37

researched myself have been the presence

1:20:39

of melanocortin receptors in the blood

1:20:41

vessels and the fact that if you knock them out you

1:20:43

get arteriosclerosis

1:20:46

, stiffening , endothelial dysfunction . There's

1:20:48

melanopsin , which you talked about , the circadian rhythm

1:20:51

. There's non-visual photoreceptor melanopsin

1:20:53

in the blood vessels , and blue light

1:20:55

mediates photorealysation of the vessels

1:20:57

. And then a biggest

1:20:59

point that I don't think anyone is talking about

1:21:01

, not in cardiology , and nor

1:21:03

else is the work of Dr

1:21:06

Geropolik , which showed that there's a biological

1:21:08

water , a fourth phase

1:21:11

water , inside the

1:21:13

blood vessels , and exposure to infrared

1:21:15

light essentially potentiates

1:21:17

this formation of a biological

1:21:20

surface inside the endothelium

1:21:22

or above the endothelium , above the endothelial

1:21:25

glycocalyx , and that is

1:21:27

incredibly potent stimulus not only

1:21:30

for blood flow but also

1:21:32

to protect the underlying endothelial

1:21:35

layer . So I think nitric oxide is one

1:21:37

part of it , but there's all these

1:21:40

other things that are mediating the natural sunlight

1:21:42

to benefit on cardiovascular health

1:21:44

.

1:21:45

Yeah , look . So I mean there's different types of

1:21:47

epidemiology mechanism . You

1:21:49

know interventional trials , so

1:21:51

the epidemiology to me is pretty robust

1:21:54

, certainly

1:21:56

those of us living in Northern Europe . The more sunlight

1:21:58

we get , the longer we live , I think for

1:22:00

whiteskin North Europeans in North Europe , that

1:22:03

data to me looks pretty robust and

1:22:07

it all has to add up . You know it's not no

1:22:09

single instrument tells you the whole tune

1:22:11

. You need an orchestra and you know

1:22:14

all of these things have to play together . We've

1:22:16

then been able very clearly in human

1:22:19

studies in man , to show , you

1:22:21

know , back to my animal model anything out

1:22:23

there able to show that nitric oxide

1:22:25

is certainly a really important causal

1:22:27

pathway . Other

1:22:30

mechanisms , you know . I

1:22:32

almost think the key thing is we know that more sunlight

1:22:34

, more sun

1:22:36

, more sunlight . We know that

1:22:38

more sunlight pretty

1:22:41

robustly ties up with

1:22:43

increased lifespan , reduced disease

1:22:45

and

1:22:48

sunlight is available for free to all of

1:22:50

us and that

1:22:52

you know we should be getting into use

1:22:54

that . I think we need to refine the message based

1:22:56

on skin color and where

1:22:58

you live . Mechanistic

1:23:00

stuff is important . I

1:23:03

only feel comfortable really talking

1:23:05

about with the mechanisms that I know

1:23:08

, but almost

1:23:10

mechanism plays

1:23:12

second part to actually an effect

1:23:14

. You know we have here a biological effect

1:23:16

and we need to agonize

1:23:18

too much over the mechanism . If

1:23:21

we can show , the increased time in UV reduces

1:23:23

risk of multiple sclerosis , cardiovascular events

1:23:26

, stroke , blood pressure etc

1:23:28

. Etc . Death from any cause

1:23:30

.

1:23:31

Yeah , and that's why your work is so important Really

1:23:34

establishing that overall

1:23:36

finding , which is those

1:23:38

mortality findings . That is the

1:23:40

hard outcome , and then I guess , yes , it's

1:23:42

up to other researchers to work

1:23:44

out there the minutiae , did you ? I'm

1:23:46

mindful of your time , richard , and I think

1:23:49

we've had such a great discussion If

1:23:51

you wanted to make mention about the effect

1:23:53

of sun on immunity

1:23:55

and disease susceptibility . But

1:23:57

if you've got to go , then that's fine too , I'm

1:24:00

going to have to take my son to football .

1:24:06

So this is association , not Aussie

1:24:08

rules , I should point out . So

1:24:11

he's not wearing a single running around the

1:24:13

freezing Scottish weather here , yeah

1:24:16

, so I think seasonal disease is big

1:24:18

. Is cardiovascular disease very clearly

1:24:20

seasonal ? Interesting infectious

1:24:23

disease , pneumonia , a very seasonal disease

1:24:25

. So

1:24:29

I'm super at Prouheart out of

1:24:31

Perth University of Western Australia , fantastic

1:24:33

stuff doing that we're setting

1:24:35

up some clinical trials that

1:24:38

we're hoping to run in the United States using

1:24:40

phototherapy to treat MS . There's

1:24:42

a whole field of things out there

1:24:45

, I think , more than we have time to go

1:24:47

on for now , I'm afraid to say .

1:24:48

Thank you so much , richard , and I can't wait to

1:24:50

get this out to people and to share

1:24:53

your very , very important message . So

1:24:55

, yeah , thank you for your time and , yes

1:24:58

, keep continue spreading the word , please

1:25:00

.

1:25:01

Okay , max , fantastic , we'll see

1:25:03

you next time .