Chronic inflammation and cancer
Originally Published:19 January 2024
Third Party Re-Publication by USA Citizens Network
Source: Chronic inflammation and cancer
Author: Dr John Campbell
INTERVIEW DATA SUMMARY
Interviewer: Dr John Campbell
Interviewee: Professor Angus Dalgleish (Oncologist, St George’s Medical School, London)
Topic: Chronic inflammation and cancer — mechanisms, viral links, and cancer development pathways
Core focus:
- Chronic inflammation as a driver of cancer
- Viral contributions (HBV, HCV, HPV, EBV, HIV-related cancers)
- Immune suppression and tumor development
- Obesity, lifestyle, and inflammatory states
- Angiogenesis and tumor progression
CORE THEMES (STRUCTURED)
- Cancer arises through multi-step mutations over decades
- Chronic inflammation creates a permissive tumor environment
- Viruses often act indirectly via immune modulation
- Immune suppression reduces cancer surveillance (T-cell function)
- Obesity and lifestyle act as systemic inflammatory drivers
- Angiogenesis supports tumor survival and expansion
- Prevention focuses on reducing chronic inflammatory burden
SELECTED QUOTES (VERBATIM)
1. Cancer as a multi-mutation process
“Cancers arise as a result of a series of mutations… at least six and in some cancers over 60.”
2. Role of chronic inflammation
“Cancers arise best in chronic inflammatory states.”
3. Viral link to cancer development
“The viruses are absolutely a great example of chronic inflammatory states.”
4. Immune suppression mechanism
“Chronic inflammation causes immune suppression and prevents an active immune response from doing its surveillance.”
5. Hepatitis B and liver cancer discovery
“All the hepatomas were Hepatitis B positive… all the controls were negative.”
6. Progression pathway in liver cancer
“Acute hepatitis… chronic hepatitis… then cirrhosis… and only then you get liver cancer.”
7. Inflammation as cancer “soil”
“Chronic inflammation is the food and the growth factor for cancer development.”
8. Immune system failure in cancer environment
“The T-cells are suppressed… and that allows mutations to survive.”
9. Prevention framing
“Reducing chronic inflammation will reduce your chances of getting cancer dramatically.”
10. Obesity as inflammatory state
“Obesity is a chronic inflammatory state.”
0:00you are most welcome to this talk and particularly a warm welcome to Professor Angus da Professor welcome back thank
0:06you for coming thank you so Professor dowlish is fairly well known to the channel now fellow of the Royal College
0:11of physicians in the United Kingdom and Australia fellow of the Royal College of Pathologists fellow of the Academy of
0:18Medical sciences and and and currently professor of oncology at St George’s medical school in London and of course a
0:24consultant oncologist uh a long-term cancer doctor
0:30so what we want to talk about this morning Professor if it’s okay with you is is the causes of
0:36cancer first of all very briefly what is cancer well cancer is a disorder of of
0:44growth and differentiation of cells basically they just escape from their
0:50programming you know they they no longer read the script as it were and decide
0:55like Escape prisoners hey this is interesting I can do what I want and so
1:01they they they start growing or spreading Etc I mean that that’s it in a nutshell the important bit though is
1:08that this is a a procedure that that is expected and heavily regulated so there
1:14are a lot of genes to try and prevent this which is one of the reasons why
1:19cancers take decades in order to manifest them having had the first touch of the blue litmus as it were it it
1:27takes a long long time and things can accelerate or switch this process off so
1:34that’s the that’s the first thing I think is really important to be aware I was just smiling there because I’ve
1:39never heard the Escape prisoner analogy before and it really just it just rang true with uh everything I know about
1:45about cancer um we want to get on to the idea shortly but um is is it basically
1:50true to say that cancers can be described as mutations well cancers arise as a result
1:59of a series of mutations so you’ll get a mutation in a cell and nothing much will
2:06happen to that except that it is less likely to die when order to do so this
2:14life cycle cells have the same life cycle as we do I mean they’re born they
2:19uh do their job whatever it is then they die and it is G having a mutation that
2:25delays that dying that allows them to continue for a bit longer and this
2:31increases just by pure random chance the chances of a second mutation occurring
2:38and that cancer is often a result of several mutations at least six and in
2:44some cancers over 60 so we know a lot of the detail and I’m not so sure that it
2:51enables us to do as much as we’d like to prevent it however that’s been in a way
2:57my sort of life’s uh um job to understand this with all the the various
3:03tools at our um neet bail on able and the the one
3:10that really got me was viruses I mean the the fact that viruses can cause cancer particularly in mice and that’s
3:17what really got me very interested in what are the real causes of cancer and
3:24the mice were the ones where they discovered the first mutations like the rat on onene uh if you have this uh
3:32mutation and this Ras enene then the cells much more likely to survive to get
3:39a second hit and then become cancerous so that is where we got a lot of our
3:44information from and interesting a lot of these viruses in mice where we
3:50studied cancer are retroviruses and so I got very
3:55interested in this and this is what I did my MD thesis on and unlike most
4:00people I did my MD thesis after I’d finished all my clinical training normally you were meant to do some
4:07registar work and then take two three years off and do thesis well I was
4:13offered many but I never found any of the projects remotely interesting and so
4:18I I just carried on doing the clinical until I got very interested in that
4:24viruses were probably causing human cancer as well but it was just much more
4:29more subtle and that’s how that’s how I got very very interested in it and I
4:35focused on retroviruses initially because that’s what you did in the laboratory and the only uh virus at that
4:42time retrovirus that was recognized was the human te- cell Leukemia Lymphoma
4:48virus htlv1 which had been found to cause uh leukemia in uh Japan and also in the uh
4:57Caribbean particularly so that was what was already known by the time I went in
5:04and then when I started and this got gets really more interesting is that uh
5:10we were able to work with the um this virus and see how it cause cancer as it
5:16were but at the time I moved in then AIDS had become really big and it was
5:24rumored that a retrovirus might cause uh uh AIDS and there was a massive search
5:30in this and as we now know both montaner in France and Gallow in America both
5:38isolated their own viruses which turned out to be the same and they were called
5:43HIV in that time now the interesting thing for me as an oncologist at that
5:49time was that aids was associated with presentations of
5:54lymphomas and capy sarcomas which were both malignancy so that
6:00I felt Justified my time delving into what was going on with this retrovirus
6:05and just tell the conclusion is it’s indirect it’s not a direct transformation turning on enogen no it
6:13was indirect by removing the immune surveillance these lymphomas and capaces
6:20popped out they’ had their policemen removed as it were and that’s so that they felt that able to uh uh multiply
6:29the didn’t have any of the restraints but the interesting thing here is what really got me is both the Lomas and the
6:36capaces and it took us decades later before we understood the capaces but
6:42both of them were driven by viruses which is sitting there very well controlled by the immune system so you
6:49can see where I’m coming from with regards how I got interested in uh how
6:55viruses cause cancer and looking around there’s viruses other than uh
7:02retroviruses so that’s how I got involved got involved very much and this is how I came across the uh the concept
7:11uh of that cancers arise best in chronic
7:17inflammatory States and the viruses are absolutely a great example of chronic
7:24inflammatory States and if I may say the the first big big example on the ward that I came
7:32across when I was working in Sydney I was working in Sydney as a senior
7:37registra uh doing medical oncology and after two years I then have the
7:42qualifications to be the consultant which I then became but I had some very interesting uh cases I was particularly
7:50interested in the hepatoma there was a lot of hepatoma in Sydney and hepatoma
7:56means the primary cancer of the liver so that’s it it was a cancer of the liver
8:02and it would kill people and there was no good treatment they’re just starting to get some uh reasonable treatments now
8:09but then it was essentially a death sentence and uh I was told uh
8:16particularly in my training as an internal medicine uh registar in general
8:21medicine when we had these cases I was told that they were due to alcoholism
8:27they’re all due to alcohol and uh I thought that was a bit odd um
8:33because we knew people who had lots to drink as it were and never got hepatomas
8:40and then I found when I was looking at some of the patients they claimed not to be interested in alcohol or have given
8:47it up years ago so I thought something’s not quite quite true here and so it been
8:54reported that a uh by that time he um
8:59that a herpes virus a hepatitis virus Hepatitis B it was called is fascinating
9:05because it had a link with Australia it was it had an Australian antigen in it
9:10because it was found in some indigenous populations but it was common in uh in
9:18Asia as was the hepatoma so I got rather irritated that
9:26everybody was being taught this fellow’s got otoma and it is due to drinking
9:32alcohol and some of these people who um have Chinese extract weren’t drinking alcohol at all
9:40so at the time I basically got hold of a very very early tests for this virus in
9:48fact it was a a pathology collaborator in the Sydney University who was developing a reliable test so they could
9:55identify this virus so I thought well what I’ll do do is I’ll get everybody
10:01who died of hepatoma uh cancer of the of the liver in Sydney in the last two or
10:08three years and we were able to identify them in their own Hospital there was over 40 and so fortunately because of
10:17the interest in this there was serum from them so I was able to get stored serum and and all I did was take the
10:24serum to the uh Pathologists who developed this test
10:30and uh some serum from other uh patients as controls obviously and uh do them so
10:37they ran through them blind and lo and behold all the hepatomas were Hepatitis
10:43B positive I mean it was really quite remarkable and all the controls were negative uh I wrote that up as one of my
10:51first what I call epidemiology papers so I started looking
10:56at what Hepatitis B does basically it causes a hepatitis acute
11:03hepatitis often which is an acute inflammation of the liver and it settles down but then it goes on to cause
11:11chronic hepatitis and then as it goes on to a more consolidating phase it’s
11:17called therosis and it’s only when you get that stage that the cancer kind of
11:24breaks breaks out so it’s taken all this time so it’s fed by or protected by this
11:31environment of chronic inflammation uh and this goes on to the point where it escapes it’s interesting
11:37in the serotic phase there’s a lot of angiogenesis there which gives gives any
11:43cell that’s had one or two mutations more growth factor it’s like it’s like
11:49watering the rose gust so so the serotic phase is when there’s fibrous tissue in the liver yes yes and and the
11:55angiogenesis means there’s something there in this very fibrous scarred liver
12:01yes that’s stimulating the production of brand new blood vessels this
12:07angiogenesis yes I don’t fully uh understand the exact mechanisms but it’s
12:12just that’s the association that you see from the pathology papers but only then
12:19do you get this uh the liver cancer now the other interesting thing was they
12:25were occasionally getting liver cancers that were hepatitis be
12:30negative but they were all from people who’d had a history of hepatitis chronic
12:38hepatitis but they hadn’t got Hepatitis B but what they had had and at this time
12:45this was called hepatitis non a nonb you remember that very well I remember it
12:51well well this there’s now a few viruses in that group but the dominant one was
12:58hepatitis to see and it did exactly the same it gave you acute hepatitis chronic
13:04hepatitis after years and then it could too could lead to a primary liver cancer
13:11now what I was very excited about is these viruses couldn’t be more different
13:17your Hepatitis B is a big complex herpes virus like with DNA multiple DNA uh and
13:24the hepatitis sees a little RNA virus and yet completely different
13:29they induce the same thing so I got very interested in pathogenesis this it was
13:34the it was the principle and the story that was required for cancers to evolve
13:42so this was the first Insight it’s not confined to a specific virus like uh
13:48Hepatitis B any virus that induces this inflammation can cause it so that’s when
13:54I got really really interested in uh the virus that cause cancer I think it’s
14:01worthwhile pointing out at this moment I’d read then realized that there were a
14:06lot of other viruses that can cause cancer and I mean the the next
14:12high-profile one is uh human papala virus which in my uh lifetime was it was
14:19and I remember reading the papers in nature saying it was caused by herpy
14:24simplex virus big complex papers saying absolute Pro
14:29and also rejection of people who said it’s due to another virus this virus
14:35turned out to be the human papiloma virus which is the cause but it it wouldn’t grow that was the problem it
14:42wouldn’t grow in the culture so that’s why it was thought not to be a real
14:47virus but it was identified with molecular biology and everything in the end and so that was another example and
14:55that virus actually is very very important it causes the the a chronic
15:01inflammation in the mucosa and that’s what leads you have to have that for quite a long time before you get the the
15:08cancer develop the same principle same story We Now Know It’s associated with uh mouth um cancers over
15:1750% of mouth cancers are are driven by he human papiloma virus esophageal
15:24cancers and throat cancers and some cancers uh have this human papiloma
15:32virus driving the cancer so at a stroke you’ve got the enormous number of
15:37cancers that we are common that we recognize caused by viruses so just to
15:44recap uh recapitulate I’ve done the hepatitis ones Hepatitis B hepatitis C
15:50and I’ve mentioned the ones associated with HIV the lymphomas which we now know
15:55is EBV driven uh Epstein bar virus and the capy sarom sooma which is driven by
16:03a herpes virus which gain is only discovered relatively recently hhv6 and they’re driving it because
16:10they’ve been released by from the the immune system now the the then you have
16:15the the papala virus is it’s clearly was a this is a mucosal transmission one so
16:23I basically was uh asked to give a a lecture in Leicester when colleague
16:29called Keno burn was there as a consultant he’s now a professor of
16:34oncology in Brisbane so we kind of switched over I done a lot of training
16:39in Brisbane and um here in the UK in Ireland and I gave this talk up there
16:46and saying that after all my HIV work that I thought that um cancers arose in
16:53imino supressed environments well we knew that from transplants Etc
16:59but that unlike HIV the immune suppression of the big common cancers
17:06lung breast uh col rectal Etc prostate
17:11what have you that the immune suppression is much more subtle and I said I think from the model
17:20of the viruses it’s due to chronic chronic um suppression by the cancer and
17:28the environment they AR rise in leads to a chronic immune
17:33suppression and afterwards I’d give this talk uh given this talk we went for a
17:39few beers afterwards as as you do as you do yeah and Keno burn says well I I
17:47agree with everything you say but I don’t think it’s the immune system’s got anything to do with it it’s obviously
17:53angiogenesis he said this is a process where angiogenesis gets to Thrive and
17:59becomes more and more enabled it makes sense because a cancer is a living tissue so you would need a blood supply
18:06otherwise it would simply go black and the crows yes absolutely so this is
18:12where so we were basically two scientists uh examining an elephant and
18:20he reckoned it was uh say the Tusk and I reckon the important part was say the
18:26year and after a couple of pipes or perhaps more we suddenly realized I said
18:33uh you Ken we’re describing the same process but from slightly different
18:38angle the only thing that causes a chronic immune suppression and
18:44stimulates chronic angiogenesis is chronic inflammation and
18:50that is what these viruses are doing in it and if this is true then we can look
18:57at all the other viruses to see if that fits their uh
19:04pathophysiology and then that that would be it and you don’t need a virus well I
19:09cut straight to the point we suddenly realized you know you got lung cancer that occurs after at least a couple of
19:17Decades of chronic bronchitis uh uh stimulation so it has
19:24the perfect chronic inflam inflammation and angen Etc the other big solid one is colar
19:32rectal cancer and colar rectal cancer we already knew was much more common 50
19:37times more common in patients with UL colitis which by definition is a chronic
19:43inflammatory state but there are patients who don’t have otive Colitis
19:48who get colon cancer and then we know there’s another predisposition polyps so
19:55I said polyps you can have familial polyps or just r random polyps but these polyps if left to grow will grow enough
20:02and then they enough mutations will occur then they become cancers and uh I
20:08asked the pathologist what what he would classify polyps as they they have
20:14certain things hereditary genetic inflammatory Etc and he said oh without
20:20a doubt they’re inflammatory lesions inflammatory ad adomas but
20:26benign but left to their own devices for 2 or three years they will become malignant which
20:32is why if you have a a propensity for these they screen you and cut them out
20:37if youve if you’ve got a familial polyposis or even if they suddenly found you’ve got a problem and they find you
20:43got polyps and they go well we better keep an eye out in case more pop up and that’s obviously the right thing to do
20:49so we suddenly realize this in fact is this is what uh is the big cursor of the
20:55majority of cancers I mean there’s not one theory for everything but this is not far off it I think this is over over
21:0290% of cers fit into this and then Ken give given his due he started to
21:10research what how chronic inflammation affects the enene cycle and the
21:17suppressor cell cycle and at this time we had uh the NIH had their National
21:25Institute of Health in America National Cancer in they released this progression of cancer
21:31uh cartoon which basically had you know one cell mutates a bit the next one
21:37lives long enough for another mutation and this is the classic you needed about six to become a Cancer and start
21:44metastasizing and we suddenly realized that this this was a lovely model just to sink into our chronic inflammation
21:52thing CU it was like planting roses into a flower bed you know this inflammation
21:58was the food and the growth factor and more importantly from my point of view
22:04of the immune system is chronic inflammation causes immune suppression
22:11and prevents an active immune response from doing its surveillance and we know
22:18te- cells can pick up an oncogene M that mutates and kill it but if it’s in a
22:23chronic inflammatory State the tea cell can’t get to it so the the the random
22:29mutation survives in this chronic inflammatory State the tea cells are
22:35suppressed they’re pushed away and that allows them to go on and get the second
22:40mutation so this explains how how you have a scenario where cancers take two
22:47three four decades in some cases before they uh they manifest so the the good
22:53thing about this is that you’ve got a long time you got a lot of warning time
22:59and from my point of view it really does say what things can you do to reduce
23:05chronic inflammation because that will reduce your chances of getting cancer
23:10dramatically just a geeky Point Professor um if if something’s inflamed
23:17I would associate that with uh an influx of white blood cells like like like cytotoxic tea cells ah very that’s very
23:25good and very true except you’ve highlighted that the immune system is quite complex
23:31and full of different different soldiers as it were it will it leads to a a a big
23:36influx of white cells like neutrophils for instance and macrofagos what have
23:42you but the t- cells can’t get there because this is becomes a very inflammatory environment it’s so and we
23:49now know that if you do have a lot of uh nutrifil in your blood with a cancer
23:55patient and very few lymphocytes that’s a very bad prognosis if you can convert that so you
24:02have a healthy te- cell and you reduce the number of white cells then you have a much better prognosis there several
24:09papers have been reported over the last two three years just pointing out this
24:14fact and saying you know I wonder why that is how does that occur because like you were say implying that lots of white
24:20cells means a good immune system means it will control it no this is a very
24:26good thing it highlights that their the immune system is a delicate balance
24:31between um tea cells the Frontline uh Warriors your front line of the army as
24:37it were and when they encounter a foreign Invader like covid for instance
24:44they charge up and they beat it up and they send signals to the uh B cells
24:50which take a while to kick in especially for a new one and then they make antibodies and uh then your program
24:58memory cells so when you meet it next time you should make the antibodies very quickly they they they program that but
25:05what we find is this Natural Balance is Disturbed and uh when we wrote these
25:11papers we’ve done many papers and books and chapters on this is when you have the chronic
25:16inflammation this balance is completely Disturbed so the tea cells are
25:22completely suppressed and we found out it was no different in patients with TB
25:28HIV and cancer a remarkable similarity
25:33and therefore a potential can you use something to restore those tea cells and
25:41uh would it work and help in HIV TB and cancer well of course that is where we
25:48realize that there was something that did that and that was these MCO bacteria
25:53uh that were being used for TB uh they were then shown uh in HIV patients to
26:00reduce their chances of getting TB big papers published in what then was a
26:06useful reliable journal the Lancet which I don’t believe in anything published
26:11there now because it seems to be a purely um political uh Journal it used
26:17to be the absolute gold standard in the old days wasn’t it absolutely it’s been totally perturbated uh I think it is
26:25tragic and a disgrace and uh so that’s that’s basically um what put them
26:32together and then out of that you know I must give credit gram rook and John
26:37Stanford John Stanford sadly has passed away now but they realized that BCG made
26:43a difference but there was a problem there was a problem with it and they wanted to make it better it’s a story in
26:50its own right but they discovered myobacterium vaki was the the the core to getting a
26:56good reliable immune response uh in TB patients exposed to TV and patients with
27:04HIV to stop them getting TV and when I looked at this what they were doing I
27:09took a great interest in this concept I realized this funny heat killed organism
27:17was able to reverse the Seesaw it was able to boost the T cells and more
27:22importantly suppress the over enthusiastic and actually dangerous
27:28chronic inflammatory responses of nutrifil and microphases and that’s exactly what it does and then I said
27:35well this is exactly what’s going on in cancer courtesy of my big interaction with kenob bur anything that boosts the
27:42te- cell response and dampens down the inflammation can only be a good thing so that’s how I ended up getting hold of
27:49the mvi and in the days before the European unan clinical trial directive
27:55which is a mechanism to stop stop Innovative creative and useful uh Studies by academics such as myself this
28:03is when you were allowed to be a doctor when you allowed to be a doctor I basically uh said I want to do a trial
28:10on this to my patients we don’t have any at that time we had nothing and they would go for anything and I was very
28:17happy to try anything providing it wasn’t non toxic course at the time we
28:22were allowed to give them interferon which I was only in the clinic for a few mon and I said this
28:28Drug’s ridiculous and remember it had been approved it had been approved I said I not impressed by any benefit but
28:35I am impressed by the side effects they’re just unacceptable particularly for patients with low volume disease so
28:42I switched to the studies and with mvi and it was no time at all you could see
28:48that there was great benefits much better than interfere on using this and
28:53that trial it I was able to to write uh you know dear sir I’ve got this stuff
29:00I’d like to try it in the cancer patients it’s been given to thousands of people with HIV and TB so there’s no
29:07problem there this that and the other and then uh at the end of the month the chairman of the Ethics Committee said we
29:14don’t see any problems with it off you go I say that because anybody will laugh
29:19at this knowing if you want to do a trial now you’re looking six months year
29:25year to get started and you got big farmer behind you who suddenly decide that they want to get this out as soon
29:32as possible then all these obstacles seem to disappear as we found with covid vaccines and things like
29:38that absolutely yeah and uh if this micro bacterium VY vaccine was available
29:44I would have it because I think it it if it boosts my t-a response it’s going to reduce the probability of cancers
29:50developing it will exactly and as I said at the time and I offered it to uh witty
29:55that we did actually have enough of the vaccine to do every Frontline Hospital staff in the covid crisis and they
30:03turned it down there’s not enough evidence can you believe it that means not enough understanding or common sense
30:09uh on the grounds of the people who should know better so it’s a Pity because not only would have these people
30:14have been protected from viral and bacterial infections by the regulation of the t- cell response we’d also
30:20potentially have a massive reduction in cancers in all Health Service employees over the next 10 20 30 years well I mean
30:28that’s a ludicrous thing solution to jump to if I may say so but it’s one that should be tested
30:35but I suspect you are right do you know why I suspect you are right because uh I’ve tried to keep busy
30:43as you know and I’ve been to uh all sorts of Immunology meetings virus
30:49meetings and cancer cancer treatment things so one of the little groups I was
30:54in which is basically uh a sort of um clinical immunology and and diseases
31:01in in humans that are difficult one of the things that staggered me because I
31:06was great became a great fan of BCG which is why I got it but you can’t use BCG more than a couple of times
31:11otherwise you you get a negative response this is the standard uh vaccine against tuberculosis exactly so I got
31:18very interested in that and I realized you needed a stimulation you gave repeatedly and that BCG doesn’t do that
31:26so that’s why we got into these heat killed ones which do so just explaining that bit but the reason I suspect you’re
31:33completely right was that at one of these meetings I think it was uh one we had in Cambridge it used to be as a nice
31:40pl we could chat and go to the local pub as usual that sort of thing and shat over it and one of the things that they
31:47had found in long-term followup for BCG uh in in done in Africa was the guy
31:55presented because they were able to do long-term followup which you can’t do most grants these days cuz they’re 5
32:00years or something so what they found and what they presented they said we’ve got some
32:07data here and it’s real and we really didn’t believe it and we can’t understand it it said but in our cohorts
32:15of uh uh children given BCG in Africa we’ve we’ve compared them to children in
32:22those countries where they wouldn’t let us give BCG I mean there are such things
32:27and it said it’s amazing it said the people who got BCG as children 50 years later they have lower
32:35incidence of heart attacks and cancer so that means at that early
32:42stage their immune systems were set like this seesaw with the te- cells a bit damped down but it had corrected
32:50it and that equilibrium was enough for them to come across all sorts of things
32:56the rest of them life and have a lower instance of heart disease and cancer so that’s why I said your your statement
33:02was ludicrous because I mean it that’s what I’d say to you know to myself
33:08because I I make those things I said but here to my amazement I must say it is
33:13the one paper at that conference I I remember I don’t even remember my own
33:21paper I’m I’m can make plenty of ludicrous statements but it’s nice to it’s nice to have it been discussed by
33:27someone who with your experience but I think you’re absolutely right but I can’t we can’t make um claims for
33:34product products you have an invested interest in they won’t allow you yeah
33:39because I’ve always you know played with the idea you have a new drug thing you could call it like Cura or
33:48wonder you’re not allowed to do that because it implies untested efficacy so
33:53that’s why I’m saying that yeah I think I’ve started to understand that cellular imbalance now because if you’ve got
33:59chronic inflammation presumably that’s going to alter the the cytokine profile of the
34:05local area of tissue MH um and cyto kindes are actually specific to particular immune cell types so it’s not
34:12you know I think it’s important actually to to to relate these things back because this does make sense in terms of
34:18basic science it does so so what you’re discussing has got complete scientific
34:24credibility as well as provisional pretty convincing empirical evidence and
34:29it just seems tragic that this isn’t being followed up especially when the risk benefit analysis is so positive
34:36exactly because what the heck is the risk of giving a few heat attenuated MCO
34:41bacteria vaki into my armor I can see pretty well no risk from that and yet
34:47yet the upsides are potentially immense no as you say there are no risks and
34:53there haven’t been any risks in all these all these studies because it is heat inactivated yeah uh um virus you’re
35:01giving a precise known dose it’s not like one of these RNA viruses where you could produce six viral particles or Six
35:08Trillion trillion trillion viral particles no it it mean it’s totally safe because it’s heat killed it can
35:14never be resurrected to life like RNA or BCG see BCG is attenuated it’s his life
35:21and I have dealt with uh two patients over my time who were on BCG and trials we in collaboration with the uh Donald
35:29Morton the John Wayne Institute a lot of the vaccines had BCG as the adant
35:34occasionally they can cause lymph noos and you find the these patients have got a very low level of TB fortunately it’s
35:43very easy to kill because it’s attenuated you can just do it with a short course of reformation you know
35:49it’s very easy but less than 1% you know so but it’s still there so the fact we
35:54don’t have to worry about that whatsoever it gives us you know confidence that
36:00we’re not going to do any harm with this one of one of my early memories about working with cancer patients as a young
36:06staff nurse is so many uh women coming in with Advanced cancers pathological
36:12fraes horrible horrible things after after cervical cancer and that’s another human papala virus yes
36:20inflamation yeah um the the term retrovirus um can you just unpack that a
36:26little what’s the difference between a virus and a retrovirus well a retrovirus is a virus
36:32first of all yeah so it’s a sub classification a sub classification most viruses that we have
36:41associated with cancer in humans have been herpes virus like the Hepatitis B
36:47virus like the epin bar virus for instance I mean they’re they’re the big big ones and the cap these are the big
36:54DNA viruses big DNA now now DNA makes RNA which makes
37:01protein which makes money as one of the uh big as one of the people in the
37:07Cambridge U molecular laboratory laboratory molecular biology in Cambridge said I can’t remember which
37:13one that was s sad but true I think it was sang or perut these big guys who
37:19were there but I me always remember them saying that because they were predicting the biotech Revolution so your DNA a
37:27makes RNA makes protein but a retrovirus is an RNA virus
37:35that codes the other way so it goes into DNA and recodes that to produce whatever
37:42it does and make make its uh proteins to replicate Etc and in that little
37:49definition that I’ve just told you I think I’ve just told you why I believe
37:54messenger RNA viruses are so so dangerous y completely utterly dangerous
38:00and why I’ve been campaigning for them to be banned and you know I’ve I’m used to all sorts of insults and I know that
38:08I was told I just a cancer doctor what do I know about viruses Etc all this but
38:14I have been well you’re just the most senior oncologist in the country but we’ll pass that point over yeah but I I
38:19I wouldn’t I wouldn’t say that but I I have been on many many scientific Boards
38:25of of companies is developing vaccines and you know gone into it great depth
38:31and I have been on the board of a company that purely focused on making
38:36messenger RNA vaccines so I mean I was on the board for 5 years and I did my
38:41cycle and I got to know that there was a big problem and that big problem I left
38:48that board seven years ago and I now know that problem’s still not been sorted and that the this p pmic
38:57was used as an excuse to get round all the problems that the regulatory people
39:02wouldn’t let them go through before that’s a terrible thing but that explains the what a retrovirus is it is
39:09actually an RNA virus that can reprogram go into the DNA and reprogram it and in
39:17mice and we know for the they’ve only got one human virus that does that H
39:23htlv1 they reprogram it and you get cancer so it’s it’s a big it’s a big
39:28risk well congratulations on leaving that when you did um now this DNA makes
39:35RNA makes protein is what we call the central dogma isn’t it of genetics you know every student learns that DNA makes
39:41RNA makes protein but we we clearly know that these retroviruses RNA makes DNA it
39:48goes the other way around and of course that DNA can make more na which makes more makes more protein
39:55now is the in order to get RNA to go to DNA
40:00we need an enzyme called reverse transcripts that’s right yeah so transcription is the DNA to the RNA the
40:06reverse transcript reverse transcription is the RNA to the DNA yes now that
40:12reverse transcriptase enzyme which is essential is that produced as a endogenous product of
40:20human cells or is that always coded for by RNA that comes in with the virus it uh where the virus is involved
40:29it encodes it itself it has its own own uh uh reverse transcriptase thing so the
40:35virus the RNA and the virus itself codes for its own reverse transcript and that is what provided the first Target for
40:43treating HIV they used reverse transcriptase Inhibitors so it wouldn’t
40:48be able to integrate and have the life cycle so that that that yeah yeah and
40:54it’s a bit of an unfair question really but is is there endogenous reverse transcripts do human cells produce
41:00reverse transcripts or do we know that I I will be very honest here I’m
41:05not sure and so I’m speculating but we do have endogenous
41:11retroviruses large number of them in the genome accumulated over millions of
41:16years of evolution accumulated over millions of years of evolution and they
41:21can they can escape as it were and we think that other viruses help these
41:28Escape because this is the pathogenesis of multiple sclerosis the uh there’s a lot of work
41:35out there to suggest that these sleeping dormant uh retroviruses which should
41:42just part of our uh genetic baggage that we come with
41:47about 90% of our genome is So-Cal baggage uh and that’s another
41:53fascinating thing is why do we carry it around and uh just for the viewers the simplest
41:59solution is I think it is if you imagine you pass all your genes on all the time
42:04and they’re just a big big baggage of jeans and how are you going to make maximum use of it whereas I think that
42:1290% of baggage is the equivalent of a library’s shelving and retrieval so it
42:19allows you to put the useful genes in an order an assembly you can retrieve them
42:24when you need them and on them I mean it’s not been proven but that that that is that’s a speculation which I I I feel
42:32most comfortable when uh discussing these so what happens with the so-called multiple sclerosis is that an enzyme
42:40sorry that another virus comes in and helps provide a re a reverse
42:48transcriptase that that virus does not have and enables it to uh wake up and
42:55start sleeping multiple SC we still don’t know exactly what’s going on but I
43:01think that’s the that’s the closest model uh to it and there’s other
43:07complications in that it’s very genetically restricted and it’s clearly got an
43:13autoimmune component to it so that’s I just wanted to answer your question but I don’t want to get into multiple
43:19sclerosis no no no I would love to because it’s we we’ll try and stick to the topic um so I think basically what
43:27we’re saying is we have this idea that uh we’re in a mure of viruses Epstein
43:34bar virus for example I assume we’ve all been exposed to that exactly um and uh
43:41we live in we live with all these viruses um most of the time they’re kept down by an active immune system chronic
43:48inflammation comes along messes up with this cellular differential we get more of these nutrifil nutrifil of course are
43:54brilliant if you got a bacterial in infection is exactly what you want exactly but it’s not it’s not what you want if you got chronic inflammation
44:01yeah suppresses the tea cells and it’s this chronic inflammation that leads to to the development of of can of cancers
44:09um and and and that kind of combines the initiator and promoter model of cancer really doesn’t it it does and can I just
44:16add an extra piece of information I forgot to show that the chronic inflammation causing cancer is a reality
44:26and that interfering with this is a reality is that the experiment has
44:32already been done rather like the BCG and TB looking beyond that how it
44:38actually reduced cancer and uh heart attacks 50 years later remember they did Big studies
44:46looking at the effect of aspirin now aspirin is a is an anti-inflammatory
44:52agent which blocks Cox’s 2 pathways and it also um blocks
44:59prostaglandins and therefore propensity to clotting in other words it reduces the production of inflammatory uh
45:06mediators so we know that it made a difference for uh for heart but once
45:12again those big studies also gave the signal that the people on the aspirin
45:17had a lower instance of colon cancer and so that’s a perfect example of
45:24serendipity you they study out to do one thing but if you broaden it and look and ask other questions and it showed that
45:31anti-inflammatories would reduce the instance of the of colon cany and aspirin was ideal unfortunately aspirin
45:39is very uh cheap but easy to to get and take it has the problem that if you take
45:46it as a uh a tablet and you don’t take it with meals it can give you gastric
45:51problems and bleeding and occasionally very occasionally the bleeding can be f F Al and the problem is that GP only
46:00needs have a one or two of these in his uh life and he gets very wary about
46:05advising aspirin at all but that is to forget that aspirin you can have it in a lowd dose for the clotting at 75 but you
46:14need higher than that for its anti-inflammatory but I’ve uh always
46:19advis that if you take the anti-inflammatory soluble with a meal mhm it greatly reduces and I do that
46:25myself I mean that uh that’s the way I would not have an aspirin in the middle of the day for a headache cuz that’ be
46:32guaranteed problems if I need a headache and sometimes sinusitis it is the best
46:38treatment for a chronic sinusitis I just pop the soluble in and
46:44I take it and if it’s urgent in the middle of the day then I’ll take a yogurt with it it’s something to protect
46:49the stomach so all these you know s sensible logical things to do can uh can
46:55work through but at the end of the day I mean I’m a great believer in Daily anti-inflammatory tablets for everybody
47:01over 40 to reduce these Pathways I mean you you you might be targeting the one
47:07for colar rectal it’s probably preventing others it looks like it has a benefit on lung cancer as well but
47:14there’s plenty of other anti-inflammatories which uh can be looked at and
47:20uh for prevention now the other causes of chronic inflammation I mean smoking
47:27is obvious so I’m not going to waste any time on that and that CA I mean most people who present with lung cancer have
47:34a history of chronic in inflammatory upper respiratory diseases every winter
47:39chronic bronchitis Etc they get admitted to aspin and eventually they’re found to
47:45have the cancer that’s that’s a um a fairly logical one it’s obvious smoking
47:51is going to contribute to the chronic inflammation isn’t it it is it absolutely is is the tyod direct
47:57carcinogen as well is it kind of a double whammy it’s double whammy I’m absolutely sure it’s it’s a double
48:02whammy in fact there’s so many carcinogens in Smoke we don’t know which one is doing it it’s just you need just
48:09increase your risk it’s as simple as that but what I wanted to get on to there is another cause of chronic
48:16inflammation which is driving up cancer of All Sorts initially the signal was
48:21for renal cancer people wonder what on Earth causes renal cancer MH uh and then
48:27it was wound cancer uterine cancer endometrial cancer what n causes these
48:33and this is I think is the most fascinating link ever MH the link is
48:39with obesity MH now obesity if you have to describe it put
48:45it in a pathologist pot as it were they only have a few pots but everything has to squeeze into one of
48:51them uh obesity squeezes into chronic and inflammatory State yes if you are
48:58obese you have far more cells than the thin person next to you and therefore
49:05they need feeding and they need turning over and they produce uh their own
49:11inflammatory growth factors Etc and so obesity is a chronic inflammatory state
49:18so probably the very best way we could reduce cancers in this country would be to prevent obesity uh and do everything
49:27that’s required for it to to reduce it because it is associated where you’re
49:32much more likely to have all the cancers all of all pretty well all of them all the common ones all the common ones yeah
49:39so that that and to me that’s this is really like reaching the peak of the Mountain of this because it is so
49:47overwhelmingly uh explains why these people have more cancers uh couple of very simple things
49:55first of all because they’re really obese and big they’ve got a lot more cells and then when you got a lot more
50:01cells you got a lot more opportunity that one of those might go malignant just on a random alone let alone the
50:08fact that the more there are like uh you know people in a room they huddle up the
50:14warmer they get and that sort of Warmness is an inflammatory State producing more Warmness more growth
50:21factors more immune suppression so that’s I wasn’t aware
50:26that I wasn’t aware of that that’s interesting I I assumed that in obesity the adap asite number was this fat cell
50:32number was fairly constant and they just kind of swelled up and got bigger and bigger but there’s actually an increase in the number of the cells present well
50:39uh that’s a very very good technical Point uh sorry and I I’m I’m not not
50:49uh qualified to answer that in I’d actually want to research that but but
50:56this let’s move to a paradigm it is certainly true that bigger people
51:01genetically without being a Beese are more likely to get cancer because they got more more likely to uh have they got
51:10more cells theyve got more cells yeah the random mutation and we know that that’s the case in dogs too bigger dogs
51:16much more likely to get cancer than the smaller dogs interesting so my thinking here would be then that
51:23that the these the amount of fat whether it’s more fat cells or whether it’s full
51:28fat cells mhm they there that’s going to cause the an abnormal in the an
51:34abnormality in the function of the cell that causes these cells to release inflammatory mediators systemically is
51:40that kind of what’s going on well it must be a way because why if you eat too much do you get fat and as you say these
51:46cells go into adpost tissue yeah and they are there to deal with excess fuel
51:54to store it in times of uh when when there is none as it were and
52:01that’s one of the reasons why people in the uh Pacific Indonesian Islands why they’re so big and the Maris because
52:09they adapted in good times they got big because they’d have to sail the oceans
52:15for several days without any food at all and that extra capacity allowed them to do that the problem is with obesity
52:23there’s no downside so keep going on storing storing storing and that interferes with all the metabolic
52:30pathways diabetes is one of the obvious very common vascular disease and
52:35everything that can go with that yeah M right so this this is so so
52:41interesting so all so all the common cancers so lung bowel prostate breast
52:47pancreas esophagus liver bladder obesity is a potential factor maybe to varying
52:53degrees of of iology but a potential factor in all of these really common cancers yes and of course in two of
53:00those breast and prostate you have a hormonal aspect uh oh yeah as well but
53:06then that the hormonal aspect can be affected you know by uh chronic inflammation and immune status so that
53:15uh that’s very comp complex I mean I think the uh breast and prostate are
53:21more complex because of the hormonal aspect uh but to me prostate is more
53:28understandable than breast I think breast is is much more complex with regards to the the real cause of in
53:37inflammation obviously hormone has a lot to do with it but males get breast cancer too obviously not nearly as
53:43common but shows that it so the hormonal aspect just makes it much more likely
53:49but the other aspects can also be affecting these tumors as well I I tend to think of the
53:56male breast as being like a prepubescent female breast in a way that there’s still like a um a basic ductal system
54:04there that can be stimulated and of course men do get breast cancer it’s yeah yeah physical activity um is that I
54:13mean it’s good obviously but in terms of cancer is it protective do you think I I
54:19don’t think I know and that’s that’s very revealing answer actually yeah
54:25um they very uh detailed results in mice
54:31where they all identical they’re all given the same stimulating factors to
54:37develop cancer they’re known to get cancer eventually so you know so it’s a very good model for what
54:44you can do to reduce the cancers so they’ve done and this has been repeated many times you’d have mice which should
54:52just walk around the cage and then there’s mice that have the opportunity to run in a wheel for you know a certain
55:00amount of time a day and this is all monitored so the ones that have a lot of exercise develop tumors far slower than
55:07those that don’t do a lot of exercise and I’m sure unlike quite a few things
55:12where the mice doesn’t quite translate The Human Condition I’m sure this is very relevant
55:18m i mean it’s good to be physically fit anyway so it’s generally just run if you
55:24don’t mind just a few minut to run through some of the common causes that we we that I used to teach my students
55:29about certainly um sun and ultraviolet
55:35radiation yes just just skin cancers or anything else could be involved in that well that’s that’s inducing a chronic
55:42inflammatory state in the skin and when I was trying to work out you know what
55:47was going on with melanoma uh I said you know know what’s causing this and I actually at a at a
55:54conference actually said there’s a great irony that all the cancers seem to be involved with chronic inflammation
56:00except the one that I’ve been given to treat melanoma and actually the
56:06pathologist came to me afterwards and said he said it’s no different he said I
56:12can tell melanoma patients just looking at their normal skin because they don’t
56:17have normal skin they have a sort of chronic inflammatory fibrous skin and he
56:24also said that is one of the reasons for your other big Quest is why do so many
56:29melanoma patients have such low vitamin D levels and he said is the skin has
56:35become inflammatory and no longer does that vital conversion for the sunshine
56:40vitamin as it were as we know from the title of one of David Grimes books yeah
56:46and so that is why so even the melanoma has it is a chronic inflammatory state
56:52which uh leads to a propensity for the melanoma wow that really fits in well
56:57and and and vitamin D of course which we know well I think I’m safe in saying that we know low vitamin D levels are
57:04involved in in the iology of of many cancers um and and that is vitamin D is an anti
57:13I mean it activates many genes and controls genetic expression but it’s also anti-inflammatory isn’t it yes it
57:19is very anti-inflammatory I mean it’s it’s absolutely vital for the immune system and it’s actually vital for the
57:26inflammation I remember when I was doing really hard research on this and I found that a very good papers of Immunology
57:33you do not have an adequate level of vitamin D then your activated cd8 cell
57:39it will latch on to an antigen on a tumor cell and it will just sort of kiss
57:44it and go away so this the C cd8 is is the T helper cell is it no the the T
57:50killer cell the activate T killer cell oh sorry yeah it’s a CD yeah I always get CD C4 and cd8 that’s yeah cd8 is the
57:57killer cell sorry the cytotoxic cell yeah and the CD4 is the helper cell that gives it all the signals that’s it y so
58:03the the cd8 won’t kill that humanum cell unless there’s a healthy level of vitamin D so vitamin D is actually
58:10required for the te cells to do their job and then I found another paper that
58:15says that uh um there’s over excessive antigen production in low levels of
58:21vitamin D well this appears to be a paradox initially but no when you look at it very carefully it’s dendritic cells
58:29presenting the primary antigens to the immune system to program it and if it
58:35low vitamin D it’s not very good at presenting just the necessary ones it
58:42presents gets sloppy and this leads to autoimmune disease and so this is why
58:48autoimmune disease is associated with low vitamin D and most people working
58:54autoimmune diseases now one of the first things they do is pick up on low vitamin D and treat it and one of the first well
59:02this is recognized was multiple sclerosis multiple sclerosis I mean your first thing you do is correct their low
59:08vitamin D levels and that’s a you know the start and the path to uh treatment
59:13and being able to help with them because it is basically an autoimmune uh disease
59:19are tackling your own melin MH yep um different radiations as a cause of
59:25cancer I mean um x-rays for example x-ray exposure or
59:32um I mean what what what would be the mechanism there can can can the radiation physically damage the the
59:38genetic material that’s what I always taught yeah yeah and it’s right it’s right yeah uh and it just it’s a matter
59:44of of dose and time I mean that’s why we can safely use x-rays uh because we know
59:50the dose is very very low and also why that we get worried about people who
59:56need x-rays frequently for long periods of time and we we go out of our way like
1:00:03people who have a lot need a lot of CT scans for instance they’re now much lower radiation but we’d switch to the
1:00:11MRI which doesn’t do that so we’ve got an alternative or Echo I mean a lot of
1:00:17tumors and things can be done with very very sophisticated Echoes and that that gives another cause
1:00:24of canc which is iatrogenesis CA caused by medical treatment MH and uh it’s
1:00:29fortunately quite quite rare now um so uh yeah I think I think it is it is very
1:00:37rare in fact the things that come to mind more radiotherapy causing other
1:00:42diseases later in life like uh heart problems and people who had their chest irradiated for Hodgkins when they were
1:00:49very young but once again we are we no longer give
1:00:55too higher dose and two we’re much better at focusing it and avoiding
1:01:00structures that might be damaged by it yeah yeah that’s good um and of course in the iatrogenic category you already
1:01:07mentioned there people that have had transplants and need chronic drugs to um suppress the the natural body’s
1:01:14natural repression is it true that they are more prone to certain cancers after years of
1:01:20imun supression absolutely especially spin uh skin cancers very interesting of All
1:01:26Sorts y um shall we recommend people to have a good diet and avoid junk food
1:01:32well obviously and this this links in with obesity because obesity is
1:01:38associated mainly with junk food I mean I I’ve done my own observations that
1:01:43what do fat people eat and they have a terrible diet I mean and and this is a
1:01:49common observation we we we see this repeatedly don’t we I mean yeah and the other thing they seem to be eating all
1:01:54the time even while driving yeah I mean I’m quite now so a good healthy diet is
1:02:00important not only to avoid go being overweight but you need a high fiber
1:02:07diet in order to have a good microbiome in the gut which basically means you
1:02:13have a good healthy immune system so the diet even helps program your uh immune
1:02:20response and your immune system and of course in the absence of the right amount of sun and everything a major
1:02:27part of that is vitamin d and vitamin D in that it’s a fat soluble vitamin well
1:02:33actually as David Grimes have pointed out the tragedy of vitamin D was it was found after vitamin c i it’s not a
1:02:41vitamin it’s far more important than a vitamin yeah yeah I agree with that and
1:02:46we’ve just done an excellent recording with Dr Grimes which will be available yeah I can’t wait to hear it actually
1:02:51cuz I oh it’s up there I’m great great fan of his it’s it’s great we we and and
1:02:58we went to the pub after for a couple of beer so it was it was a really good day um various minerals um I mean I’m
1:03:06you know I’m I’m thinking about Japan South Korea where they eat lots of seaweed high amounts of iodine um I’m
1:03:13thinking about the UK much higher rates of breast cancer where basically we don’t eat seafood do you think there
1:03:19could be anything in things like iodine being replete in iodine and other minerals
1:03:25yes I do it’s not an area I’ve researched in depth but I have engaged
1:03:31with uh others who are are convinced in the the same way that
1:03:37I’m absolutely Talisman for vitamin D in
1:03:42cancer the next thing that you get these people who’ve done a lot of research in is funnily enough iDine they talk about
1:03:50lugol’s iDine being most important because of its deficient so yes and
1:03:55there’ll be many others that we we don’t know about there are I take a drop of iodine a couple of times a week now just
1:04:02I think it’s a milligram or two right you get used to the
1:04:08taste because I mean I was working out you know if you eat kelp for example um
1:04:14you’re getting huge amounts of iodine and we get nothing like that amount of course it’s homeostatically regulated So
1:04:20within reasoning you know if you take more than the body needs it will simply be excreted in the urine so yeah and you
1:04:26you remind me that you live closer to darbishire than I do I do yeah of of
1:04:32course the reason you’re saying that is darish a neck exactly or Switzerland neck or Nepal neck where the the thyroid
1:04:38swelled up through simple lack of iodine exactly but of course the other thing that’s fascinating is this idea of the
1:04:46the amount the levels of things like vitamin D and iodine were set to prevent
1:04:52uh the amount of vitamin D was calculated on the amount to prevent rickets which of course is an extreme
1:04:58form of Bendy bone disease the amount of iodine was set to prevent Goa which is a sign of really quite extreme iodine
1:05:04deficiency there’s a difference between um the amount of substance needed to
1:05:09prevent a particular deficiency syndrome and an Optimum level MH and I think
1:05:14that’s what a lot of these blood levels and uh dietary recommendations haven’t quite come up to date with yet well
1:05:20neither have so-called experts I mean there’s a special advisory committee
1:05:25like said suban of sage which is one of the most inappropriate acronyms ever
1:05:31invented uh anything but Sage they should call it um but the other one is the special advisory committee on
1:05:38nutrition who are full of such dimwits that they feel that 400 international
1:05:43units is the maximum that should be given to the British population and I’ve chall and W he agrees with them I mean
1:05:50tiny amounts of vitamin D that that’s a good thing that you that is probably what you need for rickets because it’s
1:05:57the extreme yeah but for good health you need far more than that I you need at
1:06:03least two three times of that I mean the minimum supplementation should be a th000 international units and in the
1:06:09winter in the north the minimum is 2,000 mhm yeah and I mean if you think about
1:06:15it so we’ve got the government recommending 400 units but if you go out on a sunny afternoon without with just
1:06:22your shorts on you’re going to make 20,000 the difference is just incredible can I
1:06:28keep drinking some lger on Friday nights well I think it’s terribly important to have some uh alcohol if you’re used to
1:06:36it and Afraid so and uh I think uh that
1:06:42uh suddenly becoming righteous and stopping it in my observations isn’t
1:06:47doesn’t seem to be a very good thing to do I don’t know why but I mean a moderate amount of alcohol is is full of
1:06:54things uh I mean beer stimulates your um
1:06:59Pious patches yeah the the the yeast in in real ale I think the yeast in real
1:07:06ale particularly so that’s the justification for my beer that if you’re
1:07:13watching this video and you don’t drink please do not start based on this conversation uh but I mean it’s true
1:07:19huge amounts of alcohol though chronic inflammation that’s right huge yeah yeah huge amounts of chronic
1:07:25inflammation but the other thing about white red wine the active ingredient in
1:07:30that apart from alcohol is reservatol which is a very powerful anti-inflammatory so you know thing
1:07:37things in moderation MH are fine everything in excess I mean I mean the
1:07:43moderation is the thing isn’t it food if you don’t eat food you star if you eat too much you’re a you need something in
1:07:50between and very often in physiology we we don’t have a linear relationship between two variables like alcohol and
1:07:56cancer it’s very often an s-shaped curve isn’t it so it’s low at the bottom ENT essentially no risk then it goes up
1:08:02sharply exactly when you get to a particular critical critical dose physiology often follows this sigmoid
1:08:10sigmoid curve just workplace cancers um I mean asbestos for example I mean
1:08:18that’s a clear risk isn’t it yes and it’s very interesting as bestus
1:08:25because I I worked at the time I was involved with the MRC that they came out
1:08:32not this has nothing to do with me I was working independently but they came out and they did these big uh surveys
1:08:39because they did you know the one on lung Richard do and Etc and Pito did the
1:08:45big survey showing that smoking clearly caused lung cancer which the industry fought against for years and years and
1:08:51years so it was super obvious to everybody well there was asbestos and
1:08:58misela and that link was there for a long time and they monitored it for
1:09:05about 20 years and I remember they came out and said there was no link after I think Richard doll knew about this in in
1:09:11about 1960 I think I’m sure he would there’s no link and so that became an official report but thereafter the link
1:09:20became stronger and stronger and stronger and when became absolutely totally obvious mhm that the link was
1:09:28admitted it’s just ridiculous it it was and the interesting thing about asbestosis and Amela it is it average is
1:09:37at least 40 years 40 Years of exposure and what is the exposure it is bits of
1:09:42the asbestos that get ingested they can’t get rid of it uh they’re indigestible quite literally and that
1:09:50gives rise to a very low chronic level of inflammation so um
1:09:58misela Rises out of a mesitis basically due to the
1:10:05macras and fites having real problems trying to dispose of these particles
1:10:12melom is a totally hideous disease isn’t it plural membranes yes swells up
1:10:17occupies virtually the whole Space squashes the lung terrible it is terrible disease and I must say applied
1:10:24those principles to treatment and I have treated patients with mieloma with the IMM when I could get it
1:10:31anybody I can’t the moment because it’s going for registration trials but I was able to do that and so the IMM is one of
1:10:38these micob bacteria vac it’s it’s it’s the one that we’re focusing on now that
1:10:44yeah and maximizing anti-inflammatories uh uh which in these cases it me
1:10:50included vitamin D because vitamin D is a very strong anti-inflammatory MH and I’ve had amazing stabilizations with
1:10:57that wow in patients who refuse chemotherapy they they they look at the
1:11:02chemotherapy oh horrible and the surgery and the radiotherapy and it’s been staggering so once again it proves an
1:11:09anti-inflamatory and people will say you can’t possibly say that on a few patients but I say I can say that on a
1:11:15few patients because that is what years of being a doctor uh dealing with all these things you’re very good at
1:11:22sniffing out what what’s effective and what’s not and they only say you can say
1:11:28it when it’s been shown in a randomized trial well I have no longer got any big
1:11:33faith in randomized trials and I’ve got people who uh who agree with me ever since we when we published The Book of
1:11:41the the death of science I’ve had people contact me saying that they basically
1:11:46want to look at writing papers and doing a thing on that should be the death of the the death of the ra thank you
1:11:55the the death of the Rand is the death of the um randomized trial because now
1:12:03we know that the randomized trials for covid were completely perverted they they weren’t randomized at all I mean
1:12:10there’s nothing wrong with the principle of a randomized control trial that’s a great scientific principle you know that
1:12:16that go that go goes way back to the discovery of uh streptomycin for
1:12:22tuberculosis um that that’s great but it’s the way it’s now applied in practice and he who he who pays the
1:12:29Fiddler caus the results of the clinical trial yes yeah um briefly we we’re nearly
1:12:36finished um air pollution microparticulates are they a risk yes
1:12:42clearly clearly so um things from smoke
1:12:47incineration yeah diesel diesel fumes you here I have a little cough there but
1:12:53from time to time it’s not covid it’s none of these things I call it diesel
1:12:59lung and that’s you know after years of been exposed to Lor’s cheing out these
1:13:06part particles it does make a tiny tiny tiny particles and it does make you
1:13:11cough I mean it’s it’s possibly possibly worse than smoke but I mean the we we go
1:13:18over the top now we want all these things to be electric but actually the new diesel enges are really very very
1:13:25clean as long as long as the filters are working as long as the filters working rightly yes yeah but you’re right we’ve
1:13:31been exposed fortunately unfortunately in our generation to yeah many decades of uh abuse um is radon gas a problem
1:13:39globally or is that just a UK thing in very small pockets of the UK I’m I
1:13:45haven’t looked at this in detail I’m not an expert in it but my understanding is exactly your last bit that it’s a it’s a
1:13:51problem in small pockets in the UK where there’s very high levels and it’s been
1:13:57linked with uh lung cancer I think I think ol near me was known you have to
1:14:02test the cellers to see if it accumulates there and and cancer of course gets more common with age one
1:14:08thing I’ve never understood why are occasional cancers more common in in young people so for example you think of
1:14:14testicular cancer M more common in young men whereas the vast majority of cancers
1:14:19are are more common with with age yes they are why is there a difference
1:14:25there uh gain testicular cancer I don’t think Associated there’s exceptions to a
1:14:31general broad hypothesis of everything this of course so I I think that
1:14:36testicular definely does fall outside that the good thing about testican cancer in young men is it’s completely
1:14:43curable if you catch it very early it’s just incredibly curable um the but thank
1:14:48you for giving me that lead because it reminds me to to make it very very very clear to everybody that the your major
1:14:57risk of cancer that you can’t control are your genes you inherit from your parents yes and they’re so genetic so
1:15:04just because you get a Cancer and this is true you get lung cancer in people who’ve never smoked you get early cancer
1:15:11in all sorts of things but they’ve never been subject to chronic inflammation but we’ve known much more about that it’s
1:15:18more in the textbooks you get these these genetic conditions which make you
1:15:23much more likely to develop Cancers and they you’ve inherited those and uh I
1:15:28mean the one that Springs to mind is the braam mutations for breast and ovarian
1:15:33brca breast cancer exactly yeah yeah Y
1:15:38and of course um if we understand these causes we can take steps to to to
1:15:45prevent it which is the the entire point of this study you know I think that stuff is absolute Gold Dust I was just
1:15:51fasc that’s an hour and 50 minutes I was just riveted all the way through really it’s and it’s really good to get
1:15:58confirmation of some of the things I’ve taught over the last 30 years that they are actually correct because uh uh you
1:16:05know talking to a specialist is is really reassuring in that that respect Professor d gch as always um thank you
1:16:12so much for your time and uh giving us the benefit of of your entire medical career all canned down into one video
1:16:19absolutely amazing not that we’ve done it any kind of justice of course but but but some of
1:16:25the things I’ve just touched over 30 seconds when in fact I could go on for
1:16:30hours and hours and hours in depth of many of those things so I’m just G I’m just giving you the broad brush yeah
1:16:36well if you want to send the list I would be I would be delighted it’s many more things we can do but for for now
1:16:43thank you so much thank you for asking me thank you
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