Ep110 The Origin of the Species - and of our Viral Issue!

Ep110 The Origin of the Species - and of our Viral Issue!

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00:00
[Music] welcome to the fat emperor podcast i'm your host ivar cummins i finally caught up with gabor erdosi who has extraordinary knowledge on metabolism immunology and myriad other vectors of human health and we're going to have a fascinating discussion on this current viral issue and cover some of the key aspects a lot of people might be still wondering about including the origins of this nasty little pathogen and we do also want to get into the
00:32
origins of this pathogen and the most probable origins uh where it came from so that'll be very interesting for a lot of people but we might start off with insulin resistance leptin resistance and this whole modern massive epidemic of chronic disease driven by that issue and there's really two epidemics at least there's the epidemic of that that is exacerbating massively the epidemic of starscore v2 so maybe we'll talk for a short while on
01:03
on how one is connected to the other yeah last time i think we mentioned the collision of uh three epidemics in fact i said that it was the obesity or metabolic disease epidemic of course the viral epidemic and another one i suggested was vitamin d deficiency as kind of a third epidemic so it's a combination or collision of three different problems there are different
01:36
hypotheses about what exactly causes the this interference between obesity or metabolic diseases and uh covet 19 i think what i what i tend to buy into after looking into a lot of details and and mechanistic research is that this virus can specifically bind a tall like receptor which is called tlr tlr the tone-like receptor abbreviation
02:09
tlr4 and this receptor is kind of over activated in people with metabolic diseases already so they have this metabolic inflammation going on a lower grade of inflammation but chronic inflammation going on in their bodies and driven most likely by a bacterial imbalance in in their gut most likely again driven by poor food and lifestyle
02:40
choices so the lifestyle disease manifests in a chronic level of inflammation which is mediated by this store-like receptor for tlr-4 and downstream of tlr4 is a protein called mid-80 air mimid 88 and i think it's very important and further down there is the nf cop pop b pathway which is a
03:11
nuclear transcription factor responsible for all the immune activation observed in severe covet cases you know the interleukin-6 interleukin one beta and tnf alpha and others so this is the central hub for the initiation of uh the so-called cytokine storm in in kovid and it's it's really interviewing that people who live with these metabolic diseases
03:44
um like hypertension uh cardiovascular disease diabetes uh obesity with insulin resistance uh they all have this pathway already hyperactivated while their immune system develops some kind of a chronic tolerance to this so that they don't have higher level inflammation the immune system finds a new balance between the chronic activation of this pathway and a kind of a chronic tolerance and this is when the
04:16
virus comes in uh you have a partly suppressed partly hyperactivated a in kind of imbalanced but i like to view it as a new balance which completely or continually gradually deteriorates and there comes the virus which have rather specific uh characteristics of directly binding to this receptor this tlr-4 which is a little bit
04:46
peculiar it's not fully unique because other viruses were described to to have this characteristic of binding directly but as far as i know not for other stars like coronaviruses so it's an oval feature of this virus which we will i think link into the origins issue later and also a bit a little bit interviewingly this virus features another uh site on its spike
05:19
which is the so-called fulling cleavage site expanded the fluorine cleavage site in itself is again unique to this coronavirus to this source-like coronal virus and it means that it has higher infectivity effectivity higher virulence because of more more proteases can cut the spike from the body of the virus and initiate or mediate the the entry to the to the cell and target cells so
05:50
it increases the infectivity and if you extend the the amino acid sequences and especially how it functionally looks like in 3d it it it's very similar to a staphylococcal um super antigen the enterov and the endotoxin b the staphylococcus it's a bacterial endotoxin which uh we don't fully understand what what it does on a viral spike
06:22
but first it was uh just the hypothesis that it looks similar but later on uh other research found that specific antibodies against this seb the staphylococci endotoxin b can bind and neutralize the virus so if you have antibodies which were developed against bacterial toxin this can bind directly to the virus the viral spike right between the s1 and s2 spike 1 and
06:54
spike 2 subunits and neutralize the virus i mean how comes that a bacterium that they antibody developed against a bacterial endotoxin can neutralize this virus it's very very strange so it seems that this uh this motif it's called the motif which functions not only looks like but also functions as a bacterial endotoxin uh is there and uh and crazily enough
07:25
it the this how it stimulates the immune system goes through the same pathway it joins this mid-88 mrmyd 88 pathway downstream of tlr4 and if it wasn't enough there is another peculiar thing that this virus can do it can bind bacterial lipopolysaccharides these are some debris which the body takes up mainly from from the from the gut but also can be
07:57
taken up from the mouth or from the respiratory system if these bacteria overgrow or if the the barrier the epithelial barrier is broken or suboptimally function suboptimally and this virus can bind the ips and can aggregate these fps molecules and aggregated lps is even more inflammatory and of course this binds plr4
08:28
and goes down the same pathway all the way down to an f cup b and all the interleukins and pnf alpha and the the cytokine storm so it looks like it's specifically can amplify a a inflammatory pathway and if in people in in whom this pathway is is already hyperactive this is like a a huge boost to to a cytokine storm
08:59
so that's that's my interpretation that should be the the major pathway but of course there are other other factors too for example elevated blood glucose is known to increase the cytokine output of of innate immune cells like macrophages so if you have hyperglycemia high blood sugar if you have high leptin levels leptin is also a strong immune modulator hormone secreted by
09:30
adipose tissues from from your fat cells and if if you have too uh ma too many fat cells but especially if you have two large fat cells this leptin secretion can be very high and this again can be can tilt the immune balance towards a inflammatory status yeah that's an excellent summary and some people may need to re-watch that sequence you perfectly articulated it but again there's quite a bit in there i might unpack it a little and just parse it out and repeat it
10:02
and make sure i get it correct interestingly dr ron rosedale i interviewed believe it or not on around april 8 2020 and essentially went through this in layman's terms so that's how early the smartest low-carb guys in the room and yourself were on this thing which is quite shocking but when you mentioned their toll receptor f tlr4 nf kappa b you know we're talking tumor necrosis factor alpha tnf alpha
10:32
we're talking il1 beta il-6 and i could go on and on you know with the pathways we you primarily and myself in lectures as far back as 2017 have been talking all about all of these pathways in modern chronic disease and the driving of chronic disease and poor outcomes and here they come up again explosively now what's fascinating is that this virus kind of didn't evolve along the expected path
11:02
shall we say of the prior coronaviruses this one jumps out of nowhere in a sense and it massively exploits all of those human pathways of modern chronic disease and kind of immunocompromised nature and acceleration of of negative effects from viral uh kind of interactions it massively exploits that which is kind of unusual coincidence maybe but then the virus also as you said the fern
11:33
cleavage site it's got these very remarkable kind of properties again popped out of nowhere that link very closely to human susceptibility to infection so whoa there's two weird things you know and then you start adding on the other aspects of what you said and it's almost like you know all of this happening seems so curious or unusual and but we might get into and we'll circle back to vitamin d because i'm on the track now of the origins and i don't
12:04
think we can defer this for 10 minutes we we get into it the origins is it possible for human technology in the last 10 or 15 years because some people think it sounds like sci-fi is it eminently possible and indeed almost elementary now that you can in the laboratory put together elements to to create a virus some people think that's sci-fi but that's not really sci-fi you can do it the only thing that stops you from doing
12:34
it really is kind of regulations and rules because it's so dangerous to do that technology that it's generally banned but otherwise it's completely within the realms of our technological capability over the last 10 or 15 years is that fair to say i think it's it it doesn't even have to be very very recent technology so the kind of mutagenesis which which drives
13:07
mutations in a certain direction is at least two three decades old it's nothing new and also the gain of function uh experiments published in in the literature partly by these authors and then partly by their masters in the in the u.s they they could do it very easily you need a special tissue cultures special mice expressing the human ace to receptor for example
13:37
and then run the the um among uh certain uh planned circumstances or for a long enough period of time you can you can direct the outcome towards a certain direction and there are recombination techniques so combining different uh viruses in the same host or same cells and that that's that's a different technique and even without direct genetic editing which is the easiest to spot and then you are exposed immediately
14:10
after the first sequencing of a such a kind of weapon so to say i think it can be done relatively easily it's not rocket science anymore even i can understand some of these so it's not not so difficult oh yeah such modesty false modesty i might add but yeah so it's 30-year-old technology and if people want to view it there's two approaches one is to do genetic splicing where you take
14:40
pieces you want and you merge it with an existing viral structure or genetic structure and that one i think gabor you pointed out is kind of easy to spot right because it's a step jump if it's very modern if it's very modern then you could you could theoretically use ai artificial intelligence to substitute the human thinking how how a human would do it because that's what that's what could be spotted the most easily if ah it's a human design because i
15:11
would do it the same way put it together the same way but if you substitute the actual human design and then you use artificial intelligence to mask uh the these uh practices it could be done even with splicing and then uh just entering the the right parameters into the a ai to to to mask these human uh spots and human ways of doing it i think it could be done but we will probably never know
15:42
if if it was done or not but it it it can even be done without those extremely recent and modern practices i think i and i think that's the key thing so the splicing technology which is around for ages uh if you did it in a simple way uh it would be probably easy to spot but as you say if you used ai to design it such that it looked more natural you could probably cover but but that's still pretty complicated but entirely
16:13
doable people need to realize first and foremost it's crucial to realize we have the technology and it's entirely doable now the better way to do it if i desired to do this because i'm a smart guy you're a smart guy we get together we want to do this for whatever reason the smarter way would probably be to evolve it in an accelerated fashion kind of tilting the direction of evolution rapid evolution in the laboratory setting tilting it to end up where we want to be
16:45
and that one would leave fewer tracks by its nature because it would have technically evolved uh it might leave some uh telltale signs but it's more natural shall we say the finished product so maybe we'll talk a little more about that process of evolving a virus in the direction you desire using these humanized mice and other completely available for decades technology and i might add in as you speak
17:15
the papers you'll refer to and the evidence and probabilities i'll add them in on screen afterwards as appropriate yeah i think uh mentioning probabilities uh is a spot on thing to do because i listed all these things that uh the the spike gained a function or a site where the foreign type of proteases can cleave which the same site expanded serves as a
17:47
bacterial super antigen i mean the probability that you have a foreign cleavage site which when expanded becomes a a staphylococcal endotoxin b mimetic as uh i mean mathematically i'm not not as good at mathematics but it should be what is what is a stronger word than extremely low much stronger than extremely low so it's unbelievable yep and i'd say yeah it sounds like it's
18:19
infinitesimally uh low if you will at the same time it can buy the tlr4 directly it can buy and aggregate lps and probably many more i'm not even aware of so uh this to come together by chance i think it's it's totally unlikely well yeah and people need to understand probability the basics so if you have a one in a thousand chance
18:48
of something and independence and probability is very important uh so if you have a one one in one thousand chance of something occurring and something else is one and one thousand chance then together you'd multiply them it becomes one in a million instantly so two improbable things really massively lower probability so one in the thousand chance of the sun coming out 1 000 chance of rain occurring you know put them together it's one in a million they'll both happen if they're
19:20
independent events now if the two are intimately connected it's different but you're talking about at least two or three uh high four highly improbable things and they've all occurred together suddenly in the evolution of the sars type or the coronavirus line so it's it's enormously improbable from the moment you look at it but then there are other things to other clues within
19:50
this virus that point to you know it may not have had natural origins and i think the most striking one and i'll put it on the screen is but you'll have to explain it for me and for the audience your graph which shows the affinity or linkage between human cell lines and this virus and it also shows these mice as being very high on the graph but there isn't the we are talking about the the peptide mimicry that's the that's the proper name um
20:21
yeah uh the the interesting thing that was a really an eye-opener when i first met almost by coincidence you know sometimes i'm i'm uh deep i'm deep into some kind of research it was a immunology research i was looking into vaccine and vaccine triggered autoimmunity which is based on the mimicry the peptide mimicry and also the glycomimicry between the virus and the host the higher the mimicry the most like the more likely is
20:51
that the virus can trigger autoimmune responses in a host and then i was looking at a study and there was a there was a figure columns showing the i think six mare and seven there it means how many people how long peptides are identical and the six or seven uh peptides are identical between different uh animal animal proteins and the viral spikes protein and
21:23
of course there was a high similarity with humans because of it spent a lot of time in humans so you expect a certain level of uh of mimicry uh developing because then you can then the virus can evade the immune system avoid early recognition and so on and so forth perhaps it was a bit too high already for humans but what was really striking right next to the human column high column the same height column was the mice
21:55
musculoskeletal name put under the column the common mouse and the mouse h2 receptor which this virus uses for entry into the cells is one of the worst receptors for for the virus so mice are absolutely not susceptible to this virus unless there is a special type of mice where most strain used in research a kind of
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genetically modified mouse it's called humanized because the human h2 receptor is expressed by the mice so they the surfaces they showed the human receptor and of course the human receptor the the virus can bind very strongly and quickly so this is a this is a research tool uh in in labs and it was described i don't know 2013 14 15 so
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uh six seven eight years ago uh how researchers used it in the in the us and then this research was moved uh to china because there was a ban uh initiated in uh 2014 i think in the u.s this type of gain of function research in modern animals which tried to mimic humans in some ways i was banned in the u.s the financing funding was banned it was stopped and this research was moved to to china
23:29
but funnily enough uh it was still financed by the us mostly for some kind of circumventing this uh this ban and uh i think this this one is this one cannot be explained in any other way how the mice have how mice have uh the same level of peptide mimicry due to a viral spike as humans it's uh it can only be explained
23:58
by uh humanized genetically modified lead mice otherwise we are not aware of any i haven't heard of any natural mouse strains having very close similarity with human ace to receptors so this is just striking i mean uh and uh what was even more uh peculiar was the how the authors went about it
24:32
but perhaps not the authors but the reviewers and the editors it always happens when if you want to publish something you have to accommodate to the to the expectations so they they point out that there is extreme level mimicry between humans mouse and viral spike and then add no further comments whatsoever the only comment is that that mathematically this similarity is extremely improbable that i think that's the only comment
25:03
what they what they did i i would love to see the the original manuscript submitted and the the the exchange between the reviewers editors and the authors because that would be really telling what happened i can imagine that the original manuscript was a little bit different uh pointing out that uh okay this this uh this can have only one explanation because i we cannot come up with anything else and uh but most likely they were silenced all together
25:33
yeah and and again not silenced in a conspiracy theory way though i guess look conspiracies are part of our modern world everywhere whatever you call it i mean uh it's it's it's basic reasoning you find uh some some some figures in in a peer-reviewed uh journal uh article and uh you try to make some sense of it i mean uh you you theorize something or hypothesize something because that's what you do when you see unexpected results if you
26:04
see unexpected results you try to explain and if the if there's only one explanation that comes to mind mind one and after and again uh then probably you are not wrong because uh and i try to ask uh several scientists openly on twitter for example and and they readily respond to other questions but not to this one so yeah what do you think about this
26:34
they don't don't block me or anything like that they they just remain silent they are not ready to take an open stance on on this because they have a career in academic and whatever and probably they are worried that um this could be something which which puts them in the danger zone or whatever well well it certainly would and there's no question there um that if they acknowledged there was only one reasonable technical explanation and that was laboratory gain of function
27:06
and they would immediately and we know this from the past year they would be immediately smeared discredited and attacked all over and putting forward that i wear a team for a hat and everything no but it's it's not about you you bring the technical you know virtuosity the exceptional technical ability and knowledge in in this but you're not an academic and you're not you're not going to be attacked you unfortunately can be ignored
27:37
the data can't be ignored but saying that the data can be ignored in the mechanisms we've just discussed mechanisms are important right so the reviewers look at this they realize to their horror that even though it's just data nothing to be afraid of the implications of what the data says are unacceptable to them to publish because even the reviewers and editors will get attacked if the conclusion points massively towards gain a function because it answers the question which cannot be allowed to be answered
28:09
because the whole color of this whole thing for the last year utterly inverts if it becomes technically clear that overwhelmingly probable is that it used existing technology that's around for decades and it looks like that's where it came from and that explains the four each improbable elements which you multiply their improbabilities together and you get a huge improbability figure and then you've got this with the mouse cell line which makes no sense unless it was part
28:40
of our clearly established technology nothing crazy or sci-fi but stuff we know we can do now if you add to that the improbability or coincidence you know investigators and police are interested in coincidences of course and we should be too the coincidence that this very research is so dangerous by its nature because it will inevitably lead to a big problem that the funding was caught and then it's relocated to china and still funded from america
29:10
i mean there's no conspiracy theory here this is basic logic right nocum's razor and it ends up in uh wuhan i think is that where the laboratory ended up going yes so it's not another coincidence but of course there are only there are only i don't know four or five uh bsr uh three four laboratories um in china so the coincidence is not that high because if there are only five laboratories that
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can do this gain of function research uh it's not a it's only 25 100 chance already true but but it still divides our ridiculously improbable number by another five so at some point but the bats are a thousand miles away again the bats implicated in hosting these types of viruses are a thousand miles away from wuhan in a completely different south eastern uh province of of china so
30:14
that's another coincidence that how did they this bat made it up there it's weird probably by the mouse i think that by the mice so the bats bite the mice in uh southeast china the mice migrate to wuhan and then bite some some people at the food frozen food market so that's that's the most likely explanation what i can come up oh right so we take our tiny probability
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our infinitesimally small chance of it not being as we perceive from the data and you got to divide it by another thousand or whatever pick a number at this stage it doesn't matter how high can you stack coincidences before the whole thing topples over well i think in this case it's possible it it evolved naturally anything's possible but i think the sci-fi right the conspiracy the outrageously
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improbable ridiculous thing that's tin foily is to suggest the existing narrative right rather than the one we've described so it's quite amusing there is no existing narrative i mean even the whole uh investigation concluded with something uh totally panel i mean it's uh they they said that it might have come from frozen food or whatever which which which hadn't even been
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brought up before as a possible origin theory so it's it's just i think it's just a joke there is no alternative at the moment uh no no real alternative which could anywhere anywhere close to what uh these uh um the the data suggests yeah well you know phrases bring to mind from my corporate career and my my career as a brutal realist and the scientific thinker phrases like realities don't mention the war
32:16
you know phrases like too big to fail there's a reality in modern human world and probably going back thousands of years that some things when they're realized are just literally too big or too awkward to really have become become known it's just too big and we've seen there for the last year the enormity of this thing the absolutely disastrous response and interventions which maximize the impact of covet debt right alone maximize that with all the
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lockdowns and nonsense and then the impact of the lockdowns on general life freedoms and economy and economic determinants of health and everything we hold dear just beyond enormous negative impacts for nothing and now we've got this that if it came out let's be honest if it came out that look guys overwhelmingly on five different vectors or points of probability it's almost certain that this was part of our existing technology
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and it was call it a mistake but it happened the world cannot cannot digest that this whole thing came out of human technology i mean they can't it's too big to fail you just can't you simply cannot have that become a reality the knowledge you just can't because the implications are too horrific the con you know so it's not a conspiracy theory it's just that if i were a high level senior manager or vp involved in this whole thing
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and i realized to my horror what we're describing i would have to perforce uh get involved to make sure that this just didn't go out in the press because i would know regardless of how i feel about it and how terrible it is and unfortunate if it was a mistake i would know intuitively it can't become common knowledge not because i want to hide it but because i just know the implications are too messy
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and and at this point we simply have to bury it we have no choice even if i think it's awful and terrible and even if i would love the truth to come out i would be forced in my position to simply make it go away there is no choice politically so that that's the reality and you mentioned i'm gonna i want to segue into something that you touched on there and what you said ah it was the old bats so that's how this thing started bats right in caves
34:51
1000 miles away but how did the bats line up and the other animals in that mimetic graph of points of similarity and i'll show it again the screen how did other other animals line up because one guy is a real good guy i know in south africa or perhaps somewhere else leo looks after apes it's his life's um work and he said that apes and that species usually get hammered by human flus and there's a lot of overlap in ape
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world if there's a bad flu going in human world people have to suit up before they come into the reservations it this is known but apparently remarkably the apes seem to be clearer this one which is remarkable in itself so maybe we talk about the other animals that don't line up and including the bats yeah though the bats are actually the bats most closely implicated in uh potential uh zoonotic um
35:52
transmission uh don't really um harbor this virus i mean these wires cannot infect the the bats because uh their ace2 is so distant from from this one that the bats are no not host anymore uh to this uh virus the interesting thing you mentioned and we can refer to the same graph back again the the peptide mimicry is very low between between the
36:22
sars 2 spike and other coronavirus spikes and also non-human primate proteins and other roland with the exception of mice and rats live common lab animals also the rats not to the extent as as the mice but rats also show somewhere somewhere in between other animals and mice and humans halfway in between that's also a little bit
36:55
peculiar uh probably less experiments in redstone in mice i would say and we will go a little further with this now don't want to beat it to death but i'll ask one question before i go on to the rats if you had i don't know a million researchers who are familiar with this field and you impossible in real life but there are a million completely unbiased researchers magically a thought experiment and you bring them in one by
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one and just show them the most salient data and say what's your conclusion i'm guessing that nearly all the million if unbiased with no political or no knowledge it's a it's a it's a theoretical question and they they know nothing about any implications in real world politics or anything else would generally all the million independently look and say well yeah i guess it it it has to be gain a function
37:56
would that generally be the case i think the vast majority would ask for some time to to do their own investigation their own reading research into into this to to make sure that i'm not presenting only one half of of the findings uh in a way to to uh to confirm my my biases uh i don't really have biases but that would be that would be what i would do if i'm if i'm if i was presented with a new
38:28
hypothesis with some data i would look into the other side of of probably or hopefully refuting uh information so i would look for refuting information first and i think most of what most other researchers would do the same so have a look at how how else this could have materialized um and through natural developments recombination or whatever
38:59
but again i think they would eventually come to come to the conclusion that the probability is not on their side so yeah one or two could could happen by a complete random recombination between different viruses one harboring a foreign cleavage site another one not harboring the fooling privileged side infecting the same immunocompromised person and and then a lot of proliferation viral uh reproduction going on and then
39:30
in the same cell the the highest recombination always occurs uh in the spike so that would be natural that's not a peculiar thing at all uh so so the foreign cleavage side could be explained but then you add the the the bacterial super antigen which is an extension of the of the foreign cleavage side then the direct binding of tlr4 then then the direct binding of
40:01
polysaccharides bacterial polysaccharides then you have a look at the um the the peptide mimicry with the mice i think when you add up all this together it's it boils down to probability and then this is so minuscule probability that all this happens by a natural recombination of very different viruses that uh it's it's it's not a plausible explanation in my opinion but uh i still cannot exclude
40:31
that there is some explanation which i which i haven't found yet so i might keep thinking about it but i couldn't come up with something like that and and that's fair enough and you have in fairness always held my feet to the fire and all of my hypothesis and beliefs as well with that popery and her professor her doctor carol popper look for the black swan that undermines the hypothesis and there you will find gold there you will find you may have been incorrect and you think that way and agonized like i do
41:03
so whenever everything fits too well and i think this fits with what i expected as well confirmation bias be extremely careful look for the black swan against my own hypothesis because that's the only way you will get to scientific truth is to constantly challenge your own hypothesis so we're we're well embedded in that but let's just to finish the thought experiment with these million theoretical guys let's say that you are able to assure them for the purposes of the theoretical question that what
41:35
they see is largely what they're going to find if they research given that and assuming that what would they say and i suppose in that case you'd have all but one or two kind of cranks acknowledging well based on that data given that it's pretty complete um of course you would have to say it goes through the the human design process you would think
42:04
yeah then i think we can continue to speculate about the consequences if you accept that there is a chance at least there is a good chance that the virus you said the right way came out because it either leaked technically it either leaked or was released there are two options then i'm not saying because there is absolutely no information about this but if if you think about lab origins then the next step is considering leak or
42:37
release um and and of course the first thing one should consider is why this type of virus why directing uh the evolution of a virus in this direction and if you if you have a look at the outcome uh it's a virus which can produce disturbance it's not a killer virus i think we could the two of us could design a much better killer virus in a lab so this is not an
43:10
ultimate biological weapon to kill the highest number of enemies at all this is a virus which if it was designed it was designed to create disturbance what kind of disturbance and then uh is it a coincidence that it and virus kind of preys on old and ill people and um and what what what kind of enemy
43:42
it was it could have been designed against so if you would be uh just based on the outcomes the elderly the metabolically challenged people fall victim to this virus what is how a kind of enemy looks like and how my own homeland looks like it should be different different from the from the perspective of spread and harm disturbance done
44:15
and uh you clearly see that those populations with higher age and especially age combined with obesity metabolic diseases come out the worst from this pandemic so it's kind of uh attacking populations with high rates of of obesity diabetes cardiovascular disease and and also having a lot of old people
44:48
within the society so that's my speculation completely speculation yeah fair enough and it is speculation it well it's a reality in the fact that that's the case but then tying it to intents is speculation and of course the accidental or the intended uh kind of intentional release is will never be known but it kind of also just nicely fits if we add one more thing
45:19
that the eastern areas generally will have more t-cell cross-immunity at to prior sars you know we're assuming from many papers that there is an advantage there an immune speed of reaction and mitigation of severe impacts by having a more history with the prior sars if you add them together it kind of explains my world diagram which for me screams to me as an engineer if you draw and i'll show it on the screen if you draw a map of the world you've
45:51
got huge vast regions typified generally by what you said more older more metabolic disease more immunocompromised more autoimmune from bad foods all that stuff huge areas typified by that and also largely typified by having less exposure to prior sars perhaps but those vast regions of billions of people regardless of lockdowns or masks there's
46:21
a 30 times greater effective impact in terms of icu and mortality 30 times yeah i saw that so that many asia-pacific countries implemented different strategies different mitigation strategies japan is not the same as taiwan or or vietnam or or india or australia very different strategies
46:53
yet the outcomes are are very similar and i think that that cannot be explained by the interventions themselves because uh in my view only one thing can explain uh such such differences in outcomes is uh and it's it's immunity what kind of immunity whether it's pre-existing or it's just lower levels of of metabolic diseases different demographics much much lower
47:25
levels of elderly or a combination of these or pre-existing immunity for whatever reason you mentioned a few it could be unnoticed source like coronaviruses if there was a prior virus spread for example which didn't cause severe disease only only cold for example with with the similar but not identical antigens
47:58
especially not the antigens what we are measuring with the pcr for example or with the with the antibodies it's plausible but you don't even see the zero prevalence studies from these countries i haven't seen a a nationwide representative prevalent study from new zealand for example or or from from japan or from taiwan or from china china would be the most straightforward but nobody's doing it
48:27
why it's it's very weird because that's the information you could base some conclusions on that uh if there is uh really uh higher pre-existing immunity or or now existing immunity to to to the same or very similar virus which actually reacts uh or shows up in in antibody tests it cannot be said it cannot be no cannot be known at all because there are no studies going in looking into this it's weird it it's truly shocking that
49:00
new zealand there are no t-cell studies to show history of sars kovi to exposure or indeed what we're describing cross-immunity and i'm i'm going to come back to and i don't want to forget it back to that 30 times difference of impact to to drive it home to the listener but i must mention there's one study and it's the study i would have done as a problem solver back in march april and done all ever since and the study is to take several hundred
49:31
random people and repeatedly do antibody tests every two weeks and then you would see the tempo of the problem and answer the questions we're asking and they did it in tokyo they took around 400 people in 13 districts of tokyo where there was no lockdowns but there was kind of mask stuff and they measured their antibody status repeatedly every two weeks and the pcr went up in tokyo surge in these people and down again tailed off as expected
50:03
went up to 30 plus percent or whatever and their antibody tests nearly 50 percent of this sample group got up to positive antibody for cyrus v2 and then they began to decline so in other words tokyo this is unquestionable did not stop the spread they actually got infected in huge quantities but the impact level in icu and debt was just very small so it kind of
50:35
answers our question and isn't it incredible that there was only one such study really done the most important study of all serial antibody tracking to see the actual tempo of the problem so so there's that and i'll put that up on the screen but the other thing is to return to the example what we've got from pure logic poparian logic whatever and actually people just need to think about this really so imagine hypothetically i said to you that there's a surge in
51:06
skin cancer right but wearing black clothes all over can greatly reduce it okay that's the analogy for lockdowns and masks but then you turned around to me and showed me a map of the world and said hold on a minute okay so the skin cancer is kind of going up everywhere but the areas right europe and north america and other areas with billions of people where they're doing most black clothes wearing right they've got 30 times the rate of the skin cancer problem and you're telling
51:37
me the black clothes are the big thing to help lower and the regions that are wearing black clothes intermittently and some of them not really at all are broadly with billions of people around 30 times less skin cancer so that absolutely disproves resoundingly that the black clothes are protecting you from skin cancer and that's the analogy for lockdowns and masks i mean we have sweden we have florida and we have all the other country examples the evidence that kind of disproves the lockdown mask
52:09
effectiveness that's true but also at a global scale the people with the most lockdowns the most masks draconian by law all over have around 30 times the problem right so anyway it's just i'm pulling my hair out at this stage even though i don't have any but there we here we are yeah it's it's it's all about properly properly working the immunity i think it's uh
52:40
and then uh all the factors we mentioned vitamin d and others uh channel into this perfectly so it's not a immune immune booster per se it's a immune enabler or balancer so if you if you have it naturally you should have it because you are out in the sun we have evolved to be out in the sun and then in the northern or really southern regions uh we can store in our fat tissues uh the vitamin d so
53:12
it's coming out during the winter but you still become depleted by the time of february or early march when it uh when the sun is strong enough again uh in these areas by the way next weekend if the weather is nice i will try my first sun bath this year because it should be the time that's that's the threshold when it's high high up enough so um i encourage everybody to do that as soon as he can until that take supplements
53:44
or buy a sporty lamp or a uv lamp or whatever but anything is better than just leaving it up for for others for for politicians or scientists to to solve my own problem because my immunity is my own problem so um i wouldn't expect others to solve my own problem all the time and expect others to hide because i failed to lose 10 kilograms or 25 pounds of weight in one year
54:15
already we are approaching one year of of the outbreak the international outbreak end of february tomorrow is march so i think in one year you can lose 30 kilos if you want or 50 or whatever x axis you have 100 pounds and if you haven't done it it's not a problem of the politicians or or scientists or medical doctors this is your own problem so so they take take your health into your own health
54:46
own hands that's my my primary advice excellent now that's great way to draw to a close but we're going to come back and talk more about this and maybe talk more about vitamin d perhaps not today but there's already been a lot said about it and one thing i'll say as well is the sporty lamp is very expensive it's an excellent fda approved and human tested uv lamp but it's very expensive and a work around my wife actually got from a guy in canada
55:17
super smart guy in keto on low carb and he figured out reptile lamps so you can buy 160 watt reptile lamps which are the full sun spectrum with uv and everything in infrared perfect lamps to generate this and they use them for reptiles because reptiles drop their vitamin d their bones get brittle and they just fall apart but you can buy them for around 45 euro each get a few into an array and have yourself a pretty super cheap um you know alternative uh when
55:48
the sun isn't available or if you rather get it naturally then by taking pills uh you can do something like that so just a tip there entirely up to the individual of course it's not approved or regulated for that use but most people now are getting pretty smart in the circles we move in to look at the uv density and look at a few of the numbers and and use anything like that appropriately so great stuff gabor and i might split this one up actually into the origins
56:19
and the uh the other all the other content we talked about because i think the origins really is a self-standing discussion so i might do that afterwards and you can send me all the papers to feature on the screen so super duper as always fantastic to talk to you any last thoughts or will we leave it with the vitamin d thought and the lamp like you said i think that's that's good enough to close up the discussion really great stuff we'll be back though thanks again for having me well thank
56:50
you gabor the best content possible um with the best science and the best approaches and mechanisms and just a reminder that i do need support to continue putting together all of this content and at patreon.com forward slash ivor commons or for paypal at tinyurl.com forward slash iver commons where you can do a one-off or a monthly support so i'd really appreciate that guys and keep me getting the science out
57:23
there and countering perhaps the more biased corporate type science thank you

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