I still want to see more analysis of MHC haplotypes vs infection severity!! So much money has been thrown around these last few years and so little of it has lead to constructive, actual scientific inquiry.
Citizen funded analysis and research via substack et al (you, Kevin Mc, etc, etc) has made the efforts of the "scientific" (bah so political) establishment look mediocre at best.
Did you catch "A common allele of HLA mediates asymptomatic SARS-CoV-2 infection
https://www.medrxiv.org/content/10.1101/2021.05.13.21257065v3" - strength is that it reproduces the finding in two systems (San Fran and UK). That's more an insight into preexisting immunity than resistance to severe outcomes. For the former I still think it's mostly a tapestry of stochastic events determining whether the immune system kicks in with an early adaptive response. I.e., the lucky pre-immune are "weird," and severe outcomes are not explained by some one weird thing, but a lot of dice rolls put together among normal kids and adults.
I remember why I wanted more analysis of MHC haplotypes - it was in aid of debunking "X country filled with a specific genotype did better than country Y with a race-level delta in genotype coz [lockdowns / vaccine uptake / mask adherence/ they wuz kangz /etc]".
But as I remembered this, the goal seems moot now. Is there a single country not experiencing excess deaths? Is there a single country that did not experience remarkably similar IFR? I don't think so....
"a lot of dice rolls put together among normal kids and adults"
Batch quality IMO being a major one.
When I first read about myocarditis, it was 3 junior Belgian cyclists from the same team in one hit. Reeked of a batch-specific anomaly to me, given the popularity of cycling there, the number of riders (which requires juniors) and my memories of doing things together with friends I hung out with as a kid (ie they all went to get vaccinated together). Pure conjecture but uh yeah that was my thinking.
Have also seen couples / families suffer closely spaced reactions, indicating genetic or temporal (= batch) similarity in causes.
Apologies for asking the bleeding obvious, but does the calculation for efficacy take into account pull-forward deaths and the likelihood (my understanding only) that viruses evolve to be milder [to leave their infectees more long-lived and transmitting vs more deadly with shorter victim lives and thus less chance of transmitting]?
To test this you'd need:
1. comorbidity data for deaths (we sometimes got some of this - avg was 2.4 for Australia, from memory)
2. virus deadliness measures (No good idea how you could measure this unless with a live virus sample injected into mice?)
If we killed chunks of the comorbid patients up front, then vaccinated the less comorbid and those lesser comorbid were infected with a milder variant, it could convincingly look like vaccine efficacy.
What potentially happened is hardier / healthier people were infected with a milder variant. Vaccine still potentially does something for comabting virus, not denying that.
There's no reason to discount for pull-forward when seropositivity is low after all pre-Omicron waves. It's essentially like asking "should our 12:05 o clock lunch clients be as hungry as our 12:00 o clock ones?"
You might counter that this shouldn't apply to excess deaths because the virus is only killing those who were about to die. Says who? Again, if the seropositivity rate is low, e.g. 3% after the B.1 / spring 2020 waves, then we should assume that it has only killed 3% of the about to die. So you only have a .97 discount on daily normal deaths, and you can tell at a glance that this isn't going to eat back at your spring 2020 excess deaths spike. And by the time you get to Omicron, three years have gone by, now you are close to 100% seropositivity in some countries (very low still in others) and maybe we will start to see PFE this year.
Do you think that people who encounter the virus always have IgG seroprevalence? Seroprevalence for the entire population is not an adequate measure of how many people may have tangled with the virus, and can not tell you how much dry tinder in the vulnerable population the initial exposure may have burned. Also, the IFR is how we know it pretty much only kills the "about to die". I find a lot of your comments and reasoning confusing and somewhat difficult to parse, so sorry if I speak from a incorrect understanding of your positions
Broadly, everyone (except those who seroconvert) is getting some level of encounter without infection / antibodies at any given time after 2019. Additionally, some infections won't result in seropositivity due to assays having to use high cutoffs to achieve selectivity, plus antibodies waning.
But the burden of proof is on the assumption that susceptibles have been reduced to show why we should harbor some extremely complicated model of the virus killing everyone it can without most people getting sick. Because it is just that - an assumption - which is all I am pointing out. It is based on flu, but flu pandemics (subtype crossovers) have always been true "pandemics," basically half or more of the whole world gets sick within one or two waves. SARS-CoV-2 is transient and elusive until the Omicrons, which is why I am open to a bit of skepticism on whether the virus could really spread on its own before then.
As such, I see no reason to assume susceptibles are meaningfully depleted - the discount of previous deaths should not be assumed to outweigh gains in virulence as occurred with Alpha and Delta, so we should expect more deaths in 2021, not less. The exceptions are Italy, UK, and NYC, and I think the iatrogenecide hypothesis is strong for those outliers.
I think the IFR for Delta in the unvaccinated was rather scandalously high, but this points to suppression of early treatment and subsequent hospital mistreatment, likely killing 10s of thousands as I have said before https://unglossed.substack.com/p/the-american-unvaccinated-holocaust - these deaths go way younger than the first waves. Again we are looking at potential iatrogenecide.
So if the virus is just a cloak for a lot of murdering of people who wouldn't have died otherwise, there wouldn't be any PFE. Or if it's a mix of being deadly and being a cloak for murder (I think likely), then no PFE.
Well for 1, the north east and especially NYC, follow a gompertz curve with their ACM that seems to start before lockdowns are declared. While I agree a lot of their death is iatrogenicide, that is one of the few areas I would argue looks more like a spreading virus killing the population, than others, some that don't seem to follow said patterns and also seem to coincide with the WHO declaration of a pandemic (disruption of normal care? panic?). Second, what evidence is there that Delta was more virulent than Alpha? I was not aware of this, and it's something I find rather doubtful. If you are arguing from an exposure perspective with the ACM (amount of populace exposed due to transmissibility), then there is a trade off there. Increased transmissibility nearly always comes with less damage to the host. the host can travel farther and spread more material. A living, moderately mobible host is the evolutionary objective. There's also another big issue from my perspective (unless I still misunderstood you). The ACM for 2021 starts getting out of control in the summer months. Also, the ACM in 2020 alone clearly indicates, for at least America, that portions of the populace were well exposed. The ACM distribution being mostly elderly also shows us who died in the greatest degree, and while I do not trust the accuracy of PCRs, they ARE adequate for tracking the presence of genetic material. The viral genetic material traveled far, killed the old (and by proxy exposed the young, many of which likely didn't even seroconvert). We certainly helped a lot of them die with our care, but a lot of people were exposed. I completely fail to see how any of that would make people start getting sick again in 2021, and that it would be in the younger population, with a higher ACM. A certain percentage of the youth should have been exposed, and a large portion of the dry tinder was again, culled. Idk what the "pull forward effect" is, but if you are referring to the lack of mean reversion in the average ACM (never falling below average after being above average) then I quite simply disagree with that as well. It should have happened in 2021, the virus just isn't deadly enough to the young to account for the ACM we have seen, and what is occurring in the ACM data is not explainable by deadly viruses https://www.medrxiv.org/content/10.1101/2022.10.11.22280963v1.full.pdf
I don't mean to bust your balls though. I'm admittedly rather rusty with all this data, and I have never been great at math or statistics. But if I didn't misunderstand then I don't agree. 2021 mortality should be lower. Much lower. below the anticipated average in fact. I'm sure 2022 also shows us how shit the "vaccines" are
Previoulsy PCR+ and/or currently naturally seropositive consistently PCR+ at a lower rate than general population at all points after mid-2020, as in the Shrestha Cleveland Clinic series, multiple MOH and UKHSA reports, etc. So this means the rest of the population "doesn't have something" as far as immunity to infection going forward in late 2020 and afterward. The only question is how many future infected were always susceptible or how many become susceptible. E.g., ok Kindu et al. find that contacts who avoid infection have expansion of cross-reactive T Cells. So is it a) these people turn into next year's infections, or b) next year's infections are just the completely non-exposed? We don't know. But we do know that most of next year's infections are people who didn't PCR+ / seroconvert last year. So *at least some* people who didn't get infected are still future susceptibles. There is fuel left, regardless of what interpretations of the biology would lead us to expect.
However, what's perhaps important is whether the biology says (a) is impossible because if so, maybe we should expect diminished waves, i.e. the discount on future waves should be larger than who seroconverts / dies. Well, no, (a) is perfectly possible because innate immunity is variable, with the toggles on antiviral / antifungal / antibacterial cytokines always modulating. Expanded cross-reactive T Cells could be enough when a contact was exposed while antiviral toggles were high, but not if exposed again while antiviral toggles are low. (There's also of course viral mutation e.g. did BA.2 evade pre-existing recognition of SARS-1, leading to finally getting traction in East Asia? https://www.biorxiv.org/content/10.1101/2022.02.07.479349v3 - but mostly I want to limit to the innate immunity question.)
Finally, from an evolutionary standpoint, revolving door innate immune defenses make sense. As you say, adults have poor innate immunity. In fact immunosenescence arguably begins with puberty. So there is a window where we are still reproductive age but the front line is not as reliable at keeping us alive. It makes sense to lower the front line periodically to go ahead and see what makes it over the gate, invest in adaptive response to the same, so we don't have to worry about that thing later when innate immunity can no longer handle it. There's other biological evidence for this sort of "inside job" approach to giving our viruses a boost, e.g. Lymph Node Subcapsular Sinus Macrophages which act as virus farms inside our lymph nodes. Additionally, this kind of peace-making lets viruses thrive without having to overcome innate immunity even more than they do, which once again would seem to be evolutionary beneficial (more baby-making beyond adolescence).
So, with this and the other comment, you have mounted a case to answer my request for burden of proof. But I feel we are talking past each other a bit when it comes to "what should we expect and why should we expect it." I think this has to do with your interpretation of innate immunity which essentially does not allow for dry tinder to exist after 2020. Let's set that aside. What is actually very determinative about the existence of a gompertz curve? Nothing. A fire that only destroys a thicket will look the same as one that takes the whole forest on a graph when the y axis always scales to the top of the curve. But the supermajority of people of all ages still did not get sick and are still alive. Again, your biology argument asserts they can't get infected later so there is no need to worry about them. But without the biology argument, the case for there still being dry tinder is obvious.
The following is essentially axiomatic: As long as 1) "the killing thing" we are examining 2) "can kill not-about-to-die" and 3) "doesn't find most people" the first time it passes through, then more people are going to be killed later if it comes back. Even more if it gets better at 2. This is true regardless of IFR by age until you get to certain equilibrium points related to 1 competing with other risks (ie humans are not immortal). So you can't refute any of this with IFR by age. So like I said I think we are talking past each other because on the non-biological argument you are merely stating facts that I don't disagree with but don't find determinative. There is no actual proof that the virus only killed the about-to-die in 2020 except maybe in the aforementioned hotspots, it is just an unfounded assumption.
Delta is the most fusogenic variant in vitro thanks to P681R and is more pathogenic in animals. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8828475/ Humans are a trickier measuring stick since the vax confounds things, but studies from myriad health systems show upticks in hospitalized deaths when Delta arrives, most recently https://www.medrxiv.org/content/10.1101/2023.02.15.23285759v1 fig 5 but going all the way back to the CDC Provincetown report combining Fisman, D. Tuite, A.; Ong, S. et al.; Sheikh, A. et al. all finding the same thing.
Delta got more virulent (and maybe more contagious at the same time) regardless of whatever evolutionary theory thinks about this.
I am pressed for time, but I see a glaring issue. I am not asserting they "can't get sick later". I'm asserting that a larger portion of weak people than normal died, while also exposing a certain percentage of young, healthy people. Dry tinder comes back progressively each year and the space of time between 2020 and summer of 2021, is too short, which is when ACM picks back up. It's also too great, if a percentage of the population has gained immunity, and the elderly have been exposed. You said yourself these things take half the planet by storm in 1 to two waves (generally yearly). In a normal environment, a pandemic of this nature, will result in a mean reversion the following year, and for it not only to not occur, but to also be out of whack in the summer time, is very concerning. I am arguing from a holistic perspective: society and people obviously are more resilient to SARS 2 the second year, than the first, due to fast and abnormal removal of the normally slowly killed populace, and exposure of a certain percentage. SOme of those people were not infected in 2020. Some will still get sick despite being young and healthy. A small amount of "dry tinder" will return by winter 2021, as populations age. But again, for ACM to be HIGHER in 2021, well that's just an absolutely terrible look for the thing that was forced into everyone's arms, and the evidence for it being covid is very weak to nonexistent when you contextualize it with what age brackets are dying in 2021 and the covid IFR for those brackets, at least in my perspective.
Do you mean me? If so there there are a lot of reasons. The first being, (I don't have them on hand ATM) there are studies that show people in the same household with infected individuals, yet who do not display symptoms themselves, develop memory T and B cells to SARS 2, yet do not seroconvert. The reasons for this are actually very simple, when you have a firmer grasp on immunity in general. For starters, SARS 2, influenza, and similar respiratory viruses, are highly mutative and fast spreading, and start their infective process at a membrane barrier in your respiratory or digestive tract. You have two branches of immunity, one called the innate immune system and one called the adaptive immune system. The innate immune system, as much as they wish this were not true, is the main defense against things like res viruses. Things like mucus, the secretory IgA system (which are generalized antibodies in/on the surface of the membrane, and do not require infection with a specific pathogen to neutralize necessarily, as they tend to target conserved regions) and inflammation all come first, which of course prompt the arrival of things like dendritic cells and cytotoxic T cells. Before we continue, a thought experiment. What are antibodies? They are globular proteins. How are proteins formed? Inside cells using amino acids, which expends energy and cellular resources. So next, ask yourself a hypothetical, what is more effective, confiscating all the guns in a region, or blowing up the gun factory? These are the reasons, cytotoxic T cells and innate immunity are your main defense against these pathogens. Because late stage, humoral based IgG antibodies to specific viruses, when you are presented with hundreds of thousands if not millions/billions of different viral strains every day, are not an effective means at stopping an infection that occurs in this manner. If your body did that, your blood would be nothing but sludge due to all the antibodies. No, the body wants to identify and destroy the infected cells at the barrier, BEFORE it is compromised, you feel sick, and IgG has to be used to try and clean up the mess. This happen every single day. Not a day goes by that this system doesn't destroy cells and keep you from getting sick. Turing off things like linked recognition and the compliment cascade before they complete their processes and you are flooded with globular proteins is again, the main objective of your body. Life doesn't waste resources when it doesn't need to, or well, it wouldn't be "life". It would be "dead". This is not true for all viruses though. Some have different infective routes and mutative rates. For example SARS 2 stays so consistent because it has a proofreading helicase for its massive genome, but other viruses may be completely different. Some of those are likely early childhood disease we have effectively vaccinated against (polio maybe) but my knowledge of other vaccine tech is admittedly not great. The main point is though, if a virus is controlled by the innate immune system: generally it will harm the old, more than the young, because their innate immune systems SUCK. That is really one of the main things that kills people. Get old, T cells suck, get the flu, it goes crazy because innate immunity now sucks, and adaptive immunity is also too weak. Then you die. If it is more dependent on the adaptive immune system, then it seems likely that it will not only infect the young a lot more (poor adaptive immunity due to lack of presentation/experience) but also that it MAY be beneficial to vaccinate against said virus in that situation, though I don't KNOW that. My main point is: res viruses that are controlled by the innate immune system, doesn't give a shit about how much IgG you force produced in your blood, and your body doesn't want to make specific antibodies to one virus if it can avoid it. This translates into "people get adaptive defenses but do not seroconvert", and likely at much higher rates the younger they are. This is also, why SARS 2 doesn't generally kill kids. They have the strongest innate systems, and the weakest adaptive ones (when they are really young)
The mystery I have just described to you, is "asymptomatic infection". However the powers that be would never tell you, that pinging positive on a SARS 2 PCR yet having no symptoms (or antibodies to SARS 2), is a GOOD thing. Asymptomatic infection means your innate immune system did exactly what it was supposed to.
Edit: What I have just said about pinging positive with no symptoms only applies to the unvaccinated, especially since the vaxxed have started producing IgG4, a non inflammatory antibody that usually only is produced for allergens like pollen I believe
Anecdotal icing on the cake: I met a cancer survivor (I think? been a minute) who had "IgG deficiency", yet lived through two SARS 2 infections.
Yes, some proteins are "conserved" across viral families. Idk about nucleocapsid, but I'm pretty sure the non structural proteins are more likely to be conserved, like the polymerase which copies the RNA. There's only so many ways they can be made and changes they can undergo before they lose function, so as such they must be similar across all viruses. Spike is a structural protein that is used for receptor binding. It is the exact opposite of "conserved". Again sorry about short answers, I'm rather pressed for time
Is it possible I have not seroconverted? I think during the pandemic it was grounds for Dr loss of license if you ordered or did a seroconversion test here in Australia, not sure if it still is.
One of the first things I did when this all started was get copies of Rohit's (dry and dense, but worth it), Basic imunology (Ian Orme, brilliant read), How the immune system works (Sompayrac good read) and Janeway's Immunobiology (another good read), so there's nothing challenging in your description of innate vs adaptive immunity other than the rustiness of the passage of time.
It was my understanding that T / B cells against invaders are "taught" in our lymph nodes. I had a C19 infection after catching it from my vaccinated housemate. I got swollen tonsils (1 really bad day + an ordinary day either side) and diarrhea , they had body aches and pains, fever, fatigue, etc. As did another random person I was in conversation with 6 months later.
That to me (could also be wrong) was the classic tell of "natural" infection mediated immune response vs vaccinated infection immune response, although I wouldn't confidently state the mechanisms in any great detail. I am not young, but am fitter and healthier than probably 99% of Western society.
I'd say the inflammation is an indication you did at least do some seroconversion, though possible you still didn't reach IgG stage. People really fail to realize the sheer amount of viral material around them at a given time, especially if they are around other people. Every day you likely beat a asymptomatic infection. Swelling indicates cytokines and inflammation, which indicates that many cells have been infected in a location, and a battle is being fought there. The "taught in our lymph" you are referring to, is something called linked recognition. https://webmedia.unmc.edu/eLearning_open/COM/Linked_Recognition_Process/story_html5.html
In order for this to occur, two things must happen. Cells must be destroyed, and viral debris must be drained to the lymph. This may put out all the various types of viral proteins being produced (N protein, non structural ect.) Also, the T cells doing the destroying (or some family member of them) will acquire proteins from the site of infection. they choose specific proteins, and then migrate to the lymph. The proteins carried by your immune system, must match proteins that were drained to the lymph and picked up by B cells. This is how your body determines what proteins to fight against if it is going to use adaptive immunity, and again, this process can be cancelled/prevented if it is no longer needed, i.e. the T cells handle the infection before linked recognition occurs, and B cells that matched T cells start to proliferate.
EDIT: I can't recall the mechanisms for stopping linked recognition. I know the complement cascade has them, but linked recognition I'm not sure about. It may be that you simply don't reach this stage because enough cells were not infected or enough material was not drained, or perhaps the creation of memory B cells after can be controlled. More research needed. however anything that uses cell resources and creates proteins to fight infection, will have some type of control mechanism, to reduce or stop them when not needed. That just simply has to be true from a biological perspective, and is also how the rest of the body works with nearly every system (feedback, turn off? keep going?). It may take a lot of digging to determine exactly how linked recognition is controlled, and it may not even be well known in current science
EDIT DONE:
Now imagine, if instead of this presentation, your body started producing spike, and only spike, in muscle cells. There is no chance meeting of combative T cells with growing memory B cells. There is no nuance and additional material. There is only spike, and a shitload of it. I can find nothing about these products from a biological perspective that makes me think they are good at anything other than making a bunch of now evolutionarily irrelevant spike, and by proxy totally fucking up your normal information acquisition (natural infection)
I THINK I finally get what you meant by this sentence Brian. And I have now provided you with the explanation. It's what I posted above
"But the burden of proof is on the assumption that susceptibles have been reduced to show why we should harbor some extremely complicated model of the virus killing everyone it can without most people getting sick"
Old people died a lot because of our care and their weak innate immune responses. "most people" didn't get sick because "most people" are young, and will get defenses without even needing to seroconvert in most cases
Seropositivity might be higher for the older age cohorts who are susceptible though. In fact I think one of the main reasons why elders are at an increased risk of dying from respiratory disease is the reduced ability of their immune systems to react to new threats.
That being said I really think this culling effect might be quite a bit more grave than what we are used to from seasonal flue.
Look at the 85+ group here. We see something similar for Alzheimer proportions if I remember correctly. Ironically Alzheimer mortality is the only type of select cause I found to correlate positively with vaccination rates ever since the campaign began. So the culling effect of SARS-CoV-2 and the vaccine might actually affect different populations.
It's not just population size that's changing, it's also the composition. We might have to look more at how people are dying.
I made this website to visualize this. Just for my own reference really, but maybe this is interesting to you as well: https://cdcsucks.pervaers.com
When we praise the vaccines for their efficacy, we should keep in mind that there is a good chance we wouldn't need a vaccine anymore if it weren't for the leaky vaccines. This whole Delta wave thing is not natural. It seems the vaccines reduced the evolutionary trajectory of SARS-CoV-2 to zero. Delta was sequenced all over Europe since late March 2020. It never had a growth advantage until vaccines came along. Cost 220k people their lives within half a year in the USA alone. So really... Efficacy seems more like an individual thing here. On the population level it may as well border on -100%. Vaccine decision was sort of like an an unblinded prisoner's dilemma (probably more like extortion), without taking into account that there were also times at which vaccines reduced your chance of survival (like Q3 2021 in the USA).
A claim that it might be Vitamin D deficiency that is causing the problems, because your immune system consumes the activated form of D3 when it creates antibodies. So, if you are low to begin with, after the gene therapy treatment you will be even lower.
The paper he referred to is interesting. I am reading it but after a while my eyes glaze over and I realize that I have some really difficult software bugs to solve.
I was just in a prickly mood last night and wanted to take it out on Chesnut. It's related to the ONS releasing a terrible efficacy report immediately after I defended their mortality report, and Caul totally failing to clarify on twitter why they are not the same, just getting dunked on by the "ONS ball" team. I'm angry!
He has a Substack. That’s where I followed him. I’m no scientist and he gets very technical, but I’ll try to explain how I understood him. He says that the spike is so dangerous that it causes harm with just infection. It causes amyloid production (I think this is close) in heart and brain and I guess other places for everyone. He thinks that’s probably why Chinese were so harsh with lockdowns. They knew this. And wanted zero infections. They gave jabs, so not sure that makes sense. Anyway, that’s how I understood what he wrote. I quit following a couple of months ago, so he may have changed his views.
I even mentioned one time that, why should I bother with anything since I had Covid and I think he replied that there could be remedies. He may have posted a few remedies. I can’t remember. Maybe my brain is getting holes from the Covid. Lol
That's my read of his general vision. He does post a lot of potential remedies, but doesn't seem to be plugged into any Long Covid groups which is where I would expect the best information to come from because they are ahead of the published research.
IMO guessing what the Chinese were doing and why is highly improbable. The cultural difference is almost alien-like.
If your heart is damaged the remedies are man-made interventions. That heart muscle ain't gonna heal itself, as far as my understanding goes.
Getting stressed about potential damage is probably as bad as any actual potential damage, too. An attitude of c'est la vie seems the safest way to go.
I don't think that is true if you have taken some precautions, like keeping your D3 levels high enough. After all, Fauci is on record that he takes 6,000 IUs daily. I am following Fauci's lead in that regard but ignoring his other claims about the gene-therapy treatment. (I also have some horse paste just in case :-)
Walter is pretty firm on dying as a result of having Covid sooner rather than later. At least he was still saying that when i unsubscribed the last time. I don’t necessarily believe him, but I had to quit reading him.
Annoyingly, they use two different measures of serum D3 in the introduction, nmol/L and ng/ml. There is a conversion factor between these two but I forget its exact value ATM.
Will have to refer to the cited papers (where freely available) to see what they say.
However, this is the first hint I have seen for the mechanism behind suddenly.
"May be" is one of the most abused sentence fragments in western media IMO.
eg: ABC may be XYZ.
People subvocalise it / parse it as "ABC is XYZ" - and the headlines in media more often than not write that as the headline, only later to more honestly say "suggest it could be". They rarely link the study too.
As well as ineffectually teaching critical thinking, we appear to not even teach critical reading (3Rs!) to understand "may be" is a hypotethical.
Been wrapping my head around @FamedCelebrity 's thesis that even small p is still only correlation.
Sounds interesting. I just make sarcastic lewd gestures when "our side" fetishizes sigmas in human health outcomes. Like, we are humans, not weather, hello
Eesh, of course. ffs. I really am not this dumb, promise. Living in Australia you don't consider rarely going outside, or even if so, the sun is enough to trigger D production pretty reliably all year round. Very easy to forget this is not the case for very large populations around the world.
Curiously, as someone who used to live in Australia (Murgon, Darwin, Tennant Creek, Mt Isa, Darwin, Canberra and Adelaide, in that order) I saw an article maybe 30 years ago on The Nude Socialist, er, New Scientist that pointed out that sunlight exposure, while positively correlated skin cancers was negatively correlated with GI tract cancers and the mechanism was claimed to be Serum D3 levels.
There are hints that LNP encapsulated mRNA hangs around in the body far longer than expected, and in any event getting a second shot and then boosters will also deplete your serum D3 levels as they all cause fresh antibodies to be developed, and unless you restore those levels (sunlight, eating D2/D3-rich foods or supplements) you might be moving into very dangerous territory and I am not talking about the Northern Territory.
To where did you move, if you don't mind me asking? And how is it now?
I have had more than a few thoughts of holidaying in Mexico and crossing the border into the US and then giving birth (men can do that now, apparently, but I have not seen evidence to support this claim) to an anchor baby.
Or maybe DeSantis would grant me asylum outright. "The communist dicktatorial inmates are now running it" is surely worthy of such generosity.
I still want to see more analysis of MHC haplotypes vs infection severity!! So much money has been thrown around these last few years and so little of it has lead to constructive, actual scientific inquiry.
Citizen funded analysis and research via substack et al (you, Kevin Mc, etc, etc) has made the efforts of the "scientific" (bah so political) establishment look mediocre at best.
Did you catch "A common allele of HLA mediates asymptomatic SARS-CoV-2 infection
https://www.medrxiv.org/content/10.1101/2021.05.13.21257065v3" - strength is that it reproduces the finding in two systems (San Fran and UK). That's more an insight into preexisting immunity than resistance to severe outcomes. For the former I still think it's mostly a tapestry of stochastic events determining whether the immune system kicks in with an early adaptive response. I.e., the lucky pre-immune are "weird," and severe outcomes are not explained by some one weird thing, but a lot of dice rolls put together among normal kids and adults.
I remember why I wanted more analysis of MHC haplotypes - it was in aid of debunking "X country filled with a specific genotype did better than country Y with a race-level delta in genotype coz [lockdowns / vaccine uptake / mask adherence/ they wuz kangz /etc]".
But as I remembered this, the goal seems moot now. Is there a single country not experiencing excess deaths? Is there a single country that did not experience remarkably similar IFR? I don't think so....
No, I had not seen that one. Thank you for the link.
Only had this one in my bookmarks: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8444184/ and it has more variables than a Fauci GoF denial inquiry.
"a lot of dice rolls put together among normal kids and adults"
Batch quality IMO being a major one.
When I first read about myocarditis, it was 3 junior Belgian cyclists from the same team in one hit. Reeked of a batch-specific anomaly to me, given the popularity of cycling there, the number of riders (which requires juniors) and my memories of doing things together with friends I hung out with as a kid (ie they all went to get vaccinated together). Pure conjecture but uh yeah that was my thinking.
Have also seen couples / families suffer closely spaced reactions, indicating genetic or temporal (= batch) similarity in causes.
Apologies for asking the bleeding obvious, but does the calculation for efficacy take into account pull-forward deaths and the likelihood (my understanding only) that viruses evolve to be milder [to leave their infectees more long-lived and transmitting vs more deadly with shorter victim lives and thus less chance of transmitting]?
To test this you'd need:
1. comorbidity data for deaths (we sometimes got some of this - avg was 2.4 for Australia, from memory)
2. virus deadliness measures (No good idea how you could measure this unless with a live virus sample injected into mice?)
If we killed chunks of the comorbid patients up front, then vaccinated the less comorbid and those lesser comorbid were infected with a milder variant, it could convincingly look like vaccine efficacy.
What potentially happened is hardier / healthier people were infected with a milder variant. Vaccine still potentially does something for comabting virus, not denying that.
I think that’s why Brian called it “deathiness” rather than deadliness 😀
There's no reason to discount for pull-forward when seropositivity is low after all pre-Omicron waves. It's essentially like asking "should our 12:05 o clock lunch clients be as hungry as our 12:00 o clock ones?"
This is how I put it in my comment on "T Coddington"s post when he demo'd his awesome dashboard: https://inumero.substack.com/p/us-and-canada-examining-the-impact/comment/13288279
You might counter that this shouldn't apply to excess deaths because the virus is only killing those who were about to die. Says who? Again, if the seropositivity rate is low, e.g. 3% after the B.1 / spring 2020 waves, then we should assume that it has only killed 3% of the about to die. So you only have a .97 discount on daily normal deaths, and you can tell at a glance that this isn't going to eat back at your spring 2020 excess deaths spike. And by the time you get to Omicron, three years have gone by, now you are close to 100% seropositivity in some countries (very low still in others) and maybe we will start to see PFE this year.
Do you think that people who encounter the virus always have IgG seroprevalence? Seroprevalence for the entire population is not an adequate measure of how many people may have tangled with the virus, and can not tell you how much dry tinder in the vulnerable population the initial exposure may have burned. Also, the IFR is how we know it pretty much only kills the "about to die". I find a lot of your comments and reasoning confusing and somewhat difficult to parse, so sorry if I speak from a incorrect understanding of your positions
Broadly, everyone (except those who seroconvert) is getting some level of encounter without infection / antibodies at any given time after 2019. Additionally, some infections won't result in seropositivity due to assays having to use high cutoffs to achieve selectivity, plus antibodies waning.
But the burden of proof is on the assumption that susceptibles have been reduced to show why we should harbor some extremely complicated model of the virus killing everyone it can without most people getting sick. Because it is just that - an assumption - which is all I am pointing out. It is based on flu, but flu pandemics (subtype crossovers) have always been true "pandemics," basically half or more of the whole world gets sick within one or two waves. SARS-CoV-2 is transient and elusive until the Omicrons, which is why I am open to a bit of skepticism on whether the virus could really spread on its own before then.
As such, I see no reason to assume susceptibles are meaningfully depleted - the discount of previous deaths should not be assumed to outweigh gains in virulence as occurred with Alpha and Delta, so we should expect more deaths in 2021, not less. The exceptions are Italy, UK, and NYC, and I think the iatrogenecide hypothesis is strong for those outliers.
I think the IFR for Delta in the unvaccinated was rather scandalously high, but this points to suppression of early treatment and subsequent hospital mistreatment, likely killing 10s of thousands as I have said before https://unglossed.substack.com/p/the-american-unvaccinated-holocaust - these deaths go way younger than the first waves. Again we are looking at potential iatrogenecide.
So if the virus is just a cloak for a lot of murdering of people who wouldn't have died otherwise, there wouldn't be any PFE. Or if it's a mix of being deadly and being a cloak for murder (I think likely), then no PFE.
Well for 1, the north east and especially NYC, follow a gompertz curve with their ACM that seems to start before lockdowns are declared. While I agree a lot of their death is iatrogenicide, that is one of the few areas I would argue looks more like a spreading virus killing the population, than others, some that don't seem to follow said patterns and also seem to coincide with the WHO declaration of a pandemic (disruption of normal care? panic?). Second, what evidence is there that Delta was more virulent than Alpha? I was not aware of this, and it's something I find rather doubtful. If you are arguing from an exposure perspective with the ACM (amount of populace exposed due to transmissibility), then there is a trade off there. Increased transmissibility nearly always comes with less damage to the host. the host can travel farther and spread more material. A living, moderately mobible host is the evolutionary objective. There's also another big issue from my perspective (unless I still misunderstood you). The ACM for 2021 starts getting out of control in the summer months. Also, the ACM in 2020 alone clearly indicates, for at least America, that portions of the populace were well exposed. The ACM distribution being mostly elderly also shows us who died in the greatest degree, and while I do not trust the accuracy of PCRs, they ARE adequate for tracking the presence of genetic material. The viral genetic material traveled far, killed the old (and by proxy exposed the young, many of which likely didn't even seroconvert). We certainly helped a lot of them die with our care, but a lot of people were exposed. I completely fail to see how any of that would make people start getting sick again in 2021, and that it would be in the younger population, with a higher ACM. A certain percentage of the youth should have been exposed, and a large portion of the dry tinder was again, culled. Idk what the "pull forward effect" is, but if you are referring to the lack of mean reversion in the average ACM (never falling below average after being above average) then I quite simply disagree with that as well. It should have happened in 2021, the virus just isn't deadly enough to the young to account for the ACM we have seen, and what is occurring in the ACM data is not explainable by deadly viruses https://www.medrxiv.org/content/10.1101/2022.10.11.22280963v1.full.pdf
https://roundingtheearth.substack.com/p/excess-death-in-the-us-and-the-lack
I don't mean to bust your balls though. I'm admittedly rather rusty with all this data, and I have never been great at math or statistics. But if I didn't misunderstand then I don't agree. 2021 mortality should be lower. Much lower. below the anticipated average in fact. I'm sure 2022 also shows us how shit the "vaccines" are
2: the biology.
Previoulsy PCR+ and/or currently naturally seropositive consistently PCR+ at a lower rate than general population at all points after mid-2020, as in the Shrestha Cleveland Clinic series, multiple MOH and UKHSA reports, etc. So this means the rest of the population "doesn't have something" as far as immunity to infection going forward in late 2020 and afterward. The only question is how many future infected were always susceptible or how many become susceptible. E.g., ok Kindu et al. find that contacts who avoid infection have expansion of cross-reactive T Cells. So is it a) these people turn into next year's infections, or b) next year's infections are just the completely non-exposed? We don't know. But we do know that most of next year's infections are people who didn't PCR+ / seroconvert last year. So *at least some* people who didn't get infected are still future susceptibles. There is fuel left, regardless of what interpretations of the biology would lead us to expect.
However, what's perhaps important is whether the biology says (a) is impossible because if so, maybe we should expect diminished waves, i.e. the discount on future waves should be larger than who seroconverts / dies. Well, no, (a) is perfectly possible because innate immunity is variable, with the toggles on antiviral / antifungal / antibacterial cytokines always modulating. Expanded cross-reactive T Cells could be enough when a contact was exposed while antiviral toggles were high, but not if exposed again while antiviral toggles are low. (There's also of course viral mutation e.g. did BA.2 evade pre-existing recognition of SARS-1, leading to finally getting traction in East Asia? https://www.biorxiv.org/content/10.1101/2022.02.07.479349v3 - but mostly I want to limit to the innate immunity question.)
Finally, from an evolutionary standpoint, revolving door innate immune defenses make sense. As you say, adults have poor innate immunity. In fact immunosenescence arguably begins with puberty. So there is a window where we are still reproductive age but the front line is not as reliable at keeping us alive. It makes sense to lower the front line periodically to go ahead and see what makes it over the gate, invest in adaptive response to the same, so we don't have to worry about that thing later when innate immunity can no longer handle it. There's other biological evidence for this sort of "inside job" approach to giving our viruses a boost, e.g. Lymph Node Subcapsular Sinus Macrophages which act as virus farms inside our lymph nodes. Additionally, this kind of peace-making lets viruses thrive without having to overcome innate immunity even more than they do, which once again would seem to be evolutionary beneficial (more baby-making beyond adolescence).
Pull forward is reversion to mean, yes.
1: the epidemiology
So, with this and the other comment, you have mounted a case to answer my request for burden of proof. But I feel we are talking past each other a bit when it comes to "what should we expect and why should we expect it." I think this has to do with your interpretation of innate immunity which essentially does not allow for dry tinder to exist after 2020. Let's set that aside. What is actually very determinative about the existence of a gompertz curve? Nothing. A fire that only destroys a thicket will look the same as one that takes the whole forest on a graph when the y axis always scales to the top of the curve. But the supermajority of people of all ages still did not get sick and are still alive. Again, your biology argument asserts they can't get infected later so there is no need to worry about them. But without the biology argument, the case for there still being dry tinder is obvious.
The following is essentially axiomatic: As long as 1) "the killing thing" we are examining 2) "can kill not-about-to-die" and 3) "doesn't find most people" the first time it passes through, then more people are going to be killed later if it comes back. Even more if it gets better at 2. This is true regardless of IFR by age until you get to certain equilibrium points related to 1 competing with other risks (ie humans are not immortal). So you can't refute any of this with IFR by age. So like I said I think we are talking past each other because on the non-biological argument you are merely stating facts that I don't disagree with but don't find determinative. There is no actual proof that the virus only killed the about-to-die in 2020 except maybe in the aforementioned hotspots, it is just an unfounded assumption.
Delta is the most fusogenic variant in vitro thanks to P681R and is more pathogenic in animals. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8828475/ Humans are a trickier measuring stick since the vax confounds things, but studies from myriad health systems show upticks in hospitalized deaths when Delta arrives, most recently https://www.medrxiv.org/content/10.1101/2023.02.15.23285759v1 fig 5 but going all the way back to the CDC Provincetown report combining Fisman, D. Tuite, A.; Ong, S. et al.; Sheikh, A. et al. all finding the same thing.
Delta got more virulent (and maybe more contagious at the same time) regardless of whatever evolutionary theory thinks about this.
I am pressed for time, but I see a glaring issue. I am not asserting they "can't get sick later". I'm asserting that a larger portion of weak people than normal died, while also exposing a certain percentage of young, healthy people. Dry tinder comes back progressively each year and the space of time between 2020 and summer of 2021, is too short, which is when ACM picks back up. It's also too great, if a percentage of the population has gained immunity, and the elderly have been exposed. You said yourself these things take half the planet by storm in 1 to two waves (generally yearly). In a normal environment, a pandemic of this nature, will result in a mean reversion the following year, and for it not only to not occur, but to also be out of whack in the summer time, is very concerning. I am arguing from a holistic perspective: society and people obviously are more resilient to SARS 2 the second year, than the first, due to fast and abnormal removal of the normally slowly killed populace, and exposure of a certain percentage. SOme of those people were not infected in 2020. Some will still get sick despite being young and healthy. A small amount of "dry tinder" will return by winter 2021, as populations age. But again, for ACM to be HIGHER in 2021, well that's just an absolutely terrible look for the thing that was forced into everyone's arms, and the evidence for it being covid is very weak to nonexistent when you contextualize it with what age brackets are dying in 2021 and the covid IFR for those brackets, at least in my perspective.
Other than the stock acronym for Pfizer, what does PFE mean?
Would be interested to see your reasoning for "seroprevalance for population =/= infection of population". Assuming I read that right?
Do you mean me? If so there there are a lot of reasons. The first being, (I don't have them on hand ATM) there are studies that show people in the same household with infected individuals, yet who do not display symptoms themselves, develop memory T and B cells to SARS 2, yet do not seroconvert. The reasons for this are actually very simple, when you have a firmer grasp on immunity in general. For starters, SARS 2, influenza, and similar respiratory viruses, are highly mutative and fast spreading, and start their infective process at a membrane barrier in your respiratory or digestive tract. You have two branches of immunity, one called the innate immune system and one called the adaptive immune system. The innate immune system, as much as they wish this were not true, is the main defense against things like res viruses. Things like mucus, the secretory IgA system (which are generalized antibodies in/on the surface of the membrane, and do not require infection with a specific pathogen to neutralize necessarily, as they tend to target conserved regions) and inflammation all come first, which of course prompt the arrival of things like dendritic cells and cytotoxic T cells. Before we continue, a thought experiment. What are antibodies? They are globular proteins. How are proteins formed? Inside cells using amino acids, which expends energy and cellular resources. So next, ask yourself a hypothetical, what is more effective, confiscating all the guns in a region, or blowing up the gun factory? These are the reasons, cytotoxic T cells and innate immunity are your main defense against these pathogens. Because late stage, humoral based IgG antibodies to specific viruses, when you are presented with hundreds of thousands if not millions/billions of different viral strains every day, are not an effective means at stopping an infection that occurs in this manner. If your body did that, your blood would be nothing but sludge due to all the antibodies. No, the body wants to identify and destroy the infected cells at the barrier, BEFORE it is compromised, you feel sick, and IgG has to be used to try and clean up the mess. This happen every single day. Not a day goes by that this system doesn't destroy cells and keep you from getting sick. Turing off things like linked recognition and the compliment cascade before they complete their processes and you are flooded with globular proteins is again, the main objective of your body. Life doesn't waste resources when it doesn't need to, or well, it wouldn't be "life". It would be "dead". This is not true for all viruses though. Some have different infective routes and mutative rates. For example SARS 2 stays so consistent because it has a proofreading helicase for its massive genome, but other viruses may be completely different. Some of those are likely early childhood disease we have effectively vaccinated against (polio maybe) but my knowledge of other vaccine tech is admittedly not great. The main point is though, if a virus is controlled by the innate immune system: generally it will harm the old, more than the young, because their innate immune systems SUCK. That is really one of the main things that kills people. Get old, T cells suck, get the flu, it goes crazy because innate immunity now sucks, and adaptive immunity is also too weak. Then you die. If it is more dependent on the adaptive immune system, then it seems likely that it will not only infect the young a lot more (poor adaptive immunity due to lack of presentation/experience) but also that it MAY be beneficial to vaccinate against said virus in that situation, though I don't KNOW that. My main point is: res viruses that are controlled by the innate immune system, doesn't give a shit about how much IgG you force produced in your blood, and your body doesn't want to make specific antibodies to one virus if it can avoid it. This translates into "people get adaptive defenses but do not seroconvert", and likely at much higher rates the younger they are. This is also, why SARS 2 doesn't generally kill kids. They have the strongest innate systems, and the weakest adaptive ones (when they are really young)
The mystery I have just described to you, is "asymptomatic infection". However the powers that be would never tell you, that pinging positive on a SARS 2 PCR yet having no symptoms (or antibodies to SARS 2), is a GOOD thing. Asymptomatic infection means your innate immune system did exactly what it was supposed to.
Edit: What I have just said about pinging positive with no symptoms only applies to the unvaccinated, especially since the vaxxed have started producing IgG4, a non inflammatory antibody that usually only is produced for allergens like pollen I believe
Anecdotal icing on the cake: I met a cancer survivor (I think? been a minute) who had "IgG deficiency", yet lived through two SARS 2 infections.
"IgA <...> as they tend to target conserved regions"
By "conserved" do you mean nucleocapsid / non-spike?
Yes, some proteins are "conserved" across viral families. Idk about nucleocapsid, but I'm pretty sure the non structural proteins are more likely to be conserved, like the polymerase which copies the RNA. There's only so many ways they can be made and changes they can undergo before they lose function, so as such they must be similar across all viruses. Spike is a structural protein that is used for receptor binding. It is the exact opposite of "conserved". Again sorry about short answers, I'm rather pressed for time
Is it possible I have not seroconverted? I think during the pandemic it was grounds for Dr loss of license if you ordered or did a seroconversion test here in Australia, not sure if it still is.
One of the first things I did when this all started was get copies of Rohit's (dry and dense, but worth it), Basic imunology (Ian Orme, brilliant read), How the immune system works (Sompayrac good read) and Janeway's Immunobiology (another good read), so there's nothing challenging in your description of innate vs adaptive immunity other than the rustiness of the passage of time.
It was my understanding that T / B cells against invaders are "taught" in our lymph nodes. I had a C19 infection after catching it from my vaccinated housemate. I got swollen tonsils (1 really bad day + an ordinary day either side) and diarrhea , they had body aches and pains, fever, fatigue, etc. As did another random person I was in conversation with 6 months later.
That to me (could also be wrong) was the classic tell of "natural" infection mediated immune response vs vaccinated infection immune response, although I wouldn't confidently state the mechanisms in any great detail. I am not young, but am fitter and healthier than probably 99% of Western society.
Appreciate the reply.
I'd say the inflammation is an indication you did at least do some seroconversion, though possible you still didn't reach IgG stage. People really fail to realize the sheer amount of viral material around them at a given time, especially if they are around other people. Every day you likely beat a asymptomatic infection. Swelling indicates cytokines and inflammation, which indicates that many cells have been infected in a location, and a battle is being fought there. The "taught in our lymph" you are referring to, is something called linked recognition. https://webmedia.unmc.edu/eLearning_open/COM/Linked_Recognition_Process/story_html5.html
In order for this to occur, two things must happen. Cells must be destroyed, and viral debris must be drained to the lymph. This may put out all the various types of viral proteins being produced (N protein, non structural ect.) Also, the T cells doing the destroying (or some family member of them) will acquire proteins from the site of infection. they choose specific proteins, and then migrate to the lymph. The proteins carried by your immune system, must match proteins that were drained to the lymph and picked up by B cells. This is how your body determines what proteins to fight against if it is going to use adaptive immunity, and again, this process can be cancelled/prevented if it is no longer needed, i.e. the T cells handle the infection before linked recognition occurs, and B cells that matched T cells start to proliferate.
EDIT: I can't recall the mechanisms for stopping linked recognition. I know the complement cascade has them, but linked recognition I'm not sure about. It may be that you simply don't reach this stage because enough cells were not infected or enough material was not drained, or perhaps the creation of memory B cells after can be controlled. More research needed. however anything that uses cell resources and creates proteins to fight infection, will have some type of control mechanism, to reduce or stop them when not needed. That just simply has to be true from a biological perspective, and is also how the rest of the body works with nearly every system (feedback, turn off? keep going?). It may take a lot of digging to determine exactly how linked recognition is controlled, and it may not even be well known in current science
EDIT DONE:
Now imagine, if instead of this presentation, your body started producing spike, and only spike, in muscle cells. There is no chance meeting of combative T cells with growing memory B cells. There is no nuance and additional material. There is only spike, and a shitload of it. I can find nothing about these products from a biological perspective that makes me think they are good at anything other than making a bunch of now evolutionarily irrelevant spike, and by proxy totally fucking up your normal information acquisition (natural infection)
Final edit:
I THINK I finally get what you meant by this sentence Brian. And I have now provided you with the explanation. It's what I posted above
"But the burden of proof is on the assumption that susceptibles have been reduced to show why we should harbor some extremely complicated model of the virus killing everyone it can without most people getting sick"
Old people died a lot because of our care and their weak innate immune responses. "most people" didn't get sick because "most people" are young, and will get defenses without even needing to seroconvert in most cases
I'll fold my reply to this in the other comment to keep to one thread
Seropositivity might be higher for the older age cohorts who are susceptible though. In fact I think one of the main reasons why elders are at an increased risk of dying from respiratory disease is the reduced ability of their immune systems to react to new threats.
That being said I really think this culling effect might be quite a bit more grave than what we are used to from seasonal flue.
https://substack.pervaers.com/USA_Misc/Proportions_age_groups_65-85%2B.png
Look at the 85+ group here. We see something similar for Alzheimer proportions if I remember correctly. Ironically Alzheimer mortality is the only type of select cause I found to correlate positively with vaccination rates ever since the campaign began. So the culling effect of SARS-CoV-2 and the vaccine might actually affect different populations.
It's not just population size that's changing, it's also the composition. We might have to look more at how people are dying.
I made this website to visualize this. Just for my own reference really, but maybe this is interesting to you as well: https://cdcsucks.pervaers.com
When we praise the vaccines for their efficacy, we should keep in mind that there is a good chance we wouldn't need a vaccine anymore if it weren't for the leaky vaccines. This whole Delta wave thing is not natural. It seems the vaccines reduced the evolutionary trajectory of SARS-CoV-2 to zero. Delta was sequenced all over Europe since late March 2020. It never had a growth advantage until vaccines came along. Cost 220k people their lives within half a year in the USA alone. So really... Efficacy seems more like an individual thing here. On the population level it may as well border on -100%. Vaccine decision was sort of like an an unblinded prisoner's dilemma (probably more like extortion), without taking into account that there were also times at which vaccines reduced your chance of survival (like Q3 2021 in the USA).
Ah yes how tf I forgot about lockdowns and their impact on seropositivity (etc) , given I live in Australia ffs I will never know.
Your patient responses are appreciated.
I am going to plead senescence I tell you!! Now where are my slippers.
A claim that it might be Vitamin D deficiency that is causing the problems, because your immune system consumes the activated form of D3 when it creates antibodies. So, if you are low to begin with, after the gene therapy treatment you will be even lower.
https://twitter.com/Parsifaler/status/1634269280102502412
Chesnut generally doesn't seem to be aware that "studies say" is not how you interpret studies. He's an Abstract Tourist and I find him exhausting.
The paper he referred to is interesting. I am reading it but after a while my eyes glaze over and I realize that I have some really difficult software bugs to solve.
I was just in a prickly mood last night and wanted to take it out on Chesnut. It's related to the ONS releasing a terrible efficacy report immediately after I defended their mortality report, and Caul totally failing to clarify on twitter why they are not the same, just getting dunked on by the "ONS ball" team. I'm angry!
Abstract tourist, I love it. :D
My take after reading Chesnut is that we’re all gonna die.
Do you remember his argument for why people will die sooner post-infection? Would be interested to see a summary without trawling his twitter feed.
He has a Substack. That’s where I followed him. I’m no scientist and he gets very technical, but I’ll try to explain how I understood him. He says that the spike is so dangerous that it causes harm with just infection. It causes amyloid production (I think this is close) in heart and brain and I guess other places for everyone. He thinks that’s probably why Chinese were so harsh with lockdowns. They knew this. And wanted zero infections. They gave jabs, so not sure that makes sense. Anyway, that’s how I understood what he wrote. I quit following a couple of months ago, so he may have changed his views.
I even mentioned one time that, why should I bother with anything since I had Covid and I think he replied that there could be remedies. He may have posted a few remedies. I can’t remember. Maybe my brain is getting holes from the Covid. Lol
That's my read of his general vision. He does post a lot of potential remedies, but doesn't seem to be plugged into any Long Covid groups which is where I would expect the best information to come from because they are ahead of the published research.
Thanks for that.
IMO guessing what the Chinese were doing and why is highly improbable. The cultural difference is almost alien-like.
If your heart is damaged the remedies are man-made interventions. That heart muscle ain't gonna heal itself, as far as my understanding goes.
Getting stressed about potential damage is probably as bad as any actual potential damage, too. An attitude of c'est la vie seems the safest way to go.
That’s why I quit reading him. I have enough to ponder on!
We are. However, some will die sooner than others.
lol! You ain’t wrong. Let me clarify! We’re all gonna die much sooner if we had Covid.
I don't think that is true if you have taken some precautions, like keeping your D3 levels high enough. After all, Fauci is on record that he takes 6,000 IUs daily. I am following Fauci's lead in that regard but ignoring his other claims about the gene-therapy treatment. (I also have some horse paste just in case :-)
Walter is pretty firm on dying as a result of having Covid sooner rather than later. At least he was still saying that when i unsubscribed the last time. I don’t necessarily believe him, but I had to quit reading him.
This is the paper he refers to which is more of a review article and not primary research.
https://www.mdpi.com/2227-9059/10/6/1239
Annoyingly, they use two different measures of serum D3 in the introduction, nmol/L and ng/ml. There is a conversion factor between these two but I forget its exact value ATM.
Will have to refer to the cited papers (where freely available) to see what they say.
However, this is the first hint I have seen for the mechanism behind suddenly.
"May be" is one of the most abused sentence fragments in western media IMO.
eg: ABC may be XYZ.
People subvocalise it / parse it as "ABC is XYZ" - and the headlines in media more often than not write that as the headline, only later to more honestly say "suggest it could be". They rarely link the study too.
As well as ineffectually teaching critical thinking, we appear to not even teach critical reading (3Rs!) to understand "may be" is a hypotethical.
Been wrapping my head around @FamedCelebrity 's thesis that even small p is still only correlation.
Sounds interesting. I just make sarcastic lewd gestures when "our side" fetishizes sigmas in human health outcomes. Like, we are humans, not weather, hello
How long does that Vit D depression last? For the duration of the vaccine-induced "infection"?
Until you replace it either by getting some sunlight or taking some supplements.
Eesh, of course. ffs. I really am not this dumb, promise. Living in Australia you don't consider rarely going outside, or even if so, the sun is enough to trigger D production pretty reliably all year round. Very easy to forget this is not the case for very large populations around the world.
Curiously, as someone who used to live in Australia (Murgon, Darwin, Tennant Creek, Mt Isa, Darwin, Canberra and Adelaide, in that order) I saw an article maybe 30 years ago on The Nude Socialist, er, New Scientist that pointed out that sunlight exposure, while positively correlated skin cancers was negatively correlated with GI tract cancers and the mechanism was claimed to be Serum D3 levels.
There are hints that LNP encapsulated mRNA hangs around in the body far longer than expected, and in any event getting a second shot and then boosters will also deplete your serum D3 levels as they all cause fresh antibodies to be developed, and unless you restore those levels (sunlight, eating D2/D3-rich foods or supplements) you might be moving into very dangerous territory and I am not talking about the Northern Territory.
Nude socialist FTW.
To where did you move, if you don't mind me asking? And how is it now?
I have had more than a few thoughts of holidaying in Mexico and crossing the border into the US and then giving birth (men can do that now, apparently, but I have not seen evidence to support this claim) to an anchor baby.
Or maybe DeSantis would grant me asylum outright. "The communist dicktatorial inmates are now running it" is surely worthy of such generosity.
I moved to the most recent hell on earth (Bank collapses) otherwise known as Silicon Valley.