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What part of bollocks don´t you understand?

"crop top" 🤣

😵‍💫

Mr. Krackle does not disappoint and continues to expose his abject ignorance of medical science including immunology and the clinical trial methodology and, well, just simple English comprehension. How long to have to keep trying to educate these krackleheads.

"Please correct me if I am wrong: where's the calculation of non significance for the deaths in the publication? With such low mortality this study is underpowered for that purpose. " You essentially already gave the answer to your own question in the next sentence - it is underpowered to determine any difference in mortality, hence it is not significant. "Makes me wonder about the millions of lives saved if mortality is this low in healthy people (see exclusion criteria). I don't see the need for the vaccination of this group in this study. No lives were saved." Maybe look at the hospitalization and severe disease. THAT is the reason. Ask your employer how much money he loses every year from just one single employee being ill for one day. Then realize the vaccines reduced hospitalizations by over 90%.

​​​@@Marco-it2mrthe non significance is stated as proof of Susan's argumentation as if the study was powered fot it and that's the result. No it's not. Non significance should come with an asterix in this case not a argument of your point of view. This is misusing data the same as the vaccine sceptics are doing.

Thank you. I really appreciate your support. It is definitely disconcerting. Unfortunately pseudo-science can sound like science to people without the background to properly assess it.

Why should we take advice from a bellend?

I can't understand some of what you're trying to say but there will be obvious answers. Like your first point what was the date of the roll out or the 4months after? What is the rate of elderly deaths based on? Numbers may have increased due to delta variant being more severe or death rate in elderly might have been calculated in between dominant variant circulation. April 2020 the testing may have been very limited and at that point restrictions may have been in place where people believed there was no need to test. It may have also been a period between dominant circulating variants. When people were first vaxxed they were being made to believe it was all but impossible to be re-infected when it never prevented infection or re-infection. It was actually always re-infections because the virus was circulating long before it was ever announced. The vax was just used to stuff covid back under the rug. It was designed to give people the sense that they were safe now and in to the future despite the exact opposite being true.

Another pathetic antivax loon who doesn't understand the concept of confounding variables:

❤ Yes, so cute.

If you post them here, other people may be able to help. I would use the titles and not links as RUclips tends to delete comments with links.

@@Backtothescience Great. Ok this is gonna take a while. Please also if possible, check for it being removed, as it will be very lengthly and include my thoughts, which im not sure will/wont include censored word strings? As it might look like spam perhaps? Ok, let me just get coffee and adjust myself (I have neuro issues and ASD, so excuse the weirdness if it comes through).

@@Backtothescience First I want to start with RAS balance and covid, and the issues relating to angiotensin II peptide system becoming "unbalanced say. From what I know, the angiotensin system is not just the textbook system of vascular tension regulation to ensure proper perfusion of organs and extremities. But also HIGHLY involved in diseases of almost every organ system. (Correct me if I'm wrong at any point). Here's a breakdown of the potential consequences in different organs: Heart: High levels of Ang II can lead to hypertrophy (thickening) of the heart muscle, increased stiffness of the heart chambers, and fibrosis (scarring) of the heart tissue. These changes can impair the heart's ability to pump blood effectively and increase the risk of heart failure. Blood vessels: Chronic exposure to Ang II can cause damage and dysfunction of blood vessels, leading to atherosclerosis (hardening of the arteries) and hypertension (high blood pressure). These conditions increase the risk of heart attacks, strokes, and other cardiovascular complications. Kidneys: Ang II can directly damage the kidneys by promoting inflammation, fibrosis, and oxidative stress. It can also indirectly harm the kidneys by causing high blood pressure, which puts additional strain on the renal blood vessels and filtering units (glomeruli). Brain: High levels of Ang II have been linked to cognitive impairment, dementia, and an increased risk of stroke. Ang II can disrupt the blood-brain barrier, leading to inflammation and neuronal damage. Adrenal glands: Ang II stimulates the adrenal glands to produce aldosterone, which can contribute to high blood pressure and fluid retention. Chronically elevated aldosterone levels can also directly damage the heart and kidneys. Angiotensin II revisited: new roles in inflammation, immunology and aging Ariela Benigni, Paola Cassis, and Giuseppe Remuzzi 2010 Role of angiotensin II in aging Wenmin Yi et al. 2022 Processes involved in over activation of the downstream effects of ang II seem to be extensive and quite bad in many different organs. It increases the rate of NAD breakdown, causes mitochondrial dysregulation which I think being the main contributor to ROS will badly affect internal cell components at a faster rate. Over activation of AT1 seems to be site specific in many aspects according to what kind of things might happen. In the GI system it seems to effect protein transporters. B0AT1. Which has a knock on effect on many things possibly. GI functioning. Inflammatory response to invaders perhaps? Less precursors for serotonin? Maybe? Seems plausible. Also it seems the virus sticks around in the GI system. Which seems to be widely accepted. It was the same for COVID1 which is 20x less effective at binding to ACE2, so why would it not I guess? Also concerning is, even if its just subunits of the most likely offender, it perhaps could still have ability to reduce ACE2 function, and having a knock on effect resulting in angII build up> over AT1 activation. In the brain, it seems like it is sort of centred around its ability to alter endothelial cell function. The reducing of ace2, would create a more inflammatory phenotype and allow more to cross the BBB. I think there was a study that look at this mechanism involving malaria or something. I can't remember. The virus seems to have the ability to cause dopaminergic neuron senescence. And lessen the time these molecules "survive"? Also astrocyte involvement seems problematic. I m thinking of the seemingly large reporting of attention issues? And 4 years of adhd treatment shortages. And 7 year waiting list for ADHD. And dementia seeming to creep up. I dont like the blaming of things that to me feel lazy. Oh it's the lockdown! Oh it's trauma. Oh it's not real. RAS system is verrrry real and extremely important to keep functioning properly. These mechanism are highly conserved, so I dont see them magically becoming unimportant either. In the heart, a big concern would be remodelling? As over activation can cause many things, fibrosis/remodelling being one? Cancer. Cancer is a tough one, because many can get stuck on hard definitions. In terms of if X causes DNA damage or not. But for me I'm thinking on other levels too. As dna damage/mistakes are a constant right? So altering the cell micro environment to me seems also important. So if the balance is off with ace2 and angII builds up, we get the AT1 over activation and the changes that make a tissue more hospitable to neoplastic changes. Like the increased in VEGF and inflammatory signalling. And I think with increased VEGF in the region, this might change immune landscape also. M protein deposition might also have an effect here but in different ways. It's almost like inviting a new virus that persists in the body for a long time (according to studies) whether its active or not, seems to have specific consequences that should be studied first.? Immune. I am not totally sure, I'm not totally sure about anything, but this is all my current line of thinking until better evidence presents. So I think the body is more prone to stronger inflammatory action according to the deposition of these persistent particles that downgrade function of ace2 which leads to the angiotensin balance problem> which seems to create a phenotype more prone to inflammatory phenotypes and downstream damage and remodelling or system failure at organ level. I know there are various check measures in place (other wise we would all be dust by now), but what concerns me is the insidious nature and the siloing that social media has created. Arguably geopolitical tensions have increased this by amounts only future studies will quantify. But there seems to be a large push from social media, that proliferates into public consciousness and acceptance. Which has even affected research level direction. VERY SCARY. A difficult thing is, is that the systems in the body are time sensitive in a way, and also sensitive to variables that control biological variance. Like if a system is compartmentalised or not, and we check the blood, and only use that for something that may/may not show what is happening on an organ level in peptide systems and downstream effects? Like how long does it take for dysregulation to cause downstream reactions that have become independent of the causal mechanism? Bio peptide accumulation seems plausible to me, because angiotensin II seems to be linked directly with all the issues that seem to be increasing more and have been since covid came to be. It's such a tough issue, because so many normal problems of aging and normal life ending events are entrenched. But I think, with the world losing so much of its elderly and very sick, at the start of the pandemic, we should be in quite the negative at the moment, when it comes to excess d. Our systems may also hide details. They have very small bottle necks in many cases. Sometimes waiting lists are better, not Dx. Or disability claims? Or staff long term sick. Or if cognition/ attention, accident levels/ factory recalls? It's a lot to pick apart. But I think ANGII build up fits very well. So if it is RAS. We do have things like ace1 inhibitors to reduce some of the source accumulation factors or receptor "blockers" ARB. But perhaps the effects would be time sensitive in administration. And whether the medication is lipophilic or not. If not, perhaps it doesn't enter tissues as well, and wont cross the BBB. Strangely angiotensin system has links with the dopamine system in the brain? Weird. But might again point to some of the attention based issues/ depression. This is just an opening free ramble. Next I will post more directly about covid effects on the system and the related effects according to organs and how it suspiciously links to angiotensin II running amok

Vascular effects. Covid seems to cause some weird effect where the arterial health decreases more and more for a period of time AFTER infection resolution. 'One of the main mechanisms for the effects of SARS-CoV-2 infection on arterial stiffness is endothelial dysfunction, resulting from increased vascular inflammation and oxidative stress.6 Jul 2023' Distinct Features of Vascular Diseases in COVID-19. Alexandr Ceasovschih et al 2023 Angiotensin II and vascular inflammation Zhong et al 2005 The current data suggest that Ang II modifies several steps of inflammatory response, such as increase of vascular permeability, leukocyte infiltration, tissue hypertrophy/proliferation, and fibrosis. Ang II, via the type 1 (AT1) receptors, enhances the production of reactive oxygen species (ROS) through stimulation of NAD(P)H oxidase in the vascular wall. Increased oxidative stress contributes to endothelial dysfunction and to vascular inflammation by stimulating the redox-sensitive transcription factors (NF-kappaB) and by upregulating adhesion molecules, cytokines, and chemokines. The pro-inflammatory action of Ang II may help us to understand the molecular mechanisms of hypertension- and diabetes-induced vascular complication as well as the pleiotropic actions of drugs interfering with RAS. Known for some time? I know they also think macrophage infection is a large problem too? But it seems like angII over activation oof AT1 is enough to cause problems. I saw some studies, Im just rewinding my mind to see what about. I will google and attach. Will be back. I'm just going through the possible paths of the virus and the resulting issues according to studies

Thank you. I really appreciate your ongoing support. I think it is important to remember that the average person doesn't even hear the antivax nonsense in the first place.

Just tried a deep breath. Ouch!

@@Backtothesciencewhat we used to advise was wait about 20 minutes after taking analgesia then slowly take a deep breath in, to the point where it just starts to feel uncomfortable and slowly breathe out.

Thank you. I really appreciate your support.

❤

Mikolaj Raszek strikes again with his sponges and cows.

Of course I have heard of them. You are a little confused though - they don't have a detrimental effect. I cover them in the following video:ruclips.net/video/0JVunoNXyCk/видео.html

Susan will praise the 30 fold rise of IgG4 as a high protection against covid. Its no problem at all . Trust Susan. Really.

IgG4 is as effective as IgG1 but is not inflammatory. If you only depended on IgG1 following multiple infections of the same virus then you’d be in an inflammatory state all of the time, which is not a good state to be in. If IgG4 in the bloodstream were such a bad thing then beekeepers would not be well as IgG4 develops as a result of multiple exposures to bee venom. If IgG4 develops in solid organs then yes there can be issues, there are plenty of explanatory videos of IgG4 related diseases on this platform. Also there are lectures on antibodies and class switching on this platform.

@@Baard2000 IgG1 has an abundance of between 45% & 75% of all IgG antibodies, and has a half life of 21 days IgG2 has an abundance of between 16% & 48% and has a half life of 21 days IgG3 has an abundance of between 2% & 8% and has a half life of 7 days IgG4 has an abundance of between 1% & 12% and has a half life of 21 days According to a slide from a series of immunology lectures, which is based on a figure in “The immune system “ by Parham.

Obviously a vaccine related injury.

I hope Dr Oliver has filed an adverse event report!

I really apprciate your creative metaphor!

That is why blinded trials are used.

There’s nothing particularly magical or sinister about the spike protein, despite what people may say. Why is it different to a virus that causes cells to produce all of its proteins? The spike protein is just another protein, it cannot infect cells of its own accord, and even if it did there are multiple receptors inside the cell that can detect “foreign” molecules that are associated with pathogens.

​@@MRCAGR1 I think it was suggest that there was molecular mimicry between the spike and a cardiac proteins causing myocarditis.

You missed the important part: 16 vs 15 is not statistically significant. Got it?

How many people (of the millions) who were killed by c19 have you spoken to?

Why do you care what a bunch of gullible cookers think? Who even talks about vaccines in 2024? You are one strange oddball that's for sure.

There is a website just for peoiple like you called Sorry Antivaxxers

Please see this video: ruclips.net/video/2P8qChwZZk8/видео.html

Prasad is not a credible source.

@@Backtothescience thanks but I think the paper Prasad was refering to is a more recent one

@@Backtothescience I meant this paper : Epidemic outcomes following government responses to COVID-19: Insights from nearly 100,000 models Eran Bendavid et al. Sci Adv. 2024.

Every measure makes some kind of difference. It's just a matter of how much. The lockdowns as I saw them would have made barely any difference except to slow transmission down slightly. The virus was being treated as if it wasn't airborne or very infectious when the complete opposite was always the case. People were being told nonsense about how kids don't get it or spread it, how you can't catch it outside, how you need to spend x amount of time in close proximity, how you only need to test if you have particular symptoms etc etc. In reality people were just going about their normal business when the education and steps they'd need to take needed to be far more stringent. When the govt is in control of testing the result is whatever they tell you it is. That's why they banned importation of RAT tests until they started the vax process and admitted they didn't have control of it. I likely got the UK variant during a period where we were being told it wasn't circulating and that they just wanted to open for Christmas as if the virus cares about times and dates.

Thanks for participating in the trial 💐

"I mean, the CDC announced an average of FOUR comorbidities per death during that time but none of you 'health professionals' seemed to want to listen." You mean those comorbidities that often included conditions *directly caused by the COVID.* You seem to have missed the comment from this same CDC that in 92% of all death certificates COVID was listed as the cause of death.

@@Marco-it2mr nice try, but no, the comorbidities listed were not directly caused by COVID. These were existing ones based on the deceased's medical history. The good doctor here would already know this if she had done her due diligence, since the information is still in the public domain. Anyway, even though the CDC publicly declared this, it was largely ignored and every death certificate thereafter was conveniently signed off as C-19 being the cause of death.

@@user-pg9qj5oj8r Nice try, but yes, many were. ARDS, for example, is a common result of severe COVID. That information is indeed in the public domain, and you still decide to lie about it. "Anyway, even though the CDC publicly declared this, it was largely ignored and every death certificate thereafter was conveniently signed off as C-19 being the cause of death." And this is another lie. You sure are a good example of a malicious liar who, even when caught, just continues lying.

@@user-pg9qj5oj8r If you look at the co-morbidities it was often pneumonia and other things that were actually caused by the virus and/or ADE caused by the virus.

It's funny how you antivaxxers just blindly accept everything you read that is antivax. What you said does not even pass the pub test. Four comorbidities definitely includes those cause by the infection. So, son, it seems it was not us who didn't listen, it was YOU. The antivax loon.

Did she fall off her broomstick again?

Yes, that's why I haven't had an X-ray as the treatment is the same.

@@Backtothescience I got hit by a car years ago and was a bit battered and bruised and a rib hurt for quite a while. I didn't bother going to a doctor and everything was OK after a month or so. Someone had thrown an egg at the car and they couldn't see me when I was crossing a pedestrian crossing. The wing mirror snapped off when the car hit me so I picked it up and ran over to the car and gave it to them. The driver was really shaken up and thought she'd killed me (ha ha). They then by coincidence they turned up at the venue I was at and bought me drinks to say sorry for running me over - so it was worth getting run over in the end. I showed a friend my bruises and told her I thought I had a cracked rib. She was in stitches that I got run over on the way to the venue and was saying "a cracked rib!" over and over and laughing. I then went out with that lovely person who laughed at my cracked rib for five years. At least I have a funny story to tell.

@@MysticOblong the things people do to pick up chicks.

@@Backtothescience and get free drinks

Her paperclip is hidden, she uses it to keep her bra together, the fasteners broken.