I like to think of myself as a reasonable person. I’m a misanthrope, I don’t like humanity as a collective, but I don’t carry ill will towards individuals. I wouldn’t recommend an individual to jump off a cliff, I’d rather see them sell their car, stop flying and stop eating meat. For me this means that if I thought to myself that I had offered you bad advice in regards to the ongoing SARS-COV-2 pandemic, I would tell you so. I’ve actually gone out a few times during summer, trying to intentionally catch this virus, just to get it over with. I don’t think this ever succeeded.
To some of you this will seem terribly irresponsible. You may have heard people say that infection is virtueless, that there is no cumulative immunity, that you merely deplete your naive T cells etcetera. I don’t believe these arguments to hold value. The people who make these claims have now over time gone a step further, they now argue that all infection from respiratory viruses is effectively virtueless, that not catching RSV, noroviruses, adenoviruses, hCOv’s, rhinovirus and all the other ones out there is a good thing, that it merely protects you from damage. They’re wrong.
Before explaining the problem with their line of reasoning, I just want you to take a look with me at the outcome of a natural experiment: Which country is better off? A country that does everything “right”, or a country which allowed SARS-COV-2 to spread through the population and focused on protecting those most at risk? We can measure this by looking at cumulative excess mortality.
We’re comparing countries here in regards to excess mortality per capita. Up until early 2021, it looked like Sweden’s refusal to stop the spread of this virus caused significant excess mortality. It’s only later on, when it becomes clear that there is no significant difference. Countries that sought to reduce the spread of SARS-COV-2 (and thereby stopped other respiratory viruses from spreading too) merely ended up at the same place as Sweden later on.
If we take into consideration that Sweden in 2019 saw an unusually mild flu season, it looks as if you can have zero excess mortality from SARS-COV-2 as a country, simply by not interfering with its spread:
This virus needs to catch your body by surprise, for it to kill people who were not already in very poor health. To a body that receives constant training through exposure to other respiratory viruses, SARS-COV-2 is not able to cause the sort of damage that translates into significant excess mortality, at least not within the years of observation we have available so far.
Again, I like to think of myself as an intellectually honest person. From march 2020 onwards, I have been telling you that this virus is a nothingburger, that you should not fear it and should not implement the kind of totalitarian technocratic measures we saw implemented around the world. Had Sweden now been at the top of the charts in regards to cumulative excess mortality, I like to think I would be writing a post now, explaining that I was wrong, that you do need to painstakingly avoid running into this virus.
But when I look at the data we now have available, I can’t help but conclude that I was right. For elderly people in nursing homes with a few months of life expectancy left, SARS-COV-2 is intrinsically very dangerous. For the population as a whole, it only becomes dangerous when we engage in very stupid unprecedented experiments, like mass vaccination, wearing masks and social distancing. These experiments disrupt the natural balance that exists between humans and the community of respiratory pathogens that infect us. That’s what kills and injures people.
Of course not all measures that were implemented actually do much of anything. The masks that people were forced to wear are generally not very effective at stopping people from getting infected by respiratory viruses. But if you continue with the experiment long enough, if you move to N95’s, or those weird cyberpunk things the Zero COVID wokies wear these days, along with goggles for your eyes so you end up looking like an early 2010’s cybergoth at a German industrial dance club, you should probably be capable of preventing yourself from getting infected by any viruses at all. And that’s a terrible thing, not a good thing.
Your muscles respond to mild injuries through overrepair. This is the science behind weight-lifting. Small tears in your muscles lead your body to overcompensate and you end up with bigger stronger muscles as a result. Of course this only works if you progressively challenge your muscles with bigger weights, at the limits of what your muscles can handle. The kind of weights an experienced bodybuilder uses would merely lead to painful injuries for a novice, rather than to muscle hypertrophy.
Your bones are similar. The bones are strengthened through exposure to pressure beyond what they would normally experience. The body adjusts to such exposure. With most drugs that people expose themselves to you also see compensation, the body adjusts itself to be able to cope with such insults. Alcoholics, opioid addicts, teenagers who take Benadryl, almost every drug has effects on multiple tissues in the body, that adjust to be able to cope with the change to their environment: Enzymes that process these drugs are increased in the liver, receptors affected are downregulated, etcetera.
The effect even exists for strokes. We call it ischemic preconditioning. Temporarily reduce the supply of oxygen to a tissue and the tissue will develop adaptations that then help it to reduce the damage caused from a much stronger insult (a stroke) later on. We’re descended from organisms that have had to adjust to wildly different environments and conditions throughout the course of evolution, an outgrowth of that reality is that our bodies can learn to adjust to very extreme conditions, provided we are trained through exposure to less severe conditions.
And so I wish to ask you: If we see this effect in just about every tissue, why would the tissues affected by SARS-COV-2 be radically different? With the evidence we have available, we can say they’re not. As people living in industrialized societies, we’re able to survive outbreaks of respiratory pathogens that would decimate uncontacted hunter-gatherer tribes. The reason we are able to survive such outbreaks is because we are constantly exposed to a wide variety of other respiratory pathogens: The milder insults set us up to be able to live through bigger insults.
The best example we have, a natural experiment in which some island communities were decimated by a respiratory viruses, whereas others had comparatively low death tolls, was the 1918 outbreak of influenza. Whereas in Hawaii 0.4% of the population died, on islands that had far less contact with the outside world like Samoa, 22% of the population died. Exposure to other respiratory viruses, including other forms of influenza, trained the body to be able to deal with this highly virulent strain of Influenza. Although such prior exposure events would inevitably also have killed some people, this translated into an overall lower death toll from respiratory pathogens.
We don’t choose the era in which we are born. You and me happen to have been born into an era where we would be faced with repeat infection by a SARS corona virus. It is a source of great misery, but this virus will be part of our population’s microbiome for the foreseeable future, whether we like it or not. Unless you wish to end up like the Andaman islanders, you have no real choice: The only way to survive this storm, is to sit through it.
Most people will be familiar with T-cells and B-cells, how these cells protect you from respiratory pathogens and how they are sometimes exposed to other respiratory pathogens that provide cross-reactive immunity against SARS-COV-2. But the body’s response to respiratory pathogens extends far beyond this. There is trained immunity against pathogens.
This doesn’t just involved your NK cells, it involves tissues in your body that we generally don’t really think of as part of the immune system, like your endothelial cells and your stromal cells, which give rise to your connective tissues. Rather than being able to draw strict line when it comes to which cells in your body are part of your immune system, there’s a grey zone, with cell types about which we can argue that they play some role in defending us from pathogens. An example are your endothelial cells, which line your blood vessels.
For your lungs, the same principle applies as for other tissues, like your muscles and your bones: Insults from mild respiratory viruses prepare them to be able to cope with more dangerous respiratory viruses, like SARS-COV-2. That’s why isolated communities fared so poorly during the 1918 pandemic: They had received very little training from other respiratory viruses.
Take a look at what the authors of this study wrote:
In this review of experiences during the 1918–1920 pandemic period, influenza–pneumonia-related mortality varied by more than 50-fold during pandemic-related epidemics on various Pacific islands; mortality seemed correlated with the island’s degree of contact with outside epidemiological sources as marked by the number of steamships arriving in the major island ports. In the early 20th century, islands were connected to the outside world by trans-oceanic steamships (which travelled at <14 knots); obviously, the interconnectedness of island communities has enormously changed since then. The extreme globalization that occurred in the last century has enabled continuous circulation of antigenically diverse influenza viruses and other respiratory microbial agents; hence, the epidemiological conditions that set the stage for the extraordinarily lethal 1918–1920 pandemic are unlikely to recur.7
Other aspects such as socioeconomic status, along with living and environmental conditions, may have also played a major role in population-level mortality. In 1918, the most isolated island populations may have had more virulent clinical expressions of influenza because their lung microenvironments were not well “conditioned” by prior inflammatory events. (Figure 1) Epidemiological and animal model data demonstrate that infection with a respiratory pathogen alters subsequent immune responses to unrelated respiratory pathogens; the effect is long lasting and does not depend on T and B lymphocytes. The alteration may arise from airway remodeling of damaged tissues, alteration or redistribution of lymphatics and vascular tissues, modification of epithelial cells, and/or resetting of the activity of innate immunity.36 Islanders with a narrow range of exposures to respiratory infections prior to 1918 would have experienced the 1918 influenza virus with lungs qualitatively different from those who had had multiple respiratory infections prior to 1918 (e.g., military service veterans).
And finally, read this part:
Repeated infections with antigenically diverse respiratory agents continuously alter and further partition the memory T-cell pool; as a result, no single specificity is over-represented among the memory T cells. Over-representation of a memory T-cell clone may not benefit the host when re-exposed to the cognate T-cell epitope. For example, when CD8+ T cells lyse virally infected cells, they produce abundant quantities of pro-inflammatory cytokines with characteristic clinical manifestations, for example, cachexia, fever, vascular leakage, and respiratory failure. Successive infections may alter the relative proportions of each memory T-cell clone in an attrition process. There is limited space to accommodate memory T cells, and diverse respiratory infections progressively decrease pre-existing T-cell populations. A richly diverse T-cell repertoire, as in persons with many previous respiratory infections, could lead to a smaller clonal burst size with less immunopathologic effects.
This fits what I have sought to explain to people before: The narrowing of people’s immune repertoire from mass vaccination is dangerous. One of the most effective and simple ways we have available to undo that damage, is for affected people to be exposed to other respiratory viruses, in communities where people have not participated in this stupid experiment.
Endemic viruses that have co-evolved with their hosts for very long periods of time, are to some degree symbiotic organisms. We don’t really study the positive effects of viruses on the human body much, we mainly focus on the harm they cause. As an example, there are a number of studies that suggest a natural measles infection reduces later risk in life of cancer. As a society, we chose the path towards extermination of measles. This will have saved some children from lifelong illness and death. But is this the most effective path we could have chosen? Would we have been better off, if we had focused on controlled exposure, with access to high doses of Vitamin A? These are questions to which it’s hard to give a proper answer.
Somewhere between the extermination of smallpox and the extermination of relatively benign respiratory viruses like the hCov viruses, we begin to reduce human quality of life. There’s a large gray zone full of uncertainties, where I don’t feel comfortable voicing an opinion. I don’t claim to know whether people are better off vaccinating their children against measles or not.
What I do claim is that when we reach the outer edges of the spectrum, when you start preventing respiratory viruses that kill a handful of elderly in nursing homes every year from spreading, you start causing more harm than benefits. SARS-COV-2, whether you like it or not, is here to stay. Anyone who wants to have a normal social life, will have to be able to live through an infection from this virus.
The sort of measures that would reduce transmission of SARS-COV-2, like UVC lighting and high quality masks, can not stop the transmission of SARS-COV-2, without also stopping the transmission of other benign respiratory viruses. That’s a dangerous and harmful thing. It has the effect of making people more susceptible to severe disease, upon being infected by SARS-COV-2.