COVID-19: My Final Hypothesis

Main insights from 30 months of analysing mortality data and scratching the surface of epidemiology, virology, immunology and geography!

Introduction

I was asked recently for my top 10 insights by someone who was completely new to my work. I had been meaning to produce a summary for some time, so here it is (well 16 “insights” to be exact).

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When I first started investigating “COVID”, there was a very popular hypothetical strategy floated by Tomas Pueyo called Coronavirus: The Hammer and the Dance. Tomas seems like a really clever chap and writes eloquently. However, I said at the time that his piece was nonsense and I still believe it.

His problem (and why he appealed to so many people) was that he was blinded by the hysteria. This blindness made him overlook the single most important fact:

COVID is only a problem for people with some form of compromised immunity and/or comorbidity.

It has always been thus.

As Dr McCullough would say - “it is amenable to risk stratification and effective early treatment” (whatever “it” is, which you will understand is not actually that important if you read on).

The “hammer” approach is actually a great analogy. It’s just like this other one: “A sledgehammer to crack a nut.”

My favourite way of expressing it at the time was taking a homogenous approach to tackling a heterogeneous problem.

Absurd, illogical, inefficient, doomed to inevitably fail even absolutely let alone in terms of relative cost/benefit.

Several months later, the best epidemiologists in the world articulated it in The Great Barrington Declaration.

What’s truly incredible is that any of this needs saying. I can still clearly recollect Covidians arguing that it was not easier to protect the vulnerable (who were already mainly corralled in hospitals and care homes anyway) who numbered no more than 2% of the population, than it was to shut down the other 98%.

The second reason why the hammer strategy is nonsense is because it completely also ignores this little nugget of eternal truth:

Millennia of conflict between viruses and humans have been played out in battles that are always self-limiting for one reason or another, most importantly related to seasonality.

Any “model” that assumes exponential growth, or indeed any unfettered growth at all, as a baseline should find its way to the bin more quickly than an Expert™ can flip-flop on mask advice!

Utter nonsense.

These models and the stupid interventions imposed by the idiots in charge were all based on the false premise that COVID was novel.

It wasn’t.

And we knew it wasn’t right from the start.

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My Final Hypothesis

Fast forward 30 months (27 months since my last "final" hypothesis) and this is my final hypothesis (subject to change if new information comes to light!) based on in-depth analysis of COVID data, mortality data, and supporting science¹:

1. People die.

2. People die more frequently at certain times of the year.

3. Periods of higher mortality are typically associated with the prevalence of influenza-like pathogens (ILPs²).

4. ILPs are present all year round but may lie dormant in some hosts, reactivated at certain times when their immune systems are relatively weak.

5. ILPs impact the population (in terms of infections and illness) as a constant battle with the host population’s immune system and their metabolic health to fight off infection and disease progression.

6. The battle between ILPs varies mainly due to variation in levels of immunity of the host, and to a lesser extent due to variation in pathogenicity of the ILP (not least because nature logically selects for the most transmissible, least virulent mutation).

7. Immunity levels are a function of multiple factors but they are all related to age, general (metabolic) health of the host (which in turn is related to nutrition and stress), and the physical environment.

8. COVID exists (but isn’t really novel).

9. The virus that causes COVID (SARS-CoV-2) was re-engineered in a lab to make it more infectious (the latter part being its only novelty).

10. It is impossible to suppress the spread of a respiratory pathogen to the extent that community spread has a positive impact on severe outcomes, including death, without total isolation of every member of society. Thus, I acknowledge the theory of transmission but surmise that no lives were saved by non-pharmaceutical interventions, not even in the immediate term.

11. If COVID had been treated like all other ILPs (anti-virals, nutraceuticals, social care), the overall excess mortality would not have been unusual.

12. Acute spikes in excess mortality are due to a myriad of causes, substantially how the vulnerable/susceptible are treated (or not!), and not as a function of the amount of ILP circulating in the community (although some has to be present, which it always is).

13. Excess, non-COVID mortality arises directly from futile interventions designed to mitigate the spread of the ILP, including disruption to healthcare provision and inappropriate medical treatment.

14. The mRNA “vaccine” is not Safe or Effective™.

15. The mRNA “vaccine” causes immunosuppression (or sub-optimisation of the immunological response), leading to increase in infections and progression to severe disease (see #5 and #6).

16. If you really wanted to “save” public health systems and avoid untimely deaths, you would tackle a heterogeneous problem like COVID with a heterogeneous activity - protect the vulnerable from exposure to the ILP and do things to improve their immune systems if it’s even possible (immunosenescence probably cannot be overcome) - see #1.

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The Evidence

You can peruse my previous articles and references back to older stuff pre-Substack for the evidence that leads me to this main hypothesis.

However, I can also illustrate my hypothesis with the tale of three US states:

1. Utah

2. Colorado

3. Kansas

And some questions that public health authorities should be asking at the very least, if not working hard to answer.

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Between March and June 2020, when the ILP that causes COVID first emerges in these three neighbouring US states, notwithstanding any potential confounding due to testing rates, there appears to be plenty enough “cases” to state that it is equally prevalent in all of the communities.

Even though Colorado appears to have more COVID, all three states had very similar initial responses in an attempt to “flatten the curve” with their “hammers”. Colorado perhaps emerges as the overall “winner” but vying with Kansas over the period to end of May 2020.

And yet, Colorado is the only state that exhibits any deviation in terms of excess mortality from the activity of whatever other ILP was doing its thing up to the point that COVID took over. And it’s substantial³.

I refer to points #11, #12 and #13 of my hypothesis.

Question for Public Health: to what extent is the idiosyncratic excess death in Colorado the result of how the vulnerable were treated as opposed to the direct pathogenicity of the virus? In other words, how come the same virus did not affect mortality at all in Kansas and Utah at the time that it wreaked absolute havoc in Colorado between them?

Although it is quite apparent that the subsequent increase in COVID incidence from June 2020 manifests in relatively higher excess mortality in Utah (who ease “measures” soonest) and subsequently Kansas, this is against a backdrop of a higher general level of excess mortality in Colorado, that never returned to baseline like the other two.

It seems to me that all the communities have lower levels of immunological resistance in the battle with the ILP than they would normally have at this time of the year, probably as a result of the stresses imposed by the interventions designed to control the spread. How ironic.

I refer to points #4, #5 and #6 of my hypothesis.

Question for Public Health: to what extent do ILPs persist in the population during the summer season but never manifest as infections or disease because population-wide immunity levels have never been compromised in the past, like they were immediately after the COVID measures?

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When the incidence of ILP activity increases in the following autumn⁴, there is nothing to choose between the three states up until the end of the year.

Not only is this a clear indication that seasonality plays a part but also that these three states are very good analogues for each other in terms of climate, population density, demographics, etc., all the things that would ordinarily be expected to influence the spread of a respiratory virus.

Moreover, looking at the scale, incidence has increased five-fold. There is lots more ILP circulating in the community. And yet, there is not the same relative amount of excess death:

This is inevitable because ILP mortality is a heterogenous thing! It doesn’t matter a jot how much virus is circulating in the community, only how much gets to the susceptible population and how they respond. This should be obvious by now? It was even a logical deduction before the empirical evidence!

Question for Public Health: to what extent is relatively lower level of excess mortality in Utah, compared to Colorado and Kansas, the result of easing of “measures” sooner during the prior spring?

I find it noteworthy to mention the second spike in cases immediately post the mRNA campaign, much more so in Kansas and Utah than Colorado. But then there is an obvious bout of infections in Colorado between April and May 2021 that is not apparent in the other two states. In the latter case, could this be younger people huddled together in ski cabins?

I refer to point #15 of my hypothesis.

These waves do not manifest in equivalent new distributions of mortality.

Question for Public Health: is there no new deaths following the second and third waves of infection because community infections do not impact mortality if they do not affect the susceptible population? In other words, attempts to control community spread are futile, even if they were successful, if you don’t protect the vulnerable?

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By summer 2021, there is almost as much incidence of COVID as during the winter period, which is unusual. This is “in spite” of substantial amounts of “vaccination” across all three states that was purported to stem transmission.

OK, so that lie was well and truly exposed and only a few really stupid Covidians are still believing it even though the mantra of “protecting others” and even mandates are still being upheld in some situations.

Not only that, but the notion that the “vaccine” protects against severe disease progression and even death is also not apparent in the data:

Mortality has seemingly established a new baseline at around 20% excess rather than returning to zero and in the case of Utah and Colorado (who both have higher rates of “vaccination” compliance than Kansas), there is excess mortality that is consistently higher than that! And, excess mortality is still correlated with COVID even though it is supposed to mitigate this severest of outcomes.

I refer to point #14 of my hypothesis.

Question for Public Health: if the COVID “vaccine” is as Safe and Effective™ as claimed, how come excess mortality is no lower since the campaign was established compared to the same period the year before and how come there is relatively more death in the two states with the higher rates?

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Finally, as we come into peak season of 2022, incidence of COVID is off the charts (note had to change the three-fold from the previous year). I surmise this is what you would get if you tested any year for the common cold which is what COVID has become by this point.

How can I be so sure?

Because, in spite of there being so much more ILP in the community, the excess death rates are comparable with the prior year, with Colorado and Kansas lining back up with Utah:

I surmise this is because the extra negative impact of the interventions imposed by Colorado and Kansas has now expired. All that remains is the excess mortality associated with the compromised immunity caused by the “vaccine”.

Note again, the super excess mortality in Colorado and Utah during the most recent summer, not experienced by Kansas that has once again returned to pre-pandemic baseline before COVID-associated spike in early August. In fact, once again, all the excess mortality is associated with COVID (even though there is relatively much less of it about in the community):

It is abundantly clear that Kansas gets their summer COVID wave several weeks after Utah and Colorado which explains the delay in their excess mortality too.

Wait, what?! did I just trash my hypothesis that the COVID ILP per se is not fatal?

No, I’ve seen this misinterpretation in some of the comments of my previous articles and in debates I’ve had in various scientific forums. So, for the record:

1. I do not deny COVID exists. See point #8.

2. I do not deny that COVID causes death. See point #3.

3. I do maintain that excess death caused by COVID is due to compromised immunity. See points #4 to #7.

4. I do maintain that immunity has been impaired by the interventions designed to deal with the ILP (social distancing measures in spring 2020 and “vaccination” in 2021 and that this leads to the excess death. See points #11, #12, #13, #15 and #16.

And so, I sign off with this:

Question for Public Health: if the mRNA experiment was ended now and instead, efforts were made to improve the metabolic and immunological health of the susceptible population, what would you expect to see result in terms of all-cause mortality?

Do you think they could answer that question?

I really wish they would try because this really isn’t my job!

As Voltaire famously said, “il faut cultiver notre jardin”.

1. I was alerted to the fact that my former colleagues at HART independently did something similar a few weeks ago with consistent insights to my own - A (Possibly Unpopular) Null Hypothesis.

2. Following from “influenza-like illnesses” that result from them.

3. For context, here is the normalised excess death in the pre-COVID era:

4. Note my very careful wording. Consistent with point #4 of my hypothesis, I believe the ILP is always present. Its level of infectivity increases due to factors that compromise the immunological resistance to infection.