Sanjeev Sabhlok's blog

Thoughts on economics and liberty

An important tweet by Niccolò @lnn1910ann

THE TWEETS, the content below:

I grow ever more convinced that the pandemic of 2020 will go down in history as a point of rupture in Western society. A few thoughts in no particular order on the subject.

  1. We have been the victims of the most draconian suspensions of civil liberties since the end of WWII. Never before 2020 was it conceivable for a government in Western Europe to “lawfully” imprison citizens into their homes because they were *potentially* contagious. And yes, it was a mass house arrest, regardless of whether you think it was justified or not.
  2. The political, social, cultural, and bioethical wound that lockdowns have caused will be so hard to fix that, instead of a scar, I fear we may have an amputation: By leveraging on the citizenry’s fear—and the ability to stoke such fear through propaganda—governmental and bureaucratic power will continually increase. The state apparatus will become ever more involved in the private lives of citizens by controlling their movements and peeling away whatever is left of their autonomy over their own bodies. This is already made evident by the “Covid status checks” to access services or the divergent requirements & restrictions imposed on individuals according their vaccination status. As time goes on, I fear this will become even worse.
  3. The amputation will also be cultural. Bar a very limited number of exceptions, it has been very distressing to witness our society’s intellectual class fall in line with the bureaucracy and government. They have refused to analyze whether the dramatic suspensions of our civil liberties have been justified or proportionate, and they have failed to highlight the dangers of letting the bureaucracy encroach to such a degree on the private lives and choices of citizens. Cultural and educational institutions (universities, the media, pressure groups, religious institutions, etc.) have abdicated their role as moral compass of public opinion.
  4. Not only have they abdicated such a role, but in several cases they have also sided with the bureaucracy in promoting such invasions into private life and attacks on civil liberties. This they continue to do, without realizing the danger it poses to themselves. In addition, they are seemingly unaware that the very policies they defend go against the values they claim to defend: inclusivity, liberty, diversity, and equality and equity. It may be hypocrisy but it may also be schizophrenia. I suspect that alternative institutions able to shape public opinion are gaining ever more traction and will eventually clash with the traditional reservoir of intellectual endeavor. This clash may be traumatic for many.
  5. All this to say that the next few years may be tough under many aspects. The choices which were made over the course of 2020 have changed our lives forever, and I fear for the worse.



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Keeping track of some of the videos on Anil Ghanwat’s work







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Sorry, Alex Berenson is wrong again – for the third time

Someone shared this analysis by Alex Berenson:

People appear to die at rates 20 percent or more above normal for weeks after receiving their second Covid vaccine dose, according to data from a huge Swedish study.

The figures are buried in a preprint paper on vaccine effectiveness released last month. The headline finding of the paper was that protection against Covid, including severe cases, plunged after six months.

The researchers did not explicitly examine deaths from all causes – which have risen since the summer in many countries that have highly vaccinated populations.

But on page 32 of the 34-page report, a chart shows that 3,939 of 4.03 million Swedes who received the second dose died less than two weeks later.


Over a one-year period, that rate of death would translate into an annual mortality rate of about 2.5 percent a year – 1 person in 40 – almost three times the overall Swedish average. In a typical year, about 1 in 115 Swedes dies.

Of course, that huge gap does not account for an important confounding factor: younger people, who have a much lower risk of death, were less likely to be vaccinated.

But Sweden also provides detailed data on overall deaths nationally, making a crude baseline comparison possible.

That data shows that from an average of about 1,650 Swedes died every week between 2015 and 2019 between April 1 and early August, the period in which almost all of those 4 million Swedes in the study received their second dose. Death rates hardly varied over those years.


In other words, during the spring and summer, Sweden normally has about 3,300 deaths every two weeks – not just in the people who received vaccines, but in all 10.6 million of its people.

So let’s make an incredibly conservative assumption, one that strongly favors the vaccines. (The next couple paragraphs are a bit tricky, but I hope the payoff is worth taking the time to read and think through them.)

Assume that the group of people who received vaccines were so much older and unhealthier than those who didn’t that they would have accounted for every single death in Sweden whether or not they were vaccinated. In other words, assume that even if the vaccines did not exist, every person in Sweden who died would have been part of that group of 4.03 million people the researchers tracked – while not one other person would have died.

In that case, those 4.03 million people “should” have about 3,300 deaths every two weeks. They CANNOT HAVE MORE – because all of Sweden does not have more.

But the vaccines do exist. Those 4.03 million people received them. And in the two weeks after receiving the second vaccine dose, as a group, the researchers reported they had not about 3,300 deaths, but 3,939.

And 3,939 deaths is about 20 percent more deaths than “should” have occurred in those two post-vaccine weeks. Again, the 20 percent figure understates the real gap, because in the real world some deaths will occur in the 6.6 million unvaccinated people too, so the actual baseline number for the vaccinated group is not 3,300 deaths but somewhat lower.

Unfortunately, the researchers did not report any details on the deaths, so it is impossible to know if they are disproportionately cardiovascular. It is also impossible to know whether one particular vaccine was disproportionately linked to deaths. (Sweden used mostly the Pfizer mRNA vaccine, as well as some of AstraZeneca’s DNA/AAV vaccine, which is not available in the United States, and a small amount of Moderna’s mRNA vaccine.)

Of course, it is just possible the extra deaths are due to chance. Or that the handful of elderly Swedes who received vaccines in February and March accounted for a hugely disproportionate number of the post-vaccine deaths. (Because per-week Swedish death rates are higher in the winter, a large number of post-vaccine deaths in those months would somewhat reduce the strength of the signal, though it would still exist.)

But the caveats aside, the Swedish figures offer a very large real-world dataset apparently showing a notable increase in all-cause mortality directly following Covid vaccination.

They are yet another piece of evidence in an increasingly worrying picture – alongside case and anecdotal reports, a known link to heart inflammation in young men, the updated Pfizer clinical trial data revealing a numerical imbalance in deaths in vaccinated people, and most importantly the general rise in all-cause mortality in many countries.

And all of these red flags come for vaccines that – if the Swedish data are correct – may actually raise the risk of Covid infection after about eight months.

Yes, RAISE. See how that black line drops below the zero level on the top chart? That represents negative effectiveness, which is another way to say people who are vaccinated are MORE likely to be infected than those who aren’t.

And, as the second chart shows, effectiveness against severe Covid infection is also spiraling towards zero.

Yet the Biden Administration and governments across Europe continue to try to force more people to take these vaccines.


WELL HE’S WRONG AGAIN – for the THIRD time (for the previous two times, see this).

Alex starts off on right track here for a change – but then as usual he has missed out key issues.

Only the elderly were given vaccines in the initial stages, and their death rates are astronomically higher than that of the average population. Many of them die regardless of the vaccine. That’s what these deaths are all about.

See the age distribution of the double dose in Sweden:

In fact the signal of 20% “higher” deaths for a sample that is highly skewed towards the elderly is very low – it should have been much higher. It is low because around 3-4k of the elderly who were vulnerable have passed away due to covid – there aren’t that many left to die this year.

Overall we see from the stats that Sweden is having a HUGELY low year of deaths despite the covid pandemic spilling over into 2021. (

Let’s just say that Alex won’t be getting a job even as a junior data analyst in any analytical organisation.

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Why epidemiological models go wrong: NO ONE EVEN REMOTELY KNOWS HOW VIRUSES SPREAD. A superb paper.

This is one of the best papers for the arrogant, ignorant “modellers” to read. SCIENTISTS SIMPLY DON’T UNDERSTAND VIRUS TRANSMISSION SO WHY ARE THE FOOLS MAKING THEIR RIDUCLOUS MODELS?

Cannell, J.J., Zasloff, M., Garland, C.F. et al. On the epidemiology of influenza. Virol J 5, 29 (2008).


  1. Why is influenza both seasonal and ubiquitous and where is the virus between epidemics?
    • If influenza were surviving in an endless chain of transmissions from good transmitters to the well – the good transmitters being generally asymptomatic during times of enhanced innate immunity – the disease would be widely seeded in the population, explaining its ubiquity. Seasonal impairments in innate immunity would allow seasonal epidemics in temperate latitudes and less predictable epidemics in tropical zones, depending on viral novelty, transmissibility, virulence, and the innate immunity of the population. Non-seasonal isolated outbreaks would usually only appear in nursing homes [85] or prisons [86] where lack of sunlight impaired innate immunity; such isolated outbreaks would seldom lead to community outbreaks. More extensive out-of-season outbreaks, as occurred in 1918, would arise when novel antigenic viruses with significantly greater infectivity and virulence overwhelm innate immunity.
  2. Why are influenza epidemics so explosive?
    • Predictable fall and winter impairments in innate immunity in temperate latitudes – and less predictable recurrent impairments in subequatorial and equatorial latitudes – would cause a percentage of the non-immune population to become suddenly susceptible to background influenza virus. The size of that susceptible subpopulation would vary, not only by the size of their impairments in innate immunity, but with the transmissibility and virulence of the virus, and the percentage of the population with competent adaptive immunity. Abrupt deficiencies in innate immunity, especially when large segments of the population also have inadequate adaptive immunity, would allow quiescent influenza to erupt.
  3. Why do epidemics end so abruptly?
    • The rapid depletion of the population with both impaired innate and inadequate adaptive immunity may explain the abrupt disappearance of influenza. Impairments in innate immunity may also increase transmission, in effect, turning more infectors, symptomatic or not, into good transmitters. Furthermore, if only a small population of good transmitters – and not all the sick – usually spread the virus, and their transmission period is limited, the epidemic would end shortly after the good transmitters lose their infectivity.
  4. What explains the frequent coincidental timing of epidemics in countries of similar latitudes?
    • Simultaneous impairments of innate immunity at similar latitudes – due to seasonal sunlight deprivation – explain the almost simultaneous eruption of influenza at sites of different longitude but similar latitude. If the virus had already imbedded itself in a population and a subgroup of the infected became good transmitters when their innate immunity declines to a critical threshold, such transmitters would coincidentally infect populations at similar latitudes made susceptible by those same impairments in innate immunity.
  5. Why is the serial interval obscure?
    • Good transmitters explain the difficulty identifying influenza’s serial interval especially since influenza’s incubation period is well known. If only subpopulations of infected persons are good transmitters, and if their infectious period is limited, then the serial interval would remain obscure until we identified the good transmitters. Vitamin D induced variations in natural immunity may also affect influenza’s incubation period, further obfuscating the serial interval.
  6. Why is the secondary attack rate so low?
    • The studies we identified found a secondary attack rate of around 20%, impossibly low for a highly infectious virus spread from the sick to the well. If only a subpopulation of the infected, the good transmitters, are infective, this would explain the surprisingly low secondary attack rates. Current estimates of secondary attack rates assume the first case in the family is the index case and is spreading the disease. However, if only a subpopulation of infected persons transmit the disease, the true secondary attack rate could not be accurately determined until we identify the good infectors.
  7. Why did epidemics in previous ages spread so rapidly, despite the lack of modern transport?
    • If influenza were embedded in the population, only to erupt when impairments in innate immunity create a susceptible subpopulation, the disease would only give the appearance of spreading. Instead, it would appear in large segments of the population seasonally, and almost simultaneously, as long as good transmitters were available. Furthermore, as good transmitters traveled, populations with neither adequate innate immunity nor competent adaptive immunity may succumb. That is, the disease would actually spread, as good transmitters traveled and subsequently infected well subpopulations with impaired immunity.
  8. Why does experimental inoculation of seronegative humans fail to cause consistent illness?
    • If influenza is highly infectious, one would expect most, if not all, human volunteers iatrogenically inoculated with a novel virus to fall ill. Although the rate of illness depends on the virus used and the dose of the inoculum, variations in the innate immunity of the volunteers also explain such variable illness response. We propose individual variations in 25(OH)D levels explain some degree of the variations in illness response.
  9. Over the last 20 years, why has influenza mortality in the aged not declined with increasing vaccination rates?
    • Given that influenza vaccines effectively improve adaptive immunity, the most likely explanation is that the innate immunity of the aged declined over the last 20 years due to medical and governmental warnings to avoid the sun. While the young usually ignore such advice, the elderly often follow it [87, 88]. We suggest that improvements in adaptive immunity from increased vaccination of the aged are inadequate to compensate for declines in innate immunity the aged suffered over that same time.
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