Life insurance company: Under Covid, the number of deaths of working age in the United States has increased by 40%

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On the one hand, we may have some pleasant Covid news, because Omicron may indeed have a lower hospitalization rate. The idea that it usually does not stay in the lower lungs and produces viral pneumonia seems to be confirmed. GM provides technical explanations for people who like this kind of stuff:

I think I haven’t explained it before, but it seems that Omicron’s S1/S2 cleavage is very poor, even though FCS [furin cleavage site]If you only look at mutations, it is expected that they will actually be enhanced. But it seems that the overall conformation has changed, and the loop previously exposed to the protease is now closed most of the time. So it will not be split. This means that it now no longer depends on the TMPRSS2 protease, but only on ACE2. No one expected such a change-it seems that the ACE2+TMPRSS2 approach is always more effective, but here we are.

This also requires some explanation, but this cartoon illustrates it well:

There are basically two ways-endosomes, which require the endocytosis of the entire virus particle, which does not depend on S1/S2 cleavage, but only on ACE2, and direct fusion, which depends on ACE2+TMPRSS2.

But the interesting thing is-there is actually almost no ACE2 in the alveoli, only AT2 lung cells express it, even there it is not so high. The cause of the infection is a little bit of ACE2 plus a lot of TMPRSS2. So it uses a fusion method. Then it drives the formation of syncytia, which is very destructive.

But without S1/S2 cracking, it can only rely on ACE2.

Once again, the alveoli are not superfluous, but there are many in the bronchi.

As a result, the tropism changes, and milder respiratory symptoms may appear-lower lung infections are less, and there is less fusion between cells. An important warning is that we don’t know what’s happening in other parts of the body, how many LongCOVID there are, etc…

But then there is another question about SARS-1. Because SARS-1 is also very poor in S1/S2 cracking, but its pathogenicity is much stronger than SARS-2. So what is the mechanism there? A possible explanation is that SARS-1 is more powerful in shutting down IFN signaling, so it can replicate to higher levels in the body before innate immunity begins. This allows it to turn the lungs into mucus even without FCS…

What to see.

GM also stated in another article that this in-depth understanding of Omicron (he had no one fully sequenced the virus in the early days and made a weird explanation for the flawed shortcuts) means Omicron and Delta You cannot benefit from cross-mutation even if this happens now. If this happens, there may be adaptive gains.

However, as GM pointed out by the way above, we still don’t understand Omicron and long-term Covid. Omicron also hit the children severely. Children under five years old are one of the demonized unvaxxed because Pfizer admitted that its injection did not cause enough antibody responses in children between two and five years old:

On the other hand, even though Omicron may be less lethal, obtaining it will not bring lasting immunity. The baseline number of deaths due to Covid, especially young people who are generally considered to be less vulnerable, has been revised upwards. From the central square (Hat prompts Paul R):

Head of Indianapolis-based insurance company OneAmerica [with $100 billion in assets] It is said that the mortality rate of the working-age population is a staggering 40% higher than the pre-pandemic level.

The company’s chief executive, Scott Davidson, said at an online press conference this week: “We are now seeing the highest mortality rate in the history of this business — not just at OneAmerica.” “Everyone involved in this business The data is consistent.”…

Davidson said that the increase in the number of deaths represents a “huge number” and that it is not the elderly who died, but “mainly people of working age between 18 and 64” who were employees of a company that has a group life insurance plan through OneAmerica .

“What we saw in the third quarter, we saw it lasted until the fourth quarter, and the death rate was 40% higher than before the pandemic,” he said.

He said: “Just to let you know how bad this is, three sigma or once in 200 disasters will increase by 10% compared to before the pandemic.” “So 40% is unheard of.”…

Davidson said that most of the death claims filed are not classified as COVID-19 deaths.

“The data shows us that the number of deaths reported as COVID deaths greatly underestimates the actual number of deaths among working-age people caused by the pandemic. Their death certificates may not all be COVID-19, but the number of deaths is huge and huge. Number.”

He also stated that the company has seen a “rise” in disability claims, initially short-term disability claims, and now increasing long-term disability claims.

Now you might say, but is this inconsistent with the estimated number of excess deaths? Yes, but insurance companies are in a better position to obtain detailed information about deaths, and Davidson said his company’s experience is shared across the industry. Second, people often forget that some changes during Covid will reduce the number of deaths. For example, in the first wave of Covid in early 2020, Alabama was blocked due to an expected peak of infection, which proved to be mild compared to places like New York and California. Due to the reduction in driving and road accidents, the death toll in Alabama is negative.

Until you try to find a silver lining, this news is unlikely to be beneficial to Social Security’s solvency. Although the United States is a sovereign currency issuer, we can pay for social security if we want, but it is customary to operate as a trust. More people dying prematurely means fewer people are paying for the system. More people getting younger also means fewer payments entering the system and some (most?) receiving Social Security disability. A more serious elderly population means higher medical insurance costs.



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