All Biological life on earth is possible because of a discrete digital mechanism of preservation and replication.

The mechanism of signaling between the superorganism we know of as bacteria and its ongoing war against viruses is through a digital mechanism.
The source of innovation in biology is in this milieu of microbiome and viromes that are ubiquitous in every complex multicellular organism on earth. Humans are walking ecologies and cannot survive stripped of these ecologies.
We can picture this as a cloud of digital interaction that surrounds all of us.
The cells of multicellular creatures however do not communicate in the same way as bacteria. The DNA of mammals are sequestered from daily activity so as to prevent wear and tear.
The lifespan of mammals are related to their metabolism. The faster a mammal's heart beats the less time it has to live. A multicellular creature degrades like an analog system with each iteration error is accumulated.
Death is inevitable for multicellular creatures because our bodies have similar dynamics as non-linear systems found in chaos theory. The attractors that lead to our existence can lead to chaos and thus death.
Fortunately, evolution has gifted us with some of the digital mechanisms that bacteria have. The immune system is digital in nature. The same system that protects us from bacteria and viruses is also the same system that corrects for errors in our bodies.
At higher scales, evolution creates species that are more analog. But there is a constant tension between the drive to become analog and the need for preservation and replication.
All biological creatures balance these opposing forces by leveraging what is known as code duality. Every system has both an analog part that meets with the world and a digital part that preserves itself against the world.
In biology, the stuff that interprets the digital code of RNA are analog devices. More specifically, mechanical and electrical nano-machines.
The molecular machinery that converts energy into motion and energy into sensing are a consequence of biological innovation happening at bacteria and viral level.
But what meets the reality of physics and chemistry are analog machines. Living things require analog machinery to interpret and act within the world. The language of reality at higher scales is an analog language.
But to scale in size any organism requires digital mechanisms. Therefore this code duality must exist at many scales in a complex organism.
A common idea about the brain is that it is a dynamical system. A dynamical system is unlike a digital system like a computer. Brains have evolved to make sense of and move within their environments. They can only do so if they meet with the analog environment.
This idea however is an incomplete picture in the framing of code duality. The brain should have a digital component as predicted by this hypothesis of code duality. That digital component shares the same origin as our immune system.
Our immune system has the fascinating capability of recalling all the pathogens that have attempted to infect the body. What is the mechanism of this incredible memory system?
I've mentioned earlier that the human cognitive system consists of 3 'brains'. The nervous system, the endocrine system and the immune system. It's a very different triune brain that people conventionally think of.
The difference with biology and things that we design is that the latter has a designer that organizes things. So in a computer, the common currency is electrons. In biology, there is no common currency but a bureaucracy of transactions between different incompatible coins.
RNA has a surprisingly common currency (i.e. nucleotides). It is universal across earth originating living things. The power of digital systems come from a multitude of possible combinations. This only comes from standardization that leads to compatibility.
So evolution despite not having a designer with a mind, it has arrived at a strategy that acts like it has a mind!
@threadreaderapp unroll

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"The new answer to a 77-year-old problem"

😭


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@mugecevik is an excellent scientist and a responsible professional. She likely read the paper more carefully than most. She grasped some of its strengths and weaknesses that are not apparent from a cursory glance. Below, I will mention a few points some may have missed.
1/


The paper does NOT evaluate the effect of school closures. Instead it conflates all ‘educational settings' into a single category, which includes universities.
2/

The paper primarily evaluates data from March and April 2020. The article is not particularly clear about this limitation, but the information can be found in the hefty supplementary material.
3/


The authors applied four different regression methods (some fancier than others) to the same data. The outcomes of the different regression models are correlated (enough to reach statistical significance), but they vary a lot. (heat map on the right below).
4/


The effect of individual interventions is extremely difficult to disentangle as the authors stress themselves. There is a very large number of interventions considered and the model was run on 49 countries and 26 US States (and not >200 countries).
5/
JUST ONE PERSON—UK 🇬🇧 scientists think one immunocompromised person who cleared virus slowly & only partially wiped out an infection, leaving behind genetically-hardier viruses that rebound & learn how to survive better. That’s likely how #B117 started. 🧵 https://t.co/bMMjM8Hiuz


2) The leading hypothesis is that the new variant evolved within just one person, chronically infected with the virus for so long it was able to evolve into a new, more infectious form.

same thing happened in Boston in another immunocompromised person that was sick for 155 days.

3) What happened in Boston with one 45 year old man who was highly infectious for 155 days straight before he died... is exactly what scientists think happened in Kent, England that gave rise to #B117.


4) Doctors were shocked to find virus has evolved many different forms inside of this one immunocompromised man. 20 new mutations in one virus, akin to the #B117. This is possibly how #B1351 in South Africa 🇿🇦 and #P1 in Brazil 🇧🇷 also evolved.


5) “On its own, the appearance of a new variant in genomic databases doesn’t tell us much. “That’s just one genome amongst thousands every week. It wouldn’t necessarily stick out,” says Oliver Pybus, a professor of evolution and infectious disease at Oxford.

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