She’s 86 yet she looks like she’s in her 60s. After 35 years of Myelodysplastic Syndrome she is still beating the odds every day.
In our conversation, she explains her radical outlook and her success under the watchful eye of oncologist Dr. Azra Raza at Columbia University in New York City.
To learn more about Azra’s work, visit www.reversingcancer.org or contact John Correll [email protected].
Podcast: https://evo2.org/podcasts/donna-meyers-is-still-beating-cancer-after-35-years/
Download The First 3 Chapters of Evolution 2.0 For Free, Here – https://evo2.org/evolution/Where Did Life And The Genetic Code Come From? Can The Answer Build Superior AI? The #1 Mystery In Science Now Has A $10 Million Prize. Learn More About It, Here – https://www.herox.com/evolution2.0
Dear Perry Marshall
Hopefully, this message will get to you.
My name is Izhar Shtrom. I am a computer engineer by training, but in recent years I have been working on a hypothesis in the fields of genetics and evolution, while conducting independent research into the biological world. The hypothesis is theoretical and based on information theory, centered on the role of the DNA as information. It focuses on the question of how a single cell knows to start replicating itself, organizing spatially, and differentiating into a unique form and structure to create a living organism, while examining the information required for this process, as well as limits and theoretical lower bounds for compression.
The central argument is that the DNA in the first cell, the fertilized egg, along with its epigenetic structure, cannot theoretically contain all the information required to create a living organism. The claim is that there are gaps, on the order of magnitude, between the amount of information needed and the amount of information that can be stored. The hypothesis suggests that the central dogma of biology is incomplete and that DNA is only part of the blueprint for creating a living organism.
To clarify this in a single sentence, I would like to use an analogy. Nyquist’s theorem defines a theoretical bound for information. To ensure that a signal can be perfectly reconstructed from its samples without loss of information, the sampling rate must exceed a theoretical lower bound, the Nyquist frequency, which is twice the highest frequency in the signal. Analogously, the claim is that to ensure a living organism can be perfectly reconstructed from its ancestor, the sampled information must exceed a theoretical lower bound. The argument is that the information capacity of DNA is substantially below this theoretical boundary, and the amount of missing information is on the order of magnitude, thus necessitating the existence of an additional molecular information layer beyond DNA, governed by a mechanism not yet known to science.
The hypothesis also focuses on the question of how the spider knows to spin a web and the bird to build a nest, examining an organism’s innate knowledge and how its information was created. The main argument is that the Weismann barrier is theoretically incorrect and conceptually obscures the second cornerstone of species evolution: the transfer of information between generations.
In recent months, I have been meeting regarding this matter with many professors in the fields of biology and information theory.
In one of your YouTube lectures, you said: “Information is the central question in biology”. In your book Evolution 2.0, you claimed that Neo-Darwinism should expand beyond the framework of random mutation and natural selection. The hypothesis supports your claims, as well as those of Professor Barbara McClintock, Professor Denis Noble, Professor James A. Shapiro, Professor Alfonso Martinez, Professor David Glanzman, Professor Michael Levin, Professor Eva Jablonka, and Philip Ball.
I would be happy to discuss and present to you the main arguments and their implications.
Regards,
Izhar
Izhar,
I totally agree with you and it is abundantly clear that the Weismann Barrier is wrong. Denis Noble has written many papers about this.
It is very much true that DNA only has a fraction of the information necessary to build an organism. We have known for decades that body plans for example are not coded in DNA but reside elsewhere. People in developmental biology know this quite well.
Levin has shown that building parts in embryonic development is a live real time engineering problem, not the robotic steps of an algorithm.
I think you can cite all of this work to strengthen your case – it’s pretty easy to find – and it will be interesting to see what else comes from your mathematical proofs.
“We have known for decades that body plans for example are not coded in DNA but reside elsewhere”
There are the HOX genes
Hox genes are critical regulators of body patterning during embryonic development, but they do not provide a complete template for the entire developmental process. Large parts of development are controlled by bioelectric fields. The control mechanisms that define bioelectric fields guiding embryonic development come from a combination of tissue biomechanics and biochemical signals. These signals are changed in real time in response to what is going on around the embryo. Much of this is not coded in the genome. REF Connexin43-dependent bioelectric gradients and their role in tissue stress and Yap/Taz signaling activation ([Silver et al., 2020]).
One of the things that comes up from the hypothesis is that, in Cancer, the observed DNA mutations are not the ’cause of’ but rather the ‘result of’.
By analogy, if there is a large forest fire and the question is how it started, DNA is not the match that ignited the fire but rather the pine tree that helped it spread. The hypothesis proposes that the DNA mutations observed in cancer are a consequence of uncontrolled replication, in which the cell and its DNA error correction mechanisms do not have the time to recover after replication, leading to an accelerated accumulation of DNA mutations in the duplicated cells. In other words, the hypothesis suggests that the problem can start in a group of cells with perfectly normal DNA.
Now, if uncontrolled replication begins, DNA mutations will start to accumulate, igniting a small fire. If these mutations occur in less critical parts of the DNA, there is a good chance that the fire will extinguish itself or be put out by the firefighting forces – the immune system and the cell’s self-destruction apoptosis mechanisms. However, if one of these errors occurs in a gene that is a hallmark of cancer, such as P53, the first pine tree ignites. At this point, the firefighting forces will find it increasingly difficult to contain the fire, but still, they might succeed if they respond quickly and the conditions are favorable. But if, before the fire is put out, mutations also reach other critical genes like KRAS, MYC, BRCA1/BRCA2, additional pine trees will catch fire, and the spread may exceed the system’s ability to control it. At this stage, an out-of-control wildfire may develop, and this is the stage that, normally, we first detect the fire with our current detection tools. The hypothesis further suggests that the information driving this uncontrolled replication mainly comes from outside the cell, is not encoded in its DNA, and is part of the missing information layer that cannot be encoded in DNA.
I reviewed your Origin of Life, Evolution, Cognition and Cancer lecture at ASA 2022 and the recent meeting with Denis Noble on the Justin Brierley channel, where you discussed the Cancer Evolution Working Group, which operates under the assumption that we have been using the wrong definition of cancer for the past fifty years. The hypothesis suggests that this is not just an interesting perspective but the correct way forward.
Yes that’s where all this is headed.