I know that trauma is big among millennials and Gen Z, and that the idea has also caught on (and probably originated) with older school new agers, as an explanation to many of our world’s problems. Still I was surprised to see this pansplanation used to explain cancer by one of Michael Levin’s technicians/students.

Cancer due to trauma?

Levin is a maverick, challenging some dogmas in biology and consciousness research. He has also done some interesting experiments. But this hypothesis seems off to me, and Levin restates it here at time stamp 55 minutes (this is one example out of several). The standard explanation of cancer (a result of decades of research in molecular biology, epidemiology and evolutionary theory) is that it’s due to mutations in DNA. These can come from chemicals, radiation, viruses, or DNA replication errors made in dividing cells. If an organism suffers a traumatic injury, the organism tries to heal the resulting wound, and there will be more replication of cells than before the wound (at the site of the injury, at least if the injured cells have a low turnover rate), hence a higher probability of DNA replication errors. If this was all that Levin (or his student) was proposing, it would be quite reasonable. But they seem to be suggesting that the higher cancer probability comes not from a higher rate of mutations due to replication errors in trying to heal the wound, but from the cancer cells becoming disconnected from the rest of the organism, due to signaling defects in their gap junctions or ion channels. And the student is making an analogy to people who experience trauma either as an internal disconnection of some of their psychological parts during a traumatic experience, or getting disconnected from other people or nature.

But cancer is very different than people becoming internally or externally disconnected due to trauma. In the human trauma case, it’s about avoiding memories or situations or people, the internal (and sometimes external in avoidant attachment people) disconnection is a strategy for that, or sometimes the trauma is caused by the external disconnection from primary caretakers. The disconnection in the case of a cancer cell: 1. Does not always happen. Disconnection happens when it’s advantageous for a cancer cell to disconnect in order to be able to replicate and migrate to places with more resources, and connection happens when it is advantageous for the cell to connect so it can get resources from other cells. And 2. Is an effect of the mutated DNA, not a strategy to avoid pain, or a root cause of present pain, like it is with traumatized people. Supposedly (empirically) the disconnection can happen without a mutation in the disconnected cell, but I bet there is a mutation in the cells giving the signal to that cell to disconnect if the cancer is able to replicate. If there is no genomic difference, or if the difference is only epigenetic (regulatory changes including methylation of DNA and acetylation and phosphorylation of proteins) then the hereditability will not happen or be stable in the progeny of the cancer cells and they will revert back to normal cells.

The upstream cause of the cancer is not the disconnection but the mutation. Levin has shown experimentally (in tadpoles) that one can interfere in the causal chain between mutation and metastasis at the ion channel (cell to extra-cellular environment) signaling level (increasing resting membrane potential), which is NOT the gap junction (inter-cell) signaling so has nothing to do with connecting to other cells.

Public Relations contradicts peer reviewed publication

Indeed a closer examination of what Levin has published (in contrast to what he and his student say on YouTube) in a peer reviewed journal, shows that increasing connection to other cells INCREASES tumorigenesis, and tumorigenesis can be disrupted by reducing this connection, i.e. gap junction communication (GJC): “we were surprised to see that abrogation of GJC actually suppressed the effects of oncogenes, in contrast to prior suggestions that loss of GJC was a hallmark of incipient cancer” and “The most pronounced suppression of tumor incidence was observed upon GJC disruption taking place farther away from oncogene-expressing cells, revealing a role for GJC in distant cells in the control of tumor growth. In contrast, enhanced GJC communication through the overexpression of wild-type connexin Cx26 increased tumor incidence”.

So there is no evidence for a “stay connected” signal from the nucleus in a normal cell that is acting against cancer, and even if there were such evidence, it is no reason to come up with a new-agey theory equating cancer cells to traumatized human beings due to disconnection. Our hypothesis is that enhancing GJC allows tumor cells to more efficiently usurp resources from their neighbors, and conversely disrupting GJC, reduces this ability and allows cells to withhold resources from the tumor cells.

Evolutionary vs Functional levels

Levin’s hypothesis is that normal cells have some sort of intelligence which has the good of the organ or organism “in mind”, whereas cancer cells are only concerned with themselves (he frames it in terms of a “cognitive horizon”). There is some similarity to our model, but also some differences that might be tested empirically. In our model of the emergence of a new evolutionary level, once a new level emerges, the parts which may have been evolutionary levels prior, lose their evolvability, unless they are rogues (roughly free riders), or don’t interact much with other parts (though they could have heavily interacting internal parts). There are other possibilities which we are looking into where parts (cells in this case) can keep SOME evolvability (and experience some selective competition with each other, but not just for their own survival, also for the survival of the higher level, which offers them a gentler environment than the external environment for which there is no higher level) when a new level (an organ or organism in this case) emerges, but we will ignore those for now, as they are irrelevant to understanding the difference between cancer cells and normal cells. The important thing is that even if parts completely lose their evolvability, they can maintain a functional level structure, which involves some abstraction of information from other parts that they are forming a new level with, as well as functional specialization and probably more internal resource sharing than external resource sharing, enforced though constraints such as a membrane which regulates both energy, material and informational molecule transport across it, but also signaling to/from other cells. This is what normal cells are. Cancer cells on the other hand, keep their evolvability, because mathematically not contributing to other cells while taking resources from them allows them to have their own (higher than neighboring cells in the absence of some form of “punishment”) fitness and reproduce independently of the other cells’ signals. Our hypothesis is that cancer has to do with usurping resources, or not contributing as much resources as normal cells, in contrast to Levin’s, which says that cancer is about staying connected. Our hypothesis would predict that if a (non-neural) genetically cancerous cell can be induced to keep its resting potential high (with an “electroceutical”) across an ion channel, it will start sharing resources again with other neighboring cells or the whole organism, and (as we said above) that inducing a cancer cell to enhance its communication with neighboring cells across a gap junction would cause it to get more resources from its neighbors. This should be empirically testable, and is consistent with Levin’s observations so far, whereas Levin’s hypothesis that increasing cancer cell communication to normal cells should decrease tumor growth is contradicted by his own observations.

Neither our hypothesis nor Levins youtube hypothesis explains why there is a stronger effect of tumor suppression when gap junction disruption happens further away from the site of the tumor. The situation is complicated and could involve several different mechanisms, and Levin has a complicated hypothesis to explain it in the paper, not at all resembling the “connecting tumor cells to the rest of the organism heals the tumor” that he expresses on youtube. I doubt this hypothesis is correct either, but at least it is consistent with the data from the paper.