In my previous posts, I laid out the steps which led me to formulate the hypothesis that Hamartia, or the "sin nature," was both biological and hereditary in nature. That it came down to an abnormally formed amygdala in human beings as compared to other primates, that this malformed amygdala produced the distinctly human phenomenon called "morality," that it produced what we know as the "ego" or self-identity, and that it is directly or indirectly responsible for why all modern humans, that is, all descendants of 'adam experience death.
In this concluding post, I wanted to briefly add one more piece of information which I recently became aware of which also pertains to this discussion, and this is about the genes which are responsible for the development and formation of the human amygdala, and specifically, the STMN1 gene which is responsible for the production of Stathmin.
I had originally thought that there would be no way to discern which gene or which genes might be responsible for Hamartia in human beings. Then, testing that assumption, I did a Google search and asked the question. The answer the AI search bot gave back, and the journal links it led me to were far more than I was expecting. As it turns out, we know quite a bit about which genes are responsible, "stathmin (STMN1)" and the "serotonin transporter (SLC6A4)" gene which are linked to variations in amygdala size and function, potentially impacting emotional processing; additionally, genes related to autism spectrum disorder (ASD) like PTEN, ADNP, and FOXP1 are expressed in the developing amygdala and may play a role in its structure." (AI citation from Google Search based on journal articles from the NIH).
What's really interesting about Stathmin (produced by the gene STMN1), which is a protein that regulates the cell cytoskeleton, is that when it is deficient in mice, they have a decrease in innate and learned fear, but an increase in social interactions. Furthermore, variations in the size of the amygdala is "significantly associated with allelic variation in the stathmin (STMN1) and serotonin transporter (SLC6A4) genes, which have been linked to healthy and disordered affective processing." (Wikipedia) Stathmin is also implicated in the growth of cancerous cells as well.
I do not know all the implications of this new piece of information, but as I have previously discussed, Hamartia is the abnormal development of the human amygdala (as compared with other primates) leading to an overreactive or hyperreactive human survival response, dominated largely by the fear response; fear of not having what is needed for survival and fear of perceived threats. This fear response obstructs the brain's ability to communicate with the Logos, or God Himself who is Love, of which every human soul is a part. That a reduction in Stathmin, which is produced by a key gene in the amygdala's formation, should also decrease innate and learned fear and should result in an increase in social interaction (in addition to being associated with various disorders and illnesses) seems to me to immediately suggest a potential candidate, STMN1, for a flawed or malfunctioning gene responsible for Hamartia as I have described it. Speculating, perhaps it was originally weaker in our pre-fruit ancestors, and during human development, produced an amygdala which would only respond to genuine threats rather than everything. It is just speculation, but it's a new line of inquiry to look into, and once again, for me it lends more strength to the validity of my hypothesis.
It is my genuine hope that this cross-disciplinary approach involving the theological, the psychological, the neurological, and now the genetic will help to produce a better understanding of our inherited human flaw and ironic propensity towards negativity and self-destruction even as we seek our own survival at any cost.
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