Posit a species , of population size . Now imagine there’s exactly one member of the population that develops an inheritable, beneficial trait, through mutation. That person will have some number of offspring , and if the ratio is not significant, that trait will not persist, because even if it’s dominant, it will be bred out to extinction in a few generations. This presents the fundamental insight for a hypothesis I just came up with, which is that microorganisms, particularly contagious microorganisms, could drive our evolution. Now imagine instead that a virus spreads through population , causing a significant percentage of that population to develop the same mutation. In this case, it’s at least possible for the trait to persist, since a significant number of individuals all experience the same mutation at roughly the same time, due to an exogenous factor, in this case a virus. Then, selection can takeover, and if the trait is beneficial, it will persist, and if it is deleterious or deadly, it will die off. Finally, it is simply not credible to assume that the same random mutation will occur repeatedly in a population. Genomes are gigantic systems, with enormous numbers of possible mutations, and so the probability of the same random mutation occurring even twice, is so low that it’s not meaningful. 

As for the mechanics of this process, I noted in a previous article that it seems reasonable to assume that significant mutations are the result of already assembled strands of DNA being inserted into a sequence during replication. That is, during replication, there’s a free-floating, already complete strand of DNA that is inserted (presumably at the beginning or end of a genome). The intuition is that a healthy organism should not produce a significant number of erroneous insertions, and so it makes more sense to assume that an entire strand is inserted all at once, erroneously, which is technically a single error. This also explains the existence of the D-loop, since insertions would all occur at the “end”, causing a heterogenous portion of the genome to develop over time.

Returning to the relevance of microorganisms, I hypothesize that the source of these insertions (i.e., the strands that get appended) is the microorganisms in a given environment, which plainly interact with other organisms. As evidence for this claim, I realized that the Mongolians and some Chinese are from completely distinct heritages, with Mongolians plainly descended from Heidelbergensis (see the chart above and note HB stands for Heidelbergensis). Many Chinese are simply not related to Heidelbergensis in any meaningful way (though some are). Nonetheless, they are both plainly morphologically similar people. How could it be that two completely different heritages produce extremely similar morphologies? One explanation consistent with the facts is the hypothesis that microorganisms in the environment slowly change the morphology of people that live there long enough through mutations. The same is true of the Ancient Romans, who obviously look European, and are somehow not related to any living group of people, including Europeans. Both of these populations are evidence for the claim that environment impacts morphology, which sounds obvious, but the interesting part is the hypothesis that it’s due to microorganisms that drive specific mutations, on a sufficiently large scale to persist.

This could even explain the origin of humanity itself, specifically, the fact that it seems all species of hominin come from Africa. Why would this be the case? There’s no obvious explanation for it, though if microorganisms play a role, then similar mutations could occur in the same great apes, independently, at different points in history, producing distinct species of hominin, in the same locations. Specifically, e.g., the same or similar strands of DNA from the same or similar viruses end up appended to the same locations in the genome of an ape, which then kicks of selection, and so on.