So, let’s take this pile one steaming lump at a time.
First, here is what Zach actually wrote:
Go ahead and read it. I’ll wait.
And here is what Joanna Masel and her colleagues write on the lab website, quotemined by our apologist:
In the title of a 1995 paper, Alexey Kondrashov posed the puzzle “Why have we not died 100 times over?”. We still don’t have an answer.
Literate adults can see the difference, but I’ll spell it out for others: Zach claims that load (as described within GE) is not a “serious issue to evolution” (@talkpopgen please clarify or correct as needed), while Masel et al. are saying (at the beginning of a paragraph that poses a question; see below), that we don’t yet understand why populations persist in the face of load. Masel et al. do NOT say that this is an issue for evolution. If there is disagreement between Masel et al. and Zach, it is about the extent to which the load paradox has been solved. Zach discusses several important factors, which he seems to view as “resolutions,” but he does not claim that the paradox is “solved.” I’d love to hear from him about how he views the status of the paradox today. Here, in the meantime, is what the Masel group writes on their website, in full:
In the title of a 1995 paper, Alexey Kondrashov posed the puzzle “Why have we not died 100 times over?”. We still don’t have an answer. It should take one selective death to purge one new deleterious mutation, but the mean number of new deleterious mutations per human seems to be more than 2, exceeding the number of selective deaths available. Most work on mutation load periodically renormalizes relative fitness to deal with the fact that fitness keeps declining no matter what, or else treats only a subset of the genome. Either way, this is dodging the problem, not tackling its fundamentals, which are not specific to human mutation rates or to small population sizes. One historical solution to the mutation load paradox was synergistic epistasis, often modeled in extreme forms such as truncation selection. Since then, data has come out showing that the mean effects of two deleterious mutations are extraordinarily close to multiplicative. We are exploring models by which very weak epistasis (compatible with data) might be sufficient and/or a “ratchet” occurs in which many small-effect deleterious fixations are counterbalanced by a much smaller number of large-effect beneficial fixations.
What we can all see, then, is that the apologist either doesn’t understand what he’s reading, or has chosen to quote it in ways that obscure what both Zach and the Masel lab think and do.
Now about my son and his work in the Masel lab. (He was a grad student with Joanna and finished 3 years ago.) I dare the apologist to read the most recent preprint from my kid and Joanna (and their colleagues) and then write a summary here on the forum. The preprint is here, and I’ve mentioned it on the forum before. It needn’t take more than a half hour to read the Discussion while looking at their Figure 6.
I think they might. I don’t know if the forum is read regularly by people who – like me, twelve years ago – are descontructing their Christian faith. But those people might find your writings helpful, for reasons that I will leave unwritten.