I don’t think the issue was fully settled. @John_Harshman, @drsterncardinale and @chris_doesdna2018 need to resolve those skirmishes. We need a new thread on that, probably titled, “Genetic Entropy: Understanding Sanford’s Claims About Fitness”.
I’m not sure there’s anything to resolve–neither perspective is a strawman of GE.
Strangely it was different for me. I tended to trust non theist science sources on evolution over Christian ones at the onset, especially the ones that avoided discussing religious beliefs when unnecessary. This has changed. Its the evidence I look at now, rather than the religious backgrounds of the writers.
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But there seemed to be some disagreement on that especially between John and you both or it could be I missed the part where your seemingly conflicting views were reconciled. Is it possible for moderators to seek out the relevant parts in the GE thread opened to discuss the rebuttal article coauthored by Price, Sanford and Carter?
I seem to recall that the disagreement was about whether nearly neutral, deleterious alleles are evenly enough distributed in a population that they are not subject to selection as a group. My position (and I believe @glipsnort’s also) was that this was likely. Others disagreed. And of course this would be a necessary though not sufficient condition for GE to occur.
Since there is disagreement here, I suppose neither party has good evidence to buttress their respective positions with regards to extant human populations?
Yes, the point was that in GE they are not subject to selection. Anyone can disagree with this. But not understanding that this is part of GE, is attacking a straw man. That was my point.
There’s a difference between understanding an argument and disagreeing with it, and not understanding it and misrepresenting it, which is what some were doing.
No one in that thread disagreed that slightly deleterious mutations aren’t subject to selection.
They understood this quite well. No strawman here. I think you misunderstood John.
It seemed to me the disagreement was primarily between absolute and relative fitness. Followed by the degree of genetic variance contributing to the fitness of any given trait. It would seem, to me, unlikely to propagate enough VSDs at the same loci in the population to drown out variability in fitness. Even if that variability is small, the effects of the VSDs must necessarily take on dominant, recessive, additive, and multiplicative interactions with fitness that will be modulated further by the environment. Coupled with continuous time needed to reach fixation and population density flux, it does not seem reasonable to assume that a large population is equally affected simultaneously. Meaning selection should be able to act on that variability.
I’m not actually sure we are disagreeing.
That’s not quite the contention though. They must be subject to selection at some level of accumulation–or they can never cause an extinction event. Our discussion was exploring the degree of accumulation required and the mechanisms that would facilitate a symmetric narrowing of fitness variance simultaneously in a large population.
I don’t agree that this is a strawman.
Part of the issue may be that it’s not exactly clear what the positions held are. The few times I responded to John or Steve, it wasn’t clear that we actually disagreed.
I wouldn’t say that. I’d say we can have expectations based upon nearly neutral theory.
Well, this thread is young. And someone has disagreed, though not in this thread, that a whole lot of slightly deleterious mutations as a group aren’t subject to selection. That’s the point under contention. Oh, look:
Why not, if each mutation has only a very tiny selection coefficient such that it would take thousands of them to be noticeable to selection?
We are, specifically on the distribution of slightly deleterious mutations in the human population.
Not true. They can cause extinction with zero selection as long as the distribution within the population doesn’t vary enough for fitnesses of individuals to be significantly different. Again, it’s not variance in individual fitness that’s important here, only the portion of that variance resulting from the slightly deleterious mutations. Mutations of individually noticeable effect can be subject to selection without affecting the distribution of slightly deleterious mutations.
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Yes, this is also what I understand to be the crucial aspect of GE as a concept.
The differences in relative fitness that result from mutations of larger effect might be visible to selection, but the creeping reduction in absolute fitness is small enough that generation-to-generation decline remains effectively invisible, because everyone always suffers numerous of these VSD mutations that has some imperceptible effect on absolute fitness.
I think the idea is that these mutations would only become visible when their total number differ between individuals by hundreds, or thousands, which would only manifest as a visible fitness-difference if individuals descendants a hundred generations or more separated from their ancestors are compared.
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It appears to me that you understand the concept. Thanks. 
Really simplistic take from a physicist with a very limited biology background.
Selection is about the ability to pass on genes, so two things are most relevant: survival long enough to reproduce and success in competition for mates. (Among species with sexual reproduction.)
Something can’t cause extinction of a species without increasing mortality rates (or, e.g., infertility, reducing live births etc.) or breeding success rates.
But surely as soon as genetic changes start causing those things, they’re definitely ‘visible’ to selection? And will therefore undergo selection effects.
Quite happy to be told that, and how, I’ve missed the point. 
Yes, you’ve missed the point. If a particular variant decreases reproductive ability by a very small amount, s, where s << 1/(# of genomes in population), then it is not visible to selection. That is, the probability of the variant being fixed in the population is determined almost entirely by the fluctuations in frequency caused by the random sampling of variants that occurs every generation.
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Imagine a run in an Olympic stadium where 1,000 athletes were competing, each carrying a large empty backpack at the start. Imagine that each lap of the track, 100 grains of sand were poured into each runner’s bag. What do you think would happen after 1 lap? 2 laps? 3 laps? 10 laps? 100 laps? 1000 laps? 10000 laps? Etc… You see, VSD mutations are similar to the grains of sand in this story. They accumulate inexorably over time without natural selection being able to do anything about it, because all members of a population are affected in the same way.
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My impression, as a non-scientist, likewise “with a very limited biology background”, is that the species in the hypothesis are assumed to be in a tight bunch in terms of absolute fitness (little variation in relative fitness), so that they go ‘over the cliff’ to extinction in a tight mob, with no stragglers left to avoid extinction (or perhaps so few as to leave the species with insufficient genetic variety to survive).
Whether this is (i) a reasonably correct impression of the scenario envisioned, & (ii) a realistic scenario, I’ll leave the professional biologists to determine.
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There are only so many VSD’s possible in any given genome, so they won’t accumulate forever. Also, as the number of deleterious VSD’s accumulate it increases the probability of a mutation converting the base back to the ancestral sequence which would be a beneficial VSD. Therefore, there is an equilibrium of deleterious and beneficial VSD’s at some point.
Let’s say that we just mutated nearly all of the regions where we think VSD’s occur? Well, nature has already done that experiment. The bladderwort has a genome of just 83 million base pairs with a gene count comparable to other plants. Nearly all of what we would call junk DNA has been removed from the genome, and the plant functions just fine.
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That’s a statistical impossibility. There would be variance. We know this, because we see variance in the number of new mutations per individual.
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How do you propose causing a decline in the absolute fitness of a genotype through mutation without altering the relationship to the other genotypes in the population?