Thread by @doofgeek4011

D.D., let’s go claim by claim, because precision matters. What you’re presenting looks rhetorically forceful, but it collapses under scrutiny once the data and logic are actually examined.🧵

https://twitter.com/DivinelyDesined/status/1958552532621652330

You triumphantly seize on alignment gaps as though they disprove common ancestry. But in comparative genomics, unalignable regions (repetitive DNA, structural rearrangements, transposon insertions) are expected.

They don’t mean “15% of our DNA is alien.” Instead, they reflect differences in genome architecture layered atop a deep shared framework. Even with those regions counted, coding sequences and conserved regulatory regions remain overwhelmingly similar.

That is why synteny maps, chromosome painting, and cross-species hybridization all consistently show that humans and chimps share the vast majority of their genome.

Your math (“452 million differences”) is misleading. Neutral theory predicts mutation accumulation on the order...

...of tens of millions of substitutions over 6–7 million years, which matches the observed alignable regions. Structural variation adds complexity, but it's not some fatal anomaly and it is exactly...

...what evolutionary population genetics anticipates. Pretending otherwise is selective reading.

You misstate both the model and the literature. Durrett and Schmidt’s work explicitly shows that stepwise changes dramatically shorten waiting times, and...

...experimental systems (e.g. bacterial resistance, antifreeze proteins, or stickleback pelvic reduction) confirm that real mutations do accumulate incrementally without collapsing function.

Your claim that mutations must appear “all at once” or not at all...

...is an assumption imported from design apologetics, not biology. Proteins tolerate neutral or slightly deleterious intermediates; regulatory elements evolve modularly; and population size plus recombination makes multi-step innovation realistic.

If stepwise adaptation were impossible, we would never observe experimentally evolved binding sites, regulatory switches, or new metabolic pathways but we do, repeatedly.

What you call “speculation” is backed by mathematical models and laboratory confirmation. What you’re offering is rhetoric that assumes the conclusion.

Comparative methods aren't “assuming evolution.” They’re testing for nested hierarchies of shared changes. If humans and chimps were separately designed, we shouldn’t see the exact same endogenous retrovirus insertions, processed pseudogenes, and...

...shared neutral mutations scattered across the Y chromosome. Design could produce anything, yet what we find is constrained patterns consistent with descent. That’s explanatory power, not remotely circular.

Invoking “common designer” isn’t symmetrical. A designer can explain any outcome, which makes the hypothesis unfalsifiable. Evolution makes specific, risky predictions (e.g., broken vitamin C gene in both humans and chimps but intact in other primates),...

...which have been repeatedly confirmed.

You claim there is “no evidence” of novel function from duplication. That is flatly false.

The antifreeze glycoprotein in Antarctic notothenioid fish arose from a duplicated digestive enzyme. The immune system’s globins and MHC genes diversified through duplication. Opsin gene duplications gave primates trichromatic color vision.

Experimental work in yeast shows duplicated genes diverging under selective pressure to acquire complementary functions.

Quoting Bozorgmeh out of context doesn’t erase this mountain of evidence. Of course, duplication alone isn't a magic bullet.

However, duplication + divergence and selection is a demonstrated mechanism of innovation. Even your analogy to computer code backfires. Programmers reuse old code precisely because copying provides a starting point for novel adaptations. Biology does the same.

As for de novo genes, multiple well-documented cases exist (e.g., BSC4 in yeast, arfA in E. coli, and several human-specific ORFs). These arise from previously noncoding DNA, and we can trace the intermediates. You show no awareness of the published, replicated research.