A recent paper in bioRxiv by Jinlong Huang and colleagues, “Selection for Decreased BRCA2 Functional Activity in Homo sapiens,” presents a fascinating piece of genetic investigation. The authors report that modern humans are universally characterized by a variant of the BRCA2 gene that is approximately 20% less effective at DNA repair than the version found in chimpanzees and other primates. The study is framed as evidence for “positive selection,” suggesting that this loss of function was somehow advantageous and deliberately favored during human evolution. However, a critical analysis of the data reveals the opposite. The paper does not document the creative power of an unguided process but instead provides a stunning molecular confirmation of genetic decay. The evidence, when freed from the philosophical baggage of deep time, points directly to a history of recent origin followed by degeneration, a pattern explicitly predicted by a biblical framework.
A Fair Summary of the Research
The researchers’ stated goal was to identify genetic variations that might explain why humans have a higher incidence of certain cancers compared to non-human primates. By comparing the genomes of 21 non-human primates and 54 ancient humans against the modern human reference, they identified 299 human-specific, fixed, non-silent single nucleotide polymorphisms (SNPs) in known cancer-related genes.
Using a variety of bioinformatics tools and experimental techniques, they zeroed in on one particular SNP as uniquely significant: a change at codon 2662 of the BRCA2 gene. In this position, an ancestral methionine (M) residue has been replaced by threonine (T) in all modern humans. Through molecular modeling, co-immunoprecipitation, and two-hybrid assays, they demonstrated that this M2662T variant weakens the BRCA2 protein’s interaction with its essential partners, DSS1 and RAD51. Finally, using a direct functional assay, they confirmed that this change results in an approximately 20% reduction in the cell’s ability to repair DNA double-strand breaks (DSB). Because this less-functional version is fixed in the human population, the authors conclude that this “reduction in BRCA2 DNA repair ability was positively selected for in the course of human evolution.”
The Core Critique: Mistaking Decay for Design
The authors’ conclusion that a loss of function was “positively selected” is a textbook example of forcing data to fit a pre-committed narrative. The study’s findings are far better explained as evidence of decay, not upward evolution.
The Narrative Before the Data
The entire paper is predicated on the unproven assumption of human-chimpanzee common ancestry and a multi-million-year timescale. The phrase “after divergence from the Chimpanzee-Human Last Common Ancestor” is not a conclusion from the data; it is the ruling paradigm into which the data must be shoehorned. As we will see, this deep-time narrative is directly contradicted by real-world genetic data and is unnecessary to explain the findings.
Genetic Entropy in Action
The central, undeniable finding of this paper is a loss of specified functional information. A 20% reduction in the efficiency of a critical DNA repair machine is not an improvement; it is damage. It is a step downwards in functional integrity. This is a perfect molecular snapshot of the process of genetic entropy, whereby the accumulation of slightly deleterious mutations leads to a relentless, population-wide decline in fitness.
A critical reader might object: claiming the human gene was ‘reduced’ assumes a prior, more functional state we’ve never observed in a human. Does this not concede the premise of common ancestry? This is a vital point that reveals the profound difference between a design-based and a Darwinian interpretation. The inference of a reduction does not rely on common ancestry; it relies on common design and sound engineering principles.
Consider an analogy: a software engineer finds a specific code module is used across 99% of a company’s products, where it runs flawlessly. In one single product line, however, a version of that same module exists with a one-line error that makes it 20% less efficient. The engineer doesn’t conclude the buggy product “evolved” from the others. He correctly infers that the widespread, flawless code represents the original design specification, and the buggy version is a corrupted copy.
This is precisely the case with BRCA2. We are not comparing modern humans to apes to trace a lineage. We are comparing the modern, functionally-compromised human T-variant to the widespread, biophysically-superior M-variant (the ‘design spec’ found across primates and other vertebrates) to infer the state of the original, uncorrupted human gene. The change was a degradation from the optimal engineering standard.
Fixation by Catastrophe, Not Selection
The idea that a slightly deleterious variant was “positively selected” and driven to 100% fixation over millions of years is highly implausible. A much more powerful and scientific explanation for the fixation of this allele is the severe genetic bottleneck associated with the dispersion from the Tower of Babel, as recorded in Genesis 11. Following the global Flood, the entire human population was reduced to the small family groups that scattered across the globe. In such small, isolated populations, genetic drift—the random sampling of alleles from one generation to the next—is an overwhelmingly powerful force. Even slightly harmful mutations, like the M2662T BRCA2 variant, can rapidly become fixed by chance alone, a process that would take eons and require strong selective advantage in a large, stable population. The BRCA2 variant is not a trophy of selection’s creative power, but a molecular scar of our species’ early, tumultuous, post-Flood history.
The Better Explanation: A Record of Recent Origin and Decay
When the philosophical assumptions of Darwinism are set aside, the data from Huang et al. fit seamlessly into a model of recent, special creation and subsequent decay.
A Common Blueprint, Not Common Ancestry
The profound similarity in the BRCA2 gene and its associated repair machinery between humans and apes does not prove common descent. Rather, it points to a common Designer. An intelligent engineer will reuse elegant and effective design modules across different creations. The difference at codon 2662, therefore, is not the result of millions of years of evolutionary divergence, but of a specific mutational event that occurred within the human lineage after creation, corrupting the original, more perfect design. The original human genome would have possessed the optimal, high-function version of this gene.
The Genesis Framework Predicts the Data
The biblical model of history—a “very good” creation (Genesis 1), a subsequent Fall that introduced death and decay into the world (Genesis 3, Romans 8), and a post-Flood dispersion from Babel—provides a robust scientific framework that predicts precisely what Huang et al. discovered.
- A Perfect Origin: We begin with an engineered genome, created with fully functional, optimized DNA repair systems. The widespread, highly-conserved M-variant represents this original design standard.
- The Curse and Genetic Entropy: Following the Fall, genomes began accumulating mutations. We should expect to find molecular evidence of this decay, and a 20% decline in the function of a vital gene is a stark example.
- The Babel Bottleneck: The rapid fixation of this degraded allele is explained by the population genetics of the post-Babel dispersion.
The authors themselves introduce their paper by noting the high incidence of cancer in humans. Their finding—that a less-effective DNA repair gene is fixed in our species—provides a direct molecular link to this tragic reality. This is not a puzzle for evolution to solve; it is a direct confirmation of the biblical account of a good world gone wrong.
Conclusion
The study by Huang et al. is a valuable contribution to genetics, but its evolutionary interpretation is a failure of logic. By clinging to the narrative of deep-time, the authors are forced to describe a clear case of functional degradation as a mysterious form of progress. The evidence does not show the generation of new information or function. It shows the opposite: the loss of pre-existing, engineered function. The 20% reduction in BRCA2’s repair ability is not a sign of Darwinian selection’s creative prowess; it is a molecular testament to the universal, scientifically observable principle of genetic entropy. When interpreted through a rigorous historical science framework, the evidence points away from an unguided process and powerfully affirms a history of initial perfection followed by decay, a history whose outline is uniquely provided in the book of Genesis.