This paper perpetuates a common statistical fallacy in genetics: given the vast

This paper perpetuates a common statistical fallacy in genetics: given the vast differences between expressions, the number of variations is not indicative of the degree of difference in expression. Other than neotenic expression most other variations are all but irrelevant in social, economic, and political consequence. The evolutionary difference between populations is reducible to neotenic evolution, which accounts for group differences in phenotype, behavior and intelligence.

It’s a well-documented issue in population genetics discussions, often tied to misinterpretations of genetic diversity metrics like those in Lewontin’s 1972 analysis (where ~85% of human genetic variation occurs within populations, not between them).

This can lead to the erroneous assumption that a higher count of genetic variations (e.g., single nucleotide polymorphisms or SNPs) directly scales with the magnitude of phenotypic differences (what the statement calls “expressions,” likely referring to observable traits like morphology, physiology, or behavior).

In reality, the relationship is not linear or indicative in that way:

Most genetic variations are neutral or non-coding, having little to no impact on phenotypes or behavior; they accumulate via drift and reflect demographic history (e.g., bottlenecks in non-African populations reducing diversity outside Africa) rather than functional differences.

Phenotypic divergence often stems from a small subset of genes under selection (e.g., those influencing skin pigmentation via loci like SLC24A5 or lactose tolerance via LCT), amplified by environmental factors, even if overall genetic distance is modest.

This mismatch is indeed a common fallacy, sometimes called “Lewontin’s fallacy” in critiques (though the term is debated): people overinterpret within-group genetic diversity (e.g., higher in African populations) as implying minimal between-group phenotypic distinctions, ignoring how correlated loci or selected traits enable clear clustering.

For instance, two individuals from sub-Saharan Africa might show greater neutral genetic distance than one from Africa and one from Europe, yet share more phenotypic similarities (e.g., melanin levels) due to shared selective pressures.

Neotenic gene expression in the brain is linked to processes like neurogenesis and synaptic function, which underpin intelligence differences across individuals.

Neoteny—the retention of juvenile traits into adulthood—has been a key factor in human evolution, contributing to enhanced cognitive and behavioral flexibility.

Neoteny emerged gradually in hominins, with fossil evidence showing progressive juvenilization over millions of years (e.g., in Homo sapiens vs. Neanderthals). This aligns with many subtle variations in multiple genes, amplified by selection for sociality, cognition, and adaptability, rather than a bottleneck in one developmental process.

Compared to other primates, humans exhibit amplified neoteny, such as prolonged brain development, larger relative brain size, and extended periods of learning and plasticity.

This is evident in transcriptional patterns: about 48% of genes influencing prefrontal cortex development show delayed or prolonged expression in humans relative to chimpanzees and macaques, potentially supporting advanced linguistic and problem-solving abilities.

Behaviorally, neoteny promotes traits like reduced aggression, increased playfulness, and greater reliance on learned behaviors over instinctual ones, which facilitate social cooperation and adaptability.

For instance, neotenic features like hair loss enhance facial expressiveness for emotional communication, a cornerstone of human interaction.

In terms of intelligence, neoteny enables prolonged neuronal maturation, which correlates with higher cognitive capacity through mechanisms like increased synaptic plasticity and hypermorphosis (extension of growth phases leading to larger brains).

Cheers
CD