Rapid radiations, in which bursts of diversification yield disproportionate contributions to extant biodiversity, underlie most of the known diversity of life (Wiens & Moen, 2025). This principle holds across clades of animals, plants, fungi, and protists. We argue that a parallel process manifests in humans: our global dominance as an apex mammalian species derives from rapid internal diversification of cognition, behavior, and social interaction styles. Drawing on evolutionary genomics, epigenetics, and neuroscience, we propose that neurodiversity—including autism and related neurodivergent profiles—constitutes an adaptive radiation within a single species, sustaining variation that enables resilience, innovation, and ecological mastery. We synthesize evolutionary biology with human neuroscience to suggest that the same mechanisms responsible for generating flowering plant and arthropod hyperdiversity also operate, at a psychological and genomic scale, in Homo sapiens.
In evolutionary biology, adaptive radiation is defined as the rapid proliferation of lineages into a diversity of ecological or functional niches, often driven by key innovations (Schluter, 2000; Givnish, 2015). Rapid radiations are increasingly recognized not as exceptions but as the predominant mode of life’s diversification (Wiens & Moen, 2025). Yet, while this principle has been examined across animals and plants, its implications for human uniqueness have not been fully articulated.
Humans, unlike angiosperms or insects, have not diversified into thousands of species. Instead, our major diversifications are intraspecific—expressed through culture, cognition, and social organization. Here, we argue that human dominance originates not from uniformity but from cognitive variability as adaptive radiation, a radiation accelerated by genomic plasticity, epigenetic regulation, and the persistence of neurodivergent traits.
The study by Wiens and Moen (2025) provides the macroevolutionary foundation: across life, >80% of known biodiversity resides in clades with diversification rates in the 90th percentile, such as angiosperms, arthropods, and vertebrates. These clades are shaped by key innovations—multicellularity in eukaryotes (Chen & Wiens, 2021), pollination in flowering plants (Hernández-Hernández & Wiens, 2020), herbivory in insects (Wiens, Lapoint, & Whiteman, 2015), and terrestriality in vertebrates (Wiens, 2015b).
The principle is clear: dominance requires diversification. The clades that flourish most extensively are those that rapidly generate phenotypic and ecological diversity. This creates an interpretive lens for human evolution: if Homo sapiens has come to dominate planetary ecosystems, it is less likely through stasis or uniform specialization than through an explosion of diversified strategies sustained within the same species boundary.
Recent genomic work shows that humans have undergone accelerated evolution in the last ~20,000 years. Several mechanisms highlight diversification rather than homogeneity:
- Gene–culture coevolution: Alleles related to lactase persistence, starch digestion, and immunity show rapid expansion under agricultural and demographic shifts (Uricchio et al., 2019; Williamson & Huerta-Sánchez, 2022).
- Brain-related genes: Human-specific duplications such as SRGAP2C and changes in FOXP2 support enhanced neurogenesis, cognitive flexibility, and symbolic communication (Dennis et al., 2012; Enard, 2011).
- Polygenic adaptation: Complex traits, including educational attainment and cognitive ability, are maintained via highly polygenic architectures—suggesting selective value in variance itself (Sanchez-Roige, Palmer, & Clarke, 2023).
These processes indicate that human adaptive success required rapid diversification within the genome and brain, consistent with the radiational model described by Wiens & Moen (2025).
The concept of neurodiversity reframes neurodevelopmental conditions such as autism, ADHD, and dyslexia as naturally occurring cognitive variants rather than “deficits” (Lai, Lombardo, & Baron-Cohen, 2014). Emerging genetic and neuroscientific evidence supports this evolutionary lens:
- Persistence of autism-linked alleles: Population genomics reveals that autism-associated variants occur at non-trivial frequencies, implying balancing selection rather than uniformly deleterious trajectories (Ploeger & Galis, 2011).
- Cognitive specialization: Traits often associated with autism—enhanced perceptual discrimination, systemizing abilities, or intense focus—are advantageous in contexts requiring attention to detail, pattern detection, or innovation (Pellicano & den Houting, 2022).
- Social diversity rather than deficit: The “double empathy problem” suggests autistic–non-autistic communication difficulties are reciprocal mismatches rather than deficits, underscoring complementarity within a population radiation (Milton, 2012; Crompton et al., 2020).
- Neural variability: Functional imaging shows that connectome organization in autism exemplifies one pole of typical human brain diversity, reinforcing that cognitive “outliers” are integral parts of a broader variation spectrum (Hong et al., 2019).
These findings resonate with the ecological logic of radiations: adaptive peaks are reached not by one uniform phenotype but by a spread of complementary variants that together expand the survival envelope of a clade or species.
Epigenetic mechanisms provide the substrate for rapid, environment-tuned diversification. DNA methylation and histone modification regulate neurodevelopmental pathways, influencing cognitive outcomes and stress responses (Meaney & Szyf, 2005). Autism and other forms of neurodivergence are associated with altered epigenetic landscapes, including synaptic chromatin remodeling (Sullivan et al., 2022; Loke et al., 2015).
Far from being pathological “errors,” epigenetic sensitivity expands population-level variability. This may function as bet-hedging, increasing the likelihood that some individuals exhibit traits optimally suited to emerging social or ecological niches. This is conceptually parallel to adaptive radiations in plants or insects, where rapid trait diversification confers resilience and expansion.
Systems neuroscience provides mechanistic grounding for this variation:
- The hypothesis of altered excitation–inhibition balance explains differences in autistic cognition, but such differences can be reframed as alternative computational regimes (Sohal & Rubenstein, 2019).
- Variation in cortical connectivity indicates that neurodivergence is not random deviation but structured divergence within the species’ neural design space (Hong et al., 2019).
As in adaptive radiations, this neural heterogeneity permits a distribution of strategies, some of which may excel in environments of uncertainty, novelty, or high complexity.
Wiens and Moen (2025) demonstrate that across biology, rapid radiations explain most observed species richness. Humans exemplify the same principle intraspecifically. Variation in our genomes, epigenomes, and brains constitutes an internal adaptive radiation that sustains population-level resilience and flexibility.
This view reframes supposed anomalies—autism or ADHD—not as maladaptive noise but as positions on a radiational arc. The very success of Homo sapiens, like that of arthropods or angiosperms, lies in diversification, not uniform optimization. We are dominant precisely because our species continuously generates and sustains cognitive heterogeneity, ensuring adaptability to fluctuating social and environmental demands.
From a macroevolutionary perspective, human dominance reflects the same process identified by Wiens and Moen (2025): exceptional diversity generated through rapid radiation. In our species, this radiation lies within the mind. Differences in cognition, perception, and behavior—manifest in neurodivergence and neurodiversity—constitute adaptive specializations that collectively secure our ecological mastery. Our evolutionary story is thus not of uniform perfection but of diverse and complementary minds forming an adaptive radiation within a single species. Future work integrating genomics, epigenetics, and cognitive neuroscience will be critical to substantiating this framework and moving beyond pathology-centered interpretations of human difference.
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