Search arXivSearch

arXiv · 2508.03187

Fitness and Overfitness: Implicit Regularization in Evolutionary Dynamics

Abstract

A common assumption in evolutionary thought is that adaptation drives an increase in biological complexity. However, the rules governing evolution of complexity appear more nuanced. Evolution is deeply connected to learning, where complexity is much better understood, with established results on optimal complexity appropriate for a given learning task. In this work, we suggest a mathematical framework for studying the relationship between evolved organismal complexity and enviroenmntal complexity by leveraging a mathematical isomorphism between evolutionary dynamics and learning theory. Namely, between the replicator equation and sequential Bayesian learning, with evolving types corresponding to competing hypotheses and fitness in a given environment to likelihood of observed evidence. In Bayesian learning, implicit regularization prevents overfitting and drives the inference of hypotheses whose complexity matches the learning challenge. We show how these results naturally carry over to the evolutionary setting, where they are interpreted as organism complexity evolving to match the complexity of the environment, with too complex or too simple organisms suffering from \textit{overfitness} and \textit{underfitness}, respectively. Other aspects, peculiar to evolution and not to learning, reveal additional trends. One such trend is that frequently changing environments decrease selected complexity, a result with potential implications to both evolution and learning. Together, our results suggest that the balance between over-adaptation to transient environmental features, and insufficient flexiblity in responding to environmental challenges, drives the emergence of optimal complexity, reflecting environmental structure. This framework offers new ways of thinking about biological complexity, suggesting new potential causes for it to increase or decrease in different environments.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Hagai Rappeport, Mor Nitzan. 2025-08-05. Fitness and Overfitness: Implicit Regularization in Evolutionary Dynamics. https://arxiv.org/abs/2508.03187

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related papers

A conceptual predator-prey model with super-long transients

Drawing on the understanding of the logistic map, we propose a simple predator-prey model where predators and prey adapt to each other, leading to the co-evolution of the system. The special dynamics observed in periodic windows contribute to the coexistence of multiple time scales, adding to the complexity of the system. Typical dynamics in ecosystems, such as the persistence and coexistence of population cycles and chaotic behaviors, the emergence of super-long transients, regime shifts, and the quantifying of resilience, are encapsulated within this single model. The simplicity of our model allows for detailed analysis, reinforcing its potential as a conceptual tool for understanding ecosystems deeply.

q-bio.PE

Mutation Order and Selection Shape Intratumor Heterogeneity in Tumor Evolution

Cancer progression often requires multiple driver mutations, but the same drivers may be acquired in different orders. How these pathways jointly shape tumor clonal structure remains unclear. We develop a multitype branching-process model in which malignant transformation requires two driver mutations, distinguishing malignant cells by mutation order and the independent transformation event that founded their clone. Under a successive exponential approximation, we establish point-process limits for pathway-specific clone sizes and derive a closed-form expression for the limiting expected Simpson's index of the combined malignant population. When both mutation orders yield malignant cells with the same net growth rate, the index decomposes into effective pathway weights, determined by mutation rates and birth-death dynamics at preceding stages, and within-pathway concentration terms, determined by intermediate-to-malignant growth-rate ratios. A driver's effect on heterogeneity thus depends critically on when it is acquired. A strong driver acquired early expands the intermediate lineage and increases the supply of independent malignant founders, whereas the same driver acquired last strengthens the growth and age advantage of early-founded malignant clones. Under additive fitness effects, these opposing mechanisms can produce a non-monotone relationship between selective advantage and clonal concentration. Threshold-like non-additive fitness effects can generate highly concentrated malignant populations, while order-dependent terminal fitness causes the faster-growing pathway to dominate asymptotically. These results show how mutation order, mutational accessibility, selection, and epistasis jointly determine lineage-level intratumor heterogeneity.

q-bio.PE

Phase transitions in microbial lineage trees

Microbial populations exhibit high cell-to-cell variability, which fundamentally shapes population behavior. A striking consequence is the existence of phase transitions, where small genetic or environmental changes trigger abrupt shifts in population dynamics. While biological phase transitions have often been proposed, connecting observed behavior to the underlying physics has remained challenging. We combine population genetics with statistical physics to show how phase transitions arise naturally in microbial populations. We highlight the existence of a first-order transition in a model of bacterial plasmid engineering and find a strict lower bound on the number of plasmids that can be stably maintained in a population.

q-bio.PE