Sexual complexity as a screen for replication fidelity: the Everest effect

17 July 2026

Author: Patrick D. Shaw Stewart

The Everest Effect by Patrick Shaw Stewart

Abstract

Sexual reproduction is often accompanied by costly and very complex traits, from courtship displays and long-distance breeding migrations to gamete-recognition systems. Existing theories explain many such traits through Fisherian, handicap, good-genes, or condition-dependent processes, but they do not, however, fully address a dynamic problem in mutation-rate evolution: if environmental change favors mutator backgrounds during adaptation, what later restores high replication fidelity?

Here, I propose the Everest hypothesis, which treats short-term adaptation and replication fidelity as separate but interacting dimensions. Fidelity contributes to long-term fitness, but during environmental change, it can temporarily conflict with immediate adaptation because mutator alleles may generate beneficial variants and hitchhike with them. Roberts and Petrie’s 2022 model showed that mate choice can favor elevated mutation rates and amplify the reproductive contribution of high-performing individuals, including males carrying beneficial mutations that arise on mutator backgrounds. Everest builds on this accelerator logic but adds the corresponding brake: as adaptation proceeds and the advantage of elevated mutation declines, complex reproductive systems can amplify selection for restored replication fidelity.

The proposed key mechanism is multigenic stacking. Many reproductive systems integrate numerous gene products, regulatory functions, and behavioral or molecular steps into a single reproductive test—such as a courtship display, migration-linked breeding sequence, or biochemical compatibility system—whose outcome is mating and fertilization or, alternatively, reproductive failure. Such serial biological tests can convert many small mutator-linked defects into large differences in mating or fertilization success, thereby strengthening selection against low-fidelity backgrounds and favoring antimutator or high-fidelity genotypes. Recombination can then allow offspring to retain adaptive alleles while recovering accurate replication machinery.

The hypothesis predicts a characteristic rise-and-fall cycle in mutation rate: mutators may increase during adaptation, but complex reproductive screening can later reduce mutation rates or mutational load without erasing adaptive gains. Everest is testable through experimental evolution, manipulation of reproductive screens, parent–offspring sequencing, and comparative analyses of taxa differing in reproductive complexity. It therefore complements existing theories of sexual selection by proposing that traits elaborated by those processes can be co-opted to speed the restoration of replication fidelity after the rise of adaptive mutators.

Keywords: sexual selection; mutation-rate evolution; good genes; drift-barrier hypothesis; mutation load; recombination; experimental evolution

Figures

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1. – Graph II from van Loghem’s report on the epidemiology of respiratory illnesses in the Netherlands in the winter of 1925/26. I have superimposed ambient temperature at five Dutch weather stations (colored lines) with the temperature scale inverted (lowest temperatures at the top). From Van Loghem JJ. J Hyg 1928; 28(01):33–54.
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2. – Hope-Simpson’s record of feverish respiratory illnesses in his medical practice in Cirencester, UK, compared with notifications of such diseases in Prague, Czechoslovakia 1969–74. From Hope-Simpson RE. J Hyg 1981; 86(01):35–47.
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3. – The viruses that caused respiratory tract infections in hospitalized children in Mainz, Germany, which has an oceanic climate, 2000 – 2008. The four most frequent pathogens were, in order, rhinovirus (RV), respiratory syncytial virus (RSV), influenza A (IVA), and adenovirus (AV). From Du Prel JB et al. Clin Infect Dis 2009; 49(6):861–8.
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4. – The viruses that caused respiratory tract infections in hospitalized children in Buenos Aires, Argentina, which has humid subtropical climate, 1998 – 2003. The four most frequent pathogens were, in order, respiratory syncytial virus, influenza A, adenovirus, and parainfluenza. From Viegas M et al. J Infection 2004; 49(3):222–8.
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5. – The viruses that caused respiratory tract infections in hospitalized children in Singapore, which has a tropical climate, 1990-94. The four most frequent pathogens were, in order, respiratory syncytial virus, parainfluenza, influenza A and adenovirus. Chew FT et al. Epidemiol Infect 1998; 121 (01):121–8.
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6. – The Eurowinter Group analyzed the climate and the measures taken to protect individuals from cold in eight European regions, ranging from northern Finland to Athens. The table shows the regression coefficients (R) and their significance (p), for cause-specific indices of respiratory disease-related mortality on personal cold-exposure factors standardized at 7°C mean daily temperature. I have added labels to the plot on the right, drawing attention to some points that I found interesting. The most dangerous activities are at the top left of the plot, with the most protective at the bottom left. Activities that don’t affect the chance of dying from respiratory illness are on the right or at the middle level. Donaldson G et al. (The Eurowinter Group). Lancet 1997; 349:1341–6.
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7. – During sporting competitions people tend to crowd together in bars and at home to watch the events. The figure above shows that during the 2014 FIFA World Cup, in 18 countries in the Northern Hemisphere, there was no increase in the number of Google searches for terms related to colds and flu. It seems safe to conclude that the peaks that can be seen in winter in every country are not driven by crowding. (Notice the epidemics of colds in early autumn 2014. Autumn epidemics quite often appear when the temperature dips at the end of summer.)
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8. – Humidity: a fashionable explanation of influenza seasonality. In the last few years it has been suggested that flu seasonality is the result of the greater stability of flu virions (virus particles) in cold, dry conditions. (This comes under M2 in my categorization.) There are two major problems here: first, we have to account for the much higher levels of influenza during the rainy season in the tropics compared to other times of the year. For example, in Fortaleza (northern Brazil) influenza almost disappears outside the rainy season. Second, we would have to believe that the seasonality of influenza was driven by a different mechanism to that of many other respiratory viruses. A dozen studies, shown above, have been carried out where virus aerosols were created in rotating drums (the rotation stops the virions from settling) and the stability of virions was measured in air of different humidities. The results showed that several respiratory viruses (including influenza virus) are indeed more stable in dry air, but several others, including rhinovirus and adenovirus, are much more stable in moist air!
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Sexual complexity as a screen for replication fidelity: the Everest effect

Abstract

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