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Making the Case for Mutation Accumulation

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Modernity and Cultural Decline

Abstract

Having shown that the most salient recent case for pro-modernism is seriously flawed and that there are many apparently good reasons for anti-modernism, we investigate the distal sources of modernity’s pathological quality. We examine the possibility that deleterious mutations—that is, those that tend to impair genetic quality and thus depress fitness and/or wellness—have accumulated in modernized populations, which could have a role in the loss of mental health and the nihilization and broader cultural decline of these groups.

Certain evidence indicates that selection against these variants has indeed relaxed and that they have resultantly become more frequent in Western populations. Nevertheless, some scientists argue that this relaxation has not in fact occurred, and so arguments for this possibility are critically evaluated in this chapter.

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Notes

  1. 1.

    Developmental stability refers to an organism’s resilience to insults (genetic and environmental) that occur in the process of biological development.

  2. 2.

    Given the association between sperm count and general health (Levine et al., 2017), the massive declines in sperm count that Levine et al. (2017) find are especially troubling.

  3. 3.

    But as it happens, “there is currently very little epidemiologic evidence linking prenatal and postnatal exposure to endocrine disrupting chemicals with male reproductive disorders (including reduced sperm counts)” (Pacey, 2017; see Bonde et al., 2017).

  4. 4.

    In subsequent relevant publications, they have denied that they made any such suggestion. In the course of this chapter, we explain why we disagree.

  5. 5.

    Arslan et al. (2018a) also find evidence of grandpaternal age effects in one historical population.

  6. 6.

    For the purpose of illustration, suppose that those born in Population A to 30-year-old fathers have a 20% chance of dying in infancy due to the effects of de novo deleterious mutations and those born to 40-year-old fathers have a 40% chance of this outcome (and so the higher mortality risk for the offspring of the older fathers is due entirely to the tendency for the de novo burdens of harmful mutations that fathers bequeath to their offspring to increase with paternal age); the respective figures for Population B are 0.5% and 1% (assume that all else is equal between Population A and B, apart from differences in environmental conditions that render the same deleterious de novo variants more harmful in A compared to B). In both cases, the effect of ten additional years of paternal age is a doubling of the risk of infant death, but the overall strength of mortality selection in infancy against deleterious variants is clearly lower in B compared to A.

  7. 7.

    Some confusion here perhaps results from a claim by Woodley of Menie, Sarraf, et al. (2018) that was mistakenly not removed from their text, namely that their analysis assumes “unchanging” “generation lengths” (p. 2). In fact, the analysis does not depend on this assumption, and the claim that it does was, again, not supposed to be published. This is reflected in the use of the term “cohort” rather than “generation” in all relevant places elsewhere in the article.

  8. 8.

    Nevertheless, Ulizzi et al.’s (1979) observation makes substantial declines in the perinatal mortality rate over time especially noteworthy (see Rahman et al., 2013; Sugai, Gilmour, Ota, & Shibuya, 2017; Woods, 2008).

  9. 9.

    Arslan et al. (2018b) do not adequately acknowledge the depth of this controversy.

  10. 10.

    Type-2 diabetes prevalence has been shown to associate in the expected direction with opportunity for selection through differential mortality (Rühli, van Schaik, & Henneberg, 2016), but it is unclear if this correlation would survive relevant controls.

  11. 11.

    Arslan et al. (2018b) write the following in an endnote to their discussion of the opportunity for selection/negative selection distinction: “This confusion between opportunity (variation) and actual selection strength is also at the heart of the [sic] [Woodley of Menie, Sarraf, et al.’s] reiterated concern about a potential selective role of abortions that may compensate for selection that no longer occurs through infant mortality. Yes, the majority of abortions are elective, but in England and Wales 1–2% are therapeutic. Likewise, our estimate of the regression coefficient of paternal age on infant survival in the preindustrial populations is also only a few per cent and thus a fraction of the 12–20% infant mortality. According to our estimates, the majority of the variance in mortality and fertility is not explained by paternal age” (2018b, p. 3, n. 1). In observing that “most…abortions [in modernized populations] are elective rather than therapeutic” (p. 2), Woodley of Menie, Fernandes, et al. (2018) already conceded that some abortions are therapeutic. Furthermore, if Arslan et al.’s (2018b) point is that only the infant mortality variance “explained by paternal age” should be thought to track negative selection through infant mortality, we think that they are mistaken, for reasons given in the main text about the probable inadequacy of paternal age effects to capture the full extent of negative selection.

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Sarraf, M.A., Woodley of Menie, M.A., Feltham, C. (2019). Making the Case for Mutation Accumulation. In: Modernity and Cultural Decline. Palgrave Macmillan, Cham. https://doi.org/10.1007/978-3-030-32984-6_6

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