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Benefits of hereditarian insights for mate choice and parenting

Published online by Cambridge University Press:  11 September 2023

Geoffrey F. Miller*
Affiliation:
Psychology Department, University of New Mexico, Albuquerque, NM, USA gfmiller@unm.edu; https://psych.unm.edu/people/faculty/profile/geoffrey-miller.html

Abstract

Madole & Harden develop some good ideas about how to understand genetic causality more clearly, but they frame the benefits of behavior genetics research at a largely collective level, focused on the pros and cons of different ways to engineer the gene pool or social behavior. This neglects the individual benefits of hereditarian insights for mate choice and parenting.

Type
Open Peer Commentary
Copyright
Copyright © The Author(s), 2023. Published by Cambridge University Press

The rise of genome-wide association studies (GWASs) and polygenic scores has triggered a new moral panic about behavior genetics. In their target article, Madole & Harden (M&H) aim to neutralize some of this panic by clarifying the causal inference logic behind GWAS research. They identify some illuminating similarities between within-family genetic effects (given the sexual randomization of parental genotypes), and average treatment effects in randomized controlled trials.

However, their implicit sociopolitical framework risks handicapping the utility of behavior genetics for ordinary people. M&H write as if there are only two main ways that behavior genetics could influence humanity: collective eugenics (changing the gene pool through government policy, or through new cultural norms around embryo screening or CRISPR gene editing), or collective social engineering (using insights into gene–brain–behavior pathways to identify new biopsychosocial interventions that can nudge behavior in socially valued directions – such as reducing violent crime, mental illness, or obesity).

This collectivist viewpoint asks what behavior genetics can do for society at large – rather than for individuals making decisions about their own families. For example, M&H seek scientific insights about how to “identify novel targets for intervention,” how to “isolate steps in the causal path that serve as candidates for intervention,” and how to identify “targets for programmatic manipulation that may serve to close the gap in health disparities.”

An implicit question behind their paper seems to be: How can we make sure that behavior genetics findings are used by good liberal policymakers to solve the social problems prioritized by good liberals – rather than being turned into coercive, racist, neo-Nazi eugenics? They explicitly wish to “challenge the genetic determinism and essentialism that have historically characterized the pernicious misapplications of genetics by political extremists” on the Right (without mentioning the pernicious misapplications of Blank Slate social-constructivism by political extremists on the Left, such as Stalin, Pol Pot, Mao, etc.). Given their aversion to any kind of organized eugenics, they imply that the only other benefit of behavior genetics could be to promote “second-generation causal knowledge” that can make environmental interventions (ranging from new pharmaceuticals to new educational interventions) more effective in bio-hacking the complex genes-to-behaviors pathways.

Their distinction between “deep causes” and “shallow causes” exemplifies some hidden problems in their sociopolitical framework. “Deep causes” (with unitary, uniform, causally explanatory genetic effects) – for example, the way that homozygous mutations in the CFTR gene lead to cystic fibrosis – are seen as the gold standard. “Shallow causes” (with local, probabilistic, causally distal genetic effects) are seen as little more than stepping stones toward further mechanistic biomedical research that can identify new causal pathways for the collective melioration (or manipulation) of behavior.

The trouble is, the most heritable, stable, predictive, and important behavioral traits, such as general intelligence, the Big Five personality traits, and mental disorders, generally show “shallow” rather than “deep” genetic influences. As M&H emphasize, these massively polygenic traits are shaped by thousands of genetic variants that influence intricate neurodevelopmental systems in ways that aren't very mechanistically informative about which biomedical or sociocultural interventions might work.

So, shallow genetic influences won't help the social engineer very much in finding biopsychosocial interventions to reshape society. Yet, for an individual making important life-choices that can shape the next generation of their own family, the massively polygenic core psychological traits are much easier to influence and/or much more important to understand than severe single-gene mutations. When it comes to real-life issues in mating and parenting, where an accurately hereditarian view could guide better decision making, and where a Blank Slate view could lead to high-cost errors and lifelong regrets, “shallow causes” run pretty deep.

Mate choice has been a form of intuitive eugenics at least 540 million years, ever since the Cambrian explosion, when complex senses and centralized nervous systems started to guide sexual selection through mate choice for good genes. People tend to focus their mate choice on traits that are at least moderately heritable, such as physical health, mental health, general intelligence, personality traits, and moral, political, or religious values (Miller, Reference Miller2000). Mate choice across millions of animal species exerts a high degree of “counterfactual control” over what kinds of offspring get produced, even though animals have no conscious understanding of the “counterfactual dependence” whereby genes influence traits. However, Blank Slate ideologies (Pinker, Reference Pinker2003) have led many people to mistrust their own mate choice preferences and hereditarian intuitions, with potentially disastrous results when choosing a marriage partner, gamete donor, or child to adopt.

Likewise with parenting. In many countries, Blank Slate ideology leads parents to act as if they can micromanage the outcome of their kids' development through intensive hot-house parenting, overprotective coddling, and tiger-mothering. For example, in China there has been much debate about “involution” (内卷), meaning runaway competition in education and labor markets (Yi et al., Reference Yi, Wu, Zhang, Zeng, Wang, Liang and Cai2022). This leads parents to put enormous stress on kids to achieve at any cost – regardless of their innate abilities, personalities, and interests. The less that parents believe genes matter, the more frustrated they get by their kids' mediocrities, and the more they blame themselves for failing to provide the right shared family environment. A humbler, more hereditarian perspective allows parents to relax, trust the mate choices they made, trust their genes, and let their kids follow their own path, without the burden of trying to optimize the shared family environment in every possible way (Caplan, Reference Caplan2012).

M&H seem frustrated that they're stuck at this collective policymaking level: “Even if we concede that, at a conceptual level, genes could cause average differences in human behavior, at a practical level, it is not readily apparent what we would do with this knowledge.” Maybe the most important thing we can do with this knowledge, as individuals, is to reject the Blank Slate dogma and accept the importance of heredity when choosing our mates, raising our kids, and getting on with our lives.

Competing interest

None.

References

Caplan, B. (2012). Selfish reasons to have more kids. Basic Books.Google Scholar
Miller, G. F. (2000). The mating mind: How sexual choice shaped the evolution of human nature. Doubleday.Google Scholar
Pinker, S. (2003). The Blank Slate: The modern denial of human nature. Penguin.Google Scholar
Yi, D., Wu, J., Zhang, M., Zeng, Q., Wang, J., Liang, J., & Cai, Y. (2022). Does involution cause anxiety? An empirical study from Chinese universities. International Journal of Environmental Research and Public Health, 19, 9826. doi:10.3390/ijerph19169826CrossRefGoogle ScholarPubMed