BIOLOGY OF THE PHENOTYPE WARS

A FOUNDATIONAL DIGRESSION

As you, my much appreciated readers, have been seeing the product of my deep dive into the Canadian front in the phenotype wars (and much, much more of that to come), in real time I’ve been diverted with a research digression into the biological foundations of the phenotype wars. For those of you primarily (or exclusively) interested in the historical sociology that is the primary focus here – and has been for several years now – this may not be of much interest. If not, feel free to pass this one over. However, I do know that some of you are more interested in the deeper structures of the phenotype wars model; so you might find this of value.

As a bit of context, in my original statement of the model, in A Plea for Time in the Phenotype Wars¹, I took the approach that, given the high heritability of personality structure, the shifts across the arcs of the phenotype wars spirals were largely a matter of phenotypic selection, following something like the model of the pepper moths during the industrial revolution in England. I still expect that some amount of the biological backstory to the phenotype wars is explained precisely along these lines. However, it has also always seemed to me that there had to be more to the story: the flood of population-level support for more temporal or spatial (especially spatial) attitudes and behaviors could be simply a matter of follow-the-leader, but there could be more involved – something like a story about ontogeny and development.

Real close followers of my work will know that in my preceding book, Biological Realism² – which in many ways laid the foundations for the phenotype wars model – I discuss at length the function of what I called perceptual-cognitive-behavioral mechanisms as the generators of phenotypic variation. So, it wasn’t as though I wasn’t aware of such processes. A Plea for Time in the Phenotype Wars though was such a complex book, with such an ambitious argument, that I decided to restrict discussion of the phenotypes’ generation to the comfortable arena of more conventional selection processes. However, not only is the biology scholarship in these areas rapidly progressing, but the strength of the phenotype wars model, it seems to me, demands a more nuanced parsing. So, here, I try to do that. This will be a long one.

The following arises from both extensive conventional research and an extended discussion with my old friend Grok. We all know how Grok can hallucinate, so I have done my best to check his claims and sources, but I’m happy to hear from others on how our collaboration may have gone wrong in any of the technical details.

As a context for what I’m getting at here, consider this example. As I’ve discussed in some of my biology books, we know that various factors in early childhood (generally thought to be about 0-7 years old) can cause an individual phenotype to have a dramatically different sexual reproductive strategy – either a faster or a slower one. These are changes, forms of phenotypic plasticity, which calibrate to increase fitness likelihood, given information fed into the organism which provides cues as to what will be the more successful strategy.

I’ll say more about that regulating example below, but for now the point is that I suspect something very similar is happening around phenotypic plasticity in terms of calibrating individual phenotypes for higher/lower openness/conscientiousness in response to environmental cues. In other words, in many cases, individuals are more temporal or spatial depending upon the environment within which they find themselves. So, that’s the thesis, let’s get to the arguments.

Over the years I’ve (no doubt, on occasion, somewhat mischievously) prompted outraged responses from people through my insistence that “everything is genetic.” And of course the outrage would boil down into (sometimes sputtering) assertions of “environment!!!” What about the environment? The problem of course was that such people assumed that when I said “genetic” that I meant “heritable.” But the point, rather, was obviously that any species, to take anything (and here the thing is information) from the environment, a specific suite of genes was necessary to extract such information. This is revealed by the fact that different species take different information from the environment. Different species, for example, hear or see things that other species cannot.³ So, before we get into specific cases, let’s unpack what exactly is going on here?

We begin with hardwired adaptations which have served human fitness for our entire species history, and no doubt reach way back deeper into our hominid ancestors. Let’s start with the example of stress, which will be relevant to a couple of forthcoming cases. Stress originates in the brain’s higher-order processing centers, where sensory inputs from the environment are evaluated based on innate wiring, past experiences, and evolutionary adaptations. This hardwired evaluation then triggers the release of signaling molecules (e.g., hormones or neurotransmitters), which travel to cells and bind to receptors, initiating the chemical cascades that lead to brain changes like altered protein production.

Many proteins are involved in producing or regulating neurotransmitters like serotonin, dopamine, and norepinephrine, which modulate mood, motivation, as well as stress responses. Alterations in proteins derived from amino acids (e.g., tryptophan for serotonin) can disrupt these pathways, leading to behavioral changes. Reduced protein production in key genes can weaken synaptic strength or alter brain networks for self-reflection and decision-making. These processes can increase depression, aggression, and pain sensitivity. Artificially depleting tryptophan in healthy adults transiently heightens subjective depression and aggressive behavior, demonstrating how protein precursor changes directly affect emotional states.

So, clearly, changes in protein production then can significantly influence an adult’s behavior and personality by altering brain structure, function, and chemistry. This process is often mediated through gene expression, where genes are transcribed into RNA and translated into proteins that serve as neurotransmitters, receptors, enzymes, structural components, or signaling molecules in the brain. Disruptions or variations in this production—due to genetics, epigenetics, nutrition, stress, or disease—can reshape neural circuits, leading to shifts in mood, cognition, social interactions, and self-regulation.

To repeat, all this begins with hardwired responses to information in the environment that fitness needs have selectively molded to respond with stress responses, which themselves set off these kinds of chemical reactions manifesting in altered psychology and behavior.⁴ This would be an obvious explanation for what we conventionally think of as moods. Can the outcomes though have longer lasting effects, resulting in phenotypic diversity?

Genetic variations affecting hundreds of genes (and thus proteins) cluster to influence self-regulatory traits like self-directedness (purposeful vs. aimless), cooperativeness (empathic vs. self-centered), and self-transcendence (altruistic vs. individualistic). For example, in large-scale studies, specific protein-coding gene sets modulate brain functions for empathy, episodic memory, and goal-setting, leading to distinct personality profiles. In animal models of dominance/submissiveness, social interactions alter hippocampal protein expression, correlating with behavioral disorders like mania or depression analogs in humans. Antisocial behavior has been tied to gene-protein interactions, amplified by environmental exposures.

So, the answer seems to be yes, such processes can have longer lasting impacts. Let’s look more closely at the well studied area of diversity in human life-history, particularly as related to sexual reproduction strategies. While it’s common in biology to distinguish species as fast (e.g., turtles) or slow (e.g., elephants) in their reproductive strategies, this distinction is also found in human phenotypic diversity. The common short hand in explaining these differences is – acknowledging that all organisms are operating with a limited caloric budget – distinguishing between those phenotypes that invest more energy into mating and those which invest more energy into parenting. The former will have more children, usually starting at a younger age, and investing less in each one of them; the latter have fewer children, possibly starting at a later age, and investing more in them. As it turns out, an important contributing factor to which strategy a human female⁵ follows is significantly influenced by her early childhood environment.

Environmental cues from childhood conditions, such as parental conflict or the absence of a biological father, are translated into differential reproductive strategies through a combination of neuroendocrine signaling, epigenetic modifications, and gene expression changes. This process aligns with life-history theory, where early-life instability (perceived as a harsh or unpredictable environment) accelerates reproductive maturation to maximize fitness in potentially short-lived or resource-scarce conditions, leading to “faster” strategies (leading to not only higher number of offspring, lower parental investment per child, but even earlier menarche). Conversely, stable environments with paternal presence may cue “slower” strategies (delayed maturation, fewer offspring, higher per child investment). These adaptations occur primarily in the brain (e.g., hypothalamus-pituitary-gonadal axis).

Parenthetically, either of these phenotypes can be highly fitness enhancing, as long as the local family cues are representative of the larger social situation. So, for instance, in a society where fathers do not commit to or invest in their offspring, the young girl taking this information from her environment will be more likely to pursue a faster reproductive strategy since she will not be able to reply upon a male mating partner who will commit to aiding her in raising her children. Long term investment, waiting for such a committed male, would be a losing strategy in that situation. It is true, of course, that her local family cue may not be an accurate representation of the social situation. Her father abandoning her may have been an outlier behavior, in which case she could have found a long term committed male parenting partner, but the biology of her phenotypic plasticity, following her local family cues, led her to a lower fitness enhancing strategy then was available.

The opposite of course is also possible. In a social situation where males do not commit and invest long term in their offspring, her father could have been the outlier who did stay, commit and invest in her. In that case the biology of her phenotype plasticity would have taken the wrong cue, leading her to pursue a slower reproductive strategy of high investment, leading her to delay reproduction in waiting for a high investment male partner who was unlikely to ever appear. From a fitness perspective, that would have been the wrong strategy. The operative “assumption” is that the local family cue is more likely than not to accurately represent the social situation. An evolutionary adaptation, of course, does not have to be right every time to still on average provide the biological underpinnings for enhanced fitness.

Okay, then, so what about this biology. What exactly are we talking about? The next bit is going to be very technical. And I don’t claim to entirely understand it all, and I welcome any feedback on how this model might be better tweaked or explained. But this is what I got from Grok. (And, incidentally, anyone finding the following technically detailed discussion too much of a slog can skip down to the “Conclusion” for a broad stroke summary of what I take from everything that follows.)

1. DETECTION OF ENVIRONMENTAL CHANGES

Childhood conditions are detected as psychosocial stressors or cues of environmental quality via sensory and physiological sensors:

• Stress Receptors and Neuroendocrine Sensors: Parental conflict or father absence often manifests as chronic stress, emotional neglect, or instability, activating the hypothalamic-pituitary-adrenal (HPA) axis. This begins with sensory inputs (e.g., visual/auditory cues of arguments or paternal absence) processed in brain regions like the amygdala and prefrontal cortex, which interpret these as threats. Glucocorticoid receptors (GRs) in the hypothalamus detect elevated cortisol (stress hormone) levels, while other sensors like vasopressin receptors in the lateral septum respond to social cues of attachment or disruption. In father-absent homes, reduced paternal care is sensed as lower oxytocin or vasopressin signaling, which normally promotes bonding and security.

• Triggering Events: These cues are chronic rather than acute, occurring during sensitive developmental windows (e.g., ages 0-7 years, per evolutionary models). For instance, girls in high-conflict or father-absent families experience higher allostatic load (cumulative stress), detected via metabolic sensors (e.g., insulin-like growth factor receptors) influenced by nutrition or emotional support. This detection is rapid at the cellular level but integrates over time to form a “calibration” of life-history pace.

This phase interprets the environment as “harsh/unpredictable” (conflict/absence) vs. “stable/resource-rich” (paternal presence), setting the stage for adaptive responses.

2. TRANSMISSION OF SIGNALS TO THE GENOME

Detected signals are relayed to the nucleus through hormonal and intracellular pathways, often leading to epigenetic changes that alter gene accessibility:

• Signaling Pathways: Activation of the HPA axis releases corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH), elevating cortisol, which binds to GRs and translocates to the nucleus as a transcription factor. This activates pathways like MAPK/ERK (for stress adaptation) and PI3K/Akt (linking stress to growth/reproduction). In cases of father absence, reduced vasopressin signaling (from lower paternal bonding) triggers similar cascades in social brain areas, affecting genes for reproductive hormones. Parental conflict amplifies inflammatory pathways (e.g., NF-κB), transmitting “inflammatory memory” signals that persist.

• Epigenetic Modifications: These signals recruit enzymes for chromatin remodeling. For example:

  • DNA methylation: High stress from conflict or absence increases methylation on genes like NR3C1 (GR) or BDNF in the hippocampus and hypothalamus, silencing them and reducing resilience. In reproductive contexts, methylation affects genes like ESR1 (estrogen receptor) or AVPR1A (vasopressin receptor), accelerating HPG axis maturation. Father absence correlates with altered methylation in sperm (for intergenerational effects) and brain, potentially via miRNAs like miR-34c-5p, which regulate brain development genes (e.g., CRTC1, GBX2).

  • Histone modifications: Stress signals enhance deacetylation (tightening chromatin) via HDAC enzymes or methylation via EZH2, making reproductive genes more or less accessible. Paternal absence models in rodents show this affects lateral septum circuitry for social/reproductive behaviors. Non-coding RNAs (e.g., miRNAs, piRNAs) from stress pathways bind to mRNA, fine-tuning expression; for instance, lower miR-34c-5p in high-adversity individuals alters neural pathways for earlier puberty.

These epigenetic marks act as a “molecular memory” of childhood conditions, calibrating the HPG axis (which controls puberty and reproduction) without altering DNA sequence. In evolutionary terms, this follows the “parental conflict hypothesis,” where paternally expressed genes promote faster growth/reproduction in unstable settings.

3. TRANSLATION INTO CHANGED PROTEIN PRODUCTION AND REPRODUCTIVE STRATEGIES

Epigenetic changes modulate transcription and translation, altering proteins/hormones that drive reproductive outcomes:

• Transcription (DNA to mRNA): Modified chromatin allows transcription factors (e.g., from cortisol signaling) to upregulate genes for gonadotropin-releasing hormone (GnRH) in the hypothalamus, accelerating HPG activation. In high-conflict/absent-father scenarios, this increases mRNA for estrogen or androgen pathways, leading to earlier menarche (e.g., by 6-12 months in girls). Downregulated GR mRNA reduces stress buffering, reinforcing faster strategies.

• Translation (mRNA to Protein): Ribosomes produce more GnRH, luteinizing hormone (LH), or follicle-stimulating hormone (FSH) proteins, hastening puberty and fertility. Epigenetic silencing of growth-suppressing genes (e.g., via methylation) boosts insulin-like growth factor (IGF) proteins, promoting rapid maturation. miRNAs modulate this; e.g., altered tsRNAs/piRNAs from adversity affect protein synthesis in reproductive tissues. Feedback loops amplify: higher androgens in males from father-absent homes increase aggression proteins (e.g., testosterone-related), supporting competitive mating.

KEY EXAMPLES OF OUTCOMES

• Age of Menarche and Puberty: Father absence cues instability, epigenetically advancing HPG genes, reducing age at first menstruation via higher estrogen proteins.

• Number of Offspring and Parental Investment: Faster strategies involve altered vasopressin/oxytocin proteins, reducing pair-bonding and investment; females show earlier sexual activity, more partners, higher offspring count but lower per-child care. (Males exhibit lower paternal investment proteins, favoring quantity over quality.)

• Intergenerational Aspects: These changes can persist in germline epigenetics (e.g., sperm methylation), transmitting faster strategies to offspring.

These mechanisms are influenced by genetics (e.g., heritability of sensitivity) and can be partially reversed by later stable environments, though early marks often endure. Research emphasizes bidirectional gene-environment interplay, with human data from longitudinal studies and animal models providing causal insights.

Assuming Grok has the details correct, this provides a thorough and compelling explanation for how different phenotypes can emerge to serve evolved fitness expectations in response to environmental cues. Or, maybe better stated, how human biology is evolved to extract information from the environment to enhance the calibration of phenotypes for improved probability of enhanced fitness.

Again, this example was explored in depth because of how well these different (life-history) phenotypes are studied and understood in the literature. So, then, do the same lessons apply to the spatial and temporal phenotypes which inform my model of the phenotype wars? Can the changing niches of the two phenotypes, driving the spirals of the phenotype wars, be partially explained by not merely selection of existing options within the phenotype reaction norm but also by developmental changes in the population of individuals at any given arc of the spiral from one phenotype’s hegemony to the other. I put this prospect to Grok by asking whether the same processes resulting in different sexual reproduction strategies could be applied to different personality traits – specifically higher/lower openness/conscientiousness. With a few edits for relevance and clarity, this was the answer I got.⁶

There is substantial evidence that personality structure phenotypes, such as varying levels of conscientiousness or openness can be shaped through mechanisms similar to those influencing reproductive strategies—namely, gene-environment interactions (GxE), epigenetic modifications, and environmentally modulated gene expression. These processes allow a single genotype to produce different phenotypic outcomes in response to environmental cues, much like how childhood adversity calibrates faster or slower life-history strategies via the HPA axis, signaling pathways, and chromatin remodeling. This reflects the polygenic and poly-environmental nature of personality, where genetics provide a predisposition (heritability estimates around 40-60% for Big Five traits), but environmental factors dynamically interact to influence trait expression.

1. DETECTION OF ENVIRONMENTAL CUES

Similar to stress detection in childhood, environmental cues (e.g., family stability, socioeconomic conditions, or cultural exposures) are appraised by the brain’s sensory and cognitive systems:

• Sensory and Appraisal Processes: Inputs like social interactions, educational opportunities, or adversity are processed in regions such as the prefrontal cortex (for executive function related to conscientiousness) and temporal lobes (for creativity and openness). These are evaluated against innate and learned patterns— e.g., enriched environments might signal “safety for exploration,” while instability signals “need for caution.” This appraisal activates neuroendocrine systems, including the HPA axis for stress-related cues or dopamine/oxytocin pathways for social/novelty cues.

• Triggering Events: Chronic cues during sensitive periods (e.g., childhood or adolescence) integrate over time. For instance, supportive parenting might enhance dopamine signaling, promoting openness, while neglect activates cortisol pathways, potentially reducing conscientiousness by prioritizing survival over long-term planning. (We’ll come back to this!) This mirrors how paternal absence cues reproductive acceleration via vasopressin/oxytocin receptors.

“Knowledge” of the environment emerges from neural computations, leading to ligand release (e.g., cortisol, dopamine) that binds receptors and initiates cascades.

2. TRANSMISSION OF SIGNALS TO THE GENOME

Signals from appraised cues are relayed via pathways that lead to epigenetic changes, allowing environmental modulation of the same genotype:

• Signaling Pathways: Binding of ligands (e.g., cortisol to glucocorticoid receptors or oxytocin to OXTR) activates cascades like MAPK/ERK (for learning/novelty, influencing openness) or PI3K/Akt (for motivation/organization, tied to conscientiousness). These converge on transcription factors that regulate personality-related genes. For example, dopamine pathways (involving genes like DRD4) respond to novelty-rich environments, while serotonin pathways (e.g., 5-HTTLPR) interact with adversity to affect emotional regulation.

• Epigenetic Modifications: These signals recruit enzymes for chromatin alterations:

  • DNA methylation: Adversity can methylate promoter regions of genes like OXTR (oxytocin receptor), reducing its expression and linking to lower openness (e.g., reduced curiosity or empathy). Similarly, methylation on genes like COMT (catechol-O-methyltransferase, involved in dopamine breakdown) can vary conscientiousness by altering executive function in response to stress.

  • Histone modifications: Enrichment cues might increase acetylation via HAT enzymes, enhancing accessibility of polygenic networks for openness (e.g., loci on chromosomes 1, 2, and 12 identified in GWAS). For conscientiousness, deacetylation under instability could silence genes for organization (e.g., loci near CADM2 or MSRA).

  • Non-coding RNAs: miRNAs modulated by environment (e.g., miR-132 in response to social cues) can fine-tune mRNA stability for traits like conscientiousness, where genetic effects depend on environmental context.

These modifications create GxE effects: the same genotype (e.g., a polygenic risk score for high openness) expresses differently—higher in supportive environments, lower in adverse ones—due to interwoven genetic and environmental factors. Twin studies show heritability varies by environment (e.g., higher in stable settings), and meta-analyses indicate genetic influences decrease while environmental ones increase with age, approaching 34% heritability and 66% environmentality by adulthood.

3. TRANSLATION INTO CHANGED PROTEIN PRODUCTION AND PERSONALITY PHENOTYPES

Epigenetic changes alter transcription/translation, producing proteins that shape neural circuits for personality:

• Transcription (DNA to mRNA): Environmentally activated factors upregulate genes like those for dopamine receptors (DRD2/DRD4), increasing mRNA for openness-related proteins in exploratory contexts. For conscientiousness, stable cues might enhance mRNA for prefrontal proteins (e.g., via CADM2 loci), supporting goal-directed behavior.

• Translation (mRNA to Protein): Ribosomes produce varying protein levels—e.g., higher OXTR protein from low methylation promotes openness facets like ideas/values/actions. Feedback loops reinforce: more dopamine proteins in enriched settings amplify openness, creating stable traits.

KEY EVIDENCE AND EXAMPLES

• Openness: GWAS identify 7-14 loci (e.g., near RASA1), with heritability ~21%, but expression depends on environment. Epigenetic studies link OXTR methylation to openness; low methylation (higher expression) in supportive environments yields higher scores, while adversity increases methylation, reducing it. Twin studies show MZ/DZ correlations vary by rearing environment (e.g., .43/.23 apart vs. .51/.14 together), indicating GxE modulates the same genotype.

• Conscientiousness: 2-3 loci identified (e.g., near CADM2), with polygenic influences intertwined with environment. Adverse cues (e.g., stress) can epigenetically silence genes for executive proteins, lowering conscientiousness, while stability enhances them via acetylation. Meta-analyses show environmental effects increase from 30% in childhood to 67% in adulthood, allowing genotypes to express higher/lower levels based on cues like education or parenting.

• General Evidence: Behavioral genetics confirm GxE for all Big Five traits; e.g., environments moderate genetic variance, with no single “personality gene” but interactive polygenic networks. This parallels reproductive phenotypes, where cues like conflict calibrate outcomes via similar epigenetic pathways.

These mechanisms are adaptive (e.g., lower openness in harsh environments conserves resources), but can lead to mismatches later.

CONCLUSION

Again, I do not know enough basic molecular biology to evaluate the precise accuracy of every technical claim here. However, the reading I have done suggests to me that in broad strokes this analysis is clearly correct directionally.⁷ If that is so, then we can draw some conclusions.

First, though a helpful caveat: there is a distinction in the field between genotypes that are more robust and that are more plastic. My understanding is that this evaluation is based upon a counting of polymorphisms.⁸ Along the lines of the speculation we saw from Hibbing et. al.⁹, in a recent post, it seems plausible to suggest that there are robust spatials and temporals: those with higher heritability in their relative levels of openness and conscientiousness. These would be the hardcore base of each phenotype from a political perspective.

For the rest of the population, the ebb and flow of these phenotypic traits are explained through another story. I’d previously allowed that the majority – without a strong personality formation leaning in the direction of either political pole – probably simply followed the leader: adjusted to the prevailing political climate, giving whatever lip-service was necessary to get by without suffering as collateral damage in the phenotype wars.¹⁰ While in all likelihood a phenomena along those lines is probably part of the story, the above evidence suggests that a much more profound effect also contributes to the hegemony of either political phenotype during its reign.

For example, novelty rich environments, which feel safe for exploration, affect neurotransmitter pathways, regulating behavioral outcomes. As societies which become increasingly spatial – partially as a function of growing insulation from nature’s negative feedback loop (largely on the basis of temporals’ conscientious efforts to build social systems to optimize caloric budgets) and partially as a result of the increased prominence and prestige of uninhibited spatials associated to such gains – the conditions are established for the more plastic genotypes to express more spatial phenotypes. In this way there is a kind of snowball effect; as the more robust spatials establish a beachhead in the phenotype wars with the temporals, more and more of the bystanders morph into spatials to optimize fitness in the emerging social conditions.

The one spanner in the works here is the above emphasis upon the role of adversity and stress in reducing conscientiousness. My hypothesis has always been that it was precisely harsh Darwinian conditions that selected for higher conscientiousness, given the narrow margin of survival available to those living under such conditions. Some of the findings above complicate that hypothesis. For example: “Adverse cues (e.g., stress) can epigenetically silence genes for executive proteins, lowering conscientiousness, while stability enhances them via acetylation…” That would imply a lowering of conscientiousness under harsh Darwinian conditions.

That implication though is difficult to align with the extensive evidence showing conscientiousness highly correlated with the political right – especially when “right” is correctly associated with pluralist commitment to family, Gemeinschaft, and tradition.¹¹ But then this may not be as much of a counter-indicator in relation to the phenotype wars model as it might appear at first blush. After all, remember, the loose definition of a temporal is higher conscientiousness than openness.¹² My tendency has been to assume that that entailed high conscientiousness more globally. And that comparatively higher conscientiousness could (probably does) still exist among the more robust temporals, under harsh Darwinian conditions.

For the more plastic temporals though, perhaps their conscientiousness levels could fall, but as long as their openness levels fell even farther down, they would still qualify as temporals: higher conscientiousness than openness. And the evidence above, as I read it, does suggest that openness is even more vulnerable to adverse and unstable environments. So that way, even with declining conscientiousness, the more plastic phenotypes could become operative temporals under harsh Darwinian conditions. That of course is all speculative, but prior to this recent spate of research my model for the transitions between time-space-time-etcetera biased societies was much more speculative. All this has put considerable empirical and experimental flesh on the theoretical bones.

In any event, of course, there’s more work to do, but all this does provide considerably more substantive support and nuanced explanation for the phenotype wars model. Age and life being what it is, I’m doubtful that I’ll ever publish a second edition of A Plea for Time in the Phenotype Wars. If I did though, this material would be an important supplement to the argument made and evidence provided there. Hopefully this little digression from our discussion of the Canadian front in the phenotype wars provides some remedy to that shortcoming in the original book.

But, in the next post, we’ll be back to our regularly scheduled programming. So, if you don’t want to miss the next installment to the discussion of the Canadian front in the phenotype wars, but haven’t yet, please…

And if you know of someone who’d appreciate the kind of thing we get up to around here, please…

Meanwhile: Be seeing you!

1. Anyone interested in these topics, but unsure about the context I’m providing, should read my (must read!) book: Michael McConkey, A Plea for Time in the Phenotype Wars (Vancouver, B.C.: Biological Realist Publications, 2023).

2. Michael McConkey, Biological Realism: Foundations and Applications (Vancouver, B.C.: Biological Realist Publications, 2020).

3. Examples of all this are provided in McConkey, Biological Realism.

4. It is important to emphasize when referring to information, that “environment” means something different in natural (or sexual) selection than it does in ontogeny or development. The former usage captures objective exogenous forces, such as predation, opposite sex preference, and climate related resource availability. The later is a subjective probing of an information field for cues to enhance phenotypic plasticity in the interest of enhanced situational fitness. Such “environment” probing is only possible given the evolutionarily sculpted genetic machinery required to recognize and integrate such information. That is partly, of course, what this whole post is about.

5. There are also differences in male reproductive strategy, but I’ll focus primarily on the female as it tends to be more sweeping and dramatic in diversity.

6. Some sources worth looking at for substantiation of the claims that follow include: Ben Bar-Sadeh et al., “Unravelling the Role of Epigenetics in Reproductive Adaptations to Early-Life Environment,” Nature Reviews Endocrinology 16, no. 9 (2020): 519–33; Michael J. Meaney, “Epigenetics and the Biological Definition of Gene × Environment Interactions,” Child Development 81, no. 1 (2010): 41–79; Daniel A. Briley and Elliot M. Tucker-Drob, “Genetic and Environmental Continuity in Personality Development: A Meta-Analysis,” Psychological Bulletin 140, no. 5 (2014): 1303–31; S. Sanchez-Roige et al., “The Genetics of Human Personality,” Genes, Brain and Behavior 17, no. 3 (2018): e12439; Christian Kandler and Jana Instinske, “The Polygenic and Poly-Environmental Nature of Personality,” Current Opinion in Psychology 65 (October 2025): 102068; and Jing Luo et al., “Genetic and Environmental Pathways Underlying Personality Traits and Perceived Stress: Concurrent and Longitudinal Twin Studies,” European Journal of Personality 31, no. 6 (2017): 614–29.

7. See a nice, concise introduction to these processes, using a wide range of non-human animal examples: Cristina C. Ledon-Rettig and Erik J Ragsdale, “Physiological Mechanisms and the Evolution of Plasticity,” in Phenotypic Plasticity & Evolution: Causes, Consequences, Controversies, ed. David W. Pfennig (Boca Raton, FL: CRC Press, 2021).

8. In addition to several of the articles in Pfenning ed., Phenotypic Plasticity & Evolution, see also the classic: Mary Jane West-Eberhard, Developmental Plasticity and Evolution (New York: Oxford University Press, 2020).

9. John R. Hibbing et al., Predisposed: The Left, the Right, and the Biology of Political Differences, 2nd Edition (New York London: Routledge, 2024).

10. Though, in fairness, if you go back and look closely at the relevant discussion in A Plea for Time in the Phenotype Wars, I did ponder the prospect of epigenetic evolution, but chose for reasons of parsimony to restrict the primary discussion to phenotypic selection, as in the case of the peppered moths.

11. See my recent Hibbing et. al. post and A Plea for Time in the Phenotype Wars.

12. Though, I do think that to be a hardcore temporal, conscientiousness should be much higher than openness, and likewise in reverse for spatials.