ED as a Facultative Exit Ramp From the Reproductive Tournament

 

A selfish-gene hypothesis about status, stress, and late-life strategy

Erectile dysfunction is usually discussed as a medical problem, a vascular problem, or a psychological problem. In everyday life it is often framed as a private frustration, and in medicine it is often framed as a symptom. Those framings are useful, but they are not the only ones available. If we take an evolutionary perspective, we can ask a different question: could some forms of erectile dysfunction, especially the stress-triggered and situation-dependent kind, reflect a designed feature of the system rather than only a breakdown?

I want to propose a hypothesis that treats a subset of erectile dysfunction as a conditional strategy. The core idea is that in certain social and physiological circumstances, losing erectile function in competitive or evaluative contexts can protect an older or weaker male from costly social and physical consequences. It can reduce the pressure to compete in the reproductive tournament, lower the risk of provoking rivals, and reduce the chances of being punished, injured, or ostracized. Crucially, in this proposal, erectile dysfunction does not necessarily abolish reproduction. Instead, it can push reproduction into lower-risk contexts, meaning private, calm, supportive situations with a trusted mate, rather than public, high-pressure, status-laden sexual performance.

This is not a claim that all erectile dysfunction is adaptive. A large portion of erectile dysfunction is clearly linked to vascular disease, diabetes, medication effects, endocrine changes, neurologic issues, and the general wear and tear of aging. Those causes can be straightforward pathology or modern mismatch. My claim is narrower: psychogenic and competition-sensitive erectile dysfunction has the right properties to be a facultative switch, and we should at least consider the possibility that selection shaped that switch because it helped individuals survive and remain socially embedded long enough to gain additional reproductive and inclusive-fitness benefits.

Sneaky males and alternative reproductive tactics in primates

If you step back and look across primates, the idea of “covert reproduction” is not speculative at all. It is one of the recurring patterns you see whenever a social system produces high reproductive skew. A few males, typically those with rank, coalitions, or physical formidability, can monopolize mating opportunities. The rest do not simply become nonparticipants. They shift tactics. They mate when the dominant male is distracted, they form consortships that pull a female away from the group, they exploit moments of social ambiguity, or they rely on female choice and concealed timing. These are alternative reproductive tactics in a very literal sense.

A clean empirical example comes from rhesus macaques. There is evidence for an “audience effect” in which subordinate males and females shift mating behavior depending on who is watching, consistent with the idea that sexual behavior is strategically managed to reduce retaliation from dominants. The point is not that macaques are calculating in a human-like way. The point is that selection has had plenty of time to build behavioral rules that reduce the costs of mating under dominance constraints.

Baboons give a related pattern because they are a classic case of rank and reproductive skew. High-ranking males often obtain most mating access, but “incomplete control” is the default. There are opportunities for opportunistic or sneaky copulations, and whether those translate into paternity depends on a mix of timing, female behavior, and the practical limits of mate guarding. Long-term work on savanna baboons has explicitly grappled with the gap between mating opportunities and paternity outcomes, which is exactly where “sneaky male” strategies live.

Chimpanzees are particularly relevant because they show a menu of male tactics. Work in wild chimpanzees describes multiple mating strategies such as possessive mate guarding, opportunistic mating, consortships, and extra-group mating. The details differ by community and ecology, but the overall point is stable: even in a system with strong dominance effects, subordinate males can still achieve some reproduction by exploiting windows of access that do not require direct victory in a dominance contest.

Orangutans formalize “covert versus overt” into two male morphs. Orangutans show male bimaturism: sexually mature males can remain unflanged for long periods, while flanged males develop the prominent cheek pads and other secondary sexual characteristics associated with the classic dominant phenotype. These morphs are tied to different reproductive tactics, often described as something like “sit, call, and wait” for flanged males versus “go, search, and find” for unflanged males. In other words, one tactic is more overt and advertisement-based, and the other is more roaming and opportunistic.

What matters for this broader argument is that orangutan tactics appear to be condition-dependent rather than a simple fixed caste system. Recent long-term paternity work has tested whether these tactics map onto reproductive success in more naturalistic settings, precisely because the evolutionary logic depends on whether the “sneaky” pathway is a meaningful route to actual paternity.

If we translate this back to the ED hypothesis, the parallel is straightforward. In primates, selection often builds mechanisms that reduce direct confrontation when confrontation is too costly, while preserving some probability of reproduction through lower-visibility channels. In this framing, stress-triggered ED is not “giving up on reproduction.” It is closer to a gating mechanism that prevents conspicuous, rivalry-inviting mating effort under threat while leaving open the possibility of sexual function in private, low-threat contexts. That is the same strategic shape we see in primate alternative tactics, even though the human mechanism would be physiological and psychological rather than a discrete morph.

It is also useful to think about this in the broader logic of harem and one-male systems, where reproductive access is highly skewed. In mountain gorillas, for example, a dominant silverback can achieve disproportionate mating access while other males remain on the periphery, tolerated but reproductively constrained. In those systems, the central problem for a lower-ranking or aging male is how to remain inside the protective social umbrella without continually triggering the dominant male’s countermeasures. A context-sensitive reduction in overt sexual performance could, in principle, function as a “peripheralization” mechanism that does not require physical exile. The male is still present for kin, protection, provisioning, and group membership, but he is less legible as an active sexual rival, and therefore less likely to provoke costly retaliation. The key point is that this is not necessarily infertility or total withdrawal. It is a credible, hard-to-fake shift away from conspicuous mating effort that allows continued social embedding while preserving whatever low-risk reproductive opportunity remains.

Menopause and the evolutionary rationale for reproductive cessation

Menopause is one of the great teaching examples for evolutionary reasoning because, on its face, it looks like a direct contradiction of natural selection. If selection favors traits that increase reproduction, why would females stop reproducing well before the end of life? The modern consensus is not that there is one final answer, but that there are a small number of serious hypotheses that make distinct predictions, and the best accounts generally involve kin selection and life-history tradeoffs.

The most influential family of explanations is the grandmother hypothesis. The logic is that in humans, offspring are unusually expensive. Children remain dependent for a long time, and mothers benefit from help that increases the survival and later reproductive success of those children. If an older woman can increase her inclusive fitness more by helping existing descendants than by producing another high-risk infant late in life, then selection can favor the cessation of reproduction coupled with an extended post-reproductive lifespan. This hypothesis is tied to arguments about provisioning, skill, and the role of older females in supporting daughters and grandchildren, especially in ecologies where food acquisition and knowledge matter.

A related but distinct account is often called the mother hypothesis. Here the emphasis is not primarily on grandmaternal benefits, but on the direct fitness risk of late-life reproduction. As maternal age rises, risks to the mother and risks to dependent offspring rise. If late pregnancies increase the probability that a mother dies and leaves several dependent children without care, then continuing to reproduce can reduce total fitness. Under that logic, stopping reproduction can be favored because it protects the survival of existing offspring who still require maternal investment. This hypothesis has been explicitly modeled and tested using demographic approaches.

Then there is the reproductive conflict hypothesis, which is conceptually elegant and, in my view, underappreciated in popular discussions. It emphasizes intergenerational competition. If mothers and daughters overlap reproductively, their offspring compete for resources and care, and this conflict can reduce inclusive fitness. A mechanism that reduces reproductive overlap between generations can be favored if it resolves a conflict that would otherwise lower total descendant output. Cant and Johnstone famously formalized this logic, and it has been used to interpret patterns of unusually low reproductive overlap in humans.

One reason menopause stays so interesting is that it is rare in nature, which implies it requires special social and demographic conditions. That is why comparisons with toothed whales have become important. Killer whales and a small number of other toothed whale species show extended post-reproductive lifespans, and researchers have argued that the relevant conditions include stable kin groups and opportunities for older females to increase descendant success without continuing reproduction, while also avoiding reproductive conflict with younger females. Recent analyses continue to develop and test this framework.

If you connect all of this back to the ED analogy, you get a useful clarification. Menopause is not simply “older females stop reproducing.” It is a life-history reallocation shaped by the cost structure of late-life reproduction and the payoff structure of kin-directed investment. The proposed male analogue should therefore not be framed as a hard fertility stop, because men do not have that biology. It should be framed as a facultative shift away from the most dangerous and socially punishable forms of mating competition, paired with continued capacity for reproduction under low-threat conditions. That keeps the analogy at the level where it is strongest: strategic reallocation under changing late-life costs, rather than mechanistic symmetry.

One more nuance that matters here is the timing of selection pressure relative to the ages at which the most severe, clearly organic forms of erectile dysfunction tend to appear. In forager demography, “average lifespan” is often misleading because early mortality pulls it down, but the more relevant quantity for selection is conditional survival once someone makes it through childhood and into adulthood. Cross-cultural work on hunter-gatherer survival curves shows substantial survival into midlife and meaningful post-reproductive lifespan, even though mortality remains high compared to modern societies.

 In that context, it is plausible that a stress-sensitive, context-dependent gating system could be shaped by selection because it affects reproduction and social risk in the 20s, 30s, 40s, and 50s, which are ages where many men historically reproduced and where coalition membership still strongly determined survival and mating opportunity. At the same time, the advanced, late-life forms of ED that track vascular deterioration and generalized senescence become much more common as age increases, and those later failures are less likely to be adaptations in their own right, because selection is weaker at older ages and because many of these mechanisms reflect broader physiological decline.

This is exactly where antagonistic pleiotropy becomes a clean interpretive tool: traits that improve early-life performance and reproductive competitiveness can be favored even if they carry downstream costs that manifest later, when selection has less leverage to eliminate them.

Under that view, the early, reversible, threat-linked pattern is the best candidate for an evolved “tournament gating” feature, while the severe late-life phenotype is more plausibly senescent breakdown, mismatch, or a pleiotropic cost of earlier-life design priorities.

Why the male reproductive tournament needs an “off ramp”

In many social mammals, male reproductive success is high variance. Some males gain disproportionate mating access, and many males gain less. This creates intense selection pressure on traits that increase mating effort and competitive ability: risk-taking, aggressive dominance displays, and the willingness to engage in confrontation. The problem is that this tournament is not free. It carries a nontrivial probability of injury, social retaliation, and exclusion from valuable coalitions.

As males age, the cost-benefit ratio changes. The marginal benefit of aggressive competition can fall if status is already established, if the male’s condition is declining, or if the male’s social role has shifted toward parenting, provisioning, and alliance maintenance. At the same time, the marginal costs can rise because recovery is slower, injuries accumulate, and social tolerance for disruptive competitive behavior may drop. In a small-scale social world, the consequences of being seen as a destabilizing sexual competitor can be severe. If you lose your coalition, you do not just lose mating opportunities. You lose protection, resource access, and the social framework that makes survival reliable.

A selfish-gene logic can therefore justify a mechanism that sometimes says: do not escalate. Stop advertising. Stop competing in high-risk contexts. Keep your place in the group. If reproduction happens, let it happen in the least socially costly way.

The key observation: erectile function is context sensitive

The most important piece of phenomenology for this hypothesis is something many people already recognize, even if they have never described it in evolutionary language. A man can fail to attain an erection under pressure, scrutiny, novelty, conflict, or perceived judgment, and yet be fully capable under calm, affectionate, low-threat conditions. This is not subtle. It is one of the defining features of psychogenic erectile dysfunction, and it is strongly suggestive that sexual function is not a simple on-off state determined only by “hardware.” It is a system that is gated by threat, attention, and social meaning.

From a mechanistic perspective, this makes sense. Erection requires a physiological state consistent with safety and parasympathetic dominance. If the nervous system is treating the environment as dangerous, evaluative, or status-volatile, sympathetic activation rises. That state is excellent for vigilance and action, and it is terrible for sexual performance. The proximate mechanism is therefore already built to suppress erection when threat is high. The evolutionary question is whether that suppression is merely an inconvenient side effect, or whether it sometimes served as an adaptive control feature.

If the system suppresses erection during threat, it will inevitably suppress erection during social threats too. Social threats can be just as biologically salient as physical threats in a primate that depends on coalition membership. A humiliating failure, a public sexual challenge, or a perceived attempt to take someone else’s mate can all carry risk. In that light, situation-dependent erectile dysfunction can be reframed as a threat response that prevents an individual from entering an arena where the potential social costs exceed the expected gains.

Erectile dysfunction as an honest signal that reduces rivalry

One advantage of this kind of mechanism is that it is hard to fake. A male can verbally claim he is not competing, but claims can be strategic. An involuntary failure of performance, especially if it is reliable under stress, is not as easily manipulated. That makes it a plausible honest signal. It communicates, whether the person intends it or not, that he is not currently a reproductive threat in the public, high-status arena.

It is important to be careful here. I am not claiming that men consciously “signal” erectile dysfunction to other men in some theatrical way. The claim is that a physiological constraint can have a social meaning, and that meaning can feed back into social dynamics. If other males learn that a given male is not a consistent competitor under pressure, they may treat him as less threatening. In a dominance hierarchy, reducing perceived threat can translate into real safety. It can mean fewer challenges, less harassment, and less risk of violent escalation.

This can also help explain a subtle point that matters for the hypothesis: the mechanism does not need to abolish reproduction to have tournament effects. It only needs to suppress the type of reproduction that triggers retaliation. In many social systems, covert or low-visibility mating is tolerated differently than overt mate stealing or dominance-based sexual display. The fitness logic can be: reduce the conspicuousness of mating effort while maintaining the possibility of reproduction in low-cost contexts.

Covert reproduction and alternative tactics

This is where the analogy to alternative reproductive tactics becomes useful. In many species, males who cannot reliably win direct contests do not simply give up. They shift tactics. They may become “sneakers,” mate opportunistically, form alliances, or pursue reproduction through low-risk channels. The details vary, but the general logic is consistent: when direct competition is too costly, selection can favor mechanisms that redirect behavior toward less risky reproductive pathways.

In that framework, stress-linked erectile dysfunction can be interpreted as a gating mechanism that prevents a man from participating in the most punishing form of the tournament: high-pressure performance that carries status implications and the potential to provoke rivals. The same man may still be capable of reproduction in private, supportive contexts where there is no audience, no acute judgment, and minimal threat of retaliation. That looks less like total shutdown and more like tactical modulation.

This is also where the menopause analogy becomes both helpful and potentially misleading. Menopause is a relatively abrupt and biologically fixed shift in female fertility. The functional analogy I care about is not the mechanistic similarity, because the mechanisms are clearly different. The analogy is that both can shift late-life strategy away from the highest-risk reproduction and toward social roles that preserve survival and family success. For men, the plausible version is not a hard stop in fertility. It is a context-sensitive reduction in overt mating competition that promotes continued group membership and stable paternal or kin investment.

I also think it is worth taking seriously that the general reduction in sexuality and “horniness” that many people experience with age could itself be a strategic response to competition, not just a passive decline. In both males and females, overt sexual motivation can make you conspicuous. It puts you into the arena of rivalry, judgment, mate-guarding, and reputational hazard. If you are older, less dominant, or simply less interested in paying the costs of the tournament, there is a selfish-gene logic to turning the volume down. You become less likely to provoke conflict, less likely to trigger retaliation, and less likely to destabilize the social fabric that you still depend on for belonging and security. At the same time, you are not necessarily “out of the game.” You can remain socially embedded, maintain pair bonds, invest in offspring and kin, and still reproduce opportunistically under low-threat conditions if the opportunity exists. In that framing, reduced libido and reduced conspicuous sexual signaling can be understood, at least in part, as a calibrated shift in mating effort that lowers competitive exposure while preserving the option value of reproduction, rather than as pure maladaptive decay.

Why group membership is an individual fitness asset

A skeptic might say: why would selection ever favor a trait that reduces sexual performance? The answer is that sexual performance is not the only contributor to fitness, and it is not always the dominant one. In a social species, continued access to the group is itself a resource. It provides safety, food-sharing opportunities, alliance support, and a platform for helping offspring survive and reproduce. If an older male faces a real risk that competitive mating will trigger punishment or expulsion, then losing the ability to perform in those contexts can be protective.

This is the selfish-gene core. It is not altruistic restraint for the benefit of the group. It is self-preserving strategy under constraints. The individual survives longer, maintains access to resources, and retains the chance to reproduce when conditions permit. Even if reproduction becomes less frequent, the overall expected genetic payoff can rise if the alternative is injury, death, or social exclusion.

It also fits an intuitive observation. Many men do not want to compete indefinitely. They often want stability, respect, and family continuity more than they want constant sexual contest. In that sense, a physiological off-ramp that appears when competition becomes too costly might align with the life-history shift that an older male would benefit from making anyway.

Predictions that would support or refute the hypothesis

If this is a real evolved strategy for a subset of erectile dysfunction, it should produce patterns that differ from pure vascular aging. Several predictions follow naturally.

First, the phenomenon should be strongly context dependent. Erectile dysfunction should be most pronounced in environments that trigger social-evaluative threat: new partners, perceived judgment, unstable status, rivalry, conflict, and novelty under scrutiny. It should be less pronounced in stable, affectionate, low-pressure contexts, especially with trusted partners and high privacy.

Second, it should be at least partially reversible on short timescales, because it is mediated by stress physiology and attention, not only by long-term vascular deterioration. If it is a gating mechanism, changing the gate conditions should change the outcome.

Third, it should correlate more with perceived social threat and bargaining power than with chronological age alone. Two men of the same age should differ based on status stability, relationship security, health, and the perceived risk of rivalry. The man who is more vulnerable to sanction should show stronger gating effects.

Fourth, it should predict shifts in behavior. Men who exhibit competition-linked erectile dysfunction should, on average, invest more in kin-directed roles and alliance maintenance, not because they are morally better but because their strategy has shifted. That shift might include more parenting, more provisioning, more mentoring, more conflict avoidance, and more coalition-support behavior.

Fifth, it should show meaningful cross-cultural variation. In ecologies or social systems where male-male competition is intense and punishment for sexual provocation is high, the gating pattern should be stronger. In settings where sexual competition is low and long-term pair bonds are protected by norms that reduce rivalry, the gating pattern may be weaker.

None of these predictions are proof, but they make the hypothesis scientifically legible. They also create a way to separate the hypothesis from a simpler claim like “stress causes ED,” which is true but not explanatory in an evolutionary sense.

Alternative explanations and why they matter

Any serious discussion has to separate adaptive hypotheses from byproduct hypotheses. A byproduct account says erectile dysfunction is simply what happens when vascular health declines, when stress rises, or when hormones shift, with no special function. That account will explain a large portion of cases and should not be dismissed.

The point of the present hypothesis is that byproduct accounts do not automatically explain the specific design-like features of psychogenic ED, especially its context sensitivity and social-evaluative triggers. A system can be both constrained and designed. The same physiology that prevents erection under threat could be a simple constraint, but it could also have been tuned by selection because it prevented individuals from making dangerously costly choices in certain contexts.

To keep the argument honest, the best version of this paper treats erectile dysfunction as a heterogeneous category. Some fraction is organic pathology. Some fraction is anxiety-driven without obvious adaptive value in modern settings. Some fraction may be a misfiring of a defensive system in an environment saturated with chronic stress, sexual scripts, pornography novelty, and performance surveillance. And some fraction, especially the competition-linked pattern, could reflect an evolved gating function that once reduced severe costs in small groups.

Why this hypothesis is worth stating, even if it turns out wrong

There is a practical reason to articulate evolutionary hypotheses even when they are speculative. They change what we look for. They push us to measure context, status, threat, and coalition dynamics, rather than treating erectile dysfunction as a uniform individual defect. They also help explain why shame and performance monitoring can be so central. If the system is doing threat management, shame and monitoring are not just psychological noise. They are part of the control loop.

At minimum, this framework suggests that erectile dysfunction can sometimes be understood as a signal of safety deficit, not simply a failure of desire or masculinity. In that framing, the relevant variables are social security, trust, privacy, and stable affiliation. If those variables predict sexual function even after controlling for health, then the gating hypothesis becomes more plausible. If they do not, the hypothesis weakens.

Conclusion

I am proposing that a subset of erectile dysfunction, especially the stress-triggered and competition-sensitive form, may function as a facultative exit ramp from the reproductive tournament. In a selfish-gene sense, the advantage is not that the group benefits. The advantage is that the individual avoids injury and ostracism, preserves coalition membership, and maintains the possibility of reproduction under low-threat conditions. The mechanism does not need to eliminate sex. It only needs to suppress overt, risky, status-entangled mating effort while allowing private, supportive reproduction to remain possible.

This hypothesis makes specific predictions. It invites comparative thinking across species with alternative reproductive tactics. It also provides a psychologically realistic picture of what many men report: sexuality is not only desire and function, it is safety, status, and threat. The evolutionary question is whether that is merely how the machinery breaks under pressure, or whether it is how the machinery was built to keep individuals alive and socially embedded when competing would be a losing bet.

Postscript:

You know, there was a time back in around 2004 where I thought I came up with the evolutionary explanation for menopause. I looked into it and I found an essay by Jared Diamond that explained the consensus in the literature and, frustratingly for me, it was exactly what I wrote out a few days prior. It was very disappointing to see that my idea wasn’t novel. But this is kind of fun, 22 years later, postulating about this counterpart to female menopause. It’s kind of interesting that men don’t go through menopause and that women don’t exactly experience erectile dysfunction. But it’s interesting that those two things might be analogous on a evolutionary scale.

 

Sexual Plasticity, Maternal History, and the Missing Aversion Hypothesis: A Developmental-Evolutionary Account of Same-Sex Attraction

Abstract

Homosexuality remains challenging to explain within a simple adaptationist framework because, on its face, exclusive same-sex attraction does not directly produce offspring. A great deal of research has therefore focused on indirect evolutionary explanations, balancing selection, sexually antagonistic effects, and prenatal developmental pathways such as the fraternal birth order effect. In this article I propose a complementary account that does not require  male homosexuality to have been directly selected for as a discrete trait. The model treats same-sex attraction in males as an emergent outcome of three ingredients: (1) population-level variation in erotic category-specificity, meaning variation in how narrowly sexual arousal is canalized toward the opposite sex, (2) maternal history effects that may bias this canalization in later-born sons, and (3) a species-typical absence of a strong evolved aversion to same-sex arousal cues, shaped by ancestral social ecologies in which privacy was limited and sociosexual behavior likely served multiple social functions. This framework is intended to be testable. It makes predictions about non-exclusivity, category-specificity, and the relationships among sibling structure, development, and adult sexual phenotypes.

Introduction

When people discuss the evolutionary puzzle of male homosexuality, the conversation often becomes polarized. Either homosexuality is assumed to be a direct adaptation, which makes many researchers understandably cautious, or it is treated as a pure byproduct, which can feel unsatisfying because it leaves the developmental story vague. I think a more productive stance is to admit that we may be dealing with multiple partially overlapping pathways, some prenatal, some developmental, and some social. If the phenotype is heterogeneous, then the explanations should be as well.

My goal here is not to replace existing theories, especially not the more established prenatal accounts. My goal is to offer another piece of the puzzle that can sit alongside them and perhaps even connect them. The central move is to stop treating “homosexuality” as a single target of selection and instead treat it as one possible endpoint of a broader and plausibly selected trait: variation in sexual responsiveness and flexibility, or what I will call erotic plasticity. In this view, the evolutionary question becomes more tractable because a moderate degree of flexibility can be useful under many mating ecologies, even if one particular endpoint, exclusive same-sex attraction, does not obviously increase reproduction in a straightforward way.

Homosexuality may also be understood, in part, as an adaptive response to dominance hierarchies and to tournament-like sexual competition in primate and human groups. In many primates, high male-male competition produces steep reproductive skew, with a small number of males monopolizing access to fertile females and others adopting alternative tactics. The comparative record includes both overt dominance-based access and “sneaky” or opportunistic mating strategies, which highlights a general evolutionary principle: when the primary route to reproduction is blocked or prohibitively costly, selection often favors behavioral flexibility, risk reduction, and diversification of strategies rather than persistent head-to-head escalation. In that context, a male phenotype characterized by broader erotic responsiveness and weaker insistence on prototypical cues of high mate value could reduce costly competition and still facilitate pair bonding, affiliation, and sometimes reproduction, particularly if attraction is more easily elicited by a wider array of partner characteristics.

On this view, broadening attraction is not “settling” in a moral sense, but a shift in the salience landscape that changes what the individual experiences as compelling. Some males may be more likely to find themselves attracted to less coveted or less competitive partners within the local mating market, including older partners, less socially central partners, or partners who deviate from the most culturally idealized phenotype. The underlying idea is not that individuals consciously decide to avoid high-ranking females, but that developmental systems may be sensitive to cues of competitive difficulty and social position and respond by widening the range of cues that can acquire erotic and affiliative value. Those cues could plausibly be prenatal, such as maternal history, stress physiology, or resource constraints, and they could also be postnatal, such as chronic subordination, repeated social defeat, or environments with intense status competition. Importantly, the model allows for continued tuning across the life course. In individuals with higher baseline plasticity, the thresholds for what becomes erotically salient may remain more experience-dependent even in adulthood, making attraction patterns more responsive to the structure of the dominance hierarchy and the costs of heterosexual competition in the surrounding social ecology.

A note on what this hypothesis is not

This is not a claim that sexual orientation is chosen, learned in a simplistic sense, or reversible at will. It is also not a claim that most gay men are “really straight” and became gay through experience. Those framings are scientifically unhelpful and socially charged for good reasons. The claim is narrower and more mechanistic: individuals differ in how tightly sexual arousal and attraction are canalized toward the opposite sex, and that parameter may be influenced by prenatal and developmental factors. When canalization is weaker, developmental experience has more room to shape the final pattern of attractions, even if the person experiences that pattern as deep, early, and non-volitional.

Part I: Plasticity as a selectable trait, with homosexuality as one endpoint

In most males, sexual arousal appears relatively category-specific. The “target class” is fairly narrow, and cues that fall outside that class are much less likely to be erotically salient. But it is equally clear that there is population-level variation. Some individuals show broader attraction profiles, broader fantasy content, greater openness to atypical partners, and greater responsiveness to situational cues.

From an evolutionary perspective, it is not difficult to imagine why a distribution of erotic specificity could exist and persist. Mating markets are not uniform. In some ecologies, high-quality mates are scarce, dominance hierarchies are steep, and competition is intense. In those contexts, a male who is strictly constrained to a narrow set of preferred mates may have a higher chance of ending up unmated, socially isolated, or chronically frustrated. By contrast, a male with somewhat broader acceptability thresholds might still form pair bonds, still reproduce, and still remain socially integrated. The trait under selection here is not “same-sex attraction.” The trait is a bias toward broader partner acceptability, greater responsiveness to diverse cues, and a weaker requirement that a partner match a prototypical template.

This is where later-born sons enter the picture. A later-born male often develops under conditions that are already socially occupied. Older brothers may be larger, more established, and better positioned in status networks. Even in small-scale societies, older siblings have a head start in alliances and competence displays. A later-born male may therefore face a different competitive landscape, and selection could plausibly favor strategies that reduce costly competition and expand the feasible set of social and sexual opportunities. I am not claiming that this is the only reason plasticity would be favored, but it is a clean example of how mate-market constraints can select for flexibility without invoking selection for exclusive homosexuality.

Part II: Maternal history as a tuner of canalization

The fraternal birth order effect is one of the most discussed empirical findings in this area. The basic observation, stated cautiously, is that males with more older brothers appear, on average, more likely to be gay than males with fewer or none. The most common interpretation is prenatal. Maternal physiology may change across successive male pregnancies, potentially through immune mechanisms or related pathways, in a way that influences sexual differentiation of later male fetuses.

In the standard version of that story, the prenatal mechanism is often treated as a more direct bias toward same-sex attraction. My proposal is slightly different. I suspect that maternal history may tune a more general parameter that sits upstream of orientation categories. It may influence the strength of canalization of sexual category-specificity. Put simply, instead of “programming homosexuality,” maternal history may loosen or tighten how narrowly the developing male brain will assign sexual salience to sex-typed cues.

This matters because it creates a bridge between the prenatal story and the plasticity story. A prenatal mechanism can be real and influential without dictating a specific endpoint. It can shift the probability distribution over developmental outcomes by altering the degree to which experience-dependent learning can sculpt the sexual salience map. Under this model, two individuals could share a similar prenatal “loosening” of canalization and yet diverge in adulthood. One might become bisexual, another predominantly homosexual, another mostly heterosexual with a broader situational repertoire. The endpoint depends on the interaction between the tuned parameter and the person’s developmental environment.

This framing also makes the theory testable in a more precise way than identity categories alone. If maternal history is tuning plasticity, then birth-order effects should appear not only in who identifies as gay, but in measurable features such as exclusivity, category-specificity, and the breadth of erotic cue responsiveness.

Part III: The missing aversion hypothesis and ancestral social ecology

The final piece of the puzzle is a claim about what humans were not selected to do. Many evolutionary accounts implicitly assume that the default male design is to avoid same-sex arousal. But that is not obviously true when you look across primates and across plausible ancestral social conditions. Same-sex sexual behavior occurs in many primate species and often appears in contexts that look social rather than strictly reproductive. It can accompany tension regulation, bonding, and sometimes dominance-related interactions.

I think it is plausible that humans carry a primate-typical sociosexual repertoire in which same-sex arousal potential is not strongly suppressed by an evolved disgust-like aversion. In ancestral environments, humans likely lived in dense social groups with limited privacy. Bodies were visible. Sleep was communal. The boundary between “sexual” and “social” may have been less rigid than it is in modern private housing where sexuality is compartmentalized. If that is even partly true, then selection may never have needed to impose a hard constraint that says, “male arousal must never be triggered by male cues.” The costs of occasional same-sex arousal might have been low in many contexts, especially if it did not strongly interfere with reproduction and if it sometimes served social functions.

This is not an argument that Pleistocene life was an endless group-sex festival. That would be an overreach. The claim is more modest and more defensible: limited privacy and intense social contact may have kept the human sociosexual system more flexible than our modern moral and architectural arrangements would suggest. When you combine that baseline absence of strict aversion with individual variation in plasticity and a prenatal tuner that can loosen canalization, same-sex attraction becomes less mysterious as an outcome.

Integrating the model

The integrated hypothesis can be stated simply. Humans vary in erotic category-specificity, and that variation is at least partly heritable. Maternal history across prior male pregnancies may bias canalization strength in later-born sons, increasing the variance of developmental outcomes by making sexual salience more experience-sensitive. Humans also lack a strong evolved aversion to same-sex arousal cues, likely because our primate ancestry and ancestral social ecology did not impose consistent selection pressure to eliminate same-sex arousal potential. Under this model, modern male homosexuality is often the result of heightened plasticity plus the absence of aversion plus specific developmental and social trajectories that associate sexual reward with same-sex cues.

The model is deliberately pluralistic. It allows for the possibility that some cases are more strongly driven by prenatal biology and others by broader plasticity. It also does not require that homosexuality be directly selected for as a discrete adaptation. Selection could act on flexibility, and homosexuality could be one tail of the distribution under certain developmental regimes.

Predictions and ways to test the framework

A theory like this lives or dies on its discriminating predictions. The point is not to tell a clever story, but to specify what would make the story wrong.

First, if maternal history primarily tunes plasticity rather than directly programming a specific orientation, then the number of older brothers should correlate more strongly with measures of non-exclusivity and broader cue responsiveness than with categorical identity alone. The effect should show up in gradients of category-specificity, not only in whether someone checks a particular box.

Second, the model predicts that family structure variables should separate into biological and social components. If prenatal maternal-history mechanisms dominate, biological older brothers should matter more than step or adoptive older brothers. If postnatal competition also contributes, then co-residence and social dominance dynamics should add a smaller independent effect. This is a concrete way to disentangle prenatal tuning from social ecology.

Third, if a “missing aversion” is part of the background condition, then situational same-sex behavior should increase in contexts of reduced privacy and high social density, even when exclusive homosexuality rates do not shift proportionally. The prediction is about expression and repertoire, not identity alone.

Fourth, the framework implies trait spillovers. If the upstream variable is a general erotic flexibility parameter, then it should correlate with other measures of broader partner acceptability and perhaps with sexual novelty responsiveness, while not necessarily correlating with generalized impulsivity or psychopathology. The pattern should look like domain-specific flexibility rather than a global disinhibition phenotype.

Finally, because this model treats homosexuality as one endpoint of a distribution, it predicts heterogeneity within gay men. Some proportion should show signatures consistent with high plasticity, such as less exclusive attraction profiles or a broader range of cues that can become erotically salient. Others may show strongly canalized same-sex attraction consistent with more direct prenatal patterning. A single explanation is unlikely to fit all cases, and the model expects that.

Relationship to existing evolutionary accounts

There is a long history of evolutionary theorizing about homosexuality, including kin selection models, balancing selection, and sexually antagonistic selection. My proposal does not deny those possibilities. It reframes the question. If what persists in the population is not “genes for homosexuality” but “genes for variability in sexual canalization,” then it becomes easier to see how selection could maintain the trait even if one tail of the distribution sometimes lowers direct reproduction.

This framing also helps with a recurring confusion in public discourse. People often treat the existence of a genetic component as evidence that orientation must be strictly innate and immutable in every individual. Genetics can contribute to parameters, thresholds, and susceptibility to developmental shaping without implying volitional choice. A heritable bias toward weaker canalization can be real, and the resulting attractions can still feel foundational and stable to the person who experiences them.

Limitations and responsible framing

There are important limitations here. Much of our evidence about ancestral sexual ecology is indirect, and it is easy to overclaim. The model must therefore be presented with intellectual restraint. The correct posture is that this is a plausible synthesis that generates testable predictions, not a final answer.

There is also a social responsibility issue. Any theory that mentions plasticity risks being misread as endorsing “conversion” narratives. That is not what this is. Plasticity, in the sense used here, is about developmental sensitivity, not about coercive malleability. People do not choose their orientation, and harmful interventions are not justified by the existence of developmental influences. A responsible scientific framing needs to state this plainly.

Conclusion

I do not think we need to assume that male homosexuality was directly selected for to make sense of its persistence. A more parsimonious approach is to treat same-sex attraction as one endpoint that can emerge when three conditions coincide: higher erotic flexibility, prenatal and maternal-history factors that tune the strength of canalization, and a human sexual system that was not built with a hard aversion to same-sex arousal cues. This model respects what prenatal work is trying to explain while adding a layer that focuses on how selection could shape the underlying distribution of sexual specificity in a way that is broadly adaptive across mating ecologies.

Most importantly, it is a model that can be tested. If it is wrong, the data should be able to say so. If it is partly right, it gives us a way to unify prenatal findings, developmental variability, and primate-typical sociosexual repertoires into a coherent framework that remains academically serious while staying accessible to ordinary human intuitions about how sexuality can develop.

Postscript:

I am actually backdating this post. The true date of posting is 1/14/26. I decided to keep it from the front of my blog because of the sexual nature. I came up with this idea about homosexuality around 2005 after reading about the male birth order effect. I was embarrassed to write about it at the time and a few people close to me told me that maybe I shouldn't publish the idea because of stigma and sterotypes. I think I have matured and society in general has matured and improved, and I am happy to feel good writing about this now. Again, no offense was meant to any group in this writing and no judgments are being made. I am simply writing about a hypothesis that I thought could be true scientifically. Nature bless everyone.