Is He a Good Dad, or Does He Just Have His Mother’s Genes?

– by Thomas Felesina

The male nipple is a classic conversation starter (at least in the evo biology faculty lounge). The nipple is a feature that is functional and essential for reproductive success in females,[1] yet non-functional in males, perhaps decorative at best. We don’t spend much time agonizing over the “evolutionary function” of the male nipple. We generally accept that it exists not because it provides a fitness advantage to men, but because men and women are built from the same genetic blueprint. Men have nipples because women need them, and decoupling the genetic architecture for chest anatomy between the sexes is evolutionarily “expensive” and largely unnecessary since it imposes few costs for men. To get rid of male nipples, a mutation would first need to occur that says something like, “grow nipples ONLY if female” or “suppress nipples ONLY if male.”

However, when we move from anatomy to psychology and behavior, we often lose sight of this logic: forgetting that the shared genome governing the male and female body also governs the male and female mind. We have 23 pairs of chromosomes. Aside from the sex chromosomes (X and Y), the other 22 pairs, the autosomes, are effectively identical between the sexes. This means that most genetic variants that influence our brains and our behavior are the same for both males and females.

In my recent paper, I show that for many complex traits, the genetic correlation between the sexes (referred to as rMF) is extremely high. The genetic correlation is extremely high because when sharing genetic architecture, you cannot easily pull one sex in an evolutionary direction without dragging the other sex along with it (referred to as a correlated response). Consequently, when selection favors a trait in females, the mean trait value may increase in males as well, even if it provides no direct benefit or is slightly costly. This is the genetic equivalent of a sidecar on a motorcycle: if the driver (the sex under strong selection) turns left, the passenger (the other sex) goes left, too.

And so, when we ignore the correlated responses to selection acting on one sex, we risk falling into a trap of proposing two separate adaptive explanations: one for men, and one for women, when a single explanation might do, or at the very least, be a significant factor in the initial evolution of a trait in one of the sexes.

For instance, evolutionary psychology emphasizes that females should be “choosy” because the biological costs of a bad mating decision are high (e.g., expensive eggs, pregnancy, lactation). Males, with lower obligatory investment, are theoretically predicted (and empirically observed among many animals) to be less choosy. Yet, human men are surprisingly discriminating compared to most male mammals. Is this because men faced their own unique selection pressures to be picky? Perhaps. But it is arguably more parsimonious to suggest that strong selection for choosiness in women, driven by prolonged child-rearing demands, shifted male psychology in the same direction via our shared genome.

Take another example: humans are outliers among mammals; our fathers are unusually involved in child-rearing. Perhaps paternal care in humans increased offspring survival or improved mating opportunities, but it would be remiss to ignore the selective pressure on human mothers to be nurturing and attentive to highly dependent, altricial infants. Natural selection would have aggressively favored genetic variants that promoted responsiveness to infant cues, patience, and bonding in mothers. Because these “parental” genes likely reside on the autosomes, they are inherited by sons just as they are by daughters, leading to the emergence of paternal care. And so, the baseline capacity for human paternal care may be, at least initially, a genetic byproduct of intense selection on maternal care. Men may be nurturing dads partly because they are the sons of nurturing mothers.

While my review of the quantitative genetic literature found that high genetic correlations (often nearing 1.0) are the norm for human behavior, there are, of course, exceptions. For instance, research on extra-pair mating (infidelity) in humans has shown a surprisingly low genetic correlation between the sexes. This suggests that for cheating behavior, men and women may indeed have evolved under distinct, sex-specific pressures, allowing their genetic architectures to decouple.

Why This Matters for the Future of the Field

Acknowledging the shared genome doesn’t mean denying sex differences. Men and women differ significantly in height, yet the genetic correlation between the sexes for height is near-perfect. As I discuss in the paper, while the set of genes influencing a trait is largely the same for both sexes, the magnitude of their effect can differ for a variety of reasons; for instance, the distinct hormonal environments of men and women can amplify or dampen the effect of genes.

With this in mind, as evolutionary social scientists, we should adopt a new default assumption: unless we have evidence to the contrary, we should assume the genetic correlation between sexes is high. To claim that a trait evolved independently in both men and women requires us to devise two separate adaptive accounts, one for each sex, while also assuming the successful evolution of complex mechanisms to decouple their genetics. In contrast, assuming a high genetic correlation requires only one adaptive explanation: selection acted strongly on one sex, and the other simply inherited the trait. The latter explanation demands fewer assumptions, aligns with the biological reality of our shared genome, and should therefore be our starting point.

By respecting the constraints of our shared DNA, we can build more rigorous, parsimonious, and biologically grounded theories of human behavior. Sometimes, a dad is a dad because he evolved to be one. But sometimes, he’s a dad because his mother was a mom.

[1] While the functional nipple is a female trait, it is essential for the reproductive success of both sexes.

Thomas Felesina. (2026). The shared genome constraint: why between-sex genetic correlation matters for evolutionary social science. Evolution & Human Behavior, 47, 106773.