Monogamy And Polygamy: No Wrong Way To Love

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There is no single evolutionary pathway that results in social monogamy; rather, it has evolved separately across mammalian species (as reviewed by French et al., 2018). Social monogamy describes multiple factors, including spatial proximity of a male-female pair, exclusion of strangers, biparental care, and pair bonding (French et al., 2018). The condition of social monogamy is so complex that Carter and Perkeybile (2018) propose social monogamy can be thought of as a biological “syndrome,” with a common set of “ingredients,” which species may deviate from but still be considered socially monogamous. The evolution and maintenance of social monogamy are associated with a number of factors, including genetics, epigenetics, social structures, and neurobiology.

Lukas and Clutton-Brock (2013) show 61 independent transitions from solitary ancestors to social monogamy are required to explain the present distribution of social monogamy among mammals, though the timing of these transitions is unknown. Computational models from Opie et al. (2012) suggest harem polygyny is the ancestral state for primates. Monogamy later evolved 28 mya in Lemuroidea, 26 mya in Callicebus, and 19 mya in Hylobatidae (Opie et al. 2012).

Drivers for Social Monogamy:

Dispersal, Density, and Feeding:

About 9% of mammals are monogamous (Lukas and Clutton-Brock 2013). Opie et al. (2013) posit that monogamy remains relatively uncommon under certain ecological conditions, namely, in high population density areas where there is pressure to live in social groups as a defense against predation. Lukas and Clutton-Brock (2013) found that socially monogamous mammals live at significantly lower population densities than solitary species. I conclude that low population density is an ecological condition associated with social monogamy, as high population densities necessitate social groups rather than monogamous pair-living.

In the mammalian common ancestor, females were solitary and males controlled territories spanning several females (Lukas and Clutton-Brock 2013). Female-biased dispersal (FBD) evolved following social monogamy (Opie et al. 2013). Mabry et al. (2013) concur, finding the ancestral state for mammals was non-monogamy and male-biased dispersal (MBD) and that FBD is associated with social monogamy (Figure 1). The evolution of FBD is two-thousand times faster in socially monogamous than in non-monogamous species (Mabry et al. 2013). The character state of social monogamy combined with MBD is unstable and facilitates expeditious transitions to the ancestral state of non-monogamy with MBD or the derived state of monogamy with FBD (Mabry et al. 2013).

Dobson (1982) found MBD present in 78% of non-monogamous species, while FBD is found in 92% of monogamous species. Lukas and Clutton-Brock (2013) propose that the coevolution of FBD and social monogamy are due to dependence on a diet with calorically dense but sparsely distributed foods: 91% of socially monogamous primates rely on fruit, whereas 93% of solitary primates rely on gum, bark, fungi, and other calorie-poor foods. Logically, social monogamy will evolve where larger ranges are necessary to gather enough food, such as in the case of primates reliant on fruit. I conclude males are unable to cover ranges large enough to contain multiple females because female ranges need to be larger to get sufficient nutrition from sparsely distributed fruit, resulting in pair-living scenarios where a socially monogamous pair controls a single territory together.

Infanticide, Encephalization, and Lactation:

Ancestral state reconstructions show infanticide predates the evolution of social monogamy (Opie et al., 2013). Only about 9% of mammals are socially monogamous, whereas nearly ⅓ of primates are socially monogamous (Lukas and Clutton-Brock 2013)(Fig. 2). Opie et al. (2013) propose the increased prevalence of social monogamy in primates compared to other mammals is due to encephalization. Encephalization facilitates longer lactation periods, and thus, higher risk of infanticide (Opie et al. 2013). In contrast, social monogamy facilitates a shorter lactation period compared with gestation, reducing infanticide risk (Opie et al. 2013). So, social monogamy presents a compelling defense against infanticide.

Schillaci (2008) supports this hypothesis, finding that monogamous primate species have a larger average neocortex size to body mass ratio compared to species with multi-male/multi-female and single-male mating systems. I conclude that monogamy allows for the increased parental care investment necessary for larger brains.

Phylogenetic analysis of independent contrasts indicates there is a statistically significant negative correlation between sexual dimorphism and relative neocortex ratio (Schillaci 2008). Reduced sexual dimorphism and neocortex ratio are associated because social monogamy can attenuate the costs associated with the increased encephalization and longer infant development common in primates (French et al. 2018). Perhaps more calories overall need to be consumed to support encephalization, which is consistent with the fact that 91% of socially monogamous primates rely on calorie-dense fruit for their nutrition (Lukas and Clutton-Brock 2013). This necessity for high calorie intake increases female range size, resulting in the switch to monogamy from polygamy as males are unable to cover the territory of more than one female.

Sexually Transmitted Infections:

Another factor that selects for monogamy is the prevalence of sexually transmitted infections or STIs. Using mathematical modeling, McLeod and Day (2014) conclude pathogens causing mortality with intermediate transmission rates select for serial monogamy and sterilizing pathogens select for promiscuity. An evolutionary trade-off exists where the more sexual partners one has, the increased likelihood there is of obtaining an STI, and, conversely, the fewer sexual partners one has, the fewer opportunities for offspring (McLeod and Day 2014). Therefore, monogamy is a viable strategy for attenuation of the costs associated with STIs.

Common Features of Socially Monogamous Species:

Reduced Sexual Dimorphism:

Although mostly based on anecdotal evidence provided by field biologists rather than precise measurement, reduced sexual dimorphism is thought to be common in monogamous species (Carter and Perkeybile 2018). Schillaci (2008) found a negative relationship between sexual dimorphism and relative neocortex ratio. Perhaps encephalization provides the social awareness necessary for monogamy and reduced male competition, which is associated with reduced sexual dimorphism (Schillaci 2008).

Another factor that may contribute to the apparent reduced sexual dimorphism in monogamous species is the 5-⍺ reductase enzyme type 2 (from the SRD5A2 gene), which converts testosterone to DHT (Okeigue and Kuohung 2014). Without DHT, genital masculinization is disrupted and results in reduced sexual dimorphism (Okeigue and Kuohung 2014). Reduction in testosterone is a key feature of paternal care, which is common in monogamous species (Nunes et al. 2001). Thus, the reduced presence of testosterone, and by extension DHT, that facilitate paternal care could also result in reduced sexual dimorphism in monogamous species.

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Carter and Perkeybile (2018) agree androgen expression reduction could result in a decrease in sexual dimorphism; they posit that because the androgen receptor gene is on the x-chromosome, it is likely that mutation of the AR gene in males could occur and consequently reduce sexual dimorphism.

Paternal Care:

Paternal care is a key feature of social monogamy. Phylogenetic analysis from Lukas and Clutton-Brock (2013) suggests male care is probably a consequence of social monogamy and not a cause. Increased parental care in in monogamous prairie voles (Microtus Ochrogaster) led offspring to show increased rates of pair bonding, indicative of social monogamy, as adults (Del Razo and Bales 2016). Biparental care provides a fitness advantage, shown by the fact that socially monogamous Madoqua pairs with biparental care produced more litters per year than socially monogamous pairs without biparental care (Lukas and Clutton-Brock 2013)

Neurobiology of Socially Monogamous Characteristics:

Androgens play a key role in the regulation of paternal care and mating. Elevated testosterone levels are associated with decreased paternal behavior (Nunes et al. 2001) and lower testosterone levels are associated with decreased rates of infanticide (Perrigo et al. 1991). Androgens moderate the trade-off between mating effort and paternal care in monogamous primates (as reviewed by French et al. 2018). For example, male Leontopithecus rosalia had elevated androgen levels during mating, which subsequently decreased during birth and infant care (Bales et al. 2006). Furthermore, experienced Marmoset (Callitrichidae) fathers had decreased testosterone levels after exposure to their 2-week-old infant’s scent but not their 3-month-old infant’s or a stranger infant’s (Ziegler et al. 2016), suggesting offspring-specific olfactory signals can regulate testosterone and induce paternal behavior.

Pair bonds are the hallmark feature of social monogamy in mammals. There are many substrates responsible for pair bond formation and maintenance. One such substrate is dopamine or DA (Aragona et al. 2003). Haloperidol, a DA antagonist, prevented partner preference but didn’t disrupt mating while apomorphine, a DA agonist, induced pair bonding without mating, showing DA is necessary for the formation of the pair bond in prairie voles (Aragona et al. 2003). In addition, mating induced a 33% increase in turnover of DA in the nucleus accumbens or NAcc (Aragona et al. 2003). While this result was not statistically significant, it may indicate that mating can induce pair bond formation via the dopaminergic reward system. Prairie voles did not form pair bonds when treated with a D2 receptor antagonist (Lim et al. 2004). Smeltzer et al. (2005) also found monogamous voles (Cricetidae) had increased D2 receptor binding in the medial prefrontal cortex compared to promiscuous voles. So, DA binding with D2 receptors is necessary for pair bond formation.

Vasopressin and the regulation of the vasopressin receptor 1A (V1aR) have also been implicated in pair bond formation. Lim et al. (2004) say V1aRs in the ventral forebrain are necessary for a pair bond to form and are found in conjunction with monogamy across taxa. Cushing et al. (2003) confirm vasopressin is necessary for pair bonding; neonatal castration that disrupted pair bonding was reversed using vasopressin injections. Monogamous prairie voles have a LINE in the regulatory region of the V1aR (Young 1999) which could upregulate V1aR. In addition, Hammock and Young (2005) found voles with a long V1aR allele prefer their female partner over stranger females and that the longer microsatellite associated with the allele results in higher V1aR expression than the shorter microsatellite allele. In contrast, Solomon et al. (2009) found levels of total brain V1aR mRNA were not influenced by the V1aR allele length, but males with shorter V1aR alleles mated with significantly more females than males with the longer allele, suggesting V1aR is region specific. The ancestral state is the shorter allele according to phylogenetic analysis (Fink et al. 2006). Notably, Lim et al. (2004) found no difference in D2 receptor patterns in ventral forebrains across species of voles but did find differences in V1aR, suggesting insertion of the V1aR system into the pre-existing D2 mediated reward circuit could result in pair bonding and thus monogamy.

Lim et al. (2004) found the V1aR also regulates paternal care. Also, vasopressin results in selective aggression and protective behaviors, which are part of paternal care (Carter and Perkeybile 2018). Wang et al. (1994) found increasing vasopressin in the lateral septum of prairie voles increased paternal behavior, whereas increasing vasopressin in the lateral ventricles produced no change in paternal behavior, consistent with findings from Solomon et al. (2009). V1aR is region specific in paternal care regulation.

Paternal care plays a role in epigenetic regulation of the pair bond. Prairie vole infants that were given more parental care had increased oxytocin receptor gene (Oxtr) expression, increased Oxtr receptor density and decreased Oxtr gene methylation (Perkeybile et al. 2018), showing through upregulation of the Oxtr gene, parental care in infancy results in greater disposition for pair bond formation in adulthood. Oxtr expression is also mediated by epigenetic regulation via histone acetylation during adulthood (Carter and Perkeybile 2018). Mating upregulates Oxtr in NAcc and facilitates pair bonding (Carter and Perkeybile 2018). Thus, nurture and environment can mediate monogamous behavior.

Oxytocin evolved in mammals at least 100 mya and is related to lactation and positive sociality (Carter 2014). Oxytocin, or OT, has been found to promote sociality and “synchrony”(Jurek and Neumann 2018), making it a likely candidate to support pair bond formation. OT treatment in marmosets reduces interest in strangers of the opposite sex, time spent in proximity to strangers, and mating attempts towards strangers (Cavanuagh et al. 2014). Male prairie voles with overexpression of OT exhibit expedited pair bond formation (Ross et al. 2009). Blocking either OT or vasopressin prevents pair bonding but still leaves prairie voles very social (Cho et al. 1999). Blocking both OT and vasopressin prevents pair bonding and social behavior altogether (Cho et al. 1999). Therefore, OT in conjunction with vasopressin facilitates formation of a pair bond.

Mating is the catalyst for pair bond formation. V1aR and D2 receptor activation in the ventral forebrain during mating facilitates association between the reward of sex and the olfactory signature of a mate, resulting in pair bonding (Lim et al. 2004). Vasopressin is implicated in “postmating aggression” or mate-guarding (Winslow et al. 1993; Carter and Perkeybile 2018). This mate-guarding behavior could reinforce monogamy by preventing cuckoldry.

Social support in humans provides a fitness advantage via attenuation of the deleterious effects of excess cortisol and HPA-axis activation (Ditzen and Heinrichs 2014). Prolonged cortisol exposure due to overactivation of the HPA-axis or prolonged environmental stressors can cause reduced immune function, reduced gonadal function, loss of hippocampal neurons, and neuropsychiatric disorders (Sapolsky 2015). OT release during social support from a partner helps mitigate psychological stress in humans (Heinrichs et al. 2003). This effect is called social buffering (French et al. 2018). Male marmosets that received an OT antagonist had increased HPA-axis activity in response to a stressor than when treated with a control (Cavanaugh et al. 2016), showing the OT associated with the pair bond lessons the physiological responses to stress. Also, marmosets who previously had elevated cortisol levels spent more time in close proximity to their mate than marmosets with previously normal cortisol levels (Smith, Birnie, and French 2011). Overall, the interaction between cortisol and OT mediates the formation of pair bonding, along with vasopressin and DA.


Monogamy evolved as a defense against infanticide (Opie et al. 2013) due to the need for female-biased sex dispersal (Mabry et al. 2013), due to encephalization (Opie et al. 2013), and sexually transmitted infections (McLeod and Day 2014). It is associated with reduced sexual dimorphism (Carter and Perkeybile 2018), paternal care (Lukas and Clutton-Brock 2013), pair bonding (Lim et al. 2004), and mate-guarding (Winslow et al. 1993; Lim et al. 2004; Carter and Perkeybile 2018). Cortisol (Cavanaugh et al. 2016), oxytocin (Perkeybile et al. 2018), vasopressin (Lim et al. 2004), and dopamine (Aragona et al. 2003) are all implicated in the maintenance of socially monogamous behaviors. In conclusion, ecological, genetic, epigenetic, and social factors all affect and inform the presentation of social monogamy in mammals.

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