Commentary on Luoto & Rantala's (2022) Female Bisexuality

Previously, I reacted to Luoto et al.'s (2019a) "A Life History Approach to the Female Sexual Orientation Spectrum". This was a mistake, as I neglected to read "Response to Commentaries: Life History Evolution, Causal Mechanisms, and Female Sexual Orientation" (2019b), "Understanding the Biodevelopment of Sexual Orientation Requires a Multilevel Evolutionary Analysis" (2023), or "Female Bisexuality" (2022).

"Female Bisexuality" contains Severi Luoto's updated position on the female sexual orientation spectrum. The overall layout is similar to "A Life History Approach to the Female Sexual Orientation Spectrum", with some key changes.

The Neurodevelopmental Model of Female Sexual Orientation and Gender Identity
Luoto & Rantala (2022)

Luoto et al.'s (2019a) "pendulum" model is not included in "Female Bisexuality". Instead, Luoto & Rantala (2022) employ The Neurodevelopmental Model, depicted in the figure shown above. According to this model, female gynephilia and female masculinity are independent axes, which form a "two-dimensional space...where prenatal testosterone and estrogen vary". My previous critique ("Butches are not always Exclusively Homosexual") no longer applies, as Luoto & Rantala (2022) account for butch bisexuals.

Another one of my previous critiques ("The Sexual Malleability of Exclusively Homosexual Women") seems to no longer apply. Whereas Severi Luoto previously claimed that homosexual women "seem to lack the psychophysiological capacity for sexual malleability" (Luoto et al., 2019a), he seems to have relented on this position, claiming more recently that "it appears that bisexual women have the highest sexual fluidity, followed by homosexual women" (Luoto & Rantala, 2022). This is not to suggest that all or most homosexual women are sexually fluid, as Luoto & Rantala (2022) note: "Although some researchers have highlighted the existence of sexual fluidity in women...others have challenged this view, noting that the data do not support the view that most women are capable of sexual fluidity."

Rather than describing "Categories of Nonheterosexual Women", Luoto & Rantala (2022) describe different aspects of sexual fluidity, defined as nonexclusivity, change, and variance. They make the following important observation about reported changes of sexual orientation:

"...assessments of the prevalence or fluidity of women's sexual orientations may be confounded by the person-based nature of many nonheterosexual women's sexual attractions. In contrast to most men, most women require emotional involvement to engage in a sexual relationship...It is therefore improtant to understand that defining a bisexual woman's sexual orientation merely by asking which sex she is attracted to at an arbitrary point in time may be misleading. One may be erroneously led to believe that her sexual orientation has undergone shifts from heterosexual to homosexual or to bisexual in the course of her life. This is because romantic love causes one to focus one's energy and attention solely on the object of one's love...Should the love object be male, the woman might be inclined to identify as heterosexual. Should the love object be female, the woman may be inclined to identify as homosexual. If feelings of romantic love towards that person subside, the woman's "momentary sexual orientation" may undergo another shift, giving a muddled view about her sexual orientation. This does not ultimately boil down to sexual malleability nor to fundamental changes in the woman's sexual orientation...but to the fact that nonheterosexual women's attractions are sometimes person-based rather than sex-based...Determining women's sexual orientation through an introspective sense of their sexual orientation at an arbitrary point in time can therefore be problematic if a person-based attraction should at that specific point in time bias it to one end of the male-female gender spectrum." (Luoto & Rantala, 2022)

Ultimate-level explanations for female nonheterosexuality

Luoto et al. (2019a)

Luoto & Rantala (2022) employ a similar diagram to the one shown above, in order to explain hypothesized ultimate-level explanations for female bisexuality. There are some key differences, however. First, "Heterosexual deprivation" (symbolized by "HD" in the upper left corner) is removed, replaced with "Prosociality hypothesis" (symbolized by "P"). The radius of "Male choice" is increased to be larger than "Polygyny", while the radius of "Infanticide avoidance" (symbolized by "IA") is increased to about the same size as "Polygyny". The most notable change is the dramatic increase of the radius of "By-product", which is now considered one of the four best-supported hypotheses instead of "Alloparenting":

"Most notable and best-supported of these ultimate-level hypotheses on the evolution of female bisexuality are balanced polymorphism of masculinity, hormonally mediated fast life history strategy, sexually antagonistic selection, and the by-product hypothesis. Moderately well-supported hypotheses include alloparenting, male choice, and weak selection pressures." (Luoto & Rantala, 2022)

To describe the top four best-supported hypotheses:

Balanced polymorphism of masculinity: "Since masculinity is deemed to be a polygenic trait, higher masculinity is caused by a greater number of masculinity-inducing alleles and masculinizing environmental factors. If sufficiently masculinized, women's psychological mechanisms that deal with male choice also become masculine, leading to the development of exclusively homosexual orientation in adulthood. However...possessing only some of the masculinizing alleles would in fact be beneficial for the female both in intersexual selection and in intrasexual competition...if possessing them does not entail exclusive homosexuality. According to this hypothesis, greater masculinity could lead to enhanced male acquisition for the "tomboy" due to a reduced psychological gap between the sexes and the consequently enlarged pool of shared interests that a masculine woman would, in theory, have with men." (Luoto et al., 2019a)
Hormonally Mediated Fast Life History strategy: "This is because of the central link that sex hormones create between the development of sexual orientation...and the calibration of life history evolution...Life history strategies are a composite of developmental and psychological variables commonly represented on a fast-to-slow continuum: the fast end is occupied by species/individuals that mature quickly, reproduce early, and focus on quantity rather than quality...Ipso facto, male LH strategies are typically "faster" than those of females...This difference is largely mediated by testosterone (T)." (Luoto et al., 2019a)
Sexually antagonistic selection: "the attributes that are favored in one sex are sometimes opposite to those that are favored in the other sex...The alleles that result in a masculinized phenotype when they appear in a female body may produce more masculine physiological and behavioral traits in a male phenotype...Although these alleles may incur fitness costs for a female, the male carrying such masculinizing alleles may gain an advantage from the increased masculinity in intrasexual competition and/or intersexual selection. This advantage to the male may be sufficiently large to offset the potential cost of the alleles when they occur in the exclusively homosexual female phenotype" (Luoto & Rantala, 2022)
By-product: "Women's same-sex attractions could also simply be a by-product of high sex hormone exposure in utero - in essence being a by-product of balanced polymorphism of masculinity and sexually antagonistic selection, or other mechanisms that disrupt the prenatal hormone environment...This explanation contrasts the interpretation that such a shift in sexual orientation is adaptive at the genotypic level, as discussed earlier" (Luoto & Rantala, 2022)

The "Male choice" and "Weak selection pressures" hypotheses are both described in Apostolou's (2022) "The Evolution of Female Same-Sex Attraction".

Severi Luoto's articles provide a useful framework to make sense of evolutionary theories on female nonheterosexuality, but they are not without critique. Below are my critiques of Luoto & Rantala's (2022) "Female Bisexuality".

I. Adolescent Self-Identity is Unreliable

This first critique is a "nit-pick", and not a critique of "Female Bisexuality" per se. Luoto & Rantala (2022) claim "a large majority of self-identified lesbians have had multiple sexual encounters with men". They are right to note that these are "self-identified" lesbians, as they state this shortly before describing how "assessments of the prevalence or fluidity of women's sexual orientations may be confounded..."

The claim that "a large majority of self-identified lesbians have had multiple sexual encounters with men" is probably true, but Luoto & Rantala might have derived it from a dubious source. Elsewhere, Luoto et al. (2019b) claim that "Lesbians also have more than twice the number of male sex partners than heterosexual women (Tornello et al., 2014)". Tornello et al. (2014) studied a sample of 2,664 adolescents and young women between age 15-20. Given the "lesbian until graduation" phenomenon, the self-reported sexual identity of adolescents is not very reliable. For more reliable figures, proportions of sex partners in adult lesbians are reported by Semenyna et al. (2022).

II. Uncertainty about Sexually Antagonistic Selection

According to Luoto & Rantala (2022), sexually antagonistic selection is one of the best-supported hypothesis. In addition to providing some evidence from animal models, they claim:

"Some evidence for this hypothesis known as sexually antagonistic selection– has been provided in Italian (Camperio Ciani et al., 2018) and Australian samples (Sabia, Wooden, & Nguyen, 2017), where the reproductive success of nonheterosexual women was lower than that of heterosexual women. However, this fitness detriment can be offset by a higher number of offspring in nonheterosexual women’s kin compared with the kin of heterosexual women, as reported in the Italian sample (Camperio Ciani et al., 2018)."

However, there is some evidence for a fraternal birth order effect (FBOE) or sororal birth order effect (SBOE) in female homosexuals (Khorashad et al., 2020)(Ablaza et al., 2022)(Kabátek & Blanchard, 2025). As Raymond & Crochet (2022) explain:

"in the presence of FBOE, homosexuals have a higher birth rank (due to their higher number of older brothers), thus mimicking a higher maternal fertility if birth rank is not controlled for...due to a possible existence of an older sister effect (Ablaza et al., 2022; Blanchard & Lippa, 2007; for discussion, see Raymond et al., 2022), a similar sampling bias...could operate, as birth rank was not controlled for in this study."

As such, I am not sure there is sufficient evidence to consider sexually antagonistic selection one of the best-supported ultimate-level explanations.

III. Uncertainty about "The Estrogenic Pathway"

Luoto & Rantala (2022) build on the "estrogenic pathway" for femme lesbians, noting that: "not all parts of the brain are exposed to the same levels of aromatized estrogen. In addition, not all parts of the brain have equal numbers of estrogen receptors, nor even the same types of estrogen receptors...This means that estrogen does not influence all parts of the brain in the same way."

Luoto & Rantala (2022) also state: "It is important to note that there are two different kinds of estrogen receptors: ERα and ERβ...Thus, a mutation in one of the receptor types does not automatically mean that the other receptor type would not function (and masculinize the brain)."

My previous critique ("The "Estrogenic Pathway" for Femme Lesbians") still applies, as Luoto & Rantala (2022) rely on research of altricial rodent models to hypothesize about the "estrogenic pathway" for human women. As previously stated, Wallen (2022) notes that rats are an altricial species (born underdeveloped), while humans are a precocial species (born relatively developed): "...altricial rat and mouse models of sexual differentiation may not apply to precocial humans as they appear to use different hormonal mechanisms to produce behavioral sexual differentiation than is the case in precocial species."

Luoto & Rantala (2022) refer to Kim Wallen's research in order to claim: "Experimental evidence for estrogen's masculinizing effect on the brain does not rely only on rodent models. For example, treating rhesus macaques with flutamide (a nonsteroidal antiandrogen that blocks androgen receptors) late in gestation paradoxically hypermasculinized males' behavior despite preventing full genital masculinization (Wallen, 2005). This finding suggests that estrogen masculinizes brains also in primates: estrogen receptors, after all, would not be blocked by flutamide (which only blocks androgen receptors), while the testes will still produce testosterone that is aromatized to estrogen...When androgen receptors have been blocked, there is an increased bioavailability of testosterone to be aromatized to estrogen, leading some behaviors to become masculinized."

While this is one possible explanation, it is not the only one. Luoto & Rantala neglected to mention the alternative explanations proposed by Kim Wallen:

"There are several possible explanations for these findings. One possibility is that flutamide simply doesn’t enter the brain in sufficient amounts to occupy a significant proportion of brain androgen receptors. No in vivo studies have been done that administer flutamide peripherally (e.g., not directly administered into the brain) and measure brain levels of flutamide compared to peripheral levels. Since flutamide is a relatively weak AR ligand...any decreased neural flutamide concentration could markedly reduce its antiandrogenic behavioral effects. Probably more critically, flutamide treatment can suppress LH negative feedback resulting in increased LH secretion...This increase in LH potentially increases endogenous androgens making a neural flutamide antiandrogen blockade even less effective...Thus one possible explanation for the behavioral masculinization effects that we found with peripherally administered flutamide is that flutamide effectively blocks testicular negative feedback, resulting in either increased steroid secretion in pregnant females, such as the increased T secretion we found in our flutamide-treated mothers...or produces an increased secretion of testicular T in fetal male offspring of flutamide-treated mothers. In this regard, it may be significant that neonatally, LFM subjects had significantly higher T levels than any other group during the first 2 weeks postnatally...Whether this reflects alteration in testicular sensitivity to gonadotropins (LFM [late-treated flutamide male] subjects did not have elevated LH when their neonatal T was elevated), or some remaining effect of the late flutamide treatment on hypothalamic-pituitary-gonadal function (HPG), remains to be seen." (Wallen, 2022)

That being said, Luoto & Rantala (2022) are not wrong in hypothesizing about the possibility that estrogen masculinizes the brains of primates. Although Wallen (2022) claims that in precocial rhesus monkeys "estrogenic metabolites of androgens do not appear to play a role in behavioral sexual differentiation," she adds the following nuance to her position:

"An alternative possibility is that flutamide interferes with testicular negative feedback elevating androgens, but that estrogenic metabolites from aromatization of these elevated androgens produce increased behavioral masculinization. Given that prenatal DHT (which cannot be aromatized to an estrogen) both masculinizes and defeminizes the sexual behavior of adult female rhesus monkey...and given the moderate effects of the synthetic estrogen DESDP on juvenile behavioral masculinization, aromatization of T seems an unlikely explanation for our findings. It cannot, however, be ruled out at this time." (Wallen, 2022)

I will restate that I am not an expert on this, so I cannot determine whether altricial rodent models are applicable to precocial humans.

IV. Uncertainty about the INAH3

Luoto & Rantala (2022) assume that the INAH3 is involved in female nonheterosexuality, hypothesizing that, "if a female human fetus is exposed to high amounts of testosterone that are aromatized to estrogen at a critical point during neurodevelopment, it leads to larger and male-typical INAH3 (the human homolog of the SDN-POA), resulting in exclusive or near-exclusive homosexual orientation."

There are several reasons this hypothesis might be incorrect.

First, the INAH3 has only been studied in male homosexuals, not female homosexuals. There is some evidence that the INAH3 of male homosexuals is more female-typical, in that it tends to be smaller on average (LeVay, 1991)(Byne et al., 2001). We do not know if the reverse is true in female homosexuals, as female nonheterosexuality likely has different causes from male nonheterosexuality (Ganna et al., 2019).

Evidence from an animal model suggests otherwise. Vasey & Pfaus (2004) examined an equivalent brain structure in female Japanese macaques that display nonexclusive, same-sex sexual behavior. Contrary to Luoto & Rantala's (2022) hypothesis, this hypothalamic structure was found to be female-typical.

Even in males, a smaller INAH3 probably does not result in exclusive or near-exclusive homosexual orientation. As reported by LeVay (1991), some homosexual males had larger INAH3 volumes than some heterosexual males, just as some females had larger INAH3 volumes than some males.

Byne et al. (2001) concluded: "At present, however, we can neither ascribe any function to INAH3, nor can we interpret the functional significance of its sexual dimorphism. If INAH3 is a site related to the functional circuitry of sexual orientation, then the current data suggest that measures other than simple nuclear volume are needed to discern the relationship. Based on the results of the present study as well as those of LeVay (1991), sexual orientation cannot be reliably predicted on the basis of INAH3 volume alone."

Bailey et al. (2016) further comment: "If the true INAH-3 difference between hetero sexual and homosexual men is intermediate between LeVay’s and Byne et al.’s results, it would still be consistent with the organizational hypothesis of sexual orientation. However, even if this were true, it would be unlikely that the INAH-3 size would be a key factor regulating sexual orientation. This is because there would be too many exceptions—homosexual men with a large INAH-3 and heterosexual men with a small INAH-3—to believe that INAH-3 size is crucial."

V. Evidence that XY CAIS Women are Hyperfeminized

Luoto & Rantala (2022) state the following of XY CAIS women:"Although it is sometimes said that genetic males with CAIS have sexual interest towards males...this is not always the case..." They go on to provide some evidence that XY CAIS women are not always exclusively androphilic, arguing that "one could conclude that genetic (XY) males with CAIS seem to resemble femme bisexual women the most, supporting the hypothesis that aromatized estrogens masculinize the parts of the brain that are responsible for sexual orientation, seeing that XY CAIS individuals lack direct androgen action."

Luoto & Rantala (2022) neglected to mention the evidence that XY CAIS women are hyperfeminized in their physiological arousal patterns: "Category-specificity analyses of fMRI responses to male-preferred vs. female-preferred nude stimuli showed that men's category-specific responses differed markedly from those of both groups of women, whereas women with CAIS and control women showed highly similar responses. Brain responses of women with CAIS, while similar to those of control women, did not match them in all respects, particularly in the second analysis,in which women with CAIS showed significantly less category-specificity than did control women. Because women in general show reduced category-specificity in sexual arousal responses to sexual stimuli (Chivers, 2005; Chivers and Bailey, 2005; Chivers et al., 2004), this reduced category-specificity may reflect a heightened female-typical response due to reduced or absent response to endogenous androgens compared with control women who are functionally exposed to higher levels of adrenal and ovarian androgens. Alternatively, this could reflect a feminizing effect of prenatal estrogens derived from testosterone, which women with CAIS would be expected to have substantially greater levels of than would control women." (Hamann et al., 2014)

Luoto & Rantala (2022) concede that the androphilia of XY CAIS individuals disrupts the "estrogenic pathway" hypothesis, making the following adjustment: "It is an interesting question why XY CAIS individuals are not completely gynephilic (female-preferring) despite having similar testosterone levels as non-affected males and presumably also the same amount of aromatized estrogens in their brain during the sensitive period of sexual differentiation. It is likely that complete defeminization and masculinization also require functional androgen receptors. Thus, it appears that, in humans, both androgens and estrogens contribute to the defeminization and masculinization of the brain."

VI. Critique of The Neurodevelopmental Model

The Neurodevelopmental Model proposes that variations in female sexual orientation and gender identity arise from varying doses of prenatal androgen and estrogen exposure, modeled as orthogonal axes. Although Luoto & Rantala (2022) give some attention to these factors, their model underemphasizes the complexities of timing, dose, and regional sensitivity to gonadal hormones:

"Gonadal hormonal influences on the brain and behavior are time- and dose-dependent, mediated by differences in regional sensitivity to these hormones, and based on these variations, the effects of gonadal hormones on brain sexual differentiation are heterogeneous." (Burke et al., 2023)

Rather than dose of prenatal estrogen, it is possible that variations in female sexual differentiation are determined by the timing and dose of androgens: "androgen signaling in gestation/prenatal development, neonatal development (i.e., minipuberty) and puberty have all been found to shape sexual differentiation of the brain and sexual behavior in nonhuman animals, and different aspects of neural sexual differentiation may be mediated at different times (reviewed in Hines, 2011)...for full male-typical display of sexual behavior and preference, male-typical levels of androgens are required across all critical developmental periods, including puberty" (Burke et al., 2023) If this is also true in humans, it would explain the discrepancies described under III. Uncertainty about "The Estrogenic Pathway" and V. Evidence that XY CAIS Women are Hyperfeminized.

Moreover, there is no evidence that FTM transsexuals are more masculinized than butch lesbians. Research on the brains of transsexuals suggests that gynephilic FTMs are the same as gynephilic women, and that androphilic FTMs are less masculinized than gynephilic women (Kreukels & Guillamon, 2016) (Guillamon et al, 2016) (Burke et al., 2017) (Roselli, 2018) (Manzouri & Savic, 2019) (Skorska et al., 2020) (Frigerio et al., 2021). Where sexual orientation is associated with "shifted" brain sexual differentiation, Gender Dysphoria is not.

While The Neurodevelopmental Model is a useful starting point, it is likely flawed, and could be improved upon by accounting for the insights from animal models described by Burke et al. (2023). When it comes to female sexual orientation, VanderLaan et al.'s (2023) model might be more accurate.

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