Mate Choices Can Be Complex, But Are They Oedipal Complex?

Theory is arguably the most important part of research. A good theory helps researchers formulate better research questions as well as understand the results that their research projects end up producing.I’ve said this so often that expressing the idea is closer to a reflex than a thought at this point. Unfortunately, “theories” in psychology – if we can even call them theories – are frequently of poor quality, if not altogether absent from research, leading to similarly poorly formulated projects and explanations. Evolutionary theory offers an escape from this theoretically shallowness, and it’s the major reason the field appeals to me. I find myself somewhat disappointed, then, to see a new paper published in Evolutionary Psychology that appears to be, well, atheoretical.

No, I’m not mad; I’m just disappointed…

The paper was ostensibly looking at whether or not human children sexually imprint on the facial traits of their opposite sex parent, or, more specifically (for those of you that don’t know about imprinting):

Positive sexual imprinting has been defined as a sexual preference for individuals possessing the characteristics of one’s parents… It is said to be a result of acquiring sexual preferences via exposure to the parental phenotype during a sensitive period in early childhood.

The first sentence of that definition seems to me to be unnecessary. One could have preferences for characteristics that one’s parents also happen to possess without those preferences being the result of any developmental mechanism that uses parental phenotype as its input. So I’d recommend using the second part of the definition, which seems fine, as far as describing sexual imprinting on parents goes. As the definition suggests, such a mechanism would require (1) a specified developmental window during which the imprinting takes place (i.e. the preferences would not be acquired prior to or after that time, and would be relatively resistant to change afterwards) and (2)  that mechanism to be specifically focused on parental features.

So how did Marcinkowska & Rantala (2012) go about testing this hypothesis? Seventy subjects, their sexual partner, and their opposite sex parent (totaling 210 people) were each photographed from straight ahead and in profile. These subjects were also asked to report about their upbringing as a child. Next, a new group of subjects were presented with an array of pictures: on one side of the array was a picture of one of the opposite sex parents; on the other side there were four pictures, one of which was the partner of that parent’s child and three of which were controls. The new subjects were asked to rate how similar the picture of the parent was to the pictures of the people on the other side of the display.

The results showed that the group of independent raters felt that a man’s mother resembled slightly more closely his later partner than the controls did. The results also showed that the same raters did not feel that a woman’s father more closely resembled her later partner than the control did. Neither of these findings were in any way related to the self-reports that subjects had delivered about their upbringing either. If you’ve been following along so far, you might be curious as to what these results have to do with a sexual imprinting hypothesis. As far as I can tell, the answer is a resounding, “nothing”.

Discussion: Never mind

Let’s consider what these results don’t tell us: they certainly don’t speak to the matter of preferences. As Marcinkowska & Rantala (2012) note, actual mating preferences can be constrained by other factors. Everyone in the population might wish to monopolize the matings of a series of beautiful others, but if those beautiful others have different plans, that desire will not be fulfilled. Since the initial definition of imprinting specifically referenced preferences – not actual choices – the findings would have very little relevance to the matter of imprinting no matter how the data fell out. It’s worse than that, however: this study didn’t even attempt to look for any developmental window either. The authors seemed to just assume it existed without any demonstration that it actually does.

What’s particularly peculiar about this oversight is that, in the discussion, the authors note they did not look at any adoptive families. This suggests that the authors at least realized there were ways of testing to see if this developmental window even exists, but didn’t seem to bother running the required tests. A better test – one that might suggest such a developmental window exists – would be to test preferences of adoptive or step-children towards the features of their biological and adoptive/step-parents. If the imprinting hypothesis was true, you would expect that adoptive/step-children would prefer the characteristics of their adoptive/step-parents, not their biological ones. Further, this research could be run with respect to the time at which the new parent came into the picture (and the old one left). If there is a critical developmental window, you should only expect to see this effect when the new parent entered into the equation at a certain age; not before or beyond that point.

The problems don’t even end there, however. As I mentioned previously, this paper appears atheoretical in nature, in that the authors give absolutely no reason as to why one would expect to find a sexual imprinting mechanism in the first place, why it would operate in early childhood, let alone why that mechanism would be inclined to imprint on one’s close, biological kin. What the precise fitness benefits to such a mechanism would be are entirely unclear to me, though, at the very least, I could see it carrying fitness costs in that it might heighten the probability of incest taking place. Further, if this mechanism is presumably,active in all members of our species, and each person is looking to mate with someone who resembles their opposite sex parent, it would seem that such a preference might actively disincline people from having what would be otherwise adaptive matings. Lacking any theoretical explanation for any of this, the purpose of the research seems very confusing.

On the plus side, you can still add it to your resume, and we all know how important publications are.

All that said, even if research did find that people tended to be attracted to the traits of their opposite sex parent, such a finding could, in principle, be explained by sexual selection. Offspring inherent genes from their parents that both contributed to their parent’s phenotype as well as genes that contributed to their parent’s psychological preferences. If preferences were not similarly inherited, sexual selection would be impossible and ornaments like the peacock’s tail could never have come into existence. So, presuming your parents found each other at least attractive enough to get together and mate, you could expect their offspring to resemble them both physically and psychologically to some extent. When those offspring are then making their own mate choices, you might then expect them to make a similar set of choices (all else being equal, of course).

What can be said for the study is that it’s a great example of how not to do research. Don’t just assume the effect you’re looking to study exists; demonstrate that it does. Don’t assume that it works in a particular way in the event that it actually exists either. Most importantly, don’t formulate your research project in absence of a clearly stated theory that explains why such an effect would exist and, further, why it would work the way you expect it might. You should also try and rule out alternative explanations for whatever findings you’re expecting. Without good theory, the quality of your research will likely suffer, and suffer badly.

 References: Marcinkowska, U.M., & Rantala, M.J. (2012). Sexual Imprinting on Facial Traits of Opposite-Sex Parents in Humans. Evolutionary Psychology, 10, 621-630

Does Infidelity Pay Off (For Sparrows)?

For some species, mating can be a touch more complicated than others. In species where males provide little more than their gametes, the goal of mating for females is simple: get the best gametes available. While the specifics as to how that’s accomplished vary substantially between species, the overall goal remains the same. Since genes are all the female is getting, she may as well get the best that she can. In contrast, for some other species males provide more than just their genes; they also provide some degree of investment, which can take the form of a one-time gift through upwards of decades of sustained investment. In these species, females need to work this additional variable into their mating calculus, as the two goals do not always overlap. The male who’s willing to provide the best investment might not also happen to have the best genes, and pursuing one might risk the other.

Accordingly, it’s long been assumed that extra-pair mating (cheating) is part of the female strategy to have her cake and eat it too. A female can initiate a pair-bond with a male willing to invest while simultaneously having affairs with genetically higher-quality males, leaving the unfortunate cuckold to invest in offspring he did not sire. Undertaking extra-pair matings, however, can be risky business, in that detection by the investing male might lead to a withdrawal of investment and, in certain cases, bodily harm.

Good luck to all you parents when it comes to weaving that tidbit into your birds and bees talk.

These risks would require that offspring sired through extra-pair mating to tend to actually be fitter than offspring sired by the within-pair male, in order to be selected for. Abandonment can entail some serious risks, so females would need some serious compensating gains to offset that fact. A new paper by Sardell et al (2012) sought to determine whether extra-pair offspring would in fact be ‘fitter’ than within-pair offspring in Melospiza melodia – the song sparrow – when fitness was measured by lifetime reproductive success in number of offspring hatched, the number that survived to enter the breeding population, and the number of grand-offspring eventually produced. The results? Data gathered across 17 years, representing 2,343 hatchlings and 854 broods found that extra-pair offspring seemed to actually be less fit than their within-pair half-siblings. Well, kind of… but not really.

Over the 17 years of data collection, roughly 28% of the offspring were classed as being extra-pair offspring, and only broods with mixed paternity was considered for the present study (i.e. there was at least 1 offspring from the resident male and also at least 1 offspring from an extra-pair male). This cut the sample size down to 471 hatchlings, representing 154 mixed paternity broods across 117 pair bonds. The first point I’d like to make is that a 28% non-paternity rate seems large, and, unless it’s the result of an epidemic of forced copulations (rape), that means these female sparrows are having a lot of affairs, presumably because some mating module in their brain is suggesting they do

Within the sample of sparrows, female extra-pair offspring (the ones who were sired by the non-resident male) averaged 5.4 fewer hatched offspring over their lives, relative to their within-pair half-siblings; for extra-pair males, the corresponding average was 1.5 fewer offspring. However, not all of those hatchlings live to eventually breed. Of the 99 that did, the females that were the result of  extra-pair mating, on average, had 6.4 fewer hatchlings of their own, relative to the within-pair females; the extra-pair males also had fewer hatchlings of their own, averaging 2.6 fewer. Thus, relative to their within-pair half-siblings, extra-pair offspring seemed to produce fewer offspring of their own, and, in turn, fewer grand-offspring. (I should note at this point that any potential reasons for why extra-pair young seemed to be having fewer hatchlings are left entirely unexamined. This strikes me as something of a rather important oversight)

Are we to conclude from this pattern of results (as this article from the Huffington post, as well as the authors of the current paper did) that extra-pair mating is not currently adaptive?

And is it time for those who support the “good genes” theory to start panicking?

I don’t think so, and here’s why: when it came to the number of recruited offspring – the hatchlings who eventually reached breeding age – extra-pair females ended up having 0.2 more of them, on average, while extra-pair males had 0.2 less of them, relative to their within-pair half-siblings. While that might seem like something of a wash, consider the previous finding: within-pair offspring were having more offspring overall. If within-pair offspring tended to have more hatchlings, but a roughly equal number reach the breeding pool, that means, proportionally, more of the within-pair offspring were dying before they reached maturity. (In fact, extra-pair offspring had a 5% advantage in the number of total hatchlings that ended up reaching maturity) Having more offspring doesn’t mean a whole lot if those offspring don’t survive and then go on to reproduce themselves, and many of the within-pair offspring were not surviving.

One big area this paper doesn’t deal with is why that mortality gap exists; merely that it does. This mortality gap might even be more surprising, given that the potential risk of abandonment might mean males were less likely to have been investing when they doubted their paternity, though the current paper doesn’t speak to that possibility one way or another. Two of the obvious potential suspects for this gap are predation and parasites. Extra-pair young may be better able to either avoid predators and/or defend against pathogens because of their genetic advantages, leading to them being more likely to survive to breeding age. Then there’s also a possibility of increased parental investment: if extra-pair hatchlings are in better condition, (perhaps due to said pathogen resistance or freedom from deleterious mutations) the parents may preferentially divert scarce resources to them, as they’re a safer wager against an uncertain future. Alternatively, extra-pair offspring might have commanded a higher mating value, and were able to secure a partner more able and/or willing to invest long term. There are many unexplored possibilities.

The heart of the matter here concerns whether the female sparrows who committed infidelity would have been better off had they not done so. From the current data, there is no way of determining that as there’s no random assignment to groups and no comparison to non-mixed paternity broods (though that latter issue comes with many confounds). So not only can the data not definitely determine whether the extra-pair mating was adaptive or not, but the data even suggests that extra-pair offspring are slightly more successful in reaching breeding age. That is precisely counter to the conclusions reached by Sardell et al (2012), who state:

Taken together, these results do not support the hypothesis that EPR [extra-pair reproduction] is under positive indirect selection in female song sparrows…and in fact suggest… [that] other components of selection now need to be invoked to explain the evolution and persistence of EPR.

Their data don’t seem to suggest anything of the sort. They haven’t even established current adaptive value, let alone anything about past selection pressures. Sardell et al ‘s (2012) interpretation  of this mountain of data seems to be biting off more than they can chew.

It was a good try at least…

One final thoroughly confusing point is that Sardell et al (2012) suggest that how many grand-hatchlings the extra-pair and within-pair young had mattered. The authors concede that, sure, in the first generation within-pair sparrows had more hatchlings, proportionately more of which died, actually leaving the extra-pair offspring as the more successful ones when it came to reaching the breeding pool. They then go on to say that:

However, since EPY [extra-pair young] had 30% fewer hatched grandoffspring than WPY [within-pair young], higher recruitment of offspring of EPY does not necessarily mean that EPY had higher LRS [lifetime reproductive success] measured to the next generation. (p.790)

The obvious problem here is that they’re measuring grandoffspring before the point when many of them would seem to die off, as they did in the previous generation. So, while number of hatched grandoffspring says nothing important, they seem to think it does this time around. It’s been known that counting babies is only of limited use in determining adaptive value (let alone past adaptive value), and I hope this paper will serve as a cautionary tale for why that’s the case.

References: Sardell, R., Arcese, P., Keller, L., & Reid, J. (2012). Are There Indirect Fitness Benefits of Female Extra-Pair Reproduction? Lifetime Reproductive Success of Within-Pair and Extra-Pair Offspring The American Naturalist, 179 (6), 779-793 DOI: 10.1086/665665

What Causes (Male) Homosexuality?

My initial inspiration for starting this blog was a brief piece I had written about why Lady Gaga’s song, “Born This Way”, really got under my skin. The general premise of the song is, unless I’m badly mistaken, that homosexuality is genetic in nature, and, accordingly, should be socially accepted. The song is full of very selective logic and a poor grasp of the state of scientific knowledge, all of which is accepted in the service of furthering a political goal. For what it’s worth, I agree with that goal, but the means being used to achieve it in this case were misguided because:

“…I’m not so sure Lady Gaga – or any gay-rights supporter – wants to base their claims to equal rights on the supposition that homosexuality is a trait people are “born” with…If further research uncovers that people can come to develop a homosexual orientation for a number of reasons that have nothing to do with being “born like that”, I wouldn’t want to see the argument for equal rights slip away.”

Today, I’m going to be stepping back into that same political minefield that I did on the topic of race, and discuss a hypothesis regarding the cause of male homosexuality that some people may not like. People will not like this hypothesis for reasons extrinsic to the hypothesis itself, but do your best to contain any moral outrage you may be feeling. My first task in presenting this hypothesis will be to convince you that male homosexuality is not genetically determined – despite what an eccentric young pop-star might tell you – and is also not an adaptation.

Convincing critics is always such a pleasure.

For some, it might seem insulting that homosexuality requires an explanation, whereas heterosexuality does not. Aren’t both just different sides of a very bisexual coin? There’s a simple answer to that concern: heterosexual intercourse is the only means to achieve reproduction. An exclusive homosexual orientation is the evolutionary equivalent to sterility, and if three to five percent of the male population was consistently sterile – despite neither of anyone’s parents being sterile, by definition – that would raise some questions as to how sterility persists. There would be an intense selective pressure away from sterility, and any genes that actively promoted it would fail to reproduce themselves. That homosexuality seems to persist in the population, despite it being a reproductive dead-end, requires an explanation. Heterosexuality poses no such puzzle. 

The first candidate explanation for the persistence of homosexuality is that it’s part on an adaptation for assisting the reproduction of one’s kin. While homosexuals themselves may suffer a dramatic reduction in their lifetime reproduction, they activity assist other genetic relatives, delivering enough benefits to offset their lack of personal reproduction, similar to how ants or bees would assist the queen, forgoing reproduction themselves. This suggestion is implausible on three levels: first, it would require that homosexuals deliver enormous benefits to their relatives. For each one child a gay man wouldn’t have, they would need to ensure a brother or sister would have an additional two that they wouldn’t otherwise have without those benefits. This would require an intense amount of investment. Second, there’s no theoretical reason that’s ever been provided as to why homosexuals would develop a homosexual orientation, as opposed to, say, an asexual orientation. Seeking out intercourse with same-sex individuals doesn’t seem to add anything to the whole investment thing. Finally, this explanation doesn’t work because, as it turns out, homosexuals don’t invest anymore in their relatives than heterosexuals do (Rahman & Hull, 2005). So much for kin selection.

A second  potential explanation for homosexuality is that it’s the byproduct of sexually antagonist selection; a gene that damages the reproductive potential of males persists in the population because the same trait is beneficial when it’s expressed in female offspring (Ciani, Cermelli, & Zanzotto, 2008; Iemmola & Ciani, 2009). Another potential explanation is that a homosexual orientation is like sickle cell anemia: while it hurts the reproductive prospects of those who express it, it provides some unspecified benefit that outweighs that cost in some carriers, as sickle cell protects against malaria. Both explanations have a large issues to contend with but one of the most prominent shared issues is this: despite both hypotheses resting on rather strong genetic assumptions, half or more of the variance in male homosexual orientation can’t be attributed to genetic factors (Kirk et al., 2000; Kendler et al., 2000). Identical twins don’t seem to be concordant for their sexual orientation anymore than 30 to 50% of the time when one of the twins identifies as non-heterosexual. If homosexuality was determined solely by genes, there should be a near complete agreement. 

In fact, most of the variance appears to be due to our decadent Western lifestyle. Who knew, right?

Accordingly, any satisfying explanation for homosexuality needs to reference environmental factors, as all traits do; the picture is far from as crude as there being some genes “for” homosexuality. While there clearly are some genetically inherited components in the ontogeny of a homosexual orientation, it’s entirely unclear what those genetic factors are. It’s also far from clear how those genetic factors interact with their environment – or when, for that matter. They would seem to act sometime before puberty, but beyond that the door is open. What seems to have been established so far is that an exclusive homosexual orientation is detrimental to reproduction in a big way, and these costs are not known to be reliably offset.

There is one last hypothesis that may hold some potential, though, as I mentioned, I suspect many people won’t like it: the “gay germ” theory. The general idea is that some outside pathogen – be it a bacteria or a virus – manipulates development in some way, the end result being a homosexual orientation. This hypothesis seems to have potential for a number of reasons: first, it neatly deals with why homosexuality persists in the population, despite the massive reproductive costs. It could also account for why monozyogtic twins are often discordant for homosexual orientation, despite sharing genes and a prenatal environment. As of now, it remains an untested theory, but other lines of research suggest some preliminary success using the same basic idea to understand the persistence of disorders like schizophrenia and obsessive compulsive disorder, among many others. Of course, such a theory does come with some political baggage and questions.

Like: will two gay men ever be able to hold hands, post love-making, on top of an American flag, just like straight couples do?

The first set of questions concern the data speaking to the hypothesis: what pathogen(s) are responsible? When do they act in development? How do they alter development? Are those alterations an adaptation on the part of the pathogen or merely a byproduct? These are no simple questions to answer, especially because it won’t be clear which children will end up gay until they have matured. This makes narrowing the developmental window in which to be looking something of task. If concordance rates for monozyogtic twins are similar between adopted and reared together twins, that might point to something prenatal, depending on the age at which the twins were separated, but would not definitively rule out other possibilities. Further, this pathogen need not be specific to gay men; it could be a pathogen that much of the population carries, but, for whatever reason, only affects a sub-group of males in such a way that they end up developing a homosexual orientation.        

The second set of questions concern potential implications of this theory, were it to be confirmed. I’ll start by noting these concerns have zero, absolutely nothing, to do with whether or not the gay germ theory is true. That said, these concerns are probably where most of the resistance to the hypothesis would come from, as concerns for data (or lack thereof) are often secondary to debates. Yes, the hypothesis cries out for supporting data so it shouldn’t be accepted just yet, but I’m talking to those people who would reject it as a possibility out of hand because it sounds icky. In terms of gay rights and social acceptance, it shouldn’t matter whether homosexuality is 100% genetically determined, caused by a pathogen, or just a choice someone makes one day because they’re bored with all that vanilla heterosexual sex they’ve been having. That something may be, or is, caused by a pathogen should really have no bearing on it’s moral status. If we discovered tomorrow that it was a virus that caused men to have larger-than-average penises, I doubt many people would cheer for the potential to cure the “disease” of large-penis.         

References: Ciani, A.C., Cermilli, P., & Zanzotto, G. (2008). Sexually antagonistic selection in human male homosexuality., 3, e,2282.

Iemmola, F. & Ciani, A.C. (2009). New evidence of genetic factors influencing sexual orientation in men: Female fecundity increase in the maternal line. Archives of Sexual Behavior, 38, 393-399

Kendler, K.S., Thornton, L.M., Gilman, S.E., & Kessler, R.C. (2000). Sexual orientation in a U.S. national sample of twins and nontwin sibling pairs. American Journal of Psychiatry, 157, 1843-1846

Kirk, K.M., Bailey, J.M., Dunne, M.P., & Martin, N.G. (2000). Measurement models for sexual orientation in a community twin sample. Behavior Genetics, 30, 345-356

Rahman, Q. & Hull, M.S. (2005). An empirical test of the kin selection hypothesis for male homosexuality. Archives of Sexual Behavior, 234, 461-467 

Do “Daddy Issues” Jumpstart Menstruation?

Like me, most of you probably come from the streets. On the streets, it’s common knowledge that “daddy issues” are the root cause of women developing interests in several activities. Daddy issues are believed to play a major role in becoming a stripper, developing a taste for bad boys, and getting  a series of tattoos containing butterflies, skulls, and/or quotes with at least one glaring spelling mistake. As pointed out by almost any group in the minority at one point or another, however, that knowledge is common does not imply it is also correct. For instance, I’ve recently learned that drive-bys are not a legitimate form of settling academic disagreements (or at least that’s what I’ve been told; I still think it made me the winner of that little debate). So, enterprising psychologist that I am, I’ve decided to question the following piece of folk wisdom: is father absence really a causal variable in determining a young girl’s life history strategy, specifically with regard to the onset of menstruation?

Watch carefully now; that young boy may start to menstruate at any moment… wait; which study is this?

First, a little background is order. Life history theory deals with the way an organism allocates its limited resources in an attempt to maximize its reproductive potential. Using resources to develop one trait precludes the use of those same resources for developing other traits, so there are always inherent trade-offs that organisms need to make during development. Different species have stumbled upon different answers as to how these trade-offs should be made: is it better to be small or large? Is it better to start reproducing as soon as possible or start reproducing later? Is it better to produce many offspring and invest little in each, or produce fewer offspring and invest more? These developmental and behavioral trade-offs all need to be made under a series of ecological constraints, such as the availability of resources or the likelihood of survival. For instance, it makes no sense for a convict to refuse a final cigarette before a firing squad executes him out of concerns for his health. There’s no point worrying about tomorrow if there won’t be one. On the other hand, if you have a secure future, maybe Russian roulette isn’t the best choice for a past time.

So where do family-related issues enter into the equation?  Within each species, different individuals have slightly different answers for those developmental question, and those answers are not fixed from conception. Like all traits, their expression is contingent on the interaction between genes and the environment those genes find themselves in. A human child that finds itself with severely limited access to relevant resources is thus expected to alter their developmental trajectory according to their constraints. This has been demonstrated to be the case for obvious variables like obtaining adequate nutrition: if a young girl does not have access to enough calories, her sexual maturation will be delayed, as her body would be unlikely to successfully support the required investment a child brings.

Another of these hypothesized resources is paternal investment. The suggestion put forth by some researchers (Ellis, 2004) is that a father’s presence or absence signals some useful information to daughters regarding the availability of future mating prospects. The theory that purports to explain this association states that when young girls experience a lack of paternal investment, their developmental path shifts towards one that expects future investment by male partners to be lacking and not vital to reproduction. This, in turn, results in more sexual precociousness. Basically, if dad wasn’t there for you growing up, then, according to this theory, other men probably won’t be either, so it’s better to not develop in a way that expects future investment. That father absence has been associated with a slightly earlier onset of menarche (first menstruation) in women has been taken as evidence supporting this theory.

The basic concept also spun off into a show on MTV.

The major problem with this suggestion is that no causal link has been demonstrated. The only thing that has been demonstrated is that father absence tends to correlate with an earlier age of menstruation, and the degree to which the two are correlated is rather small. According to some correlations reported by Ellis (2004), it looks as if one could predict between 1 to 4% of the variance in timing of pubertal development on the basis of father absence, depending on which parts of the sample is under discussion. Further, that already small correlation does not control for a wide swath of additional variables, such as almost any variables that are found outside the home environments. This entire social world that exists outside of a child’s family has been known to have been of some (major) importance in children’s development, while the research on the home environment seems to suggest that family environments and parenting styles don’t leave lasting marks on personality (Harris, 1998).

As the idea that outside the home environments matter a lot has been around for over a decade, it would seem the only sane things for researchers to do are more nearly identical studies, looking at basically the same parenting/home variables, and finding the same, very small to no effect, then making some lukewarm claim about how it might be causation, but then again might not be. This pattern of research is about as tedious as that last sentence is long, and it plagues psychological research in my opinion. In any case, towards achieving that worthwhile goal of breaking through some metaphorical brick wall by just running into it enough times, Tither and Ellis (2008) set out to examine whether the already small correlation between daughter’s development and father presence was due to a genetic confound.

To do this, Tither and Ellis examined sister-pairs that contained both an older and younger sister. The thinking here is that it’s (relatively) controlled for on a genetic level, but younger sisters would experience more years of father absence following the break-up of a marriage, relative to the older sisters, which would in turn accelerate sexual maturation of the younger one. Skipping to the conclusions, this effect was indeed found, with younger sisters reporting earlier menarche than older sisters in father absent homes (accounting for roughly 2% of the variance). Among those father absent homes, this effect was carried predominately by fathers with a high reported degree of anti-social, dysfunctional behavior, like drug use and suicide attempts (accounting for roughly 10% of the variance within this subset). The moral seems to be that “good-enough” fathers had no real effect, but seriously awful parenting on the father’s part, if experienced at a certain time in a daughter’s life, has some predictive value.

So you may want to hold off on your drug-fueled rampages until your daughter’s about eight or nine years old.

First, let me point out the rather major problem here on a theoretical level. If the theory here is that father presence or absence sends a reliable signal to daughters about the likelihood of future male investment, then one would expect that signal to at least be relatively uniform within a family. If the same father is capable of signaling to an older daughter that future male investment is likely, and also signaling to a younger daughter that future male investment isn’t likely, then that signal would hardly be reliable enough for selection to have seized on.

Second, while I agree with Tither and Ellis that these results are consistent with a casual account, they do not demonstrate that the father’s behavior was the causal variable in any way whatsoever. For one thing, Ellis (2004) notes that this effect of father presence vs absence doesn’t seem to exist in African American samples. Are we to assume that father presence or absence has only been used as a signal by girls in certain parts of the world? Further, as the authors note, there tend to be other changes that go along with divorce and paternal psychotic behavior that will have an effect on a child’s life outside of the home. To continue and beat what should be a long dead horse, researchers may want to actually start to look at variables outside of the family to account for more variation in a girl’s development. After all, it’s not the family life that a daughter is maturing sexually for; it’s her life with non-family members that’s of importance.

References: Ellis, B.J. (2004). Timing of pubertal maturation in girls: An integrated life history approach. Psychological Bulletin, 130, 920-958

Harris, J.R. (1998). The Nurture Assumption: Why Children Turn Out The Way They Do. New York: Free Press

Tither, J.M., & Ellis, B.J. (2008). Impact of fathers on daughters’ age at menarche: A genetically and environmentally controlled sibling study. Developmental Psychology, 44, 1409-1420/