john hawks weblog

Usually that's a title about something related to cloning or stem cells or something. But in this case, it's about the fact that your vote may be heritable! I'm posting this because I just lectured about heritability last week. Like usual, I noted that political affiliation exhibits strong familial effects, but that these are mostly due to shared environment and not genetic variance.

Little did I know that a new study would show that genes do play a substantial role. In a twin study that numbered over 8,000 sets of twins, researchers asked questions about political hot-button topics and general political preferences.

On school prayer, for example, the identical twins' opinions correlated at a rate of 0.66, a measure of how often they agreed. The correlation rate for fraternal twins was 0.46. This translated into a 41 percent contribution from inheritance.

As found in previous studies, attitudes about issues like school prayer, property taxes and the draft were among the most influenced by inheritance, the researchers found. Others like modern art and divorce were less so. And in the twins' overall score, derived from 28 questions, genes accounted for 53 percent of the differences.

But after correcting for the tendency of politically like-minded men and women to marry each other, the researchers also found that the twins' self-identification as Republican or Democrat was far more dependent on environmental factors like upbringing and life experience than was their social orientation, which the researchers call ideology. Inheritance accounted for 14 percent of the difference in party, the researchers found.

And then there's this:

A mismatch between an inherited social orientation and a given party may also explain why some people defect from a party. Many people who are genetically conservative may be brought up as Democrats, and some who are genetically more progressive may be raised as Republicans, the researchers say.

So political party membership may not be strongly heritable, but the tendency to defect, given a conflict with the parental party, may be.

Much more good stuff in the article, including the speculation that the country may become increasingly polarized.

Reuters reports on a research study by Dr. Neri Laufer (Hadassah University Hospital, Jerusalem) into the genetic variation underlying fertility in older women. The newsworthy finding is the identification of a "select group of genes" that influence late fertility:

Using gene chip technology, [Laufer] and his team compared the genetic profiles of eight women chosen from 250 who had had children past the age of 45 with profiles of six others who had finished their families by the age of 30.

"These women appear to differ from the normal population due to a unique genetic predisposition that protects them from the DNA damage and cellular aging that helps age the ovary," he said.

Conceiving naturally past the age of 45 is rare because a womanÕs supply of eggs diminishes as she ages and approaches the menopause, which normally occurs around the age of 50.

The report implies that the alleles may be more common in some groups than others. Although it does not say, the geographic extent of the samples was almost certainly limited, so the following cannot be considered conclusive, but it is interesting:

All the super-fertile women in the study were Ashkenazi Jews, descended from the Jewish communities of central and eastern Europe. Most had had six or more children, did not use contraception and had a low miscarriage rate.

"They challenged their reproductive system until the menopause," said Laufer, who added that the distinct genetic fingerprint was not unique to them.

He found a similar profile in Bedouin women who also had children late in life.

It might be highly localized, it might be global. Whichever is the case, this is certainly interesting from the standpoint of the evolution of life history traits in humans. The persistence of fertility into later adulthood would seem to be highly adaptive, unless the allele has some cost for earlier survival or reproduction. The distribution of the allele and that of linked loci could tell us if it has been recently spreading, or if it is an ancient polymorphism. To my knowledge, this is the first examination of the determinants of fertility late in life, as opposed to genetic determinants of mortality. The shape of human life histories is affected by selection on both, so this is an important step.

From a Reuters story:

Researchers at the University of Groningen in the Netherlands have used scans to show that different areas of the brain are stimulated during an orgasm but are not activated when a woman fakes it.

"Women can imitate orgasm quite well," Gert Holstege told a fertility meeting on Monday. "But there is nothing really happening in the brain."

Not exactly earth-shattering to anyone who's watched "When Harry Met Sally." But the story buries the lede:

But they did show that different parts of the male and female brain are activated and deactivated during sexual stimulation.

The researchers found less deactivation in the males in the areas of the brain linked to emotion and fear when they were sexually stimulated.

For more speculations about the mental features related to orgasm, see my previous post. Again, this is evidence that the feature itself cannot be disentangled from the cognitive features of the brain in humans. The article further says that in females, orgasm accompanies a deactivation of cortical regions and regions of the brain involved in fear and emotion.

On the other hand, these areas might naturally be less active in people willing to climax in a clinical setting while strapped into an MRI machine...

Every introductory class in biological anthropology talks about wisdom teeth, the common name for human third molars. Around ninety percent of my students in any given semester have had these pulled, or never got them at all. Problems with the eruption or alignment of the third molars are very common, causing pain or infection. Even in cases where the teeth might ultimately not pose a long-term problem, many dentists pull them as a prophylactic. Natural cases of non-eruption are fairly common also. Sometimes these are nevertheless present, and may be removed surgically. Other times, the third molars never formed at all. As a result of both natural variation and orthodontic practice, it is increasingly rare for adults to have wisdom teeth.

Since this natural variation is so well-known to anthropologists, I was intrigued to find in a comment to a post at Gene Expression that Aristotle believed men had more teeth than women. I went in search of the essential citation, and found it in "The History of Animals," book 2, part 1 (translated by D'Arcy Wentworth Thompson):

Males have more teeth than females in the case of men, sheep, goats, and swine; in the case of other animals observations have not yet been made: but the more teeth they have the more long-lived are they, as a rule, while those are short-lived in proportion that have teeth fewer in number and thinly set.

Part 4

The last teeth to come in man are molars called 'wisdom-teeth', which come at the age of twenty years, in the case of both sexes. Cases have been known in women upwards. of eighty years old where at the very close of life the wisdom-teeth have come up, causing great pain in their coming; and cases have been known of the like phenomenon in men too. This happens, when it does happen, in the case of people where the wisdom-teeth have not come up in early years.

There may be no accounting for Aristotle's claim that men have more teeth than women, since on average they are the same. On the other hand, with the variation in third molar eruption it is quite possible that the women available for Aristotle to examine might have -- by chance -- had fewer teeth. The idea that there is a systematic difference between men and women would appear to be belied by the following section, where Aristotle clearly discusses the presence of the wisdom teeth in both sexes. This part is a vivid illustration of the problems of the posterior dentition in general -- ancient Greeks and modern Americans alike.

I was similarly fascinated to see that "wisdom teeth" was a translation from the ancient Greek. Here's the entry from the Online Etymology Dictionary:

Wisdom teeth so called from 1848 (earlier teeth of wisdom, 1668), a loan-translation of L. dentes sapientiae, itself a loan-transl. of Gk. sophronisteres (used by Hippocrates, from sophron "prudent, self-controlled"), so called because they usually appear ages 17-25, when a person reaches adulthood.

Here I thought it was just one of those old sayings nobody could account for. And did you know that "catty-corner" comes all the way from Middle English?

This week's (June 16, 2005) Nature brings yet another example of the way brain function may be modulated (see earlier posts here and here). This time, the culprit is mobile genetic elements, or retrotransposons, called LINE-1 (L1) elements.

The study, from Fred H. Gage's lab at the Salk Institute focuses on the way that these retrotransposons can alter their expression in neuronal precursor cells, ultimately resulting in changes in neural function. From the Salk Institute press release:

Brains are marvels of diversity: no two look the same -- not even those of otherwise identical twins. Scientists at the Salk Institute for Biological Studies may have found one explanation for the puzzling variety in brain organization and function: mobile elements, pieces of DNA that can jump from one place in the genome to another, randomly changing the genetic information in single brain cells. If enough of these jumps occur, they could allow individual brains to develop in distinctly different ways.

"This mobility adds an element of variety and flexibility to neurons in a real Darwinian sense of randomness and selection," says Fred H. Gage, Professor and co-head of the Laboratory of Genetics at the Salk Institute and the lead author of the study published in this week's Nature. This process of creating diversity with the help of mobile elements and then selecting for the fittest is restricted to the brain and leaves other organs unaffected. "You wouldn't want that added element of individuality in your heart," he adds.

The study may help to explain why some of these L1 elements should be there at all:

Transposable L1 elements, or "jumping genes" as they are often called, make up 17 percent of our genomic DNA but very little is known about them. Almost all of them are marooned at a permanent spot by mutations rendering them dysfunctional, but in humans a hundred or so are free to move via a "copy and paste" mechanism. Long dismissed as useless gibberish or "junk" DNA, the transposable L1 elements were thought to be intracellular parasites or leftovers from our distant evolutionary past.

It also may help to explain why their expression should be limited to germ cells and early stem cells. Nature has an accompanying editorial with this to say:

In fact, previous studies of L1 expression and mobility demonstrate L1 activity in germ cells and in early developmental cells but not in other cell types. There has been only one previous example of L1 mobility in a human somatic cell: this insertion disrupts a gene that contributes to colon cancer. Muotri et al. provide the first evidence of L1 activity in normal cells cultured directly from an animal sample, and the first evidence of somatic L1 activity late in development of a transgenic mouse.

The expression of L1s in NPCs appears to be inversely correlated with the expression of SOX2, a gene that is poorly expressed in developing NPCs but that has several vital functions in adult neural cells. The authors further demonstrate that L1 activation is related to changes in histone proteins that are associated with gene expression in general. Histones interact directly with DNA, and their acetylation and methylation pattern can determine whether a region of DNA is 'open' and transcribed. That histone modification might be a host mechanism to control L1 activity is an intriguing possibility (Ostertag and Kazazian 2005:891).

The basic idea coming out of the research is that the L1 elements may increase the diversity of expression of neuronal types. Ultimately, an adult brain incorporates only a fraction of the neuronal cells and connections among those cells that are formed during embryonic and early childhood development. If the variation among these is increased by L1 alterations, then it provides another avenue for a sort of natural Darwinian process to cull out unused neurons and connections, leaving the brain tissue composed of maximally valuable structures and communication networks. Supporting this hypothesis is the fact that cells that undergo L1 retrotransposition events are more likely to differentiate into neurons. From the press release:

Apart from their activity in testis and ovaries, jumping L1 elements are not only unique to the adult brain but appear to happen also during early stages of the development of nerve cells. The Salk team found insertions only in neuronal precursor cells that had already made their initial commitment to becoming a neuron. Other cell types found in the brain, such as oligodendrocytes and astrocytes, were unaffected.

But there is much left to be demonstrated. The conclusion of the paper includes enough to intrigue, but makes clear how little has really been shown:

Thus, our findings indicate that an engineered human L1 can retrotranspose in rat NPCs and indicate that individual neurons might be mosaic with respect to L1 content. Future experiments will focus on whether endogenous L1s naturally retrotranspose in NPCs and whether this process has any developmental significance. However, with those caveats being clearly stated, it is tempting to speculate that some of the genomic changes necessary for the uniqueness of individuals within a population, as defined by their neural circuitry, might be driven, in part, by the activities of mobile elements (Muotri et al. 2005:909).

References:

Muotri AR, Chu VT, Marchetto MCN, Deng W, Moran JV, and Gage FT. 2005. Somatic mosaicism in neuronal precursor cells mediated by L1 retrotransposition. Nature 435:903-910. Nature online

Ostertag EM and Kazazian HH, Jr. 2005. Genetics: LINEs in mind. Nature 435:890-891. Nature online

MSNBC is carrying an Associated Press article covering the Kansas State Board of Education discussions on evolution and intelligent design.

A discussion about how evolution should be taught in Kansas' public schools degenerated Wednesday into personal attacks among State Board of Education members.

Here are some excerpts:

A newsletter from [board member Connie] Morris circulated earlier this week, in which she derided evolution as an "age-old fairy tale" and criticized the four moderates by name.

...

Helping [Chairman Steve] Abrams draft the latest proposal were board members Kathy Martin, of Clay Center, and Connie Morris, of St. Francis. Morris chastised the board's four moderates for not attending the public hearings in May.

During the hearings, witnesses criticized evolutionary theory that natural chemical processes may have created the first building blocks of life, that all life has descended from a common origin and that man and apes share a common ancestor.

"Had you attended, you would have been informed," Morris said. "You would be sitting here as informed individuals and not arrogantly calling us dupes."

Instead of voting now, the board has referred the science standards to an external committee of educators. But this committee apparently doesn't know how to approach this evaluation:

The chairman of the educators' panel, Steve Case, said he's not sure what board members expect from his group. A majority of the educators supported evolution-friendly language.

"I know they don't want us to go in and take all of the changes out, which is what three-quarters of the committee will want to do," said Case, also the assistant director of the Center for Science Education at the University of Kansas.

It is essential to commencing labor contractions in pregnant women. It is implicated in behaviors related to maternal care, including milk letdown. It apparently helps to regulate social relationships in primates and other mammals.

And now, according to a study in Nature by Michael Kosfeld and colleagues (2005), oxytocin appears to be related to trust between people.

From the abstract:

Here we show that intranasal administration of oxytocin, a neuropeptide that plays a key role in social attachment and affiliation in non-human mammals causes a substantial increase in trust among humans, thereby greatly increasing the benefits from social interactions. We also show that the effect of oxytocin on trust is not due to a general increase in the readiness to bear risks. On the contrary, oxytocin specifically affects an individual's willingness to accept social risks arising through interpersonal interactions. These results concur with animal research suggesting an essential role for oxytocin as a biological basis of prosocial approach behaviour (Kosfeld et al. 2005:673).

Neuroscientist Antonio Damasio wrote an accompanying editorial.
There is also a story in the Economist on the paper. Damasio summarizes the logic of the conclusions:

Kosfeld et al. provide an engaging discussion of the possible mechanisms behind their finding. They reject the possibility that oxytocin has a nonspecific positive effect on social behaviour, because of its different influence on investors and trustees. Approach and trust possibly dominate the behaviour of investors, and that is where oxytocin works, whereas trustee behaviour is dominated by a principle of reciprocity, for which oxytocin seems irrelevant. Kosfeld et al. also reject the possibility that oxytocin merely reduces the sensitivity to risk, because in a control experiment in which the investors knew the trustee was a computer, they did not take any extra risks. The authors finally settle for an attractive pair of factors: that oxytocin overcomes the aversion to betrayal (which applies only to the investors), and that this is combined with the effects of reward that result from enhanced approach behaviour (Damasio 2005:571).

Damasio also points to some pretty interesting hypotheses about well-known pathologies, including autism and William's syndrome. The first is characterized by a relative lack of social bonding and trust; William's syndrome patients "approach strangers fearlessly and indiscriminately." He raises the question of whether this level of trust may come from excessive oxytocin release. One may alternatively ask whether it comes from an alteration in the underlying neural structures affected by oxytocin, but whether it is the first of the second, it seems likely that the trust-related mechanisms of the brain require both a structural and neurochemical input.

There has been a recent spurt of research on genes that may influence the structure or size of the brain, and their pattern of evolution in humans. These genes demonstrate the kinds of changes that may have generated the structural circuitry that underlies human behavior, although their workings are at present nearly completely unknown. But the influence of oxytocin on many aspects of human behavior illustrates an alternative route for the influence of genetic evolution. Oxytocin has multiple roles as a hormone, neuropeptide, and neurotransmitter. Instead of directly influencing the architecture of the brain, it may strongly modulate the functions of structural elements by predisposing or biasing certain kinds of outputs. Much remains to elucidate oxytocin's role, as well as that of other neuropeptides. But this kind of modulation makes it clear that the architecture of the brain must be adapted to work via the mediation of such molecules -- almost as if there were a "register shift" in the activity of certain neural substructures in response to the activity of these neuropeptides. Human brains differ from those of other primates not merely in their blueprint but also in their supply chain, as it were.

The research also points to the existence of strong subconscious influences on what might be classified as "rational" decision-making. This demonstration is not new, but it resonates as one that confounds more traditional analysis of human social bonds. Reciprocity is often conceptualized as a relation built on repeated interactions leading to trust. Humans are generally depicted within this framework as rational decision-makers who can examine their past history with other individuals (or make use of such information donated to them by other, known, individuals) and structure their future interactions accordingly. The role of oxytocin suggests that such decisions are not entirely, or perhaps even principally, made consciously. This is not to say that humans fail to make rational decisions, but instead to suggest that we have strong innate biases that reinforce certain kinds of decisions and weaken others.

Damasio's most interesting comments are in his last paragraph:

Some may worry about the prospect that political operators will generously spray the crowd with oxytocin at rallies of their candidates. The scenario may be rather too close to reality for comfort, but those with such fears should note that current marketing techniques -- for political and other products -- may well exert their effects through the natural release of molecules such as oxytocin in response to well-crafted stimuli (Damasio 2005:572).

In other words, all those pictures of babies on toilet paper advertisements are manipulating your trust. Or is that the babes in beer ads?

References:

Damasio A. 2005. Human behaviour: brain trust. Nature 435:571-572. Nature online

Kosfeld M, Heinrichs M, Zak PJ, Fischbacher U, and Fehr E. 2005. Oxytocin increases trust in humans. Nature 435:673-676. Nature online

Nicolas Rolland and Susan Crockford have a short piece in the current (June 2005) Antiquity concerning the Stegodon remains from Liang Bua (link courtesy of Jacques Cinq-Mars of the Palanth forum).

The article questions whether the Stegodon associated with the hobbits were really dwarfs:

Liang Bua Cave stands out for two remarkable findings: the first scientifically reported discovery of Pleistocene dwarf humans and a reported association of dwarf Stegodon remains, which establishes co-existence with humans (Morwood et al. 2004). The dwarf Stegodon remains (no species designated) are described, without fanfare, as an assemblage dominated by juvenile individuals. However, a Late Pleistocene dwarf Stegodon species from Flores is news indeed and calls for further clarification.

The present understanding of the succession of Stegodon species on Flores is that endemic dwarfs, represented by the Early Pleistocene species Stegodon sondaarii (from the Ola Bula Formation and Kopo Watu), became extinct by around 840 kyr (van den Bergh et al. 2001). These dwarf forms were then replaced by the medium to large-sized S. florensis, a species closely related to the S. trigonocephalus group found in Java and Wallacea islands. Thus, dwarf stegodonts became extinct before the proposed early Mid-Pleistocene peopling of Flores (Morwood 1998) and the species to co-exist with any human population on Flores should have been the normal sized Stegodon florensis. Therefore, the report that a dwarf species of Stegodon co-existed with Mid-Pleistocene hominids on Flores well after the extinction of S. sondarii is either low-key reporting at its most extreme or an error.

Rolland and Crockford "wonder" whether there actually is any evidence for dwarf size in the preserved remains, whether they may have dated to times prior to the human occupation of the cave, or their assignment as dwarfs was purely erroneous.

Remember that the initial interpretation of endemic dwarfism for the human population of Flores was argued to be credible because of the existence of other dwarf mammals, principally Stegodon. But Flores is much larger than many other islands where dwarf megafauna have been found, and the main size changes in other taxa are those of the large rodents and the Komodo dragons, who are themselves probably not phylogenetic giants.

In other words, Flores is looking less and less like the land that time forgot. Hopefully further documentation of the Stegodon remains will resolve this part of the puzzle.

I'm trying to resist becoming a hotbed of female orgasm blogging, but I just heard a promo for the story on the local news, so it seems impossible to avoid. Moreover, the issue has become a genuinely interesting debate about the role and method of evolutionary analysis. On this, I have a small contribution to make.

The Guardian is running a story on research by Kate Dunn and colleagues (2005) into the heritability of sexual response in women. Here's the abstract:

Orgasmic dysfunction in females is commonly reported in the general population with little consensus on its aetiology. We performed a classical twin study to explore whether there were observable genetic influences on female orgasmic dysfunction. Adult females from the TwinsUK register were sent a confidential survey including questions on sexual problems. Complete responses to the questions on orgasmic dysfunction were obtained from 4037 women consisting of 683 monozygotic and 714 dizygotic pairs of female twins aged between 19 and 83 years. One in three women (32%) reported never or infrequently achieving orgasm during intercourse, with a corresponding figure of 21% during masturbation. A significant genetic influence was seen with an estimated heritability for difficulty reaching orgasm during intercourse of 34% (95% confidence interval 27-40%) and 45% (95% confidence interval 38-52%) for orgasm during masturbation. These results show that the wide variation in orgasmic dysfunction in females has a genetic basis and cannot be attributed solely to cultural influences. These results should stimulate further research into the biological and perhaps evolutionary processes governing female sexual function.

At the Philosophy of Biology weblog, Elisabeth Lloyd (author of aforementioned book on female orgasm evolution) has a post generally supportive of the paper itself, but very critical of press accounts of it. She directs her greatest criticism toward the following comments by study senior author Tim Spector, which appear in the Guardian article:

Tim Spector of St Thomas's hospital in London, who led the research, said: "The theory is that the orgasm is an evolutionary way of seeing if men can prove themselves to be likely good providers or dependable, patient and caring enough to look after the kids."

Women who orgasm very easily may be more likely to be satisfied with poor quality men.

"Perhaps women who had orgasms too easily weren't very good selectors," Professor Spector said. "It paid women to be more fussy and this is one way of doing it. The simple fact is that it takes women on average 12 minutes and men two and a half minutes to reach orgasm. Adjusting to that imbalance is a test."

Lloyd has done a lot of thinking about this hypothesis, and she has a lot of ammo to unload on it. I quote from her post to give her deconstruction with some of its original clarity:

As the Guardian article makes clear, Spector is (re-)proposing a theory that orgasm is a mate-selecting device; he claims that the fact that orgasm during intercourse is difficult to attain is an evolutionary adaptation itself, making the well-known variability in orgasm among women an adaptation.

But we run into trouble immediately. The proposed adaptive state is a conditional response to quality males - have an orgasm if he's a good guy, don't if he's not - and under this theory, clearly the population of women was under selection pressure to have moved towards that optimum peak (balanced by the usual energetic costs, and so on). So why would that be an argument for the variability of orgasmic response, and not an argument for the standard result of a directional selection regime, namely, a peak at the optimum?

She goes on to summarize the data from the study, which fairly convincingly show that all females cannot have been selected to pursue this strategy -- their variability is too extensive:

If selection has been of any appreciable strength, and has been going on at least since the advent of archaic humans, we should expect that nearly all women would have such a conditional response to intercourse, and thus that nearly all women would be capable of orgasm with intercourse under the right conditions. The bad news is that there is no evidence for such a peak at all, that a full third of women rarely or never have orgasm with intercourse, and that as many as one out of ten women don't have an orgasm even once in their lives. There is a small peak in the distribution, but it is located at the non-orgasmic segment of the distribution. In other words, this is the kind of variability he needs to support his theory, and his own data show that the supporting evidence just isn't there, as I'll detail in a moment.

But there's another kind of variability, namely, that some women never have orgasm with intercourse, some women always do, and some women sometimes do and sometimes don't. This kind of variability is the kind that they do document in their study, and this kind of variability would not be selected for under his proposed hypothesis, but perversely, he implies that it would.

Heritability and alternative strategies

But I'm not sure that Lloyd and Spector are really talking about the same hypothesis. (Disclaimer: Hey, I don't know, maybe they are, in which case Lloyd's critique is more valid than I suggest.) The prologue to the Spector quote taken from the Guardian reads as follows:

The findings suggest the failure of some women to orgasm regularly is not a dysfunction, but a sophisticated mate-selection strategy that evolved during prehistoric times.

When I read that, I believed that Spector was arguing that some women (namely the ones with rarer orgasms) may have had an adaptive strategy for conditional response to male quality, leaving unstated the obvious corollary that other women may pursue different adaptive strategies.

After all, the idea that all women follow the conditional response strategy is ridiculous on its face: it cannot explain the women who reach orgasm easily and quickly most of the time, regardless of partner. If female orgasm is an adaptation, clearly there must be at least two distinct strategies: one in which orgasm is difficult and arrived at only through certain efforts, and one in which orgasm is readily achieved. There is no reason why these alternative strategies may not competed with each other in ancient human populations, considering each may have distinct advantages and drawbacks. A quick orgasm may make sex very compelling, possibly resulting in a higher frequency of inseminations -- possibly from multiple male partners. This strategy would reduce the risks associated with partnering with a single male (especially the risk of male infertility), while increasing the genetic diversity of a woman's offspring. In contrast, the conditional response strategy might have the predicted effects in encouraging female choice for male quality. Please remember that neither of these strategies has been tested, nor has the effect of their conjunction; I merely say that the hypothesis is conceivable that both of them coexisted as genetic variants within ancient human populations.

Indeed, there is no reason why there should not have been a large number of different adapted strategies toward female orgasms in past human societies. Human sexual experience must have been highly heterogenous, and the selective consequences of partially heritable mating strategies would interact in a complex way. It has the makings of a very interesting evolutionary problem.

Now, I agree that the uncritical acceptance of these hypotheses is not warranted. And I agree with Lloyd that a nonadaptive hypothesis is also very credible. The data do not point one direction or another at this point. But it is far too soon to discount the possibility that there are multiple adapted sexual strategies in human females that incorporate orgasm in differing ways.

Considering the hypothesis of alternative strategies, Lloyd's critique is mostly hollow. Consider the following passage:

The fact that this new study establishes a heritability of .45 for orgasm with masturbation (which is much more revealing than orgasm with intercourse, as far as basic orgasmic capacity goes), is also very damaging to any adaptationist account, and I'm surprised that technical people aren't saying so. Traits that are species-adaptations, such as, for example, having the capacity for language, or starting off with a good sense of taste, or having a massive brain, have heritabilities near zero. Nearly all the variability has been used up, selected out. This is just the end result of what I've just recited about the peaks in distributions. If selection is strong enough and goes on for long enough, variability around the peak gets weeded out through selection, and we're left with just one type plus random mutation and somatic, developmental, and environmental accident. Traits with heritabilities near .5 are not even close to being decent candidates for species-wide adaptations, for just this reason, as is widely known (I thought...).

FOURTH CONCLUSION: Spector's own heritability results also indicate that female orgasm is not an adaptation. Is it only population geneticists who know that species-wide adaptations have heritabilities near zero? How can it be that an expert on heritability like Spector doesn't know this? I guess this piece of knowledge might be a casualty of over-specialization.

I guess I'm as "technical" a person as has considered the issue lately, and Lloyd is just wrong about this. Certainly it is true that Fisher's Fundamental Theorem predicts that the heritability of a trait will decrease under directional selection, but Lloyd has provided us no reason to suppose that selection on female orgasm need have been directional in its pattern. Even if it were true that female orgasm were centered around a single strongly selected peak, it is far more likely that this peak would be the product of stabilizing selection rather than directional selection. The persistence of genetic variation (and thereby heritability) in such a scenario would depend on the effects of the genes themselves (e.g., is there heterosis? epistasis? antagonistic pleiotropy?). There is no simple answer to these questions, we have no knowledge whatever about the genes influencing female orgasm, and hence, it is impossible to make categorical statements about the likely heritability of the character after a history of selection.

If, as I think is a more likely scenario, there are alternative adaptive strategies toward female orgasm in humans, then it is not only likely, but necessary that the trait have substantial heritability. Unless offspring are similar to their parents, there is no sense in which alternative adaptive strategies can exist as adaptations (although under such circumstances they may well exist as cultural strategies without necessary genetic correlates).

"Species-wide adaptations"

Likewise, Lloyd's "fourth conclusion" confusingly states that "species-wide adaptations have heritabilities near zero." Remember that heritability is simply the proportion of phenotypic variance explained by genetic variance. Heritability may be near zero if phenotypic variance is high while genetic variance is very low. It may also be near zero if phenotypic variance is very low -- if the population just does not vary in the trait under consideration.

What does Lloyd mean by a "species-wide adaptation"? This is not clear to me, because her examples clearly are different in terms of variability. Humans today universally have language, and they universally have large brains (compared to, say, chimpanzees). But while the heritability of linguistic capacity is unknown, the heritability of brain size is very high in today's humans (> 0.9). Thus, it is desirable that we should be very careful in describing a trait as a "species-wide adaptation," at least if by this we mean to include some limit to the degree of potential heritability.

The example of language would seem to imply a discrete feature that differs categorically between species. A simpler example (that does not beg the question of ape linguistic capacity) is one of the human adaptations for obligate bipedality: an adducted big toe. Almost no humans have an opposable big toe; almost no chimpanzees have an adducted one. The distribution of variation of such traits nearly completely separates different species from each other, and within a species their heritability is near zero -- because their variation is near zero.

If this is the kind of trait Lloyd refers to, then it is true but trivial that such traits have heritabilities near zero. The fact that their phenotypic variance within a species is near zero allows no other conclusion. It is equally true that if we assert that female orgasm is a "species-wide adaptation" in the sense of being categorically absent from other species, then we must conclude that its heritability within humans as a categorical trait must be near zero.

But there is no reason to think that any aspect of female (or male) sexuality is a "species-wide adaptation" like an adducted big toe. As Lloyd's example of brain size makes clear, many species-typical adaptations have substantial within-species heritabilities. For example, humans have a high valgus angle, meaning the angle at the knee joint between the long axes of the femur and tibia. This angle facilitates bipedal locomotion by placing the tibia beneath the body's center of gravity during single-legged stance. This trait is clearly species-typical: human femora can easily be differentiated from chimpanzee femora by the valgus angle. But at the same time, the valgus angle itself is variable within humans. That is to say, the distribution of this continuous variable both separates humans from chimpanzees and distinguishes humans from each other. Within humans, much of the phenotypic variance is explained by underlying genetic factors, through the phenotypic correlations with other traits, such as stature, leg length, and pelvis width. Thus, this human-specific trait is moderately heritable within humans.

Human-specific traits in which alternative strategies underlie variation likewise are extensively heritable. As a case in point, human intelligence is substantially different from intelligence in any other hominoid species. Although some (hypothetical) measurement of intelligence might show some slim overlap between humans and chimpanzees in its distribution, the mean values of the two species are so different that they defy scaling. Even so, intelligence is both substantially variable in humans and substantially heritable. This heritability of intelligence may have many causes, but one of them must be the fact that intelligence itself comprises many different mental abilities that each have separate adaptive consequences. It is widely believed that such adaptive variation may in part predispose people to differing behavioral strategies, including variation in personality.

I tend to think this is not very far from the mode of evolution of human sexuality. Dunn et al. (2005:3) in fact consider mental factors as potential behavioral mediators:

Other potentially imoprtant biological factors include androgen levels or receptors, or natural variations in pleasure centres in the brain, resulting from dopamine or other psychological mood effects. All of these processes are probably mediated to some extent by genetic variations. Other associated factors, such as differences between individuals in anxiety and depression, also have heritable components and may partly contribute to the genetic component of orgasmic ability reported here.

It seems shortsighted to consider the evolution of female sexuality in isolation from the complex neurological factors that mediate female social behavior. A low frequency of orgasm during masturbation has little meaning as an adaptive character. The response to social situations, nonsexual interactions with female peers and potential male -- and female -- sexual partners, and long-term stresses must be considered in a full account of the biology of sexuality. The story does not begin or end at the clitoris, but must ultimately focus on the human as a psychological whole.

After all, the first lesson in health class is that the most important sexual organ is the one between the ears.

UPDATE 6/10/05: Elisabeth Lloyd has been kind enough to comment on this post in the comments to her original post on the subject. This has cleared up much confusion, particularly concerning the state of adaptive hypotheses for female orgasm.

Apparently, although I would never have guessed it, my hypothesis of multiple alternative strategies is novel. It seemed almost too obvious to be worth posting to me, since most of my recent thinking has been about brain evolution where these kinds of alternative strategies are common parlance. If you are a scientist reading this, take note: this is one of the great advantages of blogging, since what seems obvious to you may not be so to someone in a different field, and vice-versa.

In her comment, Lloyd acknowledges my point that only directional selection necessarily reduces heritability, but informs us that adaptive hypotheses concerning female orgasm have been framed exclusively assuming directional selection. In this case, her arguments certainly do apply to those hypotheses. This is one of the drawbacks of contemporary adaptationism that is not included in Gould and Lewontin's classic essay, "The Spandrels of San Marco": the frequent assumption that adaptations are the result of directional selection rather than other patterns. It is also a frequent confusion as applied to Sewall Wright's concept of adaptive peaks, which are not maintained by direcional selection, nor are they necessarily reached by it.

At any rate, as I mention above, I scarcely think the hypothesis of alternative strategies is testable. By introducing the possibility of many additional parameters, the hypothesis conceivably may be consistent with almost any distribution of orgasm incidence or facility. The important question is whether the hypothesized strategies may be biologically justifiable, and this will necessarily remain an impossible question to answer as long as the other behavioral correlates of such strategies are unknown. Lloyd's comment points out the problems with some such strategies as applied to the evidence. This is a bouncing ball in a sense: whenever one strategy is demonstrated to be biologically problematic, one might still propose a different set of strategies that would be commensurate with the same observations. At some point this becomes a reductio ad absurdum, but there is little chance that even the first level of two contrasting adaptive strategies can be tested with data now available.

Also note, that the more we consider correlates of female orgasm, the more we approach a non-adaptive hypothesis. That is to say, if female orgasm depends for its frequency, pattern, and existence upon other psychological or behavioral qualities, then it is possibly much simpler to argue that it is selection upon these qualities rather than orgasm itself that has shaped its distribution.

So again, this is a very much more interesting evolutionary problem than at first it might appear, and very intimately connected to the evolutionary history of the human mind.

Many thanks to Elisabeth Lloyd for her gracious and thoughtful comment. I'll never snark about orgasm-blogging again!

References:

Dunn KM, Cherkas LF and Spector TD. 2005. Genetic influences on variation in female orgasmic function: a twin study. Biol Lett (advance online). Royal Society Publications online

National Geographic News is running an interview with space scientists Seth Shostak and Bruce Betts on whether the extraterrestrial worlds in the Star Wars films are realistic. In many respects, it turns out to be more a question of biology and (gasp!) extraterrestrial anthropology than geology or physics.

For example, Shostak says:

What we might complain about is that so many of the galactic sentients [intelligent life-forms] seem determined to live on planets. Truly advanced life is likely to build its own habitats, and escape the limited area and resources of a planet. In Star Wars, it seems that only Monsieur Vader has figured this out, building his own artificial habitat, appealingly monikered the Death Star, even though it's not a star at all. But "Death Space Habitat" doesn't have as nice a ring to it.

Aside from the spoiler questions (how do all those planets have the same oxygen level, anyway?), Bett and Shostak consider the makeup of a galactic empire:

[I]t all seems unlikely, because the various inhabitants, many of which are biological, will have evolved at different times. Consequently, the top species will be many millennia ahead of the number two species, in terms of evolution, and millions and billions of years ahead of your average intelligent species. They won't want to share drinks with them in a Mos Eisley cantina.

But we need them there, to show us how Ardipithecus walked!

Much interesting consideration of the ecological makeup of different planets and whether they would be likely to occur.

But why, oh why did they have to go here:

NG News: What about Naboo, for example, the home planet of Queen Amidala? It's an idyllic world (see picture) populated by peaceful humans and an indigenous species of intelligent amphibians, the Gungans.

Shostak: We have rather few examples of two or more intelligent species simultaneously sharing a planet, but it has happened. The Neanderthals coexisted with Homo sapiens for millennia. So maybe it's possible to share, as long as neither species has the technology to obliterate, enslave, or merely cook and eat each other.

Jar-Jar a Neandertal? In the words of Darth Vader, "Nooooooooooooo!"