Link to review: The wisdom of Seinfeld.
February 8, 2011
Link to review: The wisdom of Seinfeld.
February 4, 2011
January 5, 2011
I approached Sheril Kirshenbaum’s The Science of Kissing: What Our Lips Are Telling Us with some trepidation and excitement. The former is a consequence of my hypochondria and its associated germophobia. I have no aversion to kissing in my own life (apologies for divulging personal information), but I did have some worries about having to read about other humans engaged in such an act of hygienic daring. And yet I was excited because I am interested in multidisciplinary explorations of human behavior. And of course I was familiar with the author’s oeuvre, and was expecting an engaging and wide-ranging exploration of the topic at hand.
I was not disappointed. The Science of Kissing is an intellectual full-court press; every conceivable discipline of relevance is brought into the mix. History, ethnography, ethology, neuroscience, evolutionary biology, physiology, and epidemiology, all receive attention, to name just a few of the more prominent lenses which the author fits over the course of the narrative. In other words you’re presented with an intellectual buffet. A well rounded meal will require you to sample widely, but if the lack of punctiliousness of Romans in matters of hygiene is not to your taste, you may find a discussion of the latest neuroimaging techniques and their application to matters of behavioral response more to your liking.
After the first chapter one immediately perceives that The Science of Kissing is not a tight and narrowly argued case for a positive hypothesis. Rather, it is more synoptic. Of broad scope, and yet rather tentative in its conclusions. The author makes clear in The Science of Kissing that this stance of humility of what we know is the position which is warranted by the science as it is now: the science of kissing is immature at best. In fact, this reality seems to have been one of the prods for the author’s project. Her own curiosity as to the lack of a general and accessible entry into the literature, provisional as it is, turned into the opportunity to transform her own journey of discovery into a book-length exposition.
Each chapter in The Science of Kissing is rather concise, but they are bracketed into three thematic portions. First, there is an exploration of the ultimate roots of kissing. That is, why? Naturally this entails a historical perspective, both human and natural. This is where the author immediately abdicates any pretense at making a forceful and tight argument which brooks no ambiguity or uncertainty. A book about the science of kissing might plausibly begin by asserting that the phenomenon is a human universal. No, not exactly. The author reviews a diverse range of contemporary and ancient ethnographic reports which indicate a wide variety of cultural attitudes toward kissing and its substitutes.They are often amusing, and it must be said, occasionally kinky. I have admit that the idea of foreplay not including kissing struck me as profoundly alien, but it was a reality check on the presuppositions that we bring to expectations of the plausible range of human behaviors. On the other hand, the deviations from kissing do seem to share general features with the behavior, whether it be an attention to the face or violation of norms of personal space. For example many substitutes for kissing seem to involve a sort of sniffing of the other, and it could be argued that kissing is one particular route to this general behavior of olfactory exchange. It is also notable that kissing can be found among other animals, for example the Bonobo chimpanzee.
As a social species there are a clear range of ultimate rationales for why kissing may emerge. A form of grooming, interpersonal communication, as well as ascertainment of genetic fitness. But as a complex behavior which is culturally modified and channelled the sum of human and natural historical evidence point to kissing as being a specific instantiation of a general phenomenon. Kissing seems to be on the way to becoming a human universal, but that may be a contingent fact of human history. In particular, the rise of European hegemony, and the acceptability of kissing in companionate relationships within this culture (though not exclusively within this culture, as evidenced by records of kissing in the Hebrew Bible and Hindu epics). But the contingency of the phenomenon of kissing does not entail that its emergence was arbitrary. Rather, the balance of evidence seems to suggest that kissing is a phenomenon which we humans are mildly disposed toward. Kissing exists in related taxa and has been independently practiced across disparate human societies. Ultimately kissing as a universal human phenomenon may not have been inevitable, but it was at least not improbable.
Next The Science of Kissing moves to the proximate: how the phenomenon expresses in a concrete sense. Here’s a chestnut of wisdom: men like sloppy kisses, while women do not. Another: men are much more likely to be willing to have sex with someone without kissing. The author was skeptical about the robustness of such results indicating strong sex differences, and so she decided to do a personal survey. To her surprise these sorts of sex differences were perfectly replicated in her own sample. This is where ultimate causes loom large: males and females have somewhat different sample spaces of possible reproductive strategies as a function of the number of offspring they may have. Women have about ~30 gestations available in their lives. Men on the other hand have a much higher upper bound on the number of offspring they can have via polygyny thanks to the surfeit of sperm. This tension is at the heart of much of evolutionary psychology, so the leveraging of this framework to explain sex differences in kissing seems to be on relatively solid ground.
But the differences between men and women are explored in more than just ultimate abstract causes. The Science of Kissing also delves into behavioral and cognitive neuroscience and genetics, exploring the possible links between chemistry and kissing. Earlier I noted that kissing may serve as a predictor of genetic fitness or compatibility. How? It may be an avenue by which potential mates can assess their long term compatibility, whether through pheromones, or modulation of hormones such as testosterone, oxytocin or epinephrine. Kissing in this telling may be one of the roads which leads to the Rome of pair bonding. This dovetails well with the model where kissing is one of a set of probable behavioral phenomena to facilitate necessary relations for reproductive fitness. The author is admittedly on tendentious ground in this section, but though many of the hypotheses may be falsified, it seems unlikely that all will be.
And then we move to “cooties.” Needless to say this was the chapter which discomfited me the most. And yet the lessons here are rather plain and straightforward. Follow your dentist’s advice. Those of you engaged in promiscuous polyamory may have to worry a bit more than those of us who are not so engaged. And that vampire fad? Don’t get too into biting fetishes unless you want to risk your mortality. Don’t French kiss wild animals. Seriously.
The final in depth section is perhaps one of the more peculiar, and praiseworthy, aspects of The Science of Kissing. Quite often popular science books are written by scientists who focus on their own research, scaffolded with extraneous “hooks” when necessary. If not, they are written by journalists who serve as tour guides to the world of science. Intellectual voyeurs. The author was not reviewing her own research, but she also deviated from the “outsider” viewer as well. She managed to obtain the collaboration of David Poeppel at NYU to perform a set of experiments utilizing magnetoencephalography (MEG). I won’t detail the experiments and their results, except to relay that the author had some “interesting” adventures with finding images of same sex kissing on Google Images. The Science of Kissing begins as a readable but rather conventional popular science book, if a touch on the cautious side. But through this survey of a real set of experiments inspired by the author’s curiosity in researching The Science of Kissing you get a taste of the excitement and possibilities of science as an enterprise and method, rather than a set of results and “facts.” To me this portion seems almost a challenge to the complacent preconceptions of the public as to what science is, as opposed to how science operates. Instead of an answer one is left with a series of questions.
The Science of Kissing tells its story with economy. The chapters are short and to the point. But quite often there is a density of fact which will satisfy. The qualified and nuanced take on many of the issues will appeal to the nerd, who yearns to dig between the layers of the scholarly strata. Quite often I found myself putting the book down to do further research on Wikipedia or Google Scholar. This is not a book which punches you in the face with a bold and explosive thesis. When it comes to human behavior and biology robust bold explosions are hard to come by, so I believe that this tack was the honest one. The author navigates deftly between the shoals of the “blank slate” model dominated by nearly arbitrary historical contingency and a naive genetic determinism which is hard to justify based on the empirical data.
In some ways kissing is something which has two faces. On the one hand most people would not deny its central integrity to our most personal relationships. It seems far more substantive a matter than whether you shake someone’s hand. And yet kissing may also seem a sliver of a window upon the broad expanse which is human nature. The Science of Kissing illustrates that this is not so; an exploration of the phenomenon of kissing allowed the author to shine a bright light on the gamut of the human sciences, from those which focus on the ultimate biological bases of behavior, to those which characterize its proximate manifestations. Perhaps it is the omnipresent and most personal of behaviors which may serve as the most representative windows upon how our biological inheritance interfaces with the environment in which we express our predispositions and needs. How about the science of laughing? Crying? Blinking? The possibilities are endless. But this was an excellent start.
Note: Also follow the author’s posts on the book.
December 6, 2010
Liberal Überblogger Matthew Yglesias, Pulling Back The Curtain on Human Behavior:
People sometimes seem to think that you could forestall a Gattaca-esque scenario of genetic transparency through privacy laws. But it seems to me that you’d actually need to go stronger, and not only guarantee the right to not have your genetic information disclosed. To prevent the emergence of a near-universal disclosure equilibrium in a world of cheap genetic profiling over the long run, you’d need to ban voluntary disclosure. The mere fact that you don’t want a potential partner to know your DRD4 profile will tell her all she needs to know about you.
Let’s grant the power of genomics to predict behavior in this way. Let’s also neglect the real problems of banning this sort of thing in a world of commoditized sequencing or typing.* I have some news for Matt & company, there’s already a much more powerful way to behavior genetic profile someone: look at their family. Indians have long known this. So the big short-medium term problem is that getting your hands on the biodata of anyone’s family members is one-click away….
Update: A commenter points out that Yglesias may have been advocating such a position to expose the absurdity of it. I wondered that too, but wasn’t sure and thought perhaps he was serious. In any case, I think the commenter makes good points, so I retract the charge. Though the bigger point obviously still stands.
* Unless Matt has Victorian values I assume he could anticipate that it wouldn’t be too hard to get “DNA” from a prospective partner. How exactly a ban would work when there are places overseas doing sequencing I have no idea. It isn’t as if biological material is never sent through the mail.
March 31, 2010
Below I note that sex matters when it comes to evolution, specifically in the case of how sexual reproduction forces the bits of the genome to be passed back and forth across sexes. In fact, the origin of sex is arguably the most important evolutionary question after the origin of species, and it remains one of the most active areas of research in evolutionary genetics. More specifically the existence of males, who do not bear offspring themselves but seem to be transient gene carriers is a major conundrum. But that’s not the main issue in this post. Let’s take the existence of males as a given. How do sex differences play out in evolutionary terms shaping other phenotypes? Consider Bateman’s principle:
Bateman’s principle is the theory that females almost always invest more energy into producing offspring than males, and therefore in most species females are a limiting resource over which the other sex will compete.
Female ova are energetically more expensive, and scarcer, than male sperm. Additionally, in mammals and other live-bearing species the female invests more time and energy after the point of fertilization but before the young exhibit any modicum of organismic independence (the seahorse being the exception). And, often the female is the “primary caregiver” in the case of species where the offspring require more care after birth. The logic of Bateman’s principle is so obvious when its premises are stated that it easily leads to a proliferation of numerous inferences, and many data are “explained” by its operation (in Mother Nature: Maternal Instincts and How They Shape the Human Species the biological anthroplogist Sarah Hrdy moots the complaint that the principle is applied rather too generously in the context of an important operationally monogamous primate, humans).
But the general behavioral point is rooted in realities of anatomy and life-history; in many dioecious species males and females exhibit a great deal of biological and behavioral dimorphism. But the direction and nature of dimorphism varies. Male gorillas and elephant seals are far larger than females of their kind, but among raptors females are larger. If evolution operated like Newtonian mechanics I assume we wouldn’t be theorizing about why species or sex existed at all, we’d all long ago have evolved toward perfectly adapted spherical cows floating in our own effluvium, a species which is a biosphere.
Going beyond what is skin deep, in humans it is often stated that males are less immunologically robust than females. Some argue that this is due to higher testosterone levels, which produce a weakened immune system. Amtoz Zahavi might argue that this is an illustration of the ‘handicap principle’. Only very robust males who are genetically superior can ‘afford’ the weakened immune system which high testosterone produces, in addition to the various secondary sexual characteristics beloved of film goers. Others would naturally suggest that male behavior is to blame. For example, perhaps males forage or wander about more, all the better to catch bugs, and they pay less attention to cleanliness.
But could there be a deeper evolutionary dynamic rooted in the differential behaviors implied from Bateman’s principle? A new paper in The Proceedings of the Royal Society explores this question with a mathematical model, The evolution of sex-specific immune defences:
Why do males and females often differ in their ability to cope with infection? Beyond physiological mechanisms, it has recently been proposed that life-history theory could explain immune differences from an adaptive point of view in relation to sex-specific reproductive strategies. However, a point often overlooked is that the benefits of immunity, and possibly the costs, depend not only on the host genotype but also on the presence and the phenotype of pathogens. To address this issue we developed an adaptive dynamic model that includes host–pathogen population dynamics and host sexual reproduction. Our model predicts that, although different reproductive strategies, following Bateman’s principle, are not enough to select for different levels of immunity, males and females respond differently to further changes in the characteristics of either sex. For example, if males are more exposed to infection than females (e.g. for behavioural reasons), it is possible to see them evolve lower immunocompetence than females. This and other counterintuitive results highlight the importance of ecological feedbacks in the evolution of immune defences. While this study focuses on sex-specific natural selection, it could easily be extended to include sexual selection and thus help to understand the interplay between the two processes.
The paper is Open Access, so you can read it for yourself. The formalism is heavy going, and the text makes it clear that they stuffed a lot of it into the supplements. You can basically “hum” through the formalism, but I thought I’d lay it out real quick, or at least major aspects.
This shows the birth rate of a given genotype contingent upon population density & proportions of males & females infected with a pathogen
These equations takes the first and nests them into an epidemiological framework which illustrates pathogen transmission (look at the first right hand term in the first two)
And these are the three models that they ran computations with
There are many symbols in those equations which aren’t obvious, and very difficult to keep track of. Here’s the table which shows what the symbols mean….
If you really want to understand the methods and derivations, as well how the details of how they computae evolutionarily stable strategies, you’ll have to go into the supplements. Let’s just assume that their findings are valid based on their premises.
- They assume no sexual selection
- They assume unlimited male gametes, so total reproductive skew where one male fertilizes all females is possible
- Fecundity is inversely correlated with population density
- Total population growth is ultimately dependent on females, they are the “rate limiting” sex
- Total population growth is proportional to density
- There is no acquired immunity
- There is no evolution of the pathogen in this model
Basically the model is exploring a quantitative trait which exhibits characteristics in relation to resistance of acquiring the pathogen and tolerance of it once the pathogen is acquired. In terms of the “three models,” the first is one where there is resistance to the pathogen, individuals recover from infection and decrease pathogen fitness. The second is one of tolerance, individuals are infected, but may still reproduce while infected. Note that the ability to resist or tolerate infection has a trade off, reduced lifespan (consider some forms of malaria resistance). The third model shows the trade off of tolerance and resistance.
The “pay off” of the paper is that they show that the male evolutionarily stable strategy (ESS), that is, a morph which can not be “invaded” by a mutation, may be one of reduced immune resistance in certain circumstances of high rates of infection. There is an exploration of varying rates of virulence, but there was no counterintuitive finding so I won’t cover that. In any case, here’s the figure:
The text is small, so to clarify:
1) The two panels on the top left are for model 1, and show variation in male and female recovery from infection left to right (resistance)
2) The two panels on the bottom left are for model 2, and show variation in male and female fecundity when infected left to right (tolerance)
3) The four panels on the right are for model 3, and show variation in recovery in the top two panels and fecundity in the bottom two, with male parameters varied on the left and female on the right
The vertical axis on all of the panels are male infection rate, the horizontal the female infection rate. Circled crosses (⊕) indicate regions (delimited by solid lines) where females evolve higher immunocompetence than males. The lighter shading indicates a higher value of the trait at ESS (recovery or fecundity). Note that the two top left panels show a peculiar pattern for males, the sort of counterintuitive finding which the model promises: when infection rates among males are very high their resistance levels drop. Why? The model is constructed so that resistance has a cost, and if they keep getting infected the cost is constant and there’s no benefit as they keep getting sick. In short it is better to breed actively for a short time and die than attempt to fight a losing battle against infection (I can think of possible explanations of behavior and biological resistance in high disease human societies right now). It is at medium levels of infection rates that males develop strong immune systems so that they recover. The bottom right portion of panel which shows variation in male resistance illustrates a trend where high female infection results in reduced immune state in males. Why? The argument is simple; female population drops due to disease result in a massive overall population drop and the epidemiological model is such that lower densities hinder pathogen transmission. So the cost for resistance becomes higher than the upside toward short-term promiscuous breeding in hopes of not catching the disease. Another point that is notable from the panels is that males seem to be more sensitive to variation in infection rates. This makes sense insofar as males exhibit a higher potential variance in reproductive outcomes because of the difference in behavior baked into the model (males have higher intrasexual competition).
One can say much more, as is said in the paper. Since you can read it yourself, I commend you to do so if you are curious. Rather, I would like a step back and ask: what does this “prove?” It does not prove anything, rather, this is a model with many assumptions which still manages to be quite gnarly on a first run through. It is though suggestive in joint consideration with empirical trends which have long been observed. Those empirical trends emerge out of particular dynamics and background parameters, and models can help us formalize and project abstractly around real concrete biological problems. The authors admit their model is simple, but they also assert that they’ve added layers of complexity which is necessary to understand the dynamics in the real world with any level of clarity. In the future they promise to add sexual selection, which I suspect will make a much bigger splash than this.
I’ll let them finish. From their conclusion:
We assessed the selective pressures on a subset of sex-specific traits (recovery rate, reproductive success during infection and lifespan) caused by arbitrary differences between males and females in infection rate or virulence (i.e. disease-induced death rate). In so doing, we covered a range of scenarios whereby sex-specific reproductive traits such as hormones and behaviour could plausibly affect the exposure to infection…r the severity of disease…First, we showed that changes in the traits of either sex affect the selective pressures on both sexes, either in the same or in opposite directions, depending on the ecological feedbacks. For example, an increase in male susceptibility (or exposure) to infection favours the spread of the pathogen in the whole population and therefore tends to select for higher resistance or tolerance in both sexes if the cost of immunity is constitutive. However, above a certain level of exposure, the benefit of rapid recovery in males decreases owing to constant reinfection (we assume no acquired immunity). This selects for lower resistance in males, ultimately leading to the counterintuitive situation where males with higher susceptibility or exposure to infection than females evolve lower immunocompetence…A similar pattern arises if the cost of immunity is facultative, in the form of a trade-off between rate of recovery and relative fecundity during infection (model (iii)): if males happen to be more susceptible (or exposed) to infection than females, they are predicted to evolve a longer infectious period balanced by higher sexual activity during infection than females.
Restif, O., & Amos, W. (2010). The evolution of sex-specific immune defences Proceedings of the Royal Society B: Biological Sciences DOI: 10.1098/rspb.2010.0188
March 17, 2010
Actively granting food to a companion is called pro-social behavior and is considered to be part of altruism. Recent findings show that some non-human primates behave pro-socially. However, pro-social behavior is not expected in despotic species, since the steep dominance hierarchy will hamper pro-sociality. We show that some despotic long-tailed macaques do grant others access to food. Moreover, their dominance hierarchy determines pro-social behavior in an unexpected way: high-ranking individuals grant, while low-ranking individuals withhold their partner access to food. Surprisingly, pro-social behavior is not used by subordinates to obtain benefits from dominants, but by dominants to emphasize their dominance position. Hence, Machiavellian macaques rule not through “fear above love”, but through “be feared when needed and loved when possible”.