"What jobs can't I do if I have Asperger's syndrome?"

That was a question posted on CNN.com's "Expert Q & A" today.

Luckily, the psychiatrist who answered it did not actually provide a list of jobs he thinks people with Asperger's (or any other form of autism, or any other kind of neurological difference) can't do as well as neurotypical people!

Instead, he told the person asking the question to follow her own heart:

You can do any type of job in the world that you are good at and that you enjoy. You shouldn't let a diagnosis of Asperger's syndrome hold you back from any type of employment you want to pursue. On the other hand, you shouldn't feel like you have to work in one type of job or another to meet other people's expectations.

I still thought it strange, and unfortunate, that someone would ask this question at all, and would presumably accept a list of proscribed professions, should one be put forth.

Then again, I can see how someone might come to think having Asperger's would bar them from whole categories of work, given how autism and Asperger's are usually talked about.

First, there's the negative aspect of it: the endless lists of things people with autism will never be able to do. The content of these lists will vary depending on your age of diagnosis, verbal ability and apparent intelligence, but we all hear them, from a wide variety of sources. Popular descriptions of autism --- particularly Asperger's --- also make it sound as if there's just no way in the world such a person could ever be, say, a marriage counselor, actor, nurse, schoolteacher, coach or any other job requiring "people skills".

You also hear this even in the positive treatments of Asperger's syndrome! So much of the "bright side of autism/Asperger's" literature out there focuses on stereotypical Aspie strengths, like "little-professor" pedantic immersion in particular subjects, logical thinking, precise language, spatial and mathematical virtuosity, and, probably the most commonly-cited one of all, computer proficiency.

These are all fine things, assuming one has them, but if you're an autistic person who can barely read a map, or who is regularly driven to tears trying to get your computer, or phone, or TV or whatever, to do what you want it to do, or who finds hirself quickly lost in overly technical discussions, you're probably not going to be terribly reassured by talk of how autistic people are just naturally whizzes at engineering or IT.

Quite probably, hearing that will just depress you even more.

So, with that hypothetical person (as well as the real person who posted the question on CNN.com) in mind, I am posting a list of non-stereotypical jobs held by at least one autistic person:

• Social worker (Australian blogger Linda Radfem)

Massage therapist (an Aspie male of my acquaintance does this)

Sailor (Clay Adams, at one point; as well as a different Aspie male of my acquaintance, before I met him)

Screenwriter/Playwright (yet another Aspie male of my acquaintance; Tyler Norman, who wrote and directed a movie called "Spud" just this year; David Mamet)

Fashion model (Heather Kuzmich)

Actor (Daryl Hannah; Dan Aykroyd; John Turturro)

Musician (Ladyhawke; Craig Nicholls of The Vines; Travis Meeks of Days of the New; Gary Numan; Hikari Oe; Heidi Mortensen)

Athlete (surfer Clay Marzo; marathoners Anthony Crudale, Andrew Bryant, Alex Bain and Jonathan Brunot)

Fiction writer (Caiseal Mor)

This Wikipedia page, and this somewhat recent post at Turner & Kowalski, gave me most of the people on my list, and also have a lot more I didn't include.

Patternicity, Agenticity and Autism

From what I've written on this blog so far on the subject of evolutionary psychology, you might infer that I think it's all just conventional wisdom dressed up in pseudoscientific technobabble and appeals to an evolutionary past cribbed from bad genre fiction.

While there is a lot of what passes for evolutionary psychology "research" that fits this description, I also think there are some worthwhile ideas coming out of this field, too.

The things that most intrigue me in evolutionary psychology are the explorations of the constraints that might have shaped human cognition, perception and decision-making, and how these constraints might work to encourage certain biases in human cognition, making our minds imperfect tools for grasping objective reality while at the same time doing extremely well at solving problems relevant to survival.

Anthropomorphism --- the tendency to see events, natural phenomena, animals, objects, and other nonhuman things in humanlike terms, i.e. attributing consciousness, feelings, intentions and personalities to things that may or may not have them --- is one of these biases.

Here's anthropology professor Stewart Elliott Guthrie's explanation of anthropomorphism from his chapter in the 2001 book Religion in Mind: Cognitive Perspectives on Religious Belief, Ritual, and Experience:

Theories of religion as anthropomorphism so far have failed largely because they fail to consider anthropomorphism in general. This is crucial because anthropomorphism is general, spanning all cultures and all domains (Thomson 1955 [1932]; Mitchell, Thomson and Miles 1997). It occurs spontaneously and regularly in the unconsidered experience of daily life, for instance when we hear a branch tapping at a window as someone attracting our attention, see a full garbage sack in an alley as a lurking figure, or look at a car from behind and see its headrests as the heads of occupants.

Anthropomorphism also occurs in the deliberate productions of the arts and sciences. In the sciences, it is anathema, yet as Nietzsche (1966, 316) writes, even scientists wrestle "for an understanding of the world as a humanlike thing." Indeed, they do so commonly (Liebert 1909; Kennedy 1992; Mitchell, Thompson and Miles 1997). Striking examples include Darwin's view of Nature as a stockbreeder (Young 1985); Lovelock's (1987) view of the Earth as Gaia, a living organism; and the "anthropic principle" of some physicists -- the idea that because a large number of physical properties of the universe must be just as they are for humans to exist, the existence of those properties, and of humans, can be no accident (Earman 1987).
...
[Art] combines human and non-human categories not spontaneously but self-consciously. But such art is only the tip of a cognitive iceberg, seen in the wake of conscious experience. It is a tiny fraction of an obscure whole, held up to the light of retrospect. Artists, like all of us, must encounter anthropomorphism before using it. This encounter is involuntary. It consists not in mixing cognitive categories, but in applying a template from one category to an ambiguity we later decide belongs to a different category. First we see an ambiguous shape in an alley as a person; then we think, "Oh! That's only a garbage can." It is only when we make this after-the-fact distinction that we speak of anthropomorphism. What powers religion, and what requires explanation, is this spontaneous tendency, not only in art but in all of life.

Scanning for signs of life, including signs of communication, begins early and appears intuitive and generalized. Carey and Spelke (1994, 176) note that infants "respond to objects that lack any clearly animate features (e.g., mobiles) as animate and social beings, if the behavior of those objects approximates the behavior of a responsive social agent." In a manner that parallels the Buddhist notion of karma, older children blame "illness on the victim himself or herself, rather than allow that it happened randomly, an explanation known as 'immanent justice'" (Gelman, Coley and Gottfried 1994, 345). Such interpretations apparently correspond to preconceptions that are early and powerful.

Animism is closely related to anthropomorphism and is equally widespread. Animism was first investigated experimentally by Piaget (1929), who found it universal among young children. Piaget's finding has been broadly replicated and, as Barrett notes in this volume, the dominant psychology of religion regarding concept development is still Piagetian. "A long tradition of work on animism shows that children extend psychological explanations to ... rivers, clouds and so forth" (Harris 1994, 308).

Other studies (Sheehan, Papalia-Finlay, and Hooper 1980-1981) find animism not only among children, but also among people of all ages. In addition to humans, nonhuman animals also seem to display animism. Birds peck at twigs resembling caterpillars (Hinton 1973), coyotes pounce on sticks resembling grasshoppers (Bekoff 1989), caribou avoid rockpiles resembling Inuit (American Museum of Natural History display), and chimpanzees direct threats against thunderstorms (Goodall 1992, 1994).

(I was especially intrigued by the last paragraph, about animals showing a bias towards treating ambiguous stimuli as if they were alive. That's interesting, and does add support to the idea that this is adaptive).

Several theorists have proposed evolutionary explanations for this phenomenon, most of them hinging on the relative risks and benefits of Type I (false positive) vs. Type II (false negative) errors. This reasoning is invoked to bolster claims that all sorts of quasi-related cognitive and perceptual phenomena (like patternicity, and its consciousness-seeking cousin, agenticity) might once have conferred evolutionary advantages on their possessors.

This review article (full text here) brings a long list of disparate-seeming phenomena --- among them "auditory looming," a perceptual illusion in which you hear sounds as coming from much closer to you than they actually are; superstititions; prejudices; phobias; anthropomorphism/animism; and believing that you are more in control of your fate than you really are --- together under the same vast explanatory umbrella: Error Management Theory.

Here's a description of error management theory written by the two of the idea's originators, David Buss and Martie Haselton, in this 2000 article in the Journal of Personality and Social Psychology (full text here)*:

When judgments are made under uncertainty, two general types of errors are possible --- false positives (Type I errors) and false negatives (Type II errors). A decision maker cannot simultaneously minimize both errors because decreasing the likelihood of one error necessarily increases the likelihood of the other (Green & Swets, 1966).

The costs of these two types of errors are rarely symmetrical. In scientific hypothesis testing, Type I errors are usually considered more costly than Type II errors. Scientists, therefore, typically bias their decision-making systems (e.g., inferential statistics) toward making Type II errors. Errors are also asymmetrical in warning devices like fire alarms, which are biased in the opposite direction. Missed detections (Type II errors) are more costly; therefore, the bias is toward making false alarms (Type I errors). Whenever the costs of errors are asymmetrical, humanly engineered systems should be built to be biased toward making less costly errors (Green & Swets, 1966). This bias might increase overall error rates, but it decreases overall cost.

According to error management theory (EMT; Haselton, Buss, & DeKay, 1998), decision-making adaptations have evolved through natural or sexual selection to commit predictable errors. Whenever there exists a recurrent cost asymmetry between two types of errors over the period of time in which selection fashions adaptations, they should be biased toward committing errors that are less costly. Because it is exceedingly unlikely that the two types of errors are ever identical in the recurrent costs associated with them, EMT predicts that human psychology will contain decision rules biased toward committing one type of error over another (also see Cosmides & Tooby, 1996; Nesse & Williams, 1998; Schlager, 1995; Searcy & Brenowitz, 1988; Tomarken, Mineka & Cook, 1989).

The logic of EMT extends to benefit asymmetries as well as cost asymmetries. Consider two types of correct inferences, hits and correct rejections. If the benefits associated with these two different correct inferences differ recurrently over evolutionary time, other things being equal, then selection will favor the reasoning strategy that is biased toward the more beneficial inference, even if it results in more errors overall. In cases where the costs of two different errors are the same, but the benefits are asymmetrical, the benefit asymmetry will be the driving selective force. In cases where the benefits of correct inferences are the same but the costs of errors are asymmetrical, the cost asymmetry will be the driving selective force. The key point of EMT is that selection will favor biased decision rules that produce more beneficial or less costly outcomes (relative to alternative decision rules), even if those biased rules produce more frequent errors.

And this (to go back to that review article I mentioned earlier) is how that general pattern plays out with respect to anthopomorphism in particular:

Guthrie (2001) [in the book chapter I quote an excerpt from above] used error management logic to explain one of the key features of religion --- animism. He proposed that in ambiguous circumstances to falsely assume that an intentional agent (e.g., another human) has caused some event is less costly than to miss this fact. Given that agents often have interests that compete with those of the perceiver, it is important to have a low threshold for inferring their presence. For example, if one encountered a collection of twigs arranged in an improbably neat array, Guthrie proposed that it would be better to entertain the thought that a human or other intentional agent was responsible for the arrangement --- and to increase one's vigilance to the possibility of the agent's presence --- than to casually ignore it. Guthrie (2001) and Atran and Norenzayan (in press) proposed that belief in gods may be a by-product of this adaptive bias. The proposed animacy bias is consistent with classic laboratory experiments conducted by Heider and Simmel (1944; see also Bloom & Veres, 1999). When participants view moving images of circles and squares, they find it difficult not to infer intentional states --- chasing, wanting and escaping. The tendency to infer intentional states in these stimulus arrays emerges early (age 4), and there is preliminary evidence of cross-cultural universality of the bias (in Germans and Amazonian Indians; Barrett, Todd, Miller, & Blythe, 2005), although its magnitude of expression may certainly be variable. Common features of religion across cultures (Atran & Norenzayan, 2004)are also consistent with a universal animacy bias.

So, according to this theory, our brains are biased in certain ways, not because these shortcuts were likeliest to conform to reality (they're not, and probably never were), but because the errors they tended to lead to were the least costly (and/or most beneficial) in terms of reproductive success. We err on the side of seeing patterns --- inferring direct relationships between co-occurring phenomena, for example --- because ancestral humans did not have the luxury of adopting a lifestyle of radical experimentation. We err on the side of seeing agents --- assuming that things happen because someone wanted them to happen, and took steps to ensure that they did --- because missing signs that another being (maybe a human, who might be friend or foe, or maybe a large and dangerous animal) is in the area is a much deadlier mistake to make than thinking someone is there when you're really alone.

(It's worth pointing out that this hypothesis, like many others in the field of evolutionary psychology, isn't directly falsifiable**. It can't be tested. How could it be, when the conditions it makes predictions about only existed millions of years ago?)

It's particularly interesting for me to read about the apparent universality of these biases --- agenticity, anthropomorphism, animism --- because I don't think I share them. Or, if I do, I think I have a much weaker tendency to use them.

When I think about how I understood things as a child, what sticks out to me is how impersonal, how inhuman, my world was. For most of my childhood, I made the exact opposite assumption from the one described above --- I wouldn't even necessarily think about other people in the room with me, whom I could see and hear, as intentional agents; instead, I perceived them as a cluster of different, separately-experienced phenomena that all emanated from the same source: color, movement, lots of different sounds. I perceived, but did not often draw inferences from what I perceived. Much of the time, I didn't even sort my perceptions based on where they came from. I still devote a lot more of my brainpower at any given moment to raw perception, since I cannot filter sensory input or selectively direct my attention, than I do to interpreting what I perceive. Often I will notice something, but only react to it some moments later, because it has taken me that long to transmute the raw sensory data into information.

When I would think to draw conclusions from what I saw, my conclusions tended to run in the opposite direction from what you'd expect given the human biases towards patternicity and agenticity. The world I perceived was a random, self-sufficient system. It wasn't built; it grew. (When I was little, I thought houses and roads were some kind of large plant that grew out of the ground; if you had told me people made them I would've been thunderstruck).

*This article applies EMT in a way I'm not entirely sure is valid; they make some pretty boilerplate ev-psych assumptions about optimal reproductive strategies for men and for women (and, presumably, all male and female mammals) without any regard for social organization. They seem to assume, like Enlightenment philosophers, that everyone is an island, and that the only possible deviation from this atomistic state is a monogamous marriage life partnership (however peppered with infidelities on the man's part) and nuclear family. I do not think this notion matches up very well with what we know about how modern-day hunter-gatherers, as well as our closest evolutionary kin, the great apes, live.

**Sometimes, even when a proposition isn't directly testable, it might have implications that are testable. I think this idea --- that people's minds are set up to see the world in terms of the actions of intentional agents, rather than in terms of random chance, because there is an evolutionary advantage to this bias --- is amenable to cross-species testing. If agenticity is such a useful cognitive shortcut, it would make sense for at least some other animals to have also developed it!

Commenting

Because I've been having a huge problem recently with spam comments showing up on old posts (and apparently I am not the only person this is happening to), I've decided to moderate comments on posts more than two weeks old.

I am not exactly happy with this development, since many of my old posts continue to get (legitimately) commented on, and I think having an unmoderated comment section works best for discussion purposes. I'm also not crazy about the additional work it will take for me to personally read and approve every comment. But that's less work than what I do now, which is to read them all (I get comments emailed to me), and then, if they are spam, look for the post they're attached to and delete them there.

So we'll see how this works. At present, the only comments I don't intend to approve are spam, so dissenting readers, please continue to comment. The mod queue is not there to weed you out.

I Wanna Be Sedated

(Cross-posted to Turner & Kowalski)

A few weeks ago, the German pharmaceutical company Boehringer Ingelheim completed a Phase III clinical trial (results of which were presented at the 12th Congress of the European Society for Sexual Medicine last month in Lyon, France) of a drug it hopes to market as a treatment for Hypoactive Sexual Desire Disorder in women.

The drug in question is flibanserin, which had been tested as an antidepressant in the 1990s and found not to be very effective. It has also been studied in animals, to test for anti-anxiety and anti-psychotic properties, but neither of those effects were demonstrated sufficiently to warrant any clinical trials in humans.

Flibanserin interacts with three major receptors in brain, nerve and blood-vessel tissue: first, there's the 5-HT-1A receptor (5-HT, or 5-hydroxytryptamine, being another name for serotonin), to which flibanserin binds with relatively high affinity. Though it exhibits a huge preference for this receptor in cloned tissue, it binds with about equal affinity to it and to the 5-HT-2A receptor in vivo. (See this review article for a detailed discussion of the pharmacology of flibanserin; I will attempt to summarize what I think is most relevant here).

Once it does bind to the 5-HT-1A receptor, flibanserin acts to boost its activity. This activity consists of setting the receptor's associated G proteins loose in the cell to block the production of cyclic AMP, a "second messenger" molecule that can go on to tell the cell to do all sorts of different things. (There's a cartoon illustration here of this process occurring in a neuron, with the anti-anxiety medication busiprone acting as the 5-HT-1A agonist. Though flibanserin acts a little differently than busiprone does --- it acts preferentially on somewhat different tissue types --- the general process within the cell is the same; the only difference would be where exactly it binds to the receptor, and what exact conformational changes it induces in the receptor to lead to the dissociation of the G proteins).

Though it might seem like blocking this receptor would cause the cell to do nothing, it's a bit more complicated than that. Due to the different ways in which different biological processes are regulated, the absence of a signal might activate some processes even as it suppresses others.

Some of the physiological processes which are activated by suppression of cyclic AMP (through the action of serotonin receptor 1A) include: peripheral vasodilation (i.e., dilating blood vessels throughout the body), which leads to both lower blood pressure and lower body temperature; stimulation of the vagus nerve, which causes the heart rate to slow; release of dopamine in the brain, which leads to, among other things, feelings of pleasure and satiety; faster, shallower breathing; release of norepinephrine in specific parts of the brain, which induces pupil constriction in the eyes; and reduction in extracellular levels of serotonin, glutamate and acetylcholine in the brain (the latter two of which are excitatory neurotransmitters that encourage neurons to fire; having less of them around will have a dampening effect on brain activity in general).

Flibanserin also acts on two other receptors: the aforementioned 5-HT receptor 2A, and the dopamine receptor D4.

It acts as an antagonist on 5-HT receptor 2A, binding to it and inhibiting its function. This is a somewhat complementary mechanism to its activation of 5-HT receptor 1A, since the latter receptor triggers an inhibitory cascade, while the former's action is excitatory --- i.e., rather than blocking cAMP synthesis, 5-HT receptor 2A, on ligand binding, stimulates it, leading to a variety of intracellular activities: in neurons, it leads them to fire, or to be more receptive to passing along electrical signals from adjacent neurons; in smooth muscle cells, it triggers contractions; in platelet cells, it leads them to clump together and speed up blood clotting and wound healing; through stimulation of the "pacemaker" neurons that control the heartbeat, it leads the heart to beat faster, and, through stimulation of neurons in the cortex (5-HT-2A receptors are particularly dense in sensory areas of the brain; according to Wikipedia, this receptor is a major target for a lot of powerful hallucinogenic drugs, like mescaline, psilocin and LSD), heighten sensory perception and sharpen learning, thought and emotion, particularly anxiety.

In short, both of the major pathways by which flibanserin affects the nervous system serve to slow down physiological processes, quiet the mind, and dull the senses. It's a sedative, as Borsini et al. make clear in the "Behavioral Effects" section of their review article on the "Pharmacology of Flibanserin":

Rats seem more sensitive than mice to the inhibitory effects of flibanserin on motor activity. In fact, reduced motor activity was observed at doses of 8 to 16 mg/kg, i.p. [intraperitoneally], in rats, and no reduction in motor activity was seen with doses up to 32 mg/kg, i.p., in mice. Flibanserin induced failure to grasp the wire in the traction test ... in 50% of mice at a dose of about 45 mg/kg, i.p., or 95 mg/kg, p.o. At 64 mg/kg, p.o., mice also displayed hypomotility and hypothermia. These effects were more pronounced at 128 mg/kg. At this high dose, the following additional alterations were also observed: reduced grip strength, ptosis [droopy eyelids] and head weaving, and occasional catalepsy.

Sedating effects were also apparent in the recently-released results of the clinical trials in humans, which Neuroskeptic summarizes here:

What about the side effects? There's a whole poster about them. 100 mg nightly caused 14% of patients to drop out [of the trial] due to side effects, vs. 7% of placebo - so 7% of people decided it wasn't worth it. It caused dizziness, nausea, fatigue, somnolence - and bizarrely, also insomnia. 50 mg daily was worse than 100 mg nightly, which suggests that taking this at night, rather than in the morning, is a good idea. But given what it's meant to treat, you'd want to do that anyway, right?

But this leads into my biggest problem with this data. It's obvious from the side effects data that the drug is a sedative - it makes you tired and sleepy. The animal data confirm this. It's much more likely to put you to sleep than it is to make you enjoy sex in any given month. Off the top of my head I suspect it's a sedative because it's a 5HT2A antagonist.

(Neuroskeptic also points out the cheesy names of individual trials --- the overall study was made up of several trials at different sites in North America and Europe, each one involving about five hundred participants, and each one named for a different kind of flower. DAHLIA, DAISY, VIOLET, and --- of course --- ORCHID. Subtle.)

Neuroskeptic also raises the point --- which I agree with --- that that flibanserin's mild aphrodisiac effect might be an artifact of its sedating effect. A sedative that's not so powerful it just knocks you out relaxes you, lowers your inhibitions:

Any sedative can increase sexual desire as anyone who has ever been to a bar will know. So whether this drug actually has an aphrodisiac effect, as opposed to just being a sleeping pill, is anyone's guess. To find out, you'd need to compare it to a sleeping pill, say, Valium. Or a couple glasses of wine. Until someone does that, we don't know if this drug is destined to be the next big thing or a big disappointment.

I can think of several possible instances in which that might be enough to dramatically improve someone's sex life. It might be that for women with vaginismus (a condition in which the vagina clenches and spasms, sometimes painfully, whenever anything enters it) who want to have penetrative sex but can't*, the sedating effect might allow us to relax enough to do that. Along similar lines, people who have PTSD from being raped, but who are now in a relationship they chose with a partner they trust, and genuinely want to have sex with, but who nevertheless find certain sex acts (or maybe even all sex acts) triggering, might want something to help minimize the reflexive physiological effects of their trauma. Finally, women who lose interest in sex in the context of a long-term relationship, which might well include shared spaces, shared responsibilities, and shared relationships with both/all partners' friends and relatives, might find this medication helpful in banishing everyday stresses that might otherwise kill the mood.

However, as both of those articles (as well as this one) indicate, a purely mechanical "fix" is only a good idea when the problem is also mechanical --- as in my first example, of the straight woman with vaginismus who wants to have penetrative sex but can't, because her vaginal muscles contract uncontrollably. (I would actually recommend this pill more wholeheartedly to people who are suffering from some kind of overarousal --- "arousal" here in the physiological sense, not the strictly sexual --- that actually interferes with sex, as in vaginismus, or an anxiety/overload problem, than I would to people whose libidos have greatly diminished over time for unknown reasons, because, while the latter group might be in just as much distress over their impoverished sex life, I am less confident a sedative would actually help them much in that department).

In some (most?) of the other cases, where an underlying problem in the woman's --- or the couple's --- life, like, say, an unequal distribution of household labor, leads her not to want as much sex with her partner because she's exhausted, angry, depressed, alienated or feeling unappreciated, no pill can correct that, and implying that any problems the relationship may have are the woman's fault because she's "frigid" or "wired wrong" or whatever seems to me like it would only aggravate any feelings of anger or alienation she might have.

This About Sexuality column spells out all the additional, not purely physiological factors that influence sexual desire:

Defining Sexual Desire

Sexual desire is not an easy thing to define, as even researchers involved in the flibanserin studies acknowledge. The model presented by BI [Boehringer Ingelheim] researchers involves breaking down desire into three elements, which include:

Drive, referring to spontaneous sexual interest that is somehow biological or hardwired (what this actually looks like is only a guess).

Belief & values, including social, cultural, ethnic, religious, and other factors that impact how often we might feel sexual desire, how intensely we feel it, and how comfortable we are with it.

Motivation, which considers all the psychological and interpersonal factors creating a willingness to be sexual and feel sexual desire.

The pitch from BI researchers is that while good treatments exist for low sexual desire caused by beliefs, values, and motivation, we don't have anything to treat the drive component (which they call the "biologic" component). They believe that flibanserin treats the drive component of sexual desire.

...

BI conducted several studies in North America and Europe involving over 5,000 pre-menopausal women who had been diagnosed with HSDD. In their publicity campaign, they focus on the North American studies (more on that below) and included just over 1,300 women. The average age was 35 and most of the women were married and the average length of relationships was over 10 years.

...

They haven't offered any rationale for why the drug produced statistically significant results in the "biologic" component in North America but not in Europe. I suspect the answer to that question may be messy as it would likely refer back to non-"biologic" elements of sexual desire, thus pointing out a problem with the premise of the research.

After the six month study there were participants who stopped taking the drug [and] reported that their sexual desire did not diminish. Whether this suggests that the drug is having a permanent effect on their brain chemistry, or that brain chemistry is not in fact a significant factor in most cases of low sexual desire remains to be explained.

Finally, I was interested to hear one of the researchers say that most women in the study reported that their low sexual desire crept up on them over a period of time. If, as the researchers argue, problems with low desire are drive related, hard-wired or biological, why would they appear slowly? Are they suggesting that there are precipitating factors influencing low sexual desire? If so, would effective treatment not want to address those factors before they go altering the brain chemistry of otherwise healthy women? One consideration in a low desire creep may be age, but these studies were of pre-menopausal women with an average age of 35.

Besides the brushing aside of interpersonal or environmental factors, like relationship difficulties, stress, or an unequal division of labor (whether inside the home, outside it or both), and the assumption that, in any heterosexual relationship where one partner wants sex a lot more than the other (and, of course, it's assumed that the "one partner" is male and the "other" female --- women with high levels of sexual desire and men with low levels are heavily stigmatized, and either ignored or pathologized in most discussions of sexual health), the third feminist qualm I have about a libido-boosting pill for women (and, specifically, this particular libido-boosting pill for women) relates to agency.

People who are socialized into a feminine role** in this culture are already bombarded, almost from birth, with lessons in objecthood. Our bodies, our time, our attention, our space --- none of these things are really seen as ours; they're all considered more or less public property, and the things we choose to do with them not important or legitimate in their own right. We learn to be passive, especially in the company of men. Whatever it is, he needs it more than you do. His needs, wants, ambitions, and dreams are real. What are yours?

In the face of this training, women learn to seriously second-guess their own wishes. For me, personally, this means that I set much higher minimum standards for "no" than I do for "yes." I have to be really, really averse to something to say "no" to it, while to say "yes," all I have to do is not have any serious qualms about it. Mildly ambivalent? That's a yes. Apathetic? A yes. Vague distaste that can't be explained or articulated? Yes again.

This is, of course, a very bad thing when the propositions being agreed to so dutifully, but with so little real enthusiasm or volition, involve doing fairly invasive things to one's body.

*This category, you can see in this comment thread at IBTP, does not include all women with vaginismus or vulvar pain. Many of the commenters there are perfectly happy with their penetration-free sex lives, or with their voluntary celibacy. This latter notion --- that there are people who either do not feel sexual desire, or who don't feel it particularly strongly and are more or less indifferent to sex, and that these states of being are perfectly healthy --- is still not shared by many people, as this asexual blogger demonstrates.

**Not all of whom grow up to be women

BBC Ouch! Article on Disability and Stalking

Lucy Sholl has an intriguing, but scary/disheartening, essay on BBC Ouch! about her experiences with men who seemed to be attracted to her because of her appearance of vulnerability. (Ms. Sholl has a physical disability that restricts her mobility, but is also an "invisible" disability in that she doesn't need a wheelchair, and doesn't always use a cane. So she's also had plenty of people telling her she's not really disabled, naturally).

She describes a long string of creepy, (much) older men who would latch onto her and try to court her, despite her not having shown any interest. They seemed to take her disability as an open invitation to disregard whatever boundaries she set: they'd mail her pornographic pictures with notes to her written on them, they'd ask her to be their girlfriend, their sex partner, their roommate, their wife --- even to move to their home country with them. They were all total strangers.

Here's an excerpt:

It's not that I'm complaining about the male attention; that would be an unwise thing for a single girl to do. But this type of man - the one who sends you running to the Oxford English Dictionary for the precise definition of 'stalker' - wasn't exactly what I was looking for. Despite my obvious reluctance, these men seemed sure that I was their ideal woman, as long as my personality didn't come into it. I was a blank canvas onto which they could project whatever odd, antiquated ideas they had about men and women. I was to be a romantic heroine from a Victorian novel, coughing blood into the occasional handkerchief while he, the melancholic hero, carried his burden bravely.

I suppose for a certain type of man, the idea of a disabled girlfriend carries a number of advantages. "Well," they think, "she'll always need me, she'll be grateful, and it'll be hard for her to run off with anybody else." Through friends, I also heard that a couple of men (30 years older than me, and of no fixed abode) thought that, while I'd be out of their league normally, they'd be in with a chance because of my disability. It seems your market value slips when you're
disabled, and going for a disabled woman means you'll be able to get one who's a bit prettier, cleverer and younger than you would otherwise. A win-win situation, really.

I can tell Ms. Sholl that she's not alone --- there is actually empirical research showing that disabled women are a lot likelier than their nondisabled counterparts to have male partners who espoused a philosophy of "patriarchal dominance," and that, going along with that, disabled women experience a lot more intimate-partner violence than nondisabled women do.

There really are men out there who specifically target vulnerable women, and it is often women with disabilities who end up in their sights.

Verbal Ability and Face Processing in Autism

One of the articles cited in my monster post from a couple days ago --- "Young children with Autism Spectrum Disorder look differently at positive versus negative emotional faces" (full text here) by Tessa C. J. de Wit, Terje Falck-Ytter, and Claes von Hofsten --- mentioned something I found really interesting, and certainly relevant to the continuing debate over what autism is, how to define it, and whether a coherent concept of "autism severity" exists, that I wanted to highlight, but wasn't really able to tie into the earlier post on face processing.

What they found that so intrigued me was that, when looking at photographs of emotionally expressive faces, autistic children with better social and communication skills spent more time looking at the mouth rather than the eyes:

Analyzing whether there was a negative relationship between the amount of social and communication impairment and the factors differentiating between the two groups [i.e., the autistic and control groups], we analyzed the correlation between z-transformed ADI-R scores and the looking time data for the group with ASD. As there was a high correlation between the social and communicative impairment scales of the ADI-R (r = .83, p < .01), we combined these into a single averaged z-score. This score correlated negatively with overall total looking time in the whole screen (r = -.76, p < .01, one-sided). Furthermore, there was a negative correlation between social/communication ADI-R score and percentage of looking time directed at the mouth (r = -.62, p < .05, one-sided).

In other words, the higher the children scored on measures of impairment in verbal communication and reciprocal social behavior, the less time they spent looking at the mouth.

This might seem counterintuitive, if you're used to thinking of autism in terms of poor eye contact and avoidance of strong social stimuli --- the children who were most strongly "autistic" according to their degree of social and communicative impairment were the ones who displayed the most "normal" pattern of face scanning.

I think that's interesting, and points toward the conclusion I came to in this earlier post: that there's not a straight line connecting an obviously "autistic" behavioral phenotype with any particular impairment.

The study authors hypothesize that the presence of verbal ability far in advance of social skills might bias an autistic person to look more at the mouth for social cues, because the mouth is the source of language, and a verbal autistic person might try to harness their language-processing skills to help them decode these social signals:

Contrary to what Klin et al. (2002) found for adolescents with ASD when watching complex social scenes involving conversation, we found less scanning of the mouth in the group with ASD. However, in agreement with Klin et al. (2002), we found that looking at the mouth is negatively related to the severity of social and communicative impairments (notably, Klin et al. (2002) only included social scales). Specifically, we found that the higher the social and communicative disability, the shorter the time spent looking at the mouth. Why did Klin et al. find more mouth looking in ASD while we find an opposite trend? Given that Klin et al. studied adolescents with autism that had severe socio-emotional problems but normal intelligence, one must assume they were quite verbal (the intelligence test used in Klin et al. study includes many verbal subtests). It would not be surprising if a sample of persons with ASD biased in this way looked preferentially at the mouth rather than the more emotional eyes in a complex social setting involving conversation (see also Adolphs et al., 2005). Notably, we included children at all symptom levels in our study, not only the high-functioning individuals. If our interpretation of the discrepancy between our findings and the findings of Klin et al. is correct, it predicts the direction of abnormality of mouth scanning. It is related to the balance of socio-emotive and verbal skills of the participants, where predominantly verbal individuals will be expected to look preferentially at the mouth. To test this hypothesis, the sample must be heterogeneous regarding these two symptom areas.

I think I should mention, also, that the two experiments being compared in this passage used very different kinds of stimuli; Klin et al. had their study participants watch clips from a film adaptation of Edward Albee's play "Who's Afraid of Virginia Woolf?", which naturally involved spoken dialogue as well as expressive faces, while de Wit et al. just showed a series of four still photographs of emotionally expressive faces.

(The presence of spoken language, whether in a movie or other video I'm watching or a real-life conversation, often leads me to look preferentially at the mouth of the person speaking, since I have difficulty understanding spoken language and find that reading a person's lips while also listening to their speech helps me understand it better. Maybe Klin et al.'s highly verbal autistic subjects have noticed the same thing).

One last thing: in the passage I quote from de Wit et al.'s discussion of their results, they use functional-level terminology uncritically, despite having produced evidence that somewhat perturbs that notion of an unbroken, internally-consistent hierarchy of greater to lesser autism severity. I have mentioned before that I am skeptical of functional levels as anything more than somewhat-tautological descriptors of IQ and language ability, and it is with this understanding (and also a desire to let the authors speak for themselves, even when I might not agree with them) that I have reproduced those terms here.

DEWIT, T., FALCKYTTER, T., & VONHOFSTEN, C. (2008). Young children with Autism Spectrum Disorder look differently at positive versus negative emotional faces Research in Autism Spectrum Disorders, 2 (4), 651-659 DOI: 10.1016/j.rasd.2008.01.004