"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

The Fusiform Face Area: Not a Site of Autistic Difference After All?

In a comment on one of my old posts, Amanda pointed me to this intriguing review article (full text here) questioning whether the widely-reported impairment of face processing in autistic people actually exists.

The authors review three different bodies of evidence having to do with face processing: behavioral studies (i.e., comparing autistic and neurotypical people's accuracy in identifying/distinguishing individual faces, or classifying facial expressions, from videos or photos; faces might be those of strangers, or of people known to the subjects, and might also be turned upside down or partially covered up in some experiments), electrical and magnetic evoked potential studies (i.e., doing EEGs or MEGs of people as they look at images of faces), and brain-imaging studies (doing fMRIs or PET scans of people as they look at images of faces).
The behavioral literature on how autistic people perceive faces shows that, though we are not necessarily any worse at identifying faces, or facial expressions*, we tend to go about it using different methods.

We look at different parts of the face: some studies --- like Joseph and Tanaka, 2003 (full text here); and Klin et al., 2002 --- find that we spend a lot more time looking at the lower parts of faces, particularly the mouth, while others --- among them van der Geest et al., 2002 (full text here); Dalton et al., 2005 (full text here); Lahaie et al., 2006 (full text here); Bar-Haim et al., 2006 (full text here) and de Wit et al., 2008 (full text here) --- find that we don't direct our gaze** to the lower face any more often than nonautistic people do. Some other studies have found that we attend to lots of different visual details --- both within the face and outside it --- that neurotypical subjects ignore.

Examples of studies finding a greater degree of attention to "irrelevant" visual details: Pelphrey et al. (full text here) found that the five*** autistic men they studied looked more often at "nonfeature areas of the face", like the hairline, chin, jawline, ear, temples, etc., while the five neurotypical men who served as a control group mostly looked at the triangle-shaped region in the center of the face, encompassing the eyes, nose and mouth. More recently, de Wit et al. also found this to be the case: their autistic subjects spent less time than controls did looking at either the eyes or the mouth --- about half of all their viewing was directed at areas of the face other than eyes, nose or mouth. Also, Dalton et al. found that, while the autistic young men they studied did not focus particularly on the mouth, or on any other particular feature, they definitely avoided the eyes.

Since Dalton et al. were monitoring brain activity along with gaze direction, they noticed intense activity in the amygdalae and orbitofrontal cortices of the autistic subjects whenever they focused on the eyes of the faces they were supposed to be looking at. This effect was totally absent in the nonautistic subjects, which led the authors to consider the possibility that maybe autistic people shy away from meeting people's eyes to spare themselves this nerve-wracking emotional stress:

Notably, the autistic group showed greater activation in the left amygdala and orbitofrontal gyrus than did the control group in response to the standardized emotional facial photographs, and greater right amygdala activation in response to the familiar and unfamiliar facial photographs. These are the areas associated with emotional processes, and these results suggest that processing of faces is associated with a heightened activation in affective central circuitry in autism. Together, these findings suggest that the increased activation in subjects with autism in the orbitofrontal cortex occurs specifically in response to the emotional content of the faces and not to faces in general, whereas activation in the amygdala is not specific to the emotional content of the faces but [is] a response to faces in general.

These findings indicate that the commonly reported hypoactivation in the fusiform gyrus during face processing in autism may be a function of how individuals with autism scan the face rather than a group difference in which area of the brain is used to process faces. ...
...
On the basis of these findings, we suggest that within the autistic group, eye fixation is associated with negatively valenced overarousal mediated by activation in limbic regions such as the amygdala. We propose that diminished gaze fixation within the autistic group may facilitate reduction of overarousal to social stimuli. According to this model, face-processing deficits in autism arise from hyperactivation in the central circuitry of emotion that produces hypersensitivity to social stimuli, leading to characteristic diminished gaze fixation, which in turn results in atypical activation of the fusiform gyrus. Additional studies including those involving direct measures of arousal (both self-reported and physiological) are warranted to further test this model.

This hypothesis --- that autistic people are actually hypersensitive, rather than oblivious, to the emotional content of faces, especially in the eyes --- gets some additional support from de Wit et al.'s main finding. They showed a group of autistic children and a group of typically developing children four photographs of faces --- two with "positive" emotional expressions (a calm face and a smiling face) and two with "negative" ones (a frightened face and an angry face) --- while tracking where the children directed their gaze. They found that both groups looked more at the eyes of the "negative" faces, which seems to me an indication that the autistic children were able to detect, and attend to, the socially threatening messages encoded in the angry and fearful faces. (However, the hyperarousal hypothesis does have some contradictory evidence in the findings of Pierce et al., 2004 --- they found no significant differences in amygdalar activity between autistic and nonautistic people looking at faces).

This 2006 article by Dirk Neumann, Michael Spezio, Joseph Piven and Ralph Adolphs, published in Social Cognitive and Affective Neuroscience (and not cited by Jemel, Mottron and Dawson), might help shed some light on the issue of whether or not, and in what contexts, autistic people rely on "looking you in the mouth" to decipher socially salient information: they found no differences whatsoever between their autistic and nonautistic subjects' gaze direction and accuracy at face-reading, except when they asked them to interpret images of faces that had been digitally obscured, making the task of identifying the emotion pictured very difficult.

We asked high-functioning subjects with autism to identify emotional facial expressions, a task people with autism often perform normally. In line with previous findings, we also observed normal accuracy and normal face gaze, provided that whole upright faces were used as the stimuli. When the difficulty of the task was increased and only sparse regions of a face were revealed using the bubbles technique, we still observed normal performance levels in the autism group. However, their gaze onto these sparse facial features became dramatically abnormal. People with autism looked more often and longer (autism, 27.3%; control, 8.7% of all saccades) at the mouth.

In other words, we can interpret faces one of two ways, one of which we are as good at using as nonautistic people are (i.e., the normal way, looking primarily at the eyes) and the other of which works even better, and seems to be autism-specific (i.e., looking primarily at the mouth). The study participants seemed to use the typical, eye-centered face-processing strategy as their default method, switching to the other only when the task became much more difficult, and the image from which they were to extract meaning very poorly visible.

(Fig. 4 from Neumann et al., 2006. Top image is of areas of gaze fixation for the "bubbled" images; bottom image is a graph of how much time autistic vs. nonautistic subjects spent looking at eyes vs. mouth on "bubbled" faces)

Here's what Neumann et al. have to say about their findings:

Our results are consistent with earlier findings that autism subjects are impaired when judging complex social information from the eyes, but not from the mouth (Baron-Cohen, 1995), and that they rely more on information from the mouth for emotional judgments (Spezio et al., 2006). The differences in attentional processing suggest a possible general mechanism for the neurodevelopmental progression of impaired face gaze in autism (Dawson et al., 2005). We failed to observe a deficit in using low-level visual saliency cues, or bottom-up attention, while we found differences in top-down modulation for saccades made to the mouth. We propose that this evidence is consistent with a neurodevelopmental progression that begins in infancy with a failure in directing attention to the faces and more specifically to the eyes in a face, along with preservation of bottom-up attentional processing. This is consistent with the major deficits in social engagement rather than in nonsocial areas when autism is evident in early infancy (Kanner, 1943). Reported signs of lower social engagement in infants with autism include less interest in people (Volkmar et al., 2005) and less looking at faces (Osterling et al., 2002). The abnormal top-down attentional processing of faces may be due to abnormal reward circuitry (Dawson et al., 2005) or to abnormal circuitry for emotional salience (Schultz, 2005). Over the course of development, via learning, top-down attention may cause the propensity for mouth gaze in autism. This hypothesized mechanism adds to previous hypotheses about the causes of deficits in top-down attention to the face, and draws on our findings that bottom-up attention to the face is normal in high-functioning people with autism.

Another possibility is that the bubbles stimuli reveal an impairment in how attention is directed to local vs. global features. In contrast to earlier reports, we observed a normal eye gaze to whole faces. This could also be due to a social training program most of our autism subjects participated in. Despite their overall normal gaze to whole faces, the sparse bubbles stimuli might reveal an underlying impairment in deploying attention to local (vs. global) features (Dakin and Frith, 2005).

Whatever the reasons may be for using one or another, it is certainly clear from these studies that autistic people have a wider range of face-perception strategies, the neuroanatomical correlates are unclear. So it seems to me that, unless a gaze-tracking apparatus is also used, and brain activity correlated to the part of the stimulus actually being viewed, as in Dalton et al. (2005), researchers hoping to pin down the neurophysiological underpinnings of autistic facial perception have no way of knowing that their experimental and control groups are actually doing the same task.

*Some of us are indeed "face-blind," or prosopagnosic. Prosopagnosia is not only seen in autistic people, though; it's a totally different phenomenon.

**You might be wondering how researchers can tell where their subjects are looking. There are several methods, but all the ones used in these studies seem to rely on some sort of head-mounted camera recording the infrared light that reflects off of a subject's corneas.

***The n for many of these studies is very small. I mentioned that for Pelphrey et al. (2002), n = 5; while that is the smallest sample size of any study I cite, most of the others aren't a whole lot bigger. Klin et al. (2002) have 15 autistic and 15 control subjects; Joseph and Tanaka have ~60 typically developing children and ~40 autistic ones; Neumann et al. have ten autistic subjects and ten NT ones; for van der Geest et al., the numbers are 16 autistic and 14 NT; Dalton et al. did two separate experiments, one involving eleven autistic subjects and twelve NT ones, the other involving 16 autistic subjects and 14 controls; Lahaie et al. have 16 autistic and 16 control subjects; and Bar-Haim et al. have twelve autistic and twelve typically developing subjects.

Dalton KM, Nacewicz BM, Johnstone T, Schaefer HS, Gernsbacher MA, Goldsmith HH, Alexander AL, & Davidson RJ (2005). Gaze fixation and the neural circuitry of face processing in autism. Nature neuroscience, 8 (4), 519-26 PMID: 15750588

Jemel, B., Mottron, L., & Dawson, M. (2006). Impaired Face Processing in Autism: Fact or Artifact? Journal of Autism and Developmental Disorders, 36 (1), 91-106 DOI: 10.1007/s10803-005-0050-5

Neumann D, Spezio ML, Piven J, & Adolphs R (2006). Looking you in the mouth: abnormal gaze in autism resulting from impaired top-down modulation of visual attention. Social cognitive and affective neuroscience, 1 (3), 194-202 PMID: 18985106

Pelphrey KA, Sasson NJ, Reznick JS, Paul G, Goldman BD, & Piven J (2002). Visual scanning of faces in autism. Journal of autism and developmental disorders, 32 (4), 249-61 PMID: 12199131

Neurodiversity-Themed Christmas Graphic by Kowalski

Kowalski has created this lovely holiday image (with one of my vintage magazine-illustration scans as a centerpiece --- yay teamwork!) in response to some of the more obnoxious autism- and other disability-awareness themed Christmas swag:

Why Are So Many Awesome Bloggers Named Amanda?

Seriously, it seems like a whole lot of wonderful feminist and disability-rights bloggers have that name.

There's Amanda Baggs, of course, autism/neurodiversity/anti-oppression blogger extraordinaire; she and Michelle Dawson were the first online writers I ever read, and if anybody can be said to have inspired me to do online writing, it's probably those two.

There's also Amanda Marcotte, whom I love for combining feminist blogging with atheism, skepticism and Bad-Science debunking; Amanda W. of Three Rivers Fog, whom I mostly read on FWD/Forward; Amanda Hess, who writes The Sexist; and now, most recently, I find Amanda Forest Vivian, an autistic American college student living in England, who wrote this amazing post* about an ABA school she interned at over a summer, where the staff were directed to try to stop students from stimming, or from being weird in the most harmless of ways:

...I started out thinking: wow, ABA is so cool. I've heard negative things about it from other Not Really Autistic people, but who am I to talk about what these Really Autistic kids need? They can't even talk. They might bite themselves or something. What the hell do I know about that?

And then I met Danny and the other kids in his class. High-functioning kids. Verbal kids.

Tony, who had been nonverbal a few years before, was incredibly hardworking and sweet. When he went into the school director's office and turned out the lights as a joke, I laughed, but she said, "Tony. Look at my face. How do you think that made me feel?" She stood there looking grim until he apologized.

James was stressed out and upset; one of his teachers leaned towards him, staring
fiercely into his eyes, talking with cold, strained-sounding words, the kind of voice I called "static" when I was a kid. James looked scaredly back at her, wriggling his hands around in his lap. "James," she said. "I know you're upset. But what you're doing with your hands looks silly." This boy, all the tension in him being channeled into something harmless, something she had to look under the table to see. His tension was silly. His discomfort was an inconvenience. He was eight or nine years old.

And Danny with his words. ...

Danny just liked words. When he was using his special words, the weird words he scrounged for or made up himself, he would find himself jerkily hopping across the room, speaking in a squeaky voice, his small face tense with excitement. "Presentation" was a weird word for movie, "document" was a way to talk about the letter he had typed on the computer for his parents. "I went to the barber," he said when I commented on his newly short hair, and then, with a rush of joy, "but I like to call it the hair shop!"

I like words, too. It was hard to watch Danny's teachers nudge him, sit down with him, say, "Danny, the word 'presentation' is a little weird; you need to say 'movie'." It was hard to watch the way they looked at him, pointedly, until he stilled his hopping and lowered his voice to a more standard pitch. When Danny found out my middle name is Wood, he completely tripped out on it, hammering pretend nails into my stomach and giggling, "I'm gonna build something out of you!" "Danny," a teacher said, "Don't be weird. You and Amanda were talking about names."
...
So from specific to general, from Danny to James and Tony, to Max and John. John's teacher made him walk, in stiff, clean steps, and if he started doing anything that looked like skipping or jumping, she grabbed his arm, said "No," forced him again and again. Max liked to move his arm in circles while he was watching TV, so he was hauled off into an office, pushed down into a chair, had mouthwash forced into his mouth until he cried. They told me they were narrowing it down, he was moving less and less. Max and John didn't talk. James and Tony didn't talk as well as I do. But I move too much, and I move wrong, especially when I was a kid, and in that school I saw what they do to kids who move wrong.

While I am not categorically anti-ABA --- I think it can be a valuable teaching tool, since it breaks down complicated tasks and skills into discrete, simple components --- that post (like this older post of Chaoticidealism's) does a great job of showing how some uses of ABA (yes, even without aversives) can be cruel and harmful.

In a Pedantic Linguistic Aside to this earlier post, I explain why I hate the common use of "learning" or "education" to describe methods that are essentially authoritarian in nature:

While the mental and behavioral adaptations people make to survive in a prison/institution environment ... might be called "learning," in the Skinnerian sense of that word, they also tend to sabotage a person's capacity for any other kind of learning. You get really good at surviving that hostile environment, but the price you pay is that you lose those parts of yourself that don't help you do that.

I think this also happens to kids in really intensive ABA programs. You lose initiative; you become afraid to try something before you've been told how to do it, because you're used to the teacher/therapist/whomever criticizing your attempts, telling you "No, that's wrong" whenever you do something that differs even a little bit from the response they're looking for.

So, I think that, since there is a significant cost to the kid who undergoes such training (in time if nothing else --- how're you supposed to have a childhood if you're in therapy for forty hours a week?), parents considering an ABA-based school or camp or other structured activity should ask themselves what their kid is likely to get out of it. Will they master important motor, executive, social, emotional or coping skills they've been having trouble picking up on their own? Will those skills help them become more independent (or, if you raise a skeptical eyebrow at the "independence" ideal, more productively interdependent)? Will your kid actually get something out of it that ze can use, or are you just hoping to make hir look more normal?

*Thank you, Sarah, for linking that post; I wouldn't have found it otherwise!

Health Care for All --- Except You, Lady!

On Sunday, the House of Representatives passed the Democrats' health-insurance reform bill, but not without some "collateral damage," to use Echidne's phrasing.

The bill that was passed contained an amendment, the Stupak-Pitts amendment (full text here), which would bar any government-sponsored health insurance from covering abortions. More than that, it would require any private insurance plans that might receive government subsidies, or be purchased by individuals receiving government subsidies, to strip abortion coverage from their publicly available plans, and put it into a separate category of coverage that people would have to buy for themselves (or get through their employer).

The amendment would remove all references to abortion coverage from the parts of the bill describing "Essential Benefits" (Title II, Subtitle C) --- i.e., coverage to be extended to everyone, whether directly through a government-run public insurance option or indirectly through government subsidies or exchange programs intended to make private or employer-based insurance more generally accessible --- and add this text at the end of Title II (Protections and Standards for Qualified Health Benefits Plans):

SEC. 264. LIMITATION ON ABORTION FUNDING.

a) IN GENERAL. --- No funds authorized under this Act (or an amendment made by this Act) may be used to pay for any abortion or to cover any part of the costs of any health plan that includes coverage of abortion, except in the case where a woman suffers from a physical disorder, physical injury, or physical illness that would, as certified by a physician, place the woman in danger of death unless an abortion is performed, including a life-endangering physical condition caused by or arising from the pregnancy itself, or unless the pregnancy is the results of an act of rape or incest.

b) CONSTRUCTION ON OPTION TO PURCHASE SEPARATE SUPPLEMENTAL COVERAGE OR PLAN. --- Nothing in this section shall be construed as prohibiting any non-federal entity (including an individual or a State or local government) from purchasing separate supplemental coverage for abortions for which funding is prohibited under this section, or a plan that includes coverage for such abortions, so long as ---

1. such coverage or plan is paid for entirely using only funds not authorized or appropriated by this Act; and
2. such coverage or plan is not purchased using matching funds required for a federally subsidized program, including a State's or locality's contribution of Medicaid matching funds.

c) CONSTRUCTION ON OPTION TO OFFER SEPARATE SUPPLEMENTAL COVERAGE OR PLAN. --- Notwithstanding section 303(b), nothing in this section shall restrict any [Qualified Health Benefit Plan] offering entity from offering separate supplemental coverage for abortions for which funding is prohibited under this section, or a plan that includes such abortions, so long as ---

1. premiums for such separate supplemental coverage or plan are paid for entirely with funds not not authorized or appropriated by this Act;
2. administrative costs and all services offered through such supplemental coverage or plan are paid for using only premiums collected for such coverage or plan; and
3. any nonfederal QHBP offering entity that offers a plan that includes coverage for abortions for which funding is prohibited under this section also offers a plan that is identical in every respect except that it does not cover abortions for which funding is prohibited under this section.

As Ezra Klein, Jodi Jacobson, and Jenn all point out, this will seriously aggravate the systemic inequality of access that already pervades both health care in general, and abortion and contraception in particular, in this country.

The Hyde amendment already barred women on Medicaid, women in (federal) prison, federal employees, and military personnel from receiving insurance coverage for abortion, and now the Stupak amendment will ensure that lots of other categories of women join them.

Robin Marty also points out that the amendment --- containing as it does such restrictive language surrounding when publicly-funded abortions are permissible --- could have the unintended consequence of forcing women who've miscarried to go through with their already-aborted pregnancies, because removing the dead fetus would technically be an abortion, and thus ineligible for public funding (or --- to reiterate, because I think this is the most invasive aspect of this law --- private funding by any insurance plan participating in a public insurance-exchange program or open to people receiving federal subsidies):

Hospitals and doctors in general do not have terminology to classify a difference between the termination of a live pregnancy and one in which the fetus has already died. To them, a D&C is a D&C, regardless of the state of the "conception materials" removed. Regardless of how many times I made sure to mention to the staff, either for the sake of my sanity or to spare me some sort of imagined shame, that I was ridding myself of my "dead fetus," to them it was all the same.

I also could not fail to notice the amendment's omission of mental illnesses from the list of acceptably serious health problems sufficient to justify terminating a pregnancy with federal assistance.

That omission is interesting to me, because pregnancies resulting from rape and incest are on the okay-to-abort list, even though such pregnancies may not be particularly dangerous or life-threatening. You might think that Rep. Stupak included those categories out of respect for the intense mental and emotional suffering a woman (or girl) is likely to feel, giving birth to her attacker's child, but then you wonder, if he really is so concerned about suffering, where's his consideration for women suffering suicidal depression, or terrifying psychotic breaks? Many psychiatric medications can't be taken during pregnancy, after all, and depression in particular can worsen dramatically as soon as the depressed pregnant woman gives birth.

Those incongruities suggest to me that either Rep. Stupak is really ill-informed about mental illness, pregnancy and women's health (which wouldn't surprise me --- Rep. Stupak is not a doctor), or he ascribes to the distressingly common, misogynistic view that women abort pregnancies on a whim, and that female sexuality, decoupled from marriage and socially-sanctioned procreation, is an inherently destabilizing force that must be contained.

If restricting abortion is not really about fetal life, but about female sexual agency, as Amanda Marcotte frequently --- and quite persuasively --- argues, then it makes sense that abortion bans almost always contain rape and/or incest exceptions. If the sex wasn't chosen, the woman isn't a threat; she's a pitiable victim. In the usual "elective abortion" narrative, a woman who chooses to have sex is obliged to accept the "consequences" of her decision --- i.e., pregnancy --- and any attempt by her to exert further control over her fate, say, by taking emergency contraception or, if she should become pregnant anyway, having an abortion, is an overreach; she sins, she cheats, she gets away with too much. Her impunity makes people nervous. The victim of rape or incest is not "overreaching" in this way; she's just trying to get back to normal.