Two Quick Links about Why the Fight over Evolution Matters

So, apparently Kevin Drum, a political commentator I don't read but who is apparently somewhat well-known, has written an article for Mother Jones declaring the fight over how whether biology is taught in public schools an irrelevant sideshow. 


I was nonplussed by this. Obviously, it's not the most important issue in the world --- it doesn't pose an existential threat the way climate change, peak oil/peak everything, overpopulation and hunger do, and it doesn't have the dire social consequences (or moral urgency) of, say, restricting access to contraception, the mass incarceration of people of color and poor people, increasing economic inequality or the deliberate demolition of the welfare state --- but I still felt like it had some importance that went beyond mere cultural border-policing*.


Amanda Marcotte at Pandagon and PZ Myers at Pharyngula both responded to Drum's article, and each of them made points that rang true for me, and helped explain why his statement bothered me.


Amanda:

I have to admit, I'm boggled at Kevin Drum's reaction to the news that nearly half of Americans are young Earth creationists ... . He completely misreads the situation and frankly does so in a way that I personally felt thrown under the bus.

... 

Kevin takes it as a given that fights over what's taught in high school are strictly about symbolism and have no real importance. I suspect that's a much easier view to take if you're the beneficiary of a good public school in a blue area or lucky enough to have gone through or been able to put your own kids through private school. For someone who went to a rural high school in Texas, the notion that high school doesn't matter strikes me as ridiculous in the extreme. 

The reason conservatives target high schools (and junior high schools and elementary schools) isn't because they're playing for peanuts. On the contrary, conservatives understand something liberals don't, which is that if you get people while they're young, you usually have them for life. This is also, incidentally, why conservatives pay more attention to pop culture than liberals. Liberals are great people --- I'm one of them! --- but  we have a tendency towards preening individualism and therefore discount the importance of things like what's in the classroom and what's on TV because we personally feel we're iconoclasts who aren't affected by it. Which can, in this case, cause us to neglect to remember that in fact this is the air that most people breathe, and the quality of that air matters. 

I also had strong feelings of no you're wrong when I read the paragraph in Drum's article where he dismisses "a 10th grade understanding of evolution" as something so piddling as to be dispensed with entirely, so much does it pale in comparison to the understanding of evolution one gets (presumably) in college, or in books on evolutionary biology. PZ, along with a slew of other biology professors in his comments and at Mother Jones, takes him to task for this; they write that, no, actually, they have noticed a change in how readily their students grasp what they have to teach. Almost as if high school curricula were geared toward preparing the students for college ... 


Anyway, what felt unfair to me was his assumption that, if people needed the knowledge, they could always pick it up elsewhere. This made me angry, because for many people there is no "elsewhere," or at least not one that is immediately accessible without guidance. 


(Who has tried to teach themselves a completely novel subject by checking out books on it from the library? Isn't it hard to figure out which books will be the ones you need? Technical books are often overly specific and assume you've already got a grounding in the subject, and are interested in exploring a particular question within it, and books for laypeople might not be thorough enough, and also might not be trustworthy). 


As for college, well, not everyone goes there, most of the people who go there will never encounter evolution in the classroom --- I didn't, and I majored in a biological science! --- and, again, college professors have enough to do without having to burn up lecture time with remedial material and correcting misinformation. Plus, not all colleges are created equal; some 


To top it off, what you know before college helps determine where you go, whether you go at all, and what you study! College is expensive, and for many prospective students (I know I felt this way when I was applying to colleges) the size of the scholarship you can get makes the decision for you. Scholarships for merit, as opposed to need (and there will always be more people who can't really afford college than there are people officially deemed too poor to afford college on their own), depend on how one performs on standardized tests. And what does standardized test performance depend on? What you learned in high school.


There's more: as Amanda also points out, what you're exposed to in high school shapes your interests and aspirations:

[M]y high school biology course didn't teach evolution. Without evolution, biology actually doesn't make sense, and instead it's just an anatomy class. ... I had no idea how fascinating biology actually was until I was an adult, and long past any chance of starting on that as a career path. Not that I think I would, but you can easily see someone like me making that choice as a young woman, but not really being able to because I was never offered that option in a realistic sense to begin with. 

(As someone who did study biology, and who loves Amanda's writing about science- and skepticism-related topics as much as I do her feminist writing, I can see it. Her interest in the subject is obvious, as is her commitment to find out what's true and how we know it's true. While she won't --- can't --- go into the kind of technical details I sometimes do here, her grasp of general, foundational principles is firm enough that I can easily forget she does not possess a biology degree herself.)


To shift to another aspect of why Drum's assessment is so horribly, horribly wrong, I quote PZ:

[T]his is going to be the century of dependence on the sciences. Climate change is going to hit us all; environmental crises are going to rise up all over the place; we're going to face shortages of energy and fresh water; emerging diseases will be a major concern; new biomedical technologies will cause cultural shocks; the whole world is going to change. Most people, I agree, will not be doing the research that leads to changes, and most of these problems will require political and social changes to correct, but how are you going to convince people to, for instance, change their fuel consumption habits when they're in complete denial of basic facts? How can you expect people to appreciate the importance of ecology and global interactions when you tell them that evolution doesn't matter? How will you get them to make rational decisions to control pandemics when they can't comprehend probability, epidemiology, and viral/bacterial evolution on even the most basic level? 

Most importantly, though, this utilitarian attitude that all that matters is what people can directly use in their day-to-day life is a denial of the Enlightenment and principles on which our country was founded. It's a rejection of the liberal idea that human beings should be well-rounded and informed individuals --- the informed citizenry that should be the foundation of a democracy. We can't expect everyone to be biologists or poets or political scientists, but we should expect that one outcome of a public education is an appreciation of the breadth of human endeavor, and at least a smattering of the fundamentals of a wide range of subjects, sufficient that, to make it practical again, students can make informed career decisions and understand a basic argument from evidence from an expert. We lack that now. And to wave away a simple but essential starting fact about our existence as unimportant is deeply offensive.     

I would add to his first paragraph that you don't have to wait for some futuristic nightmare scenario for these things to affect people's lives. Disease-causing bacteria are already becoming resistant to a whole lot of the antibiotics we use to fight them; lots and lots of species have disappeared or are disappearing; sensitive ecosystems are already being stressed, some to the breaking point by human activity, and humans are already failing to see why they should care***.

The picture he paints in that first paragraph has already come to pass, in the way that the proverbial camel is already in the tent, he just needs to take a few steps forward before it becomes obvious to everyone.

I would also add something else that I think denying evolution does: it makes it easier to think of humans as separate from, and above, the natural world and all those other animals. It allows us to think that what we do to it, to them, will never get back to us. 

(You don't have to deny evolution to get to that mindset, though: I see it arising just as readily from the erroneous view of evolution as a teleological process of development from simple to complex organisms, with humans sitting triumphantly at the apex. I've posted before about my annoyance with this picture of evolution.)

*This is what Andrew Sullivan, another famous political commentator whom I know to be obtuse, thanks to driftglass, an obscure political blogger who is quite acute**, has called belief in creationism a "cultural signifier" that describes the group membership of the believer rather than what that person actually believes about reality. That whole line of reasoning makes me queasy, but even if he is right that no one actually believes the Earth is six thousand years old and every animal species living on it was molded from clay and animated with the breath of a god, if that is what they decide shall be taught to children as fact, in place of the full history of life on Earth (as much of it as we know, anyway) and an explanation of how life on Earth has changed as Earth itself has changed, then those children grow up with a much poorer understanding of the world around them. An idea can have consequences in the real world whether people truly believe it or not; all they need to is act as if they believe it. Also, Andrew Sullivan is dumb.

**Hee. I made a geometry pun.

***This is not, at all, meant to be an exhaustive list, or even a primer on any of those subjects. I just put a recent news/research story in every link to make the point that, yes, this stuff is happening, and it's not just one or two isolated incidents. 

Born This Way

Some book I read a long time ago --- it may have been Steven Pinker's The Blank Slate --- maintained that, in the US, conventional wisdom has swung back and forth on whether differences between people that show up in adulthood have been present since birth, or whether they are acquired during childhood and adolescence.

It's usually intelligence that gets discussed in this way, almost always in the context of racist, sexist, or otherwise inequality-justifying theories about some groups being naturally smarter than others, but there's been a similar periodicity in thinking about other things, like personality traits. (Gender differences in cognitive style, interests, and personality are some of the things that are now widely believed to be present at birth; see Cordelia Fine's book Delusions of Gender for a lot more about these ideas' ubiquity and the still-ambiguous nature of the evidence they're supposed to be grounded in).

Right now, I want to talk about how this idea has gotten established in two different subcultures to which I belong: the autism community* and the gay community.

Autism and homosexuality have somewhat similar recent histories in US culture: both either are, or have been, considered mental disorders, both were thought in the 1950s and early '60s to be caused by some warping of the normal bond between mother and child (either, as with autism, too much distance between them, or with male homosexuality, not enough), and papers from the 1960s, '70s and '80s document various attempts to "treat," with aversion therapies that would now be considered abusive, children showing signs of either one. (One researcher even worked on both projects: O. Ivar Lovaas, who has done famous, if controversial, work adapting Applied Behavior Analysis (ABA) for use with autistic children, has also co-written several articles about "feminine boys," and using ABA to normalize their behavior).

Homosexuality was removed from the DSM in 1973, but there are still people who consider it (or anything deviating from straight, married monogamy, really) a pathological condition, and therapists who specialize in trying to turn gay people straight.

In contrast to that idea --- that gay people can change, and therefore should change --- the gay-rights movement has embraced the idea that sexual orientation is inborn. (And most mental-health professionals, including groups like the American Psychological Association, the American Psychiatric Association, the American Counseling Association, the National Association of Social Workers, and the American Medical Association, pretty much agree with them that no sexual orientation is inherently pathological, and that you can't change a person's sexual orientation through therapy).

The picture is somewhat different for autistic people. Not only is autism still considered a disease, and a pretty serious one, by almost everybody, but the idea of innateness, when it comes to autism, doesn't have the same implied corollary of "... and therefore you should accept us the way we are" that it has in reference to sexuality.

No, the shift from "psychogenic" to "biogenic" theories of autism happened for two reasons: first, and probably most important, the evidence (what little there was in the early '60s) didn't fit well with the psychogenic model**, and fit better with the biogenic one; another factor was activism by parents, who were fed up with being blamed for their children's condition, and who called for more research into potential biological causes.

Here, Boston University law professor Daniela Caruso, who has written an article on the history and legal impact of autism advocacy in the US, describes the relationship between the nascent field of biomedical research into autism and the beginnings of the US's major autism-advocacy groups:

It was only in 1964 that Bernard Rimland put forth an alternative explanation of the syndrome, based not on psychodynamics but rather on neurobiology. In 1965, Rimland founded the American Society for Autism (ASA) which is, to this day, a major center of advocacy.

Following Rimland's work, activism in the name of autism began to flourish thanks to both grassroots efforts and power houses. Some groups - most visibly Cure Autism Now (CAN) and the National Alliance for Autism Research (NAAR) - coalesced around genetic research and investigation of toxic substances potentially related to the surge of autism. It is no coincidence that such movements emerged in a context of burgeoning environmental activism. Many other capillary initiatives focused instead on the reality of living with autism by developing information centers for parents of newly diagnosed children, and starting awareness campaigns aimed at educating the public about this poorly-understood phenomenon.

(See also: this post, which discusses another article on the history of autism advocacy in the US. I also found another recent article about the role of parent activism throughout the history of autism, but I can't get at the full text of it).

I also found this snippet in Rimland's book itself (that part of it I could see on the Internet, anyway; I don't own the book), discussing why he thought so many researchers were reluctant to consider the possibility that autism had a biological basis:

In discussing the obvious prejudice against the hereditary viewpoint, Nolan Lewis (1954) points out, "It would seem that most of the prejudice against genetic inheritance stems from a feeling in the realm of wish fulfillment, based on the idea that acceptance of genetic factors would create an attitude of therapeutic hopelessness." Williams (1956) cites this point among others in his attempt to penetrate the prejudice against heredity. He notes that hopelessness is by no means justified by the evidence, and cites the ready correction of diabetes, phenylketonuria and hypothyroidism as examples.

So, that's kind of interesting --- that, at the outset, there was reluctance to adopt a conception of autism as innate and biologically based because of worries that that might mean it was impossible to eradicate through treatment --- but the answer to that wasn't, "so let's not try to make them non-autistic, let's just try to integrate them into society to the best of our, and their, ability", it was "don't be silly, of course we can make them non-autistic!"

I'd also want to point out that the two competing narratives of autism came from the same source: medical professionals, whether psychoanalysts or biomedical researchers. This is in contrast to the two competing narratives of homosexuality, one of which came from medical professionals and the other of which came straight (heh) from the people they were trying to describe. It wasn't until much later that autistic people's own viewpoints were even known to exist, much less taken into account by medical professionals and policymakers.

So, while as far as I know most autistic people do think they were born autistic, that idea doesn't have the same liberatory subtext for autism that it has for sexual orientation. (Indeed, the switch over to a mainstream view of autism as innate and biologically based had already happened when research into "extinguishing" autistic behaviors was at its peak.) The biggest thing it did was to free parents from guilt at having caused the autism, which is important and was definitely needed, but it left the position of the autistic people themselves unchanged.

*I'm using that phrase --- instead of "the autistic community" --- because I am mostly talking about parents. I've made this distinction before: the autism community, which includes parents/caregivers, healthcare workers, autism researchers, and educators; and the autistic community, which is the autistic people themselves. Sometimes the latter group is included in the former, but mostly it is not, and sometimes the two groups are at odds with each other.

**See Chapter 3 of Rimland's 1964 book, Infantile Autism, for a discussion of what those findings were and how they conflicted with the psychogenic model of autism.

Making the Genes Fit: Genetic Explanations for Autism and Their Political Implications

EXECUTIVE SUMMARY: Political-science professor Kristin Bumiller has written another long article on the politics of autism; while her earlier article focused on the neurodiversity movement, this article is mostly about mainstream autism advocacy in the vein of Autism Speaks. In it, she argues that mainstream discourse about autism assumes that autism is a genetic condition, and that this assumption is insufficiently backed by evidence. She spends most of the article detailing the political implications of this assumption, which are 1) funnelling most activism on the part of families of autistic people into relatively narrow channels of corporate-philanthropic fundraising for biomedical autism-research initiatives, rather than calling for broader social changes that might benefit autistic people; and 2) making disability an individual, rather than a social, issue.

She introduces several concepts over the course of developing those themes: "geneticization" --- a process by which the preferred explanation for sickness and disability is that some people are genetically susceptible to certain illnesses; "genetic citizenship" --- an ethic of individual responsibility for health, and for knowledge of one's genetic predispositions; and "life optimization" --- a strategy for making the most of one's (or one's child's) life chances given a certain set of genetic predispositions. She makes the case that the latter two of these things are logical responses to a genetic understanding of disease and disability in a "neoliberal welfare state" like the U.S., but also that they are inherently coercive and inegalitarian.
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Looking through the online archive of the women's-studies journal Signs, I found another article on autism by the political scientist Kristin Bumiller. (I did a series of three posts a while back about her 2008 article "Quirky Citizens: Autism, Gender and Reimagining Disability," which I thought made a lot of really good points). The more recent article, published in the summer 2009 issue of Signs, is called "The Geneticization of Autism: From New Reproductive Technologies to the Conception of Genetic Normalcy."

That odd word, "geneticization," gives you a clue as to the article's main premise: it implies treating autism as if it were genetic when it may or may not really be genetic.

Here is how Bumiller introduces the term and relates it to autism:

The term "geneticization" refers to the growth of genetics as a means to account for and explain health and disease and the process by which biological conditions constitute social definitions of normality and abnormality (Lippman 1991, 18). Abby Lippman coined this term in a feminist analysis of the growing influence of genetic determinism on public policies and private practices regarding pregnancy and health care and to emphasize the gender, race, and class implications of this trend. In particular, Lippman identified the need to study how genetic interventions affect health management in a variety of economic and social contexts. Feminist scholars have been wary of the coercive and normalizing power of medical professionals, yet they have also demonstrated the complex implications of biomedical advances. As Donna Haraway has persuasively argued, it makes little sense to be "simply oppositional" in response to this new technological future because we are deeply implicated in scientific progress (Haraway 1997, 3).

The shift in the autism field was first generated by the efforts of parents with autistic children, who were responding to regressive beliefs within the medical field. The scientific and popularized explanation for autism prior to the 1980s perpetuated a theory that pathological mothering was at the root of the disorder. Bruno Bettelheim (1979) is especially noted by critics for his view that childhood disturbances associated with autism did not arise spontaneously but resulted from extremely abnormal mother-child relations. Bettelheim's understanding of the condition is drawn from the seminal work of Leo Kanner (1943), who distinguished autism from schizophrenia as an innate or inborn disturbance of affective contact but also thought that the notable coldness and formality of the parents usually had some effect on the development of the condition. The hypothesis that autism can be attributed to a general lack of maternal warmth is called the "refrigerator mother" theory of autism, and it did not come under direct attack until Bernard Rimland criticized it in his 1964 book Infantile Autism: The Syndrome and Its Implication for a Neural Theory of Behavior. Both a parent of a child with autism and trained as a physician, Rimland undertook scientific work and activism that played a central role in recasting autism as a medical condition with distinct psychological symptoms that could potentially be remediated through diet and other therapies. In an era when parents of children with disabilities were beginning to organize and seek legitimacy, parents of autistic children embraced new biological explanations.

She goes on to describe a gradual narrowing of focus from "biological" explanations to specifically genetic ones, starting when researchers conducting twin studies found a strong pattern of heritability in autism. Later research identified a "broad autism phenotype" in parents and siblings of autistic children*, which added to the impression that it runs in families. But research into specific genes has failed to find much --- many candidate genes have been found, but each one only accounts for a tiny fraction of cases of autism. However, this review on the genetics of autism, published this month in Genetics in Medicine, estimates the total proportion of autistic people who have one of the genetic variations discovered so far at about 25%, which is actually a decent-sized chunk. Couple that with the relative newness of microarray-based comparative genomic hybridization --- the technique responsible for turning up a lot of these candidate genes --- and you see that it might be a bit premature to declare genetic research moribund**.

Kristin Bumiller thinks the continued assumption that autism must be a genetic condition has persisted beyond what the available evidence argues for, and that the idea that it may have environmental triggers is dismissed too readily. (I think the issue of whether the case for a genetic basis for autism is overstated or not is a bit more complicated; see above paragraph).

I do not argue with her assessment of the different political implications of genetic vs. environmental causes of developmental disability; if the former idea (i.e., that it's genetic) is widely believed, then each citizen is responsible for knowing hir own genetic status and making whatever reproductive choices follow from that status, while, if autism and other developmental disabilities are thought to be triggered by some environmental contaminant, then the responsibility falls to the government to enact stricter controls on neurotoxic pollutants. (Both of these scenarios presume a social context whose primary emphasis is on preventing, rather than accommodating, disability. In a less ableist society, deciding whether or not to have children if you're a carrier of [whatever] genes would be much less fraught with emotion and social pressures, although I think we'd want to limit pollution even if we weren't constantly told that developmental disability is a tragic waste of life).

Bumiller calls the individual-responsibility scenario "genetic citizenship": you become a member of a community of people affected by a given genetic disease, and that community advocates for research funding and participates in studies to help speed the development of cures or therapies:

The concept of genetic citizenship has been introduced to describe individuals in the age of biomedicalization who engage in a new style of activism related to their inheritable identities and differential embodiment (Heath, Rapp, and Taussig 2004). This concept is most frequently applied to situations in which individuals and family members affected by a genetic disease come together and take an active role in fundraising, advocating, and influencing scientists in the hope of finding a cure. In the past decade numerous disease-specific advocacy organizations have exercised significant influence over research priorities, affected capital allocation, sponsored gene banks, and demanded collaboration in the pursuit of real progress for people living with genetic diseases (Terry et al. 2007). This participation also takes advantage of new networking opportunities created by the Internet and the emergence of virtual communities. These citizens are seen as having cast off the role of passive patients to become active consumers of health services. As collectivities they have strived to maximize their influence on the development of new science, technology, and medical knowledge (Rose 2007, 23).

Autism advocacy provides an important vantage point from which to evaluate the presumed desirability of genetic citizenship because its activism is complicated by intense controversies about the significance of the genetic link and about the social identities of autistics. With the expansion of biomedical research in the field, much autism advocacy has shifted from promoting the well-being of affected families and children to searching for a cure. These new organizations, now consolidated under the banner of Autism Speaks, primarily promote biomedical research and are modeled on other fundraising campaigns that draw attention to the plight of people who suffer from rare diseases. ...
...
Prior studies of genetic citizenship have raised concerns about how the victories of new genetic movements may reflect a questionable convergence of individual interests and market forces and have noted how research priorities are driven by profit motives (Duster 2003a). Similar issues arise in the context of autism; much of this research is conducted in collaboration with high-profile genetic laboratories and large biotech corporations such as deCODE Genetics. This research is given priority despite uncertainty about whether and how genetic information will eventually be useful for pre- or postnatal genetic screening, diagnosis, or treatment methodologies. Both the irresolution about the potential benefits of genetic research and the oversimplifaction of its significance in the media diminish the power of consumers and the general public to either shift priorities or call for more transparency on the part of medical professionals. Moreover, the current focus on instrumental (and uncertain) goals rather than more broadly framed issues of social justice and welfare limits the role of disease-specific advocacy organizations in setting priorities (Stockdale 1999). Specifically in the case of autism awareness, it has been shown that since public discourse has focused on the medical paradigm --- particularly on efforts to find a cure --- there has been less focus on the rights and social welfare dimensions of the issue.

So there are good and bad things about this trend toward people organizing and cooperating with pharmaceutical and biotechnology companies to raise money and set research priorities. People are able to find other people --- whole communities of people --- who share their circumstances, and can thus pool their knowledge, resources and coping skills in ways they couldn't before, when each person essentially had to work everything out for hirself. That's a good thing; it's also a good thing that people affected by various conditions have a way to tell the scientific and medical communities what they need most.

What's not so good is the fact that the "partnership" between grassroots advocacy groups and corporations is so lopsided; this restricts disease-based activism to the corporate-philanthropic model of fundraising for biomedical research, when it might include that and campaigns for social changes geared toward creating a healthier society.

The other things Bumiller thinks are bad about the "genetic citizenship" model are its tendencies to coerce people into making certain health and reproductive choices, to exacerbate social and economic inequalities, and to put a heavy burden of responsibility on women as guardians of their families' health:

[D]isability activists have illuminated the implications of wide-scale genetic screening for the devaluing of disabled lives, particularly as the lines between state policy and individual choice are becoming increasingly blurred. Despite the well-established obligation of physicians and genetic counselors to provide nondirective advice, studies have found that patients were given information that imposes professionals' views about the usefulness of genetic knowledge and the parental responsibility to promote fetal health (Rapp 1999). This research has shown that professionals effectively delivered the message that the only rational choice is to give birth to a "normal" child. Genetic testing is now understood as a necessary component of preventative public health programs, largely as a result of the trend toward universalized testing and mandatory screening of newborns (van den Daele 2006). This shift has transformed prenatal testing from an option individual women are given to lower their risk of having a child with a genetic defect to a system of reducing overall health problems in the population (Ward 2002). ...
...
The research on prenatal counseling has also shown that professionals often frame genetic testing as necessary for socially responsible parenting. One study found that counselors presented prenatal testing as something women need in order to become good parents (Lippman 1991). In this sense, good parenting is about having the knowledge and resources provided by this testing and then following through in a socially responsible fashion. As genetic testing is fully incorporated as a standard of care for pregnant women, the act of refusal is no longer about the assumption of individual risk. Now, the noncompliant woman has failed to take advantage of an important opportunity to maximize the life chances of her child. Such actions are likely to be seen as contrary to good citizenship in an age of biopolitics, where the technologies of biomedicine have created a context in which "biology is not destiny, but opportunity" (Rose 2007, 51) and the desired course of action is to follow a strategy of life "optimization" (6). This strategy, according to Nikolas Rose, is "not eugenics but is shaped by forms of self-government imposed by the obligation of choice, the desire for self-fulfillment, and the wish of parents for the best lives for their children." He goes on to say that "its logics and its costs deserve analysis on their own terms" (69).

To see this as part of a new regime of choice is to fail to recognize the unintended consequences of life optimization in regard to the regulation of normalcy. A recent ethnographic study on the influence of new genetic knowledge on Belgian insurance companies aptly illustrates this dynamic at work. Ine Van Hoyweghen, Klasien Horstman, and Rita Schepers (2006) investigated how insurers take account of predictive medicine in the process of determining premiums. They describe the companies' decision making as a process of "making the normal deviant" because when insurers make judgments "the margin of being normal is actually quite small and the scope for deviation is quite wide" (Van Hoyweghen, Horstman, and Schepers 2006, 1229). They find that when insurers rate people with genetic predispositions they put extra emphasis on how they have managed their health. ... [I]nsurers impose a greater responsibility for optimally managing one's health on people with known risk factors. The authors' conclusions have serious implications for the social costs of life optimization: "Instead of a 'genetic determinism,' it seems more plausible that we are all subject to different levels of susceptibility. ... As a consequence, ... the individual's lifestyle habits, preventive initiatives and compliant behavior in relation to these susceptibilities could be stressed more" (Van Hoyweghen, Horstman, and Schepers 2006, 1233). The actuarial process imposes a norm that defines suitable lifestyles for people with risky genes. This creates an incentive system for genetic "deviants" to conform to normal expectations of proper lifestyles in order to satisfy social expectations.
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The concurrent forces of life optimization under conditions of biomedicalization and demands for personal responsibility in a neoliberal welfare regime make the determination of a disabled person's worthiness central to the process of gaining public health resources. The rights afforded to people with disabilities are more available to those who are good genetic citizens and can demonstrate their strict compliance with social norms. For example, special education provisions rely on eligibility and service determinations that are individualized and ad hoc rather than derived straightforwardly from medical diagnosis. As a consequence, parents with poor genetic literacy often have trouble convincing schools that their children's behavior is the result of a biological condition rather than their bad choices as parents. In social security disability determinations, each case is processed according to subjective criteria used to measure a person's ability to work. Studies show that success in claiming disability depends on a person's ability and willingness to persevere through the application process (Bilder and Mechanic 2003). Since most claims are routinely denied and these denials lead to a lengthy appeals process, only those who are unusually skilled at conveying medical knowledge, or at enlisting the assistance of medical professionals, are likely to have their applications eventually approved.

These systematic processes have the effect of distinguishing between disabled people who are at low risk and those who are at high risk for becoming dependent on the state. Social policies that rely on dividing people up according to risk groups also cut against the organic sense of solidarity that develops among people with disabilities (or among their advocates and caretakers). These systems of classification rely on distinctions that are often contrary to a dynamic and inclusive sense of citizenship among people with disabilities. The overall effect of a person's genetic status interacting with other forms of inequality is to create conditions of "cumulative social and economic disadvantage" and consequently to reduce opportunities to participate in civic life (Kelly 2002, 181).

I don't think Bumiller is endorsing any kind of conspiracy theory, or that she believes some secret cabal of biotechnology executives ever held a meeting and drew up a plan to seize control of the emerging wave of health activism. Similarly, I don't think she thinks doctors and genetic counselors are trying to "regulat[e] normalcy"; both of those things just happened, as new technologies and social movements were assimilated into a corporate-dominated, individualistic society. No human masterminds or conspiracies --- indeed, any planning or intention at all --- need ever be involved.

These are all the things I agreed with in Bumiller's article; there's also some stuff I have problems with (besides my differing assessment of the state of research into the genetics of autism), which I will write about in a later post.

Bumiller, K. (2009). The Geneticization of Autism: From New Reproductive Technologies to the Conception of Genetic Normalcy Signs: Journal of Women in Culture and Society, 34 (4), 875-899 DOI: 10.1086/597130


*Not everyone who studied relatives of autistic children found this broad autism phenotype --- this 1994 study of 44 families with multiple autistic children found that the non-autistic siblings did not display any noticeable autistic-like traits; "in the vast majority of cases, children [were] either clearly affected or clearly unaffected". But from what I can see, most of the studies published on this topic did find evidence of a broad autism phenotype, although positive results may be overrepresented among published papers just because positive results are more often published than negative results.

**You could still criticize it on other grounds, from the potential for eugenic applications of genetic research to the questionable wisdom of using limited research funds to pursue such theoretical questions ("Where does autism come from?") rather than finding out what works to improve autistic people's lives and enable them to participate in society to a greater extent.

New Open-Access E-Journal: Molecular Autism

While hunting around the Internet for autism-related research articles I might want to write about here, I found something really exciting: a free, totally open-access online journal dedicated to the molecular biology of autism.

Molecular Autism, from the look of it, was just started up this year. Its editors-in-chief are Joseph D. Buxbaum and Simon Baron-Cohen.

Here is their first editorial, a vision statement of sorts for Molecular Autism:

Molecular Autism joins other journals targeting autism and associated conditions but differs in key ways. First, Molecular Autism is both online and open access. In a field where dissemination of accurate information has become so important, where internationally, scientists, educators, clinicians, and families are tracking the developments and are looking for up-to-date, definitive and accessible sources of scientific information, Molecular Autism will provide such a forum. Open access means that the articles are freely available to all, worldwide, and at no cost to the reader. Online publication allows for no restriction on number or length of articles and for the inclusion of all available digital technologies: large data sets, unlimited use of color, slide shows, animation, video clips, and links to other web pages, all at no additional charge. Articles are published online on the day of acceptance and, very soon after, are listed in bibliographic databases and full-text article repositories. BioMed Central is a leader in online, open access journals ensuring that this mission will be seamless.
...
The second way in which Molecular Autism differs from other journals in the autism-science field is by having a focus on the molecular level. Whereas other journals have a broad remit, from clinical and educational psychological studies through cognitive experiments to neuroimaging and genetics, Molecular Autism will publish articles that have a bearing on the molecular basis of autism and related conditions. This does not preclude a behavioural or cognitive or neural study, so long as there is also a molecular measure in the study or the implications for the molecular basis of autism are considered. Our reason for this requirement is that part of our mission statement is to accelerate research into the fundamental determinants of the condition. The first 60 years of autism research have had a bias toward the psychological, and we intend - via this new journal - to correct this emphasis.

The third way in which Molecular Autism differs from other autism journals is that it aims to achieve integration across the multiple levels that these syndromes affect. We now recognize that autism will not be understood by a single discipline, be it genetics or neurology or psychology. Rather, each level has to be mapped on to the next, to reveal how mechanisms give rise to the phenotype within each system. This makes autism and related syndromes complex but the response to such a challenge has to be scientific articles that attempt to tackle such multi-level complexity.
...
We are in a transformative period in autism research. Behavioral interventions have been shown to be effective, and earlier diagnosis, using molecular and behavioral methods, becomes critical to take advantage of these interventions. In parallel, identification of etiological causes of autism has led to novel drug targets, and several large-scale clinical trials are being carried out based on these findings. We underline the important ethical issue that research into efficacy of medications should evaluate not only improvements in areas of known disability, but the lack of unwanted side effects (particularly ensuring that areas of strength in autism are not compromised). Molecular Autism will be at the forefront of these breakthroughs.

There's a lot in that editorial, and some of it (especially that last paragraph) needs unpacking.

First things first: I love, love, love free open-access journals. There's a persistent idea floating around that strong anti-science sentiment in public life is at least partially the fault of scientists themselves, who are terrible communicators walled off from the rest of the world in their insular academic and corporate R&D communities. Making the content of scientific journals freely available online to everyone* seems to me like a great way of letting the public in on what scientists are doing, although I do think it would be even better if articles could be (re)written for public consumption in more accessible language, with more detailed explanation of what individual data mean. (I understand that doing that requires a lot more work from scientists, who are very busy, though, and that if these articles were to be posted online for free, that work might well be uncompensated. I still think it would be an awesome thing to do, I'm just not sure how to make it a less onerous, thankless task for the researchers who'd be doing it).

I'm also very interested in the molecular mechanisms of autism --- I like biochemistry and molecular and cellular biology in general, and obviously I've got an existential interest in learning how my autistic nervous system differs from the standard model --- and not as interested in the fields of psychology and special education, which is where the bulk of autism-related research is being done. (Nothing against those fields, I just find molecular biology more interesting).

So, from a standpoint of pure intellectual curiosity, I'm tremendously glad there's an open-access journal dedicated to the molecular biology of autism. From a disability-rights standpoint, though, I worry about the implications of Molecular Autism's editors' stated ambition to shift the focus of autism research more onto molecular biology and away from psychology and education.

(Not that psychology and education haven't yielded some deeply problematic ideas about autism and methods to treat it --- psychology has given us both the mother-blaming "refrigerator mother" theory of autism and, more recently, the dehumanizing notion that autistic people can't feel empathy; and more educational, learning-theory approaches to autism tend to overemphasize the teaching of how to simulate "normal" behavior).

The trouble with mechanistic, biologically-based autism research, as Sarah discusses in this oldish post --- especially with research focusing on finding genes, biomarkers, or very early behavioral phenotypes characteristic of autism --- is that it's always done with an eye toward eradicating autism altogether.

No discussion of research into autism genetics can be complete without a discussion of the ethical issues of prenatal testing and screening for autism; no discussion of the neurophysiology of autism can be complete without addressing the risks and benefits (and who takes the risks, versus who reaps the benefits) of prescribing drugs to alter that neurophysiology; likewise, no discussion of early behavioral differences between autistic and non-autistic infants is complete without addressing the ethics of intensive normalization training, especially in terms of consent.

The last paragraph of the editorial I quoted does not acknowledge that there are any ethical issues with ABA (the "behavioral interventions" alluded to, which are to be implemented as early as possible), though they do tip their hat to the idea that forced drugging is problematic.

Another criticism of biological research into autism is that it won't improve quality of life for autistic people. I don't agree with this as much as I agree with the earlier criticism about ethics, and autism researchers too often ignoring the wishes, rights and concerns of actual autistic people; I think research into the neurobiology of autism has great potential to lead to better medications for neurological or psychiatric problems autistic people have. We are plagued by anxiety, depression, obsessions and compulsions, phobias, disabling sensory hypersensitivities, distortions or jumbling, and many of us have other problems, like seizures. Our autistic neurology is not always at the root of these problems, but it can certainly interfere with our attempts to treat them. If personalized medicine is the wave of the future, it makes sense that autism-specific drugs (even if those drugs are not *for* any aspect of autism) will be a part of that. Knowing how our nervous systems work, and how they differ from non-autistic people's, could lead to the development of drugs that will be more effective and less risky or loaded with unpleasant, unpredictable side effects in us.

So, while I don't want research into underlying causes of autism to be scrapped --- I want to know what autism is, on a genetic, cellular and molecular level, just as much as these researchers do; and also, I think the knowledge that molecular autism research yields might also yield drugs that could improve quality of life for some autistic people --- I would like to see active engagement with autistic people on the part of these researchers. I want autistic people weighing the ethics of various avenues of research, and I want their opinions published in Molecular Autism alongside the proposals for research they're critiquing.

*Everyone with a computer, Internet access, and the ability to read whatever language a given article is written in, that is --- and they're not all in English!

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

Drug Treatments for Autism: A Quick & Dirty History

A propos of this post at the New Republic, I've decided to do a timeline of all the different drug regimens that have been proposed --- and tested, usually on children --- as potential treatments for autism.

Autism, you were probably already aware, first came into existence as a diagnostic category in 1943, with Leo Kanner's paper "Autistic Disturbances of Affective Contact" in the journal Nervous Child*.

Kanner himself was convinced that his subjects' shared pattern of atypical development was a) a separate phenomenon from "childhood schizophrenia":

The combination of extreme autism ["autism" used here to refer only to that aloofness which makes up part of the developmental pattern being described, not --- yet --- as a name for the overall pattern itself], obsessiveness, stereotypy, and echolalia brings the total picture into relationship with some of the basic schizophrenic phenomena. ... But in spite of the remarkable similarities, the condition differs in many respects from all other known instances of childhood schizophrenia.

First of all, even in cases with the earliest recorded onset of schizophrenia, ... the histories specifically emphasize a more or less gradual change in the patients' behavior. The children in our group have all shown their extreme aloneness from the beginning of life, not responding to anything that comes to them from the outside world. ...

Second, our children are able to establish and maintain an excellent, purposeful, and "intelligent" relationship to objects that do not threaten to interfere with their aloneness, but are from the start anxiously and tensely impervious to people, with whom for a long time they do not have any kind of direct affective contact.

and b) inborn:

One other fact stands out prominently. In the whole group, there are very few really warmhearted fathers and mothers. For the most part, the parents, grandparents, and collaterals [???] are persons strongly preoccupied with abstractions of a scientific, literary, or artistic nature, and limited in genuine interest in people. ... The question arises whether or to what extent this fact has contributed to the condition of the children. The children's aloneness from the beginning of life makes it difficult to attribute the whole picture exclusively to the type of the early parental relations with our patients.

We must, then, assume that these children have come into the world with innate inability to form the usual, biologically provided affective contact with people, just as other children come into the world with innate physical or intellectual handicaps. ... [H]ere we seem to have pure-culture examples of inborn autistic disturbances of affective contact.

Disregarding Kanner's conclusions**, most psychiatrists of the time regarded autism (and schizophrenia, which was still seen as a closely related phenomenon) as a psychological response to family dynamics. Bruno Bettelheim, in particular, popularized the idea of the "refrigerator mother," which was to dominate both lay and professional understanding of autism through the 1950s, and into the '60s and '70s. By the '60s, however, some competing hypotheses had sprung up: There was Bernard Rimland's book Infantile Autism: The Syndrome and Its Implications for a Neural Theory of Behavior, which argued that autism, whether innate or not***, arose from biological rather than psychological causes, and there was Ole Ivar Lovaas, who pioneered the behavioral approach to autism --- i.e., it doesn't matter what causes it, as long as autistic children can be trained to emulate nonautistic ones.

At the same time, a number of drug therapies were being investigated, though with none too precise an idea of the mechanisms involved (see this 1942 article on the use of the powerful stimulant benzedrine in "neurotic" children displaying such eclectic symptoms as depression, "sexual tension," fear, anxiety, aggression, and "hyperkinesis"). The first drug treatment I'm aware of being proposed and tested specifically for autism is LSD (of all things!).

Here, from a 1962 study of the effects of LSD (and a similar compound, methysergide) on fourteen six- to ten-year-old children diagnosed with schizophrenia (but referred to in the article also as "autistic"), is the rationale:

[W]ith awareness of the current interest in LSD-25 as a therapeutic agent because of its psychotomimetic ["psychosis-mimicking," for you English speakers] properties, it occurred to us that LSD might be effective in breaking through the autistic defense, in chronically regressed, retarded, mute, and withdrawn children.
The theoretical interest in LSD as a serotonin inhibitor, with consideration of the possibility that serotonin is in some way related to schizophrenia, further justified this endeavor. Also, since LSD is an autonomic nervous system stimulant, it could be of particular value in treating schizophrenic children, in whom general tissue tone, especially the tone of the vascular system, and the pattern of the autonomic nervous system functions are impaired.

Since this first experiment with LSD was deemed a success, this avenue of research was pursued farther: another 1962 study of LSD in twelve "autistic schizophrenic" children; a larger study of "disturbed" children --- some autistic, some not; some verbal, some not --- coauthored by one of the authors of the study I quoted above; a pair of experiments on a set of very young autistic twin boys combining LSD dosage with a behavioral regime; and two reviews detailing a dozen or so other smallish studies were all published during the mid-1960s.

What was next? Well, in 1979 the Estonian-born neuroscientist Jaak Panksepp published "A Neurochemical Theory of Autism," in which he suggested that --- due to behavioral similarities between autistic children and animals dosed with morphine --- autism may be the external manifestation of an overactive endogenous-opioid system, and thus treatable with opiate antagonists like naltrexone or naloxone.

We recognized that much of the behaviour induced by low doses of narcotics was similar to the major symptoms of those autistic children who suffered disturbances of affective contact, as described by Kanner. Specifically, opiate-elicited symptoms corresponding to those observed in autistic children are as follows: (1) the opiate-treated animal does not appear to appreciate fully physical pain; (2) it does not cry as readily and spontaneously as normal animals; (3) it clings poorly; (4) it does not have a strong desire for social companionship; (5) it can show unusual learning effects characterized by extreme persistence of behaviour in the absence of external rewards (akin to the insistence on sameness by autistic children). The list of similarities suggests that the underlying neurochemical imbalance in autistic children may be excessive, or unusual, activity in their own endogenous brain opiate systems. Such a brain disturbance may block psychosocial development at its earliest stages - leading to failures in language acquisition and other idiosyncrasies in learning.

The opioid-excess theory, particularly its prediction that opiate antagonists would lead to more prosocial behavior in autistic patients, was tested in many, many small clinical trials throughout the 1980s and 1990s. Results of these have been uneven --- some found improvement, some found only modest, patchy improvement (particularly for decreasing self-injurious behaviors), some found no differences, and some actually found that patients taking naltrexone fared significantly worse than those on placebo. Overall, I'd call it a wash.

From the 1990s on, two trends have emerged as the dominant ones in pharmaceutical treatment of autism: antidepressants (specifically, SSRIs) and atypical antipsychotics. Here, too, effectiveness has been spotty, and the antipsychotics particularly can give rise to some truly nasty side effects. The rationale has shifted from seeking to correct any perceived underlying cause of autism (researchers are pretty sure they don't yet know what that would be) to trying to ameliorate some of the less pleasant things often associated with autism: anxiety, depression, obsessive-compulsive behaviors, self-injury, social withdrawal, hyperactivity, aggression and mood lability, among others.

(I also like how the thinking on serotonin's involvement in autism seems to have come full circle --- since the 1960s, higher levels of blood serotonin have been observed off and on in autistic people, and during the era of LSD experimentation, it was supposed that one of the ways LSD might act in a beneficial way for people with autism might be to tamp down this apparent overactivity of serotonin. Now, the approach toward serotonin is to make it more available for use in the brain, not less).

... Well, I guess I lied about the "quick" part of this Quick & Dirty History. Oh well. You win some, you lose some.

*Yes, I think that's a hilarious title for a medical journal.

**It must be pointed out that, even though he clearly states his belief that autism is probably innate, and biological, in origin, and though he often pooh-poohed Freudian notions of psychosexual development, Kanner was pretty ambiguous about this in his public pronouncements. He must have thought the interpersonal style of the autistic children's parents had some relevance, for he saw fit to emphasize it in this 1960 interview in Time magazine:

[T]here is one type of child to whom even Dr. Kanner cannot get close. All too often this child is the offspring of highly organized, professional parents, cold and rational --- the type that Dr. Kanner describes as "just happening to defrost enough to produce a child." The youngster is unable, because of regression or a failure in emotional development, to establish normal relations with his parents or other people.

Kanner then went on to write a second paper in 1949, "Problems of nosology and psychodynamics in early childhood autism," which did posit a role for "a genuine lack of maternal warmth" in causing autism. He seems to have been very much on the fence about the whole refrigerator-mother thing, evolving from believing autism to be innate, to suspecting maybe a chilly mother-child relationship might also be in play, to reiterating that autism is innate and hotly denying he ever suggested mothers might be to blame.

***Rimland later espoused the belief that vaccines could cause autism, so he clearly did not believe strongly that autism had to be genetic and inborn.