Determined, page 30
There were soon elaborations on the theory, and ones that could be vaguely considered to be liberal or humane—theoreticians in the psychodynamic fold broadened their thinking to include the possibility that a kid could be sufficiently screwed up to become schizophrenic thanks to being double-binded by the father. Nonetheless, the more general picture was of the father as passive and henpecked, culpable only insofar as he didn’t reign over that schizophrenogenic harpy of a wife loose in the house.
Things expanded even further outward with the possibility that the culprit was the entire family. By the 1970s, this “family systems” approach was embraced by the first wave of feminist psychiatrists, one proponent writing approvingly that “only recently have psychiatrists been talking about schizophrenogenic families.” Wow, progress.[19]
So What Is Actually Wrong?
Naturally, there is no empirical evidence whatsoever in support of schizophrenogenic mothering or any of its variants. Our modern understanding of schizophrenia bears no resemblance to these earlier Brothers Grimm fairy tales. We now know that schizophrenia is a neurodevelopmental disorder with strong genetic components. A great demonstration of this is the fact that if someone has the disease, their identical twin, who shares all their genes, has a 50 percent chance of having it as well (versus the usual 1–2 percent risk in the general population). The genetics of schizophrenia, however, are not about a single gene that has gone awry (as compared with classic single-gene disorders such as cystic fibrosis, Huntington’s disease, or sickle cell anemia). Instead, it arises from an unlucky combination of the variants of an array of genes, many of which are related to neurotransmission and brain development.[*] However, the collection of genes does not cause schizophrenia but, instead, increases the risk for it. This is implicit in flipping the finding just mentioned on its head—if someone has the disease, their identical twin has a 50 percent chance of not having it. In a classic gene/environment interaction, getting the disease basically requires a combination of the genetic vulnerability plus a stressful environment. What sort of stress? During fetal life, disease risk many years later is raised by prenatal malnutrition (for example, the Dutch Hunger Winter famine of 1944 greatly boosted the incidence of schizophrenia among individuals who had been fetuses at that time), exposure to any of a number of viruses by way of maternal infection, placental bleeding, maternal diabetes, or infection with the protozoan parasite Toxoplasma gondii.[*] Perinatal risk factors include premature birth, low birth weight and small head circumference, hypoxia during delivery, emergency C-section, and being born during winter months. Later during development, the risk is raised by psychosocial stressors such as loss of a parent to death, parental separation, early adolescent trauma, migration, and urban living.[20]
So the disease arises from genetic risk that leaves someone’s brain teetering on a cliff, coupled with a stressful environment that then pushes it over the edge. What abnormalities are in the brain after it’s been pushed off? The most dramatic and reliable one involves an excess of the neurotransmitter dopamine. This chemical messenger plays a role, particularly in the frontal cortex, in marking the salience of an event. Unexpected reward and we think, “Whoa, that’s great! What can I learn about what just happened to make it more likely to happen again?” Unexpected punishment, and it’s “Whoa, awful! What can I learn to make it less likely?” Dopamine is the mediator of the message “Pay attention; this is important.”[21]
The best evidence is that not only are dopamine levels elevated in schizophrenia but this is due to random bursts of its release. Producing random bursts of salience. For example, if you have schizophrenia and a pointless dump of dopamine just happens to occur when you are noting someone glancing at you, then, heavy with this faux feeling of significance in the glance, you conclude that they are monitoring you, reading your mind. Schizophrenia is a thought disorder of, as it’s termed, “aberrant salience.”[22]
Aberrant salience is thought to also contribute to another defining feature of the disease, namely the hallucinations. Most people have an internal voice in our heads, narrating events, reminding us of things, intruding with unrelated thoughts. Have a random burst of dopamine along with one of those, and it becomes marked with so much salience, so much presence, that you perceive it, respond to it as an actual voice. Most schizophrenic hallucinations are auditory, reflecting how much of our thinking is verbal. And as a truly remarkable exception that proves the rule, there have been reports of congenitally deaf individuals with schizophrenia whose hallucinations are in American Sign Language (where some hallucinate a pair of disembodied hands signing to them, or being signed to by God).[*],[23]
The disease also involves structural changes in the brain. This is a bit tricky to demonstrate. The first evidence came from postmortem comparisons of the brains of people with schizophrenia with control brains after death. The nature of the structural abnormalities raised the possibility that the finding was a “postmortem artifact” (i.e., brains of people with schizophrenia, for some reason, were more likely than control brains to get squished from being removed during autopsy). Though a little far-fetched, this worry was eliminated when neuroimaging came along, showing the same structural problems in the brains while people were still alive. The other potential confound that still needed to be eliminated concerned medications: If you observe something structurally different in the brain of, say, a forty-year-old with schizophrenia, is the difference due to the disease or to the fact that they have been taking various neuroactive drugs for decades? As a result, the gold standard in the field emerged to be neuroimages of the brains of adolescents or young adults just diagnosed with the disease, who had not been medicated yet.[*] And eventually, once it was possible to identify those genetically at risk and follow them from childhood, seeing who would develop the disease and who not, it became clear that some of the brain changes were happening well before the most serious symptoms were emerging.[24]
So these brain changes preceded and predicted the disease. The most dramatic change is that the cortex is abnormally thin, compressed (hence the worry about squishing). There are logical differences as well in the ventricles, those fluid-filled caverns inside the brain; specifically, if the cortex is thin, compressed, the ventricles enlarge, pressing outward. This raises the question of whether the problem is enlarged ventricles that squish the cortex from within or a thinned-out cortex that allows the ventricles to fill the empty space. As it turns out, the cortical thinning comes first.[25]
Very tellingly, the cortical changes are most dramatic in the frontal cortex. The thinning turns out not to be due to loss of neurons. Instead, there’s loss of the complex cables—the axons and dendrites—that allow neurons to communicate with each other.[*] The frontal cortex has a lessened ability for its neurons to communicate with each other, to coordinate their actions. To function in logical, sequential ways.[*] And in support of that, functional brain imaging shows that the thinned-out, impoverished frontal cortex in someone with schizophrenia has to work harder to pull off the same degree of efficacy at tasks than the frontal cortex of a control subject.[26]
So if one were forced to come up with a grand synthesis of the disease, based on current knowledge, it would run something like this: In schizophrenia, an array of gene variants constitute a risk for the disease, and certain times of major stress early in life regulate those genes in such a way that things divert onto the road leading to schizophrenia. These manifestations then include an excess of dopamine and sparse neuron- to-neuron connections in the frontal cortex. Why the late-adolescent/ early-adult onset typical of the disease? Because that’s when the frontal cortex is having its final burst of maturational growth (and with that being impaired in schizophrenia).[27]
Things wrong with genes, neurotransmitters, the amount of axonal wiring connecting neurons. The purpose of going through this overview of our current understanding of the disease is to hammer in this point—it’s a biological problem, it’s a biological problem. It’s the world of people in lab coats with test tubes, rather than Viennese psychoanalysts whose modus operandi would be to tell the mother that she sucks at mothering. A universe away from the idea that if you’re a teenager cursed with a schizophrenogenic mother, a descent into schizophrenic madness is your escape. In other words, this is another domain where we have managed to subtract out the notion of blame from the disease (and, in the process, become vastly more effective at treating the disease than when mothers were being given scarlet letters).
As I said, learning about the transition of epilepsy from being what happens when you enlist with Satan to being a neurological disorder is frustrating, because there’s next to no information about how the average person started thinking about the disease differently in the eighteenth and nineteenth centuries. But we know about how the transition most likely occurred in the case of schizophrenia.
A Picture Is Worth a Thousand Words—on Television
The change in the view of schizophrenia should have happened in the 1950s, when the first drugs that helped lessen the symptoms of schizophrenia came online. When dopamine is released by a neuron intent on sending a “dopaminergic” message to the next neuron in line, it works only if that next neuron has receptors that bind and respond to dopamine. Basic neurotransmitter signaling. And the first effective drugs were ones that blocked dopamine receptors. These were termed “neuroleptics” or “antipsychotics,” the most famous being Thorazine (aka chlorpromazine) and Haldol. What happens when you block dopamine receptors? The first neuron in line can release dopamine till the cows come home and still no dopaminergic signal is going to get through. And if people with the disease start acting less schizophrenic at that point, you have to logically conclude that the problem was too much dopamine on the scene in the first place.[*] The case was strengthened even more by the demonstration of the flip side—take a drug that drastically increases dopamine signaling, and people develop many schizophrenia-like symptoms; this is an amphetamine psychosis. Findings like these jump-started the dopamine hypothesis, still the most credible explanation for what is going wrong in the disease. It also caused a drastic reduction in the numbers of people with schizophrenia warehoused for life in psychiatric institutions tucked away at a genteel distance from everyone else. It was the end of asylums.[28]
This should have stopped the schizophrenogenic voodoo right in its tracks. High blood pressure can be lessened with a drug that blocks a receptor for a different type of neurotransmitter, and you conclude that a core problem was too much of that neurotransmitter. But schizophrenic symptoms can be lessened with a drug that blocks dopamine receptors, and you still conclude that the core problem is toxic mothering. Remarkably, that’s what psychiatry’s psychoanalytic ruling class concluded. After fighting the introduction of the medications tooth and nail in America and eventually losing, they came up with an accommodation: neuroleptics weren’t doing anything to the core problems of schizophrenia; they just sedated patients enough so that it is easier to psychodynamically make progress with them about the scars from how they were mothered.
The psychoanalytic scumbags even developed a sneering, pejorative term for families (i.e., mothers) of schizophrenic patients who tried to dodge responsibility by believing that it was a brain disease: dissociative-organic types. The influential 1958 book Social Class and Mental Illness: A Community Study (John Wiley), by the Viennese psychiatrist Frederick Redlich, who chaired Yale’s psychiatry department for seventeen years, and the Yale sociologist August Hollingshead, explained it all. Dissociative-organic types were typically lower-class, less educated people, for whom “It’s a biochemical disorder” was akin to still believing in the evil eye, an easy, erroneous explanation for those not intelligent enough to understand Freud.[*] Schizophrenia was still caused by lousy parenting, and nothing was to change in the mainstream for decades.[29]
The breakthrough, in the late 1970s, came at the intersections of public advocacy, neuroimaging, the influence of the media, money, and schizophrenia in the family’s closet of powerful people.
In some ways, it started with a murder. In the early seventies, a young man suffering from schizophrenia killed two people in Olympia, Washington, while in a delusional state. A local woman named Eleanor Owen, the mother, sister, and aunt of people with schizophrenia, did something that was a catalyst. She resisted the usual response of someone touched by the disease, which was to retreat into the shame and guilt that was always there but particularly searing when the rare violence committed by someone with schizophrenia confirmed the stereotype. Owen contacted seven other local people she knew who had a close family member with the disease, and they contacted the family of the killer to offer support and comfort.
Owen and cohort felt empowered by the act, and rather than shame and guilt, the main emotion they felt was rage. The antipsychotic revolution had emptied the psychiatric hospitals of chronic-care schizophrenic patients who were not much more normal and healthy in their behavior. The laudable plan was to construct community mental health clinics throughout the country that would care for these individuals and help them reintegrate into their communities. Except the funding was way slower in coming than what was needed to keep pace with the numbers of people being deinstitutionalized. By the Reagan years, funding had basically completely stopped. Most of the people deinstitutionalized, if they were lucky, wound up being dumped back on their families; otherwise, the streets. Thus the rage was at the irony of this: We’re such toxic family members that we caused the disease in the first place, and now we’re being entrusted with their care because various agencies couldn’t figure out what else to do with them? Moreover, as a group, it was easier for them to air the real source of their rage—their increasing conviction that the idea of a schizophrenogenic mother or family was sheer nonsense.
I had the opportunity to talk with Owen a few years ago, a two-hour conversation with this ninety-nine-year-old who remembered it all well. “On a primal level, I knew it was not my fault. I was operating on sheer emotional rage.”[*] Her group soon formed the Washington Advocates for the Mentally Ill, basically a support group tiptoeing into the realm of advocacy.
Meanwhile, a similar group, called the Parents of Adult Schizophrenics, had formed in San Mateo, California; it scored an early victory in winning the right for family members of individuals with schizophrenia to be on every county mental health board in the state. In Madison, Wisconsin, another group had formed, founded by Harriet Shetler and Beverly Young. They all eventually got word of each other, and by around 1979, the National Alliance on Mental Illness (NAMI) had formed. One of their first actual hires was Laurie Flynn, who became director from 1984 to 2000. A homemaker with some experience with community volunteering, she had a daughter who had starred in her high school musical and been on track to be valedictorian when a variant of schizophrenia destroyed her. She and Owen were soon joined by Ron Honberg, a lawyer and social worker who wound up running NAMI’s policy work for thirty years, despite having no family member touched by schizophrenia. The pull for him was a sense of justice: “Someone’s kid gets diagnosed with cancer, that’s one thing. Someone’s kid gets diagnosed with schizophrenia, neighbors did not come over with casseroles.”[*]
They had some successes, getting a few state legislatures to push in the direction of more medical insurance coverage of schizophrenia. Owen was the bulldog. “I have no idea how I managed to threaten them [legislators],” she recalled later. “I was a monster. It was from the pain.” Flynn described the members as “furious, in their nice Midwestern way.”
And then a catalyst happened when NAMI connected with the perfect hybrid of an individual, a first-degree family member of a schizophrenic person who also happened to be one of the world’s experts in the emerging field of biological psychiatry. E. Fuller Torrey, mentioned earlier, had decided to become a psychiatrist when his younger sister was diagnosed with schizophrenia. Schizophrenogenic theorizing struck him as deeply wrong for the same reason it did the early NAMI members, with a number of them in effect saying, “Wait, my mother mothered nine of us kids, but she only schizophrenogenically mothered one of us?” It turned him into a scathing critic of the psychoanalytic school of psychiatry. With degrees from Princeton, McGill, and Stanford, he could have settled into a comfortable, lucrative private practice. Instead, he spent some years as a physician in Ethiopia, then the South Bronx, and then an Inuit community in Alaska. He eventually became a psychiatrist in the National Institute of Mental Health, and at St. Elizabeths, the oldest federal psychiatric hospital in the U.S. In the process, he became a fierce critic of the psychodynamic stranglehold, authoring the superb books The Death of Psychiatry and Freudian Fraud (along with a highly regarded biography of Ezra Pound, a longtime patient at St. Elizabeths, and . . . eighteen other books). His outspokenness cost him at least one position, and he eventually quit the federal psychiatry establishment as well as the psychodynamically dominated American Psychiatric Association, and founded his own mental health research institute with a focus on the biological causes of schizophrenia. It was inevitable that he and NAMI would connect.
