Once upon a time there was a family with twelve children – ten sons, followed by two daughters. Six of the sons went on to be diagnosed with schizophrenia.
One tried to murder his wife by forcing her to inhale cyanide fumes. One shot his girlfriend dead, then turned the gun on himself and ended his own life. One molested his younger brother and sisters. One set fires and viciously attacked police officers, as well as patients and staff members in a mental hospital.
Are you curious to know what the Hell was going on behind the scenes while these boys were growing up? I am.
Well, don’t worry about it. The problems of this family obviously stemmed from a faulty genetic inheritance, and this has been proven by science, or at least will be proven, sometime really soon.
That is the message of Hidden Valley Road by Robert Kolker, which tells the story of the Galvin family of Colorado Springs.
The family patriarch, Don Galvin, was one of the founding fathers of the Air Force Academy and had a brilliant career, first as an Air Force Officer, then as an instructor at the Academy, and finally as Executive Director of the Federation of Rocky Mountain States. Unfortunately, it was his fate to watch helplessly as one son after another cracked up and was diagnosed with schizophrenia, the most dreaded of all those conditions known as “mental illnesses.” Kolker tells this sad story, interleaved with accounts of scientists searching for the genetic basis of this condition.
In my book Madness and Genetic Determinism: Is Mental Illness in Our Genes?, I reviewed the evidence and concluded there is no strong genetic component to schizophrenia or any other mental illness, so I was curious to see how Kolker came to the opposite position. As proof of the genetic basis of schizophrenia, he cites the Danish Adoption Study, which in fact found no correlation between a diagnosis of schizophrenia and having a schizophrenic birth mother. Zilch. Zero. The only correlation they found was with a diagnostic category they called “schizophreniform disorders,” an ill-defined grab-bag of complaints invented solely for the purposes of the study.
Moreover, the Danish Adoption Study had a large excess of mental problems in the adoptive families of index cases, and some of their “diagnostic interviews” consisted of a five-minute doorstep conversation, while others apparently never took place at all. Finally, the authors re-analyzed their own data and decided that the diagnoses of “schizophreniform disorders” which formed the very basis of the study were not reliable.
In the final analysis – literally – the study authors came up empty-handed. The results of the Danish Adoption Study were negative.
None of this is mentioned by Kolker.
Kolker also states “If one member of a pair of identical twins has schizophrenia, the chance that the twin also will have the condition is about 50 percent.” In fact, as clinical psychologist Jay Joseph has pointed out, no study performed after 1962 has reported a concordance rate for identical twins as high as even twenty-five percent. In plain English, if one member of a pair of identical twins is diagnosed with schizophrenia, the odds are better than three out of four that the other will not be. That is hardly evidence of a strong genetic basis for schizophrenia.
Now the new science of genome-wide association studies has enabled scientists to go over the human genome with a fine-toothed comb, and what have they found? The answer is: not much. To his credit, Kolker acknowledges that the claimed effect sizes of so-called “schizophrenia-associated alleles” are tiny, although he never says just how tiny.
In fact, the claimed effect sizes of these alleles is on the order of one in five hundred, or even less – one in a thousand, one in two thousand. If there are any more “schizophrenia-associated alleles” out there waiting to be discovered, their effects sizes must be even any tinier, or else the alleles themselves must be very rare. Can a gene correlated with a one in five hundred (or even less) chance of being diagnosed with schizophrenia properly be referred to as “causing” that condition? That is stretching the notion of cause and effect to utter meaninglessness.
So if faulty genes are not the cause of the complaints that fall under the diagnostic rubric of schizophrenia, what is? Since the 1980’s a mountain of evidence has accumulated showing that these complaints are caused (not “triggered”) by sexual abuse, physical abuse, and emotional abuse, along with a wide variety of other adverse childhood experiences. There is also a long and rich tradition, dating all the way back to the Eighteenth Century, of successfully treating these complaints with kindness, empathy, and compassion. Kolker seems to think that this mountain of evidence, and this long and rich tradition, can be dismissed with a single two-word phrase: the “schizophrenogenic mother.”
This is a matter that bears closer examination.
The phrase “schizophrenogenic mother” was coined by the psychiatrist Frieda Fromm-Reichmann of Chestnut Lodge as a passing aside, in a 1948 paper that was not even primarily about the etiology of schizophrenia, but which rather was devoted to the dynamics of the therapist-patient relationship. Dr. Fromm-Reichmann was a psychiatrist famed for her compassion and skill in reaching even the most seemingly intractable cases of schizophrenia, and who was immortalized by her most famous patient, Joanna Greenberg, in her semi-autobiographical novel I Never Promised You a Rose Garden. Fromm-Reichmann’s full story is told in Gail Hornstein’s masterful biography To Redeem One Person Is to Redeem the World.
Kolker bashes Dr. Fromm-Reichmann, citing the work of Thomas McGlashan, also of Chestnut Lodge, who concluded that “only” one-third of patients at the Lodge were recovered or moderately improved. He neglects Dr. Hornstein’s analysis, which showed that forty-one percent of patients exhibited a response to therapy which was rated “extremely positive” while that of an additional seventeen percent was rated “positive.”
Anyway, what of it? Many of these were patients who, given the usual standard of care of the day, likely would have spent the rest of their lives languishing in the back wards of a state hospital, abandoned and forgotten. Every single one who was restored to functioning was something little short of a miracle.
Kolker also takes a swipe at Greenberg, averring that she was misdiagnosed: “The delusional teenage girl did not have schizophrenia at all, a team of researchers declared in 1981… Schizophrenia’s star patient might not have been that sick to begin with.” But since, then as now, there are no objective biomarkers for schizophrenia, it is not clear on what basis Greenberg can be said to have been “misdiagnosed.”
And again, what of it? The fact remains that Greenberg was diagnosed with schizophrenia, and yet after three years of treatment at Chestnut Lodge went on to become a professor and a famous author. A young woman receiving such a diagnosis today might well be prescribed multiple neuroleptic drugs and end up obese and zombified, before going to an early grave. Outcomes for patients who today would be diagnosed with schizophrenia were better in the late nineteenth century, before any of the modern-day psychiatric drugs were introduced, than they are now.
All this is ignored by Kolker, who paints a one-dimensional portrait of Dr. Fromm-Reichmann as the ogre who unfairly pilloried generations of women as being solely and completely responsible for the genesis of schizophrenia in their children. Elsewhere I have argued that many of Dr. Fromm-Reichmann’s psychoanalytically-oriented contemporaries understood perfectly well that schizophrenia was the product of disturbed families, not just disturbed mothers, and that for too long the “schizophrenogenic mother” has served as a straw woman to shut down discussion of the environmental causes of schizophrenia and to promote biogenetic explanations and drug-centered treatments for that condition instead.
Kolker kicks over this straw woman again and again, as if the only alternative to drugs and electroshock is to blame the mother for everything that goes wrong in a person’s life. This is as pristine an example of a false dichotomy as one could hope to find. Kolker then goes on to preposterously undercut his own argument when he reveals that Donald Galvin, the oldest son in the family and the first to be diagnosed with schizophrenia, had been molested as a child by a priest and close family friend. Kolker doesn’t get around to dropping this bombshell until page 239 of his book, as if this were an unimportant detail.
Kolker states flatly “Sexual abuse does not cause schizophrenia.” No source is cited for this astonishing statement, but in fact study after study has shown sexual abuse is a major risk factor for schizophrenia and related complaints, with odds ratios far in excess of those of any of the so-called “schizophrenia-associated alleles” discovered through GWA studies. Can Kolker show us a single study that looked for a correlation between sexual abuse and psychotic symptoms and did not find it?
In fairness to Kolker, he does allow environmental factors a role in the genesis of schizophrenia, citing the “diathesis-stress” model of Gottesman and Shields. But the word “X” has value only if some things are not “X.” The word “diathesis” means “vulnerability to stress.” So are some people invulnerable to stress? Is there anyone out there who could never meet the criteria for a diagnosis of schizophrenia, no matter how much stress and trauma and abuse he was subjected to?
There is not an atom of evidence for this proposition, and if you think about it for a moment it should be obvious there couldn’t be. The definitive experiment in this case simply cannot be carried out (thank God).
So where does all this leave us? In the case of the Galvin family, we know the oldest son was sexually abused as a child, and that he proceeded to bully his younger brothers, who proceeded to bully and at least in some cases sexually abuse their younger siblings. We also know that at least some of the brothers experimented with LSD and an abundance of other illegal drugs as well – weed, cocaine, and God knows what else. Add to that a father’s infidelities, prolonged absences, and struggles with depression, a mother doubtless feeling overwhelmed by the task of raising twelve (!) children with almost no help from anyone else, and a mental health care system centered on drugs and electroshock rather than empathy and compassion, and that seems like plenty of fuel for this particular fire – at least to start with.
We will never know the full truth about this family. Too much time has passed, and the mother and father now are dead, as are three of the six afflicted sons – two of them as a direct result of the neuroleptic drugs they were given. Of the three remaining, two have memories impaired by decades of damaging and violent treatments. But given all we do know, is it any surprise this ended badly? Why bring genes into the argument at all?
Kolker has an answer: “By analyzing this family’s DNA and comparing it with genetic samples from the general population, researchers are on the cusp of making significant advances in treatment, prediction, and even prevention of schizophrenia.” But in fact, schizophrenia genetics researchers have been claiming to be on the “cusp” of making great discoveries for over eighty years now, and yet after all this time, they have not come up with any findings that have benefited a single patient in a clinic anywhere in the world.
The Decade of the Brain came and went two decades ago. After spending billions of dollars on brain research and gene research and generating untold petabytes of data, researchers have not come up with a single new treatment or even a diagnostic test for schizophrenia or any of the other functional disorders commonly treated by psychiatrists. At what point do we conclude the source of these patients’ problems is not in their brains, or in their genes? At what point do we consider whether we really want to continue pouring more billions into this kind of research? If not now, when?