Saturday, March 25, 2023

Comments by GPM

Showing 10 of 10 comments.

  • Sam’s unease about the term “schizophrenia” (SZ) is well placed. SZ is just the most recent inadequate placeholder to describe a process, or socioemotional/sociocognitive/sociobehavioral syndrome, that baffles the “normals” who call themselves psychiatrists and neurologists. The previous term, dementia praecox, was even worse. At least “SZ” implies some sort of dignifying and humanizing internal psychological conflict or distress actively generating the symptoms in response to social stimuli, whereas DP describes a passive, progressive and irreversible neurodegenerative condition like Alzheimer’s. In a move that Western psychiatry has mostly ignored, 20 years ago the Japanese addressed this (from Wiki):

    The old term for schizophrenia, “Seishin-Bunretsu-Byo” (Mind-Split Disease), has been replaced by “Togo-Shitcho-Sho” (Integration Disorder) in Japan.

    The Japanese apparently have more genes for psychological insight than we do. This is a step forward, but a long way to go. The term SZ should be abolished in the West and replaced by understanding. This is all part of the complete overhaul of psychiatric nosology that is desperately needed. A new edition of the DSM will not do it. The DSM needs to be trashed too. The completely failed “operationalization” or “biologization” or “geneticization” of the diagnostic criteria pushed by Insel and others is itself a type of cognitive pathology that ought to be the only entry in DSM6. The idea that suffering, worried, scared, conflicted, traumatized people have genetic brain diseases is barbaric and Medieval and even nutty. For instance, take a look at this paper, published yesterday online:

    “The genome-wide neurodevelopmental CNV burden identified explains 0.034% of the variation in PTSD symptoms.”, it says. That’s a whopping 17/50,000th of the variation “explained”. It explains nothing, but is barely non-zero, which is the threshold that apparently justifies further funding. These people are looking for a very monetizable prize: a screening test that police, military and others can use to identify those whose genes are too weak for the kind of violent work that strong-gened people can do while whistling. Such a discovery would rake in millions (or save millions from the VA budget), and that’s why funders, who are often as fooled by this grift as the general public, pony up the money. No other reason. The last thing they care about is human well being. After all, perpetual war and crime and sexual abuse are inevitable and unpreventable. Genetic intervention (genetic counseling, matchmaking, gene editing, selective abortion, career guidance, etc) is all that can be done, so press the donate button.

  • These things are hard to grasp as long as we cling to the notion that SZ is a “disease”. Rather, SZ is one of many possible responses, perhaps the most extreme short of physical suicide, to the terrors and heartbreaks that life offers to the young and vulnerable. SZ, as a form of psychosocial suicide, is as “human” as becoming Bernard Madoff or Mother Teresa, war, grief, joy, love, xenophobia, murdering cuckolders and kissing babies. Patrick Hahn asks, correctly, what other experiences might have predisposed the divorced man to “react that way”. Think of allergies, like bee stings, which cause anaphylactic shock in a minority of people, but only mild and brief irritation in most others. As in bee stings, when and why a person becomes psychotic in apparent reaction to a proximal (recent, direct) social stimulus (the affair in this case) is not merely conditioned by the apparent severity of the stressor, but also the entire life history of exposure to other stressors or trauma in the domain of social relationships. It can also be conditioned on the lack of exposure to such stressors (one of the main causes of asthma is spending infancy and childhood in an allergen-free “protected” environment). That’s why an apparently trivial stimulus can seem to precipitate a severe psychotic episode in some people. Or why a “happy” stimulus results in something very unhappy: Why one woman is overjoyed by childbirth and another plummets into a psychotic postpartum depression. The response to these transitions is conditioned on the person’s life history, which in turn is heavily conditioned by the multigenerational transmission of emotional “information”. It also helps to understand why the first major psychotic “schizophrenic” episode in a young adult is often precipitated by some upheaval in the social network and roles, such as death in the family, marriage of a sibling, leaving home, living independently, establishing separate quarters, getting married (or divorced), joining the military or having a baby. The decisive events predicating the response are buried in the past, in prior attachments and other socioenvironmental factors. Divorce can induce profound infantile rage, desperate attempts to prevent or punish abandonment, panic attacks, somatic symptoms, major depression and hysterical conversion behavior in mature adults. Or indifference, or even joy less commonly. The matter is complicated by the anecdotal nature of the case; did this man in question have a bona fide psychosis? I don’t know. Even so, I would probably trust Marie’s anecdote more than the “imaginary interviews” that the Danish adoption study fraudsters conducted. Most clinicians have seen countless cases of psychological regression and collapse associated with divorce – in the divorcing couple, and often, perhaps more commonly, in the children of the couple. Also, consider how such a profound emotional reaction could actually be adaptive, or at least preferable to some alternatives. It could have prevented a double homicide, which is far more socially destructive than privately retreating into psychosis for a while. OJ Simpson could have saved society and his children a lot of anguish and expense and prevented a few calamitous riots if he’d become psychotically incapable of the complex goal directed behavior of confrontation and decapitation. Or was it a Colombian gene cartel, as the gene hunters believe?

  • The “environment” also includes the other genes in the environment of a gene, the milieu of transcription factors etc, and above all the overall metabolic/physiologic state of the cell which calls upon genes as resources; in turn the totality of the cell is hopelessly coupled to its cellular environment, etc etc. This “cytological” or “cytosocial” environment is only partially Markovian (independent of previous state): it has a memory; previous environments affect future environments. It is also unfathomably sensitive to the sequence of environments as well their frequency, duration and magnitude. That complexity is what makes it impossible to assign a simple value to any trauma or other experience; it is historical and context dependent. It is this overwhelming complexity and sensitivity to initial and unfolding conditions, particularly in early social development, that results in the butterfly effect of stochastic experiences on personality. DNA cannot possibly contain enough information to determine this process ab initio. The DNA polymer functions as a factory organelle just like any other evolved accouterment that the earliest forms of life started tacking on. Life – that is, the living state, or “life itself” – invented DNA. The activity of genes, just like the activity of proteins and every other countless inanimate molecule in the living thing, is “controlled” by the living state, not the other way around. Life preceded DNA by millions of years. The idea that DNA is the blueprint of life is absurd. We should be worshiping (reverently pursuing the knowledge of) the living state, not a polymer. This absurdity is the twin of another absurdity, the EEA. Together, they form the porous foundation of the most colossal scientific folly in history.

  • Thanks Steve for pointing that out. I didn’t mean it that way. “Social defeat” is not caused by genetic phenotype any more than it is caused by genes. It is caused by social interaction and that is that. Children with certain neurodevelopmental CNVs – which are well characterized and highly syndromic – have exceptionally high rates of SZ, as well as social anxiety and depression. They also have exceptionally – actually phenomenally – high exposure to bullying, sexual abuse, family separation, and ridicule.

  • Good points Steve but (as you said in an earlier post in reply to Marie, I think) we don’t have “to simply understand that we have the genes and learn to work with them” because the “genes” are nonexistent. Not a single angel dances on the head of this pin. Genes (or large mutigenic structural variants, such as CNVs) that confer competitive disadvantages and social vulnerabilities may predispose to extreme social defeat in children and adolescents but they do not cause schizophrenia. Social defeat does (including fear, inferiority, abuse, abandonment, forced immigration, discrimination and so forth, in combinations that are always individually unique). As Lidz presciently said in 1958, at a time when “biological” psychiatry was just starting its rise, “schizophrenic outcome is a possibility inherent in the developmental process which must be anticipated, rather than a condition to be regarded as incomprehensible or as the manifestation of a disordered cerebral apparatus.” He also said, “I wish to remark somewhat parenthetically, in response to a question raised repeatedly, that the problem of why one child among several in a family becomes schizophrenic does not appear to be insurmountable when one grasps the dynamics of role relationships within the family, the vicissitudes of the family, and the different stresses linked to being a member of one sex or the other in the given family.” Over 95% of all cases of SZ ascertained by national registries and hospital records do not have a 1st, 2nd or even 3rd degree relative with SZ. By the way, MZTs reared together are only concordant ~13%, barely above the fraternal sibling recurrence risk (SRR, usually given as ~8%). (Furthermore, even the SRR is inflated d/t the family size effect and ascertainment biases, and of course the gratuitous definitional creep of schizophrenia that Joseph exposes in his books and papers). That small percentage (~13%) is shockingly low for a presumed genetically-based condition that encompasses every domain of personality. In contrast, in the infamous separated twin studies, Bouchard reported “separated” MZTs who were highly concordant for such trivial and arbitrary things as pet names and hair styles. This disparity is the greatest of all embarrassments to MISTRA. How is it possible that genes can control individual hair styles of “separated” twins over space and time, yet fail so miserably to produce concordance for schizophrenia in MZTs who are reared together? As so poignantly detailed in Jay Neugeboren’s autobiographical essay “Imagining Robert”, his schizophrenic twin brother was repeatedly sexually abused by someone the family trusted, a fact that didn’t come out for years after his brother’s diagnosis. And by the way, if you are an investor, the big money in GWAS/PGS phenotypic prediction is in selling test kits full of caveats and other fine print indemnifying the vendors.

  • Thoughtful observers such as Marie often make the same inferential mistake. SZ is entirely an emotionally driven reaction to social life and circumstances. Any truly genetic social disadvantage (e.g., short stature, mental slowness, speech or motor impairments, unattractiveness) merely increases the probability of social defeat and regression in response to external circumstance. There are no inherited (genetic) propensities “for” schizophrenia. Put another way, all normal humans have all the genes necessary to react to social life in the schizophrenic manner. The elusive endophenotype of schizophrenia is the normal human being.

  • Patrick,
    Somehow I missed this and just discovered it thanks to reading the comments on Jay Joseph’s current dazzling MIA article about the genetics of depression. I read HVR last year and was horrified. Kolker is an adroit hack journalist just looking for a story to tell and a book to sell. Kolker was totally out of his depth; totally incompetent to formulate and disseminate a “scientific” opinion about the Galvins. He was spoon fed the charlatanic biogenetic Koolaid of Lynn DeLisi and Robert Freedman who were convinced that the only explanation for the staggering dysfunction and unhappiness of this family had to be a rare but highly penetrant genetic variant, or some unique combination of variants, affecting neurodevelopment, the discovery of which would lead to a Lasker Prize and maybe a Nobel, and other rewards, like permanent private parking spaces at laboratories named after them, and popping champagne (see page 246). Of course they have failed but their merry genetic snark hunts are still being heavily funded, so they will continue. IOW, Kolker was a useful idiot for the behavioral genetics/biopsychiatry industry, which is heavily populated unfortunately by totally sincere, earnest and brilliant true believers. His book has done great harm, adding to the already prolific lie factory. DeLisi herself is a dangerous charlatan like David Rosenthal, who spearheaded the massive NIMH study of the Genain quads. Rosenthal considered the quads a “tragic gift of nature” and his team somehow brushed aside the horrific and inescapable environmental conditions that the quads suffered, and then added to it, subjecting them to years of demeaning scrutiny, needles, EEGs, etc like crash test dummies. DeLisi thought she could make a career out of the Galvins, just like Rosenthal and the Genains. Kolker himself, if he has any integrity, should write a second book exposing how he was both misguided to begin with and so easily deceived by the seductive genochemobabble of the industry. There’s a real story there. He would be doing the public a great service, but there of course is next to no chance of such a miracle. Instead he will continue to defend his trash and collect money, just like a biopsychiatrist telling patients they have “chemical imbalances” or “bad genes”. Kolker is profiting in his own way from the industry just like the charlatans who collect the fees for service. By the way, it is quite telling that Kolker did not hesitate to question Goodman’s diagnosis based totally on second or third hand information, yet didn’t question the diagnoses of the Galvins, who were right in front of him. HVR is not just wrong, it is toxic and disgraceful. You did a superb job cutting it down. But it’s still out there, just one nugget of plutonium in a much vaster toxic landscape. The clean up will take a long time and the resistance of this Medieval industry is tremendous.

  • Neither Engel nor the many people he inspired had such a technical definition of “model” in mind. It was more like the notion of “framework”. Reminds me of what the statistician George Box said, “All models are wrong, but some are useful.” In this case, all definitions of “model” may be wrong, but some may be more useful, or at least more commonly used, than others.

  • I applaud McLaren’s critique of Insel’s new monster, RDoC, except I am puzzled by his comments that George Engel never wrote about the biopsychosocial model and it “doesn’t exist” (“Alerted by the way everybody used the term but nobody ever provided proper references, I trolled through practically everything Engel had ever written, plus dozens of papers that cited him, to find that he had never written the model at all”). Well, it might not exist any more, having been snuffed out by the pseudobiological juggernaut, but for a while it was an inspiration to many young bloods entering the field. Engel wrote at least 3 influential papers between 1977 and 1980, two of which have the term in the title and the other which discusses it in the text, and all of which were decisive in my eventual decision to leave the profession:

    1977 The need for a new medical model: A challenge for biomedicine. Science 196:129-136

    1979 The biopsychosocial model and the education of health professionals. Annals NY Acad Sci 310: 169-181

    1980 The clinical application of the biopsychosocial model. Am. J. Psychiatry 137:535-544

    The first of these (in Science) is the most cited (nearly 2000 times). Years later, after I discovered the BPSM in my training, I corresponded with Engel near the end of his life and his words of encouragement had a lot to do with my eventual abandonment of the practice of psychiatry entirely. In some respects I am even more severe in my disdain for the industry of psychiatry than McLaren, whose outspoken stance I admire, so I just want to dispel the impression (perhaps unintended) that maybe Engel was in the same league as Insel or Gottesmann and others that dominate the industry of pseudobiological psychiatry now. Engel, by the way, was at the University of Rochester NY just down the road from his more famous contrarian contemporary, Thomas Szasz, at the NY State University branch in Syracuse. I was unable to find the full text of McLaren’s 1998 article (“A critical review of the biopsychosocial model” Australasian Psychiatry 32(1):86-92) on line so I don’t know what he actually says about Engel and the BPSM. Despite its limitations, the BPSM did restore some humanity and sanity to the profession for a while.