‘Sin your way to heaven and get slaughtered: A byzantine general problem of the self’ (part twenty-seven)

Filed under:Sin your Way to Heaven and get Slaughtered — posted by Schizostroller on August 23, 2019 @ 8:02 am

If we are to return to Rocjiewicz and Rocjiewicz Jr’s phenomenology after exploring Lisa Blackman’s ‘problem of hallucination’ it is worth exploring Ver Eecke’s ‘dualist’ view of mental health that embraces both phenomenology and the bio-medical model (he does this in his introduction to Der Waelhen’s combination of phenomenology and Lacan so a nice segue on the return through phenomenology back to Lacan’s idea of the ideal ego and ego ideal that we took a detour from some time ago).  On the face of it Ver Eecke’s argument is just another, theory that says, sure there’s a social aspect to mental health but it’s underpinned by a biological cause. This is an issue that The British Psychological Society’s Power, Threat, Meaning Framework deals with and looks at several different approaches to criticise this stance, and we will come to this after. However, Ver Eecke’s is slightly different to some of these more psychological versions in that it deals with phenomenology and Lacanian psychoanalysis. So, for that reason I would like to examine it.
Ver Eecke starts by noting a certain dual causality model to theories of psycho-somatic illnesses within the medical profession. He quotes Van Der Kolk in saying “It is thus no longer scientifically justifiable to make clear distinctions between psychologic and biologic processes; rather we need to define our understanding of the degree which genetic, developmental, toxic and social factors converge to result in certain clinical syndromes!”. He also mentions that Finnish psychiatrist Pekka Tienari suggests that it is time “to move forward to attack the question of how genetic and environmental factors transact to influence development” (p.39-40).
Ver Eecke then spends time disagreeing with the claims that neurobiological disease is the sole cause of schizophrenia, arguing that they are not as strong as they claim, and furthermore that the evidence argues positively against it. One of the first criticisms is that twin studies of monozygotic twins show a 40-50% concordance between the twins, were the cause to be solely genetic, there would be higher concordance as they are genetically the same. Moreover, with regards such genetic causation given the lower insistence of marriage and procreation amongst people with the diagnosis, the incidence of the ‘disease’ would drop, die out. Ver Eecke quotes Portin And Alanen who, after analysing twin studies, adoption studies, environmental studies, and brain imagining findings say “in the light of the evidence provided by the epidemiological studies of the genetics of schizophrenia, it seems that the present-day conclusion is that genes are neither sufficient nor a necessary cause of schizophrenia, but a risk factor for it. Interaction between the genetic factors on the one hand physical, psychological, and psychosocial factors on the other appears to be important in the aetiology of the disease.”. Ver Eecke then goes on to quote Kendler and Diehl: “Schizophrenia is clearly a complex disorder in that gene carriers need not manifest the illness (incomplete penetration), affected individuals need not have the gene (environmental forms or phenocopies), diagnostic uncertainties cannot be avoided, and different families may carry different susceptibility genes (genetic heterogeneity)… These conclusions… are not inconsistent with the hypothesis that in some individuals, schizophrenia is largely environmental in origin, while in others the disorder is caused largely by genetic factors.” (p.40-41).
Ver Eecke then turns to studies that he argues provide direct proof that genetics are not the sole cause of schizophrenia. He refers to some a Danish study that noted differences in diagnostic rates dependent on several cultural factors: increased risk for children born to Danish mothers outside Denmark; and increased risk with unknown fathers but no maternal history of schizophrenia.
Ver Eecke then looks at the dopamine hypothesis. He argues there is as yet no satisfactory dopamine hypothesis, and that dopamine hypotheses are compatible with psychosocial factors. He points out that there are two main neurological development arguments of the dopamine hypothesis as mono-causal. Neither is satisfactory, one is a neurodegenerative one which can explain increasing negative symptoms from positive symptoms but not early onset or season of birth differences. It also fails to fully account for how this neurological degeneration occurs. The other hypothesis suggests dopamine is due to early insult or trauma (including possible in utero), and this can explain early onset but not later negative symptoms. Thus Ver Eecke moves on to examine co-causality theories of the dopamine hypothesis. He notes that the dopamine hypothesis is a theory that developed out of investigating the apparent effectiveness of medications, he then notes that clinicians have observed “that at times those medications work minimally or not at all… [and] many patients continue to have cognitive deficits and negative symptoms despite having had marked response to treatment” and that “amphetamine-induced psychoses… lack a number of features commonly associated with schizophrenia, such as the presence of negative symptoms, the specific kinds of auditory hallucinations that occur in schizophrenia, and a chronic course.” (p.42). he notes that scientists using animal research have concluded that “stress-induced dopamine release could play a role in psychotic decompensation.” (p.43). Ver Eecke  notes that in such a version of the dopamine hypothesis “stress is conceptualised as a causal factor in which dopamine is the mechanism. The theory of schizophrenia presented… implies that persons with a prepsychotic structure are vulnerable to the consequences of stress. This claim goes hand in hand with claims made by Lacanian-inspired therapists that prepsychotic persons are prone to create repeated self-inflicted stress.” (p.43).
After discussing dopamine, Ver Eecke turns to theses involving norepinephrine and serotonin. With regards norepinephrine he notes research that states that studies “do not contain sufficient evidence to suggest that a defect in the norepinephrine system is primary to the development of schizophrenia… however, the studies implicate an alteration in norepinephrine metabolism or response to stress in at least some schizophrenic patients. The noradrenergic system not only is integral to the body’s response to stress but is also involved in modulating the dopaminergic system.” With regards serotonin, he notes the same researchers state that “studies of patients with schizophrenia have failed to convincingly demonstrate that abnormalities in 5-HT [serotonin] neurotransmission mediate the expression of symptoms.” (p.43). So with regarding theses involving norepinephrine and serotonin, Ver Eecke, suggests that if one were searching for “an exclusive biological explanation for schizophrenia, it is important to remember that serotonergic neurotransmission is not believed to be a causal explanation of schizophrenia and that the possible function of the neuro noradrenergic system is explicitly linked to the body’s response to stress. One can therefore conclude that consideration of the function of these two systems in the brain includes psychological stress as a possible factor in schizophrenia.” (p.43).
Ver Eecke then turns his attention to glutamate theories. He notes that Phencyclidine (PCP, angel dust) can produce schizophrenia-like symptoms by blocking one glutamate receptor (NMDA). He notes that post-mortem studies have shown that an increased number of NMDA receptors is associated with acute psychotic states from an excess of dopamine transmission as a result of a change to the nucleus accumbens from damage to the hippocampus and amygdala (potentially prenatal). Ver Eecke notes this again results in a neurobiological appeal to psychological factors relating to stress.
Ver Eecke also looks at other chemical agents, he looks at one example each from four categories. With regards biogenic amines (eg physostigimine, DFP), an increase in cholinergic activity increases negative symptoms, whereas anticholinergic agents improve negative symptoms. With regards endogenous psychotogenes, studies show schizophrenics have a relatively low incidence of allergies as well as decreased responses to histamine. As for neuropeptides, researchers have noticed that high levels of CCK (creatinine phosphokinase) in the limbic system of schizophrenics. With regards more miscellaneous chemical agents, studies have shown that gluten-poor diets decrease psychiatric admissions, or correlate with improvements in psychiatric patients.
Ver Eecke then changes the focus from chemical agents to gender, and that the sex of the person makes a difference in the age of onset as well as possibly course and recovery outcome. He notes that Wyatt claims that “some estrogens appear to have antipsychotic effects and estrogens are known antagonists of D2 receptors. Conversely, dopamine regulates the biological effects of estrogens by decreasing the binding of that hormone to its receptors…” however “there are numerous social demands that could interact with an already altered substrate to increase the risk of developing schizophrenia.” (p.44).
In conclusion to the section I am looking at here, Ver Eecke’s notes that in the conclusion to the overview article “Schizophrenia: Neurochemical, Viral, and Immunological studies” in the Comprehensive Textbook of Psychiatry, Wyatt and his coauthors claim in defence of a medication approach that “the overwhelming beneficial effect of antipsychotic medications in schizophrenia cannot be overlooked. Regardless of the original cause of illness, the neurochemical outcome appears to be a perturbation of the dopamine neurotransmitter system” (p.44). Ver Eecke notes that in investigating these issues Wyatt et al. acknowledge stress as a variable. Thus Ver Eecke argues that “a critical evaluation of the argument for a neurobiological basis of schizophrenia needs to distinguish between, on the one hand, non-interpreted facts and, on the other hand, theoretical explanations of the facts. The survey articles that summarise the theories which attempt to understand the neurobiological basis of schizophrenia do not exclude psychosocial factors. Rather, psychosocial factors are included in the reasoning of how the major neurobiological factor (dopamine system) works.” (p.44). Ver Eecke uses the acknowledgment by researchers who observe the beneficial influences of gluten-poor diets and the low incidence of allergies that these observations do not alone indicate a cause of schizophrenia. “Rather, these non-interpreted facts indicate that there is a neurobiological factor at work in schizophrenia. But such a claim can co-exist with claims derived from other observations in both the neurobiological and psychosocial domains… thus, theoretically, the neurobiological explanation for schizophrenia does not exclude the possibility of psychosocial factors. In some neurobiological explanations, positive appeal is made to these factors.” (p.45).
I will conclude this post here and continue with Ver Eecke’s dualist model in the next post. I will say here, that the purpose of this foray into biomedical theories is to dive in deeper momentarily after looking at an embodied theory, before using the Power Threat meaning Framework to look at the issues with some of the models Ver Eecke raises here (not least the dopamine model), not least that whilst Ver Eecke makes a good case for a method of taking both biological, as he argues non-interpreted facts into account, his interpretation and distinction does not go far enough, as such I will in the future also be looking at the social construction of mental illness, around diagnosis, but also around social, economic and ideological factors, not just psychological stress models. However it is clear Ver Eecke’s conclusion paves the way for this possibility.

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image: detail of installation by Bronwyn Lace