The Schizo-Stroller

It’s Mel and Colly,
The invisible cunts.
The Beth
of the Unknown Verneinung.
There’s always at least two.
The girls from another planet
Cumming to blow my world.
Boys will be boys.
Hands up if you’re not the only ones.
It’s all fucked up.
I’m not
your mum!
*you’re.

When Nietzsche writes ‘God is dead’. It is not the same sentence structure and therefore a different semantic meaning to the phrase ‘There is no God”.

Historical background for a Nietszchean exegesis:

Around that time in the burdening Wessenschaft relation between anthropology and archaeology, a theory emerged that the earliest god’s were old chieftans or Kings (Ur-Kings) when earlu differences in wealth emerged, with emerging longer periods of settlement that would be returned to, even amongst still semi-nomadic groups. These burial mounds would be then be worshipped and stories told of this King for generations after any lived memory of the King survived. Later temples would be built around these burial mounds and the dead God-King would emerge, leading to hereditary living God-Kings (eg later (but now ancient) Egypt).
This temple would also be the place that as agrarian techniques developed so would the storage of grain, this storage would soon last more than two years. The ‘clerical’ priests would be in charge of distribution and a religious ‘economy’ related to writing, maths, status and labour emerged. Thus, for example, famines were still related to religious beliefs, where the strength of the economy and thus religious faith was related to how long a drought, famine, or plague of locusts the stores could survive. Thus today in modern anthropological psychological dynamics and their relation to the economy, scapegoating is still related ot this ‘hangover’ (best described by Azazel as scapegoat in Leviticus 16 and it’s relation as a relation to the community’s fears).

So with regards such economic, social and religious organisation, this is still a relation to the phrase ‘God is dead’.
(This is related with regards to violence in Nietzsche and Freud’s mythology with regards the killing of the father by the Band of Brother’s. In these mythologies this God-King in this buriial mound was orginally killed and then mourned, as explained in Totem and Taboo. Anthropologically and archeologically the Band of Brothers theory has been put in doubt, but the burial mound theory not so much. Which leaves room for a relation to a more utility based theory of emergence, although still not to divest oneself of the entirety of any violence/ death wish theory (such as Bowlby, although there are other evidence based aspects of Bowlby etc etc)).

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.

Plays be!

I believe in Kleist!

Get you, and your war machine!

*you’re a war machine

*you’re is a war machine

We were outside the chippy
And I tried to impress her
I said

My stories are embellished
Like your
Pawn shop jewels.

I run with the pawn shop jewels
Like Goldie Lookin Chains
Newhaven State of Mind.

She looked at me,
Generic brand ketchup
smeared across her red lips
And said

*you’re porn shop jewels

My signifiyng chains
Left strung out like a
Glistening pearl necklace.
The remains of my poet’s trophy
A mere half imagined
Bukkake interruptus.

He was signifier surfing
When a shark approached.

Fortunately,
It wasn’t a Great White,
It was a Bakhtin shark

It’s not so much a demand for the sublimation of the Other, it’s more like some kind of desperate insistence on someone else’s passive aquiescence (disguised as humble acceptance) to a sub/dom subspace,
dry edged demiurge, Balian cock flicking,
nu-Protestant Ethic spirit of capitalism in the age of austerity, mindfulness for the coming Asian mode of reproduction (as we head towards the climate change End Times, with increasing inequality), unconsummated orgasm, as a relation to the symbolic, as an externalised exploitative utility, self-interested philautia disguised as the speech of the one true hubristic spokesperson for a holy agape, emotionally and behaviourally disciplined social order, as a catharsis for the failure of a narcissitic, virtue signalling performance as a ‘good person’ who lives for their faith.

Someone said to me “If you know so much about mental health, how come you are still living at the state’s expense”

I tried saying, just because you are a cancer specialist doesn’t mean you won’t get cancer.

But that was ‘too biological’ an analogy

I tried explaining that ironically what i know explains more about how come not just me, but a lot of people are not just still at the state’s expense, but need to be, rather than any magical voluntarist self-help cure.

But it wasn’t enterpreneurial, hard work of personal recovery enough a ‘story’ for him.

So i said ‘it’s like in business… it’s not what you know, it’s who you know’

An article I contributed to for the Morning Star


“ONE of the most vitriolic power struggles between professional groups is happening now and goes to the very essence of what is, or is not, mental illness.

Squaring off against each other are those who believe in a biomedical or genetic basis to mental illness (in the main, psychiatrists) and those who believe mental illness is a natural response to a threat or trauma (mainly psychologists).

At the root of it, is the battle between professions for legitimacy. Who should be controlling the narrative and who should be informing policy? Yet forgotten are the service users who are most affected by such policy arguments at this level.

The result is a confused message about mental health. For all the campaigns to reduce stigma for those with a mental illness, there is a significant crowd of voices rubbishing the very idea of mental illness, whether it is biological or from trauma

continue reading: https://morningstaronline.co.uk/article/f/traumatic-power-struggle-within-mental-health

Some unrecovery analogy imagery:

We have all played Kerplunk I hope. But as a recap there is a tube with holes, sticks are crisscrossed holding up some balls, and the trick is to remove the sticks without all the balls falling.

Our mental health is like a game of Kerplunk, and our issues are a combination of the balls and sticks. ‘Recovery’ is the ability to remove the sticks without the balls falling. As a slight adaptation to this analogy some of the balls can be removed by moving sticks, and ‘life’ adds balls all the time. The sticks are ‘safety’ adaptations that stop all the balls falling at once.

This game of Kerplunk is mostly played by us alone (in our own minds), so in this analogy the game is played in a room on your own. But we can always hear people telling us which sticks we ‘should’ remove, whilst we are sitting there looking at the problem, even though these people are not in the room with us. Government policy also demands we remove sticks, and moreover can add balls (as can other aspects of life), as well as remove sticks if we don’t keep an eye on them.

Unrecovery practices are an ad hoc practice, that is a temporary solution to keep control of our own Kerplunk game, knowing that a wrong move can send all the balls falling. ‘Bad’ recovery is procrustean and insists on this or that stick must be removed, and then blames you when the balls fall. ‘Good’ Recovery, and other therapeutic practices, listens to your knowledge of what you can see of the game, and merely supports you with your autonomy whilst you play the game. This latter ideal however from our observation seems to be at odds with current government policy and market/ capitalist needs, as it doesn’t meet the outcomes measures of outside forces.

For those who don’t know the term, that I have added some changes to the games with sticks and balls being added and removed whilst you play, like a Heath Robinson machine, is what is called an assemblage. Unrecovery is an ad hoc practice with which to deal with such an assemblage.