Some psychologists are reaching the conclusion that psychosis is often no more and no less than a natural reaction to traumatic events. For example one recent paper suggested that ‘there is growing evidence that the experiences service users report … are, in many cases, a natural reaction to the abuses they have been subjected to. There is abuse and there are the effects of abuse. There is no additional ‘psychosis’ that needs explaining’.
The Impact of Trauma
Eleanor Longden and John Read take a long hard look at the evidence for the involvement of trauma in the incidence of psychosis, and look carefully at the implications of that in their article The Role of Social Adversity in the Etiology of Psychosis. A degree of patience will be required here as some quotes are a bit technical. Hopefully your patience will be rewarded by the insights gained. Later posts in this sequence will return to easier terrain!
They are not impressed by the proponents of mainstream thinking (page 6):
Neither the NIMH nor the UK’s National Health Service (NHS, 2014) websites cite the considerable research that implicates traumatic or adverse events as causes of psychosis.
So, while the increased presence of voices that argue against the view that dismisses psychosis as a self-contained abnormality is encouraging, there is still a long way to go. Moreover, it’s of critical importance that we shift the consensus towards normalising psychosis. Exactly what I mean by that will become clear as I go along.
They quote rigorous analyses of multiple studies (meta-analyses in the jargon) that demonstrate beyond dispute in their view that (page 7) ‘individuals with a history of childhood trauma (child sexual abuse, physical abuse, emotional abuse, neglect, bullying, parental death) were shown to be 2.8 times more likely to develop psychotic symptoms than those who had not.’ They also explain that (pages 7-8):
Large-scale population studies have shown that associations between adversity and psychotic experience remain significant when controlling for possible confounders, including: family history of psychosis and other mental health problems (which negates the notion that psychosis only occurs in those genetically predisposed), age, sex, ethnicity, marital status, exposure to discrimination, other psychiatric diagnoses, education level, neuroticism, and substance use.
Moreover they feel the evidence proves that ‘the likelihood of psychosis increases relative to the extent of adversity exposure.’
They explain in detail why they think that patients’ accounts of abuse and trauma cannot be dismissed as deluded fabrications. Patient testimonies, in their view, hold up as well as those provided by people without any diagnosis.
Shields, in a paper I will be discussing in more detail later adds head injuries into the mix in a particularly interesting way (Pages 148-9:
One classic and commonly discussed risk factor for psychosis is a head injury (Symonds, 1937). Although there are conflicting data (cf. David & Prince, 2005), there is good reason to believe that a traumatic brain injury does indeed predispose individuals to psychosis (Molloy, Conroy, Cotter, & Cannon, 2011). However, why and how traumatic brain injuries bring about the occurrence of psychosis is unknown. This paper proposes that this predisposition is due to damage of the lateral prefrontal cortex (lPFC) or connectivity to it. The lPFC is responsible for suppressing unwanted thoughts and memories (Anderson et al., 2004). A consequence of this is that impairing the lPFC entails a diminished ability to avoid dealing with unwanted thoughts and memories. Therefore, an individual who has incurred a head injury that damaged or impaired his or her lPFC cannot avoid dealing with unwanted thoughts or issues to the same degree that a healthy individual can. Because of that, when faced with existentially distressing issues, an individual with an injured lPFC who chooses to try to avoid these issues would suffer psychotic breaks when a healthy individual faced with the same issues would not – as the weight of these issues would not press down as hard on healthy individuals who can repress them.
Shields also has an unusual take on the idea that drug use is one of the causes of psychosis (page 149):
Drug use – particularly cannabis use– is associated with an increased risk of developing psychosis (Moore et al., 2007). [My] hypothesis, however, notes that drug use is often an attempt by an individual to escape from reality. Rather than drug use being the cause of psychosis, then, drug use would be a symptom of an inability to deal with reality as it is – which is a clear precursor to psychosis on this view.
Longden and Reid, to come back to their perspective, also give short shrift to the genetic argument and quote a powerful piece of evidence to support their scepticism (page 11):
A particularly shocking demonstration of the limitations of the genetic argument is an epidemiological analysis of the prevalence and incidence of schizophrenia in Nazi Germany, wherein it is estimated between 220,000 and 269,500 citizens with the diagnosis were forcibly sterilized or murdered by the Nazi regime (Read & Masson, 2013; Torrey & Yolken, 2010). Contrary to everything that is known about genetic, heritable conditions, the rates of schizophrenia diagnoses in Germany did not diminish after the war but increased. The analysis showed this atrocity provided proof against the very reasoning used to instigate it.
Because they are convinced by the evidence suggesting that trauma is a major trigger of psychosis they can make a telling point against simplistic claims that genes lead to defective brains that make you psychotic. They write (page 12):
To assume that brain differences exist in a social vacuum, and are solely and causally responsible for schizophrenia, has the same logic as suggesting neural changes during bereavement are the causes of sadness rather than the loved one’s loss.
They continue by describing an explanatory model that states clearly that trauma as the child grows damages the brain in ways that are likely to create psychotic experiences (ibid):
The traumagenic neurodevelopmental (TN) model of psychosis (Read, Perry, Moskowitz, & Connolly, 2001) synthesises biological and psychological research to emphasise the similarities between structural and functional abnormalities in the brains of abused children and those of adult patients with psychosis (which, correspondingly, reflect the differences between patients with psychosis and healthy adults, and traumatised and non-traumatised children). A major premise of the TN model is that the heightened stress sensitivity consistently found in patients with psychosis is not necessarily inherited, but caused by formative exposure to abuse and neglect.
They discuss in more technical detail than it is appropriate to include here exactly what kind of damage has been done to the brain. In a later sequence of posts I will be unpacking a powerful explanatory model (Mike Jackson in Psychosis and Spirituality – pages 139-153), which attempts to pinpoint, from a psychological rather than a biological point of view, the issue of exactly why the trajectory of some people’s experience of psychosis is quite positive while that of others is so negative.
Longden and Reid then move on to discussing the problems surrounding the currently preferred treatment, which is based on the idea that excess brain dopamine or dopamine sensitivity is the cause of psychosis (page 15):
. . . . the dopamine hypothesis was crafted from indirect evidence—the seemingly beneficial sedative effects of neuroleptics. On discovering their main mode of action was blocking dopamine receptors, the argument developed that schizophrenia itself must therefore result from dopamine overactivity. Thus rather than designing a therapeutic agent to treat a disorder, a disorder was hypothesised to fit the drug; and, as pointed out by Jackson (1986), is as logically tenable as claiming headaches are induced by a lack of aspirin.
They do not deny that dopamine could well be implicated in reactions to stress. They do though feel that the efficacy of medication has been falsely explained and possibly overstated, especially as (page 17) ‘long-term medication use may lead to some of the neurological anomalies traditionally ascribed to psychosis itself (Moncrieff & Leo, 2010; Smieskova et al., 2009).’ These anomalies include shrinkage of the frontal lobes.
Grant S Shields, in a paper to which we will be returning shortly, suggests their scepticism is warranted (page 42):
[B]iological treatments of psychosis are somewhat ineffective: the efficacy of antipsychotic drugs to reduce psychotic symptoms and prevent relapse is only 41% (Leucht, Arbter et al., 2009; Leucht, Corves et al., 2009).
If medication is at best only a partial solution with potentially damaging side-effects, where do we go next. The authors of this paper argue for Compassion Focused Therapy but admit the evidence-base supporting its use is thin up till now. This needn’t stop us looking more closely at why some form of psychotherapy could well work.
Next time I will be looking at what the purpose of a psychotic experience might be.
 This can be found in the American Journal of Psychotherapy, Vol. 70, No. 1, 2016
 To be found in Existential Analysis 25.1: January 2014.
 To be found in Existential Analysis 25.1: January 2014.