Is there a link between schizophrenia and work-related stress: has evolving medical science been able to establish any connection between the two?

Schizophrenia is consistently ranked by the World Health Organisation (WHO) as one of the top 10 causes of disability worldwide. It results from the cumulative effects of several risk factors, rather than a single cause, including genetic predisposition, early environmental factors, environmental influences and biological processes. Schizophrenia has a significant developmental component, and numerous scientific articles have been published which look at how developmental and environmental factors contribute to the risk of developing schizophrenia. This includes stressful life events.

Background

Schizophrenia is a long-term mental health condition often described as a psychotic illness. It causes a variety of symptoms, such as hallucinations, delusions, disorganised behaviour/speech and lack of emotion. It is commonly associated with impairments in cognitive, social and occupational functioning.

Identifying the mechanisms that can lead to development or worsening of these disorders to promote functional recovery is an area of interest and focus for mental health research. The most powerful indicator of risk is having a relative with schizophrenia. The lifetime risk for schizophrenia increases from about 1% in the general population to about 10% in the first-degree relatives of patients with schizophrenia, to over 40% in identical co-twins of schizophrenic individuals and to nearly 50% in those who have two parents with the disorder. Twin studies were the first studies to provide compelling evidence for the role of genetic factors in the aetiology of schizophrenia, demonstrating that it is shared genes that determine this familial aggregation. However, the specific genes involved have not been identified.

Some studies have explored the link between environmental risk factors and the development of schizophrenia including pregnancy and birth complications, prenatal exposure to rubella, and prenatal malnutrition. Such studies indicated that epidemiological risk factors for schizophrenia include living in an urban area, immigration, employment and educational difficulties, drug abuse and adverse life events. There is evidence to suggest that the pathophysiology of schizophrenia proceeds from a complex interaction between genes and the environment which complicates efforts to differentiate the relative contributions of each.
 

Does stress play a role?

Some studies have reported an excess of stressful life events in the few weeks before the onset or relapse of schizophrenia illness.

Evidence gleaned from existing studies indicates that stress may serve as both a precipitating factor and an aggravating influence in the development of latent psychotic disorders. Evidence suggests that sustained or significant exposure to stress can adversely affect individuals with an existing vulnerability, increasing the likelihood that such disorders will surface.

A number of mechanisms have been proposed to explain the relationship between stress and the onset of psychotic symptoms. Notably, activation of the hypothalamic–pituitary–adrenal (HPA) axis during periods of stress can alter cortisol levels, subsequently impacting cerebral functioning in regions commonly associated with psychosis, including the prefrontal cortex and the hippocampus. Stress is also understood to disrupt dopaminergic pathways, which play a central role in the presentation of psychotic phenomena. Such disruption may heighten dopamine receptor sensitivity or increase dopamine release, creating conditions in which psychotic episodes may emerge or intensify.

The vulnerability–stress (or diathesis–stress) model is widely regarded as relevant in this context. It proposes that individuals with a genetic or biological predisposition to psychosis are more susceptible to developing symptoms when exposed to substantial psychosocial stressors. The interplay between genetic vulnerability, environmental pressures and individual resilience ultimately influences whether a psychotic disorder is likely to manifest under stress.

There is conflicting evidence on whether people with schizophrenia experience more stressful life events than unaffected individuals, but evidence indicates that the risk for schizophrenia-spectrum psychopathology increases as one experiences more stressful life events. Further, people at varying points along the schizophrenia spectrum tend to experience elevated negative affect and elevated perceptions of uncontrollability in response to everyday stress. However, stress remains one of the lowest risk environmental risk factors identified with other factors being more prevalent.
 

What this means for Defendants and Insurers

Whilst claims are few and far between, Clyde & Co has seen a small number of stress related claims in which schizophrenia is alleged to have been caused, contributed to and/or accelerated. Thus far, these claims have not been progressed due to the lack in persuasive medical evidence on the link between work related stress and psychotic illness.

Whilst there is evidence out there to support a link between stressful life events and the onset of psychotic disorders, including schizophrenia, proving such a link is going to be challenging for Claimants. Claimants will need to prove that on the balance of probability, the work related stress reported caused, or contributed to the development of the Claimant’s psychotic condition. Multi factorial aetiology always complicates causation when it comes to civil litigation, and in the case of schizophrenia, studies to date have shown that familial and genetic factors carry by far the greatest risk and that the effect of individual environmental factors is modest. There are also added complications for Claimants in this area.
 

The significance of the prodromal phase

Psychotic illnesses are often preceded by a prodromal phase which can last months or years, and in which symptoms vary over time. For schizophrenia, ICD 11 states that “A prodromal phase often precedes the onset of psychotic symptoms by weeks or months. The characteristic features of this phase often include loss of interest in work or social activities, neglect of personal appearance or hygiene, inversion of the sleep cycle and attenuated psychotic symptoms, accompanied by negative symptoms, anxiety/agitation, or varying degrees of depressive symptoms.” It is therefore entirely possible, and no doubt likely, that Claimants will be experiencing this phase throughout the duration of any perceived work-related problems.
 

Difficulties with retrospective attribution

There is the additional problem in that people naturally look for explanations in life. Brown and Birley did studies in the late 1960s about acute onset of schizophrenia. They specifically looked at individuals with an acute onset so that they could see exactly when the onset of the illness was and then interview patients and relatives about the three month period before then. They also had a comparison group. The acute onset illness group did report more “threatening” stressful events in the three weeks prior to their acute presentation.

It is worth noting that the events included were overtly threatening, such as physical trauma or threat and emotional abuse, and not the kind of stressors typically reported in claims for work related stress.

Further, there are more general studies and observations which have pointed to contradictory findings. For example, hospital admissions with psychosis did not increase in England during the blitz, and there was not a grossly increased rate of psychosis in concentration camp survivors, or in US soldiers in World War II. There were increases in neurotic illnesses in some of these situations.

There is also the very unfortunate fact that a Claimant suffering from a psychotic illness is unlikely to be a reliable historian. It is widely accepted that psychotic beliefs interfere with reality-based recall.
 

Conclusion

In summary, whilst there is evidence linking stress with the onset of psychosis, including an association with adverse life events and biochemical changes, based on medical research to date, it is going to be an uphill challenge for Claimant’s to prove that work related stress directly caused or contributed to the onset of illness in any individual case. Studies have made progress in identifying environmental risk factors for schizophrenia and the beginning of an understanding as to how such factors may interact with genetic predisposition.

Clarifying the exact nature of gene-environment interaction is likely to have to wait for the identification of the susceptibility genes for schizophrenia. The extent to which genetic predisposition is compounded by environmental effects cannot be fully explored until susceptibility genes for schizophrenia are identified.