The Role Of Nature And Nurture In The Development Of Psychosis
When looking at the contributions of nature and nurture on adolescent mental health, it is likely that the causes of illnesses such as Psychosis, are not nature or nurture individually, but actually a combination of the two; therefore it is important to discuss how they interact on an epigenetic and biopsychosocial basis.
Genetics play a large role in the development of psychosis, as adolescents are more likely to be affected if a family member has been prior. Twin studies suggest the concordance rates for psychotic mental illnesses (like schizophrenia) for monozygotic twins are around 45% and heritability estimates are around 80%. Therefore, although there is a clear genetic correlation, there must be some external influences on psychosis, as monozygotic twins share 100% of their DNA. In studies looking at the effects of stressful life events on psychosis, the overall conclusion states that stressful life experiences, like victimization or even trauma can predict psychotic episodes later in adolescence. Analysis of genetic influences explained most, but not all slight differences in SLE’s, suggesting genetic factors are potentially being influential on individual’s subjection to certain stressful environments (as well as the extent to how much stress they evoke), meaning the environmental factors are somewhat heritable. The ‘LEAP’ study used a self-report method of assessing SLEs, and a questionnaire (SPEQ) for measuring psychotic experiences on monozygotic and dizygotic twins, was done to assess the extent to which single phenotypes can be attributed to genetic and environmental factors. The study showed that all types of SLEs were moderately associated with positive psychotic symptoms, whether it be in our out of personal control.
In adolescence, social stresses experienced daily can build up and increase the risk of experiencing psychotic episodes however, there must be a present genetic propensity to be triggered. A biopsychological explanation is the vulnerability of the adolescent brain, which has a high sensitivity to cortisol, so adolescents feel stress more intensely and quickly. As well as this, adolescents have a less developed Pre- frontal cortex, which is responsible for stopping the stress response; it is likely they feel stress for a longer period of time, so have a larger window for a potential spur of psychosis.
Studies have found a correlative link between the use of cannabis in adolescence and the onset of psychosis. It has been found that those who use cannabis regularly in early adolescence, had more psychotic symptoms later in their adolescent years compared to a control group. (Harkany et al, 2008). Cannabis can be particularly harmful to those with a family history of psychosis, and due to past stigma may be unknowingly at risk. In adolescence, cannabis can affect the neurodevelopmental processes (like synaptic plasticity), and interfere with usual development of processes, potentially including the dysfunction of dopamine. The endocannabinoid system is responsible for ‘neuronal cell proliferation, migration and differentiation’, so the use of THC may lead to irreversible neurobiological changes affecting functions and behaviour. Neuroplastic changes that take place in cannabis users (especially the effects on BDNF), can be linked to a potential mechanism causing the consequences of exposure to cannabis, including disorders showing interference with neurodevelopment, such as psychosis.
A possible explanation for this, in terms of epigenetics, could be that external factors can influence gene expression, causing physiological changes, that subsequently increase the risk of developing psychosis. Overall, this would suggest and underlying biological input of cannabis that can subsequently cause psychosis, however it is the lifestyle choices made by individuals that triggers such adversity which involves a nurture aspect. The choice to use cannabis could be due to pressures from the individuals lives (living environment) or a copying mechanism for their intense emotions. For this reason, again, psychosis can’t be attributed solely to nature or nurture.
Brain scans have revealed that reduced grey matter may be linked with psychotic symptoms, which can affect thought processing. Adolescents brain areas develop at different rates; the more basic functions first, followed impulse control later. Subsequently, adolescents feel emotions more intensely and may react strongly to situations, especially during the stressful years of adolescence. This is related to rewards system of the brain, meaning there is an abundance of hormones such as dopamine, so intense situations will cause even higher amounts of the neurotransmitter. Studies have shown that ‘dopamenic agonists’ can induce psychosis in healthy individuals, and worsen psychosis in those with schizophrenia, so we assume high levels cause psychosis.
A gene that regulates levels of dopamine is the COMT gene, found on the 22nd chromosome. Individuals that seem to lack in this area are 30 times more likely to develop schizophrenic and psychotic symptoms. There are studies which show COMT can predict schizophrenia, based on a genetic association approach, whereby variabilities of the gene are screened to observe whether any variation is more common in schizophrenics. In addition, studies have also investigated the variation in the amino acid sequence of the COMT enzyme and noticed that the amino acid valine at position-108, is replaced with methionine. Because this polymorphism is co-dominant, it causes a decrease in the molecular thermo-stability of the protein, hindering its ability to break down dopamine. Furthermore, it was found that individuals with valine in place of methionine at position 158, have decreased cognitive function and are also more likely to develop schizophrenia. This would suggest an overlying genetic factor may be linked to the causes of schizophrenia.
Empirical evidence, focusing on biological brain functions, shows there is a predisposition for psychosis. Therefore, the extent to which the environment influences our risk of developing it, can be inflated by our gene expression in certain situations. However, saying nature alone is responsible for the cause of schizophrenia, would be a gross simplification of the matter, as gene expression can be influenced by external factors such as stress and lifestyle choices. The cause of psychosis must be an interplay between the two.
