In the context of the nature-nurture debate, interactionism is the view that all human behavioral traits develop from the interaction of both "nature" and "nurture", that is, from both genetic and environmental factors.
This view further holds that genetic and environmental influences on organismal development are so closely interdependent that they are inseparable from one another.
[2] Historically, interactionism has presented a limited view of the manner in which behavioral traits develop, and has simply demonstrated that "nature" and "nurture" are both necessary.
[7] Critics of interactionism include major figures in behavioral genetics such as Arthur Jensen, Robert Plomin, and philosopher Neven Sesardic.
Both genetic and environmental factors work accompanied to transform a vulnerability to depression to be expressed in its actuality.
[11] As MDD is a polygenic trait its development is dependent on variations of a range of genes each exhibiting small effect sizes.
[12] In the instance of personal life events however, whether they were passive or active trauma has a mediating effect on the heritability of the disorder.
Contrarily, Mullins found whilst polygenic risk scores and stressful events were predictors of depression, however he believed them to be isolated factors acting independently.
[14] Whilst results in the field are unreliable, research generally points in favour of the compatibility between genetic and environmental contributors to psychopathology and depression.
As inherent vulnerability increases the threshold for the environmental trauma to trigger the disorder decreases.
Residual stress is a key factor in the expression of PTSD, it is the initial and prolonged effects of trauma and a catalyst in its development.
Ecological and biological pathways are also preceding factors that increase the likelihood of PTSD following trauma and residual stress.
Ecological pathways include both personal and environmental influences such as coping mechanisms, interpersonal support, and the individual’s environment.
Ecological and biological factors provide a predisposition whilst residual stress triggers its onset.
Greater trauma leads to greater levels of residual stress, and trauma can be divided into pre-trauma i.e., childhood abuse, and post-trauma i.e., social support, in which females are more influenced by post-trauma than their male counterparts in the development of PTSD.
For example, survivors of sexual abuse found PTSD was influenced considerably by familial nature of support, negative parental reactions were found to intensify PTSD whereas high levels of social support helped diminish psychological fallout and recovery time.
These environmental factors aside from residual stress generate maladaptive cognitive patterns that provide a ‘breaking point’ to individuals with genetic vulnerability to PTSD to exhibit the disorder.
Furthermore, structural alterations increase the susceptibility of PTSD, for example, sexually abused adolescent girls and those generally maltreated in comparison to a control group had dysregulation within their hypothalamic pituitary adrenal axis (HPA) alongside decreased hippocampal volume.
[23][24][25] This interactionism approach explains why people with similar genes or traumatic experiences, do not necessarily develop schizophrenia together.
[32][33] Houston[33] found that sexual abuse had a significant correlation with the development of schizophrenia, only if the patients used cannabis.
However, combined therapy demonstrates statistically significant improvement in reducing schizophrenia symptoms compared to a single treatment.