Interactionism (nature versus nurture)

Perspective that human behavior is caused by interaction of genetic and environmental factors

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.[1] Historically, it has often been confused with the statistical concept of gene-environment interaction.[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.[3] Among the first biologists to propose an interactionist theory of development was Daniel Lehrman.[4] Since then, numerous interactionist perspectives have been proposed, and the contradictions between many of these perspectives has led to much controversy in evolutionary psychology and behavioral genetics.[5][6] Proponents of various forms of interactionist perspectives include Philip Kitcher, who refers to his view as "causal democracy", and Susan Oyama, who describes her perspective as "constructive interactionism".[7] Critics of interactionism include major figures in behavioral genetics such as Arthur Jensen, Robert Plomin, and philosopher Neven Sesardic.[8][6][9][10]

## Interactionist perspective to depression[edit]

Depression is not dependent entirely on genetic nor environmental influences alone to trigger its onset. Both genetic and environmental factors work accompanied to transform a vulnerability to depression to be expressed in its actuality. Research has demonstrated the synchrony of polygenic scores of major depressive disorders (MDD) with stressful life events and social support to increase the probability of developing depression. Although Monroe and Simons criticize interactionism for a lack of precise measurement to grasp its ‘conceptual essence’, there’s been numerous studies surrounding gene by environment interaction commonly focussing on candidate genes such as genetic variation within the serotonin transporter (SLC6A4) gene.[11] As MDD is a polygenic trait its development is dependent on variations of a range of genes each exhibiting small effect sizes. Peyrot et al also found increased polygenic risk scores and genetic vulnerability in the presence of childhood trauma demonstrating the collaboration between environmental and genetic stressors.[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. When passive, meaning the individual played less of an active in their trauma i.e., illness or accident, the heritability wasn’t as severe than when active i.e., in cases of separation, relationship conflict, financial or legal trouble. Contrarily, Mullins found whilst polygenic risk scores and stressful events were predictors of depression, however he believed them to be isolated factors acting independently.[13]

The combined therapy (psychotherapy with pharmacotherapy) for depression did show statistically significant improvement compared with psychotherapy[14] and pharmacotherapy.[15] This is the value of considering both genetic and environmental factors in the explanation for depression. However, the effectiveness depends on severity and chronicity. In mild and moderate non-chronic depression, the combined therapy has no differences from single therapy.[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.[16]

## Interactionist perspective to PTSD[edit]

Ecological, biological, and residual stress pathways interact in order to manifest post-traumatic stress disorder (PTSD), the experience of trauma being the primary contributor to PTSD. The severity of trauma is a prime factor to the onset of PTSD but the question as to why only a fraction of individuals who experience trauma develop a pathological response whilst others do not rest in the assumptions that it is the combination of both genetic vulnerability that exhibit PTSD in alliance with environmental trauma. Among those who experience extreme severities of PTSD such as violent crimes, assault, severe accidents, approximately 3-35% develop symptoms. 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. And biological pathways include neurological anomalies, inherited traits, and structural anomalies such as hippocampal atrophy. 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. Ecological pathways include factors such as a history of abuse, physical and sexual. Women with a history of physical abuse were found to be 5x more likely to have a history of PTSD, 10x more susceptible to experiencing it then controls. Parental abuse is a predictor for future anti-social behaviour and decreased social skills, and maladaptive social information processing increasing sensitivity to PTSD. 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.

Biological pathways include a diversity of factors including hormonal and neurotransmitter abnormalities, and alterations in neural structure. Male adults of PTSD were found to have higher urinary biproduct of norepinephrine and epinephrine (adrenaline), lower cortisol levels, and abnormalities in neurotransmitter levels associated with anger, hostility and depression related to PTSD. Increased norepinephrine is involved with the activation of traumatic memories, and increased catecholamines are what lead to increased levels of stress-related hormones such as cortisol, and neurotransmitters associated with PTSD, which in the instance of trauma increases one’s vulnerability to it. 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. Furthermore, corticotropin releasing hormone (CRH) increases heart rate and enhances fear conditioning and is also the hormone responsible for regulating the HPA axis which corresponds with symptoms of PTSD.[17]

## Interactionist perspective to Schizophrenia[edit]

### Background information[edit]

The twin study that investigated the development of schizophrenia found that identical twins are at risk of developing schizophrenia than non-identical twins.[18][19] However, in those research, none of them found identical twins 100% developed schizophrenia together. This suggests the development of schizophrenia is not only due to genetic causes but also impacted by environmental factors. On the other hand, in an adoption study, the participants were all adopted by a family without schizophrenia history at an early age. Children with a genetic schizophrenia mother are more sensitive to negative child-raring style than those with no genetic risk. Have genetic risk children are more likely to develop schizophrenia in such families.[20] This suggested the role of biological factors in the development of schizophrenia. Therefore, researchers consider the interaction of genetic and environmental factors to explain schizophrenia. This is also the tendency of psychologists to research mental disorders.

### Diathesis stress model[edit]

A diathesis-stress model is an interactionism approach. In the context of schizophrenia, diathesis is the vulnerability. This vulnerability can be either biological predisposing or early experiences, or both.[21] The stressor could be any event that can trigger schizophrenia. This stressor can trigger a schizophrenia vulnerability individual to the onset of the condition.[22][23][24] This interactionism approach explained why people with similar genes or traumatic experiences, did not develop schizophrenia together.

#### Early diathesis-stress model[edit]

The early diathesis-stress model[25] suggested that diathesis is a single gene, called schizogene. It leads to a personality development. He named it schizotypic personality. Individuals who do not have schizotypic personality would not express the symptoms of schizophrenia, no matter what stress they experience. However, once a schizotypic personality, the stress from the family can trigger schizophrenia. This model is over-simple. First, more recent research found that 108 genes are associated with the development of schizophrenia.[26] No schizogene determines schizophrenia, it is a polygenic mental disorder. Second, the stressor is not limited to the family environment, but any negative experience in life.[27] For example, childhood traumas, low socioeconomic status, substance misuse…

#### Modern diathesis-stress model[edit]

However, the idea of the diathesis-stress model did not be given up. More recent research developed a more comprehensive model. The research suggests that genetic defect leads to individuals becoming sensitive to stress, and create biological vulnerability.[24] Their dopamine (DA) receptor is an abnormality and hippocampal damage. Then, stressors can activate the hypothalamic pituitary adrenal (HPA) axis of vulnerable individuals.[23][24] This would lead to the release of cortisol and hippocampal damage. The release of cortisol can further disrupt that abnormal DA system. According to the dopamine hypothesis, the DA system abnormality is associated with the symptoms of schizophrenia. Also, the stressor will further damage the hippocampus, and this is associated with schizophrenia symptoms.[24] It also causes patients hypersensitive to stressors in everyday life,[22][24] this is a negative cycle. Stress is not just a trigger of schizophrenia, but also leads to deterioration.

More recent research found that diathesis is not just biological. Early childhood traumas can also lead to psychological vulnerability.[28][29][22] This traumatic experience could be child abuse and neglect (CACN). For example, Read found that 69% of women and 59% of male patients experienced childhood abuse (physical abuse, sexual abuse or both).[28] They impact the early development of the brain and disrupt the HPA, DA and hippocampal systems.[29] This created a similar vulnerability as the gene.

More recent research found that stressor is not just a negative life experience. For example, Using cannabis could be a stressor that triggers the vulnerability of individuals who develop schizophrenica.[30][31] One significant finding in Houston[31] found that sexual abuse only has a significant correlation with the development of schizophrenia if the patients use cannabis. This could be because cannabis affects the dopamine system[21] and triggers that vulnerability. However, to the patients, the reason for using substances such as cannabis is for enjoyment.[32][33] Stressors are now defined as all events that can trigger vulnerability. Also, not all smokers develop schizophrenia, thus using cannabis only counts as a stressor.

### Application of interactionism approach to schizophrenia[edit]

The diathesis-stress model supports a reason for the combination treatment for schizophrenia.[27][29] If not approved the interactionism approach, there is unreasonable use of the combination treatment. The combination of CBT and drug treatment showed statistically significant improvement in reducing schizophrenia symptoms than a single treatment.[20] However, it did not show the effect of reducing the relapse rate.

#### Criticism of the application[edit]

Although recent research has a better understanding of the diathesis-stress model to explain schizophrenia. They still did not fully understand the mechanisms behind how vulnerability and stressors produce schizophrenia symptoms. Therefore, the interactionist treatment just simply combines biological and psychological treatment. However, combined therapy does not always have statistically significant improvement in mitigating schizophrenia symptoms compared to drug therapy. The combination treatment needs to pay for both drug and psychological treatment, but the effect is unstable. Thus, it is lack of cost-effectiveness.

## See also[edit]

* Flynn effect
* Heritability
* Diathesis-stress model
* Social information processing

## References[edit]

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