Interactionism (nature versus nurture)

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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]

Contents

Interactionist perspective to depression

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 demonstrates 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, its effectiveness depends on the severity and chronicity of depression. For mild and moderate non-chronic depression, the combined therapy has no differences from a 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

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

Background

Twin studies that investigated the development of schizophrenia found that identical twins have a higher concordance rate for schizophrenia than non-identical twins. [18] [19] [20] However, none of them found a 100% concordance rate from identical twins. Identical twins have exact genes. This suggests the development of schizophrenia is not only due to genetic factors but also environmental factors. On the other hand, in an adoption study, participants were adopted at a young age by families without a schizophrenia history. Children with genetic risks (such as having a genetic schizophrenia mother) were more sensitive to negative child-raring styles than those with no genetic risk. They are more likely to develop schizophrenia in undesirable child-raring style families. [21] This suggests the role of genetic 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

The diathesis-stress model is an interactionism approach. In the context of schizophrenia, diathesis is the vulnerability. Vulnerabilities can be either genetic predisposition or early experiences, or both. [22] Stressors are any event that can trigger a schizophrenia-vulnerable individual to the onset of the condition. [23] [24] [25] This interactionism approach explains why people with similar genes or traumatic experiences, do not necessarily develop schizophrenia together.

Early diathesis-stress model

The early diathesis-stress model was developed by Meehl. [26] It suggested that diathesis was a single gene, called schizogene. It led to a personality development, called schizotypic personality. Individuals who did not have schizotypic personality would not express the symptoms of schizophrenia, no matter what stress they experienced. However, once a schizotypic personality, the stress from the family could trigger schizophrenia. This model is over-simple. First, more recent research found that 108 genes are associated with the development of schizophrenia. [27] No schizogene determines schizophrenia, it is a polygenic mental disorder. [18] Second, the stressors are not limited to the problematic family environment. They can be any negative experience in life. [28] For example, childhood traumas, low socioeconomic status, substance misuse…

Modern diathesis-stress model

However, the concept of the diathesis-stress model did not be given up. Researchers make it more comprehensive. The research suggests that genetic defect leads to biological vulnerability. [25] This schizophrenia–vulnerable individual’s dopamine (DA) receptors and hippocampus area were abnormal. Later, stressful experiences (the stressor) can activate their hypothalamic pituitary adrenal (HPA) axis. [24] [25] This leads to the release of cortisol. This 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. Stressors also further damage the hippocampus of vulnerable individuals. Schizophrenia patients have a smaller volume of the hippocampus compared with a typical brain [18] [29] [25] Moreover, stressors also cause patient more sensitive to stress in everyday life, [23] [25] this is a vicious cycle. Therefore, the stressors are not just a trigger of schizophrenia but also lead to deterioration.

In the more comprehensive model, diathesis is not just genetic. Early childhood traumas can also lead to psychological vulnerability. [18] [30] [31] [23] This traumatic experience can be child abuse and neglect. For example, Read found that 69% of women and 59% of male schizophrenia patients experienced childhood abuse (physical abuse, sexual abuse or both). [30] This experience impacts the early development of the brain. For example, disrupts the HPA, DA and hippocampal systems. [31] This can create a similar vulnerability to that created by genes.

Similarly, stressors are not just subjective negative life experiences. For example, using cannabis can be a stressor that triggers schizophrenia-vulnerable individuals to develop schizophrenics. [32] [33] Houston [33] found that sexual abuse had a significant correlation with the development of schizophrenia, only if the patients used cannabis. This can be because cannabis influences the dopamine system. [22] However, to the patients, the reason for using substances such as cannabis is for enjoyment. [34] [35] Therefore, stressors are now defined as all events that can trigger vulnerable individuals to express schizophrenia symptoms. However, not all smokers develop schizophrenia. Thus, using cannabis is only considered as a stressor but not a cause.

Application of interactionism approach to schizophrenia

The diathesis-stress model supports a reason for using combined therapy for schizophrenia treatment. [28] [31] If not approved the interactionism approach, there is no reason to use the combined therapy. For example, if therapists propose schizophrenia is due to genetic reasons. Then, it is difficult to convince the patients to participate in drug treatment followed by psychological treatment, and vice versa. However, combined therapy demonstrates statistically significant improvement in reducing schizophrenia symptoms compared to a single treatment. [36] [37] [38] Although it did not indicate the effect of reducing the relapse rate.

Criticism of the application

Recent research has a better understanding of the diathesis-stress model to explain schizophrenia. However, the mechanism by which vulnerability and stressors contribute to the development of schizophrenia remains unclear. [22] Therefore, the interactionist treatment (combined therapy) just simply combines psychotherapy and pharmacotherapy. This may be attributed to the reason why combined therapy does not always have statistically significant improvement in mitigating schizophrenia symptoms compared to drug therapy. [36] [37] In the case of combined therapy, it is more expensive than a single therapy. This unstable effectiveness can impact its promotion because it lacks cost-effectiveness.

Moreover, the significant improvement of the combined therapy can simply be because the effect of their own is added up. It does not necessarily mean there is an interaction effect between these two treatments. There can be a treatment causation fallacy. [22]

See also

Related Research Articles

<span class="mw-page-title-main">Schizophrenia</span> Mental disorder with psychotic symptoms

Schizophrenia is a mental disorder characterized by reoccurring episodes of psychosis that are correlated with a general misperception of reality. Other common signs include hallucinations, delusions, disorganized thinking, social withdrawal, and flat affect. Symptoms develop gradually and typically begin during young adulthood and are never resolved. There is no objective diagnostic test; diagnosis is based on observed behavior, a psychiatric history that includes the person's reported experiences, and reports of others familiar with the person. For a diagnosis of schizophrenia, the described symptoms need to have been present for at least six months or one month. Many people with schizophrenia have other mental disorders, especially substance use disorders, depressive disorders, anxiety disorders, and obsessive–compulsive disorder.

<span class="mw-page-title-main">Causes of mental disorders</span> Etiology of psychopathology

A mental disorder is an impairment of the mind disrupting normal thinking, feeling, mood, behavior, or social interactions, and accompanied by significant distress or dysfunction. The causes of mental disorders are very complex and vary depending on the particular disorder and the individual. Although the causes of most mental disorders are not fully understood, researchers have identified a variety of biological, psychological, and environmental factors that can contribute to the development or progression of mental disorders. Most mental disorders result in a combination of several different factors rather than just a single factor.

Post-traumatic stress disorder (PTSD) is a mental and behavioral disorder that develops from experiencing a traumatic event, such as sexual assault, warfare, traffic collisions, child abuse, domestic violence, or other threats on a person's life or well-being. Symptoms may include disturbing thoughts, feelings, or dreams related to the events, mental or physical distress to trauma-related cues, attempts to avoid trauma-related cues, alterations in the way a person thinks and feels, and an increase in the fight-or-flight response. These symptoms last for more than a month after the event. Young children are less likely to show distress, but instead may express their memories through play. A person with PTSD is at a higher risk of suicide and intentional self-harm.

Abnormal psychology is the branch of psychology that studies unusual patterns of behavior, emotion, and thought, which could possibly be understood as a mental disorder. Although many behaviors could be considered as abnormal, this branch of psychology typically deals with behavior in a clinical context. There is a long history of attempts to understand and control behavior deemed to be aberrant or deviant, and there is often cultural variation in the approach taken. The field of abnormal psychology identifies multiple causes for different conditions, employing diverse theories from the general field of psychology and elsewhere, and much still hinges on what exactly is meant by "abnormal". There has traditionally been a divide between psychological and biological explanations, reflecting a philosophical dualism in regard to the mind–body problem. There have also been different approaches in trying to classify mental disorders. Abnormal includes three different categories; they are subnormal, supernormal and paranormal.

<span class="mw-page-title-main">Diathesis–stress model</span> Psychological theory

The diathesis-stress model, also known as the vulnerability–stress model, is a psychological theory that attempts to explain a disorder, or its trajectory, as the result of an interaction between a predispositional vulnerability, the diathesis, and stress caused by life experiences. The term diathesis derives from the Greek term (διάθεσις) for a predisposition or sensibility. A diathesis can take the form of genetic, psychological, biological, or situational factors. A large range of differences exists among individuals' vulnerabilities to the development of a disorder.

<span class="mw-page-title-main">Gene–environment interaction</span> Response to the same environmental variation differently by different genotypes

Gene–environment interaction is when two different genotypes respond to environmental variation in different ways. A norm of reaction is a graph that shows the relationship between genes and environmental factors when phenotypic differences are continuous. They can help illustrate GxE interactions. When the norm of reaction is not parallel, as shown in the figure below, there is a gene by environment interaction. This indicates that each genotype responds to environmental variation in a different way. Environmental variation can be physical, chemical, biological, behavior patterns or life events.

Complex post-traumatic stress disorder is a stress-related mental disorder generally occurring in response to complex traumas, i.e., commonly prolonged or repetitive exposures to a series of traumatic events, within which individuals perceive little or no chance to escape.

The trauma model of mental disorders, or trauma model of psychopathology, emphasises the effects of physical, sexual and psychological trauma as key causal factors in the development of psychiatric disorders, including depression and anxiety as well as psychosis, whether the trauma is experienced in childhood or adulthood. It conceptualises people as having understandable reactions to traumatic events rather than suffering from mental illness.

Gender is correlated with the prevalence of certain mental disorders, including depression, anxiety and somatic complaints. For example, women are more likely to be diagnosed with major depression, while men are more likely to be diagnosed with substance abuse and antisocial personality disorder. There are no marked gender differences in the diagnosis rates of disorders like schizophrenia and bipolar disorder. Men are at risk to suffer from post-traumatic stress disorder (PTSD) due to past violent experiences such as accidents, wars and witnessing death, and women are diagnosed with PTSD at higher rates due to experiences with sexual assault, rape and child sexual abuse. Nonbinary or genderqueer identification describes people who do not identify as either male or female. People who identify as nonbinary or gender queer show increased risk for depression, anxiety and post-traumatic stress disorder. People who identify as transgender demonstrate increased risk for depression, anxiety, and post-traumatic stress disorder.

Childhood trauma is often described as serious adverse childhood experiences (ACEs). Children may go through a range of experiences that classify as psychological trauma; these might include neglect, abandonment, sexual abuse, emotional abuse, and physical abuse, witnessing abuse of a sibling or parent, or having a mentally ill parent. These events have profound psychological, physiological, and sociological impacts and can have negative, lasting effects on health and well-being such as unsocial behaviors, attention deficit hyperactivity disorder (ADHD), and sleep disturbances. Similarly, children whose mothers have experienced traumatic or stressful events during pregnancy have an increased risk of mental health disorders and other neurodevelopmental disorders.

Schizophrenia is a neurodevelopmental disorder with no precise or single cause. Schizophrenia is thought to arise from multiple mechanisms and complex gene–environment interactions with vulnerability factors. Risk factors of schizophrenia have been identified and include genetic factors, environmental factors such as experiences in life and exposures in a person's environment, and also the function of a person's brain at it develops. The interactions of these risk factors are intricate, as numerous and diverse medical insults from conception to adulthood can be involved. Many theories have been proposed including the combination of genetic and environmental factors may lead to deficits in the neural circuits that affect sensory input and cognitive functions.

Memory and trauma is the deleterious effects that physical or psychological trauma has on memory.

The differential susceptibility theory proposed by Jay Belsky is another interpretation of psychological findings that are usually discussed according to the diathesis-stress model. Both models suggest that people's development and emotional affect are differentially affected by experiences or qualities of the environment. Where the Diathesis-stress model suggests a group that is sensitive to negative environments only, the differential susceptibility hypothesis suggests a group that is sensitive to both negative and positive environments. A third model, the vantage-sensitivity model, suggests a group that is sensitive to positive environments only. All three models may be considered complementary, and have been combined into a general environmental sensitivity framework.

<span class="mw-page-title-main">Transgenerational trauma</span> Psychological trauma

Transgenerational trauma is the psychological and physiological effects that the trauma experienced by people has on subsequent generations in that group. The primary modes of transmission are the uterine environment during pregnancy causing epigenetic changes in the developing embryo, and the shared family environment of the infant causing psychological, behavioral and social changes in the individual. The term intergenerational transmission refers to instances whereby the traumatic effects are passed down from the directly traumatized generation [F0] to their offspring [F1], and transgenerational transmission is when the offspring [F1] then pass the effects down to descendants who have not been exposed to the initial traumatic event - at least the grandchildren [F2] of the original sufferer for males, and their great-grandchildren [F3] for females.

A cognitive vulnerability in cognitive psychology is an erroneous belief, cognitive bias, or pattern of thought that predisposes an individual to psychological problems. The vulnerability exists before the symptoms of a psychological disorder appear. After the individual encounters a stressful experience, the cognitive vulnerability shapes a maladaptive response that increases the likelihood of a psychological disorder.

The genetic influences of post-traumatic stress disorder (PTSD) are not understood well due to the limitations of any genetic study of mental illness; in that, it cannot be ethically induced in selected groups. Because of this, all studies must use naturally occurring groups with genetic similarities and differences, thus the amount of data is limited. Still, genetics play some role in the development of PTSD.

Epigenetics of anxiety and stress–related disorders is the field studying the relationship between epigenetic modifications of genes and anxiety and stress-related disorders, including mental health disorders such as generalized anxiety disorder (GAD), post-traumatic stress disorder, obsessive-compulsive disorder (OCD), and more. These changes can lead to transgenerational stress inheritance.

Ming Tso Tsuang is an American psychiatrist and Distinguished Professor of Psychiatry at the University of California, San Diego. He is considered a pioneering researcher in the genetic epidemiology of schizophrenia and other severe mental disorders. Tsuang has authored and co-authored more than 600 publications and serves as founding and senior editor of the American Journal of Medical Genetics Part B.

Gene-environment interplay describes how genes and environments work together to produce a phenotype, or observable trait. Many human traits are influenced by gene-environment interplay. It is a key component in understanding how genes and the environment come together to impact human development. Examples of gene-environment interplay include gene-environment interaction and gene-environment correlation. Another type of gene-environment interplay is epigenetics, which is the study of how environmental factors can affect gene expression without altering DNA sequences.

Robert Keers was a British psychologist conducting innovative research on individual differences in mental health problems with a specific focus on psychiatric genetics.

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  35. ↑ Buadze, Anna; Stohler, Rudolf; Schulze, Beate; Schaub, Michael; Liebrenz, Michael (December 2010). "Do patients think cannabis causes schizophrenia? - A qualitative study on the causal beliefs of cannabis using patients with schizophrenia". Harm Reduction Journal. 7 (1): 22. doi: 10.1186/1477-7517-7-22 . PMC   2954921 . PMID   20920183.
  36. 1 2 Morrison, Anthony P; Law, Heather; Carter, Lucy; Sellers, Rachel; Emsley, Richard; Pyle, Melissa; French, Paul; Shiers, David; Yung, Alison R; Murphy, Elizabeth K; Holden, Natasha; Steele, Ann; Bowe, Samantha E; Palmier-Claus, Jasper; Brooks, Victoria; Byrne, Rory; Davies, Linda; Haddad, Peter M (May 2018). "Antipsychotic drugs versus cognitive behavioural therapy versus a combination of both in people with psychosis: a randomised controlled pilot and feasibility study". The Lancet Psychiatry. 5 (5): 411–423. doi:10.1016/S2215-0366(18)30096-8. PMC   6048761 . PMID   29605187.
  37. 1 2 Malmberg, Lena; Fenton, Mark; Rathbone, John (23 July 2001). "Individual psychodynamic psychotherapy and psychoanalysis for schizophrenia and severe mental illness". Cochrane Database of Systematic Reviews. 2012 (2): CD001360. doi:10.1002/14651858.CD001360. PMC   4171459 . PMID   11686988.
  38. ↑ [ citation needed ]
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