Diathesis-stress Model Research Articles

The weight of childhood adversity: evidence that childhood adversity moderates the impact of genetic risk on waist circumference in adulthood.

The present study tested the interactive effects of childhood adversity and polygenic risk scores for waist circumference (PRS-WC) on waist circumference (WC). Consistent with a diathesis-stress model, we hypothesize that the relationship between PRS-WC and WC will be magnified by increasing levels of childhood adversity. Observational study of 7976 adults (6347 European Americans and 1629 African Americans) in the Health and Retirement Study with genotyped data. PRS-WC were calculated by the HRS administrative core using the weighted sum of risk alleles based on a genome-wide association study conducted by the Genetic Investigation of Anthropometric Traits (GIANT) consortium. Childhood adversity was operationalized using a sum score of three traumatic events that occurred before the age of 18 years. There was a statistically significant interaction between PRS-WC and childhood adversity for European Americans, whereby the magnitude of PRS-WC predicting WC increased as the number of adverse events increased. This study supports the idea of the interactive effects of genetic risks and childhood adversity on obesity. More epidemiological studies, particularly with understudied populations, are needed to better understand the roles that genetics and childhood adversity play on the development and progression of obesity.

Analysis of COVID-19-related psychiatric disorders: clinical manifestations and therapeutic considerations

During the COVID-19 pandemic, neuropsychiatric disorders have been diagnosed both in the acute phase, and in the aftermath of this disease. Inpatients, as well as outpatients recently diagnosed with mild, moderate or severe forms of Coronavirus infection have reported neuropsychiatric manifestations with variable duration, symptoms that could be directly or indirectly related to the viral pathogenic agent. Patients who are recovering from the acute phase of COVID-19 also may exhibit various psychopathological manifestations, during the so-called “post-COVID-19 syndrome” or “long COVID-19 syndrome”. Explanations regarding the onset of this type of clinical manifestations and the SARS-CoV-2 infection are extremely diverse, ranging from biological factors (e.g., direct central nervous system viral activity, cerebral hypo-oxygenation, high level of inflammatory response) to psycho-social stressors (e.g., isolation, fear of death, anxiety related to possible somatic complications or sequelae). Objectives: The primary objective of this article was to analyze psychiatric manifestations in patients with acute COVID-19 disease and in patients during post-COVID-19 phase. The secondary objective was to propose a conceptual framework for the evaluation and treatment of these patients. Methods: Patients included in this analysis were screened positive for COVID-19 infection in the last 6 months before their first psychiatric examination. These patients were further evaluated to detect any personal history of psychiatric disorders, somatic comorbidities, or significant concomitant pharmacological treatments. Specific scales for the measurement of symptoms severity and functional impairment were administered in all patients. Results: Five patients were included in this analysis, one during the acute phase of COVID-19 infection, and four patients were evaluated after the complete remission of this disease. Hyperactive delirium, mild neurocognitive disorder, major depressive episode, panic disorder with agoraphobia, or acute psychotic disorder were the main diagnoses in these patients. All patients received adequate treatment and they were monitored using psychological scales until symptoms remission or stabilisation. Conclusions: Psychosocial stressors, neurobiological changes, systemic inflammatory reaction, and individual vulnerability factors may contribute to a diathesis-stress model for psychiatric disorders onset within the acute phase or after the remission of acute manifestations in COVID-19-diagnosed patients

Psychological Issues among Individuals with Chronic Illnesses: A Multi-Informant Perspective

Background and Objective. Individuals with chronic illnesses exhibit number of psychological issues, but their significance in worsening the situation is always ignored. It has been highlighted that psychological issues are deteriorating the quality of life of individuals with chronic illness (Awopetu, Omadu & Abikoye, 2017). Current study was conducted to discover the psychological issues of individuals with chronic illnesses (i.e., cardiac, diabetes and cancer). Method. Focus Group discussions were conducted by using multi-informant approach to provide a broader picture. The focus group guides were prepared following the Self-determination Theory (Deci & Ryan, 2004), the Diathesis–stress model (Ingram & Luxton, 2005), and the Disability-Stress-Coping Strategy (Wallander & Varni, 1998). Twenty-four focus group discussions (1-6 focus groups with individuals having chronic illnesses, six with caregivers of the individuals having chronic illnesses, six with the doctors treating these patients and six were conducted with nurses and paramedical staff) comprised of 6-9 members each. Analyses. After the collection of data, it’s organization and coding was done after which themes were generated by using the content analysis approach (Berelson, 1952). Generated themes have provided the major indicators of psychological issues and these are crying spells, sleeping difficulty, sadness, hopelessness, loss of interest in life, appetite problems and loss of interest in everything, aggression (physical and verbal). Implications. Findings have implications for caregivers and professionals working with the patients i.e. the doctors, nurses, paramedical staff etc. It may also help the doctors to consider the psychological condition of the patients while treating their physiological problems.

Interaction of recent stressful life events and childhood abuse on orbitofrontal grey matter volume in adults with depression

BackgroundThe diathesis-stress model of major depressive disorder (MDD) predicts interactions of recent stressful life events (SLEs) in adulthood and early developmental risk factors. We tested, for the first time, the diathesis stress model on brain structure in a large group of MDD patients. MethodsStructural magnetic resonance imaging data of 1465 participants (656 with lifetime diagnosis MDD; 809 healthy controls) were analyzed using voxel-based morphometry to identify clusters associated with recent SLEs (Life Events Questionnaire). Those clusters were then examined for group (healthy/MDD) × early developmental risk (operationalized as childhood abuse [Childhood Trauma Questionnaire] and a major psychiatric disorder [i.e., MDD, bipolar disorder, schizophrenia, and schizoaffective disorder] in a first-degree relative) × recent SLEs three-way interactions on grey matter volume. ResultsThere was a group × childhood abuse × recent SLEs interaction on left medial orbitofrontal cortex grey matter volume. This three-way interaction arose because childhood abuse and recent SLEs interacted in MDD subjects but not in healthy subjects. LimitationsWe are not able to draw conclusions about the cause and effect relationship due to our cross-sectional study design. ConclusionsOur data provides evidence for an interplay between orbitofrontal cortex structure, childhood abuse and recent SLEs. These factors have previously been linked to MDD and their complex interaction contributes to the pathogenesis of MDD.

Integrating the Gut Microbiome and Stress-Diathesis to Explore Post-Trauma Recovery: An Updated Model.

Musculoskeletal conditions of traumatic and non-traumatic origin represent an ongoing health challenge. While the last three decades have seen significant advancement in our understanding of musculoskeletal conditions, the mechanisms of a delayed or lack of recovery are still a mystery. Here, we present an expansion of the integrated stress-diathesis model through the inclusion of the gut microbiome. Connecting the microbiome with known adverse neurobiologic, microbiologic and pathophysiologic sequelae following an injury, trauma or stressful event may help improve our knowledge of the pathogenesis of poor recovery. Such knowledge could provide a foundation for the exploration and development of more effective interventions to prevent the transition from acute to chronic pain.

The interplay between parental care and OPRM1 in reward responsiveness

The Reinforcement Sensitivity Theory (RST) explains a variety of reward-motivated behaviors as the result of the activation of biologically-based systems. Inspired by the influences of parental bonding and opioid peptide on reward system, we investigated the contributions of parental bonding and mu-opioid receptor gene (OPRM1) towards motivation systems (i.e., the BAS, BIS-anxiety, and FFFS-fear). Results indicated that (1) parental care was negatively related to FFFS-fear, but parental overprotection was positively related to both FFFS-fear and BIS-anxiety; (2) parental care significantly interacted with OPRM1 rs1799971 in reward responsiveness with diathesis-stress model. Poor parental care reduced reward responsiveness among individuals with the G allele, but not those with the AA genotype. These findings from this study demonstrate a new gene-environment interactive mechanism of the RST.

Using Crisis Theory in Dealing With Severe Mental Illness-A Step Toward Normalization?

The perception of mental distress varies with time and culture, e.g., concerning its origin as either social or medical. This may be one reason for the moderate reliability of descriptive psychiatric diagnoses. Additionally, the mechanisms of action of most psychiatric treatments and psychotherapeutic interventions are generally unknown. Thus, these treatments have to be labeled as mostly unspecific even if they help in coping with mental distress. The psychiatric concept of mental disorders therefore has inherent limitations of precision and comprises rather fuzzy boundaries. Against this background, many people question the current process of diagnosing and categorizing mental illnesses. However, many scholars reject new approaches discussed in this context. They rather hold on to traditional diagnostic categories which therefore still play a central role in mental health practice and research and. In order to better understand the adherence to traditional psychiatric concepts, we take a closer look at one of the most widely adopted traditional concepts – the Stress-Vulnerability Model. This model has originally been introduced to tackle some problems of biological psychiatry. However, it has been misapplied with the result of drawing attention preferentially to biological vulnerability instead of a wider array of vulnerability factors including social adversity. Thus, in its current use, the Stress-Vulnerability Model provides only a vague theory for understanding mental phenomena. Therefore, we discuss the advantages and allegedly limited applicability of Crisis Theory as an alternative heuristic model for understanding the nature and development of mental distress. We outline the problems of this theory especially in applying it to severe mental disorders. We finally argue that an understanding of Crisis Theory supported by a systemic approach can be applied to most types of severe psychological disturbances implying that such an understanding may prevent or manage some negative aspects of the psychiatrization of psychosocial problems.

The Vulnerability-Stress-Model-Holding Up the Construct of the Faulty Individual in the Light of Challenges to the Medical Model of Mental Distress.

In the late 1970s, the course seemed to be set for a reconciliation of the controversy around the somatic vs. the social nature of mental distress. The biopsychosocial model and the vulnerability-stress-model were influential agents in this move, but a medicalized somatic view on mental distress persisted nonetheless. The reasons for this persistence are complex, and naturally include questions of structural power. However, the adherence to a certain fundamental framing of a problem may continue to be transmitted not only out of conviction, but also unwittingly. The vulnerability-stress-model allowed those who used it to effectively stick to the implications of a medicalized somatic view of the faulty individual who falls ill, while also allowing them to believe they integrated the social dimensions of the problem. A close reading and hermeneutical interpretation of the text by Zubin and Spring (1977) and an analysis of its use in psychoeducation serve as a case study in this respect. The vulnerability-stress-model (simply called “vulnerability model” by Zubin and Spring; more often “stress-vulnerability model” by English speaking recipients, and “vulnerability-stress-model” by German authors) seems to have been a success story: since its publication by Zubin and Spring (1977), it has been the point of reference for numerous scholarly and popular (“psychoeducational”) adaptations. It was soon extended from the diagnosis of schizophrenia to various psychiatric diagnoses, understanding mental distress as the result of a trait/state-interaction in the shape of “deviant coping patterns” (Zubin and Spring, p. 112). Recipients appraised the integration of environmental and dispositional factors, some of them opposing the supposed originally integrative intention of the VSM to reduced applications of it (Schmidt, 2012). However, it can be argued that this integration is a matter of rhetorics rather than argumentative essence. Their argument which significantly depends on the use of metaphors, as well as their referencing amounts to a confirmation of a medicalized view on mental distress and a dismissal of the role played by societal factors. Applied to psychoeducation, this paradoxical combination reinforced a view of the persons in question as individually vulnerable, rather than socially wounded. The consequences in terms of what appears as remedy are significant and contribute to turning individual difference into disability.

The stress-vulnerability model on the path to schizophrenia: Interaction between BDNF methylation and schizotypy on the resting-state brain network

The interplay between schizophrenia liability and environmental influences has been considered to be responsible for the development of schizophrenia. Recent neuroimaging studies have linked aberrant functional connectivity (FC) between the default-mode network (DMN) and the frontoparietal network (FPN) in the resting-state to the underlying neural mechanism of schizophrenia. By using schizotypy as the proxy for genetic-based liability to schizophrenia and methylation of brain-derived neurotrophic factor (BDNF) to represent environmental exposure, this study investigated the impact of the interaction between vulnerability and the environment on the neurobiological substrates of schizophrenia. Participants in this study included 101 healthy adults (HC) and 46 individuals with ultra-high risk for psychosis (UHR). All participants were tested at resting-state by functional magnetic resonance imaging, and group-independent component analysis was used to identify the DMN and the FPN. The Perceptual Aberration Scale (PAS) was used to evaluate the schizotypy level. The methylation status of BDNF was measured by pyrosequencing. For moderation analysis, the final sample consisted of 83 HC and 32 UHR individuals. UHR individuals showed reduced DMN-FPN network FC compared to healthy controls. PAS scores significantly moderated the relationship between the percentage of BDNF methylation and DMN-FPN network FC. The strength of the positive relationship between BDNF methylation and the network FC was reduced when the schizotypy level increased. These findings support the moderating role of schizotypy on the neurobiological mechanism of schizophrenia in conjunction with epigenetic changes.

The Interaction Between POMC rs2071345 Polymorphism and Alcohol Dependence in Anxiety Symptoms Among Chinese Male Problem Drinkers.

ObjectiveAlcohol dependence can increase the level of anxiety. A growing body of research has identified a link between anxiety symptoms of problem drinkers and their genetic or environment factors, respectively. However, to date few studies have directly examined gene-environment (G × E) interaction on their anxiety symptoms during the acute alcohol withdrawal. The present study aims to examine the interaction between the proopiomelanocortin (POMC) rs2071345 polymorphism and alcohol dependence on anxiety symptoms of male problem drinkers, and further test the exact form of interaction on two competing models: the diathesis-stress model vs. the differential susceptibility model.MethodsA total of 440 male problem drinkers (Mage = 44.5 years, SD = 9.45) were recruited from nine main psychiatric hospitals of northern China during acute alcohol withdrawal. Blood samples were collected for genotyping, self-reported anxiety symptoms, and levels of alcohol dependence were assessed.ResultsResults indicated that the POMC rs2071345 polymorphism significantly moderated anxiety symptoms associated with alcohol dependence. A region of significance (RoS) test showed that male problem drinkers with T allele were more likely to experience more anxiety symptoms than those with CC homozygote when the standardized score of concurrent alcohol dependence was above 0.31. Confirmatory model evaluation indicated that the interaction effect involving POMC gene polymorphism conformed to the diathesis-stress model rather than differential-susceptibility model of person × environment interaction.ConclusionsThis study suggested that the SNP in POMC rs2071345 was associated with alcohol dependence in anxiety symptoms of male problem drinkers and further provided evidence in support of the diathesis-stress hypothesis of alcohol dependence in terms of anxiety symptoms.

Cognitive Behavioral Therapy for Psychosis

Cognitive behavioral therapy for psychosis (CBTp) is recommended by the National Treatment Guidelines in both the U.K. and the U.S. Consistent reports of moderate effect sizes have led to such interventions being suggested as part of routine clinical practice. However. Access to CBTp is poor due to a variety of factors, including training and resources. Therapeutic developments should be based on the theoretical understanding of cognitive models and psychological process associated with stress-vulnerability model. Cognitive models of psychosis incorporate the role of negative core beliefs, hypervigilance for threat, scanning for confirmatory evidence and safety behavior. The current evidence about CBTp is reviewed regarding various methods such as low-intensity of CBTp, different formats of therapy (e.g., individual or group), and phase of illness (e.g., acute or treatment-resistant) of subjects. This review suggests that that patients with psychosis with various disease phase need to be derived more benefit from appropriate adjunctive CBTp.

Association between stressful life events and grey matter volume in the medial prefrontal cortex: A 2‐year longitudinal study

Stressful life events (SLEs) in adulthood are a risk factor for various disorders such as depression, cancer or infections. Part of this risk is mediated through pathways altering brain physiology and structure. There is a lack of longitudinal studies examining associations between SLEs and brain structural changes. High‐resolution structural magnetic resonance imaging data of 212 healthy subjects were acquired at baseline and after 2 years. Voxel‐based morphometry was used to identify associations between SLEs using the Life Events Questionnaire and grey matter volume (GMV) changes during the 2‐year period in an ROI approach. Furthermore, we assessed adverse childhood experiences as a possible moderator of SLEs‐GMV change associations. SLEs were negatively associated with GMV changes in the left medial prefrontal cortex. This association was stronger when subjects had experienced adverse childhood experiences. The medial prefrontal cortex has previously been associated with stress‐related disorders. The present findings represent a potential neural basis of the diathesis‐stress model of various disorders.

The effect of early trauma on suicidal vulnerability depends on fronto-insular sulcation.

Improving our understanding of pathophysiology of suicidal behavior (SB) is an important step for prevention. Assessment of suicide risk is based on socio-demographic and clinical risk factors with a poor predictivity. Current understanding of SB is based on a stress-vulnerability model, whereby early-life adversities are predominant. SB may thus result from a cascade of developmental processes stemming from early-life abuse and/or neglect. Some cerebral abnormalities, particularly in fronto-limbic regions, might also provide vulnerability to develop maladaptive responses to stress, leading to SB. We hypothesized that SB is associated with interactions between early trauma and neurodevelopmental deviations of the frontal and insular cortices. We recruited 86 euthymic women, including 44 suicide attempters (history of depression and SB) and 42 affective controls (history of depression without SB). The early development of prefrontal cortex (PFC) and insula was inferred using 3D magnetic resonance imaging-derived regional sulcation indices, which are indirect markers of early neurodevelopment. The insula sulcation index was higher in emotional abused subjects; among those patients, PFC sulcation index was reduced in suicide attempters, but not in affective controls. Such findings provide evidence that SB likely traced back to early stages of brain development in interaction with later environmental factors experienced early in life.

Family therapy for persons with schizophrenia: neglected yet important

Since the 1950s, the observed disturbances in family relationships in which a member has been diagnosed as having schizophrenia has led many systemic family therapists to the hypothesis that these family interactions may have preceded the onset of illness and contributed to it. However, attempts at using traditional family therapy with families of patients with schizophrenia were not successful or widely adopted. With the introduction of neuroleptic medication, the treatment of schizophrenia changed dramatically, and patients often returned to their family in varying stages of partial remission, increasing the burden on relatives. Furthermore, research based on the expressed emotion concept demonstrated that the chance of relapse increases by a factor of 2.5 when a patient returns to a high-EE-family in contrast to a low-EE-family environment; consequently, the vulnerability–stress model started to guide treatment development. Based on these developments, since 1980, several psychoeducational family management programs have been evaluated showing a significant reduction in relapse when compared to standard psychiatric care from 49 to 13%. To date, at least 50 RCT studies have been published showing the effectiveness of family interventions in various culturally diverse countries. Therefore, according to the NICE and other guidelines, family intervention should be offered to all families of people with psychosis who live with or are in close contact with the patient, in conjunction with neuroleptic treatment. Despite this strong recommendation, family involvement is under-implemented in mental health care, despite its strong scientific, economic, legal and moral basis. To improve the psychosocial health of patients with psychotic disorders and their relatives, more research is necessary, as well as more training for professionals in effective family interventions.

Beyond the diathesis-stress paradigm: Effect of the environmental sensitivity × pubertal tempo interaction on depressive symptoms.

Based on the Differential Susceptibility Theory, we examined whether the relationship between pubertal maturation and depressive symptoms can be moderated by individual differences in environmental sensitivity. The current article used the three-wave data collected from Japanese adolescents aged from 12 to 15 years (girls=111, boys=98). Consequently, a significant Sensitivity × Pubertal Development interaction was observed in 12- to 13-year-old boys, but not girls. Sensitive boys who experienced accelerated physical maturation reported decreased depressive symptoms, while those who experienced less maturation had increased depressive symptoms. The shape of the interaction supported both the Differential Susceptibility Theory and the Diathesis-Stress Model. Our findings suggest that sensitivity during early puberty among boys could be reconsidered as susceptibility rather than vulnerability.

Combining transplant professional’s psychosocial donor evaluation and donor self-report measures to optimise the prediction of HRQoL after kidney donation: an observational prospective multicentre study

ObjectivesLiving donor kidney transplantation is currently the preferred treatment for patients with end-stage renal disease. The psychosocial evaluation of kidney donor candidates relies mostly on the clinical viewpoint of transplant...

Management of Psychiatric Disorders in Patients with Endocrine Disorders.

The neuropsychiatric symptoms and disorders among endocrine disorders are discussed in the context of current global and local epidemiological data. Neuropsychiatric symptoms, clinical differentials in hypothyroidism, hyperthyroidism, and parathyroid disorders, and relevant management protocols are described. HPT axis and its interaction with psychotropic usage are mentioned. Stress diathesis, depression, anxiety disorders, and severe mental illnesses and their respective association with diabetes, the relevant mechanisms, and management protocols are stated. The metabolic syndrome, its definition, and its relationship to psychotropic usage are laid out. Moreso, best clinical practices for scenarios such as hyperprolactinemia and psychiatric illnesses, and steroid-induced psychosis are mentioned.

A diathesis-stress rat model induced suicide-implicated endophenotypes and prefrontal cortex abnormalities in the PKA and GABA receptor signaling pathways

Suicide is one of the leading causes of death and represents a significant public health problem worldwide; however, the underlying mechanism of suicide remains unclear, and there is no animal model with suicide-implicated endophenotypes for investigating the etiology, course and potential treatment targets of suicide. Thus, we generated a diathesis-stress rat model to simulate suicide-implicated endophenotypes. First, two hundred rats were screened in two rounds of learned helplessness (LH) tests and selected as learned helplessness-sensitive (LHS) rats (n = 37) and learned helplessness-resistant (LHR) rats (n = 39). Then, all LHS rats and half of the rats (randomly selected) in the LHR group were exposed to four weeks of social defeat stress (SDS) (LHS + SDS group, n = 37 and LHR + SDS group, n = 20, respectively). The remainder of the LHR rats were handled as controls (LHR + CON group, n = 19). The LHS + SDS group showed significantly more suicide-implicated endophenotypes than the LHR + CON group, including longer immobile times in the forced swim test (hopelessness), higher scores in the irritability test (irritability), shorter latencies to attack (impulsivity), longer total attack times in the resident-intruder test (aggression), and lower sucrose preference indices (anhedonia). Proteomic analyses revealed that the canonical pathways that were the most common between the LHS + SDS and LHR + CON groups were the PKA and GABA receptor pathways in the prefrontal cortex. A diathesis-stress paradigm would be a useful way to establish a rat model with suicide-implicated endophenotypes, providing novel perspectives for revealing the potential mechanism of suicide.

Suicide: Allostatic regulation and resilience

Suicide is a complex public health problem that is the result of a number of intertwined biopsychosocial factors. The diathesis-stress model suggests that suicide is the result of an interaction between genetic vulnerability and environmental stressors. Chronic stress and trauma contribute to biologic adaptations, including hypothalamus-pituitary-adrenal axis dysregulation, that contribute to the degradation of regulatory mechanisms and promote wear and tear the body, represented by allostatic load (AL). AL has been associated with a number of negative outcomes, including mental health problems and suicide. Fortunately, there are pharmacological and non-pharmacological interventions that are effective at reducing AL and reversing its effects. Thus, AL may provide a construct for supporting early risk identification, prevention, and treatment of suicide. AL biomarkers that are amenable to measurable change, effective treatments to reduce AL and perhaps help prevent suicide, and how to best tailor them to the individual and societal levels are important avenues of therapeutic inquiry.

Using the stress–vulnerability model to better understand suicide in prison populations

Suicide is the culmination of the interaction of a number of factors with the critical component being distress. The contribution of mental illness as a vulnerability factor in an individual case of suicide by a prisoner may be significant, marginal or non-existent. Because of the high prevalence in prison populations of all risk factors for suicide, relying solely on those factors is of little use in elaborating the risk of suicide for a given prisoner. Whilst a current mental illness or past history of a suicide attempt are two factors that appear to be strongly associated with completed suicide, no screening or risk assessment tool has any proven efficacy in predicting suicide in prison populations. The stress–vulnerability model offers a more sophisticated and comprehensive assessment and also informs a more individualised needs-based management of the risk of suicide with an emphasis on detecting and responding to a prisoner’s distress.