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The Link Between Low Socioeconomic Status and Psychopathology. Article. Explaining the Link Between Low Socioeconomic Status and Psychopathology: Testing Two Mechanisms of Social Causation Hypothesis Martha E. Wadsworth Thomas M. Achenbach. Review of the Literature.
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The Link Between Low Socioeconomic Status and Psychopathology
Article Explaining the Link Between Low Socioeconomic Status and Psychopathology: Testing Two Mechanisms of Social Causation Hypothesis Martha E. Wadsworth Thomas M. Achenbach
Review of the Literature • Rates of psychopathology and mental disorders are higher among individuals of lower socioeconomic status. • This has been found for: • Major Depressive Disorder • Antisocial Personality Disorder • Anxiety Disorders • Substance Use Disorders • Also found for measures of: • Demoralization • Depressive symptoms • Nonspecific distress • What is interestingabout the disorders found to be more prominent in lower SES individuals?
Both Internalizing and Externalizing Disorders • Internalizing Disorders • Major Depressive Disorders • Anxiety Disorders • Externalizing Disorders • Antisocial Personality Disorder • Substance Use Disorder • Robust support for the social causation hypothesis in both Internalizing and Externalizing disorders
Two Leading Hypotheses • Social Selection Hypothesis or “Downward Drift” Hypothesis • Social Causation Hypothesis
Social Selection Hypothesis • Individuals with psychological problems “drift” downward because their impairment prevents them from functioning in society and meeting societal role expectations. • Initial causes of psychopathology are unrelated to SES (i.e., genetic liabilities) • What example was mentioned in the article? • Support for hypothesis: • SES differences in rates of schizophrenia (Dohrenwend et al., 1992) • Possibly rates of ADHD (Miech et al., 1999)
Social Causation Hypothesis • People with low SES develop psychological problems as a result of the stress caused by economic difficulties. • Poverty = an adverse event that may activate a diathesis (i.e., genetic predisposition) • Support for this hypothesis: • High levels of environmental stress have been shown to produce PTSD, depression, and anxiety • High incidence rates of mental disorders among people with low SES
Like the age-old adage: Which came first, the chicken or the egg?
What would the diathesis stress model for the social causation hypothesis look like?
Diathesis Stress Model Stressful situation(s) related to low SES Example: Not having enough money to pay for basic needs (i.e., rent or utility bills) Genetic Predisposition Mental Disorder
Clip • What are your thoughts on the news story you just saw? • Does it help you understand how low SES can create stresses that may lead to psychological problems?
Social Causation Hypothesis • Differential incidence hypothesis – • Previous studies testing the social causation hypothesis have typically compared incidence rates. • Additional interpretation: Individuals from all SES levels are susceptible to psychological problems, but low-SES individuals do not recover as quickly because they do not have the same access to treatment as middle and higher SES individuals • Differential cumulative prevalencehypothesis – • There is an accumulation of low-SES cases as new cases occur and existing ones do not recover.
Previous studies have not tested cumulative prevalence rates • Would provide information on: • whether social causation effects are solely due to increased incidence rates among low SES individuals OR • whether low SES individuals are less likely to recover than higher SES individuals due to differences in access to effective treatment (differential cumulative prevalence)
What can be learned from children and adolescents? • Better test of social causation hypothesis since children’s behaviors do not affect a family’s SES • Longitudinal studies: • Can track the child over time and examine the course of psychological problems and referrals for mental health treatment. • Can examine differential incidence and cumulative prevalence hypotheses
Current Study • Extended previous research of the social causation hypothesis by testing both the differential incidence and cumulative prevalence hypotheses • Longitudinal data for children and youth aged 8-17 • 3 SES levels: Low, Middle, High • 4 assessment time points in 3-yr Intervals • Compared the new case incidence rates of seven forms of psychopathology • Compared utilization of mental health services after the first time point • Examined cumulative prevalence findings for clinically elevated cases by SES level • Also looked at remission rates by SES levels • Also tested for changes in syndrome scores at time points 2, 3, 4.
Findings- Syndrome Scores • Looked at syndrome scores on thought problems, somatic complaints, attention problems, delinquent behavior, and aggressive behavior. • There were no significant differences between the middle and high SES groups in differences of syndrome scores over time • Syndrome scores for the low SES groups increased over time • Refer to Figure 1 in article (pg. 1149)
Findings • A different pattern was found for anxious/depressed scores: • See Figure 2 (on pg. 1149) • Scores were higher for the low SES group only at time point 4. • How do the authors explain this finding?
Low SES children are no more at risk for anxious/depressed problems than higher SES children until young adulthood • Different finding may be due to proximal factors associated with low SES (i.e., parental depression) • Does anyone have an example of this from the clip? • Adults are more likely to be vulnerable to the demoralization and stress that can arise from low status jobs or marital dissolution.
Finding- Cumulative Prevalence • An accumulation of elevated scores among individuals from low SES for all syndromes except anxious/depressed and somatic complaints • No differences in remission rates by SES on thought problems, delinquent behavior, or aggressive behavior • Thus, the larger numbers of low-SES individuals reflect higher incidence rates of elevated syndrome scores. • This result was not due to worse remission rates followed by accumulation of cases • However, data indicated that low SES individuals did not get well as quickly or to the same extent as middle and high SES individuals with somatic complaints (at Time 2) and withdrawn (at Time 3).
Finding- Differential Mental Health Referrals • Although the low SES group had higher problem scores on 5 of the 7 syndromes, there were no differences between groups in utilization of mental health services
Conclusions • Low SES appears to contribute to more new cases of several forms of psychopathology. • Low SES appears to limit access to mental health care for some individuals who have high problem scores. • These results combined with previous studies showing social selection effects may provide support for a temporal course.
Support for a temporal course of psychological problems Initial psychological problems (activates a diathesis) Social causation effects Failure to recover Downward drift found in adult samples (Social Selection effects)
Important to Note • Social causation by itself does not imply causation of psychopathology: • Not all low SES individuals have mental disorders- resiliency • Implies that stresses resulting from having a low SES can contribute to various levels of psychopathology • What do results of this study show us in light of the lecture on Nature vs. Nurture debate? • Results of this study further support the Multiplicative/Interactive Approach • Genes and the environment interact to produce psychopathology • Therefore, it is nature AND nurture, not one or the other.
As aspiring clinicians, what are some clinical implications of the present study?
Clinical Implications and Future Directions • Increase access to effective healthcare and mental health services- • more mental health providers and prevention programs in low income communities • more affordable mental healthcare • Treatments should address the stress and adversity related to having a low SES • Clinicians should be aware of potential biases they have with regard to low SES individuals • More research on prevention programs that address economic stress, stress reactivity, and coping