Do racial patterns in psychological distress shed light on the Black–White depression paradox? A systematic review

Purpose

Major epidemiologic studies in the US reveal a consistent “paradox” by which psychiatric outcomes such as major depressive disorder (MDD) are less prevalent among Blacks relative to Whites, despite greater exposure to social and economic stressors and worse physical health outcomes. A second paradox, which has received less attention and has never been systematically documented, is the discrepancy between these patterns and Black–White comparisons in psychological distress, which reveal consistently higher levels among Blacks. By systematically documenting the latter paradox, this paper seeks to inform efforts to explain the first paradox.

Methods

We conduct a systematic review of the literature estimating the prevalence of MDD and levels of psychological distress in Blacks and Whites in the US.

Results

The literature review yielded 34 articles reporting 54 relevant outcomes overall. Blacks have a lower prevalence of MDD in 8 of the 9 comparisons observed. In contrast, Blacks have higher levels of psychological distress (in terms of “high distress” and mean scores) than Whites in 42 of the 45 comparisons observed. Tests of statistical significance, where available, confirm this discrepant pattern.

Conclusions

A systematic review of the epidemiologic evidence supports the existence of a “double paradox” by which Blacks’ lower prevalence of MDD relative to Whites’ is inconsistent with both the expectations of social stress theory and with the empirical evidence regarding psychological distress. Efforts to resolve the Black–White depression paradox should account for the discordant distress results, which seem to favor artifactual explanations.

     

Is it time to reassess the BDNF hypothesis of depression?

The brain-derived neurotrophic factor (BDNF) hypothesis of depression postulates that a loss of BDNF is directly involved in the pathophysiology of depression, and that its restoration may underlie the therapeutic efficacy of antidepressant treatment. While this theory has received considerable experimental support, an increasing number of studies have generated evidence which is not only inconsistent, but also directly contradicts the hypothesis. This article provides a critical review of the clinical and preclinical studies which have been responsible for this controversy, outlining pharmacological, behavioural and genetic evidence which demonstrates the contrasting role of BDNF in regulating mood and antidepressant effects throughout the brain. I will also review key studies, both human and animal, which have investigated the association of a BDNF single-nucleotide polymorphism (Val66Met) with depression pathogenesis, and detail the number of inconsistencies which also afflict this novel area of BDNF research. The article will conclude by discussing why now is a critical time to reassess the original BDNF hypothesis of depression, and look towards the formation of new models that can provide a more valid account of the complex relationships between growth factors, mood disorders and their treatment.     

Does smoking reduce akathisia? Testing a narrow version of the self-medication hypothesis

BACKGROUND: The self-medication hypothesis proposes that schizophrenia patients smoke to decrease their schizophrenia symptoms or antipsychotic side effects, but they usually start smoking before their illness and heavy smoking is not consistently associated with fewer symptoms or side effects. A narrow version of the self-medication hypothesis, heavy smoking reduces akathisia, is explored. METHOD: The sample included 250 outpatients with DSM-IV schizophrenia assessed with the Positive and Negative Syndrome Scale (PANSS) and the Barnes Akathisia Scale. Prevalences were 69% (173/250) for smoking, 39% (98/250) for heavy smoking (> or =30 cigarettes/day), 7% (17/250) for akathisia (Barnes Global score>1), 14% (35/250) for a broader akathisia definition (Barnes Global score>0) and 20% for excited symptoms (>1 on the PANSS factor score). RESULTS: Heavy smoking was not associated with akathisia (41% of patients with akathisia were heavy smokers versus 39% of patients without akathisia; chi2=0.3, df=1, p=0.86), even after correcting for confounding factors and/or using a broader akathisia definition. Heavy smoking was associated with excited schizophrenia symptoms (possibly reflecting agitation). Particularly in patients taking lower doses of typical antipsychotics, excited symptoms, with or without akathisia, were strongly associated with heavy smoking and appear to interact with patients' reports of smoking's calming effect as the main reason for smoking. CONCLUSION: The self-medication hypothesis does not explain increased smoking and heavy smoking in schizophrenia. Moreover, heavy smoking may be associated with more disturbed brain homeostatic mechanisms. Prospective studies need to explore whether temporary increases in cigarette smoking may be associated with periods of higher agitation, with or without akathisia.     

The role of body dissatisfaction as a risk factor for depression in adolescent girls: are the differences Black and White?

Body dissatisfaction, disordered eating and depression differentially affect adolescent girls (compared to boys); however, these variables have not been examined in relation to ethnicity. A review of the literature finds that Black adolescent girls are more satisfied with their bodies than White adolescent girls and engage much less frequently in dieting or disordered eating than do White girls in the US. A central question raised by this review is whether body dissatisfaction and pubertal timing are as relevant to our understanding of the etiology of depression in Black girls as they appear to be in White girls. Based on the available data, it does not seem that a risk factor model supporting the role of early pubertal timing, weight increases and body dissatisfaction in the development of depression applies to Black adolescent girls. This review underscores the need for future research with a variety of ethnic minority groups to better understand the etiology of adolescent depression.     

Testing the PROMIS® Depression measures for monitoring depression in a clinical sample outside the US

The Patient Reported Outcomes Measurement Information System (PROMIS) was devised to facilitate assessment of patient self-reported health status, taking advantage of Item Response Theory. We aimed to assess measurement properties of the PROMIS Depression item bank and an 8-item static short form in a Spanish clinical sample. A three-month follow-up study of patients with active mood/anxiety symptoms (n = 218) was carried out. We assessed model unidimensionality (Confirmatory Item Factor Analysis), reliability (internal consistency and Item Information Curves), and validity (convergent-discriminant with correlations; known-groups with comparison of means and effect sizes; and criterion validity with Receiver operating Characteristics (ROC) analysis). We also assessed 3-month responsiveness to change (Cohen's effect sizes (d) in stable and recovered patients). The unidimensional model showed adequate fit (CFI = 0.97, RMSEA = 0.08). Information Curves had reliabilities over 0.90 throughout most of the score continuum. As expected, we observed high correlations with external self-reported depression, and moderate with self-reported anxiety and clinical measures. The item bank showed an increasing severity gradient from no disorder (mean = 48, SE = 0.6) to depression with comorbid anxiety (mean = 55.8, SE = 0.4). PROMIS detected depression disorder with great accuracy according to the area under the curve (AUC = 0.89). Both formats, item bank and short form, were highly responsive to change in recovered patients (d > 0.7) and had small changes in stable patients (d < 0.2). The good metric properties of the Spanish PROMIS Depression measures provide further evidence of their adequacy for monitoring depression levels of patients in clinical settings. This double check of quality (within countries and populations) supports the ability of PROMIS measures for guaranteeing fair comparisons across languages and countries in specific clinical populations.     

From the Binet–Simon to the Wechsler–Bellevue: Tracing the History of Intelligence Testing

The history of David Wechsler's intelligence scales is reviewed by tracing the origins of the subtests in the 1939 Wechsler–Bellevue Intelligence Scale. The subtests originated from tests developed between 1880 and World War I, and was based on approaches to mental testing including anthropometrics, association psychology, the Binet–Simon scales, language-free performance testing of immigrants and school children, and group testing of military recruits. Wechsler's subtest selection can be understood partly from his clinical experiences during World War I. The structure of the Wechsler–Bellevue Scale, which introduced major innovations in intelligence testing, has remained almost unchanged through later revisions.     

Is low IQ related to risk of death by homicide? Testing a hypothesis using data from the Vietnam Experience Study

Lower IQ test scores are related to an increased risk of violent assault. We tested the relation between IQ and death by homicide. In a prospective cohort study of 14,537 men (21 homicides), the association between lower IQ and an increased risk of homicide was lost after multiple adjustment.     

Racial differences in depression in the United States: how do subgroup analyses inform a paradox?

Purpose

Non-Hispanic Blacks in the US have lower rates of major depression than non-Hispanic Whites, in national household samples. This has been termed a “paradox,” as Blacks suffer greater exposure to social stressors, a risk factor for depression. Subgroup analyses can inform hypotheses to explain this paradox. For example, it has been suggested that selection bias in household samples undercounts depression in Blacks; if selection is driving the paradox, Black–White differences should be most pronounced among young men with low education.

Methods

We examined Black–White differences in lifetime major depression in subgroups defined simultaneously by sex, age, and education using data from the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) and the Collaborative Psychiatric Epidemiology Surveys (CPES).

Results

In NESARC and CPES, Blacks had lower odds than Whites of lifetime major depression in 21 and 23 subgroups, respectively, of 24. All statistically significant differences were in subgroups favoring Blacks, and lower odds in Blacks were more pronounced among those with more education.

Conclusions

These results suggest that hypotheses to explain the paradox must posit global mechanisms that pertain to all subgroups defined by sex, age, and education. Results do not lend support for the selection bias hypothesis.     

Exploring the relations between depression, somatization, dissociation and alexithymia--overlapping or independent constructs?

BACKGROUND: The aim of this study was to extend our knowledge of associations among the constructs of alexithymia, depression, somatization and dissociation. SAMPLING AND METHODS: 924 nonclinical subjects answered questions about depression (21-item Beck Depression Inventory), somatization (13-item somatization part of Symptom Check List-90), dissociation (28-item Dissociative Experiences Scale) and alexithymia (20-item Toronto Alexithymia Scale). In addition, a 12-item General Health Questionnaire (GHQ-12) was administered to detect psychiatric distress among subjects. RESULTS: The results suggested that there was a significant clinical correlation between somatization, dissociation, depression and alexithymia (rho varied from 0.31 to 0.56). The principal component analysis revealed the presence of four components: depression, somatization, dissociation and alexithymia. The use of factor scores diminished the covariance between measures (rho varied from -0.10 to 0.01 between the factor scores). There was almost no correlation between the dissociation factor (rho = 0.06) and alexithymia factor (rho = 0.09) scores and general distress (GHQ-12). CONCLUSIONS: This study suggests that while somatization, dissociation, depression and alexithymia are distinct constructs, they correlate to a considerable extent. The use of factor analysis and factor scores should be considered to diminish covariance between the above constructs. Comparing results between factored and unfactored results may prove illuminating. As a case in point, the results suggest that the part of dissociation that coincides with other constructs (overlaps) is associated with distress, whereas the distinct part of dissociation (no shared covariance) is not associated with distress. The same applies to the alexithymia construct. Longitudinal studies are needed to show whether there is a trait such as a relatively stable dissociation component and also whether a separate state-dependent dissociation component exists that is associated with coincident distress, somatization and depression.     

Is late onset depression a prodrome to dementia?

BACKGROUND: Recent research suggests there are clinical and biological differences between late onset depression (LOD) and early-onset depression (EOD). OBJECTIVES: In this paper we review clinical, epidemiological, structural neuroimaging and genetic investigations of late life depression that have been performed over the past two decades and offer evidence that LOD is often a prodromal disorder for dementia. RESULTS: LOD patients are more likely to have cognitive impairment and to have more deep white matter lesions (DWMLs). Evidence concerning cortical and temporal lobe atrophy is conflicting, while the ApoE 4 allele is not associated with LOD. CONCLUSIONS: It is likely that LOD is not a prodrome for a particular type of dementia, but the majority of patients who do develop dementia will acquire Alzheimer's disease (AD) or a vascular dementia, as these are by far the most common causes of dementia. This issue requires further clarification with follow-up of patients over the long term.     

Electroconvulsive therapy-induced Wolff–Parkinson–White syndrome: a case report

Objective

Wolff–Parkinson–White (WPW) syndrome is characterized by premature ventricular excitation due to the presence of an abnormal accessory pathway. Electrocardiography (ECG) of patients with WPW syndrome portrays a short PR interval and a wide QRS interval with a delta wave.

Methods

Herein, we report the case of a patient with schizophrenia who developed a wide QRS interval with a delta wave immediately following electroconvulsive therapy (ECT).

Results

Initially, the delta wave disappeared within 2 days after ECT. However, the duration of the delta wave increased exponentially to 4 months when ECT was repeated.

Conclusion

Although the patient's cardiocirculatory dynamics remained normal, we continued to monitor her ECG until the delta wave disappeared because WPW syndrome can lead to serious arrhythmia.     

Is the serotonin hypothesis/theory of depression still relevant? Methodological reflections motivated by a recently published umbrella review

European Archives of Psychiatry and Clinical Neuroscience -