Joseph M. Boden

Relation of Threatened Egotism to Violence and Aggression: The Dark Side of High Self-Esteem

Conventional wisdom has regarded low self-esteem as an important cause of violence, but the opposite view is theoretically viable. An interdisciplinary review of evidence about aggression, crime, and violence contradicted the view that low self-esteem is an important cause. Instead, violence appears to be most commonly a result of threatened egotism--that is, highly favorable views of self that are disputed by some person or circumstance. Inflated, unstable, or tentative beliefs in the selfs superiority may be most prone to encountering threats and hence to causing violence. The mediating process may involve directing anger outward as a way of avoiding a downward revision of the self-concept.

Exposure to childhood sexual and physical abuse and adjustment in early adulthood

OBJECTIVE This research examined linkages between exposure to childhood sexual abuse (CSA) and childhood physical punishment/abuse (CPA) and mental health issues in early adulthood. METHOD The investigation analyzed data from a birth cohort of over 1,000 New Zealand young adults studied to the age of 25. RESULTS Exposure to CSA and CPA was associated with increased risks of later mental disorders including depression, anxiety disorder, conduct/anti-social personality disorder, substance dependence, suicidal ideation, and suicide attempts at ages 16-25. Control for social, family, and individual factors reduced the associations between CPA and mental health outcomes to the point of statistical non-significance. However, there was a consistent finding for CSA to remain associated with increased risks of later mental health problems. After adjustment, those exposed to CSA including attempted or completed sexual penetration had rates of disorder that were 2.4 times higher than those not exposed to CSA. Those exposed to harsh or abusive physical punishment had rates of disorder that were 1.5 times higher than those exposed to no or occasional physical punishment. It was estimated that exposure to CSA accounted for approximately 13% of the mental health problems experienced by the cohort. Findings showed that exposure to CPA had only weak effects on later mental health. It was estimated that exposure to CPA accounted for approximately 5% of the mental health problems experienced by the cohort. CONCLUSIONS Exposure to CSA was associated with consistent increases in risks of later mental health problems. Exposure to CPA had weaker and less consistent effects on later mental health. These findings suggest that much of the association between CPA and later mental health reflects the general family context in which CPA occurs, whereas this is less the case for CSA.

Alcohol and depression

AIMS To examine the literature on the associations between alcohol use disorders (AUD) and major depression (MD), and to evaluate the evidence for the existence of a causal relationship between the disorders. METHODS PsycInfo; PubMed; Embase; Scopus; ISI Web of Science database searches for studies pertaining to AUD and MD from the 1980 to the present. Random-effects models were used to derive estimates of the pooled adjusted odds ratios (AOR) for the links between AUD and MD among studies reporting an AOR. RESULTS The analysis revealed that the presence of either disorder doubled the risks of the second disorder, with pooled AORs ranging from 2.00 to 2.09. Epidemiological data suggest that the linkages between the disorders cannot be accounted for fully by common factors that influence both AUD and MD, and that the disorders appear to be linked in a causal manner. Further evidence suggests that the most plausible causal association between AUD and MD is one in which AUD increases the risk of MD, rather than vice versa. Potential mechanisms underlying these causal linkages include neurophysiological and metabolic changes resulting from exposure to alcohol. The need for further research examining mechanisms of linkage, gender differences in associations between AUD and MD and classification issues was identified. CONCLUSIONS The current state of the literature suggests a causal linkage between alcohol use disorders and major depression, such that increasing involvement with alcohol increases risk of depression. Further research is needed in order to clarify the nature of this causal link, in order to develop effective intervention and treatment approaches.

Tests of causal links between alcohol abuse or dependence and major depression.

CONTEXT There has been a great deal of research on the comorbidity between alcohol abuse or dependence (AAD) and major depression (MD). However, it is unclear whether AAD increases the risk of MD or vice versa. OBJECTIVE To examine the associations between AAD and MD using fixed-effects modeling to control for confounding and using structural equation models to ascertain the direction of causality. DESIGN Data were gathered during the course of the Christchurch Health and Development Study, a 25-year longitudinal study of a birth cohort of children from New Zealand (635 boys, 630 girls). SETTING General community sample. PARTICIPANTS The analysis was based on a sample of 1055 participants with available data on AAD and MD at ages 17 to 18, 20 to 21, and 24 to 25 years. MAIN OUTCOME MEASURES Symptom criteria for AAD and MD from the DSM-IV at ages 17 to 18, 20 to 21, and 24 to 25 years as well as measures of life stress, cannabis use, other illicit drug use, affiliation with deviant peers, unemployment, partner substance use, and partner criminality at ages 17 to 18, 20 to 21, and 24 to 25 years. RESULTS There were significant (P < .001) pooled associations between AAD and MD. Controlling for confounding factors using conditional fixed-effects models and time-dynamic covariate factors reduced the magnitude of these associations, but they remained statistically significant. Structural equation modeling suggested that the best-fitting causal model was one in which AAD led to increased risk of MD. CONCLUSIONS The findings suggest that the associations between AAD and MD were best explained by a causal model in which problems with alcohol led to increased risk of MD as opposed to a self-medication model in which MD led to increased risk of AAD.

Cannabis use and later life outcomes

AIM To examine the associations between the extent of cannabis use during adolescence and young adulthood and later education, economic, employment, relationship satisfaction and life satisfaction outcomes. DESIGN A longitudinal study of a New Zealand birth cohort studied to age 25 years. MEASUREMENTS Measures of: cannabis use at ages 14-25; university degree attainment to age 25; income at age 25; welfare dependence during the period 21-25 years; unemployment 21-25 years; relationship quality; life satisfaction. Also, measures of childhood socio-economic disadvantage, family adversity, childhood and early adolescent behavioural adjustment and cognitive ability and adolescent and young adult mental health and substance use. FINDINGS There were statistically significant bivariate associations between increasing levels of cannabis use at ages 14-21 and: lower levels of degree attainment by age 25 (P < 0.0001); lower income at age 25 (P < 0.01); higher levels of welfare dependence (P < 0.0001); higher unemployment (P < 0.0001); lower levels of relationship satisfaction (P < 0.001); and lower levels of life satisfaction (P < 0.0001). These associations were adjusted for a range of potentially confounding factors including: family socio-economic background; family functioning; exposure to child abuse; childhood and adolescent adjustment; early adolescent academic achievement; and comorbid mental disorders and substance use. After adjustment, the associations between increasing cannabis use and all outcome measures remained statistically significant (P < 0.05). CONCLUSIONS The results of the present study suggest that increasing cannabis use in late adolescence and early adulthood is associated with a range of adverse outcomes in later life. High levels of cannabis use are related to poorer educational outcomes, lower income, greater welfare dependence and unemployment and lower relationship and life satisfaction. The findings add to a growing body of knowledge regarding the adverse consequences of heavy cannabis use.

Cigarette smoking and depression: tests of causal linkages using a longitudinal birth cohort

BACKGROUND Research on the comorbidity between cigarette smoking and major depression has not elucidated the pathways by which smoking is associated with depression. AIMS To examine the causal relationships between smoking and depression via fixed-effects regression and structural equation modelling. METHOD Data were gathered on nicotine-dependence symptoms and depressive symptoms in early adulthood using a birth cohort of over 1000 individuals. RESULTS Adjustment for confounding factors revealed persistent significant (P<0.05) associations between nicotine-dependence symptoms and depressive symptoms. Structural equation modelling suggested that the best-fitting causal model was one in which nicotine dependence led to increased risk of depression. The findings suggest that the comorbidity between smoking and depression arises from two routes; the first involving common or correlated risk factors and the second a direct path in which smoking increases the risk of depression. CONCLUSIONS This evidence is consistent with the conclusion that there is a cause and effect relationship between smoking and depression in which cigarette smoking increases the risk of symptoms of depression.

The developmental antecedents of illicit drug use: evidence from a 25-year longitudinal study.

BACKGROUND The present study examined the developmental antecedents of illicit drug use and abuse/dependence. METHODS A 25-year prospective longitudinal study of the health, development, and adjustment of a birth cohort of 1265 New Zealand children. Measures included assessments of adolescent and young adult illicit drug use and abuse/dependence; cannabis use to age 25; measures of parental adjustment; measures of exposure to childhood sexual abuse, physical abuse, and interparental violence; novelty-seeking; childhood and early adolescent adjustment and substance use; and affiliation with substance-using peers. RESULTS Illicit drug use and abuse/dependence from ages 16 to 25 were significantly associated (all p values<.05) with a range of parental adjustment measures; exposure to abuse in childhood; individual factors; and measures of childhood and early adolescent adjustment. Analyses using repeated measures logistic regression models suggested that parental illicit drug use, gender, novelty-seeking, and childhood conduct disorder predicted later illicit drug use and abuse/dependence. Further analyses revealed that these pathways to illicit drug use and abuse/dependence were mediated via cannabis use, affiliation with substance-using peers, and alcohol use during ages 16-25. CONCLUSIONS The current study suggested that the illicit drug use and abuse/dependence were associated with a range of early life circumstances and processes that put individuals at greater risk of illicit drug use and abuse/dependence. However, the use of cannabis in late adolescence and early adulthood emerged as the strongest risk factor for later involvement in other illicit drugs.

Anxiety disorders and suicidal behaviours in adolescence and young adulthood: findings from a longitudinal study

BACKGROUND The aim of this study was to estimate the extent to which anxiety disorders contribute to an increase in suicidal behaviour after controlling for both observed and non-observed sources of confounding. METHOD Data were collected from the Christchurch Health and Development Study (CHDS), a 25-year longitudinal study of over 1000 participants. Measures of anxiety disorders [phobia, generalized anxiety disorder (GAD), panic disorder], major depression (MD), substance use disorders, conduct/antisocial personality disorder, stressful life events, unemployment, and suicidal ideation/attempts for subjects aged 16-18, 18-21 and 21-25 years were used to fit random and fixed effects regression models of the associations between anxiety disorders and suicidal behaviours. RESULTS Anxiety disorders were strongly associated with suicidal ideation/attempts. Any single anxiety disorder increased the odds of suicidal ideation by 7.96 times [95% confidence interval (CI) 5.69-11.13] and increased the rate of suicide attempts by 5.85 times (95% CI 3.66-9.32). Control for co-occurring mental disorders, non-observed fixed confounding factors and life stress reduced these associations [suicidal ideation odds ratio (OR) 2.80, 95% CI 1.71-4.58; suicide attempts incidence rate ratio (IRR) 1.90, 95% CI 1.07-3.39]. Rates of suicidal behaviour also increased with the number of anxiety disorders. Estimates of the population attributable risk suggested that anxiety disorders accounted for 7-10% of the suicidality in the cohort. CONCLUSIONS Anxiety disorders may be a risk factor for suicidality, even after controlling for confounding, with risks increasing with multiple anxiety disorders. Management of anxiety disorders may be an important component in strategies to reduce population rates of suicide.

Cannabis and psychosis

The UK government is considering reclassifying cannabis because of concerns about links with mental health problems. What does the evidence show?

Repressive coping : Distraction using pleasant thoughts and memories

To avoid exposure to unpleasant or unwanted emotional material, some people may distract themselves by summoning up pleasant thoughts such as happy memories. Manipulation of negative affect might therefore result in heightened accessibility of pleasant thoughts and memories, contrary to hypotheses of mood-congruent recall. In Experiment 1, repressors were faster to recall happy memories after watching an unpleasant film than after watching a neutral film. Nonrepressors showed the opposite effect (i.e., mood-congruent memory). In Experiment 2, after an unpleasant film, repressors were faster to recall a happy memory than to recall a sad memory. In Experiment 3, repressors spontaneously generated pleasant thoughts after watching an unpleasant film, whereas nonrepressors did not. Thus, repressors apparently cope with exposure to negative affective material by accessing pleasant thoughts. Results are discussed in terms of cognitive defenses against emotional distress and the associative structure of repression.