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The extent to which exposure to childhood sexual and physical abuse increases the risk of psychotic experiences in adulthood is currently unclear.
To examine the relationship between childhood sexual and physical abuse and psychotic experiences in adulthood taking into account potential confounding and time-dynamic covariate factors.
Data were from a cohort of 1265 participants studied from birth to 35 years. At ages 18 and 21, cohort members were questioned about childhood sexual and physical abuse. At ages 30 and 35, they were questioned about psychotic experiences (symptoms of abnormal thought and perception). Generalised estimating equation models investigated covariation of the association between abuse exposure and psychotic experiences including potential confounding factors in childhood (socioeconomic disadvantage, adverse family functioning) and time-dynamic covariate factors (mental health, substance use and life stress).
Data were available for 962 participants; 6.3% had been exposed to severe sexual abuse and 6.4% to severe physical abuse in childhood. After adjustment for confounding and time-dynamic covariate factors, those exposed to severe sexual abuse had rates of abnormal thought and abnormal perception symptoms that were 2.25 and 4.08 times higher, respectively than the ‘no exposure’ group. There were no significant associations between exposure to severe physical abuse and psychotic experiences.
Findings indicate that exposure to severe childhood sexual (but not physical) abuse is independently associated with an increased risk of psychotic experiences in adulthood (particularly symptoms of abnormal perception) and this association could not be fully accounted for by confounding or time-dynamic covariate factors.
Few studies have examined the contribution of specific disaster-related experiences to post-traumatic stress disorder (PTSD) symptoms.
To examine the roles of peri-traumatic stress and distress due to lingering disaster-related disruption in explaining linkages between disaster exposure and PTSD symptoms among a cohort exposed to the 2010–2011 Canterbury (New Zealand) earthquakes.
Structural equation models were fitted to data obtained from the Christchurch Health and Development Study at age 35 (n=495), 20–24 months following the onset of the disaster. Measures included: earthquake exposure, peri-traumatic stress, disruption distress and PTSD symptoms.
The associations between earthquake exposure and PTSD symptoms were explained largely by the experience of peri-traumatic stress during the earthquakes (β=0.189, P<0.0001) and disruption distress following the earthquakes (β=0.105, P<0.0001).
The results suggest the importance of minimising post-event disruption distress following exposure to a natural disaster.
Traumatic brain injury (TBI) occurs frequently during child and early adulthood, and is associated with negative outcomes including increased risk of drug abuse, mental health disorders and criminal offending. Identification of previous TBI for at-risk populations in clinical settings often relies on self-report, despite little information regarding self-report accuracy. This study examines the accuracy of adult self-report of hospitalized TBI events and the factors that enhance recall.
The Christchurch Health and Development Study is a birth cohort of 1265 children born in Christchurch, New Zealand, in 1977. A history of TBI events was prospectively gathered at each follow-up (yearly intervals 0–16, 18, 21, 25 years) using parental/self-report, verified using hospital records.
At 25 years, 1003 cohort members were available, with 59/101 of all hospitalized TBI events being recalled. Recall varied depending on the age at injury and injury severity, with 10/11 of moderate/severe TBI being recalled. Logistic regression analysis indicated that a model using recorded loss of consciousness, age at injury, and injury severity, could accurately classify whether or not TBI would be reported in over 74% of cases.
This research demonstrates that, even when individuals are carefully cued, many instances of TBI will not recalled in adulthood despite the injury having required a period of hospitalization. Therefore, screening for TBI may require a combination of self-report and review of hospital files to ensure that all cases are identified. (JINS, 2016, 22, 717–723)
The public health burden of alcohol is unevenly distributed across the life course, with levels of use, abuse, and dependence increasing across adolescence and peaking in early adulthood. Here, we leverage this temporal patterning to search for common genetic variants predicting developmental trajectories of alcohol consumption. Comparable psychiatric evaluations measuring alcohol consumption were collected in three longitudinal community samples (N = 2,126, obs = 12,166). Consumption-repeated measurements spanning adolescence and early adulthood were analyzed using linear mixed models, estimating individual consumption trajectories, which were then tested for association with Illumina 660W-Quad genotype data (866,099 SNPs after imputation and QC). Association results were combined across samples using standard meta-analysis methods. Four meta-analysis associations satisfied our pre-determined genome-wide significance criterion (FDR < 0.1) and six others met our ‘suggestive’ criterion (FDR <0.2). Genome-wide significant associations were highly biological plausible, including associations within GABA transporter 1, SLC6A1 (solute carrier family 6, member 1), and exonic hits in LOC100129340 (mitofusin-1-like). Pathway analyses elaborated single marker results, indicating significant enriched associations to intuitive biological mechanisms, including neurotransmission, xenobiotic pharmacodynamics, and nuclear hormone receptors (NHR). These findings underscore the value of combining longitudinal behavioral data and genome-wide genotype information in order to study developmental patterns and improve statistical power in genomic studies.
Recent studies have examined gene×environment (G×E) interactions involving the monoamine oxidase A (MAOA) gene in moderating the associations between exposure to adversity and antisocial behaviour. The present study examined a novel method for assessing interactions between a single gene and multiple risk factors related to environmental and personal adversity.
To test the hypothesis that the presence of the low-activity MAOA genotype was associated with an increased response to a series of risk factors.
Participants were 399 males from the Christchurch Health and Development Study who had complete data on: (a) MAOA promoter region variable number tandem repeat genotype; (b) antisocial behaviour (criminal offending) to age 30 and convictions to age 21; and (c) maternal smoking during pregnancy, IQ, childhood maltreatment and school failure.
Poisson regression models were fitted to three antisocial behaviour outcomes (property/violent offending ages 15–30; and convictions ages 17–21), using measures of exposure to adverse childhood circumstances. The analyses revealed consistent evidence of G x E interactions, such that those with the low-activity MAOA variant who were exposed to adversity in childhood were significantly more likely to report offending in late adolescence and early adulthood.
The present findings add to the evidence suggesting that there is a stable G x E interaction involving MAOA, a range of adverse environmental and personal factors, and antisocial behaviour across the life course. These analyses also demonstrate the utility of using multiple environmental/personal exposures to test G×E interactions.
Recent studies have raised issues concerning the replicability of gene ×
environment (G × E) interactions involving the monoamine oxidase A
(MAOA) gene in moderating the associations between
abuse or maltreatment exposure and antisocial behaviour. This study
attempted to replicate the findings in this area using a 30-year
longitudinal study that has strong resemblance to the original research
To test the hypothesis that the presence of the low-activity
MAOA genotype was associated with an increased
response to abuse exposure.
Participants were 398 males from the Christchurch Health and Development
Study who had complete data on: MAOA promoter region
variable number tandem repeat genotype; antisocial behaviour to age 30;
and exposure to childhood sexual and physical abuse.
Regression models were fitted to five antisocial behaviour outcomes
(self-reported property offending; self-reported violent offending;
convictions for property/violent offending; conduct problems; hostility)
observed from age 16 to 30, using measures of childhood exposure to
sexual and physical abuse. The analyses revealed consistent evidence of G
× E interactions, with those having the low-activity
MAOA variant and who were exposed to abuse in
childhood being significantly more likely to report later offending,
conduct problems and hostility. These interactions remained statistically
significant after control for a range of potentially confounding factors.
Findings for convictions data were somewhat weaker.
The present findings add to the evidence suggesting that there is a
stable G × E interaction involving MAOA, abuse exposure
and antisocial behaviour across the life course.
Recent meta-analyses have raised concerns about the replicability of gene
× environment interactions involving the serotonin transporter gene
(5-HTTLPR) in moderating the associations between adverse life events and
To use data gathered over the course of a 30-year longitudinal study of a
New Zealand birth cohort to test the hypothesis that the presence of
short (‘s’) alleles of 5-HTTLPR are associated with an increased response
to life stress.
Participants were 893 individuals from the Christchurch Health and
Development Study who had complete data on: the 5-HTTLPR genotype;
psychiatric disorders up to the age of 30; and exposure to childhood and
adult adverse life events.
A series of 104 regression models were fitted to four mental health
outcomes (depressive symptoms, major depression, anxiety disorder and
suicidal ideation) observed at ages 18, 21, 25 and 30 using 13 measures
of life-course stress that spanned childhood and adult stressors. Both
multiplicative and additive models were fitted to the data. No evidence
was found that would support the hypothesis that ‘s' alleles of 5-HTTLPR
are associated with increased responsivity to life stressors.
The present findings add to the evidence suggesting that it is unlikely
that there is a stable gene × environment interaction involving 5-HTTLPR,
life stress and mental disorders.
Marriage is known to be associated with improved mental health, but little research has examined whether the duration of a cohabiting relationship is associated with mental health.
To examine the associations between relationship duration and mental health problems in a birth cohort of 30-year-olds.
Associations between relationship duration and mental health were examined using a generalised estimating equation approach. Associations were adjusted for covariates, including prior mental health problems.
Longer relationship duration was significantly associated with lower rates of depression, suicidal behaviour and substance abuse/dependence, even after adjustment for covariates. In most cases the associations did not vary with gender. Legal relationship status (legally or de facto married) was not significantly related to mental health once due allowance was made for relationship duration.
Increasing relationship duration, but not legal relationship status, has a protective effect on mental health for men and women.
Psychiatric disorders are common during young adulthood and comorbidity is frequent. Individual psychiatric disorders have been shown to be associated with negative economic and educational outcomes, but few studies have addressed the relationship between the total extent of psychiatric disorder and life outcomes.
To examine whether the extent of common psychiatric disorder between ages 18 and 25 is associated with negative economic and educational outcomes at age 30, before and after controlling for confounding factors.
Participants were 987 individuals from the Christchurch Health and Development Study, a longitudinal study of a birth cohort of individuals born in Christchurch, New Zealand, in 1977 and followed to age 30. Linear and logistic regression models were used to examine the associations between psychiatric disorder from age 18 to 25 and workforce participation, income and living standards, and educational achievement at age 30, before and after adjustment for confounding factors.
There were significant associations between the extent of psychiatric disorder reported between ages 18 and 25 and all of the outcome measures (all P<0.05). After adjustment for confounding factors, the associations between psychiatric disorder and workforce participation, income and living standards remained significant (all P<0.05), but the associations between psychiatric disorder and educational achievement were not significant (all P>0.10).
After due allowance had been made for a range of confounding factors, psychiatric disorder between ages 18 and 25 was associated with reduced workforce participation, lower income and lower economic living standards at age 30.
Research on the comorbidity between cigarette smoking and major depression has not elucidated the pathways by which smoking is associated with depression.
To examine the causal relationships between smoking and depression via fixed-effects regression and structural equation modelling.
Data were gathered on nicotine-dependence symptoms and depressive symptoms in early adulthood using a birth cohort of over 1000 individuals.
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.
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.
There has been continued interest in the extent to which women have positive and negative reactions to abortion.
To document emotional reactions to abortion, and to examine the links between reactions to abortion and subsequent mental health outcomes.
Data were gathered on the pregnancy and mental health history of a birth cohort of over 500 women studied to the age of 30.
Abortion was associated with high rates of both positive and negative emotional reactions; however, nearly 90% of respondents believed that the abortion was the right decision. Analyses showed that the number of negative responses to the abortion was associated with increased levels of subsequent mental health disorders (P<0.05). Further analyses suggested that, after adjustment for confounding, those having an abortion and reporting negative reactions had rates of mental health disorders that were approximately 1.4–1.8 times higher than those not having an abortion.
Abortion was associated with both positive and negative emotional reactions. The extent of negative emotional reactions appeared to modify the links between abortion and subsequent mental health problems.
Research on the links between abortion and mental health has been limited by design problems and relatively weak evidence.
To examine the links between pregnancy outcomes and mental health outcomes.
Data were gathered on the pregnancy and mental health history of a birth cohort of over 500 women studied to the age of 30.
After adjustment for confounding, abortion was associated with a small increase in the risk of mental disorders; women who had had abortions had rates of mental disorder that were about 30% higher. There were no consistent associations between other pregnancy outcomes and mental health. Estimates of attributable risk indicated that exposure to abortion accounted for 1.5% to 5.5% of the overall rate of mental disorders.
The evidence is consistent with the view that abortion may be associated with a small increase in risk of mental disorders. Other pregnancy outcomes were not related to increased risk of mental health problems.
This paper examines the relationship between self-esteem in adolescence and later mental health, substance use, and life and relationship outcomes in adulthood. The investigation analyzed data from a birth cohort of approximately 1,000 New Zealand young adults studied to the age of 25. Lower levels of self-esteem at age 15 were associated with greater risks of mental health problems, substance dependence, and lower levels of life and relationship satisfaction at ages 18, 21, and 25. Adjustment for potentially confounding factors reduced the strength of these associations to either moderate or statistically nonsignificant levels. It was concluded that the effects of self-esteem during adolescence on later developmental outcomes were weak, and largely explained by the psychosocial context within which self-esteem develops.
It is unclear how the recurrence of major depression in adolescence affects later life outcomes.
To examine the associations between the frequency of major depression at ages 16–21 and later outcomes, both before and after controlling for potentially confounding factors.
Data were gathered from a 25-year longitudinal study of a birth cohort of New Zealand children (n=982). Outcome measures included DSM–IV symptom criteria for major depression and anxiety disorders, suicidal ideation and attempted suicide, achieving university degree or other tertiary education qualification, welfare dependence and unemployment, and income at ages 21–25 years.
There were significant (P<0.05) associations between the frequency of depression at ages 16–21 years and all outcome measures. After adjustment for confounding factors, the association between frequency of depression and all mental health outcomes, and welfare dependence and unemployment, remained significant (P<0.05).
The frequency of depression in adolescence and young adulthood is associated with adverse mental health and economic outcomes in early adulthood.
Debate surrounds the underlying structure of internalising disorders
including major depression, generalised anxiety disorder, phobias and
To model the within-time and across-time relationships of internalising
symptoms, incorporating effects from generalised internalising and
disorder-specific components of continuity.
Data were gathered from a 25-year longitudinal study of a birth cohort of
953 New Zealand children. Outcome measures included DSM–IV symptom scores
for major depression, generalised anxiety disorder, phobia and panic
disorder at the ages of 18, 21 and 25 years.
Structural equation modelling showed that, within-times, a common
underlying measure of generalised internalising explained symptom score
comorbidities. Across-time correlation of symptom scores was primarily
accounted for by continuity over time in generalised internalising.
However, for major depression and phobia there was also evidence of
across-time continuity in the disorder-specific components of
Internalising symptoms can be partitioned into components reflecting both
a generalised tendency to internalising and disorder-specific
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.
Data gathered over the course of a 25-year longitudinal study of 1,055
young people was used to examine gender differences in the onset of early
parenthood and the developmental processes that place males and females at
risk of becoming a young parent. Results revealed clear gender differences
in the timing of early parenthood, with females being twice as likely as
males to become a parent between the ages of 16 and 25 years. In contrast,
the risk factors and life course processes that placed males and females
at risk of an early transition to parenthood were very similar. Two
exceptions were a gender-specific effect for maternal age and exposure to
parental change, suggesting that having been raised by a younger mother
and having experienced parental changes in your family of origin increased
risks of early parenthood for females but not males. These findings
contribute to our understanding of the effects of gender on life course
development.This research was funded by
grants from the Health Research Council of New Zealand, the National Child
Health Research Foundation, the Canterbury Medical Research Foundation and
the New Zealand Lottery Grants Board.