A TPB-Based Smoking Intervention among Chinese High School Students.

OBJECTIVES: China is the world's largest tobacco consumer and its adolescent smoking rate is increasing. Smoking interventions among high school students are limited. The aim of this study was to deliver and evaluate a brief theory-based smoking intervention in China, with a focus on anti-smoking cognitions. METHODS: The intervention was based on the constructs of an extended theory of planned behavior and life skills training. Using class-level randomization sampling, 106 tenth graders from two high schools in Kunming, China received a four-session intervention; 101 students were assigned as control group members. Surveys were conducted at three time-points (1 week before the intervention, 1 week post-intervention, and 6 months post-intervention). MANOVA and latent class analysis were used to test the intervention's effectiveness and personal change trajectories over time. RESULTS: The intervention failed to change smoking behavior, intention or willingness, but improved anti-smoking attitudes and perceived control over smoking. Skills showed a general enhancement, consistent with participants' qualitative feedback. Trajectories of smoking behavior, intention, and willingness all assumed two distinct but constant latent classes independent of the intervention. CONCLUSIONS: This study suggests that addressing attitudinal and control beliefs among adolescents and building on assertiveness via additional strategies in life skills such as appropriate refusal skills may be beneficial. The absence of a successful change in subjective norm should be a focus for future anti-smoking programs in China.

A randomised controlled trial of a theory-based intervention to improve sun protective behaviour in adolescents ('you can still be HOT in the shade'): study protocol.

BACKGROUND: Most skin cancers are preventable by encouraging consistent use of sun protective behaviour. In Australia, adolescents have high levels of knowledge and awareness of the risks of skin cancer but exhibit significantly lower sun protection behaviours than adults. There is limited research aimed at understanding why people do or do not engage in sun protective behaviour, and an associated absence of theory-based interventions to improve sun safe behaviour. This paper presents the study protocol for a school-based intervention which aims to improve the sun safe behaviour of adolescents. METHODS/DESIGN: Approximately 400 adolescents (aged 12-17 years) will be recruited through Queensland, Australia public and private schools and randomized to the intervention (n = 200) or 'wait-list' control group (n = 200). The intervention focuses on encouraging supportive sun protective attitudes and beliefs, fostering perceptions of normative support for sun protection behaviour, and increasing perceptions of control/self-efficacy over using sun protection. It will be delivered during three × one hour sessions over a three week period from a trained facilitator during class time. Data will be collected one week pre-intervention (Time 1), and at one week (Time 2) and four weeks (Time 3) post-intervention. Primary outcomes are intentions to sun protect and sun protection behaviour. Secondary outcomes include attitudes toward performing sun protective behaviours (i.e., attitudes), perceptions of normative support to sun protect (i.e., subjective norms, group norms, and image norms), and perceived control over performing sun protective behaviours (i.e., perceived behavioural control). DISCUSSION: The study will provide valuable information about the effectiveness of the intervention in improving the sun protective behaviour of adolescents.

Identifying critical sun-protective beliefs among Australian adults.

We investigated critical beliefs to target in interventions aimed at improving sun-protective behaviours of Australian adults, a population at risk for skin cancer. Participants (N = 816) completed a Theory of Planned Behaviour belief-based questionnaire and a 1-week follow-up of sun-protective behaviour. A range of behavioural, normative and control beliefs correlated with sun-protective behaviour, with no and only minimal differences observed in correlations between beliefs and behaviour by gender and age, respectively. A range of key beliefs made independent contributions to behaviour; however, the behavioural belief about being less likely to tan (ß = 0.09); normative belief about friends (ß = 0.20); and control beliefs about forgetfulness (ß = -0.14), inconvenience (ß = -0.17), knowing I will be in the sun for a long time (ß = 0.16) and more fashionable sun-protective clothing (ß = 0.13) were significant critical beliefs guiding people's sun-protective behaviour. Our study fills a gap in the literature by investigating an at-risk population for skin cancer and using an established theoretical framework to identify critical beliefs that guide Australian adults' decisions to sun protect. Attention to these critical beliefs will assist health campaigns and interventions aimed at combating the increasing rates of skin cancer for adults.

Investigation of C-reactive protein and AIM2 methylation as a marker for PTSD in Australian Vietnam veterans.

Chronic inflammation is a key factor in symptomology and comorbidities of post-traumatic stress disorder (PTSD). Levels of a proinflammatory marker, C-reactive protein (CRP) are increased in individuals with PTSD but it is not clear if this is due to trauma exposure or PTSD. Our study aimed to assess the relationship between serum CRP levels, CRP SNPs, methylation, mRNA expression and PTSD in a homogenous trauma exposed Australian Vietnam veteran cohort. We hypothesized that decreased DNA methylation would be associated with increased gene expression and increased peripheral CRP levels in PTSD patients and that this would be independent of trauma. Participants were 299 Vietnam veterans who had all been exposed to trauma and approximately half were diagnosed with PTSD. We observed higher levels of serum CRP in the PTSD group compared to the non-PTSD group but after controlling for BMI and triglycerides the association did not remain significant. No association was found between CRP SNPs and PTSD or CRP levels. Absent in Melanoma 2 (AIM2) which is a mediator of inflammatory response and a determinant of CRP levels was analysed for DNA methylation and mRNA expression. We observed a trend level association between PTSD and AIM2 methylation after controlling for age, smoking, triglycerides, BMI and cell types. There was no significant interaction between PTSD and CRP levels on AIM2 methylation after controlling for covariates. We observed that as AIM2 methylation levels decreased, AIM2 mRNA expression increased. Elevated CRP levels were associated with AIM2 mRNA in the trauma exposed cohort but there was no significant interaction effect with PTSD. Our results could not confirm that CRP is a marker of PTSD independent of trauma in this group of older veterans. CRP may be a broad marker of disease risk, or a marker of PTSD in younger cohorts than those in this study.

NLRP3 is associated with coronary artery disease in Vietnam veterans.

BACKGROUND: Previous studies have established that coronary artery disease is associated with excess inflammation. These studies have shown an elevation of both pro and anti-inflammatory cytokines in sufferers of coronary artery disease. There is increasing interest in the role played by the inflammasome Nod Like Receptor family pyrin domain containing 3 (NLRP3) in the aetiology of coronary artery disease. Increased severity of coronary artery disease correlates with higher levels of expression of NLRP3. Does NLRP3 polymorphisms play a role in the aetiology of coronary artery disease? METHOD: In a cohort of Vietnam War (n-299) veterans who have been previously exposed to trauma, NLRP3 polymorphisms were analysed for association with coronary calcium scores using analyses of variance. Independent t-test was used to analyse genotypes. In samples with a small representation of minor homozygotes, genotypes were combined and analysed using independent t-test. If any of the genotype analysis suggested the potential for a dominant or a recessive model the model was further explored. Hardy-Weinberg Equilibrium was calculated using Hardy-Weinberg equilibrium calculator including analysis for ascertainment bias. RESULTS: The NLRP3 polymorphism, rs10159239 was significantly associated (p = 0.001) with a higher raised coronary calcium score. The Single Nucleotide Polymorphism rs10159239 was examined by logistic regression with known risk factors for Coronary artery disease and remained significant (0.035). This is the first time rs10159239 A-allele has been associated with raised coronary calcium score. CONCLUSIONS: This is the first time rs10159239 A-allele has been associated with raised coronary calcium score. Further research is needed to replicate our results in larger well-characterised cohorts.

Craving mediates the effect of impulsivity on lapse-risk during alcohol use disorder treatment.

Rash impulsiveness, the propensity for approach behaviour despite potential negative consequences, is associated with stronger alcohol craving in patients with Alcohol Use Disorder (AUD). This relationship is poorly understood and implications for treatment response are unexamined. This study explored the relationship between rash impulsiveness, craving, and treatment response among 304 outpatients enrolled in a 12-week abstinence-based Cognitive-Behavioural Therapy (CBT) program for AUD. Assessments were completed pre-and-post treatment, with craving and alcohol consumption monitored at each treatment session. Higher rash impulsiveness predicted more frequent craving over treatment (b = 0.95, 95% CI = 0.40, 1.50). Higher craving was associated with greater lapse-risk (b = 0.04, 95% CI = 0.03, 0.05), with the association between craving and lapse-risk increasing as treatment progressed (b = 0.01, 95% CI = 0.01, 0.02). Craving positively mediated the relationship between rash impulsiveness and lapse-risk (µâ€¯= 0.38, 95% CI = 0.10, 0.70). Contrary to hypotheses, the risk of lapse in response to craving was not moderated by rash-impulsiveness. These results suggest that AUD patients with a predisposition for rash impulsiveness are more vulnerable to alcohol craving, and subsequently, poorer treatment outcomes.

Correlation between interferon γ and interleukin 6 with PTSD and resilience.

Posttraumatic Stress Disorder (PTSD) is a debilitating psychiatric disorder with decreased general health prognosis and increased mortality. Inflammation has been hypothesised to be a link between PTSD and the most common co-morbid medical disorders. However, the relationship between inflammation and PTSD is not clear. Individual inflammatory markers have shown variable associations with PTSD. This study investigates the correlations between serum cytokines, PTSD and resilience in a cohort of Caucasian Vietnam combat veterans (n = 299). After correction for multiple testing, PTSD severity was correlated with small but significant decreases in interleukin 6 and interferon γ (p = 0.004, p = 0.013, respectively) whereas resilience was correlated with increased levels of interleukin 6 and interferon γ (p = 0.023; p = 0.007, respectively). Analyses of sub-symptoms of PTSD revealed that mood and arousal symptoms showed the most significant effect on interleukin 6 and interferon γ. More research is needed to further elucidate the mechanisms underlying the relationship between cytokine levels, PTSD sub-symptoms and trauma outcomes to improve the knowledge base of differences in trauma response and the biological system.

Detailed Polysomnography in Australian Vietnam Veterans With and Without Posttraumatic Stress Disorder.

STUDY OBJECTIVES: Recent results from the PTSD Initiative, a cross-sectional cohort study in Australian Vietnam veterans (VV) with and without posttraumatic stress disorder (PTSD), demonstrated an increased prevalence of self-reported sleep disturbances in those with PTSD. This study aimed to objectively assess the prevalence of sleep disorders in the same cohort using detailed polysomnography (PSG). METHODS: Participants from the PTSD Initiative were recruited to undergo PSG. PTSD status was determined with the Clinician Administered PTSD Scale for DSM-5 (CAPS-5). Subjective sleep information was attained via structured questionnaires. Data from single night PSG were compared between trauma-exposed VV with and without PTSD. RESULTS: A total of 74 trauma-exposed male VV (40 with PTSD) underwent PSG (prospective n = 59, retrospective n = 15). All PSG parameters were similar between groups. No difference was seen in PSG-diagnosed obstructive sleep apnea (OSA) or periodic limb movements of sleep (PLMS). VV with PTSD showed a trend toward increased duration of sleep with oxygen saturations < 90% (10% versus 1.8%; P = .07). VV with PTSD reported increased sleep onset latency (42.4 versus 13.3 minutes; P < .01); were less likely to report sleeping well (32.5% versus 67.5%; P < .01); had higher OSA risk using Berlin Questionnaire (BQ) (70% versus 38.2%; P < .01); and had higher rates of partner-reported limb movements (56.4% versus 17.6%; P < .01). No association between PSG-diagnosed OSA and PTSD severity was evident. CONCLUSIONS: In Australian VV with and without PTSD, no difference was seen across all PSG parameters including the diagnosis and severity of OSA and PLMS. However, VV with PTSD demonstrated an increased perception of sleep disturbances.

Is acamprosate use in alcohol dependence treatment reflected in improved subjective health status outcomes beyond cognitive behavioural therapy alone?.

OBJECTIVE: To examine whether the addition of acamprosate to Cognitive Behavioural Therapy (CBT) outpatient alcohol dependence treatment impacted on subjective health status. METHOD: Among 268 patients consecutively treated for alcohol dependence, 149 chose CBT alone. A matched design was used. From a possible pool of 119 Acamprosate + CBT and 149 CBT-only patients, 86 Acamprosate + CBT subjects were individually matched with 86 CBT-only patients on parameters of gender, age, prior detoxification and alcohol dependence severity. Health Status (SF-36) and Psychological Well-Being (GHQ-28) was assessed pre- and post-treatment. RESULTS: Pre-treatment, both self-reported health status and psychological well-being was markedly below normative (community) ranges. Program completers significantly improved across both measures over 12 weeks of treatment and some health domains approximated community levels. No treatment group differences were observed. CONCLUSIONS: Participants who completed the CBT-based treatment showed significant improvement in self-reported health status. The use of acamprosate did not register additional improvement on either SF-36 or GHQ-28, beyond CBT alone.

The profile of psychiatric symptoms exacerbated by methamphetamine use.

BACKGROUND: Methamphetamine use can produce symptoms almost indistinguishable from schizophrenia. Distinguishing between the two conditions has been hampered by the lack of a validated symptom profile for methamphetamine-induced psychiatric symptoms. We use data from a longitudinal cohort study to examine the profile of psychiatric symptoms that are acutely exacerbated by methamphetamine use. METHODS: 164 methamphetamine users, who did not meet DSM-IV criteria for a lifetime primary psychotic disorder, were followed monthly for one year to assess the relationship between days of methamphetamine use and symptom severity on the 24-item Brief Psychiatric Rating Scale. Exacerbation of psychiatric symptoms with methamphetamine use was quantified using random coefficient models. The dimensions of symptom exacerbation were examined using principal axis factoring and a latent profile analysis. RESULTS: Symptoms exacerbated by methamphetamine loaded on three factors: positive psychotic symptoms (suspiciousness, unusual thought content, hallucinations, bizarre behavior); affective symptoms (depression, suicidality, guilt, hostility, somatic concern, self-neglect); and psychomotor symptoms (tension, excitement, distractibility, motor hyperactivity). Methamphetamine use did not significantly increase negative symptoms. Vulnerability to positive psychotic and affective symptom exacerbation was shared by 28% of participants, and this vulnerability aligned with a past year DSM-IV diagnosis of substance-induced psychosis (38% vs. 22%, χ(2)(df1)=3.66, p=0.056). CONCLUSION: Methamphetamine use produced a symptom profile comprised of positive psychotic and affective symptoms, which aligned with a diagnosis of substance-induced psychosis, with no evidence of a negative syndrome.

D2 dopamine receptor gene polymorphism: paroxetine and social functioning in posttraumatic stress disorder.

This study examined whether allelic status of the D2 dopamine receptor (DRD2) gene was associated with response to a selective serotonin reuptake inhibitor, paroxetine, in the treatment of posttraumatic stress disorder (PTSD). Sixty-three Caucasian war veterans with combat-related PTSD were treated with paroxetine for 8 weeks. Patients were assessed at baseline and at follow-up using the General Health Questionnaire-28 (GHQ). TaqI A DRD2 alleles were determined by PCR. Before paroxetine treatment, patients with the DRD2 A1+ allele (A1A2 genotype) compared to those with the A1- allele (A2A2 genotype) had higher total GHQ psychopathological scores (P=0.040) and higher GHQ subscale scores for anxiety/insomnia (0.046), social dysfunction (P=0.033) and depression (P=0.011). In an intention-to-treat analysis, paroxetine was associated with significant improvement in total GHQ scores (P=0.014) and in the factor scores of social dysfunction (P=0.033), anxiety (P=0.009) and depression (P=0.026). Furthermore, there was a significant allele by time interaction on the social dysfunction scale, with A1+ allelic patients showing significant improvement in social functioning compared to A1- allelic patients (P=0.031), an effect independent of changes in depression or anxiety. This suggests changes in social functioning induced by paroxetine may be, in part, mediated via D2 dopamine receptors. The DRD2 A1 allele may prove to be a useful marker to assist clinicians in predicting which patients with PTSD are likely to obtain improvements in social functioning with paroxetine treatment.

Impulsivity-related cognition in alcohol dependence: Is it moderated by DRD2/ANKK1 gene status and executive dysfunction?

Perceived impaired control over alcohol use is a key cognitive construct in alcohol dependence that has been related prospectively to treatment outcome and may mediate the risk for problem drinking conveyed by impulsivity in non-dependent drinkers. The aim of the current study was to investigate whether perceived impaired control may mediate the association between impulsivity-related measures (derived from the Short-form Eysenck Personality Questionnaire-Revised) and alcohol-dependence severity in alcohol-dependent drinkers. Furthermore, the extent to which this hypothesized relationship was moderated by genetic risk (Taq1A polymorphism in the DRD2/ANKK1 gene cluster) and verbal fluency as an indicator of executive cognitive ability (Controlled Oral Word Association Test) was also examined. A sample of 143 alcohol-dependent inpatients provided an extensive clinical history of their alcohol use, gave 10ml of blood for DNA analysis, and completed self-report measures relating to impulsivity, impaired control and severity of dependence. As hypothesized, perceived impaired control (partially) mediated the association between impulsivity-related measures and alcohol-dependence severity. This relationship was not moderated by the DRD2/ANKK1 polymorphism or verbal fluency. These results suggest that, in alcohol dependence, perceived impaired control is a cognitive mediator of impulsivity-related constructs that may be unaffected by DRD2/ANKK1 and neurocognitive processes underlying the retrieval of verbal information.

KPNA3 variation is associated with schizophrenia, major depression, opiate dependence and alcohol dependence.

KPNA3 is a gene that has been linked to schizophrenia susceptibility. In this study we investigated the possible association between KPNA3 variation and schizophrenia. To investigate a wider role of KPNA3 across psychiatric disorders we also analysed major depression, PTSD, nicotine dependent, alcohol dependent and opiate dependent cohorts. Using a haplotype block-based gene-tagging approach we genotyped six KPNA3 single nucleotide polymorphisms (SNPs) in 157 schizophrenia patients, 121 post-traumatic stress disorder patients, 120 opiate dependent patients, 231 alcohol dependent patients, 147 nicotine dependent patients and 266 major depression patients. One SNP rs2273816 was found to be significantly associated with schizophrenia, opiate dependence and alcohol dependence at the genotype and allele level. Major depression was also associated with rs2273816 but only at the allele level. Our study suggests that KPNA3 may contribute to the genetic susceptibility to schizophrenia as well as other psychiatric disorders.

Effectiveness of current treatment approaches for benzodiazepine discontinuation: a meta-analysis.

AIMS: To assess the effectiveness of current treatment approaches to assist benzodiazepine discontinuation. METHODS: A systematic review of approaches to benzodiazepine discontinuation in general practice and out-patient settings was undertaken. Routine care was compared with three treatment approaches: brief interventions, gradual dose reduction (GDR) and psychological interventions. GDR was compared with GDR plus psychological interventions or substitutive pharmacotherapies. RESULTS: Inclusion criteria were met by 24 studies, and a further eight were identified by future search. GDR [odds ratio (OR) = 5.96, confidence interval (CI) = 2.08-17.11] and brief interventions (OR = 4.37, CI = 2.28-8.40) provided superior cessation rates at post-treatment to routine care. Psychological treatment plus GDR were superior to both routine care (OR = 3.38, CI = 1.86-6.12) and GDR alone (OR = 1.82, CI = 1.25-2.67). However, substitutive pharmacotherapies did not add to the impact of GDR (OR = 1.30, CI = 0.97-1.73), and abrupt substitution of benzodiazepines by other pharmacotherapy was less effective than GDR alone (OR = 0.30, CI = 0.14-0.64). Few studies on any technique had significantly greater benzodiazepine discontinuation than controls at follow-up. CONCLUSIONS: Providing an intervention is more effective than routine care. Psychological interventions may improve discontinuation above GDR alone. While some substitutive pharmacotherapies may have promise, current evidence is insufficient to support their use.