Gender determinants of smoking practice in Indigenous communities: an exploratory study.

Despite the need to urgently reduce smoking rates among Indigenous Australians, in order to close-the-gap in life expectancy, little is known regarding how this can be achieved. This study aimed to explore whether a focus on gender specific determinants of smoking among Indigenous Australians could be identified, thus providing a potentially novel approach to underpin future efforts at intervention. A qualitative research design was employed. Eighty-two participants, comprised of 43 Indigenous women (mean age 32.15, SD, 12.47) and 39 Indigenous men (mean age 34.91, SD, 11.26), participated in one of 12 focus groups held in metropolitan, regional and rural locations in South Australia. Facilitators prompted discussion in response to the question: 'What is it like being a smoker these days?' Two experienced coders assessed data for themes using Attride-Stirling's (2002) method of analysis. Two global themes emerged for men and women. The first theme, 'It's Harder to Smoke Nowadays', encompassed sub-themes capturing changed smoking practices in response to tobacco control strategies implemented in Australia. Sub-themes of 'smoking in secrecy' coupled with an 'awareness of the effects of passive smoking' were identified among women. Among men, sub-themes that depicted tension between 'a desire to be a role model' and 'guilt about smoking' emerged. The second theme, 'Push and Pull Factors', identified a range of gender specific determinants of smoking. While similar reasons for smoking ('pull factors') were identified in men and women (e.g. addiction, boredom, stress, pleasure, mood stabiliser), different 'push factors' (reasons for not wanting to smoke) emerged. For men, sport, fitness and children were identified as reasons for not wanting to smoke, whereas women identified factors such as respect for non-smokers, and body image concerns. The current findings suggest that there may be fundamental differences in the determinants of smoking (pull factors) as well as reasons for wanting to quit (push factors) between Indigenous men and women. A focus on interventions that target gender specific determinants, or motivators of smoking, offers a novel, and potentially efficacious approach to reduce smoking rates among Indigenous Australians.

COMT polymorphism modulates the resting-state EEG alpha oscillatory response to acute nicotine in male non-smokers.

Performance improvements in cognitive tasks requiring executive functions are evident with nicotinic acetylcholine receptor (nAChR) agonists, and activation of the underlying neural circuitry supporting these cognitive effects is thought to involve dopamine neurotransmission. As individual difference in response to nicotine may be related to a functional polymorphism in the gene encoding catechol-O-methyltransferase (COMT), an enzyme that strongly influences cortical dopamine metabolism, this study examined the modulatory effects of the COMT Val158Met polymorphism on the neural response to acute nicotine as measured with resting-state electroencephalographic (EEG) oscillations. In a sample of 62 healthy non-smoking adult males, a single dose (6 mg) of nicotine gum administered in a randomized, double-blind, placebo-controlled design was shown to affect α oscillatory activity, increasing power of upper α oscillations in frontocentral regions of Met/Met homozygotes and in parietal/occipital regions of Val/Met heterozygotes. Peak α frequency was also found to be faster with nicotine (vs. placebo) treatment in Val/Met heterozygotes, who exhibited a slower α frequency compared to Val/Val homozygotes. The data tentatively suggest that interindividual differences in brain α oscillations and their response to nicotinic agonist treatment are influenced by genetic mechanisms involving COMT.

Mindfulness-based cancer stress management: impact of a mindfulness-based programme on psychological distress and quality of life.

Within the area of cancer care, mindfulness-based therapeutic interventions have been found to be efficacious in reducing psychological distress related to a cancer diagnosis; however, the impact of mindfulness-based interventions on quality of life is unclear. This study explores the impact of a Mindfulness-Based Cancer Stress Management programme on psychological distress and quality of life. Research methodology included a single-group quasi-experimental study of 26 participants experiencing distress related to a cancer diagnosis, including carers, who completed an MBCSM programme and all assessments. Participants completed the Functional Assessment of Cancer Therapy - General version 4 (FACT-G) and its associated spirituality index (FACIT-Sp-Ex), Hospital Anxiety and Depression Scale (HADS), Freiburg Mindfulness Inventory (FMI), and the Distress Thermometer at baseline, post-intervention, and three months after programme completion. Significant improvements were observed on all measures (ranges: P ≤ 0.001 to 0.008, r = -0.53 to -0.79) following the intervention, which were maintained at 3-month follow-up. Mindfulness was significantly correlated with all main outcome measures at post-intervention (range: r = -0.41 to 0.67) and 3-month follow-up (range: r = -0.49 to 0.73), providing evidence for the internal validity of the study. Our findings indicate that the MBCSM programme is effective in reducing psychological distress and improving quality of life, including spiritual well-being.

Complementary medicine and recovery from cancer: the importance of post-traumatic growth.

Many users of Complementary and Alternative Medicines (CAMs) claim that participation leads to improved well-being; however, contradictory evidence exists, with some studies linking CAM use with poorer quality of life (QoL) or increased distress. This study explored whether an individual's experience of post-traumatic growth (PTG) following cancer may play a role in explaining these disparate outcomes. One hundred and sixty-one cancer survivors (mean age = 58.96, SD = 12.12) completed measures comprised of PTG (Post-Traumatic Growth Inventory), CAM use, QoL (Functional Assessment of Cancer Therapy scale + Functional Assessment of Chronic Illness Therapy Spiritual Well-Being Scale), post-traumatic stress disorder symptoms (Impact of Event Scale Revised) and depression, anxiety and stress (21-item short-form Depression Anxiety Stress Scale). A multiple regression controlling for gender, age, general and cancer-specific distress indicated support for PTG as a mediator of the relationship between CAM and QoL. An individual's experience of PTG following cancer may be an important determinant of gaining benefit from participation in CAMs. Future research aimed at identifying potential facilitators of PTG may result in increased benefits of interventions aimed at improving adjustment among cancer survivors.

Effects of nicotine on visuospatial attentional orienting in non-smokers.

Nicotine is a highly addictive substance, suggested to be in part due to its cognitive enhancing effects in the attentional domain. Improvements in stimulus selection with nicotine have been reported but its effects on visual-spatial selective attention are unclear. This study utilized event-related potentials (ERPs) to examine the acute effects of nicotine on selective attention in non-smokers performing a Posner-type visuo-spatial task. The attentional processing of visual-spatial locations is reflected in the P1 ERP component, which represents earlier stages of visual analysis. 24 non-smokers received nicotine gum (6 mg) in a randomized, double-blind, placebo-controlled, repeated measures design. Behavioral performance and ERPs were assessed in response to target locations preceded by valid, invalid and neutral cues. Nicotine did not affect behavioral performance indices. P1 amplitudes were greater in valid and neutral cue trials compared to invalid cue trials and acute nicotine administration (vs. placebo) was found to increase P1 amplitudes in the right hemisphere, particularly in valid cue trials. In addition, in high symptomatic subjects (as indexed by greater increases in heart rate post-administration), nicotine (vs. placebo) produced greater P1 amplitudes in valid cue trials. The study concludes that nicotine enhanced visuospatial selective attention with regards to early visual encoding and analysis. These results demonstrate support in general for the attentional effects of nicotine and nicotinic agonists and they specifically extend these effects to include orienting of visual-spatial attention.

Effects of COMT genotype on sensory gating and its modulation by nicotine: Differences in low and high P50 suppressors.

Elevated smoking rates seen in schizophrenia populations may be an attempt to correct neuropathologies associated with deficient nicotinic acetylcholine receptors and/or dopaminergic systems using exogenous nicotine. However, nicotine's effects on cognitive processing and sensory gating have been shown to be baseline-dependent. Evidence of a restorative effect on sensory gating deficits by nicotine-like agonists has been demonstrated, however, its underlying mechanisms in the context of dopamine dysregulation are unclear. Catechol-O-methyltransferase (COMT), a key dopamine regulator in the brain, contains a co-dominant allele in which a valine-to-methionine substitution causes variations in enzymatic activity leading to reduced synaptic dopamine levels in the Val/Val genotype. Using a randomized, double-blind, placebo-controlled design with 57 non-smokers, this study examined the effects of COMT genotype on sensory gating and its modulation by nicotine in low vs. high suppressors. The results were consistent with the hypothesis that increased dopamine resulting from nicotine stimulation or Met allelic activity would benefit gating in low suppressors and impair gating in high suppressors, and that this gating improvement with nicotine would be more evident in Val carriers who were low suppressors, while the gating impairment would be more evident in Met carriers who were high suppressors. These findings reaffirm the importance of baseline-dependency and suggest a subtle relationship between COMT genotype and baseline-stratified levels of sensory gating, which may help to explain the variability of cognitive abilities in schizophrenia populations.

Promoting positive change in the face of adversity: experiences of cancer and post-traumatic growth.

The increasing population of cancer survivors underscores the need to develop a complete understanding of the survivorship experience, including positive aspects. The aim of this study was to explore people's experiences of cancer to assess the relevance of the post-traumatic growth (PTG) construct and to identify potentially modifiable factors that may promote PTG. Group interviews were conducted with 15 people (eight men, seven women) aged between 36 and 85 who had been diagnosed with cancer and completed treatment. Participants identified that while a cancer diagnosis is a traumatic event and has an immense impact, there is potential for PTG. Participants described examples of positive change within their relationships, perceptions of self and life in general perception, and spirituality. Various modifiable factors were identified as enabling participants to experience growth including social support, finding information, complementary therapy use, lifestyle changes and physical activity. Modifiable factors such as physical activity and searching for information have the potential to influence the development of PTG by providing cancer survivors with an opportunity to regain control. Encouraging and developing research that examines the relationship between modifiable factors and PTG will assist in the development of interventions that address the unique needs of cancer survivors.

A review of community engagement in cancer control studies among Indigenous people of Australia, New Zealand, Canada and the USA.

This review aimed to address studies of cancer control in Indigenous populations, with a focus on: (1) the nature and extent of community engagement; and (2) the extent to which community engagement has facilitated successful outcomes. Articles addressing Indigenous cancer control using some degree of community engagement were identified by a search of the following electronic databases: MEDLINE (via Ovid and Pubmed), psycINFO, CINAHL and Google Scholar. Relevant studies were scored and analysed according to Green et al.'s guidelines for participatory research. Studies often engaged the community only minimally. Where studies resulted in successful outcomes, they tended to have included Indigenous community members in genuine research roles, from planning, to implementation, to presentation of results at conferences. Studies with positive health outcomes were often initiated by a combination of academic researchers and community members or organisations. This narrative review highlighted significant scope for improvement in community-based studies addressing Indigenous cancer control. Increased attention to the philosophical underpinnings of community engagement is required to ensure that the benefits of this approach are translated to achieve improved cancer control outcomes. An increased awareness of the benefits of community engagement may prove effective in conducting cancer control research that leads to improved outcomes in Indigenous communities.

Why people choose to not use complementary therapies during cancer treatment: a focus group study.

While 50% of cancer patients use complementary therapies (CT) during treatment, few studies have examined why individuals choose not to use CT. This study aimed to address this gap in knowledge using a focus group methodology, where 36 participants took part in one of eight groups; participants were recruited until saturation of themes was achieved. Three categories of participants were investigated: patients/recent survivors (n= 14); volunteers/advocates (n= 16), the majority of whom were also long-term survivors; and health professionals (n= 6). Focus groups were digitally audio-recorded, transcribed, and coded thematically using NVivo software. Reasons for non-use fell into four broad themes: (1) Resource barriers, particularly the cost and lack of time; (2) fear and distrust, including the potential for drug interactions; (3) lack of evidence, including the unproven nature of many CT practices; and (4) satisfaction with conventional treatment. Two further themes related to the benefits of non-use and reasons for discontinuation. A sub-analysis indicated that reasons for non-use differed by CT category, with non-use being mentioned more frequently for biologically based and body-based therapies. Differences in understanding CT non-use emerged between patients, volunteers and health professionals. Findings have clinical implications regarding tailoring information for patients during and after cancer.

The moderating role of the dopamine transporter 1 gene on P50 sensory gating and its modulation by nicotine.

Although schizophrenia has been considered primarily a disease of dopaminergic neurotransmission, the role of dopamine in auditory sensory gating deficits in this disorder and their amelioration by smoking/nicotine is unclear. Hypothesizing that individual differences in striatal dopamine levels may moderate auditory gating and its modulation by nicotine, this preliminary study used the mid-latency (P50) auditory event-related potential (ERP) to examine the single dose (6 mg) effects of nicotine (vs. placebo) gum on sensory gating in 24 healthy nonsmokers varying in the genetic expression of the dopamine transporter (DAT). Consistent with an inverted-U relationship between dopamine level and the drug effects, individuals carrying the 9R (lower gene expression) allele, which is related to greater striatal dopamine levels, tended to evidence increased baseline gating compared to 10R (higher gene expression) allele carriers and showed a reduction in gating with acute nicotine. The present results may help to understand the link between excessive smoking and sensory gating deficits in schizophrenia and to explain the potential functional implications of genetic disposition on nicotinic treatment in schizophrenia.

Differential effects of nicotine on P50 amplitude, its gating, and their neural sources in low and high suppressors.

Sensory gating impairment in schizophrenia has been documented in the form of aberrant middle latency P50 event-related brain potential responses to S(1) and/or S(2) stimuli in a paired (S(1)-S(2)) auditory stimulus paradigm. Evidenced by a failure to suppress S(2) P50 or by attenuated S(1) P50s, these sensory deficits have been associated with increased smoking behaviour in this disorder, and may be related to the putative ameliorating effects of smoke-inhaled nicotine on neural mechanisms regulating gating. Comparison of healthy controls with low versus high gating efficiency has been forwarded as a model for investigating the actions of antipsychotic agents on aberrant gating functions. In the current study, the effect of a single dose (6 mg) of nicotine gum on P50, gating indices, and their cortical sources indexed with sLORETA (standardized low resolution electromagnetic tomography), was examined in healthy non-smokers (n=24) stratified for low and high gating levels. Scalp surface recordings revealed nicotine modulation of P50 and its gating to be differentially exhibited in high (decreasing gating) and low (increasing gating) suppressors while the underlying cortical sources influenced by nicotine (middle frontal gyrus, inferior/superior parietal lobules, pre- and post-central gyri) were seen only in low suppressors. These findings suggest that nicotine impacts sensory gating in healthy volunteers and as the gating enhancing effects were dependent on low baseline gating efficiency, nicotinic receptor agonists may be associated with unique P50 modulating actions in schizophrenia.

Effects of nicotine on the amplitude and gating of the auditory P50 and its influence by dopamine D2 receptor gene polymorphism.

Evidence of normalized auditory P50 suppression with acute nicotine in schizophrenia has supported the contention that elevated smoking rates in this disorder may be an attempt to correct a nicotinic receptor pathophysiology that may underly impaired sensory gating in these patients. There is very little information regarding the neurochemical or genetic pathways through which nicotine regulates P50 amplitude and its suppression in human studies. In a randomized, double-blind, placebo-controlled design with 24 non-smokers, this study examined the influence of TaqIA dopamine D2 receptor gene polymorphisms on P50 and its inhibition during nicotine gum (6 mg) administration. Within a paired click (S(1)-S(2)) paradigm, placebo treated A1(+) and A1(-) allele groups differed with respect to P50 amplitude and gating. While nicotine (relative to placebo) attenuated S(1) P50 amplitude in A1(+) allele carriers, in the A1(-) carriers it increased S(2) P50 amplitude and increased P50 gating as indexed by an augmented gating difference wave (GDW). These findings suggest that nicotine exerts mixed gating properties in healthy nicotine naive volunteers and that dopamine functions to alter both P50 and its gating as well as their response to acute nicotine agonist treatment.

Nicotine and smoker status moderate brain electric and mood activation induced by ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist.

As the increased smoking prevalence in schizophrenics may be interpreted as an adaptive response to an underlying biological defect, investigations into nicotine's actions within N-methyl-d-aspartate (NMDA) antagonist drug models of schizophrenia may improve our understanding of the role of glutamatergic neurotransmission in initiating and maintaining nicotine dependence in this disorder. In this double-blind, placebo-controlled, randomized study, the electroencephalographic (EEG) and subjective response to a sub-psychotomimetic intravenous dose of the NMDA antagonist ketamine was examined in 20 regular smokers and 20 non-smokers pretreated with placebo or nicotine gum. Although nicotine increased EEG arousal, ketamine produced electrocerebral signs of brain activation (decreased slow wave power) and sedation (decreased fast wave power and frequency), which were not affected by nicotine pretreatment and were evident only in non-smokers. Ketamine increased a number of self-report indices of subjective arousal, some of which were attenuated and potentiated by nicotine in smokers and non-smokers, respectively. These findings suggest that long-term (evidenced by smoker vs. non-smoker comparisons) and short-term (acute) nicotine exposure may alter NMDA receptor-mediated arousal and mood systems in a way that promotes nicotine dependence in smokers, and addresses neurobiological deficiencies in smokers with schizophrenia.

Acute effects of cholecystokinin tetrapeptide on brain stem auditory evoked potentials in healthy volunteers.

This study investigated the effects of continuous slow intravenous infusion of cholecystokinin tetrapeptide (CCK-4) on brain stem auditory evoked potentials (BSAEP) in healthy subjects. Twenty-four subjects, 15 females and 9 males, were assigned to infusion with either placebo or CCK-4 in a randomized, double-blind, parallel group design. BSAEPs, mood, physical symptoms, and vital signs were assessed once before infusion and at 10 min and 40 min after the onset of infusion. In the 16 subjects (N = 8, CCK-4; N = 8, placebo) CCK-4, compared to placebo, delayed peak I latency during early infusion, slowed the latencies of peaks III and V, and decreased the amplitude of peak III throughout the infusion. No significant treatment differences were observed with respect to symptoms, mood, or cardiovascular measures. These preliminary findings suggest that CCK-4 may interfere with information processing in the brain stem auditory pathways and that prolonged intravenous CCK-4 administration may be a useful challenge paradigm for investigating CCK's modulatory role on brain stem mechanisms mediating anxiety and panic in humans.