42 research outputs found

    Social prescribing for suicide prevention: a rapid review

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    This rapid review delves into the realm of social prescribing as a novel approach to suicide prevention by addressing the social determinants of health. Through an exploration of various databases including MEDLINE, PsychInfo, WILEY, and Sage, a total of 3,063 articles were initially identified as potentially relevant to the research. Following a meticulous screening process, 13 articles were included in the final review, shedding light on the potential effectiveness and impact of social prescribing interventions on suicide prevention. Key findings indicate the need for additional monitoring and support for individuals at risk of suicide, emphasising warm referrals and sustained connections after referral to enhance the efficacy of social prescribing models. The review also highlights the importance of social capital and trust among vulnerable populations, underscoring the significance of community-based referrals in suicide prevention initiatives. Overall, this review identifies the potential of social prescribing as a valuable tool in mitigating suicide risk factors and promoting mental health and wellbeing in diverse populations

    The Potential Impact of a Public Health Approach to Improving the Physical Health of People Living with Mental Illness

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    With already wide disparities in physical health and life expectancy, COVID-19 presents people with mental illness with additional threats to their health: decreased access to health services, increased social isolation, and increased socio-economic disadvantage. Each of these factors has exacerbated the risk of poor health and early death for people with mental illness post-COVID-19. Unless effective primary care and preventative health responses are implemented, the physical illness epidemic for this group will increase post the COVID-19 pandemic. This perspective paper briefly reviews the literature on the impact of COVID-19 on service access, social isolation, and social disadvantage and their combined impact on physical health, particularly cancer, respiratory diseases, heart disease, smoking, and infectious diseases. The much-overlooked role of poor physical health on suicidality is also discussed. The potential impact of public health interventions is modelled based on Australian incidence data and current research on the percentage of early deaths of people living with mental illnesses that are preventable. Building on the lessons arising from services’ response to COVID-19, such as the importance of ensuring access to preventive, screening, and primary care services, priority recommendations for consideration by public health practitioners and policymakers are presented

    Failure to deactivate the default mode network indicates a possible endophenotype of autism.

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    BACKGROUND: Reduced activity during cognitively demanding tasks has been reported in the default mode network in typically developing controls and individuals with autism. However, no study has investigated the default mode network (DMN) in first-degree relatives of those with autism (such as siblings) and it is not known whether atypical activation of the DMN is specific to autism or whether it is also present in unaffected relatives. Here we use functional magnetic resonance imaging to investigate the pattern of task-related deactivation during completion of a visual search task, the Embedded Figures Task, in teenagers with autism, their unaffected siblings and typically developing controls. FINDINGS: We identified striking reductions in deactivation during the Embedded Figures Task in unaffected siblings compared to controls in brain regions corresponding to the default mode network. Adolescents with autism and their unaffected siblings similarly failed to deactivate regions, including posterior cingulate and bilateral inferior parietal cortex. CONCLUSIONS: This suggests that a failure to deactivate these regions is a functional endophenotype of autism, related to familial risk for the condition shared between individuals with autism and their siblings.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are

    You talkin' to me? Communicative talker gaze activates left-lateralized superior temporal cortex during perception of degraded speech.

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    Neuroimaging studies of speech perception have consistently indicated a left-hemisphere dominance in the temporal lobes' responses to intelligible auditory speech signals (McGettigan and Scott, 2012). However, there are important communicative cues that cannot be extracted from auditory signals alone, including the direction of the talker's gaze. Previous work has implicated the superior temporal cortices in processing gaze direction, with evidence for predominantly right-lateralized responses (Carlin & Calder, 2013). The aim of the current study was to investigate whether the lateralization of responses to talker gaze differs in an auditory communicative context. Participants in a functional MRI experiment watched and listened to videos of spoken sentences in which the auditory intelligibility and talker gaze direction were manipulated factorially. We observed a left-dominant temporal lobe sensitivity to the talker's gaze direction, in which the left anterior superior temporal sulcus/gyrus and temporal pole showed an enhanced response to direct gaze - further investigation revealed that this pattern of lateralization was modulated by auditory intelligibility. Our results suggest flexibility in the distribution of neural responses to social cues in the face within the context of a challenging speech perception task

    5-HTTLPR-environment interplay and its effects on neural reactivity in adolescents

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    It is not known how 5-HTTLPR genotype x childhood adversity (CA) interactions that are associated with an increased risk for affective disorders in population studies operate at the neural systems level. We hypothesized that healthy adolescents at increased genetic and environmental risk for developing mood disorders (depression and anxiety) would demonstrate increased amygdala reactivity to emotional stimuli compared to those with only one such risk factor or those with none. Participants (n=67) were classified into one of 4 groups dependent on being homozygous for the long or short alleles within the serotonin-transporter-linked polymorphic region (5-HTTLPR) of the SLC6A4 gene and exposure to CA in the first 11 years of life (present or absent). A functional magnetic resonance imaging investigation was undertaken which involved viewing emotionally-salient face stimuli. In addition, we assessed the role of other variables hypothesized to influence amygdala reactivity, namely recent negative life-events (RNLE) assessed at ages 14 and 17, current anxiety symptoms and psychiatric history. We replicated prior findings demonstrating moderation by gene variants in 5-HTTLPR, but found no support for an effect of CA on amygdala reactivity. We also found a significant effect of RNLE aged 17 with amygdala reactivity demonstrating additive, but not interactive effects with 5-HTTLPR. A whole-brain analysis found a 5-HTTLPR×CA interaction in the lingual gyrus whereby CA appears to differentially modify neural reactivity depending on genotype. These results demonstrate that two different forms of environmental adversities interplay with 5-HTTLPR and thereby differentially impact amygdala and cortical reactivity

    Australia’s Health Tracker by Socio-Economic Status

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    A brief report card on preventable chronic diseases, conditions and their risk factors. Tracking progress for a healthier Australia by 202

    Mitchell Institute Comment: The National Commission of Audit, May 2014

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    Title listed in Mitchell Institute Reports webpage: Response to The National Commission of Audi
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