There is minimal knowledge about the impact of large-scale epidemics on community mental health, particularly during the acute phase. This gap in knowledge means we are critically ill-equipped to support communities as they face the unprecedented COVID-19 pandemic. This study aimed to provide data urgently needed to inform government policy and resource allocation now and in other future crises. The study was the first to survey a representative sample from the Australian population at the early acute phase of the COVID-19 pandemic. Depression, anxiety, and psychological wellbeing were measured with well-validated scales (PHQ-9, GAD-7, WHO-5). Using linear regression, we tested for associations between mental health and exposure to COVID-19, impacts of COVID-19 on work and social functioning, and socio-demographic factors. Depression and anxiety symptoms were substantively elevated relative to usual population data, including for individuals with no existing mental health diagnosis. Exposure to COVID-19 had minimal association with mental health outcomes. Recent exposure to the Australian bushfires was also unrelated to depression and anxiety, although bushfire smoke exposure correlated with reduced psychological wellbeing. In contrast, pandemic-induced impairments in work and social functioning were strongly associated with elevated depression and anxiety symptoms, as well as decreased psychological wellbeing. Financial distress due to the pandemic, rather than job loss per se , was also a key correlate of poorer mental health. These findings suggest that minimizing disruption to work and social functioning, and increasing access to mental health services in the community, are important policy goals to minimize pandemic-related impacts on mental health and wellbeing. Innovative and creative strategies are needed to meet these community needs while continuing to enact vital public health strategies to control the spread of COVID-19.

Objectives To estimate initial levels of symptoms of depression and anxiety, and their changes during the early months of the COVID‐19 pandemic in Australia; to identify trajectories of symptoms of depression and anxiety; to identify factors associated with these trajectories. Design, setting, participants Longitudinal cohort study; seven fortnightly online surveys of a representative sample of 1296 Australian adults from the beginning of COVID‐19‐related restrictions in late March 2020 to mid‐June 2020. Main outcome measures Symptoms of depression and anxiety, measured with the Patient Health Questionnaire (PHQ‐9) depression and Generalised Anxiety Disorder (GAD‐7) scales; trajectories of symptom change. Results Younger age, being female, greater COVID‐19‐related work and social impairment, COVID‐19‐related financial distress, having a neurological or mental illness diagnosis, and recent adversity were each significantly associated with higher baseline depression and anxiety scores. Growth mixture models identified three latent trajectories for depression symptoms (low throughout the study, 81% of participants; moderate throughout the study, 10%; initially severe then declining, 9%) and four for anxiety symptoms (low throughout the study, 77%; initially moderate then increasing, 10%; initially moderate then declining, 5%; initially mild then increasing before again declining, 8%). Factors statistically associated with not having a low symptom trajectory included mental disorder diagnoses, COVID‐19‐related financial distress and social and work impairment, and bushfire exposure. Conclusion Our longitudinal data enabled identification of distinct symptom trajectories during the first three months of the COVID‐19 pandemic in Australia. Early intervention to ensure that vulnerable people are clinically and socially supported during a pandemic should be a priority.

Background The COVID-19 pandemic has been highly disruptive, with the closure of schools causing sudden shifts for students, educators and parents/caregivers to remote learning from home (home-schooling). Limited research has focused on home-schooling during the COVID-19 pandemic, with most research to date being descriptive in nature. The aim of the current study was to comprehensively quantify the psychosocial impacts of home-schooling on parents and other caregivers, and identify factors associated with better outcomes. Methods A nationally representative sample of 1,296 Australian adults was recruited at the beginning of Australian COVID-19 restrictions in late-March 2020, and followed up every two weeks. Data for the current study were drawn from waves two and three. Surveys assessed psychosocial outcomes of psychological distress, work and social impairment, and wellbeing, as well as a range of home-schooling factors. Results Parents and caregivers who were home-schooling during the COVID-19 pandemic experienced significantly higher levels of psychological distress and work/social impairment compared to those who were not home-schooling or had no school-aged children. A current mental health diagnosis or lower levels of perceived support from their child’s school negatively affected levels of psychological distress, work and social impairment, and wellbeing in parents and caregivers involved in home-schooling. Conclusions The mental health impacts of home-schooling were high and may rise as periods of home-schooling increase in frequency and duration. Recognising and acknowledging the challenges of home-schooling is important, and should be included in psychosocial assessments of wellbeing during periods of school closure. Emotional and instrumental support is needed for those involved in home-schooling, as perceived levels of support is associated with improved outcomes. Proactive planning by schools to support parents may promote better outcomes and improved home-schooling experiences for students.

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The incidence and prevalence of inflammatory bowel disease (IBD) are increasing worldwide. Some ecological studies show increasing incidence with increasing latitude. Ambient ultraviolet radiation varies inversely with latitude, and sun exposure of the skin is a major source of vitamin D. Vitamin D deficiency is common in patients with IBD. Sun exposure and vitamin D have immune effects that could plausibly reduce, or be protective for, IBD. One quarter of new IBD cases are diagnosed in childhood or adolescence, but most research is for adult-onset IBD. Here, we review the evidence for low sun exposure and/or vitamin D deficiency as risk factors for IBD, focusing where possible on pediatric IBD, where effects of environmental exposures may be clearer. The literature provides some evidence of a latitude gradient of IBD incidence, and evidence for seasonal patterns of timing of birth or disease onset is inconsistent. High prevalence of vitamin D deficiency occurs in people with IBD, but cannot be interpreted as being a causal risk factor. Evidence of vitamin D supplementation affecting disease activity is limited. Further research on predisease sun exposure and well-designed supplementation studies are required to elucidate whether these potentially modifiable exposures are indeed risk factors for IBD.

In this study we explored the relationship between hypnotic susceptibility measured with the Harvard Group Scale of Hypnotic Susceptibility (HGSHS) and cardiovascular parameters. After assessing their degree of hypnotic susceptibility, we induced 21 female students into happy mood states and into sad mood states. During the mood state induction we monitored blood pressure, heart rate, and cardiac vagal tone continuously. The study demonstrated a strong relationship between hypnotic susceptibility and both cardiac vagal tone and heart rate reactivity. Subjects with lower heart rate and greater vagal tone during baseline and greater heart rate increases during mood induction were more susceptible to hypnosis. Multiple regression analyses indicated that approximately 40% of the individual difference variance of hypnotic susceptibility was accounted for by baseline cardiac vagal tone and heart rate reactivity during mood state. The data demonstrate that autonomic tone, assessed by cardiac vagal tone and heart rate reactivity, are related to hypnotic susceptibility as measured by the HGSHS.

Background: The D-Health Trial aims to determine whether monthly high-dose vitamin D supplementation can reduce the mortality rate and prevent cancer. We did not have adequate statistical power for subgroup analyses, so could not justify the high cost of collecting blood samples at baseline. To enable future exploratory analyses stratified by baseline vitamin D status, we developed a model to predict baseline serum 25 hydroxy vitamin D [25(OH)D] concentration. Methods: We used data and serum 25(OH)D concentrations from participants who gave a blood sample during the trial for compliance monitoring and were randomised to placebo. Data were partitioned into training (80%) and validation (20%) datasets. Deseasonalised serum 25(OH)D concentrations were dichotomised using cut-points of 50 nmol/L, 60 nmol/L and 75 nmol/L. We fitted boosted regression tree models, based on 13 predictors, and evaluated model performance using the validation data. Results: The training and validation datasets had 1788 (10.5% <50 nmol/L, 23.1% <60 nmol, 48.8 <75 nmol/L) and 447 (11.9% <50 nmol/L, 25.7% <60 nmol/L, and 49.2% <75 nmol/L) samples, respectively. Ambient UV radiation and total intake of vitamin D were the strongest predictors of low serum 25(OH)D concentration. The area under the receiver operating characteristic curves were 0.71, 0.70, and 0.66 for cut-points of <50 nmol/L, <60 nmol/L and <75 nmol/L respectively. Conclusions: We exploited compliance monitoring data to develop models to predict serum 25(OH)D concentration for D-Health participants at baseline. This approach may prove useful in other trial settings where there is an obstacle to exhaustive data collection.

If environmental exposures are shown to cause an adverse health outcome, reducing exposure should reduce the disease risk. Links between exposures and outcomes are typically based on ‘associations’ derived from observational studies, and causality may not be clear. Randomized controlled trials to ‘prove’ causality are often not feasible or ethical. Here the history of evidence that tobacco smoking causes lung cancer—from observational studies—is compared to that of low sun exposure and/or low vitamin D status as causal risk factors for the autoimmune disease, multiple sclerosis (MS). Evidence derives from in vitro and animal studies, as well as ecological, case-control and cohort studies, in order of increasing strength. For smoking and lung cancer, the associations are strong, consistent, and biologically plausible—the evidence is coherent or ‘in harmony’. For low sun exposure/vitamin D as risk factors for MS, the evidence is weaker, with smaller effect sizes, but coherent across a range of sources of evidence, and biologically plausible. The association is less direct—smoking is directly toxic and carcinogenic to the lung, but sun exposure/vitamin D modulate the immune system, which in turn may reduce the risk of immune attack on self-proteins in the central nervous system. Opinion about whether there is sufficient evidence to conclude that low sun exposure/vitamin D increase the risk of multiple sclerosis, is divided. General public health advice to receive sufficient sun exposure to avoid vitamin D deficiency (<50 nmol/L) should also ensure any benefits for multiple sclerosis, but must be tempered against the risk of skin cancers.