A Policy-Ready Public Health Guidebook of Strategies and Indicators to Promote Financial Well-Being and Address Financial Strain in Response to COVID-19

Introduction The COVID-19 pandemic has adversely affected the financial well-being of populations globally, escalating concerns about links with health care and overall well-being. Governments and organizations need to act quickly to protect population health relative to exacerbated financial strain. However, limited practice and policy-relevant resources are available to guide action, particularly from a public health perspective, that is, targeting equity, social determinants of health, and health-in-all policies. Our study aimed to create a public health guidebook of strategies and indicators for multisectoral action on financial well-being and financial strain by decision makers in high-income contexts. Methods We used a multimethod approach to create the guidebook. We conducted a targeted review of existing theoretical and conceptual work on financial well-being and strain. By using rapid review methodology informed by principles of realist review, we collected data from academic and practice-based sources evaluating financial well-being or financial strain initiatives. We performed a critical review of these sources. We engaged our research–practice team and government and nongovernment partners and participants in Canada and Australia for guidance to strengthen the tool for policy and practice. Results The guidebook presents 62 targets, 140 evidence-informed strategies, and a sample of process and outcome indicators. Conclusion The guidebook supports action on the root causes of poor financial well-being and financial strain. It addresses a gap in the academic literature around relevant public health strategies to promote financial well-being and reduce financial strain. Community organizations, nonprofit organizations, and governments in highincome countries can use the guidebook to direct initiative design, implementation, and assessmen

Gambling disorder and suicide: An overview of the associated co-morbidity and clinical characteristics

Context: A high prevalence of suicide and attempted suicide in relation to gambling disorder is in increasing evidence in current scientific data. The objective of this review was to explore if there was a primary correlation between psychiatric co-morbidities and gambling and/or a secondary correlation with suicide acts. Evidence Acquisition: We performed a critical analysis of the most recent papers in the scientific literature in this regard and report on the most significant findings. Results: A direct relationship between gambling and suicidality was highlighted in a number of European, American, and Asian countries. However, it was not clear whether or not gambling increased the risk of suicidal behavior. Twogeneral trends were noted. The first was that gamblers with extreme gambling behavior incurred economic losses and debts to such an extent that suicidal acts appeared to be the only solution. The second was that suicidal acts by gamblers were precipitated by interpersonal and/or working challenges, in conjunction with personality traits of impulsivity and psychiatric co-morbidities. Conclusions: A combination of impulsivity, certain psychiatric disorders, and social factors may explain the frequent occurrence of suicidal behavior in gamblers

Decreases in Community Viral Load Are Accompanied by Reductions in New HIV Infections in San Francisco

BACKGROUND: At the individual level, higher HIV viral load predicts sexual transmission risk. We evaluated San Francisco's community viral load (CVL) as a population level marker of HIV transmission risk. We hypothesized that the decrease in CVL in San Francisco from 2004-2008, corresponding with increased rates of HIV testing, antiretroviral therapy (ART) coverage and effectiveness, and population-level virologic suppression, would be associated with a reduction in new HIV infections. METHODOLOGY/PRINCIPAL FINDINGS: We used San Francisco's HIV/AIDS surveillance system to examine the trends in CVL. Mean CVL was calculated as the mean of the most recent viral load of all reported HIV-positive individuals in a particular community. Total CVL was defined as the sum of the most recent viral loads of all HIV-positive individuals in a particular community. We used Poisson models with robust standard errors to assess the relationships between the mean and total CVL and the primary outcome: annual numbers of newly diagnosed HIV cases. Both mean and total CVL decreased from 2004-2008 and were accompanied by decreases in new HIV diagnoses from 798 (2004) to 434 (2008). The mean (p = 0.003) and total CVL (p = 0.002) were significantly associated with new HIV cases from 2004-2008. CONCLUSIONS/SIGNIFICANCE: Reductions in CVL are associated with decreased HIV infections. Results suggest that wide-scale ART could reduce HIV transmission at the population level. Because CVL is temporally upstream of new HIV infections, jurisdictions should consider adding CVL to routine HIV surveillance to track the epidemic, allocate resources, and to evaluate the effectiveness of HIV prevention and treatment efforts

The Neurotropic Parasite Toxoplasma Gondii Increases Dopamine Metabolism

The highly prevalent parasite Toxoplasma gondii manipulates its host's behavior. In infected rodents, the behavioral changes increase the likelihood that the parasite will be transmitted back to its definitive cat host, an essential step in completion of the parasite's life cycle. The mechanism(s) responsible for behavioral changes in the host is unknown but two lines of published evidence suggest that the parasite alters neurotransmitter signal transduction: the disruption of the parasite-induced behavioral changes with medications used to treat psychiatric disease (specifically dopamine antagonists) and identification of a tyrosine hydroxylase encoded in the parasite genome. In this study, infection of mammalian dopaminergic cells with T. gondii enhanced the levels of K+-induced release of dopamine several-fold, with a direct correlation between the number of infected cells and the quantity of dopamine released. Immunostaining brain sections of infected mice with dopamine antibody showed intense staining of encysted parasites. Based on these analyses, T. gondii orchestrates a significant increase in dopamine metabolism in neural cells. Tyrosine hydroxylase, the rate-limiting enzyme for dopamine synthesis, was also found in intracellular tissue cysts in brain tissue with antibodies specific for the parasite-encoded tyrosine hydroxylase. These observations provide a mechanism for parasite-induced behavioral changes. The observed effects on dopamine metabolism could also be relevant in interpreting reports of psychobehavioral changes in toxoplasmosis-infected humans

Epigenetic understanding of gene-environment interactions in psychiatric disorders: a new concept of clinical genetics

Epigenetics is a mechanism that regulates gene expression independently of the underlying DNA sequence, relying instead on the chemical modification of DNA and histone proteins. Although environmental and genetic factors were thought to be independently associated with disorders, several recent lines of evidence suggest that epigenetics bridges these two factors. Epigenetic gene regulation is essential for normal development, thus defects in epigenetics cause various rare congenital diseases. Because epigenetics is a reversible system that can be affected by various environmental factors, such as drugs, nutrition, and mental stress, the epigenetic disorders also include common diseases induced by environmental factors. In this review, we discuss the nature of epigenetic disorders, particularly psychiatric disorders, on the basis of recent findings: 1) susceptibility of the conditions to environmental factors, 2) treatment by taking advantage of their reversible nature, and 3) transgenerational inheritance of epigenetic changes, that is, acquired adaptive epigenetic changes that are passed on to offspring. These recently discovered aspects of epigenetics provide a new concept of clinical genetics

Proteasome inhibition for treatment of leishmaniasis, Chagas disease and sleeping sickness

Chagas disease, leishmaniasis and sleeping sickness affect 20 million people worldwide and lead to more than 50,000 deaths annually. The diseases are caused by infection with the kinetoplastid parasites Trypanosoma cruzi, Leishmania spp. and Trypanosoma brucei spp., respectively. These parasites have similar biology and genomic sequence, suggesting that all three diseases could be cured with drugs that modulate the activity of a conserved parasite target. However, no such molecular targets or broad spectrum drugs have been identified to date. Here we describe a selective inhibitor of the kinetoplastid proteasome (GNF6702) with unprecedented in vivo efficacy, which cleared parasites from mice in all three models of infection. GNF6702 inhibits the kinetoplastid proteasome through a non-competitive mechanism, does not inhibit the mammalian proteasome or growth of mammalian cells, and is well-tolerated in mice. Our data provide genetic and chemical validation of the parasite proteasome as a promising therapeutic target for treatment of kinetoplastid infections, and underscore the possibility of developing a single class of drugs for these neglected diseases

Effects of Heparin and Enoxaparin on APP Processing and Aβ Production in Primary Cortical Neurons from Tg2576 Mice

Alzheimer's disease (AD) is caused by accumulation of Aβ, which is produced through sequential cleavage of β-amyloid precursor protein (APP) by the β-site APP cleaving enzyme (BACE1) and γ-secretase. Enoxaparin, a low molecular weight form of the glycosaminoglycan (GAG) heparin, has been reported to lower Aβ plaque deposition and improve cognitive function in AD transgenic mice

Family social environment in childhood and self-rated health in young adulthood

<p>Abstract</p> <p>Background</p> <p>Family social support, as a form of social capital, contributes to social health disparities at different age of life. In a life-course epidemiological perspective, the aims of our study were to examine the association between self-reported family social environment during childhood and self-reported health in young adulthood and to assess the role of family functioning during childhood as a potential mediating factor in explaining the association between family breakup in childhood and self-reported health in young adulthood.</p> <p>Methods</p> <p>We analyzed data from the first wave of the Health, Inequalities and Social Ruptures Survey (SIRS), a longitudinal health and socio-epidemiological survey of a random sample of 3000 households initiated in the Paris metropolitan area in 2005. Sample-weighted logistic regression analyses were performed to determine the association between the quality of family social environment in childhood and self-rated health (overall health, physical health and psychological well-being) in young adults (n = 1006). We used structural equation model to explore the mediating role of the quality of family functioning in childhood in the association between family breakup in childhood and self-rated health in young adulthood.</p> <p>Results</p> <p>The multivariate results support an association between a negative family social environment in childhood and poor self-perceived health in adulthood. The association found between parental separation or divorce in childhood and poor self-perceived health in adulthood was mediated by parent-child relationships and by having witnessed interparental violence during childhood.</p> <p>Conclusion</p> <p>These results argue for interventions that enhance family cohesion, particularly after family disruptions during childhood, to promote health in young adulthood.</p

The 'antisocial' person: an insight in to biology, classification and current evidence on treatment

<p>Abstract</p> <p>Background</p> <p>This review analyses and summarises the recent advances in understanding the neurobiology of violence and empathy, taxonomical issues on defining personality disorders characterised by disregard for social norms, evidence for efficacy of different treatment modalities and ethical implications in defining 'at-risk' individuals for preventive interventions.</p> <p>Methods</p> <p>PubMed was searched with the keywords 'antisocial personality disorder', 'dissocial personality disorder' and 'psychopathy'. The search was limited to articles published in English over the last 10 years (1999 to 2009)</p> <p>Results</p> <p>Both diagnostic manuals used in modern psychiatry, the <it>Diagnostic and Statistical Manual </it>published by the American Psychiatric Association and the <it>International Classification of Diseases </it>published by the World Health Organization, identify a personality disorder sharing similar traits. It is termed antisocial personality disorder in the diagnostic and statistical manual and dissocial personality disorder in the <it>International Classification of Diseases</it>. However, some authors query the ability of the existing manuals to identify a special category termed 'psychopathy', which in their opinion deserves special attention. On treatment-related issues, many psychological and behavioural therapies have shown success rates ranging from 25% to 62% in different cohorts. Multisystemic therapy and cognitive behaviour therapy have been proven efficacious in many trials. There is no substantial evidence for the efficacy of pharmacological therapy. Currently, the emphasis is on early identification and prevention of antisocial behaviour despite the ethical implications of defining at-risk children.</p> <p>Conclusions</p> <p>Further research is needed in the areas of neuroendocrinological associations of violent behaviour, taxonomic existence of psychopathy and efficacy of treatment modalities.</p