Climate Change and Health: Transcending Silos to Find Solutions

Background: Climate change has myriad implications for the health of humans, our ecosystems, and the ecological processes that sustain them. Projections of rising greenhouse gas emissions suggest increasing direct and indirect burden of infectious and noninfectious disease, effects on food and water security, and other societal disruptions. As the effects of climate change cannot be isolated from social and ecological determinants of disease that will mitigate or exacerbate forecasted health outcomes, multidisciplinary collaboration is critically needed. / Objectives: The aim of this article was to review the links between climate change and its upstream drivers (ie, processes leading to greenhouse gas emissions) and health outcomes, and identify existing opportunities to leverage more integrated global health and climate actions to prevent, prepare for, and respond to anthropogenic pressures. / Methods: We conducted a literature review of current and projected health outcomes associated with climate change, drawing on findings and our collective expertise to review opportunities for adaptation and mitigation across disciplines. / Findings: Health outcomes related to climate change affect a wide range of stakeholders, providing ready collaborative opportunities for interventions, which can be differentiated by addressing the upstream drivers leading to climate change or the downstream effects of climate change itself. / Conclusions: Although health professionals are challenged with risks from climate change and its drivers, the adverse health outcomes cannot be resolved by the public health community alone. A phase change in global health is needed to move from a passive responder in partnership with other societal sectors to drive innovative alternatives. It is essential for global health to step outside of its traditional boundaries to engage with other stakeholders to develop policy and practical solutions to mitigate disease burden of climate change and its drivers; this will also yield compound benefits that help address other health, environmental, and societal challenges

Familial forms of diabetes insipidus: clinical and molecular characteristics

Over the past two decades, the genetic and molecular basis of familial forms of diabetes insipidus has been elucidated. Diabetes insipidus is a clinical syndrome characterized by the excretion of abnormally large volumes of diluted urine (polyuria) and increased fluid intake (polydipsia). The most common type of diabetes insipidus is caused by lack of the antidiuretic hormone arginine vasopressin (vasopressin), which is produced in the hypothalamus and secreted by the neurohypophysis. This type of diabetes insipidus is referred to here as neurohypophyseal diabetes insipidus. The syndrome can also result from resistance to the antidiuretic effects of vasopressin on the kidney, either at the level of the vasopressin 2 receptor or the aquaporin 2 water channel (which mediates the re-absorption of water from urine), and is referred to as renal or nephrogenic diabetes insipidus. Differentiation between these two types of diabetes insipidus and primary polydipsia can be difficult owing to the existence of partial as well as complete forms of vasopressin deficiency or resistance. Seven different familial forms of diabetes insipidus are known to exist. The clinical presentation, genetic basis and cellular mechanisms responsible for them vary considerably. This information has led to improved methods of differential diagnosis and could provide the basis of new forms of therapy