Biological Models for Suicide Prevention – Online Course
March 14, 2019 - December 31, 2019
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Course Presenter: James Greenblatt, MD
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Course Description:
…..Suicide is the observable result of what is often a complex array of problems. Strong scientific evidence suggests that suicide risk is moderated by underlying biochemical abnormalities and environmental factors, which together can impact brain function and alter the structure of the brain itself. Brain alterations that accrue as a result can place an individual along a path towards tragedy. In being a phenomenon that science has shown to involve myriad endogenous and exogenous factors, however, suicidality – and psychiatric disorders that confer increased risk – invites an integrative approach that may offer at-risk patients the very best opportunity for recovery.
This three-module course will introduce an integrative model for suicide prevention, one in which the concept of suicidality as the result of underlying biochemical, nutritional, genetic, and environmental factors is explored. Research illustrating the benefits of nutritional supplementation to mitigate risk factors will be presented; evidence-based interventions will be described; and a treatment approach centred upon objective biologic measurement and a concept of biochemical individuality will be presented.
Upon completion, participants will be able to elucidate the clinical utility of an integrative approach for suicide prevention, and safely incorporate evidence-based, individually-tailored augmentation strategies into treatment protocols to maximize the rehabilitative trajectories of the patients they serve.
This intermediate level course is intended for: doctors, psychiatrists, nurse practitioners, nurses, social workers, psychologists, and other mental health professionals.
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Course Learning Objectives
Upon completion of the course, participants will be able to:
- Identify nutritional, biochemical, genetic, epigenetic, and environmental factors associated with suicidality, and explain how these factors affect changes in brain structure and/or function to confer increased risk
- Explain how exogenous and intrinsic factors can trigger systemic inflammation, and how inflammation negatively affects biochemical processes relating to neurotransmitter synthesis and immune response
- Appreciate the scientifically-established risks associated with the use of antidepressant and antipsychotic medications
- Describe the clinical utility of objective biologic testing as part of an integrative treatment approach
- Elucidate the biologic, psychiatric, and clinical ramifications of biochemical individuality
- Incorporate evidence-based testing and augmentation strategies into an integrative suicide prevention protocol
Continuing Education Credits:
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Module 1 will begin with an exploration of the suicide crisis: its scope and escalation, factors contributing to the global increase in incidence, and current prevention initiatives. Treatment approaches constituent of reigning therapeutic paradigms will be reviewed, with a special focus on pharmaceutical medications. Empirical evidence highlighting the risks and side-effects of antidepressant and antipsychotic medication will be presented, alongside data that challenge the notion that symptomatic suppression through reactive polypharmacy is an adequate stratagem. Finally, the role of trauma and genetics in the etiology of suicidal behaviors will be reviewed within a functional medicine context, and a new, biologic model of suicide prevention will be introduced.
Complimentary Live Webinar on March 14. Course registration is required for on demand (MP4 recording).
Registration – https://register.gotowebinar.com/register/8569589625174726915
Module 2 provides an in-depth exploration of a phenomenon that research has associated with a variety of psychiatric disorders and suicidality: inflammation. Intrinsic and biochemical factors that contribute to localized and systemic inflammatory response will be discussed, along with mechanisms whereby inflammation may progress from acute to chronic and thus confer elevated depression and suicide risk. The role of fats and lipids in the maintenance of mental health will be elucidated, with an emphasis on essential fatty acids, omega-3 fatty acids, and cholesterol. Scientific evidence linking cholesterol and suicide will be reviewed, as well as the biologic mechanisms by which low cholesterol may precipitate alterations in brain function. This module will invite a new perspective as to the roles that nutrition and biochemistry play in the pathophysiology of psychiatric disorders, and the ways in which underlying biochemical abnormalities can increase suicide risk
Course registration is required. This module will be presented as a live webinar and available on demand (MP4 recording).
In this module, the exploration of biochemical factors that underlie psychiatric illness and suicidality will be continued, with analyses as to the significance and ramifications of sleep deprivation and hypovitaminosis D (vitamin D deficiency). Factors contributing to these phenomena will be examined, and scientific evidence will be presented that places disordered sleep and hypovitaminosis D firmly in the list of factors to be considered as part of an integrative approach to suicide prevention. The module will then turn to an exploration of the history, biologic actions, and therapeutic potential of one of Nature’s ‘miracle minerals’: lithium. Research demonstrating the efficacy of nutritional lithium as part of an integrative protocol will be reviewed, with an emphasis on the biologic mechanisms postulated to underlie lithium’s documented neuroprotective and anti-inflammatory effects. Finally, a roadmap to suicide prevention will be presented, inviting participants to rethink current treatment approaches in light of evidence that suicidal behavior arises from underlying biologic abnormalities that, if rectified, can offer patients true hope for recovery.
Course registration is required. This module will be presented as a live webinar and available on demand (MP4 recording).