Course Description:

When it comes to eating disorders, there is an ever-widening gap between research and practice.  Despite a fast-growing body of scientific evidence implicating specific biologic abnormalities as etiologic factors, mainstream treatments continue to adhere to psychodynamic models that prioritize the treatment of psychologic issues and rely heavily on pharmaceutical interventions.  The inadequacy of these models, in tandem with epidemiologic data indicating that rates of eating disorders are on the rise, underscores a dire need for a field-wide paradigm shift.

Over the course of four modules, this course presents clinicians with an opportunity to immerse themselves in an integrative, empirically substantiated, functional medicine model for the treatment of anorexia nervosa, binge-eating disorder, and food addiction.  An objective review of standard treatment methods will segue into an in-depth exploration of the neural, genetic, and metabolic correlates of disordered eating, and the biologic pathways through which intrinsic and environmental factors can precipitate appetite dysregulation.  Research and experience-informed treatment recommendations will be presented, with an emphasis on objective testing and biochemical individuality.  The implications of this integrative model, which does not discount psychodynamic factors but rather establishes the rectification of biologic imbalances as a top priority, are significant, and open the doors to the realization of effective, lasting solutions for eating disorders.

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1. A Biologic Model of Eating Disorder Pathogenesis

Hope on the Horizon: A Biologic Model of Eating Disorder Pathogenesis
Module 1 will begin with an examination of the global tragedy that is eating disorder incidence, morbidity, and treatment inadequacy, informed by epidemiologic studies revealing rates of anorexia and other disorders rising sharply worldwide.  Next, developments in our understanding as to the biologic underpinnings of disordered eating, including genetic factors, celiac disease, and lipid deficiencies, will be explored, providing strong empirical support for a functional medicine model of eating disorder pathogenesis.  Current treatment practices and standards of care, which do not account for biologic causality and continue to rely on psychodynamic models and pharmaceutical interventions, will be critically reviewed, highlighting a critical need for today’s integrative practitioners to redefine therapeutic priorities and focus on the rectification of biochemical imbalances as a necessary prerequisite for recovery.

2. Targeting Micronutrient Deficiencies in Treatment

Module 2 will explore diet and unique dietary habits that research has associated with eating disorder pathologies, with a focus on biologic pathways through which nutritional imbalances precipitate neurologic and behavioral dysfunction.  The implications of veganism and vegetarianism, commonly observed in anorexic populations, will be discussed as they relate to the essential mineral zinc and symptomatic constellations associated with zinc deficiency.  Dietary and metabolic factors that influence zinc absorption will be reviewed, along with the mechanisms through which zinc modulates neurotransmitter synthesis.  Next, research evidence supporting etiologic connections between psychiatric disorders and members of the B vitamin family – vitamin B12, folate, vitamin B3, and thiamine – and the clinical implications of B vitamin deficiency will be presented, with a special focus on the physiologic and neurologic ramifications of vitamin B3 deficiency (pellagra) and thiamine deficiency (beriberi).  The module will conclude with a review of clinical case studies highlighting the therapeutic significance of achieving B vitamin repletion through integrative protocols, and a discussion about Postural Orthostatic Tachycardia Syndrome (POTS, a form of dysautonomia associated with thiamine deficiency).

3. Amino Acids and Probiotics for Eating Disorders

Healing the Gut, Helping the Mind: Amino Acids and Probiotics for Eating Disorders
Module 3 will begin with a look at protein, and the physical, neurologic, and behavioral consequences of dietary patterns that minimize or exclude protein consumption.  After an overview of the biochemical functions of amino acid precursors, the lecture will turn to an examination of intrinsic and exogenous factors capable of modulating amino acid status.  Diet, age, the essential mineral zinc, and digestive enzymes will be discussed in regard to their influences on amino acid absorption and bioavailability, and studies highlighting the neurologic sequelae of amino acid depletion will be presented.  Clinical recommendations for the rectification of amino acid deficiencies in eating disorder patients through free-form amino acid supplementation will be provided and integrated into a functional protocol that emphasizes objective testing.

The lecture will then turn to one of the most exciting frontiers in modern psychiatry – gut microbiota and the gut-brain axis – and elucidate the clinical ramifications of new research illuminating the significant functional interconnections between human health, behavior, and bacteria.  The roles of gut microbes in digestion, immune modulation, and neuroendocrine function will be explored, as will the physiology and function of the gut-brain-axis.  The implications of gut dysbiosis and Clostridia overgrowth will be discussed as they pertain to eating disorder pathologies, and the therapeutic applications of probiotics substantiated in light of promising empirical evidence.

4. Integrative Solutions for Binge-Eating

Module 4 is devoted to redefining binge-eating disorder (BED) – a widely prevalent and destructive mental illness characterized by recurrent episodes of bingeing – according to an integrative functional medicine model.  In this new model, BED is defined as a diverse range of physiologically generated food addictions arising from dysregulation in reward and satiety control pathways, pathways influenced by a variety of factors that can be modified via orthomolecular interventions.

The module will begin with an exploration of the mechanisms through which the brain and body establish functional parameters for hunger and satiety, and how these mechanisms relate to neural correlates of addiction.  Scientific evidence supporting the hypothesis that food addiction is associated with similar patterns of brain activation as are observed in substance abuse will be critically assessed, lending empirical support for a biologic model of BED pathogenesis.  Dietary factors capable of influencing feeding behavior, such as MSG, sugar, and opioid peptides derived from dairy and wheat, will be examined, as will the biochemical pathways through which they modulate hunger and satiety.  Next, current options for the pharmacologic management of BED will be objectively reviewed, as will new studies which implicate genetic polymorphisms in BED etiology.  Finally, guidelines for applying a functional medicine protocol for the treatment of BED will be reexamined, and clinical recommendations for nutritional supplementation to optimize neurotransmitter synthesis and address micronutrient imbalances presented.

Learning Objectives:

Upon completion of this course, registrants will be able to:

  • Explain why many young people diet, but relatively few develop eating disorders
  • Elucidate the biologic pathways and mechanisms underlying associations between celiac disease and anorexia nervosa
  • Describe the essential biologic functions of lipids, elucidate the neurologic consequences of essential fatty acid and cholesterol deficiencies, and relate lipid deficiencies to eating disorder presentations in terms of a functional medicine model
  • Elucidate an evidence-based rationale for prioritizing micronutrient repletion over psychotherapeutic interventions in the treatment of eating disorders
  • Identify dietary and environmental factors capable of inhibiting zinc absorption, and describe how zinc deficiency can contribute to anorexia-type symptomatic presentations
  • Describe genetic and dietary factors that can contribute to low folate levels
  • Explain how poor diet and/or disordered eating behaviors can precipitate paresthesia and neurologic decline associated with POTS
  • Identify and elucidate the neural correlates of food addiction
  • Safely and effectively implement functional medicine protocols for micronutrient repletion, neurotransmitter optimization, and digestive optimization in eating disorder presentations
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