Presenter: David Perlmutter, MD,FACN, ABIHM Format: MP4 Video file of Slides and Audio
Immune and inflammatory mechanisms play pivotal roles in a vast array of degenerative conditions including Alzheimer’s disease, autism, multiple sclerosis, depression, Parkinson’s disease, coronary heart disease, diabetes and cancer. In general, these conditions are at best, medically managed over the lifetime of the patient with attention focused on symptom management. And these efforts are almost exclusively directed at the segment of our being that is represented by mammalian cells ? on a cellular level representing only ten percent of our holobiont selves. From a purely numerical perspective, ignoring the other 90% represented by microorganisms paints a myopic approach which appears further restrictive when recognizing that our endogenous microbes leverage huge sway precisely in the areas that underlie our most pernicious disease entities ? immune regulation and inflammation.
This presentation will focus on the role of decreased microbial diversity as a correlate to immune dysregulation and enhanced inflammation that characterize degenerative issues, with an emphasis on the role of modifiable challenges to the microbiome including diet, xenobiotics, stress, method of birth, antibiotics and gliadin. These modifiable factors will be explored through the lens of their effects upon microbial diversity. The important role of bowel permeability as a requisite event in this process will be explored with an introductory discussion of applicable laboratory analysis showing clinical utility.
Learning Objectives:
- Understand the fundamental role of inflammation and immune dysregulation in various degenerative conditions.
- Appreciate how various environmental and thus modifiable issues impact the microbiome from a functional perspective.
- Understand the roles of multiple microbiota related products in both health and disease including short chain fatty acids, “small molecules,” neurotransmitters, lipopolysaccaride (LPS) and cytokines.
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