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Join us for this one-day seminar in London on Saturday 8th October at the prestigious Royal Society of Medicine in London.
Price: £125 + VAT (concessions available for students)
Timings: 9.30am – 5.30pm
To book, call 0333 241 4289 or use our online booking form and someone will be in touch to register you onto the seminar.
6 hours of NNA CPD Approved
What is it about?
The role of the complex community of microbial dwellers inside our digestive tract remains a valuable, but still poorly understood resource in which changes to density and variety can have significant effects on human function and health. One of the roles of these organisms is in the generation of endogenous defence molecules including the master antioxidant, glutathione.
The synthesis of glutathione in each cell in our body is an important rate limiting step in the progression of cellular damage and its role in human health is well recognized. Challenges to its production and utilization include genetic abnormalities such as methylation and histone deacetylase activity, the production of key intermediates, and, diet including consumption of suitable fermentable fibres and digestible proteins. Additionally, infections, heavy metals, medications and others not only alter glutathione synthesis but create increased demands for it through the induction of pro-inflammatory molecules. It has been recently shown that non-genetic loss of formation of the glutathione-producing enzymes can decrease glutathione and is associated with several health conditions.
This one day event is designed to explore some of the clinically relevant evolving events in microbiology, mucosal immunity and functional medicine as it relates to inflammation and health. The presenters are well known for their many years of work in research, analysis, practice and lecturing. They will present substantive evidence of these evolving trends and how they impact on clinical decisions, describing where evidence is preliminary, novel, or of greater substantiation. The day will have a strong clinical bias and provide a welcome opportunity for questions and answers.
The speakers will:
- Stimulate new ideas
- Reinforce current best practice methods
- Challenge entrenched beliefs with evolving comprehension
- Offer new and substantive clinical ideas
- Support the functional medicine approach to patient care
- Diminish the temptation to be protocol driven in treatment plans
- Provoke discussion and review
- Provide networking opportunities
- Make you feel positive about the opportunities for helping more people recover their health safely
Michael Ash – DO ND BSc RNT
A number of contemporaneous studies have highlighted the importance of the gut microbiota for human health through the regulation of host immune response and energetic metabolism. Microbiota it is becoming clear, interact with host cells in particular by modulating the mitochondrial activities. This mitochondria – microbiota cross-talk is of interest because mitochondria and bacteria share numerous common structural and functional features. Recently a range of studies have exposed a strong association between microbiota quality and diversity and mitochondrial function.
The mitochondrial production of Reactive Oxygen Species does of course play an important role during the innate immune response and inflammation and is often targeted by pathogenic bacteria. The gut epithelial barrier homeostasis is regulated by microbiota through the production of mitochondrial ROS amongst a range of other factors.
In addition, microbiota released metabolites can directly interfere with mitochondrial respiratory chain and ATP production. Some of them, particularly Short Chain Fatty Acids (SCFAs) have beneficial effects on mitochondrial activity, gene transcription and immune homeostasis. All these data suggest that microbiota target mitochondria to regulate its interaction with the host. Imbalance of this cross-talk may results in pathogenic state as observed in many common non communicable illnesses. Strategies to modulate the quality and diversity of microbiota, improve metabolite induction, and associated microbial capabilities, mediate mitochondrial fitness and competence, improvement in transcription expression and metabolic and metabolite management will be explored as clinical methods for multiple intervention approaches. Food, food concentrates and related molecular pathways will be explored and discussed in context.
David Quig PhD MS BS
A considerable amount of research has moved beyond trying to define the human GI microbiome to identification of core ecological functions that many microbes can perform. The GI metabolome entails a complex network of interactions among and between microbes, and their environment. The environment (terrain) is a complex ecosystem referred to as the intestinal barrier, that includes resident microbial guilds, resident and recruited immune cells, antimicrobial entities, and it’s very own glycobiome. The GI glycobiome includes variably glycosylated proteins (mucins) and lipids that provide a first wave of protective barriers.
Specific membrane-bound mucins impart selective microbial adhesion that in turn affects microbe-induced alterations in mucin and mucus production and metabolism, and molecular signaling and communication with the host. As such the protective mucus barrier and the glycocalyx provide barriers and surveillance for the underlying epithelial barrier.
Dysregulation of the glycan-rich and the epithelial barriers contribute to insufficiency dysbiosis that can adversely affect systemic innate detoxification processes that can result in excessive systemic oxidative stress and inflammation. A greater appreciation of the supramucosal barrier can lead to more comprehensive clinical intervention for GI issues and compromised innate detoxification. Definitive ways to assess increased permeability of the epithelial cell barrier, including that induced by gluten, will also be discussed.
Additional Speakers – Antony Haynes BA Hons, Dip ION mBANT and Dr Elisabeth Philipps PhD
The role of the gastrointestinal tract in the generation of metabolites and neurotransmitters and their impact on mental and neurological health.
Experimental studies demonstrate effects of commensal intestinal bacteria on behaviour and brain function that are contextually meaningful and which appear to be biologically significant. For example, gut bacteria have been shown to influence reactivity of the HPA axis and the induction and maintenance of REM sleep. They may also influence mood, pain sensitivity and normal brain development.
Several mechanisms, though none mutually exclusive, may enable commensal gut bacteria to influence function or dysfunction in the central nervous system (CNS) via (1) stimulation of host immune responses leading to diverse patterns of systemic cytokine activation and (2) alterations in neuronal circuitry by direct microbial effects on the enteric nervous system (ENS), with CNS transmission through vagal and other routes.
A third mechanistic area garnering increasing interest is the generation of absorbable neuroactive metabolites, including neurotransmitters, via the fermentation of foods by the resident bacteria; short chain fatty acids, inflammatory cytokines and tryptophan appear to confer considerable local and systemic advantages including in the brain and mood.
Elisabeth will explore the key cause and effect elements associated with metabolic and neurogenic molecules derived from gut fermentation and Antony will discuss clinical interventions that will provide you with a practical approach to managing people with an altered gut brain axis.