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With host Dr Nirala Jacobi BHSc ND, Chief Medical Officer, SIBOTest.com

Apr 17, 2017

In this episode Dr Nirala Jacobi speaks with Dr Bradley Bush about the fascinating and complex world of neurotransmitters.

Dr Bush received his Naturopathic Doctorate degree from the National College of Naturopathic Medicine.  He is co-owner and clinic director of Natural Medicine of Stillwater and its online consumer direct website for practitioners, neurovanna.com.

The Bush practice focuses on fatigue, insomnia, GI disorders, mood disorders, and lyme disease. Dr Bush has over 16 years of industry experience. He is the owner of Natural Health Insights, providing consulting services to the naturopathic products and laboratory testing industry.

Dr Bush speaks nationally and regularly publishes on the topics of neuroimmunology, brain-gut connections, neuroendocrinology, and lyme disease.  Dr Bush sits on two non profit boards, The Naturopathic Education and Research Consortium, and Compass Centre for Health.

In this episode topics discussed include:

  • Who are the major players in the enteric nervous system for neurotransmitter regulation?
  • Does low serotonin in the gut mean low serotonin in the brain?
  • The sympathetic-parasympathetic rhythm, and how important this is in calibrating the smooth muscle movement in the gastrointestinal tract.
  • Underlying factors to sympathetic dominance in a person, such as chronic infection, dysbiosis, and/or inflammation.
  • The complex presentations of sympathetic overdrive, ranging from anxiety and insomnia, to exhaustion, and why this is.
  • Why increased norepinephrine in conjunction with normal or low epinephrine is a worse situation than just high epinephrine, due to the lack of counter balance for inflammation and an upregulated innate immunity.
  • Repercussions of high epinephrine in conjunction with low norepinephrine.
  • The multiple actions of cortisol, epinephrine, and norepinephrine in the body and their roles in acute and chronic conditions.
  • Urinary transmitter analysis, stability, and recommended labs.
  • Nutrients used to support synthesis of the various neurotransmitters.
  • L-dopa v.s. tyrosine use, and the various benefits of each.
  • Clinical indications for L-dopa use.
  • How depleted catecholamines can be related to low secretory IgA.
  • Genetic mutations (MTHFR) and how this relates to neurotransmitter dysfunction.
  • Does serum C-reactive protein (CRP) directly correlate to SIBO activity?
  • Myeloperoxidase measurement as a marker of neutrophil activity, and how it can be a useful monitoring tool for irritable bowel syndrome (IBS) and irritable bowel disease (IBD) patients.
  • How does inflammation turn down the synthesis of serotonin and catecholamines?
  • How the indoleamine 2,3-dioxygenase enzyme (IDO) conducts “The Tryptophan Steal” as an outcome of chronic inflammation, and the implications of this.
  • What solutions are there to address the tryptophan steal?
  • The benefit of using supplemental 5-HTP over tryptophan in light of chronic inflammation and impacted adrenal health.
  • Doses, dose timing, and length of time to use 5-HTP.
  • SIBO as a common underlying factor for the inflammatory state that can drive neurotransmitter dysfunction.
  • What is the role of glutamate?
  • Glutamate versus glutamine, and how is this relevant to supplementation.
  • How is glutamate measured, what do high levels indicate, and how does it impact the nervous system?
  • Glutathione as the biggest byproduct of L-glutamine metabolism.
  • Powder V.S. tablet for L-glutamine use, and the dose recommended.
  • What is urinary neurotransmitter testing reflecting?
  • The blood-brain barrier, and how the brain is not a closed system.
  • MTHFR and COMT genetic testing as indicated by low monoamine neurotransmitters and high catecholamines on urinary neurotransmitter panels.
  • What to do with patients on medications being used to conventionally regulate neurotransmitters?
  • Tactics of improving neurotransmitter markers prior to SIBO treatment in order to offset the flaring of the symptoms during die off.

 

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