Download: Grand Rapids Schedule
Ward Dean, MD: The Neuroendocrine Theory of Aging
The Neuroendocrine Theory of Aging is based on the work of Professor Vladimir Dilman, former Director, NN Petrov Institute of Oncology, St Petersburg, Russia. Dilman proposed that development, aging and the diseases of aging are due to a loss of hypothalamic receptor sensitivity to negative feedback inhibition. These programmed changes result in a constant shifting of homeostasis and aging-related biochemical and physiological parameters, which result in what Dilman designated as the metabolic pattern of aging. He proposed that aging and the diseases of aging could be delayed or reversed by: (1) restoring hypothalamic and peripheral receptor sensitivity; (2) normalizing biochemical and endocrine parameters; and (3) restoring mitochondrial bioenergetics. Specific drugs and nutriceuticals discussed include metformin, selegiline, nicotinic acid, methylene blue, and appropriate hormones, bio-peptides, and mitochondrial enhancers.
1. Understand the concept of negative feedback inhibition as it applies to the endocrine system, and the relationship between hormone levels and hormone receptor sensitivity and concentration.
2. Understand the neuroendocrine changes that result in the diseases of aging, including type III diabetes (Alzheimer’s disease).
3. Identify pharmaceuticals and nutriceuticals that enhance hormone receptor sensitivity, restore hormone levels and activity to more youthful levels, reverse and delay the onset of age-related degenerative diseases, and possibly extend the maximum lifespan.
1.How is MS diagnosed. How is MRI used to diagnose MS early. The use of MRI as a bio-marker for MS .
2. Learn about the basics of MS. Incidence, demographics, prognostic features, genetic predisposition, cause of MS- working hypothesis.
3. Role of Immunology in the pathogenesis of MS
4. How is MS classified.
5.Symptomatic management of MS: Bowel/Bladder; Spasticity; Weakness; Cognitive Dysfunction; Fatigue; What is a relapse and Treatment of a relapse
6. Preventive therapies. Will discuss all of the therapies which are approved by FDA, efficacy, side effects & complications.
7. Research updates.
Paul Harch MD: Hyperbaric Oxygen Therapy: Scientific Foundation & Applications to Neurological Disease
This lecture is an overview of hyperbaric therapy in neurodegenerative diseases with a review of the literature. The lecture will begin with a presentation of the scientific foundations of hyperbaric therapy (HBT). HBT will first be defined historically and then scientifically as a combination therapy of increased pressure and increased oxygen whose mechanism of action is epigenetic modulation of gene expression and suppression, particularly those genes controlling inflammation. The activity of this therapy will be shown to be most prevalent in acute, subacute, and chronic wound conditions. The literature on etiology of neurodegenerative disease will be reviewed to show that neurodegenerative diseases result from a combination of genetic and cumulative environmental factors that generate central nervous system wounds. Many of these diseases are characterized by the end-products of inflammation/wounding, namely scar (multiple sclerosis-MS, chronic traumatic encephalopathy-CTE) or protein aggregation (Alzheimers, Parkinson’s Disease-PD). Lastly, the literature will be reviewed on HBT in inflammation and neurodegenerative and developmental diseases, including Parkinson’s Disease, dementia (Alzheimer’s and others), amyotrophic lateral sclerosis (ALS), CTE, MS, and autism spectrum disorder (ASD).
Learning objective #1: To learn and understand the historical definition of HBOT, its inadequacies, and the newer scientific definition of hyperbaric therapy as a combination therapy with gene modulation effects.
Learning objective #2: To learn and understand HBOT as a treatment of acute, subacute, and chronic wounds in any location in the body.
Learning objective #3: To learn and understand that neurodegenerative diseases result from a combination of genetic factors and cumulative environmental factors that generate central nervous system wounds. Inflammation will be shown to be a dominant pathophysiology in the wounding.
Learning objective #4: To learn and understand the positive and negative literature on HBOT in a variety of neurodegenerative and neurodevelopment diseases and the effects of HBOT on inflammation.
Jean-Ronel Corbier, MD: Autism and the Restoration Model
Autism represents an ideal medical condition for exploring the role of genetic versus environmental triggers in neurodevelopment. Understanding the impact of these triggers in the context of the developing brain, synaptic plasticity, various regulatory systems in the body and the functioning of other organ systems that are involved in autism is key. Genetic and environmental triggers also play a role in other fields that are related to autism and interface with the nervous system including toxicology, neuroimmunology, gastroenterology to name a few. All of these factors can lead to neuroinflammation, neurometabolic changes (e.g. mitochondrial dysfunction), alterations in the microbiome and other pathological states that can and should be addressed when trying to tackle autism from an etiological perspective.
My learning objects include:
1- Explain the role of genetic (and epigenetic) factors in autism
2- Discuss the role of environmental triggers with autism and how they interact with genetic expression
3- Show that autism is a multi-systemic condition (not just one that affects the nervous system)
4- Discuss how the above factors can lead to pathological problems that result in autism system
5- Provide a mode (I call the Restoration Model) that takes into account all of the above in approaching autism from a therapeutic perspectives.
Andrea Gruszecki, ND: Environmental exposures and neurotransmitter disruptions-Everyday exposures, oxidative stress and neurodegeneration.
The presentation will review a variety of environmental exposures that may alter neurotransmission and increase neurodegeneration and the use of urinary neurotransmitter assessments as a clinical tool in the evaluation and monitoring neurotransmission, environmental exposures and detoxification.
Urinary neurotransmitters may serve as functional biomarkers for the enzymes of neurotransmission. Increased oxidative stress from environmental exposures may contribute to neurodegenerative disorders. Changes in urinary serotonin, dopamine, and glutamate levels have been suggested as biomarkers in neurobehavioral toxicology to assess symptoms from chemical or toxic element exposures. Information gained through neurotransmitter assessments may provide therapeutic opportunities that improve clinical success and patient health outcomes. Neurotransmitter metabolism requires a variety of enzymes, including catechol-O-methyltransferase (COMT), monoamine oxidase (MAO). Patterns of neurotransmitters and their metabolites may provide functional information about these important detoxification enzymes. Altered patterns of urinary neurotransmitters may also highlight the need for precursor amino acids or nutritional cofactors essential for neurotransmitter synthesis and metabolism. Strategies for the assessment of neurotransmitters and precursor nutrients vital for normal neurologic function will be summarized. Nutritional support that may optimize the function of neurotransmission enzymes, support normal neurologic functions and decrease oxidative stress will be reviewed.
Increased familiarity with neurotransmitter synthesis and metabolism and the metabolism of neurotransmitters and the integral roles of COMT and MAOA in detoxification.
Increased familiarity the effects toxicant exposures may have on enzymes of neurotransmission, neurologic functions, and neurodegeneration.
Increased familiarity with nutritional supports for neurotransmitter synthesis and metabolism.
- To understand the role of environmental triggers in the induction of OCD, PANDAS, and ANDAS
- To learn that Group A Streptococcus is not the only infectious agent that contributes to OCD, PANDAS, and ANDAS
- To observe that many food components cross-react with D1, D2, and NMDA receptor, and therefore may contribute to the symptomatologies of PANDAS
- To understand about the importance of measuring levels of antibodies against pathogens, food antigens, and neuronal antigens in the blood, and how it can help practitioners manage the treatment of patients with PANDAS
The group of behavior and movement disorders known as pediatric autoimmune neuropsychiatric disorders associated with streptococci (PANDAS) has an association with infections and the immune response against them. PANDAS is a subset of the condition called obsessive-compulsive disorder (OCD) and tic disorders. The main symptoms of PANDAS are motor and vocal tics and obsessive-compulsive behavior. In OCD, PANDAS and the adult version, ANDAS, the onset and development of neuropsychiatric symptoms is preceded by infection with Group A Streptococcus (GAS).
Group A Streptococcus (GAS) or Streptococcus or Streptococcus pyogenes, is a pathogen that causes a wide variety of significant human diseases. Starting out as a throat infection, Streptococcus can present as self-limiting infections of the pharynx and skin in some individuals, while others experience more serious manifestations resulting in behavioral disorders and neuroautoimmunity. In a subgroup of patients with OCD, PANDAS and ANDAS, antibody response may play a role in the development of neuropsychiatric abnormalities due to mimicry and other mechanisms.
Molecular mimicry between streptococcal M protein and human tissue antigens is not the only mechanism for the induction of autoimmunity. Streptococcal antigens have the capacity to bind to a number of human serum proteins. This occurs due to the expression of a variety of receptors on GAS that can bind to these blood proteins. Perhaps this binding of GAS antigens to blood proteins may serve as an additional mechanism in the pathogenesis of autoimmune diseases, including rheumatic diseases, nephropathy, phospholipid syndrome and others. Recent research has shown how streptococcal infection can facilitate the migration of GAS-specific Th17 cells from the nasal-associated lymphoid tissue (NALT) into the brain. This can lead to serum IgG deposition, microglial activation, and loss of excitatory synaptic proteins, while no bacteria can be detected in central nervous system tissue.
This strong immune reaction against streptococcal antigens has become the basis for immunological assays for the detection of GAS. The use of these immunological assays are becoming important for the diagnosis of various disorders associated with these infectious agents.
Marty Heinz MD: Compensating for neurotoxin-induced dysregulation
Since this research project started 20 years ago, in 1997, there has been many people and groups who have come and gone while expounding virtues of “neurotransmitter testing” that were not supported by the science. With 22 peer-reviewed papers relating to the topic, this research project has the only current scientific publications on the topic of urinary neurotransmitter testing. This talk will present highlights from these peer-reviewed papers (see bibliography).
1. The participant will understand why baseline neurotransmitter testing is documented in the medical literature as being of no value in definitive clinical decision making.
2. The participant will understand urinary neurotransmitter renal physiology including neurotransmitter synthesis and the OCT-2 transporter role in determination of neurotransmitters concentrations in the final urine.
3. The participant will understand why urinary neurotransmitters have never been in the peripheral or central systems.
4. The participant will understand how relative nutritional deficiencies can be induced by disease, drugs and nutrients.
Boyd Haley PhD: An evaluation of heavy metal chelation by various commercially available compounds
Most currently available compounds used to treat animals and humans for heavy metal toxicity, primarily mercury and lead toxicity, are charged, hydrophilic compounds that are not effective at reaching the intracellular sites where most of the heavy metal is bound that causes the toxic effects. Some of these compounds have sulfhydryls on adjacent carbons that sterically prevent them from chelating Hg2+ in a 1;1 complex. Instead they form weaker sandwich complexes with Hg2+. Charged heavy metal complexes are excreted through the kidneys into the urine. In weaker binding complexes with Hg2+ the mercury being excreted can exchange with more reactive sulfhydryls on proteins in the kidney causing a deterioration of kidney function. Since these compounds are charged they do not effectively cross cell membranes or enter the central nervous system where the heavy metal binding and toxic effects are mostly occurring. They therefore mostly bind to blood located Hg2+ reducing the levels by about 25-30%. This reduction in blood Hg2+ levels is re-established quickly by equilibrium with the intracellular Hg body burden which is much larger. While this approach seems to work it takes many treatments over a long period of time to have a significant effect on total mercury body burden. There is also a concern about translocation of Hg2+ into the kidney causing renal deterioration. Recently, a new class of uncharged, hydrophobic chelator has been developed that enters cells, crosses the blood brain barrier and forms a true 1:1 chelate with Hg2+ that is very stable and non-reactive, and does not translocate Hg to other tissues. This new chelator has a structure that consists of two naturally occurring compounds used as food preservatives or antioxidants. The animal and human testing at levels effective and safe for chelation has little to no toxic side effects and does not cause a depletion in any essential metal. It has been tested and shown to be efficacious in preventing death and toxicity in animals subjected to multiple lethal dose of HgCl2 and in Phase II efficacy studies on mercury toxic miners with no significant adverse effects occurring. In a Phase I safety and pharmacokinetics study no significant adverse effects were recorded and no depletion of essential metals.
Richard Nahas MD: Blockages: the missing link in environmental toxicity
Blockages are disturbances in the nervous system left behind after injury and trauma, and they are the single most important and under-treated cause of chronic disease in the world. This is the premise behind this lecture, which will help participants understand what blockages are and how they affect the psycho-immuno-neuro-endocrine (PINE) system in environmental toxicity. Dr Nahas will summarize many different elements of integrative medicine, including acupuncture meridians, homeopathy, myofascial release, applied kinesiology and other systems of bioenergetic testing and treatment. These ‘dots’ will be connected to present a general theory of vibrational medicine and present it as the basis for a new paradigm for the prevention and treatment of neurodegenerative diseases.
David Steenblock DO, MS: Alzheimer’s Disease and Environmental Toxins
Evidence for Alzheimer’s disease and environmental risk factors include air pollutants (with nitrogen dioxide, carbon monoxide, particulate matter, diesel exhaust, and ozone) aluminum, pesticides and electric and magnetic fields. These toxins promote oxidative stress, mitochondrial dysfunction and brain disorders, including Alzheimer’s disease. Therapies may include detoxification, chelation therapy, hyperbaric oxygen, nocturnal oximetry, PEMF, and pharmaceutical and nutraceutical products.
1. List four diagnostic tests for environmental toxins and injuries.
2. List five symptoms related to brain disorders arising from environmental toxins.
3. What is a “green space” and how does it reduce air pollution?
4. List four nutraceuticals that detoxify pesticides.
Mark Morningstar DC, PhD: NeuroREgeneration: Strategies to Use It, Not Lose It
Mark Morningstar, DC, PhD, of the Natural Wellness& Pain Relief Center, will be speaking on the role of functional medicine and functional rehabilitation treatments for neurodegeneration. The main purpose of this talk will be to provide attendees with information they can use first thing Monday morning to help patients suffering from Parkinson’s disease, Alzheimer’s disease, dementia, etc. In addition to covering the more well-known functional medicine strategies for these disorders, activities to promote neurological activation in various brain areas will be described.
In treating patients with chronic neurodegenerative symptoms, it is important to design treatment plans that try to address any root underlying causes of their respective condition, while at the same time offer treatments that help them manage the day-to-day symptoms of the condition that improves their quality of life.
My talk will discuss the 3 requirements of neurons, and the various strategies and treatments that may be used to fulfill these 3 requirements. Many integrative and functional medicine providers will tend to focus on 1 or 2 of these requirements, but rarely have I seen an emphasis on all 3 simultaneously.
The presentation will highlight specific key aspects of working with neurodegenerative disorders, including:
Mechanical contributions to neurodegeneration;
Functional medicine therapies for neurodegenerative disorders;
Low-tech rehabilitation strategies for improved ADLs and neuro-activation;
- Discuss the definition of volatile organic compounds such as xylene, ethylbenzene and other BTEX compounds.
- Discuss the chemical properties of xylene: 3 isomers which occur naturally in petroleum products and coal tar and can be made synthetically; can be found in air, water, soil and food; background levels in food, indoor and outdoor air.
- Discuss how xylene can enter the environment and how people might be exposed to xylene.
- Explain how xylene affects adult and child health, symptoms, and body systems affected.
- Briefly discuss tests to determine exposure, what agencies regulate xylene and what levels the US government has approved.
- Discuss how people/families can reduce the risk of exposure to xylene (per the US federal government) and from a physician’s perspective.
- Discuss the chemical properties of hydrogen sulfide (H2S).
- Discuss sources of H2S: what environments it can be found in, background levels.
- Describe symptoms of low level exposure to H2S.
- Describe symptoms and known health effects from exposure to high levels of H2S.