Speakers
Your speakers are dedicated to bring together a synthesis of knowledge regarding the role of NAFLD and methylation in human health.
Day one will address the pandemic juvenile and adult non-alcoholic fatty liver disease (NAFLD) that may under certain conditions progress to end-stage liver disease and hepatocellular carcinoma. The presentations will focus on the mechanisms associated with the array of causative factors, and objective laboratory testing that addresses many of the risk factors and outcomes and clinical applications.
Aberrant Methionine Metabolism: Clinical Implications and Intervention
These presentations will define the clinically relevant aspects of abnormal methionine metabolism, and present case studies with initial assessments and follow up after clinical intervention. Basic protocols will be provided based upon objective laboratory testing and clinical experience. Methionine, an essential amino acid, is considered by many to be of utmost importance due to its vital roles in methylation, transsulfuration and transmethylation of homocysteine. On first pass through the liver about 50% of dietary methionine is metabolized to s-adenosyl methionine (SAM) which is the donor of methyl groups to DNA/RNA, proteins, neurotransmitters, and phospholipids. Methylation of DNA is a major mechanism for the regulation of gene expression. After methyl group donation SAM is converted to s-adenosylhomocysteine (SAH). SAH is a very potent inhibitor of all methylation reactions in the body, and the ratio of SAM to SAH has been described as the methylation index. Subsequently SAH is reversibly converted to homocysteine which is a branch point whereby homocysteine can conditionally be metabolized through the transsulfuration pathway ultimately to form taurine, cysteine, glutathione (GSH) and essential sulfate ions. Alternatively homocysteine can be metabolized through the transmethylation pathway back to methionine. SAH is also emerging as a risk factor for cardiovascular disease and has been implicated in NAFLD. There are many genetic (single nucleotide polymorphisms (SNPs) and epigenetic factors (nutrients, oxidative stress and environmental toxicants) that can adversely affect methionine metabolism at a variety of enzymatic steps. Clinical consequences of aberrant methionine metabolism are common and may result in a plethora of consequences including: aberrant neurotransmitter metabolism, developmental delay, psychiatric disorders, oxidative stress, compromised DNA synthesis and repair, immune dysregulation, carcinogenesis, impaired innate detoxification, and perhaps increased risk for autism spectrum disorder. The most common SNPs and epigenetic disruptors of methionine metabolism will be discussed, and protocols for successful remediation will be provided. The second talk will present case studies. The case studies will provide patient symptoms and comprehensive laboratory testing before and after clinical intervention.
Our commitment to you during the day is to make this journey fun, intense, rich in content and experience, and, most of all, valuable on Monday morning when you return to your clinic.
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.
![]() |
Lyn Patrick, NDLyn Patrick ND graduated from Bastyr University in 1984 with a doctorate in naturopathic medicine and has been in private practice as a state licensed naturopathic physician in Arizona and Colorado for the last 30 years. Dr. Patrick is a published author of numerous articles in peer-reviewed medical journals and has been a Contributing Editor for Alternative Medicine Review, a Medline-indexed journal of complementary/alternative medical research. She speaks internationally on the integrative medical treatment of chronic hepatitis C, environmental medicine, liver disease, endocrine disruption, metal toxicology and other topics. She is a current member of the Board of Directors of the American College for the Advancement of Medicine (ACAM) and a planner and faculty member for ACAM’s continuing medical education conferences, lecturing in the area of chelation and metal toxicology. She is a founding partner and educator for Progressive Medical Education, an online continuing education site for primary care providers Progressive Medical Education. She is also a founding partner and presenter at the Environmental Health Symposium, an international environmental medicine conference based in the United States.In her spare time she enjoys biking, hiking and kayaking the mountains, lakes, and rivers of southwestern Colorado. |
![]() |
David Quig PhD, MS, BSDavid Quig, PhD David Quig received his BS and MS degrees in Human Nutrition from Virginia Tech and a PhD in Nutritional Biochemistry from the University of Illinois. After a five year stint as a Research Associate studying lipid biochemistry and cardiovascular disease at Cornell University, he was a Senior Cardiovascular Pharmacologist for seven years with a major pharmaceutical company. For the past 22 years David has served as the Vice President of Scientific Support for Doctor’s Data, Inc. He has focused on toxic elements, methylation and amino acid metabolism, the clinical application of the biochemistry of endogenous detoxification, and the influence of the gastrointestinal metabolome on health and sustained adverse health conditions. David regularly speaks at national and international medical conference, and has facilitated and co-authored an array of clinical studies spanning exposure and retention of environmental toxicants, nutritional status and gastrointestinal dysbiosis. Biomedical research aside, David is an adrenal seeker who is insatiably attracted to a variety of activities that are propelled only by the forces of nature. |