This exciting educational presentation shines light on the methylation cycle and discusses the role of nutrients as a clinical strategy. This event will be in a round table format including in-studio discussion surrounding the topics presented. In this round-table, Dino Celeda, Ph.D is accompanied by Amy Pieczarka, RD, LDN, CCN, CDE and Andrew Campbell, M.D.
Key Topics covered during this presentation:
• Learn about methylation and methylation potential
• Discover how methylation potential is correlated with neurotransmitter balance
• Learn the significance of the methionine and homocysteine ratio
• See how the MTHFR gene affects homocysteine balance
• Understand patient methylation with the Methyl Detox Profile
2. As Always…
Tonight’s discussion does not take into consideration
your patient’s medical history, drug/supplement
interactions and/or allergies/sensitivities. It is the
responsibility of the practitioner to determine
appropriate supplement and dosing choices for each
patient.
3. About the Commentators
Amy Pieczarka, RD,LDN,CCN,CDE
Director of Nutrition Services
PreviMedica
Andrew W. Campbell, M.D.
Medical Advisor
Cell Science Systems
4. About the Speaker
• Friedrich Schiller Universitaet – Heidelberg, Germany
• Institut National de La Recherche Agronomique - France
• Krankenhaus Harlaching -Germany
Dr. Dino Celeda holds a Ph.D in Biology specialized in
Human Genetics from the Ruprecht Karls Universitaet,
Heidelberg, Germany. He completed his training and held
positions at many renowned institutions including:
Dr. Celeda has authored numerous publications in the field of Human Genetics. Included in
his experience are Senior R&D, Scientific Advisor, Director of Genetic Testing and Director of
Science positions.
Dr. rer. nat. Dino Celeda (Ph.D)
Scientific Officer
7. Genetic Polymorphism (SNP)
A SNP can lead to a change in protein sequence and thus influence the 3-D conformation. In
the example here, the SNP disrupts hemoglobin formation and causes sickle cell anemia.
8. Functional Genetic Test Results
The individual’s functional genetic test results are shown on a level
of functionality and/or expression of the corresponding enzyme.
• homozygous positive, -;-, both alleles from both parents show
mutation. Reduced function/expression.
• heterozygous +;-, one allele from one parent shows mutation,
the other allele shows the normal, wild-type. 50% of the genes
are normal
• homozygous negative +;+, both alleles from both parents have
no mutation and show the normal, wild type. 100% of the genes
are normal.
9. Genomic Insights TM
– TEST
Individual’s current status: testing of relevant SNPs and
corresponding metabolic markers in blood
– TARGET
Targeted intervention: personalized, specific supplementation
according to individual results of relevant of SNPs, and
corresponding metabolic markers in blood
– MONITOR
Individual progress: monitoring and maintaining the progress
of personalized, specific supplementation with measurement
of metabolic markers in blood
Applying Functional Genetics for targeted intervention by
personalized, specific supplementation
10. Genomic Insights TM
Importance of personalized targeted nutrition
Overload of Supplements
can impact metabolic process and lead to side effects.
Individual Genetic SNPs
may require personalized supplementation of specific vitamins, minerals, trace elements and
/or amino acids for the maintenance and optimization of metabolic processes.
Side Effects
can influence a variety of functions in the organism like immune responses (reduced NK-
cytotoxicity).
11. Genes in the Methionine/Homocysteine Cycle
• MTHFR (Methylenetetrahydrofolate reductase)
C677T and A1298C mutations in the MTHFR gene are known to cause a diminished methylation
capacity, by a reduction in 5-MethylTHF synthesis.
• Methionine synthase (MS)
MS is encoded by the 5-methyltetrahydrofolate-homocysteine-methyltransferase gene (MTR). Its task
is to generate methionine from homocysteine by using methylcobalamin (methylated vitamin B12)
obtained when 5-MethylTHF donates its methyl group to vitamin B12. The mutation at position
C3518T in the gene is described with a reduced activity of the resulting enzyme.
• COMT (Catechol-O-Methyltransferase)
COMT is responsible for the transfer of the methyl group from SAMe to specific substances (e.g.
catecholamines) for removal. COMT is also involved in drug metabolism/clearance, neurotransmitter
regulation, gene expression as well as in the detoxification of a variety of environmental toxins.
The mutations at position G472A (Val108/158Met) and G304A (Ala52/102Thr) are described with a
reduced activity of the resulting enzyme.
31. Pre-Webinar Survey Questions
• What would be a ‘red flag’ for a practitioner to prompt the ordering of the
Methyl Detox Profile?
• How do you know when someone is under or over methylating?
• Does someone with a SNP require lifelong supplementation?
• How does the SAD vs. Paleo diet affect this?
• How does one decide which methylating supplement to use?
• How do I specifically use the MTHFR results on pharmacogenomics
testing to help mental health patients?