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Health & Wellness Services

L_113 Methylation Panel Testing – Blood

£790.00

Methylation is one of the important epigenetic processes by which gene activity is turned on or off, up or down, often in response to environmental triggers and can then impact our health. Epigenetic’s is the study of changes to an organism caused by modification of gene expression.

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Description

Includes your full personal report and plan from Jo, with a Zoom consultation to run through the diagnosis and prognosis.

What is Methylation and why is it important to test?

Methylation is one of the important epigenetic processes by which gene activity is turned on or off, up or down, often in response to environmental triggers and can then impact our health. 

Epigenetics is the study of changes to an organism caused by modification of gene expression, rather than by changes to the DNA itself. In other words, these changes affect our health by “dialing” genes activity up or down without altering the genes. As methylation affects how genes express, methylation can accelerate disease or slow it down or stop it. It’s important to have the right amount of methylation …. Not too much and not too little.

All the cells in our bodies have the same DNA sequence: a cell from your heart has the same DNA as one from your stomach. That means some other process decides how individual cells develop and differentiate.

(All information has come from Dr Ann Shippy MD)

Methylation Example Report

The Science Bit…

What is Methylation?

Methylation is a chemical process that happens billions of times per second in every cell of the body.1Methyl groups are transferred and donated between many different molecules which change their structure and function. Methyl groups act like billions of switches which turn genes on or off, help regulate mood, detoxify hormones, produce energy, and promote healthy ageing.

Vitamins, minerals, and amino acids from the diet are needed to keep this process running smoothly. There are also genetic factors and oxidative stressors which can affect how well this pathway works.2

Why is Methylation important?

Methylation is needed to create DNA and RNA and regulate gene expression. It helps make creatine, which is needed for skeletal muscle contraction. Methylation is involved in basic energy production, fat metabolism, immune responses, vascular health, and cell membrane repair. It produces and metabolises neurotransmitters to regulate mood. Methylation also works to neutralise toxins and hormones.

Methylation defects have been associated with many clinical conditions including, but not limited to cancer, autism, ADHD, congenital and neural tube defects, cognitive decline, depression, cardiovascular disease, and schizophrenia.3-11

What advantage does the Methylation Panel offer compared to other diagnostics?

Genova’s Methylation Panel combines biomarkers with genetic information in one profile. Some genetic predispositions are not always expressed, therefore seeing combined results offers greater insight.

Not only does the Methylation Panel assess the methylation cycle, but it also incorporates the folate cycle and transsulfuration. Because these three processes are interconnected, the Methylation Panel is able to provide a complete picture regarding methylation status.

How are the results of the Methylation Panel helpful?

The Methylation Panel can uncover needs for nutritional support such as amino acids, vitamins, and minerals. Knowing this can help guide dietary and nutraceutical treatment plans. Additionally, knowing genetic predispositions can help focus supplementation to override potential methylation defects.

References

  1. Baric I, Staufner C, Augoustides-Savvopoulou P, et al. Consensus recommendations for the diagnosis, treatment and follow-up of inherited methylation disorders. J Inherit Metab Dis. 2017;40(1):5-20.
  2. Locasale JW. Serine, glycine and one-carbon units: cancer metabolism in full circle. Nature Rev Cancer. 2013;13(8):572.
  3. Duthie SJ. Folic acid deficiency and cancer: mechanisms of DNA instability. Br Med Bull. 1999;55(3):578-592.
  4. Refsum H, Ueland PM, Nygard O, Vollset SE. Homocysteine and cardiovascular disease. Ann Rev Med. 1998;49:31-62.
  5. Miller AL. The methylation, neurotransmitter, and antioxidant connections between folate and depression. Alt Med Rev. 2008;13(3):216-227.
  6. Troesch B, Weber P, Mohajeri MH. Potential Links between Impaired One-Carbon Metabolism Due to Polymorphisms, Inadequate B-Vitamin Status, and the Development of Alzheimer’s Disease. Nutrients. 2016;8(12).
  7. Schalinske KL, Smazal AL. Homocysteine imbalance: a pathological metabolic marker. Adv Nutr. 2012;3(6):755-762.
  8. Grayson DR, Guidotti A. The dynamics of DNA methylation in schizophrenia and related psychiatric disorders. Neuropsychopharmacology. 2013;38(1):138.
  9. Dayon L, Guiraud SP, Corthésy J, et al. One-carbon metabolism, cognitive impairment and CSF measures of Alzheimer pathology: homocysteine and beyond. Alzheimers Res Ther. 2017;9(1):43.
  10. Castro R, Rivera I, Blom HJ, Jakobs C, Tavares de Almeida I. Homocysteine metabolism, hyperhomocysteinaemia and vascular disease: an overview. J Inherit Metab Dis. 2006;29(1):3-20.
  11. Nardone S, Sharan Sams D, Reuveni E, et al. DNA methylation analysis of the autistic brain reveals multiple dysregulated biological pathways. Transl Psychiatry. 2014;4(9):e433.
  12. Zakhari S. Alcohol Metabolism and Epigenetics Changes. Alcohol Res. 2013;35(1):6-16.
  13. Kharbanda KK. Alcoholic liver disease and methionine metabolism. Semin Liver Dis. 2009;29(2):155-165.
  14. Bardag-Gorce F, Oliva J, Wong W, et al. S-adenosylmethionine decreases the peak blood alcohol levels 3 h after an acute bolus of ethanol by inducing alcohol metabolizing enzymes in the liver. Exp Mol Pathol. 2010;89(3):217-221.
  15. Zhao Y, Li JS, Guo MZ, Feng BS, Zhang JP. Inhibitory effect of S-adenosylmethionine on the growth of human gastric cancer cells in vivo and in vitro. Chin J Cancer. 2010;29(8):752-760.
  16. Pouliot MC, Labrie Y, Diorio C, Durocher F. The Role of Methylation in Breast Cancer Susceptibility and Treatment. Anticancer Res. 2015;35(9):4569-4574.
  17. Pascale RM, Feo CF, Calvisi DF, Feo F. Deregulation of methionine metabolism as determinant of progression and prognosis of hepatocellular carcinoma. Transl Gastroenterol Hepatol. 2018;3:36.
  18. Wang X, Falkner B, Zhu H, et al. A genome-wide methylation study on essential hypertension in young African American males. PLoS One. 2013;8(1):e53938.
  19. Obeid R, Herrmann W. Homocysteine and lipids: S-adenosyl methionine as a key intermediate. FEBS letters. 2009;583(8):1215-1225.
  20. Lai CQ, Parnell LD, Troen AM, et al. MAT1A variants are associated with hypertension, stroke, and markers of DNA damage and are modulated by plasma vitamin B-6 and folate. Am J Clin Nutr. 2010;91(5):1377-1386.
  21. Papakostas GI, Cassiello CF, Iovieno N. Folates and S-adenosylmethionine for major depressive disorder. Can J Psychiatry. 2012;57(7):406-413.
  22. Sugden C. One-carbon metabolism in psychiatric illness. Nutr Res Rev. 2006;19(1):117-136.
  23. Obeid R, Schadt A, Dillmann U, Kostopoulos P, Fassbender K, Herrmann W. Methylation status and neurodegenerative markers in Parkinson disease. Clin Chem. 2009;55(10):1852-1860.
  24. Dayon L, Guiraud SP, Corthésy J, et al. ONE-CARBON METABOLISM, COGNITIVE IMPAIRMENT AND CSF MARKERS OF ALZHEIMER PATHOLOGY: HOMOCYSTEINE AND BEYOND. Alzheimers Dement. 2017;13(7):P705.
  25. Smith AD, Refsum H. Homocysteine, B vitamins, and cognitive impairment. Annu Rev Nutr. 2016;36:211-239.
  26. de Vega WC, Vernon SD, McGowan PO. DNA methylation modifications associated with chronic fatigue syndrome. PLoS One. 2014;9(8):e104757.

This page was created using the information from Genova Lab and Dr Ann Shippy websites.

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