Summary of MTHFR, APOE, and TNF-alpha | PDF

Summary

This document provides summaries of the MTHFR, APOE, and TNF-alpha genes, outlining their functions, clinical indications, and implications of abnormal results. It explores the relationship between genes, nutrition, and clinical medicine and stresses the need for a holistic approach involving nutrigenetic testing.

Full Transcript

## MTHFR Summary Snapshot 1. What is it? * key enzyme involved in methylation 2. When is it clinically indicated? * Hyperhomocysteinemia, low B vitamin level, mainly folate; increased risk of venous thrombosis, CVD, HTN, stroke, diabetic neuropathy or retinopathy, depression, autism, and sch...

## MTHFR Summary Snapshot 1. What is it? * key enzyme involved in methylation 2. When is it clinically indicated? * Hyperhomocysteinemia, low B vitamin level, mainly folate; increased risk of venous thrombosis, CVD, HTN, stroke, diabetic neuropathy or retinopathy, depression, autism, and schizophrenia; increased risk of birth defects (NTDs or congenital heart defects, cleft lip and/or palate, and Down syndrome); increased risk of recurrent pregnancy loss; increased risk of fracture and/or low BDM; increased risk of all cancers; NAFLD 3. How does it compare to other commonly used diagnostics? * Should be used in combination with other markers, not as a standalone 4. What are the clinical implications of an abnormal result? * Possible impaired methylation, low B vitamins, high Hcy 5. What are other nutrients to consider? * $Mg, Zn, Fe, B2, B6, B12$, Folate/5-MTHF, TMG/Betaine 6. What is the treatment for impaired activity? * Dietary and supplemental sources of B vitamins, health lifestyle ## APOE Summary Snapshot 1. What is it? * key protein involved in transport of lipids 2. When is it clinically indicated? * plasma lipid abnormalities such as high TGs, high LDL-C, low, HDL-C; increased risk for T2DM, atherosclerosis, MI, stroke; indications of high inflammation such as elevated C-RP and hyperuricemia; low BMD or increased risk for OP and fractures; indications of oxidative stress/low antioxidant status and heavy metal toxicity. 3. How does it compare to other commonly used diagnostics? * Should be used in combination with other markers, not as a standalone 4. What are the clinical implications of an abnormal result? * Possible increased risk of high lipids, CVD, and/or dementia 5. What are other nutrients to consider? * Cardiovascular and neurological supportive nutrients 6. What is the treatment for impaired activity? * Minimize stress, healthy diet low in sugar and high in nutrients ## TNF-alpha Summary Snapshot 1. What is it? * Proinflammatory cytokine 2. When is it clinically indicated? * Presence of all (chronic) inflammatory conditions 3. How does it compare to other commonly used diagnostics? * Should be used in combination with other markers of inflammation, not as a standalone 4. What are the clinical implications of an abnormal result? * Possible increased risk of inflammation/inflammatory conditions 5. What are other nutrients to consider? * Nutrients to reduce inflammation 6. What is the treatment for impaired activity? * Minimize stress, low-inflammation diet ## Summary * There is a lot we now know about genes * There is a lot we still don't know about genes and modulation of the epigenome * There is still less we know about nutrigenomic application to clinical medicine, but there is some recent data emerging * Food (and eating) is (are) filled with informational signals delivered to our cells * Nutrigenetic testing should be coupled with laboratory nutrient assessment for clinical application * Note how nutrients come together with genes for a more complete. Picture/assessment * MTHFR, COMT, APOE, and TNF-a are some important genes that will assist with clinical therapeutic strategies