The topic of methylation is getting its fair share of attention lately, and rightfully so. Methylation is a biochemical process involving addition of a methyl group to a substrate. Methylation has over 200 functions with the body. When optimal methylation occurs, it is responsible for mitochondrial function and cellular energy, cell division, recovery and turnover, immune regulation, neurotransmitter production and synchronization, detoxification, DNA and RNA production, gene regulation, hormone regulation, myelination and much more.Methylation

Methylation deficiency can play a role in common symptoms experienced by adults such as: Migraines, headache, vertigo, dizziness. Chronic fatigue, fibromyalgia, Chronic pain, neuralgias, neuropathies, adult attention deficit disorder (ADD), adult attention deficit hyperactivity disorder (ADHD), anxiety disorders, depression, bi-polar, Alzheimer’s disease and dementias, Infertility and hormonal regulation issues, asthma, food sensitivities, auto-immune disorders (lupus, rheumatoid, Hashimoto’s, etc.), chronic immune dysfunction (yeast, viral, Lyme’s disease, etc.), diabetes and cardiovascular disease.

Methylation occurs with the help of the universal methyl donor SAMe (S-adenosyl-L-methionine). SAMe is synthesized in the methionine cycle using dietary precursors namely: methionine, folate, choline, betaine, vitamins B2, B6 and B12. Genetic and acquired factors can predispose people to developing methylation deficiency including western diet, restricted diets, alcohol, certain medications, stress, environmental toxicity, disease and everyone’s favorite single nucleotide polymorphisms (SNPs).

A SNP is a genetic variation in a single nucleotide that leads to appreciable differences in enzyme or protein function. SNPs can confer an increased or decreased activity of a particular enzyme and we all have them. There is a lot of press about MTHFR nowadays. MTHFR is an enzyme that is responsible for converting dietary folic acid into an active and usable form within the body to be used in the methylation cycle to create the universal methyl donor, SAMe. A genetic mutation or SNP anywhere along the gene or methylation cycle can affect the production of SAMe and can lead to hypomethylation. Complicating it even further, a low dietary intake of cofactors named above, can further lead to hypomethylation and can further change expression of the gene.

When the methylation cycle is hypo functioning and we have reduced levels of SAMe, a number of important modules are not sufficiency produced. One chemical of great importance is glutathione (a powerful antioxidant) which is made from homocysteine. Homocysteine is converted via transsulfaration to cysteine or remethylation into methionine. Breakdown in either process leads to hyperhomocysteinemia. Homocysteine is an inflammatory chemical that causes neuronal damage and death, microvascular damage and have been associated with memory loss and cognitive decline.

While knowing our individual SNPs are important, the study of how these SNPs have a biochemical effect on our nutrient absorption, delivery, metabolism, elimination, or biological action are of greater value. This study is called Nutrigenomics. Good news, you can have a simple and easy genetic test to find out if and which SNPs you have and determine you overall methylation status and methyl factor need. This knowledge can help override the deleterious effects of predisposing factors and prevent problems associated with methylation deficiencies.


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