Methylation & ADD

A Methylation Deficiency appears to be the primary abnormality in patients suffering from ADD/ADHD. The methylated form of folic acid (ie methylfolate) is essential in the conversion of tyrosine to dopamine. By genetically limiting the production of methylfolate, the patient secondarily limits the production of dopamine. Low dopamine levels affect focus, concentration, organization, short term memory, vestibulo-visual interaction, sleep patterns, emotional stability and even hormonal regulation. Altered levels of dopamine additionally affect the levels of epinephrine and norepinephrine. Imbalances in this biochemical region, dopamine, epinephrine and norepinephrine are implicated in ADD/ADHD. One can envision that methylation cycle function is needed to produce SAMe as a methyl donor for the dopamine/ norepinephrine / epinephrine pathways to help to recover ADD/ADHD.