Pushing methylation beyond optimal creates problems.
More isn't better. The therapeutic window follows a U-shaped curve where both deficiency and excess cause pathology.
The overmethylation pattern
45-46% of schizophrenia cases show severe overmethylation. Anxiety, insomnia, mood swings—all can be triggered by too much methylation support.
Excess SAMe converts to toxic compounds that actually inhibit methylation.
MTHFR variants aren't roadblocks. They're signals.
40-50% of people have MTHFR polymorphisms
This is too common to be a disease. It's a variation.
Riboflavin (B2) is the cofactor for MTHFR
Many with "genetic weakness" simply need more B2. Studies show riboflavin normalizes homocysteine even with MTHFR variants.
The same variant can cause over OR under methylation
Depending on compensatory mechanisms and environment. Genetic tests alone can't tell you.
Recognizing overmethylation.
Red flag: Initial improvement followed by severe side effects in week two of methylfolate supplementation suggests accumulation overwhelming compensatory mechanisms.
Safe methylation support starts foundational.
Address nutrient deficiencies through whole foods first
Optimize gut health—microbiome affects methylation
Remove methylation inhibitors (toxins, certain medications)
Reduce methylation competitors (stress, inflammation)
Start low, go slow with any supplementation
Methylation adaptogens
Curcumin, sulforaphane, quercetin, and dark berries naturally regulate methylation bidirectionally—without overstimulation risk.
The goal isn't maximizing methylation. It's optimizing balance.
Precision approaches that honor individual biochemistry, not blanket supplementation based on genetic tests.
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