The COMT Gene Diet is a personalized nutritional strategy tailored to support the function of the Catechol-O-Methyltransferase (COMT) enzyme, which is critical for metabolizing catecholamines and estrogen metabolites. Polymorphisms in the COMT gene can lead to reduced enzyme activity, resulting in slower clearance of these neurohormones and estrogens. This dietary protocol aims to provide specific micronutrients that serve as cofactors for the COMT enzyme or support alternative detoxification pathways.
Origin
This concept is rooted in neuroendocrinology and pharmacogenetics, recognizing the COMT enzyme’s role in neurotransmitter homeostasis and estrogen clearance. The gene’s common variant, a SNP that exchanges valine for methionine (Val158Met), was identified as a major determinant of enzyme efficiency. Clinical application of the “COMT Gene Diet” arose from the need to manage the physiological consequences of slower catecholamine and estrogen breakdown through targeted nutritional support.
Mechanism
COMT requires S-adenosylmethionine (SAMe) as a methyl donor to catalyze the inactivation of catecholamines like dopamine and norepinephrine, and to facilitate the clearance of estrogen’s active metabolites. A key dietary mechanism involves ensuring adequate intake of methyl-donor nutrients, such as folate, B12, and betaine, to support SAMe production. Furthermore, the diet may limit intake of substances that compete with or inhibit COMT activity, thereby optimizing the clearance kinetics of crucial neuroendocrine signaling molecules.
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