What is the Origin of COMT Val158Met?

The name is a precise genetic nomenclature: COMT identifies the enzyme, Val158Met indicates the amino acid change, and SNP signifies its origin as a naturally occurring variation in the human genome. The enzyme itself is critical for deactivating neurotransmitters like dopamine and norepinephrine. Understanding this polymorphism is a key aspect of personalized medicine and genetic screening.

What is the Mechanism of COMT Val158Met?

Individuals with the Met allele typically possess a COMT enzyme with up to four times lower activity compared to those with the Val allele. This reduced function leads to a slower breakdown of catecholamines, which can result in higher and more prolonged levels of these stress hormones in the prefrontal cortex. Clinically, this genetic profile may require tailored approaches to stress management and hormonal detoxification support.

COMT Val158Met

Meaning

COMT Val158Met is a common single nucleotide polymorphism (SNP) in the Catechol-O-Methyltransferase (COMT) gene, which affects the enzyme’s ability to metabolize catecholamines and certain estrogen metabolites. The variation involves a substitution of the amino acid valine (Val) with methionine (Met) at position 158, resulting in a clinically significant reduction in enzymatic activity. This genetic variation can influence an individual’s neuroendocrine response to stress, pain sensitivity, and the detoxification of estrogenic compounds.

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∞ COMT Val158Met
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Can Lifestyle Interventions Mitigate the Effects of a Slow COMT Gene Polymorphism?

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COMT Val158Met

Meaning

Origin

Mechanism

How Do Genetic Variations Affect Estrogen Clearance Rates?

How Do Individual Genetic Variations Influence Hormone Therapy Effectiveness?

Can Genetic Testing Reveal a Predisposition to Poor Estrogen Metabolism and Guide Lifestyle Choices?

What Are the Clinical Considerations for Genetically Guided Hormone Protocols?

What Are the Clinical Implications of Genetic Markers for Estrogen Metabolism?

How Do Genetic Variations Influence Estrogen Metabolism during Hormone Therapy?

Can Lifestyle Interventions Mitigate the Effects of a Slow COMT Gene Polymorphism?

Can Genetic Predispositions Influence Hormonal Fatigue Susceptibility?

How Do Individual Genetic Variations Influence Responses to Hormonal Interventions for Cognition?

How Do Individual Responses to Hormonal Therapies Vary?

How Do Individual Genetic Variations Influence Responses to Hormonal Protocols for Cognition?

How Do Genetic Variations Influence Individual Responses to DIM?

How Do Genetic Variations Influence Estrogen Metabolism?

Can Hormonal Therapies Counteract Genetic Predispositions in Dopamine Response?

What Role Do Genetic Polymorphisms Play in Estrogen Metabolism and Therapy Response?

How Do Genetic Differences Impact Estrogen Clearance Pathways?

What Are the Clinical Implications of COMT Gene Polymorphisms for Male Estrogen Levels?

What Specific Genes Influence Cognitive Responses to TRT?

What Are the Long-Term Safety Implications of Enzyme Variations in Hormone Therapy?

How Do Genetic Variations Influence Estrogen Therapy Safety?

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