Methylation Profile; plasma
Normal metabolism of methionine is critical for cellular methylation of DNA, proteins and neurotransmitters. Aberrant methionine metabolism can occur in anyone at any age and can be associated with numerous health consequences including cardiovascular disease and cancer. The Methylation Profile provides a functional assessment of the phenotypic expression of common SNPs (MTHFR, MS, CBS) by evaluating the plasma levels of methionine, cysteine, SAM, SAH, homocysteine, adenose and cystathionine. It also provides the important "methylation index", a ratio of SAM to SAH.
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5 to 7 days
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This test is useful for
- Birth Defects
- Cardiovascular Disease
- Congenital Heart Disease
- Detoxification Impairment
- Down Syndrome
- General Health and Longevity
- Genetic Disorders
- Immune Dysfunction
- Neurodegenerative Diseases
- Nutritional Deficiencies
- Psychiatric Disorders
Normal methionine metabolism is absolutely critical for
methylation, transsulfuration and folate-dependent transmethylation.
Abnormal metabolism of methionine can be found in anyone at any age. It
is usually associated with genetic or nutritional deficiencies, aging
and exposures to environmental toxicants. For example, lead can inhibit
methyltransferase enzymes and transmethylation of homocysteine via
inhibition of the enzyme methylene-tetrahydrofolate reductase (MTHFR).
Conditions associated with untreated, aberrant methionine metabolism include, but are not limited to:
- Abnormal neurotransmitter metabolism and psychiatric disorders such as schizophrenia and bipolar disorder
- Neurodegenerative diseases
- Dysregulation of nitric acid homeostasis
- Oxidative stress
- Global under-methylation, synthesis and repair of DNA
- Immune dysregulation/autoimmunity
- Cardiovascular disease
- Congenital heart disease and birth defects
- Impaired endogenous detoxification processes
- Increased risk for Down's syndrome
Methylation: Methionine is first enzymatically
converted to S-adnosylmethionine (SAM), the principal methyl donor for
methylation of DNA, RNA, protein, phospholipids, creatinine and
neurotransmitters. S-adenosylhomocysteine (SAH) is generated as a
product of all SAM-dependent methylation reactions and is hydrolyzed to
homocysteine (Hcy) and adenosine through a reversible reaction (AHCY).
SAH is a potent inhibitor of all SAM-dependent methylation reactions.
Efficient removal of adenosine and Hcy is imperative to prevent
accumulation of SAH. The enzymatic activities of adenosine kinase,
adenosine deaminase and 5'-nucleosidases contribute to maintaining
normal levels of adenosine.
Transmethylation: Hcy is normally primarily
removed or recycled by remethylation to methionine through a series of
reactions that require 5-methyltetrahydrofolate, B-12 and betaine to
complete the normal methionine cycle. A low ratio of SAM to SAH is a
sensitive indicator of under-methylation. Elevated plasma Hcy is an
independent risk factor for cardiovascular disease (CVD). Recent
research suggests that elevated SAH may be an even better predictor of
risk for CVD.
Transsulfuration: Methionine > Homocysteine
> Cysteine. The methionine transsulfuration pathway occurs primarily
in the liver and kidneys, and diverts Hcy away from remethylation to
methionine toward synthesis of conditionally essential amino acid
cysteine, essential sulfate, taurine and glutathione. Homocysteine in
the presence of serine and B6 is enzymatically converted to
cystathionine and ultimately cysteine. Cysteine is the rate-limiting
amino acid in the biosynthesis of quintessential glutathione (GSH). GSH
is pivotal in the regulation of intracellular redox homeostasis,
oxidative stress, immune function, DNA synthesis and repair, apoptosis
and detoxification of metals and chemicals. The DDI Methylation Profile
evaluates the plasma levels of methionine, cysteine, SAM, SAH, Hcy,
adenosine and cystathionine, and provides the important "methylation
index," a ration of SAM to SAH. The test results can facilitate
appropriate individualized interventions to improve or normalize
methionine metabolism and ameliorate or prevent adverse consequences
associated with inadequate methylation and/or transsulfuration capacity.