Clinical
Microbiology

Toxic & Essential
Elements

Nutritional
Environmental
Exposure &
Detoxification

Cardiovascular

     
    

        

 
Does your patient base present any of the conditions above? 
Did you know that these and other conditions may be exacerbated by
poor methylation?
 

 
 
 
It has been suggested that the most sensitive indicator of poor methylation is the relative plasma concentrations of SAM to SAH (methylation index). Impaired methylation may be remedied with appropriate intake/supplementation of nutrients such as methionine, folate, B-12, B-6, betaine, zinc, and magnesium.

The results of the Plasma Methylation Profile from Doctor's Data can be used to determine suitable nutritional support to normalize methionine metabolism and ameliorate or prevent the potential adverse consequences associated with inadequate methylation and transsulfuration capacity.

 
Do you have questions about this or any of our other tests? Click the button below to complete our contact request form and your territory representative will reach out to you shortly.
  
 

 
 

 
Limited Estrogen Detoxification
The 2-OH and 4-OH metabolites (catechol estrogens) are readily oxidized to quinones which, as you know, are highly reactive.  2,4-hydroxy estrones can be significant mechanisms of estrogen quinone cell damage.  This harmful pathway can be minimized through detoxification and excretion of the catechol estrogens by methyl groups donated by S-adenosylmethionine (SAM).  The inability to efficiently detoxify these estrogen metabolites has been linked to an increased susceptibility to postmenopausal estrogen sensitive cancers and overall prostate cancer risk.
  
Neurotransmitter Imbalance
Methylation defects are associated with altered neurotransmitter metabolism. SAM is an essential cofactor both for synthesis and metabolism of neurotransmitters. Normal SAM levels may also be required for the maintenance of myelin (the fatty layer of insulation that surrounds each nerve).  
  
Mitochondrial Dysfunction
Coenzyme Q10 (CoQ10) and carnitine are two cellular nutrients required in order to produce sufficient mitochondrial energy.  CoQ10 is important for its role in ATP production in the mitochondrial respiratory chain while carnitine is involved in the transport of fatty acids into the mitochondrial matrix.  Synthesis of both nutrients relies heavily upon the methyl donating capacity of SAM.  Compromised methionine metabolism may decrease levels of SAM, thusresulting in impaired methylation and decreased cellular energy.
  
Toxic Element Exposure

Epigenetics is the study of heritable changes in gene expression that occur without changes in DNA sequence. Epigenetic mechanisms are flexible genomic parameters that can change genome function under environmental influence. Toxic element exposure may contribute to epigenetic mechanisms which are known to affect enzymatic action required for proper methionine synthesis.  
  
Cardiovascular Disease
Plasma homocysteine and S-adenosylhomocysteine (SAH) are positively associated with occlusive artery and cardiovascular disease and homocysteine has been historically considered to be an independent risk factor for cardiovascular disease.  SAH is the immediate precursor of homocysteine, and although present in blood at less than 1/500th the concentration ofhomocysteine, recent research has suggested that SAH may be an even stronger indicator of vascular disease.

Type 2 Diabetes
A recent study showed that increased plasma concentrations of homocysteine and other methylation pathway intermediates are related to disturbed renal function in patients with type 2 diabetes.  Additionally, patients with renal failure had a much lower methylation index SAM/SAH ratio and elevated SAH.
   

 
Want to see the latest research on this topic?

  
Zhang CX, Ho SC, Chen YM, Lin FY, Fu JH, Cheng SZ.  Dietary folate, vitamin B6, vitamin B12 and methionine intake and the risk of breast cancer by estrogen and progesterone receptor status.  BMC Medical Genomics 2014, 7:5.

Bottiglieri T, Laundy M, Crellin R, Toone BK, Carney MW, Reynolds EH.  Homocysteine, folate, methylation, and monoamine metabolism in depression.  J Neurol Neurosurg Psychiatry. 2000 Aug;69(2):228-32

Phillipson OT.   Management of the aging risk factor for Parkinson's disease.   Neurobiol Aging. 2014 Apr;35(4):847-57.

Baccarelli A and V. Bollati V.  Epigenetics and environmental chemicals.  Curr Opin Pediatr. 2009 Apr; 21(2): 243–251.

Baccarelli A and Ghosh S.  Environmental Exposures, Epigenetics and Cardiovascular Disease.  Curr Opin Clin Nutr Metab Care. 2012 Jul; 15(4): 323–329.

Herrmann W, Schorr H, Obeid R, Makowski J, Fowler B, Kuhlmann MK. Disturbed homocysteine and methionine cycle
intermediates S-adenosylhomocysteine and S-adenosylmethionine are related to degree of renal insufficiency in type 2 diabetes.
Clin Chem. 2005 May;51(5):891-7

 
  
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Why Choose Doctor's Data, Inc.?
 
Doctor's Data, Inc. has provided innovative specialty testing to healthcare practitioners around the world from our advanced CLIA-licensed clinical laboratory since 1972 A specialist and pioneer in essential and toxic elemental testing, the laboratory provides a wide array of functional testing to aid in decision making and better patient outcomes.  Choose DDI to help you assess and treat heavy metal burden, nutritional deficiencies, gastrointestinal function, cardiovascular risk, liver and metabolic abnormalities, and more.