Sarcosine is an amino acid made within the methylation cycle when S-adenosylmethionine (SAM) is conjugated with glycine.
It can also be made by catabolism of dimethylglycine (DMG).
There are many dietary sources of sarcosine including eggs, legumes, nuts, and meats.
Sarcosine is also available as an over-the-counter supplement, and it is widely used in cosmetic formulations (toothpaste, creams, and soaps) and detergents.
In the methylation cycle, sarcosine is created by the GNMT enzyme, which functions to control SAM excess. Some clinicians use sarcosine elevation as a marker of ‘excess methyl supplementation’ or ‘over-methylation.’ Currently, there is no literature to support this hypothesis, but rather it is based on physiology.
Sarcosine can also be produced through the breakdown of DMG.
Sarcosine is a natural glycine transport inhibitor in the CNS, enhancing N-methyl-D-aspartate (NMDA) receptors. NMDA synaptic receptors are not only important for basic CNS functions (breathing, motor function), but also learning, memory, and neuroplasticity. Decreased NMDA function results in cognitive defects, and overstimulation causes excitotoxicity.
Abnormalities in these receptors are implicated in many diseases and targeted for pharmacologic therapy. Sarcosine has been shown to be a co-agonist for NMDA receptors. For this reason, there are many studies evaluating sarcosine as an adjunct treatment for psychiatric diseases, such as schizophrenia, which is characterized by decreased NMDA function. In addition, using sarcosine to enhance NMDA function can improve depression-like behaviors.
Since DMG is essentially sarcosine with an extra methyl group, research shows that they have similar effects. Some studies have evaluated urinary and serum sarcosine’s use as a prostate cancer progression marker; however, the data is mixed. These studies are based on nonspecific metabolomic profiling, which followed random metabolite elevation patterns.
- Strzelecki D, Podgorski M, Kaluzynska O, et al. Supplementation of Antipsychotic Treatment with the Amino Acid Sarcosine Influences Proton Magnetic Resonance Spectroscopy Parameters in Left Frontal White Matter in Patients with Schizophrenia. Nutrients. 2015;7(10):8767-8782.
- Luka Z, Mudd SH, Wagner C. Glycine N-methyltransferase and regulation of S-adenosylmethionine levels. J Biol Chem. 2009:jbc. R109. 019273.
- Lee M-Y, Lin Y-R, Tu Y-S, Tseng YJ, Chan M-H, Chen H-H. Effects of sarcosine and N, N-dimethylglycine on NMDA receptor-mediated excitatory field potentials. J Biomed Sci. 2017;24(1):18.
- Frontiers in Neuroscience. In: Van Dongen AM, ed. Biol NMDA Receptor. Boca Raton (FL): CRC Press/Taylor & Francis Group, LLC.;2009
- Kemp JA, McKernan RM. NMDA receptor pathways as drug targets. Nat Neurosci. 2002;5:1039.
- Lucarelli G, Fanelli M, Larocca AMV, et al. Serum sarcosine increases the accuracy of prostate cancer detection in patients with total serum PSA less than 4.0 ng/ml. Prostate. 2012;72(15):1611-1621.
Jentzmik F, Stephan C, Miller K, et al. Sarcosine in Urine after Digital Rectal Examination Fails as a Marker in Prostate Cancer Detection and Identification of Aggressive Tumours. Eur Urol. 2010;58(1):12-18.
- Sreekumar A, Poisson LM, Rajendiran TM, et al. Metabolomic profiles delineate potential role for sarcosine in prostate cancer progression. Nature. 2009;457(7231):910.
- Allen RH, Stabler SP, Lindenbaum J. Serum betaine, N, N-dimethylglycine and N-methylglycine levels in patients with cobalamin and folate deficiency and related inborn errors of metabolism. Metabolism. 1993;42(11):1448-1460.
- Steenkamp DJ, Husain M. The effect of tetrahydrofolate on the reduction of electron transfer flavoprotein by sarcosine and dimethylglycine dehydrogenases. Biochem J. 1982;203(3):707-715.
- MacMillan L, Lamarre SG, daSilva RP, Jacobs RL, Brosnan ME, Brosnan JT. Riboflavin Deficiency in Rats Decreases de novo Formate Production but Does Not Affect Plasma Formate Concentration. J Nutr. 2017;147(3):346-352.
- Blom W, Fernandes J. Folic acid dependent hypersarcosinaemia. Clin Chim Acta. 1979;91(2):117-125.
- Luka Z, Mudd SH, Wagner C. Glycine N-methyltransferase and regulation of S-adenosylmethionine levels. J Biol Chem. 2009;284(34):22507-22511.
- Scriver CR, Beaudet AL, Sly WS, et al. Metab Molec Bases Inherited Disease, 4 Volume Set. McGraw-Hill Professional Publishing; 2000.
- Hashimoto K. Glycine transporter inhibitors as therapeutic agents for schizophrenia. Recent Patents CNS Drug Discovery. 2006;1(1):43 53.
- Gropper S SJ, Groff J. Adv Nutr Human Metab. 5th ed. Belmont, CA: Wadsworth, Cengage Learning; 2009.
The clinical significance of low sarcosine is unknown. This group of markers relates to the intake of meat, poultry and fish, and may be decreased in vegetarians/vegans.
Elevated sarcosine may be seen with methyl donor supplementation.
Dietary intake of sarcosine-rich foods (i.e. eggs, legumes, nuts, and meats) and environmental sources (i.e. toothpaste, creams, and soaps) may result in elevated levels.
Nutrient cofactor deficiencies within the methylation cycle (folate, vitamin B12, and vitamin B2) can contribute to elevated levels.
In fact, folate therapy has been used to normalize sarcosine. Upregulation or a SNP in the GNMT enzyme within the methylation cycle may contribute to sarcosine elevations. Sarcosine has no known toxicity, as evidenced by the lack of phenotypic expression of inborn errors of sarcosine metabolism.
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