Vanilmandelic Acid

Optimal Result: 0.4 - 3.6 mmol/mol creatinine.

Vanilmandelic acid (VMA) is formed in the liver by the oxidation of 3-methoxy-4-hydroxyphenylglycol.

As a downstream metabolite of tyrosine-derived catecholamines, levels of VMA can reflect the overall synthesis and metabolism of catecholamines.

Whether norepinephrine or epinephrine are metabolized into VMA or 3-methoxy-4-OH-phenylglycol (MHPG) depends on the presence and specificity of various available aldehyde reductase and dehydrogenase enzymes.


- Eisenhofer G, Kopin IJ, Goldstein DS. Catecholamine Metabolism: A Contemporary View with Implications for Physiology and Medicine. Pharmacol Rev. 2004;56(3):331.

- Kopin IJ. Evolving views of the metabolic fate of norepinephrine. Endocrinol Exp. 1982;16(3-4):291-300.

- Maas J. MHPC: Basic Mech Psychopathol. Academic Press; 2012.

- Grouzmann E, Lamine F. Determination of catecholamines in plasma and urine. Best Pract Res Clin Endocrinol Metab. 2013;27(5):713-723.

- Alam N, Wasi N, Naeem S, et al. Methylphenidate increases the urinary excretion of vanillylmandelic acid in rats that is attenuated by buspirone co-administration. Pak J Pharm Sci. 2019;32(2 (Supplementary)):895-898.

- Garvey MJ, Noyes R, Jr., Woodman C, Laukes C. The association of urinary 5-hydroxyindoleacetic acid and vanillylmandelic acid in patients with generalized anxiety. Neuropsychobiology. 1995;31(1):6-9.

- Williams CM, Greer M. Homovanillic Acid and Vanilmandelic Acid in Diagnosis of Neuroblastoma. JAMA. 1963;183(10):836-840.

- Sunderman FW, Jr. Measurements of Vanilmandelic Acid for the Diagnosis of Pheochromocytoma and Neuroblastoma. Am J Clin Pathol. 1964;42(5):481-497.

- Gregianin L, McGill A, Pinheiro C, Brunetto A. Vanilmandelic acid and homovanillic acid levels in patients with neural crest tumor: 24-Hour urine collection versus random sample. Ped Hematol Oncol. 2009;14:259-265.

- Januszewicz W, Wocial B. Urinary excretion of catecholamines and their metabolites in patients with renovascular hypertension. Jap Heart J. 1978;19(4):468-478.

- Helin P, Kuoppasalmi K, Laakso J, Harkonen M. Human urinary biogenic amines and some physiological responses during situation stress. Int J Psychophysiol. 1988;6(2):125-132.

- Brantley PJ, Dietz LS, McKnight GT, Jones GN, Tulley R. Convergence between the Daily Stress Inventory and endocrine measures of stress. J Consult Clin Psychol. 1988;56(4):549-551.

- Dikanovic M, Kadojic D, Demarin V, et al. The effect of stress hormones on cerebral hemodynamics in patients with chronic posttraumatic stress disorder. Acta Clin Croat. 2009;48(4):405-411.

- Pequignot JM, Peyrin L, Mayet MH, Flandrois R. Metabolic adrenergic changes during submaximal exercise and in the recovery period in man. J Appl Physiology. 1979;47(4):701-705.

- Takeda A. Manganese action in brain function. Brain Res Rev. 2003;41(1):79-87.

- Ai LB, Chua LH, New AL, et al. Urinary homovanillic acid (HVA) and vanillymandelic acid (VMA) in workers exposed to manganese dust. Biol Trace Elem Res. 1998;64(1-3):89-99.

- Chen P, Chakraborty S, Mukhopadhyay S, et al. Manganese homeostasis in the nervous system. J Neurochem. 2015;134(4):601-610.

What does it mean if your Vanilmandelic Acid result is too high?

Centrally-acting medications, such as antidepressants and stimulants used for ADHD can elevate overall catecholamines and therefore urinary metabolites.

Urinary levels have been shown to correlate with generalized anxiety disorder.

VMA is sometimes used in the work up of pheochromocytoma, neural crest tumors, renovascular hypertension, and neuroblastoma in the right clinical context.

Elevations in catecholamine urinary metabolites have been shown to correlate with the physiologic stress response, exercise, and PTSD.

What does it mean if your Vanilmandelic Acid result is too low?

Low levels of catecholamine metabolites can reflect insufficient amino acid precursors for neurotransmitter production, nutrient cofactor insufficiencies for enzymatic conversion, and genetic abnormalities in enzyme function. Methylation is required for neurotransmitter creation and metabolism. Thus, methylation defects or lack of methylation cofactors may contribute to abnormal levels. Copper is an important cofactor for dopamine beta-hydroxylase, which forms norepinephrine from dopamine. In copper deficiency, norepinephrine formation can be impaired and potentially lower VMA levels. Manganese released into the synaptic cleft may influence synaptic neurotransmission. Dietary manganese deficiency, which may enhance susceptibility to epileptic functions, appears to affect manganese homeostasis in the brain, probably followed by alteration of neural activity.

There are studies which evaluate the neurotoxicity of manganese. Elevated levels of VMA and HVA have been seen in manganese toxicity from occupational exposure which induces a CNS condition similar to Parkinson’s disease.

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