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Functional Assessment of Urinary Neuro-biogenic Amines—A COMPREHENSIVE GUIDE 

115

Phenylethylamine (PEA)

P h e n y l e t h y l a m i n e

(B-phenylethylamine or PEA) is one of

several trace amines present in the cen-

tral nervous system at low (nanomolar)

concentrations. The interaction of trace

amines, and their receptors, in the brain

may play a role in psychiatric and neuro-

logical disease processes. Experimental

evidence suggests that dysregulation of

trace amines may alter levels of dopa-

mine, norepinephrine or serotonin, and

thereby contribute to neuropsychiatric

disorders such as attention deficit hyper-

activity disorder (ADHD), schizophre-

nia, depression and neurodegenerative

diseases. PEA may potentiate neuron

responses to dopamine and norepineph-

rine. PEA excretion may be influenced

by diurnal rhythms; larger amounts are

excreted during the late evening and

early morning hours. Clinically, trace

amines are generally considered sym-

pathomimetic (they mimic the action

of sympathetic nerve stimulation), they

may affect vasoconstriction and blood

pressure. In large, supra-physiologic dos-

es, the effects of trace amines are similar

to amphetamines.

Effects:

Decreased

PEA levels have been as-

sociated with Parkinson’s disease, de-

pression, attention deficit hyperactivity

disorder (ADHD) and autism. In stud-

ies of ADHD patients, low levels of the

precursor amino acid phenylalanine or

decreased activity of aromatic L-amino

acid decarboxylase (AADC), the en-

zyme that converts phenylalanine into

PEA, may decrease PEA levels. AADC

requires pyridoxal phosphate (vitamin

B6) as a cofactor. Reserpine may deplete

CNS levels of trace amines.

Excess

PEA may occur due to sup-

plementation. Elevated PEA levels have

been reported during the use of mono-

amine oxidase inhibitors (MAOIs)

or antipsychotic medications. Excess

PEA may be the only clue to mono-

amine oxidase B (MAO-B) deficiency.

Experiments in humans and animals

associate PEA elevations with stress or

anxiety. Elevations in PEA may con-

tribute to anxiety disorders (animal

studies). Very high levels may have am-

phetamine-like effects, and may induce

seizures (animal studies). Patients with

hypertension or bone disease may have

elevated PEA levels. Exercise or high

protein diets may also increase PEA

levels. Inhibition of PEA catabolism

(breakdown) has been associated with

schizophrenia, as have elevated lev-

els of PEA. Increased urinary excretion

of PEA has been observed in paranoid

schizophrenia.

PEA may be naturally occurring in

plant foods, or may be incorporated

into foods through deliberate bacteri-

al fermentation. Trace amines may be

generated in the gastrointestinal tract

by protein-fermenting gut bacteria af-

ter a protein-rich meal, and they may

be found in a variety of foods as the re-

sult of food spoilage or fermentation.

Dietary trace amines are usually metab-

olized quickly by MAO enzymes. PEA is

preferentially oxidized by MAO-B, and

may be the only elevated urinary bio-

marker if MAOB is deficient. Dietary

PEA is able to cross the blood brain

barrier into the CNS. Elevated levels of

trace amines may occur due to phenyl-

ketonuria (PKU), ergot poisoning or the

use of medications such as MAO inhib-

itors (MAOIs).