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Researchers at Rush University and the Center for Creative Development in Chicago conducted a study demonstrating PEA’s anti-depressant effects:

“Phenylethylamine (PEA), an endogenous neuroamine, increases attention and activity in animals and has been shown to relieve depression in 60% of depressed patients. It has been proposed that PEA deficit may be the cause of a common form of depressive illness. Fourteen patients with major depressive episodes that responded to PEA treatment (10-60 mg orally per day were reexamined 20 to 50 weeks later. The antidepressant response had been maintained in 12 patients. Effective dosage did not change with time. There were no apparent side effects. PEA produces sustained relief of depression in a significant number of patients, including some unresponsive to the standard treatments.”

1) Sabelli H; Fink P; Fawcett J; Tom C. Sustained antidepressant effect of PEA replacement. J Neuropsychiatry Clin Neurosci, 1996 Spr, 8:2, 168-71.

In the book Natural Remedies for Depression by Donald Brown, N.D., Alan R. Gaby, M.D., and Ronald Reichert, N.D., the L form of phenylalanine is discussed:

“L-Phenylalanine, the naturally occurring form of phenylalanine, is converted in the body to L-tyrosine. D-phenylalanine, which does not normally occur in the body or in food, is metabolized to phenylethylamine (PEA), a compound that occurs normally in the human brain and has been shown to have mood-elevating effects. Decreased urinary levels of PEA (suggesting a deficiency) have been found in some depressed patients.7 Although PEA can be synthesized from L-phenylalanine, a large proportion of this amino acid is preferentially converted to L-tyrosine. Dphenylalanine is therefore the preferred substrate for increasing the synthesis of PEA—although L-phenylalanine would also have a mild antidepressant effect because of its conversion to L-tyrosine and its partial conversion to PEA. Because D-phenylalanine is not widely available, the mixture D,L-phenylalanine is often used when an antidepressant effect is desired."

Hector Sabelli, MD, PhD, studied PEA while a professor at Chicago’s Rush University. Now director of the Chicago Center for Creative Development, Sabelli says that the new findings fit exactly with all of his own experiments.

“What we have seen is that PEA metabolism is reduced in people who are depressed,” Sabelli tells WebMD. “If you give PEA to people with depression, about 60% show an immediate recovery -- very fast, a matter of half an hour.”

So what about the natural substances called endorphins, which have previously been linked to runners’ high? Billett says that endorphins don’t penetrate the brain as easily as PEA does -- so she thinks PEA may be the true basis for the good mood one gets from a workout. Sabelli is not so quick to rule out endorphins, however, and says that the natural compounds probably interact in various ways. “We think PEA is part of the reward of exercise,” Billett says, adding that it might be affecting other brain chemicals and that it’s likely there are normal differences between individuals. “Some will respond to exercise, some won’t.”

The "Love Molecule" (PEA) is Safe.
Research Abstract from the Centre for Molecular Design in Beerse, Belgium: “...Despite its short half-life, phenylethylamine attracts attention since it can potentiate catecholaminergic neurotransmission and induce striatal hyperreactivity. Subnormal phenylethylamine levels have been linked to disorders such as attention deficit and depression; the use of selegiline (Deprenyl) in Parkinson’s disease may conceivably favor recovery from deficient dopaminergic neurotransmission by a monoamine oxidase-B inhibitory action that increases central phenylethylamine. . The importance of phenylethylamine in mental disorders is far from fully elucidated but the evolution of phenylethylamine concentrations in relation to symptoms remains a worthwhile investigation for individual psychotic patients.

PEA Replacement
In a 1996 study, the effects of phenylethylamine (PEA) replacement were studied. It was found that PEA, an endogenous neuroamine, increased attention and activity in animals and has been shown to relieve depression in 60% of depressed patients. It has been proposed that PEA deficit may be the cause of a common form of depressive illness. Fourteen patients with major depressive episodes that responded to PEA treatment (10-60 mg orally per day, with 10 mg/day selegiline to prevent rapid PEA destruction) were reexamined 20 to 50 weeks later. The antidepressant response had been maintained in 12 patients. Effective dosage did not change with time. There were no apparent side effects. PEA produces sustained relief of depression in a significant number of patients, including some unresponsive to the standard treatments. PEA improves mood rapidly but does not produce tolerance.

ADHD & PEA Human Studies
In a number of controlled studies, by measuring urinary excretion levels, PEA was found to be significantly lower in children with ADHD and LD (learning disability). A decreased level of PEA is considered to potentially play an important role for the pathogenesis of LD and ADHD.2 Beta-phenylethylamine (b-PEA), a biogenic trace amine, acts as a neuromodulator in the nigrostriatal dopaminergic pathway and stimulates the release of dopamine.

Animal Studies
In a number of animal studies, neurotransmitters were shown to be depressed. Trace amines (TAs) are present in the central nervous system in which they up-regulate catecholamine release and are implicated in the pathogenesis of addiction, attentiondeficit/ hyper-activity disorder, Parkinson’s disease, and schizophrenia.