PEA & The Case for Chocoholics

Chocolate bar

The Case for Chocoholics by Tom Rayhawk

Extending beyond the multitude of delectable forms that this manna of candy exists in, the tickling of your taste buds and heart racing effects are only part of the story of this cocoa-derived treat. Containing antioxidants, phytonutrients and blood-pressure reducing compounds, chocolate does not fit nicely under the category of “empty calories” inherent to most sugar-laden food. One compound, in particular, is associated with the addictive and mood-elevating characteristics that many feel after consuming chocolate. This constituent is phenylethylamine or PEA.

Although relatively simple in its chemical structure, PEA influences a great number of neurotransmitter and hormonal systems. Noradrenergic, Dopaminergic and Acetylcholinergic receptors all show binding affinity to and are impacted by phenylethylamine. The underlying behavioral ramifications of this interaction are divergent and include anorexic, or appetite suppression, anti-depressant and mood enhancement, and elevation in attention and overall cognition. However, abnormally high concentrations of PEA have been associated with schizophrenic-like behavior, anxiety, and insomnia. The complex process of addiction also implicates PEA as a culprit. Humans manufacture beta-phenylethylamine via the removal of a carboxyl group (CO2) from l-phenylalanine by phenylalanine decarboxylase (3). As a biogenic amine, PEA shares some chemical characteristics with amino acids, namely that it contains an amine or –NH2 constituent attached to the phenyl group. Unlike amino acids, however, PEA does not have the carboxylic group (-CO2H) in its backbone. Following synthesis, the amine has a very short half-life as it is not stored in neurons and is subject to rapid degradation by monoamine oxidase b (MAO-b) and – in the liver – by aldehyde dehydrogenase and aldehyde oxidase (10). It is oxidized by these enzymes to phenylacetic acid and 2-phenylethanol via the intermediate, phenylacetaldehyde. The “aldehydes” are at work in the periphery meaning that when using an oral route of administration, your PEA has to make it past these enzymes before it can reach the brain. Present in the mitochondria of the gut, mao-b enzymes are another obstacle to PEA entry into the central nervous system. So as you can see, supplements containing phenylethylamine have to somehow circumvent these pathways for one to garner its effects. As with all trace amines, beta-phenylethylamine, is naturally present in small quantities in humans and is found in highest concentrations in the hypothalamus (2). The hypothalamus is the “thermostat” of many regulatory systems including satiety. Specific receptors here, the (+)-[3H] amphetamine binding sites, binds to amphetamine, PEA and phenylethylamine related compounds. Upon binding, a decrease in self-regulated feeding occurs. Interestingly, glucose also binds to these receptors indicating that glucose flux through the hypothalamus is mimicked by PEA and thus satisfies the “glucostatic” or “fed” signal to this drive-oriented brain region (1). In short, PEA “tricks” the brain into thinking glucose levels are abundant, food seeking behaviors are not warranted, and hunger levels thus decrease. PEA is a psychomotor stimulant meaning that it positively enhances the interplay between motor – or muscular – and mental activities or processes. A slowing in this process is typical of depressive disorders. This psychomotor activation, some research supports, is one of the driving forces behind addictive behaviors. A specific pathway of dopaminergic neurons present in the midbrain, limbic, cortical regions, nucleus accumbens, and amygdala of the brain is altered during self-reinforcing activities (13). These regions, termed the mesocorticolimbic system, are the “drive” centers of the brain that function in incentive motivation and reward. Alcohol, barbiturates, nicotine, opiates, benzodiazepines, marijuana and yes, psychomotor stimulants, (i.e. PEA) all trigger this pathway (11, 12). By prolonging the activity and levels of dopamine and other neurotransmitters, PEA can produce changes in the motivational pathways making an individual more prone to drug-seeking behaviors. These pathways are actually very similar to those that mature during memory formation and the learning process. Glutamate is the major excitatory neurotransmitter in the brain and alterations occur in its expression and in neurons to which it binds when these rewarding habits or new skills are developing (15). PEA’s ability to enhance cognition and concentration are evident by the amine’s positive relationship in those treated for attention-deficit disorder (ADD) and attention-deficit with hyperactivity disorder (ADHD). One method used to gage the levels of phenylethylamine in the blood is to measure the amount excreted in the urine. PEA levels in urine have been shown to be significantly lower in those with ADHD than in control subjects (4, 5, 6). Japanese researcher Kusaga and colleagues have published many works supporting this. In one of their studies from 2002 they administered methylphenidate – Ritalin – to subjects and deduced that one of the underlying differences was that responders to the drug had elevated beta-phenylethylamine compared to non-responders (4).

Dopamine (DA) is undoubtedly the neurotransmitter most impacted by PEA. Many of PEA’s functions are attributed to its capacity to augment dopamine function. The most straightforward evidence of this is that PEA directly increases dopamine release (8,9). Typically, dopamine is released by neurons to exert its biological activity and is taken back by these same cells via the dopamine transporter (DAT) leading to its inactivation. One of the means by which both cocaine and amphetamine work is by displacing this transporter, thus prolonging the activity of dopamine (14).

Initially, it was thought that PEA worked similarly. However this hypothesis has been called into question by recent studies which demonstrated that when exogenous dopamine is applied that PEA does not enhance dopaminergic activity (7,8). This might seem confusing but this simply means that PEA does not enhance the effects of dopamine already active within the human nervous system. It does, however, promote its secretion and it generates many of the same actions as DA. Instead, a new theory has evolved showing that PEA interacts with autoreceptors on certain portions of dopaminergic neurons, increasing the secretion of DA. Essentially, PEA “turns on” certain portions of the cells that release dopamine, leading to a greater than normal DA pool. PEA and other trace amines co-exist with dopamine and are released from dopaminergic neurons of the nigrostriatal system. It thus follows that PEA shares many of the same similar physiological actions as dopamine. Its structure bears great resemblance to amphetamine and as one might deduce, it shares many of the same characteristics including an increase in motor activity and anorexic tendencies.


1.Itzchak Angel, Richard L. Hauger, My Do Luu, Bridget Giblin, Phil Skolnick, Steven M. Paul. Glucostatic Regulation of (+)-[3H]amphetamine binding in the Hypothalamus: Correlation with Na{+},K{+}-ATPase Activity. Proceedings of the National Academy of Sciences of the United States of America, Vol. 82, No. 1. 8 (Sep. 15, 1985), pp. 6320-6324 2.A. J. Greenshaw, A. V. Juorio and T. V. Nguyen. Depletion of striatal â-phenylethylamine following dopamine but not 5-HT denervation. Brain Research Bulletin, Volume 17, Issue 4, October 1986, Pages 477-484. . 3. Sidney Udenfriend and Jack R. Cooper. Assay of l-phenylalanine as phenylethylamine after enzymatic decarboxylation; Application to isotopic studies. J Biol Chem. 1953 Aug;203(2):953-60. 4.Kusaga A, Yamashita Y, Koeda T, Hiratani M, Kaneko M, Yamada S, Matsuishi T. Increased urine phenylethylamine after methylphenidate treatment in children with ADHD.Ann Neurol 2002 Sep;52(3):372-4 5. Kasuga A. Decreased beta-phenylethylamine in urine of children with attention deficit hyperactivity disorder and autistic disorder. No To Hattatsu. 2002 May;34(3):243-8 6. Baker GB, Bornstein RA, Rouget AC, Ashton SE, van Muyden JC, Coutts RT.. Phenylethylaminergic mechanisms in attention-deficit disorder. Biol Psychiatry 1991 Jan 1;29(1):15-22 7. Geracitano R, Federici M, Prisco S, Bernardi G, Mercuri NB. Inhibitory effects of trace amines on rat midbrain dopaminergic neurons. Neuropharmacology. 2004 May;46(6):807-14 8. Mauro Federici, Raffaella Geracitano, Alessandro Tozzi, Patrizia Longone, Silvia Di Angelantonio, C. Peter Bengtson, Giorgio Bernardi, and Nicola B. Mercuri. Trace Amines Depress GABAB Response in Dopaminergic Neurons by Inhibiting G–Gated Inwardly Rectifying Potassium Channels. Mol Pharmacol 67:1283-1290, 2005.… 9. Kota Ishida, Mikio Murata, Nobuyuki Katagiri, Masago Ishikawa, Kenji Abe, Masatoshi Kato, Iku Utsunomiya, and Kyoji Taguchi. Effects of -Phenylethylamine on Dopaminergic Neurons of the Ventral Tegmental Area in the Rat: A Combined Electrophysiological and Microdialysis Study. Journal of Pharmacology And Experimental Therapeutics. 314:916-922, 2005. 10. Panoutsopoulos GI, Kouretas D, Gounaris EG, Beedham C. Metabolism of 2-phenylethylamine and phenylacetaldehyde by precision-cut guinea pig fresh liver slices. Eur J Drug Metab Pharmacokinet. 2004 Apr-Jun;29(2):111-8.… 11. Terry E Robinson, Kent C Berridge (2000) The psychology and neurobiology of addiction: an incentive-sensitization view Addiction 95 (8s2), 91–117. 12. Pan, Wynn H. T., Hsieh, Min-Chien, Wu, Hsiao-Hua & Lin, Shi-Kwang Difference in magnitude of psychostimulant-induced extracellular norepinephrine in the ventral tegmental area contributes to discrepant prefrontal dopamine outflow. Addiction Biology 12 (1), 51-58. 13. Kalivas PW, Nakamura M (1999) Neural systems for behavioral activation and reward. Curr Opin Neurobiol 9:223–227. 14. Jones SR, Joesph JD, Barak LS, Caron MG, Wightman RM (1999) Dopamine neuronal transport kinetics and effects of amphetamine. J Neurochem 73:2406–2414.

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