Review articles

By Ms. Meredith Irsfeld , Mr. Matthew Spadafore , Dr. Birgit Pruess
Corresponding Author Ms. Meredith Irsfeld
North Dakota State University, - United States of America
Submitting Author Dr. Birgit Pruess
Other Authors Mr. Matthew Spadafore
North Dakota State University, - United States of America

Dr. Birgit Pruess
North Dakota State University, Fargo ND 58108 - United States of America 58108


neurotransmitter, antimicrobial, food spoilage

Irsfeld M, Spadafore M, Pruess B. A-phenylethylamine, a small molecule with a large impact. WebmedCentral BIOCHEMISTRY 2013;4(9):WMC004409
doi: 10.9754/journal.wmc.2013.004409

This is an open-access article distributed under the terms of the Creative Commons Attribution License(CC-BY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Click here
Submitted on: 28 Sep 2013 06:31:08 PM GMT
Published on: 30 Sep 2013 07:42:44 AM GMT


During a screen of bacterial nutrients as inhibitors of Escherichia coli O157:H7 biofilm, the Pruβ research team made an intriguing observation: among 95 carbon and 95 nitrogen sources tested, β-phenylethylamine (PEA) performed best at reducing bacterial cell counts and biofilm amounts, when supplemented to liquid beef broth medium (Lynnes et al., 2013a). This review article summarizes what is known about PEA.

After some starting information on the chemistry of the molecule, we focus on PEA as a neurotransmitter and then move on to its role in food processing. PEA is a trace amine whose molecular mechanism of action differs from biogenic amines, such as serotonin or dopamine. Especially low or high concentrations of PEA may be associated with specific psychological disorders. For those disorders that are characterized by low PEA levels (e.g. attention deficit hyperactivity disorder), PEA has been suggested as a ‘safe’ alternative to drugs, such as amphetamine or methylphenidate, which are accompanied by many undesirable side effects. On the food processing end, PEA can be detected in food either as a result of microbial metabolism or thermal processing. PEA’s presence in food can be used as an indicator of bacterial contamination.


ß-phenylethylamine (PEA) is a small molecule that exhibits an array of intriguing and seemingly unrelated functions. The purpose of this review is to summarize general information about PEA, as well as detailing a selection of the functions, namely its role as a neurotransmitter and in food processing. General information is summarized in Chapter I, including the chemical properties of PEA (1.1), its natural occurrence and biological synthesis (1.2), and its chemical synthesis (1.3). Chapter II describes PEA’s functions as a neurotransmitter and details its impact on attention deficit hyperactivity disorder (2.1), depression (2.2), and schizophrenia (2.3) as three examples of psychological disorders. A comparison of PEA’s action to that of other trace and biogenic amines is provided (Illustration 3). Finally, Chapter III describes the role of PEA in food processing, starting with its occurrence in fermented food and meat as the result of microbial metabolism (3.1) and its occurrence in chocolate as the result of thermal processing (3.2). The article concludes with the recently described use of PEA as an antimicrobial to be used in the processing of beef meat (3.3).

Throughout this manuscript, we mention companies that sell PEA. We are not in any way affiliated with any of these and do not mean to discriminate. The list of companies is incomplete and exemplary.


I.General Information

1.1 Chemical Properties of PEA

PEA is known under a variety of names including ?-phenylethylamine, ?-phenethylamine, and phenylethylamine. According to the International Union of Pure and Applied Chemistry (IUPAC), the proper name of PEA is 2-phenylethylamine. Its molecular formula is denoted by C8H11N.

The general information on and the chemical properties of PEA are summarized in Illustration 1. Briefly, PEA has a molecular weight of 121.17964 g/mol, a high solubility in ddH2O (Cashin, 1972; Shannon et al., 1982), and a short half life (Shannon et al., 1982). These chemical characteristics impact PEA’s biological functions. In particular, the lack of a methyl group distinguishes PEA from its structural relative amphetamine:

1.2 Natural Occurrence and Biological Synthesis of PEA

The occurrence of PEA and its derivatives has previously been reviewed  (Bentley, 2006). PEA can be found in many algae (Guven et al., 2010), fungi and bacteria (Kim et al., 2012) as well as a variety of different plant species (Smith, 1977). PEA is the decarboxylation product of phenylalanine.

In several bacterial species, the above reaction is catalyzed by the enzyme tyrosine decarboxylase, which also converts tyrosine to another trace amine, tyramine (Marcobal et al., 2012; Pessione et al., 2009). Intriguingly, PEA synthesized by fungi and bacteria can also be found in food products (Onal et al., 2013), where it serves an indicator of food quality and freshness. This includes the Korean natto (Kim et al., 2012) and commercial eggs (Figueiredo et al., 2013). Another food that contains PEA is chocolate, where it is not produced by bacteria, but during the thermal processing of cocoa (Granvogl et al., 2006). As one example of PEA in plants, PEA can be found in members of the family Leguminosae, which is the second-largest family of seed plants and is comprised of trees, shrubs, vines, herbs (such as clover), and vegetables (such as beans and peas). The various different species found within this family have been used as food, green manure, and for medicinal purposes (Sanchez-Blanco et al., 2012). A hypothesis was formulated that plant synthesized PEA may serve as a defense mechanism against insects and foraging animals (Smith, 1977).

PEA has also been found in the brains of humans and other mammals (Paterson et al., 1990; Philips et al., 1978), which is facilitated by its high solubility in plasma and its ability to cross the blood-brain barrier (Oldendorf, 1971). Like its ?-methylated derivative, amphetamine, PEA has stimulant effects which lead to the release of so called biogenic amines, including dopamine and serotonin (Bailey et al., 1987; Rothman & Baumann, 2006). Unlike amphetamine, PEA has difficulties maintaining high concentrations in the human body, due to its oxidative deamination to phenylacetic acid by the enzyme B monoamine oxidase (MAO) (Yang & Neff, 1973). Phenylacetic acid,has an effect that is similar to the activity of the natural endorphins, an effect that is known as a “runner’s high”.

Due to its impact on the levels of several ‘feel good hormones’ (see above), PEA has recently gained popularity as a nutritional supplement that is sold by numerous health stores to improve mood. Since it also decreases the amount of water intake, it aids weight loss efforts (Hoffman et al., 2006). Naturodoc describes PEA as “an immediate shot of happiness, pleasure, and emotional wellbeing” (, Serenity Station describes the effects of PEA as “feeling happier, more alive and even having a better mood and attitude” ( Altogether, PEA appears to have a number of positive effects on human health without the risks of its structural relatives.

1.3 Chemical Synthesis of PEA

Two different pathways that lead to the chemical synthesis of PEA have been established in the 40s and 50s of the past century. First, PEA is produced by reduction of a nitrile into an amine (Robinson & Snyder, 1955). Specifically, 1 kg of benzyl cyanide is mixed with 1 tablespoon of the Raney-Nickel catalyst in a calorimeter bomb. The formation of secondary amines in this reaction is reduced by the addition of ammonia. The reaction occurs at 13.9 Mpa and 130oC under hydrogen, the cooled down liquid is removed from the catalyst by filtration. This procedure has a yield of about 860 to 890 g of PEA, equaling 83 to 87%. 

A second, simpler way of producing PEA is to reduce w-nitrostyrene with lithium aluminum hydride in ether (Nystrom & Brown, 1948). The experimental procedure that employs the use of lithium aluminum in reduction reactions follows the mechanism used in a Grignard synthesis. w-nitrostyrene is added to the previously prepared lithium aluminum hydride in ether while stirring. This results in an alcoholate precipitate, which thickens the solution requiring more ether to be added. Finally, using acid hydrolysis the metal alcoholate is decomposed and the product can be isolated and extracted from the ether.

Recent literature focuses on the biological synthesis of PEA, rather than the chemical one. 1-phenylethylamine can be synthesized by Escherichia coli overexpressing ?-transaminase (Cardenas-Fernandez et al., 2012). Likewise, the PEA biosynthetic enzyme from Enterococcus faecium can be expressed in E. coli, which leads to large amounts of L-phenylalanine and tyrosine decarboxylase activity (Marcobal et al., 2006). Intriguingly, PEA can serve as a substrate for the synthesis of other drugs, such as sulfonamides that are being used as anti-microbials (Rehman et al., 2012).

II.  PEA as a Neurotransmitter

PEA is a member of the so called trace amines (reviewed by Premont et al., 2001). The expression ‘trace amine’ is used to refer to a group of amines that occur at much lower intra- and extra-cellular concentrations than the chemically and functionally related biogenic amines and neurotransmitters epinephrine, norepinephrine, serotonin, dopamine, and histamine. The molecular mechanism of the trace amines involves binding to a novel G protein-coupled receptor, called TAAR (trace amine-associated receptor) (Borowsky et al., 2001; Bunzow et al., 2001), the most studied of which, TAAR1, can be activated by the drug amphetamine as well (Borowsky et al., 2001). The downstream events that follow the initial interaction of PEA and TAAR1 are not nearly as well understood as the receptors and their various ligands themselves (Zucchi et al., 2006), it is however believed that binding of PEA to TAAR1 results in an alteration of the monoamine transporter functions, which leads to inhibition of the re-uptake of dopamine, serotonin, and norepinephrine (Xie & Miller, 2008). Eventually, this will cause an increased concentration of these neurotransmitters at the synapses. A similar increase in the synaptic concentrations of dopamine can be accomplished by blocking the dopamine transporter directly. Methylphenidate is an example of a class of drugs that can perform this blockage (Gatley et al., 1999).

The chemical properties of the biogenic amines, trace amines, and structurally related drugs are summarized in Illustration 2. Illustration 3 is a graphic representation of the regulatory pathway from the trace amine PEA to the increased concentration of the biogenic amines and neurotransmitters dopamine and serotonin. The effects of the drugs amphetamine and methylphenidate are included. Chapter II summarizes the impact of PEA on three psychological disorders, attention deficit hyperactivity disorder, depression, and schizophrenia.

2.1 Attention deficit hyperactivity disorder

A common disease that an estimated 4-9% of young children suffer from is attention deficit hyperactive disorder (ADHD) (reviewed by (Cormier, 2008).  ADHD is a chronic child hood disorder which is characterized by a number of behavioral symptoms, including a small attention span, increased frustration, distractibility, and often depression and anxiety (American Psychiatric Association, 2000). ADHD often is paralleled by co-existing psychiatric disorders and patients can have problems that are attributable to ADHD way into their adulthood (Brassett-Harknett & Butler, 2007). While diagnosis of ADHD is usually done by analysis of the symptoms (American Psychiatric Association, 2000), PEA was recently described as a biomarker for ADHD (Scassellati et al., 2012). This novel discovery will improve the confidence of the diagnostic efforts, possibly leading to reduced misdiagnosis and overmedication. Specifically, the urinary output of PEA was lower in a population of children suffering from ADHD, as compared to the healthy control population, an observation that was paralleled by reduced PEA levels in ADHD individuals (Baker et al., 1991; Kusaga, 2002). In a consecutive study (Kusaga et al., 2002), those of the children suffering with ADHD were treated with methylphenidate, also known as Ritalin. Patients whose symptoms improved in response to treatment with methylphenidate had a significantly higher PEA level than patients who did not experience such an improvement in their condition (Kusaga et al., 2002).

While this is encouraging by the first view, amphetamine and methylphenidate based drugs demonstrate many undesirable side effects, including mild headaches, nausea, insomnia, and constipation. Overdose, whether accidental or intentional, of any of the amphetamine of methylphenidate drugs has been associated with cardiovascular effects, which was attributed to increased levels of extracellular dopamine, norepinephrine, and serotonin (Spiller et al., 2013). While the connection between stimulant drugs as a treatment for ADHD and cardiovascular disease at this time still appears controversial (Olfson et al., 2012), naturopathic professionals have started to recommend PEA as a treatment for ADHD because of the assumed lack of side- and long-term effects (for an example, see resources/Documents/Phenylethylamine).

2.2 Depression

Depression is a very common, sometimes serious disease that affects a wide range of people. It is currently the second leading cause of disability in the age group of 15 to 44. By the year 2030, depression is predicted to be the primary cause of disability (World Health Association, 2008).  While depression may be most common in the age group of 15 to 44, it can affect people of all ages and backgrounds. Among the characteristics of depression that were summarized in a review article (Voinov et al., 2013), women are 50%  more likely to be affected  by depression than  men and depression can shorten a person’s life by 25-30 years (Voinov et al., 2013). 

Most medication that is currently available is about 80% effective for those suffering from depression (Voinov, 2013).  Selective serotonin re-uptake inhibitors (SSRI) are the most popular antidepressant prescribed worldwide (Artigas, 2013).  SSRI function by blocking the serotonin transporter and thus inhibiting the re-uptake of serotonin (Gutman & Owens, 2006; Peremans et al., 2006). This will result in an increase of the synaptic concentration of serotonin (see Illustration 3). However, SSRI act very slowly at the beginning of the treatment, while exhibiting a range of side effects upon long term use. These long-term side effects include insulin resistance (Chen et al., 2012), bone density loss (Haney et al., 2007), and  some poorly understood effects on the offspring of mothers with maternal depression (Olivier et al., 2013). Overall, the question has been raised where to go from here (Artigas, 2013) and a need for the novel approaches to depression treatment is evident. The study by Xie and Miller (Xie & Miller, 2008), that had shown that PEA altered the serotonin transporter by interacting with TAAR, may point towards a safer alternative to SSRI treatment of depression in the form of PEA.       

2.3 Schizophrenia

Schizophrenia is rare mental disorder that could potentially be related to PEA.  About 1% of the world’s population is affected by schizophrenia, which is characterized by problematic thinking and perception (Rossler et al., 2005). Typically, schizophrenia starts around adolescence and will stay with the patient for the rest of their life, though life expectancy can be largely reduced due to suicide. An additional complication is community attitude because many people perceive schizophrenic patients as potentially dangerous (Stuart & Arboleda-Florez, 2001). 

There are different ideas on how one develops schizophrenia.  One hypothesis proposes that dopamine contributes to the development of schizophrenia (Howes & Kapur, 2009). In agreement with this hypothesis, patients suffering from schizophrenia are hyper-sensitive to drugs (e.g. methylphenidate) that block the dopamine receptor (Lieberman et al., 1987). A new perspective is given by the TAAR1 receptor (Illustration 3). TAAR1 activation improves the symptoms that are associated with both schizophrenia and depression (in rodent and primate models), without causing the range of negative effects that result from direct blockage of the dopamine receptor (Revel et al., 2013).

Among other factors that may contribute to schizophrenia are inflammatory cytokines (Zakharyan & Boyajyan, 2013) and phospholipase (Koh, 2013) . Altogether, schizophrenia may be the most complex of the here discussed psychological disorders and it is quite apparent that many factors contribute to its development.

III. PEA and other Amines in Food

PEA and other amines can be found in food as a result of two fundamentally different processes, metabolic activity of bacteria (3.1) or thermal processing of the food (3.2).  In the cases of metabolic activity, amines can be used as a marker for contamination of food by the respective bacteria. Most recently, it has been found that PEA can be added to food intentionally to reduce bacterial cell counts of E. coli O157:H7 (3.3).

3.1 PEA and other amines in food as a result of microbial contamination

Some foods that contain microorganisms can release high levels of amines, including the trace amines  PEA, tyramine,and  tryptamine, the biogenic amine histamine, and the polyamines putrescine and cadaverine (Shalaby, 1996).  Such amines are formed by bacteria of the genera Lactobacillus, Clostridium, Pseudomonas, and Enterobacteriaceae that contain amino acid decarboxylases which remove an ?-carboxyl group from the respective amino acid (Giraffa, 2003; Shalaby, 1996).   

This increased concentration of amines is due to bacterial metabolic processes and is commonly associated with foods and food products made through the process of fermentation (Bunkova et al., 2013).  A good example of this is the ‘cheese reaction’ which refers to high levels of tyramine as a result of elevated levels of tyrosine in cheese that has had increased storage times at temperatures higher than recommended by the producer. As mentioned earlier (Chapter 1.2), PEA can be a by-product of the tyrosine decarboxylase reaction because the same enzyme that is capable of converting tyrosine to tyramine can also metabolize phenylalanine to PEA (Marcobal et al., 2012). In individuals taking monoamine oxidase inhibiting drugs, the ‘cheese reaction’ can result in a hypertensive crisis (Boulton et al., 1970; Da et al., 1988; Deftereos et al., 2012).

A second group of food or food product that contains elevated levels of amines is meat and/or fish (Kulawik et al., 2013; Li et al., 2012; Liu et al., 2013), where amine production is part of the food spoilage reaction and can be used as an indicator of food freshness and quality. Specifically, bacteria from the families Enterobacteriaceae and Pseudomonadaceae can produce cadaverine and putrescine in spoiled turkey meat. It was suggested to use tyramine, putrescine, and cadaverin to quantify meat freshness (Fraqueza et al., 2012). In vegetables, high levels of tyramine were only seen in brine, unless the vegetables were contaminated prior to processing or the temperature and storage time were extreme (Moret et al., 2005).

Since elevated levels of amines are usually an indicator of food spoilage, it is possible use detection of amines as an indicator of food freshness. One such techniques is thin-layer chromatography to separate and identify amounts of tyramine and PEA (Garcia-Moruno et al., 2005).

3.2 PEA in chocolate as a result of thermal processing

The connection between “food and mood” has been recognized long time ago (Ottley, 2000). In particular, chocolate craving has been the focus of intense research (Durkin et al., 2012; Hormes & Timko, 2011; Werthmann et al., 2013). Lately, the combination of chocolate with coffee has been proposed as “a novel elixir for a long and happy life”  (Dal Moro, 2013). Besides a number of other beneficial substances (e.g. antioxidants), chocolate also contains trace amounts of PEA (Ziegleder et al., 1992), a result of the thermal processing and fermentation of cocoa (Granvogl et al., 2006). Since we mentioned earlier that PEA is promoted to aid weight loss, one may conclude that if a person eats enough chocolate they will lose weight! Careful readers: in a study that attempted to determine the concentration of PEA in chocolate, the detection limit for PEA was 3 mg/kg of chocolate and the concentration of PEA in their chocolate samples was below this limit (Pastore et al., 2005).  In contrast, the recommendation for PEA as a nutritional supplement is currently 500 mg/day (for an example, please, see http://www.bodybuilding This means that the concentration of PEA in chocolate is not high enough to induce weight loss, so eating chocolate will still lead to weight gain.

One interesting controversy around chocolate and PEA is the question whether chocolate can cause migraine and whether this may be due to PEA. Of course, food in general can trigger migraine (Finocchi & Sivori, 2012). Also, individual studies point towards chocolate as one of those foods (Fukui et al., 2008), but other studies are in contrast with these findings (Marcus et al., 1997). The fact that other foods that contain PEA, tyramine, or histamine (e.g. cheese and wine) may also trigger migraine (Werthmann et al., 2013) raised the question whether dietary amines may be responsible for this response. This question is justified, considering that PEA causes the release of nor-epinephrine into the synaptic space, which consequently constricts the aorta and the coronary arteries (Broadley et al., 2009). However, results among various studies are inconclusive (Jansen et al., 2003) and the connection between chocolate and migraines remains a mystery.

3.3 PEA as an anti-microbial

In Chapter 3.1, we discussed contamination and food spoilage by bacteria. One such initially contaminated food can cross-contaminate additional food products through the food processing chain because of  the bacteria’s ability to attach to food contact surfaces and form biofilm  (Giaouris et al., 2013). Recent research advances that are aimed at the prevention of biofilm formation include the manipulation of the bacteria’s bacterial signal transduction pathways, including quorum sensing (Bassler, 2010) and two-component signaling (Lynnes et al., 2013b). One such environmental signal that bacteria can respond to is PEA, whose signal transduction pathway may include the flagellar and global regulator complex FlhD/FlhC (Stevenson et al., 2013). In our own research lab, PEA was found to be most inhibitory of the 95 carbon and 95 nitrogen sources screened for their effect on E. coli O157:H7 growth, bacterial cell counts, and biofilm amounts. Bacterial cell counts of E. coli O157:H7 were determined from beef meat pieces that were treated with different dilutions of PEA and subsequently inoculated with the bacteria; this resulted in a 90% reduction of bacterial cell counts when the beef was treated with a concentration of PEA at 150 mg/ml. This demonstrates how PEA could be good candidate as a beef treatment to reduce E. coli O157:H7 bacterial infections associated with contaminated meat (Lynnes et al., 2013a).


The authors thank the NIH/NIAID for funding B.M.P. through grant 1R15AI089403. Dr. Shelley Horne (NDSU) is thanked for critically reading the manuscript and helpful discussions. Laura Nessa (NDSU) is thanked for helpful discussions and valuable ideas.

Authors Contribution(s)

All authors contributed equally to the work.


1. American Psychiatric Association (2000) Diagnostic and statistical manual of mental disorder. (4h ed ), Washington DC.
2. Artigas F (2013) Developments in the field of antidepressants, where do we go now? Eur Neuropsychopharmacol: doi: 10.1016/j.euroneuro.2013.04.013. Epub ahead of print.
3. Bailey BA, Philips SR & Boulton AA (1987) In vivo release of endogenous dopamine, 5-hydroxytryptamine and some of their metabolites from rat caudate nucleus by phenylethylamine. Neurochem Res 12: 173-178.
4. Baker GB, Bornstein RA, Rouget AC, Ashton SE, Van Muyden JC & Coutts RT (1991) Phenylethylaminergic mechanisms in attention-deficit disorder. Biol Psychiatry 29: 15-22.
5. Bassler BL (2010) Small cells-big future. Molecular Biology of the Cell 21: 3786-3787.
6. Bentley KW (2006) ß-Phenylethylamines and the isoquinoline alkaloids. Nat Prod Rep 23: 444-463.
7. Borowsky B, Adham N, Jones KA, Raddatz R, Artymyshyn R, Ogozalek KL, Durkin MM, Lakhlani PP, Bonini JA, Pathirana S, Boyle N, Pu X, Kouranova E, Lichtblau H, Ochoa FY, Branchek TA & Gerald C (2001) Trace amines: identification of a family of mammalian G protein-coupled receptors. Proc Natl Acad Sci U S A 98: 8966-8971.
8. Boulton AA, Cookson B & Paulton R (1970) Hypertensive crisis in a patient on MAOI antidepressants following a meal of beef liver. Can Med Assoc J 102: 1394-1395.
9. Brassett-Harknett A & Butler N (2007) Attention-deficit/hyperactivity disorder: an overview of the etiology and a review of the literature relating to the correlates and lifecourse outcomes for men and women. Clin Psychol Rev 27: 188-210.
10. Broadley KJ, Akhtar Anwar M, Herbert AA, Fehler M, Jones EM, Davies WE, Kidd EJ & Ford WR (2009) Effects of dietary amines on the gut and its vasculature. Br J Nutr 101: 1645-1652.
11. Bunkova L, Adamcova G, Hudcova K, Velichova H, Pachlova V, Lorencova E & Bunka F (2013) Monitoring of biogenic amines in cheeses manufactured at small-scale farms and in fermented dairy products in the Czech Republic. Food Chem 141: 548-551.
12. Bunzow JR, Sonders MS, Arttamangkul S, Harrison LM, Zhang G, Quigley DI, Darland T, Suchland KL, Pasumamula S, Kennedy JL, Olson SB, Magenis RE, Amara SG & Grandy DK (2001) Amphetamine, 3,4-methylenedioxymethamphetamine, lysergic acid diethylamide, and metabolites of the catecholamine neurotransmitters are agonists of a rat trace amine receptor. Mol Pharmacol 60: 1181-1188.
13. Cardenas-Fernandez M, Neto W, Lopez C, Alvaro G, Tufvesson P & Woodley JM (2012) Immobilization of Escherichia coli containing omega-transaminase activity in LentiKats(R). Biotechnol Prog 28: 693-698.
14. Cashin CH (1972) Effect of sympathomimetic drugs in eliciting hypertensive responses to reserpine in the rat, after pretreatment with monoamineoxidase inhibitors. Br J Pharmacol 44: 203-209.
15. Chen X, Margolis KJ, Gershon MD, Schwartz GJ & Sze JY (2012) Reduced serotonin reuptake transporter (SERT) function causes insulin resistance and hepatic steatosis independent of food intake. PLoS One 7: e32511.
16. Cormier E (2008) Attention deficit/hyperactivity disorder: a review and update. J Pediatr Nurs 23: 345-357.
17. Da PM, Zurcher G, Wuthrich I & Haefely WE (1988) On tyramine, food, beverages and the reversible MAO inhibitor moclobemide. J Neural Transm Suppl 26: 31-56.
18. Dal Moro F (2013) A sweet piece of dark chocolate in a hot cup of dark coffee: a novel elixir for a long and happy life. Food Chem Toxicol 59: 808.
19. Deftereos SN, Dodou E, Andronis C & Persidis A (2012) From depression to neurodegeneration and heart failure: re-examining the potential of MAO inhibitors. Expert Rev Clin Pharmacol 5: 413-425.
20. Durkin K, Rae K & Stritzke WG (2012) The effect of images of thin and overweight body shapes on women's ambivalence towards chocolate. Appetite 58: 222-226.
21. Figueiredo TC, Viegas RP, Lara LJ, Baiao NC, Souza MR, Heneine LG & Cancado SV (2013) Bioactive amines and internal quality of commercial eggs. Poult Sci 92: 1376-1384.
22. Finocchi C & Sivori G (2012) Food as trigger and aggravating factor of migraine. Neurol Sci 33 Suppl 1: S77-S80.
23. Fraqueza MJ, Alfaia CM & Barreto AS (2012) Biogenic amine formation in turkey meat under modified atmosphere packaging with extended shelf life: Index of freshness. Poult Sci 91: 1465-1472.
24. Fukui PT, Goncalves TR, Strabelli CG, Lucchino NM, Matos FC, Santos JP, Zukerman E, Zukerman-Guendler V, Mercante JP, Masruha MR, Vieira DS & Peres MF (2008) Trigger factors in migraine patients. Arq Neuropsiquiatr 66: 494-499.
25. Garcia-Moruno E, Carrascosa AV & Munoz R (2005) A rapid and inexpensive method for the determination of biogenic amines from bacterial cultures by thin-layer chromatography. J Food Prot 68: 625-629.
26. Gatley SJ, Volkow ND, Gifford AN, Fowler JS, Dewey SL, Ding YS & Logan J (1999) Dopamine-transporter occupancy after intravenous doses of cocaine and methylphenidate in mice and humans. Psychopharmacology (Berl) 146: 93-100.
27. Giaouris E, Heir E, Hebraud M, Chorianopoulos N, Langsrud S, Moretro T, Habimana O, Desvaux M, Renier S & Nychas GJ (2013) Attachment and biofilm formation by foodborne bacteria in meat processing environments: Causes, implications, role of bacterial interactions and control by alternative novel methods. Meat Sci: doi:10.10106/j.meatsci.2013.05.023. Epub ahead of print.
28. Giraffa G (2003) Functionality of enterococci in dairy products. Int J Food Microbiol 88: 215-222.
29. Granvogl M, Bugan S & Schieberle P (2006) Formation of amines and aldehydes from parent amino acids during thermal processing of cocoa and model systems: new insights into pathways of the strecker reaction. J Agricult Food Chem 54: 1730-1739.
30. Gutman DA & Owens MJ (2006) Serotonin and norepinephrine transporter binding profile of SSRIs. Essent Psychopharmacol 7: 35-41.
31. Guven KC, Percot A & Sezik E (2010) Alkaloids in marine algae. Mar Drugs 8: 269-284.
32. Haney EM, Chan BK, Diem SJ, Ensrud KE, Cauley JA, Barrett-Connor E, Orwoll E & Bliziotes MM (2007) Association of low bone mineral density with selective serotonin reuptake inhibitor use by older men. Arch Intern Med 167: 1246-1251.
33. Hoffman JR, Kang J, Ratamess NA, Jennings PF, Mangine G & Faigenbaum AD (2006) Thermogenic effect from nutritionally enriched coffee consumption. J Int Soc Sports Nutr 3: 35-41.
34. Hormes JM & Timko CA (2011) All cravings are not created equal. Correlates of menstrual versus non-cyclic chocolate craving. Appetite 57: 1-5.
35. Howes OD & Kapur S (2009) The dopamine hypothesis of schizophrenia: version III--the final common pathway. Schizophr Bull 35: 549-562.
36. Jansen SC, van DM, Bottema KC & Dubois AE (2003) Intolerance to dietary biogenic amines: a review. Ann Allergy Asthma Immunol 91: 233-240.
37. Kim B, Byun BY & Mah JH (2012) Biogenic amine formation and bacterial contribution in Natto products. Food Chem 135: 2005-2011.
38. Koh HY (2013) Phospholipase C-beta1 and schizophrenia-related behaviors. Adv Biol Regul: doi: 10.1016/j.jbior.2013.08.002. Epub ahead of print.
39. Kulawik P, Ozogul F & Glew RH (2013) Quality properties, fatty acids, and biogenic amines profile of fresh tilapia stored in ice. J Food Sci 78: S1063-S1068.
40. Kusaga A (2002) Decreased ß-phenylethylamine in urine of children with attention deficit hyperactivity disorder and autistic disorder. No To Hattatsu 34: 243-248.
41. Kusaga A, Yamashita Y, Koeda T, Hiratani M, Kaneko M, Yamada S & Matsuishi T (2002) Increased urine phenylethylamine after methylphenidate treatment in children with ADHD. Ann Neurol 52: 372-374.
42. Li K, Bao Y, Luo Y, Shen H & Shi C (2012) Formation of biogenic amines in crucian carp (Carassius auratus) during storage in ice and at 4 degrees C. J Food Prot 75: 2228-2233.
43. Lieberman JA, Kane JM & Alvir J (1987) Provocative tests with psychostimulant drugs in schizophrenia. Psychopharmacology 91: 415-433.
44. Liu F, DU L, Xu W, Wang D, Zhang M, Zhu Y & Xu W (2013) Production of tyramine by Enterococcus faecalis strains in water-boiled salted duck. J Food Prot 76: 854-859.
45. Lynnes T, Horne SM & Prüß BM (2013a) ß-phenylethylamine as a novel nutrient treatment to reduce bacterial contamination due to Escherichia coli O157:H7 on beef meat. Meat Sci 96: 165-171.
46. Lynnes T, Prüß BM & Samanta P (2013b) Acetate metabolism and Escherichia coli biofilm: new approaches to an old problem. FEMS Microbiol Lett 344: 95-103.
47. Marcobal A, De las Rivas B, Landete JM, Tabera L & Munoz R (2012) Tyramine and phenylethylamine biosynthesis by food bacteria. Crit Rev Food Sci Nutr 52: 448-467.
48. Marcobal A, De las Rivas B & Munoz R (2006) First genetic characterization of a bacterial ß-phenylethylamine biosynthetic enzyme in Enterococcus faecium RM58. FEMS Microbiol Lett 258: 144-149.
49. Marcus DA, Scharff L, Turk D & Gourley LM (1997) A double-blind provocative study of chocolate as a trigger of headache. Cephalalgia 17: 855-862.
50. Moret S, Smela D, Populin T & Conte LS (2005) A survey on free biogenic amine content of fresh and preserved vegetables. Food Chem 89: 355-361.
51. Nystrom RF & Brown WG (1948) Reduction of organic compounds by lithium aluminum hydride; halides, quinones, miscellaneous nitrogen compounds. J Am Chem Soc 70: 3738-3740.
52. Oldendorf WH (1971) Brain uptake of radiolabeled amino acids, amines, and hexoses after arterial injection. Am J Physiol 221: 1629-1639.
53. Olfson M, Huang C, Gerhard T, Winterstein AG, Crystal S, Allison PD & Marcus SC (2012) Stimulants and cardiovascular events in youth with attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry 51: 147-156.
54. Olivier JD, Akerud H, Kaihola H, Pawluski JL, Skalkidou A, Hogberg U & Sundstrom-Poromaa I (2013) The effects of maternal depression and maternal selective serotonin reuptake inhibitor exposure on offspring. Front Cell Neurosci 7: 73.
55. Onal A, Tekkeli SE & Onal C (2013) A review of the liquid chromatographic methods for the determination of biogenic amines in foods. Food Chem 138: 509-515.
56. Ottley C (2000) Food and mood. Nurs Stand 15: 46-52.
57. Pastore P, Favaro G, Badocco D, Tapparo A, Cavalli S & Saccani G (2005) Determination of biogenic amines in chocolate by ion chromatographic separation and pulsed integrated amperometric detection with implemented wave-form at Au disposable electrode. J Chromatogr A 1098: 111-115.
58. Paterson IA, Juorio AV & Boulton AA (1990) 2-Phenylethylamine: a modulator of catecholamine transmission in the mammalian central nervous system? J Neurochem 55: 1827-1837.
59. Peremans K, Goethals I, De VF, Dobbeleir A, Ham H, Van Bree H, Van Heeringen C & Audenaert K (2006) Serotonin transporter and dopamine transporter imaging in the canine brain. Nucl Med Biol 33: 907-913.
60. Pessione E, Pessione A, Lamberti C, Coisson DJ, Riedel K, Mazzoli R, Bonetta S, Eberl L & Giunta C (2009) First evidence of a membrane-bound, tyramine and ß-phenylethylamine producing, tyrosine decarboxylase in Enterococcus faecalis: a two-dimensional electrophoresis proteomic study. Proteomics 9: 2695-2710.
61. Philips SR, Rozdilsky B & Boulton AA (1978) Evidence for the presence of m-tyramine, p-tyramine, tryptamine, and phenylethylamine in the rat brain and several areas of the human brain. Biol Psychiatry 13: 51-57.
62. Premont RT, Gainetdinov RR & Caron MG (2001) Following the trace of elusive amines. Proc Natl Acad Sci U S A 98: 9474-9475.
63. Rehman AU, Afroz S, Abbasi MA, Tanveer W, Khan KM, Ashraf M, Ahmad I, Afzal I & Ambreen N (2012) Synthesis, characterization and biological screening of sulfonamides derived form 2-phenylethylamine. Pak J Pharm Sci 25: 809-814.
64. Revel FG, Moreau JL, Pouzet B, Mory R, Bradaia A, Buchy D, Metzler V, Chaboz S, Groebke ZK, Galley G, Norcross RD, Tuerck D, Bruns A, Morairty SR, Kilduff TS, Wallace TL, Risterucci C, Wettstein JG & Hoener MC (2013) A new perspective for schizophrenia: TAAR1 agonists reveal antipsychotic- and antidepressant-like activity, improve cognition and control body weight. Mol Psychiatry 18: 543-556.
65. Robinson JC & Snyder HR (1955) ß-phenylethylamine. Org Synth 3: 720-721.
66. Rossler W, Salize HJ, Van Os J & Riecher-Rossler A (2005) Size of burden of schizophrenia and psychotic disorders. Eur Neuropsychopharmacol 15: 399-409.
67. Rothman RB & Baumann MH (2006) Balance between dopamine and serotonin release modulates behavioral effects of amphetamine-type drugs. Ann N Y Acad Sci 1074: 245-260. Sanchez-Blanco J, Sanchez-Blanco C, Sousa M & Espinosa-Garcia F (2012) Assessing introduced Leguminosae in Mexico to identify potentially high-impact invasive species. Acta Botan Mexicana 100: 41-77.
68. Scassellati C, Bonvicini C, Faraone SV & Gennarelli M (2012) Biomarkers and attention-deficit/hyperactivity disorder: a systematic review and meta-analyses. J Am Acad Child Adolesc Psychiatry 51: 1003-1019.
69. Shalaby AR (1996) Significance of biogenic amines to food safety and human health. Food Res Internat 29: 675-690.
70. Shannon HE, Cone EJ & Yousefnejad D (1982) Physiologic effects and plasma kinetics of ß-phenylethylamine and its N-methyl homolog in the dog. J Pharmacol Exp Ther 223: 190-196.
71. Smith TA (1977) Phenethylamine and related compounds in plants. Phytochemistry 16: 9-18.
72. Spiller HA, Hays HL & Aleguas A, Jr. (2013) Overdose of drugs for attention-deficit hyperactivity disorder: clinical presentation, mechanisms of toxicity, and management. CNS Drugs 27: 531-543.
73. Stevenson LG, Szostek BA, Clemmer KM & Rather PN (2013) Expression of the DisA amino acid decarboxylase from Proteus mirabilis inhibits motility and class 2 flagellar gene expression in Escherichia coli. Res Microbiol 164: 31-37.
74. Stuart H & Arboleda-Florez J (2001) Community attitudes toward people with schizophrenia. Can J Psychiatry 46: 245-252.
75. Voinov B, Richie WD & Bailey RK (2013) Depression and chronic diseases: it is time for a synergistic mental health and primary care approach. Prim Care Companion CNS Disord 15: doi: 10.4088/PCC.12r01468. Epub ahead of print.
76. Werthmann J, Roefs A, Nederkoorn C & Jansen A (2013) Desire lies in the eyes: attention bias for chocolate is related to craving and self-endorsed eating permission. Appetite 70C: 81-89.
77. World Health Association WHO (2008) The global burden of disease: 2004 update. WHO Library Cataloguing-in-Publication Data ISBN 978 92 4 156371 0.
78. Xie Z & Miller GM (2008) Beta-phenylethylamine alters monoamine transporter function via trace amine-associated receptor 1: implication for modulatory roles of trace amines in brain. J Pharmacol Exp Ther 325: 617-628.
79. Yang HY & Neff NH (1973) ß-phenylethylamine: a specific substrate for type B monoamine oxidase of brain. J Pharmacol Exp Ther 187: 365-371.
80. Zakharyan R & Boyajyan A (2013) Inflammatory cytokine network in schizophrenia. World J Biol Psychiatry: doi:10.3109/15622975.2013.830774. Epub ahead of print.
81. Ziegleder G, Stojacic E & Stumpf B (1992) Occurrence of ß-phenylethylamine and its derivatives in cocoa and cocoa products. Zeitschrift fur Lebensmittel-Untersuchung und Forschung 195: 235-238.
82. Zucchi R, Chiellini G, Scanlan TS & Grandy DK (2006) Trace amine-associated receptors and their ligands. Br J Pharmacol 149: 967-978.

Source(s) of Funding

The research was funded by grant 1R15AI089403 from the NIH/NIAID.

Competing Interests

The authors declare no competing interests.

5 reviews posted so far

A-phenylethylamine, a small molecule with a large impact
Posted by Dr. Josephine Anthony on 27 Dec 2013 04:37:41 AM GMT
This review will not be counted towards final review score for this article and for its inclusion into WebmedCentral Peer Reviewer articles because reviewer did not feel he/she had sufficient experience and knowledge to review the article.

A-Phenylalanine, a small molecules with a large impact
Posted by Dr. Ranjith N Kumavath on 29 Oct 2013 10:09:17 AM GMT Reviewed by WMC Editors
This review will not be counted towards final review score for this article and for its inclusion into WebmedCentral Peer Reviewer articles because reviewer did not feel he/she had sufficient experience and knowledge to review the article.

A-phenylethylamine, a small molecule with a large impact
Posted by Dr. Oluyomi S Adeyemi on 17 Oct 2013 03:36:20 PM GMT Reviewed by WMC Editors

A-phenylethylamine, a small molecule with a large impact
Posted by Dr. Miranda Bader on 10 Oct 2013 08:57:48 PM GMT Reviewed by Author Invited Reviewers

A-phenylethylamine, a small molecule with a large impact
Posted by Dr. L. Caetano M Antunes on 06 Oct 2013 02:57:16 AM GMT Reviewed by WMC Editors

0 comments posted so far

Please use this functionality to flag objectionable, inappropriate, inaccurate, and offensive content to WebmedCentral Team and the authors.


Author Comments
0 comments posted so far


What is article Popularity?

Article popularity is calculated by considering the scores: age of the article
Popularity = (P - 1) / (T + 2)^1.5
P : points is the sum of individual scores, which includes article Views, Downloads, Reviews, Comments and their weightage

Scores   Weightage
Views Points X 1
Download Points X 2
Comment Points X 5
Review Points X 10
Points= sum(Views Points + Download Points + Comment Points + Review Points)
T : time since submission in hours.
P is subtracted by 1 to negate submitter's vote.
Age factor is (time since submission in hours plus two) to the power of 1.5.factor.

How Article Quality Works?

For each article Authors/Readers, Reviewers and WMC Editors can review/rate the articles. These ratings are used to determine Feedback Scores.

In most cases, article receive ratings in the range of 0 to 10. We calculate average of all the ratings and consider it as article quality.

Quality=Average(Authors/Readers Ratings + Reviewers Ratings + WMC Editor Ratings)