Phenylethylamine, usually shortened to PEA, is a trace amine: a small molecule built from phenylalanine, an amino acid, and present in the body at far lower levels than dopamine or serotonin. Your cells make it, and so do microbes, which is why it turns up in fermented and aged foods such as cheese and wine and in cocoa. A 1983 review described it as the body’s natural amphetamine. It is not palmitoylethanolamide, a fat-derived compound that is also abbreviated PEA and studied for chronic pain. This page is about phenylethylamine only.
The popular story says chocolate makes you feel in love because of PEA. Three findings sit awkwardly with it. In one test of real chocolate, PEA was below the 3 mg/kg detection limit. When two volunteers took 250 mg of PEA by mouth, their urinary PEA rose only modestly, because the body breaks it down. And in a craving study, cocoa capsules matching chocolate’s active ingredients had virtually no effect, while white chocolate partly eased the craving.
The thing most readers do not know is how fast PEA disappears. Injected into rat brain, its half-life was 3.8 minutes. Drugs that block the enzyme MAO-B, such as selegiline, raise urinary PEA in people, and the few reports of PEA relieving depression gave it together with selegiline. That is a drug effect, not a food effect.
Health benefits of phenylethylamine
No benefit of eating phenylethylamine is proven. The best-supported finding is a negative one: in controlled challenge tests, chocolate and PEA did not trigger headache more than a look-alike. The mood data are old and small. The reports of PEA relieving depression gave it with selegiline, a prescription drug, and describe no comparison group. Exercise raises a PEA breakdown product in urine, and cell work shows PEA acts on the TAAR1 receptor, but neither shows a benefit from food or supplements. Nothing here reaches strong or moderate evidence. Here is what 18 studies found, strongest evidence first, including the ones that found nothing.
A review of oral challenge studies found that in the one conclusive chocolate trial, the amount of PEA was not related to headache attacks
Review of 13 oral challenge studies of biogenic amines in susceptible people (5 positive, 8 negative), searched up to August 2001. Three positive ones were ineligible and 6 of the other 10 were inconclusive. The 4 conclusive studies were all negative. The authors found no scientific basis for diet advice on biogenic amines. Newer work is not covered.
In 63 women with chronic headache, chocolate was no more likely than carob to provoke headache
Double-blind provocation trial. After 2 weeks on a diet low in vasoactive amine foods, each woman ate two chocolate and two carob samples in random order. Half had migraine, 37.5% tension-type headache and 12.5% both. The result (p = 0.83) did not depend on what the women believed about chocolate. The abstract does not give the PEA content of the chocolate.
A review found that all three provocation studies failed to show chocolate triggers migraine more than a placebo
Review of 25 studies of chocolate as a self-reported trigger and 3 provocation studies, searched to January 2020. In 23 studies chocolate was named as a trigger by a small share of people (1.3 to 33%). The authors say it is unclear whether eating chocolate before an attack is a cause or an early craving, and that evidence is insufficient to tell patients to avoid it. Chocolate holds many compounds besides PEA.
After 250 mg of PEA by mouth, urinary PEA rose only modestly while a breakdown product rose far more
Study in only 2 healthy men given one oral dose of PEA hydrochloride. The authors read the result as extensive metabolism, and the ratio of one breakdown product to PEA reached 9.4. The same paper checked 10,190 routine doping-control urine samples and found PEA above about 500 ng/mL in 31 (0.3%). PEA was added to the World Anti-Doping Agency Prohibited List in January 2015.
Show 14 more studies
Oral chocolate or PEA changed the brain-wave recordings of people with migraine little
A 1977 study of EEG recordings after oral amines. Tyramine switched on abnormal activity in people with epilepsy, but little changed in the recordings of migraine patients after chocolate or beta-phenylethylamine. The abstract gives no doses or group sizes.
A 30-minute treadmill run raised a PEA breakdown product in urine by 77% in 20 healthy men
Pilot study. The men gave 24-hour urine on a rest day and on a day with 30 minutes on a treadmill at 70% of maximal heart rate reserve. It measured phenylacetic acid, which the authors take to reflect PEA, not PEA itself. It did not measure mood, so the link to the antidepressant effect of exercise is the authors’ idea.
PEA at 10 to 60 mg a day, taken with the drug selegiline, kept depression relief in 12 of 14 responders
Follow-up report of 14 people with major depression who had responded to oral PEA given with 10 mg a day of selegiline, a prescription MAO-B inhibitor used to slow PEA breakdown. They were re-examined 20 to 50 weeks later. No comparison group is described, and the effect cannot be credited to PEA alone. The author reports no apparent side effects.
The drug L-deprenyl (selegiline) at 10 to 30 mg a day raised urinary PEA in atypical depression, but the authors doubt that explains its antidepressant effect
Biochemical study in people with atypical depression. Urinary PEA rose significantly and platelet MAO activity almost vanished. Between 25 and 33% of the dose came out as methamphetamine or amphetamine. The authors suggest the antidepressant effect works by some other mechanism, or in addition to MAO-B inhibition. This was a drug study, not a PEA study.
Selegiline raised urinary PEA in a dose-dependent way in depressed patients, while the MAO-A blocker clorgyline did not
Clinical comparison of three prescription MAO inhibitors given for 3 or more weeks. Selegiline at 10, 30 or 60 mg a day produced marked rises in urinary PEA and two tyramines. Pargyline at 90 mg a day matched the top selegiline dose, while clorgyline at 30 mg a day changed trace amines negligibly. That fits MAO-B being the main route of PEA breakdown. These are drug doses, not food amounts.
A meta-analysis found 13.9% of migraine patients name chocolate as a trigger and 8.0% name cheese
Meta-analysis of patient-reported trigger rates from 8 observational studies (7 pooled). Chocolate 13.9% (95% CI 7.0 to 21.0), cheese 8.0% (3.0 to 12.0) and caffeine 12.0%, with very large variation between studies. Self-reports cannot show cause, and the studies did not isolate PEA. The author advises headache diaries over blanket avoidance.
People with major depression excreted less of the PEA breakdown product phenylacetic acid, 78.2 against 141.1 mg a day
Urine from 144 patients with major depression was compared with urine from 48 healthy volunteers, and plasma levels in 23 drug-free patients (300.33 ng/mL) with 12 volunteers (491.83 ng/mL). The authors suggest low levels may mark depression. The same paper reports that the amino acid phenylalanine, PEA’s building block, lifted mood in 31 of 40 depressed people, and the abstract describes no control group.
Urinary PEA was not low in depression: 7 of 53 patients had values over three times the highest control
Two groups of hospitalized depressed patients were compared with 16 healthy controls. The seven high excretors were all women and were not otherwise distinguishable. In a subgroup, PEA did not track phenylacetic acid. The authors conclude depression is not linked to a general PEA deficit.
Plasma PEA did not differ between depressed and healthy people
Average plasma PEA in 32 healthy people was 1.19 ng/mL. In 14 depressed patients, PEA was negatively correlated with MHPG, a norepinephrine breakdown product (r = -0.73), which the author reads as PEA possibly regulating noradrenergic function. A correlation in a small group cannot show that.
When injected into rat brain, PEA was lost with a half-life of 3.8 minutes
Rat study with injections into the brain’s fluid spaces. Half-lives were 5.1 minutes for p-tyramine, 7.4 for m-tyramine and 8.0 for dopamine. Blocking MAO with pargyline slowed the loss. Direct brain injection skips the gut, so this shows the speed of breakdown, not how much dietary PEA arrives.
In rats, injected PEA crossed the blood-brain barrier readily (brain-uptake index 83, with water as 100)
Rat study with an injected 100 µg dose. The index was 83 for PEA and 98 for amphetamine, and the authors conclude PEA enters by passive diffusion. Together with the half-life above, this suggests breakdown rather than the barrier limits how much PEA reaches the brain.
High doses of PEA injected into mice caused depression-like behavior and lowered striatal dopamine, but doses by mouth in rats did not
Mice received 25 to 75 mg/kg by injection for up to 7 days. They showed depression and anxiety-like behavior and movement problems, and PEA blocked a mitochondrial enzyme (complex I) and made hydroxyl radicals. Rats given 75 to 125 mg/kg by mouth for 7 days showed no such effects, which the authors take to mean food rich in PEA is safe for most people.
In mice with stress-hormone-induced depression-like behavior, PEA at 50 mg/kg eased the behavior
Mice got corticosterone (20 mg/kg) for 21 days and PEA in the last four days. PEA reversed the drop in two growth-signal proteins, BDNF and TrkB, in the hippocampus. In cultured neurons, 100 µM PEA rescued dendritic spines. It is a mouse model, and the dose is not a human dose.
A gut bacterium’s PEA and tryptamine went with insulin resistance in patients and impaired insulin signaling in mice and monkeys
Levels of the gut bacterium Ruminococcus gnavus, tryptamine and phenethylamine were linked to insulin resistance in people with type 2 diabetes and irritable bowel syndrome. Treating healthy mice and monkeys with the two compounds impaired insulin signaling through the TAAR1 receptor. It concerns PEA made in the gut, was tested together with tryptamine, and says nothing about PEA from food.
Foods high in phenylethylamine
Phenylethylamine forms in food when microbes strip the carboxyl group from phenylalanine, so it turns up in fermented and aged foods such as ripened cheese and wine, and in cocoa. Amounts are small and vary a lot. The ranking below comes from the Danish food database Frida, which lists few foods with a PEA value.
Chocolate is the food everyone names, and the measurements are modest. In a 2005 method paper, PEA was not found in real chocolate samples, and the test could not detect less than 3 mg/kg. A German study found PEA rose during cocoa fermentation and fell during roasting and alkalizing, and that a chocolate’s level depends on its non-fat cocoa content. A Brazilian processing study saw it rise during roasting, up to 2.47 mg/kg of dry weight in cocoa nibs, and found most amines did not reach the finished chocolate. By the 3 mg/kg limit, a 40 g bar would hold under about 0.12 mg of PEA, more than 2,000 times less than the 250 mg oral dose in the study above.
Cheese and wine are less clear than their reputation. PEA was not detected in any of 112 dairy products bought in the Czech Republic, including 55 farm cheeses. In 160 bottles of Primitivo wine it was found in only two, at less than 2.12 mg per liter. In ripened imported cheeses, histamine made up most of the amines: about 86% in Pecorino Romano and 77% in Grana Padano.
Per serving. No daily amount is set, so bars compare each food with the top food.
Per 100 g. No daily amount is set, so bars compare each food with the top food.
Per 100 kcal: the same calories of each food, for a fair comparison. Bars compare each food with the top food.
Food labels have no Daily Value or Reference Intake for phenylethylamine, so the % compares each food with the top food.
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Sources
- Natrella G, Vacca M, Minervini F, et al. A Comprehensive Review on the Biogenic Amines in Cheeses: Their Origin, Chemical Characteristics, Hazard and Reduction Strategies. Foods. 2024.
- Pastore P, Favaro G, Badocco D, et al. 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. 2005.
- Ziegleder G, Stojacic E, Stumpf B. [Occurrence of beta-phenylethylamine and its derivatives in cocoa and cocoa products]. Z Lebensm Unters Forsch. 1992.
- Silveira PTS, Glória MBA, Tonin IP, et al. Varietal Influence on the Formation of Bioactive Amines during the Processing of Fermented Cocoa with Different Pulp Contents. Foods. 2023.
- Silva GS, Dala-Paula BM, Bispo ES, et al. Bioaccessibility of bioactive amines in dark chocolates made with different proportions of under-fermented and fermented cocoa beans. Food Chem. 2023.
- Buňková L, Adamcová G, Hudcová K, et al. Monitoring of biogenic amines in cheeses manufactured at small-scale farms and in fermented dairy products in the Czech Republic. Food Chem. 2013.
- Patrignani F, Ndagijimana M, Belletti N, et al. Biogenic amines and ethyl carbamate in primitivo wine: survey of their concentrations in commercial products and relationship with the use of malolactic starter. J Food Prot. 2012.
- Kandasamy S, Yoo J, Yun J, et al. Quantitative Analysis of Biogenic Amines in Different Cheese Varieties Obtained from the Korean Domestic and Retail Markets. Metabolites. 2021.
- Sigmund G, Dib J, Tretzel L, et al. Monitoring 2-phenylethanamine and 2-(3-hydroxyphenyl)acetamide sulfate in doping controls. Drug Test Anal. 2015.
- Langwagen M, Jacobsen J, Christensen T, Poulsen A. The Danish Food Composition Database, Frida version 5.5. National Food Institute, Technical University of Denmark. 2025.
How phenylethylamine works
Most of what we know about how phenylethylamine acts comes from cells and animals. Three ideas matter: the body breaks it down within minutes, it switches on a receptor called TAAR1, and gut microbes make some of it. Here is each one, and what has been seen in people.
It is broken down within minutes
Monoamine oxidase (MAO) enzymes clear PEA fast. When PEA was injected into rat brain, half of it was gone in 3.8 minutes, sooner than dopamine at 8.0 minutes. Blocking MAO with a drug slowed the loss.
Drawn to scale, from the half-lives in one 1988 rat study. Injecting into the brain skips the gut, so it shows how fast PEA is broken down, not how much of a food dose arrives.
In depressed patients, selegiline and pargyline, which block MAO-B more than MAO-A, raised urinary PEA in a dose-dependent way, while clorgyline, which blocks MAO-A, barely did. That fits MAO-B being the main route. It is also why MAO inhibitors matter for safety (see below). After 250 mg of PEA by mouth, urinary PEA rose only modestly in two men.
What happened to urinary PEA with three prescription MAO inhibitors in one clinical comparison. The drawing shows direction only; the paper reports the size as marked for selegiline and negligible for clorgyline.
It switches on a receptor called TAAR1
PEA is one of the trace amines that activate TAAR1, a receptor first cloned in 2001. Switching it on raises the cell signal cAMP, and TAAR1 sits where it can influence how dopamine and serotonin cells fire and release. Amphetamine-like effects of trace amines were seen only at concentrations many orders above normal body levels, according to one review, so the role of PEA at everyday levels is still a hypothesis.
How a trace amine such as PEA is thought to act through TAAR1, as described in a review of cell and animal work.
Gut microbes make it too
Microbes make PEA from phenylalanine, in fermented food and in the gut. In one study, a gut bacterium that makes tryptamine and phenethylamine was linked to insulin resistance in patients, and the two compounds impaired insulin signaling in mice and monkeys. That is a lab and association result for PEA made inside the body, not evidence about food.
What has been seen in people
In people, the data are thin. Challenge tests found no link between chocolate or PEA and headache. A 250 mg dose barely moved urinary PEA. Urinary and plasma PEA were not low in depression as a group, and the relief reports used selegiline. A 30-minute run raised a breakdown product by 77% in 20 men, with no mood measured. In a craving study, cocoa capsules had virtually no effect, and a review concluded that any mood benefit of chocolate is ephemeral. Most of these are among the study cards above.
Sources
- Durden DA, Nguyen TV, Boulton AA. Kinetics of intraventricularly injected trace amines and their deuterated isotopomers. Neurochem Res. 1988.
- Murphy DL, Karoum F, Pickar D, et al. Differential trace amine alterations in individuals receiving acetylenic inhibitors of MAO-A (clorgyline) or MAO-B (selegiline and pargyline). J Neural Transm Suppl. 1998.
- Grandy DK. Trace amine-associated receptor 1-Family archetype or iconoclast?. Pharmacol Ther. 2007.
- Pei Y, Asif-Malik A, Canales JJ. Trace Amines and the Trace Amine-Associated Receptor 1: Pharmacology, Neurochemistry, and Clinical Implications. Front Neurosci. 2016.
- Berry MD. Mammalian central nervous system trace amines. Pharmacologic amphetamines, physiologic neuromodulators. J Neurochem. 2004.
- Zhai L, Xiao H, Lin C, et al. Gut microbiota-derived tryptamine and phenethylamine impair insulin sensitivity in metabolic syndrome and irritable bowel syndrome. Nat Commun. 2023.
- Wolf ME, Mosnaim AD. Phenylethylamine in neuropsychiatric disorders. Gen Pharmacol. 1983.
- Borah A, Paul R, Mazumder MK, et al. Contribution of β-phenethylamine, a component of chocolate and wine, to dopaminergic neurodegeneration: implications for the pathogenesis of Parkinson’s disease. Neurosci Bull. 2013.
- Sabelli HC, Fawcett J, Gusovsky F, et al. Clinical studies on the phenylethylamine hypothesis of affective disorder: urine and blood phenylacetic acid and phenylalanine dietary supplements. J Clin Psychiatry. 1986.
- Michener W, Rozin P. Pharmacological versus sensory factors in the satiation of chocolate craving. Physiol Behav. 1994.
- Parker G, Parker I, Brotchie H. Mood state effects of chocolate. J Affect Disord. 2006.
Is phenylethylamine safe? Supplements, dose and interactions
We found no reports of harm from PEA at food amounts. In rats, doses of 75 to 125 mg/kg by mouth for 7 days caused no overt effects, and a review of challenge studies found no relation between dietary biogenic amines and intolerance reactions. We found no acceptable daily intake or upper intake level for PEA from an official body. In the US, a February 2022 FDA warning letter told one seller that PEA capsules marketed with ADHD and antidepressant claims were an unapproved new drug. PEA has also been on the World Anti-Doping Agency Prohibited List since January 2015.
- Doses and side effects. The mood reports gave 10 to 60 mg a day by mouth with 10 mg of selegiline, in 14 people, with no apparent side effects reported. One 250 mg dose has been given to two men. We found no controlled trial of PEA alone, so a safe supplement dose is not established.
- MAO inhibitors. MAO inhibitors, including selegiline, stop the breakdown of PEA, and urinary PEA rose in a dose-dependent way. People on them are warned about foods high in tyramine because of hypertensive crisis, and a 1986 review says 6 mg of tyramine may produce a mild crisis. We found no case report or trial of a PEA supplement with an MAO inhibitor, so the blood pressure risk is inferred from how the enzyme works. Do not combine them without a doctor.
- Look-alike stimulants. Weight-loss and sports supplements do not always match the label. In 21 supplements labeled as containing Acacia rigidula, FDA scientists found phenethylamine at 710 to 171,620 µg/g and BMPEA, a different compound and an amphetamine isomer, in 9. Another analysis found BMPEA in 11 of 21 brands, up to 93.7 mg a day at the maximum serving. In rats, BMPEA raised blood pressure. FDA says BMPEA is not a dietary ingredient, so products listing it are misbranded. Those findings are about BMPEA, not PEA.
- Pregnancy, children and animals. We found no studies of PEA supplements in pregnancy, breastfeeding or children, so ask your doctor. In mice, high-dose injections of 25 to 75 mg/kg caused depression-like behavior and lowered striatal dopamine, a lab result with no human counterpart.
How to get more phenylethylamine
- Food gives little. The chocolate test found less than 3 mg/kg, and PEA was not detected in the Czech cheese samples, so foods will not reach the doses used in the mood reports.
- Eating it does little. After 250 mg by mouth, urinary PEA rose only modestly in two men, and in rat brain its half-life was 3.8 minutes.
- Exercise may raise it. A 30-minute treadmill run at 70% of maximal heart rate reserve raised urinary phenylacetic acid by 77% in 20 men. That is a breakdown product, in a pilot study without a mood measure.
Sources
- Sengupta T, Mohanakumar KP. 2-Phenylethylamine, a constituent of chocolate and wine, causes mitochondrial complex-I inhibition, generation of hydroxyl radicals and depletion of striatal biogenic amines leading to psycho-motor dysfunctions in Balb/c mice. Neurochem Int. 2010.
- Jansen SC, van Dusseldorp M, Bottema KC, et al. Intolerance to dietary biogenic amines: a review. Ann Allergy Asthma Immunol. 2003.
- U.S. Food and Drug Administration. Warning letter to Crystal Clear Supplements, 620285. February 4, 2022.
- U.S. Food and Drug Administration. BMPEA in dietary supplements. Content current as of February 22, 2023.
- Sigmund G, Dib J, Tretzel L, et al. Monitoring 2-phenylethanamine and 2-(3-hydroxyphenyl)acetamide sulfate in doping controls. Drug Test Anal. 2015.
- Piper T, Krombholz S, Thevis M. Carbon isotope ratios of phenethylamine and its urinary metabolite phenylacetylglutamine. Drug Test Anal. 2024.
- Sabelli H, Fink P, Fawcett J, et al. Sustained antidepressant effect of PEA replacement. J Neuropsychiatry Clin Neurosci. 1996.
- Murphy DL, Karoum F, Pickar D, et al. Differential trace amine alterations in individuals receiving acetylenic inhibitors of MAO-A (clorgyline) or MAO-B (selegiline and pargyline). J Neural Transm Suppl. 1998.
- Flockhart DA. Dietary restrictions and drug interactions with monoamine oxidase inhibitors: an update. J Clin Psychiatry. 2012.
- McCabe BJ. Dietary tyramine and other pressor amines in MAOI regimens: a review. J Am Diet Assoc. 1986.
- Pawar RS, Grundel E, Fardin-Kia AR, et al. Determination of selected biogenic amines in Acacia rigidula plant materials and dietary supplements using LC-MS/MS methods. J Pharm Biomed Anal. 2014.
- Cohen PA, Bloszies C, Yee C, et al. An amphetamine isomer whose efficacy and safety in humans has never been studied, β-methylphenylethylamine (BMPEA), is found in multiple dietary supplements. Drug Test Anal. 2016.
- Schindler CW, Thorndike EB, Rice KC, et al. The Supplement Adulterant β-Methylphenethylamine Increases Blood Pressure by Acting at Peripheral Norepinephrine Transporters. J Pharmacol Exp Ther. 2019.
- Avula B, Bae JY, Chittiboyina AG, et al. Liquid chromatography-quadrupole time of flight mass spectrometric method for targeted analysis of 111 nitrogen-based compounds in weight loss and ergogenic supplements. J Pharm Biomed Anal. 2019.
- Szabo A, Billett E, Turner J. Phenylethylamine, a possible link to the antidepressant effects of exercise?. Br J Sports Med. 2001.
- Pastore P, Favaro G, Badocco D, et al. 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. 2005.
- Buňková L, Adamcová G, Hudcová K, et al. Monitoring of biogenic amines in cheeses manufactured at small-scale farms and in fermented dairy products in the Czech Republic. Food Chem. 2013.
History of phenylethylamine
Phenylethylamine was first isolated by Marceli Nencki in 1876 and first synthesized in 1909 by Treat Johnson and Herbert Guest. In 1974 a paper in Nature proposed a PEA-oxidizing defect in migraine, and a 1975 letter re-examined chocolate, beta-phenethylamine and migraine. That tied PEA to the idea that chocolate triggers headaches, which the 1997 double-blind chocolate and carob trial did not support.
In the 1980s and 1990s, Sabelli and colleagues proposed that low PEA might underlie some depression, and tested PEA given with selegiline. In 2001, two papers described the cloning of a receptor for trace amines, now called TAAR1, which gave PEA a known target. Some authors have proposed that PEA explains romantic love, but we found no direct evidence for it.
PEA has since moved from the lab into supplements marketed for mood and weight loss. The World Anti-Doping Agency added it to its Prohibited List in January 2015, and in 2022 FDA told one seller that its PEA capsules were an unapproved drug.
Sources
- Sandler M, Youdim MB, Hanington E. A phenylethylamine oxidising defect in migraine. Nature. 1974.
- Schweitzer JW, Friedhoff AJ, Schwartz R. Letter: Chocolate, beta-phenethylamine and migraine re-examined. Nature. 1975.
- Marcus DA, Scharff L, Turk D, et al. A double-blind provocative study of chocolate as a trigger of headache. Cephalalgia. 1997.
- Grandy DK. Trace amine-associated receptor 1-Family archetype or iconoclast?. Pharmacol Ther. 2007.
- Piper T, Krombholz S, Thevis M. Carbon isotope ratios of phenethylamine and its urinary metabolite phenylacetylglutamine. Drug Test Anal. 2024.
- Sigmund G, Dib J, Tretzel L, et al. Monitoring 2-phenylethanamine and 2-(3-hydroxyphenyl)acetamide sulfate in doping controls. Drug Test Anal. 2015.
- Sabelli H, Fink P, Fawcett J, et al. Sustained antidepressant effect of PEA replacement. J Neuropsychiatry Clin Neurosci. 1996.
- Lang-Illievich K, Klivinyi C, Lasser C, et al. Palmitoylethanolamide in the Treatment of Chronic Pain: A Systematic Review and Meta-Analysis of Double-Blind Randomized Controlled Trials. Nutrients. 2023.
- U.S. Food and Drug Administration. Warning letter to Crystal Clear Supplements, 620285. February 4, 2022.
- Phenethylamine. Wikipedia.
Frequently asked questions about phenylethylamine
Is phenylethylamine the chocolate love chemical?
No study shows it. In one test of real chocolate, PEA was below the 3 mg/kg detection limit, and 250 mg by mouth raised urinary PEA only modestly. In a craving study, cocoa capsules had virtually no effect, while white chocolate partly eased the craving. A review of chocolate and mood concluded that any benefit is ephemeral.
Which foods contain phenylethylamine?
Fermented and aged foods and cocoa, in small amounts. The ranking above shows the Danish data. In papers, PEA was not detected in 112 Czech dairy products, appeared in only two of 160 Primitivo wines at less than 2.12 mg per liter, and was under the 3 mg/kg detection limit in real chocolate.
Does dietary phenylethylamine reach the brain?
Very little is known to. Injected PEA entered rat brain easily (uptake index 83, water 100) but was lost with a half-life of 3.8 minutes, and 250 mg by mouth raised urinary PEA only modestly in two men. We found no study measuring brain PEA in people after eating chocolate or cheese.
Does phenylethylamine cause migraines?
Controlled tests say not clearly. In 63 women with chronic headache, chocolate was no more likely than carob to provoke headache (p = 0.83), and a review of challenge studies found no relation between PEA in chocolate and attacks. Still, 13.9% of migraine patients name chocolate as a trigger, so a headache diary is the better guide for you.
Do phenylethylamine supplements help mood or weight loss?
No controlled trial of PEA alone is known to us. The mood reports used 10 to 60 mg a day with 10 mg of selegiline in 14 responders, with no comparison group described. We found no weight-loss trials. FDA told one seller that PEA capsules marketed with ADHD and antidepressant claims were an unapproved drug.
Can you take phenylethylamine with an MAO inhibitor?
Ask your doctor first. MAO inhibitors raise urinary PEA, with selegiline doing so in a dose-dependent way. People on them are warned about tyramine-rich foods, and a review says 6 mg of tyramine may produce a mild hypertensive crisis. We found no direct study of PEA with an MAO inhibitor, so the risk is inferred.
Is phenylethylamine the same as phenylalanine?
No. Phenylalanine is an amino acid, and PEA is made from it, in the body and by microbes in food. In one report, phenylalanine lifted mood in 31 of 40 depressed people, but the abstract describes no control group. PEA itself is broken down within minutes.
Does exercise raise phenylethylamine?
It may. In 20 healthy men, 24-hour urinary phenylacetic acid, which the authors take to reflect PEA, was 77% higher after a 30-minute treadmill run. It was a pilot study, the control was the same men on a rest day, and no mood was measured.