Contribution of β-phenethylamine, a component of chocolate and wine, to dopaminergic neurodegeneration: implications for the pathogenesis of Parkinson’s disease

Migraine Triggers and Oxidative Stress: A Narrative Review and Synthesis

“…β‐phenylethylamine, a biogenic amine derived from phenylalanine, is a suspected active ingredient in such possible migraine trigger foods as chocolate, wine, and some cheeses . Also, phenylethylamine is a minor metabolite of phenylalanine, of which aspartame is a significant source .…”

“…Also, phenylethylamine is a minor metabolite of phenylalanine, of which aspartame is a significant source . Phenylethylamine functions as an excitatory neuromodulator, and with acute administration it potentiates dopamine release and increases motor behavior . It is also a norepinephrine and dopamine reuptake inhibitor …”

“…With long‐term administration or at high doses, however, it inhibits complex 1 of the mitochondria in the dopamine‐containing cells of the substantia nigra, leading to release of hydroxyl radicals, oxidative stress‐mediated damage, and Parkinsonian symptoms in laboratory animals . In fact, at high doses, β‐phenylethylamine behaves similarly to rotenone and MPTP, used as neurotoxic models of Parkinson disease …”

Monitoring 2‐phenylethanamine and 2‐(3‐hydroxyphenyl)acetamide sulfate in doping controls

“…Moreover, urinary PEA levels are increased in patients undergoing anti‐depressant therapy with the monoamine oxidase A and B inhibitor phenelzine, and varying urine concentrations of PEA were also the subject of studies concerning psychiatric disorders in the past . Despite the fact that the oral bioavailability of PEA is considered extremely limited due to extensive first‐pass metabolic degradation and studies calling into question whether long‐term over‐consumption of PEA represents a neurological risk factor, PEA is widely sold as a dietary supplement. Consequently, it appeared relevant for adequate doping control analyses to study the correlation of orally administered PEA and its urinary concentration and to probe for metabolic products potentially enabling a differentiation of PEA of natural endogenous origin and that resulting from an application of the product.…”

“…[5] Moreover, urinary PEA levels are increased in patients undergoing anti-depressant therapy with the monoamine oxidase A and B inhibitor phenelzine, [6] and varying urine concentrations of PEA were also the subject of studies concerning psychiatric disorders in the past. [7] Despite the fact that the oral bioavailability of PEA is considered extremely limited due to extensive first-pass metabolic degradation [2,8] and studies calling into question whether long-term over-consumption of PEA represents a neurological risk factor, [9] PEA is widely sold as a dietary supplement.…”