The Role and Use of PEA in Depression & Neurobehavioral Disorders by DR RICHARD CLARK KAUFMAN The Phenylethylamine Hypothesis of Depression According to the "Phenylethylamine Hypothesis of Depression" proposed in 1974, the endogenous trace amine Beta- Phenylethylamine (PEA) sustains psychological energy just as thyroid hormone sustains physical energy And a deficit of PEA produces depressions. The Phenylethylamine hypothesis goes on to state that PEA is a neuromodulator of mood, attention, pleasure-seeking behavior, and libido. The phenylethylamine hypothesis led to simple safe and effective way of treating depression and other affective disorders by based on years of research conducted by Dr. Hector Sabelli and colleagues. Take an oral replacement of PEA as replacement to correct an underlying deficiency or defect in neural transmitter functioning. The majorities of depressed individuals show a significant reduction in their symptoms or have complete recovery without any adverse reactions. Plus, there're is significant increases in cognitive performance functions, attention, awareness, and feelings of pleasure, libido, normal social behavior and sense of wellbeing. PEA. More than Endogenous Amphetamine in our Brain The Phenylethylamine Hypothesis of Depression stems from the observation that amphetamines increased energy and relieved depressive symptoms of depressive patients. Amphetamine is essentially phenylethylamine with an added methyl group. Studies show that PEA induces behavioral and electrophysiological effects similar to those of amphetamine. Unlike amphetamine, PEA is endogenous to the brain and does not develop tolerance or dependency, or produce any side effects. The stimulant effects of amphetamines and PEA are attributed to the release of catecholamines (noradrenalin, dopamine). This is the basis for the catecholamine hypothesis of depression. However current research shows that PEA is significantly more effective than amphetamine in relieving depression and has therapeutic value in a wide range of neurological and behavioral disorders, Endogenous Mesencephalic Enhancer and Transmitter Signal Amplifier Starting around 1995, Dr Joesph Knoll and his colleagues began presenting their evidence of PEA as an endogenous "mesencephalic enhancer". There are enhancer-sensitive neurons in the brain work in a split-second on a high activity level due to endogenous enhancer substances. The mesencephalic enhancer PEA enhancers of the impulse propagation mediated release of catecholamines (dopamine, epinephrine) and serotonin in the brain.