Citation

Van Winkle E. Med. Hypotheses 2000; 54(1): 146-156.

Affiliation

Millhauser Laboratories of the Department of Psychiatry, New York University School of Medicine, New York 10016, USA. rotuneol@popmail.med.nyu.edu

Copyright

(Copyright © 2000, Elsevier Publishing)

DOI

10.1054/mehy.1998.0834

PMID

10790741

Abstract

The continual suppression of emotions during fight or flight reactions results in atrophy and endogenous toxicosis in noradrenergic neurons. Toxic metabolites interfere with neurotransmission, causing depression. During periodic detoxification crises, excess norepinephrine floods synapses overexcite postsynaptic neurons, and cause symptoms ranging from mild anxiety to violent behavior. When toxic metabolites, which may include excess dopamine, epinephrine, serotonin, gamma-aminobutyric acid, peptides, amino acids, and various metabolic waste products, are bound to noradrenergic receptor sites, these sites become unavailable to norepinephrine. Excitation of postsynaptic neurons is diminished and depression returns. The diverse proteins in receptor sites presumed to be specific for false neurotransmitters may instead encode specific memories. The shift in depressive and excitatory behavior is characteristic of most psychiatric disorders, addictions, Alzheimer's disease, Parkinson's disease, and psychosomatic disorders. Recovery is a detoxification process and can be facilitated by therapy that involves re-experiencing childhood traumas, releasing, and redirecting repressed emotions.

Language: en