Citation

Van Winkle E. Med. Hypotheses 2000; 55(4): 356-368.

Copyright

(Copyright © 2000, Elsevier Publishing)

DOI

10.1054/mehy.2000.1146

PMID

unavailable

Abstract

The continual suppression of emotions during fight or flight reactions results in atrophy and endogenous toxicosis in noradrenergic neurons. Diminished synaptic levels of norepinephrine are associated with depression. During periodic detoxification crises excess norepinephrine and other metabolites flood synapses. The norepinephrine overexcites postsynaptic neurons and causes symptoms ranging from mild anxiety to violent behavior. Some of the other metabolites, which may include dopamine, epinephrine, serotonin, gamma-aminobutyric acid, peptides, amino acids, and various metabolic waste products, are bound by noradrenergic receptors and alter neurotransmission. When they prevent norepinephrine from exciting postsynaptic neurons, depression returns. A mechanism is proposed for the binding of norepinephrine and for the effects of the other metabolites, many of which have been thought to be neurotransmitters. The diverse receptor proteins presumed to be specific for false neurotransmitters may instead encode specific memories. The shift in depressive and excitatory behavior is characteristic of nearly all nervous and mental disorders, including addictions, Alzheimer's disease, Parkinson's disease, and psychosomatic disorders. When toxins accumulate in regions of the brain that control specific activities, the symptoms observed will be related to those activities, giving rise to supposedly distinct disorders that represent the same detoxification process. Recovery can be facilitated by therapy and self-help measures that involve the releasing and redirecting of repressed emotions. Full text: http://homepages.nyu.edu/[small tilde]er26/toxicmind.html