Endorphins and psychiatry.

The term 'endorphin' (a combination of endogenous-morphine) is used to designate the entire group of peptides found in the brain and pituitary that mimic the biological properties of opiates. 'Endogenous opioid peptides', 'endogenous opioids' 'opioid peptide' and 'endopioids' can be considered as synonymous. Since the identification of stereospecific opiate receptors2J and the pentapeptides methionine and leucine enke~halin,~ more than 20 endogenous peptides have. been discovered and additional synthetic analogues have been developed. Although their precise function remains unknown evidence suggests they may act as neurotransmitters, neurohormones or neuromodulators. The link between endorphins and the pathogenesis of schizophrenic and affective states has been made on the observations and findings that: 1. endogenous opiates produce mood changes and schizophrenic-like symptoms, 2. anecdotal evidence of their prophylactic use against psychotic symptoms in heroin users, 3. the distribution of these peptides follows closely pathways involved in the mediation of pain and emotional behaviour 4. depressive and schizophrenic patients have higher pain thresholds. Two seemingly paradoxical hypotheses have been advanced following the observation that intracerebral administration of B-endorphin produced catatonic-like state in rodents. Bloom et a/.5 speculated that the catatonia was similar to motor abnormalities characteristic of some schizophrenias and was related to an excess of endorphin levels at receptor binding sites. Jacquet and Marks,6 on the other hand, compared the catatonia with the extrapyramidal rigidity produced by neuroleptics. They suggested a deficiency of endorphin activity in schizophrenia. The evidence in support of either hypothesis is inconclusive. Administration of B-endorphin, enkephalins or synthetic analogues to test the deficiency hypothesis has resulted in symptomatic improvement, deterioration or no change. A similar confused picture has emerged following the administration of the opiate antagonists, naloxone and naltrexone, to reduce assumed high endorphin levels.' Factors contributing to this confusion are the varied doses used on diagnostically heterogenous patients, the concurrent medication taken by some patients, the small sample sizes and the adequacy of assessment measures or procedures used. Gerner et a1.,* for example, investigated the effects of B-endorphin infusion in 10 depressed and eight schizophrenic subjects. While several measures were used and changes rated by different assessors at different times, only the overall ratings of psychopathology as determined by one scale, the modified Bunney-Hamburg scale, were reported on and discussed. The reader is left to assume that changes in other measures remained insignificant. Whether double-blind investigations were maintained in these studies is also open to question. Administration of B-endorphin …