Tryptophan and serotonin in schizophrenia.
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Biomedical subjects
Publications and source records attributed to D A Bender.
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The records of a selected group of 215 subjects who had successfully lost surplus weight were followed-up for periods of one to six years. Mean initial weight was 131% of standard (19.5 kg surplus) and the mean time taken to achieve 'goal weight' was 7.05 months (range two to 20 months) at a mean rate of 2.9 kg per month (range 1.85 to 5 kg). Altogether 121 subjects (56.3%) maintained goal weights within plus or minus 2.3 kg of goal; 79 subjects (36.7%) maintained within plus or minus 4.5 kg. At time of examination of the records, 39 subjects (18.8%) had maintained constant weight for more than four years, 22 subjects (10.6%) for three to four years, 65 subjects (31.4%) for two to three years, 58 subjects (28.5%) for one to two years, and 23 subjects (11.1%) for periods of up to one year.
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The concentration of tryptophan not incorporated into protein or polypeptides in the pancreas of male rats rose two- to three-fold in response to a 24 hrs period of food deprivation. On refeeding or intra-peritoneal administration of glucose the level of tryptophan in the pancreas fell, while that in the serum rose. The pancrease B-cytotoxic agents alloxan and streptozotocin both abolished this response to fasting, while neutral red (an A-cytotoxic agent) had no effect. It therefore appears that the tryptophan which accumulates in the pancreas during fasting is located mainly in the B-cells of the Islets of Langerhans. In female rats, the concentration of tryptophan in the pancreas was greater at dioestrus than at any other stage of the oestrous cycle. The increase in pancreatic tryptophan was maximal at metoestrus and minimal at oestrus.
Withdrawal of drug from a group of chlorpromazine-treated chronic male schizophrenics led to a significant rise in the initially low serum tryptophan concentration, and a rise in the fraction freely diffusible. These changes, which would be expected to lead to an increase in tryptophan influx into the brain, and hence to an increase in cerebral serotonin synthesis, could be related to the clinical effects of drug withdrawal.
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