Symptoms, disorders and chemistry.
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Biomedical subjects
Publications and source records attributed to S N Young.
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To determine whether the composition of feedings would affect newborn behavior independently of the act of feeding itself, 53 two- to three-day-old normal newborns were randomly assigned to receive an extra feeding of water, carbohydrate (lactose), or balanced formula 3 hours after their usual early morning feeding. Previous studies in adult humans and animals, and a single study in human newborns, have indicated that more sleep might be expected following the carbohydrate feed compared with the water and balanced-formula feeds because of recruitment of centrally mediated serotonergic systems. Behavioral effects were assessed for 40 minutes postfeeding by direct observation of the newborn's states (quiet, active, and indeterminate sleep; drowsiness; non-cry wakefulness; and fret/cry). Feed composition did affect behavior, and the effects were fairly specific to particular newborn states. Non-cry wakefulness and drowsiness were unrelated to the presence or type of nutrients, but they tended to occur soon after the meal in all groups. Crying was increased in water-fed newborns relative to both carbohydrate- and formula-fed newborns. Sleeping showed specific patterns of change in all three groups. Sleep duration was increased in the balanced-formula group compared with the water group throughout the observation period. Contrary to the prediction, sleeping duration in carbohydrate-fed newborns never exceeded that of formula-fed newborns; rather, it resembled that of water-fed newborns early in the postprandial period, but formula-fed newborns later. These effects could not easily be explained by potential confounding factors such as handling, volume ingested, caloric intake, or plasma glucose concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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In a double-blind controlled study lasting 4 weeks 25 newly admitted severely depressed patients were randomly assigned to tryptophan-nicotinamide or imipramine or tryptophan-nicotinamide-imipramine combination. Nicotinamide was given to reduce peripheral breakdown of tryptophan. Although there were no substantial differences between the three treatments, the efficacy of tryptophan-nicotinamide tended to diminish after 2 weeks when the dose of tryptophan was increased from 4 g/day to 6 g/day and that of nicotinamide from 1.0 g/day to 1.5 g/day. The therapeutic response of patients treated with tryptophan-nicotinamide was significantly correlated with the rise in plasma tryptophan. For the tryptophan-nicotinamide-imipramine group, however, therapeutic response and rise in plasma tryptophan were negatively correlated, implying that tryptophan levels were too high in some patients. The data suggest that tryptophan-nicotamide may be as effective as imipramine in unipolar patients providing the dose is kept within the therapeutic window, and that at low doses it could also potentiate the action of tricyclic antidepressants. Bipolar patients seem to require higher doses of tryptophan than unipolar patients.
Growth hormone antagonizes the induction of tryptophan pyrrolase and tyrosine amino-transferase by cortisol. We have shown that contrary to previous reports, growth hormone is also capable of antagonizing the induction of these enzymes by tryptophan and alpha-methyl tryptophan. As alpha-methyl tryptophan is not metabolized appreciably in the rat, our data show that growth hormone does not act indirectly through changes in the liver tryptophan content as was suggested previously. Growth hormone decreases the rate of tryptophan catabolism in vivo after induction of tryptophan pyrrolase by tryptophan and alpha-methyl tryptophan. Because the rate of catabolism of a tryptophan is slower in animals treated with growth hormone, tissue tryptophan levels and the rate of synthesis of 5-hydroxyltryptamine in the brain are higher in these animals than in those receiving tryptophan alone. Thus, although tryptophan administration raises brain 5-hydroxytryptamine levels, induction of tryptophan pyrrolase in the liver, by the load, limits the extent and duration of the rise in brain 5-hydroxytryptamine synthesis. This has important implications for the clinical use of tryptophan in psychiatric disorders, where tryptophan is given to produce long-lasting elevations of brain 5-hydroxytryptamine.
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To assess the possible role of amine neurotransmitters in human epilepsy, we measured metabolites of serotonin (5-hydroxyindoleacetic acid [5-HIAA]), dopamine (homovanillic acid [HVA]), and norepinephrine (3-methoxy-4-hydroxyphenylethylene glycol [MHPG]) in the lumbar cerebrospinal fluid (CSF) of patients with partial complex seizures and in neurologic controls. Untreated epileptic patients had lower concentrations of 5-HIAA and HVA in the lumbar CSF than the controls, but the differences were not statistically significant. Among epileptic patients receiving effective antiepileptic drug treatment, the HVA concentration was within the control range. Mean MHPG concentrations were similar in patients and controls. From the epileptic patients whose CSF was obtained at pneumoencephalography we obtained a second sample of CSF that was originally in the basal cisterns. No significant differences between treated and untreated patients were found for any of the three metabolites. The concentrations of HVA and 5-HIAA were higher in cisternal than in lumbar CSF, but there was no such gradient for MHPG.
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