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Biomedical subjects

S N Young

Publications and source records attributed to S N Young.

At least 19 recordsLinked to original sources
PubMed1995

Acute effect of altered tryptophan levels and alcohol on aggression in normal human males.

Normal males received amino acid mixtures designed to raise or lower tryptophan availability, and thus to raise or lower brain serotonin synthesis. They also received alcoholic or non-alcoholic drinks. The subjects were tested in the Taylor Competitive Reaction Time Task in which they competed against a (non-existent) partner in a reaction time task. The magnitude of electric shocks that the subjects were willing to give to their bogus partner was used as a measure of aggression. Lowered tryptophan levels and ingestion of alcohol were associated with increased aggression. Our data support the idea that low serotonin levels may be involved in the etiology of aggression. They suggest that subjects with low brain serotonin levels may be particularly susceptible to alcohol-induced violence.

Adolescent↗
PubMed1995

Maternal dietary carbohydrate restriction influences the developmental profile of postnatal rat brain indoleamine metabolism.

Dietary glucose restriction during pregnancy can retard fetal brain development, lower term brain glycogen levels and adversely affect the serotonergic neurotransmitter system in the fetus. To study if the postnatal profile of brain indoles continues to respond to these diet-induced changes, pregnant rats were fed graded levels (0, 12, 24, 60%) of glucose from impregnation to day 15 postpartum, and neonatal brain measurements were made. A steady decrease in tryptophan levels, a steady increase in 5-hydroxytryptamine (5-HT) levels and a U-shaped change in 5-hydroxyindoleacetic acid (5-HIAA) were observed during the first 15 postpartum days. Superimposed on these development profiles was a temporary surge in the concentrations of all three indoles 24 h after birth, which was dramatic for tryptophan and more modest for 5-HT and 5-HIAA. The level of carbohydrate in the maternal diet significantly influenced the magnitude of this increase in tryptophan, 5-HT and 5-HIAA at 24 h: the values were significantly higher in the carbohydrate-restricted (12 or 24%) rat pups when compared with control or carbohydrate-free (0% glucose) offspring. No effects of dietary treatment were apparent by day 6. However, the reemergence of a significant difference in brain 5-HT content at day 15 postpartum indicates that even when energy intake is adequate the level of carbohydrate in the maternal diet may continue to play a role in modulating serotonergic neurotransmitter levels later in development.

Animals↗
PubMed1995

"Sucrose analgesia" and diphtheria-tetanus-pertussis immunizations at 2 and 4 months.

In human newborns, small amounts of sucrose reduce crying with procedural pain by about 50%. To determine whether "sucrose analgesia" could be extended to painful procedures beyond the newborn period, 57 infants were randomly assigned to receive three 250-microliters doses of 50% sucrose solution (g/100 mL) or water before their diphtheria-tetanus-pertussis immunizations at 2 and 4 months of age. Crying during and after injection was measured separately to determine whether sucrose modified crying during the noxious stimulus, recovery from the stimulus, or both. Sucrose was effective in reducing crying only from 83 to 69%, and the reduction was limited to the postinjection period. We conclude that, although sucrose continues to have some effect beyond the newborn period, the effect is limited to recovery from the noxious stimulus, is clinically modest, and is probably smaller than in the newborn period.

Crying↗
PubMed1994

Caffeine and propranolol block the increase in rat pineal melatonin production produced by stimulation of adenosine receptors.

The adenosine agonist 5'-N-ethylcarboxamidoadenosine (NECA) injected i.p. during the light period increased rat pineal melatonin levels and this increase was blocked by simultaneous administration of the non-selective adenosine receptor antagonist caffeine. A single dose of the adenosine A1 agonist cyclopentyladenosine had no effect on nocturnal melatonin production. The NECA-stimulated increase was also blocked by the beta-adrenergic receptor antagonist propranolol. Given alone, neither caffeine nor propranolol had any effect on melatonin levels. The results point to an intermediate role for beta-adrenergic receptors in the adenosine-stimulated increase of melatonin production.

Adenosine↗
PubMed1994

Mood-lowering effect of tryptophan depletion. Enhanced susceptibility in young men at genetic risk for major affective disorders.

METHODS: A double-blind placebo-controlled cross-over study in which plasma tryptophan was manipulated by administration of a tryptophan-deficient amino acid mixture. In the placebo condition, all subjects received a nutritionally balanced amino acid mixture that contained tryptophan. To further standardize baseline amino acids, each subject was provided with a low-protein diet the day before amino acid challenges. Subjects were euthymic, healthy men aged 18 to 30 years with either a multigenerational family history of affective illness or no family history of psychiatric illness in the present or in the two previous generations. Each subject was screened with a structured clinical interview to rule out a personal history of psychiatric illness. RESULTS: Plasma tryptophan was reduced by 89% 5 hours after the administration of the tryptophan-deficient amino acid mixture. Six of 20 subjects with a family history of affective illness and none of 19 subjects without a family history of psychiatric illness showed a lowering of mood of 10 or more points on the Profile of Mood States depression scale (P = .012, Fisher's Exact Test) 5 hours after tryptophan depletion. No significant mood changes were observed following the control treatment (balanced amino acid mixture) in either group. CONCLUSIONS: Our data support the hypothesis that subjects with no prior depressive episodes but with a multigenerational family history of major affective disorder show a greater reduction in mood after tryptophan depletion. They are also consistent with theories that implicate deficient serotonergic function as one possible etiological factor in major depressive disorders.

Adolescent↗
PubMed1994

Effects of intra-oral sucrose on crying, mouthing and hand-mouth contact in newborn and six-week-old infants.

To determine whether a single intra-oral administration of sucrose would calm infants and elicit mouthing and hand-mouth contact, crying newborn and six-week-old infants were given sucrose solution before one feed and sterile water before another in a cross-over trial. Six-week-old infants were also given sucrose and water after feeding. For the newborn infants, the calming effect was rapid, substantial and lasted for at least four minutes. Mouthing and hand-mouth contact increased, but for shorter durations. For the six-week-old infants, sucrose calmed for one minute only before feeding, but had no effects on mouthing or hand-mouth contact. The results imply that intra-oral sucrose has acute age-related effects on crying and suckling-feeding behaviour mediated by a pre-absorptive mechanism. Sucrose may tap a functional system for reducing distress related to feeding and/or regulation of infant state.

Administration, Oral↗
PubMed1994

Tryptophan in the treatment of late luteal phase dysphoric disorder: a pilot study.

Thirteen patients diagnosed during two menstrual cycles as suffering from late luteal phase dysphoric disorder were then followed in an open pilot study for a further three cycles. During one complete cycle, baseline levels of symptoms were obtained. During the next three cycles, the patients were treated with L-tryptophan, six grams per day. L-tryptophan treatment was associated with a significant amelioration of symptoms with only mild side effects. These data suggest that L-tryptophan should be tested at a dose of six grams of L-tryptophan per day in a placebo-controlled study in patients with late luteal phase dysphoric disorder who suffer from symptoms such as depression, irritability, insomnia and carbohydrate craving, which may respond to potentiation of serotonin function.

Adult↗
PubMed1993

Restriction of maternal dietary carbohydrate decreases fetal brain indoles and glycogen in rats.

In spite of evidence that dietary carbohydrate can increase brain tryptophan and 5-hydroxytryptamine in adult rats, the possible influence of maternal dietary carbohydrate on fetal brain indoles has received little attention. We studied the effect of graded levels (0, 4, 12 and 60%) of maternal dietary fructose or glucose fed throughout pregnancy on fetal brain glycogen and indoles. The diets were isoenergetic and met the NRC energy requirements for pregnant rats. The results demonstrated that low maternal dietary carbohydrate, with adequate energy intake, reduced fetal brain weight and concentrations of glycogen, tryptophan, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid. There were no significant differences between glucose and fructose feeding at any dietary carbohydrate level for any fetal brain measurements, showing that it was the level and not the type of dietary carbohydrate that was important. Significant correlations between fetal brain 5-hydroxytryptamine and brain glycogen, and between fetal brain 5-hydroxytryptamine and brain weight, suggested that lowered brain 5-hydroxytryptamine was only one symptom of disrupted brain development in fetuses of dams fed low levels of carbohydrate. The results show that dietary carbohydrate restriction during pregnancy can have adverse effects on fetal brain development, glycogen levels, and neurotransmitter synthesis even when maternal dietary protein and energy intake are adequate.

Animals↗
PubMed1993

The use of diet and dietary components in the study of factors controlling affect in humans: a review.

Although one of the first biological treatments of a major psychiatric disorder was the dietary treatment of pellagra, the use of diet and dietary components in the study of psychopathology has not aroused much interest. This article reviews three areas in which the dietary approach has provided interesting information. The tryptophan depletion strategy uses a mixture of amino acids devoid of tryptophan to lower brain tryptophan in order to study the symptoms that can be elicited. One effect of tryptophan depletion is a lowering of mood, the magnitude of which seems to depend on the baseline state of the subject. Therefore, recovered depressed patients often undergo an acute relapse, while normal subjects show more moderate changes of mood. Totally euthymic subjects show no lowering of mood, but subjects with high normal depression scale scores or subjects with a family history of depression show a moderate lowering of mood. These data indicate that low serotonin levels alone cannot cause depression. However, serotonin does have a direct effect on mood, and low levels of serotonin contribute to the etiology of depression in some depressed patients. Folic acid deficiency causes a lowering of brain serotonin in rats, and of cerebrospinal fluid 5-hydroxyindoleacetic acid in humans. There is a high incidence of folate deficiency in depression, and there are indications in the literature that some depressed patients who are folate deficient respond to folate administration. Folate deficiency is known to lower levels of S-adenosylmethionine, and S-adenosylmethionine is an antidepressant that raises brain serotonin levels. These data suggest that low levels of serotonin in some depressed patients may be a secondary consequence of low levels of S-adenosylmethionine. They also suggest that the dietary intake and psychopharmacological action of methionine, the precursor of S-adenosylmethionine, should be studied in patients with depression. Normal meals have definite effects on mood and performance in humans. The composition of the meal, in terms of protein and carbohydrate content, can influence these behaviors. Because protein and carbohydrate meals can influence brain serotonin in rats, these effects in humans have usually been interpreted in terms of altered serotonin functioning. However, the current balance of evidence is against the involvement of serotonin in the acute effects of protein and carbohydrate meals in humans. The underlying mechanisms involved are unknown, but there are a variety of possibilities.(ABSTRACT TRUNCATED AT 400 WORDS)

Affect↗
PubMed1992

Acute tryptophan depletion blocks morphine analgesia in the cold-pressor test in humans.

The effects of depletion of the serotonin precursor, L-tryptophan, on the threshold and tolerance to cold pressor pain, and the analgesic effect of morphine (10 mg intramuscularly), were tested in a double blind trial on human volunteers. Effects on mood were also assessed using the Profile of Mood States and the Addiction Research Center Inventory (ARCI) Scales. To deplete tryptophan, subjects were fed a tryptophan-deficient amino acid mixture 4.5 h before morphine was administered. Controls received the mixture with tryptophan, which is equivalent to a nutritionally balanced protein. The tryptophan-deficient meal reduced plasma tryptophan more than 70% but had no effect on threshold or tolerance to cold pressor pain. After morphine, tolerance to cold pressor pain increased in controls. Tryptophan depletion abolished this analgesic effect. Pain threshold was not altered by morphine. In subjects with normal tryptophan, the analgesic effect of morphine was predicted by the level of plasma morphine-6-glucuronide, but not by the level of morphine. Morphine increased scores on the LSD scale of the ARCI, but had no effect on other measures of mood. Tryptophan depletion also failed to alter mood in these subjects, who had unusually low depression scores before tryptophan depletion.

Adolescent↗
PubMed1992

Short-term effects of feed composition on sleeping and crying in newborns.

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)

Crying↗