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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The sleep-wake cycle of 12 tryptophan dietary deficient rats and their non-deficient paired controls were observed for a 8:00 a.m. to 8:00 p.m. period. EEG, EMG and body activity were continuously monitored on polygraphic recordings throughout the 12 hr observation period. The results indicate no significant difference between the tryptophan deficient and sufficient animals in time spent awake, slow-wave or parodoxical sleep. There was a non-significant trend among the tryptophan deficient animals to be less active and spend more time in both slow-wave and paradoxical sleep, which is in contrast to an expected insomnia effect. The results do not support the suggested relationship between reduced serotonin levels and the occurrence of insomnia, questioning the serotonergic theory of sleep.
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PMID:Effect of a chronic tryptophan dietary deficiency on the rat's sleep-wake cycle. 20 99

The author states that the use of the amino acid L-tryptophan as a hypnotic might avoid the problems of nonspecificity in the currently used CNS depressants because L-tryptophan is chosen on the basis of the chemistry of normal sleep rather than on a purely empirical basis. He reviews nine studies from his laboratory dealing with the effects of L-tryptophan on sleep. Studies in rats, normal human subjects, and subjects with mild insomnia all demonstrate that L-tryptophan reduces sleep latency. Polygraphic studies demonstrate that L-tryptophan, unlike hypnotics, does not produce distortions of sleep physiology when first administered, on long-term administration, or after withdrawal.
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PMID:L-tryptophan: a rational hypnotic with clinical potential. 32 Aug 87

The authors report a case of eosinophilia-myalgia syndrome with a progressive neuromyopathy. Progressive weakness, myalgia, and dermatitis developed in the patient described after chronic ingestion of high-dose L-tryptophan for insomnia. Laboratory, electrophysiologic, and muscle biopsy results support the diagnosis of an inflammatory myopathy consistent with that of eosinophilia-myalgia syndrome. The patient's weakness led to wheelchair dependency. A review of the literature regarding this disorder shows inconsistent results with steroid and other modes of therapy. After a course of high-dose steroids with long-term tapering and vigorous inpatient and outpatient rehabilitation, the patient was able to walk and function independently within 2 months.
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PMID:Clinical improvement of the myopathy in eosinophilia-myalgia syndrome with steroids and rehabilitative therapy. 142 67

Several developments in serotonin neuropharmacology have implications for psychiatric disorders and have already begun to impact their treatment. Selective inhibitors of serotonin uptake, which enhance serotonergic function by preventing the removal of serotonin from the synaptic cleft via the membrane transporter, have been introduced for the treatment of depression and may be effective in other disorders. Precursor loading can increase serotonin concentrations in the synaptic cleft, and tryptophan--which has been available in health food stores and drug stores--had become increasingly used for self-medication of depression, insomnia, and premenstrual syndrome. Conversion to serotonin is not the major metabolic pathway for tryptophan, and large increases in other tryptophan metabolites (such as quinolinic acid, a substance that is excitotoxic at high concentrations) accompany small increases in extracellular serotonin. The recent epidemic of the eosinophilia-myalgia syndrome associated with tryptophan now appears due to a trace contaminant in the product from a single manufacturer. A major advance in serotonin pharmacology has been the elucidation of serotonin receptor heterogeneity. At least seven receptor subtypes (5-HT1A, 5-HT1B, 5-HT1C, 5-HT1D, 5-HT2, 5-HT3, 5-HT4) have been identified in brain. Direct-acting agonists and antagonists can have selective affinity for specific receptor subtypes. Selective activation of 5-HT1A receptors seems to cause anxiolytic and possibly antidepressive effects. Selective antagonists of 5-HT2 or 5-HT3 receptors may be useful in treating anxiety and schizophrenia. Drugs that enhance serotonergic function suppress aggression in animals, but the specific receptor subtypes involved are not known. The advances being made in serotonin pharmacology will help define the role of this brain neurotransmitter in psychiatric and other disorders and can be expected to lead to further therapeutic advances.
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PMID:Role of serotonin in therapy of depression and related disorders. 167 51

An association between the ingestion tryptophan and a syndrome characterized by scleroderma-like skin abnormalities, fasciitis, and eosinophilia has recently been recognized in the United States. We report the clinical and histopathological findings in nine patients and the results of biochemical analyses of tryptophan metabolism in seven patients with this syndrome. Edema of the extremities, frequently accompanied by pruritus, paresthesia, and myalgia, developed in the nine patients (six women and three men; age range, 30 to 66 years) 1 to 18 months after the start of therapy with tryptophan (1.5 to 3.0 g daily) for insomnia, depression, or obesity. Five patients were taking drugs (benzodiazepines) known to inhibit hypothalamic-pituitary-adrenal function, and one had adrenal insufficiency. All had blood eosinophilia in the acute phase of their illness (mean eosinophil count [+/- SD], 3.62 +/- 2.87 X 10(9) cells per liter). All had histopathological changes in the dermis and subcutaneous tissue typical of scleroderma, and seven patients had eosinophils. The fascia was inflamed and fibrotic, and adjacent skeletal muscle often showed perifascicular inflammation. Tryptophan was discontinued in all patients, and eight received prednisone. The cutaneous symptoms improved, but only two patients had complete resolution of their illness. The patients had plasma levels of tryptophan before and after an oral dose of tryptophan that were similar to those in normal subjects. Plasma levels of L-kynurenine and quinolinic acid, which are metabolites of tryptophan, were significantly higher in four patients with active disease than in three patients studied after eosinophilia had resolved or in five normal subjects (P less than 0.001)--findings consistent with the activation of the enzyme indoleamine-2,3-dioxygenase. This illness resembles eosinophilic fasciitis and probably represents one aspect of the recently reported eosinophilia-myalgia syndrome. The development of the syndrome may result from a confluence of several factors, including the ingestion of tryptophan, exposure to agents that activate indoleamine-2,3-dioxygenase, and possibly, impaired function of the hypothalamic-pituitary-adrenal axis.
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PMID:Scleroderma, fasciitis, and eosinophilia associated with the ingestion of tryptophan. 231 25

In a single-blind study six male patients (mean age 39.5 years) with moderate insomnia were treated with placebo for three nights, 100 mg indole-3-pyruvic acid (IPA) for three nights, 200 mg IPA for three nights, 100 mg IPA for two nights and placebo for two nights. Polygraphic recordings were made and total sleep time, sleep efficiency, sleep latency, slow wave sleep latency, rapid eye movement (REM) sleep latency, number of arousals (greater than 1 min), percentage and duration of wakefulness after sleep onset, percentage and duration of wakefulness after sleep onset, percentage and duration of sleep stages 1, 2, 3, 4 and REM were recorded. At the end of 13 days, total sleep time, duration of stage 2 sleep and total non-REM were significantly increased when compared with baseline. Total sleep time and duration of stage 2 and total non-REM sleep on completion were significantly decreased when compared with after 200 mg IPA (night 9). Results suggest an action of IPA on human sleep similar to that of exogenous melatonin and L-tryptophan, thus confirming that IPA could be used to increase serotonin and melatonin turnover.
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PMID:Indole-3-pyruvic acid as a possible hypnotic agent in insomniac subjects. 174 33

Recently there have been reports that long-term use of estrogen- containing oral contraceptives (OCs) can induce folic acid and vitamin B deficiency which can lead to hematopoiesis. The symptoms are paleness, forgetfulness, sleeplessness, and euphoric and depressive states. This deficiency occurs when serum folic content falls below 8 nmol/1 or 3 ng/ml. According to a nutrition group blood folic acid level declined up to 40% in patients taking OCs. In a Sri Lanka study of healthy women aged 20-45 taking Ovulen 50 (.05 mg of ethinyl estradiol and 1 mg of ethynodiol diacetate) folic acid level dropped in the 1st 6 months stabilizing at 2.2 ng/ml in those from the lowest social classes and at 2.9 ng/ml in those from privileged classes. Prophylactic substitution of folic acid in the diet was recommended by WHO, but it is less effective since it appears in the diet as polyglutamate that has to be broken down to absorbable monoglutamate. A US study found that taking OCs for 60 months resulted in a 40% reduction of the vitamin B12 serum level, while vitamin B12 concentrations in erythrocytes and peripheral blood stayed normal. Vitamin B12 helps recover tetrahydrofolic acid from N-methyltetrahydrofolic acid. Possibly this is another manifestation of OC-induced folic acid hypovitaminosis. OCs can also influence tryptophan metabolism reducing its blood concentration whereby less 5-hydroxytryptamine (serotonin) is produced. This results in headache, concentration decreases irritability, and sleep disturbances. In addition, lower riboflavin (vitamin B2) and thiamin concentration in erythrocytes was reported after using OCs. Counseling on the possible effect on vitamin stores and on proper nutrition including folic acid as monoglutamate is necessary for women who use OCs or estrogen substitution therapy for postmenopause or for osteoporosis prophylaxis.
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PMID:[Folic acid and vitamin deficiency caused by oral contraceptives]. 192 42

L-tryptophan is an essential amino acid taken as an over-the-counter nutritional supplement for a variety of conditions including chronic pain, insomnia, and depression. In October 1989 several patients were reported having eosinophilia-myalgia syndrome (EMS) who had taken L-tryptophan in large doses. Little is known about the long-term outcomes of EMS. A patient with EMS who developed contractures of the upper extremities because of severe myalgias is discussed. Early aggressive rehabilitative intervention may prevent contractures in patients with EMS.
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PMID:Upper extremity contractures in a patient with eosinophilia-myalgia syndrome. 195 17

We describe a patient who developed fever, fatigue, muscle weakness, dyspnea, skin rash, and eosinophilia after taking "high doses" of tryptophan for insomnia for two years. A gallium-67 scan revealed diffuse increased uptake in the lung and no abnormal uptake in the muscular distribution. Bronchoscopy and biopsy confirmed inflammatory reactions with infiltration by eosinophils, mast cells, and lymphocytes. CT scan showed an interstitial alveolar pattern without fibrosis. EMG demonstrated diffuse myopathy. Muscle biopsy from the right thigh showed an inflammatory myositis with eosinophilic and lymphocytic infiltrations.
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PMID:Gallium uptake in tryptophan-related pulmonary disease. 199 38

The dexamethasone suppression test (DST), the thyrotropin releasing hormone (TRH) test, and the ratio of plasma L-tryptophan to competing amino acids (L-TRP/CAA) were studied in relation to the 21 items of the Hamilton Depression Rating Scale (HDRS) in 123 depressed patients categorized according to DSM-III. The relationships between the biological data and the items or item clusters of the HDRS were assessed by multivariate analyses. The psychopathological correlates of increased post-dexamethasone cortisol and decreased thyroid stimulating hormone (TSH) responsivity to TRH were middle and delayed insomnia and weight loss. The symptom correlates of decreased availability of L-TRP to the brain were psychic anxiety, depersonalization, obsessions and paranoid symptoms. Core depressive symptoms, i.e. depression, loss of interest, feelings of guilt and suicidal thoughts, were not related to the biological markers.
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PMID:Symptom profiles of biological markers in depression: a multivariate study. 211 48


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