Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with tuberculous meningitis developed a pellagra-like skin eruption after treatment with isoniazid. Administration of the drug was continued, and a topical preparation of niacinamide (nico-tinamide) was applied to one half of the face and the back of one hand. The areas treated responded rapidly, and subsequently all affected areas of the patient were treated, with almost complete resolution of the rash. At the same time, there was noticeable improvement in the patient's depression and apathy. We suggest that all of these changes could be due to percutaneous absorption of niacinamide.
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PMID:Topically applied niacinamide in isoniazid-induced pellagra. 12 35

Young rats were fed a niacin-deficient diet with and without 15 g/kg supplementary L-leucine. Both groups grew slowly for 5 wk and showed no difference in the severity of their condition. Nor did their 14CO2 production differ after intraperitoneal dosing with [methylene-14C]tryptophan. In a 2 X 3 X 3 multifactorial trial with a niacin-free basal diet, the effects of 15 g/kg supplementary leucine were compared with isonitrogenous glycine supplements. Half of the diets were also marginally deficient in pyridoxine and resulted in slower growth, but no interactive effect with leucine. The leucine supplement depressed excretion of N1-methylnicotinamide only in the groups receiving supplementary tryptophan. It was also associated with a depression in the level of nicotinamide nucleotides in the rats' livers that was not eliminated by addition of either 25 mg/kg nicotinic acid or 1 g/kg L-tryptophan. The existence of pellagra in Hyderabad, India, has been hypothesized to result from excessive leucine in the diet rather than from a deficiency of niacin/tryptophan. Neither our results with rats nor those of others appear to provide support for this hypothesis.
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PMID:Leucine excess and niacin status in rats. 295 74

Deficiencies of specific vitamins produce consistent symptoms of psychiatric disorder. Thiamine deficiency, which is common in alcoholism, can produce confusion and psychotic symptoms, in addition to neurological signs. Vitamin B12 and folate deficiency may contribute symptoms of disorientation, depression or psychosis; their measurement is a part of routine dementia work-ups. Pyridoxine deficiency results in seizures, although the effects of exogenously administered pyridoxine are not clearly understood in depression and anxiety - the disorders in which it is most frequently used clinically. The use of vitamins has been most prominent in psychiatry in the treatment of schizophrenia, where large doses of nicotinic acid were initially given alone and later combined with other vitamins and minerals. Several theoretical models were described to support the use of vitamins in schizophrenia. These included: the parallels of schizophrenia to the psychiatric symptoms of pellagra; hypotheses of a defect in adrenaline metabolism; and the accumulation of psychotoxic substances which produce psychotic symptoms. Initially, positive results were reported over 30 years ago, but have not been replicated by thorough investigations. An extensive series of comprehensive placebo-controlled trials failed to show efficacy for any of the vitamin therapies tested. Although clearly less effective than antipsychotic drug treatment, vitamin therapy is not without risks - adverse effects have been reported with nicotinic acid, pyridoxine and vitamin C.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vitamins in psychiatry. Do they have a role? 389 44

Three experiments were carried out to determine the effects of feeding a niacin-free diet (NFD) to immature quail. The first two experiments demonstrated that the results were influenced by the age of the birds. Birds placed on test at 4 weeks of age (57 g) had reduced growth rates but did not readily develop niacin deficiency symptoms. In contrast, newly hatched chicks (7.2 g) were highly sensitive as all birds died within 9 days of being fed the NFD. In the third experiment the NFD was fed to birds that were intermediate in weight (19 g) to those in the first two experiments. Niacin deficiency led to a marked depression in growth, closure of eyes, reduced activity and a marked atrophy of the pectoral muscle. There was a dramatic reduction in the level of NAD and NADPH in the pectoral muscle but not in other tissues. The niacin status of quail did not affect the activity levels of metabolically related or unrelated enzymes in liver or pectoral muscle. It may be concluded that niacin deficiency reduces pyridine nucleotide levels in muscle tissue but not other tissues and that it does not affect the activity level of certain enzymes in muscle or liver tissue.
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PMID:Effects of niacin deficiency on pyridine nucleotide levels and enzyme activities in various organs of young growing quail. 707 17

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)
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PMID:The use of diet and dietary components in the study of factors controlling affect in humans: a review. 829 22

Some diseases develop dementia, but they may be dementia-like-situation, such as depression and drugs induced one. There are many causes as an etiology of dementia. Among them a lots of diseases are treatable dementia, like chronic subdural hematoma, normal pressure hydrocephalus, brain abscess, syphilis, herpetic encephalitis, Wilson's disease, hypothyroidism, parathyroid disease, vitamin B12 deficiency, pellagra etc. In examination of patients with dementia, exact history taking, physical examination and laboratory examination should be done carefully. In the patients with Alzheimer's dementia and cerebrovascular disease's dementia, as many risk factors are known, we must try to treat and exclude each risk factor and protect the dementia. Inactivity of physical and mental function is reported to induce the dementia, so activation of them could prevent the development and the progression of dementia. In future the methods of the prevention of apoptosis and cell death would be found in order to prevent the dementia. Free radical scavenger, nerve trophic factor, cytokine, antagonist of glutamate etc. will have the possibility to become the medicine for the dementia. The nerve transplantation, nerve transmitter, nerve peptide etc. might serve as the allopathic treatment for the dementia.
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PMID:[Aging of brain and the maintenance of the function]. 875 27

The history of pharmacotherapy of mental illness can be divided into three periods. Introduction of morphine, potassium bromide, chloral hydrate, hyoscine, paraldehyde, etc., during the second half of the 19th century (first period), led to the replacement of physical restraint by pharmacological means in behavior control. Introduction of nicotinic acid, penicillin, thiamine, etc., during the first half of the 20th century (second period), led to significant changes in the diagnostic distribution of psychiatric patients; psychoses due to cerebral pellagra, and dementia due to syphilitic general paralysis virtually disappeared from psychiatric hospitals, and the prevalence of dysmnesias markedly decreased. Treatment with therapeutically effective drugs of mania, schizophrenia, depression, bipolar disorder, generalized anxiety disorder, panic disorder, obsessive compulsive disorder, Alzheimer's disease, etc., during the second half of the 20th century (third period), brought to attention the heterogeneity of the populations within the diagnostic categories of schizophrenia and depression. Introduction of the first set of psychotropics and the spectrophotofluorimeter during the 1950s triggered the development of neuropsychopharmacology. Introduction of genetic technology for the separation of receptor subtypes in the 1980s opened the path for the "tailoring" of psychotropic drugs by the dawn of the 21st century, to receptor affinities.
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PMID:Pharmacotherapy of mental illness--a historical analysis. 1138 74

Previous work has shown that niacin deficiency in rats increases the severity of ethylnitrosourea (ENU)-induced anemia and leukopenia and the long-term development of cancer. The current study was initially designed to characterize changes in bone marrow cell populations during ENU treatment in this model. Weanling Long-Evans rats were fed diets containing 0 or 30 mg/kg of added niacin for a period of 2-3 wk. ENU treatment started after 1 wk of feeding and consisted of either 4 or 8 doses of ENU delivered by gavage, every other day. Niacin deficiency (ND) alone caused a significant depression in nucleated red blood cells (30%), and a sporadic effect on granulocytes (+23% after 4 doses of vehicle, -29% after 8 doses of vehicle). ENU treatment, after only 4 doses, caused a large decline in the numbers of bone marrow cells, and this effect was enhanced by ND (ENU decreased lymphocytes by 66% in pair-fed (PF) and 86% in ND, granulocytes by 41% in PF and 64% in ND, and nucleated red blood cells by 63% in PF and 71% in ND). Cell cycle distribution suggested that bone marrow cells in niacin-adequate rats, but not ND rats, mounted a compensatory proliferative response during chronic ENU exposure. ND alone caused an 80% decrease in bone marrow NAD+ levels at all time points. Surprisingly, chronic exposure to ENU (which should cause DNA damage and NAD+ utilization) led to a 2.8-fold increase in NAD+ content in ND marrow cells. This finding led to a second study in which ND and niacin-adequate PF control rats received 7 doses of ENU or vehicle (CON), after which all rats received 1 dose of ENU. In this study, modestly enhanced bone marrow NAD+ in chronically treated PF rats was used to synthesize 2-fold greater amounts of poly(ADP-ribose) than seen after one acute dose of ENU, while this did not occur in chronically treated ND rats, in spite of a 2.8-fold increase in bone marrow NAD+. This study has shown that bone marrow cell populations are sensitized to ENU treatment by ND, that NAD+ pools are regulated in response to DNA damage, and that NAD+ localization and/or utilization in the nucleus is altered during ND and chronic DNA damage.
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PMID:Chronic DNA damage and niacin deficiency enhance cell injury and cause unusual interactions in NAD and poly(ADP-ribose) metabolism in rat bone marrow. 1279 12

Pellagra is a systemic disturbance caused by a cellular deficiency of niacin, resulting from inadequate dietary nicotinic acid and/or its precursors, the essential amino-acid tryptophan. In Europe and North America cases of pellagra are rarely encountered, but in some developing countries this disease is frequent, and is the most frequent clinical feature of nutritional deficiency of adult. The principal causes of pellagra are: nutritional niacin deficiency; chronic alcoholism; gastro-intestinal malabsorption; some medications (5-fluoro-uracil, isoniazid, pyrazinamide ehtionamide, 6-mercaptopurine, hydantoins, phenobarbital and chloramphenicol). The diagnosis of pellagra is based on the patient's history and the presence of "3 D syndrome": dermatitis, diarrhea, and dementia. The dermatitis caused by pellagra is a bilaterally symmetrical erythema at the sites of solar exposure. The dermatitis begins in the form of an erythema with acute or intermittent onset gradually changing to an exsudative eruption on the dorsa of the hand, face, neck, and chest with pruritus and burning. Acute dermatitis of pellagra resembles sunburn in the first stages, sometimes with vesicles and bullae. The gastro-intestinal disturbances are: anorexia, nausea, epigastric discomfort and chronic or recurrent diarrhea. Anorexia and malabsorbative diarrhea lead to a state of malnutrition and cachexia. Stools are typically watery, but occasionally can be bloody and mucoid. Neuropsychologic manifestation included photophobia, asthenia, depression, hallucinations, confusions, memory loss and psychosis. As pellagra advances, patient become disoriented, confused and delirious; then stuporous and finally die. Pathological changes in the skin is non-specific, there are no chemical tests available to definitively diagnose pellagra. However low levels of urinary excretion of N-methylnicotinamide and pyridone indicates niacin deficiency. The treatment of pellagra consisted to exogenous administration of niacin or nicotinamide cures. Topical management of skin lesions with emollients may reduce discomfort. The therapy should also include other B vitamins, zinc and magnesium as well as a diet rich in calories. The prevention is based in the nutritional education (food sources of niacin: eggs, bran, peanuts, meat, poultry, fish, red meat, legumes and seeds), and the eviction of alcohol.
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PMID:[Pellagra]. 1620 85

Niacin is converted in tissues to NAD(+), which is required for synthesis of the intracellular calcium signaling molecule cyclic ADP-ribose (cADPR). cADPR is involved in many aspects of cognitive function, including long-term depression, in the hippocampus, a brain region that regulates spatial learning ability. The objective of this study was to determine whether niacin deficiency and pharmacological nicotinamide supplementation have an effect on spatial learning ability in young male Long-Evans rats as assessed by the Morris Water Maze, and whether brain NAD(+) and cADPR are modified by dietary niacin intake. We investigated 3 models of niacin deficiency: niacin deficient (ND) vs. pair fed (PF), ND vs. partially feed restricted (PFR), and ND vs. niacin recovered (REC). ND rats showed an improvement in spatial learning ability relative to PF, PFR, and REC rats. ND rats also showed a decrease in both NAD(+) and cADPR relative to PF and REC rats. We also investigated 1 model of pharmacological supplementation, niacin-supplemented vs. control. The niacin-supplemented group showed a small but significant spatial learning impairment relative to controls, and an increase in brain cADPR and NAD(+). Changes in neural function related to the NAD(+) associated calcium signaling molecule, cADPR, may be the link between diet and behavior.
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PMID:Water maze performance in young male Long-Evans rats is inversely affected by dietary intakes of niacin and may be linked to levels of the NAD+ metabolite cADPR. 1737 75


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