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)

Nitrous oxide interacts with vitamin B12 resulting in selective inhibition of methionine synthase, a key enzyme in methionine and folate metabolism. Thus, nitrous oxide may alter one-carbon and methyl-group transfer most important for DNA, purine and thymidylate synthesis. Long-term exposure to high concentrations of nitrous oxide may cause megaloblastic bone-marrow depression and neurological symptoms. Exposure to higher doses for less than 6 hours, as in clinical anaesthesia, are considered harmless. Recent studies seem to suggest a correlation between nitrous oxide anaesthesia and hyperhomocysteinaemia which is accepted to be an independent risk factor for coronary artery disease. As for today, available data do not support the notion that exposure to trace amounts of nitrous oxide is associated with impaired fertility or an increased risk of developing cancer. Emission of nitrous oxide from medical use is estimated to contribute less than 0.05% to total annual greenhouse gas emission.
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PMID:Toxicity of nitrous oxide. 1275 48

Starved larvae of Rhodnius prolixus, when challenged with Enterobacter cloacae B12, had their mortality related to their period of starvation. R. prolixus larvae fed on plasma alone, compared with insects fed on whole blood, had their immune reactivity affected as shown by: (i) a significant reduction in the ability to produce cecropin-like and lysozyme activities in the haemolymph when inoculated with E. cloacae; (ii) a reduction in numbers of haemocytes and nodule formation following challenge with bacteria; (iii) a decreased ability of plasma-fed insects in destroying their infection caused by inoculation of E. cloacae cells; and (iv) alpha-ecdysone therapy counteracted the immune depression in Rhodnius larvae fed on plasma alone. However, unlike other immune reactions, this set of experiments failed to demonstrate any interference of the plasma feeding on the prophenoloxidase-activating system, since melanin production was not reduced when the system was stimulated by the presence of bacteria in the haemolymph. The significance of these data is discussed in relation to the effect of diet components and the moulting hormone on the immune reactivity in insects.
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PMID:Immune responses in Rhodnius prolixus: influence of nutrition and ecdysone. 1277 Apr 13

The aim of this study was to gain a deeper understanding of the development of burning mouth syndrome (BMS). Eighteen females (43-80 yr old), referred to the Clinic of Oral Medicine, formed the study group. Oral examination did not reveal any mucosal lesion or dental pathology, blood analyses of vitamin B12 and serum iron levels were within normal reference values, and no allergies to dental materials were reported. Reported pain/discomfort was 49.4 (mean) on a 100-mm visual analog scale and duration of symptoms was, on average, 8.1 yr (median = 1.5 yr). Taped semistructured interviews were transcribed and analysed in line with grounded theory methodology. In the analysis, a core category emerged, labeled communicating psychological discomfort. This category indicated musings about the meaning of life and interacted with a personality characterized by a strong need for conscientiousness, a life style including long-standing struggle with psychosocial overload, and external social and cultural influences. The debut of the BMS was then preceded by an acutely stressful event. A psychosocial history, in addition to a detailed dental and medical history, seems to be crucial in diagnosing patients. If a psychological disorder and somatization of anxiety and depression is suggested, as indicated in our study, the patient should be offered counseling by a psychologist.
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PMID:Burning mouth syndrome: experiences from the perspective of female patients. 1288 95

Strenuous bouts of prolonged exercise and heavy training are associated with depressed immune cell function. Furthermore, inadequate or inappropriate nutrition can compound the negative influence of heavy exertion on immunocompetence. Dietary deficiencies of protein and specific micronutrients have long been associated with immune dysfunction. An adequate intake of iron, zinc and vitamins A, E, B6 and B12 is particularly important for the maintenance of immune function, but excess intakes of some micronutrients can also impair immune function and have other adverse effects on health. Immune system depression has also been associated with an excess intake of fat. To maintain immune function, athletes should eat a well-balanced diet sufficient to meet their energy requirements. An athlete exercising in a carbohydrate-depleted state experiences larger increases in circulating stress hormones and a greater perturbation of several immune function indices. Conversely, consuming 30-60 g carbohydrate x h(-1) during sustained intensive exercise attenuates rises in stress hormones such as cortisol and appears to limit the degree of exercise-induced immune depression. Convincing evidence that so-called 'immune-boosting' supplements, including high doses of antioxidant vitamins, glutamine, zinc, probiotics and Echinacea, prevent exercise-induced immune impairment is currently lacking.
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PMID:Exercise, nutrition and immune function. 1497 37

Psychiatric manifestations are frequently associated with pernicious anemia including depression, mania, psychosis, dementia. We report a case of a patient with vitamin B12 deficiency, who has presented severe depression with delusion and Capgras' syndrome, delusion with lability of mood and hypomania successively, during a period of two Months. Case report - Mme V., a 64-Year-old woman, was admitted to the hospital because of confusion. She had no history of psychiatric problems. She had history of diabetes, hypertension and femoral prosthesis. The red blood count revealed a normocytosis with anemia (hemoglobin=11,4 g/dl). At admission she was uncooperative, disoriented in time and presented memory and attention impairment and sleep disorders. She seemed sad and older than her real age. Facial expression and spontaneous movements were reduced, her speech and movements were very slow. She had depressed mood, guilt complex, incurability and devaluation impressions. She had a Capgras' syndrome and delusion of persecution. Her neurologic examination, cerebral scanner and EEG were postponed because of uncooperation. Further investigations confirmed anemia (hemoglobin=11,4 g/dl) and revealed vitamin B12 deficiency (52 pmol/l) and normal folate level. Antibodies to parietal cells were positive in the serum and antibodies to intrinsic factor were negative. An iron deficiency was associated (serum iron=7 micromol/l; serum ferritin concentration=24 mg/l; serum transferrin concentration=3,16 g/l). This association explained normocytocis anemia. Thyroid function, hepatic and renal tests, glycemia, TP, TCA, VS, VDRL-TPHA were normal. Vitamin B12 replacement therapy was started with hydroxycobalamin 1 000 ng/day im for 10 days and iron replacement therapy. Her mental state improved dramatically within a few days. After one week of treatment the only remaining symptoms were lability of mood, delusion of persecution, Capgras' syndrome but disappeared totally 9 days after the beginning of the treatment. A neurologic examination was possible because of cooperation. All the tendon reflexes of inferior members were absent. The plantars were in flexion and there was a left inferior member hypoesthesia. The cerebral scan and EEG were normal. Fundic biopsy, realized by fibroscopy, revealed fundic atrophia and intestinal metaplasia compatible with Biermers' disease. The iron deficiency exploration concluded diet deficiency. Mme V. appeared euphoric, her speech was very rapid with play on words and overactivity. This hypomania state totally disappeared 3 days after. Six Months after her hospitalisation, she presented an hypothyroidism (TSH=3,780; T3=1,35; T4=1,08). A thyroid hormones replacement was started and she continued to receive Monthly B12 replacement. Discussion - This case report illustrates psychiatric manifestations of Biermers' disease. The clinical arguments in favour are: white woman, more than 60 Years old, no history of psychiatric problems, atypical symptoms (confusional state with psychiatric symptoms), fluctuation of symptoms (severe depression with confusional state, delusion of persecution and Capgras' syndrome; delusion with lability of mood and hypomania), dramatic improvement after 9 days of vitamin B12 replacement therapy. The biological arguments are: anemia, vitamin B12 deficiency, normal folate level, atrophia and fundic metaplasia, positive antibodies to parietal cells in the serum, association between Biermers' disease and autoimmune disease (Haschimoto thyroidite). Psychiatric manifestations can occur in the presence of low serum B12 levels but in the absence of the other well recognized neurological and haematological abnormalities of pernicious anemia. Mental or psychological changes may precede haematological signs by Months or Years. They can be the initial symptoms or the only ones. Verbank et al. described the case of a patient with vitamin B12 deficiency in whom hypomania, paranoia and depression had been successively presented during a period of 5 Years before anemia have been developed. The case of Mme V. is similar in the succession of severe depression with delusion of persecution and Capgras' syndrome, delusion with lability of mood and hypomania, during a period of two Months. This report seems to be the first one of a sequence of several psychiatric states with pernicious anemia during a period of two Months with normocytosis anemia. To illustrate this illness we reviewed the literature regarding psychopathology associated with B12 deficiency. The most common psychiatric symptoms were depression, mania, psychotic symptoms, cognitive impairment and obsessive compulsive disorder. The neuropsychiatric severity by vitamin B12 deficiency and the therapeutic efficacy depends on the duration of signs and symptoms. Conclusion - We recommend consideration of B12 deficiency and serum B12 determinations in all the patients with organic mental disorders, atypical psychiatric symptoms and fluctuation of symptomatology. B12 levels should be evaluated with treatment resistant depressive disorders, dementia, psychosis or risk factors for malnutrition such as alcoholism or advancing age associated with neurological symptoms, anemia, malabsorption, gastrointestinal surgery, parasite infestation or strict vegetarian diet. In first intention, B12 deficiency should be researched by serum B12 determination (normal 200-950 pg/ml). Studies of methylmalonic acid and homocysteine showed that they are very sensitive functional indicators of cobalamin status especially when other evidence of cobalamin (B12) deficiency was equivocal. Measurement of methylmalonic acid (normal 73-271 nmol/l) and homocysteine (normal 5,4-13,9 micromol/l) should not replace the measurement of serum cobalamin.
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PMID:[Psychiatric manifestations of vitamin B12 deficiency: a case report]. 1502 91

We examined individual-difference variables in relation to the rate of change in global cognitive performance, measured by the MMSE, from 3 years prior to diagnosis of Alzheimer's disease (AD) to the time of diagnosis. The population-based sample consisted of 230 incident AD persons who were followed over a 3-year interval. The average annual decline in MMSE was 1.81 points. Being older and acquiring additional diseases during the 3 years preceding diagnosis predicted a faster rate of decline in global cognitive functioning. However, other individual difference variables such as sex, education, depression, vitamin levels (vitamin B12 and folic acid), apolipoprotein status, and social network did not precipitate the rate of decline in the preclinical phase of AD.
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PMID:Predictors of cognitive change from preclinical to clinical Alzheimer's disease. 1525 92

Elevated total homocysteine (tHcy) concentrations have been found to be associated with cardiovascular disease and dementia in old age. The present study was performed to identify the prevalence of hyperhomocysteinemia (HHcy) and to analyze the association between tHcy concentration and sociodemographic characteristics, nutritional parameters, and cognitive and functional status in this sample of hospitalized geriatric patients. A total of 214 patients (77% females) 65+ years old admitted into an acute care geriatric ward of an internal medical department in the Northern Italy were studied. tHcy concentration was measured using a high-performance liquid chromatography with fluorescence detection (HPLC-F). Information about nutrition (body mass index [BMI], serum albumin, cholesterol, and transferrin) was collected on admission. Functional status was investigated with the Basic Activities of Daily Living scale (ADL) and the Instrumental Activities of Daily Living scale (IADL); cognitive and affective status were assessed by the Mini-Mental State Evaluation (MMSE) and the Geriatric Depression Scale (GDS). The mean tHcy concentration was 18.4 +/- 13.1 micromol/L; 74.2% of males and 68.9% of females had HHcy (> 12 micromol/L). Sixty-four percent of patients with normal serum vitamin B12 and folate concentrations had HHcy. Elevated tHcy concentrations were associated with older age, male gender, increasing serum creatinine, lower MMSE score, and disability. The mean tHcy concentration depended on the occurrence of different diseases. Patients affected by atherosclerotic diseases, such as ischemic heart diseases, cerebrovascular diseases, and dementia had higher mean tHcy concentration than those without diagnosed vascular diseases. In multivariate analysis, vitamin B12, folate, serum albumin, creatinine, and disability emerged as factors associated with tHcy, adjusted for age, gender, education, MMSE score, and atherosclerotic diseases. Our results suggest that the prevalence of HHcy in hospitalized patients is very high, even in subjects with normal cobalamin and folate concentrations. High Hcy concentration can be associated with functional impairment.
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PMID:Homocysteine and disability in hospitalized geriatric patients. 1528 Oct 11

The brain is an organ elaborated and functioning from substances present in the diet. Dietary regulation of blood glucose level (via ingestion of food with a low glycemic index ensuring a low insulin level) improves the quality and duration of intellectual performance, if only because at rest the adult brain consumes 50 p. 100 of dietary carbohydrates, 80 p. 100 of them for energy purposes. The nature of the amino acid composition of dietary proteins contributes to good cerebral function; tryptophan plays a special role. Many indispensable amino acids present in dietary proteins help to elaborate neurotransmitters and neuromodulators. Omega-3 fatty acids provided the first coherent experimental demonstration of the effect of dietary nutrients on the structure and function of the brain. First it was shown that the differentiation and functioning of cultured brain cells requires omega-3 fatty acids. It was then demonstrated that alpha-linolenic acid (ALA) deficiency alters the course of brain development, perturbs the composition and physicochemical properties of brain cell membranes, neurones, oligodendrocytes, and astrocytes (ALA). This leads to physicochemical modifications, induces biochemical and physiological perturbations, and results in neurosensory and behavioral upset. Consequently, the nature of polyunsaturated fatty acids (in particular omega-3) present in formula milks for infants (premature and term) conditions the visual and cerebral abilities, including intellectual abilities. Moreover, dietary omega-3 fatty acids are certainly involved in the prevention of some aspects of cardiovascular disease (including at the level of cerebral vascularization), and in some neuropsychiatric disorders, particularly depression, as well as in dementia, notably Alzheimer's disease. Their deficiency can prevent the satisfactory renewal of membranes and thus accelerate cerebral aging. Iron is necessary to ensure oxygenation, to produce energy in the cerebral parenchyma, and for the synthesis of neurotransmitters. The iodine provided by the thyroid hormone ensures the energy metabolism of the cerebral cells. The absence of iodine during pregnancy induces severe cerebral dysfunction, leading to cretinism. Manganese, copper, and zinc participate in enzymatic mechanisms that protect against free radicals, toxic derivatives of oxygen. The use of glucose by nervous tissue implies the presence of vitamin B1. Vitamin B9 preserves memory during aging, and with vitamin B12 delays the onset of signs of dementia, provided it is administered in a precise clinical window, at the onset of the first symptoms. Vitamins B6 and B12, among others, are directly involved in the synthesis of neurotransmitters. Nerve endings contain the highest concentrations of vitamin C in the human body. Among various vitamin E components, only alpha-tocopherol is involved in nervous membranes. The objective of this update is to give an overview of the effects of dietary nutrients on the structure and certain functions of the brain.
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PMID:[The role of nutritional factors on the structure and function of the brain: an update on dietary requirements]. 1545 64

Homocysteine (Hcy) is harmful to neurons and blood vessels, including the cerebral microvasculature. It is possible that such effects contribute to the cascade of events that leads to cognitive decline, dementia, and depression in later life. Hcy is produced during the metabolism of the essential amino-acid methionine, which also involves a methyl group transfer derived from folate and choline metabolism. Its plasma level can be influenced by factors such as age, vitamin deficiency, renal function, and a common mutation in the methylenetetrahydrofolate reductase (MTHFR) gene, where cytosine is replaced by thymidine (C-->T) at nucleotide position 677. Subjects with the TT genotype have higher homocysteine levels and may be particularly prone to experiencing depression as a result of high plasma Hcy and dysfunction of methylation metabolic pathways critical to the synthesis of noradrenaline and serotonin. We designed the present study to investigate whether older women with the TT genotype would have higher depression and lower cognitive scores than women with CT and CC genotypes. A total of 240 community-dwelling women aged 70 years or over volunteered to take part in the study - 29 carried the TT genotype, 113 the CT and 98 the CC genotype. The Beck Depression Inventory (BDI) score for subjects with the TT genotype was statistically similar to the other groups (P = 0.609). Plasma Hcy showed a modest and significant correlation with BDI scores (r = 0.21) that was independent from age, B12 and folate levels. There was no association between beck anxiety inventory (BAI) scores and MTHFR genotype or homocysteine levels. The cognitive assessment of participants included measures of verbal memory, memory for faces, verbal fluency, visuo-spatial abilities and the cognitive section of the Cambridge Examination For Mental Disorders Of The Elderly (CAMCOG)-MTHFR genotype had no clear association with cognitive scores. These results indicate that, in isolation, the MTHFR C677T gene variation does not play an important role in the modulation of mood and cognitive performance in later life.
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PMID:Contribution of the MTHFR gene to the causal pathway for depression, anxiety and cognitive impairment in later life. 1558 52

We review the findings in major depression of a low plasma and particularly red cell folate, but also of low vitamin B12 status. Both low folate and low vitamin B12 status have been found in studies of depressive patients, and an association between depression and low levels of the two vitamins is found in studies of the general population. Low plasma or serum folate has also been found in patients with recurrent mood disorders treated by lithium. A link between depression and low folate has similarly been found in patients with alcoholism. It is interesting to note that Hong Kong and Taiwan populations with traditional Chinese diets (rich in folate), including patients with major depression, have high serum folate concentrations. However, these countries have very low life time rates of major depression. Low folate levels are furthermore linked to a poor response to antidepressants, and treatment with folic acid is shown to improve response to antidepressants. A recent study also suggests that high vitamin B12 status may be associated with better treatment outcome. Folate and vitamin B12 are major determinants of one-carbon metabolism, in which S-adenosylmethionine (SAM) is formed. SAM donates methyl groups that are crucial for neurological function. Increased plasma homocysteine is a functional marker of both folate and vitamin B12 deficiency. Increased homocysteine levels are found in depressive patients. In a large population study from Norway increased plasma homocysteine was associated with increased risk of depression but not anxiety. There is now substantial evidence of a common decrease in serum/red blood cell folate, serum vitamin B12 and an increase in plasma homocysteine in depression. Furthermore, the MTHFR C677T polymorphism that impairs the homocysteine metabolism is shown to be overrepresented among depressive patients, which strengthens the association. On the basis of current data, we suggest that oral doses of both folic acid (800 microg daily) and vitamin B12 (1 mg daily) should be tried to improve treatment outcome in depression.
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PMID:Treatment of depression: time to consider folic acid and vitamin B12. 1567 Nov 30


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