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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Folic acid, a water-soluble vitamin, has been used since the 1940s to treat some cases of macrocytic anemia without neurologic disease. Folate deficiency is best diagnosed with red blood cell folate levels along with macrocytosis and/or megaloblastic anemia. In addition to reversing overt deficiency, the vitamin may reduce the incidence of neural tube defects by 45% in women who receive 400 micrograms per day. It is recommended that all women of childbearing age take 400 micrograms of folate per day. Elevations in homocysteine levels, a metabolite intimately associated with folate, are also being found with increasing regularity in those with cardiovascular diseases. Homocysteine levels are reduced by folic acid administration. Therefore, there is some biologic plausibility, but not currently direct proof, for the assumption that folate supplements may prevent heart disease, stroke, and peripheral arterial disease. Controlled trials should take place before widespread food supplementation with folate is carried out on a large scale because of the possibility of outbreaks of permanent B12-related neurologic damage in those with undiagnosed pernicious anemia. However, if a patient has a premature cardiovascular event and has minimal risk factors, ordering a test to determine homocysteine level may be advisable, and if elevated, treating with folic acid supplement as long as B12 deficiency does not coexist.
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PMID:The role of folic acid in deficiency states and prevention of disease. 904 May 15

Fasting hyperhomocysteinemia is an independent risk factor for coronary artery disease, stroke, peripheral vascular atherosclerosis, and for arterial and venous thromboembolism. The risk for cardiovascular disease with homocysteine is similar to conventional risk factors. The interaction of hyperhomocysteinemia with hypertension and smoking is strong and the combined effect is more than multiplicative. The combined effect of homocysteine and cholesterol is additive. Homocysteine produces atherosclerosis, thromboembolism, and vascular endothelial cell injury. Vascular dysfunction produced by homocysteine may be due to endothelial cell damage. Homocysteinemia-induced atherosclerosis is probably due to various factors including endothelial cell injury, inability to sustain S-nitroso-homocysteine formation because of imbalance between production of nitric oxide by dysfunctional endothelium and homocysteine, smooth muscle cell proliferation, and thromboembolism. There is strong evidence that endothelial cell injury is associated with oxidative stress produced by homocysteine. Hyperhomocysteinemia is associated with numerous conditions, including coronary disease, stroke, peripheral vascular disease (carotid artery and cerebrovascular atherosclerosis), venous thrombosis, renal disease, diabetes mellitus, and organ transplant. Folic acid, vitamin B12 and B6 have been shown to be beneficial in reducing plasma homocysteine levels. Folic acid is specifically very effective, safe and inexpensive.
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PMID:Homocysteine, a Risk Factor for Cardiovascular Disease. 982 15

A study involving results of the PGA Tour, Senior PGA Tour, and the LPGA Tour investigated whether "choking under pressure" occurs among professional golfers. Players were individuals who either were leading going into the final round or within five strokes of the lead. It was hypothesized that players who were one stroke from the lead and to a lesser extent players who were leading should have higher final round scores than those players who were two or more strokes from the lead ("choking"). However, the results did not support the choking hypothesis. Players who were leading going into the final round won the majority of the time.
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PMID:Do professional golfers "choke"? 1218 33

Folate is a cofactor in one-carbon metabolism, during which it promotes the remethylation of homocysteine -- a cytotoxic sulfur-containing amino acid that can induce DNA strand breakage, oxidative stress and apoptosis. Dietary folate is required for normal development of the nervous system, playing important roles regulating neurogenesis and programmed cell death. Recent epidemiological and experimental studies have linked folate deficiency and resultant increased homocysteine levels with several neurodegenerative conditions, including stroke, Alzheimer's disease and Parkinson's disease. Moreover, genetic and clinical data suggest roles for folate and homocysteine in the pathogenesis of psychiatric disorders. A better understanding of the roles of folate and homocysteine in neuronal homeostasis throughout life is revealing novel approaches for preventing and treating neurological disorders.
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PMID:Folate and homocysteine metabolism in neural plasticity and neurodegenerative disorders. 1259 Dec 16

Prostaglandins (PGs) originate from the degradation of membranar arachidonic acid by cyclooxygenases (COX-1 and COX-2). The prostaglandin actions in the nervous system are multiple and have been suggested to play a significant role in neurodegenerative disorders. Some PGs have been reported to be toxic and, interestingly, the cyclopentenone PGs have been reported to be cytoprotective at low concentration and could play a significant role in neuronal plasticity. They have been shown to be protective against oxidative stress injury; however, the cellular mechanisms of protection afforded by these PGs are still unclear. It is postulated that the cascade leading to neuronal cell death in acute and chronic neurodegenerative conditions, such as cerebral ischemia and Alzheimer's disease, would be mediated by free radical damage. We tested the hypothesis that the neuroprotective action of cyclopentanone could be caused partially by an induction of heme oxygenase 1 (HO-1). We and others have previously reported that modulation of HO total activity may well have direct physiological implications in stroke and in Alzheimer's disease. HO acts as an antioxidant enzyme by degrading heme into iron, carbon monoxide, and biliverdin that is rapidly converted into bilirubin. Using mouse primary neuronal cultures, we demonstrated that PGs of the J series induce HO-1 in a dose-dependent manner (0, 0.5, 5, 10, 20, and 50 micro g/ml) and that PGJ(2) and dPGJ(2) were more potent than PGA(2), dPGA(2), PGD(2), and PGE(2). No significant effects were observed for HO-2 and actin expression. In regard to HO-3 expression found in rat, with its protein deducted sequence highly homologous to HO-2, no detection was observed in HO-2(-/-) mice, suggesting that HO-3 protein would not be present in mouse brain. We are proposing that several of the protective effects of PGJ(2) could be mediated through beneficial actions of heme degradation and its metabolites. The design of new mimetics based on the cyclopentenone structure could be very useful as neuroprotective agents and be tested in animal models of stroke and Alzheimer's disease.
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PMID:Regulation of heme oxygenase expression by cyclopentenone prostaglandins. 1270 76

Coronary syndromes are induced by atherosclerosis which results from lipid deposit as well as inflammatory cells in vascular walls triggered by oxidative modification of LDL cholesterol. Treatment with antioxidant vitamins (vitamin C and E) has no evident effect on coronary events whereas aspirin and statins treatments result in a 25 to 30% reduced rate of fatal and non fatal myocardial infarction in primary and in secondary prevention trials. Both drugs are highly recommended in secondary prevention. In primary prevention they are useful and cost effective if the estimated risk of coronary event is 1.5% per year or higher. They are not cost-effective if this risk is 0.6% per year or less. With aspirin there is a 1.5 fold increase of hemorrhagic stroke and a 2 fold increase of gastrointestinal hemorrhage. Aspirin is less efficient in younger patients (< 50 years of age), in those with high blood pressure (> 145 mmHg) and those with low serum hsCRP (< 1 mg/l.). Statins are well tolerated and they could reduce not only C-V and global mortality but also the risk of stroke and of macular degeneration. They could also delay the occurrence of diabetes and kidney failure. Folate administration can lower elevated serum homocysteine level, which is a risk factor for C-V and Alzheimer's disease. However the clinical benefit resulting from folate treatment must still be demonstrated.
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PMID:[Prevention of cardiovascular and degenerative diseases: I. Aspirin, statins, or vitamins?]. 1509 4

Elevated plasma homocysteine is associated with an increased risk of myocardial infarction, stroke, and venous thromboembolism. Folic acid and other B vitamins lower plasma homocysteine levels, but whether this therapy confers a clinical benefit has yet to be determined. Until we know the results of ongoing clinical trials of homocysteine-lowering therapy, testing for and treating elevated homocysteine is probably justified only in patients with known cardiovascular disease or who are at high risk.
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PMID:Homocysteine: is it a clinically important cardiovascular risk factor? 1547 4

Dietary supplementation with B-vitamins that lower plasma total homocysteine concentrations are expected to lower the risk of cardiovascular disease. Folic acid and vitamin B (12) lower blood homocysteine concentrations by about 25-30% in populations without folic acid fortification, but by only 10-15% in populations with fortification. In observational studies, 25% lower homocysteine is associated with about 10% less coronary heart disease (CHD) and about 20% less stroke. This review examines the current status of 12 large-scale randomized trials of B-vitamin supplementation and risk of cardiovascular disease. Seven of these trials are being performed in populations without fortification (five involving participants with prior CHD, two with prior stroke) and five in populations with fortification (two with prior CHD, two with renal disease, and one with prior stroke). Many of these trials may not have included a sufficient number of people or lasted long enough to have adequate power to exclude false-negative results. Taken together, however, these trials involve 32,000 patients with prior vascular disease in unfortified populations and 20,000 (14,000 with vascular disease and 6000 with renal disease) patients in fortified populations. A metaanalysis of these trials should have adequate power to determine whether homocysteine-lowering vitamin supplements can reduce the risk of cardiovascular disease.
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PMID:Homocysteine-lowering trials for prevention of heart disease and stroke. 1604 74

Folic acid fortification of grain products was mandated in the USA by January 1998 and in Canada by November 1998. It was hypothesized that screening total plasma homocysteine levels adjusted for age, sex, race and country that were drawn in stroke patients for the Vitamin Intervention for Stroke Prevention trial from 1997 to 2001 would be steady when fortification was completed. Samples were grouped by years 1997/1998, 1999 and 2000/2001, and adjusted means were calculated using a general linear regression model. In 2,612 US and 1,059 Canadian patients, levels showed no consistent trend in the USA alone, while Canadian levels declined (p = 0.06 overall, 0.0003 in the oldest age group). US levels were 0.39 micromol/l (95% CI: -0.08, 0.85) lower than in Canada. Neither fasting nor time since stroke affected the results.
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PMID:Plasma total homocysteine levels in stroke patients screened for the vitamin intervention for stroke prevention clinical trial in the era of folate fortification. 1625 53

Both prostaglandin A(1) (PGA(1)) and lithium have been reported to protect neurons against excitotoxic and ischemic injury. The present study was undertaken to examine the effects of lithium and PGA1 on heat shock proteins (HSP) and the growth arrest and DNA-damage-inducible gene (GADD153) and to evaluate if lithium could potentiate PGA(1)'s neuroprotective effects against cerebral ischemia. Rats were pretreated with a subcutaneous injection of lithium for 2 days and a single intracerebral ventricle administration of PGA(1) 15 min before ischemic insult. Brain ischemia was induced by a permanent middle cerebral artery occlusion. The infarct volume, motor behavior deficits and brain edema were analyzed 24 h after ischemic insult. The result showed that PGA(1) significantly reduced infarct volume, neurological deficits and brain edema. Except for neurological deficit, lithium enhanced PGA(1)'s neuroprotection. The neuroprotective effects of PGA(1) were associated with an up-regulation of cytoprotective heat shock proteins HSP70 and GRP78 in the ischemic brain hemisphere as determined by immunoblotting and immunofluorescence. The induction of HSP70 and GRP78 was enhanced by lithium. However, although the expression of GADD153 was enhanced significantly after pMCAO, it was not influenced by either PGA(1) or lithium or their combination. These studies suggest that lithium can potentiate PGA(1)'s neuroprotective effects and thus may have potential clinical value for the treatment of stroke in combination with other neuroprotective agents.
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PMID:Enhancement of neuroprotection and heat shock protein induction by combined prostaglandin A1 and lithium in rodent models of focal ischemia. 1679 96


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