The effect of folic acid fortification on plasma folate and total homocysteine concentrations.
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BACKGROUND: In 1996, the Food and Drug Administration issued a regulation requiring all enriched grain products to be fortified with folic acid to reduce the risk of neural-tube defects in newborns. Fortification (140 microg per 100 g) began in 1996, and the process was essentially complete by mid-1997. METHODS: To assess the effect of folic acid fortification on folate status, we measured plasma folate and total homocysteine concentrations (a sensitive marker of folate status) using blood samples from the fifth examination (January 1991 to December 1994) of the Framingham Offspring Study cohort for baseline values and the sixth examination (January 1995 to August 1998) for follow-up values. We divided the cohort into two groups on the basis of the date of their follow-up examination: the study group consisted of 350 subjects who were seen after fortification (September 1997 to March 1998), and the control group consisted of 756 subjects who were seen before fortification (January 1995 to September 1996). RESULTS: Among the subjects in the study group who did not use vitamin supplements, the mean folate concentrations increased from 4.6 to 10.0 ng per milliliter (11 to 23 nmol per liter) (P<0.001) from the baseline visit to the follow-up visit, and the prevalence of low folate concentrations (<3 ng per milliliter [7 nmol per liter]) decreased from 22.0 to 1.7 percent (P< 0.001). The mean total homocysteine concentration decreased from 10.1 to 9.4 micromol per liter during this period (P<0.001), and the prevalence of high homocysteine concentrations (>13 micromol per liter) decreased from 18.7 to 9.8 percent (P<0.001). In the control group, there were no statistically significant changes in concentrations of folate or homocysteine. CONCLUSIONS: The fortification of enriched grain products with folic acid was associated with a substantial improvement in folate status in a population of middle-aged and older adults. (+info)
Impaired anticoagulant response to infusion of thrombin in atherosclerotic monkeys associated with acquired defects in the protein C system.
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To examine the effects of atherosclerosis on the protein C anticoagulant pathway in vivo, we measured anticoagulant responses to intravenous administration of human alpha-thrombin or activated protein C (APC) in cynomolgus monkeys. Two groups of monkeys were fed either a control diet (n=18) or an atherogenic diet (n=12) that produces both hypercholesterolemia and moderate hyperhomocyst(e)inemia. A third group (n=8) was fed an atherogenic diet for 15 months, and then fed the atherogenic diet supplemented with B vitamins for 6 months to correct the hyperhomocyst(e)inemia. The plasma homocyst(e)ine level was higher in monkeys fed the atherogenic diet (9.6+/-1.0 micromol/L) than in monkeys fed the control diet (3.7+/-0.2 micromol/L) or the atherogenic diet with B vitamins (3.6+/-0.2 micromol/L) (P<0.001). Infusion of thrombin produced a much greater prolongation of the activated partial thromboplastin time in monkeys fed the control diet (52+/-10 seconds) than in monkeys fed the atherogenic diet either with (24+/-4 seconds) or without (27+/-5 seconds) supplemental B vitamins (P<0.02). Thrombin-dependent generation of circulating APC was higher in control (294+/-17 U/mL) than in atherosclerotic (240+/-14 U/mL) monkeys (P<0.05), although levels of fibrinogen, plasminogen, D-dimer, and thrombin-antithrombin complexes were similar in each group. Injection of human APC produced a similar prolongation of the activated partial thromboplastin time in control (31+/-3 seconds) and atherosclerotic (29+/-2 seconds) monkeys. These findings provide evidence for impaired anticoagulation, due partly to decreased formation of APC, in atherosclerosis. The blunted anticoagulant response to thrombin in hypercholesterolemic monkeys was not corrected by supplementation with B vitamins. (+info)
Vitamin B status in patients with chronic fatigue syndrome.
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Some patients with chronic fatigue syndrome say they benefit from taking vitamin supplements. We assessed functional status for the B vitamins pyridoxine, riboflavin and thiamine in 12 vitamin-untreated CFS patients and in 18 healthy controls matched for age and sex. Vitamin-dependent activities--aspartate aminotransferase (AST) for pyridoxine, glutathione reductase (GTR) for riboflavin, transketolase (TK) for thiamine--were measured in erythrocyte haemolysates before and after in-vitro addition of the relevant vitamin. For all three enzymes basal activity (U/g Hb) was lower in CFS patients than in controls: AST 2.84 (SD 0.62) vs 4.61 (1.43), P < 0.001; GTR 6.13 (1.89) vs 7.42 (1.25), P < 0.04; TK 0.50 (0.13) vs 0.60 (0.07), P < 0.04. This was also true of activated values: AST 4.91 (0.54) vs 7.89 (2.11), P < 0.001; GTR 8.29 (1.60) vs 10.0 (1.80), P < 0.001; TK 0.56 (0.19) vs 0.66 (0.08), P < 0.07. The activation ratios, however, did not differ between the groups. These data provide preliminary evidence of reduced functional B vitamin status, particularly of pyridoxine, in CFS patients. (+info)
Adrenocorticotropic hormone increases hydrolysis of B-6 vitamers in swine adrenal glands.
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Shipping stress is an economic problem because of its effect on meat quality. Because shipping increases plasma cortisol and pyridoxal 5'-phosphate interacts with steroid hormones, we examined the interaction between adrenocorticotropic hormone (ACTH) and vitamin B-6 metabolism in pigs. Six crossbred pigs with ear vein catheters received 50 IU of porcine ACTH intravenously at 3-h intervals from 0800 to 2100 h on d 1-3 and 100 IU intramuscularly at 0800, 1400 and 2000 h on d 6 and 7. Controls received saline. ACTH had no effect on pyridoxal 5'-phosphate in adrenal tissue but decreased pyridoxamine 5'-phosphate from 6.1 +/- 0.7 to 4.7 +/- 1.0 nmol/g (P < 0.05). Adrenal pyridoxal and pyridoxamine concentrations were 0.4 +/- 0.1 nmol/g in controls and 1.1 +/- 0.3 and 1.3 +/- 0.5 nmol/g, respectively, in ACTH-treated pigs (P < 0.01). Pyridoxal 5'-phosphate phosphatase activity [median (25-75 percentile value)] at pH 7.4 in adrenal tissue was 66.6 (47.8-75.5) nmol/(g. min) in the controls and 764 (626-771) in the ACTH-treated pigs (P < 0.01). There was no significant difference in pyridoxal kinase activity. However, kinase activity in the adrenals was about twice as high as in other tissues. These data suggest an active turnover of vitamin B-6 in adrenal tissue. (+info)
A survey of the current clinical practice of psychiatrists and accident and emergency specialists in the United Kingdom concerning vitamin supplementation for chronic alcohol misusers.
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Although it is well known that B-vitamin deficiencies directly affecting the brain are common in alcohol misuse, no concise guidelines on the use of vitamin supplements in alcohol misusers currently exist in the UK. The purpose of this study was to assess current practice and opinion among UK physicians. Questionnaires were completed by a total of 427 physicians comprising Accident and Emergency (A&E) specialists and psychiatrists, with a response rate of 25%. The main findings were that vitamin deficiency was perceived as being uncommon amongst alcohol misusers (<25%) and there was no consensus as to which B vitamins are beneficial in treatment or the best method of administration of B-vitamin supplementation. The majority of psychiatrists favoured oral administration for prophylaxis against the Wernicke-Korsakoff syndrome in chronic alcohol misusers and parenteral therapy in patients with signs of Wernicke-Korsakoff syndrome. Whilst only just over half the A&E specialists expressed a preference, most favoured parenteral therapy in both cases. Most respondents did not currently have a unit policy/protocol on the management of vitamin supplementation in chronic alcohol misusers. Overall, the findings suggest that there is wide variation in current practice and highlight the need for guidelines in this area. (+info)
Alzheimer disease: protective factors.
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Approximately 6-8% of all persons aged >65 y have Alzheimer disease and the prevalence of the disease is increasing. Any intervention strategy aimed at decreasing risks or delaying the onset of the disease will therefore have a substantial effect on health care costs. Nutrition seems to be one of the factors that may play a protective role in Alzheimer disease. Many studies suggest that oxidative stress and the accumulation of free radicals are involved in the pathophysiology of the disease. Several studies have shown the existence of a correlation between cognitive skills and the serum concentrations of folate, vitamin B-12, vitamin B-6, and, more recently, homocysteine. However, nutritional factors have to be studied not alone but with the other factors related to Alzheimer disease: genetics, estrogen, antiinflammatory drug use, and socioeconomic variables. The objective of this article was to review recent studies in this field. (+info)
Nutrients and HIV: part two--vitamins A and E, zinc, B-vitamins, and magnesium.
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There is compelling evidence that micronutrient deficiencies can profoundly affect immunity; micronutrient deficiencies are widely seen in HIV, even in asymptomatic patients. Direct relationships have been found between deficiencies of specific nutrients, such as vitamins A and B12, and a decline in CD4 counts. Deficiencies appear to influence vertical transmission (vitamin A) and may affect progression to AIDS (vitamin A, B12, zinc). Correction of deficiencies has been shown to affect symptoms and disease manifestation (AIDS dementia complex and B12; diarrhea, weight loss, and zinc), and certain micronutrients have demonstrated a direct anti-viral effect in vitro (vitamin E and zinc). The previous article in this series focused on selenium and beta carotene deficiencies in HIV/AIDS. This literature review elucidates how deficiencies of the micronutrients zinc, magnesium, vitamins A, E, and specific B vitamins relate to HIV symptomology and progression, and clearly illustrates the need for nutritional supplementation in HIV disease. (+info)
Correlation between plasma total homocysteine and copper in patients with peripheral vascular disease.
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BACKGROUND: Increased concentrations of both plasma total homocysteine and copper are separately associated with cardiovascular disease. Correlations between plasma total homocysteine, trace elements, and vitamins in patients with peripheral vascular disease have not been investigated. METHODS: The concentrations of trace elements in plasma were determined by the multielement analytical technique of total-reflection x-ray fluorescence spectrometry. Plasma total homocysteine was determined by HPLC. RESULTS: In the univariate and multivariate regression analyses, copper was positively correlated with plasma total homocysteine in all subjects (coefficient +/- SE, 0.347 +/- 0.113; P = 0.0026 and coefficient +/- SE, 0.422 +/- 0.108; P = 0.0002, respectively), and in patients with peripheral vascular disease (coefficient +/- SE, 0.370 +/- 0.150; P = 0.016; and coefficient +/- SE, 0.490 +/- 0.151; P = 0.0025, respectively). Correlation between copper and plasma total homocysteine was not detected in healthy control subjects. The concentration of calcium in plasma (67.5 vs 80. 8 microg/g) was significantly lower in the patients than in the control subjects (P = 0.02). When the patients were divided into groups, the patients with suprainguinal lesions had significantly higher copper concentrations (P = 0.04) and significantly lower selenium and calcium concentrations (P = 0.01 and 0.008, respectively) than the healthy subjects. Patients had higher concentrations of autoantibodies against oxidized LDL and concentrations of thiobarbituric acid-reactive substance than the healthy subjects (P <0.0001 and P = 0.001, respectively). The concentrations of plasma total homocysteine and alpha-tocopherol were significantly higher, and the concentrations of vitamin B(6) and beta-carotene were lower in the patients than the healthy subjects. CONCLUSION: Our findings suggest that the atherogenicity of homocysteine may be related to copper-dependent interactions. (+info)