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PubMed1992

Hyperhomocyst(e)inaemia: an independent risk factor for intermittent claudication.

The aim of this study was to test the question of hyperhomocyst(e)inaemia as a risk factor for intermittent claudication (IC) independent of other important risk factors for peripheral atherosclerotic disease, such as smoking, hypertension, diabetes mellitus, hypercholesterolaemia, hypertriglyceridaemia, low levels of high-density-lipoprotein (HLD) cholesterol and age. The study population was recruited from an epidemiological study in Linköping County, Sweden, where all middle-aged men (n = 15,253, 45-69 years of age) were screened for IC. Seventy-eight subjects with verified IC and 98 healthy sex- and age-matched controls were randomly selected. Plasma levels of homocyst(e)ine (including the sum of free and bound forms of homocysteine and their disulphide oxidation products, homocystine, and homocysteine-cysteine mixed disulphide) were significantly higher (16.74 +/- 5.45 mumol l-1, mean value +/- SD, P = 0.0002) in IC subjects than in controls (13.80 +/- 3.21 mumol l-1), with 23% of the claudicants above the 95th percentile for controls. Stepwise logistic regression analysis revealed that the difference in plasma homocyst(e)ine was independent of the other above-mentioned risk factors. Moreover, the elevation of plasma homocyst(e)ine in claudicants was mainly confined to subjects with serum folate levels of less than or equal to 11.0 nmol l-1. The results suggest that folic acid supplementation should be tried in IC subjects with hyperhomocyst(e)inaemia.

Aged↗
PubMed2004

Autonomic function and serum erythropoietin levels in chronic fatigue syndrome.

OBJECTIVE: Given previous findings, we wished to investigate whether there was evidence of autonomic dysfunction in patients with chronic fatigue syndrome, and whether this could be related to reduced erythropoietin levels and altered red blood cell indices. METHODS: We assessed autonomic function and analysed blood parameters (including erythropoietin) in 22 patients with chronic fatigue syndrome who were medication-free and without comorbid depression or anxiety. Results were compared to 23 iron-deficiency anaemia patients and 18 healthy individuals. RESULTS: Autonomic testing in patients with chronic fatigue syndrome yielded a significantly greater increase in heart rate together with a more pronounced systolic blood pressure fall on standing compared to healthy individuals. Heart rate beat-to-beat variation on deep breathing and responses to the Valsalva manoeuvre were normal. Two of 22 patients with chronic fatigue had mild normochromic normocytic anaemia with normal ferritin, vitamin B12 and folate levels. Serum erythropoietin levels were within reference range. CONCLUSION: Some autonomic dysfunction is present in chronic fatigue syndrome (CFS) patients; the explanation remains uncertain, but could relate to cardiovascular deconditioning. There were no major haematological, biochemical or immunological abnormalities in these patients.

Adult↗
PubMed1982

Folate metabolism in the ethanol-fed rat.

The effect of long-term ethanol supplementation on folate metabolism was studied in McCollum rats receiving approximately 30% of their caloric intake as ethanol. Ethanol did not significantly affect hepatic or plasma total folate levels. The net hepatic uptake and metabolism of a labeled folate dose to polyglutamate forms were unimpaired by ethanol administration. In fact, the ethanol-fed animals metabolized hepatic pteroylmonoglutamates to polyglutamate forms, predominantly the pentaglutamate, at a slightly faster rate than the control animals, and the net hepatic uptake of the labeled dose was higher than in the controls. Tetrahydrofolate derivatives were the predominant one-carbon form of folate in the livers of ethanol-fed and control animals, although the proportion of folate in the 5-methyltetrahydrofolate form was slightly increased after ethanol supplementation. Although hepatic metabolism of folate appears to be unimpaired in the ethanol-fed rat, an increased rate of pteroylpolyglutamate synthesis, with a resulting increase in the tissue storage of folate, might be a contributing factor to the low serum folate levels reported in alcoholics.

Alcoholism↗
PubMed2004

Is there a role for folate determinations in current clinical practice in the USA?

Our objectives were to determine the likelihood of true folate deficiency among patients tested for this disorder, to identify whether there were differences between the clinical indications for folate testing in folate-normal and folate-deficient patients and to assess the impact of a diagnosis of folate deficiency on patient management. The results of all blood samples analyzed for serum and erythrocyte folate levels during the year 2001 at the Cleveland Clinic Foundation were retrieved. Folate deficient patients were identified and their medical charts were reviewed to determine the indications, patient characteristics, and impact of this diagnosis on patient management. For comparison, medical chart review was also conducted on a control group composed of an equal number of randomly selected patients with normal serum folate values. A total of 6024 (4689 serum and 1335 erythrocyte) samples from 4985 patients were collected. In the study, 77 (1.6%) of the serum folate levels, from 74 patients, were identified as low. When compared with the control group, patients with low serum folate levels had lower hemoglobin and a greater red cell distribution width. Mean corpuscular volume, however, did not differ between the two groups. No significant differences in the clinical indications for serum folate level determinations could be identified. Only 39 of the 74 patients with low serum folate levels were given folate replacement, representing only 0.9% of the clinically suspected and tested patients. We conclude that determination of serum folate level infrequently led to appropriate folate replacement therapy. Moreover, even when suspected, true folic acid deficiency is rare and clinical indications are not helpful in diagnosis.

Adult↗
PubMed1991

B complex vitamin patterns in geriatric and young adult inpatients with major depression.

This study compared the B complex vitamin status at time of admission of 20 geriatric and 16 young adult non-alcoholic inpatients with major depression. Twenty-eight percent of all subjects were deficient in B2 (riboflavin), B6 (pyridoxine), and/or B12 (cobalamin), but none in B1 (thiamine) or folate. The geriatric sample had significantly higher serum folate levels. Psychotic depressives had lower B12 than did non-psychotic depressives. Poorer blood vitamin status was not associated with higher scores on the Hamilton Depression Rating Scale or lower scores on the Mini-Mental State Examination in either age group. The data support the hypothesis that poorer status in certain B vitamins is present in major depression, but blood measures may not reflect central nervous system vitamin function or severity of affective syndromes as measured by the assays and scales in the present study.

Adult↗
PubMed2003

Folic acid with or without vitamin B12 for cognition and dementia.

BACKGROUND: Folates are vitamins essential to the development of the central nervous system. Insufficient folate activity at the time of conception and early pregnancy can result in congenital neural tube defects. In adult life folate deficiency has been known for decades to produce a characteristic form of anaemia ("megaloblastic"). More recently degrees of folate inadequacy, not severe enough to produce anaemia, have been found to be associated with high blood levels of the amino acid homocysteine. Such degrees of folate inadequacy can arise because of insufficient folates in the diet or because of inefficient absorption or metabolic utilisation of folates due to genetic variations. Conventional criteria for diagnosing folate deficiency may be inadequate for identifying people capable of benefiting from dietary supplementation. High blood levels of homocysteine have been linked with the risk of arterial disease, dementia and Alzheimer's disease. There is therefore interest in whether dietary supplements of folic acid (an artificial chemical analogue of naturally occurring folates) can improve cognitive function of people at risk of cognitive decline associated with ageing or dementia, whether by affecting homocysteine metabolism or through other mechanisms. There is a risk that if folic acid is given to people who have undiagnosed deficiency of vitamin B12 it may lead to neurological damage. Vitamin B12 deficiency produces both an anaemia identical to that of folate deficiency but also causes irreversible damage to the central and peripheral nervous systems. Folic acid will correct the anaemia of vitamin B12 deficiency and so delay diagnosis but will not prevent progression to neurological damage. For this reason trials of folic acid supplements may involve simultaneous administration of vitamin B12. Apparent benefit from folic acid given in the combination would therefore need to be "corrected" for any effect of vitamin B12 alone. A separate Cochrane review of vitamin B12 and cognitive function is being prepared. OBJECTIVES: To examine the effects of folic acid supplementation, with or without vitamin B12, on elderly healthy and demented people, in preventing cognitive impairment or retarding its progress. SEARCH STRATEGY: Trials were identified from a search of the Cochrane Dementia and Cognitive Improvement Specialized Register Group on 9 April 2003 using the terms: folic acid, folate, vitamin B9, leucovorin, methyltetrahydrofolate, vitamin B12, cobalamin, cyanocobalamin, dementia, cognitive function, cognitive impairment, Alzheimer's disease, vascular dementia, mixed dementia and controlled trials. MEDLINE and EMBASE (both all years) were searched for additional trials on healthy people. SELECTION CRITERIA: All double-blind placebo-controlled randomized trials, in which supplements of folic acid with or without vitamin B12 were compared with placebo for elderly healthy people or people with any type of dementia or cognitive impairment. DATA COLLECTION AND ANALYSIS: The reviewers independently applied the selection criteria and assessed study quality. One reviewer extracted and analysed the data. In comparing intervention with placebo, weighted mean differences, and standardized mean difference or odds ratios were estimated. MAIN RESULTS: Four randomized controlled trials fulfilled the inclusion criteria for this review. One trial (Bryan 2002) enrolled healthy women, and three (Fioravanti 1997; Sommer 1998; VITAL 2003) recruited people with mild to moderate cognitive impairment or dementia with or without diagnosed folate deficiency. Fioravanti 1997 enrolled people with mild to moderate cognitive impairment or dementia as judged by scores on the Mini-Mental State Examination (MMSE) and Global Deterioration Scale and with serum folate level<3ng/l. One trial (VITAL 2003) studied the effects of a combination of vitamin B12 and folic acid on patients with mild to moderate cognitive impairment due to Alzheimer's disease or mixed dementia. The analysis from the included trials found no benefit from folic acid with or without vitamin B12 in comparison with placebo on any measures of cognition and mood for healthy or cognitively impaired or demented people: Folic acid effect and healthy participants: there was no benefit from of oral 750 mcg folic acid per day for five weeks compared with placebo on measures of cognition and mood of 19 healthy women aged 65 to 92. Folic acid effect and people with mild to moderate cognitive decline or dementia: there were no statistically significant results in favour of folic acid with or without vitamin B12 on any measures of cognitive function. Scores on the Mini-Mental State Examination (MMSE) revealed no statistically significant benefit from 2 mg per day folic acid plus 1mg vitamin B12 for 12 weeks when compared with placebo (WMD 0.39, 95% CI -0.43 to 1.21, P=0.35). Cognitive scores on the Alzheimer's Disease Scale (ADAS-Cog) showed no statistically significant benefit from 2 mg /day folic acid plus 1 mg /day vitamin B12 for 12 weeks compared with placebo (WMD 0.41, 95% -1.25 to 2.07, P=4.63). The Bristol Activities of Daily Living Scale (BADL) revealed no benefit from 2mg per day of folic acid plus 1 mg vitamin B12 for 12 weeks in comparison with placebo (WMD -0.57, 95%CI -1.95 to 0.81, P=0.42). None of the sub tests of the Randt Memory Test (RMT) showed statistically significant benefit from 15 mg of folic acid orally per day for 9 weeks when compared with placebo. One trial (Sommer 1998) reported a significant decline compared with placebo in two cognitive function tasks in demented patients who had received high doses of folic acid (10 mg /day) for unspecified periods. One trial (VITAL 2003) showed that 2 mg folic acid plus 1 mg vitamin B12 daily for 12 weeks significantly lowered serum homocysteine concentrations (P <0.0001). REVIEWER'S CONCLUSIONS: There was no beneficial effect of 750 mcg of folic acid per day on measures of cognition or mood in older healthy women. In patients with mild to moderate cognitive decline and different forms of dementia there was no benefit from folic acid on measures of cognition or mood. Folic acid plus vitamin B12 was effective in reducing the serum homocysteine concentrations. Folic acid was well tolerated and no adverse effects were reported. More studies are needed.

Cognition↗
PubMed2007

Vitamin B6, B12, and folic acid supplementation and cognitive function: a systematic review of randomized trials.

BACKGROUND: Despite their important role in cognitive function, the value of B vitamin supplementation is unknown. A systematic review of the effect of pyridoxine hydrochloride (hereinafter "vitamin B(6)"), cyanocobalamin or hydroxycobalamin (hereinafter "vitamin B(12)"), and folic acid supplementation on cognitive function was performed. METHODS: Literature search conducted in MEDLINE with supplemental articles from reviews and domain experts. We included English language randomized controlled trials of vitamins B(6) and/or B(12) and/or folic acid supplementation with cognitive function outcomes. RESULTS: Fourteen trials met our criteria; most were of low quality and limited applicability. Approximately 50 different cognitive function tests were assessed. Three trials of vitamin B(6) and 6 of vitamin B(12) found no effect overall in a variety of doses, routes of administration, and populations. One of 3 trials of folic acid found a benefit in cognitive function in people with cognitive impairment and low baseline serum folate levels. Six trials of combinations of the B vitamins all concluded that the interventions had no effect on cognitive function. Among 3 trials, those in the placebo arm had greater improvements in a small number of cognitive tests than participants receiving either folic acid or combination B-vitamin supplements. The evidence was limited by a sparsity of studies, small sample size, heterogeneity in outcomes, and a lack of studies that evaluated symptoms or clinical outcomes. CONCLUSION: The evidence does not yet provide adequate evidence of an effect of vitamin B(6) or B(12) or folic acid supplementation, alone or in combination, on cognitive function testing in people with either normal or impaired cognitive function.

Cognition↗
PubMed1980

Folate and mineral metabolism in poorly nourished epileptic children.

Ninety poorly nourished, ambulant, epileptic children, who had been receiving anticonvulsant medications for at least one year, were studied in respect to their folic acid and vitamin D metabolism. Only 11 (12.2%) had borderline or low folate levels. Serum vitamin D levels were low in five (8.9%); serum calcium levels were low in nine (10%); and serum phosphorus levels were low in three (3.3%). Alkaline phosphatase levels were elevated in 19 (21.1%), but whether these arose from bone or liver was ot determined. Height retardation did not correlate with abnormal mineral metabolism.

Adolescent↗
PubMed2006

Tracking the prevention of folic acid-preventable spina bifida and anencephaly.

BACKGROUND: The fortification of wheat flour with folic acid prevents most cases of spina bifida and anencephaly by raising serum folate levels among women capable of bearing children, as does encouraging women to consume folic acid supplements prior to pregnancy. Unfortunately, surveillance is conducted in few countries where the need is greatest. METHODS: A method for assessing the prevention of these birth defects is presented that combines fortification program information with country case prevalence estimates. RESULTS: This approach suggests that about 70% of all cases could be prevented within a year of implementation of fortification programs, were it not for the inertia of regulatory agencies. CONCLUSIONS: Professional researchers and clinicians can help combat this situation by becoming advocates for child health in their respective countries.

Anencephaly↗
PubMed2006

Dietary folate is associated with p16(INK4A) methylation in head and neck squamous cell carcinoma.

Inactivation of the p16(INK4A) (CDKN2A) gene in the Rb pathway is among the most common somatic alterations observed in tobacco-related solid tumors, including head and neck squamous cell carcinoma (HNSCC). In addition, a low folate diet is an important risk factor for HNSCC. Decreased dietary folate in an animal model of hepatocellular carcinoma has been associated with the induction of epigenetic silencing of the p16(INK4A) gene. In an ongoing population-based study of HNSCC, we sought to extend this observation to human disease testing the hypothesis that p16(INK4A) methylation is associated with decreased dietary folate. We also investigated the association of methylation silencing with functional polymorphisms in the folate metabolism enzyme methylene tetrahydrofolate reductase (MTHFR). In 169 HNSCCs, the odds ratio for p16(INK4A) methylation among those with low dietary folate intake was 2.3 (95% CI = 1.1-4.8) when compared with those with high folate intake. Furthermore, this increased risk for epigenetic silencing at p16(INK4A) was modified by the MTHFR alleles previously associated with diminished serum folate levels. Hence, in HNSCC low dietary intake of folate is associated with p16(INK4A) methylation, and this relationship is modified by the MTHFR genotype. Our data provides important evidence for a mechanism of action of folate deficiency in cancer.

Adult↗
PubMed1980

Impairment of folic acid absorption by oral pancreatic extracts.

Higher serum folate levels were found among newly diagnosed, untreated patients with pancreatic insufficiency than among treated patients despite greater fat malabsorption in the former group. In vivo folate absorption tests using Tritium-labeled pteroylmonoglutamatic acid showed folate absorption to be enhanced in pancreatic insufficiency patients as compared to control subjects (P less than 0.01). Moreover, pancreatic extract significantly inhibited folate absorption in both normal subjects (P less than 0.05) and pancreatic insufficient patients (P less than 0.001). In vitro testing showed pancreatic extract to form insoluble complexes with folate. Such complex formation may diminish absorption of dietary folate and lead to folate deficiency. Since both pancreatic extract and bicarbonate are used in the treatment of pancreatic insufficiency and both are known to impair folate absorption, folate status should be monitored in patients being treated for pancreatic insufficiency; supplementation may be indicated.

Administration, Oral↗
PubMed1992

Evidence for the induction and release of pancreatic folylpolyglutamate hydrolase by the ingestion of folyl polyglutamates in the rat.

Pteroyl polyglutamate hydrolase (folyl conjugase), which hydrolyses the dietary polyglutamyl folates into simple forms prior to absorption, has been shown to be induced in rat pancreas in response to dietary polyglutamyl folates but not by ingestion of synthetic unconjugated folates. Folate absorption, as measured by the rise in serum folate levels after ingestion, of dietary conjugated folates is impaired in pancreatectomised animals whereas absorption of synthetic simple folate is not. A severe build-up of folyl conjugase is observed in the lumen of control but not in pancreatectomised animals after dietary folate ingestion. These results taken together would suggest that dietary folates are hydrolysed to monoglutamyl forms suitable for absorption in the lumen; the hydrolysis is catalysed by a luminal folyl conjugase of pancreatic origin induced by dietary conjugated folates.

Animals↗
PubMed1986

Folic acid malabsorption in atrophic gastritis. Possible compensation by bacterial folate synthesis.

Folic acid absorption was studied in 12 elderly subjects with atrophic gastritis and 10 elderly normal controls using tritium-labeled pteroylmonoglutamic acid. Two folic acid absorption tests were carried out on each subject with 120 ml of either water or 0.1 N HCl. Folic acid absorption was significantly lower in subjects with atrophic gastritis than in normal controls (31% vs. 51%, respectively; p less than 0.01). In subjects with atrophic gastritis, folic acid absorption rose significantly to 54% (p less than 0.001) when administered with acid, but did not change in normal controls (50%). Serum folate levels were normal in all subjects. Proximal small intestinal pH was higher in atrophic gastritis subjects than in normal controls (7.1 vs. 6.7, respectively; p less than 0.05), as were bacterial counts of small intestinal fluid (p less than 0.01). Bacteria cultured from the aspirates of subjects with atrophic gastritis were able to synthesize folate in vitro when incubated in a folate-free medium. Atrophic gastritis results in folic acid malabsorption but not in folate deficiency, possibly due to increased bacterial synthesis of folate in the small intestine.

Aged↗
PubMed2004

Second trimester folate status and preterm birth.

OBJECTIVE: The purpose of this study was to show that maternal folate status during pregnancy may be related to preterm birth. STUDY DESIGN: Women were recruited at 24 to 29 weeks' gestation from 1995 to 2000 into the Pregnancy, Infection, and Nutrition Study. Those who completed an interview and a food frequency questionnaire, or provided a blood sample for radioassay of serum (n = 2026) and red blood cell (n = 1034) folate were included. RESULTS: Mean daily dietary folate intake was 463 microg (SD +/- 248). Intake </=500 microg was associated with increased preterm delivery (RR = 1.8, 95% CI 1.4-2.6) controlling for total energy intake. Serum folate levels <16.3 ng/mL and red blood cell folate levels </=626.6 ng/mL yielded adjusted risk ratios of 1.8 (95% CI 1.3-2.5) and 1.7 (95% CI 1.1-2.6), respectively. Patterns were similar for spontaneous and overall preterm birth. CONCLUSION: These results support the hypothesis that low folate levels during the second trimester of pregnancy are associated with an increased risk of preterm birth.

Adult↗
PubMed2002

Preconception counseling improves folate status of women planning pregnancy.

OBJECTIVE: To assess whether counseling women planning pregnancy to start or continue folic acid supplementation improves folate status. METHODS: Women and their partners reported folic acid supplement intake in a preconceptional health questionnaire, and the women were categorized as reported "users" or "nonusers" of supplements before counseling. The use of periconceptional folic acid was addressed at a subsequent preconceptional consultation. Differences between reported supplement users and nonusers before counseling as well as between assumed users and nonusers of folic acid (with precounseling red cell and serum folate levels above and below 590 nmol/L and 20 nmol/L, respectively) were analyzed. RESULTS: A total of 111 (66%) of 168 eligible women participated. Estimated mean red cell folate levels of women who reported no use of folic acid supplements before counseling increased significantly after 4 months from 540 nmol/L to 680 nmol/L. Red cell folate levels of women who reported taking supplements (44%) remained stable up to 1 year after counseling. Women with low precounseling folate levels showed a highly significant mean increase in red cell folate from 475 nmol/L to 689 nmol/L 4 months after counseling. CONCLUSION: Addressing periconceptional folic acid use at a preconceptional consultation improves folate status among women planning to conceive.

Adult↗
PubMedDate not supplied

Mood disorder with mixed features due to vitamin B(12) and folate deficiency.

Vitamin B(12) and folate deficiency is often associated with affective disorders mainly of the depressive type. We report a case of a 42-year-old woman with a mood disorder with mixed depressed/manic features that was due to vitamin B(12) and folate deficiency. The psychopathology developed over a five-year period without hematologic or other overt clinical characteristics of pernicious anemia. Replacement treatment with vitamin B(12) and folate was rapidly followed by full clinical remission, electroencephalographic normalization and neuropsychological improvement. At a one-year follow-up this condition was stable. Consequently, patients who respond poorly to psychopharmacologic treatment and/or present with atypical mood symptoms would warrant determination of vitamin B(12) and folate serum levels.

Adult↗
PubMed1997

Acute folate deficiency in a critically ill patient.

A 19-year-old male patient developed thrombocytopenia and leukopenia due to acute folate deficiency while recovering from a multiple organ failure syndrome. Risk factors for acute folate deficiency are extensive tissue damage due to sepsis, trauma or surgery and acute renal failure requiring renal replacement therapy. The diagnosis is based on bone marrow examination showing marked megaloblastic changes whereas serum folate levels and red cell folate levels are normal. Recognition of this serious complication of critical illness is important because it should be readily prevented by folic acid therapy.

Acute Disease↗