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Results for “FOLIC ACID DEFICIENCY”

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PubMed1986

Cumulative excess urinary excretion of folate in rats after repeated ethanol treatment.

The folate deficiency that is produced by chronic alcohol ingestion results from poor dietary intake and from effects of ethanol on folate metabolism and absorption. Previous studies in fasted rats showed that singular treatment with ethanol produces an increase in urinary folate levels, in amounts that account for a subsequent decrease in plasma folate levels. The effects of subacute administration of ethanol on urinary folate excretion were studied in fed and fasted rats treating for 1, 2, 3 or 4 d either with ethanol orally in four doses of 1 g/kg each at hourly intervals or with glucose in isocaloric doses. Urine was collected at timed intervals up to 12 h after each daily dose. Rats were fed daily except for the evening prior to the final treatment day. Ethanol treatment produced an increase in urinary folate excretion in fed and in fasted rats, although the effect in fed rats was less marked. The increased excretion was similar on each final day, whether rats were treated for 1, 2, 3 or 4 d, indicating that there was no adaptation to the loss of folate during this subacute treatment. The excess urinary folate excretion accumulated so that the longer the rats were exposed to ethanol, the greater the urinary loss. These results suggest that when animals are chronically treated with ethanol, urinary folate loss could contribute to the development of folate deficiency.

Animals↗
PubMed1986

Mechanisms of vitamin deficiencies in alcoholism.

Chronic alcoholic patients are frequently deficient in one or more vitamins. The deficiencies commonly involve folate, vitamin B6, thiamine, and vitamin A. Although inadequate dietary intake is a major cause of the vitamin deficiency, other possible mechanisms may also be involved. Alcoholism can affect the absorption, storage, metabolism, and activation of many of these vitamins. Possible factors which cause alterations in the absorption, storage, and metabolism of these vitamins are discussed. Suggestions for management of vitamin deficiencies in chronic alcoholics are also discussed.

Alcoholism↗
PubMed2004

Folate and DNA methylation: a mechanistic link between folate deficiency and colorectal cancer?

Epidemiological, clinical, and animal studies collectively indicate that dietary folate intake and blood folate levels are inversely associated with colorectal cancer risk. Folate plays an essential role in one-carbon transfer involving remethylation of homocysteine to methionine, which is a precursor of S-adenosylmethionine, the primary methyl group donor for most biological methylations. DNA methylation is an important epigenetic determinant in gene expression, maintenance of DNA integrity and stability, chromosomal modifications, and development of mutations. Dysregulation and aberrant patterns of DNA methylation are generally considered to be mechanistically involved in colorectal carcinogenesis. Aberrant DNA methylation has been considered as a leading mechanism by which folate deficiency enhances colorectal carcinogenesis. However, currently available data pertaining to the effects of folate deficiency on DNA methylation are inconsistent and incomplete. The portfolio of evidence from animal, human, and in vitro studies suggests that the effects of folate deficiency on DNA methylation are highly complex; appear to depend on cell type, target organ, and stage of transformation; and are gene and site specific. In addition, the pattern of site- and gene-specific DNA methylation induced by folate deficiency may not be in concert with the direction of changes in genomic DNA methylation. Collectively, currently available evidence indicates that genomic DNA hypomethylation in the colorectum is not a probable mechanism by which folate deficiency enhances colorectal carcinogenesis. However, there is still a possibility that sequence-specific alterations of DNA methylation in critical cancer-related genes might be mechanistically involved in the folate deficiency-mediated colorectal carcinogenesis.

Colorectal Neoplasms↗
PubMed1986

Iron, folate and vitamin B12 nutrition and anaemia in black preschool children in the northern Transvaal.

The prevalence of anaemia and deficiencies of iron, folate and vitamin B12 were investigated in 140 rural black preschool children aged 3-5 years living in five different villages in the Letaba area, near Tzaneen. Anaemia was highly prevalent, 39.2% of the children having haemoglobin levels below 11.1 g/dl. Approximately 10% were considered to be iron-deficient. On the basis of subnormal red cell folate values, 1 in 4 children was folate-deficient, suggesting the need for intervention at the community level such as enrichment of the staple foodstuff, maize meal, with folic acid.

Black or African American↗
PubMed1985

Folate and nutrition.

The main causes of nutritional folate deficiency are reviewed as well as the consequential effects of this vitamin deficiency; some are well defined such as hematological consequences, others are less known: possible effects on immune and non-immune systems, influence on the central and peripheral nervous system, on the outcome of pregnancy and newborns. This paper emphasizes at-risk physiological and pathological situations of deficiency: pregnancy, premature infants, elderly, alcoholics, patients admitted to intensive care units. In these high risk populations, the benefit of folic acid prophylaxis is raised.

Adolescent↗
PubMed1975

Recurrent aphthae: treatment with vitamin B12, folic acid, and iron.

A series of 130 consecutive outpatients with recurrent aphthous stomatitis were screened at the oral medicine department, Glasgow Dental Hospital, for deficienciesin vitamin b12, folic acid, and iron. In 23 patients (17.7%) such deficiencies werefound; five were deficient in vitamin B12, seven in folic acid, and 15 in iron. Four had more than one deficiency. Out of 130 controls matched for age and sex 11 (8.5%) were found to have deficiencies. The 23 deficient patients with recurrent aphthaewere treated with specific replacement therapy, and all 130 patients were followed up for at least one year. Of the 23 patients on replacement therapy 15 showed complete remission of ulceration and eight definite improvement. Of the 107 patientswith no deficiency receiving local symptomatic treatment only 33 had a remission or wereimproved. This difference was significant (P less than 0.001). Most patients withproved vitamin B12 or folic acid deficiency improved rapidly on replacement therapy;those with iron deficiency showed a less dramatic response. The 23 deficient patientswere further investigated to determine the cause of their deficiencies and detect the presence of any associated conditions. Four were found to have Addisonian perniciousanaemia. Seven had a malabsorption syndrome, which in five proved to be a gluten-induced enteropathy. In addition, there were single patients with idiopathic proctocolitis, diverticular disease of the colon, regional enterocolitis, and adenocarcinoma of thecaecum. We suggest that the high incidence of deficiencies found in this series andthe good response to replacement therapy shows the need for haematological screening of such patients.

Adenocarcinoma↗