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PubMedDate not supplied

[Vitamin and mineral deficiency in Mexico. A critical review of the state of the art. II. Vitamin deficiency].

We carried out a review of the studies related to vitamin deficiencies in the Mexican population published since 1950. Forty four studies were published from which we can conclude that: a) dietary intake data suggest that ascorbic acid, riboflavin and retinol intake are deficient: reported intakes were 40-70%, 35-64% and 20-72% of the recommended daily amounts respectively; niacin intake was also deficient in some studies; b) about 10% of Mexican children in rural areas had deficient values of plasma retinol (< 100 ng/ml) and about 25 to 30% had low values (100-200 ng/ml); this prevalence is reduced in children with a higher socioeconomic level; c) some studies were found that show the existence of marginal deficiencies of vitamin E, riboflavin and vitamin B12 in apparently healthy populations. Further studies are required to identify the magnitude of these and perhaps other vitamin deficiencies and their potential effects on the health and function of the Mexican population.

Adult↗
PubMed1992

Effects of folate deficiency and supplementation on methylnitrosourea-induced rat mammary tumors.

BACKGROUND: There are metabolic and epidemiologic data consistent with the hypothesis that folate deficiency increases the likelihood of cancer. Conversely, it is also known that folate is necessary for cancer growth, but few experiments in laboratory animals have evaluated the effects of folate deficiency on the development of chemically induced cancers. PURPOSE: Our purpose was to determine the effects of nutritional folate deficiency in female Fischer 344 rats on initiation and early promotion of methylnitrosourea (MNU)-induced mammary cancer. METHODS: Rats (age, 27 days) were fed a folic acid-deficient diet (AIN-76A) supplemented with glycine and succinylsulfathiazole [FA(0)]; the FA(0) diet supplemented with 2 or 40 mg of folic acid per kilogram [FA(2) or FA(40), respectively]; or the FA(0) diet supplemented with 20 mg of folinic acid per kilogram [FL(20)]. At 57 days of age, each diet-treated group (30 rats in each group) received MNU (50 mg/kg) by intravenous injection. Immediately after MNU treatment, all animals were fed the AIN-76A complete diet containing 2 mg of folic acid per kilogram. Control groups were fed the AIN-76A complete diet throughout the entire experiment. RESULTS: After 4 weeks, folate deficiency, but not anemia or growth suppression, was documented by lower folate levels in plasma and red blood cells in the group receiving the FA(0) diet. Cancer multiplicity (i.e., number of mammary cancers per number of tumor-bearing animals) at 180 days after MNU injection was 1.32, 1.90, 2.14, and 2.73 mammary cancers per tumor-bearing animal in the FA(0), FA(2), FA(40), and FL(20) groups, respectively; the value in the FA(0) group was statistically significant compared with the values in the other groups. The time required for 50% of the rats to develop palpable mammary cancer was 170, 142, 100, and 85 days, respectively. The value of 170 days for the FA(0) group was statistically significant compared with the values of 100 and 85 days. Mammary cancer incidence was 63%, 70%, 72%, and 73%, respectively; these percentages were not significantly different. CONCLUSIONS: Folate deficiency suppresses and folate supplementation enhances initiation or early promotion of MNU-induced mammary cancer in rats, even when the folate-deficient rats do not have anemia or growth suppression. IMPLICATION: Since the rat is relatively resistant to folate deficiency anemia, other animal models should be used to test the effect of folate nutriture on carcinogenesis.

Animals↗
PubMed1980

Methionine synthesis, aminoimidazole carboxamide excretion and folate levels in pregnant rats.

The capacity for tetrahydrofolate regeneration through folate-linked methionine synthesis and for purine-ring closure through formylation of aminoimidazole carboxamide ribotide was studied in pregnant female rats fed diets containing either methionine or homocystine with or without folic acid. Plasma and liver folates, serine transhydroxymethylase, 5,10-methylene tetrahydrofolate dehydrogenase and glutamate formiminotransferase activities were also assayed. Pregnancy proceeded normally in all groups. Hypotrophic fetuses were observed only with the diet containing homocystine and no folic acid. Plasma folates were severely depleted at the end of pregnancy even when folic acid was present in the diet. Hepatic stores of folate were twice as high in the methionine as in the homocystine-fed pregnant females supplemented with folic acid. This favorable effect of methionine was not observed in folic acid-deficient females. No change in levels of serine transhydroxymethylase, 5,10-methylenetetrahydrofolate dehydrogenase, glutamate formimino-transferase activities was observed. Pregnancy did not stimulate methionine synthetase activity, the level of which was primarily affected by the nutritional conditions. Because of its low output and narrow range of adaptativity, methionine synthetase cannot be the sole regulatory factor of THF regeneration. Urinary excretion of aminoimidazole carboxamide was enhanced in folic acid-deficient pregnant females and was not prevented by supplying methionine.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed2001

[Homocysteine, endothelial dysfunction and cardiovascular risk: pathomechanisms and therapeutic options].

Elevated homocyst(e)ine plasma concentrations are an independent risk factor for cardiovascular disease. Hyperhomocyst(e)inaemia is common in patients with peripheral arterial occlusive disease, coronary heart disease, cerebrovascular disease, carotid artery stenosis and venous thromboembolism. Endothelial dysfunction may be one underlying cause leading to proatherogenic effects associated with hyperhomocyst(e)inaemia. However, the mechanisms which lead to impaired endothelial function in hyperhomocyst(e)inaemia are not fully understood. Recent evidence suggests that homocyst(e)ine may interact with physiological mediators of the endothelial matrix. Oxidative mechanisms and decreased biological activity of endothelium-derived nitric oxide (NO) may also contribute to homocyst(e)ine-associated endothelial dysfunction. B vitamins are essential cofactors in the metabolism of homocyst(e)ine to methionine via the remethylation-pathway (vitamin B12, folic acid) and to cystathionine via the transsulphuration-pathway (vitamin B6). Dietary deficiencies of folic acid, vitamin B12, and vitamin B6 appear to be common among elderly people in the western world and represent one pathogenic factor related to the incidence of hyperhomocyst(e)inaemia. Several studies have demonstrated that dietary supplementation with folic acid and the vitamins B12 and B6 is an efficient means to decrease plasma homocyst(e)ine. No clinical studies are available to date to prove whether reducing homocyst(e)ine levels to the normal range by supplementary B vitamins will also beneficially affect vascular function or cardiovascular risk. Furthermore it is unknown whether moderately elevated homocyst(e)ine concentrations per se may predispose to development of vascular disease, or whether homocyst(e)ine is an indirect marker of cardiovascular disease. Further investigations will be necessary to elucidate the causal relationship between elevated homocyst(e)ine plasma concentrations and the incidence of cardiovascular events, especially since the therapeutic strategies in hyperhomocyst(e)inaemia would differ depending on the underlying pathophysiological mechanisms.

Adult↗
PubMed1991

[Anemia in pregnancy. Review].

Pregnancy anemia occurs when the concentration of hemoglobin in pregnant women is less than 11 g/dl, provided that they live at sea level. Nutritional deficiencies of iron and folic acid, combined or isolated, are the main causes of this type of anemia, due to increased demands of nutrients to satisfy the needs of the fetus and the growing tissues during pregnancy. Nutritional deficiency of vitamin B12 is infrequent during pregnancy unless there are coexistant gastrointestinal abnormalities or immunological processes. The recommended therapy for iron or folic acid deficiency is oral administration of ferrous salts or folic acid, in daily doses that should not be higher than 60 mg of elemental iron or 2.5 mg of folic acid.

Anemia, Hypochromic↗