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PubMed1998

Homocysteine and cardiovascular disease.

An elevated level of total homocysteine (tHcy) in blood, denoted hyperhomocysteinemia, is emerging as a prevalent and strong risk factor for atherosclerotic vascular disease in the coronary, cerebral, and peripheral vessels, and for arterial and venous thromboembolism. The basis for these conclusions is data from about 80 clinical and epidemiological studies including more than 10,000 patients. Elevated tHcy confers a graded risk with no threshold, is independent of but may enhance the effect of the conventional risk factors, and seems to be a particularly strong predictor of cardiovascular mortality. Hyperhomocysteinemia is attributed to commonly occurring genetic and acquired factors including deficiencies of folate and vitamin B12. Supplementation with B-vitamins, in particular with folic acid, is an efficient, safe, and inexpensive means to reduce an elevated tHcy level. Studies are now in progress to establish whether such therapy will reduce cardiovascular risk.

Arteriosclerosis↗
PubMed2006

Distribution of anemia associated with micronutrient deficiencies other than iron in a probabilistic sample of Mexican children.

BACKGROUND: This investigation aims to explore the association among anemia and vitamins A, C, and folate deficiencies in a probabilistic sample of Mexican children. METHODS: Data on hemoglobin, serum vitamins A and C and folate concentrations and percent transferrin saturation (PTS) in children 0.5-11 years (n = 1,770) were extracted from the database of the probabilistic Mexican National Nutrition Survey 1999 (NNS-99). RESULTS: Overall, 16.6% of children were anemic. Iron deficiency children with or without anemia had more frequent low serum retinol (40.6 vs. 16% and 27.7 vs. 11.9%, p < 0.05, respectively) and lower hemoglobin folate (11.5 vs. 22%, p < 0.05) than their non-iron deficiency counterparts. Mean concentrations of serum iron (p < 0.01), folate (p < 0.001) and retinol (p < 0.0001), but not ascorbic acid (p < 0.6), were significantly lower in anemic than in nonanemic children. In a linear regression model, 15% of hemoglobin variation in children was explained by retinol, folate and PTS, but not vitamin C (p <0.0001). CONCLUSION: Anemia was mostly associated with iron deficiency and with a lesser proportion of folate and vitamin A deficiencies. Vitamin A deficiency might be overestimated since iron deficiency may lower serum retinol concentrations. Interventions aimed to reduce anemia in this population must consider interactions between those micronutrients in designing strategies.

Adolescent↗
PubMed1996

Vascular dysfunction in monkeys with diet-induced hyperhomocyst(e)inemia.

Elevated plasma homocyst(e)ine may predispose to complications of vascular disease. Homocysteine alters vasomotor regulatory and anticoagulant properties of cultured vascular endothelial cells, but little is known about effects of hyperhomocyst(e)inemia on vascular function in vivo. We tested the hypothesis that diet-induced moderate hyperhomocyst(e)inemia is associated with vascular dysfunction in cynomolgus monkeys. Plasma homocyst(e)ine increased from 4.O +/- O.2 microM when monkeys were fed normal diet to 10.6 +/- 2.6 microM when they were fed modified diet (mean +/- SE; P = 0.02). Vasomotor responses were assessed in vivo by quantitative angiography and Doppler measurement of blood flow velocity. In response to activation of platelets by intraarterial infusion of collagen, blood flow to the leg decreased by 42 +/- 9% in monkeys fed modified diet, compared with 14 +/- 11% in monkeys fed normal diet (P = 0.008), Responses of resistance vessels to the endothelium-dependent vasodilators acetylcholine and ADP were markedly impaired in hyperhomocyst(e)inemic monkeys, which suggests that increased vasoconstriction in response to collagen may be caused by decreased vasodilator responsiveness to platelet-generated ADP. Relaxation to acetylcholine and, to a lesser extent, nitroprusside, was impaired ex vivo in carotid arteries from monkeys fed modified diet. Thrombomodulin anticoagulant activity in aorta decreased by 34 +/- 15% in hyperhomocyst(e)inemic monkeys (P = 0.03). We conclude that diet-induced moderate hyperhomocyst(e)inemia is associated with altered vascular function.

Animals↗
PubMed1998

Ability of endogenous folate from soy protein isolate to maintain plasma homocysteine and hepatic DNA methylation during methyl group depletion in rats.

We investigated different means of achieving methyl depletion by feeding weanling rats modified AIN diets depleted of folate (FD), folate + choline (FCD), and folate + choline + methionine (FCMD), and examined the consequent effects on folate status, homocysteine levels, and methylation status. Control rats were fed a 12% protein diet consisting of either casein or soy protein isolate (SPI) and containing 2 mg/kg folate, 0.2% choline, and 0.4% methionine. After the rats had been on the diets for 4 and 8 weeks, whole blood folate concentration was measured and found to be significantly depleted in the folate deficient treatments compared with controls at 4 weeks (p < 0.001), this reduction being significantly greater (p < 0.03) in casein-fed rats (60%) than in SPI-fed rats (32%). The omission of choline and methionine from the diet had no further influence on whole blood folate. A significant inverse correlation was observed in the casein-fed rats after 8 weeks between mean plasma homocysteine concentration and decreasing methyl content of the diet (r2 = 0.978, p < 0.002), an effect not seen in the corresponding SPI-fed rats. Hypomethylation of hepatic DNA evidenced by a reduction in 5-methylcytosine content was present in the casein rats fed FCD and FCMD relative to control (p < 0.05). No hepatic DNA methylation changes were observed in the SPI-fed rats. The results obtained in the present work demonstrate that a soy-based diet can compensate against methyl group depletion by maintaining plasma homocysteine levels and an adequate level of DNA methylation, a result we attribute to endogenous folate content.

5-Methylcytosine↗
PubMed2002

Monitoring dietary compliance in coeliac disease using red cell distribution width.

Red cell distribution width (RDW) as measured on modern blood analysers is a sensitive marker of nutritional deficiency affecting red blood cell production and maturation. Such deficiencies are common in coeliac disease and it may therefore be possible indirectly to assess response to a gluten-free diet by monitoring the RDW. We measured RDW, iron, B12, folate and endomysial antibodies (EMA) in 46 newly diagnosed coeliac patients at diagnosis and after a gluten-free diet. RDW was elevated in 76% of patients at diagnosis. There was a significant decrease in RDW (17.3% vs 13.8%) after 12 months of diet, corresponding to sero-conversion of EMA and normalisation of serum iron, B12 and folate levels. We conclude that monitoring RDW is a simple indirect means of assessing response to a gluten-free diet in coeliac disease.

Anemia, Iron-Deficiency↗
PubMed1977

[Anemia in terminal kidney failure. Pathogenesis and therapy].

Various factors are involved in the pathogenesis of anemia in dialysis patients. Reduced erythropoiesis is mainly attributed to erythropoietin deficiency. Stimulation of erythropoiesis may be promoted by androgens. Substitution of iron is recommended in case of iron deficiency. As a rule, supplementation of vitamin B12 is not necessary, but administration of folic acid is recommended. Treatment of anemia in renal failure is rendered more effective by increased technical efficiency in hemodialysis permitting a relatively protein-rich diet. Blood transfusions are not necessary during routine treatment of dialysis. Since bilateral nephrectomy will always provoke severe anemia, it should be reserved to special cases of severe hypertension. Until now, no conservative therapy has been developed which would allow optimal treatment of anemia in dialysis patients. Successful renal transplantation still is, and will be, the best therapeutic intervention.

Androgens↗
PubMed1995

Case report: subacute combined degeneration of the spinal cord from folate deficiency.

Subacute combined degeneration of the spinal cord is a rare neurologic complication of folate deficiency. Progressive gait disturbance, weakness, confusion, and depression developed in a 39-year-old man. He had taken phenobarbital for more than 2 years. He was bedbound, with new loss of position and vibration senses in the lower extremities. His hemoglobin was 2.9/dl, mean corpuscular volume 122 fl, vitamin B12 428 pg/ml, and folate 1 ng/ml. Peripheral blood and bone marrow showed megaloblastic anemia. Serum methylmalonic acid and homocysteine levels were consistent with folate deficiency, not B12 deficiency. Treatment with folate and packed erythrocytes resulted at 4 months in overall improvement, including walking. Position sense was restored, and vibration sense had become nearly normal. The authors found no cause for folate deficiency except phenobarbital.

Adult↗
PubMed1994

Sensitivity of serum methylmalonic acid and total homocysteine determinations for diagnosing cobalamin and folate deficiencies.

PURPOSE: Patients with cobalamin (vitamin B12) deficiency usually lack many of the classic features of severe megaloblastic anemia; because of the low diagnostic specificity of decreased serum cobalamin levels, demonstrating the deficiency unequivocally is often difficult. We examined the sensitivity of measuring serum concentrations of methylmalonic acid and total homocysteine for diagnosing patients with clear-cut cobalamin deficiency and compared the results with those of patients with clear-cut folate deficiency. PATIENTS AND METHODS: Serum metabolites were measured for all patients seen from 1982 to 1989 at two university hospitals who met the criteria for cobalamin and folate deficiency states and for such patients seen from 1968 to 1981 from whom stored sera were available. In all, 406 patients had 434 episodes of cobalamin deficiency and 119 patients had 123 episodes of folate deficiency. Criteria for deficiency states included serum vitamin levels, hematologic and neurologic findings, and responses to therapy. Responses were documented in 97% of cobalamin-deficient patients and 76% of folate-deficient patients. Metabolite levels were measured by modified techniques using capillary-gas chromatography and mass spectrometry. RESULTS: Most of the cobalamin-deficient patients had underlying pernicious anemia; two thirds were blacks or Latinos. Hematocrits were normal in 28% and mean cell volumes in 17%. Of the 434 episodes of cobalamin deficiency, 98.4% of serum methylmalonic acid levels and 95.9% of serum homocysteine levels were elevated (greater than 3 standard deviations above the mean in normal subjects). Only one patient had normal levels of both metabolites. Serum homocysteine levels were increased in 91% of the 123 episodes of folate deficiency. Methylmalonic acid was elevated in 12.2% of the folate-deficient patients; in all but one, the elevation was attributable to renal insufficiency or hypovolemia. CONCLUSIONS: For the cobalamin-deficient patients, measuring serum metabolite concentrations proved to be a highly sensitive test of deficiency. We conclude that normal levels of both methylmalonic acid and total homocysteine rule out clinically significant cobalamin deficiency with virtual certainty.

Female↗