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PubMed1988

Elevation of total homocysteine in the serum of patients with cobalamin or folate deficiency detected by capillary gas chromatography-mass spectrometry.

To determine if levels of serum total homocysteine are elevated in patients with either cobalamin or folate deficiency, we utilized a new capillary gas chromatographic-mass spectrometric technique to measure total homocysteine in the serum of 78 patients with clinically confirmed cobalamin deficiency and 19 patients with clinically confirmed folate deficiency. Values ranged from 11 to 476 mumol/liter in the cobalamin-deficient patients and 77 of the 78 patients had values above the normal range of 7-22 mumol/liter as determined for 50 normal blood donors. In the cobalamin-deficient patients, serum total homocysteine was positively correlated with serum folate, mean corpuscular volume, serum lactate dehydrogenase, serum methylmalonic acid, and the degree of neurologic involvement, and inversely correlated with platelets and hematocrit. In the folate-deficient patients, values for serum total homocysteine ranged from 17 to 185 mumol/liter and 18 of the 19 patients had values above the normal range. Some patients with pernicious anemia who were intermittently treated with cyanocobalamin were found to have elevated serum levels of total homocysteine while they were free of hematologic and neurologic abnormalities. The measurement of serum total homocysteine will help define the incidence of cobalamin deficiency and folate deficiency in various patient populations.

Adult↗
PubMed1992

Methyl group metabolism in the pancreas of folate-deficient rats.

Several studies have suggested that the metabolism of one-carbon compounds may have a special role in the function of the exocrine pancreas. An amino acid-defined diet was used to produce folate deficiency in a group of male rats. These rats were compared with a group of rats pair-fed the same diet supplemented with adequate folate and with a third group fed the folate-supplemented diet with ad libitum access. Pancreatic folate concentrations were already severely depleted after 4 wk of feeding the deficient diet (0.95 +/- 0.10, 5.81 +/- 0.29 and 4.58 +/- 0.30 nmol/g for the deficient, pair-fed control and ad libitum-fed control groups, respectively). The level of folate present in the pancreas of nondeficient animals was second only to that reported for liver. Urinary amylase excretion by animals in the deficient group was higher than that by the other groups (245.5 +/- 21.9, compared with 181.9 +/- 14.5 and 195.3 +/- 10.9 units/mg creatinine for the deficient, pair-fed control and ad libitum-fed control groups, respectively) after 4 wk. The ratio of S-adenosylmethionine to S-adenosylhomocysteine was 18.6 +/- 1.6 and 14.5 +/- 1.0 after 4 wk for the ad libitum-fed control and pair-fed control groups, respectively, but was significantly lower at 6.3 +/- 1.1 for the deficient group. These results indicate a profound effect of folate deficiency upon methyl group metabolism of the pancreas and suggest that this may result in decreased pancreatic function.

Animals↗
PubMed1993

Dietary folate requirement determined for channel catfish, Ictalurus punctatus.

Juvenile channel catfish, Ictalurus punctatus, were fed semipurified basal diets containing 0, 0.2, 0.5, 1.0, 4.0 or 10.0 mg/kg of folic acid or 10 g/kg of succinylsulfathiazole in aquaria for 15 wk. Fish fed the sulfonamide showed higher mortality, lower weight gain, lower thrombocyte counts, higher hemocytoblast and neutrophil counts, and lower liver folate concentrations than did control fish (0 folic acid), indicating that significant intestinal bacterial synthesis of folate occurs in channel catfish. There were positive quadratic regressions of weight gain, hematocrit, erythrocyte and leukocyte numbers, and positive linear regressions of plasma and liver folate on dietary folic acid concentrations. Broken-line analysis showed that the dietary requirements for folic acid for optimum weight gain, hematocrit, and erythrocyte and leukocyte numbers were 1.01, 1.17, 1.12 and 1.15 mg/kg, respectively. Plasma and liver concentrations of folate associated with normal growth and hematopoiesis were 22.9 nmol/L and 20.0 nmol/g, respectively. Ratios of leukocytes and lymphocytes to erythrocytes were maximal in fish fed 4.0 mg folic acid/kg, indicating that immunocompetence may increase as the dietary dose exceeds that required for normal growth. Anemia in folate-deficient channel catfish was characterized by pale livers, spleens, gills and kidneys, and by poikilocytosis, anisocytosis, pyknosis, cytoplasmic clearing, increased numbers of hemocytoblasts, macrocytosis, and binucleated erythrocytes or "spectacle" cells.

Animals↗
PubMed2001

Anemia in children.

Anemia in children is commonly encountered by the family physician. Multiple causes exist, but with a thorough history, a physical examination and limited laboratory evaluation a specific diagnosis can usually be established. The use of the mean corpuscular volume to classify the anemia as microcytic, normocytic or macrocytic is a standard diagnostic approach. The most common form of microcytic anemia is iron deficiency caused by reduced dietary intake. It is easily treatable with supplemental iron and early intervention may prevent later loss of cognitive function. Less common causes of microcytosis are thalassemia and lead poisoning. Normocytic anemia has many causes, making the diagnosis more difficult. The reticulocyte count will help narrow the differential diagnosis; however, additional testing may be necessary to rule out hemolysis, hemoglobinopathies, membrane defects and enzymopathies. Macrocytic anemia may be caused by a deficiency of folic acid and/or vitamin B12, hypothyroidism and liver disease. This form of anemia is uncommon in children.

Adolescent↗
PubMed1999

Can reduced folic acid and vitamin B12 levels cause deficient DNA methylation producing mutations which initiate atherosclerosis?

Atherosclerosis of the vascular system has classically been attributed to elevated serum cholesterol concentrations. Recently, it has been found that reduced serum levels of folic acid, vitamin B12, and vitamin B6 are related to the etiology of atherosclerosis and coronary heart disease. These deficiencies lead to inadequate production of S-adenosyl-methionine, creating a condition of hypomethylation. It is hypothesized that this causes hypomethylation of the DNA in cells in the arterial intima resulting in mutation and proliferation of smooth-muscle cells which lead to the formation of atheroma. It is further hypothesized that such action can be reversed by supraphysiological doses of these three vitamins to reduce or remove existing atheroma. It is recommended that all patients suffering from atherosclerosis and having deficiencies of any of these three vitamins and/or an elevation of serum homocysteine receive supplementation to prevent worsening of their condition.

Arteriosclerosis↗
PubMed1998

Candidate noninfectious disease conditions.

Important micronutrient deficiencies in at-risk populations can be addressed simultaneously with programmatically cost-effective results. Because of the interaction between many micronutrients, this would also be biologically effective. With adequate investment and political support, the chances of eliminating iodine deficiency as a problem in women of reproductive age and young children and of eliminating vitamin A deficiency as a problem in young children in the future are high. To eliminate iron deficiency and folic-acid-dependent neural tube defects (FADNTDs) in low-income populations, a new set of approaches will have to be developed. These same approaches, if successful, could be used to tackle other important micronutrient deficiencies.

Anemia, Iron-Deficiency↗
PubMed2000

Homocysteine and renal disease.

Hyperhomocysteinemia refers to an elevated circulating level of the sulfur-containing amino acid homocysteine and has been shown to be a risk factor for vascular disease in the general population. In patients with renal failure, hyperhomocysteinemia is a common feature. The underlying pathophysiological mechanism for this phenomenon is unknown. Proposed mechanisms include reduced renal elimination of homocysteine and impaired nonrenal disposal, possibly because of inhibition of crucial enzymes in the methionine-homocysteine metabolism by the uremic milieu. Absolute or relative deficiencies of folate, vitamin B6, or vitamin B12 may also play a role. Several case-control and prospective studies have now indicated that hyperhomocystenemia is an independent risk factor for atherothrombotic disease in patients with predialysis and end-stage renal disease. In renal patients, plasma homocysteine concentration can be reduced by administration of folic acid in doses ranging from 1 to 15 mg per day. In more than 50% of the cases, however, the homocysteine concentration remains above 15 micromol/L. The effects of vitamin B12 or vitamin B6 are unclear. Large intervention trials are now needed to establish whether homocysteine-lowering therapy will reduce atherothrombotic events in patients with renal failure. These studies are now planned or are ongoing.

Adult↗
PubMed1982

Folate and iron deficiencies in mothers and their newborn children.

Iron and folate status was assessed in 79 multiparous French women and 21 immigrant parturient women, previously defined as belonging to a high risk population for nutritional deficiencies, and their newborn infants. Maternal hemoglobin was correlated with ferritinemia and with serum folate values; weight gain during pregnancy appeared to be correlated with mother's iron status at start of labour and gestation duration with folate status. The need of iron and folic supplementation is emphasized for such groups. While a correlation appeared between maternal and newborn values for serum and red blood cell folates and for the RBC indices, no statistical difference was found between the infants born to iron or folate deficient mothers when compared with others.

Female↗
PubMed2003

News and views on folate and elderly persons.

Elderly persons are especially exposed to folate deficiency, where normal/subnormal folate levels do not exclude tissue deficiency. Accompanying diseases, medication, and lifestyle factors may contribute to/cause deficiency. Symptoms of deficiency can be hematological, neurological, or neuropsychiatric, but it is likely that there are also cardiovascular manifestations as well as associations with malignancies. The physician should make an individualized investigation to establish the probable cause. Among the available determinants of the folate/cobalamin state, plasma homocysteine (Hcy) is a swift and sensitive marker and has the strongest connection to cognitive function. The association is generally stronger between Hcy levels and symptoms than between vitamin-related levels and symptoms. The duration as well as the severity of symptoms are of importance in terms of the improvement of neurological and neuropsychiatric symptoms when substitution is performed. The issue of general folate fortification of flour is complex, and there are as many pros and cons as there are countries in which it is considered to be launched. It is important to bear in mind that in our modern society, deficiency of folate/cobalamin--overt or latent--mainly is a problem of the elderly and a challenge to the doctor.

Aged↗
PubMed1980

The neuropsychiatry of megaloblastic anaemia.

The neuropsychiatric states of 50 patients with vitamin B12 deficiency and 34 patients with folate deficiency presenting with megaloblastosis in a general hospital were examined and compared. Abnormalities of the nervous system were found in two-thirds of both groups. Peripheral neuropathy was the most common condition associated with vitamin B12 deficiency and affective disorder with folate deficiency. The proportions of patients with organic mental change were similar in the two groups. Subacute combined degeneration of the cord was an uncommon complication and occurred only in the patients with vitamin B12 deficiency. There was no relation between haematological and neuropsychiatric abnormalities. The neuropsychiatry of megaloblastic anaemia seen in this study of patients presenting to haematologists or general physicians contrasts with that reported previously, before haematological techniques for separating the two deficiencies were introduced.

Adolescent↗
PubMed1998

Acquired mitochondrial impairment as a cause of optic nerve disease.

BACKGROUND: Blindness from an optic neuropathy recently occurred as an epidemic affecting 50,000 patients in Cuba (CEON) and had clinical features reminiscent of both tobacco-alcohol amblyopia (TAA) and Leber's hereditary optic neuropathy (Leber's; LHON). Selective damage to the papillomacular bundle was characteristic, and many patients also developed a peripheral neuropathy. Identified risk factors included vitamin deficiencies as well as exposure to methanol and cyanide. In all 3 syndromes, there is evidence that singular or combined insults to mitochondrial oxidative phosphorylation are associated with a clinically characteristic optic neuropathy. PURPOSE: First, to test the hypothesis that a common pathophysiologic mechanism involving impairment of mitochondria function and, consequently, axonal transport underlies both genetic optic nerve diseases such as Leber's and acquired toxic and nutritional deficiency optic neuropathies. According to this hypothesis, ATP depletion below a certain threshold leads to a blockage of orthograde axonal transport of mitochondria, which, in turn, leads to total ATP depletion and subsequent cell death. Second, to address several related questions, including (1) How does impaired energy production lead to optic neuropathy, particularly since it seems to relatively spare other metabolically active tissues, such as liver and heart? (2) Within the nervous system, why is the optic nerve, and most particularly the papillomacular bundle, so highly sensitive? Although there have been previous publications on the clinical features of the Cuban epidemic of blindness, the present hypothesis and the subsequent questions have not been previously addressed. METHODS: Patients in Cuba with epidemic optic neuropathy were personally evaluated through a comprehensive neuro-ophthalmologic examination. In addition, serum, lymphocytes for DNA analysis, cerebrospinal fluid (CSF), sural nerves, and eyes with attached optic nerves were obtained from Cuban patients, as well as from Leber's patients, for study. Finally, we developed an animal model to match the low serum folic acid and high serum formate levels found in the CEON patients, by administering to rats low doses of methanol after several months of a folic acid-deficient diet. Optic nerves and other tissues obtained from these rats were analyzed and compared with those from the Cuban patients. RESULTS: Patients from the Cuban epidemic of optic neuropathy with clinical evidence of a selective loss of the papillomacular bundle did much better once their nutritional status was corrected and exposure to toxins ceased. Patients with CEON often demonstrated low levels of folic acid and high levels of formate in their blood. Histopathologic studies demonstrated losses of the longest fibers (in the sural nerve) and those of smallest caliber (papillomacular bundle) in the optic nerve, with intra-axonal accumulations just anterior to the lamina cribrosa. Our animal model duplicated the serologic changes (low folic acid, high formate) as well as these histopathologic changes. Furthermore, ultrastructural examination of rat tissues demonstrated mitochondrial changes that further matched those seen on ultrastructural examination of tissues from patients with Leber's. CONCLUSION: Mitochondria can be impaired either genetically (as in Leber's) or through acquired insults (such as nutritional or toxic factors). Either may challenge energy production in all cells of the body. While this challenge may be met through certain compensatory mechanisms (such as in the size, shape, or number of the mitochondria), there exists in neurons a threshold which, once passed, leads to catastrophic changes. This threshold may be that point at which mitochondrial derangement leads to such ATP depletion that axonal transport is compromised, and decreased mitochondrial transport results in even further ATP depletion. Neurons are singularly dependent on the axonal transport of mitochondria. (

Adult↗
PubMed1997

Folate deficiency and cervical intraepithelial neoplasia.

The presence of HPV, using the Digene Hybrid Capture System, was identified in a group of 324 women with CIN and in 228 women with normal cytological smears. Risk of occurrence of CIN was 40 times higher for high risk HPV types. The serum folic acid level and the level of antioxidant compounds in plasma (retinol, alpha-tocopherol, vitamins C and E) in women of the studied and control group was determined by HPLC (high-performance liquid chromatography-reversed phase). Statistically lower levels of folic acid were found in the women with CIN-HPV (+) (OR: 7.5: 95% CI: 1.2-9.7). Studies have shown that lower levels of antioxidants coexisting with low levels of folic acid increases the risk of CIN development.

Antioxidants↗