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This compacted overview of the nutrition-immune response connection underscores the role of nutrition as a deterrent to infection. Malnutrition enhances the propensity to and heightens the intensity of infections by weaknening the various host defense mechanisms. Thus: 1. Deficiencies of vitamin A, niacin, riboflavin, folic acid, vitamin B12, pyridoxine, ascorbic acid, iron and protein disrupt the tissue barriers to infection. 2. Protein-calorie, folate, iron, pyridoxine and zinc deprivations markedly depress the cell-mediated immune system. 3. Deficiencies of protein, pyridoxine, folic acid, pantothenic acid, thiamine, biotin, riboflavin, niacin-tryptophan, vitamin A and ascorbic acid inhibit humoral antibody formation in mammalian systems. 4. Vitamin A lack prevents the formation of lacrimal, salivary and sweat gland lysozymes. 5. Complement, properdin, interferon and transferrin concentrations are reduced in those nutritional deficiencies that interfere with protein synthesis. 6. Protein-calorie, iron and folate deficiencies impair phagocytosis by interfering with phagocyte microbial killing power or with phagocyte production. 7. Protein, ascorbic acid and zinc deficiencies retard wound healing that prevents spread of infectious lesions. [2]

In this double-blind study, the effects of ascorbic acid, vitamin B6, vitamin B12, and folate supplementation on the maternal nutritional status and vitamin content of breast milk in 16 low socioeconomic lactating women were studied. Nine subjects were administered a commercial multivitamin-multimineral supplement and seven were given placebos. Milk samples were collected four times per day at 4-h intervals from 5 to 7 and 43 to 45 days postpartum. Fasting blood samples were taken from all mothers at the end of each milk collection period. Dietary records of all foods consumed were kept from 4 to 7 and 42 to 45 days postpartum. There were no significant differences in milk or plasma levels of ascorbic acid between the unsupplemented and supplemented groups. Both the EGPT index and milk concentration of vitamin B6 were significantly different (p less than 0.01) between the unsupplemented and supplemented groups. The milk concentrations of vitamin B12 increased significantly (p less than 0.05) in the supplemented group, as did the milk concentrations of folate (p less than 0.01). Because of consistently low levels of dietary vitamin B6 and folic acid in this group of low socioeconomic lactating women, either dietary changes or supplements could be necessary to maintain recommended levels of these vitamins in the womens' breast milk [3]

In this double-blind study, the effects of ascorbic acid, vitamin B6, vitamin B12, and folate supplementation on the maternal nutritional status and vitamin content of breast milk in 16 low socioeconomic lactating women were studied. Nine subjects were administered a commercial multivitamin-multimineral supplement and seven were given placebos. Milk samples were collected Diet as a key factor in determining genomic stability is more important than previously imagined because we now know that it impacts on all relevant pathways, namely exposure to dietary carcinogens, activation/detoxification of carcinogens, DNA repair, DNA synthesis and apoptosis. Current recommended dietary allowances for vitamins and minerals are based largely on the prevention of diseases of deficiency such as scurvy in the case of vitamin C. Because diseases of development, degenerative disease and aging itself are partly caused by damage to DNA it seems logical that we should focus better our attention on defining optimal requirements of key minerals and vitamins for preventing damage to both nuclear and mitochondrial DNA. To date, our knowledge on optimal micronutrient levels for genomic stability is scanty and disorganised. However, there is already sufficient evidence to suggest that marginal deficiencies in folate, vitamin B12, niacin and zinc impact significantly on spontaneous chromosome damage rate. The recent data for folate and vitamin B12 in humans with respect to micronucleus formation in blood and epithelial cells provide compelling evidence of the important role of these micronutrients in maintenance of genome integrity and the need to revise current RDAs for these micronutrients based on minimisation of DNA damage. Appropriately designed in vitro studies and in vivo placebo controlled trials with dose responses using a complementary array of DNA damage biomarkers are required to define recommended dietary allowances for genomic stability. Furthermore these studies would have to be targeted to individuals with common genetic polymorphisms that alter the bioavailability of specific micronutrients and the affinity of specific key enzymes involved in DNA metabolism for their micronutrient co-factor. That there is a need for an international collaborative effort to establish RDAs for genomic stability is self-evident. [4]

Inadequate folate status is associated with an increased risk for chronic diseases that may have a negative impact on the health of the aging population. Folate, a water-soluble vitamin, includes naturally occurring food folate and synthetic folic acid in supplements and fortified foods. Inadequate folate status may result in hyperhomocysteinemia, a significant risk factor for atherosclerotic vascular disease, changes in DNA that may result in pro-carcinogenic effects and increased risk for cognitive dysfunction. Folate status may be negatively influenced by inadequate intake, genetic polymorphisms and interactions with various drugs. In the US, folic acid is now added to enriched grain products and continues to be included in the majority of ready-to-eat breakfast cereals. Recent data indicate that the folate status in the US population has improved significantly, presumably due to the effects of fortification. Folic acid (not food folate) intake in excess of the Tolerable Upper Intake Level may mask the diagnosis of a vitamin B(12) deficiency, which is more prevalent in the elderly than younger individuals. When folic acid supplements are recommended, a multivitamin that includes vitamin B(12) should also be advised. To safely and effectively increase folate intake in the elderly, naturally occurring folate- rich food sources should be promoted. Folate-rich foods include orange juice, dark green leafy vegetables, asparagus, strawberries and legumes. These foods are also excellent sources of other health-promoting nutrients associated with chronic disease risk reduction. [5]

BACKGROUND: The bioavailability of dietary folate has been estimated to be approximately 50% of that of synthetic folic acid. Folate in the diet is linked to a polyglutamate chain that may restrict folate absorption. OBJECTIVE: Our goal was to quantify the bioavailability and bioefficacy of low doses of polyglutamyl folic acid relative to that of monoglutamyl folic acid. DESIGN: In total, 180 men and women aged 50-75 y ingested capsules containing 323 nmol heptaglutamyl folic acid/d or 262 nmol monoglutamyl folic acid/d or placebo in a randomized parallel trial. Serum and erythrocyte folate and plasma homocysteine concentrations were measured after an overnight fast at baseline and after 12 wk of intervention. RESULTS: Mean serum and erythrocyte folate concentrations increased less in the polyglutamyl folic acid group [6.1 (95% CI: 5.3, 7.0) and 155 (122, 188) nmol/L, respectively] than in the monoglutamyl folic acid group [11.8 (10.3, 13.3) and 282 (246, 318) nmol/L, respectively]. Differences remained statistically significant (P < 0.05) after correction for the difference in the amount of folic acid administered. The decrease in plasma homocysteine concentrations did not differ significantly between treatment groups [polyglutamyl: -12.1% (-14.8%, -9.3%); monoglutamyl: -14.1% (-16.3%, -11.9%)]. The relative bioavailability of polyglutamyl folic acid was 64% (52%, 75%) on the basis of serum folate and was 68% (51%, 84%) on the basis of erythrocyte folate concentrations. Bioefficacy, determined by changes in plasma homocysteine concentrations, was 106% (77%, 134%). CONCLUSION: The polyglutamate chain of folates in the diet reduces their bioavailability. [6]

During three decades of neurological practice I have witnessed a remarkable change in attitudes to the benefits and risks of folic acid therapy in nervous system disorders. In the 1960s all that was known and taught was that folic acid was harmful to the nervous system, especially in precipitating or exacerbating the neurological complications of vitamin B12 deficiency. So deeply held was this view that the possibility of neuropsychological benefits from this vitamin was initially viewed with considerable scepticism. In 30 years we have moved from a view of all risks and no benefits to one of all benefits and little or no risks! The experience of a whole generation of physicians who painfully learned the risks of folic acid to the nervous system in the 1940s and 1950s, to which the risk of aggravating epilepsy was later added, is in danger of being overlooked, and a more balanced approach is needed. Over the past 35 years numerous studies have shown a high incidence of folate deficiency and a correlation with mental symptoms, especially depression and cognitive decline, in epileptic, psychiatric, and psychogeriatric populations [7]

BACKGROUND: The effectiveness of nutritional supplementation in improving cognitive functioning is evaluated in elderly people. METHODS: The authors systematically reviewed randomized controlled trials that compared nutritional supplementation with a placebo treatment. Trials were identified from a MEDLINE search and from reference lists of identified studies and review articles. From each trial, information was gathered on the number and age of persons studied; the type, dosage, and duration of the intervention; and the assessed outcome measures. RESULTS: From 1086 titles, 571 articles were excluded based on their titles. Of the remaining 467 articles, the abstracts were read and 422 articles were excluded based on information found there. The remaining articles were screened for quality aspects of the study design, leaving 21 proper randomized, controlled trials. These trials are discussed in three groups according to the type of supplementation: multinutrient intervention or single components with or without a putative mechanism. Twelve studies, which were evenly distributed among the three supplement groups, found significantly positive effects of nutritional intervention on cognitive functioning, whereas nine studies did not. None of the studies found a significantly negative effect of nutritional intervention. CONCLUSIONS: Shortcomings in methodology varying from the duration of intervention to outcome measures partly explain discrepancies in findings. Despite the heterogeneity in trial design, the results of this review suggest that nutritional supplements may improve the cognitive functioning of elderly persons and do no harm. Further well-designed studies are needed to support these findings [8]

BACKGROUND: The effectiveness of nutritional supplementation in improving cognitive functioning is evaluated in elderly people. METHODS: The authors systematically reviewed randomized controlled homocysteine, an alternative risk factor of cardiovascular disease, may play a role in the pathogenesis of essential hypertension. The mechanism of this disease has not been elucidated, but it may be related to impairment of vascular endothelial and smooth muscle cell function. Therefore, the occurrence of endothelial dysfunction could contribute to alterations of the endothelium-dependent vasomotor regulation. Elevated homocysteinemia diminishes the vasodilation by nitric oxide, increases oxidative stress, stimulates the proliferation of vascular smooth muscle cells, and alters the elastic properties of the vascular wall. Thus, homocysteine contributes to elevate the blood pressure. Also it is known that elevated plasma levels of homocysteine could lead to oxidant injury to the endothelium. The correction of elevated homocysteinemia by administration of vitamins B12 and B6 plus folic acid, could be a useful adjuvant therapy of hypertension. However, further controlled randomized trials are necessary to establish the efficacy and tolerability of these potentially therapeutic agents. [9]

A common genetic variant in the methylenetetrahydrofolate reductase (MTHFR) gene involving a cytosine to thymidine (C-->T) transition at nucleotide 677 is associated with reduced enzyme activity, altered folate status and potentially higher folate requirements. The objectives of this study were to investigate the effect of the MTHFR 677 T allele on folate status variables in Mexican women (n = 43; 18-45 y) and to assess the adequacy of the 1998 folate U.S. Recommended Dietary Allowance (RDA), 400 micro g/d as dietary folate equivalents (DFE). Subjects (14 CC, 12 CT, 17 TT genotypes) consumed a low folate diet (135 micro g/d DFE) for 7 wk followed by repletion with 400 micro g/d DFE (7 CC, 6 CT, 9 TT) or 800 micro g/d DFE (7 CC, 6 CT, 8 TT) for 7 wk. Throughout repletion with 400 micro g/d DFE, the TT genotype had lower (P 0.05) in their response relative to the CC genotype. Throughout repletion with 800 micro g/d DFE, the CT genotype had lower (P 0.05) in the measured variables between the TT and CC genotypes. Repletion with 400 micro g/d DFE led to normal blood folate and desirable plasma tHcy concentrations, regardless of MTHFR C677T genotype. Collectively, these data demonstrate that the MTHFR C-->T variant modulates folate status response to controlled folate intakes and support the adequacy of the 1998 folate U.S. RDA for all three MTHFR C677T genotypes. [10]

Choline and folate share methylation pathways and, in studies of rats, were shown to be metabolically inter-related. To determine whether choline status is related to folate intake in humans, we measured the effect of controlled folate depletion and repletion on the plasma choline and phosphatidylcholine concentrations of 11 healthy men (33-46 y) and 10 healthy women (49-63 y) fed low-choline diets in two separate metabolic unit studies. Total folate intake was varied by supplementing low folate (25 and 56 microg/d for men and women, respectively) and low choline (238 and 147 mg/d for men and women, respectively) diets with pteroylglutamic acid for 2-6 wk following folate-depletion periods of 4-5 wk. The low folate/choline intakes resulted in subclinical folate deficiencies; mean plasma choline decreases of 28 and 25% in the men and women, respectively; and a plasma phosphatidylcholine decrease of 26% in the men (P < 0. 05). No functional choline deficiency occurred, as measured by serum transaminase and lipid concentrations. The decreases in choline status measures returned to baseline or higher upon moderate folate repletion and were more responsive to folate repletion than plasma folate and homocysteine. Feeding methionine supplements to the men did not prevent plasma choline depletion, indicating that folate is a more limiting nutrient for these methylation pathways. The results indicate that 1) choline is utilized as a methyl donor when folate intake is low, 2) the de novo synthesis of phosphatidylcholine is insufficient to maintain choline status when intakes of folate and choline are low, and 3) dietary choline is required by adults in an amount > 250 mg/d to maintain plasma choline and phosphatidylcholine when folate intake is low. [11]

In 1996 the Food and Drug Administration (FDA) issued a regulation to take effect in January 1998 that all enriched cereal grain products include 140 microg of folic acid/100 g. The present cross-sectional study was undertaken to assess the effect of this fortification on RBC folate concentrations in the Framingham Offspring Cohort. Among those who did not take B-vitamin supplements, we compared RBC folate in 561 individuals who were examined before implementation of the FDA mandatory folic acid fortification (not exposed) vs. 354 individuals who were examined after implementation of fortification (exposed). We calculated the prevalence of deficient (<160 microg/L, 362.6 nmol/L) and acceptable (>200 microg/L, 453.2 nmol/L) RBC folate concentrations in both groups. Those exposed to folic acid fortification had a mean RBC folate of 450.0 microg/L (1019.7 nmol/L), a value 38% higher than the mean RBC folate of 325.3 microg/L (737.1 nmol/L) in those who were not exposed to fortification (P < 0.001). The prevalence of individuals with deficient RBC folate was 4.9% in the group not exposed to fortification [12]

Many microorganisms in the large intestine are capable of synthesizing folate. Preliminary evidence suggests that this folate may be absorbed. The purpose of the 2 experiments reported herein was to estimate the pool of folate in the feces of human infants and piglets and to ascertain, if absorbed, whether the quantity and form of folate are sufficient to potentially affect the folate status of the host organism. The folate content of milk fed to and of fecal solids collected from exclusively human milk-fed (n = 12) and formula-fed (n = 10) term infants (1-6 mo old) was determined microbiologically before (short-chain folates) and after folate conjugase (total folate) treatment. The folate content of formula fed and of feces collected from 10-d-old piglets (n = 10) was also determined microbiologically. The roportion of 5-methyltetrahydrofolate (5-methylTHF) in feces of human infants and piglets that was monoglutamylated was determined by HPLC analysis. The folate content of fecal solids collected from infants was 93.2 +/- 92.8 nmol/d (mean +/- SD), representing on average 50% (8.0-170.1%) of their mean estimated dietary folate intake. Fecal folate was largely present as short-chain folate (66 +/- 21.3%) with the predominant form being 5-methylTHF, 52.5 +/- 30.1% of which was monoglutamylated. In piglets, the folate content of feces was 301.3 +/- 145.7 nmol/d, representing 36% of their dietary folate intake. Piglet fecal folate was largely present as short- chain folate (68.1 +/- 12.6%) with the predominant species being 5-methylTHF, 29.3 +/- 33.2% of which was monoglutamylated. Collectively, these data suggest that the quantity and form of folate (monoglutamylated) in the large intestine of human infants and piglets are sufficiently large to potentially affect folate status. [13]

The natural folate derivative, 5-methyltetrahydrofolate ([6S]-5-MTHF), could be an option for supplementation and fortification but its bioavailability remains unclear. This study compared the bioavailability of [6S]-5-MTHF with that of folic acid (FA) by measuring plasma folate responses after a single ingestion of equivalent doses of the two folate forms. In a double-blind, crossover study, 13 men (presaturated with FA) received in random order each of the following treatments administered orally at 1-wk intervals: 1) placebo capsule; 2) 500 micro g FA capsule; and 3) 500 micro g [6S]-5-MTHF capsule. Plasma total folate concentrations were measured before and up to 10 h after each treatment (n = 10 samples per treatment). Plasma folate concentrations increased significantly (compared with baseline) from 0.5 to 5 h after both folate treatments. The maximum plasma folate response did not differ between the two treatments (mean +/- SEM, 33.4 +/- 3.9 vs. 31.8 +/- 3.9 nmol/L, P = 0.7, for FA and [6S]-5-MTHF, respectively) and typically occurred in individuals between 0.5 and 3 h postprandially. The area under the plasma folate response curve was significantly greater after both folate treatments compared with placebo, and the response did not differ between the treatments. These results indicate that the short-term bioavailabilities of [6S]-5-MTHF and FA are equivalent. Supplementation with the natural folate derivative could have all the beneficial effects associated with FA, but without the potential disadvantage of masking the anemia of vitamin B-12 deficiency. [14]

Low blood folate concentrations have been associated with cardiovascular disease, neural tube defects and selected cancers, but little is known about folate status in Chinese adults. In a cross-sectional study we measured the plasma and red blood cell folate concentrations in 2422 Chinese men and women aged 35 to 64 y, living in the North and South of China, who provided blood samples either in March or September of 2001. The geometric mean concentrations of plasma and red blood cell folate were lower among Northerners than Southerners (adjusted geometric means, 8.4 and 502, and 16.7 and 811 nmol/L, respectively) controlling for age, gender, season (spring and fall), area (urban and rural), BMI, multivitamin use, alcohol intake and current smoking status. We estimated that approximately 40% of the Northerners and approximately 6% of the Southerners had plasma folate concentrations lower than the 6.8 nmol/L (3 microg/L), and approximately 30% of the Northerners and approximately 4% of the Southerners had red blood cell folate concentrations lower than the 363 nmol/L (160 microg/L), levels used to define folate deficiency. Within each region, men had lower plasma folate concentrations than women (6.9 versus 9.8 nmol/L in the North, and 14.5 versus 19.6 nmol/L in the South). In men, current smokers had a higher risk of folate deficiency compared with nonsmokers [adjusted odds ratios, 1.9 (95% CI, 1.4-2.6) for plasma folate deficiency and 2.5 (95% CI, 1.7-3.6) for red blood cell folate deficiency (P < 0.001)]. Our findings suggest that a large proportion of Chinese adults have a low folate status, especially those living in northern China where 60% of the men are plasma folate deficient in the spring. Further studies are needed to elucidate the factors that influence folate concentrations among middle-aged Chinese and to evaluate possible intervention strategies. [15]

DNA double-strand breaks, the most serious DNA lesion caused by ionizing radiation, are also caused by several vitamin or mineral deficiencies, such as for folate. Primary human lymphocytes were either irradiated or cultured at different levels of folate deficiency to assess cell proliferation, apoptosis, cell cycle, DNA breaks, and changes in gene expression. Both radiation and folate deficiency decreased cell proliferation and induced DNA breaks, apoptosis, and cell cycle arrest. Levels of folate deficiency commonly found resulted in effects similar to those caused by 1 Gy of radiation, a relatively high dose. Though both radiation and folate deficiency caused DNA breaks, they affected the expression of different genes. Radiation activated excision and DNA double-strand break repair genes and repressed mitochondrially encoded genes. Folate deficiency activated base and nucleotide excision repair genes and repressed folate-related genes. No DNA double-strand break repair gene was activated by folate deficiency. These findings suggest that a diet poor in folate may pose a risk of DNA damage comparable to that of a relatively high dose of radiation. Our results also suggest that research on biological effects of low-dose radiation should take into account the nutritional status of the subjects, because folate deficiency could confound the effects of low-dose radiation. [16]

References

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Nutrition and the immune response -- a review

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Bioavailability of heptaglutamyl relative to monoglutamyl folic acid in healthy adults.

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Benefits and risks of folic acid to the nervous system

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Methylenetetrahydrofolate reductase 677C-->T variant modulates folate status response to controlled folate intakes in young women

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Folate nutriture alters choline status of women and men fed low choline diets

12 J Nutr. 2001 Dec;131(12):3277-80 Folic acid fortification increases red blood cell folate concentrations in the Framingham study. Choumenkovitch SF, Jacques PF, Nadeau MR, Wilson PW, Rosenberg IH, Selhub J. Vitamin Metabolism and Aging Laboratory, and Epidemiology Program, Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University

Folic acid fortification increases red blood cell folate concentrations in the Framingham study

13 J Nutr. 2004 Jun;134(6):1389-94. A large pool of available folate exists in the large intestine of human infants and piglets. Kim TH, Yang J, Darling PB, O'Connor DL. Department of Nutritional Sciences, University of Toronto and The Hospital for Sick Children

A large pool of available folate exists in the large intestine of human infants and piglets

14 J Nutr. 2004 Mar;134(3):580-5. The short-term bioavailabilities of [6S]-5-methyltetrahydrofolate and folic acid are equivalent in men. Pentieva K, McNulty H, Reichert R, Ward M, Strain JJ, McKillop DJ, etal Northern Ireland Centre for Food and Health, University of Ulster

The short-term bioavailabilities of [6S]-5-methyltetrahydrofolate and folic acid are equivalent in men

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16 FASEB J. 2004 Jan;18(1):209-11. Epub 2003 Nov 3. Folate deficiency and ionizing radiation cause DNA breaks in primary human lymphocytes: a comparison. Courtemanche C, Huang AC, Elson-Schwab I, Kerry N, Ng BY, Ames BN. Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley, California, USA.

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