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1
Shulpekova, Yulia, Vladimir Nechaev, Svetlana Kardasheva, Alla Sedova, Anastasia Kurbatova, Elena Bueverova, Arthur Kopylov, Kristina Malsagova, Jabulani Clement Dlamini, and Vladimir Ivashkin. "The Concept of Folic Acid in Health and Disease." Molecules 26, no. 12 (June 18, 2021): 3731. http://dx.doi.org/10.3390/molecules26123731.
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Folates have a pterine core structure and high metabolic activity due to their ability to accept electrons and react with O-, S-, N-, C-bounds. Folates play a role as cofactors in essential one-carbon pathways donating methyl-groups to choline phospholipids, creatine, epinephrine, DNA. Compounds similar to folates are ubiquitous and have been found in different animals, plants, and microorganisms. Folates enter the body from the diet and are also synthesized by intestinal bacteria with consequent adsorption from the colon. Three types of folate and antifolate cellular transporters have been found, differing in tissue localization, substrate affinity, type of transferring, and optimal pH for function. Laboratory criteria of folate deficiency are accepted by WHO. Severe folate deficiencies, manifesting in early life, are seen in hereditary folate malabsorption and cerebral folate deficiency. Acquired folate deficiency is quite common and is associated with poor diet and malabsorption, alcohol consumption, obesity, and kidney failure. Given the observational data that folates have a protective effect against neural tube defects, ischemic events, and cancer, food folic acid fortification was introduced in many countries. However, high physiological folate concentrations and folate overload may increase the risk of impaired brain development in embryogenesis and possess a growth advantage for precancerous altered cells.
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Kulkarni, Medha V., C. P. Parameswaran Nair, and Gomathy Viswanathan. "Varying Folate Pattern in Different Strains of Mice Fed Coconut Oil and Sesame Seed Oil Diet." Pteridines 7, no. 4 (November 1996): 143–47. http://dx.doi.org/10.1515/pteridines.1996.7.4.143.
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Summary The effect of coconut oil feeding with and without cholesterol on folate metabolism in the two strains of mice, C57BL/6 and AKR have been studied. Liver total folate levels are higher in AKR mice. Coconut oil feeding markedly decreased the ratio of nonmethyl/methyl folates in C57BL/6 strain but not in AKR. Cholesterol supplementation to the coconut oil diet increased the percentage of monoglutamyl folates at the expense of polyglutamyl folates in both strains. Only C57BL/6 strain showed growth retardation on coconut oil feeding. The differences in hepatic folate metabolism between the two strains could possibly have an important role in determining their differences in susceptibility to diet induced atherosclerosis.
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Crivellenti, Lívia de Castro, Patrícia Barbieri, and Daniela Saes Sartorelli. "Folate inadequacy in the diet of pregnant women." Revista de Nutrição 27, no. 3 (June 2014): 321–27. http://dx.doi.org/10.1590/1415-52732014000300006.
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OBJECTIVE: To estimate food and dietary folate inadequacies in the diets of adult pregnant women. METHODS: A prospective study was conducted with 103 healthy pregnant adult users of the Public Health Care System of Ribeirão Preto, São Paulo, Brazil. The present study included the 82 women with complete food intake data during pregnancy, which were collected by three 24-hour dietary recalls. Food folate (folate naturally present in foods) and dietary folate (food folate plus folate from fortified wheat flour and cornmeal) inadequacies were determined, using the Estimated Average Requirement as cutoff. RESULTS: The diets of 100% and 94% of the pregnant women were inadequate in food folate and dietary folate, respectively. However, fortified foods increased the medium availability of the nutrient by 87%. CONCLUSION: The large number of pregnant women consuming low-folate diets was alarming. Nationwide population studies are needed to confirm the hypothesized high prevalence of low-folate diets among pregnant women.
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Sanderson, Peter, Helene McNulty, Pierpaolo Mastroiacovo, Ian F. W. McDowell, Alida Melse-Boonstra, Paul M. Finglas, and Jess F. Gregory. "Folate bioavailability: UK Food Standards Agency workshop report." British Journal of Nutrition 90, no. 2 (August 2003): 473–79. http://dx.doi.org/10.1079/bjn2003889.
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The UK Food Standards Agency convened a group of expert scientists to review current research investigating folate bioavailability. The workshop aimed to overview current research and establish priorities for future research. Discrepancies were observed in the evidence base for folate bioavailability, especially with regard to the relative bioavailability of natural folates compared with folic acid. A substantial body of evidence shows folic acid to have superior bioavailability relative to food folates; however, the exact relative bioavailability still needs to be determined, and in particular with regard to mixed diets. The bioavailability of folate in a mixed diet is probably not a weighted average of that in the various foods consumed; thus the workshop considered that assessment of folate bioavailability of whole diets should be a high priority for future research.
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Silaste, Marja-Leena, Maire Rantala, Georg Alfthan, Antti Aro, and Y. Antero Kesäniemi. "Plasma homocysteine concentration is decreased by dietary intervention." British Journal of Nutrition 89, no. 3 (March 2003): 295–301. http://dx.doi.org/10.1079/bjn2002776.
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High plasma total homocysteine (tHcy) concentration is reported to be a risk factor for vascular diseases. We investigated the extent to which serum folate and plasma tHcy respond to a high intake of natural folate from food. Thirty-seven healthy females volunteered to participate in a crossover dietary intervention. The study included a baseline period and two 5-week diet periods (low- and high-folate diets) with a 3-week washout in between. The low-folate diet contained one serving of both vegetables and frui/, while during the high-folate diet the subjects ate at least seven servings of vegetables, berries, and citrus frui/. Serum and erythrocyte (RBC) folate, serum vitamin B12, and plasma tHcy concentrations were measured at the baseline and at the end of each diet period. The mean concentrations of serum and RBC folate were 11·0 (sd 3·0) nmo/ and 412 (sd 120) nmo/ at the end of the low-folate diet and 78 (95 % CI 62, 94) % and 14 (95 % CI 8, 20) % higher in response to the high-folate diet (P<0·001). The serum concentration of vitamin B12remained unchanged during the intervention. The mean plasma tHcy concentration was 8·0 μmo/ at the end of the low-folate diet and decreased by 13 (95 % CI 9, 18) % in response to the high-folate diet (P<0·001). In conclusion, a diet high in fresh berries, citrus fruit, and vegetables effectively increases serum and RBC folate and decreases plasma homocysteine.
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Mason, Joel B. "Diet, folate, and colon cancer." Current Opinion in Internal Medicine 1, no. 3 (June 2002): 240–45. http://dx.doi.org/10.1097/00132980-200201030-00005.
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Mason, Joel B. "Diet, folate, and colon cancer." Current Opinion in Gastroenterology 18, no. 2 (March 2002): 229–34. http://dx.doi.org/10.1097/00001574-200203000-00013.
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Bills, ND, MJ Koury, AJ Clifford, and EN Dessypris. "Ineffective hematopoiesis in folate-deficient mice." Blood 79, no. 9 (May 1, 1992): 2273–80. http://dx.doi.org/10.1182/blood.v79.9.2273.2273.
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Abstract A folate-free amino acid-based diet provided an opportunity to characterize the effects of folate depletion on growth, tissue folate levels, and hematopoiesis of mice under well-standardized conditions. Weanling mice were fed a folate-free, amino acid-based diet supplemented with either 0 or 2 mg folic acid/kg diet for 35 to 48 days. Folate concentrations were decreased in liver, kidney, serum, and erythrocytes in mice fed the folate-free diet. The folate-deficient mice had anemia, reticulocytopenia, thrombocytopenia, and leukopenia, all of which reverted to normal after folic acid was reintroduced to the diet. Hematopoietic organs of folate-deficient mice had alterations that were similar to those seen in folate-deficient humans except that in mice, the hyperplasia of hematopoietic tissue occurred in the spleen rather than in the marrow. Ferrokinetic studies showed a normal 59Fe- transferrin half-life, but the percentage of 59Fe-incorporation into red blood cells at 48 hours was markedly subnormal. The number of committed hematopoietic progenitors at the stages of erythroid colony- forming units (CFUs), megakaryocyte CFUs, and granulocyte-macrophage CFUs were all increased in folate-deficient mice. However, the progeny of these progenitors was markedly decreased in folate-deficient mice. Thus, the folate-deficient mice had “ineffective hematopoiesis” leading to pancytopenia, and they therefore provide a murine model of megaloblastic anemia.
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Bills, ND, MJ Koury, AJ Clifford, and EN Dessypris. "Ineffective hematopoiesis in folate-deficient mice." Blood 79, no. 9 (May 1, 1992): 2273–80. http://dx.doi.org/10.1182/blood.v79.9.2273.bloodjournal7992273.
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A folate-free amino acid-based diet provided an opportunity to characterize the effects of folate depletion on growth, tissue folate levels, and hematopoiesis of mice under well-standardized conditions. Weanling mice were fed a folate-free, amino acid-based diet supplemented with either 0 or 2 mg folic acid/kg diet for 35 to 48 days. Folate concentrations were decreased in liver, kidney, serum, and erythrocytes in mice fed the folate-free diet. The folate-deficient mice had anemia, reticulocytopenia, thrombocytopenia, and leukopenia, all of which reverted to normal after folic acid was reintroduced to the diet. Hematopoietic organs of folate-deficient mice had alterations that were similar to those seen in folate-deficient humans except that in mice, the hyperplasia of hematopoietic tissue occurred in the spleen rather than in the marrow. Ferrokinetic studies showed a normal 59Fe- transferrin half-life, but the percentage of 59Fe-incorporation into red blood cells at 48 hours was markedly subnormal. The number of committed hematopoietic progenitors at the stages of erythroid colony- forming units (CFUs), megakaryocyte CFUs, and granulocyte-macrophage CFUs were all increased in folate-deficient mice. However, the progeny of these progenitors was markedly decreased in folate-deficient mice. Thus, the folate-deficient mice had “ineffective hematopoiesis” leading to pancytopenia, and they therefore provide a murine model of megaloblastic anemia.
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Kim, Kyong-Chol, Hyeran Jang, Julia Sauer, Ella M. Zimmerly, Zhenhua Liu, Aurelie Chanson, Donald E. Smith, Simonetta Friso, and Sang-Woon Choi. "Folate supplementation differently affects uracil content in DNA in the mouse colon and liver." British Journal of Nutrition 105, no. 5 (January 21, 2011): 688–93. http://dx.doi.org/10.1017/s0007114510004332.
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High folate intake may increase the risk of cancer, especially in the elderly. The present study examined the effects of ageing and dietary folate on uracil misincorporation into DNA, which has a mutagenic effect, in the mouse colon and liver. Old (18 months; n 42) and young (4 months; n 42) male C57BL/6 mice were pair-fed with four different amino acid-defined diets for 20 weeks: folate deplete (0 mg/kg diet); folate replete (2 mg/kg diet); folate supplemented (8 mg/kg diet); folate deplete (0 mg/kg diet) with thymidine supplementation (1·8 g/kg diet). Thymidylate synthesis from uracil requires folate, but synthesis from thymidine is folate independent. Liver folate concentrations were determined by the Lactobacillus casei assay. Uracil misincorporation into DNA was measured by a GC/MS method. Liver folate concentrations demonstrated a stepwise increase across the spectrum of dietary folate levels in both old (P = 0·003) and young (P < 0·001) mice. Uracil content in colonic DNA was paradoxically increased in parallel with increasing dietary folate among the young mice (P trend = 0·033), but differences were not observed in the old mice. The mean values of uracil in liver DNA, in contrast, decreased with increasing dietary folate among the old mice, but it did not reach a statistically significant level (P < 0·1). Compared with the folate-deplete group, thymidine supplementation reduced uracil misincorporation into the liver DNA of aged mice (P = 0·026). The present study suggests that the effects of folate and thymidine supplementation on uracil misincorporation into DNA differ depending on age and tissue. Further studies are needed to clarify the significance of increased uracil misincorporation into colonic DNA of folate-supplemented young mice.
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Thoma, Green, and Ferguson. "Citrus Pectin and Oligofructose Improve Folate Status and Lower Serum Total Homocysteine in Rats." International Journal for Vitamin and Nutrition Research 73, no. 6 (December 1, 2003): 403–9. http://dx.doi.org/10.1024/0300-9831.73.6.403.
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Low folate status leads to increased total homocysteine (tHcy) concentration, and this has been associated with an increased risk of several diseases. Many colonic bacteria are capable of synthesizing folate, and certain dietary fibers may enhance this effect. We assessed the ability of non-fermentable (cellulose) and fermentable (citrus pectin and oligofructose) fibers to improve folate status and lower tHcy in rats. Weanling Sprague-Dawley rats were fed a folate-deficient diet with 5% cellulose for four weeks. Rats were then randomly assigned to one of five folate-adequate (400 mug/kg diet) test diets for 24 days. Diets were as follows: Basal; Basal + Sulfa Drug (succinylsulfathiazole); Cellulose; Citrus Pectin; and Oligofructose. High-fiber diets were formulated by diluting the basal diet such that the final diets contained 10% of the added fiber. Twenty-one days later, 3H-r-aminobenzoic acid was injected into the cecum, and rats were terminated three days later. Rats receiving the Citrus Pectin diet had significantly higher plasma (p = 0.011), erythrocyte (p = 0.035), and colonic tissue folate concentrations (p = 0.013) and lower tHcy (p = 0.003) than rats given the Cellulose diet. Rats receiving the Oligofructose had significantly higher plasma folate (p < 0.001) and lower tHcy (p = 0.032) concentrations than rats receiving the Cellulose diet. 3H-folate was detected in the livers of all rats except those receiving Sulfa Drug. Our study indicates that Citrus Pectin and Oligofructose, but not Cellulose, can significantly increase indices of folate status in rats and lower tHcy. It also confirms the ability of the large bowel to absorb folate.
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Wang, Xinyan, Wen Li, Zhenshu Li, Yue Ma, Jing Yan, John X. Wilson, and Guowei Huang. "Maternal Folic Acid Supplementation During Pregnancy Promotes Neurogenesis and Synaptogenesis in Neonatal Rat Offspring." Cerebral Cortex 29, no. 8 (August 23, 2018): 3390–97. http://dx.doi.org/10.1093/cercor/bhy207.
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Abstract Maternal folic acid supplementation during pregnancy is associated with improved cognitive performances in offspring. However, the effect of supplementation on offspring’s neurogenesis and synaptogenesis is unknown, and whether supplementation should be continued throughout pregnancy is controversial. In present study, 3 groups of female rats were fed a folate-normal diet, folate-deficient diet, or folate-supplemented diet from 1 week before mating until the end of pregnancy. A fourth group fed folate-normal diet from 1 week before mating until mating, then fed folate-supplemented diet for 10 consecutive days, then fed folate-normal diet until the end of pregnancy. Offspring were sacrificed on postnatal day 0 for measurement of neurogenesis and synaptogenesis by immunofluorescence and western blot. Additionally neural stem cells (NSCs) were cultured from offspring’s hippocampus for immunocytochemical measurement of their rates of proliferation and neuronal differentiation. The results demonstrated that maternal folic acid supplementation stimulated hippocampal neurogenesis by increasing proliferation and neuronal differentiation of NSCs, and also enhanced synaptogenesis in cerebral cortex of neonatal offspring. Hippocampal neurogenesis was stimulated more when supplementation was continued throughout pregnancy instead of being limited to the periconceptional period. In conclusion, maternal folic acid supplementation, especially if continued throughout pregnancy, improves neurogenesis and synaptogenesis in neonatal offspring.
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Qiu, Andong, Sang Hee Min, Michaela Jansen, Usha Malhotra, Eugenia Tsai, Diane C. Cabelof, Larry H. Matherly, Rongbao Zhao, Myles H. Akabas, and I. David Goldman. "Rodent intestinal folate transporters (SLC46A1): secondary structure, functional properties, and response to dietary folate restriction." American Journal of Physiology-Cell Physiology 293, no. 5 (November 2007): C1669—C1678. http://dx.doi.org/10.1152/ajpcell.00202.2007.
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This laboratory recently identified a human gene that encodes a novel folate transporter [ Homo sapiens proton-coupled folate transporter ( HsPCFT); SLC46A1] required for intestinal folate absorption. This study focused on mouse ( Mus musculus) PCFT ( MmPCFT) and rat ( Rattus norvegicus) PCFT ( RnPCFT) and addresses their secondary structure, specificity, tissue expression, and regulation by dietary folates. Both rodent PCFT proteins traffic to the cell membrane with the NH2- and COOH-termini accessible to antibodies targeted to these domains only in permeabilized HeLa cells. This, together with computer-based topological analyses, is consistent with a model in which rodent PCFT proteins likely contain 12 transmembrane domains. Transport of [3H]folates was optimal at pH 5.5 and decreased with increasing pH due to an increase in Km and a decrease in Vmax. At pH 7.0, folic acid and methotrexate influx was negligible, but there was residual (6 S)5-methyltetrahydrofolate transport. Uptake of folates in PCFT-injected Xenopus oocytes was electrogenic and pH dependent. Folic acid influx Km values of MmPCFT and RnPCFT, assessed electrophysiologically, were 0.7 and 0.3 μM at pH 5.5 and 1.1 and 0.8 μM at pH 6.5, respectively. Rodent PCFTs were highly specific for monoglutamyl but not polyglutamyl methotrexate. MmPCFT mRNA was highly expressed in the duodenum, proximal jejunum, liver, and kidney with lesser expression in the brain and other tissues. MmPCFT protein was localized to the apical brush-border membrane of the duodenum and proximal jejunum. MmPCFT mRNA levels increased ∼13-fold in the proximal small intestine in mice fed a folate-deficient vesus folate-replete diet, consistent with the critical role that PCFT plays in intestinal folate absorption.
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Koury, Mark J., Donald W. Horne, Zoe A. Brown, Jennifer A. Pietenpol, Benjamin C. Blount, Bruce N. Ames, Robert Hard, and Stephen T. Koury. "Apoptosis of Late-Stage Erythroblasts in Megaloblastic Anemia: Association With DNA Damage and Macrocyte Production." Blood 89, no. 12 (June 15, 1997): 4617–23. http://dx.doi.org/10.1182/blood.v89.12.4617.
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Abstract An in vitro model of folate-deficient erythropoiesis has been developed using proerythroblasts isolated from the spleens of Friend virus-infected mice fed an amino acid-based, folate-free diet. Control proerythroblasts were obtained from Friend virus-infected mice fed the same diet plus 2 mg folic acid/kg diet. Our previous studies showed that, after 20 to 32 hours of culture in folate-deficient medium with 4 U/mL of erythropoietin, the folate-deficient proerythroblasts underwent apoptosis, whereas control erythroblasts survived and differentiated into reticulocytes over a period of 48 hours. The addition of folic acid or thymidine to the folate-deficient medium prevented the apoptosis of the folate-deficient erythroblasts, thereby implicating decreased thymidylate synthesis as the main cause of apoptosis in the folate-deficient erythroblasts. In the study reported here, we examined intracellular folate levels, uracil misincorporation into DNA, p53 and p21 proteins, and reticulocyte formation in erythroblasts cultured in folate-deficient or control medium. In all experiments, the folate-deficient erythroblasts cultured in folate-deficient medium gave results that varied significantly from folate-deficient erythroblasts cultured in control medium or control erythroblasts cultured in either folate-deficient or control media. Folate-deficient erythroblasts cultured in folate-deficient medium had marked decreases in all coenzyme forms of folate that persisted throughout culture, increased uracil misincorporation into DNA, persistent accumulations of p53 and p21, and decreased reticulocyte production but increased size of individual reticulocytes. A model of folate-deficient erythropoiesis based on apoptosis of late stage erythroblasts is presented. This model provides explanations for the clinical findings in megaloblastic anemia.
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de Visser, Huub M., Nicoline M. Korthagen, Cristina Müller, Ruud M. Ramakers, Gerard C. Krijger, Floris P. J. G. Lafeber, Freek J. Beekman, Simon C. Mastbergen, and Harrie Weinans. "Imaging of Folate Receptor Expressing Macrophages in the Rat Groove Model of Osteoarthritis: Using a New DOTA-Folate Conjugate." CARTILAGE 9, no. 2 (November 3, 2017): 183–91. http://dx.doi.org/10.1177/1947603517738073.
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Objective To evaluate the presence and localization of folate receptor expressing macrophages in the rat groove model of osteoarthritis and determine the suitability of a new folate conjugate with albumin-binding entity (cm09) for in vivo SPECT (single-photon emission computed tomography) analysis. Design In male Wistar rats, local cartilage damage was induced in addition to a standard ( n = 10) or high-fat diet ( n = 6). After 12 weeks, 111In labeled folate conjugates were administered, and SPECT/CT (computed tomography) imaging was performed after 24 hours. Subsequently, osteoarthritis severity and folate receptor expression were assessed using (immuno)-histological sections. Results In vivo SPECT/CT imaging of the new folate conjugate (cm09) was as useful as a folate conjugate without albumin-binding entity in the groove model of osteoarthritis with less renal accumulation. Induction of cartilage damage on a standard diet resulted in no effect on the amount of folate receptor expressing macrophages compared with the contralateral sham operated joints. In contrast, inducing cartilage damage in the high-fat diet group resulted in 28.4% increase of folate receptor expression as compared with the nondamaged control joints. Folate receptor expressing cells were predominantly present in the synovial lining and in subchondral bone as confirmed by immunohistochemistry. Conclusions Folate receptor expression, and thus macrophage activation, can clearly be demonstrated in vivo, in small animal models of osteoarthritis using the new 111In-folate conjugate with specific binding to the folate receptor. Increased macrophage activity only plays a role in the groove model of osteoarthritis when applied in a high-fat diet induced dysmetabolic condition, which is in line with the higher inflammatory state of that specific model.
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Norsidah, Ku-Zaifah, Ahmad Yusof Asmadi, Ayob Azizi, Othman Faizah, and Yusof Kamisah. "Palm Tocotrienol-Rich Fraction Improves Vascular Proatherosclerotic Changes in Hyperhomocysteinemic Rats." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/976967.
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This study investigated the effects of palm tocotrienol-rich fraction (TRF) on aortic proatherosclerotic changes in rats fed with a high methionine diet. Forty-two male Wistar rats were divided into six groups. The first group was the control (fed with a basal diet). Another five groups were fed with 1% methionine diet for 10 weeks. From week 6 onward, folate (8 mg/kg diet) or palm TRF (30, 60, and 150 mg/kg diets) was added into the diet of the last four rat groups, respectively. The high methionine diet raised the plasma total homocysteine and aortic lipid peroxidation, which were reduced by the palm TRF and folate supplementations. Plasma nitric oxide was reduced in the high methionine group compared to the control (3.72±0.57versus6.65±0.53 μmol/L,P<0.05), which reduction was reversed by the palm TRF (60 and 150 mg/kg) and folate supplementations. The increased aortic vascular cell adhesion molecule-1 expression in the methionine group (2.58±0.29) was significantly reduced by the folate (1.38±0.18) and palm TRF at 150 mg/kg (1.19±0.23). Palm TRF was comparable to folate in reducing high methionine diet-induced plasma hyperhomocysteinemia, aortic oxidative stress, and inflammatory changes in rats.
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Engeham, Sarah F., Andrea Haase, and Simon C. Langley-Evans. "Supplementation of a maternal low-protein diet in rat pregnancy with folic acid ameliorates programming effects upon feeding behaviour in the absence of disturbances to the methionine–homocysteine cycle." British Journal of Nutrition 103, no. 7 (November 27, 2009): 996–1007. http://dx.doi.org/10.1017/s0007114509992662.
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Maternal protein restriction in rat pregnancy is associated with altered feeding behaviour in later life. When allowed to self-select their diet, rats subject to prenatal undernutrition show an increased preference for fatty foods. The main aim of the present study was to evaluate the contribution of folic acid in the maternal diet to programming of appetite, since disturbances of the folate and methionine–homocysteine cycles have been suggested to impact upon epigenetic regulation of gene expression and hence programme long-term physiology and metabolism. Pregnant rats were fed diets containing either 9 or 18 % casein by weight, with folate provided at either 1 or 5 mg/kg diet. Adult male animals exposed to low protein (LP) in fetal life exhibited increased preference for high-fat food. Providing the higher level of folate in the maternal diet prevented this effect of LP, but offspring of rats fed 18 % casein diet with additional folate behaved in a similar manner to LP-exposed animals. Among day 20 gestation fetuses, it was apparent that both protein restriction and maternal folate supplementation could have adverse effects upon placental growth. Examination of methionine–homocysteine and folate cycle intermediates, tissue glutathione concentrations and expression of mRNA for methionine synthase, DNA methyltransferase 1 and methyltetrahydrofolate reductase revealed no gross disturbances of folate and one-carbon metabolism in either maternal or fetal tissue. The present findings indicated that any role for DNA methylation in programming of physiology is not related to major perturbations of folate metabolism, and is likely to be gene-specific rather than genome-wide.
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Vrentzos, George E., John A. Papadakis, Niki Malliaraki, Evagelos A. Zacharis, Elias Mazokopakis, Andreas Margioris, Emmanuel S. Ganotakis, and Anthony Kafatos. "Diet, serum homocysteine levels and ischaemic heart disease in a Mediterranean population." British Journal of Nutrition 91, no. 6 (June 2004): 1013–19. http://dx.doi.org/10.1079/bjn20041145.
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Homocysteine (Hcy) is recognised as a risk factor for IHD. Serum Hcy is negatively correlated with serum folate levels, the main sources of which are fruits, vegetables and legumes. The present case–control study was designed to examine the relationship between serum Hcy levels and IHD and to assess the role of dietary factors in the southern Mediterranean population of Crete, Greece. Serum Hcy, folate, vitamin B12, creatinine and glucose levels and a full lipid profile were measured in 152 patients with established IHD, median age 64 (range 33–77) years, and 152 healthy control subjects, age- and sex-matched. Dietary data were assessed using a 3 d food intake record. Compared with controls, patients with IHD had significantly higher daily intakes of vitamin B12and MUFA and significantly lower intakes of carbohydrate, fibre, folate, cholesterol,n-3 fatty acids and totaltransunsaturated fatty acids. Moreover, patients had significantly higher serum Hcy, vitamin B12and creatinine levels, but significantly lower folate. Serum folate concentrations in both groups had a significant positive correlation with dietary fibre consumption and a significant inverse correlation with vitamin B12intake. IHD patients should be encouraged to increase their daily dietary intake of fibre, folate andn-3 fatty acids, which are significant components of the traditional Cretan Mediterranean diet. Where dietary folate intake is inadequate, folate supplements are recommended to reduce elevated Hcy levels.
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Balaghi, M., D. W. Horne, and C. Wagner. "Hepatic one-carbon metabolism in early folate deficiency in rats." Biochemical Journal 291, no. 1 (April 1, 1993): 145–49. http://dx.doi.org/10.1042/bj2910145.
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Glycine N-methyltransferase (GNMT) is inhibited by 5-methyltetrahydrofolate polyglutamate in vitro. It is believed to play a regulatory role in the synthesis de novo of methyl groups. We have used the amino-acid-defined diet of Walzem and Clifford [(1988) J. Nutr. 118, 1089-1096] to determine whether folate deficiency in vivo would affect GNMT activity, as predicted by the studies in vitro. Weanling male rats were fed on the folate-deficient diet or a folate-supplemented diet pair-fed to the deficient group. A third group was fed on the folate-supplemented diet ad libitum. Development of folate deficiency rapidly resulted in decreased levels of S-adenosylmethionine (SAM) and elevation of S-adenosylhomocysteine (SAH). The ratios of SAM to SAH were 1.8, 2.7 and 1.5 in the deficient group for weeks 2, 3 and 4 of the experiment, and the values were 9.7, 7.1 and 8.9 for the pair-fed control group and 10.3, 8.8 and 8.0 for the control group ad libitum fed. The activity of GNMT was significantly higher in the deficient group than in either of the two control groups at each time period. This was not due to increased amounts of GNMT protein, but reflected an increase in specific enzyme activity. Levels of folate in both the cytosol and mitochondria were severely lowered after only 2 weeks on the diet. The distribution of folate coenzymes was also affected by the deficiency, which resulted in a marked increase in the percentage of tetrahydrofolate polyglutamates in both cytosol and mitochondria and a very large decrease in cytosolic 5-methyltetrahydrofolate. The increased GNMT activity is therefore consistent with decreased folate levels and decreased inhibition of enzyme activity.
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Hill, Sarah A., Nicholas J. Cave, and Sandra Forsyth. "Effect of age, sex and body weight on the serum concentrations of cobalamin and folate in cats consuming a consistent diet." Journal of Feline Medicine and Surgery 20, no. 2 (March 22, 2017): 135–41. http://dx.doi.org/10.1177/1098612x17699680.
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Objectives Multiple feline diseases involving the gastrointestinal tract, pancreas, liver and biliary tract are known to cause abnormal serum cobalamin and folate concentrations. Measuring the serum concentration of these vitamins can therefore be a helpful diagnostic tool. However, factors other than disease, in particular age, have also been suggested to have an effect on the serum concentration of cobalamin and folate. In previous studies, the dietary intake was not standardised, or even known, despite diet being the prinicpal source of both vitamins. Therefore, we evaluated the effect of age, sex and body weight on the serum concentration of folate and cobalamin in cats fed the same diet. Methods The serum cobalamin and folate concentrations were measured in 65 apparently healthy cats in a nutrition colony that had been fed an identical diet. A linear model was used to test the relationship between the serum concentration of cobalamin and folate with the variables age, sex and body weight. Results There was a large variation in the serum concentration of both folate and cobalamin, despite identical intake. Serum cobalamin was inversely associated with age ( P = 0.002), and males had higher concentrations than females ( P = 0.039). Serum folate was positively associated with age ( P = 0.01). Conclusions and relevance Independent of diet, serum cobalamin concentration decreases with age. Changes in gastrointestinal function, microflora or metabolism may be responsible. Older cats may be more susceptible to cobalamin deficiency secondary to inappetence or gastrointestinal disease.
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Czarnowska-Kujawska, Marta, Elżbieta Gujska, and Joanna Michalak. "Folate determination in livers of different animal species." Czech Journal of Food Sciences 38, No. 1 (February 29, 2020): 43–48. http://dx.doi.org/10.17221/78/2019-cjfs.
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The liver is the main storage organ for folate. In the study the folate content in chicken, turkey, pig, and beef livers was evaluated with the use of the HPLC (high performance liquid chromatography) method which allowed various folate vitamers differentiation. The total folate content in the tested livers ranged from 419 to 1289 µg 100 g–1 in pork and chicken livers, respectively, and was several times higher than in folate rich vegetables, which are the most common folate sources in the human diet. Additionally, good stability of two folate abundant forms, tetrahydrofolate and 5-methyltetrahydrofolate, under frying was shown in the chicken liver samples. The obtained results contribute well to the general need of promoting the folate intake from various natural sources, not only of plant origin.<br /><br />
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Kato, Dnistrian, Schwartz, Toniolo, Koenig, Shore, Zeleniuch-Jacquotte, Akhmedkhanov, and Riboli. "Epidemiologic Correlates of Serum Folate and Homocysteine Levels among Users and Non-users of Vitamin Supplement." International Journal for Vitamin and Nutrition Research 69, no. 5 (September 1, 1999): 322–29. http://dx.doi.org/10.1024/0300-9831.69.5.322.
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Lower serum folate and higher serum homocysteine levels are known risk factors for various conditions. Thus, epidemiologic correlates with these measurements were studied for 256 multivitamin users and 230 non-users who were middle-aged women. Both serum folate and homocysteine levels increased with advancing age in both multivitamin users (P < 0.01 and P < 0.01) and non-users (P = 0.08 and P < 0.01). Among non-users, higher intake of vegetables, fruits, cold cereals and total protein were associated positively with serum folate and inversely with homocysteine levels. There were 25–74% increases in serum folate and 10–15% decreases in serum homocysteine between 1st and 4th quartiles of intake of these food/nutrients. In addition, 26% lower serum folage and 18% higher serum homocysteine were observed for those smoking 20 or more cigarettes per day compared with non-smokers. Among multivitamin users, body weight was correlated inversely with serum folate (P < 0.01) and positively with serum homocysteine levels (P = 0.04), while no correlates were found among lifestyle factors. Regular use of multivitamins increased serum folate about fourfold and decreased homocysteine twofold. These results suggest that multivitamin use can offset the effects of an unhealthy lifestyle on these serum markers, and that levels of serum folate and homocysteine can also be favorably influenced by healthier diet and abstinence from smoking.
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Ramaekers, Vincent T., Jeffrey M. Sequeira, Nenad Blau, and Edward V. Quadros. "A milk-free diet downregulates folate receptor autoimmunity in cerebral folate deficiency syndrome." Developmental Medicine & Child Neurology 50, no. 5 (May 2008): 346–52. http://dx.doi.org/10.1111/j.1469-8749.2008.02053.x.
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Chan, Yen-Ming, Susanne Aufreiter, Stephen J. O’Keefe, and Deborah L. O’Connor. "Switching to a fibre-rich and low-fat diet increases colonic folate contents among African Americans." Applied Physiology, Nutrition, and Metabolism 44, no. 2 (February 2019): 127–32. http://dx.doi.org/10.1139/apnm-2018-0181.
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How dietary patterns impact colonic bacterial biosynthesis of vitamins and utilization by humans is poorly understood. Our aim was to investigate whether a reciprocal dietary switch between rural South Africans (traditionally high fibre, low fat) and African Americans (Western diet of low fibre, high fat) affects colonic folate synthesis. Colonic evacuants were obtained from 20 rural South Africans and 20 African Americans consuming their usual diets at baseline. For 2 weeks thereafter, rural South Africans were provided with a Western diet (protein, 27%; fat, 52%; carbohydrate, 20%; and fibre, 8 g/day) and African Americans were provided with a high fibre, low-fat diet (protein, 16%; fat, 17%; carbohydrate, 63%; and fibre, 43 g/day). Colonic evacuants were again collected. No difference between groups at baseline in the folate content of 3-h evacuants was observed. The high-fibre, low-fat diet consumed by African Americans during the intervention produced a 41% increase in mean total folate content compared with baseline values (p = 0.0037). No change was observed in rural South Africans consuming a Western diet. Mean total folate content of colonic evacuants was higher among African Americans at the end of the dietary switch (3107 ± 1811 μg) compared with rural South Africans (2157 ± 1956 μg) (p = 0.0409). In conclusion, consistent with animal studies, switching from a Western diet to one higher in fibre and lower in fat can be expected to result in greater colonic folate content. Future research should confirm that these observations are not transitory and understand the contribution of transit-time to the findings.
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Farrell, Colleen, Siya Khanna, Md Tozammel Hoque, Nancy Basset, Aneta Plaga, Ishba Syed, Susanne Aufreiter, et al. "Folate Transporters Are Found Throughout the Colon of Humans and Their mRNA Expression Appears to Be Unaffected by Low Dose Folic Acid Supplementation." Current Developments in Nutrition 5, Supplement_2 (June 2021): 1309. http://dx.doi.org/10.1093/cdn/nzab059_010.
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Abstract Objectives A large depot of folate resides in the colon and can exceed dietary intake. Little is known about the capacity of the colon to absorb folate. We aimed to determine the expression of key folate transporters, reduced folate carrier (RFC) and proton-coupled folate transporter (PCFT), throughout the colon of healthy adults and the impact of low dose folic acid (FA) supplementation. Methods In this 16 wk open-labelled randomized control trial, healthy adults (n = 25) from a colonoscopy waiting list were randomized to receive daily a multivitamin plus a 400 μg FA (400FA, n = 12) or no FA supplement (0FA, n = 13). Subjects were provided with low FA bread and pasta and instructions how to follow a low FA containing diet. Six 24-hr diet recalls were administered throughout the study and blood samples were collected at baseline, 8 and 16 wk. At colonoscopy (16 wk), 4 tissue biopsies were collected from the terminal ileum, cecum, ascending and descending colon. Blood folates were determined by microbial assay; mRNA levels of folate transporters were assessed using qPCR. Results One subject was removed from analysis due to missing data (0FA). No group differences in age, sex, BMI, dietary intake, vitamin B12, red blood cell (RBC) and plasma folate levels at baseline were observed. Mean ± SD FA supplement adherence was 92 ± 12% and 96 ± 9% at 8 and 16 wk, respectively. Subjects in the 400FA group had higher total folate intake (P < 0.05) and higher RBC and plasma folate levels (P < 0.01) at 8 and 16 wk compared to 0FA subjects. RBC values at 16 wk were 1764 ± 636 and 865 ± 190 nmol/L in the 400FA and 0FA group, respectively. RFC and PCFT were detected in terminal ileum and colon biopsies (n = 96) and their mRNA levels in each section did not differ between groups. However, expression of RFC was markedly higher than PCFT across all biopsy sections (P < 0.05) and highest in the terminal ileum, compared to the cecum, ascending and descending colon in both groups (P < 0.05). Conclusions We demonstrated expression of folate transporters, RFC and PCFT, throughout the human colon suggesting their potential contribution to overall folate absorption. mRNA expressions were not affected by a low dose FA supplement. A deeper understanding of how FA and folate status affect colonic transporter regulation may inform future revisions of folate intake recommendations. Funding Sources Natural Sciences and Engineering Research Council.
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Fila, Michal, Cezary Chojnacki, Jan Chojnacki, and Janusz Blasiak. "Is an “Epigenetic Diet” for Migraines Justified? The Case of Folate and DNA Methylation." Nutrients 11, no. 11 (November 14, 2019): 2763. http://dx.doi.org/10.3390/nu11112763.
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Migraines are a common disease with limited treatment options and some dietary factors are recognized to trigger headaches. Although migraine pathogenesis is not completely known, aberrant DNA methylation has been reported to be associated with its occurrence. Folate, an essential micronutrient involved in one-carbon metabolism and DNA methylation, was shown to have beneficial effects on migraines. Moreover, the variability of the methylenetetrahydrofolate reductase gene, important in both folate metabolism and migraine pathogenesis, modulates the beneficial effects of folate for migraines. Therefore, migraine could be targeted by a folate-rich, DNA methylation-directed diet, but there are no data showing that beneficial effects of folate consumption result from its epigenetic action. Furthermore, contrary to epigenetic drugs, epigenetic diets contain many compounds, some yet unidentified, with poorly known or completely unknown potential to interfere with the epigenetic action of the main dietary components. The application of epigenetic diets for migraines and other diseases requires its personalization to the epigenetic profile of a patient, which is largely unknown. Results obtained so far do not warrant the recommendation of any epigenetic diet as effective in migraine prevention and therapy. Further studies including a folate-rich diet fortified with valproic acid, another modifier of epigenetic profile effective in migraine prophylaxis, may help to clarify this issue.
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Berrocal-Zaragoza, Maria I., Jeffrey M. Sequeira, Michelle M. Murphy, Joan D. Fernandez-Ballart, Samah G. Abdel Baki, Peter J. Bergold, and Edward V. Quadros. "Folate deficiency in rat pups during weaning causes learning and memory deficits." British Journal of Nutrition 112, no. 8 (September 3, 2014): 1323–32. http://dx.doi.org/10.1017/s0007114514002116.
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Folate is essential for fetal development, and its deficiency during gestation causes behavioural deficits in the offspring. The present study investigated its influence during weaning on brain function in the pups of rats that were put on a folate-deficient (FD) diet on postnatal day (PND) 1. Systemic folate deficiency in pups on the FD diet (n 15) was evident from the dramatically lower hepatic folate concentrations (median 23·7, range 8·1–48·4 ng/mg protein) and higher homocysteine concentrations (median 27·7, range 14·7–45·5 pmol/mg protein), respectively, compared with those of pups on the normal diet (ND; n 9) (median 114·5, range 64·5–158·5 ng/mg protein and median 15·5, range 11·6–18·9 pmol/mg protein) on PND 23. Brain folate concentrations although low were similar in pups on the FD diet (median 10·5, range 5·5–24·5 ng/mg protein) and ND (median 11·1, range 7·1–24·2 ng/mg protein). There was a high accumulation of homocysteine in the brain of FD pups, mostly in the hippocampus (median 58·1, range 40·8–99·7 pmol/mg protein) and cerebellum (median 69·1, range 50·8–126·6 pmol/mg protein), indicating metabolic folate deficiency despite normal brain folate concentrations. Developmental deficits or autistic traits were more frequent in the FD group than in the ND group and repetitive self-grooming occurred, on average, three times (range 1–8) v. once (range 0–3) during 5 min, respectively. Long-term memory or spatial learning and set-shifting deficits affected 12 to 62 % of rats in the FD group compared with none in the ND group. Post-weaning folic acid supplementation did not correct these deficits. These observations indicate that folate deficiency during weaning affects postnatal development even when gestational folate supply is normal.
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Wani, Nissar Ahmad, Abid Hamid, Krishan Lal Khanduja, and Jyotdeep Kaur. "Folate malabsorption is associated with down-regulation of folate transporter expression and function at colon basolateral membrane in rats." British Journal of Nutrition 107, no. 6 (August 24, 2011): 800–808. http://dx.doi.org/10.1017/s0007114511003710.
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Folates, an essential component (important B vitamin) in the human diet, are involved in many metabolic pathways, mainly in carbon transfer reactions such as purine and pyrimidine biosynthesis and amino acid interconversions. Deficiency of this micronutrient leads to the disruption of folate-dependent metabolic pathways that lead to the development of clinical abnormalities ranging from anaemia to growth retardation. Folate deficiency due to alcohol ingestion is quite common, primarily due to malabsorption. The present study dealt with the mechanistic insights of folate malabsorption in colonic basolateral membrane (BLM). Wistar rats (n 12) were fed 1 g/kg body weight per d ethanol (20 %) solution orally for 3 months and folate transport was studied in the isolated colonic BLM. The folate exit across colon BLM shows characteristics of carrier-mediated process with the major involvement of reduced folate carrier (RFC). The chronic ethanol ingestion decreased the uptake by decreasing the affinity by 46 % (P < 0·01) and the number of transport molecules by 43 % (P < 0·001) at the colon BLM. The decreased uptake was associated with down-regulation of proton-coupled folate transporter (PCFT) and RFC expression at mRNA and protein levels. The extent of decrease was 44 % (P < 0·01) and 24 % (P < 0·05) for PCFT and 23 % (P < 0·01) and 57 % (P < 0·01) for RFC at mRNA and protein levels, respectively. Moreover, folate transporters were associated with lipid rafts (LR) of colon BLM, and chronic alcoholism decreased the association of these transporters with LR.
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Chen, Ta-Fu, Ming-Jang Chiu, Chou-Tz Huang, Ming-Chi Tang, Sue-Jane Wang, Chia-Chuan Wang, and Rwei-Fen Syu Huang. "Changes in dietary folate intake differentially affect oxidised lipid and mitochondrial DNA damage in various brain regions of rats in the absence/presence of intracerebroventricularly injected amyloid β-peptide challenge." British Journal of Nutrition 105, no. 9 (January 5, 2011): 1294–302. http://dx.doi.org/10.1017/s0007114510005052.
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Accumulating evidence suggests that changes in dietary folate intake may modulate the risks of Alzheimer's disease (AD) through as yet unknown mechanisms. The aims of the present study were to investigate how dietary folate affects the brain folate distribution, levels of oxidised lipid and DNA damage in the absence/presence of β-amyloid(25–35)(Aβ) peptide challenge, a pathogenic hallmark of AD. Male Wistar rats were assigned to diets with folic acid at 0 (folate deprivation; FD), 8 (moderate folate; MF) and 8 mg folic acid/kg diet+0·003 % in drinking-water (folate supplementation; FS) for 4 weeks. A single injection of Aβ peptide (1 mg/ml) or the vehicle solution was intracerebroventricularly (icv) administrated to rats a week before killing. Brain folate, a marker of oxidative injury, and neuronal death were assayed. In the absence of an Aβ injection, FD rats showed reduced folate levels, and increased 2-thiobarbituric acid-reactive substances and a mitochondrial (mt)DNA 4834 bp large deletion (mtDNA4834deletion) in the hippocampus compared with the counterpart brains of control rats (P < 0·05). A single icv injection of Aβ peptide potentiated lipid peroxidation in the medulla of FD rats, which was ameliorated by feeding FD rats with the MF and FS diets (P < 0·05). Feeding the FS diet to Aβ-injected rats enriched brain folate levels and reduced mtDNA4834deletion in the hippocampal and medullary regions compared with corresponding tissues of Aβ+FD rats (P < 0·05). Aβ+FS rats had reduced rates of neuronal death in the frontal cortex compared with Aβ+FD rats (P < 0·05). Taken together, our data revealed that folate deprivation differentially depleted brain folate levels, and increased lipid peroxidation and mtDNA4834deletions, particularly, in the hippocampus. Upon Aβ challenge, the FS diet may protect various brain regions against lipid peroxidation, mitochondrial genotoxicity and neural death associated with folate deprivation.
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Mudryj, Adriana N., Margaret de Groh, Harold M. Aukema, and Nancy Yu. "Folate intakes from diet and supplements may place certain Canadians at risk for folic acid toxicity." British Journal of Nutrition 116, no. 7 (September 9, 2016): 1236–45. http://dx.doi.org/10.1017/s000711451600307x.
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AbstractTo examine the prevalence of folate inadequacy and toxicity based on usual intakes from food and supplements, as well as biomarkers of folate, secondary data analyses were performed using cross-sectional, nationally representative data from the Canadian Community Health Survey, Cycle 2.2 (n32 776), as well as biomarker data from the Canadian Health Measures Survey, Cycles 1, 2 and 3 (n15 754). On the basis of unfortified food sources, Canadians would struggle to consume adequate amounts of folate. When folate intakes from all food sources were considered, the overall prevalence of folate inadequacy was low across all age/sex groups, with the exception of females >70 years. However, >10 % of supplement users were above the tolerable upper intake level, increasing to almost 18 % when overage factors were accounted for. In addition, between 20 and 52 % of supplement users had elevated erythrocyte folate concentrations, depending on the cut-off used. Results from this study suggest that insufficient dietary intakes of folate in Canadians have been ameliorated because of the fortification policy, although folate inadequacy still exists across all age groups. However, supplement users appear to be at an increased risk of folic acid (FA) overconsumption as well as elevated erythrocyte folate. As such, the general population should be informed of the potential risks of FA overconsumption resulting from supplement use. This study suggests a need for more careful assessment of the risks and benefits of food fortification, particularly fortification above mandated levels, and FA supplement use in the general population.
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Cho, Clara E. "Role of methyl group vitamins in hypothalamic development of food intake regulation in Wistar rats." Applied Physiology, Nutrition, and Metabolism 39, no. 7 (July 2014): 844. http://dx.doi.org/10.1139/apnm-2014-0094.
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High multivitamin diets (HV; 10-fold AIN-93G) fed during pregnancy to Wistar rats produce offspring with increased food intake, obesity, and characteristics of metabolic syndrome. The hypothesis that methyl group vitamins in HV gestational and pup diets modify expression of the obesogenic phenotypes in the offspring through their effects on hypothalamic feeding pathways was tested by 4 studies. In studies 1 and 2, dams were fed the AIN-93G diet with recommended vitamin (RV), HV, high methyl vitamins (10-fold folate, vitamin B12 and vitamin B6) (HMethyl), or HV with normal folate (HVNF) and male offspring were weaned to a high-fat diet for 8 weeks. In studies 3 and 4, dams were fed RV, HV, or high 10-fold folate (HFol), and male offspring were weaned to RV, HV, or HFol diets for 29 weeks. The results were as follows: (i) HV and HMethyl diets increased obesogenic phenotypes and altered hypothalamic regulation of food intake and metabolism concurrent with epigenetic effects on gene expression. (ii) Removing folate additions to the HV diet showed that folate contributes to the obesogenic phenotype in the offspring and epigenetic alterations in the hypothalamus that favour increased food intake. (iii) Matching pup diet vitamin content with that of the HV and HFol diet-fed dams prevented their increased food intake, body weight, and insulin resistance when weaned to the RV diet. (iv) Both HFol gestational and pup diets altered hypothalamic feeding pathways through DNA methylation, showing that epigenetic effects of these vitamins occur not only in utero but also postnatally. In conclusion, methyl group vitamins in HV gestational and pup diets modify expression of the obesogenic phenotypes and hypothalamic food intake regulatory systems in the Wistar rat offspring.
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Doyle, Wendy, Apama Srivastava, Michael A. Crawford, Rupinda Bhatti, Zoeé Brooke, and Kate L. Costeloe. "Inter-pregnancy folate and iron status of women in an inner-city population." British Journal of Nutrition 86, no. 1 (July 2001): 81–87. http://dx.doi.org/10.1079/bjn2001376.
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The purpose of the present study was to evaluate whether micronutrient supplementation improved the nutritional status of women with poor diets during the inter-pregnancy interval. Fifty-five women who had given birth to a low birth weight baby (<2·5 kg), and who planned to have a further pregnancy, were recruited to a prospective randomised study in East London, UK. Of the fifty-five mothers recruited, forty-four (78 %) met fewer than four of sixteen dietary reference values according to the information provided in a 7 d diet diary, and were categorised as having an ‘inadequate’ diet. Half of the mothers in the ‘inadequate’-diet group were randomly assigned to receive a micronutrient and a single cell oil supplement containing docosahexaenoic acid. All participants received dietary advice based on analysis of their diet diaries, and general lifestyle advice on preparing for pregnancy. Mothers had a blood sample taken at 3 and 9 months post-partum to measure their folate, Fe stores and fatty acid status. Mean serum and erythrocyte folate levels increased significantly between 3 and 9 months post-partum in both the adequate-diet group and the supplemented group. At 9 months post-partum, over half of the unsupplemented, inadequate-diet group remained severely deficient in folate (serum folate <230 nmol/l) and had low serum ferritin levels (<15 μg/l). The high prevalence of inadequate diets in this inner-city population and the low motivation of women to participate in a nutrition programme suggests that consideration should be given to the provision of free folate and Fe supplements to all women in this and similar populations, or at least to women who have delivered a low birth weight baby, who plan further pregnancies.
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DeWolfe, Judy. "Folate Intake of Older Adults Before and After Fortification of Grain Products." Canadian Journal of Dietetic Practice and Research 68, no. 4 (December 2007): 218–20. http://dx.doi.org/10.3148/68.4.2007.218.
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Purpose: To determine whether fortification allowed older adults in the Kingston, Frontenac, and Lennox & Addington (KFL&A) Public Health area to obtain adequate amounts of food folate, and the proportion at risk of consuming more than the upper limit (UL) of folic acid (1,000 mcg). Methods: Dietary intake of a convenience sample of 103 healthy, active older adults (age range: 65 to 95 years) was measured using three 24-hour recalls. Dietary folate preand post-fortification was estimated. Results: Mean dietary folate increased from pre- to postfortification, but 43.4% of women and 20% of men still consumed less than the Estimated Average Requirement of 320 mcg dietary folate equivalent. No intakes exceeded the UL. Participants whose diet met grain products and vegetable and fruit recommendations of Canada's Food Guide to Healthy Eating consumed significantly more folate. Conclusions: Despite fortification, some older adults in the KFL&A area may not be obtaining enough folate to meet their nutritional needs, and may be at risk for health problems associated with folate deficiency. However, without concomitant serum folate measurements, the proportion is not known. Dietitians need to continue promoting foods naturally rich in folate, along with folic acid-fortified foods. While none of the older adults consumed more than the UL, some could exceed this amount if folic acid supplements were added to a folic acid-rich diet.
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Duthie, Susan J. "Epigenetic modifications and human pathologies: cancer and CVD." Proceedings of the Nutrition Society 70, no. 1 (November 11, 2010): 47–56. http://dx.doi.org/10.1017/s0029665110003952.
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Epigenetic changes are inherited alterations in DNA that affect gene expression and function without altering the DNA sequence. DNA methylation is one epigenetic process implicated in human disease that is influenced by diet. DNA methylation involves addition of a 1-C moiety to cytosine groups in DNA. Methylated genes are not transcribed or are transcribed at a reduced rate. Global under-methylation (hypomethylation) and site-specific over-methylation (hypermethylation) are common features of human tumours. DNA hypomethylation, leading to increased expression of specific proto-oncogenes (e.g. genes involved in proliferation or metastasis) can increase the risk of cancer as can hypermethylation and reduced expression of tumour suppressor (TS) genes (e.g. DNA repair genes). DNA methyltransferases (DNMT), together with the methyl donor S-adenosylmethionine (SAM), facilitate DNA methylation. Abnormal DNA methylation is implicated not only in the development of human cancer but also in CVD. Polyphenols, a group of phytochemicals consumed in significant amounts in the human diet, effect risk of cancer. Flavonoids from tea, soft fruits and soya are potent inhibitors of DNMT in vitro, capable of reversing hypermethylation and reactivating TS genes. Folates, a group of water-soluble B vitamins found in high concentration in green leafy vegetables, regulate DNA methylation through their ability to generate SAM. People who habitually consume the lowest level of folate or with the lowest blood folate concentrations have a significantly increased risk of developing several cancers and CVD. This review describes how flavonoids and folates in the human diet alter DNA methylation and may modify the risk of human colon cancer and CVD.
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O'Leary, K., and P. J. A. Sheehy. "Influence of folic acid-fortified foods on folate status in a folate depletion–repletion rat model." British Journal of Nutrition 85, no. 4 (April 2001): 441–46. http://dx.doi.org/10.1079/bjn2000288.
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An increasing number of foods fortified with varying levels of folic acid are appearing in the market place, targeted either at the general population or at specific consumer groups. Although it is assumed that the folate in these products should be highly bioavailable, there is a need to carry out studies to ascertain that this is, in fact, the case. The present study investigated the ability of selected folic acid-fortified foods (targeted at different types of consumer) to increase the folate status of folate-deficient rats. Forty-two weanling male rats (Wistar strain) were fed a folate-deficient diet containing 1 % succinyl sulfathiazole (w/w) for 28 d. Following depletion, seven rats were randomly assigned to each of five repletion diets containing folic acid, Complan®, Slim Fast®, Opti-Fuel2®or Cola Coa®calculated to provide 200 μg folate/kg of each diet. Calculations were based on folate information from the product labels. After a further 28 d, plasma, liver and kidney folate concentrations were determined by microbiological assay. Plasma homocysteine was measured by HPLC as a functional indicator of folate status. The folate content of the foods was measured by tri-enzyme extraction followed by microbiological assay. Our analyses suggest that there may be considerable inaccuracies on the part of the manufacturers in relation to the folate declarations on the product labels. Despite this, the four foods evaluated were highly effective in elevating plasma, liver and kidney folate and lowering plasma homocysteine concentrations in rats. These results lend support to the policy of food fortification with folic acid as a means of raising the folate status of the population, and in particular to the fortification of specific foods which may target areas of the population where increased folate status is most needed.
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Huot, Pedro S. P., David W. Dodington, Rebecca C. Mollard, Sandra A. Reza-López, Diana Sánchez-Hernández, Clara E. Cho, Justin Kuk, Wendy E. Ward, and G. Harvey Anderson. "High Folic Acid Intake during Pregnancy Lowers Body Weight and Reduces Femoral Area and Strength in Female Rat Offspring." Journal of Osteoporosis 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/154109.
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Rats fed gestational diets high in multivitamin or folate produce offspring of altered phenotypes. We hypothesized that female rat offspring born to dams fed a gestational diet high in folic acid (HFol) have compromised bone health and that feeding the offspring the same HFol diet attenuates these effects. Pregnant rats were fed diets with either recommended folic acid (RFol) or 10-fold higher folic acid (HFol) amounts. Female offspring were weaned to either the RFol or HFol diet for 17 weeks. HFol maternal diet resulted in lower offspring body weights (6%,P=0.03) and, after adjusting for body weight and femoral length, smaller femoral area (2%,P=0.03), compared to control diet. After adjustments, HFol pup diet resulted in lower mineral content (7%,P=0.01) and density (4%,P=0.002) of lumbar vertebra 4 without differences in strength. An interaction between folate content of the dam and pup diets revealed that a mismatch resulted in lower femoral peak load strength (P=0.01) and stiffness (P=0.002). However, the match in folate content failed to prevent lower weight gain. In conclusion, HFol diets fed to rat dams and their offspring affect area and strength of femurs and mineral quantity but not strength of lumbar vertebrae in the offspring.
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Banjari, Ines, Vlatka Matokovic, and Vedrana Skoro. "The question is whether intake of folic acid from diet alone during pregnancy is sufficient." Medical review 67, no. 9-10 (2014): 313–21. http://dx.doi.org/10.2298/mpns1410313b.
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Pregnancy and Folic Acid. Pregnancy is the most important period in life of every woman, partially for the number of physiological adaptations she is going through, partially for the expectance of new life. In addition, pregnancy is the ?critical window? for development later in childhood, as a period of foetal programming during which nutrition plays one of crucial roles. Despite the general belief that nutrition through pregnancy is adequate and characterized by better nutritional habits, a number of studies do not corroborate this belief. Role of Folic Acid. An adequate folate blood level is necessary for normal cell growth, synthesis of several compounds including deoxyribonucleic acid and ribonucleic acid, proper brain and neurologic functions; it is included in the regulation of homocysteine level, and closely related to the vitamin B12 metabolism. Folate deficiency in pregnancy is related to neural tube defects, other neurological disorders, preterm delivery and low birth weight. Food sources. A correlation between folate and the prevention of broad spectrum of chronic diseases has been confirmed. Emerging evidence from the epigenetic studies is now bringing even more light on the level of significance of folic acid. A wide range of plant and animal foods are the natural sources of folate; liver, yeast, mushrooms, and green leafy vegetables being the most significant. Different ways of food preparation influence the folate stability and its bioavailability varies from 25 to 50% from foods, 85% from enriched foods or 100% from supplements. Conclusion. A great amount of scientific results has led to official recommendations for folic acid supplementation in pregnant women as well as in a number of obligatory or voluntary fortification programmes in order to prevent the folate deficiency on the level of different population groups. Nevertheless, there must be a certain level of precaution for elderly because folate can mask the vitamin B12 deficiency with possible fatal outcomes.
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Sauer, Julia, Hyeran Jang, Ella M. Zimmerly, Kyong-chol Kim, Zhenhua Liu, Aurelie Chanson, Donald E. Smith, Joel B. Mason, Simonetta Friso, and Sang-Woon Choi. "Ageing, chronic alcohol consumption and folate are determinants of genomic DNA methylation, p16 promoter methylation and the expression of p16 in the mouse colon." British Journal of Nutrition 104, no. 1 (March 8, 2010): 24–30. http://dx.doi.org/10.1017/s0007114510000322.
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Older age, dietary folate and chronic alcohol consumption are important risk factors for the development of colon cancer. The present study examined the effects of ageing, folate and alcohol on genomic and p16-specific DNA methylation, and p16 expression in the murine colon. Old (aged 18 months; n 70) and young (aged 4 months; n 70) male C57BL/6 mice were pair-fed either a Lieber-DeCarli liquid diet with alcohol (18 % of energy), a Lieber-DeCarli diet with alcohol (18 %) and reduced folate (0·25 mg folate/l) or an isoenergetic control diet (0·5 mg folate/l) for 5 or 10 weeks. Genomic DNA methylation, p16 promoter methylation and p16 gene expression were analysed by liquid chromatography–MS, methylation-specific PCR and real-time RT-PCR, respectively. Genomic DNA methylation was lower in the colon of old mice compared with young mice (P < 0·02) at 10 weeks. Alcohol consumption did not alter genomic DNA methylation in the old mouse colon, whereas it tended to decrease genomic DNA methylation in young mice (P = 0·08). p16 Promoter methylation and expression were higher in the old mouse colon compared with the corresponding young groups. There was a positive correlation between p16 promoter methylation and p16 expression in the old mouse colon (P < 0·02). In young mice the combination of alcohol and reduced dietary folate led to significantly decreased p16 expression compared with the control group (P < 0·02). In conclusion, ageing and chronic alcohol consumption alter genomic DNA methylation, p16 promoter methylation and p16 gene expression in the mouse colon, and dietary folate availability can further modify the relationship with alcohol in the young mouse.
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McKay, Jill A., Elizabeth A. Williams, and John C. Mathers. "Gender-specific modulation of tumorigenesis by folic acid supply in the Apc+/Min mouse during early neonatal life." British Journal of Nutrition 99, no. 3 (March 2008): 550–58. http://dx.doi.org/10.1017/s0007114507819131.
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Epidemiological studies suggest an inverse association between folic acid intake and colorectal cancer risk. Conversely, conventional treatment of existing tumours includes the use of folate antagonists. This suggests that the level of exposure to folate and its timing in relation to stage of tumorigenesis may be critical in determining outcomes. We hypothesised that folic acid depletion in utero and during early neonatal life may affect tumorigenesis in offspring. To investigate this hypothesis, female C57Bl6/J mice were randomised to a folic acid adequate (2 mg folic acid/kg diet) or folic acid depleted diet (0·4 mg folic acid/kg) from mating with Apc+/Min sires and throughout pregnancy and lactation. At weaning the Apc+/Min offspring were randomised to a folic acid adequate (2 mg folic acid/kg diet) or depleted (0·26 mg folic acid/kg diet) diet, creating four in utero/post-weaning dietary regimens. At 10 weeks post-weaning, mice were killed and the intestinal tumour number and size were recorded. Folic acid depletion during pregnancy and post-weaning reduced erythrocyte folate concentrations in offspring significantly. Folic acid depletion during pregnancy and lactation did not affect tumour multiplicity or size. However, female mice fed normal folic acid diets post-weaning had more, and larger, tumours when compared with depleted females and both depleted and adequate folic acid fed males. These data suggest that folate depletion post-weaning was protective against neoplasia in female Apc+/Min mice and highlights the need for further investigation of the optimal timing and dose of folic acid supplementation with regard to colorectal cancer risk.
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Maxwell, M. H., C. C. Whitehead, and J. Armstrong. "Haematological and tissue abnormalities in chicks caused by acute and subclinical folate deficiency." British Journal of Nutrition 59, no. 1 (January 1988): 73–80. http://dx.doi.org/10.1079/bjn19880011.
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1. Haematological, histological and ultrastructural findings in young chicks fed on a purified diet severely deficient in folate are reported.2. Growth of the birds was greatly depressed and they had a macrocytic anaemia. Other haematological changes included abnormal nuclear formations in erythrocytes, numerous mitoses and hypersegmented granulocytes.3. Megaloblasts were observed in bone marrow and their fine structure is described for the first time in an avian species.4. Morphological changes occurred also in the liver. The parenchyma had damaged sinusoidal endothelium, inflammatory cells and no glycogen. Mitochondria were damaged and many were associated with unusual crystalline structures.5. Chickens fed on a semi-purified diet of low folate content showed no growth depression or clinical signs of deficiency but had abnormal haematological values and morphological changes that resembled those seen in birds fed on the purified diet.6. These abnormalities responded to dietary supplements of pteroylmonoglutamic acid in a dose-related manner and may be useful in diagnosing subclinical folate deficiency.
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Gomes, Sandra, Carla Lopes, and Elisabete Pinto. "Folate and folic acid in the periconceptional period: recommendations from official health organizations in thirty-six countries worldwide and WHO." Public Health Nutrition 19, no. 1 (April 16, 2015): 176–89. http://dx.doi.org/10.1017/s1368980015000555.
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AbstractObjectiveTo summarize the recommendations on folate intake and folic acid supplementation and fortification in the periconceptional period, aimed at prevention of neural tube defects (NTD), provided by official health organizations in different countries worldwide and WHO.DesignInformation on recommendations for folate and folic acid intake in the periconceptional period was gathered from the websites of official national health organizations of several countries worldwide and from the WHO website.SettingWHO, selected developed countries and emerging economies, totalling thirty-six countries worldwide (some European, BRICS, G8, Asian Tiger/Asian Dragon and Australia).ResultsRecommendations differ between countries, although the majority (69·4 %) recommend a healthy diet plus a folic acid supplement of 400 µg/d from preconception (4–12 weeks) until the end of the first trimester of pregnancy (8–12 weeks). The same recommendation is issued by the WHO. Dosages for women at high risk of NTD are up to 4–5 mg/d (for 41·7 % of studied countries). The recommended intake for folate is in the range of 300–400 µg/d for women of childbearing age and 500–600 µg/d for pregnant women in different countries and WHO. Five countries emphasize the importance of a healthy diet rendering supplementation needless. By contrast, five others advise a healthy diet and supplementation plus mandatory fortification. Only one mentions the importance of ensuring an adequate folate status and refers to checking with a health-care provider on the need for supplements.ConclusionsDifferent recommendations regarding folate and folic acid, seeking NTD prevention, are available worldwide; however, most countries and WHO focus on a healthy diet and folic acid supplementation of 400 µg/d periconceptionally.
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Višekruna, Ivona, Ivana Rumbak, Ivana Rumora Samarin, Irena Keser, and Jasmina Ranilović. "Homocysteine Levels Show Significant Differences among Mediterranean Dietary Quality Index Variables Compared to Folate and Vitamin B12 Status in Women." International Journal for Vitamin and Nutrition Research 85, no. 3-4 (December 2015): 202–10. http://dx.doi.org/10.1024/0300-9831/a000237.
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Abstract. Results of epidemiologic studies and clinical trials have shown that subjects following the Mediterranean diet had lower inflammatory markers such as homocysteine (Hcy). Therefore, the aim of this cross-sectional study was to assess female diet quality with the Mediterranean diet quality index (MDQI) and to determine the correlation between MDQI, homocysteine, folate and vitamin B12 levels in the blood. The study participants were 237 apparently healthy women (96 of reproductive age and 141 postmenopausal) between 25 and 93 years. For each participant, 24-hour dietary recalls for 3 days were collected, MDQI was calculated, and plasma Hcy, serum and erythrocyte folate and vitamin B12 levels were analysed. Total MDQI ranged from 8 to 10 points, which represented a medium-poor diet for the subjects. The strength of correlation using biomarkers, regardless of group type, age, gender and other measured parameters, was ranked from best (0.11) to worst (0.52) for olive oil, fish, fruits and vegetables, grains, and meat, in this order. Hcy levels showed the best response among all markers across all groups and food types. Our study shows significant differences between variables of the MDQI and Hcy levels compared to levels of folate and vitamin B12 in participants with medium-poor diet quality, as evaluated according to MDQI scores.
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Achón, M., E. Alonso-Aperte, L. Reyes, N. Úbeda, and G. Varela-Moreiras. "High-dose folic acid supplementation in rats: effects on gestation and the methionine cycle." British Journal of Nutrition 83, no. 2 (February 2000): 177–83. http://dx.doi.org/10.1017/s0007114500000222.
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There is new evidence that a good folate status may play a critical role in the prevention of neural-tube defects and in lowering elevated homocysteine concentrations. This adequate folate status may be achieved through folic acid dietary supplementation. Folate is a water-soluble vitamin with a low potential toxicity. However, the possible consequences of long-term high-dose folic acid supplementation are unknown, especially those related to the methionine cycle, where folate participates as a substrate. With the aim of evaluating such possible effects, four groups of Wistar rats were classified on the basis of physiological status (virgin v. pregnant) and the experimental diet administered (folic-acid-supplemented, 40 mg/kg diet v. control, 2 mg folic acid/kg diet). Animals were fed on the diets for 3 weeks. Results showed that gestation outcome was adequate in both groups regardless of the dietary supplementation. However, there were reductions (P < 0·001) in body weight and vertex-coccyx length in fetuses from supplemented dams v. control animals. Folic acid administration also induced a higher (P < 0·01) S-adenosylmethionine : S-adenosylhomocysteine value due to increased S-adenosylmethionine synthesis (P < 0·01). However, hepatic DNA methylation and serum methionine concentrations remained unchanged. Serum homocysteine levels were reduced in supplemented dams (P < 0·05). Finally, pregnancy caused lower serum folate, vitamin B6 and vitamin B12 levels (P < 0·05). Folic acid administration prevented the effect of pregnancy and raised folate levels in dams, but did not change levels of vitamins B12 and B6. These new findings are discussed on the basis of potential benefits and risks of dietary folic acid supplementation.
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Choi, S.-W., Y.-I. Kim, J. N. Weitzel, and J. B. Mason. "Folate depletion impairs DNA excision repair in the colon of the rat." Gut 43, no. 1 (July 1, 1998): 93–99. http://dx.doi.org/10.1136/gut.43.1.93.
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Background/Aims—Diminished folate status appears to promote colonic carcinogenesis by, as of yet, undefined mechanisms. Impaired DNA repair plays a significant role in the evolution of many colon cancers. Since folate is essential for thede novo synthesis of nucleotides and since folate depletion has previously been associated with excessive DNA strand breaks, it was hypothesised that folate depletion may impair DNA repair. Studies were therefore performed to examine whether folate depletion affects the two major categories of DNA repair.Methods—Study 1: eight weanling male Sprague-Dawley rats were fed on diets containing either 0 or 8 mg folate/kg diet with 1% succinylsulphathiazole for four weeks. After viable colonocytes had been harvested, DNA excision repair was evaluated by a single cell gel electrophoresis assay. Study 2: eighteen animals were fed on similar diets for five weeks. Also in study 2, 18 additional rats were fed on the same defined diet without succinylsulphathiazole for 15 weeks. Weekly injections with the procarcinogen, 1,2-dimethylhydrazine (20 mg base/kg), were administered to the latter group of animals. Five microsatellite loci from different chromosomes were investigated for instability in hepatic and colonic DNA.Results—In study 1, a significantly retarded rate of DNA excision repair was observed in the folate deficient colonocytes compared with controls (p<0.05). In study 2, there was no evidence of instability at the five microsatellite loci associated with either short or long term folate depletion.Conclusions—Folate deficiency impairs DNA excision repair in rat colonic mucosa; a similar degree of deficiency, even when administered in conjunction with a colonic carcinogen, did not produce evidence of a widespread defect in mismatch repair.
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Moore, Caroline J., Maude Perreault, Michelle F. Mottola, and Stephanie A. Atkinson. "Diet in Early Pregnancy: Focus on Folate, Vitamin B12, Vitamin D, and Choline." Canadian Journal of Dietetic Practice and Research 81, no. 2 (June 1, 2020): 58–65. http://dx.doi.org/10.3148/cjdpr-2019-025.
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Purpose: Prenatal multivitamins are recommended in pregnancy. This study assessed food and supplement intakes of folate, vitamin B12 (B12), vitamin D, and choline in pregnant women living in Southern Ontario in comparison with current recommendations. Methods: Women recruited to the Be Healthy in Pregnancy RCT (NCT01693510) completed 3-day diet/supplement records at 12–17 weeks gestation. Intakes of folate, B12, vitamin D, and choline were quantified and compared with recommendations for pregnant women. Results: Folate intake (median (min, max)) was 1963 μg/day dietary folate equivalents (153, 10 846); 90% of women met the Estimated Average Requirement (EAR) but 77% exceeded the Tolerable Upper Intake Level (UL) (n = 232). B12 intake was 12.1 μg/day (0.3, 2336); 96% of women met the EAR with 7% exceeding the EAR 100-fold (n = 232). Vitamin D intake was 564 IU/day (0.0, 11 062); 83% met the EAR, whereas 1.7% exceeded the UL (n = 232). Choline intake was 338 mg/day (120, 1016); only 18% met the Adequate Intake and none exceeded the UL (n = 158). Conclusion: To meet the nutrient requirements of pregnancy many women rely on prenatal vitamins. Reformulating prenatal multivitamin supplements to provide doses of vitamins within recommendations to complement a balanced healthy diet would ensure appropriate micronutrient intakes for pregnant women.
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Lentz, Steven R., Rochelle A. Erger, Sanjana Dayal, Nobuyo Maeda, M. René Malinow, Donald D. Heistad, and Frank M. Faraci. "Folate dependence of hyperhomocysteinemia and vascular dysfunction in cystathionine β-synthase-deficient mice." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 3 (September 1, 2000): H970—H975. http://dx.doi.org/10.1152/ajpheart.2000.279.3.h970.
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Hyperhomocysteinemia is a risk factor for stroke, myocardial infarction, and venous thrombosis. Moderate hyperhomocysteinemia is associated with impaired endothelial function, but the mechanisms responsible for endothelial dysfunction in hyperhomocysteinemia are poorly understood. We have used genetic and dietary approaches to produce hyperhomocysteinemia in mice. Heterozygous cystathionine β-synthase-deficient mice (CBS +/−), which have a selective defect in homocysteine transsulfuration, and wild-type (CBS +/+) littermates were fed either a control diet or a diet that is relatively deficient in folic acid for 6 wk. Plasma total homocysteine was 5.3 ± 0.7 μM in CBS +/+ mice and 6.4 ± 0.6 μM in CBS +/− mice ( P = 0.3) given the control diet. Plasma total homocysteine was 11.6 ± 4.5 μM in CBS +/+ mice and 25.1 ± 3.2 μM in CBS +/− mice ( P = 0.004) given a low-folate diet. In mice fed the control diet, relaxation of aortic rings in response to the endothelium-dependent vasodilator acetylcholine did not differ significantly between CBS +/+ mice and CBS +/− mice. In contrast, in mice fed a low-folate diet, maximal relaxation to acetylcholine was markedly impaired in CBS +/− mice (58 ± 9%) compared with CBS +/+ mice (84 ± 4%) ( P = 0.01). No differences in relaxation to the endothelium-independent vasodilator sodium nitroprusside were observed among the four groups of mice. These data indicate that CBS-deficient mice are predisposed to hyperhomocysteinemia during dietary folate deficiency, and moderate hyperhomocysteinemia is associated with marked impairment of endothelial function in mice.
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McKillop, Derek J., Kristina Pentieva, Donna Daly, Joseph M. McPartlin, Joan Hughes, J. J. Strain, John M. Scott, and Helene McNulty. "The effect of different cooking methods on folate retention in various foods that are amongst the major contributors to folate intake in the UK diet." British Journal of Nutrition 88, no. 6 (December 2002): 681–88. http://dx.doi.org/10.1079/bjn2002733.
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Folate intake is strongly influenced by various methods of cooking that can degrade the natural forms of the vitamin in foods. The aim of the present study was to determine the effect of different cooking methods on folate retention in various foods that contribute to folate intake in the UK diet. Typical purchasing and cooking practices of representative food folate sources were determined from a questionnaire survey of local shoppers (n 100). Total folate was determined by microbiological assay (Lactobacillus casei NCIMB 10463) following thermal extraction and tri-enzyme (α-amylase, protease and conjugase) treatment in raw foods and after typical methods of cooking. Boiling for typical time periods resulted in only 49 % retention of folate in spinach (191·8 and 94·4 μg/100 g for raw and boiled spinach respectively; P<0·005), and only 44 % in broccoli (177·1 and 77·0 μg/100 g for raw and boiled broccoli respectively, P<0·0001). Steaming of spinach or broccoli, in contrast, resulted in no significant decrease in folate content, even for the maximum steaming periods of 4·5 min (spinach) and 15·0 min (broccoli). Prolonged grilling of beef for the maximum period of 16·0 min did not result in a significant decrease in folate content (54·3 and 51·5 μg/100 g for raw and grilled beef respectively). Compared with raw values, boiling of whole potatoes (skin and flesh) for 60·0 min did not result in a significant change in folate content (125·1 and 102·8 μg/100 g for raw and boiled potato respectively), nor was there any effect on folate retention whether or not skin was retained during boiling. These current results show that the retention of folate in various foods is highly dependent both on the food in question and the method of cooking. Thus, public health efforts to increase folate intake in order to improve folate status should incorporate practical advice on cooking.
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Barkow, B., J. J. Matte, H. Böhme, and G. Flachowsky. "Influence of folic acid supplements on the carry-over of folates from the sow to the piglet." British Journal of Nutrition 85, no. 2 (February 2001): 179–84. http://dx.doi.org/10.1079/bjn2000238.
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This experiment aimed to investigate the influence of folic acid supplements on the carry-over of folates from the sow to the fetus during late gestation and to the suckling piglet. Two groups of sixteen German Landrace sows received, during gestation and lactation, a diet supplemented with either 0 or 10 mg folic acid/kg. Increased folic acid concentrations in the serum of sows were detected only at the end of gestation (day 100) and at the end of lactation (day 28). The supplementation with folic acid to the sows' diet improved the folic acid supply of the fetus compared with unsupplemented controls; values were respectively 92.6v.56.2 nmol folates/l serum in newborn piglets and 171.9v.76.3 μmol folates/g fresh liver in stillborn piglets (P< 0.05). Folate concentrations in colostrum and milk (day 28) were 3.6- and 5.0-times higher in supplemented than unsupplemented sows. This treatment effect was also reflected in the serum of piglets until weaning. Therefore, the folic acid supply for the suckling piglet is dependent mainly upon the carry-over of maternal folates via colostrum and milk.
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Sharma, Jaspreet, Blake Rushing, Natalia Krupenko, Susan Sumner, and Sergey Krupenko. "Effect of Folate Diet on Liver Metabolomics in Wild Type and Aldh1l1 Knockout Mice." Current Developments in Nutrition 5, Supplement_2 (June 2021): 949. http://dx.doi.org/10.1093/cdn/nzab050_016.
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Abstract Objectives The goal of the present study was to investigate whether dietary folate restriction exacerbates the metabotype associated with the KO. Methods Hepatic tissues from wildtype (Aldh1l1+/+) and KO (Aldh1l1−/−) mice fed a control (CD), or folate deficient diet (FDD) for 16 weeks were profiled using untargeted metabolomics to identify metabolite changes and affected pathways. Results PCA plots of the 6595 peaks in the preprocessed liver datasets show tight clustering of samples within the groups and clear separation between genotypes, and diets. OPLS-DA analysis showed strong separation between pairwise comparisons of the groups with model statistics (R2X, R2Y, and Q2) all greater than 0.5, indicating that dietary folate and Aldh1l1 alone or in combination have a significant effect on the liver metabolomes in male and female mice. Using MetaboAnalyst for pathway analysis significant differences in bile acid metabolism, nucleotide metabolism, and protein synthesis/amino acid metabolism (aminoacyl-tRNA biosynthesis; alanine, aspartate and glutamate metabolism; valine, leucine and isoleucine biosynthesis) were observed in males. Similarly, in females many perturbations in amino acid metabolism, nucleotide metabolism, carbohydrate metabolism (pyruvate metabolism; fructose and mannose metabolism), sphingolipid metabolism, bile acid metabolism and microbiome metabolism (propanoate metabolism; butanoate metabolism) were noted. Conclusions Dietary folate elicits liver metabolome response depending on Aldh1l1 genotype. Funding Sources NIH, R01
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Nowjack-Raymer, R. E., and A. Sheiham. "Numbers of Natural Teeth, Diet, and Nutritional Status in US Adults." Journal of Dental Research 86, no. 12 (December 2007): 1171–75. http://dx.doi.org/10.1177/154405910708601206.
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Evidence that dental status affects diet is equivocal. The hypothesis of this study was that diet was affected by dental status. The objective was to assess the relationship between numbers of teeth and diet and nutritional status in US adult civilians without prostheses. We examined 6985 NHANES (1988–1994) participants. Data included socio-economics, demographics, dental status, and diet and nutritional status. Dietary data were obtained from food frequency questionnaires and 24-hour dietary recall. Serum levels of beta carotene, folate, and vitamin C were measured with isocratic high-performance liquid chromatography. The population was classified by numbers of teeth. Covariance and Satterthwaite F-adjusted statistical comparisons were made between tooth groupings and the fully dentate population. Multilinear regression models adjusted for covariates. People with fewer than 28 teeth had significantly lower intakes of carrots, tossed salads, and dietary fiber than did fully dentate people, and lower serum levels for beta carotene, folate, and vitamin C. Dental status significantly affects diet and nutrition.