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PubMed2005

Biochemical indexes of the B vitamins in cord serum are predicted by maternal B vitamin status.

BACKGROUND: The concentration of total homocysteine (tHcy) is higher in newborns than in older children. Vitamin B-12 is the major determinant of tHcy in newborns. Maternal status of folate, vitamin B-12, and vitamin B-6 during pregnancy may affect the biochemical markers of these micronutrients in newborns. OBJECTIVE: Our objective was to study the relation between concentrations of the metabolites and B vitamins in maternal sera and concentrations in the umbilical venous blood of the corresponding newborns. DESIGN: We studied healthy pregnant women at the time of labor who were expecting healthy, full-term, appropriate-birth-weight babies. Samples were available from 82 mother-infant pairs. RESULTS: Concentrations of B vitamins were higher in cord samples than in maternal blood (folate, 2-fold; vitamin B-12, 1.5-fold; and vitamin B-6, 6-fold). Concentrations of cystathionine and methylmalonic acid (MMA) were also higher in the infants than in the mothers (x +/- SD: cystathionine, 462 +/- 189 and 343 +/- 143 nmol/L; MMA, 353 +/- 144 and 233 +/- 110 nmol/L). No significant differences in tHcy concentrations were observed between fetal and maternal samples. Concentrations of vitamin B-12 did not differ significantly between mothers of infants from different quartiles of cord MMA. Higher fetal MMA concentrations were related to higher maternal MMA and vitamin B-12 concentrations and lower fetal concentrations of vitamin B-12. Fetal concentrations of cystathionine were predicted by maternal cystathionine, gestational age, fetal vitamin B-6, and fetal tHcy. CONCLUSIONS: Maternal concentrations of the metabolic markers of B vitamins predict values in fetal blood at delivery. Fetal tHcy concentrations were low but were predicted by the vitamin status of the mother. The effect of increasing maternal intake of vitamins B-12 and B-6 during pregnancy on the fetal concentrations of the metabolites should be investigated.

Adult↗
PubMed1981

An increase in vitamin E requirement induced by high supplementation of vitamin C in rats.

Weanling rats were maintained on purified diets with graded levels of vitamin E at 50, 60, 100, 200, or 500 IU/kg diet; each group was further divided into two subgroups, each with six rats and received vitamin C at 0 or 1.5 g/kg diet. After 1 or 2 months, the determination of antioxidant status showed that the high supplementation of vitamin C at the marginally adequate vitamin E level significantly increased in vitro erythrocyte hemolysis and liver lipid peroxidation, and significantly lowered erythrocyte level of reduced glutathione and plasma level of vitamin E; thus lowering the overall antioxidant potential of the animals. A small increase in vitamin E level counteracted the hemolytic and peroxidative effect of the high supplementation of vitamin C. A greater increase in vitamin E level counteracted the effect of high supplementation of vitamin C in decreasing glutathione level and plasma vitamin E level. These results indicate that the adverse effect of the high supplementation of vitamin C on tissue antioxidant potential may be overcome by increasing the supplementation level of vitamin E, and suggest that vitamin E requirement may be increased with increased vitamin C supplementation.

Animals↗
PubMed2000

Assessment of vitamin B-12, folate, and vitamin B-6 status and relation to sulfur amino acid metabolism in neonates.

BACKGROUND: Total serum homocysteine (tHcy) has been used as an indicator of intracellular vitamin B-12, vitamin B-6, and folate status in adults, but data for neonates and infants are lacking. Vitamin B-12 deficiency may have fatal effects on neurologic development in infants; therefore, early diagnosis is crucial. OBJECTIVE: Our aim was to provide a reference range for tHcy in neonates and to explore the relation of tHcy to 1) serum vitamin concentrations, 2) the product of the transsulfuration pathway (cysteine), and 3) nutritional factors. DESIGN: tHcy, cysteine, folate, vitamin B-12, and vitamin B-6 were measured in 123 healthy, breast-fed neonates. The influence of nutrition (formula or human milk) on these variables was investigated in 60 infants. RESULTS: The mean (+/-SD) tHcy concentration was 7.8 +/- 3.1 micromol/L. tHcy showed a linear association with log vitamin B-12 (r = -0.64, P: < 0. 001), red blood cell folate (r = -0.33, P: < 0.001), and cysteine (r = 0.36, P: < 0.001). The strongest linear association was found between tHcy and the ratio of log cysteine to log vitamin B-12 (r = 0.71, P: < 0.0001). We found more neonates with probable tissue deficiencies of vitamin B-12 and folate on the basis of tHcy measurements than was expected from the analysis of serum vitamin concentrations alone (15.4% compared with 9.7%). Breast-fed infants had significantly lower vitamin B-12 concentrations and significantly higher serum tHcy and cysteine concentrations and ratios of log cysteine to log vitamin B-12 than did formula-fed infants (P: < 0.001). CONCLUSIONS: tHcy can be used as a functional indicator of vitamin B-12 and folate status in neonates. The ratio of cysteine to vitamin B-12 can be used as an additional index of impaired intracellular Hcy metabolism. tHcy and cysteine concentrations in infants are affected by nutritional factors.

Amino Acids↗
PubMed2003

Fortification of orange juice with vitamin D: a novel approach for enhancing vitamin D nutritional health.

BACKGROUND: Fortification of milk with vitamin D may not be adequate for satisfying the vitamin D requirement because of variability in vitamin D content after fortification and because many persons have milk allergy or lactose intolerance. Additional foods need to be fortified with vitamin D. OBJECTIVE: We determined whether vitamin D, a fat-soluble vitamin, is bioavailable in orange juice and skim milk, 2 nonfat beverages. DESIGN: On 3 separate occasions, 18 adults ingested 25 000 IU vitamin D(2) in 240 mL whole milk or skim milk or in 0.1 mL corn oil applied to toast. A separate, double-blind, randomized, controlled trial investigated whether the consumption of orange juice fortified with vitamin D(3) would increase serum 25-hydroxyvitamin D [25(OH)D] concentrations: 14 subjects ingested 240 mL orange juice fortified with 1000 IU vitamin D, and 12 subjects ingested a control orange juice daily for 12 wk. RESULTS: Peak serum vitamin D(2) concentrations did not differ significantly after the ingestion of vitamin D(2) in whole milk, skim milk, or corn oil on toast. After subjects consumed orange juice fortified with 1000 IU vitamin D(3) daily for 12 wk, serum 25(OH)D(3) concentrations increased by 150%, and serum parathyroid hormone concentrations decreased by 25% compared with baseline; control subjects had a seasonal increase of 45% in 25(OH)D and no significant change in serum parathyroid hormone. CONCLUSIONS: The fat content of milk does not affect vitamin D bioavailability. Vitamin D fortification at 1000 IU/240 mL orange juice for 12 wk safely increased 25(OH)D(3) concentrations in adults.

Adult↗
PubMed1979

Association between plasma and liver vitamin A levels in the calf; weanling pig, rabbit and rat; and adult goat fed fixed intakes of vitamin A.

To reexamine the relationship between plasma and liver vitamin A levels, data from various species of animals fed fixed intakes of vitamin A ester (expressed as retinol equivalents/kg liver weight/day) were vitamin A ester (expressed as retinol equivalents/kg live weight/day) were studied. The intakes ranging from deficient to toxic were for 48 calves, 4 to 17,600 micrograms; 39 pigs, 17.6 to 19,842 micrograms; 86 rabbits, 4.5 to 287 micrograms; 138 rats, 4 to 16,384 micrograms; and 40 goats, 1 to 17,640 micrograms. Following the feeding of these intakes for periods of between 5 and 133 weeks, blood and liver samples were taken for vitamin A determinations. Plasma vitamin A concentrations reached minimum values at low liver vitamin A levels whereas liver vitamin A levels reached maximum values at high plasma vitamin A concentrations. Upon elimination of data pairs at the extremes, linear regressions of log10 (total liver vitamin A) on plasma vitamin A concentrations and of plasma vitamin A concentrations on log10 (total liver vitamin A) were statistically significant. Therefore it was possible to estimate within limits the log10 (total liver vitamin A) from plasma vitamin A. Applicable limits were for the calf 8 to 46 micrograms/100 ml of plasma, for the pig 14 to 32, for the rabbit 14 to 74, for the rat 5 to 51 and for the goat 22 to 55. Simple correlation coefficients were 0.92, 0.60, 0.93, 0.92 and 0.75.

Aging↗
PubMed2001

The amino bisphosphonate ibandronate prevents vitamin D toxicity and inhibits vitamin D-induced calcification of arteries, cartilage, lungs and kidneys in rats.

Experiments were carried out to determine whether the doses of the amino bisphosphonate ibandronate that inhibit bone resorption inhibit soft tissue calcification and death in rats treated with a toxic dose of vitamin D. These studies were prompted by the recent discovery that ibandronate doses that inhibit bone resorption potently inhibit artery calcification induced by treatment with the vitamin K antagonist warfarin. All 16 rats treated with the toxic dose of vitamin D (12.5 mg cholecalciferol x kg(-1)) died by d 6 after the first vitamin D injection (median survival: 4.5 d), whereas the 12 rats treated with vitamin D plus ibandronate (0.25 mg x kg(-1) x d(-1)) were alive and in good health at d 10. Rats treated with vitamin D alone and examined at d 4 had extensive Alizarin red staining for calcification in the aorta, the carotid, hepatic, mesenteric, renal and femoral arteries, kidneys and lungs, whereas rats treated with vitamin D plus ibandronate had no evidence for calcification at any of these tissues when examined at d 7 and 10. Ibandronate treatment also inhibited the dramatic increase in the levels of calcium and phosphate seen in the abdominal aorta, kidneys, lungs and trachea of the vitamin D-treated rats (P < 0.001). Serum calcium levels were, however, not different in rats treated with vitamin D alone (3.4 +/- 0.2 mmol x L(-1)) and in rats treated with vitamin D plus ibandronate (3.5 +/- 0.2 mmol x L(-1)). Treatment with vitamin D alone increased levels of matrix Gla protein, an inhibitor of soft tissue calcification, in the arteries, kidneys, lungs and trachea by 10- to 100-fold, and ibandronate treatment prevented this increase. The importance of these studies in the rat model is that they identify a class of drugs in current clinical use that can be used to treat patients with vitamin D toxicity and that they identify the dose of the drug that is predicted to be effective, namely the dose that inhibits bone resorption. Because there is no other known treatment for vitamin D toxicity, there would seem to be good reason to try bisphosphonates such as ibandronate in future studies aimed at treating patients who have been exposed to toxic levels of vitamin D.

Animals↗
PubMed2003

Diversity in rat tissue accumulation of vitamin B12 supports a distinct role for the kidney in vitamin B12 homeostasis.

BACKGROUND: Vitamin B(12) in plasma is complexed to the carrier proteins transcobalamin (TC) and haptocorrin. The TC-B(12) complex is filtered in the glomeruli and reabsorbed in the renal tubules by receptor-mediated endocytosis, providing a route for a significant renal accumulation of vitamin B(12). The present study investigates the role of the rodent kidney in B(12) homeostasis by examining the distribution of vitamin B(12) in rats during vitamin B(12) depletion or B(12) load, and compares kidney accumulation with the vitamin distribution in other tissues including brain, liver, testes, intestine, spleen and plasma. METHODS: Fifteen rats were fed on a diet containing different concentrations of B(12) supplemented with s.c. injections of B(12). Twenty four hours prior to sacrifice, all animals were injected with [(57)Co]B(12). The vitamin contents of kidneys, liver, spleen, brain, testis, intestine, skeletal muscle, serum and urine were analysed. Both total tissue vitamin B(12) accumulation and [(57)Co]B(12) were determined to compare steady-state B(12) and the distribution of an acutely injected dose. In the kidney, free and protein-bound B(12) was determined by gel filtration. RESULTS: The rat kidneys accumulated more B(12) during normal and loaded conditions than any other tissue. A 110-fold increase in vitamin content was observed from the deficient to the loaded conditions in the kidney compared with a 3.5-fold increase in the liver. In contrast to all other organs, significantly smaller amounts of acutely injected B(12) accumulated in the kidneys in the vitamin-deprived state compared with both the normal and the vitamin-loaded condition. CONCLUSIONS: The present study suggests a significant role for the rodent kidney in vitamin B(12) metabolism. We propose a model for rat tissue uptake consistent with the presence of two different TC-B(12) receptors and renal uptake following filtration of TC-B(12) in the glomeruli. The presented model allows for the reduced renal uptake and accumulation in vitamin-deprived conditions, thus reserving the vitamin for other tissues, including nerve tissue and bone marrow, which are more sensitive to vitamin B(12) deficiency.

Animals↗
PubMed1983

Cyclic interconversion of vitamin K1 and vitamin K1 2,3-epoxide in man.

The disposition of a single intravenous bolus dose of 10 mg vitamin K1 and vitamin K1-2,3-epoxide were studied in two healthy subjects without and with 12 h pretreatment dose of phenprocoumon (0.4 mg/kg). For each compound administered alone the plasma concentration-time profile was adequately fitted by a biexponential equation, with an average terminal half-life of 2.0 and 1.15 h for the administered vitamin K and its 2,3-epoxide respectively. While vitamin K1 was measurable in plasma following administration of vitamin K1-2,3-epoxide, the epoxide was not detectable following administration of vitamin K1. Following pretreatment with phenprocoumon and after intravenous administration of vitamin K1, both the average half-life and area under the plasma concentration-time profile of vitamin K1 were marginally reduced to 1.5 h and 1.76 mg l-1 h respectively, while the plasma concentration of vitamin K1-2,3-epoxide was readily measurable and its half-life markedly prolonged to 14.7 h. Following pretreatment with phenprocoumon and after oral administration of vitamin K1-2,3-epoxide, no vitamin K1 was detectable in plasma and the half-life of the epoxide was 13.8 h. Based on area considerations the data suggest that either phenprocoumon does more than just inhibit the reduction of vitamin K1-2,3-epoxide to vitamin K1, or that the simple model describing the interconversion between vitamin K1 and its epoxide is inadequate. The same conclusion is drawn from the analysis of comparable data in dogs, obtained by Carlisle & Blaschke (1981).

Adult↗
PubMed1986

Vitamin E deficiency and vitamin C supplements: exercise and mitochondrial oxidation.

The effects of dietary antioxidant vitamins E and C on exercise endurance capacity and mitochondrial oxidation were investigated in rats. The endurance capacity of both vitamin E-deficient and vitamin C-supplemented, E-deficient rats was significantly (P less than 0.05) lower (38.1 and 33.6%, respectively) than control animals. Compared with the normal and vitamin E-deficient rats, there was a significant (P less than 0.05) increase in the concentration of vitamin C in blood and liver of the vitamin E-deficient, C-supplemented animals. Hence dietary vitamin C supplementation does not prevent the inhibition of exercise endurance capacity or increased hemolysis seen in vitamin E deficiency. The mitochondrial activities for the oxidation of palmitoyl carnitine and alpha-ketoglutarate were significantly (P less than 0.05) decreased by a single bout of exercise in brown adipose tissue but not in muscle, heart, or liver from vitamin C-supplemented, E-deficient groups of rats when compared with the activities in the tissue from the same group of rats killed at rest. Similar results were also seen in brown adipose tissue from vitamin E-deficient rats. The results suggest a tissue-specific role for vitamins E and C in substrate oxidation and show that the poor endurance capacity of vitamin E-deficient rats cannot be attributed to any changes in the mitochondrial activity in skeletal or cardiac muscles. It is also concluded that vitamin C supplementation, at least at the dose employed in the present study, cannot counteract the detrimental effects associated with vitamin E deficiency.

Adipose Tissue, Brown↗
PubMed2000

Long-term effects of vitamin E, vitamin C, and combined supplementation on urinary 7-hydro-8-oxo-2'-deoxyguanosine, serum cholesterol oxidation products, and oxidation resistance of lipids in nondepleted men.

We studied the long-term effects of vitamins E and C and their combination on lipid peroxidation in vivo and in vitro. The Antioxidant Supplementation in Atherosclerosis Prevention (ASAP) trial is a double-masked placebo-controlled randomized clinical trial to study the effects of vitamin C (500 mg of slow release ascorbate per day), vitamin E (182 mg of RRR-alpha-tocopherol acetate per day), and the combination of both antioxidants. Lipid peroxidation measurements were carried out for 48 male participants at entry and at 12 and 36 months. Compared with placebo, vitamin E and the vitamin combination increased plasma lipid-standardized alpha-tocopherol during the first 12 months by 68.2% and 65.2% (P:<0. 001 for both), respectively, and reduced serum 7beta-hydroxycholesterol by 50.4% (P:=0.013) and 44.0% (P:=0.041), respectively. The net change of lipid standardized alpha-tocopherol was 63.8% after 36 months of vitamin E supplementation and 43.3% for the combination. Vitamin C supplementation elevated plasma total ascorbate level by 30.1% (P:=0.043) in 12 months and by 91.1% (P:=0. 001) in 36 months. Neither vitamin E, vitamin C, nor the combination influenced the urinary excretion rate of 7-hydro-8-oxo-2'-deoxyguanosine or the antioxidative capacity of plasma. Vitamin E and the combination of vitamins E and C enhanced the oxidation resistance of isolated lipoproteins and total serum lipids. Our data indicate that long-term supplementation of nondepleted men with a reasonable dose of vitamin E alone or in combination with slow release vitamin C reduces lipid peroxidation in vitro and in vivo, whereas a relatively high dose of vitamin C alone does not.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1972

The role of the pancreas in vitamin B 12 absorption: studies of vitamin B 12 absorption in partially pancreatectomized rats.

The effect of partial pancreatectomy (80-90%) on vitamin B(12) absorption was studied in the rat. The absorption of 5 ng of (57)Co-labeled vitamin B(12) was significantly reduced from 70 +/-2.5% (mean +/-SE) in control and sham-operated rats to 32 +/-2.6% in partially pancreatectomized rats. Hog pancreatic extract (0.17 g/kg) improved vitamin B(12) absorption from 30.0 to 61.0% in partially pancreatectomized rats but did not alter vitamin B(12) absorption in control rats. Chloramphenicol did not enhance vitamin B(12) absorption in partially pancreatectomized rats with pancreatic extract-improved vitamin B(12) malabsorption. The partially pancreatectomized rats with pancreatic extract-improved vitamin B(12) malabsorption were sacrificed and the stomach and small bowel studied in vitro to further define the pathogenesis of the vitamin B(12) malabsorption. Rat gastric intrinsic factor stimulated vitamin B(12) uptake by intestinal sacs prepared from partially pancreatectomized rats 3.1-fold. Gastric intrinsic factor prepared from partially pancreatectomized rats was as effective in promoting vitamin B(12) uptake by rat intestinal sacs as intrinsic factor prepared from control rats. These data indicate that partially pancreatectomized rats develop an abnormality in the absorption of labeled vitamin B(12) which can be corrected by pancreatic extract. The vitamin B(12) malabsorption is due to neither an alteration in gastric intrinsic factor activity nor an impairment of the intrinsic factor-vitamin B(12) receptor in the intestine. It is suggested that in the partially pancreatectomized rats the intrinsic factor-vitamin B(12) complex exists in a form which is not available for absorption.

Animals↗
PubMed1980

Vitamin D metabolites in serum from hypoparathyroid patients treated with vitamin D2 and 1 alpha-hydroxyvitamin D3.

Vitamin D and its metabolites 25-hydroxyvitamin D (25OHD), 24,25-dihydroxyvitamin D [24,25-(OH)2D], 25,26-(OH)2D, and 1,25-(OH)2D were measured after separation on high pressure liquid chromatography in sera from two hypoparathyroid patients treated with high doses of vitamin D2. Fractions with displacement activities in the competitive protein-binding assays were found which were not detectable in sera from controls not supplemented with vitamin D2. These fractions, presumably representing vitamin D2 metabolites, were quantitated separately from the vitamin D3 metabolites. After a change of treatment from milligram doses of vitamin D2 to microgram doses of 1 alpha OHD3, the serum metabolites of vitamin D2 and vitamin D3 were followed from 8-13 months. During the first 2-3 months, there was an initial relatively rapid fall in serum vitamin D2 levels and metabolites, followed by a slower decline. High levels of vitamin D2 metabolites were still present after 13 months. Taking into account the marked preponderance of 25OHD2 to 25OHD3, the relative concentration of (OH)2D3 metabolites were higher than expected, which might indicate a preferential 25OHD3 hydroxylation or alternatively, a more rapid degradation of vitamin D2 metabolites in these patients. The high and sustained release of vitamin D2, presumably from fat stores, more than a year after vitamin D2 ingestion was stopped has obvious clinical implications and should be considered in the long term follow-up of patients shifted from the traditional high doses of vitamin D to the newly synthesized 1 alpha OHD3 or 1,25(OH)2D3.

Adult↗
PubMed1991

Interaction between dietary vitamin A and single oral doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the TCDD-induced toxicity and on the vitamin A status in the rat.

The effect of dietary vitamin A on the toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and the effect of TCDD on the tissue vitamin A levels in 8-week-old male Sprague-Dawley rats of variable vitamin A status, were investigated. Rats were fed purified casein based diets containing 2,000, 5,000, 8,000, or 21,000 IU of vitamin A/kg from weaning and throughout the experiment. The study was terminated 44 days after the administration of a single oral dose of 0, 15, 30, 60, or 120 micrograms TCDD/kg body wt. With this dietary regimen it was possible to obtain healthy animals of the same age with a vitamin A status that varied within a physiological range. LD50-values for TCDD could not be calculated in any dietary group due to the unexpectedly low mortality rate. The obtained data, however, suggest that low dietary intake of vitamin A impairs the ability to tolerate the lethal effect of TCDD and/or decreases the survival time. Some TCDD-related effects, i.e. body weight loss, liver enlargement and decreased testes weight, were more pronounced in the groups receiving low levels of dietary vitamin A, whereas the decrease in thymus weight was as severe in all dietary groups. Exposure to TCDD had a pronounced effect on tissue vitamin A contents. The effect differed between tissues and was dependent upon the dose of TCDD and on the vitamin A status of the animal. Generally, exposure to TCDD results in the reduction of vitamin A in most organs; very likely because the capacity for vitamin A storage is diminished. The kidney is an exception because it accumulates vitamin A in response either to TCDD itself or to the altered vitamin A status which TCDD induces. Data presented in this study are not sufficient to conclude if the observed changes of tissue vitamin A contents are sufficient to explain the spectrum of morphological changes, which is typical of TCDD exposure.

Animals↗
PubMed1992

Vitamin profiles of eggs as indicators of nutritional status in the laying hen: vitamin B12 study.

Hens of a type used for egg production were fed a corn and soybean meal diet supplemented with no vitamin B12 or with vitamin B12 levels to provide one, two, or four times the National Research Council (1984) breeding hen requirement of 4 micrograms/kg diet for 27 wk. All hens were placed on a recovery diet containing one and one-half times the requirement level of vitamin B12 from Weeks 27 through 30. Egg yolk vitamin B12 concentrations were determined frequently by radioisotope dilution analysis. Egg production records were kept continuously, and eggshell thickness, egg weight, hatchability of eggs, and hen body weights were measured at selected times. Although egg yolk vitamin B12 concentrations were high at the outset, they decreased markedly in 2 wk from hens fed the two lowest dietary levels. After 12 wk on the diets, egg concentrations of vitamin B12 stabilized and were proportional to the amount of vitamin added to the diet. Egg concentrations of vitamin B12 between 1.3 and 2.6 micrograms/100 g yolk appeared to be needed to support maximum hatchability and egg weight. Egg production was reduced after 12 wk on the diets in the hens fed the two lowest vitamin B12 levels. As vitamin B12 level increased, shell thickness decreased and egg weight, hen weight, and hatchability increased. Maximum egg production, egg weight, hen weight, and hatchability were obtained when the diet contained 8.0 micrograms/kg of vitamin B12. Egg yolk vitamin B12 concentrations respond rapidly to dietary changes in the level of this vitamin and are indicative of the vitamin B12 status of the hen.

Animals↗
PubMed1999

Relation of consumption of vitamin E, vitamin C, and carotenoids to risk for stroke among men in the United States.

BACKGROUND: Antioxidants increase the resistance of low-density lipoprotein to oxidation and may thereby reduce risk for atherosclerosis. OBJECTIVE: To determine whether intake of vitamin E, vitamin C, or carotenoids predict risk for total or ischemic stroke. DESIGN: Prospective observational study. SETTING: The Health Professionals Follow-up Study. PARTICIPANTS: 43,738 men 40 to 75 years of age who did not have cardiovascular disease or diabetes. MEASUREMENTS: Repeated and validated dietary assessments were done by using a self-administered 131-item food-frequency questionnaire, which included questions on dose and duration of vitamin supplement use. The follow-up period was 8 years. RESULTS: A total of 328 strokes occurred: 210 ischemic, 70 hemorrhagic, and 48 unclassified. After adjustment for age, smoking, hypertension, hypercholesterolemia, body mass index, physical activity, parental history of myocardial infarction, alcohol consumption, and total energy intake, the relative risk for ischemic stroke in the top quintile of vitamin E intake (median, 411 IU/d) compared with the bottom quintile (5.4 IU/d) was 1.18 (95% CI, 0.77 to 1.82). The relative risk for ischemic stroke in the top quintile of vitamin C intake (1167 mg/d) compared with the bottom quintile (95 mg/d) was 1.03 (CI, 0.66 to 1.59). Results for total stroke were similar. Associations of vitamin intake with hemorrhagic stroke were also nonsignificant, but the CIs were wide. Neither dose nor duration of vitamin E or vitamin C supplement use was related to risk for total or ischemic stroke. The relative risk for ischemic stroke was 1.16 (CI, 0.81 to 1.67) in men using 250 IU or more of vitamin E supplementation per day compared with men who used no vitamin E supplements and was 0.93 (CI, 0.60 to 1.45) in men using 700 mg or more of vitamin C supplementation per day compared with men who used no vitamin C supplements. A significant inverse relation between lutein intake and risk for ischemic stroke was seen but was not independent of other dietary factors. CONCLUSIONS: Vitamin E and vitamin C supplements and specific carotenoids did not seem to substantially reduce risk for stroke in this cohort. Modest effects, however, cannot be excluded.

Adult↗
PubMed1981

Synthesis and biological activity of vitamin D3 3 beta-sulfate. Role of vitamin D3 sulfates in calcium homeostasis.

To determine the biological activity of vitamin D sulfates, we synthesized vitamin D3 3 beta-sulfate and tested its biological activity in vitamin D-deficient hypocalcemic rats. When vitamin D3 sulfate was administered as a single oral dose of 208,000 or 416,000 pmol (100 micrograms or 200 micrograms), it increased active calcium transport in the duodenum and was also able to mobilize calcium from bone and soft tissue. Dose levels below this failed to elicit a response. Vitamin D3 itself was active at doses as low as 260 pmol when administered in this manner. In order to test the biological activity of vitamin D3 sulfate in various doses when administered chronically, we tested the biological activity of vitamin D3 sulfate after 5 days or oral dosing: vitamin D3 sulfate was active at doses of 52,000 pmol/day (25 microgram), whereas vitamin D3 was active at doses of 65 to 260 pmol/day over a period of 5 days. When administered as a single intravenous dose, vitamin D3 sulfate exhibited no biological activity in doses as high as 52,000 pmol. Vitamin D3, however, was active at a dose of as low as 65 pmol. We conclude that vitamin D3 sulfate, a metabolite of vitamin D3 of heretofore unknown biological activity, is considerably less active than vitamin d3 itself.

Animals↗
PubMed1997

[Vitamin A concentration in maternal milk: the effect of intake and serum levels of vitamin A during the third trimester of pregnancy].

BACKGROUND: Breast fed newborns depend on maternal milk for their supply of vitamin A. A deficiency of this vitamin is associated with increased morbidity and mortality. The present study investigates whether the nutritional status of the mother during pregnancy conditions vitamin A levels in maternal milk. SUBJECTS AND METHOD: 57 healthy, lactating mothers aged between 18 and 35 were studied. Vitamin A intake during the third trimester of pregnancy was recorded using a 5 day dietary record (including a Sunday) and by registering nutrients supplied by supplements. Vitamin A levels in maternal serum during this stage of pregnancy and in transition milk (days 13-14 of lactation) and mature milk (day 40 of lactation) were determined using high performance liquid chromatography. RESULTS: The effect of vitamin A intake during pregnancy on maternal milk composition was particularly noticeable in mothers with intakes below recommended values. These subjects showed lower vitamin A concentrations in transition (60.9 micrograms/dl) and mature milk (47.2 micrograms/dl) than those with adequate intakes of this vitamin (90.8 micrograms/dl and 79.2 micrograms/dl, respectively). Subjects with serum vitamin A concentrations below 30 micrograms/dl (22.8%) during the third trimester of pregnancy also showed lower levels of the vitamin in mature milk (50 micrograms/dl) compared with those with higher serum levels (74.8 micrograms/dl). CONCLUSIONS: Diet and the nutritional status of vitamin A during pregnancy seem to condition concentrations of this vitamin in maternal milk. This, in turn, will affect the intake of vitamin A by the newborn. Given that deficiencies were detected both in serum and in maternal milk, the monitorization of the vitamin A levels in pregnant women is recommendable and if necessary, would be improved.

Adult↗
PubMed2006

High frequency of maternal vitamin B12 deficiency as an important cause of infantile vitamin B12 deficiency in Sanliurfa province of Turkey.

BACKGROUND: Vitamin B12 deficiency in infancy may cause failure to thrive, severe neurological disorders and megaloblastic pancytopenia. It is well known that infants born with deficient vitamin B12 storage have increased the risk of vitamin B12 deficiency. Vitamin B12 deficiency is more prevalent in infancy in Sanliurfa province (at the southeast region of Turkey). AIM OF THE STUDY: The aim of this study was to determine the frequencies of vitamin B12, folic acid and iron deficiencies in pregnants and their babies at birth and to what extend the mothers' deficiency becomes effective on babies' deficiencies. METHODS: The study groups were constituted by 180 pregnant women and their single and term babies. Venous blood samples of pregnants were obtained 1-3 h before delivery and babies' cord bloods were collected at birth. Vitamin B12 and folic acid levels were measured with electro chemiluminiscence method; serum iron and iron binding capacities were measured by colorimetric method and complete blood counts were performed by automatic blood counter. RESULTS: Mean vitamin B12 levels in maternal and cord blood serum were 130 +/- 61.7 pg/ml and 207 +/- 141 pg/ml; mean folic acid levels were 8.91 +/- 6.46 ng/ml and 17.8 +/- 11.8 ng/ml; mean serum iron levels were 56.9 +/- 37.5 microg/dl and 147 +/- 43.2 microg/dl; and mean transferrin saturations were 11.8 +/- 8% and 65.6 +/- 24%, respectively. There were vitamin B12 deficiency (<160 pg/ml) in 72% of the mothers and 41% of the babies, and severe deficiency (<120 pg/ml) in 48% of the mothers and 23% of the babies. Folic acid deficiency was found in 12% of the mothers, but was not found in the babies. There were iron deficiency in 62% of the mothers and 1% of the babies. There were statistically significant correlation between maternal and cord blood serum vitamin B12 levels (r = 0.395, P < 0.001) and folic acid levels (r = 0.227, P = 0.017), while there were no correlation between maternal and cord blood iron levels and transferrin saturations. CONCLUSION: The study results showed that vitamin B12 deficiency is prevalent in pregnants in this region and that 41% of infants have born with deficient vitamin B12 storages. Therefore, prophylactic use of vitamin B12 by pregnant women in Sanliurfa and other poor communities could have considerable benefits to prevent vitamin B12 deficiency and its complications in infants.

Adult↗