Excessive Amounts Of Vitamin Research Articles

Deprescribing: What About Vitamins, Minerals, and Other Nutritional Supplements?

Deprescribing: What About Vitamins, Minerals, and Other Nutritional Supplements?

Assessing the Relationship between Individual Level Dietary Intake and the Occurrence of Preeclampsia/Eclampsia and Haemorrhage among Pregnant Women in Eastern Region of Ghana: A Prospective Cohort Study

Pre-eclampsia/eclampsia (PE-E) and haemorrhage are dangerous diseases that occur in pregnancy. This study seeks to assess the relationship between individual-level dietary intake and the occurrence of pre-eclampsia/eclampsia and haemorrhage among pregnant women in the Eastern Region of Ghana. The prospective cohort study involved all pregnant women in their third trimester of pregnancy (>28 weeks gestational age) reporting for antenatal care (ANC) in seven Hospitals in the Eastern Region of Ghana. The study used a 24-hour repeated dietary recall to elicit dietary intake information from pregnant women until delivery. The majority of pregnant women in this study had adequate consumption of phosphorus far above the RDI, coupled with an inadequate intake of calcium, excess intake of sodium, and manganese. The average dietary intake for carbohydrates in this study was rather higher than the RDA. There was a statistically significant association between PE-E and the intake of vitamin C. A statistically significant association exists between the intake of calcium and vitamin A and haemorrhage. The findings show that pregnant women who consumed adequate and excess amounts of vitamin C reduced their odds of developing PE-E by 41.7% and 39.8%, respectively. The results show that pregnant women who had an excess intake of calcium were 6.128 times the odds of developing haemorrhage compared to those who had inadequate intake. Again, pregnant women who had adequate intake of vitamin A were 4.351 times the odds of developing haemorrhage compared to those who had inadequate intake. It is recommended that more nutrition specialists to be trained and posted to counsel pregnant women on nutrition in pregnancy to avert the consequences of PE-E and haemorrhage.

Monitored Supplementation of Vitamin D in Preterm Infants: A Randomized Controlled Trial.

Appropriate supplementation of vitamin D can affect infections, allergy, and mental and behavioral development. This study aimed to assess the effectiveness of monitored vitamin D supplementation in a population of preterm infants. 109 preterm infants (24 0/7–32 6/7 weeks of gestation) were randomized to receive 500 IU vitamin D standard therapy (n = 55; approximately 800–1000 IU from combined sources) or monitored therapy (n = 54; with an option of dose modification). 25-hydroxyvitamin D [25(OH)D] concentrations were measured at birth, 4 weeks of age, and 35, 40, and 52 ± 2 weeks of post-conceptional age (PCA). Vitamin D supplementation was discontinued in 23% of infants subjected to standard treatment due to increased potentially toxic 25(OH)D concentrations (>90 ng/mL) at 40 weeks of PCA. A significantly higher infants’ percentage in the monitored group had safe vitamin D levels (20–80 ng/mL) at 52 weeks of PCA (p = 0.017). We observed increased vitamin D levels and abnormal ultrasound findings in five infants. Biochemical markers of vitamin D toxicity were observed in two patients at 52 weeks of PCA in the control group. Inadequate and excessive amounts of vitamin D can lead to serious health problems. Supplementation with 800–1000 IU of vitamin D prevents deficiency and should be monitored to avoid overdose.

Hypervitaminosis A: A Rare Cause of Hypercalcemia

Abstract Introduction: Hypercalcemia is a rather common clinical problem and a majority of cases are found to be secondary to primary hyperparathyroidism and malignancy. A rare cause of hypercalcemia is associated with high levels of vitamin A and thought to be secondary to the effect of vitamin A on bone to stimulate osteoclastic resorption or inhibit osteoblastic formation. Clinical Case: A 54 year-old male with a past medical history of CKD stage 3 secondary to medullary sponge kidney presented for hypercalcemia. He complained of chronic constipation, joint pain, mood changes and recurrent kidney stones. Reported multivitamin use (including 1000mcg of vitamin A) for years but was discontinued one year prior to visit. Lab work showed calcium of 11.5 mg/dL (8.7–10.2mg/dL), albumin 4.9 g/dL (3.8–4.9g/dL), elevated 24h urine calcium, eGFR 40 mL/min/1.73, parathyroid hormone 5 pg/mL (15-65pg/mL,) normal 1,25-OH vit D and 25-OH vit D, PTHrP <2.0 pmol/L, serum protein electrophoresis unremarkable. His vitamin A level was elevated to 103 ug/dL (20.1–62.0ug/dL). CT chest showed no findings concerning for sarcoidosis. Bone density scan showed normal bone mineral density. Patient diagnosed with hypercalcemia secondary to elevated vitamin A levels. Current limited literature shows stopping the vitamin A supplement will normalize vitamin A levels and correct the hypercalcemia. This patient had discontinued his multivitamin 1 year prior and vitamin A remained elevated, thought to be due to his poor kidney function. Treatment was targeted at improving his hypercalcemia and reducing his symptoms. He was prescribed a one-week course of prednisone 40 mg daily. His calcium level improved to 10.5 mg/dL. Prednisone was reduced to 20 mg daily with normalization of calcium to 10.3 mg/dL (8.7–10.2mg/dL). Conclusion: Hypercalcemia is a rare but known complication of vitamin D toxicity. The liver, kidney and adrenal glands store vitamin A and it is excreted in the urine. Liver and kidney disease pose higher risk of vitamin A toxicity. We present a unique case of Hypercalcemia secondary to elevated vitamin A levels in a patient with moderate chronic kidney disease who was not taking excessive amounts of vitamin A and whose calcium and vitamin A did not normalize once vitamin A supplements were discontinued. The CKD 3 may have reduced vitamin A clearance and increased its toxicity. Hypercalcemia is not the only concern regarding vitamin A toxicity, the increasing use of dietary supplements and over the counter medications may pose significant risks for osteoporosis and bone fractures. A high clinical suspicion and thorough workup to exclude other causes of hypercalcemia is warranted to diagnose hypervitaminosis A as the etiology. Steroids can reduce gastrointestinal absorption of calcium, however, its role in vitamin A toxicity remains unclear. Further research is needed to investigate the appropriate treatment for these patients.

Uptake of beta‐carotene by the maternal‐fetal barrier: influences of maternal vitamin A regimens and its mechanisms

Synthesis of vitamin A by cleavage of β‐carotene, its most abundant precursor in human diet, is regulated by nutrient availability in adult tissues. Intact β‐carotene is transported in association with various lipoprotein particles in circulation. Local de novo biosynthesis of retinoids from β‐carotene can be an important source of retinoids during embryonic development. Retinoids, especially transcriptionally active retinoic acid, are essential for normal embryonic development.This study examines effects of different maternal vitamin A regimens on uptake of supplemented β‐carotene by maternal‐fetal barrier. Wild‐type mice were maintained on diets containing sufficient, deficient and excess amounts of vitamin A during pregnancy. At 13.5 days of gestation, dams were supplemented with 10–30 μg/gbody weight of β‐carotene by intraperitonial injection. Maternal serum, liver, placenta, embryos were collected after 24 hours and analyzed by HPLC. Pregnant females injected with vehicle were controls.Well detectable β‐carotene levels were observed in maternal serum, liver, placenta and embryos in all supplemented mice. Serum and liver β‐carotene levels were unaltered under different vitamin A regimens. Embryonic β‐carotene levels were reduced when dams were maintained on vitamin A‐excess diet, but placental levels were not altered under any of the dietary regimens. This suggests a protective action of placenta that limits the transfer of β‐carotene from maternal circulation to embryo under vitamin A excess conditions. mRNA expressions of placental LDL receptor, SRBI (HDL receptor) were unchanged upon β‐carotene supplementation, however LRP1 (chylomicron remnants receptor) was dramatically downregulated upon β‐carotene supplementation, at least when dams were on vitamin A‐sufficient diet.Grant Funding Source : NIH

Inhibiting Effects of Hypervitaminosis A on Development of Fetal Rat Adrenal Glands1)

Administration of pregnant rats with excess amounts of vitamin A from the 8th to the 10th day of pregnancy induced destruction in fetal brain. On the last day of pregnancy, fetuses of treated mothers have smaller weight of adrenal glands as compared with intact fetuses. Maternal treatment with high amounts of vitamin A significantly reduced protein and nucleic acids levels and inhibited cell multiplication in fetal rat adrenal glands. Adrenal glands of fetuses from vitamin A treated mothers synthetized in vitro from 4-14C progesterone less amounts of radioactive 11-deoxycorticosterone, corticosterone, 18-hydroxy-11-deoxycorticosterone and aldosterone than adrenal glands of intact fetuses on the last day of intrauterine development. These results showed that maternal hypervitaminosis A depressed morphological and functional development of fetal rat adrenal glands on the last day of pregnancy.

Patients Previously Treated for Lymphoma Consume Inadequate or Excessive Amounts of Five Key Nutrients

Adequate amounts of nutrients such as folate, vitamin A, iron, selenium and calcium are essential for general health including prevention of cancer. Yet, excess amounts of vitamin A, folate, and iron may also promote cancer. This study sought to determine whether adults who had completed initial treatments for B-cell lymphoma from 1 to 3 years earlier were consuming recommended amounts of these key nutrients and their interests in nutritional education. We surveyed 141 patients undergoing follow-up in the Lymphoma/Myeloma Clinic at The University of Texas M. D. Anderson Cancer Center using a validated food frequency questionnaire and supplemental questionnaire regarding nutritional interest. Nutrient intakes were estimated based on national databases of average content in foods and compared with recommended guidelines. One hundred forty-one participants returned complete questionnaires, but errors limited some nutrient estimates to 134 participants. Participants' mean age was 50, 55% were male, and 80% were non-Hispanic whites. Most participants (94%) were consuming either inadequate or excessive amounts of one or more of these key nutrients. Half of the participants were interested in receiving nutritional education. These findings are of concern because of their potential impact upon recovery and maintenance of general health and possibly cancer-related pathways after treatment.

Hypervitaminosis A resulting in DNA aberration in fetal transgenic mice (Muta ™ Mouse)

Treatment with excessive amounts of Vitamin A during maternity induces fetal malformations. However, it is unclear whether these malformations are due to gene mutations or not. Using transgenic mice (containing lacZ gene showing β-galactosidase enzymatic activity), we planned to observe whether gene mutations occur in the fetal tissues after treatment during maternity with Vitamin A (retinol palmitate). On the 11th day of pregnancy, mothers were given 30 mg (group 2), 150 mg (group 3) and 300 mg (group 4) of Vitamin A/kg body weight orally. Fetuses obtained on the 18th day of gestation showed malformations, such as cleft palate, origodactyly, brachydactyly and ectromeria. Most notably, cleft palate occurred dose dependently. The incidental rates were 100% in group 4, 58% in group 3 and 6% in group 2. The number of dead and absorbed fetuses also increased dose dependently with the treatments. DNA (integrated vectors containing lacZ genes) extracted from each fetus showed Vitamin A-induced lacZ mutations, especially in the malformed fetuses. The mutation frequencies were 4.99 × 10 −5 in group 4, 5.28 × 10 −5 in group 3 and 4.26 × 10 −5 in group 2. The frequencies of group 3 were significantly higher ( p < 0.05) than that of the controls (group 1), 2.79 × 10 −5. Maternal treatment with Vitamin A (150 mg/kg of body weight) was carried out on the 11th day of pregnancy. Fetuses obtained on the 14th day of gestation showed a much higher incidence of mutation, approximately 8.91 × 10 −5 (group 6) that was significantly highter ( p < 0.0001) than those from the controls (group 5), 2.94 × 10 −5. The present study indicates a possibility that hypervitaminosis A-induced fetal malformation and death might be caused by gene mutations.

Hypercalcaemia in two dogs caused by excessive dietary supplementation of vitamin D

A three-year-old Border collie was presented with a two-week history of lethargy, stiff gait, polydipsia and polyuria. Biochemical analysis revealed hypercalcaemia. Serum concentrations of 25-hydroxyvitamin D (25[OH]D) and 1,25-dihydroxyvitamin D (1,25[OH]2D) were markedly elevated and parathyroid hormone was undetectable. Subsequent analysis of the dog's diet revealed that the food contained excessive amounts of vitamin D. The hypercalcaemia resolved following treatment with bisphosphonates and dietary change. Hypervitaminosis D was diagnosed in a second unrelated dog, which had been fed the same brand of dog food as case 1. The dog was also hypercalcaemic and had markedly elevated serum concentrations of 25(OH)D and 1,25(OH)2D. Hypervitaminosis D in dogs has been reported to occur secondarily to ingestion of either rodenticides containing cholecalciferol or antipsoriatic ointments that contain vitamin D analogues. Hypervitaminosis D has also been reported following the treatment of hypoparathyroidism. To the authors' knowledge, this is the first report of hypervitaminosis D in dogs following the accidental over supplementation of a commercial diet with vitamin D. While the benefits of adequate dietary vitamin D are well established in dogs, the potential deleterious effects of over supplementation of vitamin D should also be acknowledged.

Micronutrients, probiotics and the liver

Abstract The liver is the main gateway to the passage of nutrients from the gut to systemic sites. The organ is affected by the deficiencies of many vitamins and trace elements and excess amounts of vitamin A, iron, copper and zinc. Recent work has documented the beneficial role of probiotic organisms for many parts of the body including the liver. This knowledge is finding clinical and public health significance in the prevention and management of many human diseases.

Dietary Vitamin C and Vitamin E Interact to Influence Growth and Tissue Composition of Juvenile Hybrid Striped Bass (Morone chrysops ♀ × M. saxatilis ♂) but Have Limited Effects on Immune Responses

Juvenile hybrid striped bass (initially 12.0 g) were fed diets containing deficient, adequate or excessive amounts of vitamin C and/or vitamin E in a factorial arrangement to investigate potential nutritional interaction and effects on immune responses. Nine semipurified diets were supplemented with 0, 25 or 2500 mg vitamin C/kg and 0, 30 or 300 mg vitamin E/kg and fed to fish in triplicate aquaria for 10 wk. Weight gain, feed efficiency, mortality and tissue vitamin levels were significantly (P < or = 0.05) affected by dietary vitamin levels. In addition, a significant interaction between vitamin C and vitamin E was observed. At inclusion levels of 25 and 2500 mg/kg, dietary vitamin C improved feed efficiency and protected fish fed vitamin E-deficient diets from growth depression and mortality. At inclusion levels of 30 and 300 mg/kg, vitamin E prevented mortality in fish fed vitamin C-deficient diets; however, 300 mg vitamin E/kg was necessary to prevent growth depression in vitamin C-deficient fish but was unable to improve feed efficiency. Lysozyme, bacterial killing ability, as well as plasma protein and total immunoglobulin levels of fish were not affected by dietary vitamin levels, whereas respiratory burst activity increased with vitamin E supplementation. Thus, interactions between vitamin C and vitamin E were observed in hybrid striped bass. These interactions may be due to the ability of vitamin C to regenerate vitamin E to its functional form but also suggest an ability of vitamin E to spare vitamin C.

Effects of Simultaneous Treatment with Excess Amounts of Vitamin A and Goitrogens on Thyroid Tumorigenesis in Rats.

In order to investigate the effects of vitamin A (VA) supplementation on thyroid proliferative lesions associated with goitrogens other than thiourea, F344 rats were given VA in the diet at 0.1% and drinking water containing sulfadimethox-ine, propylthiouracil, potassium thiocyanate or phenobarbital for 19 weeks after initiation with N-bis (2-hydroxypropyl) nitrosamine. At the end of the treatment period, serum T3, T4, and TSH levels, T4-uridinedi phosphate glucuronosyltransferase (UDP-GT) activity in the liver, and thyroid weights were determined. In addition, thyroid proliferative lesions were histologically examined and evaluated for their PCNA labeling indices. Although serum T4 levels were lowered by VA in all goitrogen-treatment cases, serum levels of TSH, which is responsible for control of proliferation of thyroid follicular cells, were not elevated by the VA supplementation. There were also no enhancing effects of VA in terms of the other parameters, suggesting that the enhancement observed ealier with thiourea is a special case.

キャットフードに起因した猫のビタミンD過剰症

Vitamin D toxicosis caused by commercially available cat food was examined clinically and experimentally. Four patient cats which had been primarily fed on the same dry cat food were referred for evaluation to Iwate University Veterinary Hospital. The vitamin D content of the cat food was 5, 290 IU/100g. X-ray examinations in all cases revealed mineral depositions of various sizes in the lung, trachea, stomach and small intestine. Plasma Ca concentration was more than 11 mg/dl in all cases except case 1 and plasma 25 (OH) D concentration was more than 100 ng/ml in all cases. Subsequently, plasma concentrations of Ca and 25 (OH) D in Case 1 increased to 16.0 mg/dl and 311.9 ng/ml, respectively. Cases 1 and 2 developed uremia and the other cases showed a moderate increase in plasma concentrations of BUN and creatinine. Histopathologically, systemic calcification was observed in the soft tissues of Cases 1 and 2. Four healthy cats were experimentally fed on the same commercially available cat food to determine the changes in plasma concentrations of vitamin D metabolites and minerals. The concentrations of Ca and 25 (OH) D had increased by 40 days later. These findings suggest that all patient cats may have developed vitamin D toxicosis due to eating cat food containing excessive amounts of vitamin D.

Antioxidant role of cellular reduced coenzyme Q homologs and α-tocopherol in free radical-induced injury of hepatocytes isolated from rats fed diets with different vitamin E contents

Reduced coenzyme Q 9 (CoQ 9H 2) and reduced coenzyme Q 10 (CoQ 10H 2) as well as α-tocopherol (α-Toc) are known to be potent lipid-soluble antioxidants in mammalian tissues. Reduced coenzyme Q homolog (CoQ n H 2) appears to show antioxidant activity independent of that of α-Toc (Matsura, T., Yamada, K. and Kawasaki, T. (1992) Biochim. Biophys. Acta 1123, 309–315). To further confirm this, we have studied the antioxidant role of cellular CoQ n H 2 and α-Toc using hepatocytes isolated from rats fed diets containing deficient, sufficient, and excess amounts of vitamin E(VE). Cellular damage was induced with a hydrophilic radical initiator. 2,2′-azobis(2-amidinopropane) dihydrochloride (AAPH). The concentration of α-Toc in VE-deficient hepatocytes was approximately 1/12 that in VE-sufficient hepatocytes, whereas the concentration of α-Toc in VE-excess hepatocytes was approximately 7-fold that in VE-sufficient hepatocytes. The molar ratios of α-Toc to CoQ n H 2 (CoQ 9H 2 plus CoQ 10H 2) in VE-deficient, sufficient and excess cells were 0.03, 0.33 and 2, respectively. In the hepatocytes in these three dietary groups, α-Toc status had little effect on the concentration of CoQ homologs. These hepatocytes were incubated with 50 mM AAPH for 4 h. The cell viability in all groups of hepatocytes decreased rapidly after 3 h of AAPH treatment, and was associated with the increase of lipid peroxides. The loss of cell viability and the increase of lipid peroxidation in VE-deficient cells were more pronounced than those in the hepatocytes of the other two groups. The endogenous CoQ 9H 2 content of each group of hepatocytes decreased linearly with a reciprocal increase in oxidized CoQ 9 after addition of AAPH, whereas the decrease of endogenous CoQ 10H 2 in each group during AAPH treatment was much less than that of endogenous CoQ 9H 2. α-Toc in the three VE dietary groups of hepatocytes was also consumed without a time lag addition of AAPH, and it was not spared by CoQ n H 2, even VE-deficient cells where the CoQ n H 2 concentration was 38-fold that of α-Toc. These results indicate that CoQ n H 2, especially CoQ 9H 2, is a lipid-soluble antioxidant, which is as effective as α-Toc in rat hepatocytes under the conditions employed in this study, and acts independently of α-Toc to inhibit lipid peroxidation.

Hyperechoic renal medullary pyramids in infants and children.

Fifty-five children (34 boys, 21 girls; age range, 1 day to 18 years) with increased echogenicity of the renal medullary pyramids at ultrasound evaluation were identified. The clinical diagnoses associated with hyperechoic medullary pyramids could be separated based on the presence or absence of hypercalciuria. Patients with drug-induced hypercalciuria included 10 infants treated with furosemide, two treated with long-term steroid therapy, and one treated with excessive amounts of vitamin D. Other clinical conditions associated with hypercalciuria included renal tubular acidosis (n = 10), Bartter syndrome (n = 5), hyperparathyroidism (n = 3), Williams syndrome (n = 2) and medullary sponge kidney (n = 2). Ten children with transient renal insufficiency and three with sickle cell disease had normal urine calcium concentration. Isolated disease entities accounted for the remainder of cases. A specific diagnosis can usually be made in a patient with hyperechoic renal medullary pyramids by using a systematic clinical approach that includes evaluation of patient age, serum and urine calcium concentration, and renal function.

Serum factors which alter cell membranes.

Mammalian cell membranes are much more sensitive to changes in serum ion concentrations than they are to serum cholesterol. Because of this, arterial cells function normally only in a very narrow range of serum ion concentrations. Unfortunately, new introductions into the food supply have been made in the diet since 1920 which may perturb the delicate relationships between arterial cell membranes and the blood serum to which they are exposed. For example, powerful surface active agents are used to emulsify fats in a host of popular food items. None of them have been adequately tested for their possible role in changing phospholipid head group composition of arterial or myocardial cell membranes. Ocean salt has been replaced by refined table salt removing a rich source of magnesium from the diet of Northern Europeans and Americans. Excessive amounts of Vitamin D, which may calcify soft tissue, have been added to the diet as a means of preventing a disease that does not develop in babies exposed to sunshine. The introduction of hydrogenated vegetable oil to the diet has helped to stimulate per capita fat consumption to almost twice the level of 1920. How the introduction of such technology has changed arterial cell membrane structure or function has not been considered. It is now possible to consider the influence of this technology on the food supply by the application of modern genetic engineering methods. The application of this type of methodology in the study of cholesterol metabolism and its role in atherosclerosis may help to find means of preventing heart disease and strokes.

Effect of supplements on the nutrient intake of children

Daily intakes of nutrients were calculated from records of food eaten at home, as school lunches, and morning milk, of boys and girls in second and sixth grades. Vitamin/mineral supplementations were also calculated. Comparisons were made (with and without supplementation) with the Recommended Dietary Allowances (RDAs). Analyses of variance between sexes and between grade levels showed second graders consumed better diets than sixth and boys better diets than girls. Although many received supplements, intakes of several nutrients were below the 67 per cent level. The milk program played a significant role in calcium consumption. Excessive amounts of vitamin A and ascorbic acid were consumed by some children.

Gas-liquid chromatographic determination of vitamin D in multivitamin preparations containing excess amounts of vitamin E.

Gas-liquid chromatographic (GLC) determination of vitamin D in multivitamin preparations containing excess amounts of vitamin E (a more than 2,500 weight ratio of dl-alpha-tocopheryl acetate to vitamin D) was investigated and a simplified routine method was established because the method reported previously (1) could not be applied to such special preparations. After applying the unsaponifiable matters of a sample to a phosphate-treated alumina column chromatography prepared according to MULDER et. al. (2), the eluate was evaporated and the residue was subjected to thin-layer chromatography (TLC) and GLC. When this method was applied to model preparations made by mixing vitamin D2 and dl-alpha-tocopheryl acetate (excess amounts), good results were obtained. Since the results on a commercial multivitamin preparation containing excess amounts of vitamin E were also satisfactory, it was confirmed that the proposed method could be used for simplified routine determinations.

"Uncomplicated" Hyperbilirubinemia of Prematurity

The role that bilirubin plays in brain damage associated with prematurity has not been completely defined. The hazards in these infants of hyperbilirubinemia in association with isoimmunization and excessive amounts of vitamin K analogue,1are well known; it has also been shown that when sulfisoxazole2is given to jaundiced premature infants, a significant proportion die with kernicterus. However, the magnitude of the risk of hyperbilirubinemia in the absence of these known complicating factors has not been established. Meyer3and Crosse et al.4stated that hyperbilirubinemia is harmful to the newborn premature infant, and suggested that 18 mg/100 ml be considered the concentration of bilirubin in the blood, above which brain damage is likely to occur. Corner,5Dundon,6and Newns et al.7agreed in principle but believed that the critical concentration is higher. Another group8found a correlation between increasing concentrations of