Dietary biotin intake modulates the pool of free and protein-bound biotin in rat liver

The current studies were undertaken to analyze the relationships among dietary biotin intake, hepatic free biotin and hepatic protein-bound biotin in rats. The biotin status of rats was manipulated through dietary intervention to model moderate biotin deficiency, adequacy, supplementation and pharmacologic biotin supplementation (0, 0.06, 0.6 and 100 mg/kg, respectively). Urinary biotin excretion was directly related to biotin intake, but no difference between biotin-adequate and biotin-supplemented rats was detected. In contrast, plasma biotin was directly and significantly regulated by biotin intake at every intake level. A hepatic free biotin pool was directly demonstrated in these studies, and like plasma, its size was directly related to dietary biotin intake. The relationship between dietary biotin intake and protein-bound biotin was also analyzed. Moderate biotin deficiency markedly decreased the abundance of each biotinylated polypeptide in rat liver. Biotin supplementation did not significantly elevate the abundance of biotinylated pyruvate, propionyl CoA, methylcrotonyl CoA or acetyl CoA carboxylase 1. The abundance of biotinylated acetyl CoA carboxylase 2, however, was significantly higher in biotin-supplemented rats. Pharmacologic biotin intake significantly reduced the abundance of biotinylated propionyl CoA and methylcrotonyl CoA carboxylase. These results indicate the following: 1) moderate biotin deficiency reduces free and protein bound biotin; 2) biotin intakes in rats that mimic the currently recommended daily value (DV) do not result in full protein biotinylation; and 3) pharmacologic supplementation may reduce the abundance of functional carboxylases.     

Excretion of organic acids associated with biotin deficiency in chronic anticonvulsant therapy

Urinary organic acids, known to be elevated in children with biotin deficiency, were determined in 7 epileptics under long-term therapy with anticonvulsants and in three controls. Four patients administered phenytoin, primidone, phenobarbital, or carbamazepine, alone or in combination, had reduced plasma biotin levels (less than 250 ng/l) and an elevated excretion of certain organic acids indicating a possibly decreased activity of propionyl CoA carboxylase (3-OH-propionate, methylcitrate) and 3-methylcrotonyl CoA carboxylase (3-methylcrotonate and the glycine conjugate, 3-OH-isovalerate). Two epileptics receiving sodium valproate alone had normal circulating biotin levels and no changes in level of the investigated urinary acids were found. These findings indicate that the reduced biotin levels seen in epileptics receiving other anticonvulsants than sodium valproate lead to an elevated excretion of certain organic acids in urine.     

Lymphocyte propionyl-CoA carboxylase and its activation by biotin are sensitive indicators of marginal biotin deficiency in humans

BACKGROUND: Marginal biotin deficiency may be a human teratogen. A biotin status indicator that is not dependent on renal function may be useful in studies of biotin status during pregnancy. A previous study of experimental biotin deficiency suggested that propionyl-coenzyme A carboxylase (PCC) activity in peripheral blood lymphocytes (PBLs) is a sensitive indicator of biotin status. OBJECTIVE: We examined the utility of measuring PCC activity and the activation of PCC by biotin in detecting marginal biotin deficiency. DESIGN: Marginal biotin deficiency was induced in 7 adults (3 women) by egg-white feeding for 28 d. Blood and urine were obtained on days 0, 14, and 28 (depletion phase) and 44 and 65 (repletion phase). PBLs were incubated with (activated) or without (control) biotin before PCC assay. The activation coefficient of PCC is the ratio of PCC activity in activated PBLs to that in control PBLs. The significance of differences for all measurements was tested by repeated-measures analysis of variance with Fisher's post hoc test and Bonferroni correction. RESULTS: Changes in the urinary excretion of biotin and of 3-hydroxyisovaleric acid confirmed that marginal biotin deficiency was successfully induced. By day 14, PCC activity had decreased (P < 0.0001) to below the lower limit of normal in all subjects. By day 28, the activation coefficient of PCC had increased significantly (P = 0.003) and was above the upper limit of normal in 6 of 7 subjects. CONCLUSION: PCC activity is the most sensitive indicator of biotin status tested to date. In future pregnancy studies, the use of lymphocyte PCC activity data should prove valuable in the assessment of biotin status.     

The abundance and function of biotin-dependent enzymes are reduced in rats chronically administered carbamazepine

The effect of dietary antiepileptic drug administration on the metabolism and function of the water-soluble vitamin biotin was analyzed in a physiologically relevant rat model of biotin nutriture. Administration of carbamazepine (CBZ) in semipurified rat diet at 1.5 and 2.9 g/kg for 19 d did not reduce growth rate or food intake. After this dietary treatment, brain lactic acid and ammonia concentrations were significantly elevated, but no changes in these metabolites occurred in the liver. Urinary biotin excretion was altered and the concentrations of biotin sulfoxides and biocytin in the serum were elevated. Brain biotin was unaffected, but concentrations of bisnorbiotin and biocytin were significantly reduced by dietary administration of CBZ. The relative abundance of hepatic acetyl CoA carboxylase 1 and 2, pyruvate carboxylase (PC), methylcrotonyl CoA carboxylase and propionyl CoA carboxylase was significantly reduced by CBZ, whereas the relative abundance of biotinylated PC was significantly reduced in the brain. In agreement with the carboxylase abundance data, the activity of hepatic PC was significantly reduced in rats consuming CBZ-containing diets. These data demonstrate that administration of the antiepileptic medication CBZ, even with food, reduces the abundance and function of biotin-dependent enzymes in the liver and brain, partially accounting for the metabolic alterations, including organic acidemia, that are observed clinically.     

Biotin deficiency blocks thymocyte maturation, accelerates thymus involution, and decreases nose-rump length in mice

Biotin deficiency in experimental animals causes low body weight as well as several phenomena suggestive of an altered immune system. We reported previously that chronic biotin deficiency in mice decreases body weight and alters the number and proportion of lymphocyte subpopulations in the spleen. To further characterize the effects of biotin deficiency, we studied in detail the maturation of thymocytes and the status of biotin in the thymus, as well as the body length of biotin-deficient mice. Male Balb/cAnN mice were fed for up to 20 wk either standard control diet, a biotin-deficient diet, or a biotin-sufficient diet. At different times, nose-rump length, weight of the thymus, spleen and liver, total number of cells in the spleen and thymus, pyruvate carboxylase (PC) and propionyl CoA carboxylase (PCC) activity in thymus cells, and the proportion of distinct thymocyte subsets were determined. These variables did not differ between mice fed the control and biotin-sufficient diets. In contrast, biotin-deficient mice differed from biotin-sufficient mice in all of the analyzed variables. PC and PCC specific activities of thymocytes of mice fed the biotin-depleting diet decreased during the first 4 wk by 84.5%. The maturation of thymocytes in biotin-deficient mice was arrested at the double-negative stage. Our results suggest that biotin deficiency in mice causes an accelerated involution of the thymus and decreases nose-rump length, but these effects do not correlate in magnitude or in temporality with the sharp decrease in the activity of the biotin-dependent carboxylases. As such, the possibility that the aforementioned effects are not related directly to the prosthetic function of biotin should be considered.     

Effects of biotin on pyruvate carboxylase, acetyl-CoA carboxylase, propionyl-CoA carboxylase, and markers for glucose and lipid homeostasis in type 2 diabetic patients and nondiabetic subjects

BACKGROUND: Several studies have shown that biotin affects glucose homeostasis. Serum biotin concentrations are lower in subjects with type 2 diabetes than in control subjects. Lymphocyte propionyl-CoA carboxylase (PCC; EC 6.4.1.3) activity has proved to be a sensitive indicator of biotin status that is more accurate than is serum biotin concentration. OBJECTIVE: We studied the activity of PCC, pyruvate carboxylase (PC; EC 6.4.1.1), and acetyl-CoA carboxylase (ACC; EC 6.4.1.2) in type 2 diabetic and nondiabetic subjects. The effect of biotin administration (6.14 micro mol/d) on the activity of these enzymes and on several plasma metabolites was also studied. DESIGN: We compared the activities of carboxylases in circulating lymphocytes from patients with type 2 diabetes (n = 24) with those in circulating lymphocytes from nondiabetic subjects (n = 30). We also assessed the effect of biotin administration for 14 and 28 d on the activity of these enzymes and on the concentrations of several metabolites (type 2 diabetic patients, n = 10; nondiabetic subjects, n = 7). RESULTS: No significant differences in lymphocyte carboxylase activities were found between the type 2 diabetic patients and the nondiabetic subjects. Biotin administration increased the activity of PCC, PC, and ACC in all the subjects. No significant change in glucose, insulin, triacylglycerol, cholesterol, or lactate concentration was observed with the treatment in either the diabetic or the nondiabetic subjects. CONCLUSIONS: The activity of carboxylases does not differ significantly between type 2 diabetic and nondiabetic subjects. Pharmacologic doses of biotin increase lymphocyte PCC, PC, and ACC activities.     

Vitamin status during total parenteral nutrition

Plasma concentrations of vitamins A and E, serum and erythrocyte folic acid, serum B12 and erythrocyte enzyme activations (to assess vitamins B1, B2 and B6 status) were measured at the start and finish of 39 courses of total parenteral nutrition (TPN). The daily regimen was standard. Plasma vitamin A, E, and folate concentrations and vitamin B6 status improved significantly during TPN. Three patients developed low levels of vitamin A and two patients developed high transketolase activations (B1 depletion) during therapy. The adequacy of vitamin replacement and the monitoring of vitamin status during TPN is discussed.     

Marginal biotin deficiency is teratogenic in ICR mice

The incidence of marginal biotin deficiency in normal human gestation is approximately one in three. In ICR mice, maternal biotin deficiency results in cleft palate, micrognathia, microglossia and limb hypoplasia. However, the relationships among the severity of maternal biotin deficiency, fetal biotin status and malformations have not been reported. This study utilized validated indices of biotin status to investigate the relationships among maternal biotin status, fetal biotin status and the rate of fetal malformations in ICR mice. Biotin status was controlled by feeding diets with varying egg white concentration. In dams and fetuses, biotin status was assessed by hepatic biotin content and hepatic activity of the biotin-dependent enzyme propionyl-CoA carboxylase; in dams, status was also assessed by urinary excretion of biotin and 3-hydroxyisovaleric acid. Malformations were assessed morphologically. Biotin was measured by HPLC/avidin-binding assay. Propionyl-CoA carboxylase (PCC) activity was determined by H(14)CO(3) incorporation. 3-Hydroxyisovaleric acid concentration was determined by GC/MS. Although no overt signs of deficiency appeared, metabolic disturbances caused by biotin deficiency were detectable in dams and fetuses. These disturbances increased with increasing egg white. Fetal biotin status correlated significantly with maternal biotin status (fetal vs. dam hepatic biotin, r = 0.671; fetal vs. dam PCC activity, r = 0.70). The incidences of malformations were strikingly dependent on egg white concentration. We conclude that in ICR mice, marginal maternal biotin deficiency causes fetal biotin deficiency. We speculate that the fetal malformations are primarily the consequence of fetal biotin deficiency. Because murine malformations appeared at degrees of biotin deficiency that are similar to those in human gestation, we speculate that some human fetal malformations may be caused by biotin deficiency.     

Plasma and red blood cell vitamin E status of patients on total parenteral nutrition

Plasma and red blood cell (RBC) tocopherol isomer (alpha, beta, delta, and gamma) concentrations were measured prior to, and following total parenteral nutrition (TPN), with Intralipid. Before feeding, nine of 13 patients had plasma total tocopherol levels less than 0.6 mg/dl (normal range 0.63-1.24 mg/dl) and 10 of 13 had total RBC tocopherol levels less than 0.2 mg/dl (normal range (0.20-0.39 mg/dl). Following 7 days TPN plasma vitamin E status increased significantly (p less than 0.001). However, this was due mostly to increases in the circulating level of beta + gamma-tocopherols. RBC vitamin E status was also significantly increased (p less than 0.001) following TPN, however, this was again due to incorporation of non-alpha-tocopherols. In a second study a alpha-tocopherol supplement, Vitlipid N, (9.1 mg alpha-tocopherol/day) was included in the feed. In these patients, large increases in plasma concentrations of non-alpha-tocopherol isomers were accompanied by an apparent improvement in alpha-tocopherol status (0.64 vs 0.44 mg/dl after 7 days). However, RBC alpha-tocopherol concentration did not change appreciably in these patients following either 7 or 14 days feeding. It is concluded that RBC vitamin E status is markedly influenced by the available plasma tocopherol pool and that provision of a small supplement of alpha-tocopherol is not sufficient to compete with the high concentration of non-alpha-isomers present in Intralipid. TPN utilizing fat emulsions containing high levels of non-alpha-tocopherol isomers (even when accompanied by alpha-tocopherol supplements) does not improve alpha-tocopherol status.     

Plasma vitamin levels in patients on prolonged total parenteral nutrition

Vitamins are essential in total parenteral nutrition (TPN), their importance being highlighted by repeated past documentation of various vitamin deficiencies particularly in patients on long-term parenteral nutrition therapy. This study evaluated the efficacy of water- (Soluvit) and fat-soluble (Vitalipid) vitamin supplementation in patients receiving total parenteral nutrition using the three in one 3-liter bag system. All patients received water-soluble vitamin supplements daily. Fat-soluble vitamin supplements were administered on a daily or twice weekly basis. Twenty-two patients were studied. In seven of the 22 patients vitamin status was assessed on more than one occasion during TPN support, thus bringing the total number of observations to 30. The mean duration of TPN support was 35 days. Eight of the observations were made during less than 10 days, three between 11-19 days, 15 between 20-60 days, and four during more than 60 days of TPN support. Biochemical deficiency as judged by subnormal enzyme activity or vitamin levels were present in 10% of the patients for thiamin, 3% for riboflavin, and 6% for nicotinic acid. By contrast 83% of the patients had low plasma vitamin C and B6 levels. Low plasma vitamin A and E levels were also present in 43 and 40% of the patients, respectively. According to the plasma concentrations of the vitamins studied it would appear that the commercial vitamin preparations used in this study are inadequate in maintaining optimal vitamin status.(ABSTRACT TRUNCATED AT 250 WORDS)     

Visual function in patients undergoing long-term total parenteral nutrition

To evaluate the effects of long-term total parenteral nutrition (TPN) on eye function, 27 adults and 12 children in the UCLA Home TPN Clinic underwent ophthalmoscopic examination and visual-function testing. Direct inspection of the fundus showed a marked granularity of the retinal pigmented epithelium in some patients. About one-half of the children and one-third of the adults tested had at least one and usually two abnormalities in their electroretinogram. Determination of blood nutrients thought to affect vision revealed that zinc and vitamin E were within normal range. Vitamin A concentrations were above normal in 10 of 19 adults and selenium concentrations were below normal in 10 of 10 children and 17 of 21 adults tested. Linoleic and linolenic acid concentrations were low; plasma, platelet, and urine taurine concentrations were significantly lower than normal. Despite these diffuse nutrient abnormalities, only zinc and vitamin E concentrations correlated significantly with any index of visual function.     

Zinc status and vitamin A transport in cystic fibrosis

Zinc status and the retinol transport system were examined in 18 retinol supplemented cystic fibrosis (CF) patients and 40 age-matched controls. Plasma vitamin A was significantly lower in the CF group as compared to the controls and correlated positively with plasma retinol-binding protein (RBP) in both the CF and control groups. Plasma zinc of the CF group was not significantly lower than controls whereas hair zinc was. Plasma zinc was positively correlated with plasma RBP, vitamin A, and albumin in the CF group but not in the controls. Plasma concentrations of vitamin A, RBP, albumin, and zinc decreased with age in the CF group but not in the controls. The data support previous suggestions that low plasma vitamin A levels in CF are due to defects in the retinol transport system. The zinc status of the CF groups as a whole was judged to be low-normal however a subgroup of CF patients were in the marginal to deficient category. This subgroup also had lower levels of plasma vitamin A and RBP. The data suggest that zinc may be a contributing factor in the low plasma vitamin A/RBP levels of CF patients with marginal or deficient zinc status.     

The effect of total enteral tube feeding on the vitamin status of malnourished patients with inflammatory bowel disease

Eight malnourished patients (5 men and 3 women, mean age 26.5 +/- 0.4 years) suffering from Inflammatory Bowel Disease were prospectively included at admission to study the effect on protein-energy and vitamin status of a specially designed enterally tube fed formula diet. Eighty nine healthy individuals (36 men and 53 women, mean age 34 +/- 2 years) were used as controls. All but one patient were on steroids. The mean caloric supply was 58.2 +/- 2.4 kcal/kg/day with a mean nitrogen content of 0.37 +/- 0.02 gN/kg/day. The mean Total Enteral Nutrition period lasted 20.8 +/- 2.3 days (range 12 to 28 days). Fat- and water-soluble vitamins were studied at admission and after the nutritional period. Likewise both the protein-energy nutritional status and the activity of the disease were evaluated. At admission, plasma levels of folate, biotin, beta-carotene and vitamins A, C and E were significantly lower in patients than in controls. Tocopherol/cholesterol ratio, and vitamin B1, B2, B6, and B12 status were normal. At the end, plasma values of folate, biotin and vitamin C remained unchanged. However, the protein-energy nutritional status and the activity of the disease significantly improved. At admission, 4 out of 8 patients were at risk of developing hypovitaminosis for vitamins A, C, biotin, beta-carotene, and folate. At the end, a similar percentage remained at risk for these vitamins except for vitamin A. The content of some vitamins in the best designed formula diets does not meet the needs for patients with Inflammatory Bowel Disease.     

Plasma vitamin and mineral status in home parenteral nutrition patients

Home parenteral nutrition (HPN) provides long-term nutritional support for persons whose absorptive capacity is compromised by a variety of intestinal malabsorption problems. However, the presence of vitamin and mineral deficiency syndromes that normally would not have time to develop in the hospitalized patient receiving total parenteral nutrition has been reported in patients receiving HPN. This study entails a longitudinal survey of plasma concentrations of vitamins A, E, and 1,25-dihydroxyvitamin D, as well as the minerals zinc, copper, and selenium, in patients receiving HPN. Plasma samples from eight patients who had been on HPN for 1-92 months before the study began were obtained once a month over a 12-month period. The blood was drawn immediately before their evening infusion of TPN in order to approximate fasting plasma nutrient concentrations. Patient values were compared to fasting control values and to published norms. Values for vitamin A, 1,25-dihydroxyvitamin D, and zinc all were within the normal range, and there was no evidence of metabolic bone disease. Plasma vitamin E and copper concentrations exceeded the normal range for most of the 12-month period. Of all of the nutrients studied, only plasma selenium concentrations were consistently in the low-normal to below-normal range. Selenium levels in patients on HPN should be monitored regularly, and supplementation may be necessary if clinical conditions warrant.     

The effects of acute infection on indices of zinc status

Various indices of zinc status were assessed in 12 patients with acute urinary tract or chest infections on Day 1 and Day 7 of the infection. Leucocyte counts were raised on Day 1 but had returned to near normal by Day 7. Plasma zinc was decreased on Day 1 in conjunction with depressed plasma albumin concentrations (r = 0.71, p < 0.001) but both had returned to normal by Day 7. Mononuclear cell zinc was raised in all patients on Day 1 compared to Day 7 and control values, but polymorphonuclear cell zinc remained unchanged. However, polymorphonuclear cell alkaline phosphatase activity was grossly increased on Day 1 and correlated with leucocyte count (r = 0.61, p < 0.01). Plasma alkaline phosphatase activity was variable. These results indicate that in patients with infections measurement of plasma mononuclear cell zinc concentration and alkaline phosphatase activity are misleading indicators of zinc status. Polymorphonuclear cell zinc is unaffected by leucocytosis, inflammation and stress and may therefore provide a more reliable index of zinc status in such patients.     

Problems of trace elements and vitamins during long-term total parenteral nutrition: a case report of idiopathic intestinal pseudo-obstruction

An 8-year-old girl with chronic idiopathic intestinal pseudo-obstruction (CIIP), who is the first case of CIIP in Japan, has been receiving total parenteral nutrition (TPN) for more than 6 years. During this time, she experienced deficiencies of copper, zinc, vitamin A, vitamin B12, folic acid, and biotin, and an excess of vitamin A; she exhibited a series of signs and symptoms due to these deficiencies and vitamin A overdosage. Nevertheless, careful monitoring of serum levels of trace elements and vitamins and appropriate therapy have almost solved these problems. She has achieved normal physical and mental development and goes to school, while receiving home parenteral nutrition with an ambulatory infusion system.     

Home parenteral nutrition in children: bioavailability of vitamins in binary mixtures stored for 8 days

Vitamin supply in children on long-term parenteral nutrition depends on the specific age-related needs and on the bioavailability of vitamins when introduced into nutritional bags. The present study aimed to investigate the vitamin status in children on home TPN receiving nutritional bags which had been stored during a prolonged period of 8 instead of 4 days and where the new vitamin preparation Cernevit has been introduced. 19 children aged from 5 months to 11 years receiving home parenteral nutrition, for 42 months on average, were studied. Daily vitamin supply for children above 2 years of age was: A 1050 ug, D 5.5 ug, E 10.2 mg plus 0.6 mg/g lipid (Intralipid), C 125 mg, B1 3.5 mg, B2 4.1 mg, B6 4.5 mg, biotine 69 mug; children who were younger than 2 years received half of these intakes. Water soluble vitamin status was only measured in children over 3 years old. Plasma levels remained stable and adequate for age, for most of the studied vitamins. Vitamin A concentration was inferior to 200 mug/l in 1 patient with hepatopathy. Plasma concentrations of vitamin E, which were initially below 6 mg/l in 4 patients, returned to normal during the study. Plasma levels of vitamin C were below 6.2 mg/l in several infants either temporarily (5 patients) or during the whole study period (2 patients). These results support a prolongation of the intervals between preparing batches of nutritional bags and also between deliveries. This results in a considerable reduction of costs, provided that plasma vitamin levels, specially vitamin C, are regularly monitored.     

Choline and vitamin B12 deficiencies are interrelated in folate-replete long-term total parenteral nutrition patients

BACKGROUND: Choline has recently been recognized as an essential nutrient, in part based on deficiency data in long-term home total parenteral nutrition (TPN) patients. Choline, a methyl donor in the metabolism of homocysteine, is intricately related to folate status, but little is known about choline and vitamin B12 status. Long-term TPN patients are also subject to vitamin B12 deficiency. OBJECTIVE: The objective of the study was to evaluate any interaction between choline, vitamin B12, and folate in patients with severe malabsorption syndromes, requiring long-term TPN. DESIGN: Plasma free choline, serum and red blood cell (RBC) folate, serum vitamin B12 methylmalonic acid, B6, and plasma total homocysteine concentrations were assayed by standard methods. Low choline was defined as values that fall 1 to < or =3 and marked low choline concentration as >3 SD below the control mean. RESULTS: Both low choline concentrations (52% were marked low, 33% low, 14% normal) and elevated methylmalonic acid concentrations (47%) were prevalent. Choline concentration was significantly lower and RBC folate higher in patients with elevated methylmalonic acid. Total homocysteine elevations were rare (3 of 21) and mild. CONCLUSIONS: These data suggest a strong interaction between vitamin B12 and choline deficiencies and folate status in this population, which may be due in part to variations in vitamin and choline delivery by TPN. Folate adequacy may increase B12 use for homocysteine metabolism, thus limiting B12 availability for methylmaIonic acid metabolism. Choline use may also increase, and choline deficiency may worsen if choline substitutes when the vitamin B12 side of the homocysteine metabolic pathway cannot be used.     

Blood levels of water-soluble vitamins in pediatric patients on total parenteral nutrition using a multiple vitamin preparation

Although guidelines for the parenteral use of vitamin preparations in pediatric patients have been published, there are very limited data on the efficiency of these preparations and on the exact needs of infants and children on total parenteral nutrition (TPN). We report here an open, prospective, study of the blood levels of water-soluble vitamins in infants and children on TPN before and during supplementation with a new water-soluble multivitamin formula containing per vial unit: B1, 3 mg; B2, 3.6 mg; B6, 4 mg; niacin, 40 mg; pantothenate, 15 mg; ascorbate, 100 mg; biotin, 60 micrograms; folic acid, 400 micrograms; B12, 5 micrograms. Thirteen children, 9 months to 15 yr old, on home TPN for 1.5 months to 7 yr, and 17 hospitalized infants and children, 1 week to 15 yr old, receiving TPN were studied for 2 weeks to 4 months. Daily doses were given according to age: 1/2 vial if less than 18 months; 1 vial if greater than 18 months and less than 10 years; 1.5 vials if greater than 10 years. Assays for B1, B2, biotin, niacin, plasma and red blood cell (RBC) folates were performed by microbiologic methods, B12 was measured by radioimmunoassay. During the study, B1 levels were consistently above the upper limit of the normal range, B2 and B12 remained in the normal range although there was a slight decrease in B12 values. Almost half of the patients had initially low levels of biotin, niacin, and folates. Biotin, after a significant sharp rise during the first month of supplementation returned to normal range. Niacin levels were initially low in infants and rose toward normal values during treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Vitamin status of eating disorder patients: Relationship to clinical indices and effect of treatment

Vitamin abnormalities in eating disorder patients may contribute to altered neuropsy-chological status and the development of sequelae such as cognitive dysfunction. We examined the relationship between vitamin status and clinical indices in 13 low-weight patients with anorexia or bulimia nervosa at admission to a treatment program. Vitamin status was evaluated again at discharge (2–6 weeks later) in nine of these patients. Four patients (31%) initially had erythrocyte enzyme activity indices suggesting deficiency for riboflavin and for vitamin B-6. Patients with biochemical evidence for riboflavin deficiency had lower relative body weight than those with normal riboflavin status (p < .02). Three patients (23%) had elevated plasma cholesterol concentrations (>5.69 mmol/L). Plasma retinol concentrations were within the normal range. Plasma alphatocopherol concentrations were positively associated with serum albumin (p < .04), cholesterol (p < .0003), and total lipids (p < .0003), and were inversely associated with body mass index (p < .04). At discharge, thiamin, riboflavin and vitamin B-6 status indicators were normal in all cases examined. Suboptimal vitamin status is common in eating disorder patients but is normalized with dietary intervention and nutritional rehabilitation. © 1995 by John Wiley & Sons, Inc.