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Effect of vitamin B6 on the side effects of a low-dose combined oral contraceptive.Contraception (UNITED STATES) Apr 1997, 55 (4) p245-8 Analogous to recommendations for treatment of side effects of early pregnancy and premenstrual syndrome, use of vitamin B6 has been recommended for the treatment of side effects of oral contraceptive (OC) use. A randomized, triple-blinded controlled trial of 124 women was done to evaluate the effect of taking 150 mg of vitamin B6 daily for 30 days on the severity of nausea, headache, vomiting, dizziness, depression, and irritability associated with the initiation of low-dose (30 micrograms norgestrel and 30 micrograms ethinyl estradiol) OG use. The severity of the symptoms was measured on a scale from 0 to 3 (not present to severe), and was evaluated at one month after admission. The two treatment groups (vitamin B, and placebo) had comparable baseline characteristics. From admission to follow up, there was a decrease in the severity of all symptoms in both groups. There was no statistically significant difference in the reductions found in the vitamin B6 and the placebo groups, although reductions in the severity of headache and dizziness were greater in the B6 group. The decrease in the severity of all OC side effects can be explained more by a placebo effect than by a marginal pharmacological effect of the vitamin B6. Vitamin B6 in the treatment of the premenstrual syndrome - Review (1) BR. J. OBSTET. GYNAECOL. (United Kingdom), 1991, 98/3 (329-330) BR. J. CLIN. PRACT. (United Kingdom), 1988, 42/11 (448-452) We present a survey summarising the retrospective reports of the therapeutic effect of pyridoxine (vitamin B6) in 630 women suffering from premenstrual syndrome (PMS) who attended a PMS clinic during the period 1976-1983. The daily doses of pyridoxine hydrochloride varied from 40 to 100 mg early in the study and from 120 to 200 mg in the later period of the investigations. The response to treatment was recorded as good (no significant residual complaints) in 40 per cent of more of patients taking 100-150 mg pyridoxine daily and in 60 per cent of patients treated with 160-200 mg daily. Together with partial response (useful benefit but still some significant complaints), the positive effect of the treatment increased to 65-68 per cent and 70-88 per cent respectively. No symptoms consistent with a diagnosis of peripheral neuropathy were reported. Effect of vitamin B-6 on plasma and red blood cell magnesium levels in premenopausal women ANN. CLIN. LAB. SCI. (USA), 1981, 11/4 333-336) The effect of 100 mg of vitamin Bsub 6 twice a day on plasma and red blood cell (RBC) magnesium was evaluated in nine premenopausal subjects during the period of one month. According to reported normal ranges for plasma and RBC magnesium (1.7 to 2.3 and 4.7 to 7.0, mg per dl, respectively), three subjects had low plasma magnesium, and all subjects had low RBC magnesium during the control period. Following vitamin Bsub 6 administration, the mean plasma and RBC magnesium levels were significantly elevated, with a doubling of RBC levels after four weeks of therapy. These results support the postulate that vitamin Bsub 6 plays a fundamental role in the active transport of minerals across cell membranes. EGYPT AMER.J.CLIN.NUTR. (USA), 1975, 28/1 (4-9) Studies on the interrelation between female hormones associated with reproduction and the vitamin Bsub 6 dependent enzymes along the kynurenin pathway of tryptophan metabolism were carried out in girls with an age less, and more than 10 yr (just before the onset of the first menstrual cycle), and in postmenopausal women with and without relative (excess) production of estradiol from the adrenal cortex. It is found that most of the determined metabolites are retained by the girls with age less than 10 yr after tryptophan loading without and with vitamin Bsub 6 supplementation. Estradiol from either the ovaries (in girls just before menarche), or the adrenal cortex, in postmenopausal women with relative (excess) production of this hormone, interferes with the further degradation of 3 hydroxyanthranilic acid. However, this interference could be completely restored by vitamin Bsub 6 supplementation. The extra presence of a partial impairment in the kynureninase enzyme is also suggested in these postmenopausal women. In the latter case, this enzymatic activity could be partially restored by vitamin Bsub 6 supplementation. On the contrary, the enzymes kynureninases and transaminases, are inhibited in postmenopausal women without (excess) production of adrenocortical estradiol. Pyridoxine supplementation partially corrected the inhibition, especially that of 3 hydroxykynurenine transaminase enzyme. ITALY MINERVA ANESTESIOL. (ITALY), 1984, 50/11 (573-576) The physiopathological background to senile osteoporosis in women is reviewed with a reminder of possible complications like vertebral fractures and incident pain. The treatment protocols developed from these premises include the administration of oestroprogestins, vitamins D2, B1 and B6 and calcitonin. They also incorporate exposure to electromagnetic pulsation fields, ultraviolet and infrared rays as well as FANS and antidepressant treatment. Vitamins and metals: Potential dangers for the human being Schweizerische Medizinische Wochenschrift (Switzerland), 1996, 126/15 (607-611) Administration of vitamins or metals may cause severe side effects. Retinoids (derivatives of vitamin A) used for the treatment of various skin disorders are teratogenic, hepatotoxic and may induce a substantial increase in serum lipids. A case report demonstrates that vitamin D supplementation in a patient under total parenteral nutrition can cause hypercalcemia. The isolated administration of vitamin B1, without concomitant vitamin B6 and nicotinamide may precipitate potentially life-threatening pellagra encephalopathy. Repeat blood transfusions may produce clinically overt organ hemosiderosis, e.g. cirrhosis of the liver, diabetes mellitus or myocardiopathy. The literature contains reports on a few cases of sarcoma associated with orthopedic metal implants. The controversial issue of the potential dangers of dental amalgams is briefly mentioned. Vitamin B6 status in cirrhotic patients in relation to apoenzyme of serum alanine aminotransferase CLIN. BIOCHEM. (Canada), 1988, 21/6 (367-370) Plasma levels of pyridoxal-5'-phosphate (PLP) in cirrhotic patients were significantly lower than in control subjects. However, the plasma total pyridoxal level and urinary 4-pyridoxic acid excretion were not decreased in non-alcoholic patients but in alcoholic patients. In the latter, the percentage of apo alanine aminotransferase was not related to the plasma PLP level, but was significantly correlated with plasma total pyridoxal level and urinary 4-pyridoxic acid excretion. We conclude that alcoholic cirrhotic patients have vitamin B6 deficiency, which is at least responsible for low serum alanine aminotransferase activity. Vitamin B6 concentrations in patients with chronic liver disease and hepatocellular carcinoma BR. MED. J. (UK), 1986, 293/6540 (175) Recently a method permitting estimation of concentrations of pyridoxal-5-phosphate from direct measurement of plasma total pyridoxal and free (that is, non-phosphorylated) pyridoxal concentrations was described, and we applied this to patients with chronic liver diseases. Because of the high risk of hepatocellular carcinoma in patients with chronic liver disease we also studied patients with hepatocellular carcinoma with or without associated cirrhosis. We studied 17 patients with cirrhosis, 10 of whom had histologically confirmed hepatocellular carcinoma; five patients with hepatocellular carcinoma but without cirrhosis; and nine healthy control subjects. Total pyridoxal concentrations ranged from 10 to 51 pmol/ml in the nine normal subjects. Although seven of the patients with hepatocellular carcinoma had concentrations below the lowest values recorded in the control group, there was no significant difference overall between either patient group and the control subjects. The concentrations of pyridoxal-5-phosphate, however, were much lower in the patients with uncomplicated liver disease, being unrecordable in seven (p < 0.01, Wilcoxon's rank sum test). The proportion of total pyridoxal existing as active pyridoxal-5-phosphate was more than 50% in all control subjects but less than 50% in all patients with liver disease apart from one with cirrhosis and three with hepatocellular carcinoma. The normal concentrations of total pyridoxal in most of the patients with cirrhosis suggest that deficient intake and poor absorption of vitamin B6 are not the major cause of the deficiency of pyridoxal-5-phosphate in such patients found in this and other studies. This deficiency may be due either to failure of hepatic conversion of vitamin B6 or to enhanced degradation of pyridoxal-5-phosphate. The possibility that vitamin B6 deficiency is a risk factor for the development of hepatocellular carcinoma in cirrhosis cannot be excluded, particularly as seven of the patients had lower concentrations of pyridoxal-5-phosphate than any normal subject. Abnormal vitamin B6 status in childhood leukemia. Cancer. 1990 Dec 1. 66(11). P 2421-8 Vitamin B6 is involved in many biological processes of potential relevance to carcinogenesis and tumor growth, including DNA synthesis and maintenance of immunocompetence, yet very little information exists on B6 nutritional status in childhood leukemia. Using a radioenzymatic assay, the authors measured plasma pyridoxal 5'-phosphate (PLP), the biologically active form of B6, in 11 newly diagnosed untreated children with leukemia and 11 age-matched controls. The children with leukemia had significantly lower PLP levels than the controls. In 26 additional leukemia patients and 26 additional controls, a high-performance liquid chromatography assay also demonstrated lower plasma PLP levels in childhood leukemia compared with controls. These differences were significant for both acute lymphoblastic leukemia (ALL) and for acute nonlymphoblastic leukemia (ANLL). The PLP values did not correlate with indices of leukemia cell burden, but did correlate with reported B6 intake, suggesting that illness-related diet changes are at least partially responsible for the low PLP levels. Before any chemotherapy, overall nutritional status was suboptimal in 53% of ALL cases and 57% of ANLL cases. Newly diagnosed children with leukemia have suboptimal overall nutrition as well as suboptimal vitamin B6 status. Hyperhomocysteinaemia and end stage renal disease Journal of Nephrology (Italy), 1997, 10/2 (77-84) Vascular disease is a major cause of morbidity and mortality in end stage renal failure patients and cannot be explained entirely by the prevalence of traditional risk factors for atherosclerosis. A high plasma homocysteine concentration, which is a risk factor for vascular disease is found in patients with end stage renal disease. The exact cause for the hyperhomocysteinaemia seen in these patients is unknown, al metabolism of homocysteine. High homocysteine concentrations may also be attributable to a deficiency of folate, vitamin B6 or vitamin B12 although, because of supplementation, these vitamins may be present in high concentrations in renal patients. The occurrence of hyperhomocysteinaemia despite high plasma vitamin concentration could be due to altered metabolism or inhibition of intracellular vitamin activity. A number of studies have now established hyperhomocystinaemia to be an independent risk factor for atherosclerosis in patients with end-stage renal disease. Plasma homocysteine concentrations can be reduced by administration of folic acid either alone or combined with vitamin B12 or vitamin B6. The effects of such reduction on vascular risk in renal failure patients needs further study. Circulation (UNITED STATES) Dec 1 1996, 94 (11) p2743-8 BACKGROUND: A high level of total plasma homocysteine is a risk factor for atherosclerosis, which is an important cause of death in renal failure We evaluated the role of this as a risk factor for vascular complications of end-stage renal disease. METHODS AND RESULTS: Total fasting plasma homocysteine and other risk factors were documented in 176 dialysis patients (97 men, 79 women; mean age, 56.3 14.8 years). Folate, vitamin B12, and pyridoxal phosphate concentrations were also determined. The prevalence of high total homocysteine values was determined by comparison with a normal reference population, and the risk of associated vascular complications was estimated by multiple logistic regression. Total homocysteine concentration was higher in patients than in the normal population (26.6 1.5 versus 10.1 1.7 mumol/L; P < .01). Abnormally high concentrations (> 95th percentile for control subjects, 16.3 mumol/L) were seen in 149 patients (85%) with end-stage renal disease (P < .001). Patients with a homocysteine concentration in the upper two quintiles (> 27.8 mumol/L) had an independent odds ratio of 2.9 (CI, 1.4 to 5.8; P = .007) of vascular complications. B vitamin levels were lower in patients with vascular complications than in those without. Vitamin B6 deficiency was more frequent in patients than in the normal reference population (18% versus 2%; P < .01). CONCLUSIONS: A high total plasma homocysteine concentration is an independent risk factor for atherosclerotic complications of end-stage renal disease. Such patients may benefit from higher doses of B vitamins than those currently recommended. High dose-B-vitamin treatment of hyperhomocysteinemia in dialysis patients. Kidney Int (UNITED STATES) Jan 1996, 49 (1) p147-52 Hyperhomocysteinemia, an arteriosclerotic risk factor, persists in 75% of dialysis patients despite routine low dose supplementation with the B-vitamin co-factors/substrates for homocysteine (Hcy) metabolism, and normal or supernormal plasma status of these vitamins (Atherosclerosis 114:93, 1995). We conducted a placebo-controlled eight-week trial of the effect on plasma homocysteine of adding supraphysiologic dose folic acid (15 mg/day), B-6 (100 mg/day), and B-12 (1 mg/day) to the usual daily dosing of 1 mg folic acid, 10 mg B-6, and 12 micrograms B-12, in 27 hyperhomocysteinemic dialysis patients. Total plasma homocysteine was measured at baseline, and after four and eight weeks. Blinded analyses revealed no evidence of toxicity in the group randomized to supraphysiologic dose B-vitamin supplementation. Plasma homocysteine was significantly reduced after both four weeks (-29.8% vs. -2.0%; P = 0.0024) and eight weeks (-25.8% vs. .6%; P = 0.0009) of active versus placebo treatment. Also, 5 of 15 treated versus 0 of 12 placebo group patients had their plasma Hcy reduced to within the normative range (< 15 mumol/liter). Supraphysiologic doses of B-vitamins may be required to correct hyperhomocysteinemia in dialysis patients. The activities of coenzyme Q10 and vitamin B6 for immune responses. Biochem Biophys Res Commun (UNITED STATES) May 28 1993, 193 (1) Coenzyme Q10 (CoQ10) and vitamin B6 (pyridoxine) have been administered together and separately to three groups of human subjects. The blood levels of CoQ10 increased (p < 0.001) when CoQ10 and pyridoxine were administered together and when CoQ10 was given alone. The blood levels of IgG increased when CoQ10 and pyridoxine were administered together (p < 0.01) and when CoQ10 was administered alone (p < 0.05). The blood levels of T4-lymphocytes increased when CoQ10 and pyridoxine were administered together (p < 0.01) and separately (p < 0.001). The ratio of T4/T8 lymphocytes increased when CoQ10 and pyridoxine were administered together (p < 0.001) and separately (p < 0.05). These increases in IgG and T4-lymphocytes with CoQ10 and vitamin B6 are clinically important for trials on AIDS, other infectious diseases, and on cancer. J Natl Cancer Inst (UNITED STATES) May 1987, 78 (5) p951-9 Effects of dietary vitamin B6 at levels ranging from deficiency to megadoses on the development of herpes simplex virus type 2-transformed (H238) cell-induced tumors and on in vitro responses relating to cell-mediated immunity were examined. Male BALB/cByJ mice (n = 260), 5 weeks of age, were fed 20% casein diets containing pyridoxine (PN) at 0.2, 1.2 for the control diet, 7.7, or 74.3 mg/kg diet for 4-11 weeks. After 4 weeks of dietary treatment, 120 of the mice received an injection of H238 cells; mice without H238 injection served as controls. At 4, 8, and 11 weeks, animals from each group were euthanized and blood and spleen samples obtained. Mice fed 0.2 mg PN developed mild deficiency symptoms and gained significantly less weight than those fed 1.2-, 7.7-, and 74.3-mg PN diets. Thirteen to 16 days after tumor cell injection, primary tumor incidence was lowest in mice fed 74.3 mg PN; later, incidence among groups was similar. Mice fed 1.2 mg PN had the largest primary tumor volume, the highest incidence of lung metastases, and the greatest number of metastatic nodules per animal at 7 weeks post injection. Overall, lower tumor volumes were found in animals fed 7.7 and 74.3 mg PN (14 and 32% less than the tumor volume for those fed 1.2 mg PN, respectively); mice fed 0.2 mg PN had the lowest tumor volume. Blood and spleen lymphoproliferative response to stimulation by phytohemagglutinin or concanavalin A generally tended to be higher in mice fed 7.7 and 74.3 mg PN as compared to that in animals fed either 0.2 or 1.2 mg PN. However, decreased mitogen-stimulated responsiveness was observed in all animals with progressive tumor growth. Tumor growth also resulted in splenomegaly and increased thymic atrophy. Significant negative relationships between tumor volume and tumor pyridoxal 5-phosphate (PLP) concentrations were observed for 1.2-, 7.7-, and 74.3-mg PN diet groups. These data suggest that high dietary intake of vitamin B6 may have suppressed tumor development by either immune enhancement or PLP growth regulation of this tumor. Homocysteine: Relation with ischemic vascular diseases. Piolot A.; Nadler F.; Parez N.; Jacotot B. Serv. de Med. Int.-Nutr.-Metab., CHU Henri-Mondor, 94010 Creteil Cedex France Revue de Medecine Interne (France), 1996, 17/1 (34-45) Homocysteine, a sulfur-containing amino acid, is an intermediate metabolite of methionine. Patients with homocystinuria and severe hyperhomocysteinemia develop premature arteriosclerosis and arterial thrombotic events, and venous thromboembolism. Studies suggest that moderate hyperhomocysteinemia can be considered as an independent risk factor in the development of premature cardiovascular disease. In vitro, homocysteine has toxic effects on endothelial cells. Homocysteine can promote lipid peroxidation and damage vascular endothelial cells. Moreover, homocysteine interferes with the natural anticoagulant system and the fibrinolytic system. Homocysteinemia should be known in patients with premature vascular diseases, especially in subjets with no risk factors. Folic acid, vitamin B6 can lower homocysteine levels. Journal of Mental Deficiency Research 1985 Sep Vol 29(3) 233-240 19 infants with Down's syndrome participated in a double-blind study of the clinical effects of pharmacological doses of vitamin B-sub-6 administration, starting under 8 wks of age and continuing until 3 yrs of age. 10 Ss received the vitamin and 9 the placebo. No statistically significant differences were found between the 2 groups in mental age, height, weight, cranial circumference, or tongue protrusion. Vitamin B-sub-6 significantly elevated whole blood 5-hydroxytryptamine during the 1st yr. A study of side effects conducted on a larger open population of 400 Down's syndrome patients (from infants to aged 12 yrs) found vitamin B-sub-6 to be relatively safe when administered over long periods of time, with photosensitive blisters as the major complication. Journal of Mental Deficiency Research 1985 Sep Vol 29(3) 241-246 Recorded cortical auditory evoked potentials (CAEPs) at 1 and at 3 yrs of age in 19 children with Down's syndrome participating in a double-blind trial of vitamin B-sub-6 and placebo that was begun in early infancy and continued for 3 yrs. CAEPs have previously been shown to have abnormally high amplitude in Down's syndrome patients. The CAEPs of the Ss in the B-sub-6-treated and placebo groups were compared. Only minor effects were found in the CAEPs recorded at 1 yr of age. At 3 yrs of age, however, comparison of the B-sub-6-treated group and the placebo group revealed significant differences in both amplitudes and latencies of CAEP components. Peak-to-peak amplitudes of prominent components were significantly lower in B-sub-6-treated Ss than in their placebo controls. Amplitude correlated in some cases with whole blood serotonin levels. Latencies for several prominent evoked peaks were significantly longer in B-sub-6-treated Ss. Findings suggest a difference in neurodevelopmental trajectories that seems to be a pharmacological effect of B-sub-6 administration. (17 ref) Miner Electrolyte Metab (SWITZERLAND) 1996, 22 (1-3) p106-9 Moderate hyperhomocysteinemia, a risk factor for premature atherosclerosis, is present in chronic uremic patients. We prospectively evaluated the effects of sequential supplementation with pyridoxine (70 mg/day) and folic acid (10 mg/day) for two 3-month periods in 37 nondialyzed patients (29 males) with creatinine clearance (Ccr) ranging from 10 to 80 ml/min, whose plasma vitamin B12 and folate level was in the normal range. Mean ( SD) baseline plasma total homocysteine (Hcy) was 14.9 5.2, 16.5 5.1 and 26.1 12.1 mumol/l (upper limit in 45 healthy controls 14.1 mumol/l) in patients with CCr 40-80, 20-40 and < 20 ml/min, respectively. Following pyridoxine Hcy did not significantly decrease whereas following folic acid Hcy decreased significantly to 9.9 2.9 (-33% vs. baseline), 10.3 3.4 (-37%) and 15.4 5.5 (-40%), respectively (Student's paired t test, p < 0.001) in the 3 groups. We conclude that folate (but not pyridoxine) pharmacologic supplementation is effective in lowering elevated plasma Hcy in chronic renal failure patients, thus suggesting that enhancing the Hcy remethylation pathway may overcome hyperhomocysteinemia in such patients. In view of the potential atherogenic effects of hyperhomocysteinemia, long-term folate supplementation should be considered in uremic patients. Prospects for nutritional control of hypertension Med Hypotheses (ENGLAND) Mar 1981, 7 (3) p271-83 Sodium restriction is not the only nutritional measure likely to prove valuable in the treatment and prevention of hypertension. The hypotensive effects of central adrenergic stimulation can be promoted by supplementary tyrosine, insulin potentiation (as with GTF), and (possibly) high-dose pyridoxine. Insulin potentiators (GTF) and prostaglandin precursors (essential fatty acids) should have direct relaxant effects on vascular muscle. A high potassium, low sodium diet, coenzyme Q, and prevention of cadmium toxicity (as with dietary selenium) may act to offset renally-mediated pressor influences. Functional combinations of these measures might prove to be substantially effective, in which case they would offer considerable advantages over potentially toxic drug therapies. Unrecognized pandemic subclinical diabetes of the affluent nations: Causes, cost and prevention Journal of Orthomolecular Medicine (Canada), 1996, 11/2 (95-99) Regarding populations on the industrialized 'western affluent diet', arguments are made that: (1) plasma glucose values commonly seen and accepted as normal are abnormal; (2) their glucose tolerance is innately unstable; (3) most of their morbidity and mortality is produced by hyperglycemia far below glycosuria and/or arteriosclerosis which can occur independently or together; (4) simple low cost methods for preventing and treating both have been in the literature for decades (correction of the sugar, fat and protein excesses; and controlled supplementation of pyridoxine (vitamin B6). Mg, Cr and coenzyme Q10); and (5) these lessons were missed by main stream medicine because of the vast size of the literature, enforcement of 'treatment of choice', and lack of computer aided diagnosis. Cited as striking evidence of this tragic situation is the failure of mainstream clinical medicine to understand the cause of the remarkable decline in CVD in the 1960s and 1970s that followed U.S. enrichment of cereals with pyridoxine (vitamin B6). Recommendations are made for correction of unnecessary costly delays between publication and implementation of such research findings. Vitamin and mineral deficiencies which may predispose to glucose intolerance of pregnancy Journal of the American College of Nutrition (USA), 1996, 15/1 (14-20) There is an increased requirement for nutrients in normal pregnancy, not only due to increased demand, but also increased loss. There is also an increased insulin resistant state during pregnancy mediated by the placental anti-insulin hormones estrogen, progesterone, human somatomammotropin; the pituitary hormone prolactin; and the adrenal hormone, cortisol. If the maternal pancreas cannot increase production of insulin to sustain normoglycemia despite these anti-insulin hormones, gestational diabetes occurs. Gestational diabetes is associated with excessive nutrient losses due to glycosuria. Specific nutrient deficiencies of chromium, magnesium, potassium and pyridoxine may potentiate the tendency towards hyperglycemia in gestational diabetic women because each of these four deficiencies causes impairment of pancreatic insulin production. This review describes the pathophysiology of the hyperglycemia and the nutrient loss in gestational diabetes and further postulates the mechanism whereby vitamin/mineral supplementation may be useful to prevent or ameliorate pregnancy-related glucose intolerance. Vitamin B6 alleviates the vascular complications of insulin-treated STZ-induced diabetic rats Nutritional Sciences Journal (Taiwan), 1996, 21/3 (235-248) The purpose of this study is to investigate whether vitamin B6 alleviates the vascular complications of insulin-treated streptozotocin (STZ)-induced diabetes in rats. Diabetic animals were treated with or without vitamin B6 and/or insulin. Platelet aggregation induced by ADP (10 microM) or thrombin (0.05 D/mL) was measured in platelet rich plasma of normal and diabetic animals. 14C-Thromboxane B2 (14C-TxB2) production of platelets, using 14C-Arachidonic Acid (14C-AA) as a precursor, was assayed by means of scanning radiochromatography and autoradiography. 14C-TxB2 was quantitied by scintillation counter. The results showed that vitamin B6 in conjuction with insulin treatment resulted in lower blood glucose than either vitamin B6 or insulin treatment alone. Similarly, platelet aggregation and TxB2 production in diabetics with vitamin B6 and insulin treatment were significantly decreased. These data indicated that vitamin B6 in conjunction with insulin treatment seemed to be better than vitamin B6 or insulin treatment alone in controlling blood glucose, inhibiting platelet aggregation and decreasing TxA2 production. Vopr Med Khim (RUSSIA) Apr-Jun 1996, 42 (2) p153-8 Metabolism of vitamins C, B2, B6 and niacin in children with insulin-dependent diabetes mellitus was distinctly different from that of healthy persons of the same age as shown by studies of the correlation between content of vitamins or their coenzyme forms in blood, excretion of the vitamins with urine and content of the vitamins in a diet. These data corroborated once again that in estimation of the vitamins consumption suitable for ill children, the criteria of healthy children requirements for vitamins should not be taken into consideration. Dissimilar metabolism in healthy and impaired persons may also demonstrate some differences in consumption of these vitamins. Preliminary data showed that requirements of the impaired children for vitamin C were slightly increased, for vitamin B2--similar or slightly decreased as compared with healthy children. These results suggest that additional investigations are required for evaluation of vitamins consumption in children with diabetes mellitus of the I type. The endocrine pancreas in pyridoxine deficient rats. Med (JAPAN) Jul 1981, 134 (3) p331-6 Because the supplementation of pyridoxine (vitamin B6) improves the glucose tolerance in gestational diabetes and adult onset diabetes, pyridoxine deficiency has been considered to be one of the factors that cause diabetes mellitus. We produced pyridoxine deficient rats by giving pyridoxine-free food with deoxypyridoxine which competitively the activity of pyridoxal phosphate. In these pyridoxine deficient rats plasma insulin during the glucose tolerance test was significantly low as compared with controls. In vitro experiments of pancreas perfusion showed that secretion of insulin and glucagon was impaired in the pyridoxine deficiency. Since the restriction of diet-calorie caused a decrease in arginine- nduced secretion of insulin and glucagon from the isolated pancreas, the impairment of the endocrine pancreas may depend on malnutrition. Pyridoxine deficiency is surely one of the factors that impair the endocrine pancreas by multifactorial derangement of metabolism besides the tryptophan-nicotinic acid pathway. Diabetes (UNITED STATES) Jul 1989, 38 (7) p881-6 The effects of vitamin B6 on erythrocyte metabolism, erythrocyte hemoglobin O2 affinity (P50), and nonenzymatic glycosylation were studied in 15 Caucasian men with type II (non-insulin-dependent) diabetes mellitus. A control group of 13 healthy Caucasian men was also evaluated. Before treatment, diabetic subjects had low mean cell hemoglobin concentration values and increases in both erythrocyte 2,3-diphosphoglycerate (2,3-DPG) levels and erythrocyte hexokinase activities. Although all three of these changes are associated with a decrease in hemoglobin O2 (Hb-O2) affinity, P50 values were normal in diabetic subjects. Moreover, P50 values normalized to pH 7.4 (P50(7.4] were inversely related to the level of glycosylated hemoglobin (HbA1c). Both erythrocyte 2,3-DPG and erythrocyte ATP were also inversely related to HbA1c. Vitamin B6 nutriture, as determined by erythrocyte aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, was normal in all diabetic subjects before vitamin B6 therapy. Nonetheless, HbA1c levels decreased after 6 wk of treatment with 150 mg/day pyridoxine and increased again during placebo administration. These changes were not explained by changes in fasting blood glucose. Pyridoxine therapy also decreased P50(7.4) values and increased erythrocyte AST and ALT activities but had no effect on 2,3-DPG, ATP, or the activities of hexokinase, glucose-6-phosphate dehydrogenase, and 6-phosphogluconate dehydrogenase. These observations suggest that 1) nonenzymatic glycosylation may play a role in regulating both erythrocyte metabolism and Hb-O2 affinity in diabetic subjects, and 2) vitamin B6 therapy may modify nonenzymatic glycosylation of hemoglobin in this population. [Criteria of supply of vitamins B1, B2, and B6 in children with insulin-dependent diabetes mellitus] Vopr Med Khim (RUSSIA) Nov-Dec 1995, 41 (6) p58-62 By mathematically analysing the curves of urinary excretion of vitamins, their plasma and erythrocytic concentrations or of TDP-effect, by constructing and mathematically interpreting the variation curves of distribution of a given plasma concentration of riboflavin and pyridoxal phosphate for 10-14-old-year children suffering from insulin-dependent diabetes mellitus after supplementation of vitamin, as a criterion of normal requirement for vitamin B2, the authors are prone to recommend the concentration of riboflavin over 10 micrograms/ml in plasma and over 96 micrograms/ml in erythrocytes, the hourly excretion of more than 27 micrograms. It has been ascertained that the criteria for the optimal body's requirements for vitamins in diabetes mellitus children do not differ from those in healthy age-matched children. Thus, the value of TDP-effect is less than 1.25, the concentration of pyridoxal phosphate is over 8.4 micrograms/ml plasma, the excretion values of thiamine and 4-pyridoxic acid are 13.5 and 64.0 micrograms/h, respectively. Articles about vitamins Vitamin B6
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