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Diet is a modifiable factor that ensures optimal growth, biochemical performance, improved mood and mental functioning. Lack of nutrients, notably vitamin B, has an impact on human health and wellbeing. The United Arab Emirates is facing a serious problem of micronutrient deficiencies because of the growing trend for bariatric surgery, including Roux-en-Y gastric bypass and sleeve gastrectomy. People undergoing bariatric surgery are at high risk of developing neurological, cognitive, and mental disabilities and cardiovascular disease due to deficiency in vitamin B. Vitamin B is involved in neurotransmitter synthesis, including γ-aminobutyric acid, serotonin, dopamine, and noradrenaline. Deficiency of vitamin B increases the risk of depression, anxiety, dementia and Alzheimer's disease. In addition, vitamin B deficiency can disrupt the methylation of homocysteine, leading to hyperhomocysteinemia. Elevated homocysteine levels are detrimental to human health. Vitamin B deficiency also suppresses immune function, increases the production of pro-inflammatory cytokines and upregulates NF-κB. Considering the important functions of vitamin B and the severe consequences associated with its deficiency following bariatric surgery, proper dietary intervention and administration of adequate supplements should be considered to prevent negative clinical outcomes.

Aim: In this study, we aimed to determine the incidence of hair loss in patients who underwent laparoscopic sleeve gastrectomy (LSG), and to observe whether use of Biotin has an impact on hair loss. Methods: This study included 156 female patients who underwent LSG for obesity and completed a 1-year follow-up. All patients with vitamin deficiency were screened in the pre- and postoperative period. Hair loss was defined as the subjective perception of the women of losing a higher amount of hair when compared with normal situation. Results: Hair loss was observed in 72% of the patients after LSG ( n  = 112). Seventy-nine percent of the patients reported hair loss between the third and fourth-month interval, and continued for an average of 5.5 ± 2.6 months. Permanent alopecia was not observed in any of the patients. Patients who experienced hair loss and Biotin deficiency after LSG were prescribed 1000 mcg/day of Biotin for 3 months. Of these 22 patients; only 5 (23%) patients reported a remarkable decline in hair loss. İn addition, 29 patients were found to take 1000 mcg/day of Biotin for average 2.5 months after onset of hair loss by their own initiative, despite optimal blood Biotin levels. Eleven (38%) patients reported a remarkable decline in hair loss. The effect of biotin use on hair loss in patients with and without biotin deficiency was compared. There was no significant difference ( P  = .2). Conclusion: Temporary hair loss after LSG is common. It was found that biotin supplementation used to prevent hair loss does provide low efficacy.

Numerous recent studies show that vitamin D deficiency potentiates various chronic physical and psychiatric disorders and diseases. It has been shown that a similar range of disorders is also associated with latent infection with Toxoplasma gondii (Nicolle et Manceaux, 1908). For instance, among cancer, diabetes and schizophrenia patients, we find a higher prevalence of both toxoplasmosis and vitamin D deficiency. Theoretically, therefore, vitamin D deficiency could be the missing link between toxoplasmosis and these disorders. We tested this hypothesis by searching for decreased vitamin D levels in the serum of subjects infected with T. gondii (furthermore called Toxoplasma-infected subjects) in two cross-sectional and one case-control study. Results of the first cross-sectional study (N = 72) suggest that Toxoplasma-infected neurasthenic patients have non-significantly lower levels of calcidiol than Toxoplasma-free patients (study A: P = 0.26 in women, P = 0.68 in men). However, two other studies (study B: N = 400; study C: N = 191) showed a non-significantly higher concentration of vitamin D in Toxoplasma-infected subjects than in Toxoplasma-free subjects both in men (study B: P = 0.70, study C: P = 0.55) and in women (study B: P = 0.64, study C: P = 0.12). Taken together, our preliminary results thus do not support the hypothesis that toxoplasmosis could be associated with vitamin D decrease.

Background: Epidemiologic evidence regarding niacin, folate, vitamin B-6, and vitamin B-12 intake in relation to cognitive function is limited, especially in midlife. Objective: We hypothesize that higher intake of these B vitamins in young adulthood is associated with better cognition later in life. Design: This study comprised a community-based multicenter cohort of black and white men and women aged 18-30 y in 1985-1986 (year 0, i.e., baseline) from the Coronary Artery Risk Development in Young Adults (CARDIA) study ( n = 3136). We examined participants' CARDIA diet history at years 0, 7, and 20 to assess nutrient intake, including dietary and supplemental B vitamins. We measured cognitive function at year 25 (mean ± SD age: 50 ± 4 y) through the use of the Rey Auditory Verbal Learning Test (RAVLT) for verbal memory, the Digit Symbol Substitution Test (DSST) for psychomotor speed, and a modified Stroop interference test for executive function. Higher RAVLT and DSST scores and a lower Stroop score indicated better cognitive function. We used multivariable-adjusted linear regressions to estimate mean differences in cognitive scores and 95% CIs. Results: Comparing the highest quintile with the lowest (quintile 5 compared with quintile 1), cumulative total intake of niacin was significantly associated with 3.92 more digits on the DSST (95% CI: 2.28, 5.55; P -trend < 0.01) and 1.89 points lower interference score on the Stroop test (95% CI: -3.10, -0.68; P -trend = 0.05). Total folate was associated with 2.56 more digits on the DSST (95% CI: 0.82, 4.31; P -trend = 0.01). We also found that higher intakes of vitamin B-6 (quartile 5 compared with quartile 1: 2.62; 95% CI: 0.97, 4.28; P -trend = 0.02) and vitamin B-12 (quartile 5 compared with quartile 1: 2.08; 95% CI: 0.52, 3.65; P -trend = 0.02) resulted in better psychomotor speed measured by DSST scores. Conclusion: Higher intake of B vitamins throughout young adulthood was associated with better cognitive function in midlife., (© 2017 American Society for Nutrition.)

Introduction: The aim of this study was to assess the incidence, clinical presentation, and outcomes of neurologic disorders secondary to vitamin B deficiencies following bariatric surgery., Methods: Patients at a single academic institution who underwent bariatric surgery and developed neurologic complications secondary to low levels of vitamins B1, B2, B6, and B12 between the years 2004 and 2015 were studied., Results: In total, 47 (0.7%) bariatric surgical patients (Roux-en-Y gastric bypass n = 36, sleeve gastrectomy n = 9, and duodenal switch n = 2) developed neurologic manifestations secondary to vitamin B deficiencies. Eleven (23%) patients developed postoperative anatomical complications contributed to poor oral intake. Median duration to onset of neurologic manifestation following surgery was 12 months (IQR, 5-32). Vitamin deficiencies reported in the cohort included B1 (n = 30), B2 (n = 1), B6 (n = 12), and B12 (n = 12) deficiency. The most common manifestations were paresthesia (n = 31), muscle weakness (n = 15), abnormal gait (n = 11), and polyneuropathy (n = 7). Four patients were diagnosed with Wernicke-Korsakoff syndrome (WKS) which was developed after gastric bypass (n = 3) and sleeve gastrectomy (n = 1). Seven patients required readmission for management of severe vitamin B deficiencies. Overall, resolution of neurologic symptoms with nutritional interventions and pharmacotherapy was noted in 40 patients (85%). The WKS was not reversible, and all four patients had residual mild ataxia and nystagmus at the last follow-up time., Conclusions: Nutritional neurologic disorders secondary to vitamin B deficiency are relatively uncommon after bariatric surgery. While neurologic disorders are reversible in most patients (85%) with vitamin replacements, persistent residual neurologic symptoms are common in patients with WKS.

Background: Laparoscopic sleeve gastrectomy (LSG) has gained popularity as the leading bariatric procedure for the treatment of morbid obesity. Due to the rising numbers of bariatric surgeries, neurologic complications have become increasingly recognized. Our aim was to examine biochemical and hormonal factors that are associated with neuropathy post-LSG., Methods: Thirty-two patients were included: 16 patients with neuropathy in the neuropathic group (NG) and 16 patients without neuropathy in the control group (CG). Diagnosis was made by a consultant neurologist, and blood samples were taken to examine vitamin deficiencies and hormones involved in neuropathy., Results: There was no significant difference between the BMI (p = 0.1) in both groups as well as excess weight loss percentages post-LSG at 12 months (p = 0.6). B12 levels were within normal range, but higher in NG (p = 0.005). Vitamin B1 and B2 levels were significantly lower in NG; p values are 0.000 and 0.031, respectively. Vitamin B6 levels were significantly higher in NG (p = 0.02) and copper levels were lower in NG (p = 0.009). There was no significant difference in GLP-1 response in both groups., Conclusion: Our data showed post-LSG neuropathy is associated with lower levels of vitamin B1, B2, and copper, plus patients who are older in age. Vitamin B6 was significantly higher in the NG, which is, at toxic levels, associated with neuropathy. No difference in preoperative BMI, excess weight loss percent at 1 year, and GLP-1 levels was found. Larger data is required to validate our results.

Background & Aims: The relationship between vitamin D levels and chronic hepatitis B (CHB) infection and treatment outcomes are poorly elucidated. We measured pre-treatment serum vitamin D (25-hydroxyvitamin D3; 25[OH]D3) levels and determined their association with clinical parameters and treatment outcomes in active CHB patients without advanced liver disease enrolled in a global clinical trial., Methods: Patients were randomly assigned to either 48 weeks of tenofovir disoproxil fumarate (TDF) plus peginterferon alfa-2a (PegIFN), TDF plus PegIFN for 16 weeks followed by TDF for 32 weeks, PegIFN for 48 weeks, or TDF for 120 weeks. Univariate and multivariate analyses were conducted to determine associations between vitamin D, baseline factors, and week 48 clinical outcome., Results: Of 737 patients, 35% had insufficient (⩾20 but <31 ng/ml) and 58% had deficient (<20 ng/ml) vitamin D levels. In univariate analysis, lower vitamin D levels were significantly associated with the following baseline parameters: younger age, lower uric acid levels, HBeAg-positive status, lower calcium levels, blood draw in winter or autumn, and HBV genotype D. On multivariate analysis, only HBV genotype, season of blood draw, calcium level, and age retained their association. High baseline level of vitamin D was associated with low HBV DNA, normal ALT and HBsAg at week 48 independent of treatment groups, but the association, with the exception of ALT, became statistically insignificant after adjusting for age, gender, HBeAg and HBV genotype., Conclusions: Abnormally low vitamin D levels are highly prevalent among untreated, active CHB patients. Baseline vitamin D levels are not associated with treatment outcomes, but were associated with normal ALT., (Copyright © 2015 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.)

An 11-year-old male with autism became less responsive and was hospitalized with hepatomegaly and liver dysfunction, as well as severe lactic acidosis. His diet for several years was self-limited exclusively to a single "fast food"-a particular type of fried chicken-and was deficient in multiple micronutrients, including the B vitamins thiamine and pyridoxine. Lactic acidosis improved rapidly with thiamine; 2 weeks later, status epilepticus-with low serum pyridoxine-resolved rapidly with pyridoxine. Dietary B vitamin deficiencies complicated the care of this critically ill autistic child and should be considered in this setting., (© 2014 American Society for Parenteral and Enteral Nutrition.)

Background: Bariatric surgery is considered an effective method for sustained weight loss, but may cause various nutritional complications. The aim of this study was to evaluate the nutritional status of minerals and vitamins, food consumption, and to monitor physiologic parameters in patients with obesity before and 6 months after Roux-en-Y gastric bypass surgery (RYGB)., Methods: Thirty-six patients who had undergone RYGB were prospectively evaluated before and 6 months after surgery. At each phase their weight, height, body mass index (BMI), Electro Sensor Complex (ES Complex) data, food consumption, and total protein serum levels, albumin, prealbumin, parathyroid hormone (PTH), zinc (Zn), B12 vitamin (VitB12), iron (Fe), ferritin, copper (Cu), ionic calcium (CaI), magnesium (Mg), and folic acid were assessed., Results: The mean weight loss from baseline to 6 months after surgery was 35.34±4.82%. Markers of autonomic nervous system balance (P<.01), stiffness index (P<.01), standard deviation of normal-to-normal R-R intervals (SDNN) (P<.01), and insulin resistance (P<.001) were also improved. With regard to the micronutrients measured, 34 patients demonstrated some kind of deficiency. There was a high percentage of Zn deficiency in both pre- (55.55%) and postoperative (61.11%) patients, and 33.33% of the patients were deficient in prealbumin postoperatively. The protein intake after 6 months of surgery was below the recommended intake (<70 g/d) for 88.88% of the patients. Laboratory analyses demonstrated an average decrease in total protein (P<.05), prealbumin (P = .002), and PTH (P = .008) between pre- and postsurgery, and a decrease in the percentage of deficiencies for Mg (P<.05), CaI (P<.05), and Fe (P = .021)., Conclusion: Despite improvements in the autonomic nervous system balance, stiffness index markers and insulin resistance, we found a high prevalence of hypozincemia at 6 months post-RYGB. Furthermore, protein supplements were needed to maintain an adequate protein intake up to 6 months postsurgery., (Copyright © 2014 American Society for Bariatric Surgery. Published by Elsevier Inc. All rights reserved.)

We report a case of a 49-year-old Japanese man, who was admitted to our hospital because of severe dyspnea. He was found to have severely low serum folate and megaloblastic anemia, which was at first suspected to cause his dyspnea. It was assumed that severely low serum folate might be related to his malnutrition, probably caused by habitual alcohol consumption. He died in several days because of acute respiratory distress syndrome. Autopsy revealed diffuse alveolar damage (DAD) in the lungs and systemic lymph node swelling by EBV-positive diffuse large B-cell lymphoma, in addition to megaloblastic anemia in the bone marrow. Together with histological hemophagocytosis and high level of serum iron and ferritin, DAD was considered to be caused by hypercytokinemia triggered by the presence of EBV-positive diffuse large B-cell lymphoma. On the other hand, pathological findings suggestive of habitual alcohol consumption were not apparent. We considered that low serum folate in this case was not by the low intake but by increased consumption of folate by rapid progression of the lymphoma.

Objective: Bariatric surgery can reduce the risk of obesity-related complications of pregnancy, but may cause essential nutrient deficiencies. To assess adherence to laboratory testing guidelines, we examined frequency of testing for and diagnosis of deficiency during preconception and pregnancy using claims data in women with a delivery and bariatric surgery., Methods: Retrospective analysis of claims from seven Blue Cross/Blue Shield plans between 2002 and 2008. We included women with a delivery and bariatric surgery within the study period. We used common procedural terminology (CPT) and ICD-9 codes to define laboratory testing and deficiencies for iron, folate, vitamin B12, vitamin D, and thiamine. Using Student's t-test and chi-square testing, we compared frequency of laboratory tests and diagnoses during 12 months preconception and 280 days of pregnancy between women with pregnancy before versus after surgery. We used multivariate logistic regression to evaluate for predictors of laboratory testing., Results: We identified 456 women with pregnancy after bariatric surgery and 338 before surgery. The frequency of testing for any deficiency was low (9%-51%), but higher in those with pregnancy after surgery (p<0.003). The most common deficiency was vitamin B12 (12%-13%) with pregnancy after surgery (p<0.006). Anemia and number of health provider visits were independent predictors of laboratory testing., Conclusion: Women with pregnancy after bariatric surgery were tested for and diagnosed with micronutrient deficiencies more frequently than those with pregnancy before surgery. However, most laboratory testing occurred in less than half the women and was triggered by anemia. Increased testing may help identify nutrient deficiencies and prevent consequences for maternal and child health.

Alcoholism plays a major role in the insufficient utilization or deficiency of the vitamin B-complex molecules, and the pathologies resulting therefrom. Thiamine, pyridoxamine, and folic acid, each contain primary amine functional groups, whereas nicotinamide and vitamin B12 contain amide groups, each of which are potential reactants with acetaldehyde (AcH), the primary intermediate in the metabolism of ethanol. In this current study, it is reported that prothrombin time (PT), which is prolonged in a fraction of the alcoholic population, can be modified (in the laboratory) when several B-complex vitamins and AcH are added successively to human plasma or are premixed prior to the addition to plasma. Particularly, thiamine, pyridoxamine, and folic acid, at 0.01 mol/l, when added successively with 44.7 mmol/l AcH to plasma, or when premixed prior to addition to plasma, produced a marked reduction in the anticoagulant effect of AcH. Nicotinamide had no effect on PT nor did mixtures with AcH effect PT. However, NAD, which contains a primary amine in its AMP moiety, reacted with AcH, lowering the latter's anticoagulant activity upon addition to plasma. Vitamin B12 did not affect PT. Interestingly, successive mixtures of vitamin B12 and AcH to plasma resulted in a small but statistically significant increase (P≤0.05) in the anticoagulant effect of AcH, whereas premixtures had no statistically significant effect (P>0.05). The decrease in anticoagulant activity of AcH in the presence of B-complex vitamins and NAD suggests that the primary amines in these molecules may form Schiff bases with AcH, thereby lowering both the free AcH concentration as well as the ability of the free vitamins/coenzymes to partake in essential physiological reactions.

Background: Carnitine transports fatty acids from the cytoplasm to the mitochondrial matrix, where the fatty acids are oxidized. Chronic alcohol consumption reduces the concentration of carnitine and interferes with oxidative processes occurring in the cell., Aim: The assessment of carnitine concentrations in plasma of chronically intoxicated alcohol dependent persons in a 49-day abstinence period., Material/methods: The study included 31 patients (5 women and 27 men) aged from 26 to 60 years (44.6 ± 8.9) and 32 healthy subjects (15 women and 17 men) aged 22-60 years (39.8 ± 9.4). The patients' alcohol dependence ranged from 2 to 30 years (13.6 ± 7.5). Examined subjects consumed 75-700 g of ethanol/day (226.9 ± 151.5). Plasma concentrations of free and total carnitine were measured three times: at the first (T0), 30th (T30) and 49th (T49) day of hospital detoxification. Free (FC) and total (TC) carnitine were determined by the spectrophotometric method. Plasma acylcarnitine (AC) concentration was calculated from the difference between TC and FC; then the AC/FC ratio was calculated. To determine statistically significant differences for related variables, Student's t-test was used., Results: At T0, alcoholics had significantly lower concentration of FC and TC (p < 0.05) in plasma, as compared to the control group. In comparison to controls, at T30, plasma TC and FC (p < 0.01) as well as AC (p < 0.001) were reduced. The lowest concentration of TC, FC and AC (p < 0.001)was found at T49. The ratio of AC/FC at T0 had a tendency to be higher in alcoholics than in the control group (p = 0.05), whereas at T49 it was significantly lower in alcoholics as compared to the control subjects (p < 0.05)., Conclusions: Chronic alcohol intoxication causes a plasma deficiency of carnitine. Forty-nine days of abstinence showed a significant decrease in the concentration of TC, FC and AC. Further research is necessary to clarify whether a low level of plasma carnitine after chronic alcohol intoxication is caused by the uptake of blood carnitine by tissues such as liver or muscles. In alcoholics the supplementation of carnitine is recommended in the case of a low level of plasma carnitine.

Background: The role of one-carbon metabolism nutrients in colorectal carcinogenesis is not fully understood. Associations might be modified by mandated folic acid (FA) fortification or alcohol intake., Objective: We investigated associations between intakes of folate, riboflavin, vitamin B-6, and vitamin B-12 and colorectal cancer (CRC) in the Women's Health Initiative Observational Study, stratified by time exposed to FA fortification and alcohol intake., Design: A total of 88,045 postmenopausal women were recruited during 1993-1998; 1003 incident CRC cases were ascertained as of 2009. Quartiles of dietary intakes were compared; HRs and 95% CIs were estimated by Cox proportional hazards models., Results: Dietary and total intakes of vitamin B-6 in quartile 4 compared with quartile 1 (HR: 0.80; 95% CI: 0.66, 0.97 and HR: 0.80; 95% CI: 0.66, 0.99, respectively) and total intakes of riboflavin (HR: 0.81; 95% CI: 0.66, 0.99) were associated with reduced risk of CRC overall and of regionally spread disease. In current drinkers who consumed <1 drink (13 g alcohol)/wk, B vitamin intakes were inversely associated with CRC risk (P-interaction < 0.05). Dietary folate intake was positively associated with CRC risk among women who had experienced the initiation of FA fortification for 3 to <9 y (P-interaction < 0.01)., Conclusions: Vitamin B-6 and riboflavin intakes from diet and supplements were associated with a decreased risk of CRC in postmenopausal women. Associations of B vitamin intake were particularly strong for regional disease and among women drinkers who consumed alcohol infrequently. Our study provides new evidence that the increased folate intake during the early postfortification period may have been associated with a transient increase in CRC risk.

Several studies have shown that blood vitamin levels are lower in alcoholic patients than in control subjects. Acute ethanol exposure enhances the release of vitamins from liver cells in vitro. The aim of the present study is to confirm the effects of ethanol consumption on vitamin contents in vivo. We compared the contents of B-group vitamins in the liver, blood and urine between ethanol-fed and control rats fed a diet containing a sufficient- and low-vitamin mixture. The experimental rats were fed a 15 % ethanol solution freely for 28 d, and then 24 h urine samples were collected, after which the animals were killed. The B-group vitamin contents in the liver, blood and urine were measured. No differences in liver, blood and urine contents were observed between the control and ethanol-fed rats fed a diet containing a sufficient-vitamin mixture. On the contrary, in rats fed a diet containing a low-vitamin mixture, consumption of ethanol caused a decrease in the contents of vitamins B₁, B₂ and pantothenic acid in the liver; however, the contents of the other vitamins did not decrease. In the blood, the contents of vitamins B₁, B₂, B₆ and pantothenic acid were lower in the ethanol-fed rats than in the controls. Urinary excretion of the B-group vitamins, except for niacin, was lower in the ethanol-fed rats. These results show that ethanol consumption affects the absorption, distribution and excretion of each of the vitamins in rats fed a diet containing a low-vitamin mixture.

Parenteral nutrition (PN) is a relatively recent life-saving development in medicine but brings with it a range of new potential complications. Much of our knowledge about the signs and symptoms of individual micronutrient deficiencies comes from observations of patients receiving PN, and an example of this is the pivotal paper by Velez and colleagues published in Journal of Parenteral and Enteral Nutrition in 1985. This case report was the first published study to identify acute thiamine deficiency with cardiopathy and metabolic acidosis occurring in adult patients receiving vitamin-free PN. Although the importance of thiamine has been recognized since the late 19th century, it is still unclear exactly what dose is required for full repletion of a deficient patient, and further research would be useful to elucidate this question.

Glycogen storage disease type I is an autosomal recessive disorder caused by the defect in the glucose-6-phosphate enzyme system. Frequent intake of glucose-containing glycogen storage disease formula, uncooked cornstarch, or both, are usually needed to maintain normal blood glucose level. We report a glycogen storage disease type 1b girl with biotin deficiency caused by an exclusive glucose-containing glycogen storage disease formula for years, presenting with the appearance of severe skin lesions, and diagnosed by urinary organic acid analysis by gas chromato-spectrometry, and blood acylcarnitine analysis by tandem mass-spectrometry., (© 2011 Wiley Periodicals, Inc.)

We have previously shown that a nutritional model of B vitamin deficiency and homocysteine cycle alteration could lead to increased amyloid β deposition, due to PSEN1 and BACE over-expression and consequent increase in secretase activity. We hypothesize that nutritional factors causing homocysteine cycle alterations (i.e. hyperhomocysteinemia) could induce sequence-specific DNA hypomethylation and "aberrant" gene activation. Aim of present study was to analyze the methylation pattern of PSEN1 promoter in SK-N-BE neuroblastoma cells and TgCRND8 mice, in a B vitamin (folate, B12 and B6) deficiency paradigm. PSEN1 methylation status has been evaluated through bisulphite modification and genomic sequencing. We demonstrate that B vitamin deficiency induces hypomethylation of specific CpG moieties in the 5'-flanking region; S-adenosylmethionine has been supplemented as methyl donor to reverse this effect. PSEN1 promoter methylation status is correlated with gene expression. These findings pinpoint a direct relationship between B vitamin-dependent alteration of homocysteine cycle and DNA methylation and also indicate that PSEN1 promoter is regulated by methylation of specific CpG moieties., (Copyright © 2009 Elsevier Inc. All rights reserved.)

Frailty is a geriatric syndrome characterized by muscle weakness, sarcopenia, and fatigue, and is associated with several adverse health outcomes, including disability. Design of therapeutic interventions for geriatric frailty has been challenging and may be because of inadequate understanding of its biological underpinnings. Carnitine is important for energy production in skeletal muscles and there seems to be a negative correlation between advancing age and muscle carnitine levels. Carnitine deficiency may therefore contribute to geriatric frailty. Age-associated carnitine deficiency from a variety of etiologies, including organic cation transporter (OCTN2) mutation and carnitine palmitoyltransferase II (CPT) deficiency, may potentially explain the relationship between carnitine-associated mitochondrial dysfunction and geriatric frailty. Development of therapeutic agents capable of prevention or reversal of carnitine deficiency in older adults may minimize the occurrence of frailty in geriatric populations., (2010 Elsevier Ireland Ltd. All rights reserved.)

Objective: The aims of this study were to determine the prevalence of nutrient deficiencies in patients who present for bariatric surgery, assess nutritional status after surgery, and compare these with preoperative levels., Methods: A retrospective study was conducted to identify preoperative and 1-year postoperative nutrition deficiencies in patients undergoing bariatric surgery. The screening included serum ferritin, vitamin D, vitamin B(12), homocysteine, folate, red blood cell folate, and hemoglobin. Results were available for 232 patients preoperatively and 149 patients postoperatively. Two-tailed chi(2) tests and paired-sample t tests were used., Results: Preoperatively, vitamin D deficiency was noted at 57%. The prevalence of abnormalities 1 year after roux-en-Y gastric bypass was higher compared with preoperative levels (P < .05). After surgery, anemia was detected in 17%, elevated homocysteine levels (women only) in 29%, low ferritin in 15%, low vitamin B(12) in 11%, and low RBC folate in 12%. Mean hemoglobin, ferritin, and RBC folate levels deteriorated significantly but remained well within normal ranges. The prevalence of vitamin D deficiencies decreased, but not significantly. In sleeve gastrectomy patients, mean ferritin levels decreased (P < .05), without any patient developing a deficiency., Conclusion: Vitamin D deficiency is common among morbidly obese patients seeking bariatric surgery. Because the prevalence of micronutrient deficiencies persists or worsens postoperatively, routine nutrition screening, recommendation of appropriate supplements, and monitoring adherence are imperative in this population.

Reports of nutritional deficiencies after Bariatric surgery have lead investigators to inquire about the preoperative nutritional status of morbidly obese patients. Interestingly, numerous reports demonstrated a pattern of low levels of various micronutrients among overweight and obese patients, even in comparison with normal weight population. In this article we reviewed the literature for micronutrient deficiencies in obese patients prior to weight reduction surgery.

Thiamine deficiency can occur in any disease that results in inadequate intake or excessive loss of vitamin B1. In addition to increased thiamine consumption secondary to high cell turnover, cancer patients frequently have reduced oral intake as a direct result of their cancer or from cancer treatments. However, Wernicke encephalopathy (cerebral Beriberi), a clinical manifestation of thiamine deficiency, has rarely been associated with cancer patients. We report a case of Wernicke encephalopathy in a nonalcoholic patient with lymphoma. Although thiamine deficiency rarely potentiates clinical sequelae in cancer patients, it is important to recognize the risk and the clinical signs and manifestations so that prompt therapy can be initiated to reverse morbidity.

Carnitine is an amino acid derivative that has a key role in the regulation of fatty acid metabolism and ATP formation. Carnitine deficiency has been described in various conditions, including chronic kidney disease (CKD) and end stage renal disease (ESRD). The deficiency of this micronutrient is postulated to lead to adverse effects across multiple organ systems. There is a paucity of information on carnitine deficiency and its effects in the pediatric CKD and ESRD populations. Currently, there is no evidence supporting the routine use of carnitine supplementation in children with ESRD. In this article, we review the pathophysiology, pharmacokinetics and the potential effects of levo-carnitine supplementation with a focus on the pediatric CKD and ESRD populations. Finally, potential future directions of research are discussed.

Background: A vegetarian diet is considered to promote health and longevity and reduce the risk of cardiovascular diseases and cancer. However, a vegetarian diet may be deficient in some nutrients. Exclusion of animal products in vegetarian diets may affect the status of certain B-vitamins, and further cause the rise of plasma homocysteine concentration., Objective: The nutritional status of various B-vitamins (B(1), B(2), B(6), B(12), folic acid) and the concentration of homocysteine in blood plasma of omnivores (n = 40), vegetarians (n = 36) and vegans (n = 42) in Austria was evaluated., Methods: The evaluation was done using the functional parameters erythrocyte transketolase (ETK), glutathione reductase (EGR) and glutamic oxaloacetic transaminase (EGOT) activation coefficients. Enzyme activity was measured photometrically. The quantity of vitamins B(1), B(2) and B(6) in urine and the concentrations of vitamin B(6) and homocysteine in plasma were determined by HPLC methods with fluorescence detection. Plasma concentration of vitamin B(12) and folic acid were measured with radioimmunoassay., Results: Most of the subjects showed a satisfying vitamin B(1) status. Vegans presented a significantly lower mean plasma vitamin B(12) concentration than omnivores and vegetarians and deficiency in 2.4% of the volunteers but the highest mean value of plasma folate among the investigated groups. A deficient status of folate was found in 18% of omnivores and in approximately 10% of vegans and vegetarians. The status of riboflavin is considered to be deficient in about 10% of omnivores and vegetarians and in over 30% of vegans. According to the activation coefficient of GOT, approximately one third of all subjects showed vitamin B(6) deficiency. Elevated homocysteine concentration in plasma was observed in 66% of the vegans and about 45-50% of the omnivores and vegetarians. Vegan subjects had significantly higher mean plasma homocysteine levels than omnivores., Conclusion: Thiamin and folate need not be a problem in a well-planned vegan diet. Vitamins B(12) and B(2) may need attention in the strict vegan diet, especially regarding elevated homocysteine levels in plasma. Pyridoxine status appeared to be independent of the diet., (Copyright 2006 S. Karger AG, Basel.)

In a pilot study we measured the effect of three different combinations of the vitamins B6, folate and B12 on the serum concentrations of homocysteine, cystathionine and methylmalonic acid in five healthy young men without hyperhomocysteinemia. The results indicate that there are still undescribed interactions between vitamin B6 and folate, suggesting that these two vitamins should be given together to avoid depletion of the one not given. With regard to the well known metabolic pathways of methionine and cysteine, this confirms the hypothesis that a combined supplementation with the vitamins B6 and folate (and B12) is superior to folate alone in order to lower homocysteine.

Objectives: To study the prevalence of iron and vitamin deficiencies, endocrine disorders and immunological parameters in patients with primary Sjogren's syndrome (1 degree SS)., Design and Subjects: At the time of the establishment of the diagnosis of 1 degree SS in 43 consecutive patients, a clinical examination including haematological analyses was performed. The patients' medical records were also reviewed., Setting: Patients referred for diagnosis to The University Hospital, Linköping, a secondary or tertiary referral hospital serving the middle part of southern Sweden., Results: In total, current or previously treated iron and vitamin deficiencies were registered for 63% of the 1 degree SS patients (iron 51%, vitamin B12 25%, folate 9%). Current low ferritin was noted in 24%, low iron saturation in 37%, decreased vitamin B12 in 13% and folate in 9%. Thyroid disease was found in a total of 33% and 30% had had autoimmune thyroiditis. Three patients (7%) had verified diabetes mellitus. Erythrocyte sedimentation rate (ESR) was raised in 65% of the patients and 84% had a polyclonal increase of Ig. Rheumatoid factor (RF) was detected in 85%, antinuclear antibody (ANA) in 74%, anti-SS-A in 88% and anti-SS-B in 73% of the patients., Conclusion: Iron and vitamin deficiencies and thyroid diseases are common in patients with 1 degree SS. Since these disorders often are treatable and may affect the patients' distress as well as their immune and exocrine function, an active, recurrent search for deficiencies, endocrine diseases and other frequently recorded disorders is recommended.

Objective: This study compared food intake among patients with recurrent aphthous stomatitis (RAS) and control patients., Study Design: A total of 2129 outpatients of a dental hospital were enrolled. Of these, 118 patients reporting RAS experiences 4 times or more during the past year (RAS group) were selected with age-matched and sex-matched control patients. The patients filled out a questionnaire about the frequency intake of 33 foods., Results: Principal component factor analysis extracted 2 food intake patterns (Factor I and II). The factor weight for Factor I showed a significantly positive correlation with consumption ratios of calcium, iron, vitamin B1, and vitamin C intake to total daily intake. The median factor score for Factor I, which was calculated based on the factor weight, was significantly lower in the patients with RAS than that in the controls., Conclusion: We hypothesize that not only iron and vitamin B1 might be deficient in these patients but also calcium and vitamin C.

Celiac disease is a genetically-based intolerance to gluten. In the past, celiac disease has been considered a rare disease of infancy characterized by chronic diarrhea and delayed growth. Besides the overt enteropathy, there are many other forms which appear later in life; target organs are not limited to the gut, but include liver, thyroid, skin and reproductive tract. It is now recognized that celiac disease is a relatively frequent disorder; the overall prevalence is at least 1:300 in Western Europe. Celiac disease may impair the reproductive life of affected women, eliciting delayed puberty, infertility, amenorrhea and precocious menopause. Clinical and epidemiological studies show that female patients with celiac disease are at higher risk of spontaneous abortions, low birth weight of the newborn and reduced duration of lactation. No adequate studies are available on the rate of birth defects in the progeny of affected women; however, celiac disease induces malabsorption and deficiency of factors essential for organogenesis, e.g. iron, folic acid and vitamin K. The overall evidence suggests that celiac disease patients can be a group particularly susceptible to reproductive toxicants; however, the pathogenesis of celiac disease-related reproductive disorders still awaits clarification. At present, like the other pathologies associated with celiac disease, the possible prevention or treatment of reproductive effects can only be achieved through a life-long maintenance of a gluten-free diet.

This article discusses the metabolism of homocysteine, factors affecting its plasma level, and the evidence for its role in the pathogenesis of vascular disease. The treatment of hyperhomocysteinemia and its possible impact on vascular disease prevention and progression are described also.

In contrast to the classic, slowly progressive polyneuropathy in alcoholic patients, acute forms, clinically mimicking Guillain-Barré syndrome, are rare. We present a patient who developed motor weakness and sensory loss in all four limbs within four days. Laboratory data were consistent with long-term alcohol abuse and documented thiamine deficiency. Repeated cerebrospinal fluid examinations were normal. Electrophysiological studies showed an acute sensorimotor polyneuropathy with predominantly axonal involvement. We conclude that acute alcoholic neuropathy has to be distinguished from Guillain-Barré syndrome and other forms of acute polyneuropathy by using clinical, laboratory, and electrophysiological data. Both ethanol toxicity and vitamin deficiency could play a role in the pathogenesis.

We present a patient with type 1 diabetes mellitus, who had severe, progressive macrovascular disease despite an optimal control of modifiable risk factors. Screening for other risk factors revealed a markedly elevated plasma homocysteine level, that was secondary to pernicious anemia. The biological and clinical implications of this association are discussed.

An amino acid formula produced in Japan is not supplemented with biotin since biotin is not permitted as a food additive. Biotin deficiency developed in an 11-month-old Japanese infant who had been diagnosed as a neonate with cow milk and soy bean allergy and fed with an amino acid formula and hypoallergenic rice processed by protease. Serum levels of zinc, essential fatty acids and biotinidase were within the normal range while that of biotin was below the normal range. Urinary 3-hydroxy-isovalerate and slightly elevated levels of plasma branched-chain amino acids disappeared 1 week after oral supplementation with 1 mg day-1 of biotin as did the symptoms of orificial skin lesions, lethargy, hypotonia and alopecia later. In summary, to prevent biotin deficiency, biotin should be added to the Japanese amino acid formula.

Although the general health and development of vegan and vegetarian children seem to be normal, there may be subtle differences compared with omnivores. They are at increased risk of iron deficiency, and impaired psychomotor development associated with iron deficiency has been reported in macrobiotic infants. Fortunately, this impairment is not permanent, and follow-up studies have reported higher-than-average intelligence quotients among older macrobiotic children. Several other hazards of vegetarian diets have been identified, including vitamin B12 deficiency, rickets, and a bulky diet that can restrict energy intake in the first few years of life; however, these pitfalls can be avoided easily, and children can be successfully reared on vegetarian diets.

Carnitine is essential for muscle energy production and is required for the transport of long chain fatty acids and acyl co-enzyme A derivatives across the inner mitochondrial membrane. Recently, an absorptive transport mechanism was discovered at the small bowel level suggesting the possibility of a carnitine deficient state in patients with mucosal damage. Therefore, this study investigated carnitine concentrations in serum of patients with coeliac disease. Serum samples were obtained from 12 patients with active coeliac disease and seven with non-active disease, and compared with serum samples of 17 children with gastrointestinal symptoms but with a small bowel normal on biopsy examination and 33 normal controls. Total serum carnitine concentration was significantly lower in the patients with coeliac disease compared with the other two groups and to reference values. When the degree of atrophy of coeliac intestinal mucosa was numerically graded, serum carnitine concentrations did not correlate to the degree of the intestinal lesion but were significantly lower in the damaged intestine compared with the group with normal mucosa. It is suggested that coeliac disease should be considered as a potential cause of secondary carnitine deficiency.

Objective: To evaluate carnitine (3-hydroxy-4-N-trimethyl-ammoniobutanoate) deficiency in AIDS patients by measuring serum total, free and short-chain carnitine concentrations., Design: We conducted an open study., Setting: All patients were seen at the Infectious Diseases Clinic, Università 'La Sapienza', Rome, Italy., Patients, Participants: Twenty-nine AIDS patients, aged 27-41 years, with a previous history of drug use; and 14 healthy age- and sex-matched controls were studied., Interventions: Study subjects were administered 500-800 mg zidovudine daily for 2 to 28 months (8 +/- 6 months)., Main Outcome Measures: Carnitine deficiency was suspected in study participants prior to data collection because of previously reported cardiac symptoms, muscle weakness, hypometabolism and/or cachexia., Results: A marked decrease in total and free carnitine was observed in 21 (72%) subjects. Nine of these patients also had low levels of short-chain carnitine., Conclusions: AIDS patients may become carnitine-depleted and therefore at risk for alterations in fatty-acid oxidation and energy supply.

Vitamin B1, B2 and B6 status were determined in 90 male heroin addicts admitted to Pramongkutklao Army Hospital. Their age (Mean +/- S.D.) was 25.5 +/- 7.8 years. Their activation coefficients of the enzyme transketolase, glutathione oxidoreductase and aspartate aminotransferase (ETK AC, EGR AC and EAST AC respectively) were significantly increased for addicts who were on drugs for a long time which indicated a biochemical deficiency. In addition, 26 follow-up cases treated with methadone for a period of one and two weeks were compared before and after treatment and it was found that ETK AC, EGR AC, and EAST AC were significantly decreased. This means that improvement in the vitamin B1, B2 and B6 status was obtained during admission.

Although specific vitamin deficiency syndromes are relatively rare in the United States, primary care physicians may encounter them in elderly patients and persons who consume minimal diets. Knowledge of such deficiencies is crucial in the evaluation of these patients. The authors discuss manifestations of deficiency of vitamins A, B, and C and recommend appropriate methods of diagnosis and treatment.

Cancer often causes malnutrition and specific vitamin and protein deficiencies. Chemotherapy also causes deficiencies by promoting anorexia, stomatitis, and alimentary tract disturbances. Antimetabolite drugs in particular inhibit synthesis of essential vitamins, purines, and pyrimidines. Because vitamin levels in the blood are often nondiagnostic, nutritional deficiency is identified almost exclusively on the basis of clinical signs and symptoms and the patient's response to therapy. Signs and symptoms of cachexia and hypoalbuminemia are common in patients with advanced cancer. Deficiencies of vitamins B1, B2, and K and of niacin, folic acid, and thymine also may result from chemotherapy. Nutritional deficiencies are chemically correctable; however, the tumor must be eradicated to relieve cachexia.

In conclusion we may state that a borderline vitamin deficiency exists in many population groups as well as in single persons even in industrialized countries. The reason for this fact is mainly the low education which is often associated with a low socioeconomic status and certain food patterns which derive from tradition, emotion or from other reasons not yet well understood. We have proved that the avoidance of pork and whole-wheat bread leads to a borderline vitamin B1 deficiency and the avoidance of citrus fruits, fruits, vegetables, viscera and potatoes to a broderline vitamin C deficiency. On the other hand, preference of meat did not show any adverse effect in respect to the vitamin B6 status. We believe that this kind of studies has to be continued, since the aim of nutritional surveys should consist in improving the nutritional status of the general population or of population groups. Therefore, it should be investigated why in certain population groups poor nutrition exists. Only the answer to this question could help us to combat malnutrition in industrialized countries in the best way.

Carnitine deficiency has been claimed to be responsible for the myo- and cardio-myopathy observed in dialysis patients and has been attributed to the loss of carnitine during dialysis. To quantitate carnitine loss, we determined the carnitine concentrations in 29 patients on chronic hemodialysis, 10 patients on chronic hemofiltration, and 8 patients on CAPD. Mean plasma carnitine levels in hemodialysis and hemofiltration patients (39.8 +/- 2.7 mumoles/liter; N = 39) were significantly lower (P less than 0.01) than in controls (49.8 +/- 2.0 mumoles/liter; N = 43). Hemodialysis or hemofiltration led to a further reduction (33.2 +/- 3.5 mumoles/liter; P less than 0.001). There was no significant difference in the mean plasma carnitine level between CAPD patients (40.0 +/- 5.7 mumoles/liter) and controls. Hemofiltration treatment resulted in a weekly loss of 795 +/- 84 mumoles of carnitine. This was significantly lower (P less than 0.0001) than the urinary carnitine excretion in healthy controls (1534 +/- 134 mumoles per week; N = 27) and the carnitine elimination in the dialysate of CAPD patients (1905 +/- 236.6 mumoles per week; N = 8). It is concluded that carnitine deficiency in dialysis patients cannot be explained by loss into dialysate or filtrate. Because intestinal reabsorption of carnitine does not seem to be impaired, decreased endogenous carnitine synthesis is considered as the most plausible explanation for the moderate degree of carnitine deficiency observed in dialysis patients.