vitamin-b-12 and Autism-Spectrum-Disorder

Topics: Adolescent; Autism Spectrum Disorder; Child; Dietary Supplements; Folic Acid; Humans; Retrospective Studies; Vitamin B 12; Vitamins; Water

Autism Spectrum Disorder (ASD) has become a major public health concern due to its rapidly rising incidence over the past few years. Disturbances in folate or methionine metabolism have been identified in many individuals with ASD, suggesting that the folate-methionine cycle may play an essential role in the pathogenesis of autism. Thus, changes in metabolite concentrations associated with this cycle could be used as potential biomarkers and therapeutic targets for ASD. The aim of this systematic review is to elucidate the perturbations of this cycle and the possible interventions that may be proposed in this context. Several studies have shown that high levels of homocysteine and low levels of vitamins B12 and folate are associated with ASD. These changes in serum metabolites are influenced by poor diet. In fact, children with ASD tend to eat selectively, which could compromise the quality of their diet and result in nutrient deficiencies. Moreover, these disturbances may also be caused by genetic predispositions such as polymorphisms of the

Topics: Autism Spectrum Disorder; Child; Dietary Supplements; Folic Acid; Humans; Methionine; Racemethionine; Vitamin B 12

Autism spectrum disorder (ASD) is characterized by early-appearing social communication deficits, with genetic and environmental factors potentially playing a role in its etiology, which remains largely unknown. During pregnancy, certain deficiencies in critical nutrients are mainly associated with central nervous system impairment. The vitamin B9 (folate) is primarily related to one-carbon and methionine metabolism, participating in methyl donor generation. In addition, supplementation with folic acid (FA) is recommended by the World Health Organization (WHO) in the first three gestational months to prevent neural tube defects. Vitamin B12 is related to folate regeneration, converting it into an active form. Deficiencies in this vitamin have a negative impact on cognitive function and brain development since it is involved in myelin synthesis. Vitamin D is intimately associated with Ca

Topics: Autism Spectrum Disorder; Female; Folic Acid; Humans; Hydrocortisone; Pregnancy; Retrospective Studies; Vitamin A; Vitamin B 12; Vitamin D; Vitamin K; Vitamins

Cobalamin C disease is the most common complementation class of cobalamin disorders. Here, we present a case of a 14-yr-old male with early-onset cblC disease and autism spectrum disorder (ASD) admitted to our inpatient medical service for behavioral decompensation. We use this case to highlight key aspects of the neurodevelopmental and neuropsychiatric disorders associated with cblC disease. By incorporating a comprehensive review of existing literature, we highlight salient domains of psychological impairment in cblC disease, discuss the full range of neuropsychiatric presentations, and review clinical management implications unique to cblC disease.

Topics: Amino Acid Metabolism, Inborn Errors; Autism Spectrum Disorder; Carrier Proteins; Homocystinuria; Humans; Male; Methylmalonic Acid; Mutation; Vitamin B 12; Vitamin B 12 Deficiency

Recently, connections have been made between feeding and eating problems and autism spectrum disorder (ASD) and between autism pathophysiology and diet issues. These could explain some of the mechanisms which have not yet been discovered or are not sufficiently characterized. Moreover, there is an increased awareness for micronutrients in ASD due to the presence of gastrointestinal (GI) problems that can be related to feeding issues. For example, levels of vitamins B

Topics: Autism Spectrum Disorder; Avitaminosis; Child; Correlation of Data; Female; Humans; Male; Micronutrients; Pyridoxine; Thiamine; Vitamin A; Vitamin B 12; Vitamin D

Children with autism spectrum disorders show higher food selectivity, which restricts consumption of some foods and may cause nutritional deficiencies. The aims of this meta-analysis are to determine the overall differences in nutritional intake and food consumption between children with autism spectrum disorder and control (typical development) children, as well as determine the extent to which the nutritional intake and food consumption of autistic children comply with the dietary recommendations. Children with autism spectrum disorder consume less protein (standardized mean difference = -0.27, 95% confidence interval (-0.45, -0.08)), calcium (-0.56 (-0.95, -0.16)), phosphorus (-0.23 (-0.41, -0.04)), selenium (-0.29 (-0.44, -0.13)), vitamin D (-0.34 (-0.57, -0.11)), thiamine (-0.17 (-0.29, -0.05)), riboflavin (-0.25 (-0.45, -0.05)) and vitamin B12 (-0.52 (-0.95, -0.09)) and more polyunsaturated fat acid (0.27 (0.11, 0.44)) and vitamin E (0.28 (0.03, 0.54)) than controls. Autistic children also consume less omega-3 (-0.83 (-1.53, -0.16)) and more fruit (0.35 (0.12, 0.59)) and vegetables (0.35 (0.09, 0.61)) than control children; however, these results must be considered with care due to the low number of studies included in the analysis and the high heterogeneity. The results also suggest a lower intake of calcium, vitamin D and dairy and a higher intake of fruit, vegetables, protein, phosphorus, selenium, thiamine, riboflavin and vitamin B12 than recommended.

Topics: Adolescent; Autism Spectrum Disorder; Calcium, Dietary; Case-Control Studies; Child; Child, Preschool; Diet; Dietary Fats; Dietary Fats, Unsaturated; Dietary Proteins; Eating; Fatty Acids, Omega-3; Feeding Behavior; Food Preferences; Fruit; Humans; Infant; Nutrition Policy; Phosphorus, Dietary; Riboflavin; Selenium; Thiamine; Trace Elements; Vegetables; Vitamin B 12; Vitamin D; Vitamin E; Vitamins

Children with autism spectrum disorder (ASD) have been reported to have reduced ability to methylate DNA and elevated markers of oxidative stress. We sought to determine if methyl B12, a key metabolic cofactor for cellular methylation reactions and antioxidant defense, could improve symptoms of ASD.. A total of 57 children with ASD were randomly assigned to 8 weeks of treatment with methyl B12 (75 μg/kg) or saline placebo every 3 days in a subcutaneous injection. The primary outcome measure was overall improvement in symptoms of ASD as measured by the Clinical Global Impressions-Improvement (CGI-I) score. Secondary outcome measures included changes in the Aberrant Behavior Checklist (ABC) and the Social Responsiveness Scale (SRS). Laboratory measures of methionine methylation and antioxidant glutathione metabolism were assessed at baseline and 8 weeks.. A total of 50 children (mean age 5.3 years, 79% male) completed the study. The primary outcome measure - the clinician rated CGI-I score - was statistically significantly better (lower) in the methyl B12 group (2.4) than in the placebo group (3.1) (0.7 greater improvement in the methyl B12 group, 95% CI 1.2-0.2, p = 0.005). Clinical improvement among children treated with methyl B12 was positively correlated with increases in plasma methionine (p = 0.05), decreases in S-adenosyl-l-homocysteine (SAH) (p = 0.007) and improvements in the ratio of S-adenosylmethionine (SAM) to SAH (p = 0.007), indicating an improvement in cellular methylation capacity. No improvements were observed in the parent-rated ABC or SRS.. Methyl B12 treatment improved clinician-rated symptoms of ASD that were correlated with improvements in measures of methionine metabolism and cellular methylation capacity. Clinical Trial Registry: Efficacy Study of Subcutaneous Methyl B12 in Children with Autism: NCT01039792 ( clinicaltrials.gov1 ).

Topics: Antioxidants; Autism Spectrum Disorder; Biomarkers; Child; Child, Preschool; Double-Blind Method; Female; Follow-Up Studies; Glutathione; Humans; Male; Methionine; Oxidative Stress; Psychiatric Status Rating Scales; Treatment Outcome; Vitamin B 12

Folate and vitamin B

Topics: Adolescent; Autism Spectrum Disorder; Case-Control Studies; Child; Child, Preschool; Female; Folic Acid; Humans; Neural Tube Defects; Pregnancy; Retrospective Studies; Vitamin B 12; Vitamins

Topics: Adult; Autism Spectrum Disorder; Autistic Disorder; Case-Control Studies; Child; Female; Humans; Mothers; Pregnancy; Vitamin B 12

Topics: Autism Spectrum Disorder; Child; Developmental Disabilities; Humans; Infant, Newborn; Infant, Newborn, Diseases; Nervous System Malformations; Vitamin B 12

Autism spectrum disorders (ASDs) are neurodevelopmental disorders with an increasing prevalence but lack reliable biomarkers for early diagnosis. The present study investigated 13 serological metabolites and 2 genetic variants related to folate metabolism in a total of 89 ASD cases and 89 matched controls. Fisher discriminant analysis was used to establish the classification model to recognize ASD cases and controls. Ten metabolites were significantly different between the groups, of which six metabolites were used as predictors to determine the discriminant prediction model: vitamin B12, 5-methylene-tetrahydrofolate, methonine, the ratio of S-adenosylmethionine/S-adenosylhomocysteine, methionine synthase and transcobalamin II. The model had statistical significance (lambda=0.520, χ

Topics: 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase; Autism Spectrum Disorder; Biomarkers; Case-Control Studies; Child; Child, Preschool; Discriminant Analysis; Female; Folic Acid; Homocysteine; Humans; Male; Polymorphism, Single Nucleotide; S-Adenosylhomocysteine; Tetrahydrofolates; Transcobalamins; Vitamin B 12

Autism spectrum disorder (ASD) is characterized by severe and persistent difficulties in social communication and social interaction at multiple levels. Recently, metabolic disorders have been associated with most cases of patients with ASD. The aim of this study was to investigate, through a new and more sophisticated mass technique, such as UHPLC-mass spectrometry (Q-exactive analyzer), alteration in metabolisms analyzing ASD children urine samples from children showing simultaneous vitamin B6, B9 and B12 deficiencies. This in order to study how these concurrent deficiencies may influence some phenotypic aspects of autistic disorder. Thus, urinary metabolic patterns specific to ASD were explored at an early age in 60 children with ASD, showing lower three vitamins levels, and 60 corresponding controls (age group 3-8, M: F=42:18). The results showed significant block of cystathionine formation with consequent accumulation of homocysteine. A lower glutathione levels (GSH), with reduction of essential intracellular reducing environment required for normal immune function, detoxification capacity and redox-sensitive enzyme activity. Increased concentration of 5-methyltetrahydrofolate, which leads to a lower availability of methyl group and significant decrease in urinary methionine and S-adenosyl-L-methionine (SAM) concentrations, the major methyl donor. The latter justify the well-known reduction in protein and DNA methylation reported in autistic children. As a final consideration, the concomitant deficiencies of all three B vitamins, recorded in a significant number of autistic children, suggests that intestinal dysbiosis in these patients may be the main cause of a reduction in their absorption, in addition to the genetic mutation of a specific gene.

Topics: 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase; Autism Spectrum Disorder; Child; Child, Preschool; Chromatography, High Pressure Liquid; Cystathionine; Female; Folic Acid; Glutathione; Homocysteine; Humans; Male; Mass Spectrometry; Methionine; Methylation; Mutation; Oxidation-Reduction; Phenotype; Vitamin B 12; Vitamin B 6

To examine the prospective association between multivitamin supplementation during pregnancy and biomarker measures of maternal plasma folate and vitamin B. This report included 1257 mother-child pairs, who were recruited at birth and prospectively followed through childhood at the Boston Medical Center. ASD was defined from diagnostic codes in electronic medical records. Maternal multivitamin supplementation was assessed via questionnaire interview; maternal plasma folate and B. There was a 'U shaped' relationship between maternal multivitamin supplementation frequency and ASD risk. Extremely high maternal plasma folate and B

Topics: Adult; Autism Spectrum Disorder; Biomarkers; Child; Dietary Supplements; Female; Folic Acid; Humans; Interviews as Topic; Male; Pregnancy; Prospective Studies; Risk Factors; Vitamin B 12; Vitamins

BACKGROUND Both genetic and environmental factors play a role in the development of autism spectrum disorder (ASD). This case-control study examined the association between childhood ASD and single-nucleotide polymorphisms (SNPs) in genes involved with vitamin B12 and folate metabolism. MATERIAL AND METHODS Genotypes of transcobalamin 2 (TCN2) rs1801198, methionine synthase (MTR) rs1805087, methionine synthase reductase (MTRR) rs1801394, and methylene tetrahydrofolate reductase (MTHFR) rs1801133 were examined in 201 children with ASD and 200 healthy controls from the Han Chinese population. RESULTS Our results showed no association of all examined SNPs with childhood ASD and its severity. CONCLUSIONS None of the examined SNPs were a risk factor for the susceptibility to childhood ASD and severity of the disease in a Han Chinese population.

Topics: 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase; Adolescent; Alleles; Asian People; Autism Spectrum Disorder; Case-Control Studies; Child; China; Ethnicity; Female; Ferredoxin-NADP Reductase; Folic Acid; Genetic Association Studies; Genetic Predisposition to Disease; Genotype; Haplotypes; Humans; Male; Methylenetetrahydrofolate Reductase (NADPH2); Polymorphism, Single Nucleotide; Risk Factors; Transcobalamins; Vitamin B 12

BACKGROUND The purpose of this study was to assess the values of the mean platelet volume (MPV) in children with attention deficit hyperactivity disorder (ADHD) and with autism spectrum disorders (ASDs) to determine the risk of cardiovascular disease in these 2 disorder groups. MATERIAL AND METHODS The study included a total of 79 patients with ADHD or ASDs and controls in the Van region of Turkey. The control group included subjects of matching age and sex with no ADHD, ASDs, or chronic disease and taking no vitamins. The hematological parameters of the patients, including MPV, vitamin B12, and vitamin D, were assessed. RESULTS The study included a total of 79 children and adolescents aged 2-18 years (32 females and 47 males). Of the patients, 36 were in the ADHD group, 18 in the ASDs group, and 25 in the control group. There was no statistically significant difference in hematological parameters between the groups, but there were significant differences in terms of vitamin D and vitamin B12. The patient groups showed lower levels of vitamin B12 and vitamin D. In the ADHD group, there was a negative correlation between both vitamins and MPV (p<0.05). Partial correlation analysis of the ADHD group showed that MPV in particular was negatively correlated to vitamin D, and not to vitamin B12 (p: 0.03). CONCLUSIONS Both ADHD and ASDs may accompany increased risk for cardiovascular disease due to the presence of vitamin B12 and D deficiency and their own characteristics. Therefore, these disorders should be closely followed up.

Topics: Adolescent; Attention Deficit Disorder with Hyperactivity; Autism Spectrum Disorder; Avitaminosis; Biomarkers; Cardiovascular Diseases; Child; Female; Humans; Male; Mean Platelet Volume; Risk Factors; Vitamin B 12; Vitamin D

Cobalamin (vitamin B12 [Cbl]) is an essential cofactor for many biochemical pathways. Transcobalamin (TC) is required to internalize Cbl into the cells through membrane receptor-mediated endocytosis. Cbl is then processed in the cytoplasm and mitochondria by complementation factors leading to its active metabolites; methylcobalamin and 5-deoxyadenosyl-cobalamin. Deficiency of TC results in an elevation in methylmalonic acid and homocysteine. Patients usually present with macrocytic anemia, pancytopenia, failure to thrive, gastrointestinal symptoms, and neurological dysfunction. In this study, we report 4 patients from 2 unrelated families, with confirmed diagnosis of TC deficiency. Patients initially had a typical presentation of TC deficiency: severe diarrhea and vomiting, recurrent infections, stomatitis, macrocytic anemia, and neutropenia. Interestingly one of the patients was diagnosed at 3 months of age and developed ataxic gait related to cerebellar atrophy at the age of 14 months. His elder affected sibling was diagnosed at 5 months of age was completely normal. Two sibs, diagnosed at 2 months of age and immediately after birth, had autism spectrum disorder. Molecular investigations showed 2 novel mutations in TCN2 gene. Patients were treated and stayed stable on weekly injection of Cbl. In conclusion, TC deficiency has a wide heterogeneity in clinical phenotype, genotype, laboratory, and radiologic findings. Early detection of the disease and early initiation of aggressive parenteral treatment is probably associated with better prognosis and disease control.

Topics: Autism Spectrum Disorder; Biomarkers; Brain; Child, Preschool; DNA Mutational Analysis; Fibroblasts; Follow-Up Studies; Genetic Association Studies; Genetic Predisposition to Disease; Humans; Infant; Infant, Newborn; Magnetic Resonance Imaging; Male; Mutation; Transcobalamins; Vitamin B 12

Foley et al. (2014) published their findings in this journal on the role of prenatal exposure to propionic acid (PPA) and behavioral outcomes in treated rat pups. The authors show that PPA treated pups displayed subtle differences in behavior including nest seeking, novel object recognition, and locomotor activity. Others have previously proposed that PPA infusion in rat could represent a valid animal model of ASD since many of the diagnostic criteria for the disorder spectrum manifest under such conditions. A pathogenic makeover of gut microbiome to facilitate the growth of microbes capable of producing PPA, like Clostridia species, has been proposed as an infectious contributing etiology to the PPA model of ASD, however the reason for this pathogenic microbial overgrowth is not clear. This discussion highlights a previously identified novel environmental factor (i.e., nitrous oxide, N

Topics: Animals; Animals, Newborn; Autism Spectrum Disorder; Disease Models, Animal; Environment; Nitrous Oxide; Propionates; Rats; Vitamin B 12

Fatty acids are critical for pediatric neurodevelopment and are abnormal in autism, although prior studies have demonstrated conflicting results and methodological differences. To our knowledge, there are no published data on fatty acid in Canadian children with autism. The aim of this study was to investigate red blood cell and serum fatty acid status to identify whether abnormalities exist in Canadian children with autism, and to enhance future cross-study comparison.. Eleven Canadian children with autism (3 girls, 8 boys; age 3.05 ± 0.79 y) and 15 controls (9 girls, 6 boys; age 3.87 ± 1.06 y) met inclusion criteria, which included prior Diagnostic and Statistical Manual diagnosis of autism spectrum disorder, no recent medication or supplements, no specialty diets, and no recent illness.. The children with autism demonstrated lower red blood cell docosahexaenoic acid (P < 0.0003), eicosapentaenoic acid (P < 0.03), arachidonic acid (P < 0.002), and ω-3/ω-6 ratios (P < 0.001). They also demonstrated lower serum docosahexaenoic acid (P < 0.02), arachidonic acid (P < 0.05), and linoleic acid (P < 0.02) levels.. Fatty acids in both serum and red blood cells were abnormal in this small group of Canadian children with autism than in controls, underlining a need for larger age- and sex-matched investigations in this community. A potential role for fatty acid abnormalities within the complex epigenetic etiology of autism is proposed in relation to emerging understanding of relationships between cobalamin metabolism, gut microbiota, and propionic acid production.

Topics: Arachidonic Acid; Autism Spectrum Disorder; Autistic Disorder; Canada; Case-Control Studies; Child, Preschool; Cross-Sectional Studies; Docosahexaenoic Acids; Eicosapentaenoic Acid; Erythrocytes; Fatty Acids; Fatty Acids, Omega-6; Female; Humans; Linoleic Acid; Male; Propionates; Vitamin B 12

In our study, we aimed to reveal pathophysiologic mechanisms in ASD by comparing plasma amino acid levels between patients and healthy controls while considering vitamin B12 and D levels.. The study included 21 patients aged 2-18 years-old who were followed with a diagnosis autism spectrum disorder (ASD) and 21 age and sex-matched healthy children from our outpatient clinic as control group.. The study included 42 children and adolescents aged 2-18 years-old (19 girls and 23 boys). There were no significant differences in terms of body weight and height between the groups. We found significant differences in levels of ammonium, phosphoethanolamine, histidine, homocysteine, carnosine, methionine, cystathionine, cystine, threonine, 3-methyl histidine and phenylalanine/tyrosine ratio between patient and control groups. Both vitamin B12 and D were significantly lower in the ASD group compared to controls. In the variance analysis with vitamin B12 and D as covariates, significant differences persisted for only phosphoethanolamine (p=0.04), cystathionine (p<0.001), cystine (p=0.006) and threonine (p=0.02).. Further studies are needed on the amino acids that show variations in children with ASD in order to reveal their role in the etiology and therapeutic use in ASD.

Topics: Adolescent; Amino Acids; Autism Spectrum Disorder; Case-Control Studies; Child; Child, Preschool; Female; Humans; Male; Vitamin B 12; Vitamin D