Steroid hormone pathways, vitamin D and autism: a systematic review.

The origins of the male preponderance in autism incidence remain unclear. The idea that perinatal factors associated with sex differentiation (e.g., steroid hormone pathways) may increase the possibility of the emergence of autism is complementary to the hypothesis that female individuals are intrinsically less likely to develop autism. Empirical evidence for the mechanistic roles of in utero steroid hormones in autism etiology is accumulating but inconsistent. We conducted a systematic review using rigorous criteria for the measurements of steroids and vitamin D exposure, to summarize the potential contributing roles of prenatal and early postnatal steroids and vitamin D alterations to the emergence of autism. We searched PubMed, PsychInfo, Scopus, and included 22 studies for qualitative synthesis. Among them, six studies examined the association of autism diagnoses in offspring and levels of steroids and precursor steroid hormones in the fetal environment, eight studies examined the associations between autism and maternal and fetal blood vitamin D levels during pregnancy and at birth, and eight studies examined the associations between offspring autism diagnoses and maternal hyperandrogenemia diagnosed before pregnancy. We identified promising and complex results regarding the relations between steroid metabolism and autism. The interpretation of findings was limited by the mostly observational study designs, insufficient investigation of the effects of offspring sex, confounders and their cumulative effects on the development of the child, and unclear impact of the timing of steroids exposure and their effects on fetal neurodevelopment.

Supplementation with selenium attenuates autism-like behaviors and improves oxidative stress, inflammation and related gene expression in an autism disease model.

Autism spectrum disorder (ASD) refers to a group of neurodevelopmental disorders. The etiology and pathological mechanisms of ASD are still unknown, and its prognosis is poor. This study investigated the effects of selenium (Se) supplementation on abnormal behavior and cognitive function in ASD model mice, as well as the potential action pathways. BTBR mice were randomly assigned to either a model group (BTBR group), a model selenium supplement group (BTBR+Se group), a normal control group (B6 group) or a normal selenium supplement group (B6+Se group). Sodium selenite, at a dosage of 1 mg/kg/day, was administered to the selenium supplementation groups by gavage. The mice in the BTBR group and the B6 group received the same amount of 0.9% saline by gavage. After 4 weeks of continuous intervention, the social functions and cognitive behaviors of the mice and the selenium concentration in hippocampal tissue were assessed. Hippocampal tissue structures were observed. Changes in neurotransmitter levels, oxidative stress and neuroinflammatory indicators were detected. SelP protein expression was significantly lower in hippocampal tissue from BTBR mice than in hippocampal tissue from B6 mice. The administration of sodium selenite in BTBR mice: (1) increased the expression of SelP; (2) attenuated spatial learning, memory impairment and improved social behaviors; (3) changed the serum levels of 5-HT, DA and Glu; (4) decreased the levels of inflammatory cytokines IL-6, IL-1ß, and TNF-α in serum and hippocampal tissue; (5) reduced the ROS and MDA contents and significantly increased SOD activity, CAT activity, GSH-px activity, and antioxidant GSH levels; and (6) protected against neuronal loss in the hippocampus. Se supplementation significantly improved the social functioning, repetitive stereotyped behavior and cognitive function in BTBR mice. Se may play a protective role in the hippocampus of BTBR mice by regulating neurotransmitter levels, reducing oxidative stress, alleviating neuroinflammation and rescuing neural cell damage.

Increased Expression of Kv10.2 in the Hippocampus Attenuates Valproic Acid-Induced Autism-Like Behaviors in Rats.

The role of potassium channels provides suggestive evidence for the etiology of autism. The voltage-gated potassium channel Kv10.2 (KCNH5) is widely expressed in the brain. However, the inherent relationship between Kv10.2 and autism is still unclear. Herein, a rat valproic acid (VPA)-induced autism spectrum disorder model was established. The expression level of Kv10.2 was obviously decreased in the hippocampus of VPA rats. Kv10.2 was mainly localized in neurons. Subsequently, a recombinant lentivirus expressing Kv10.2 was used to upregulate the expression of Kv10.2 in the hippocampus of VPA-exposed rats. The results were promising as injection of the Kv10.2 lentivirus in the hippocampus relieved anxiety and stereotypical behavior, and improved the social and exploratory abilities of rats that were prenatally exposed to VPA. In addition, spectral analysis of electroencephalogram data revealed that animals exposed to VPA exhibited increased high-frequency activity compared with the control rats, and this activity recovered to a certain extent after upregulation of Kv10.2 expression by lentivirus injection. These results suggest that changes in Kv10.2 may play an important role in the etiology of autism, thus providing a promising direction for further research on autism.

Folic acid improves abnormal behavior via mitigation of oxidative stress, inflammation, and ferroptosis in the BTBR T+ tf/J mouse model of autism.

The aim of this study was to examine the effects of folic acid (FA) on the autistic phenotypes in BTBR T+ Itpr3tf/J (BTBR) mice and to investigate underlying mechanisms. Mice received FA (0.2 mg/kg/day) orally from postnatal days 14 to 35. Mice were then tested for stereotyped and repetitive behaviors, social interaction, and spatial learning and memory at the end of FA supplementation. Oxidative stress, neuroinflammatory responses and ferroptosis-related proteins in the brain were also evaluated. FA supplementation in BTBR mice reduced repetitive and stereotyped behavior, improved social communication, and enhanced memory and spatial learning. FA supplementation also reduced neuronal loss in hippocampal CA1 regions of the brain and decreased the levels of the proinflammatory cytokines such as interleukin-1ß (IL-1ß), Iba-1, IL-18, tumor necrosis factor-a, and IL-6 and glial fibrillary acidic protein in the hippocampus. FA supplementation changed the malondialdehyde and glutathione levels and superoxide dismutase (SOD) and glutathione peroxidase activities in the hippocampus. FA supplementation inhibited the elevation of the SOD1 and TFR protein levels and enhanced the relative expression levels of glutathione peroxidase 4 and ferroportin 1 in the hippocampus and increased the relative levels of phospho-Ca2+/calmodulin-dependent protein kinase II and phospho-cAMP-response element binding protein in the hippocampus. FA oral supplementation to BTBR mice rescued stereotyped and repetitive behaviors, social deficit, and spatial learning and memory impairments, likely by improving the oxidative-stress and inflammatory responses by altering the ferroptosis signaling pathways.

The Independent and Combined Effects of Omega-3 and Vitamin B12 in Ameliorating Propionic Acid Induced Biochemical Features in Juvenile Rats as Rodent Model of Autism.

Metabolites of proper fatty acids modulate the inflammatory response and are essential for normal brain development; equally, abnormal fatty acid metabolism plays a critical role in the pathology of autism. Currently, dietary supplements are often used to improve the core symptoms of Autism spectrum disorder (ASD). The present study analyzed the effects of orally supplemented omega-3 (ω-3) and vitamin B12 on ameliorating oxidative stress and impaired lipid metabolism in a propionic acid (PPA)-induced rodent model of autism, together with their effect on the gut microbial composition, where great fluctuations in the bacterial number and strains were observed; interestingly, polyunsaturated fatty acids such as omega-3 induced higher growth of the gram-positive bacterium Staphylococcus aureus and decreased the survival rates of Clostridia sp. as well as other enteric bacterial strains. Thirty-five young male western albino rats were divided into five equal groups. The first group served as the control; the second group was given an oral neurotoxic dose of PPA (250 mg/kg body weight/day) for 3 days. The third group received an oral dose of ω-3 (200 mg/kg body weight/day) for 30 days after the 3-day PPA treatment. Group four was given an oral dose of vitamin B12 (16.7 mg/kg/day) for 30 days after PPA treatment. Finally, group five was given a combination of both ω-3 and vitamin B12 at the same dose for the same duration after PPA treatment. Biochemical parameters related to oxidative stress and impaired fatty acid metabolism were investigated in the brain homogenates of each group. The effects of the dietary supplements on the gut microbiota were also observed. The PPA-treated autistic model expressed significantly higher levels of lipid peroxides and 5-lipoxygenase (5-LOX) and significantly less glutathione (GSH), glutathione S-transferase (GST), and cyclooxygenase 2 (COX2) than the control group. However, a remarkable amelioration of most of the impaired markers was observed with oral supplementation with ω-3 and vitamin B12, either alone or in combination. Our results concluded that impairment at various steps of the lipid metabolic pathways may contribute to the development of autism; however, supplementation with ω-3 and vitamin B12 can result in a positive therapeutic effect.

Association of Folic Acid Supplementation During Pregnancy With the Risk of Autistic Traits in Children Exposed to Antiepileptic Drugs In Utero.

Importance: Strategies to prevent autism in children exposed to antiepileptic drugs (AEDs) during pregnancy are important. Objective: To explore whether folic acid supplementation and folate status in pregnancy are associated with reduced risk of autistic traits owing to in utero AED exposure. Design, Setting, and Participants: The population-based, prospective Norwegian Mother and Child Cohort Study approached Norwegian-speaking women attending routine ultrasonographic examinations from June 1999 through December 31, 2008 (163 844 of 277 702 women refused). No exclusion criteria were applied beyond language. Questionnaires during and after pregnancy, analysis of blood samples, and linkage to the Medical Birth Registry of Norway were performed. Children aged 18 to 36 months of women with available information on use of AEDs and of folic acid supplementation (n = 104 946) were included in the analysis from March 1, 2016, through June 13, 2017. Exposures: Maternal folic acid supplementation 4 weeks before to 12 weeks after conception. Plasma folate concentration was analyzed at gestational weeks 17 to 19. Main Outcomes and Measures: Autistic traits were evaluated using the Modified Checklist for Autism in Toddlers and Social Communication Questionnaire. Odds ratios (ORs) for autistic traits in children by maternal use vs nonuse of folic acid supplements were adjusted for maternal health and socioeconomic factors. Folate concentrations and folic acid doses were associated with the degree of autistic traits. Results: The overall mean (SD) age of the 104 946 mothers of participating children was 29.8 (4.6) years, with complete information available for analysis in 103 868. Mean (SD) age of women with epilepsy who received AED treatment was 29.4 (4.9); women with epilepsy who did not receive AED treatment, 29.1 (4.9); and without epilepsy, 29.8 (4.6) years. In the 335 children exposed to AEDs, the risk for autistic traits was significantly higher at 18 months of age (adjusted OR [AOR], 5.9; 95% CI, 2.2-15.8) and 36 months of age (AOR, 7.9; 95% CI, 2.5-24.9) when their mothers had not used folic acid supplements compared with children of mothers who had used supplements. Among women without epilepsy, the corresponding risks were lower at 18 months of age (AOR, 1.3; 95% CI, 1.2-1.4) and 36 months of age (AOR, 1.7; 95% CI, 1.5-1.9); among the 389 children of women with untreated epilepsy, the corresponding risks were not significant at 18 months of age (AOR, 1.0; 95% CI, 0.4-3.0) and 36 months of age (AOR, 2.5; 95% CI, 0.4-16.6). Degree of autistic traits was inversely associated with maternal plasma folate concentrations (ß = -0.3; P = .03) and folic acid doses (ß = -0.5; P < .001). Concentrations of AEDs were not associated with the degree of autistic traits. Conclusions and Relevance: Risk of autistic traits in children exposed to AEDs in utero may be mitigated by periconceptional folic acid supplementation and folate status. Fertile women using AEDs should take folic acid supplements continuously.

Gestational vitamin D deficiency and autism-related traits: the Generation R Study.

There is intense interest in identifying modifiable risk factors associated with autism-spectrum disorders (ASD). Autism-related traits, which can be assessed in a continuous fashion, share risk factors with ASD, and thus can serve as informative phenotypes in population-based cohort studies. Based on the growing body of research linking gestational vitamin D deficiency with altered brain development, this common exposure is a candidate modifiable risk factor for ASD and autism-related traits. The association between gestational vitamin D deficiency and a continuous measure of autism-related traits at ~6 years (Social Responsiveness Scale; SRS) was determined in a large population-based cohort of mothers and their children (n=4229). 25-hydroxyvitamin D (25OHD) was assessed from maternal mid-gestation sera and from neonatal sera (collected from cord blood). Vitamin D deficiency was defined as 25OHD concentrations less than 25 nmol l-1. Compared with the 25OHD sufficient group (25OHD>50 nmol l-1), those who were 25OHD deficient had significantly higher (more abnormal) SRS scores (mid-gestation n=2866, ß=0.06, P<0.001; cord blood n=1712, ß=0.03, P=0.01). The findings persisted (a) when we restricted the models to offspring with European ancestry, (b) when we adjusted for sample structure using genetic data, (c) when 25OHD was entered as a continuous measure in the models and (d) when we corrected for the effect of season of blood sampling. Gestational vitamin D deficiency was associated with autism-related traits in a large population-based sample. Because gestational vitamin D deficiency is readily preventable with safe, cheap and accessible supplements, this candidate risk factor warrants closer scrutiny.

Vitamin A Deficiency Induces Autistic-Like Behaviors in Rats by Regulating the RARß-CD38-Oxytocin Axis in the Hypothalamus.

SCOPE: Vitamin A (VA) is an essential nutrient for the development of the brain. We previously found that children with autism spectrum disorder (ASD) have a significant rate of VA deficiency (VAD). In the current study, we aim to determine whether VAD is a risk factor for the generation of autistic-like behaviors via the transcription factor retinoic acid receptor beta (RARß)-regulated cluster of differentiation 38 (CD38)-oxytocin (OXT) axis. METHODS AND RESULTS: Gestational VAD or VA supplementation (VAS) rat models are established, and the autistic-like behaviors in the offspring rats are investigated. The different expression levels of RARß and CD38 in hypothalamic tissue and serum retinol and OXT concentration are tested. Primary cultured rat hypothalamic neurons are treated with all-trans retinoic acid (atRA), and recombinant adenoviruses carrying the rat RARß (AdRARß) or RNA interference virus RARß-siRNA (siRARß) are used to infect neurons to change RARß signal. Western blotting, chromatin immunoprecipitation (ChIP), and intracellular Ca2+ detections are used to investigate the primary regulatory mechanism of RARß in the CD38-OXT signaling pathway. We found that gestational VAD increases autistic-like behaviors and decreases the expression levels of hypothalamic RARß and CD38 and serum OXT levels in the offspring. VAS ameliorates these autistic-like behaviors and increases the expression levels of RARß, CD38, and OXT in the gestational VAD pups. In vitro, atRA increases the Ca2+ excitability of neurons, which might further promote the release of OXT. Different CD38 levels are induced in the neurons by infection with different RARß adenoviruses. Furthermore, atRA enhances the binding of RARß to the proximal promoter of CD38, indicating a potential upregulation of CD38 transcriptional activity by RARß. CONCLUSIONS: Gestational VAD might be a risk factor for autistic-like behaviors due to the RARß signal suppression of CD38 expression in the hypothalamus of the offspring, which improves with VAS during the early-life period. The nutritional status during pregnancy and the early-life period is important in rats.

Brain carnitine deficiency causes nonsyndromic autism with an extreme male bias: A hypothesis.

Could 10-20% of autism be prevented? We hypothesize that nonsyndromic or "essential" autism involves extreme male bias in infants who are genetically normal, but they develop deficiency of carnitine and perhaps other nutrients in the brain causing autism that may be amenable to early reversal and prevention. That brain carnitine deficiency might cause autism is suggested by reports of severe carnitine deficiency in autism and by evidence that TMLHE deficiency - a defect in carnitine biosynthesis - is a risk factor for autism. A gene on the X chromosome (SLC6A14) likely escapes random X-inactivation (a mixed epigenetic and genetic regulation) and could limit carnitine transport across the blood-brain barrier in boys compared to girls. A mixed, common gene variant-environment hypothesis is proposed with diet, minor illnesses, microbiome, and drugs as possible risk modifiers. The hypothesis can be tested using animal models and by a trial of carnitine supplementation in siblings of probands. Perhaps the lack of any Recommended Dietary Allowance for carnitine in infants should be reviewed. Also see the video abstract here: https://youtu.be/BuRH_jSjX5Y.

Vitamin D and autism, what's new?

An increasing amount of evidence points to the possibility that gestational and early childhood vitamin D deficiency [25(OH)D < 40 ng/ml] cause some cases of autism. Vitamin D is metabolized into a seco-steroid hormone that regulates about 3% of the 26,000 genes in the coding human genome. It is also a neurosteroid that is active in brain development, having effects on cellular proliferation, differentiation, calcium signaling, neurotrophic and neuroprotective actions; it also appears to have an effect on neurotransmission and synaptic plasticity. Children who are, or who are destined to become, autistic have lower 25(OH)D levels at 3 months of gestation, at birth and at age 8 compared to their unaffected siblings. Two open label trials found high dose vitamin D improves the core symptoms of autism in about 75% of autistic children. A few of the improvements were remarkable. The vitamin D doses used in these children were 300 IU/KG/day up to a maximum of 5000 IU/day (highest final 25(OH)D level reached was 45 ng/ml). The other study used 150,000 IU/month IM as well as 400 IU/day [highest final 25(OH)D level was 52 ng/ml]. These two open label trials were recently confirmed with a randomized controlled trial (RCT) using 300 IU/kg/day with a maximum of 5000 IU/day and resulted in effects similar to the two open label studies. In terms of prevention, a recent small study showed vitamin D supplementation during pregnancy (5000 IU/day) and during infancy and early childhood (1000 IU/day) significantly reduced the expected incidence of autism in mothers who already had one autistic child from 20% to 5%. Vitamin D is safe; for example, over the last 15 years, Poison Control reports there have been approximately 15,000 cases of vitamin D overdose. However only three of these 15,000 people developed clinical toxicity and no one died. Given those facts, practitioners might consider treating autism with 300 IU/kg/day, and seek to prevent autism by supplementing pregnant and lactating women (5000 IU/day) and infants and young children (150 IU/kg/day) checking 25(OH)D levels every 3 months. These doses will increase 25(OH)D blood levels to those recommended by the Endocrine Society. As the American Academy of Pediatrics recommends vitamin D supplementation during infancy and childhood, pediatricians and family practitioners should evaluate the current evidence on autism and vitamin D and act accordingly.

[Vaccines: history and stories between reality and imagination]. / La Storia e le storie sui vaccini. Un piano tra veridicità e fantasia.

Vaccinations and the controversy around them always go in parallel. We identified four categories blending in various amounts of truth and imagination: history, myths, shams and frauds. Over the years, they have alternated and sometimes transformed into one another. This sharp separation into categories is certainly academic and forced. In fact, the line between these aspects is not clear enough to allow a rigid and well-defined division. Our work starts from the category containing the most truthfulness: history, and goes on to analyze two categories that add fantasy to facts: myths and shams (or better, "old wives' tales"). The history deals with the topics of variolation and the first anti-vaccine activists' disputes. Myths that arose around immunization include immune overload, homeoprophylaxis, and excessive hygiene. In this context, immunization itself risked becoming a myth, being considered not amenable to improvements. In the category of old wives' tales we find rumors about the presence in the vaccines of considerable quantities of supposedly toxic components such as aluminum, squalene, Thimerosal and nanoparticles, as well as the existence of secret techniques of vaccine preparation that involve unethical procedures. The last category, fraud, is the poorest in both truth and fantasy but it is still hard to confront. The most famous fraud is the supposed link between vaccines and autism. In this frame, disinformation is certainly a fertile substrate for the emergence both of elements close to reality and of very imaginative ones. Vaccine hesitancy is believed to be responsible for decreasing vaccine coverage and increasing the risk of vaccine-preventable disease outbreaks and epidemics. The role of communication in immunization is essential to its success, especially taking into account the deep transformations the world of information is going through. The great multitude of voices seem to carry the same weight, but it is not so in science. Web searches are influenced by the filter bubble phenomenon, which contributes to the radicalization of people's opinion through cognitive isolation. A new, more effective strategy of communication is required in order to regain the trust of populations in immunization in a context characterized by the presence of groups impervious to scientific evidence.

The maternal body as environment in autism science.

Research on autism and environmental risk factors has expanded substantially in recent years. My analysis draws attention to the regimes of perceptibility that shape how the environment is materialized in post-genomic science. I focus on how more complex narratives of autism's causes and social anxieties surrounding child development have helped situate autism risk in women's bodies before and during pregnancy. This has resulted in what I call the maternal body as environment in autism science. I show that this figure involves three characteristics: the molecularization of the environment, an individualization of risk, and the internalization of responsibility. I argue that these three features point to a new spatial and temporal politics of risk and responsibility that may heighten social and medical surveillance of women's bodies and decisions, eclipsing larger questions about the uneven distribution of exposures in society and more holistic understandings of health that include neurodiversity. I conclude by considering what the maternal body as environment signals for women, social justice, and the politics of environmental health in the post-genomic era.

Autism: Pathophysiology and Promising Herbal Remedies.

Autism is a comprehensive growth abnormality in which social skills, language, communication, and behavioral skills are developed with delay and as diversionary. The reasons for autism are unclear, but various theories of genetics, immunity, biological, and psychosocial factors have been proffered. In fact, autism is a complex disorder with distinct causes that usually co-occur. Although no medicine has been recognized to treat this disorder, pharmacological treatments can be effective in reducing its signs, such as self-mutilation, aggression, repetitive and stereotyped behaviors, inattention, hyperactivity, and sleeping disorders. Recently, complementary and alternative approaches have been considered to treat autism. Ginkgo biloba is one of the most effective plants with an old history of applications in neuropsychological disorders which recently is used for autism. The present review discusses the recent findings, pathophysiology, and etiology of autism and thereafter addresses the promising results of herbal remedies.

Vitamin D hormone regulates serotonin synthesis. Part 1: relevance for autism.

Serotonin and vitamin D have been proposed to play a role in autism; however, no causal mechanism has been established. Here, we present evidence that vitamin D hormone (calcitriol) activates the transcription of the serotonin-synthesizing gene tryptophan hydroxylase 2 (TPH2) in the brain at a vitamin D response element (VDRE) and represses the transcription of TPH1 in tissues outside the blood-brain barrier at a distinct VDRE. The proposed mechanism explains 4 major characteristics associated with autism: the low concentrations of serotonin in the brain and its elevated concentrations in tissues outside the blood-brain barrier; the low concentrations of the vitamin D hormone precursor 25-hydroxyvitamin D [25(OH)D3]; the high male prevalence of autism; and the presence of maternal antibodies against fetal brain tissue. Two peptide hormones, oxytocin and vasopressin, are also associated with autism and genes encoding the oxytocin-neurophysin I preproprotein, the oxytocin receptor, and the arginine vasopressin receptor contain VDREs for activation. Supplementation with vitamin D and tryptophan is a practical and affordable solution to help prevent autism and possibly ameliorate some symptoms of the disorder.

A focus on homocysteine in autism.

Homocysteine is an amino acid, which plays several important roles in human physiology. A wide range of disorders, including neuropsychiatric disorders and autism, are associated with increased homocysteine levels in biological fluids. Various B vitamins: B6 (pyridoxine), B12 (cobalamin), and B9 (folic acid) are required as co-factors by the enzymes involved in homocysteine metabolism. Therefore, monitoring of homocysteine levels in body fluids of autistic children can provide information on genetic and physiological diseases, improper lifestyle (including dietary habits), as well as a variety of pathological conditions. This review presents information on homocysteine metabolism, determination of homocysteine in biological fluids, and shows abnormalities in the levels of homocysteine in the body fluids of autistic children.

Low serum levels of 25-hydroxyvitamin D (25-OHD) in children with autism / Baixos níveis séricos de 25-hidroxivitamina D (25-OHD) em crianças com autismo

Objective: To confirm previous evidence suggesting an association between autism and low vitamin D serum levels. Methods: This preliminary exploratory study assessed the circulating levels of 25-hydroxyvitamin D (25-OHD) in pediatric patients with autism and in typically developing controls from Juiz de Fora, Brazil. Results: Serum levels of 25-OHD were lower in children with autism (26.48 ± 3.48 ng mL-1) when compared to typically developing subjects (40.52 ± 3.13 ng mL-1) (p < 0.001). Conclusion: Our findings attest to the importance of vitamin supplementation during pregnancy and in the treatment of children with autism, who tend to present low vitamin D consumption rates (AU)

Objetivo: Confirmar evidências prévias indicando uma associação entre autismo e baixos níveis séricos de vitamina D. Métodos: Este estudo preliminar avaliou os níveis circulantes de 25-hidroxivitamina D (25-OHD) em pacientes pediátricos com autismo e em controles apresentando desenvolvimento típico em Juiz de Fora, Brasil. Resultados: Os níveis séricos de 25-OHD foram menores em crianças com autismo (26,48 ± 3,48 ng mL-1) em comparação com indivíduos com desenvolvimento típico (40,52 ± 3,13 ng mL-1) (p < 0,001). Conclusão: Nossos resultados confirmam a importância da suplementação de vitamina durante a gravidez e no tratamento de crianças com autismo, que costumam apresentar um baixo consumo de vitamina D (AU)

Lack of correlation between metallic elements analyzed in hair by ICP-MS and autism.

A cross-sectional case-control study was carried out to evaluate the concentrations of metallic elements in the hair of 44 children with diagnosis of autism and 61 age-balanced controls. Unadjusted comparisons showed higher concentrations of molybdenum, lithium and selenium in autistic children. Logistic regression analysis confirmed the role of risk factor for male gender and showed a slight association with molybdenum concentrations. Unconventional chelation and vitamin-mineral supplementation were ineffective on elemental hair concentrations. A meta-analysis including the present and previous similar studies excluded any association of autism with hair concentrations of mercury, cadmium, selenium, lithium and copper. A slight association was found for lead only, but it was very weak, as strictly dependent on the worst data from one study.