Manual Vitamin D handbook: structures, synonyms, and properties

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Supplementary Table 1 provides details of the distributions of the demographic variables before and after imputation. Table 2 summarises the prevalence of 25OHD deficiency in mid-gestation and cord blood for those samples for which SRS scores were available. On average, 25OHD concentrations from cord blood were lower compared with concentrations at mid-gestation mean 25OHD concentration in maternal serum at mid-gestation: Scores on the SRS were available for children.

Scores higher than 1. Mean gender-weighted scores s.

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Mean SRS s. Supplementary Table 3 also provides an overview of the SRS scores for different vitamin D deficiency categories. Table 3 shows the results of the main analyses for the SRS including ethnicity as a covariate. These results imply that, after correcting for confounding variables see notes under Table 3 , those who were deficient at time of birth had on average 0. When treating SRS as a dichotomous outcome, that is, comparing children with SRS scores above the suggested cutoff with children below the suggested cutoff, those who were vitamin D deficient at mid-gestation were 3.

The comparison of SRS scores of those that were deficient at two time points mid-gestation and cord blood versus those that were not deficient at either time point showed that being 25OHD deficient at both time points was predictive of higher SRS scores. When we treated 25OHD concentrations as continuous variables we observed a significant increase in SRS scores with decreasing concentrations of 25OHD for both mid-gestation and cord samples, that is, a similar pattern as observed in the association between vitamin D deficiency categories and SRS Table 3C.

In the analyses restricted to offspring with European ethnicity, we found that the pattern of findings persisted with significant increase in SRS scores for those deficient versus sufficient both Midgestion and Cord and for those insufficient vs sufficient mid-gestation Supplementary Table 5.

Similarly, when we replaced ethnicity with the genetic component that captures both population stratification and family-relatedness, the pattern of findings identified in the main analyses persisted, suggesting that the observed association was free from confounding with ethnicity Supplementary Table 6. The results persisted after adjusting the models for season of blood sampling that is, season at mid-gestation or at time of birth for respective analyses. Results shown in Supplementary Table 7. There was no significant difference in the gender of the child Supplementary Table 8.


In our population-based cohort study sample of children, we show that gestational vitamin D deficiency was associated with higher scores on the SRS. We report for we believe the first time an association between mid-gestational 25OHD deficiency and variation in a widely used, continuous measure of autism-related traits in the general population. The pattern of findings persisted when we restricted the analyses to the offspring of European ethnicity and when we accounted for sample structure using individual level genetic data of the offspring.

These analyses strongly reduce the chance that our main analyses were confounded by ethnic diversity within the sample. When we examined the two time-point measures of vitamin D deficiency we found only mother—infant pairs with deficiency at both time points had higher scores on the SRS. This finding suggests that infants exposed to persistent low vitamin D from mid-gestation until birth may be at risk for autism-related traits, whereas this was not identified in those with deficiency at only one time point.

In light of the a significant relationship between 25OHD when assessed as a continuous variable versus SRS, and b the significant relationship between both mid-gestation deficient and insufficient 25OHD concentration versus SRS, we speculate that the exposure may operate as a continuous graded risk factor, without a critical threshold. Our study, based on a large, population-based, multi-ethnic cohort, was well suited to test our hypotheses. Vitamin D is a fat-soluble vitamin that, in humans, is obtained from exposure to sunlight and, to a lesser extent, from diet.

Several other ligands operating via nuclear receptors are known to be important in brain development for example, retinoic acid, glucocorticoids, thyroid hormone, sex hormones. Both the vitamin D receptor and the rate-limiting enzyme required for the production of 1,25 dihydroxyvitamin D, are expressed in neurons and glial cells in the brain. Rodent models based on transient prenatal exposure to vitamin D deficiency have found a range of persistent molecular gene and protein expression , neurochemical and behavioural changes of interest to neuropsychiatry. These convergent clues may provide insights into the etiopathogenesis of neurodevelopmental disorders.

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For example, the active form of vitamin D 1,25 dihydoxyvitamin D is known to impact on the function of voltage-gated calcium channels. With respect to study limitations, although we had measures of 25OHD concentrations at two developmental time points, we lacked information at other stages of gestation and early life.

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Defining the precise critical window during which developmental vitamin D deficiency adversely impacts on brain development would be premature. Differential attrition is known to impact on the representativeness of modern birth cohorts. It should also be noted that we do not believe that low gestational 25OHD concentration is solely linked to higher scores on the SRS that is, specificity between the exposure and the outcome.

There is evidence linking low prenatal vitamin D status with increased risk of other neurodevelopmental disorders such as schizophrenia 13 and attention deficit and hyperactivity disorder. Randomised controlled trials of vitamin D supplementation during pregnancy will be needed in order to confidently link vitamin D and an increased risk of autism-related conditions.

In light of the evidence linking prenatal vitamin D with general growth and bone health 68 , 69 , 70 such trials should be designed with several primary outcomes. In our data, we observe a more pronounced association for those who were deficient at two time points that is, mid-gestation and at time of birth compared with deficiency at only one time point. We also detected an association between the continuous measure of vitamin D concentrations and autism-related traits, letting us hypothesise that vitamin D is operating as a continuous grade risk factor without a critical threshold.

Randomised controlled trials will be required to test this hypothesis. Future research should focus on specificity of the effect of early life vitamin D deficiency in relation to neurodevelopmental disorders. Alongside animal studies that aim to elucidate the biological mechanisms linking vitamin D deficiency and brain development, human studies could focus on endophenotypes to better understand the pathway from vitamin D deficiency to various neurodevelopmental disorders for example, structural and functional magnetic resonance imaging 44 , This study has several important strengths.

Our sample was based on a large representative multi-ethnic cohort. We used a gold standard assessment of 25OHD concentrations, and a widely used measure of autism-related traits. We had access to infant genotypes and were able to explore innovative models that can more precisely adjust for ancestral differences and family-relatedness in the cohort.

Our findings require replication in independent samples. We are aware of several case—control studies currently underway that will examine the association between neonatal 25OHD and ASD.

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The association between developmental vitamin D deficiency and autism-related traits may have important implications from a public health perspective. It is feasible that a safe, cheap and publicly accessible vitamin D supplement in at-risk groups may reduce the prevalence of this risk factor. Just as prenatal folate supplementation has reduced the incidence of spina bifida, we speculate that prenatal vitamin D supplementation may reduce the incidence of ASD.

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Vitamin D Handbook: Structures, Synonyms, and Properties by G. W. A. Milne, M. Delander -

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Citations Publications citing this paper. References Publications referenced by this paper. Regulation of the vitamin D receptor and cornifin beta expression in vaginal epithelium of the rats through vitamin D3. Persistent trefoil factor 1 expression imprinted on mouse vaginal epithelium by neonatal estrogenization Fujiko Masui , Keiko Kurosaki , Takao Mori , Manabu Matsuda.

CYP2R1 is a major, but not exclusive, contributor to hydroxyvitamin D production in vivo. Extrarenal expression of the hydroxyvitamin Dhydroxylase.