自闭症与维生素D。

Autism and vitamin D.

作者信息

Cannell John Jacob

机构信息

Atascadero State Hospital, Psychiatry, 10333 El Camino Real, Atascadero, CA 93423, United States.

出版信息

Med Hypotheses. 2008;70(4):750-9. doi: 10.1016/j.mehy.2007.08.016. Epub 2007 Oct 24.

Abstract

UNLABELLED

Any theory of autism's etiology must take into account its strong genetic basis while explaining its striking epidemiology. The apparent increase in the prevalence of autism over the last 20 years corresponds with increasing medical advice to avoid the sun, advice that has probably lowered vitamin D levels and would theoretically greatly lower activated vitamin D (calcitriol) levels in developing brains. Animal data has repeatedly shown that severe vitamin D deficiency during gestation dysregulates dozens of proteins involved in brain development and leads to rat pups with increased brain size and enlarged ventricles, abnormalities similar to those found in autistic children. Children with the Williams Syndrome, who can have greatly elevated calcitriol levels in early infancy, usually have phenotypes that are the opposite of autism. Children with vitamin D deficient rickets have several autistic markers that apparently disappear with high-dose vitamin D treatment. Estrogen and testosterone have very different effects on calcitriol's metabolism, differences that may explain the striking male/female sex ratios in autism. Calcitriol down-regulates production of inflammatory cytokines in the brain, cytokines that have been associated with autism. Consumption of vitamin D containing fish during pregnancy reduces autistic symptoms in offspring. Autism is more common in areas of impaired UVB penetration such as poleward latitudes, urban areas, areas with high air pollution, and areas of high precipitation. Autism is more common in dark-skinned persons and severe maternal vitamin D deficiency is exceptionally common the dark-skinned.

CONCLUSION

simple Gaussian distributions of the enzyme that activates neural calcitriol combined with widespread gestational and/or early childhood vitamin D deficiency may explain both the genetics and epidemiology of autism. If so, much of the disease is iatrogenic, brought on by medical advice to avoid the sun. Several types of studies could easily test the theory.

摘要

未标注

任何关于自闭症病因的理论在解释其显著的流行病学特征时都必须考虑到其强大的遗传基础。在过去20年中,自闭症患病率的明显上升与避免日晒的医学建议增加相对应,这种建议可能降低了维生素D水平,并且理论上会大幅降低发育中大脑的活性维生素D(骨化三醇)水平。动物数据反复表明,孕期严重维生素D缺乏会使数十种参与大脑发育的蛋白质失调,并导致幼鼠脑容量增加和脑室扩大,这些异常与自闭症儿童中发现的异常相似。患有威廉姆斯综合征的儿童在婴儿早期骨化三醇水平可能会大幅升高,其表型通常与自闭症相反。患有维生素D缺乏性佝偻病的儿童有几种自闭症标志物,在高剂量维生素D治疗后这些标志物显然会消失。雌激素和睾酮对骨化三醇的代谢有非常不同的影响,这些差异可能解释了自闭症中显著的男女比例。骨化三醇会下调大脑中与自闭症相关的炎性细胞因子的产生。孕期食用富含维生素D的鱼类可减少后代的自闭症症状。自闭症在紫外线B穿透受损的地区更为常见,如极地地区、城市地区、空气污染严重的地区和降水量高的地区。自闭症在肤色较深的人群中更为常见,而严重的母体维生素D缺乏在肤色较深的人群中尤为常见。

结论

激活神经骨化三醇的酶的简单高斯分布,再加上广泛存在的孕期和/或儿童早期维生素D缺乏,可能解释自闭症的遗传学和流行病学特征。如果是这样,那么这种疾病很大程度上是医源性的,是由避免日晒的医学建议导致的。几种类型的研究可以很容易地检验这一理论。

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