推翻传统观点!高水平维生素D并不能预防痴呆
2018/07/17
上半年,探索君先后报道了维生素D降低患癌风险、治疗糖尿病、提高出生几率等方面的好消息。然而,7月9日发表的一项新成果却给维生素D泼了点冷水。研究称,维生素D不太可能保护个体免受多发性硬化症、帕金森病、阿尔茨海默症或其他大脑相关疾病的侵害。


图片来源:Nutritional Neuroscience

这篇发表在Nutritional Neuroscience上题为“Are the protective benefits of vitamin D in neurodegenerative disease dependent on route of administration? A systematic review”的研究表明,科学家们未能找到确凿的临床证据证明,维生素D可作为一种神经保护剂。

参与该研究的Krystal Iacopetta说:“我们的工作反驳了一种观点,即,较高水平的维生素D能够对大脑健康产生积极影响。”

具体来说,在这项研究中,基于对超过70篇临床前和临床研究的系统性回顾,Iacopetta等调查了维生素D在各种神经退行性疾病中的作用。


Krystal Iacopetta. Credit: CNBP

过去的研究发现,与健康人群相比,神经退行性疾病患者的维生素D水平往往较低。这导致了一种假设,即通过更多的紫外线和阳光照射或服用维生素D补充剂来提高维生素D水平,可能会产生积极的影响。一个被广泛认可的观点是,这些补充剂可能能够降低患大脑相关疾病的风险或限制这些疾病的进展。

不过,通过对所有科学文献的深入分析,这项新研究表明,情况并非如此。没有令人信服的证据表明维生素D是大脑的保护剂。

“我们对方法、样本大小以及治疗效果的分析表明,维生素D与大脑疾病可能是相关的,但两者并不是直接的因果关系。对于我们所研究的任何一种疾病,我们都无法确定维生素D的神经保护作用。”Iacopetta解释道。


Credit: CC0 Public Domain

领导该研究的Mark Hutchinso教授说:“这一结果非常重要,它是对当前数据和相关科学出版物极为全面的回顾和分析。我们打破了一种普遍持有的观念,即阳光照射产生的维生素D对大脑是有益的。”

不过,Hutchinson教授也强调,可能会有证据表明,紫外线(阳光照射)对大脑有益,但这种益处与维生素D的水平无关。

“虽然维生素D对健康的生活至关重要,但它似乎并不能像一些人所期待的那样,成为对抗脑部疾病的神奇‘阳光片’(sunshine tablet)。”他说。

参考资料:

Vitamin D no defence against dementia

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  • Are the protective benefits of vitamin D in neurodegenerative disease dependent on route of administration? A systematic review

    Background: The clinical and preclinical exploration of the therapeutic properties of vitamin D have significantly increased in the past decade, owing to the growing associative evidence suggesting vitamin D is neuroprotective. However, whether depletion of vitamin D contributes to the onset of neurological disorders or is a symptom of neurological disease has yet to be defined. Much remains unclear about the causal role of vitamin D and the method of use and forms of vitamin D. Objectives: We sought to quantitatively assess if neuroprotective benefits from vitamin D in neurodegenerative diseases are dependent on route of administration: comparing the effect of endogenously sourced vitamin D from UV exposure to exogenously derived vitamin D through synthetic supplementation. Design: We systematically searched PubMed, Embase and PsycInfo databases which included both pre-clinical and clinical studies investigating vitamin D in neurodegenerative diseases. Articles were subject to strict inclusion criteria and objectively assessed for quality. Additionally, Medline data was analysed to identify trends in topic publications and linguistic characteristics of papers. Results: From a total of 231 screened articles, we identified 73 appropriate for review based on inclusion criteria: original studies that investigated vitamin D levels or levels of vitamin D supplementation in neurodegenerative diseases or investigated past/present sun exposure in disease cohorts. Results indicate there is insufficient evidence to comprehensively reflect on a potential neuroprotective role for vitamin D and if this was dependent on route of administration. The majority of current data supporting neuroprotective benefits from vitamin D are based on pre-clinical and observational studies. Solid evidence is lacking to support the current hypothesis that the beneficial effect of UV exposure results from the synthesis of vitamin D. Sun exposure, independent of vitamin D production, may be protective against multiple Sclerosis, Parkinson’s disease and Alzheimer’s disease. Yet, further research is required to elucidate the beneficial mechanism of actions of UV exposure. The literature of vitamin D and amyotrophic lateral sclerosis was limited, and no conclusions were drawn. Therefore, in cases where UV-derived vitamin D was hypothesized to be the beneficial mediator in the neuroprotective effects of sun exposure, we propose results are based only on associative evidence. Conclusion: On the basis of this systematic review, strong recommendations regarding therapeutic benefits of vitamin D in neurodegenerative disease cannot be made. It is unclear if vitamin D mediates a protective benefit in neurodegenerative disease or whether it is an associative marker of UV exposure, which may contribute to as of yet unidentified neuroprotective factors.

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