Vitamin D in Synaptic Plasticity, Cognitive Function, and Neuropsychiatric Illness

　

Trends in Neurosciences
Volume 42, Issue 4, April 2019, Pages 293-306

Vitamin D in Synaptic Plasticity, Cognitive Function, and Neuropsychiatric Illness
Author links open overlay panelPhoebe E.Mayne1Thomas H.J.Burne12
1
Queensland Brain Institute, the University of Queensland, St Lucia, QLD 4072, Australia
2
Queensland Centre for Mental Health Research, Wacol, QLD 4076, Australia

Vitamin D plays various roles in normal brain physiology, including modulating synaptic plasticity.

Converging evidence suggests that vitamin D deficiency affects multiple brain processes, including cognitive functioning, in both healthy people and those afflicted with neuropsychiatric illness. The underlying mechanisms, however, are poorly understood.

Evidence suggests that vitamin D deficiency impacts synaptic plasticity through a plethora of avenues, including l-type voltage-gated calcium channels and regulation of various neurotransmitters, including NO.

An emerging concept is that vitamin D deficiency may weaken the integrity of PNNs, aggregates of the ECM, through modulation of MMPs.

PNNs have been reported to play essential roles in cognitive processes such as learning and memory. As such, dysregulation of PNNs is likely to disturb neural-circuit function and impair cognitive functioning.

Assessing the molecular mechanisms that underpin the roles of vitamin D in cognition is pertinent to informing preventive and intervention strategies for persons with cognitive disturbances, including patients with schizophrenia.

Over a billion people worldwide are affected by vitamin D deficiency. Although vitamin D deficiency is associated with impaired cognition, the mechanisms mediating this link are poorly understood. The extracellular matrix (ECM) has now emerged as an important participant of synaptic plasticity and a new hypothesis is that vitamin D may interact with aggregates of the ECM, perineuronal nets (PNNs), to regulate brain plasticity. Dysregulation of PNNs caused by vitamin D deficiency may contribute to the presentation of cognitive deficits. Understanding the molecular mechanisms underpinning the role of vitamin D in brain plasticity and cognition could help identify ways to treat cognitive symptoms in schizophrenia and other neuropsychiatric conditions.

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Keywords
vitamin D deficiencycognitionneuropsychiatric illnesssynaptic plasticityperineuronal nets

Vitamin D in Synaptic Plasticity, Cognitive Function, and Neuropsychiatric Illness - ScienceDirect
https://www.sciencedirect.com/science/article/abs/pii/S0166223619300062

　

The Effect of Vitamin D on Psychosis and Schizophrenia ...
https://www.greatplainslaboratory.com/articles-1/2016/5/18/the-effect-of-vitamin-d-on...
May 18, 2016 · The risk of schizophrenia and vitamin D status vary with season of birth, latitude, and skin pigmentation. The UV rays required to make vitamin D are reduced in the months most associated with an increase in the birth of individuals who later develop schizophrenia.

Prenatal Vitamin D Deficiency Linked to Schizophrenia Risk
https://articles.mercola.com/.../2018/12/20/vitamin-d-deficiency-schizophrenia.aspx
Dec 20, 2018 · There is a lifelong impact for children born of vitamin D deficient mothers, ranging from childhood allergies and more frequent colds and flu, to a greater risk for diabetes, cardiovascular disease and, as recently confirmed, schizophrenia; Children who were vitamin D deficient at birth had a 44 percent increased risk of developing schizophrenia as adults; vitamin D status could account for 8 percent of the schizophrenia …

　

Vitamin D and brain health: New mechanism may explain link

New research finds that vitamin D deficiency affects a type of brain “scaffolding” that supports the neurons. This finding could lead to new therapies for the neurological symptoms of mental health conditions such as schizophrenia.

Our bodies produce vitamin D in response to sun exposure. New research helps explain why this vitamin is key for brain health.
Vitamin D, which people sometimes refer to as the “sunshine vitamin,” is necessary for maintaining healthy bones. It also benefits the immune and cardiovascular systems, as well as endocrine function.

For instance, research has suggested that insufficient vitamin D may compromise the immune system, raise the risk of hypertension, and negatively affect insulin secretion in people with type 2 diabetes.

Newer studies have focused on the potential link between vitamin D and brain health. For example, a recent study that Medical News Today reported on reinforced the notion that there may be an association between vitamin D deficiency and a higher risk of schizophrenia.

Other studies have shown that depriving middle-aged rodents of vitamin D led them to develop brain damage and perform less well on cognitive tests. Researchers have also found that people who survive sudden cardiac arrest are less likely to recover brain function if they have low levels of vitamin D.

A new study delves deeper into this link between vitamin D and brain function to find a potential reason why the nutrient may be key to memory function.

Thomas Burne, an associate professor at the University of Queensland Brain Institute in St. Lucia, Australia, led the new research. Burne and his colleagues published their findings in the journal Trends in Neurosciences.

Vitamin D and brain health: New mechanism may explain link
https://www.medicalnewstoday.com/articles/324541

　

维生素D对精神病和精神分裂症的影响
May 18, 2016 Vit D Resources
JAMES GREENBLATT, MD
维生素D缺乏已被链接到一个宽范围的主要精神疾病的，并且是为研究人员关注的新兴领域。从我的经验用在住院和门诊精神病和精神分裂症的个人工作，我经常在这一患者群体，其中症状的严重程度呈负相关血清维生素D水平发现维生素D水平低。最近，患有精神分裂症，精神病，选修缄默症和双相情感障碍的个体化验检查低于20毫微克/毫升血清一致维生素D水平。由于维生素D水平恢复正常，症状好转。虽然机制尚不清楚，最近的研究表明，维生素D对炎症和免疫过程的调控作用可能会影响临床症状和精神分裂症患者（蒋，纳塔拉，与范，2016年）治疗反应的表现。

维生素D缺乏症和精神分裂症的发展的链接已被世界各地的各年龄段的患者中研究。一个荟萃分析回顾1988年和2013年间发表的19项研究发现维生素D缺乏症和精神分裂症有很大的关系。从这些研究中的2804名参与者中，患有精神分裂症的参与者超过65％的维生素D缺乏。维生素D缺乏参与者的2.16倍更可能有精神分裂症比维生素D充足的参与者（Valipour，Saneei，与Esmaillzadeh，2014年）。

精神分裂症和维生素D的风险与出生，纬度和皮肤色素沉着的季节而变化。使维生素D所需的紫外线在与增加个人谁以后开发精神分裂症的诞生最相关的个减少。一项综述在内共437710人患有精神分裂症的发现，大多数人都出生在一月和二月。因此，这些新生儿暴露于产前和围产期期间较低水平的紫外线。精神分裂症的发生率增加也可以看出在高纬度地区，尤其是移民中。这同样可以与紫外线可用性和随后的维生素D状态。在高纬度地区，一个黑皮肤的个体也将在维生素D更明显的减少比浅色皮肤的个体。较轻的皮肤个人将有较少的黑色素，让肌肤更有效地吸收紫外线。据估计，肤色较深的人在高纬度地区更可能发展精神分裂症比一般人群（Chiang等，2016）。

瑞典研究人员回顾病历在精神科门诊，以确定维生素D缺乏可能预测。的117精神病患者85％以上有次优的维生素D水平。这些与精神分裂症和自闭症的最低水平。中东，地中海，东南亚或非洲人种是低维生素D的预测强接受维生素D补充剂来纠正自己的不足的患者取得了相当大的改进的精神病和抑郁症状（谦卑等，2010）。

维生素D的浓度在50精神分裂症患者在以色列19-65岁的测量。较低的平均患者与对照相比（20毫微克/毫升）精神分裂症（15毫微克/毫升）之间进行检测维生素D的浓度调整为太阳照射和补充的影响后（Itzhaky等人，2012）。同样，在新西兰102成人精神科住院病人92％，也有不理想的维生素D水平，并均超过两倍，可能欧洲人有以下严重缺乏的水平<10毫微克/毫升（门克斯等，2012）。

在3,182孩子在英国的一个前瞻性的出生队列，研究人员测量了在年龄维生素D水平9.8年和年龄12.8年评估精神病经验。儿童时期的维生素D浓度青春期早期时有精神病的经历有关。如果精神病的经验都涉及到精神分裂症的发展，这种支持更高的维生素D的浓度与精神分裂症的可能保护协会（Tolppanen等人，2012）。

维生素D缺乏与更严重的症状。横断面分析在12-18岁既需要住院或部分住院谁患有精神病的青少年进行。评估的104例患者中，72％没有足够的维生素D水平。维生素D状态是有关心理疾病的严重程度。那些维生素D缺乏是3.5倍更可能有幻觉，妄想，妄想或（仁慈等，2012）。第二项研究支持这一结论。维生素D是从20例首发精神分裂症分析。（刻板思维迟钝影响，情绪退缩，关系差，被动冷漠的社会退缩，抽象思维和）的阴性症状更严重是紧密联系在一起较低的维生素D水平相关。较低的维生素D水平也与更严重的全面认知缺陷相关的（Graham等，2015）。

麦格拉思等。（2010）研究新生儿维生素D状态和精神分裂症的后来风险之间的关系。他们确定424箱子与精神分裂症来自丹麦精神病中央登记册，并分析了他们的新生儿干血点。不出意料，他们发现维生素D状态和显著季节变化谁移民到丹麦的母亲的后代维生素D显著较低水平。他们还发现，那些与维生素D低级新生儿浓度有精神分裂症的风险增加。研究人员估计，如果所有这些新生儿有最佳的维生素D水平，精神分裂症病例40％以上的可能是可以避免的。

同一组研究人员还发现，在生命的第一年服用维生素D补充剂与精神分裂症的男性风险降低相关。他们看着芬兰出生队列，并收集关于婴儿期的频率和补充维生素D的剂量数据。男性谁经常服用维生素D补充剂不得不相比，谁从来没有补充88％降低患精神分裂症的风险（麦格拉思等，2004）。

这背后营养疾病的关系的机制只能在推测。那些患有精神分裂症通常有炎症的标志物升高。细胞是维生素D的低产生高水平的炎性细胞因子，而细胞充足的维生素D释放显著少这些细胞因子。因此，有可能是一种抗炎机构（Chiang等人，2016）。维生素D调节参与精神分裂症牵连通路的许多基因，包括参与突触可塑性基因，神经元发育和对抗氧化应激的保护的转录（Graham等，2015）。动物研究表明，在妊娠期间缺乏维生素D会影响多巴胺代谢和改变多巴胺系统在发育中的大脑。多巴胺已经涉及到精神分裂症的发病机理。在妊娠期间的维生素D缺乏症也可能会影响与精神分裂症（Valipour，Saneei，＆Esmaillzadeh，2014年）相关的大脑结构。

尽管缺乏临床试验在精神病和治疗精神分裂症的分析维生素D补充剂，这个患者人群中维生素D水平低的个体往往会从补充中受益。基于超过25年的临床经验，我已经在使用维生素D 5000至10000国际单位，每日一次作为一种辅助疗法的治疗效果观察显著改善。血清中维生素D含量应每两个月重新评估，直到最佳水平得以实现。

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谦虚，MB，古斯塔夫森，S.，＆Bejerot，S.（2010）。精神科门诊中25-羟基维生素D（25-OHD）在瑞典的低血清水平：随季节，年龄，种族和精神病诊断的关系。作者：类固醇生物化学与分子生物学，121（14日维生素D研讨会论文集），467-470。

Itzhaky，D.，Bogomolni，A.，Amital，D.，Arnson，Y.，Amital，H.，和戈登，K.（2012）。低血清维生素D浓度与精神分裂症患者。以色列医学协会杂志，14（2），88-92。

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麦格拉思，JJ，Eyles，DW，彼得森，CB，安德森，C，柯，P.，伯恩，TH，＆...莫滕森，PB（2010）。新生儿维生素D水平与患精神分裂症的风险：基于人群的病例对照研究。档案馆普通精神病学，（9），889。

门克斯，D.，沼泽，河，兰开斯特，K.，格兰特，M.，院长，P.，＆杜伊特，S.（2012）。在新西兰的怀卡托地区精神科住院患者的维生素D状态。 BMC精神病学，12，68。

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标签：詹姆斯·格林布拉特博士，维生素ð ，精神病，精神分裂症

对精神病维生素D和精神分裂症的影响 - 大平原实验室，公司
https://www.greatplainslaboratory.com/articles-1/2016/5/18/the-effect-of-vitamin-d-on-psychosis-and-schizophrenia

　

Cureus. 2018 Jul; 10(7): e2960.
Published online 2018 Jul 10. doi: 10.7759/cureus.2960
PMCID: PMC6132681
PMID: 30214848
The Role of Vitamin D in Brain Health: A Mini Literature Review
Monitoring Editor: Alexander Muacevic and John R Adler
Ibrar Anjum,1 Syeda S Jaffery,2 Muniba Fayyaz,3 Zarak Samoo,4 and Sheraz Anjumcorresponding author5

Abstract
Vitamin D is vital for our body as it regulates calcium homeostasis and maintains bone integrity. In this article, we will discuss how vitamin D aids in the function of neuronal and glial tissue and the many health consequences in a person with vitamin D deficiency. Some of the effects of vitamin D deficiency that will be discussed include the development of dementia caused by the increase of cerebral soluble and insoluble amyloid-β (Aβ) peptides and a decrease of its anti-inflammatory/antioxidant properties, the link to depression by a reduction of the buffering of increased calcium in the brain, and vitamin D deficiency in expecting mothers linking to the development of autism and schizophrenic-like disorders, hypoxic brain injury, and other mental illnesses. Lastly, we will discuss how vitamin D deficiency is linked to the development of diabetes mellitus, its role in neuronal development and a decrease of microglial inflammatory function leading to increased brain infections.

Keywords: vitamin d deficiency, dementia, depression, diabetes mellitus, autism, schizophrenia
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Introduction and background
Vitamin D a lipid soluble vitamin, also known as sunshine vitamin synthesized in our skin in the presence of sunlight [1]. This vitamin strongly known for its role in calcium and bone metabolism and maintaining bone integrity, has been deduced to have more functions than just that [2]. Scientists with the support of multiple types of research have linked the hormone-like vitamin to some disorders throughout the body such as cardiovascular disease, cancer, stroke, metabolic disorders including diabetes [3]. Cognitive impairment, dementia, psychosis, and autism have been added to the list as well now in the interchange of decreased vitamin D levels [4]. The importance of vitamin D3 in reducing the risk of these diseases continues to rise due to the increasing portion of the population in developed countries having a significant vitamin D deficiency [5]. The older population is at an unusually high risk for vitamin D deficiency due to the decreased cutaneous synthesis, and dietary intake of vitamin D. Vitamin D receptors are widespread in brain tissue, and vitamin D's biologically active form (1,25(OH)(2)D3) has shown neuroprotective effects including the clearance of amyloid plaques, a hallmark of Alzheimer's disease [6]. Recent studies have confirmed an association between cognitive impairment, dementia, and vitamin D deficiency. A growing body of literature also suggests that higher serum 25-hydroxyvitamin D (25(OH)D) concentrations, either in utero or early life, may reduce the risk of autism [7]. Indeed, vitamin D was reported to modulate the biosynthesis of neurotransmitters and neurotrophic factors; moreover, its receptor was found in the central nervous system. Vitamin D deficiency was therefore assessed as a risk factor for the multiple diseases aforementioned [8]. In this review, we will discuss and summarize the current knowledge of vitamin D’s role in improving brain function and the relation of vitamin D deficiency to various central nervous system disorders.

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Review
Vitamin D is an essential micronutrient for bone growth and regulation of calcium homeostasis. It not only plays a vital role in skeletal growth but also has other critical biological actions in neurodevelopment and function. The primary source of vitamin D is sunlight; it is also obtained from a few foods such as oily fish and fortified margarine. Vitamin D carries a cholesterol backbone and has steroid-like effects. It is the fat-soluble hormone that plays an essential role in brain health [9]. Recently vitamin D is increasingly recognized as a necessary neuro-steroid with various actions in the brain [10]. Circulating 25(OH) vitamin D crosses the blood-brain barrier and enters glial cells and neuronal cells to be converted into 1,25(OH) 2 D, which is the active form of vitamin D [11]. In this article, we will discuss the active form of vitamin D, calcitriol which mediates its effects by binding to the vitamin D receptor (VDR), which is principally located in the nucleus of target cells [12]. VDR is a nuclear steroid receptor through which it performs its functions in the brain. It has been found that synthesis and destruction of vitamin D occur in the brain and VDR which is required for vitamin D to show its effect is seen in different regions of the brain.

In the last decades, several studies were conducted which shows the association between vitamin D and brain health and the impact of vitamin D deficiency on the brain. In 2016, Miller BJ et al. conducted a human study which shows that vitamin D increases plasma Aβ in older adults, indicative of decreased brain Aβ [13]. In March 2016, Annweiler C et al. conducted a study which demonstrates the neurosteroid actions of vitamin D in the regulation of calcium homeostasis, β-amyloid deposition, antioxidant and anti-inflammatory properties. It also discusses neuroprotection action of vitamin D against neurodegenerative process associated with Alzheimer’s disease and cognition [14].

A meta-analysis conducted in 2017 shows the hypothesis that 25(OH) D concentrations less than 25 nmol/l increases risk for dementia especially in adults and patients above 65 years of age [15-16]. A study conducted by Durk MR et al. on mice investigates the role of vitamin D3 receptor in reducing cerebral soluble and insoluble amyloid-β (Aβ) peptides. It shows that VDR is a potent therapeutic target in the prevention and treatment of Alzheimer’s disease [17]. Furthermore, a study conducted by Annweiler et al. shows that hypovitaminosis D is commonly seen in adults and 65-year-old patients. They show sign of dementia and cognition impairment [18].

Several studies show the link between vitamin D and depression. A study conducted in 2015 shows the low levels of serotonin in the hippocampus seen in depression [19]. Evidence from animal studies shows the behavioural and anatomical changes in the hippocampus in animals with low vitamin D [20]. Berridge conducted a study in 2017 which have evidenced that depression caused by an imbalance between excitatory and inhibitory pathways in the brain. Hypothesis argues that vitamin D reduces the increase in neuronal levels of calcium (CA +2) that are driving depression. Vitamin D plays a role in maintaining the expression of the CA 2+ pumps and buffers that reduce CA 2+ levels, which may explain how it acts to reduce the onset of depression [21].

In 2014, Gezen-AK et al. conducted a study which shows that vitamin D regulates the release of nerve growth factor (NGF), an essential molecule for the neuronal survival of hippocampal neurons as well as cortical neurons [22]. Kelly L conducted a study which demonstrated that vitamin D insufficiency might relate to higher levels of anxiety and depression, in turn contributing to the elevated risk of psychosis in children with chromosome 22q11.2 deletion syndrome (22q11.2DS). This syndrome is a complex developmental disorder with serious medical, cognitive and emotional symptoms in their lifespan [23].

In early life, vitamin D plays a vital role in neuronal development. Some studies conducted recently shows the effect of vitamin D on early life brain development. In May 2018, a study conducted by Yates et al. shows that deficiency of vitamin D in maternal and offspring shows some disabilities in early life including learning and memory problems and grooming behaviours. There was also some evidence of increased lateral ventricle volume and altered neural expression of genes involved in dopamine and glucocorticoid-related pathways suggesting autism and schizophrenic-like disorders [24]. In March 2018, Freedman et al. performed a systematic review of prenatal nutrients and childhood emotional development and later mental illness. The result shows prenatal nutrients including vitamin A and D are required in pregnancy to decrease the risk for schizophrenia and other mental illness in later life of offspring [25]. Vitamin D plays a vital role in neonatal hypoxic-ischemic brain injury. In February 2018, Stessman et al. conducted a study which demonstrates pregnant mothers are at higher risk for developing vitamin D deficiency. Babies born to vitamin D deficient mothers developed hypoxic-ischemic brain injury [26].

Di Somma et al., in a study, shows optimal levels of vitamin D in the bloodstream are necessary to preserve the neurological development and protect the adult brain [27]. Balanced dietary intake is a well-established lifestyle factor in maintaining cognition during ageing. A recent study shows that vitamin D helps in keeping cognitive function in older adults [28]. An interesting study conducted by Harrison et al. shows the association of vitamin D deficiency and the development of diabetes mellitus through paraventricular hypothalamic nuclei. It shows the positive relationships between them [29]. In November 2017, Kesby JP et al. conducted a study showing the effect of vitamin D on both widespread neurotransmitter changes (glutamine/noradrenaline) and regionally selective neurotransmitter changes (dopamine/serotonin). It concluded that developmental vitamin D deficiency leads to these brain changes [30-31]. Due to its effect on dopamine pathway in the brain, vitamin D can be a useful therapeutic agent used as an intervention therapy to be combined with existing treatments for Parkinson’s disease [32]. Staphylococcal enterotoxin B (SEB) is a superantigen and can initiate inflammation. Microglial cells in brain fight against these types of inflammation. Vitamin D deficiency affects the inflammatory process in the brain causing exposure of the brain to these vulnerable pathogens [33].

Go to:
Conclusions
In conclusion, vitamin D is essential to maintain important functions of the body such as calcium homeostasis, maintenance of skeleton integrity, and neurodevelopment. Its deficiency has been linked to many problems such as dementia, depression, diabetes mellitus, autism, and schizophrenia. It is important that this topic is emphasized since correcting the deficiency state can help prevent many negative health consequences.

Go to:
Notes
The content published in Cureus is the result of clinical experience and/or research by independent individuals or organizations. Cureus is not responsible for the scientific accuracy or reliability of data or conclusions published herein. All content published within Cureus is intended only for educational, research and reference purposes. Additionally, articles published within Cureus should not be deemed a suitable substitute for the advice of a qualified health care professional. Do not disregard or avoid professional medical advice due to content published within Cureus.

　

The Role of Vitamin D in Brain Health: A Mini Literature Review
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6132681/

　

The combination of vitamins and omega-3 fatty acids has an enhanced anti-inflammatory effect on microglia

Author links open overlay panelE.KurtysaU.L.M.EiselbJ.M.VerkuylcL.M.BroersencR.A.J.O.DierckxaE.F.J.de Vriesa
a
Department of Nuclear Medicine and Molecular Imaging, University of Groningen, University Medical Center Groningen, PO Box 30.001, 9700 RB Groningen, The Netherlands
b
Department of Molecular Neurobiology, Center for Life Sciences, University of Groningen, Groningen, The Netherlands
c
Nutricia Research, Uppsalalaan 12, 3584 CT Utrecht, The Netherlands
Received 26 April 2016, Revised 1 July 2016, Accepted 18 July 2016, Available online 25 July 2016.

Highlights
• Combining nutrients acting on converging anti-inflammatory pathways may enhance their anti-inflammatory properties.

• Increased anti-inflammatory action can be achieved when vitamins A, D and fatty acids are combined.

• Retinoic acid receptor a plays a pivotal role in the anti-inflammatory action of vitamin A on LPS-activated BV-2 cells.

Abstract
Neuroinflammation is a common phenomenon in the pathology of many brain diseases. In this paper we explore whether selected vitamins and fatty acids known to modulate inflammation exert an effect on microglia, the key cell type involved in neuroinflammation. Previously these nutrients have been shown to exert anti-inflammatory properties acting on specific inflammatory pathways. We hypothesized that combining nutrients acting on converging anti-inflammatory pathways may lead to enhanced anti-inflammatory properties as compared to the action of a single nutrient. In this study, we investigated the anti-inflammatory effect of combinations of nutrients based on the ability to inhibit the LPS-induced release of nitric oxide and interleukin-6 from BV-2 cells. Results show that omega-3 fatty acids, vitamins A and D can individually reduce the LPS-induced secretion of the pro-inflammatory cytokines by BV-2 cells. Moreover, we show that vitamins A, D and omega-3 fatty acids (docosahexaenoic and eicosapentaenoic) at concentrations where they individually had little effect, significantly reduced the secretion of the inflammatory mediator, nitric oxide, when they were combined. The conclusion of this study is that combining different nutrients acting on convergent anti-inflammatory pathways may result in an increased anti-inflammatory efficacy.

The combination of vitamins and omega-3 fatty acids has an enhanced anti-inflammatory effect on microglia - ScienceDirect
https://www.sciencedirect.com/science/article/abs/pii/S0197018616302273

　

60 ng维生素D如何促进怀孕-个人故事
通过约翰-2011年7月
我妻子反复流产，直到维生素D水平提高到60ng以上。
专家告诉我们，由于她检测出阳性的染色体疾病，我们永远不可能有男孩。
现在我们有1个女孩和1个双胞胎男孩！
详细的故事
从2005年开始，我妻子在7至10周内发生了4次流产。这些反复发生的流产是在她的维生素D水平提高到60ng以上后停止的。专家告诉我们，我们有无法解释的流产原因。一位遗传学专家说，由于她的两个X染色体上的染色体异常，我们永远不可能有男孩。一个女孩将是可行的，因为它可以从我的X染色体中获取丢失/损坏的DNA，但是我的Y染色体不可能填写必要的X信息。流产中的三个被确定为男孩（X＆Y.）

一时兴起，我决定增加维生素D。对我们来说，别无选择，因为流产是“无法解释的”。虽然她喜欢阳光，但也虔诚地使用防晒霜。她不是棕褐色的，也不使用维生素D补充剂，所以我认为她维生素D缺乏。她停止使用防晒霜，除非她认为自己可能会被烧伤。她去海滩上了阳光明媚的假期，以获取阳光中的维生素。她还使用室内日晒沙龙增加维生素D。她将辅助因子镁，维生素K2和磷虾油以及IU的D3含量从20,000升高到150,000，以增加维生素D的血清水平。

当我们在2006年末进行的妊娠试验呈阳性时，我们感到兴奋和恐惧。她服用了额外的叶酸，并继续服用D3，K2和磷虾油。她继续获得尽可能多的紫外线照射，但注意不要灼伤。她继续经常去室内日光浴沙龙，但将疗程时间限制在7分钟以内（并确保自己永远不会变得太热。）她的怀孕很顺利，非常受欢迎。在冬季，她的维生素D水平经测试为60.02 ng，通常是一年中的最低水平。

2007年7月，她生下了一个美丽的女孩。她长8磅，11盎司，21.5英寸长！

几年过去了，但她继续服用维生素D补充剂，并在少量使用防晒霜的情况下暴露于紫外线。 2010年又进行了一次阳性妊娠试验。这次被证实为双胞胎，都是男孩。由于她以前的流产男孩历史，我们感到恐惧。她在海滩和日光浴沙龙保持维生素D的补充和紫外线的照射。她被诊断出患有妊娠期糖尿病，并服用了低剂量的胰岛素。但是，除此之外，这次怀孕也很顺利。

还应注意，她没有典型的怀孕口罩。
我一直想知道这种面膜是否会在维生素D缺乏的人群中出现。
也许它应该被称为维生素D缺乏面膜？

2010年12月，她在39周内阴道分娩了两个健康的男孩。
双方在Apgars测试中得分均为9/9。
两个婴儿都很强壮，每个人长20英寸，一个为6 1/2磅，另一个为7。（双胞胎非常大。）
第二天母亲和婴儿出院。
母亲也没有缝线或妊娠纹。

我坚信，增加维生素D对这些婴儿的健康有着深远的影响。
有生育问题的任何人都应考虑进行维生素D测试，并在怀孕前和怀孕期间优化其水平。

　

Recurrent spontaneous abortions associated with low vitamin D levels – Nov 2013 | VitaminDWiki
https://vitamindwiki.com/Recurrent+spontaneous+abortions+associated+with+low+vitamin+D+levels+%E2%80%93+Nov+2013

　

How 60 ng of vitamin D enabled pregnancy - a personal story | VitaminDWiki
https://vitamindwiki.com/How+60+ng+of+vitamin+D+enabled+pregnancy+-+a+personal+story

　

　