Vitamin D, Depressive Symptoms, and Covid-19 Pandemic.
Vitamin D, Depressive Symptoms, and Covid-19 Pandemic.
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DOI：
10.3389/fnins.2021.670879
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发表时间：
2021
影响因子：
4.3
通讯作者：
Moreira JD
中科院分区：
文献类型：
--
作者：
Ceolin G;Mano GPR;Hames NS;Antunes LDC;Brietzke E;Rieger DK;Moreira JD
自2019冠状病毒病爆发以来，不同国家的研究都强烈指出了心理健康危机的出现，抑郁性精神病理学和自杀倾向的患病率急剧增加。维生素D缺乏与心理健康问题的风险增加以及个人对压力的反应有关。研究已经讨论了低血清维生素D浓度和抑郁症状之间的关系，这表明保持足够的血清维生素D浓度似乎对它有保护作用。在抑郁症的实验模型中，维生素D通过调节5-羟色胺代谢有助于改善多巴胺能神经传递。维生素D的活性形式1，25-二羟维生素D3通过维生素D受体（VDR）的信号传导诱导色氨酸羟化酶2（TPH 2）基因的表达，影响5-羟色胺再摄取转运蛋白（SERT）的表达以及负责5-羟色胺催化的单胺氧化酶-A（MAO-A）的水平。维生素D还与时间生物学相互作用存在相关联系，当光暗周期之间发生不平衡时，这可能会影响抑郁症状的发展。在这一观点中，我们讨论了维生素D在COVID-19大流行期间与压力相关的抑郁症状加剧中的重要作用。建议在COVID-19大流行期间持续封锁和社会隔离程序期间，维生素D监测以及在检测到缺乏时补充维生素D可被视为一项重要的医疗保健措施。维生素D在抑郁症状发展中的作用。在COVID-10疫情期间，世界各地政府实施的封锁和社交距离措施削弱了从阳光中合成维生素D的能力。当7-脱氢胆固醇（7-DHC）转化为前维生素D3，然后转化为维生素D3 [25（OH）D3]时，内源性维生素D合成在皮肤中启动。它通过血液循环由维生素D结合蛋白（VDBP）运输到肝脏，肾脏和大脑，在那里可以转化为活性形式[1，25（OH）2D 3]。在脑中，1，25（OH）2D 3的生物学效应主要由维生素D受体（VDR）通过基因组机制介导，其影响5-羟色胺代谢的几个方面，例如通过诱导色氨酸羟化酶2（TPH 2）基因表达增加5-羟色胺合成;影响5-羟色胺再摄取转运体（SERT）的表达和单胺氧化酶-A（MAO-A）的水平，从而引起5-羟色胺的抑制;间接调节褪黑素的合成，改善昼夜节律。这种机制可能在社会隔离期间受损，并因大流行期间阳光照射量低而导致维生素D减少，这可能有助于抑郁症状的发展。
Since the COVID-19 outbreak, studies across diverse countries have strongly pointed toward the emergence of a mental health crisis, with a dramatic increase in the prevalence of depressive psychopathology and suicidal tendencies. Vitamin D deficiency has been associated with an increased risk of mental health problems as well as individual responses to stress. Studies have discussed the relationship between low serum vitamin D concentrations and depressive symptoms, suggesting that maintaining adequate concentrations of serum vitamin D seems to have a protective effect against it. Vitamin D was found to contribute to improved serotonergic neurotransmission in the experimental model of depression by regulating serotonin metabolism. The signaling of 1,25-dihydroxyvitamin D3, the active form of vitamin D, through vitamin D receptor (VDR) induces the expression of the gene of tryptophan hydroxylase 2 (TPH2), influences the expression of serotonin reuptake transporter (SERT) as well as the levels of monoamine oxidase-A (MAO-A), the enzyme responsible for serotonin catabolism. Vitamin D also presents a relevant link with chronobiological interplay, which could influence the development of depressive symptoms when unbalance between light-dark cycles occurs. In this Perspective, we discussed the significant role of vitamin D in the elevation of stress-related depressive symptoms during the COVID-19 pandemic. It is suggested that vitamin D monitoring and, when deficiency is detected, supplementation could be considered as an important healthcare measure while lockdown and social isolation procedures last during the COVID-19 pandemic. Role of vitamin D in the development of depressive symptoms. The synthesis of vitamin D from sunlight is impaired by lockdown and social distance measures imposed by the governments around the world during COVID-10 pandemic. Endogenous vitamin D synthesis initiates in the skin when 7-dehydrocholesterol (7-DHC) is converted in pre-vitamin D3 and then vitamin D3 [25(OH)D3]. It is transported through blood circulation by the vitamin D binding protein (VDBP) to the liver, the kidney, and the brain, where can be converted in its the active form [1,25(OH)2D3]. In the brain, the biological effects of 1,25(OH)2D3 are largely mediated by vitamin D receptor (VDR) through genomic mechanisms, which influence several aspects of serotonin metabolism, such as increasing serotonin synthesis by induction of the tryptophan hydroxylase 2 (TPH2) gene expression; influencing the expression of serotonin reuptake transporter (SERT) and the levels of monoamine oxidase-A (MAO-A), responsible to serotonin catabolism; and indirectly may regulate the synthesis of melatonin that improve the circadian rhythm. This mechanism can be impaired during social isolation and consequent reduction of vitamin D due to low sun exposure during the pandemic, which could contribute to the development of depressive symptoms.
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影响因子：
3.7
作者：
Di Nicola, Marco;Dattoli, Luigi;Sani, Gabriele
通讯作者：
Sani, Gabriele
影响因子：
5
作者：
Jorde, Rolf;Sneve, Monica;Grimnes, Guri
通讯作者：
Grimnes, Guri
影响因子：
6.3
作者：
Alavi, Negin Masoudi;Khademalhoseini, Saeed;Assarian, Fatemeh
通讯作者：
Assarian, Fatemeh
影响因子：
5.4
作者：
Ceolin G;Matsuo LH;Confortin SC;D'Orsi E;Rieger DK;Moreira JD
通讯作者：
Moreira JD
DOI：
10.1093/advances/nmab012
发表时间：
2021-10-01
期刊：
Advances in nutrition (Bethesda, Md.)
影响因子：
--
作者：
Kazemi A;Mohammadi V;Aghababaee SK;Golzarand M;Clark CCT;Babajafari S
通讯作者：
Babajafari S