Vitamin D, effects on brain development, adult brain function and the links between low levels of vitamin D and neuropsychiatric disease
TL;DR: The preclinical findings revealing that vitamin D can regulate catecholamine levels and protect against specific Alzheimer-like pathology increase the plausibility of this link.
About: This article is published in Frontiers in Neuroendocrinology.The article was published on 2013-01-01. It has received 571 citations till now. The article focuses on the topics: vitamin D deficiency & Vitamin D and neurology.
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01 Jul 2013
TL;DR: There is potentially a great upside to increasing the vitamin D status of children and adults worldwide for improving musculoskeletal health and reducing the risk of chronic illnesses, including some cancers, autoimmune diseases, infectious diseases, type 2 diabetes mellitus, neurocognitive disorders and mortality.
Abstract: It is now generally accepted that vitamin D deficiency is a worldwide health problem that affects not only musculoskeletal health but also a wide range of acute and chronic diseases. However, there remains cynicism about the lack of randomized controlled trials to support the association studies regarding the nonskeletal health benefits of vitamin D. This review was obtained by searching English-language studies published up to April 1, 2013, in PubMed, MEDLINE, and the Cochrane Central Register of Controlled Trials (search terms: vitamin D and supplementation) and focuses on recent challenges regarding the definition of vitamin D deficiency and how to achieve optimal serum 25-hydroxyvitamin D concentrations from dietary sources, supplements, and sun exposure. The effect of vitamin D on fetal programming epigenetics and gene regulation could potentially explain why vitamin D has been reported to have such wide-ranging health benefits throughout life. There is potentially a great upside to increasing the vitamin D status of children and adults worldwide for improving musculoskeletal health and reducing the risk of chronic illnesses, including some cancers, autoimmune diseases, infectious diseases, type 2 diabetes mellitus, neurocognitive disorders, and mortality.
994 citations
Cites background from "Vitamin D, effects on brain develop..."
...In vivomouse studies found that in utero hypovitaminosis D impairs brain development and leads to persistent changes in the adult brain.(192) The 1,25(OH)2D3 is rapidly incorporated into embryonic hippocampal cells, moves into the nucleus, and then returns to the cytoplasm....
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...At birth, rats with prenatal vitamin D deficiency had heavier and longer brains, enlarged lateral ventricles, and decreased cortical thickness.(5,192,194-196) Evidence fromhuman studies is scanty....
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TL;DR: More studies are needed to definitively conclude that vitamin D can offer preventive and therapeutic benefits across a wide range of physiological states and chronic nonskeletal disorders.
Abstract: Significant controversy has emerged over the last decade concerning the effects of vitamin D on skeletal and nonskeletal tissues. The demonstration that the vitamin D receptor is expressed in virtually all cells of the body and the growing body of observational data supporting a relationship of serum 25-hydroxyvitamin D to chronic metabolic, cardiovascular, and neoplastic diseases have led to widespread utilization of vitamin D supplementation for the prevention and treatment of numerous disorders. In this paper, we review both the basic and clinical aspects of vitamin D in relation to nonskeletal organ systems. We begin by focusing on the molecular aspects of vitamin D, primarily by examining the structure and function of the vitamin D receptor. This is followed by a systematic review according to tissue type of the inherent biological plausibility, the strength of the observational data, and the levels of evidence that support or refute an association between vitamin D levels or supplementation and maternal/child health as well as various disease states. Although observational studies support a strong case for an association between vitamin D and musculoskeletal, cardiovascular, neoplastic, and metabolic disorders, there remains a paucity of large-scale and long-term randomized clinical trials. Thus, at this time, more studies are needed to definitively conclude that vitamin D can offer preventive and therapeutic benefits across a wide range of physiological states and chronic nonskeletal disorders.
650 citations
TL;DR: There remains some controversy regarding what blood level of 25-hydroxyvitamin D should be attained for both bone health and reducing risk for vitamin D deficiency associated acute and chronic diseases and how much vitamin DShould be supplemented.
Abstract: Vitamin D, the sunshine vitamin, has received a lot of attention recently as a result of a meteoric rise in the number of publications showing that vitamin D plays a crucial role in a plethora of physiological functions and associating vitamin D deficiency with many acute and chronic illnesses including disorders of calcium metabolism, autoimmune diseases, some cancers, type 2 diabetes mellitus, cardiovascular disease and infectious diseases. Vitamin D deficiency is now recognized as a global pandemic. The major cause for vitamin D deficiency is the lack of appreciation that sun exposure has been and continues to be the major source of vitamin D for children and adults of all ages. Vitamin D plays a crucial role in the development and maintenance of a healthy skeleton throughout life. There remains some controversy regarding what blood level of 25-hydroxyvitamin D should be attained for both bone health and reducing risk for vitamin D deficiency associated acute and chronic diseases and how much vitamin D should be supplemented.
575 citations
Cites background from "Vitamin D, effects on brain develop..."
...vitamin D for a plethora of physiological functions and health outcomes including neuropsychiatric disorders [246], justifying the recommendation to enhance children’s and adults’ vitamin D status by following recommendations for sensible sun exposure, ingesting foods that contain vitamin D and...
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University of Melbourne1, Swinburne University of Technology2, University College London3, French Institute of Health and Medical Research4, University of Valencia5, Harvard University6, National Institutes of Health7, Columbia University8, University of Canterbury9, University of Las Palmas de Gran Canaria10, China Medical University (Taiwan)11
TL;DR: A viewpoint from an international collaboration of academics is presented, in which a context and overview of the current evidence in this emerging field of research is provided, and the future direction of recognition of diet and nutrition as central determinants of both physical and mental health is advocated.
375 citations
TL;DR: This review summarizes estrogen actions in the brain from the standpoint of their effects on synapse structure and function, noting also the synergistic role of progesterone.
Abstract: Estrogen facilitates higher cognitive functions by exerting effects on brain regions such as the prefrontal cortex and hippocampus. Estrogen induces spinogenesis and synaptogenesis in these two brain regions and also initiates a complex set of signal transduction pathways via estrogen receptors (ERs). Along with the classical genomic effects mediated by activation of ER α and ER β, there are membrane-bound ER α, ER β, and G protein-coupled estrogen receptor 1 (GPER1) that can mediate rapid nongenomic effects. All key ERs present throughout the body are also present in synapses of the hippocampus and prefrontal cortex. This review summarizes estrogen actions in the brain from the standpoint of their effects on synapse structure and function, noting also the synergistic role of progesterone. We first begin with a review of ER subtypes in the brain and how their abundance and distributions are altered with aging and estrogen loss (e.g., ovariectomy or menopause) in the rodent, monkey, and human brain. As there is much evidence that estrogen loss induced by menopause can exacerbate the effects of aging on cognitive functions, we then review the clinical trials of hormone replacement therapies and their effectiveness on cognitive symptoms experienced by women. Finally, we summarize studies carried out in nonhuman primate models of age- and menopause-related cognitive decline that are highly relevant for developing effective interventions for menopausal women. Together, we highlight a new understanding of how estrogen affects higher cognitive functions and synaptic health that go well beyond its effects on reproduction.
273 citations
References
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Book•
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01 Jan 1979
TL;DR: In what case do you like reading so much? What about the type of the vitamin d the calcium homeostatic steroid hormone book? The needs to read? Well, everybody has their own reason why should read some books as discussed by the authors.
Abstract: In what case do you like reading so much? What about the type of the vitamin d the calcium homeostatic steroid hormone book? The needs to read? Well, everybody has their own reason why should read some books. Mostly, it will relate to their necessity to get knowledge from the book and want to read just to get entertainment. Novels, story book, and other entertaining books become so popular this day. Besides, the scientific books will also be the best reason to choose, especially for the students, teachers, doctors, businessman, and other professions who are fond of reading.
3,998 citations
Book•
19 Mar 2013
TL;DR: The evidence supported a role for these nutrients in bone health but not in other health conditions, and there is emerging evidence that too much of these nutrients may be harmful.
Abstract: The charge to the committee (Institute of Medicine Committee to Review Dietary Reference Intakes for Vitamin D and Calcium) was to assess current relevant data and update, as appropriate, the DRIs (Dietary Reference Intakes) for vitamin D and calcium. The review was to include consideration of chronic disease indicators (e.g., reduction in risk of cancer) and other (non-chronic disease) indicators and health outcomes. The definitions of these terms are discussed below. Consistent with the framework for DRI development, the indicators to assess adequacy and excess intake were to be selected based on the strength and quality of the evidence and their demonstrated public health significance, taking into consideration sources of uncertainty in the evidence. Further, the committee deliberations were to incorporate, as appropriate, systematic evidence-based reviews of the literature.Specifically, in carrying out its work, the committee was to: Review evidence on indicators to assess adequacy and indicators to assess excess intake relevant to the general North American population, including groups whose needs for or sensitivity to the nutrient may be affected by particular conditions that are widespread in the population such as obesity or age-related chronic diseases. Special groups under medical care whose needs or sensitivities are affected by rare genetic disorders or diseases and their treatments were to be excluded; Consider systematic evidence-based reviews, including those made available by the sponsors as well as others, and carefully document the approach used by the committee to carry out any of its own literature reviews; Regarding selection of indicators upon which to base DRI values for adequate intake, give priority to selecting indicators relevant to the various age, gender, and life stage groups that will allow for the determination of an Estimated Average Requirement (EAR); Regarding selection of indicators upon which to base DRI values for upper levels of intake, give priority to examining whether a critical adverse effect can be selected that will allow for the determination of a so-called benchmark intake; Update DRI values, as appropriate, using a risk assessment approach that includes (1) identification of potential indicators to assess adequacy and excess intake, (2) selection of the indicators of adequacy and excess intake, (3) intake-response assessment, (4) dietary intake assessment, and (5) risk characterization. Identify research gaps to address the uncertainties identified in the process of deriving the reference values and evaluating their public health implications.
3,110 citations
TL;DR: This review critically summarizes the neuropathology and genetics of schizophrenia, the relationship between them, and speculates on their functional convergence via an influence upon synaptic plasticity and the development and stabilization of cortical microcircuitry.
Abstract: This review critically summarizes the neuropathology and genetics of schizophrenia, the relationship between them, and speculates on their functional convergence. The morphological correlates of schizophrenia are subtle, and range from a slight reduction in brain size to localized alterations in the morphology and molecular composition of specific neuronal, synaptic, and glial populations in the hippocampus, dorsolateral prefrontal cortex, and dorsal thalamus. These findings have fostered the view of schizophrenia as a disorder of connectivity and of the synapse. Although attractive, such concepts are vague, and differentiating primary events from epiphenomena has been difficult. A way forward is provided by the recent identification of several putative susceptibility genes (including neuregulin, dysbindin, COMT, DISC1, RGS4, GRM3, and G72). We discuss the evidence for these and other genes, along with what is known of their expression profiles and biological roles in brain and how these may be altered in schizophrenia. The evidence for several of the genes is now strong. However, for none, with the likely exception of COMT, has a causative allele or the mechanism by which it predisposes to schizophrenia been identified. Nevertheless, we speculate that the genes may all converge functionally upon schizophrenia risk via an influence upon synaptic plasticity and the development and stabilization of cortical microcircuitry. NMDA receptor-mediated glutamate transmission may be especially implicated, though there are also direct and indirect links to dopamine and GABA signalling. Hence, there is a correspondence between the putative roles of the genes at the molecular and synaptic levels and the existing understanding of the disorder at the neural systems level. Characterization of a core molecular pathway and a 'genetic cytoarchitecture' would be a profound advance in understanding schizophrenia, and may have equally significant therapeutic implications.
1,879 citations
"Vitamin D, effects on brain develop..." refers result in this paper
...Like other animal models, the DVD-deficient model does not replicate every aspect of schizophrenia but it has several attractive features when compared to other animal models of this disease: (a) it is based on clues from epidemiology; (b) it reproduces the increase in lateral ventricle size (one of the most consistent neurobiological correlates of schizophrenia (Harrison and Weinberger, 2005); and (c) it reproduces two crucial behavioral endophenotypes associated with schizophrenia, i....
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TL;DR: It is shown that renin expression and plasma angiotensin II production were increased severalfold in vitamin D receptor-null (VDR-null) mice, leading to hypertension, cardiac hypertrophy, and increased water intake, and 1,25(OH)(2)D(3) is a novel negative endocrine regulator of the renin-angiotens in system.
Abstract: Inappropriate activation of the renin-angiotensin system, which plays a central role in the regulation of blood pressure, electrolyte, and volume homeostasis, may represent a major risk factor for hypertension, heart attack, and stroke. Mounting evidence from clinical studies has demonstrated an inverse relationship between circulating vitamin D levels and the blood pressure and/or plasma renin activity, but the mechanism is not understood. We show here that renin expression and plasma angiotensin II production were increased severalfold in vitamin D receptor-null (VDR-null) mice, leading to hypertension, cardiac hypertrophy, and increased water intake. However, the salt- and volume-sensing mechanisms that control renin synthesis are still intact in the mutant mice. In wild-type mice, inhibition of 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] synthesis also led to an increase in renin expression, whereas 1,25(OH)(2)D(3) injection led to renin suppression. We found that vitamin D regulation of renin expression was independent of calcium metabolism and that 1,25(OH)(2)D(3) markedly suppressed renin transcription by a VDR-mediated mechanism in cell cultures. Hence, 1,25(OH)(2)D(3) is a novel negative endocrine regulator of the renin-angiotensin system. Its apparent critical role in electrolytes, volume, and blood pressure homeostasis suggests that vitamin D analogues could help prevent or ameliorate hypertension.
1,744 citations
"Vitamin D, effects on brain develop..." refers background in this paper
...Such studies would appear necessary because VDR knockout mice have a number of abnormalities outside the CNS which may confound interpretation of behavioral data, including hypertension and increased fluid intake (Li et al., 2002), cardiac hypertrophy (Xiang et al....
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TL;DR: FGF‐23 is a potent regulator of the vitamin D and phosphate metabolism and caused a reduction in serum 1,25‐dihydroxyvitamin D by altering the expressions of key enzymes for the vitaminD metabolism followed by hypophosphatemia.
Abstract: We analyzed the effects of an FGF-23 injection in vivo. FGF-23 caused a reduction in serum 1,25-dihydroxyvitamin D by altering the expressions of key enzymes for the vitamin D metabolism followed by hypophosphatemia. This study indicates that FGF-23 is a potent regulator of the vitamin D and phosphate metabolism.
Introduction: The pathophysiological contribution of FGF-23 in hypophosphatemic diseases was supported by animal studies in which the long-term administration of recombinant fibroblast growth factor-23 reproduced hypophosphatemic rickets with a low serum 1,25-dihydroxyvitamin D [1,25(OH)2D] level. However, there is no clear understanding of how FGF-23 causes these changes.
Materials and Methods: To elucidate the molecular mechanisms of the FGF-23 function, we investigated the short-term effects of a single administration of recombinant FGF-23 in normal and parathyroidectmized animals.
Results: An injection of recombinant FGF-23 caused a reduction in serum phosphate and 1,25(OH)2D levels. A decrease in serum phosphate was first observed 9 h after the injection and was accompanied with a reduction in renal mRNA and protein levels for the type IIa sodium-phosphate cotransporter (NaPi-2a). There was no increase in the parathyroid hormone (PTH) level throughout the experiment, and hypophosphatemia was reproduced by FGF-23 in parathyroidectomized rats. Before this hypophosphatemic effect, the serum 1,25(OH)2D level had already descended at 3 h and reached the nadir 9 h after the administration. FGF-23 reduced renal mRNA for 25-hydroxyvitamin D-1α-hydroxylase and increased that for 25-hydroxyvitamin D-24-hydroxylase starting at 1 h. In addition, an injection of calcitriol into normal mice increased the serum FGF-23 level within 4 h.
Conclusions: FGF-23 regulates NaPi-2a independently of PTH and the serum 1,25(OH)2D level by controlling renal expressions of key enzymes of the vitamin D metabolism. In conclusion, FGF-23 is a potent regulator of phosphate and vitamin D homeostasis.
1,611 citations
"Vitamin D, effects on brain develop..." refers background in this paper
...FGF23 is a hormone that regulates vitamin D metabolism by down-regulating the vitamin Dsynthesizing enzyme CYP27B1 and up-regulating the vitamin Dcatabolizing enzyme CYP24A1 in kidney (Shimada et al., 2004)....
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