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What Is Vitamin D Used For In The Human Body

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What Are Dangers Of Taking Vitamin D And B Complex Together?

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Received: 1 January 2019 / Revised: 21 February 2019 / Accepted: 18 March 2019 / Published: 11 May 2019

Recent advances in vitamin D research indicate that this vitamin, a secosteroid hormone, has beneficial effects on several body systems other than the musculoskeletal system. Both 25 dihydroxy vitamin D [25(OH)

Vitamin D Benefits—and How To Get More D In Your Diet

D] is essential for human physiological functions, including reducing inflammation and excessive intracellular oxidative stress. Vitamin D is one of the main regulators of systemic inflammation, oxidative stress and mitochondrial respiration, and thus, the aging process in humans. In turn, molecular and cellular actions generate 1, 25(OH).

De-oxidative stress, cell and tissue damage and slows the aging process. On the other hand, hypovitaminosis D impairs mitochondrial functions, and increases oxidative stress and systemic inflammation. Interaction of 1, 25(OH).

D with its intracellular receptors modulates vitamin D-dependent gene transcription and activation of vitamin D-responsive elements, which trigger multiple second messenger systems. Thus, it is not surprising that hypovitaminosis D increases the incidence and severity of many common age-related diseases, such as metabolic disorders associated with oxidative stress. These include obesity, insulin resistance, type 2 diabetes, hypertension, pregnancy complications, memory disorders, osteoporosis, autoimmune diseases, certain cancers, and systemic inflammatory diseases. Adequacy of vitamin D leads to less oxidative stress and improves mitochondrial and endocrine functions, reducing the risks of disorders, such as autoimmunity, infections, metabolic derangements and impairment of DNA repair; All of these contribute to a healthy, graceful aging process. Vitamin D is also a potent anti-oxidant that facilitates balanced mitochondrial activities, preventing oxidative stress-related protein oxidation, lipid peroxidation and DNA damage. New understanding of vitamin D-related advances in metabolomics, transcriptomics, epigenetics in relation to its ability to control oxidative stress in association with micronutrients, vitamins and antioxidants after normalization of serum 25(OH)D and tissue 1, 25(OH)

Vitamin D is a micronutrient that is metabolized into a multifunctional secosteroid hormone essential for human health. Globally, its deficiency is a major public health problem affecting all age and ethnic groups; It has surpassed iron deficiency as the world’s most common nutritional deficiency. An increased prevalence of vitamin D deficiency and associated complications is prominent in countries farthest from the equator. However, in people living within 1,000 km of the equator (e.g. Sri Lanka, India and Far Eastern, Middle Eastern, Central American and Persian Gulf countries) due to a combination of climatic conditions, ethnic and cultural habits, and darker skin color [1, 2, 3, 4].

How Much Vitamin D Should You Take To Be Healthy

Most of the vitamin D needed by the human body can be produced by a person’s exposure to sunlight, such as in summer, with dietary sources playing a supporting role when exposure to sunlight is limited or ineffective for vitamin D production. Despite the above, more than 50% of the population of the mentioned group of countries is vitamin D deficient [5, 6]. If effective public health guidelines are implemented, vitamin D deficiency can be easily and cost-effectively treated and prevented, saving millions of dollars and lives. Although excessive sun exposure does not cause hypervitaminosis D, it can cause other damage due to damage to skin cell DNA [7, 8, 9]. Thus, guidelines for safe sun exposure are needed for each country.

During the last decade, many advances have emerged in the understanding of the physiology and biology of vitamin D and its receptor ecology [10]. Vitamin D metabolism and functions are modulated by many factors. Accumulating evidence supports a biological association of vitamin D with reduced disease risk and improved physical and mental functions. This field is advancing rapidly, including knowledge of the physiology of vitamin D-vitamin D receptor (VDR) interactions and the biology and metabolism of vitamin D and their effects on the vitamin D axis and gene polymorphisms [11]. Together these data have facilitated our understanding of new ways to intervene to prevent and treat human diseases.

However, what is lacking are adequately powered, of sufficient duration, well-designed randomized controlled clinical studies (RCTs) conducted unbiasedly with nutritional vitamin D as the main intervention and predefined hard endpoints/primary outcomes. holds [12] . In addition, such studies should recruit individuals with vitamin D deficiency [ie, serum 25(OH)D concentrations less than 20 ng/mL (50 nmol/L)] and a daily pre-determined target serum 25( OH)D concentrations should be obtained. oral administration and/or safe exposure to ultraviolet rays; Not just depending on the orally administered dose. The goal of this review is to explore vitamin D-modulated gene interactions and the effects of hypovitaminosis-induced, mitochondria-dependent oxidative stress on aging.

D], produced not only in renal tubular cells (endocrine functions as hormones) but also in extrarenal target tissue cells, providing autocrine and paracrine functions. However, because it resides within target tissue cells, the intracellular concentrations achieved are unclear. In addition, the catabolism activity of 24-hydroxylase in target tissues plays an important role in the regulation of both 25-hydroxy vitamin D [25(OH)D); calcidiol], and 1, 25(OH)

Vitamin D Synthesis Within The Body Including Precursors, Enzymes,…

D generated in the renal tubules and target cells can vary from person to person and from day to day and is difficult to quantify. Although circulating calcitriol is modulated by parathyroid hormone (PTH) and serum ionized calcium concentration [13], intracellular content is largely controlled by serum 25(OH)D availability and hydroxylation upon hydroxylation by calcidiol and calcitriol catabolism. 24 and C-23 by a specific 24-hydroxylase (CYP24A1) [14].

After exposure to ultraviolet B (UVB) rays, skin cells actively synthesize vitamin D. As a feedback mechanism, additional precursors produced are catabolized in dermal cells by the same UVB rays. In addition, the skin also contains the inactive enzyme 24-hydroxylase, which also inhibits overproduction of vitamin D through 24-hydroxylation of vitamin D [15]. This process of homeostasis is regulated by UVB, PTH and serum ionized calcium concentration [16]. When a person is overexposed to ultraviolet rays, the mentioned built-in protective mechanism prevents excessive retention of vitamin D in the skin. Therefore, sun exposure does not increase serum 25(OH)D pathological levels, leading to hypervitaminosis D or its complications, such as hypercalcemia.

In addition, vitamin D synthesized in the skin from excess UVB exposure is catabolized in part by 20-hydroxylation by the cholesterol side chain cleavage enzyme CYP11A1 [17]. Thus, multiple intrinsic mechanisms are present to prevent excess vitamin D from reaching the circulation. The efficiency of vitamin D synthesis in the skin is affected by many factors, including melanin pigment density, skin condition and age, and the use of sunscreen and UV-blocking makeup, creams and ointments, and clothing. In addition, older age or scarred skin, as well as time of day or year and duration of sun exposure affect vitamin D synthesis in the skin [18, 19, 20, 21].

Although solar radiation is the source of vitamin D production in the skin, excessive exposure, especially to those who are genetically susceptible, can cause skin cancer [22, 23, 24]. On the other hand, optimal vitamin D status protects against various types of internal cancer, melanoma, and several other diseases. Therefore, there is a need to balance sun exposure in favor of benefits while avoiding potential harmful effects [25, 26, 27].

Things That Can Undermine Your Vitamin D Level

D regulates many genes within the human genome [28]. Tissue vitamin D concentrations and its receptor gene polymorphisms, not only influence the mechanism of action and modulate the second messenger system, but also modulate the ability of ligand-bound VDR to bind to vitamin D response elements (VDREs) at promoter regions in genes and starts second messenger systems [29]. The National Human Genome Research Institute (NHGRI) is a public research consortium, ENCODE [Encyclopedia of DNA Elements; http://www.genome.gov/10005107] [30] to answer related questions.

On the formation rates of proteins, such as the insulator protein CTCF (transcriptional repressor CTCF; 11-zinc finger protein, CCCTC-binding factor, etc.) and VDR [31, 32]. These findings

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