Moreover, in the presence of vitamin D deficiency, DNA damage, impair DNA repair systems, premature cell death, and accelerated aging get accelerated. Abnormal mitochondria produce suboptimal amounts of ATP while generating excess ROS a double whammy, creating a vicious cycle of enhancing the effects from excessive oxidative stress.

In addition to hypovitaminosis D, toxins, metabolic abnormalities, and the aging process itself causes mitochondrial dysfunction. Diseases that get worsen by vitamin D inadequacy include, insulin resistance, type 2 diabetes, obesity, hypertension, memory disorders, osteoporosis, certain cancers, and systemic inflammatory diseases, and pregnancy-associated complications. Consequently, vitamin D deficiency increases the incidence and/or severity of many age-related metabolic disorders that are linked to oxidative stress and accelerates the aging process. Hypovitaminosis D, on the other hand, accelerates these processes. Role of Calcitriol on Inflammation and Oxidative StressД¬alcitriol dampen inflammation, oxidative stress, cell/tissue damage, and thereby, the aging process. Recent data support less known, key functions of vitamin D on non-musculoskeletal functions, particularly on mitochondrial respiratory functions/energy generation, oxidative stress, and the aging process. Vitamin D is a potent anti-oxidant that improves mitochondrial activity, preventing oxidative stress-related protein oxidation, lipid peroxidation, and DNA damage.

Both 25 dihydroxy vitamin D and its active hormonal form, 1,25-dihydroxyvitamin D are essential for human physiological functions, including damping down inflammation and the excessive intracellular oxidative stresses. Vitamin D affects all systems in the body. New understandings of vitamin D-related advances in metabolomics, transcriptomics, epigenetics, in relation to its ability to control oxidative stress in conjunction with micronutrients, vitamins, and antioxidants, following normalization of serum 25(OH)D and tissue 1,25(OH)2D concentrations, likely to promise cost-effective better clinical outcomes in humans. Vitamin D is also a potent anti-oxidant that facilitates balanced mitochondrial activities, preventing oxidative stress-related protein oxidation, lipid peroxidation, and DNA damage. Vitamin D adequacy 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 this aids a healthy, graceful aging process. These include obesity, insulin resistance, type 2 diabetes, hypertension, pregnancy complications, memory disorders, osteoporosis, autoimmune diseases, certain cancers, and systemic inflammatory diseases. Thus, it is not surprising that hypovitaminosis D increases the incidence and severity of several age-related common diseases, such as metabolic disorders that are linked to oxidative stress. The interaction of 1,25(OH)2D with its intracellular receptors modulates vitamin DвЂ“dependent gene transcription and activation of vitamin D-responsive elements, which triggers multiple second messenger systems. On the other hand, hypovitaminosis D impairs mitochondrial functions, and enhances oxidative stress and systemic inflammation. In turn, molecular and cellular actions form 1,25(OH)2D slow down oxidative stress, cell and tissue damage, and the aging process.

Vitamin D is one of the key controllers of systemic inflammation, oxidative stress and mitochondrial respiratory function, and thus, the aging process in humans. 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.

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