Great article on the relationship between vitamin D and aging. Numerous studies have shown a direct relationship between all-cause mortality and vitamin D deficiency. High levels of vitamin D are associated with a lower mortality rate among patients with T2DM. Patients with vitamin D levels less than 30 nmol/L had significantly higher all-cause mortality. Vitamin D deficiency was more severe in patients with neoplasia: 17 ng/mL, versus 21.3% ng/mL ( p = 0.0005).
Vitamin D decreases inflammatory markers (C-reactive protein, interleukin 10) and oxidative stress markers (free radicals, nitric oxide), thus influencing atherosclerosis. The role of calcitriol in reducing renin synthesis was demonstrated, as well as its important role in the proliferation process of cardiomyocytes and vascular muscle cells. myocardial infarction is 2.4 times higher in those with a vitamin D level less than 15 ng/mL compared to those with values greater than 30 ng/mL
Vitamin D can modulate the expression of neurotrophic factors, such as nerve growth factor and glial cell line-derived neurotrophic factor, which are essential for nerve survival and regeneration. Additionally, vitamin D can inhibit the production of pro-inflammatory cytokines, such as tumor necrosis factor-alpha and interleukin-6, which are involved in nerve inflammation and degeneration [56].
Additionally, vitamin D may improve the function of calcium channels, which are important for nerve conduction and neurotransmission. Regarding diabetic macroangiopathy, vitamin D participates in the reduction of chronic inflammation and oxidative stress, which are important factors in endothelial dysfunction, atherosclerosis and the modulation of angiogenesis, which is altered in diabetes. Consequently, the healing of vascular lesions is impaired.
In recent years, researchers have shown that vitamin D and its active metabolites are useful in preventing or treating various forms of cancer through many mechanisms, such as regulation of gene transcription, tumor cell apoptosis, repair of DNA, antioxidant protection and immunomodulation. ].
Vitamin D plays a crucial role in the prevention and treatment of dementia. One of the mechanisms that confirms this hypothesis is that it positively regulates the production of several neurotrophic factors, which promote the survival, development and function of neurons. Furthermore, in animal studies, chronic vitamin D supplementation appears to protect against the neurotoxicity of glutamate exposure.
Vitamin D deficiency is associated with several comorbidities that reduce quality of life. It is useful for this blood test to become routine in practice in those at risk of overweight, obesity, hypertension, dyslipidemia, non-alcoholic steatohepatitis and metabolic syndrome. Vitamin D is the sunshine vitamin. During exposure to sunlight, 7-dehydrocholesterol in the skin absorbs ultraviolet B (UVB) radiation and converts it to previtamin D3. Previtamin D3, being thermodynamically unstable, isomerizes within a few hours to form vitamin D3. Prolonged exposure to UVB rays leads to transformation into tachysterol or lumisterol, which can be further metabolized into biologically active hydroxyforms. Exposure to sunlight also provides other health-related benefits that are independent of vitamin D production. These include the activation of central neuroendocrine mediators, including the activation of the hypothalamic-pituitary-adrenal (HPA) axis or its elements and the production of nitric oxide. The latter would lead to a reduction in blood pressure.
Great article on the relationship between vitamin D and aging. Numerous studies have shown a direct relationship between all-cause mortality and vitamin D deficiency. High levels of vitamin D are associated with a lower mortality rate among patients with T2DM. Patients with vitamin D levels less than 30 nmol/L had significantly higher all-cause mortality. Vitamin D deficiency was more severe in patients with neoplasia: 17 ng/mL, versus 21.3% ng/mL ( p = 0.0005).
Vitamin D decreases inflammatory markers (C-reactive protein, interleukin 10) and oxidative stress markers (free radicals, nitric oxide), thus influencing atherosclerosis. The role of calcitriol in reducing renin synthesis was demonstrated, as well as its important role in the proliferation process of cardiomyocytes and vascular muscle cells. myocardial infarction is 2.4 times higher in those with a vitamin D level less than 15 ng/mL compared to those with values greater than 30 ng/mL
Vitamin D can modulate the expression of neurotrophic factors, such as nerve growth factor and glial cell line-derived neurotrophic factor, which are essential for nerve survival and regeneration. Additionally, vitamin D can inhibit the production of pro-inflammatory cytokines, such as tumor necrosis factor-alpha and interleukin-6, which are involved in nerve inflammation and degeneration [56].
Additionally, vitamin D may improve the function of calcium channels, which are important for nerve conduction and neurotransmission. Regarding diabetic macroangiopathy, vitamin D participates in the reduction of chronic inflammation and oxidative stress, which are important factors in endothelial dysfunction, atherosclerosis and the modulation of angiogenesis, which is altered in diabetes. Consequently, the healing of vascular lesions is impaired.
In recent years, researchers have shown that vitamin D and its active metabolites are useful in preventing or treating various forms of cancer through many mechanisms, such as regulation of gene transcription, tumor cell apoptosis, repair of DNA, antioxidant protection and immunomodulation. ].
Vitamin D plays a crucial role in the prevention and treatment of dementia. One of the mechanisms that confirms this hypothesis is that it positively regulates the production of several neurotrophic factors, which promote the survival, development and function of neurons. Furthermore, in animal studies, chronic vitamin D supplementation appears to protect against the neurotoxicity of glutamate exposure.
Vitamin D deficiency is associated with several comorbidities that reduce quality of life. It is useful for this blood test to become routine in practice in those at risk of overweight, obesity, hypertension, dyslipidemia, non-alcoholic steatohepatitis and metabolic syndrome. Vitamin D is the sunshine vitamin. During exposure to sunlight, 7-dehydrocholesterol in the skin absorbs ultraviolet B (UVB) radiation and converts it to previtamin D3. Previtamin D3, being thermodynamically unstable, isomerizes within a few hours to form vitamin D3. Prolonged exposure to UVB rays leads to transformation into tachysterol or lumisterol, which can be further metabolized into biologically active hydroxyforms. Exposure to sunlight also provides other health-related benefits that are independent of vitamin D production. These include the activation of central neuroendocrine mediators, including the activation of the hypothalamic-pituitary-adrenal (HPA) axis or its elements and the production of nitric oxide. The latter would lead to a reduction in blood pressure.
https://www.mdpi.com/2077-0383/13/5/1390 (2024).--
https://www.biorxiv.org/content/10.1101/2024.02.13.580162v1.abstract (2024).--
https://www.sciencedirect.com/science/article/abs/pii/B9780323913867000064 (2024).--