Vitamin D deficiency accelerates hardening of the arteries
Relation of vitamin D deficiency to cardiovascular risk factors, disease status, and plaque in human carotid artery visualised by scanning electron microscope. Many studies show a 25(OH)D inverse relationship in serum and different cholesterol Figure 1: Cardiovascular pathophysiology of vitamin D deficiency. . vitamin D3 did not appear to alter coronary artery calcified plaque burden among. In approximately 15% of human atherosclerotic plaque, the calcium deposits A link between vitamin D signaling and vascular calcification is suggested by the.
In the human genome, approx. The vitamin D receptor present in most human tissues and cells has also been located in the cells of the cardiovascular system endothelial cells, vascular smooth muscle cells, myocytes and fibroblasts ; moreover, the ability of these cells has been proved in the autocrine and paracrine synthesis of active vitamin D metabolite regardless of the hydroxycholecalciferol level in the body .
Under the influence of ultraviolet radiation having a wavelength of nm UVB 7dehydrocholesterol is converted to pre-vitamin D3.
Is Vitamin D a New Therapeutic Option in Coronary Artery Disease? Overview Data
Regular exposure to UVB radiation increases the concentration of vitamin D levels in plasma, without risking the toxic effects of vitamin D on the body because its excessive amounts are converted into inactive isomers. In autumn and winter the source of vitamin D is diet.
Currently, recommended limits for exposure to sunlight may lead to increasing vitamin D deficiency [ 6 ]. Another reason for the growing epidemic of vitamin D deficiency is the aging population, as has been shown in the effectiveness of skin synthesis which weakens with body ageing; in people over 70 years of age it is four times lower than in young people with the same exposure to the sun [ 78 ].
Lower levels of vitamin D have also been reported within women [ 910 ] and patients with chronic kidney disease who are considered to be patients with a high cardiovascular risk. Another factor increasing the risk of inadequate levels of vitamin D is living in northern regions, the autumn and winter period, low physical activity, being in a nursing home, black skin colour, smoking, obesity, gastrointestinal malabsorption disorders, liver disease, use of glycocorticosteroids, immunosuppressants and also anti-retroviral therapy [ 11 ].
The essence of atherosclerosis is the inflammation of the artery walls as a response to the damage of the vascular endothelium [ 12 ].
It has been shown that chronic treatment with the hydroxycholecalciferol has a positive influence on endothelial cells by reducing the production of reactive oxygen compounds, stimulating production of superoxide dismutase [ 13 ],increasing the endothelial activity of nitric oxide synthase [ 1314 ], as well as protection against the glycosylation end product effects [ 15 ].
Anti-inflammatory effects are exerted through the inhibition of prostaglandin and cyclooxygenase-2 synthesis, and by stimulating the synthesis of cytokines with anti-inflammatory activity [ 16 - 19 ]. Further research is required for the yet unexplained effect of vitamin D on the process of calcification of the vascular wall.
It has been shown that at low concentrations, it reduces the calcification of the middle and inner membrane of coronary arteries [ 2021 ] and in high concentrations it stimulates the conversion of mesenchymal cells into osteoblasts and thereby contributes to the formation of calcifications in the central membrane of the artery [ 22 ] which leads to the stabilization of existing atherosclerotic plaques.
Vitamin D Supplements May Make Arteries Healthier
In the process of destabilization of the atherosclerotic plaque, the decisive role is played by a thin connective tissue cover, large lipid core, high activity of inflammatory cells and increased neovascularization [ 12 ]. In addition to the anti-inflammatory effect, vitamin D inhibits the conversion of macrophages into foam cells [ 23 ], reduces the neovascularization process by inhibiting the vascular endothelial growth factor and stimulating the apoptosis of epithelial cells, decreases the metalloproteinase activity responsible for the remodelling of the vascular wall and the cardiac muscle leading to the destabilization of atherosclerotic plaques [ 24 - 26 ].
The atherosclerotic plaque rupture is followed by the release of its lipid content, which initiates blood clotting [ 12 ]. The anticoagulant effect of vitamin D exerts by reducing the expression of the procoagulant tissue factor, increasing the anticoagulant production of thrombomodulin [ 27 ], and inhibition of platelet adhesion to vascular endothelial cells [ 28 ].
In addition, the results of recent years show an independent compound of low vitamin D levels and documented risk factors for the cardiovascular system such as hypertension [ 29 ], atherogenic lipid profile [ 30 ], diabetes [ 31 ] and obesity [ 32 ]. As shown, the deficiency of vitamin D leads to the activation of the renin-angiotensin-aldosterone system RAASwhile high levels of vitamin D reduces the plasma renin activity, leading to a reduction of angiotensin II concentration.
This leads to a reduction in blood pressure and control of inflammatory processes in the vascular endothelium, which also reduces the progression of atherosclerosis [ 29 ]. Particularly noteworthy is the effect of vitamin D on the lipid profile. A compound of high levels of total cholesterol and LDL-C with coronary atherosclerosis is clearly documented.
It was further found that the reduction in total cholesterol and low density lipoprotein below recommended levels significantly reduces the cardiovascular risk [ 3334 ].
- Coronary artery disease and its association with Vitamin D deficiency
Many studies show a 25 OH D inverse relationship in serum and different cholesterol fractions [ 30 ]. The explanation for these results may be a common metabolic pathway for vitamin D and cholesterol. Both of these are formed from a single precursor - 7dehydrocholesterol.
In addition, the hydroxycholecalciferol can inhibit CYP51A1, which also participates in the synthesis of cholesterol. A deficiency of hydroxycholecalciferol increases reductase activity and raises the CYP51A1 cholesterol levels [ 35 ]. Moreover increased 25 OH D levels during treatment with statins have been observed, shedding new light on the effects of these drugs [ 36 - 38 ].
It is believed that blocking HMG-CoA reductase for preventing the cholesterol synthesis pathway promotes the synthesis of cholecalciferol from 7-dehydrocholesterol and is responsible for at least part of the pleiotropic effect of statins.
A separate issue concerns the impact of the 25 OH level on statin therapy. It has been shown that within patients with normal serum and a slight deficiency of 25 OH D, there is significantly greater reduction in total cholesterol levels and triglyceride levels which have been achieved during treatment with atorvastatin compared to patients with deep deficiency  the mechanism of this phenomenon is likely to effect CYP3A4 and requires further research. The study participants were placed into four groups.
The fourth group took inactive placebos. The researchers chose 2, IU because they suspected that might be the best dose, and 4, IU because that's the highest level before people start experiencing toxic effects.
Vitamin D Supplements May Make Arteries Healthier
Also, previous studies have shown that, taken daily, 2, IU and 4, IU doses of vitamin D can bring a vitamin-deficient person's levels of vitamin D back within a normal range, the study authors noted. Those in the study who took 4, IU daily -- more than six times the currently recommended amount -- experienced a Those who took 2, IU a day experienced a 2 percent decrease in arterial stiffness during the same timeframe.
People who took the currently recommended dose of IU had a slight increase in arterial stiffness -- about 0. Those who took the placebos had a 2. No toxic effects were observed among people who took the larger doses of the vitamin, Dong said. Vitamin D might help arterial health by blocking a hormone system that increases constriction of blood vessels, the researchers said.
It also helps reduce inflammation, which has been linked to hardened arteries. Dong expects that some whites also would benefit from vitamin D supplementation. However, taking handfuls of vitamin D will not excuse a person from eating right or exercising for their heart health, Dong added.