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At the present time, where generally accepted to refer to different possible, "states that" the case of vitamin D are: [46]
Deficiency (less than 30nmol / L or 12 ng / ml, leading to rickets in children and osteomalacia in adults)
Insufficieny (between 30-50nmol / L, and a group of 12-20ng / ml)
Suitable (between 50-125mol / L, or 20-50ng / ml)
High (above 125nmol / L or 50 ng / ml)
(Where 2.5 nmol / L is approximately equal to 1 ng / ml and 1 microgram (ug g) of vitamin D3 about 40 international units [47])
Guidelines for vitamin D generally accepted and used as a reference for this article is above. "Optimal levels of vitamin D" is not a legal term for one of the four bands.
The one goal of 75nmol / L optimal for bone health in the elderly [48] and bone-related conditions, such as dental health or reduce the risk of falls and fractures in the elderly. [49] This also seems to be a target for the prevention of colorectal cancer. [49]
Even in studies that recommend oral intake high (5,000IU), and the ultimate goal still it seems to be about 75-80nmol / L [11]
The recommended levels of vitamin D are more or less 75nmol / L (30 ng / ml) to certain conditions.
2.2. The lack of (predictable)
Vitamin D deficiency seems to rise from 1988 onwards. Using 75nmol / L as a cut, and the percentage of the population below this level has risen from 55% to 77% in 2004. [50] seems to have stabilized somewhat, with 79% less than 80nmol / L [51]
It seems that the lack of rates in the population has increased over the past two decades, but it has stabilized in recent years.
Using other interruption, in 2010 29% of the US population was less than 50 nmol / L (clinical failure) and 3% lower than the 20nmol / L (clinical deficiency). [51] These levels vary depending on the season, and the use of 50 nmol / L as a cut again, and 11% of people under this line at the end of summer (sand Boston, and the latitude of 42 degrees north), while at the end of the winter, and this number more than 30%. [52] There are still a small area to the north on the other side of the world (Britain, a latitude of 53.1 degrees north) deficiency rates to rise. To evaluate serum levels of 25, 50 and 75nmol / L ratio of the population under the increase of 3.2%, 15.4%, and 60.9% at the end of the summer to 15.5%, 46.6% and 87.1% at the end of the winter values. [53] Estonia (59 ° N) is the ratio of the population scoring less than 25 nmol / L and 50 nmol / l were recorded in 8% and 73% at the end of the winter, respectively. [54]
Vitamin D deficiency still occur in the vicinity of Ecuador places. A study conducted in the city of Isfahan, Iran (32 ° N) percentage of the population is registered under 25.50, and 75 nmol / L to 26.9%, 50.8% and 70.4%, respectively. [55] cultural and religious issues can come into play with this study, where the population is composed of both sexes, women included the wearing of religious clothing in public places in this region. South Florida (Miami, 25 ° N) registered 38% and 40% of men and women, respectively, less than 50 nmol / L [56]
Despite the importance of the above presentation, and at least one study has suggested that this could only account for five saw the contrast. [57]
Latitude plays an important role, but the lack of (as defined by serum levels of 25 nmol / L or less) and palaces (50 nmol / L) and spread all over the world.
Deficiency is common in patients, with 22% of patients with serum levels less than 20 nmol / L, and was 57% lower than the levels of 37.5 nmol / l in the study. [58]
Finally, some studies comparing the quarterly of vitamin D found (that divides the population quarter based on the amount of vitamin D circulating) that 50.3% of African-Americans are in the lowest quarter of vitamin D levels (in this study, without 17.3ng / ml [ 59]) and 7.8% in the top quarter (32.1%); whites were at least 9.5% in the quarter and 43.5% in the top quarter, with Mexican Americans and all others are split about 20% / 20% of these quartiles. [59] These results indicate that the low rates associated with the synthesis of vitamin D of dark-skinned hold practical importance.
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Generally, it must be 2,000IU sufficient to meet the needs of most individuals completely in doses between 2,000-10,000IU do not necessarily provide more public interest, but do not be toxic either.
[63] The meta-analysis of 76 trials on vitamin D levels in the blood serum was carried out (for more than 50 people, taking either D2 or D3) with daily doses of vitamin D 5-53.5mcg variables in most tests with two tests using 124-250 micrograms daily [64] or 225mcg [65] by dividing the experiments were complemented by the amount of vitamin D, and was associated with an average increase of 10mcg 9NG / ml and a spring (RIC; 25-75 C). Of 7.2-14.8ng / ml with a double oral dose (20 micrograms) that are associated with an increase in the average serum 12.9ng / ml and quarterly from 9.2-20.4ng / ml. [63] This study calculated (based off meta-analysis) to sign 0.78ng / ml (1.95nmol / L) in micrograms of vitamin D3 supplement daily increase does not exceed 20 micrograms (in the elderly without calcium supplements) has been observed [63] and similar results with other critical, pointing out that 100 IU of vitamin D3 serum vitamin D increases 1-2nmol / L [66] and increase 10-25nmol / L with 1000 IU. [67] Although the first meta-analysis are only in the more than 50 people, and this dose-response in general through a period of time there seems to be for all age groups. [68] [69] [70] [71]
Home is used to predict the serum levels of vitamin D used (vitamin D3 overcome vitamin D2) and a dose of vitamin D, and both were statistically significant. Coingested calcium and vitamin D supplements basal serum (less than that resulting in a further increase after supplementation) both showed a tendency to increase the bioavailability, but were not statistically significant. [63] This study can not determine the age, sex or because of external factors. [63]
With respect to the dose, lower doses of oral look more efficient in increasing serum levels of vitamin D, with still higher dosages increased serum levels, but not both (reduced absorption at high doses), the contrast between the primary individuals. In dose ranges less than the mouth, vitamin D appears to increase linearly with each increase of 100 IU of serum in approximately that 1-2nmol / L and 1,000 international units are involved in a range of 10-25nmol / L (2, 000IU 20 -50nmol / L).
20,000IU daily has been associated with toxicity, [62], while the daily supplements of 10,000 IU does not seem to induce toxicity, [72]
Bowling used sharp sometimes on a weekly or monthly basis, and has been associated with toxicity bolus 300,000IU. [62]
Preloading a large bolus of vitamin D (in this study, 50,000-100,000IU) before the maintenance period seems to provide more benefits than just taking a daily dose maintenance. [73]
Toxicity was observed in the very high daily doses of vitamin D, which is about 10 times the daily dose 2,000IU above.
When comparing against vitamin D2 D3, meta-analysis found that, when it was controlled on the basis of weight (micrograms rather than IU) of vitamin D3 was associated with an average increase of serum, which 4.29ng / ml greater than vitamin D2. [63]
Vitamin D3 seems to be a more reliable form of vitamin D, relative to D2, and increased serum levels of the appropriate group.
3. Life Extension
And mortality in the area of research tend to refer to the deaths of all causes, and is establishing an association through surveys and epidemiological research, since death is uncommon. Rarely made causality in these cases. Vitality is a general term, and especially slang used to refer to physical fitness and wellness, and independent of the reality of life. And it looks at the longevity sometimes a combination of avoidance and mortality, and at the same time enhance the vitality.
3.1. death rate
It linked low levels of vitamin D independently with increased mortality in the general population. [59] smaller sample size (derived from data from the NHANES) indicate that this partnership with mortality is not affected by sex, race, and rely only on circulating levels of vitamin D, [74] despite the fact that (because of the lower skin installation rates) It has been shown to increase the frequency of low vitamin D in the blood black to increase the overall risk of death in a cohort of the elderly. [75] Further analysis of data from NHANES found that the reduction of the dose-dependent in all causes of mortality of 6.11% in the 10 nmol increase / L in circulating levels of vitamin D, although this association was borderline factors little time taken confusion in the mind [ 74] (an increase of 10 nmol / L can be obtained by eating about 1000IU per day [61]).
Compared with the lowest circulating vitamin D levels against higher levels traded in cohort studies, a relationship between the risk of death and lower levels of circulating. The study found that those with 50 nmol / L (20 ng / ml) or less have a relative risk (RR) of death from any cause of 1.65. [74] Another study, pointing out that at least the quarter to measure 17.8ng / ml was independently associated with a 26% increased risk of death with respect to the highest quarter (which was higher than the 32.1ng / ml serum levels). [59] Moreover, in the fragility of 1.98 it was higher at least once a quarter, compared noninstitutionalized elderly to the top of the quarter, and was associated positively with mortality; the lowest quarter was 2.98 higher relative risk of death compared with the top quarter. [76] It is important to note also suspected to be the biggest benefit of deaths with vitamin D supplementation is to reduce the vulnerability of the elderly. [76]
Review fixed major systematic meta-analysis of clinical trials have confirmed (mainly older) evaluating all forms of vitamin D This studies the results of monitoring the impact of vitamin D 's in all causes of death, search the relative risk (RR) of deaths each -Cause with supplements 0.97 (95% CI 0,94-0,99); when the analysis of a specific form of vitamin D, found that vitamin D3 granted to only cut a great risk (RR 0.94, 95% CI 0.91 to .98). [77]
Many observational studies have found an inverse relationship between vitamin D levels in the blood serum and all causes of death. Clinical study the effect of supplementation on the mortality experience seems to confirm a slight decrease in the mortality rate, especially in the elderly population. It seems vitamin D3 supplementation with the most effective supplements that means with respect to reductions in mortality.
In general, complete with 1000 IU of vitamin D3 per day (seen as an estimate low dose) is estimated to reduce the medical costs to treat cancer billion to about $ 16- $ 25 for the exercise of a protective effect and general deterrence. [78]
3.3. Longevity
She research study of the descendants of nonagenarian (90 and over) with the brothers room (to take longevity hereditary) that when you consider the vitamin D levels of their children, and vitamin D levels do not rise beyond it; their spouses. [79] Specifically, it was the descendants of nonagenarian 6% vitamin D and significantly reduced the frequency of genes CYP2R1, it is that makes people to higher levels of vitamin D. [79]
It makes sense that vitamin D could be a biomarker for something that is associated with longevity, although there is no evidence to suggest vitamin D may improve life simply indirect mortality, and reduce the risk of premature death.
4. Pharmacy
4.1. Mechanisms (General)
Vitamin D3 is practiced most of its effects either directly through its own future (vitamin D receptor, known as the black box), who works in the nucleus and promote protein synthesis, or through the work of "non-genomic" may still be through the black box is not localized in the nucleus, but caveolae cell membrane. [80]
Despite the traditional black box and is believed to exert only work in the heart by gene transcription, it was later found to move from the core to the cytoplasmic membrane when activated by vitamin D3 hormonally active, suggesting that VDR may play a role in all the genetic work and non-genetic of vitamin D. [81] further evidence of the dual role of the VDR from another study in spermatids, who pointed out that the VDR-induced changes in the cell that was quashed by VDR activation inhibitors that have not yet become genetic in nature. [82] At the same time, it appears that additional receptors bound to the membrane is VDR- of vitamin D, which may play a role in non-genomic action of vitamin D, such as 1,25 (OH) 2D3 associated membrane, and rapid response steroid binding protein (1, 25D3-MARRS, also known as the RER network stress protein 57, or ERp57), which has no sequence similarity to the classic VDR. [83] These two proteins sometimes can work together; for example, each of the VDR was observed and 1,25 D3-MARRS to work side-by-side in the case of the photoresist. [84]
Vitamin D is practiced in the activation of the side effects of receptors. Classic vitamin D receptors can operate all the genetic and non-genetic, while another receptor known as 1,25D3-MARRS can work not genomically.
4.2. Enzyme reactions
Hormones is an enzyme expressed in multiple tissues; and one of its main tasks is to produce estrogen locally, and that can have a beneficial to bone growth and matainance effect, but can promote the growth of breast cancer tumors. [85] The active form hormonally of vitamin D3 seems to be a specific modulator hormones tissue, and increased expression in the builder of bone cells and fibroblasts in the bone, [86] and the cells adrenocortical [87] and prostate cancer (one beneficial effect), [87] [88 and a decrease in breast cancer cells. [87] Vitamin D3 also appears to induce the activity of hormones in the placenta cells. [89]
Knockout mutation of the vitamin D receptor in mice reduces the action of hormones enzyme (CYP19) to varying degrees. It has been reduced activities in the ovary and testis and epididymis by 24% .58% and 35% with low attendant in gene expression. [90] This may be secondary to stop the metabolic process of calcium, as calcium supplements to these mice to normalize the actions of hormones. [90]
In MCF-7 cells (a cell line of breast cancer cells), and can be 100 Nm of vitamin D3 active limit flexible hormones to control 60% and the elimination of nearly cultured cell growth in response to alcohol custody, breed MCF-7 cells. [91]
Interestingly, synthetic analogue of vitamin D3 (known as EB1089) prevents hormones currently through the new inhibitory path. [91] This is the analog which also showed effective in reducing breast cancer in animal models. [92] [93]
Vitamin D appears to be selective modulator tissue hormones, are able to increase or decrease the activity of hormones depends on the tissue in question.
In people who use pharmaceutical grade hormone inhibitors (usually the treatment of breast cancer), you may deplete levels of vitamin D, which prepares them musculoskeletal symptoms. [94], though this does not seem to be the most predictive biomarker, with deliberate depletion of estrogen (as a treatment of breast) cancer being the most predictive causal, and is believed to be. [95] [96] However, the reduction in cases of joint pain significantly (odds ratio 0.12, 95% CI 0,03-0,40), which achieved serum above 40 ng / ml levels of vitamin D supplements daily 800IU 16, 000IU followed by twice a month. [97] large doses (in this study, vitamin D2 weekly 50,000IU) appear to be more effective in the reduction of thematic reports of pain in the joints. [98]
Vitamin D can reduce joint pain caused by powerful hormones inhibitors (AI). This may be secondary to strong inhibitors hormones depleting vitamin D.
The most plausible reason for the pain of arthritis with the use of AI remains estrogen depletion, depletion of estrogen, which is closely associated with the induction of articular and joint pain.
5.1. Mechanisms
Nerve cells in the brain appear to express an enzyme necessary for bioactivate vitamin D [99] with the highest concentration of this enzyme that occurs in the hypothalamus nerve and dopamine from the substantia nigra. [100] most of the cells express the vitamin D receptor (VDR), but it seems to be absent in the basal cells and nerve Nucelar Meynert in the cerebellum, [100] and expressed in glial cells in the brain. [100]
It seems calcium metabolism to underlie neuronal cell death by excessive stimulation, [101] [102] [103] [104] and hormonally active vitamin D given a protective effect in the laboratory in concentrations relevant physiologically up to 100 Nm, but not above . [105] It seems that the protection mechanism to be mediated through the organization to the bottom of CA2 + L-type ion channels sensitive to the effort [105] an effect that was also observed in bone cells. [106] [107] These channels have been implicated L- type in excess stimulation. [108] [109]
Study in rodents noticed these effects of living nerves, suggesting the slowdown in the rate of decline in the density of neurons in the hippocampus during aging in long-term treatment with vitamin D, which indicates to maintain nerve cells. [110]
Vitamin D seems to be able to modify a subset of the calcium channels in nerve cells, and cell death control through excess stimulation in the laboratory based on data from a group of animals.
5.2. Knowledge
In young adults vitamin D insufficient (76.6 +/- 19.9nmol / L), adding vitamin D 5000IU diet for a period of one month can not affect the working memory, inhibition response or cognitive flexibility despite the fact that increased serum vitamin D at a rate of 98nmol levels / L [111], anxiety and anger tens been similarly affected. [111]
5.3. Depression
Inverse relationship between vitamin D and depression has emerged (low-linked vitamin D with more symptoms of depression) said for the first time in 1979 [112] and associations in at risk of accidents cardiovascular, [113] Fibromyalgia [114] and in women during the winter. [115]
Blood levels of vitamin D is inversely associated with symptoms of depression in some cohorts.
I noticed study a correlation between inadequate vitamin D (35-50nmol / L) and symptoms of depression in adolescents 54 As noted in the relief of symptoms after 4000IU 2000IU supplements for a month next two months, with serum vitamin D rose to 90-91nmol / L (high enough group) ; it observed a decrease by 42%, according to assess the size classification WHO-5, and seemed overall improvement. [116] were observed improvements in symptoms of depression in any other place in a small pilot study of women with low (link despite the fact that some evidence suggests that there is a relationship between vitamin D levels and depression symptoms, evidence is mixed this vitamin can supplements D helps with these symptoms, and the positive results tend to be in the population with low VITAMIND D to start.
5.4. MS
Multiple sclerosis (MS) is a neurological disease, and pro-inflammatory that affect the myelin sheath of nerve cells, and is a condition most common in developed countries neurological infections. [117] [118] assumed a connection between multiple sclerosis and vitamin D comes from the associations between MS and the show, which is also highly correlated with vitamin D [119] [120] and exposure to the sun during childhood is inversely related to the risk of MS in adulthood. [121] [122] and there is no relationship between maternal vitamin D levels during pregnancy and the risk of MS in the offspring was found, however. There [123] and the evidence points to a protective effect of sun exposure, [120] [121] [122] with a descriptive study for the establishment of a protective connection between multiple sclerosis and vitamin D serum levels directly. [123]
Multiple sclerosis (MS) is associated with the spread of longitude and sun exposure, which in turn are associated with levels of vitamin D.
In animal models of inflammation of the brain and spinal experimental autoimmune (a model for MS), it could be vitamin D and thus reduces the incidence of [124] and delay progression of the disease. [125] Moreover, there may be synergies between vitamin D and MS standard treatment, interferon beta. [126] The benefits of vitamin D may be associated with ease of demyelination of nerve cells in the laboratory. [127]
Vitamin D seems to exert protective effects in an animal model of multiple sclerosis.
5.5. Alzheimer's disease
Alzheimer's disease (AD) is a neurological disorder associated with a cholinergic deficiency signals and synaptic function. Vitamin D mechanisms seem therapeutic promise for Alzheimer's disease [128] as is the case in other neurological diseases, vitamin D appears in the blood serum to be inversely linked with risk of AD; [129] It seems that the risk to be a little less than Parkinson's, who have low levels....
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