Use of Vitamin D Supplement as an Adjunct Therapy for Treating Stroke

Use of Vitamin D Supplement as an Adjunct Therapy for Treating Stroke
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Use of Vitamin D Supplement as an Adjunct Therapy for Treating Stroke
Having a low vitamin D status is a common forms of health problems owing to the fact that it affects almost one in every two people and it has adverse effects on one’s health. Existing findings from previous studies shows that vitamin D deficiency exposes an individual to musculoskeletal, cardiovascular, infectious, malignant diseases, renal diseases, and autoimmune diseases (Garg et al. 2013; Langlois et al. 2010; Bodnar et al. 2013). The findings also show that a poor vitamin D also leads to increased risks of stroke and poor health outcomes among post-stroke patients. This is important because stroke has been established as the third highest cause of death and among the leading in causing disability among patients (Dickens et al. 2011). Owing to its high incidence, it is important to establish approaches of preventing and treating stroke so as to help in reduction of the related mortality, morbidity, and healthcare costs.
PICOT Question
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PopulationI
InterventionC
ComparatorO
OutcomeSearchPatients with stroke. Vitamin D supplementation. Different effects of vitamin D supplementation.
Effects of vitamin D deficiency. Treatment of stroke.
Reduction of risk factors to stroke.What is the impact of using vitamin D supplement as a adjunct therapy for treating stroke on healthcare outcomes among stroke patients?
Literature
Sufficient epidemiological evidence demonstrates that the lack of adequate vitamin D is closely linked with high risk of strokes. Remarkably, several researchers have focused on establishing regional and seasonal stroke incidence differences (Matsuda and Shimomura 2013). Although their submissions were inconsistent, most studies showed that the incidences of stroke are likely to rise during wintertime and at low elevations. This is because of the general presence of low UV-B radiation at lower altitudes and in winter and consequently lowers levels of 25(OH)D. There are several probable explanations for the concluding findings but the opinions postulated in this research are suitable in the hypothesis that 25(OH)D levels present risks for cerebrovascular occurrences (Donley et al. 2014). Similarly, studies found that after 30 days of the initial stroke incidence ever, patients showed notably inferior level 25(OH)D in comparison to healthy elder subjects. This research is supported by other works that found out that people bearing records of stroke and cases with MRI cerebrovascular infection signs had minimized levels of 25(OH)D.
Some hopeful researchers such as Koizumi et al. (2011) have now explicitly offered solutions to the inquiry if the levels of 25(OH)D are predictors of future stroke risks. A previous research by Ketteler et al. (2012) examined 755 elderly subjects and followed their history for ten years in which 70 strokes were witnessed during the observation duration, but the levels of 25(OH)D were not significant between examinations (11.9±7.2 ng/ml) and control experiments (12.5±7.8 ng/ml). Nevertheless, in comparison to the least tertile in the levels of 1,25(OH)2 D, the stroke risks were notably minimized in the largest tertile where the relative risk factor was 0.41 (95% CI; 0.22-0.77). Another study by Michaud et al. (2014) focused on 1471 healthy women of the average age of 74 who lived in the community and engaged in a 5-year random selected placebo control experiment with calcium supplements. Stroke hazard ratios (HR) with ((95% CI) in a crude model and another design customized for the risk of cardiovascular agents showed 1.7 and 1.4 each, in women whose levels of 25 (OH) D were seasonally adjusted below 20 ng/ml in comparison with females who had higher levels of 25 (OH) D. During experimentation, the increase in the dangers for stroke was elevated in women who had calcium allocation, which demonstrated an HR for stroke in 2.5 group deficient in vitamin D in unregulated analyses (Michaud et al. 2014). However, after modifications, all associations observed for low levels of 25(OH)D and higher chances of stroke became insignificant. The issue is discussed in the LURIC study, which is a proposed follow-up review amid 3299 subjects admitted for coronary angiography. In an average study period of 7.75 years, deadly stroke claimed the lives of 42 experimental subjects (Block et al. 2017). In addition, the threat of fatal stroke was minimized considerably per increment in a month of sampling blood adjusted z values of both 1,25(OH)2 D and 25(OH)D. The hazard ratios (with 95% CI) modified for cardiovascular peril circumstances were 0.72 in the case of 1,25(OH)2D and 0.67 in the case of 25(OH)D (Block et al. 2017).
Information from the Mini-Finland Health test of 6219 cardiovascular free subjects aged at least 30 years also adds to the existing literature (Kilkkinen et al. 2009). However, with average observation duration of 27.1 years, the survey recorded 293 deaths caused by cerebrovascular diseases. After adjustments for risk factors associated with cardiovascular disease were made, the hazard ratios for cerebrovascular mortality was 0.48 in the topmost versus the least 25(OH)D quintile. Extra analysis indicated that the modified hazard ratios for ischemic stroke and hemorrhagic stroke were 0.60 (0.38-0.93) and 0.61 (0.26-1.46) sequentially. Another yet important study was conducted at the American Heart Association where a prospective follow up was done for 27686 patients who had no history of cardiovascular disease and were 50 years and above (Takahashi et al. 2014). A one-year observation of respondents whose 25(OH)D levels were below 15 ng/ml showed that their stroke death risks were 78% higher than those whose 25(OH)D levels were higher than 30 ng/ml.
Randomized experimental tests are infrequent and were not satisfactorily conducted to exhibit the alterations in the occurrence of strokes. In postmenopausal female experimentation in the Women’s Health Initiative (WHI), 362 subjects were randomly allocated to placebo or 1000 mg plus 400 IU vitamin D on daily basis (Ivarsson et al. 2015). In an observational time of 7 years, 739 strokes were witnessed and the hazard ratios in the actual against placebo cohort were 0.95. Evaluations of the WHI experiment constrained to death occurrences of cerebrovascular, the hazard ratio was 0.89 in the treatment of the placebo group. Analyses of subgroups showed a corresponding hazard ratio of 0.62 in subjects below 70 years and an HR of 1.20 in the adult experimental population (Lin et al. 2014). Interpreting the aforementioned insignificant falls in the levels of strokes in the calcium plus vitamin D cohort is difficult. The contributors of the WHI research admitted that the major limits such as the poor adherence to medication and extremely low daily dosage of 400 IU were noteworthy inhibitors of their study, which disqualify any ultimate deduction on the gains of vitamin D in addition to calcium supplements (Fukagawa et al. 2017). Furthermore, a different experimentation involved randomly controlled tests among 2686 elderly population in a period of 4 months with 100,000 IU supplement of vitamin D. The observation recorded just 54 deaths through stroke after a 5-year follow up with no significant deviations between the placebo and treatment cohort (26 fatal strokes against 28). One major restriction of large vitamins interventional experimentation is the nonexistence of PTH measurements that are necessary to make a conclusion if the achieved levels of 25(OH)D were adequate for cure or prevention of possibly detrimental PTH elevations (Scholl, Chen, and Stein 2013). Generally, the controlled random trials failed to consider variations in each individual responding to the supplements of vitamin D. This is a crucial note when dealing with obese patients since they are at higher risks of stroke, hence require an estimated 10, 000 IU daily to replete their status of vitamin (Ureсa-Torres et al. 2013). Considering all findings, observational studies largely favor the assumption that vitamin D prevents strokes, but there are limited interventional studies while the available ones have limitations based on methodology. Therefore, whether vitamin D prevents stroke occurrence is yet to be confirmed in controlled random tests.
Research findings also demonstrate that vitamin D supplementation can effectively treat low levels of 25(OH)D. Projections suggest that supplementation of 1,000 IU vitamin D on a daily basis raises the level of 25(OH)D by around 10 ng/ml (Daga et al. 2012; Kozlov et al. 2014). However, individuals respond contrarily to supplementation of vitamin D and this should be considered; therefore, the amount of 25(OH)D should be re-measured after every 3 months to evaluate the effectiveness of the supplementation. For instance, individuals with obesity are at an augmented risk of getting affected by stroke and; thus, they require more quantities of vitamin D when compared to an individual with normal weight for the obese to attain a sufficient level of 25(OH)D in their body. Notably, supplementation of vitamin D can be done on a daily basis, weekly, or monthly, and whichever plan is selected the results obtained are the same in terms of increasing the level of 25(OH)D (Angel et al. 2013). Exposure to the sun can also help in increasing the levels of vitamin D to the same increase that would have been acquired if one consumes routine vitamin D supplements of up to 20,000 IU. However, it is important to consider the potential negative impacts of excessive exposure to sunlight. Patients diagnosed with end-stage renal diseases are mainly treated through treatment of active vitamin D with 1,25-(OH)2D. As opposed to natural vitamin D, the therapeutic window of supplementation of 1,25-(OH)2 D is moderately narrow and could result in hypercalcemia in the event of overdose of 1,25(OH)2 D (Zahedirad, Nikooyeh, and Neyestani 2015). Therefore, there are countless analogues of vitamin D that have been developed and have a reduced calcemic effect and are; thus, considered more beneficial to 1,25-(OH)2D.
Several epidemiological studies such as Sprinzl et al. (2013) that have been conducted have shown that the prevalence of dyslipedia has increased among patients who have low levels of 25(OH)D. Available literature on the same by Gacci et al. (2015) has shown that supplementation of vitamin D helps in increasing HDL-cholesterol and lowering triglycerides, but the randomized controlled trials also showed there was a slight increase in the level of LDL-cholesterol. Owing to the fact that statin therapy contributes to reduced incidence of stroke, it is worth noting that a recent trial showed that lipid response is better to atorvastatin in patients who have high levels of 25(OH)D than in those with low levels of the same. Additionally, previous findings also show that statin treatment can increase the levels of 25(OH)D, but there is inconsistency in the data available for this topic. Observational studies like Lehmann and Schmieder (2011) and Gonzalez et al. (2013) have also shown that deficiency of vitamin D contributes to increase in the body mass index and increase in the ratio of waist to hip. Data acquired from interventional trials performed are inclusive but they also fail to that vitamin...