Vitamin D deficiency has been mechanistically and clinically linked to neurological diseases and neuropsychological disorders, cognitive impairment, and neurodegenerative diseases.22 Our current study has emphasized that 32% of participants had deficit serum Vitamin-D level, 48% of subjects had insufficient and 20% of participants had sufficient serum level of vitamin-D.
Studies carried across different countries in South and South East Asia showed, with few exceptions, widespread prevalence of hypovitaminosis D, in both sexes and all age groups of the population.23 High prevalence of hypovitaminosis D in South Asia can be explained by skin pigmentation and traditional clothing. Air pollution and limited outdoor activity further compounds this problem in the urban population.24 The current study stated that there is lower degree of positive relationship of BMI with Serum Vitamin-D level (r=0.162, p=0.094), that is statistically not significant at p<0.05. In another way there is no statistically significant association between BMI and vitamin D (χ2=12.474, p=0.071). The finding is supported by a study on the effect of vitamin D supplementation on serum 25OHD in thin and obese women as the result showed a significant inverse relation between total body fat mass and serum 25-OHD (p<0.0001) and serum 1,25(OH)2D (p=034). There was no significant change in total body fat mass after treatment with vitamin D or calcitriol in randomized trials.25 Similarly the finding is contradicted by the study aimed to find association between BMI and vitamin D supplement the result stated that there was significant differences in mean 25(OH)D levels of vitamin D supplementation doses were consistently seen across BMI categories.26 Again contradicted by another cross-sectional study on serum vitamin D level in different 222 socio-demographic population The mean difference between normal and obese population was statistically significant (p= 0.007).27
Present study revealed that serum vitamin-D level was significantly associated with gender (χ2=0.233, p=0.003), marital status (χ2=0.562, p=0.014), address (i.e. Terai, Hilly and mountain region) (χ2=4.431, p=0.009) and physical activity (χ2=0.193, 0.013). Several national and international previous studies supported the finding as an ecological study conducted to assess association of vitamin D status with socio-demographic factors in Calgary, Canada, result of the study revealed that there is significant association between 25-hydroxyvitaminD level and all the predictors i.e. age, gender and educational status (all p<0.0001).28 Another study on determinants of vitamin D status in young adults; influence of lifestyle, sociodemographic and anthropometric factors among 738 subjects revealed that the relative risk (RR) for vitamin D deficiency was highest for men 2.09 (1.52, 2.87); subjects who exercised 0-½ hours a week 1.88 (1.21, 2.94).29 A study aimed to assess the association between vitamin D deficiency and depression in Nepalese population stated significant association of gender, geographical location of residence, marital status, religion and vitamin D status with clinically significant depression.30 Other study has been observed a direct relationship between latitude and the prevalence of Multiple Sclerosis (MS), which suggests a role for UV radiation and vitamin D in MS development.31
There was poor level of positive relation of Smoker (r=0.02, p=0.805 and Alcoholism (r=0.059, p=0.534) with serum vitamin D level, but statistically not significant. Smoke (χ2=0.355, p=0.048) was significantly associated with serum level of vitamin-D whereas no association of alcohol with vitamin-D level at p<0.05. A cross-sectional study on determinants of vitamin D status in young adults; influence of lifestyle, sociodemographic and anthropometric factors among 738 subjects supports as the result of study revealed that 238 subjects had vitamin D insufficiency, 135 had vitamin D deficiency of which 13 had severe vitamin D deficiency (S-25[OH]D < 12.5 nmol/L). The relative risk (RR) for vitamin D deficiency was highest for smokers 1.33 (1.02, 1.73). Smoking was associated with a higher RR = 1.33 (1.02, 1.73) for vitamin D deficiency compared with nonsmoking. Whereas contradicted the result of alcohol as alcohol intake was associated with a lower RR = 0.68 (0.47, 0.90) for vitamin D deficiency compared to non-drinker, an increase of one unit of alcohol was associated with RR = 0.81 (0.68 - 0.97).29 Another study on interaction of vitamin D and smoking on inflammatory markers, the data was collected from Korean Elderly Environmental Panel Study that included 560 subjects. The result of the study was that association of vitamin D deficiency and hs-CRP in smokers was stronger than that in nonsmokers (smokers: β=-0.375, p=0.013; non-smokers: β=-0.060, p=0.150). Smoking status was an effect modifier that changed the association between vitamin D deficiency and hs-CRP (interaction estimate: β=-0.254, p=0.032). There was a stronger significant association of smokers and vitamin D deficiency than non-smokers.32 A review on Vitamin D and alcohol aimed to evaluate the association between alcohol use and vitamin D serum levels alcohol intake was found to be positively associated with vitamin D status in 15 articles and negatively associated with vitamin D in 18 articles.33 the finding is contradicted by another study on chronic ethanol exposure effects on vitamin D levels among subjects with alcohol use disorder stated that levels of inactive vitamin D (25(OH)D3), active vitamin D (1, 25(OH)2D3), cathelicidin/LL-37, and CYP27B1 proteins were significantly reduced (p < 0.05). Chronic exposure to alcohol has the potential to reduce the levels of vitamin D.34
Several evidence suggests that vitamin D acts like a neurosteroid and is required for normal brain development and function.35 An endocrine review on Vitamin D and neurological diseases, aimed to highlight the relationship between vitamin D and neurological diseases stated that there is association between low levels of 25(OH)D and a wide spectrum of neurodegenerative conditions such as multiple sclerosis, Alzheimer’s disease, Parkinsons’s disease and neurocognitive disorders, is supported by in vitro and in vivo data.35 Other studies showed that the risk of MS decreases with increasing intake of vitamin D36, and serum 25(OH)D levels are significantly lower in patients with MS as compared to healthy controls.37 These studies directly support the results of our current study as history of chronic illness (χ2=0.10, p=0.03), timing of occurrence of stroke (χ2=11.41, p=0.017) and diagnosis (χ2=21.19, p=0.011) had significant association with Serum vitamin-D level at p<0.05. There was lower degree of positive relation of chronic illness (r=0.053, p=0.579) and diagnosis (r=0.012, p=0.902) with serum Vitamin-D level. Whereas the Serum Vitamin-D level was not significantly associated with History of stroke (χ2=11.62, p=0.06) and type of stroke (χ2=4.84, p=0.21) at p=0.05.
Another cross-sectional study to evaluate the association between Vitamin-D and hypertension among 520 people supports the study as the result stated that Severe vitamin D deficiency was highly prevalent in people with hypertension than in people without hypertension (p value <0.001). The study concluded that Vitamin D deficiency was associated with an increased risk of having hypertension.38 In our current study subjects 25% (27) had chronic illness history with hypertension and the Karl pearson correlation coefficient showed positive relation as well significant association with Serum Vitamin D level of Nepalese residents. A Similar Case-control study aimed to assess the serum level of vitamin D in cerebral stroke patients and secondly, to examine if its deficiency was associated with stroke severity and outcome result revealed that studied stroke patients had statistically significant lower levels of vitamin D. Multivariable analysis of the significant variables showed that old age (OR = 1.072), dyslipidemia (OR = 3.588), vitamin D deficiency (OR = 4.790), and large infarction size (OR = 7.462) was independently associated with stroke severity. The study concluded that stroke patients suffer from vitamin D deficiency, which was associated with both stroke severity and poor outcome.39
A study on reduced Vitamin D in acute stroke compared the serum 25-dihydroxyvitamin D levels with first-ever stroke the result revealed no relationship between 25OHD level and the length of time between stroke and 25OHD sampling (adjusted r2=−0.02; P=0.77). The mean Z score of vitamin D in acute stroke was −1.4 SD units (95% CI, −1.7, −1.1), with 77% of patients falling in the insufficient range concluded that reduced vitamin D was identified in the majority of patients with acute stroke throughout the year and may have preceded stroke.40 A vitamin D deficiency and incident stroke risk in community living black and white, supports the finding as the study revealed there was no statistically significant differences in the association of lower 25-hydroxyvitamin D with higher risk of stroke in black i.e. (95% CI1.18, 5.83) vs. white i.e. (95% CI 0.83, 3.24) participants.41 Another study on Vitamin D in amyotrophic lateral sclerosis represented that in chronic neurological diseases levels of vitamin D in blood appeared low but there was no significant differences found between the level of vitamin D and Amyotrophic lateral sclerosis patients (18.8±12.2) and the healthy subjects (20.7±10.1).42 Similarly, Cross-sectional associations of plasma vitamin D with cerebral β-amyloid in older adults at risk of dementia, the study didn’t find the association between baseline 25(OH)D levels and cerebral Aβ in any of the brain regions studied.43 Vitamin D is not associated with incident dementia or cognitive impairment over an 18 years period of time another study presented as the result showed that the adjusted HR for the continuous GRS for all cause dementia was 1.04 (95% CI:0.91, 1.19).44 A study to investigate association between serum concentration of vitamin D and 1-year mortality in stroke patients presents that out of the 382 stroke patients, 16.5% died in a year, and the mean 25(OH)D level was lower in those patients (32.3±22.0 vs. 44.6±28.7 nmol/l, p<0.001) and survival at 1 year was worse in patients in the lowest tertile of 25(OH)D levels (i.e. <25.7nmol/l). The study concluded that low level serum 25(OH)D level at stroke onset association was with higher mortality at 1 year in patient.45
The finding from this study may supports for the implementation of measures to determine the real state of vitamin D and its implication on Neurological disorders. We recognize some limitations of our study as the study completed with small size of 108 due to rigorous inclusion and exclusion criteria. As it was a hospital-based study, sample might not be enough to represent the total population of our country. The study should be continued with similar control groups.